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    World Health Orgnization
    Geneva, 1987

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    1.1. Identity, physical and chemical properties, analytical 
    1.2. Sources of human and environmental exposure
    1.3. Environmental transport, distribution, and transformation 
    1.4. Environmental levels and human exposure
    1.5. Effects on organisms in the environment
    1.6. Kinetics and metabolism
    1.7. Effects on experimental animals and  in vitro test systems
    1.8. Effects on man


    2.1. Identity
         2.1.1. Pentachlorophenol (PCP)
         2.1.2. Sodium pentachlorphenate (Na-PCP)
         2.1.3. Pentachlorophenyl laurate
    2.2. Impurities in pentachlorophenol
         2.2.1. Formation of PCDDs and PCDFs during thermal 
    2.3. Physical, chemical, and organoleptic properties
    2.4. Conversion factors
    2.5. Analytical methods
         2.5.1. Sampling methods
         2.5.2. Analytical methods


    3.1. Natural occurrence
    3.2. Man-made sources
         3.2.1. Industrial production
        Manufacturing processes
        Emissions during production
        Disposal of production wastes
        Production levels
    3.3. Uses
         3.3.1. Commercial use
         3.3.2. Agricultural use
         3.3.3. Domestic use
         3.3.4. Use for control of vectors
         3.3.5. Formulations


    4.1. Transport and distribution between media
         4.1.1. Volatilization
         4.1.2. Adsorption
         4.1.3. Leaching
    4.2. Biotransformation
         4.2.1. Abiotic degradation

         4.2.2. Microbial degradation
        Aquatic degradation
        Degradation in soil
    4.3. Degradation by plants
    4.4. Ultimate fate following use
         4.4.1. General aspects
         4.4.2. Disposal of waste water
         4.4.3. Incineration of wastes


    5.1. Environmental levels
         5.1.1. Air
         5.1.2. Water and sediments
         5.1.3. Soil
         5.1.4. Aquatic and terrestrial organisms
        Aquatic organisms
        Terrestrial organisms
         5.1.5. Drinking-water and food
         5.1.6. Consumer products
         5.1.7. Treated wood
    5.2. Occupational exposure
    5.3. General population exposure
    5.4. Human monitoring data


    6.1. Absorption
         6.1.1. Animal studies
         6.1.2. Human studies
    6.2. Distribution
         6.2.1. Animal studies
         6.2.2. Human studies
    6.3. Metabolic transformation
         6.3.1. Animal studies
         6.3.2. Human studies
    6.4. Elimination and excretion
         6.4.1. Animal studies
         6.4.2. Human studies
    6.5. Retention and turnover
         6.5.1. Animal studies
         6.5.2. Human studies
    6.6. Reaction with body components


    7.1. Microorganisms
    7.2. Aquatic organisms
         7.2.1. Plants
         7.2.2. Invertebrates
         7.2.3. Vertebrates
    7.3. Terrestrial organisms
         7.3.1. Plants
         7.3.2. Animals

    7.4. Population and ecosystem effects
    7.5. Biotransformation, bioaccumulation, and
         7.5.1. Aquatic organisms
         7.5.2. Terrestrial organisms


    8.1. Acute toxicity
    8.2. Short-term toxicity
         8.2.1. Pure or purified PCP
         8.2.2. Technical grade PCP
         8.2.3. Comparative studies
    8.3. Long-term toxicity
    8.4. Effects on reproduction and fetal development
    8.5. Mutagenicity
    8.6. Carcinogenicity
    8.7. Other studies
    8.8. Contaminants affecting toxicity
         8.8.1. Octachlorodibenzodioxin (OCDD)
         8.8.2. Heptachlorodibenzodioxin (H7CDD)
         8.8.3. Hexachlorodibenzodioxin (H6CDD)
         8.8.4. Polychlorinated dibenzofurans (PCDFs)
         8.8.5. Polychlorodiphenyl ethers (PCDPEs)
         8.8.6. Other microcontaminants
    8.9. Mechanism of toxicity


    9.1. Acute toxicity - poisoning incidents
    9.2. Effects of short- and long-term exposures
         9.2.1. Occupational exposure
        Skin and mucous membranes
        Liver and kidney
        Blood and haemopoetic system
        Nervous system
        Immunological system
        Cytogenetic effects
        Other systems
         9.2.2. General population exposure


    10.1. Evaluation of human health risks
          10.1.1. Occupational exposure
          Exposure levels and routes
          Toxic effects
          Risk evaluation
          10.1.2. Non-occupational exposure
          Exposure levels and routes
          Risk evaluation
          10.1.3. General population exposure
          Exposure levels and routes

          Risk evaluation
    10.2. Evaluation of effects on the environment
    10.3. Conclusions


    11.1. Environmental contamination and human exposure
    11.2. Future research
          11.2.1. Human exposure and effects
          11.2.2. Effects on experimental animals and  in vitro test 
          11.2.3. Effects on the ecosystem





Dr U.G. Ahlborg, Unit of Toxicology, National Institute of 
   Environmental Medicine, Stockholm, Sweden 

Dr R.C. Dougherty, Department of Chemistry, Florida State 
   University, Tallahassee, Florida, USA 

Dr H.H. Dieter, Federal Health Office, Institute for Water, Soil, 
   and Air Hygiene, Berlin (West) 

Dr A.H. El Sabae, Pesticide Division, Facultry of Agriculture,
   University of Alexandria, Alexandria, Egypta

Dr A. Furtado Rahde, Ministry of Public Health, Porto Alegre, 

Dr S. Gupta, Department of Zoology, Faculty of Basic Sciences, 
   Punjab Agricultural University, Ludhiana, Punjab, Indiaa

Dr L.V. Martson, All Union Scientific Research Institute of the
   Hygiene and Toxicology of Pesticides, Polymers, and
   Plastics, Kiev, USSRa

Dr U.G. Oleru, Department of Community Health, College of Medicine,
   University of Lagos, Lagos, Nigeria

Dr Shou-Zheng Xue, Toxicology Programme, School of Public Health, 
   Shanghai Medical University, Shanghai, China 


Dr F.F. Hertel, Fraunhofer Institute for Toxicology and
   Aerosol Research, Hanover, Federal Republic of Germany

Dr E. Kramer (European Chemical Industry Ecology and Toxicology 
   Centre), Dynamit Nobel A.G., Cologne, Federal Republic of 

Dr D. Streelman (International Group of National Associations of 
   Agrochemical Manufacturers), Agricultural Chemicals Registration 
   and Regulatory Affairs, Philadelphia, Pennsylvania, USA 

Mr G. Ozanne (European Chemical Industry Ecology and Toxicology 
   Centre), Rhone Poulenc DSE/TOX, Neuilly-sur-Seine, France 

Mr V. Quarg, Federal Ministry for Environment, Nature Conservation 
   and Nuclear Safety, Bonn, Federal Republic of Germany 

a  Invited but unable to attend.

 Observers (contd)

Dr U. Schlottmann, Chemical Safety, Federal Ministry for 
   Environment, Nature Conservation and Nuclear Safety, Bonn, 
   Federal Republic of Germany 

Dr M. Sonneborn, Federal Health Office, Berlin (West)

Dr W. Stober, Fraunhofer Institute for Toxicology and Aerosol
   Research, Hanover, Federal Republic of Germany


Dr K.W. Jager, International Programme on Chemical Safety, World 
   Health Organization, Geneva, Switzerland  (Secretary) 

Mrs B. Bender, International Register for Potentially Toxic
   Chemicals, Geneva, Switzerland

Dr A. Gilman, Industrial Chemicals and Product Safety Section, 
   Health Protection Branch, Department of National Health and 
   Welfare, Tunney's Pasture, Ottawa, Ontario, Canada  (Temporary 
    Adviser) (Rapporteur) 

Dr L. Ivanova-Chemishankska, Institute of Hygiene and Occupational 
   Health, Medical Academy, Sofia, Bulgaria  (Temporary Adviser) 

Dr E. Johnson, Unit of Analytical Epidemiology, International
   Agency for Research on Cancer, Lyons, France

Dr G. Rosner, Fraunhofer Institute for Toxicology and Aerosol
   Research, Hanover, Federal Republic of Germany  (Rapporteur)

Dr G.J. Van Esch, Bilthoven, Netherlands  (Temporary Adviser)


    Every effort has been made to present information in the 
criteria documents as accurately as possible without unduly 
delaying their publication.  In the interest of all users of the 
environmental health criteria documents, readers are kindly 
requested to communicate any errors that may have occurred to the 
Manager of the International Programme on Chemical Safety, World 
Health Organization, Geneva, Switzerland, in order that they may be 
included in corrigenda, which will appear in subsequent volumes. 

                       *    *    *

    A detailed data profile and a legal file can be obtained from 
the International Register of Potentially Toxic Chemicals, Palais 
des Nations, 1211 Geneva 10, Switzerland (Telephone no. 988400 - 


    A WHO Task Group on Environmental Health Criteria for 
Pentachlorophenol met at the Fraunhofer Institute for Toxicology 
and Aerosol Research, Hanover, Federal Republic of Germany from 20 
to 24 October, 1986.  Dr W. Stber opened the meeting and welcomed 
the members on behalf of the host Institute, and Dr U. Schlottmann 
spoke on behalf of the Federal Government, who sponsored the 
meeting.  Dr K.W. Jager addressed the meeting on behalf of the 
three co-operating organizations of the IPCS (UNEP/ILO/WHO).  The 
Task Group reviewed and revised the draft criteria document and 
made an evaluation of the risks for human health and the 
environment from exposure to pentachlorophenol. 

    The drafts of this document were prepared by DR G. ROSNER of 
the Fraunhofer Institute for Toxicology and Aerosol Research, 
Hanover, Federal Republic of Germany, and DR A. GILMAN of the 
Health Protection Branch, Ottawa, Canada. 

    The efforts of all who helped in the preparation and 
finalization of the document are gratefully acknowledged. 

                         * * *

    Partial financial support for the publication of this criteria 
document was kindly provided by the United States Department of 
Health and Human Services, through a contract from the National 
Institute of Environmental Health Sciences, Research Triangle Park, 
North Carolina, USA - a WHO Collaborating Centre for Environmental 
Health Effects.  The United Kingdom Department of Health and Social 
Security generously supported the costs of printing. 


1.1.  Identity, Physical and Chemical Properties, Analytical Methods

    Pure pentachlorophenol (PCP) consists of light tan to white, 
needlelike crystals and is relatively volatile.  It is soluble in 
most organic solvents, but practically insoluble in water at the 
slightly acidic pH generated by its dissociation (pKa 4.7).  
However, its salts, such as sodium pentachlorophenate (Na-PCP), 
are readily soluble in water.  At the approximately neutral pH of 
most natural waters, PCP is more than 99% ionized. 

    Apart from other chlorophenols, unpurified technical PCP 
contains several microcontaminants, particularly polychlorinated 
dibenzo- p-dioxins (PCDDs) and polychlorinated dibenzofurans 
(PCDFs), of which H6CDD is the most relevant congener 
toxicologically.  2,3,7,8-T4CDD has only once been confirmed in 
commercial PCP samples (0.25 - 1.1 g/kg).  Depending on the 
thermolytic conditions, thermal decomposition of PCP or Na-PCP may 
yield significant amounts of PCDDs and PCDFs.  The use and the 
uncontrolled incineration of technical grade PCP is one of the most 
important sources of PCDDs and PCDFs in the environment. 

    Most of the analytical methods used today involve acidification 
of the sample to convert PCP to its non-ionized form, extraction 
into an organic solvent, possible cleaning by back-extraction into 
a basic solution, and determination by gas chromatography with 
electron-capture detector (GC-EC) or other chromatographic methods 
as ester or ether derivatives (e.g., acetyl-PCP).  Depending on 
sampling procedures and matrices, detection limits as low as 
0.05 g/m3 in air or 0.01 g/litre in water can be achieved. 

1.2.  Sources of Human and Environmental Exposure

    PCP is mainly produced by the stepwise chlorination of phenols 
in the presence of catalysts.  Until 1984, Na-PCP was partly 
synthesized by means of the alkaline hydrolysis of 
hexachlorobenzene, but it is now produced by dissolving PCP flakes 
in sodium hydroxide solution. 

    World production of PCP is estimated to be of the order of 
30 000 tonnes per year.  Because of their broad pesticidal efficiency
spectrum and low cost, PCP and its salts have been used as 
algicides, bactericides, fungicides, herbicides, insecticides, and
molluscicides with a variety of applications in the industrial, 
agricultural, and domestic fields.  However, in recent years, most 
developed countries have restricted the use of PCP, especially for
agricultural and domestic applications. 

    PCP is mainly used as a wood preservative, particularly on a 
commercial scale.  The domestic use of PCP is of minor importance 
in the overall PCP market, but has been of particular concern 
because of possible health hazards associated with the indoor 
application of wood preservatives containing PCP. 

1.3.  Environmental Transport, Distribution, and Transformation

    The relatively high volatility of PCP and the water solubility 
of its ionized form have led to widespread contamination of the 
environment with this compound.  Depending on the solvent, 
temperature, pH, and type of wood, up to 80% of PCP may evaporate 
from treated wood within 12 months. 

    The adsorption and leaching behaviour of PCP varies from soil 
to soil.  Adsorption of PCP decreases with rising pH and so PCP is 
most mobile in mineral soils, and least mobile in acidic clay and 
sandy soils. 

    Solid or water-dissolved PCP can be photolysed by sunlight 
within a few days, yielding aromatic (lower chlorinated phenols, 
etc.) and nonaromatic fragments, as well as hydrogen chloride (HCl) 
and carbon dioxide (CO2).  Traces of PCDDs, mainly OCDD are formed 
photochemically on irradiation of Na-PCP in aqueous solution. 

    PCP degrading microorganisms have been isolated from waters and 
soils.  High organic matter and moisture content, median 
temperatures, and high pH enhance microbial breakdown in soil 
(half-life = 7 - 14 days).  Low oxygen conditions are generally 
unfavourable for the biodegradation of PCP, allowing it to persist 
in soil (half-life = 10 - 70 days under flooded conditions), water 
(half-life = 80 - 192 days in anaerobic water), and sediments (10% 
decomposition within 5 weeks to almost no degradation).  Several 
studies have proved that PCP can be degraded by activated sludge.  
However, in full-scale treatment plants the treatment efficiency is 
often reduced. 

    Numerous metabolites have been identified resulting from the 
methylation, acetylation, dechlorination, or hydroxylation of PCP.  
Of the possible metabolites, at least tetrachlorocatechol seems to 
be relatively persistent.  However, there is a lack of data 
concerning the fate of the intermediate products of both the 
abiotic and biotic degradation of PCP. 

1.4.  Environmental Levels and Human Exposure

    The ubiquitous occurrence of PCP is indicated by its detection, 
even in ambient air of mountain rural areas (0.25 - 0.93 ng/m3).  In 
urban areas, PCP levels of 5.7 - 7.8 ng/m3 have been detected. 

    While elevated PCP concentrations can be found in groundwater 
(3 - 23 g/litre) and surface water (0.07 - 31.9 g/litre) within 
wood-treatment areas, the PCP level of surface waters is usually in 
the range of 0.1 - 1.0 g/litre, with maximum values of up to 11 
g/litre.  PCP concentrations in the mg/litre range can be 
encountered near industrial discharges. 

    Sediments of water bodies generally contain much higher levels 
of PCP than the overlying waters.  Soil samples from PCP or 
pesticide plants contain around 100 g PCP/kg (dry weight); heavily 
contaminated soil (up to 45.6 mg PCP/kg) can be found in the 
vicinity of wood-treatment areas. 

    Residues of PCP in the aquatic invertebrate and vertebrate 
fauna are in the low g/kg range (wet weight).  Very high levels 
(up to 6400 g/kg) are found in fish from waters that are 
contaminated with wood preservatives, while sediment-dwelling 
organisms, such as clams, show PCP levels of up to 133 000 g/kg.  
Fish kills result in PCP residues in fish of between 10 and 
30 mg/kg. 

    After agricultural PCP application, birds can be highly 
contaminated (47 mg/kg wet weight in liver).  Exposure of farm 
animals to PCP-treated wood shavings used as litter causes a musty 
taint of the flesh as a result of contamination with 
pentachloroanisole, a metabolite of PCP biodecomposition.  PCP 
levels ranging from not detectable to 8571 g/kg have been found in 
the muscle tissue of wild birds. 

    The general population is exposed to PCP through the ingestion 
of drinking-water (0.01 - 0.1 g/litre) and food (up to 40 g/kg in 
composite food samples).  Apart from the daily dietary intake (0.1 
- 6 g/person per day) resulting from direct food contamination 
with PCP, continuous exposure to hexachlorobenzene and related 
compounds in food, which are biotransformed to PCP, may be another 
important source. 

    In addition, because of its widespread use, the general 
population can be exposed to PCP in treated items such as textiles, 
leather, and paper products, and above all, through inhalation of 
indoor air contaminated with PCP.  Generally, PCP concentrations of 
up to about 30 g/m3 can be expected, for up to the first month, 
after indoor treatment of large surfaces; considerably higher 
levels (up to 160 g/m3) cannot be excluded under unfavourable 
conditions.  In the long term, values of between 1 and 10 g/m3 are 
typical PCP concentrations after extensive treatments, though 
higher levels, up to 25 g/m3, have been found in rooms treated one 
to several years earlier.  For comparison, PCP indoor air levels in 
untreated houses are generally below 0.1 g/m3. 

    According to the usage pattern, the main sources of 
occupational exposure to PCP are the treatment of lumber in 
sawmills and treatment plants, and exposure to treated wood during 
carpentry and other wood-working activities.  Most of the reported 
air concentrations at the work-place are below the TWA MAC value of 
500 g/m3 that has been established by several countries.  
Occupational exposure to PCP mainly occurs via inhalation and 
dermal exposure. 

    Since the PCP concentrations in the sources (air, food) do not 
directly indicate the actual PCP intake by the different routes, 
extrapolation from urine residue data has been used to estimate 
human total body exposure.  Mean or median urine-PCP levels range 
around 10 g/litre for the general population without known 
exposure, around 40 g/litre for non-occupationally exposed 
persons, and around 1000 g/litre for occupationally exposed 

    The ranges of urine levels observed in exposed and unexposed 
persons overlap considerably.  This overlap probably occurs because 
occupational exposure does not necessarily involve high loading, 
while non-occupationally exposed people may, in some instances, be 
exposed to PCP at levels encountered at the work-place. 

1.5.  Effects on Organisms in the Environment

    As a result of its biocidal properties, PCP negatively affects 
non-target organisms in soil and water at relatively low 
concentrations.  Algae appear to be the most sensitive aquatic 
organisms; as little as 1 g/litre can cause significant inhibition 
of the most sensitive algal species. Less sensitive species show 
EC50 values of around 1 mg/litre. 

    Most aquatic invertebrates (annelids, molluscs, crustacea) and 
vertebrates (fish) are affected by PCP concentrations below 1 
mg/litre in acute toxicity tests.  Generally, reproductive and 
juvenile stages are the most sensitive, with LC50 values as low as 
0.01 mg/litre for fish larvae.  Low levels of dissolved oxygen, low 
pH, and high temperature increase the toxic effects of PCP.  
Concentrations causing sublethal effects on fish are in the low 
g/litre range.  As PCP contamination in many surface waters is in 
this range, population and community effects cannot be ruled out.  
This is also indicated by the substantial alterations in the 
community structure of model ecosystems that are induced by PCP. 

    PCP is accumulated by aquatic organisms.  Fresh-water fish show 
bioconcentration factors of up to 1000 compared to < 100 in marine 
fish.  The portion of PCP taken up, either through the surrounding 
water or along the food chain, is probably species specific. 

    PCP taken up by terrestrial plants remains in the roots and is 
partly metabolized. 

1.6.  Kinetics and Metabolism

    PCP is readily absorbed through the intact skin and respiratory 
and gastrointestinal tracts, and distributed in the tissues.  
Highest levels are observed in liver and kidney, and lower levels 
are found in body fat, brain, and muscle tissue.  There is only a 
slight tendency to bioaccumulate, and so relatively low PCP 
concentrations are found in tissues.  In rodent species, 
detoxication occurs through the oxidative conversion of PCP to 
tetrachlorohydroquinone, to a small extent also to 
trichlorohydroquinone, as well as through conjugation with 
glucuronic acid.  In rhesus monkeys, no specific metabolites have 
been detected.  In man, metabolism of PCP to 
tetrachlorohydroquinone seems to occur only to a small extent. 

    Rats, mice, and monkeys excrete PCP and their metabolites, 
either free or conjugated with glucuronic acid, mainly in urine 
(rodents, 62 - 83%; monkeys, 45 - 75%) and to a lesser extent with 
the faeces (rodents, 4 - 34%; monkeys, 4 - 17%).  The 
pharmacokinetic profile following single doses depends on the 

species and possibly on the sex of the test animals.  Rats and mice 
eliminate PCP rapidly, with a half-life of 6 - 27 h.  The kinetics 
in rats follow a biphasic elimination scheme with a comparatively 
slow second elimination phase (half-life, 33 - 374 h), perhaps 
because extensive enterohepatic circulation retains PCP in the 
liver.  Retention may also be the result of plasma-protein binding 
of PCP, which seems to become stronger at lower PCP concentrations. 

    In rats, 90% of an applied single oral dose is excreted by day 
3 with small amounts still remaining in the liver (0.3%) and kidney 
(0.05%) after 9 days.  On the other hand, monkeys show a much 
slower elimination rate (half-life, 41 - 92 h), apparently because 
they do not metabolize PCP; even 15 days after oral application of 
a single dose (10 mg/kg bodyweight), about 11% of the total dose 
remained in the body, particularly in the intestines and liver. 

    The elimination kinetics of PCP in human beings are a 
controversial subject.  A study on 4 male volunteers ingesting a 
single oral dose of water-soluble Na-PCP at 0.1 mg/kg body weight 
showed a rapid elimination of PCP both in urine (half-life, 33 h) 
and plasma (30 h).  Within 168 h, 74% of the dose was excreted in 
urine as free PCP and 12% as its glucuronide, while about 4% was 
eliminated in the faeces.  In contrast to this study, the 
application of oral doses of between 0.016 and 0.31 mg PCP/kg body 
weight in 40% ethanol revealed a substantially slower PCP 
excretion rate, with elimination half-lives of 16 days (plasma) and 
18 - 20 days (urine).  These low elimination rates have been 
ascribed to the high protein binding tendency of PCP. 

    Some animal data indicate that there may be long-term 
accumulation and storage of small amounts of PCP in human beings.  
The fact that urine- or blood-PCP levels do not completely 
disappear in some occupationally exposed people, even after a long 
absence of exposure, seems to confirm this, though the 
biotransformation of hexachlorobenzene and related compounds 
provides an alternative explanation of this phenomenon.  However, 
there is a lack of data concerning the long-term fate of low PCP 
levels in animals as well as in man.  Furthermore, no data are 
available on the accumulation and effects of microcontaminants 
taken up by people together with PCP. 

1.7.  Effects on Experimental Animals and  In Vitro Test Systems

    In the main, mammalian studies have been relatively consistent 
in their demonstration of the effects of exposure to PCP.  In rats, 
lethal doses induce an increased respiratory rate, a marked rise in 
temperature, tremors, and a loss of righting reflex.  Asphyxial 
spasms and cessation of breathing occur soon before cardiac arrest, 
which is in turn followed by a rapid, intense rigor mortis. 

    PCP is highly toxic, regardless of the route, length, and 
frequency of exposure.  Oral LD50 values for a variety of species 
range between 27 and 205 mg/kg body weight according to the 
different solvent vehicles and grades of PCP.  There is limited 

evidence that the most dangerous route of exposure to PCP is 
through the air. 

    PCP is also an irritant for exposed epithelial tissue, 
especially the mucosal tissues of the eyes, nose, and throat. Other 
localized acute effects include swelling, skin damage, and hair 
loss, as well as flushed skin areas where PCP affects surface blood 
vessels.  Exposure to technical formulations of PCP may produce 
chloracne.  Comparative studies indicate that this is a response to 
microcontaminants, principally PCDDs, present in the commercial 
product.  The parent molecule appears responsible for immediate 
acute effects, including irritation and the uncoupling of oxidative 
phosphorylation with a resultant elevated temperature. 

    Short- and long-term studies indicate that purified PCP has a 
fairly limited range of effects in test organisms, primarily rats.  
Exposure to fairly high concentrations of PCP may reduce growth 
rates and serum-thyroid hormone levels, and increase liver weights 
and/or the activity of some liver enzymes.  In contrast, technical 
formulations of PCP usually at much lower concentrations can 
decrease growth rates, increase the weights of liver, lungs, 
kidneys, and adrenals, increase the activity of a number of liver 
enzymes, interfere with porphyrin metabolism, alter haematological 
and biochemical parameters and interfere with renal function. 
Apparently microcontaminants are the principal active moities in 
the nonacute toxicity of commercial PCP. 

    PCP is fetotoxic, delaying the development of rat embryos and 
reducing litter size, neonatal body weight, neonatal survival, and 
the growth of weanlings.  The no-observed-adverse-effect-level 
(NOAEL) for technical PCP is a maternal dose of 5 mg/kg body weight 
per day during organogenesis.  The NOAEL for purified PCP is lower. 
In one study, it was reported that purified PCP was slightly more 
embryo/fetotoxic than technical PCP, presumably because 
contaminants induced enzymes that detoxified the parent compound. 

    PCP is not considered teratogenic, though, in one instance, 
birth defects arose as an indirect result of maternal hyperthermia.  
The NOAEL in rat reproduction studies is 3 mg/kg body weight per 
day.  This value is remarkably close to the NOAEL mentioned in the 
previous paragraph, but there are no corroborating studies in other 
mammalian species. 

    PCP has also proved immunotoxic to mice, rats, chickens, and 
cattle; at least part of this effect is caused by the parent 

    Neurotoxic effects have also been reported, but the possibility 
that these are due to microcontaminants has not been excluded. 

    PCP is not considered carcinogenic for rats.  Mutagenicity 
studies support this conclusion in as much as pure PCP has not been 
found to be highly mutagenic.  Its carcinogenicity remains 
questionable because of shortcomings in these studies.  The 
presence of at least one carcinogenic microcontaminant (H6CDD) 

suggests that the potential for technical PCP to cause cancer in 
laboratory animals cannot be completely ruled out. 

Note: Since the publication of this monograph in 1987, however, the 
results of adequate carcinogenicity studies with commercial-grade 
pentachlorophenol have been published. The conclusions of these studies 
are indicated in the addendum to 8.6 Carcinogenicity.

1.8.  Effects on Man

    The effects of PCP on man are very similar to those reported in 
experimental animals.  Human data have been obtained primarily from 
accidental exposures and from the work-place.  Unfortunately, there 
are few precise estimates of exposure, hence dose-response 
relationships are difficult to establish in human beings. 

    It is clear that the use of PCP may pose a significant hazard 
with regard to specific aspects of the health of workers employed 
in the production or use of PCP.  Chloracne, skin rashes, 
respiratory diseases, neurological changes, headaches, nausea, and 
weakness have been documented in workers at numerous production and 
manufacturing sites. Similar symptoms have been reported in some 
inhabitants of houses treated internally with PCP.  Acute 
intoxications leading to hyperpyrexia and death have been clearly 
associated with exposure to the chlorophenol molecule itself, 
whereas chloracne appears to be an effect of the PCDD and PCDF 
microcontaminants.  Changes in industrial practice have resulted 
in fewer high-dosage, acute exposures, but deaths due to 
occupational overexposure to PCP are still being reported. 

    Studies designed to examine biochemical changes in wood-workers 
exposed to high levels of PCP for extended periods have failed to 
indicate statistically significant effects on major organs, neural 
tissues, blood elements, the immune system, or reproductive 
capacity.  However, many of these studies were based on small 
sample sizes; hence, analyses of trends indicating effects on liver 
enzymes, kidney function, T-cell suppression, nerve conduction 
velocity, etc., have not been statistically significant.  Others 
have been non-specific in the search for signs of intoxication in 
large groups of workers.  However, there are mounting indications 
that long-term exposure to relatively high levels of PCP leading to 
blood-plasma concentrations as high as 4 ppm is likely to cause 
borderline effects on some physiological processes. Some of these 
effects, especially those involving the liver and the immune 
system, may be caused, in whole or in part, by the 
microcontaminants of these chlorophenols, especially H6CDD. 

    Several epidemiological studies from Sweden and the USA have 
indicated that occupational exposure to mixtures of chlorophenols 
is associated with increased incidences of soft tissue sarcomas, 
nasal and nasopharyngeal cancers, and lymphomas.  In contrast, 
surveys from Finland and New Zealand have not detected such 
relationships.  The major deficiency in all of these studies 
appears to be a lack of specific exposure data. 

    There are no conclusive reports of increased incidences of 
cancers in workers exposed specifically to PCP; however, there have 
not been any carefully conducted studies of a suitably exposed 

occupational group large enough to provide the necessary 
statistical power to identify an increase in cancer mortality.  
Furthermore, there are few occupational groups that have been 
exposed to a single chemical, such as PCP.  Finally, the various 
levels of microcontaminants in different formulations make 
inferences to PCP in general difficult. 

    Persons non-occupationally exposed to technical PCP in rooms 
complained about relatively unspecific symptoms (headache, fatigue, 
hair loss, tonsillitis, etc.); a causative connection with PCP 
could not be proved or disproved. 


    Pentachlorophenol (PCP) and its salt, sodium pentachlorophenate 
(Na-PCP), are the most important forms of pentachlorophenol in 
terms of production and use.  Other derivatives such as the 
potassium salt, K-PCP, and the lauric acid ester, L-PCP are of 
minor importance.  Reflecting this minor role, few data on the 
physical and chemical properties of K-PCP and L-PCP are reported in 
the literature.  Hence, this section primarly concerns PCP and its 
sodium salt. 

2.1.  Identity

2.1.1.  Pentachlorophenol (PCP)
Chemical Structure

Molecular formula:       C6HCl5O

CAS chemical name:       Pentachlorophenol

Common synonyms:         chlorophen; PCP; penchlorol; penta; 
                         pentachlorofenol; pentachlorofenolo; 
                         pentachlorphenol; 2,3,4,5,6-

Common trade names:      Acutox; Chem-Penta; Chem-Tol; Cryptogil 
                         ol; Dowicide 7; Dowicide EC-7; Dow 
                         Pentachlorophenol DP-2 Antimicrobial; 
                         Durotox; EP 30; Fungifen; Fungol; Glazd 
                         Penta; Grundier Arbezol; Lauxtol; Lauxtol 
                         A; Liroprem; Moosuran; NCI-C 54933; NCI-C 
                         55378; NCI-C 56655; Pentacon; Penta-Kil; 
                         Pentasol; Penwar; Peratox; Permacide; 
                         Permagard; Permasan; Permatox; Priltox; 
                         Permite; Santophen; Santophen 20; 
                         Sinituho; Term-i-Trol; Thompson's Wood 
                         Fix; Weedone; Witophen P 

CAS registry number:     87-86-5

2.1.2.  Sodium pentachlorphenate (Na-PCP)
Chemical Structure

Molecular formula:       C6Cl5ONa
                         C6Cl5ONa x H2O (as monohydrate)

Common synonyms:         penta-ate; pentachlorophenate sodium; 
                         pentachlorophenol, sodium salt; 
                         pentachlorophenoxy sodium; pentaphenate; 
                         phenol, pentachloro-, sodium derivative 
                         monohydrate; sodium PCP; sodium 
                         pentachlorophenate; sodium 
                         pentachlorophenolate; sodium 

Common trade names:      Albapin; Cryptogil Na; Dow Dormant 
                         Fungicide; Dowicide G-St; Dowicide G; 
                         Napclor-G; Santobrite; Weed-beads; 
                         Xylophene Na; Witophen N 

CAS registry number:     131-52-2 (Na-PCP);
                         27735-64-4 (Na-PCP monohydrate)

2.1.3.  Pentachlorophenyl laurate

    The molecular formula of pentachlorophenyl laurate is 
C6Cl5OCOR; R is the fatty acid moiety, which consists of a mixture 
of fatty acids ranging in carbon chain length from C6 to C20, the 
predominant fatty acid being lauric acid (C12) (Cirelli, 1978b). 

2.2.  Impurities in Pentachlorophenol

    Technical PCP has been shown to contain a large number of 
impurities, depending on the manufacturing method (section 3.2.1).  
These consist of other chlorophenols, particularly isomeric 
tetrachlorophenols, and several microcontaminants, mainly 
polychlorodibenzodioxins (PCDDs), polychlorodibenzofurans (PCDFs), 
polychlorodiphenyl ethers, polychlorophenoxyphenols, chlorinated 
cyclohexenons and cyclohexadienons, hexachlorobenzene, and 
polychlorinated biphenyls (PCBs).  Table 1 presents analyses of PCP 
formulations taken from several publications.  According to Crosby 
et al. (1981), the quality of PCP is depends on the source and date 
of manufacture.  Furthermore, analytical results may be extremely 
variable, particularly with regard to earlier results, which should 
be considered with caution.  Jensen & Renberg (1972) detected 
chlorinated 2-hydroxydiphenyl ethers, which obviously may transform 
to dioxins during gas chromatography, thus giving a false 
indication of a higher level of PCDDs.  Unlike these "predioxins", 
other isomers are not direct precursors of dioxins, and are 
labelled "isopredioxins". 

Table 1.  Impurities (mg/kg PCP) in different technical PCP products
Component                           Specification, producer, PCP content  (%)                      
                      Tech-      Tech-     Tech-      Techni-    Techni-  Techni-     Technicalf
                      nicala     nicalb    nicalb,e   calc,g,h   cald,i   cale      
                      Monsanto   Dow       Dow        Dow        Dow      Dyn. Nobel  Rhne-Poulenc
                      (84.6%)    (88.4%)   (98%)      (90.4%)    (ns)j    (87%)       (86%)
  Tetrachloro-        30 000     44 000    2700       10 4000    ns       50 000      70 000
  Trichloro-          ns         < 1000    500        < 1000     ns       20          ns
  Higher chlorinated  ns         62 000    5000       ns         ns       ns          70 000

  Tetrachloro-        < 0.1      < 0.05    < 0.05     < 0.05     < 0.2k   < 0.001     < 0.01
  Pentachloro-        < 0.1      ns        ns         ns         < 0.2    ns          ns
  Hexachloro-         8          4         < 0.5      1          9        3.5         5
  Heptachloro-        520        125       < 0.5      6.5        235      130         150
  Octachloro-         1380       2500      < 1.0      15         250      600         600

  Tetrachloro-        < 4        ns        ns         ns         < 0.2    ns          ns
  Pentachloro-        40         ns        ns         ns         < 0.2    0.2         ns
  Hexachloro-         90         30        < 0.5      3.4        39       10          ns
  Heptachloro-        400        80        < 0.5      1.8        280      60          ns
  Octachloro-         260        80        < 0.5      < 1.0      230      150         ns

 Hexachlorobenzene     ns         ns        ns         400        ns       ns          ns
a   From: Goldstein et al. (1977).
b   From: Schwetz et al. (1974).
c   From: Schwetz et al. (1978).
d   From: Buser (1975).
e   From: Umweltbundesamt (1985).
f   From: Anon (1983b).
g   Purified.
h   Dowicide EC-7.
i   Dowicide 7.
j   ns = not specified.
k   < = below detection limit.
    In Fig. 1, the structures and numbering system for the 
polychlorinated dibenzodioxins (PCDDs) and dibenzofurans (PCDFs) 
are illustrated. 


    Since the toxicity of PCDDs and PCDFs depends not only on the 
number but also on the position of chlorine substituents, a precise 
characterisation of PCP impurities is essential. The presence of 
highly toxic 2,3,7,8-tetrachlorodibenzo- p-dioxin (2,3,7,8-T4CDD) 
has only been confirmed once in commercial PCP samples.  In the 
course of a collaborative survey, one out of five laboratories 
detected 2,3,7,8-T4CDD in technical PCP and Na-PCP samples at 
concentrations of 250 - 260 and 890 - 1100 ng/kg, respectively 
(Umweltbundesamt, 1985).  Buser & Bosshardt (1976) found detectable 
amounts of T4CDD (0.05 - 0.23 mg/kg) in some samples of different 
technical PCP products, but on re-analysis were unable to confirm 
the compound's identity.  In other cases, T4CDD has not been 
identified at detection limits of 0.2 - 0.001 mg/kg (Table 1). 

    The higher polychlorinated dibenzodioxins and dibenzofurans 
are more characteristic of PCP formulations (Table 1). 
Hexachlorodibenzo- p-dioxin (H6CDD), which is also considered 
highly toxic and carcinogenic (section 8), was found at levels of 
0.03 - 35 mg/kg (Firestone et al., 1972), 9 - 27 mg/kg (Johnson et 
al., 1973), and < 0.03 -  10 mg/kg (Buser & Bosshardt, 1976).  
According to Fielder et al. (1982), the 1,2,3,6,7,9-, 1,2,3,6,8,9-, 
1,2,3,6,7,8-, and 1,2,3,7,8,9-isomers of H6CDD have been detected 
in technical PCP.  The 1,2,3,6,7,8and 1,2,3,7,8,9-H6CDDs 
predominated in commercial samples of technical PCP (Dowicide 7) 
and Na-PCP.  Octachloro-dibenzo- p-dioxin (OCDD) is present in 
relatively high amounts in unpurified technical PCP (Table 1). 

    Recently, the identification of 2-bromo-3,4,5,6-
tetrachlorophenol as a major contaminant in three commercial PCP 
samples (ca. 0.1%) has been reported.  This manufacturing by-
product has probably not been detected in other analyses because it 
is not resolved from the PCP peak by traditional chromatographic 
methods (Timmons et al., 1984). 

2.2.1.  Formation of PCDDs and PCDFs during thermal decomposition

    The thermal decomposition of PCP or Na-PCP yields significant 
amounts of PCDDs and PCDFs, depending on the thermolytic 
conditions.  For pure PCP, dimerization of PCP has been suggested 
as an underlying reaction process; in technical PCP, additional 
reactions, i.e., dechlorination of higher chlorinated PCDDs and 
cyclization of predioxins are involved in forming various and 
different PCDD isomers (Rappe et al., 1978b). 

    Pyrolysis of alkali metal salts of PCP at temperatures above 
300 C results in the condensation of two molecules to produce 
OCDD.  PCP itself forms traces of OCDD only on prolonged heating in 
bulk and at temperatures above 200 C (Sandermann et al., 1957; 
Langer et al., 1973; Stehl et al., 1973). 

    Although present in original technical PCP products, a number 
of PCDDs, other than OCDD, are generated during thermal 
decomposition (290 - 310 C) in the absence of oxygen (Table 2) 
(Buser, 1982). 

Table 2.  PCDDs (mg/kg PCP) in the 
pyrolysate of technical PCP and Na-PCPa
                     PCP       Na-PCP
2,3,7,8-T4CDD        -b        -c
1,2,3,7,8,9-H6CDD    53        2.1
1,2,3,6,7,8-H6CDD    66        0.95
Total H6CDD          455       10.5
H7CDD                5200      65
OCDD                 15 000    200
a   From: Buser (1982).
b   Detection limit (1 mg/kg).
c   Detection limit (0.25 mg/kg).

2.3.  Physical, Chemical, and Organoleptic Properties

    Pure pentachlorophenol consists of light tan to white, 
needlelike crystals.  It has a pungent odour when heated (Windholz, 
1976).  Its vapour pressure suggests that it is relatively 
volatile, even at ambient temperatures.  Since PCP is practically 
insoluble in water at the slightly acidic pH generated by its 
dissociation, readily water-soluble salts such as Na-PCP are used 
as substitutes, where appropriate. 

    Na-PCP is non-volatile; its sharp PCP odour results from slight 
hydrolysis (Crosby et al., 1981).  Technical PCP consists of 
brownish flakes or brownish oiled, dustless flakes, coated with a 
mixture of benzoin polyisopropyl and pine oil.  Technical Na-PCP 
consists of cream-coloured beads (Anon., 1983a,b).  Technically 
pure L-PCP consists of a brown oil that is insoluble in water and 
alcohols, and soluble in non-polar solvents, oils, fats, waxes, and 
plasticizers (Cirelli, 1978b). 

    PCP is non-inflammable and non-corrosive in its unmixed state, 
whereas a solution in oil causes deterioration of rubber (Mercier, 

    Because of the electron withdrawal by the ring chlorines, PCP 
behaves as an acid, yielding water-soluble salts such as sodium 
pentachlorophenate.  Due to nucleophilic reactions of the hydroxyl 
group, PCP can form esters with organic and inorganic acids and 
ethers with alkylating agents, such as methyl iodide and 
diazomethane (Crosby et al., 1981).  This property has been used 
for analytical purposes (section 2.5.2). 

    PCP may exist in two forms: the anionic phenolate, at neutral 
to alkaline pH, and the undissociated phenol at acidic pH.  At pH 
2.7, PCP is only 1% ionized; at pH 6.7, it is 99% ionized (Crosby 
et al., 1981).  Other relevant properties of pure PCP and Na-PCP 
are shown in Table 3. 

    PCDDs and PCDFs may also be formed during the combustion of 
materials treated with either purified or technical PCP. Smoke from 
birch leaves impregnated with purified Na-PCP and burnt on an open 
fire showed considerably increased amounts of PCDDs compared with 
the original sample (Table 4).  The mass fragmentograms revealed 14 
of the 22 possible T4CDD isomers with 1,3,6,8- and 1,3,7,9-T4CDD as 
the main and 2,3,7,8- T4CDD as minor isomers.  The formation of 
PCDFs, including small amounts of  2,3,7,8-T4CDF, during either 
combustion or micropyrolysis (280 C, 30 min) was only observed in 
technical PCP samples; purified Na-PCP was negative in this respect 
(Rappe et al., 1978b). 

Table 3.  Physical, chemical, and organoleptic properties of PCP 
and Na-PCP
                             PCP                      Na-PCP
Boiling pointa               310 C (decomposition)

Relative molecular massb     266.4                    288.3

Melting pointa               191 C

Density (d422 in g/ml)b      1.987                    2

Vapour pressure kPa (mmHg)
  at 20 Cc                  2 x 10-6 (1.5 x 10-5)
  at 19 Cd                  6.7 x 10-7 (5 x 10-6)

Saturation vapour density    220
(g/m3) (20 C)c

Steam volatilitye            0.167
(g/100 g water vapour)
(100 C)

Table 3 (contd.)
                             PCP                      Na-PCP
Solubility in fat            213
(g/kg) (37 C)f

 n-Octanol/water partition    4.84 (pH 1.2);               
coefficient (log P)g         3.56 (pH 6.5); 
                             3.32 (pH 7.2);
                             3.86 (pH 13.5)

pKa (25 C)e                 4.7

Solubility in water:
  0 C, pH 5                 0.005
  20 C, pH 5                0.014
  30 C, pH 5                0.020
  20 C, pH 7                2
  20 C, pH 8                8
  20 C, pH 10               15                       > 200
  25 C                                               330

Solubility in organic 
solvents (g/100 g) 
(25 C)b:
  acetone                    50                       35
  benzene                    15                       insoluble
  ethanol (95%)              120                      65
  ethylene glycol            11                       40
  isopropanol                85                       25
  methanol                   180                      25

Odour threshold              1.6 (in water)

Olfactory threshold          0.03 (in water)
a   From: IRPTC (1983).
b   From: Cirelli (1978b).
c   From: Zimmerli (1982).
d   From: Dobbs & Grant (1980).
e   From: Crosby et al. (1981).
f   From: Rippen (1984).
g   From: Kaiser & Valdmanis (1982).
h   From: Gunther et al. (1968).
i   From: Bundesamt fr Umweltschutz (1982).
j   From: Dietz & Traud (1978a).

    Jansson et al. (1978) observed a very wide range of PCDD 
concentrations in the smoke from burning wood chips impregnated 
with a technical PCP formulation (Table 4).  The formation of PCDDs 
was favoured by temperatures below 500 C, oxygen deficit, and 
lower gas-retention time.  The results given in Table 4 are 
corrected for the very low background values obtained by burning 
untreated wood chips. 

    When technical PCP was burnt in a quartz reactor (600 C, 10 
min), Lahaniatis et al. (1985) identified the following thermolytic 
products: pentachlorobenzene, hexachlorobenzene, octachlorostyrole, 
octachloronaphthaline, decachlorobiphenyl, H6CDF, OCDF, and OCDD.  
2,3,7,8-T4CDD was not detected at a detection limit of 1 mg/kg PCP. 

    Olie et al. (1983) found only slightly higher levels of PCDDs 
and PCDFs in the fly ash of burned new wood treated with PCP 
compared with painted wood, which was more than 60 years old.  
However, because data were missing on PCDD/PCDF levels in the 
original samples and on the conditions of burning, meaningful 
interpretation of these results is not possible. 

2.4.  Conversion Factors

    1 ppm = 10.9 mg PCP/m3 (25 C, 101.3 kPa)
    1 mg PCP/m3 = 0.09 ppm

Table 4.  Amount of PCDDs in the original sample and in 
the smoke from combusted materials treated with purified 
Na-PCP or technical PCP
         Birch leavesa           Wood chipsb
         (mg PCDDs/kg Na-PCP     (mg PCDDs/kg PCP
         (purified))             (technical))             
         Original     Smokec     Original    Smokec,d
         sample                  sample
T4CDD    < 0.02       5.2        nde         < 4.7 - 47
P5CDD    < 0.03       14         nd          < 1.2 - 419
H6CDD    < 0.03       56         7           < 9.3 - 93
H7CDD    0.3          172        93          < 4.7 - 279
OCDD     0.9          710        186         < 0.9 - 442
a   Adapted from: Rappe et al. (1978b).
b   Adapted from: Jansson et al. (1978).
c   Smoke trapped on charcoal filter.
d   Depending on combustion conditions.
e   nd = not determined.

2.5.  Analytical Methods

    A number of methods have been used to determine PCP in a 
variety of media.  The earlier procedures were reviewed by Bevenue 
& Beckman (1967).  They were mostly based on colour reactions, 
which are not very specific and relatively insensitive.  For 
several years, more sophisticated devices have been available to 
analysts, of which gas chromatography has become the method of 
choice (Table 5). 

Table 5.  Analytical methods for the determination of PCP
Medium   Sampling method        Analytical method             Detec-   Detection     Reco-   Reference
                                                              tion     limit         very

Air-     Impinger collection    Derivatization with diazo-    ECa      0.22 mg/m3    nsc     Hoben et al.
aerosol  with KOH; hexane       methane; purification in                                     (1976a)
         extraction             chromatoflex Florisil
                                column; GCd analysis

Air      Filter and bubbler     HPLCe analysis; column:       UV254b   0.27 mg/m3    95.3-   NIOSH
         collection; ethylene    Bondapack C18; mobile                              100.9%  (1978)
         glycol extraction      phase: methanol/water

Air      Bubbler collection;    Derivatization with acetyl    EC       0.05 g/m3    ns      Dahms &
         absorption in K2CO3    chloride; GC analysis                                        Metzner
         solution; hexane                                                                    (1979)

Air      Adsorption on to       GC analysis                   EC       0.5 g/m3    ns      Zimmerli &
         filter papers                                                                       Zimmermann
         impregnated with                                                                    (1979)
         adsorbant extraction
         concentration in ether

Air      Impinger collection;   HPLC analysis; column:        UV225    0.5 g/m3     ns      Woiwode et
         absorption in K2CO3-   Lichrosorb C18; mobile                                       al. (1980)
         solution; benzene      phase: methanol

Air      Air from wood samples  GC analysis                   EC       ns            89.7-   Warren et
         in reactor tube ads-                                          (< 1.5        99.9%   al. (1982)
         orbed on silica gel;                                          g/m3)
         desorption with benzene

Air      Impinger collection;   Derivatization with acetic    EC       ns            ns      Kauppinen &
         absorption in          anhydride in presence of                                     Lindroos
         toluene                pyridine; GC analysis                                        (1985)

Table 5.  (contd.)
Medium   Sampling method        Analytical method             Detec-   Detection     Reco-   Reference
                                                              tion     limit         very
 Biological tissues and fluids

Blood    Benzene extraction     Derivatization with diazo-    EC       20 g/litre   87-     Bevenue et
(human)  from acidified         methane; GC analysis                                 100%    al. (1968)

Blood,   Ethyl ether extrac-   No derivatization; GC anal-   EC-3H    0.1 ng        90-     Barthel et
urine,   tion from acidified     ysis; column: 3% diethylene   EC-63Ni  0.02 ng       100%    al. (1969)
tissue   solution; NaOH ex-     glycol succinate + 2% H3PO4;
(human)  traction; benzene      confirmation by MS and TLC

Organic  Hexane/isopropanol     Der. with acetic anhydride    EC       ns            81-91%  Rudling
tissues  extraction from        in presence of pyridine;                                     (1970)
         acidified sample;      GC analysis
         borax extraction

Urine    Ethyl ether extrac-   Derivatization with diazo-    EC       10 g/litre   92-     Shafik et
(rat)    tion from acidified     ethane; GC analysis                                  98%     al. (1973)

Adipose  NaOH extraction;       Derivatization with diazo-    EC       5 g/kg       75%     Shafik
tissue   diethyl ether          methane; GC analysis                                         (1973)
(human)  extraction from
         acidified solution

Urine,   Acidic hydrolysis      No derivatization; negative   MSf      1 ng          90%     Dougherty &
seminal  (urine); hexane/2-     chemical ionization (NCI)                                    Piotrowska
fluid    propanol or hexane/    mass spectrometry; internal                                  (1976a;b)
(human)  ether extraction from  standard:  p-chlorobenzophenone
         acidified solution

Tissue,  Hexane or benzene      Derivatization with diazo-    EC       20 g/kg      91.4-   Hoben et al.
plasma,  extraction             ethane (urine) or diazo-                             95.3%   (1976a)
urine                           methane; purification in
(rat)                           chromatoflex Florisil column;
                                GC analysis

Table 5.  (contd.)
Medium   Sampling method        Analytical method             Detec-   Detection     Reco-   Reference
                                                              tion     limit         very
Tissues  Acetone extraction     (a) TLCg analysis on silica   Radio-   ns            ns      Glickman et
(fish)                              gel UV254; mobile phase:  active                         al. (1977)
                                    methylene chloride

         Acetone extraction     (b) Derivatization with       MS       ns            ns      Glickman et
                                    methyl iodide and K2CO3;                                 al. (1977)
                                    GC analysis

Urine    Hexane extraction      Derivatization with acetyl    EC       10 g/litre   ns      Dahms &
(human)  from acidified         chloride in the presence of                                  Metzner
         solution               pyridine; GC analysis                                        (1979)

Urine    Benzene extraction     Derivatization with diazo-    EC       1 g/litre    93.2-   Edgerton
(human,  from acidified         methane; separation of                               97.2%   et al.
rat)     solution               methylated phenols in acid                                   (1979)
                                alumina column; GC analysis;
                                GC-MS confirmation

Plasma   Benzene extraction     Derivatization with acetic    EC       50 g/litre   91-     Eben et
(human)                         anhydride; GC analysis                               102%    al. (1981)

Urine    Acidic or enzymatic    Derivatization with acetic    EC       20 g/litre   77-     Eben et
(human)  hydrolysis; ethyl      anhydride; GC analysis                               98%     al. (1981)
         ether extraction;
         benzene extraction

Tissues, Diethyl ether (ethyl   Purification on Hypersil-     UV216    1 g/kg       62-     Mundy &
serum,   acetate-hexane)        cartridge; mobile phase:                             108%    Machin
egg      extraction from NaOH   methanol; HPLC analysis                                      (1981)
yolk/    (hydrochloric acid)
white    solution; concentra-
         tion by evaporation

Table 5.  (contd.)
Medium   Sampling method        Analytical method             Detec-   Detection     Reco-   Reference
                                                              tion     limit         very
Urine    Acidic hydrolysis;     HPLC analysis; column: Sphe-  UV313    10 g/litre   102%    Drummond
(human)  distillation; methy-   risorb-ODS; mobile phase:                                    et al.
         lene chloride ex-      acetonitrile; internal stan-                                 (1982)
         traction from acidi-   dard: 3,5-dichloro-2,3,6-
         fied solution;         tribromophenol (DTP)
         evaporation and
         redistillation in

Urine    Acidic hydrolysis;     LC analysis; column: Spheri-  UV254    0.1           83.3   Pekari &
(human)  hexane/isopropanol     sorb-ODS; mobile phase:                mol/litre    3.7%    Antero
         extraction; evap-      methanol                               (27 g/litre)         (1982)
         oration and redis-
         tillation in methanol

Urine    Acidic hydrolysis;     Derivatization with acetic    SIM-MSh  1 nmol/litre  ns      Harge-
(human)  int.standard (4,6-     or propionic anhydride;       (0.27                          sheimer &
         dibromo- o-cresol)      GC analysis                   g/litre)                      Coutts
         added; methylene                                                                    (1983)
         chloride extraction


Milk     Benzene extraction;    Derivatization with acetic    EC       5 g/litre    80-     Erney
(bovine) extraction with        anhydride; GC analysis                               87.2%   (1978)
         K2CO3 solution

Milk     Sulfuric acid          Purification in BioSil        EC       10 - 15       80%     Lamparski
(bovine) digestion; hexane      A-column; derivatization               g/litre              et al.
         extraction             with diazomethane; GC                                        (1978)

Carrots, Soxhlet extraction     Derivatization with diazo-    EC       0.2 g/kg     80-     Bruns &
potatoes (carrots) or blending  ethane; purification in                              108%    Currie
         with acidified         Florisil-column; GC                                          (1980)
         acetone                analysis

Table 5.  (contd.)
Medium   Sampling method        Analytical method             Detec-   Detection     Reco-   Reference
                                                              tion     limit         very
Canned   Methylene chloride     Derivatization with diazo-    EC       ns            92-     Heikes &
food and extraction from        methane; purification in               (< 0.3        103%    Griffitt
jar lids acidified solution;    Florisil-column; GC analysis           g/kg)                (1980)
         clean-up by gel perme-
         ation chromatography

Edible   Alkaline hydrolysis;   Direct GC analysis on DEGS/   EC       5 - 10 g/kg  83-     Stijve
gelatins iso-octane extraction  phosphoric acid column; con-                         108%    (1981)
         from acidified         firmation by GC analysis of
         solution               acetate derivative

Plant    Maceration with acidi- Derivatization with diazo-    EC       ns            94.2%   Fuchs-
mater-   fied acetone;          methane; purification in                                     bichler
ials     chloroform extr.;      Florisil-column; GC analysis                                 (1982)
         cleanup by automated
         gel chromatography

Mush-    Steam distillation     (a) Derivatization with ace-  EC       0.5 g/kg     92%     Schnhaber
rooms    from acidified sample;     tic anhydride GC analysis          fresh weight          et al.
         dichloromethane        (b) HPLC analysis; column:    UV220    0.5 g/kg             (1982)
         extraction                 LiChrosorb RP-8; mobile
                                    phase: methanol/ o-phos-
                                    phoric acid


Soil     NaOH extraction;       Derivatization with diazo-    EC       0.1 - 1       > 97%   Renberg
         clean-up by ion        methane; GC analysis                   g/kg                 (1974)

Soil     Nielsen-Kryger steam   Direct GC analysis on fused   EC       ns            58-     Narang et
         distillation from      silica SE 54 column                                  95%     al. (1983)
         acidified soil;
         chloride extraction

Table 5.  (contd.)
Medium   Sampling method        Analytical method             Detec-   Detection     Reco-   Reference
                                                              tion     limit         very

Raw and  Petroleum ether        TLC analysis on Al2O3         Colori-  0.5 g/litre  75-     Zigler &
treated  extraction from        plates; mobile phase:         metric                 100%    Phillips
water    acidified sample;      (a) benzene;(b) NaOH/acetone;                                (1967)
         evaporation;           chromogenic agent: AgNO3/2-
         drying; evaporation    phenoxyethanol

Natural, Benzene extraction     Derivatization with acetic    EC       0.01          84-     Chau &
waste    and K2CO3-solution     anhydride; hexane extrac-              g/litre      93%     Coburn
water                           tion; GC analysis                                            (1974)

River    Hexane/ethyl ether     Derivatization with boron     MS       0.01          ns      Matsumoto
water    extraction; ethyl      trifluoride methanol and               g/litre              et al.
         acetate extraction     trimethylsilyl; GC analysis                                  (1977)
         from acidified

Surface  Toluene extraction;    Derivatization with acetic    EC       0.01          85%     Wegman &
water    extraction with        anhydride; petroleum ether             g/litre              Hofstee
         K2CO3-solution         extraction; GC analysis                                      (1979)

Waste    Chloroform extraction  Direct HPLC analysis of       UV254    10 g/litre   ns      Ervin &
water    from acidified sample; chloroform extract; column:                                  McGinnis
         rotary evaporation     silica gel; mobile phase:                                    (1980)
                                cyclohexane-acetic acid and
                                other solvents

Surface  Diethyl ether          Direct HPLC analysis          UV215    20 g/litre   > 80%   Ivanov &
water    extraction; evapor-                                                                 Magee
         ation; dissolution in                                                               (1980)

Surface  Chloroform extraction  Direct analysis in double     Absorp-  5 - 10        92-     Carr et
water    from acidified         beam UV spectrophotometer     tion     g/litre      102%    al. (1982)
         sample;NaOH extraction                               (320 nm)

Table 5.  (contd.)
Medium   Sampling method        Analytical method             Detec-   Detection     Reco-   Reference
                                                              tion     limit         very
Surface  Concentration by       GC analysis (no deriviti-     EC       0.01          95     Rbelt et
water    extraction, ads-       zation); column: Carbowax              g/litre      3%      al. (1982)
         orption, rotary        20 M plus phosphoric acid;
         evaporation            confirmation by MS

Surface, Addition of Na2HPO4    Extraction and derivitzation  EC       1 ng/litre    98-     Abrahams-
waste,   buffer solution        by adding hexane containing                          100%    son & Xie
drinking-(for acid waste water  internal standard (2,6-dibro-                                (1983)
water    pH adjustment to 7     mophenol) and acetic anhy-
         with NaOH              dride directly to sample;
                                GC analysis

Water    Samples prepared from  HPLC analysis with isocratic  UV280    21 ng         ns      Buckman et
         stock solutions in     elution of various substitu-                                 al. (1984)
         acetonitrile           ted phenols


Wood     Chloroform extraction  TLC analysis on silica gel    UV       0.06 g       ns      Henshaw et
         from wood shavings     plates; developing solvent:                                  al. (1975)

Wood-    Soxhlet extraction     Derivatization with diazo-    EC       ns            30-70%  Levin &
dust     with ether ether;      methane; GC analysis                                         Nilsson
         evaporation; dissol-                                                                (1977)
         ution in acetone;
         TLC separation;
         hexane elution

Lumber   Pulverization of wood  HPLC analysis; column: Sphe-  UV230    0.1 g/cm2    ns      Daniels &
(sur-    sample; extraction     risorb-ODS; mobile phase:                                    Swan
face     with acetonitrile      water-acetonitrile-acetic                                    (1979)
treated) containing internal    acid
         standard; ultrasonic

Table 5.  (contd.)
Medium   Sampling method        Analytical method             Detec-   Detection     Reco-   Reference
                                                              tion     limit         very
Sawdust, Extr. with acetic      TLC analysis; different sol-  Colour   2 mg/kg       ns      Ting &
wood-    acid-methanol; evap-   vent systems; sprayed with    reaction                       Quick
shavings oration; conversion    tetrabase reagent                                            (1980)
         to chloranil in warm
         nitric acid

 Various materials

Toy      Soxhlet extraction     Direct GC analysis; confirm-  FIDi     1 - 4 mg      70-     von
paints   with acetone; concen-  ation by TLC analysis                  /litre        100%    Langeveld
         tration by evaporation                                                      (1975)

PCP      Dioxane extraction     HPLC analysis; column: Bon-   UV254    ns            97%     Hayes
formula-                        dapakC18; mobile phase:                                      (1979)
tions                           methanol/PIC A (paired ion
                                chromatography A reagent)
                                and water/PIC A

Sedi-    Homogenization;        Derivatization: pyrolytic     EC       0.5 - 25      92.8-   Butte et
ment,    toluene extraction     ethylation with triethyl               g/kg         97.6%   al.
clams    from acidified sample  sulfonium-iodide; GC anal-                                   (1983)
         containing 2,4,6-      ysis; confirmation by MS
         tribromophenol as
         internal standard

Table 5.  (contd.)
Medium   Sampling method        Analytical method             Detec-   Detection     Reco-   Reference
                                                              tion     limit         very
Tallow   Vortex mixing; auto-   Derivatization with diazo-    EC       1 g/kg       80-     Lee et
         mated gel permeation   methane; Florisil-column;                            107%    al.
         chromatographic clean- GC analysis; confirmation                                    (1984)
         up; rotary evapora-   with MS
         tion; solution in 

Indus-   Hexane extraction      Derivatization with penta-             0.1 pg        ns      Sha &
trial    (for starch: after     fluorobenzyl bromide; GC      EC                             Duffield
starch,  steam distillation)    analysis and negative ion                                    (1984)
surface                         chemical ionization MS        MS
water                           (NICI-MS) analysis
a   EC = electron-capture detector.
b   UV = ultraviolet.
c   ns = not specified.
d   GC = gas chromatography.
e   HPLC = high-performance liquid chromatography.
f   MS = mass spectrometry.
g   TLC = thin-layer chromatography.
h   SIM = selected ion monitoring.
i   FID = flame ionization detector.
j   NICI = negative ion chemical ionization.
    The determination of PCP is based on the distinctive properties 
of this substance: steam distillation is possible because of its 
volatility; its acidic behaviour is used in extracting it into a 
base and in ion-exchange chromatography; the electro-positive ring 
reinforces selective chromatographic adsorption and the absorption 
of ultraviolet radiation; finally, the reactivity of PCP with 
certain organic compounds to form esters, ethers, and coloured 
derivatives is of great importance for its detection and 
measurement (Crosby et al., 1981). 

    Most of the analytical methods used today involved 
acidification of the sample to convert PCP to its non-ionized form, 
extraction into an organic solvent, possible cleanup by back-
extraction into basic solution, and analysis by gas chromatography 
or other chromatographic methods as ester or ether derivatives.  In 
the following section, the sampling and analytical methods is 
described as reviewed mainly by Bevenue & Beckman (1967), Gebefuegi 
et al. (1979), and Crosby et al. (1981).  In addition, the more 
recently published methods for PCP determination in various 
matrices are summarized (Table 5). 

2.5.1.  Sampling methods

    In principle, the sampling techniques summarized by Bevenue & 
Beckman (1967) are still the methods of choice; more recent methods 
are included in Table 5. 

    The first step in preparing a sample consisting of a solid 
material is a thorough pulverization or homogenization in special 
mills or blenders.  Maceration of the sample in a blender with an 
organic solvent is more rapid than Soxhlet extraction and similar 
efficiencies can be achieved with both procedures (Bruns & Currie, 

    For cellulose materials, adhesives, agricultural commodities, 
biological tissues, and water, an initial extraction with dilute 
sodium hydroxide solution at room temperature for several hours, 
followed by acidification and steam distillation may be preferable.  
For samples that contain components strongly complexed with PCP, 
such as soybean oil, treatment with hot concentrated sulfuric acid 
is recommended prior to steam distillation.  Liquid-liquid 
partitioning or distillation of the filtered extract at the boiling 
point of water may also be used to isolate PCP (Bevenue & Beckman, 

    When alkaline soil extracts are acidified, gel formation can 
occur at pH values lower than 6, resulting in interference with the 
extraction of PCP.  According to Renberg (1974), proper separation 
is possible if the acidic substances are bound, under alkaline 
conditions, to an anion ion exchanger. 

    When analysing liquid materials, particularly urine samples, 
the sample should first be hydrolysed by heating the acidified 
urine to free the PCP moiety of its sulfate and glucuronide 
conjugates (Edgerton & Moseman, 1979; Drummond et al., 1982; Butte, 

1984).  Enzymatic hydrolysis is questionable, because the metabolite 
tetrachlorohydroquinone strongly inhibits the enzyme 
beta-glucuronidase (Ahlborg et al., 1974). 

    For determining the PCP content of air several possible 
sampling procedures are described by Gebefuegi et al. (1979) 
including: absorption in liquids, such as potassium carbonate 
(K2CO3) solution or ethylene glycol; adsorption on activated 
charcoal or silica gel; freezing and condensing by sucking the air 
through cooling traps; or derivatization by phenolate formation in 
alkaline solution.  By pumping high volumes of air through the 
sample-collecting device, PCP is concentrated in the collector, 
thus enhancing the detection limit. 

    Concentration is also required for other matrices with 
relatively low PCP contents.  For water samples, procedures used 
involve the separation of PCP from the water by distillation, 
sublimation, freeze-drying, adsorption, and extraction (Rbelt et 
al., 1982).  The extraction solvents, in turn, are concentrated by 
distillation or evaporation. 

    Only a few investigators have used internal standards, adding 
specific substances to the samples to check for completeness of 
recovery during the extensive solvent extractions and manipulative 
steps required.  Drummond et al. (1982) used 3,5-dichloro-2,3,6-
tribromophenol, while Needham et al. (1981) incorporated 2,4,6-
tribromophenol, and Hargesheimer & Coutts (1983) spiked the samples 
with 4,6-dibromo- o-cresol. 

    Most recovery data given in Table 5 were obtained by spiking 
samples with known amounts of PCP and carrying them through the 
entire analytical procedure.  Ernst & Weber (1978a) used 14C-PCP 
for this purpose.  To check the efficiency of acetylation, Rudling 
(1970) compared spiked samples with a pentachlorophenyl acetate 
standard.  According to NIOSH (1978), an appropriate correction 
factor should be used if recovery of PCP in air samples is less 
than 95%. 

    Using the analytical method of Erney (1978) (Table 5), Zimmerli 
et al. (1980) found that only about 8% of "endogenous" PCP was 
extractable from raw bovine milk, though 82.5% of known amounts of 
PCP added had been recovered on average.  A complete extraction was 
only achieved by acid or alkaline pretreatment of the milk (cf., 
Lamparski et al., 1978) (Table 5), which probably releases the PCP 
bound to proteins. Zimmerli et al. (1980) concluded from this 
finding that recovery data may indicate values that do not 
correspond to the true recovery. 

2.5.2.  Analytical methods

    Earlier methods, which have been thoroughly reviewed by Bevenue 
& Beckman (1967), were based on the formation of coloured 
derivatives from the reaction of PCP with either nitric acid or 4-
aminoantipyrine.  Other reagents commonly used in this respect are 

 p-nitraniline, sulfanilic acid, and 3-methyl-2-benzenethiazoline-
hydrazine (Koppe et al., 1977).  As already mentioned, these 
colorimetric or spectrometric methods are not very specific and 
comparatively insensitive, and therefore only suitable for pure 
solutions or for production and routine controls.  They may be of 
some importance in determining total phenolics, for example, in the 
monitoring of levels of phenolics in surface and waste waters. 
However, comparative studies, in which 45 laboratories within the 
European Communities participated, revealed that photometric 
procedures gave rather different results, depending on specific 
laboratory conditions (Sonneborn, 1976; Rbelt et al., 1982).  
According to Crosby et al. (1981), colorimetric or 
spectrophotometric procedures achieve a sensitivity that is, at 
best, in the low ppb-range (1:109). 

    Gas chromatography, particularly when combined with an 
electron-capture detector, substantially lowers the detection 
limits to the ppt-range (1:1011 - 1:1012) and is therefore the
preferred method today.  Very few investigators have applied direct
gas chromatography after the extraction procedures.  To reduce peak
tailing, derivatization of PCP with appropriate compounds prior to
analysis is preferred.  Diazomethane is most commonly used to
produce the methyl ether.  As shown in Table 5, this method, which
is based on the work of Bevenue et al. (1966), has been used to
determine PCP in a variety of matrices including blood, urine,
fish, soil, and water.  According to Crosby et al. (1981), it is
an official method for regulatory analysis in the USA.  The
procedure for measuring PCP in blood and urine samples as
recommended by the National Institute for Occupational Safety and
Health (NIOSH), USA, is described by Eller (1984a,b). 

    Other alkyl ethers have been produced as derivatives of PCP, 
including the ethyl, propyl, 1-butyl, isobutyl, amyl, and isoamyl-
PCP (Cranmer & Freal, 1970).  Besides the potential health risk 
incurred when using hazardous reagents such as diazomethane or 
dimethyl sulfate, the alkylation method is subject to interferences 
from other compounds with active H-atoms, e.g., carboxy acid 
herbicides such as 2,4-dichloro-and 2,4,5-trichlorophenoxyacetic 
acid (Chau & Coborn, 1974; Crosby et al., 1981).  These drawbacks 
are avoided by the acetylation of PCP with acetic anhydride to give 
acetyl-PCP as reported by Rudling (1970), Chau & Coborn (1974), and 
other research workers (Table 5). 

    Several techniques, other than gas chromatography, have been 
used in connection with electron-capture detection. These include 
thermal conductivity and microcoulometric detectors (Bevenue & 
Beckman, 1967), thin-layer chromatography (TLC), gas chromatography 
in connection with mass spectrometry (MS), and high-performance 
liquid chromatography (HPLC) equipped with UV detectors.  In 
particular, the last two methods have become more and more 
prevalent as reflected by Table 5.  In many cases, mass 
spectrometry has been used to confirm the identity of PCP peaks 
determined by EC detectors.  Dougherty & Piotrowska (1976a) and 
Kuehl & Dougherty (1980) screened environmental and tissue samples 
for PCP using negative chemical ionization (NCI) mass spectrometry.  

This method provides a sensitivity of detection comparable to GC-
ECD analysis.  Moreover, it can be used for compound 
identification.  Since both of these methods require an extensive 
amount of pretreatment, a procedure had to be adopted for PCP 
determination by which samples could be measured simply and 
precisely, without the tedious extraction and formation of 
derivatives needed for the other methods.  High-performance liquid 
chromatography offers these advantages, as using this method direct 
determination of PCP is possible, giving peaks of constant height 
and high resolution.  Comparative GC-ECD and HPLC analyses of 
mushrooms conducted by Schnhaber et al. (1982) resulted in similar 
detection limits (Table 5). 

    Detection limits depend not only on the sensitivity of the 
detection systems, but also, to a great extent, on the volume of 
the sample.  The detection limits given in Table 5 refer to the 
smallest amounts of PCP detectable using the procedure and sample 
size described by the authors.  In many cases, it would be possible 
to lower the detection limit by taking larger samples, particularly 
in the case of gaseous and fluid matrices. 

    Analytical interferences may become a problem in PCP analysis 
for residues, particularly at low measurement levels.  Bevenue & 
Ogata (1971) reported errors during the determination of PCP in the 
picogram range, because of analytical-grade reagents such as sodium 
hydroxide.  Arsenault (1976) observed an apparent contamination of 
samples with PCP from the general laboratory atmosphere.  However, 
measuring blank samples as controls and purifying reagents should 
exclude false data.  For example, Dietz & Traud (1978b) distilled 
the extraction solvent diethyl ether to remove the antioxidant BHT 
(2,6-di- tert-butyl-4-methyl-phenol).  Similarly, the authors 
recommended the distillation of dioxan prior to its use as 
extraction solvent; otherwise, some volatile impurities could 
interfere with the measurement of PCP. 

    Substances interfering during gas chromatography may cause more 
of a problem.  These include chloronaphthalenes, polychlorinated 
biphenyls (PCBs), pesticides such as diuron, and  p-methoxytetra-
chlorophenol.  Arsenault (1976) therefore questioned the GC-ECD 
method in the g range.  In a thorough study on phenolics in water 
(Rbelt et al., 1982), derivatization was omitted because non-
specific reactions might occur in complex mixtures, e.g., in 
polluted waters.  The working group achieved best results in terms 
of separation of chlorophenols with a column of 10% Carbowax 20 M 
plus 2% phosphoric acid, the mobile phase being nitrogen enriched 
with formic acid.  The latter was found to prevent tailing 
resulting from adsorption of chlorophenols on the packing material 
of the column.  For quantitative analysis with an unequivocal 
identification, it has been recommended that after gas 
chromatographic separation the carrier gas should be split and 
conducted to both an electron capture detector (ECD), and a flame 
ionization detector (FID), as well as to a mass spectrometer (MS). 


3.1.  Natural Occurrence

    Arsenault (1976) hypothesized the existence of a natural 
background level of PCP or analytically similar compounds.  He 
suggested this on the basis that paramethoxytetrachlorophenol, a 
metabolite of a fungus, could interfere with the GC-EC analysis of 
PCP, because of its similar molecular size, shape, and retention 
time.  The hypothesis of a natural background level of PCP has not 
been examined further.  Unsuccessful attempts to produce higher 
chlorophenols by enzymatic conversion (Siuda, 1980) suggest that 
sources of environmental PCP are exclusively related to human 

3.2.  Man-Made Sources

3.2.1.  Industrial production  Manufacturing processes

    PCP was first synthesized by Merz & Weith (1872) using a 
similar preparation method to that currently used during commercial 
production (Prager et al., 1923).  The use of PCP as a wood 
preservative started in the late 1930s (Doedens, 1964). 

    PCP is produced by one of two methods: direct chlorination of 
phenols and hydrolysis of hexachlorobenzene.  The direct 
chlorination is carried out in two steps.  First, liquid phenol, 
chlorophenol, or a polychlorophenol is bubbled with chlorine gas at 
30 - 40 C to produce 2,4,6-trichlorophenol, which is then 
converted to PCP by further chlorination at progressively higher 
temperatures in the presence of catalysts (aluminum, antimony, 
their chlorides, and others).  The second method involves an 
alkaline hydrolysis of hexachlorobenzene (HCB) in methanol and 
dihydric alcohols, in water and mixtures of different solvents in 
an autoclave at 130 - 170 C (Melnikov, 1971).  In the Federal 
Republic of Germany, PCP is synthesized by means of stepwise 
chlorination of phenols. Na-PCP was produced until 1984 using 
hexachlorobenzene hydrolysis; now, it is produced by dissolving PCP 
flakes in sodium hydroxide solution (BUA, 1986).  In the USA, the 
general reaction used is the chlorination of phenols (Crosby et 
al., 1981). 

    In addition to the formation of PCP, numerous by-products are 
generated, as reflected by analytical profiles in Table 1. The 
chlorination procedure yields a technical product that usually 
contains a considerable amount of tetrachlorophenols (4 - 12%) due 
to incomplete chlorination reactions.  The formation of 
microcontaminants is favoured by elevated temperatures and 
pressure.  With both manufacturing methods, toxic by-products, such 
as chlorinated ethers, dibenzofurans, and dibenzo- p-dioxins, are 
formed.  In addition, the alkaline HCB hydrolysis method can result 
in the presence of hexachlorobenzene in the resulting PCP (Jensen 
& Renberg, 1973; Plimmer, 1973; Firestone, 1977; Jones, 1981).  Emissions during production

    Some data are available concerning the loss of phenolic and 
nonphenolic compounds into the environment during the normal 
production of PCP or Na-PCP (Umweltbundesamt, 1985). The following 
air emission concentrations (mg/m3) and mass flow values (g/h) were 
reported: PCP 0.7 mg/m3, 9 g/h; tetrachlorophenols 0.2 mg/m3, 0.8 
g/h; trichlorophenols 0.02 mg/m3, 0.04 g/h; hexachlorobenzene 23.9 
mg/m3, 12 g/h; pentachlorobenzene 2 mg/m3, 15.5 g/h; 
tetrachlorobenzene 2.8 mg/m3, 66.5 g/h; OCDD 0.05 mg/m3, 0.04 g/h; 
OCDF 0.02 mg/m3, 0.002 g/h. 

    The annual air emission values resulting from the production 
of approximately 2000 tonnes of PCP or Na-PCP, respectively, per 
annum are given in Table 6. 

Table 6.  Air emissions of phenolic and non-phenolic 
compounds during production (maximum values)a
                       Annual air emissions (kg/year) 
                       during production of:         
                       2000 tonnes     2000 tonnes            
                       PCP/year        Na-PCP/year
PCP                    18              65
Other chlorophenols    9               5
Hexachlorobenzene      -               105
Other chlorobenzenes   1               700
OCDD                   0.2             0.2
a   Adapted from: BUA (1986).

    While no waste water occurs during the production of PCP, the 
annual loss of various compounds resulting from Na-PCP production 
into the waste water was as follows: PCP, 60 kg; OCDD, 0.34 g; 
H7CDDs, 0.1 g; H6CDDs, 0.001 g; OCDF, 0.1 g; H7CDFs, 0.026 g; 
H6CDFs, 0.002 g (BUA, 1986).  Disposal of production wastes

    The volume of contaminated waste water generated during the 
production of Na-PCP is small, because manufacturers and regulatory 
agencies have emphasized efficient process design (Jones, 1981). 

    During the production of approximately 2000 tonnes PCP/year, 
about 8 tonnes of washing methanol, 4 tonnes of activated charcoal, 
and 2 tonnes of other wastes occur.  These wastes, as well as the 
filtration sludge resulting from Na-PCP production, contain 
considerable amounts of hazardous chemicals (Table 7).  They are 
generally disposed of by either storage in underground disposal 
sites (filtration sludge) or incineration at temperatures above 
1200 C (BUA, 1986). 

Table 7.  Phenolic and non-phenolic compounds in the combined 
wastes (PCP production) and filtration sludge (Na-PCP production)
Compound                   Combined wastes    Filtration sludge
                           (kg/year)          (kg/year)
PCP                        1350               900
Other chlorophenols        0.7                nsb
Hexachlorobenzene          ns                 6000
Decachlorobiphenyl         ns                 3400
Decachlorophenoxybenzene   ns                 44
OCDD (OCDF)                0.98               0.67 (0.67)
H7CDDs (H7CDFs)            0.13               0.17 (0.045)
H6CDDs (H6CDFs)            0.013              0.092 (0.015)
P5CDDs (P5CDFs)            0.003 x 10-3       0.016 (0.005)
T4CDDs (T4CDFs)            0.002 x 10-3       0.007 (0.001)
2,3,7,8-T4CDD              ns                 0.001
a   Adapted from: BUA (1986).
b   ns = not specified.

    US EPA (1985) proposed that wastes from the production and 
manufacturing use of PCP should be classifed as acutely hazardous 
wastes, on the basis of the presence of substantial concentrations 
of the carcinogenic congener H6CDD and the chronic toxicity 
potential of PCP itself.  Production levels

    No precise estimates can be made of the total world production 
of PCP and Na-PCP.  According to the data profile of IRPTC (1983), 
90 000 tonnes of PCP per year are produced globally.  The Economist 
Intelligence Unit (1981) estimated world production to be of the 
order of 50 000 - 60 000 tonnes per year, based on the North 
American and European Community output.  However, the production 
figures presented in Table 8 indicate a total production of only 
30 000 tonnes per year. The production, foreign trade, and 
consumption figures given in this summary table can give only a 
rough idea of the true PCP market.  Recent restrictions on the use 
of PCP (section 3.3), a decline in the forestry industry, and the 
increasing use of alternative means of wood preservation have 
probably reduced the demand for PCP over the last few years. 

    The major PCP producers operating in 1980 are shown in Table 9 
together with the plant locations and their capacities.  Some 
additional factories exist in which PCP is mixed or formulated to 
yield special end-use products.  There are also chemical producers 
who sell pure, analytical grade PCP, but do not produce PCP for 
technical purposes.  The Monsanto Company, which had a capacity of 
11.8 kilotonnes in the USA, stopped PCP production in their plant 
at Sauget, Illinois, in 1978 (Jones, 1981).  Dow Chemical closed 
down its manufacturing plant at Midland, Michigan in October 1980 
(Jones, 1984).  Similarly, the only PCP producing plant in the 
United Kingdom, also operated by the Monsanto Company, was closed 
down in the same year (Economist Intelligence Unit, 1981), while 

Reichhold Chemicals Inc., at Tacoma, Washington, USA ceased PCP 
production in 1985.  In the Federal Republic of Germany, the 
production of PCP and Na-PCP was stopped in 1986. 

3.3.  Uses

    The main advantages of PCP and its derivatives are that they 
are effective biocides and soluble in oil (PCP) or water (Na-PCP).  
Few pesticides show a similarly broad efficiency spectrum at low 
cost.  Therefore, PCP and its salts have a variety of applications 
in industry, agriculture, and in domestic fields, where they have 
been used as algicides, bactericides, fungicides, herbicides, 
insecticides, and molluscicides. 

3.3.1.  Commercial use

    In Table 10, the major registered commercial uses of PCP are 
broken down for the United Kingdom and the USA.  Although PCP and 
its derivatives have many uses, by far the major application is 
wood preservation.  Cirelli (1978a), Hoos (1978), and Jones (1981) 
have reported on commercial use patterns in North America.  In the 
USA, about 80% of PCP is used for commercial wood treatment, 6% is 
in use for slime control in pulp and paper production, and 3% 
accounts for non-industrial purposes, such as weed control, fence-
post treatment and paint preservation (Crosby et al., 1981); 
however, the last two cases imply wood treatment as well.  The 
remaining 11% is converted to Na-PCP, which in turn is partly used 
for wood preservation, mainly sapstain control in waterborne 
conditions, e.g., for treating pressboard. Overall, some 95 - 98% 
of American PCP production is used directly or indirectly in wood 
treatment (Economist Intelligence Unit, 1981). 

Table 8.  Production, foreign trade, and consumption of PCP and Na-PCP (tonnes per year)
according to data available from government authorities and producers
             Belgium/    Francea   Germany,      Italya    Nether-    United     Canadac   USAd
             Luxemburga            Federal                 landsa     Kingdoma
                                   Republic ofb  (year     (year      (year
             (year na)e  1979      1979   1984   na)e      na)e       na)e       1981      1977
  PCP        0           1700      2450   1550   0         0          0          1700      20 349
  Na-PCP     0           2800      2100   1750   0         0          0          70

  PCP        150-        insigni-  0      0      250 -     30 -       na         500       na
  Na-PCP     160         ficant    300    0      280       40         na         0         na

  PCP        0           300-      1950   1360   0         0          300        600       approxi-
  Na-PCP     0           700       2150   1710   0         0                     0         mately

  PCP        approxi-    1000      500    190    250-      30-        500        1536      na
  Na-PCP     mately      2500      250    40     280       40                    32        na
a   From: Economist Intelligence Unit (1981).
b   From: BUA (1986).
c   From: Jones (1984).
d   From: Jones (1981).
e   na = not available.
f   Approximately 1% of domestic sales.
Table 9.  Pentachlorophenol producers and their capacities in 1980
Producer                   Country       Plant           Capacity 
                                         Location        (tonnes)           
                                                         (total PCP)
Uniroyal Chemical,a        Canada        Clover Bar,     1800
Division of Uniroyal, Ltd                Alta

Rhne-Poulencb             France        Pont-de-Claix   4500

Dynamit Nobelb             Germany,      Rheinfelden     4000
                           Republic of

Dow Chemical, USAa         USA           Midland,        13 500

Table 9 (contd.)
Producer                   Country       Plant           Capacity 
                                         Location        (tonnes)           
                                                         (total PCP)

Reichhold Chemicalsa       USA           Tacoma,         8100
Inc.                                     Washington

Vulcan Materiala           USA           Wichita,        9000
Company Chemical Division                Kansas
a   From: Jones (1981).
b   From: Economist Intelligence Unit (1981).

    Data from Canada and the Federal Republic of Germany confirm 
the main use of PCP as a wood preservative.  In Canada, about 95% 
of the PCP is used for this purpose (Jones, 1981).  Approximately 
61% of the volume of PCP used in the Federal Republic of Germany in 
1983 was used for wood preservation, while considerable amounts of 
PCP were used by the textile (13%), leather (5%), mineral oil (6%), 
and glue (6%) industries, respectively (Angerer, 1984).  No PCP was 
used in the paint or pulp industry whereas, in 1974, as much as 3% 
or 7%, respectively, were used in these branches.  PCP used on 
textiles is usually in the form of the PCP ester rather than PCP or 

    Pentachlorophenyl laurate (L-PCP) was developed especially for 
application on fabrics (Hueck & LaBrijn, 1960; Bevenue & Beckman, 
1967).  The estimates of L-PCP use in the United Kingdom in Table 
10 are based on a publication from the year 1974 (HMSO, 1974).  
According to an unpublished note submitted to the IPCS by Catomance 
Limited, Hertfordshire, the sole manufacturer of pentachlorophenyl 
laurate in the United Kingdom, the usage pattern in the United 
Kingdom has not changed following the cessation of production of 
PCP in 1978.  However, most of the PCP ester used there today is 
said to be for domestic timber preservation; the use of L-PCP for 
textile preservation is supposed to be mainly confined to tropical 
or semi-tropical countries. 

    In the USSR, PCP is used for the preservation of commercial 
timber, paints, varnishes, paper, textiles, ropes, and leather 
(IRPTC, 1984). 

    Na-PCP is also used to inhibit algal and fungal growth in 
cooling tower waters at electric generating plants (Hoos, 1978); in 
1976, about 30% of the Na-PCP used in Canada was for this purpose 
(Jones, 1981). 

Table 10.  Major commercial (non-agricultural) uses of PCP in the
United Kingdom and the USAa
Use                                                         Active 
 United Kingdom
  Anti-mildew agent in the wool textile industry            L-PCP, Na-PCP
  Mothproofing carried out by dyers and cleaners            L-PCP
  Wood preservation                                         PCP, L-PCP,
  Paint additives                                           PCP
  Antimicrobial (slimicide) agents in paper and board       PCP
  Antifungal agent in textiles other than wool (cotton,
  Flax and jute fabric, ropes, cordage and tentage)         L-PCP
  Cable impregnation                                        L-PCP
  Anti-mildew agent in leather                              nsb
  Fungicide in adhesives                                    Na-PCP
  Bactericide in drilling fluids                            nsb

  Microbiostat for commercial and industrial water cooling  Na-PCP
  Microbiocide for leather                                  K-PCP, PCP
  Microbiocide for burlap, canvas, cotton, rope, and twine  PCP
  Microbiocide and insecticide for wood treatment           PCP, Na-PCP
  Preservative for oil and water-based paint                PCP
  Slime control for pulp and paper                          PCP
  Microbiocide for petroleum drilling mud and flood water   PCP
  Fumigant for shipping-van interiors                       PCP
  Preservative for hardboard and particle-board             PCP
a   From: Crosby et al. (1981).
b   ns = not specified.

    Alterations in the use pattern have taken place during the last 
few years as a result of the increased concern about the potential 
health hazards from PCP and its impurities.  In Japan, the 
production of PCP was 14.5 kilotonnes in 1966 and 3.3 kilotonnes in 
1971, after which production ceased entirely (IARC, 1979a).  In the 
Federal Republic of Germany, 3300 tonnes of total PCP were produced 
in the year 1984, of which 93% was exported, leaving 230 tonnes for 
use in the country (BUA, 1986).  Nine years earlier (1974), 4100 
tonnes of PCP were produced, 60% of which were exported; in 1979, 
84% of the 4503 tonnes produced were sold abroad (Angerer, 1984).  
These figures indicate a drastic decrease in the consumption of PCP 
in the Federal Republic of Germany during the last few years.  In 
Canada, the Federal Republic of Germany, and Sweden, where PCP had 
been heavily used as a slime control agent in the paper mills, the 
use of chlorinated phenols for this purpose was prohibited in 
recent years as a consequence of the discharges, which had toxic 
effects on the aquatic environment.  In Sweden, all use of PCP was 
banned in 1977 (Ahlborg & Thunberg, 1980; Jones, 1981).  The US 
Environmental Protection Agency does not intend to prohibit the use 

of PCP in oil-well water or in pulp and paper mills, provided that 
impermeable gloves are worn during application and that the H6CDD 
content will be reduced to 1 ppm (US EPA, 1984b).  Similarly, the 
use of PCP (including its salts) for wood protection has not been 
cancelled in the USA.  However, the US EPA (1984a) intends to 
establish certain changes in the terms and conditions of 

3.3.2.  Agricultural use

    Significant quantities of PCP were previously used in a number 
of agricultural applications.  These resembled industrial uses in 
that most were to prevent wood decay, in farm buildings, fences, 
and storage facilities (Jones, 1981).  However, PCP or its sodium 
salt have also been used as a herbicide and dessicant for forage 
seed crops, a herbicide for non-food vegetation control, a biocide 
in the post-harvest washing of fruit, and as an insecticide for use 
in beehives, seed plots, and greenhouses (Crosby et al., 1981).  
PCP was formerly used as a herbicide in paddy and upland rice 
fields, particularly in Japan (Kobayashi, 1978; Crosby et al., 
1981).  In addition, PCP and Na-PCP have been approved for a number 
of applications in the food industry, such as biocides in packaging 
materials and glues (Table 11). 

    In the USSR, PCP is applied as a nonselective herbicide and as 
a desiccant on cotton plants.  At least 10 days should lapse 
following cotton plant treatment (IRPTC, 1984). 

Table 11.  Other uses of PCP and its salts as a potential 
source of food contaminationa
Use                                         Specific compound
Slime control on paper and paperboard       K-PCP, Na-PCP
Preservative in can-end cement              Na-PCP
Defoaming agents                            Na-PCP
Paper contacting aqueous and fatty food     Na-PCP
Animal glue for containers                  Na-PCP
Sealing gaskets for containers              K-PCP, Na-PCP
Preservative for wood products              PCP, Na-PCP
Preservative in coatings                    Na-PCP
Rubber antioxidant                          Na-PCP
Preservative for ammonium alginate          Na-PCP
a   Adapted from: Firestone (1973).

    Recently, regulations to limit or even ban some uses of PCP 
have been established in a number of countries.  The Canadian 
government suspended agricultural applications of PCP and Na-PCP in 
mushroom culture, above-ground interior woodwork of farm buildings, 
and as herbicides and soil sterilants (Jones, 1984).  Japan 
restricted herbicidal use of PCP because of its high toxicity to 
fish (Kobayashi, 1979; Crosby et al., 1981).  The paper industry of 
the Federal Republic of Germany and Sweden no longer use PCP in 
packaging paper (Ahlborg & Thunberg, 1980; Angerer, 1984). 

    US EPA (1984b) proposed cancelling the registration of 
pesticide products containing PCP as the active ingredient for non-
wood preservative uses, i.e., herbicidal and antimicrobial uses.  
In addition, PCP-containing wood preservatives for home and farm 
use must not be applied where there may be direct contact with 
domestic animals or livestock or close contact with food or feed 
(US EPA, 1984a). 

3.3.3.  Domestic use

    The largely uncontrolled use of PCP by private individuals is 
almost exclusively related to the treatment of wood, both outdoors 
and indoors.  PCP is the main active ingredient in certain wood 
preservatives for home use, and is added to products such as stains 
and paints.  Although this category of products plays only a minor 
role in the overall PCP market, it has been of particular concern, 
since cases of apparent PCP intoxication after indoor application 
in private homes have been reported (section 5).  As a consequence 
of such incidents, the use of PCP for the preservation of interior 
timber has been banned in Canada (Jones, 1981) and the Netherlands 
(Economist Intelligence Unit, 1981).  Since 1986, the use of PCP as 
a biocide for indoor application has been forbidden in the Federal 
Republic of Germany by government regulatory action (FRG, 1986).  
Furthermore, there is a gentlemen's agreement between the 
government and industry to suspend the use of PCP in wood 
preservatives in general (BUA, 1986).  The US EPA (1984a) intends 
to limit the use of PCP-containing wood preservatives in interiors 
to certain support structures.  This is also true for the indoor 
use of PCP-treated wood.  The sale and use of PCP is restricted to 
certified applicators.  Thus, the domestic use of PCP is not as 
significant as it was some years ago. 

    Other reported applications of PCP include health-care products 
and disinfectants for use in the home, farms, and hospitals.  PCP 
may also be contained in dental-care products (Jones, 1981), 
bactericidal soaps, laundry products, and medical products for the 
skin (Crosby et al., 1981). 

3.3.4.  Use for control of vectors

    The application of Na-PCP to control vectors of pathogens has 
been of some relevance in tropical and subtropical areas. Na-PCP 
has been used as a herbicide to control  Salvinia sp., a host plant 
of  Mansonia mosquitos, which transmit the elephantiasis-causing 
filarias to man (Chow et al., 1955). 

    Na-PCP has also been used for control of the intermediate snail 
hosts of schistosomiasis (Berry et al., 1950; Toledo et al., 1976).  
After World War II, Hunter et al. (1952) proposed Na-PCP as the 
molluscicide of choice for use in Japan.  In China, Na-PCP is still 
in use for this purpose today (Xue, 1986)a. 
a  Personal communication to the Task Group on Pentachlorophenol.

3.3.5.  Formulations

    In the treatment of wood, PCP is usually administered as a 5% 
solution in a mineral spirit solvent, such as No. 2 fuel oil or 
kerosene (Cirelli, 1978a), or methylene chloride, isopropyl 
alcohol, or methanol (Ingram et al., 1981a).  Since PCP is not very 
soluble in hydrocarbon solvents, and tends to migrate to, and 
crystallize on, treated wood surfaces (a phenomenon known as 
"blooming"), formulations may also contain co-solvents and anti-
blooming agents (David, 1985a).  Most commercial formulations also 
contain other chlorophenols, mainly  tetrachlorophenol (Nilsson et 
al., 1978).  The  aim  of such mixtures is to prevent blooming on 
treated wood by lowering the melting point of the chlorophenols.  
An aqueous solution of Na-PCP is used for commercial sapstain 
control (Konasevich et al., 1983). 

    Chlorophenols may be combined with other active components such 
as methylene bisthiocyanate and copper naphthenate in the 
formulation of PCP pesticides (von Rmker et al., 1974). 
Conversely, PCP is added to biocides, the primary active ingredient 
of which is another compound; for example, sodium fluoride 
formulations for wooden poles and posts may contain up to 10% 
technical PCP (US EPA, 1973). 

a   Personal communication, Catomance Ltd, Welwyn Garden City,
    Hertfordshire, United Kingdom.


4.1.  Transport and Distribution Between Media

    Several physical and chemical parameters affect the transport 
and distribution of PCP in soil, water, and air.  Volatilization 
and adsorption are the major mechanisms; leaching and movements on 
surfaces and in air are of minor importance (Jones, 1981). 

4.1.1.  Volatilization

    Volatilization can be an important source of loss of PCP from 
water and soil surfaces as well as from PCP-treated materials.  
Dip- or brush-treating coniferous wood may lead to a 30 - 80% loss 
of PCP, due to evaporation, within 12 months (Morgan & Purslow, 
1973; Petrowitz, 1981). 

    Several factors influence the rate of volatilization of PCP 
from wood.  Ingram et al. (1981b) showed that certain solvents or 
mixtures of solvents may either reduce or increase the 
volatilization of PCP.  Such solvents, as well as resins, are used 
to achieve a timely release of PCP through solubilization and/or 
occlusion, e.g., PCP evaporation was decreased by about 20%, when 
15% of an alkyd resin was added to a wood preservative containing 
5% PCP (Petrowitz, 1981).  Temperature appeared to be the external 
variable that had the greatest effect on volatilization; a rise in 
temperature from 20 to 30 C caused a 3- to 4-fold increase in 
volatilization. Relative humidity and rate of air flow had only a 
minor influence on PCP volatilization from wood.  The loss of PCP 
from pine-wood samples was half as much as that from spruce wood 
samples after 21 days, apparently because pine is much more easily 
impregnated than spruce.  Thus, the depth of penetration of PCP in 
wood, the species of wood, and the process of treatment appear to 
be other external variables influencing diffusion and 
volatilization.  As an example, immersion of small blocks of pine 
sapwood with a 5% PCP solution leads to a PCP loss of 20% after 6 
months compared with only 4%, 9 months following double vacuum 
treatment (Morgan & Purslow, 1973). 

    Evaporation is used for the disposal of PCP in waste water at 
some wood-preserving plants (section 4.4).  Extensive studies on 
the volatilization of PCP from water or soil have not been carried 
out, but Klpffer et al. (1982) studied this process in an aqueous 
solution in the absence of other pathways of removal.  Temperature 
and pH of the solution were the most important factors influencing 
the evaporation rate. Since only the un-ionized form of PCP seems 
to be volatile, at pH 5.1, when 13.2% of the PCP was present as the 
free acid, the 50% residence time was 328 h at 30 C, whereas, at 
pH 6, with more than 98% PCP dissociated to its phenate, a one-half 
residence time of 3120 h was measured.  These findings suggest that 
evaporation of PCP from surface waters with a pH above 6 should be 
quite low. 

4.1.2.  Adsorption

    The extent of adsorption of a pesticide governs its 
biovailability in soil; hence, both the rate of degradation and the 
biocidal activity are likely to be reduced by strong adsorption.  
In addition, though possessing a reduced activity, a highly 
adsorbed compound would exert a prolonged effect (Su & Lin, 1971; 
Choi & Aomine, 1972). 

    pH seems to be the major factor controlling the magnitude of 
PCP adsorption.  Choi & Aomine (1974a) investigated PCP retention 
in a range of soil types, and determined that adsorption was 
maximal in strongly acidic soils, relatively minor in moderately 
acidic soils, and absent in weakly acidic or neutral soils.  Other 
research workers have observed the same relationship between soil 
pH and PCP retention (Green & Young, 1970; Kaufmann, 1976). 

    The organic matter content and surface area of soils exert a 
minor, but significant, effect on PCP adsorption.  Choi & Aomine 
(1974a) found that the magnitude of adsorption decreased in the 
following order: humusallophanic, allophanic, montmerillonitic, and 
halloysitic soils.  This finding confirms the binding of PCP by 
organic matter reported by other authors (Su & Lin, 1971; Choi & 
Aomine, 1972). 

    Under the weakly acidic to neutral conditions characterizing 
most soils, adsorption is likely to exert a minor effect on PCP 
dynamics.  In this regard, it is noteworthy that Choi & Aomine 
(1974b) studied adsorption using hexane as a solvent, because the 
amount of the pesticide sorbed onto soils from aqueous solution was 
too small to determine. 

4.1.3.  Leaching

    Leaching of a chemical through the soil is interrelated with 
factors such as adsorption, water solubility of the substance, soil 
type, moisture, percolation velocity, and pH (Haque & Freed, 1974).  
Thus, the leaching behaviour of PCP will vary, depending on the 
soil under examination. 

    Leaching is an important means of transport for PCP, in some 
instances.  Kuwatsuka (1972) noted that much of the PCP applied to 
flooded rice paddies was carried through the soil in solution, and 
the Weed Science Society of America Herbicide Handbook (WSSA, 1974) 
reported that Na-PCP also leaches readily in soil.  This is 
consistent with the observation that leaching of PCP occurs more 
easily in alkaline soils than in both acidic clay and sandy soils 
(Kaufman, 1976). 

    In addition, substantial quantities of PCP are found in waters 
leaching from contaminated sites.  For example, 2.05 and 3.35 mg 
PCP/litre were detected in groundwater from a wood preservation 
plant near Lake Superior (Thompson et al., 1978), and PCP in the 
g/litre range was detected in water seeping from a landfill 
(Kotzias et al., 1975). 

    Some  in vitro studies have revealed little or no PCP in soil 
leachate (Arsenault, 1976; Weiss et al., 1982b), but these are 
difficult to interpret, as residence times are either extremely 
long, or not reported.  In other percolation tests, PCP did not 
leach in the profile of a brown earth-Lessiv within one month, but 
was detected in the water seeping from a podzol (1.5 mg PCP/litre) 
after two days (Frnzle, 1982). 

    From the sorption and leaching behaviour of PCP, it can be 
concluded that organic matter serves as a reversible storage 
compartment, allowing desorption of PCP at elevated soil-water 
content and, hence, accumulation of PCP in the soil solution and 
eventually, in the groundwater (BUA, 1986). 

    Stranks (1976) stated that PCP does not leach readily from 
treated wood, particularly if applied via an oil carrier. 

4.2.  Biotransformation

4.2.1.  Abiotic degradation

    Both PCP and Na-PCP are subject to abiotic (photochemical) 
degradation in water, organic solvents, and on solid surfaces.  In 
the photolysis pathway (Fig. 2) suggested by Wong & Crosby (1978), 
three types of degradation products occur: (a) lower chlorinated 
phenols, mainly 2,3,4,6- and 2,3,5,6-tetrachlorophenol together 
with trichlorophenols; (b) chlorinated dihydroxybenzenes, primarly 
tetrachlororesorcinal and tetrachlorocatechol; and (c) non-aromatic 
fragments, mostly dichloromaleic acid.  Irradiation of the last 
compound, in turn, yielded carbon dioxide (CO2) and chloride ions. 


    Wong & Crosby (1978, 1981) discovered that photolysis of PCP 
(100 mg/litre) in aqueous solutions took place much faster at pH 
7.3 than at pH 3.3.  The ionized PCP disappeared completely within 
20 h (half-life, 3.5 h), whereas the half-life of the un-ionized 
form was about 100 h.  The increasing rate of photodecomposition 
with increasing pH, reported also by Wang (1965), provides evidence 
of an ionic mechanism, the initial and rate-limiting reaction being 
the photo-nucleophilic replacement of PCP chlorine atoms by 
hydroxyl groups (Crosby et al., 1972). 

    PCP photodegradation proved to be primarily oxidative in the 
studies described.  However, in natural waters, reduction processes 
seem to prevail in an acid, high organic load environment and under 
the influence of organic proton-donors. Wong & Crosby (1981) 
concluded this from the absence of oxidized substances, such as 
dichloromaleic acid, and the detection of reduced products. 

    Gb et al. (1975) and Gb (1981) simulated photochemical 
decomposition in, or on, aerosol surfaces, dust particles etc., in 
the troposphere, using a mercury high-pressure lamp to match 
tropospherical sunlight.  Adsorption of PCP on silica gel resulted 
in markedly accelerated photodecomposition because of the 
bathochromic shift of the maxima of absorption from 210 to 310 nm; 
about 14% of 80 mg solid PCP was mineralized to HCl and CO2 within 
7 days, while, under otherwise identical conditions, 88% of PCP 
deposited on silica gel was decomposed. 

    Photodecomposition of PCP is even accelerated if catalysed by 
semiconductors such as zinc (ZnO) and titanium dioxide (TiO2) in 
aqueous suspensions (Barbeni et al., 1985).  Under direct summer 
sunlight, the half-life of PCP was about 8 min (12 mg PCP/litre 
with 2 TiO2/litre, pH 3).  Under laboratory conditions, the half-
life was 15 min at 45 - 50 C, pH 10.5, and lambda > 330 nm; 
mineralization of PCP was more than 95%. 

    Na-PCP, like its parent compound, is readily photolysed.  Hiatt 
et al. (1960) investigated photodecomposition of Na-PCP as a 
possible factor reducing its efficacy as a molluscicide in South 
African streamwaters.   In vitro exposure to UV radiation (290 - 330 
nm) caused chemical degradation of Na-PCP, which was directly 
proportional to light intensity, and a corresponding loss of 
molluscicidal activity. Similarly, Na-PCP applied to rice paddies 
in order to control barnyard grass ( Panicum crusgalli L.) was 
readily decomposed by sunlight (Kuwahara et al., 1966a).  Aqueous 
solutions of Na-PCP exposed to sunlight broke down to form mainly 
chloroanilic acid and 3,4,5-trichloro-6-(2'-hydroxy-3',4',5',6'-
tetrachlorophenoxy)- o-benzoquinone (Kuwahara et al., 1966a), and 
minor amounts of tetrachlororesorcinol and three benzoquinones 
(Kuwahara et al., 1966a,b; Munakata & Kuwahara, 1969). 

    Field evidence indicates that photolysis is an important means 
of PCP loss  in situ.  In their study of PCP contamination in the Bay 
of Quinte, Lake Ontario, Fox & Joshi (1984) found the proportions 
of 2,3,4,6- and 2,3,5,6-tetrachlorophenol in environmental samples 
to be enriched relative to PCP.  Since these compounds are products 
of the photodegradation of PCP, they suggested that photolysis was 

dominating PCP breakdown. Similarly, Yunker (1981) concluded that 
photolysis was the most important pathway for the removal of 
pentachlorophenate from enclosed marine pelagic enclosures off the 
west coast of Canada. 

    Crossland & Wolf (1985) found evidence that direct photo-
transformation was mainly responsible for the loss of PCP from 
experimental outdoor ponds (50 - 100 g PCP/litre).  They observed 
half-lives for the loss of PCP in the range of 2 - 4.7 days (pH 7.3 
- 10.3; 10 - 21 C); decomposition was most rapid in relatively 
clear water. 

    The formation of PCDDs as a result of photochemical reaction 
has been described.  Crosby & Wong (1976) irradiated Na-PCP in 
aqueous solution.  Traces of OCDD were found, while 2,3,7,8-T4CDD 
was not detectable, presumably because of its rapid photoreduction 
(Crosby et al., 1971).  The photolysis of OCDD yields a variety of 
chlorinated dibenzodioxins with decreasing numbers of chlorine 
atoms (Crosby et al., 1971, 1973; Buser, 1976). 

    This is consistent with the findings of Lamparski et al. 
(1980), who observed H6CDD and H7CDD in the course of photolysis 
studies with wood samples treated with PCP in methylene chloride.  
The OCDD content increased from the initial concentration of 3 mg 
OCDD/kg Dowicide EC-7 (containing low initial PCDD concentrations) 
or non-detectable amounts of OCDD/kg purified PCP (Aldrich Chemical 
Company), respectively, to yield up to about 70 mg OCDD/kg PCP on 
the surface of wood in both PCP specifications, while controls 
stored in the dark showed no increase in OCDD.  Use of a 
hydrocarbon oil as a solvent significantly reduced OCDD formation 
during irradiation to yield 4.4 mg OCDD/kg Dowicide EC-7 or 2.2 mg 
OCDD/kg purified PCP, respectively.  Moreover, OCDD concentrations 
only slightly increased in wood samples treated with a technical 
PCP containing relatively high initial PCDD concentrations (OCDD - 
1100 mg/kg). 

    These results agree with those reported by Cull & Dobbs (1984), 
who found no evidence of the formation of OCDD in technical PCP 
(solvent - hydrocarbon oil) or Na-PCP (solvent - water).  This has 
been attributed to the photolytic destruction and volatilisation 
of OCDD dominating its formation when the initial OCDD 
concentration is relatively high. 

4.2.2.  Microbial degradation

    The microbial degradation of PCP has been studied using natural 
and artificial media with mixed or single microbial cultures.  Lyr 
(1963) demonstrated that fungi were able to attack PCP by means of 
phenol oxidase.  Cserjesi (1967) observed PCP decomposition by 
fungi of the genus  Trichoderma in malt extract solution at a 
concentration of approximately 10 mg/litre.  Similar studies have 
also been carried out with a number of other fungal species (Duncan 
& Deverall, 1964; Cserjesi, 1972). 

    Numerous PCP degrading bacterial strains, which are partly 
capable of using PCP as a sole source of organic carbon, have been 

isolated (Chu & Kirsch, 1972; Kirsch & Etzel, 1973; Watanabe, 1973; 
Suzuki, 1977; Reiner et al., 1978; Edgehill, 1982; Stanlake & Finn, 
1982; Trevors, 1982a). 


    Several pathways of PCP degradation have been suggested. 
Because of the tremendous number of microbial strains, numerous 
metabolites have been identified as degradation products (Table 
12).  The possible steps of PCP decomposition as reported by 
several authors are summarized in Fig. 3.  The major metabolic 
processes degrading PCP or its sodium salt are as follows (Suzuki, 
1977; Kaufman, 1978; Reiner at al., 1978; Murthy et al., 1979; Rott 
et al., 1979): 

    (a)  methylation to yield the methylether of PCP,

    (b)  acylation of the hydroxyl group resulting in
         pentachlorophenol acetate;

    (c)  dechlorination to tetrachlorophenols; and

    (d)  hydroxylation to tetrachlorodihydroxybenzenes.

The metabolites originating from these initial steps are subject to 
further transformations as depicted in Fig. 3. Thus, a number of 
substances may arise, which accumulate to different extents; the 
limiting step is the ring fission to chlorinated aliphatic 
compounds such as tetrachloromuconic acid (Lyr, 1962).  Further 
dechlorination may result in further transformations of the 
aliphatic compounds (Janke & Fritsche, 1978) to form low molecular 
substances such as acetic acid or succinate, which then enter the 
tricarboxylic acid cycle.  Suzuki (1983) reported that 34% of the 
14C resulting from 14C-PCP microbial decomposition was recovered as 
14CO2, the remaining compounds being unidentified 14C-metabolites. 

Table 12.  Metabolites formed by the microbial transformation of PCPa
Substance                            Reference
(1)   pentachlorophenol acetate      Rott et al. (1979)

(2)   2,3,4,5-tetrachlorophenol      Ide et al. (1972); Kuwatsuka &
                                     Igarashi (1975); Murthy et al.

(3)   2,3,5,6-tetrachlorophenol      Ide et al. (1972); Kuwatsuka &
                                     Igarashi (1975); Murthy et al.

(4)   2,3,4,6-tetrachlorophenol      Ide et al. (1972); Kuwatsuka &
                                     Igarashi (1975)

(5)   2,4,5-trichlorophenol          Ide et al. (1972); Kuwatsuka &
                                     Igarashi (1975)

(6)   2,3,6-trichlorophenol          Kuwatsuka & Igarashi (1975);
                                     Murthy et al. (1979)

(7)   2,3,4-trichlorophenol          Kuwatsuka & Igarashi (1975)

(8)   2,3,5-trichlorophenol          Ide et al. (1972); Kuwatsuka &
                                     Igarashi (1975)

(9)   2,4,6-trichlorophenol          Kuwatsuka & Igarashi (1975)

(10)  3,4-dichlorophenol             Ide et al. (1972); Kuwatsuka &
                                     Igarashi (1975)

(11)  3,5-dichlorophenol             Ide et al. (1972); Kuwatsuka &
                                     Igarashi (1975)

Table 12.  (contd.)
Substance                            Reference
(12)  2,3,4,5-tetrachloroanisole     Ide et al. (1972); Rott et al.
      (acetate)                      (1979)b

(13)  2,3,5,6-tetrachloroanisole     Ide et al. (1972); Rott et al.
      (acetate)                      (1979)b

(14)  2,3,4,6-tetrachloroanisole     Engel et al. (1966); Ide et al.
      (acetate)                      (1972); Rott et al. (1979)b

(15)  2,3,5-trichloroanisole         Ide et al. (1972)

(16)  2,4,5-trichloroanisole         Ide et al. (1972)

(17)  3,4-dichloroanisole            Ide et al. (1972)

(18)  3,5-dichloroanisole            Ide et al. (1972)
(19)  3-chloroanisole                Ide et al. (1972)

(20)  pentachloroanisole             Cserjesi & Johnson (1972); Ide et
                                     al. (1972); Kuwatsuka & Igarashi
                                     (1975); Murthy et al. (1979);
                                     Rott et al. (1979)

(21)  tetrachlorocatechol            Suzuki (1977); (Rott et al.
      (diacetate)                    (1979)b

(22)  tetrachlorohydroquinone        Suzuki (1977)

(23)  tetrachlororesorcinol          Rott et al. (1979)b

(24)  tetrachlorohydroquinone        Rott et al. (1979)
      dimethylether (diacetate)

(25)  tetrachlorobenzoquinone        Reiner et al. (1978)

(26)  trichlorohydroxybenzoquinone   Reiner et al. (1978)

(27)  2,3,6-trichlorohydroquinone    Reiner et al. (1978)

(28)  2,6-dichlorohydroquinone       Reiner et al. (1978)

(29)  2-chlorohydroquinone           Reiner et al. (1978)

(30)  14CO2                          Chu & Kirsch (1972); Kirsch &
                                     Etzel (1973); Suzuki (1977)

Table 12.  (contd.)
Substance                            Reference
(31)  Cl-                            Watanabe (1973); Suzuki (1977)

(32)  tetrachloromuconic acid        Lyr (1962)

(33)  beta-hydroxytrichloromuconic   Lyr (1962)
a   Adapted from: Kaufman (1978).
b   Reference refers to acetate form.  Aquatic degradation

    Boyle et al. (1980) studied the effects of dissolved oxygen 
supply, light, pH, and the presence of hydrosoil on the aquatic 
biodegradation of PCP.  Light, high pH, and high oxygen 
concentrations led to the most rapid and complete breakdown of PCP.  
PCP disappeared from the pond water of aquaria at differential 
rates, with half-lives ranging from 12.8 to 18.6 days, except for 
the anaerobic aquarium without hydrosoil (79.8 days).  The absence 
of light and mud associated with low pH and anaerobic conditions 
favoured the persistence of PCP, indicating that the phenolic form 
of PCP is more persistent than the phenate form and that the 
oxidative pathway is the major mechanism for PCP degradation in 
simulated lake environments.  Thus, PCP may be most persistent in 
the deoxygenated hypolimnion of stratified lakes. 

    This effect of oxygen on biotransformation was confirmed by Liu 
et al. (1981), who calculated the half-lives of PCP in aerobic and 
anaerobic metabolic fermentors to be 0.36 and 192 days, 
respectively.  These half-lives are much lower than those reported 
by Boyle et al. (1980), probably because Liu et al. (1981) used an 
acclimatized culture whereas in the other studies natural pond 
water was employed.  This illustrates how important the 
preadaptation of microorganisms is for their capacity to degrade 

    Pignatello et al. (1983) showed that the aquatic micro-flora 
can adapt to PCP and can become the most important factor for 
clearing contaminated surface water of PCP, particularly in deeper 
waters where the photolytic contribution is minimized. 

    Liu et al. (1981) investigated the impact of co-metabolites 
and of different nitrogen sources on PCP biodegradability.  
Peptone, glucose, and the sodium salt of 4-chlorophenol suppressed 
the degradation rate while yeast extracts stimulated PCP 
decomposition; the basis for these various effects is not clear. 

    In a report by Pierce & Victor (1978), levels of PCP in a man-
made lake in Mississippi increased from background levels (0.3 
g/litre) to 150 - 277 g/litre, immediately after an accidental 
overflow from a pole-treatment plant, decreasing to 5 - 16 g/litre 
within 4 months.  Long-term influx of PCP from the contaminated 

watershed and persistence in organically rich sediments (4 - 1518 
g/kg dry weight) were thought to provide a source of long-term 
pollution of the aquatic ecosystem (sections 5.1.4 and 6.5.1). 

    Since anaerobic biodegradation of PCP is relatively slow, PCP 
persists in sediments considerably longer than in water. 
Accordingly, high concentrations of PCP have been measured in river 
and lake sediments (section 5.1.2). 

    The fate of PCP in estuarine sediments was investigated 
following contamination with 11 tonnes of PCP after a ship 
collision (De Laune et al., 1983).  Although the contaminated 
sediments had been removed by vacuuming 2 weeks after the accident, 
as much as 1.6 mg/kg (dry weight) could be detected 1 1/2 years 
later compared with < 5 g/kg at remote sampling points.  
Laboratory studies showed a much faster breakdown under aerobic 
conditions (70% decomposition at pH 8 within 5 weeks) compared with 
anaerobic conditions (10% decomposition). 

    The high persistence of PCP in the sediment has been confirmed 
by studies on the fate of PCP in a bay of Lake Ontario (Canada), 
which has been contaminated by a wood-preserving plant since the 
1940s (Fox & Joshi, 1984).  The rather constant T4CP:PCP ratio 
throughout the core (depth of 15 cm corresponding to the year 1949) 
indicates that almost no degradation of these chlorophenols 
occurred, once they had been incorporated into sediments. 

    Of the possible PCP metabolites, tetrachlorocatechol seems to 
be among the most persistent.  Compared with all other chlorinated 
phenols studied, this substance showed the highest levels in the 
sediment (3.2 - 348 g/kg dry weight) or plankton (108 g/kg wet 
weight) of Finnish lakes contaminated with wood preservatives and 
chlorobleaching wastes (Paasivirta et al., 1980).  Degradation in soil

    As in water, the biodegradability of PCP in soil depends on the 
type and the physiological state of the microorganisms, but several 
environmental factors also influence this process, such as a high 
amount of organic matter or high moisture content, which enhance 
the biodegradation of PCP (Young & Carrol, 1951; Kuwatsuka, 1972).  
Low temperatures (O C, 4 C) have proved unfavourable for the 
growth of  Pseudomonas species and hence their PCP breakdown 
activity, while, at 20 C, PCP (50 mg/litre) was degraded to about 
50% within 8 days (Trevors, 1982a).  Low pH values also reduced the 
microbial breakdown of PCP (Stanlake & Finn, 1982). 

    The effects of oxygen on biodegradation vary: in some 
instances, anaerobic conditions in soils increase the rate of 
degradation, apparently as reducing conditions promote reductive 
dechlorination (Ide et al., 1972).  On the other hand, 
biodegradation in terms of formation of the intermediate 
pentachloroanisole was significantly greater in aerobic than in 
anaerobic soil (Murthy et al., 1979).  An average loss of 88% of 
100 mg PCP/kg from clay soil was detected under aerobic conditions 
(over 160 days at 23 C) compared with only 7% loss under anaerobic 
conditions (Baker & Mayfield, 1980). 

    The half-life of PCP in moist farm soils (initial 
concentration, 100 mg/kg) ranged from 7 to 14 days, depending on 
the soil varieties.  PCP degradation was inhibited by certain 
fungicides and also under submerged conditions (Suzuki, 1983).  
Other half-lives reported are 10 - 70 days, under flooded 
conditions, and 20 - 120 days under upland conditions (Kaufman, 

    Edgehill & Finn (1983) investigated the use of PCP-degrading 
bacteria as a prophylactic measure to decontaminate soil after 
accidental PCP spills or when PCP-treated poles are set up near 
surface waters.  Direct inoculation of acclimated  Arthrobacter 
cells into the soil enhanced the disappearance of PCP at least 10-
fold; the half-life of PCP in the soil incubated at 30 C in the 
laboratory was reduced from 12 - 14 days to about 1 day.  However, 
outdoor trials demonstrated that the efficacy of this measure was 
limited under natural conditions, as thorough mixing of the soil at 
the time of inoculation was required to achieve a 85% reduction of 
the extractable PCP at 12 days compared with only 15 - 30% without 

4.3  Degradation by Plants

    Degradation of PCP may also take place in plants.  Rice plants 
were found to absorb about 3% of the radioactivity of 14C-PCP 
applied on the soil, of which 50% could be extracted, mainly as 
unchanged PCP, 9% as unidentified conjugates, and about 1% as a 
tetrachlorophenol-isomer (Haque et al., 1978). 

    Weiss et al. (1982a) also studied the metabolism of 14C-PCP 
(23 kg/ha) in rice plants.  Rice roots contained 0.14% of the 
applied radioactivity as unchanged PCP, 3.95% as unextractable 
residues, and 1.08% as various metabolites.  The influence of soil 
microorganisms was not excluded, but the authors regarded the 
detection of hydroxylated and methoxylated tetrachlorobenzenes as 
evidence of plant metabolism, because these substances were not 
found in soil (Weiss et al., 1982a,b). 

    The metabolism of PCP was also investigated under aseptic 
conditions using soybean ( Glycine max L.) and wheat ( Triticum 
 aestivum L.) cell suspension cultures in which the isolated 
conversion products could be attributed to the metabolic activity 
of the plant cell cultures themselves (Langebartels & Harms, 1984).  
The beta-D-glucoside of PCP was identified as the main conjugate 
formed by the cell suspensions.  Anisoles and lower chlorinated 
phenols were not detected; however, some PCP was incorporated into 
a non-extractable fraction.  Sandermann et al. (1984) isolated 
polar conjugates from wheat and soybean cell cultures, and 
demonstrated that covalent incorporation of PCP into lignin takes 

4.4  Ultimate Fate Following Use

4.4.1  General aspects

    The amount of PCP entering the environment and its subsequent 
fate can be controlled at point sources where high amounts of PCP 
are used, such as preservation plants.  However, because of its many 
applications, PCP is released into the environment from a number of 
diffuse sources and is subject to transport and transformation in 
different environmental compartments, as outlined in the previous 
sections. The evaporation data cited above (section 4.1.1) suggest 
that a significant fraction of the entire production of PCP will 
ultimately enter the atmosphere. 

4.4.2  Disposal of waste water

    As shown in Table 13, municipal sewage discharges contain only 
low PCP concentrations, whereas effluents from wood-treating 
factories may contain considerable amounts of PCP, depending on the 
intensity and efficacy of treatment measures prior to discharge.  
One method of handling wood preservation effluents in Canada is to 
store waste water on company property and allow it to evaporate, 
which obviously contributes to air pollution.  The disposal of 
waste water is also achieved by incineration (section 4.4.3) and by 
secondary treatment before discharge into the receiving water 
(Hoos, 1978). 

    Most small wood-treatment plants handle wastes by incineration 
or lagooning, while larger manufacturers treat their wastes.  
Primary treatment is often applied when PCP is dissolved in a 
carrier oil: gravity separation is used to recover oil and PCP for 
recycling or treatment, while some plants remove oil droplets or 
wood particles by filtration (Richardson, 1978). 

    Several laboratory and treatment-plant studies have shown that 
PCP can be degraded by activated sludge (Dust & Thompson, 1973; 
Kirsch & Etzel, 1973; Etzel & Kirsch, 1974; Moos et al., 1983; 
Guthrie et al., 1984; Hickman & Novak, 1984).  However, in full-
scale treatment plants, the treatment efficiency is often reduced.  
For example, according to a US EPA survey, 8 out of 14 publicly-
owned treatment plants could not remove any of the PCP load.  Most 
of the removal efficiency of the remaining plants (6 - 87%) was 
attributed to adsorption on solids (Feiler, 1980). 

    Biodegradability strikingly decreases when commercial PCP is 
introduced unless the input concentrations are reduced (Reiner et 
al., 1978).  In the presence of more readily degradable substrates, 
PCP degradation is suppressed. Moreover, activated sludge is not 
usually protected from shock loads, unless acclimatized to PCP 
(Hickman & Novak, 1984). 

    Some other treatment systems appear to be appropriate for the 
treatment of PCP-contaminated waste water, but their suitability 
has not as yet been demonstrated on a large scale.  Degradation of 
PCP in a biofilm reactor only occurred when the microflora was 
attached to solid support material, such as soft-wood bark 

(Apajalahti & Salkinoja-Salonen, 1984; Salkinoja-Salonen et al., 
1983, 1984).  PCP concentrations exceeding 1 mmol (266 mg/litre), 
and also some toxic solvents, such as chloroform, inhibited PCP 

Table 13.  Levels of PCP in industrial and municipal discharges in
different countries
Country    Type of waste water          PCP               Reference
Canada     Effluents from wood          0.6               Environment
           preservation industry at     225               Canada (1979)
           4 sites in British           NDa
           Columbia                     2760

Canada     Industrial and municipal                       Garrett (1980)
           discharges in the Greater
           Vancouver Area:
           - average from 22 sites      5.1
           - range                      (0.2 - 42.5)
           - drainage ditches           6000

Denmark    Municipal sewage                               Folke & Lund
           - influents                  0.2 - 0.7         (1983)
           - effluents                  0.1 - 2.4

Germany,   Effluents from sewage        20 - 680          Dietz &
Federal    treatment plant receiving                      Traud (1978b)
Republic   waste water from paper mill
           Effluents from various       1 - 130

USA        Municipal sewage                               Buhler et al.
           - influents                  1.4 - 4.6         (1973)
           - effluents                  1 - 4.4

USA        Samples from wood-treating                     Ervin &
           factories                                      McGinnis
           - untreated waste water      17 000 - 32 000   (1980)
           - treated waste water        160 - 75 000

USA        Effluents from wood-         25 000 - 15 0000  Thompson &
           treatment factories                            Dust (1971)
a   ND = not detectable.

    Hakulinen & Salkinoja-Salonen (1982) reported on the efficiency 
of a fluidized bed reactor in removing chlorophenols from pulp and 
paper industry bleaching effluents.  Chlorophenols including PCP 
were completely mineralized in the anaerobic reactor.  The aerobic 
part of the system served as an after treatment unit to remove the 
remaining organic load. 

    Adsorption on to activated carbon has also been used in 
treating contaminated waste waters; removal of PCP approaches 100% 
using this method (Richardson, 1978). 

4.4.3  Incineration of wastes

    As considerably increased amounts of PCDDs can be emitted 
during the combustion of PCP-treated material compared with 
untreated samples (section 2.2.1), the incineration of PCP-
containing wastes is problematical.  Since temperature of burning 
and the residence time cannot be controlled in the fire-places of 
private homes, the incineration of wood treated with chlorophenols 
is a potential source of PCDD/PCDF emission.  Moreover, accidental 
burning of chlorophenols can lead to considerable emissions of 
these compounds: Kauppinen & Lindroos (1985) estimated that the 
burning of 100 kg chlorophenol formulation during a saw-mill fire 
would result in 20 g of PCDDs. 

    According to Powers (1976), "the complete and controlled high 
temperature oxidation coupled with adequate scrubbing and ash 
disposal facilities offers the greatest immediate potential for the 
safe disposal of concentrated pentachlorophenol".  The destruction 
of PCP in treated wood in a controlled air incinerator was achieved 
with efficiencies greater than 99.99% at combustion temperatures of 
between 916 and 1032 C (Stretz & Vavruska, 1984).  The analytical 
results showed no evidence of T4CDD or T4CDF, both in the hot zone 
between primary and secondary chambers and in the offgas, at 
detection limits of 1 ppb or 5 ppb, respectively. 

    There are many other sources of PCDDs and PCDFs from
combustion processes.  The incineration of municipal waste may be 
the largest source of PCDD and PCDF emissions into the environment 
(Ballschmiter et al., 1983; Chiu et al., 1983; Tiernan et al., 
1983).  The various sources of these compounds are discussed in 
more detail in the corresponding reviews on PCDDs and PCDFs, e.g., 
Umweltbundesamt (1985), Karasek & Hutzinger (1986), and in 
Boddington et al. (1985). 

    The thermal conversion of organochlorine compounds, e.g., 
polyvinylchloride and polyvinylidene chloride, can be a source of 
atmospheric chlorophenols including PCP (Ahlborg et al., 1986; 
Dougherty, 1986a). 

    Other common methods of waste disposal such as deep-sea or 
deep-well disposal, landfill sites, or open pits should not be 
considered as a means for disposing of PCP-containing wastes, 
because of the mobility of PCP (Powers, 1976; Crosby et al., 1981). 

a  Personal communication to the Task Group on Pentachlorophenol.


5.1.  Environmental Levels

5.1.1.  Air

    While PCP concentrations in the air at industrial sites and in 
rooms contaminated with PCP have been reported (section 5.2), there 
is apparently little information on PCP levels in the ambient air. 

    Cautreels et al. (1977) sampled airborne particulate matter 
near La Paz, Bolivia, at an altitude of 5200 m and in a residential 
city area of Antwerp, Belgium.  At a detection limit of 0.02 ng/m3, 
the atmosphere of the Bolivian mountain rural area contained 0.25 - 
0.93 ng/m3 and that of the Antwerp urban area 5.7 - 7.8 ng/m3 air, 
respectively.  More recent analytical results (Bundesamt fr 
Umweltschutz, 1983) showed PCP air concentrations ranging between 
0.9 and 5.1 ng/m3 in Switzerland. 

    The ubiquitous occurrence of PCP in ambient air can also be 
shown from rain water and snow analyses.  Rain water collected in 
Canada (Jones, 1981), Hawaii (Bevenue et al., 1972) and West Berlin 
(Rosskamp, 1982) contained between 0.002 and 0.3 g PCP/litre.  
Water melted from snow in southern Finland revealed PCP 
concentrations of 0.15 and 0.98 g/litre, respectively.  PCP 
fallout as calculated from Finnish snow samples ranged from 1.49 to 
136.0 g/m2 (Paasivirta et al., 1985). 

5.1.2.  Water and sediments

    Levels of industrial and municipal discharges in different 
countries are shown in Table 13 (section 4.4.2).  Municipal sewage 
discharges contain PCP concentrations at levels comparable with 
those in surface waters.  However, wood-treating factories may 
contribute substantially to the PCP load in surface waters, which 
ranges from non detectable to 10 500 g PCP/litre (Table 14), 
depending on the extent of pollution by different sources. 

    The majority of the water samples analysed for PCP contained 
less than 10 g/litre, most contained less than 1  PCP/litre.  The 
extreme PCP levels of up to 10 500 g/litre reported by Fountaine 
et al. (1976) were found in a highly polluted stream near an 
industrial area in the vicinity of Philadelphia, USA. 

    Ernst & Weber (1978b) calculated the PCP input into the German 
Bight via the river Weser to be of the order of 1000 kg per year, 
assuming an average PCP level of 0.1 g PCP/litre and a water flow 
of 300 m3/second.  Taking an average concentration of 0.5 g 
PCP/litre in the surface waters of the Federal Republic of Germany 
(Foquet & Theisen, 1981), the total load in all surface waters of 
the Federal Republic of Germany was estimated by Fischer (1983) to 
be in the range of 60 tonnes per year, of which 30 - 40 tonnes are 
transported by the Rhine river. 

Table 14.  PCP concentrations in surface waters of different countries
Country    Surface water              PCP (g/litre)     Reference
           and location               (range, mean)
Canada     Fresh-water sites in       trace - 0.30       Environment,
           British Columbia (BC)                         Canada (1979)

           Marine sites in BC         NDa - 7.3

Germany,   Weser river and estuary    0.05 - 0.5         Ernst & Weber
Federal                                                  (1978b)
Republic   German Bight               < 0.002 - 0.026
           Ruhr river                 < 0.1 - 0.2        Dietz & Traud
                                      (0.1)              (1978b)

           Rhine river, Cologne       0.1                Fischer & Slem-
                                                         rova (1978)

Japan      Tama river, Tokyo          0.1 - 0.9          Matsumoto et
                                      0.01 - 0.09        al. (1977)

           Sumida river, Tokyo        1 - 9

           River water, Tokyo         0.18  0.14        Matsumoto
           area                                          (1982)

Nether-    Rhine river 1976           Max.b 2.4 (0.7)    Wegman &
lands      Rhine river 1977           Max. 11.0 (1.1)    Hofstee (1979)
           River Meuse 1976           Max. 1.4 (0.3)
           River Meuse 1977           Max. 10.0 (0.8)

South      124 sampling points        ND - 0.85          Van Rensburg
Africa                                                   (1981)

Sweden     River water downstream     9                  Rudling (1970)
           from pulp mill

           Lake receiving             3

Table 14.  (contd.)
Country    Surface water              PCP (g/litre)     Reference
           and location               (range, mean)
USA        Willamette river           0.1 - 0.7          Buhler et al.

           Highly polluted stream                        Fountaine et
           near Philadelphia                             al. (1976)
           - factory location         4500 - 10 500
           - downstream               49 - 240

           Estuary in the             ND - 0.01          Murray et al.
           Galveston Bay, Texas                          (1981)

           Pond in Mississippi        < 1 - 82           Pierce et al.
           contaminated by waste                         (1977)
           from pole-treatment 
a   ND = not detectable.
b   Max. = maximum values.

    Wong & Crosby (1981) reported PCP concentrations ranging from 1 
to 800 g/litre (average, 227 g/litre) in the surface pond water 
near a local wood-treatment factory and of about 20 g PCP/litre in 
agricultural drainage.  Elevated PCP concentrations were also found 
in groundwater (3.03 - 23.3 g/litre) and surface water samples 
(0.07 - 31.9 g/litre) within saw-mill areas.  Around these sites, 
PCP levels ranged between not detectable and 0.6 g/litre in 
groundwater and between 0.01 and 0.07 g/litre in the water of a 
nearby lake (Valo et al., 1984).  PCP in the g/litre range was 
detected in the water seeping from a landfill (Kotzias et al., 
1975).  A level as high as 3.35 mg/litre was found in groundwater 
from a monitoring well near a wood-preservation factory (Thompson 
et al., 1978). 

    A PCP-monitoring study in water was performed by Rahde & Della 
Rosa (1984, 1986) in a region of the Amazon jungle (Tucurui, 
Brazil).  The construction of a dammed reservoir affected a large 
area (2430 km2) with sawmills and PCP-treated wood.  Water samples 
collected from the main river and its affluents before the flooding 
in 1984 contained between 5 and 14 g PCP/litre.  In 1984-85, after 
the flooding, the area had been covered with about 46 billions m3 
of water, PCP was not detectable at a detection limit of 4 g/litre. 

    In general, the sediments of a water body contain much higher 
levels of PCP than the overlying waters.  At several fresh-water 
and marine sites in British Columbia, Canada, receiving effluents 
from the wood-treatment industry, average PCP levels in the 
sediments ranged from not detectable to 590 g/kg, while the 
corresponding range in the overlying waters was from not detectable 
to 7.3 g/litre (Table 14).  During a 1978 survey of toxic 
substances in the Great Lakes of Canada, sediment samples from the 

Thunder Bay, Marathon, and Michipicoten areas of Lake Superior 
contained averages of 16 900, 7300, and 2300 g PCP/kg dry 
sediment, respectively.  In another study of contamination from a 
wood preservation facility on the Bay of Quinte, Lake Ontario, Fox 
& Joshi (1984) analysed water and sediment samples for PCP.  At a 
site distant from the plant discharge, sediment PCP levels ranged 
from 1 to 61 g/kg dry weight, while surface waters contained only 
0.015 g/litre.  Sediments from the Mississippi lake monitored by 
Pierce & Victor (1978) averaged 364 g/kg dry sediment, compared 
with levels in the lake water of only 0.1 g/litre.  A similar 
distribution was observed in surface waters in the Netherlands 
(Wegman & van den Broek, 1983); sediment samples from Lake 
Ketelmeer, a deposition area for Rhine river sediments, contained a 
median PCP concentration of 8.4 g/kg dry weight, while the 
overlying water contained 0.41 g/litre.  PCP concentrations in 
sediment samples collected in the vicinity of a paper mill 
discharge pipe in a North Sea bight, two years after going out of 
use (Butte et al., 1985) and in Finnish lakes contaminated by wood 
preservatives (Paasivirta et al., 1980) were of the same order of 

    These examples indicate that PCP and Na-PCP adsorb on 
sediments, which concurs with findings from experimental work.  
Strufe (1968) reported a study in which 65% of added Na-PCP 
adsorbed on river mud within 20 h. 

5.1.3.  Soil

    Soil samples, taken at 4 sites in the vicinity of a Swiss PCP-
producing facility (Dynamit Nobel), contained between 25 and 140 g 
per kg (dry weight) at a depth of 0 - 10 cm and between 33 and 184 
g/kg at 20 - 30 cm.  These levels are higher than  the PCP 
concentrations of 35 g/kg (0 - 10 cm) and 26 g/kg (20 - 30 cm) 
determined in soil samples from a "reference site".  The 
simultaneous presence of some PCDDs and PCDFs (maximum values: 
H7CDD, 0.6 g/kg; OCDD, 7.68 g/kg; P5CDF, 1 g/kg at 0 - 10 cm) in 
sample sites near the chemical factory compared to only one 
positive sample (H7CDF, 0.51 g/kg) at the remote site confirmed 
the contamination (Bundesamt fr Umweltschutz, 1983). 

    The soil surrounding Finnish sawmills was found to be heavily 
contaminated with up to 45.6 mg/kg (0 - 5 cm) or 1 mg PCP/kg fresh 
weight (80 - 100 cm) near the treatment basin, up to 0.14 mg/kg in 
the storage area for preserved wood and 0.012 mg/kg outside the 
storage area.  The vertical distribution of chlorophenols including 
PCP explains the ground-water contamination observed (Valo et al., 

    In Canada, soil samples from the former site of a pesticide 
plant contained less than 50 g PCP/kg (Garrett, 1980).  The PCP 
levels in the leachate and in soil in the vicinity of 3 waste-
disposal sites were also in the g/kg range (Kotzias et al., 1975).  
Samples of agriculturally used soils in Bavaria (Federal Republic 
of Germany) contained about 100 g PCP/kg (Gebefuegi, 1981). 

    PCP concentrations in soil samples taken at a distance of 2.5, 
30.5, and 152.5 cm from poles treated with PCP were 658, 3.4, and 
0.26 mg/kg, respectively.  Arsenault (1976) considered the last 
value as a "natural background level", which he derived from the 
blank of 0.2 - 0.4 ppm found in unexposed soil samples.  However, 
such a level seems very high for a substance that does not appear 
to occur naturally.  This high level could be the result of the 
contamination of the soil or of the reagents used for analysis. 

5.1.4.  Aquatic and terrestrial organisms  Aquatic organisms

    Levels of PCP in aquatic organisms from various collection  
sites are listed in Table 15.  No data are available on the 
background levels of PCP in biota.  All sampling sites in Table 15 
were more or less contaminated with industrial effluents.  
Relatively low contamination is reflected by residues of PCP in 
aquatic invertebrate and vertebrate fauna in the low g/kg-range.  
For example, Zitko et al. (1974) found a range of < 0.5 - 4 g 
PCP/kg wet weight in the muscle tissue of different fish species 
(Table 15).  Higher levels were detected in organisms collected in 
surface waters that were thought to be contaminated with wood 
preservatives: up to 2100 g PCP/kg wet weight were found in marine 
fish in British Columbia, Canada (Environment Canada, 1979) and up 
to 6400 g/kg in fresh-water fish from Finnish lakes (Paasivirta et 
al., 1981) (Table 15). Some sediment-dwelling organisms showed the 
highest residues: polychaetes from the Weser estuary contained 
between 103 - 339 g PCP/kg wet weight (Ernst & Weber, 1978a).  
Even higher levels (266 - 133 000 g/kg) were found in clams from a 
North Sea bight, near the end of a waste-water pipe from which 
about 26 tonnes of PCP were discharged into the mud flats until 
1978 (Butte et al., 1985). 

    Residues of PCP in biota associated with toxic PCP water 
concentrations are in the mg/kg range.  Following extensive 
application of Na-PCP as a molluscicide in rice fields in Surinam, 
Vermeer et al. (1974) found 8.1 mg PCP/kg wet weight in dead frogs 
 (Pseudis paradoxa) and between 31.2 and 59.4 mg/kg in three species 
of fish, which were also found dead.  Composite samples of snails 
 (Pomacea glauca) contained, on average, 36.8 mg PCP/kg wet weight. 

    Whole samples of small fish collected from a river in British 
Columbia, Canada, during an accidental fish kill resulting from the 
spraying of hydropoles, had levels of 16.3 mg PCP/kg; two large 
cutthroat trout  (Salmo clarki) contained 10.3 mg/kg (Jones, 1981). 

Table 15.  PCP residues in aquatic animalsa
Organism        Type of   Location of sample    Sample   Concentration   Basis  Reference
                sample                          date     (g/kg)a

  Jellyfish     whole     Gulf of Mexico        1979     0.1 - 1         wet    Kuehl & Dougherty (1980)

  Sponge        whole     Finnish lakes         Summer   1.9 - 13        wet    Paasivirta et al. (1980)
                          contaminated with     1978
                          wood preservatives

   Sagartia      whole     Weser estuary and     1976-77  2.7 - 7         wet    Ernst & Weber (1978a)
   troglodytes             German Bight

  Polychaete    whole                           1978     103 - 339       wet

  Mussel        muscle    Finnish lakes         Summer   1.7 - 5.6       wet    Paasivirta et al. (1980)
                          contaminated with     1978
                          wood preservatives

  Clam          muscle    Marine sites near     Autumn   ND - 12         wet    Environment Canada
  ( Macoma sp.)            wood-preservation     1978                            (1979)
                          factories in British
                          Columbia, Canada

  Clam          whole     Wadden sediment of    1980-81  266 - 133 000   dry    Butte et al. (1985)
   (Mya          (without  Jadebusen, bight of            (median: 800)
   arenaria)     shells)   the North Sea, PCP
                          discharged area until

                          Reference site                 266 - 532

  Crayfish      muscle    Fresh-water sites     Autumn   ND - trace      wet    Environment Canada
  ( Pacifas-               near wood-preserv-    1978                            (1979)
   tacus sp.)              ation factories in
                          British Columbia,

Table 15.  (contd.)
Organism        Type of   Location of sample    Sample   Concentration   Basis  Reference
                sample                          date     (g/kg)a
  Crab          muscle    Marine sites near     Autumn   ND - 20         wet    Environment Canada
   (Cancer                 wood-preservation     1978                            (1979)
   magister)               factories in
                          British Columbia,

  Crab          muscle    Marine sites near     Autumn   trace - 7       wet
   (Cancer                 wood-preservation     1978
   productus)              factories in
                          British Columbia,

  Brown shrimp  whole     Estuary of the        1980     4 - 17          wet    Murray et al. (1981)
   (Penaeus                Galveston Bay area
   aztecus)                of Texas

  Blue crab     soft                                     1.9 - 4.1       wet
   (Calinectes   tissues

  Dwarf squid   whole                                    1.4 - 4.3       wet


  Sculpin       muscle    Marine sites near     Autumn   trace - 84      wet    Environment Canada
  (marine)      liver     wood-preservation     1978     trace - 2100    wet    (1979)
   (Leptocottus            factories in
   armatus)                British Columbia,

  Sculpin       muscle    Fresh-water sites              5 - 100         wet
  (freshwater)  liver     near wood-preserv-             trace - 600     wet
   (Cottus                 ation factories in
   asper)                  British Columbia,

Table 15.  (contd.)
Organism        Type of   Location of sample    Sample   Concentration   Basis  Reference
                sample                          date     (g/kg)a
  Pike          muscle    Finnish lakes         Summer   6.5 - 8         wet    Paasivirta et al. (1980)
   (Esox                   contaminated with     1978
   lucius)                 wood preservatives

  Roach         muscle                                   0.9 - 12.8      wet

  Pike          muscle    Finnish lakes         May      11.9 - 94.3     wet    Paasivirta et al. (1981)
   (Esox                   contaminated with     1980     (maximum 6400)
   lucius)                 wood preservatives

  Pike          muscle    Finnish lakes         Spring/  15.9 - 18.9     wet    Paasivirta et al. (1983)
   (Esox                   contaminated with     Summer
   lucius)                 wood preservatives    1981

  Pike          muscle    Finnish lakes         Summer   8.2 - 17.3      wet    Paasivirta et al. (1985)
   (Esox                   contaminated with     1982
   lucius)                 wood preservatives    
                                                1983     1.2             wet
  Crab          muscle                          1982     9.4 - 41.5      wet
   (Rutilus                                      1983     0.5             wet

  Baltic        muscle                          1983     1.8 - 4.7       wet

  Winter        muscle    Estuaries in New      Autumn   1.8 - 4         wet    Zitko et al. (1974)
  flounder                Brunswick, Canada     1972

Table 15.  (contd.)
Organism        Type of   Location of sample    Sample   Concentration   Basis  Reference
                sample                          date     (g/kg)a
  Cod           muscle                                   0.8             wet

  Sea raven     muscle                                   < 0.5           wet

  Atlantic      whole     Estuaries in New      Autumn   0.5 - 1.3       wet    Zitko et al. (1974)
  salmon                  Brunswick, Canada     1972
   (Salmo salar)           

  White shark   liver                                    10.8            wet

  Flounder      whole     Estuary in the        1980     1.6 - 3.5       wet    Murray et al. (1981)
                          Galveston Bay

  Longnose      whole                                    4.7 - 5.6       wet
a   ND = not detectable.  Terrestrial organisms

    As with aquatic plants, almost no data are available on 
residues of PCP in terrestrial plants.  Grass samples taken in the 
vicinity of a PCP producer at Rheinfelden, Switzerland, contained 
between 67 - 87 g PCP/kg dry weight, comparable to the PCP 
concentration of 87 g/kg found in grass from a reference site 
(Bundesamt fr Umweltschutz, 1983). 

    Reported residue levels in terrestrial vertebrates are mainly 
related to domestic animals exposed to PCP: the tissues and blood 
of cows and calves of dairy herds in the USA showed unquantified 
PCP contamination (Hoeting, 1977).  One herd housed in a PCP-
treated wooden barn had blood-PCP levels of 270 - 570 g/litre (US 
EPA, 1978). 

    Pentachloroanisole, a metabolite of the PCP biodecomposition, 
causes a musty taint in broiler chicken tissues.  It appears that 
the chloroanisole arises through the microbial methylation of PCP 
in wood shavings used as chicken litter (Curtis et al., 1972; Parr 
et al., 1974; Harper & Banave, 1975).  Wood shavings have been used 
as litter not only for broiler chickens, but also for turkeys, 
ducks, pigs, and cattle. 

    Neidert et al. (1984) found low residue levels of PCP in all 
1072 chicken liver and 723 fat samples examined (most < 0.01 
mg/kg), indicating an overall exposure of poultry to PCP. Only 
0.75% of the liver samples contained PCP levels higher than 0.1 

    In the field study of Vermeer et al. (1974) mentioned earlier, 
PCP was detected in liver samples of birds (0.06 - 0.19 mg/kg wet 
weight) residing in the vicinity of PCP-treated rice fields.  High 
PCP residues were found in the brain (mean, 11.3 mg/kg wet weight), 
liver (46.6 mg/kg), and kidney (20.3 mg/kg) of dead snail kites 
 (Rostrhamus sociabilis), which had probably ingested Na-PCP 
contaminated snails. 

    Only a few data on PCP residues in terrestrial animals, 
apparently not exposed to PCP, have been reported: purple martin 
fledglings from Alberta, Canada, contained 31 g PCP/kg (Jones, 
1981).  The muscle tissue of juvenile starlings, collected from 
their nests in South Finland in 1982 and 1983, contained PCP levels 
ranging from not detectable to 59 g/kg wet weight (mean, 5.9 
g/kg) (Paasivirta et al., 1985).  The pectoral muscles of white-
tailed eagles, also collected in Finland, contained between 14 and 
8571 g PCP/kg wet weight, while levels in eggs ranged from not 
detectable to 25 g/kg.  Eggs of osprey contained between 1 and 803 
g PCP/kg. 

5.1.5.  Drinking-water and food

    PCP concentrations ranging from < 1 to 50 g/litre were 
detected in domestic well water (Oroville, California) (Wong & 
Crosby, 1981).  Buhler et al. (1973) analysed drinking-water 

obtained from the Willamette river (USA).  They found 0.06 g 
PCP/litre in the finished water.  PCP was found at a level of 0.1 
g/litre in one water sample (Dougherty & Piotrowska, 1976b).  
Concentrations of 0.01 - 0.02 g PCP/litre were detected in 
drinking-water in the Ruhr area of the Federal Republic of Germany 
(Dietz & Traud, 1978b).  PCP levels in Florida drinking-water 
supplies ranged from 0.003 to 0.34 g/litre (Morgade et al., 1980).  
Detrick (1977) suggested that the chlorination of phenol in water 
supplies might be responsible for the wide occurrence of PCP. The 
chlorination of 1 mg phenol/litre by 10 mg chlorine/litre is said 
to yield about 0.2 g PCP/litre, which is comparable with the 
levels found in drinking-water.  However, the odour threshold for 
phenol is in the g/litre range, thus low levels of phenol can 
generally be detected in water. 

    Most data on PCP residues in food have been collected in the 
USA, where a number of pesticides, including PCP, have been 
routinely monitored in the FDA Market Basket Survey.  In 1973-74, 
PCP was found in 10 out of 360 composite food samples, at 
concentrations ranging from 10 to 30 g/kg (Manske & Johnson, 
1977).  In 1975, 5.4% of a total of 240 samples were contaminated 
with PCP at 10 - 40 g/kg (Johnson & Manske, 1977).  Values for the 
period 1965-70 are shown in Table 16.  PCP concentrations measured 
in daily diet samples in the Federal Republic of Germany 
(Gebefuegi, 1981) are similar, averaging 16.3 g/kg (range, 2.6 - 
27.5 g/kg).  Krause (1982) found elevated PCP concentrations in 
the food-basket samples of persons applying wood preservatives in 
private homes. Two-thirds of the samples analysed contained between 
2 and 13 g PCP/kg with a median of about 6 g PCP/kg, whereas the 
control samples fell between less than 0.1 and 5 g/kg. 

    Samples of agricultural produce taken by the Alberta Department 
of Agriculture (Canada), consisting mainly of potatoes and raw 
milk, contained PCP levels of less than 10 g/kg.  In isolated 
samples, PCP levels of up to 2700 g/kg occurred, as a result of 
contamination from storage containers made of treated wood (Jones, 

    In southern Ontario, Canada, 45 bovine milk samples collected 
from bulk transports hauling milk were analysed for chlorophenols 
(Frank et al., 1979).  PCP was not detected in whole milk at a 
detection level of 0.1 g/litre. 

    In analysing commercial mushrooms for PCP residues, Meemken et 
al. (1982) found that levels in 11 out of 17 fresh mushroom samples 
exceeded the recommended limit of 10 g/kg set in the Federal 
Republic of Germany for certain food items.  Residues apparently 
originated from the treated wooden cases used for culturing 
mushrooms, which contained up to 3900 mg PCP/kg. 

Table 16.  Average incidence of PCP residues 
in food composites and daily dietary intake of 
PCP in the USAa
Year     Number of     Percent       Daily PCP       
         composites    positive      intake             
         examined      composites    (g/person 
                                     per day)
1965     216           1.4           -b
1966     312           3.3           6
1967     360           2.2           1
1968     360           1.9           1
1969     360           2.8           2
1970     360           nsc           nsc
a   From: Duggan & Corneliussen (1972).
b   < detection limit (1 g).
c   ns = not specified.

    PCP can also enter food during processing, transportation, or 
storage.  Heikes & Griffitt (1980) demonstrated that canned fruit 
and vegetables in Mason jars can be contaminated with PCP due to 
PCP residues in sealing gaskets, lids, and enamel. Levels in the 
jar lid, sealing gaskets, and enamel were as high as 198 g/lid, 
125 mg/kg, and 4.4 mg/kg, respectively. Six fruits and vegetables 
originally free from PCP, contained between 0.29 and 1.1 g/litre 
in the liquid and between 1.4 and 38 g/kg in the solids, after 
being canned and stored for 4 days in contaminated jars. 

    Kroyer et al. (1982) modelled the transfer of PCP from wooden 
storage containers to flour experimentally.  Within 24 h, 
remarkable quantities of PCP can be adsorbed by flour in contact 
with PCP-treated wood: applied wood preservative could be detected 
in the foodstuff at levels ranging from 0.2 to 1 mg PCP/kg. 

    PCP levels in the range of 240 - 1090 g/kg were found in the 
flesh grease from hides treated with PCP.  Collagen material 
derived from hides, pigskin, and decalcified bones is used for the 
manufacture of edible gelatins, and Stijve (1981) detected PCP in 
each of 50 samples of commercially available gelatins tested.  
Products from western Europe and the USA generally contained less 
than 100 g/kg, while those from tropical countries contained from 
1000 to 5000 g PCP/kg.  The US Food and Drug Administration (FDA) 
has proposed prohibiting "the use of animal bones, hides, or skins 
that have been exposed to pentachlorophenol" (Federal Register, 

    A calculated daily dietary intake of PCP for the period 1965-70 
is shown in Table 16.  The values ranging from 1 to 6 g/person per 
day were based on a market-basket survey of 117 retail food items.  
Each market basket represented a 2-week diet, constructed according 
to consumer behaviour.  The foods were prepared as for eating and 
then analysed (Duggan & Corneliussen, 1972).  In another survey 

(Krause, 1982), in contrast to the above food collection procedure, 
samples of complete meals prepared and eaten by different families 
were collected over a period of 3 - 7 days and pooled.  This 
sampling procedure is more realistic, as it takes into 
consideration the fact that food may be contaminated during storage 
in PCP-contaminated rooms.  In fact, in households where PCP-
containing wood preservatives had been applied, meals averaged 6 g 
PCP/kg (2/3 range, 2 - 13 g/kg), while the meals of a control 
group were less contaminated (< 0.1 - 5 g/kg).  According to 
Fischer (1983), the daily dietary intake on the basis of these data 
is 0.1 - 1 g/person per day for people without known exposure and 
6 g/person per day for persons exposed to PCP-treated interiors. 

5.1.6.  Consumer products

    On the basis of the diverse applications of PCP, it would be 
expected that a large number of consumer products contain this 
compound.  Furthermore, PCP from the indoor atmosphere can 
contaminate a number of household items.  However, there are few 
data on PCP levels in consumer products.  In one example, van 
Langeveld (1975) analysed 65 commercial samples of paints used on 
children's toys and found that 14% contained PCP in the range of 
100 - 2700 mg/kg. 

    The Swiss Federal Office of Health (Siegwart, 1983) found PCP 
in various clothes including socks, pantyhose, and insoles, with 
PCP concentrations between 0.015 and 0.96 mg/kg; one insole 
contained 13.2 mg PCP/kg (Siegwart, personal communication, 1986). 

5.1.7.  Treated wood

    Obviously, PCP-treated wood contains substantial quantities of 
the compound itself.  The Ontario Ministry of Agriculture detected 
tetrachlorophenol and PCP in samples of wood shavings used as 
livestock litter in southern Ontario (Jones, 1981); PCP levels were 
as high as 628 mg/kg in fresh litter, but fell off sharply, after 
56 days use to 96 mg/kg or less.  In the United Kingdom, Parr et 
al. (1974) found an average PCP concentration of 12 mg/kg (range, 
1 - 83 mg/kg) in fresh broiler house litter, while spent litter 
contained an average of 0.3 mg/kg.  Curtis et al. (1972) found as 
much as 40 mg PCP/kg in samples of shavings and sawdust.  Levin & 
Nilsson (1977) assayed for tetrachlorophenol, PCP, and several 
contaminants in wood dust from a Swedish  sawmill.  PCP levels in 
dust from wood treated with 2% Na-2,3,4,6-tetrachlorophenol ranged 
from 30 to 100 mg/kg. 

    Analysis of timber samples taken from homes in the Federal 
Republic of Germany, several years after it had been recom-mended 
to avoid the indoor use of PCP, revealed PCP levels ranging from 
0.1 to 615 mg/kg (mean, 35 mg/kg) (Ruh et al., 1984).  This means 
that the timber had either been treated with PCP or that it was 
contaminated.  In this context, it is noteworthy that Ruh & 
Gebefuegi (1984) also analysed wooden material which, according to 
consumer information, was supposed to be untreated.  Only 30% of 
the samples were PCP-free, 40% contained from 0.05 to 0.8 mg 
PCP/kg, and 31% contained from 1 to 20 mg/kg. 

    Untreated wood samples from furniture in a living room  in 
which panelling had been painted with a wood preservative (6% PCP) 
according to instructions, were analysed by Gebefuegi et al. 
(1979). PCP concentrations ranged from 15.5 to 26 mg/kg in the top 
layer (0 - 1.5 mm) and from 2.5 to 7 mg/kg at 3 - 8 mm.  For 
comparison, treated wood samples contained between 1570 and 2754 
mg/kg in the top layer, 612 - 1800 mg/kg in the middle layer (1.5 - 
3 mm), and 117 - 340 mg/kg in the bottom layer (3 - 8 mm).  Freshly 
treated wood surfaces showed PCP concentrations of between 4000 and 
6000 mg/kg. 

5.2.  Occupational Exposure

    A list of potential sources of occupational exposure to PCP is 
presented in Table 17.  However, the actual PCP concentrations that 
workers are exposed to during such industrial or commercial 
activities are rarely measured. 

    Since PCP is extensively used for wood protection and 
preservation, most studies of occupational exposure have been 
conducted in this field of industry.  If the pressure treating 
method is used, respiratory exposure to PCP occurs mainly when the 
door of the pressure vessel is opened and PCP can escape into the 
breathing zone of the worker.  With non-pressure treatment, 
continuous evaporation of PCP into the air takes place, since the 
tanks or vats are open.  With both processes, dermal exposure of 
workers is possible during the handling of the treated wood 
(Williams, 1982).  The polychlorinated impurities in PCP may be 
enriched relative to freshly prepared PCP solution during the 
recirculation of the preservatives (Levin et al., 1976; Lamberton 
et al., 1979).  Hence, during the periodic tank and cylinder 
cleaning processes, much higher exposures to PCP impurities may 
occur than expected theoretically. 

    In Table 20, a number of PCP air concentrations as measured in 
the course of human monitoring studies is shown.  In addition, air 
samples taken at the breathing zone in 11 wood-treating factories 
in the USA ranged from 10 to 510 g/m3 (Todd & Timbie, 1983).  Most 
of the data in Table 20 are below the TWA or MAC value of 500 g 
PCP/m3 (IRPTC, 1983), which has been established by several 
countries.  However, this value is derived "by analogy with other 
compounds of similar action and toxicity in addition to the 
specific available information" (ACGIH, 1980).  With lumber 
treatment, exposure to airborne PCP is generally below 100 g/m3; 
concentrations higher than the TWA value commonly occur during PCP 
or Na-PCP production. 

Table 17.  Potential sources of occupational exposure to 
PCP or its sodium salta
Manufacture and shipping of industrial chlorophenols
Wood-treatment plants
Carpentry and other timber and wood-working
Termite control
Agricultural pesticide application
Industrial cooling towers and evaporative condensers
Treatment and handling of wool
Treatment and handling of burlap, canvas, rope, leather
Paper manufacture
Petroleum and other drilling
Paint and adhesive manufacture and use
Telephone and electrical line work
Dyeing and cleaning of garments
a   Adapted from: Crosby et al. (1981).

    Extremely high occupational exposures have been reported as a 
result of the agricultural use of PCP.  Following PCP application 
on cotton fields over a 2-year period, Demidenko (1969) reported 
that unusually high concentrations of up to 38 000 g PCP/m3 air 
were found where the sprayers were working and that the workers 
exhibited typical symptoms of PCP intoxication (eye and nasal 
irritation, headaches, fatigue).  In the breathing zone of the 
workers formulating the spray, air-PCP levels of 320 g/m3 were 
measured.  Pilots in spraying aircraft were exposed to an average 
of 880 g PCP/m3.  Air levels, at a distance of 10 - 50 m from the 
treated field, varied from 960 to 4400 g/m3. 

    The magnitude of PCP exposure depends particularly on the 
methods used in handling the chemical, and on measures to minimize 
PCP levels in the work-place.  According to Wood et al. (1983), 
automated processes and closed systems have greatly reduced the 
exposure level in large-scale manufacturing and wood-treatment 
factories.  However, in small-scale operations, overexposure may 
occur through inadequate control measures.  In addition to 
measurements of ambient PCP levels during industrial or 
agricultural use, several attempts have been made to estimate 
exposure on the basis of urine-PCP levels in workers involved in 
the direct and controlled application of PCP (section 5.4). 

5.3.  General Population Exposure

    Because of the widespread use of PCP products, the general 
population also comes into contact with this substance.  PCP has 
been detected at the g/litre level in the urine of people, not 
occupationally exposed, in widely different groups and locations 
(section 5.4).  It is likely that this wide-spread occurrence of 
PCP in human populations results from PCP intake or from the 
metabolism of other chlorinated compounds rather than from the 
natural occurrence of PCP. 

    Some possible sources of non-occupational exposure to PCP in 
the home, work, and outdoor environments are listed in Table 18.  
In such cases, the general population can be incidentally exposed 
to PCP-treated items such as textiles, leather, and paper products 
(Jones, 1981, 1984).  In addition, a variety of consumer products 
including food may contain PCP, though no direct PCP application 
has been involved, if they are stored in PCP-treated wooden 
containers or exposed to PCP in the atmosphere of rooms where 
woodwork has been treated with PCP.  This is consistent with the 
laboratory studies of Morgan & Purslow (1973), Ingram et al. 
(1981a,b), and Petrowitz (1981) who observed considerable losses of 
PCP from wood samples (section 4.1.1). 

Table 18.  Some possible sources of non-occupational 
exposure to PCP or its sodium salta
Use of retail trade pesticide products containing PCP
  (for wood preservation, termite control, etc.)
Use of PCP-treated lumber for construction of dwellings
Smoke from sawmills and burning scrap lumber
Sawdust (fuel, floor covering, particle-board, etc.)
Burlap, canvas, and rope
Wool and other textiles
Leather products
Paper products
Contact with adhesives, paint, and painted surfaces
Used telephone poles and railroad ties
Ornamental wood-chips
Fat trimmed from treated hides (used as feed additive)
Water treated for mollusc control
Contaminated food
a   Adapted from: Crosby et al. (1981).

    Wood preservatives containing PCP or its sodium salt have been 
widely applied in the domestic field both indoors and outdoors.  In 
some countries, the indoor use of PCP-containing wood preservatives 
has been regulated by government authorities (section 3.3.3).  
Cases of PCP intoxication in persons residing in treated houses 
have roused public concern as to whether the general population 
might be endangered by domestic applications of PCP and have led to 
investigations of PCP levels in rooms and the evaluation of 
potential health effects. 

    In one instance, volatilization of PCP within a room from 
treated interior wood led to PCP deposition on untreated wood, 
furniture, and curtains at levels of between 23 and 26 mg/kg and to 
residues (mg/kg) on other household items such as carpets, books, 
oil paintings, and cassette tapes.  The air levels of PCP varied 
between 50 and 100 g/m3 in the living room of the house, which had 
been under examination since 1974, because of reported PCP 
intoxications (Gebefuegi et al., 1979). 

    Krause & Englert (1980), Aurand et al. (1981), and Krause 
(1982) reported the results of a survey in the Federal Republic of 
Germany, which included the analysis of indoor air samples in 104 
homes and of the urine of more than 1000 persons.  Depending on the 
intensity of, and the time elapsed since, indoor PCP application, 
PCP concentrations in the air ranged from not detectable to about 
25 g/m3, frequently from 2 to 10 g/m3.  The median value of 5 g 
PCP/m3 is 1000 times higher than the outdoor air levels found in 
residential areas (section 5.1.1).  For comparison, indoor air 
levels of PCP in houses of a control group without known exposure 
were generally below the detection limit of 0.1 g PCP/m3. 

    Air concentrations of PCP of between 1 and 10 g/m3 have been 
reported in the living- and bedrooms of Swiss homes (Zimmerli et 
al., 1979).  Similar levels (1 - 25 g/m3) were found in rooms 
treated one to several years earlier; levels of 25 and 30 g/m3 
were found in rooms a few weeks after treatment (Dahms & Metzner, 

    In an unpublished study carried out in the United Kingdom in 
1980 and cited by Dobbs & Williams (1983), PCP air concentrations 
were monitored as a function of time.  During the first week after 
treatment of the roof void of a house, PCP levels were as follows: 
16 - 67 g/m3 in the treated roof void, 3.9 - 15 g/m3 in the 
landing, and 1.6 - 2.8 g/m3 in the bedroom; 5 - 10 weeks after 
treatment, PCP concentrations in the treated roof void ranged from 
1.7 to 6.7 g/m3 compared with 0.6 - 5 g/m3 in the landing and 
1.6 - 2.8 g/m3 in the bedroom.  Although the PCP air concentration 
in or near the treated room rapidly decreased, levels in the 
untreated bedroom remained stable, perhaps as a result of adsorption 
and desorption processes. 

    To follow the volatilization of PCP from treated wood in 
enclosed environments, studies were conducted in a building with an 
enclosed swimming pool, the walls and ceiling of which had been 
treated with PCP (Gebefuegi, 1981; Gebefuegi et al., 1983). Within 
a fortnight, an estimated 178.5 mg PCP had diffused from the 
wooden panels (210 m2), based on detection of 1 g/litre in the 
water of the swimming pool, 60 g/litre in the water condensed from 
the heat pump, and 4 g/m3 in the air of the hall housing the 
swimming pool.  Air levels of PCP inside this building ranged from 
1 to 160 g/m3, one year after the application of the wood 
preservative.  Two years later, PCP concentrations in the indoor 
air averaged 4 g/m3, and, even after 7 - 8 years, PCP was still 
present at about 0.4 g/m3, though, in the interim, the wood panels 
had been painted with another wood preservative, which undoubtedly 
reduced the rate of PCP diffusion. 

    In a study conducted in the USA, PCP vapour levels were 
measured in the air of treated wooden structures.  The highest 
level detected was 38 g/m3 in the basement of the building where 
there was the highest ratio of treated wood surface area to room 
volume, and no ventilation.  PCP levels were higher in the main 
floor of this house (8.8 g/m3) and in a warehouse (3.52 g/m3) 

than in 11 other rooms of different buildings, which ranged from 
0.09 to 1 g/m3.  Variability in PCP concentrations was mainly 
attributable to ventilation differences (Saur et al., 1982). 

    Compared with the aforementioned studies, the values (0.06 - 
1.6 g/m3) reported by Dobbs & Williams (1983) from houses in the 
United Kingdom represent rather low PCP levels.  Generally, PCP 
concentrations of up to about 30 g/m3 can be expected during the 
first month following treatment; considerably higher levels (up to 
160 g/m3) may not be excluded under unfavourable conditions.  In 
the long term, values of between 1 and 10 g/m3 are typical PCP 
concentrations after extensive treatments. 

    Krause (1982) considered household dust to be very suitable for 
screening purposes, because it accumulates PCP and can be easily 
collected.  Household dust collected in the houses of residents 
using PCP contained about 1000 times more PCP (mean, 15 mg/kg; 2/3 
range, 6 - 20 mg/kg) than that of control households (mean, 0.008 
mg/kg; 2/3 range, 0.003 - 0.013 mg/kg). 

    In similar, more recent studies, relatively high PCP levels 
(range, 0.2 - 217.3 mg/kg; mean, 28.5 mg/kg) were found in 
household dust samples, indicating indoor air contamination 
resulting from PCP contaminated surfaces (Ruh et al., 1984). 

    The concentration of PCDDs or PCDFs in PCP-contaminated 
interiors has not yet been determined.  However, it may be assumed 
that the ratio of their air concentrations will be proportional to 
their rates of volatilization.  Because of their lower vapour 
pressure (e.g., H6CDD, 8.8 x 10-5 Pa), volatilization of PCDDs will 
be lower than that of PCP.  According to Cull et al. (1983), the 
following PCDD concentrations can be predicted in houses where PCP 
air concentrations range from 1 to 10 g/m3: OCDD, 0.2 - 20 ng/m3; 
H6CDD, 0.007 - 0.7 ng/m3; H7CDD, 0.04 - 4 ng/m3. 

    First reports of indoor air analyses of PCDDs and PCDFs in a 
house in the Federal Republic of Germany (Eckrich, 1986), which had 
been treated with PCP-containing wood preservatives several years 
before, seem to confirm these estimates; however, the data 
reported are still insufficient for a conclusion to be drawn.  
Further studies are under way that could be used to characterize 
the PCDD and PCDF levels in indoor air of PCP-treated homes. 

    Residues of PCP in the general population may arise not only 
from oral, dermal, or inhalation uptake of PCP, but also from the 
metabolic transformation of other chlorinated compounds (Table 19).  
In studying the biotransformation of hexa- and pentachlorobenzene 
in the rat, mouse, guinea-pig, laying hen, and rainbow trout, Koss 
& Koransky (1978) found PCP and other metabolites in both the 
excreta and tissues of the animals.  Considering the substantial 
residues of hexachlorobenzene in the human body and in human milk, 
PCP intake arises via this route in both adults and new-born 
children. Similarly, the continuous low-level PCP excretion from 
people, who apparently are not exposed to PCP, might be partly due 
to continuous exposure to hexachlorobenzene and related compounds. 

Table 19.  Chlorinated compounds metabolized to PCP
Source                         Reference
hexachlorobenzene              Mehendale et al. (1975); Engst et
                               al. (1976); Rozman et al. (1977);
                               Sanborn et al. (1977); Koss &
                               Koransky (1978); van Ommen et al.

pentachloronitrobenzene        Murthy & Kaufman (1978); Koegel et
                               al. (1979)

BHC isomers (i.e., lindane)    Balba & Saha (1974); Engst et al.

5.4.  Human Monitoring Data

    Exposure levels as measured in the indoor air or in consumer 
products may provide indirect indications of exposure to PCP.  
However, it is not possible to separate oral, respiratory, and 
dermal exposures, under non-experimental conditions.  Thus, the PCP 
concentrations of the sources do not directly indicate the actual 
human PCP intake by the different routes. 

    Several investigations have been carried out to relate the 
human body burden to the urinary-PCP level.  These are summarized 
in Tables 20, 21, and 22) distinguishing between occupationally 
exposed workers and the general population.  The latter has, in 
turn, been divided into individuals exposed non-occupationally, 
such as persons exposed to PCP-containing wood preservatives 
applied to the interior of private homes, offices, public 
facilities etc., and people without known exposure. 

    In many cases, values for populations without known exposure 
overlap those of exposed populations, perhaps because persons 
designated as unexposed might unknowingly have been exposed to 
obscure sources of PCP.  In addition, occupational exposure does 
not always involve high loading, for, as pointed out in section 
5.2, both very low and very high air levels of PCP have been found 
in work-places.  Conversely, people exposed non-occupationally, 
particularly those who apply PCP-containing wood preservatives 
indoors, may be exposed to air levels of PCP encountered at work-
places or even higher levels. 

    Analytical improvements in the last few years have 
substantially lowered the detection limits (section 2.5.2) and, 
combined with different methods, this makes the comparability of 
analytical data questionable, particularly when urinary-PCP levels 
have been determined without hydrolysis, as in the survey of Krause 
& Englert (1980), since, under these conditions, PCP levels will 
have undoubtedly been underestimated.  According to Zimmerli et al. 
(1979) and Butte (1984), analysis for total PCP yields 
concentrations about 3 times higher than those for only free PCP. 

    For these reasons, it is not possible to derive exact ranges of 
PCP levels in different exposure groups from the data in Tables 20, 
21, and 22.  However, the mean or median urine-PCP levels are 
likely to range around 0.01 mg/litre for the general population 
without known exposure, around 0.04 mg/litre for persons exposed 
non-occupationally, and around 1 mg/litre for occupationally 
exposed people. 

    Only two particularly detailed studies of domestic PCP exposure 
provide comparative data.  Comparing the mean urine-PCP levels, 
Hernandez & Strassmann-Sundy (1980) (No. 3 in Table 21, No. 5 in 
Table 22) observed that residents of log homes treated with PCP had 
a body burden that was between 5 and 60 times higher than that of 
residents of untreated log homes or conventional homes. 

    The most thoroughly designed survey (Krause & Englert, 1980; 
Aurand et al., 1981; Krause, 1982) included air analyses in the 
houses of a control group showing PCP concentrations generally 
below the detection limit of 0.1 g/m3 (No. 6 in Table 22).  The 
mean urine-PCP level of this group was about 3.5 times lower than 
that of the corresponding exposure group (No. 5 in Table 21). Much 
greater differences are encountered, if the highest concentrations 
measured are compared with the control levels.  No significant 
correlation was established between the PCP levels in air and in 
urine, which again casts doubt on the validity of air-PCP levels as 
an exposure parameter.  Nevertheless, on subdividing the exposed 
persons into 2 groups with PCP exposure either lower and equal to 
5 g PCP/m3 or higher than 5 g PCP/m3, urinary-PCP levels seem to 
be elevated at the higher indoor concentrations.  In addition, 
younger residents are obviously more exposed to PCP than older 
ones, perhaps because, on average, children spend more time at 

    When comparing PCP concentrations in the urine and blood, the 
levels in serum or plasma generally exceed those in urine, the 
extent of this difference varying according to the exposed group.  
The blood-PCP:urine-PCP ratio in people without known exposure or 
in persons exposed non-occupationally is considerably higher than 
that in occupationally exposed individuals.  For comparison, in most 
of the cases of lethal intoxication summarized in Table 24 (section 
6.2.2), urine-PCP levels even exceeded the corresponding blood 
levels.  This pattern may be the result of heterogenous plasma-
protein binding of PCP (section 6.6). 

    Shafik (1973) detected significant amounts of PCP (mean, 0.025 
mg/kg; range, 0.005 - 0.052 mg/kg) in human adipose tissue samples 
from the general population.  Similar values (mean, 0.0145 mg/kg) 
(Table 25, section 6.3.1) were reported by Grimm et al. (1981), 
whereas higher PCP contents (mean, 0.14 mg/kg; range, not 
detectable - 0.57 mg/kg) were found in adipose tissue samples from 
subjects with "no occupational contacts" (Ohe, 1979). 

Table 20.  Levels of PCP in the air, and in the serum or plasma, and urine of
individuals exposed occupationally
Number Activity            Sample    Length of  Air (g/m3)   Serum (mg/litre)  Urine (mg/litre)  Reference
of                         size      exposure   mean (range)  mean (range)      mean (range)
study                      (number)  (years)
(1)    Lumber, carpentry   1         ns         na            na                0.024             Cranmer &
                                                                                (0.022 - 0.025)a  Freal (1970)

(2)    Lumber, closed      11        1          na            na                1.6 (ns)          Casarett et
       tank procedure                                                                             al. (1969)

(3)    Lumber, dipping     11        1          na            na                2.6 (ns)          Casarett et
                                                                                                  al. (1969)

(4)    Lumber, dipping     ns        ns         19            na                2.83              Arsenault
                                                (3 - 63)                        (0.12 - 9.68)     (1976)

(5)    Lumber, dipping     18 - 22   ns         na            3.78              0.95              Klemmer et
                                                              (0.15 - 17.4)     (< 0.01 - 7.80)   al. (1980)

(6)    Lumber, dipping,    18        ns         na            5.14              1.31              Begley et
       spraying, or                                           (0.43 - 14)       (0.09 - 3.3)      al. (1977)
       - 6th day of        18        ns         na            4.92              1.36
         vacation                                             (0.50 - 13)       (0.18 - 3.5)
       - 20th day of       18        ns         na            2.19              0.59
         vacation                                             (0.32 - 5.3)      (0.05 - 1.4)
       - 51st day of       13        ns         na            2.61              0.95
         renewed work                                         (0.19 - 8.1)      (0.03 - 3.6)

(7)    Lumber, generalb    3         5          1             1.11              0.15              Wyllie et
                                     (2 - 11)   (< 1 - 15)    (0.35 - 3)        (0.044 - 0.47)    al. (1975)

(8)    Lumber industry     20        ns         na            ns                ns                Gossler &
                                                              (0.4 - 4.8)       (0.07 - 0.57)c    Schaller

(9)    Lumber, officeb     1         10         2             0.65              0.06              Wyllie et
                                                (< 1 - 3)     (0.42 - 0.75)     (0.04 - 0.11)     al. (1975)

Table 20.  (contd.)
Number Activity            Sample    Length of  Air (g/m3)   Serum (mg/litre)  Urine (mg/litre)  Reference
of                         size      exposure   mean (range)  mean (range)      mean (range)
study                      (number)  (years)
(10)   Lumber, pressure    1         5          6             2.29              0.30              Wyllie et
       treatmentb                               (< 1 - 15)    (1.51 - 3.55)     (0.09 - 0.76)     al. (1975)

(11)   Lumber, pressure    ns        ns         14            na                1.24              Arsenault
       treatment                                (4 - 1000)d                     (0.17 - 5.57)     (1976)

(12)   Lumber, pressure    23 - 24   ns         na            1.72              0.27              Klemmer et
       treatment                                              (0.02 - 7.70)     (< 0.01 - 2.40)   al. (1980)

(13)   Lumber, pressure                                                                           Embree et
       treatment                                                                                  al. (1984)
       - Airborne +        10        5 - 10     55.6          0.71              0.11
         dermal                                 ( 89)        ( 0.38)          ( 0.02)
       - Airborne          8         5 - 10     66.7          0.24              0.05
         exposure                               ( 100)       ( 0.23)          (0.02)
       - No known          5         5 - 10     ns            0.06              ns
         exposure                                             ( 0.02)

(14)   Lumber, spraying    2         ns         na            na                0.20              Cranmer &
                                                                                (0.13 - 0.27)a    Freal

(15)   Lumber, spraying    ns        ns         6             na                0.98              Arsenault
                                                (3 - 69)d                       (0.13 - 2.58)     (1976)

(16)   PCP processing      18        12         ns            0.25e             0.112e            Triebig et
       factory                       (0.3 -     (2.2 - 55.5)  (0.02-1.5)f       (0.013 - 1.224)   al. (1981)g

(17)   PCP application     23        3e         2.4           1e                ns                Zober et
                                     (0.5 -     (0.3 - 8)     (0.2 - 2.4)f                        al. (1981)
(18)   PCP processing      18        10e        17.5          0.25e             ns                Zober et
                                     (0.2 -     (2 - 50)      (0.02 - 1.5)f                       al. (1981)

Table 20.  (contd.)
Number Activity            Sample    Length of  Air (g/m3)   Serum (mg/litre)  Urine (mg/litre)  Reference
of                         size      exposure   mean (range)  mean (range)      mean (range)
study                      (number)  (years)
(19)   PCP production      8         ns         < 100 -       4.73  3.41       2.38  1.91       Bauchinger
                                                > 500h                                            et al.
       Na-PCP production   14        ns         < 100 -       2.23  1.51       0.84  0.65       (1982)
                                                > 500i

(20)   PCP production      18        ns         270 - 4000    na                0.72  0.55       Ning (1984)
       Na-PCP production   50        ns         0 - 50        na                0.35  0.30

(21)   PCP synthesis,      9         ns         na            na                1.2               Siqueira &
       full time activity                                                       (0.34 - 3.4)      Fernicola
       - same factory,     12        ns         na            na                0.15              (1981)
         reduced PCP                                                            (0.032 - 0.4)

(22)   Pesticide,          130       ns         na            na                1.80              Bevenue et
       spraying                                                                 (0.003 - 35.7)    al. (1967b)

(23)   Farmers and pest    210 -     ns         na            0.25              0.01              Klemmer et
       control operators   280                                (< 0.01 - 8.4)    (< 0.01 - 0.040)  al. (1980)
a   Range of replicate analyses of single urine samples.
b   Mean concentrations shown are calculated from sampling data collected over a 5-month period. Mean air 
    level for workers listed as "lumber, general", is calculated from data provided for all 11 sites over a 
    5-month period by Wyllie et al. (1975).
c   Assuming a daily urine volume of 1.4 litre.
d   Mean "average exposure levels" encountered by employees.  Air at "maximum exposure" sites, next to sources, 
    contained 26 g/m3 (lumber spraying site) and 297 g/m3 (pressure treatment site).
e   Median.
f   Plasma.
g   Data partly identical with those from Zober et al. (1981).
h   From 67 samples, 18 were < 100 and 10 > 500 g/m3.
i   From 55 samples, 7 were < 100 and 8 > 500 g/m3.
na = Not analysed.
ns = Not specified.
Table 21.  Levels of PCP in the air, and in the serum or plasma, and urine of individuals 
exposed non-occupationally
Number Exposure/             Sample    Length    Air       Serum        Urine         Reference
of     comments              size      of        (g/m3)   (mg/litre)   (mg/litre)
study                        (number)  exposure  mean      mean         mean
                                       (months)  (range)   (range)      (range)
(1)    Miscellaneous groups  117       ns        na        na           0.04          Bevenue et 
       including house-                                                 (nd -         al. (1967b)
       holds and pesticide                                              1.84)
(2)    Indoor application    16        ns        ns        na           ns            Zimmerli et 
       of PCP solutions                          (1 - 10)               (0.030 -      al. (1979)

(3)    Residents of log      5         ns        0.29      1.126        0.084         Hernandez &
       homes treated with                        (0.20 -   (0.580 -     (0.047 -      Strassmann-
       PCP solutions                             0.38)a    1.750)       0.216)        Sundy (1980)
                             32        ns        na        0.330        0.013
                                                           (0.116 -     (0.002 -
                                                           1.084)       0.087)

(4)    "No occupational      32        ns        na        0.32         0.03          Klemmer et 
       exposure"; control                                  (0.002 -     (< 0.01 -     al. (1980)
       group for Number 5                                  7.20)        1)
       in Table 20                                        

Table 21.  (contd.)
Number Exposure/             Sample    Length    Air       Serum        Urine         Reference
of     comments              size      of        (g/m3)   (mg/litre)   (mg/litre)
study                        (number)  exposure  mean      mean         mean 
                                       (months)  (range)   (range)      (range)
(5)    Indoor application    989       ns        6.1       na           0.044         Krause & 
       of an average of                          (nd -                                Englert 
       40 litre PCP                    (< 9      25)b                                 (1980)  
       solutions                       years)    4.9c                   0.029c            
                                                 (2.5 -                 (0.013 - 
                                                 9.5)                   0.071)
       - Subgroups:                                  
         1. m < 18 years     16        ns        < 5       na           0.047c
                                                                        (0.017 - 
         2. m > 18 years     39        ns        < 5       na           0.023c
                                                                        (0.011 - 
         3. f < 18 years     22        ns        < 5       na           0.033c
                                                                        (0.016 - 
         4. f > 18 years     39        ns        < 5       na           0.026c
                                                                        (0.015 - 
         5. m < 18 years     23        ns        > 5       na           0.079c
                                                                        (0.014 - 
         6. m > 18 years     31        ns        > 5       na           0.043c
                                                                        (0.011 - 
         7. f < 18 years     25        ns        > 5       na           0.059c
                                                                        (0.011 - 
         8. f > 18 years     43        ns        > 5       na           0.039c
                                                                        (0.021 - 

Table 21.  (contd.)
Number Exposure/             Sample    Length    Air       Serum        Urine         Reference
of     comments              size      of        (g/m3)   (mg/litre)   (mg/litre)
study                        (number)  exposure  mean      mean         mean 
                                       (months)  (range)   (range)      (range)
(6)    Indoor application                                                             Sangster et 
       of about 70 litres                                                             al. (1982)
       PCP solution
       - before ventilation  6         6         0.60      na           0.0032
                                                 (0.14 -                (0.0007 - 
                                                 1.20)                  0.0078)
       - after ventilation   6         -         0.08      0.080        0.0033
                                                 (nd -     (0.025 -     (0.0018 -        
                                                 0.24)     0.190)d      0.0080)

       Indoor application    2         0.5       0.15      0.033        na
       of about 100 litres                       (nd -     (0.031 -
       PCP solution                              0.40)     0.034)d
       about 75 litres PCP

       Indoor application    2         1         0.67      0.565        na
       of about 100 litres                       (0.44 -   (0.47 -
       PCP solution                              0.95)     0.66)d

Table 21.  (contd.)
Number Exposure/             Sample    Length    Air       Serum        Urine         Reference
of     comments              size      of        (g/m3)   (mg/litre)   (mg/litre)
study                        (number)  exposure  mean      mean         mean 
                                       (months)  (range)   (range)      (range)
(7)    "Workers non-         27        ns        na        na           0.009         Siqueira &
       occupationally                                                   (nd -         Fernicola
       exposed"; control                                                0.034)        (1981)
       group for Number 21
       in Table 20

(8)    Indoor application    80        ns        na        (0.0025 -    (0.002 -      Janssens &
       PCP solutions                                       0.5)         0.075)        Schepens

(9)    Residents in buil-    46        ns        na        (0.001 -     na            Ruh et al.
       dings with PCP con-                                 0.110)e                    (1984)
       taminated wood

(10)   Residents in homes    204       ns        na        0.058c       0.014c        Grimm et al.
       treated with PCP      (234)                                                    (1985)
a   Air samples taken on the 1st and 2nd floor of a 2-story log house.
    A sample of interior surface wood contained 1132 mg PCP/kg (0.11%).
b   104 air indoor samples taken.
c   Median (2/3 range).
d   Plasma.
e   Whole blood.
na = Not analysed.
nd = Not detectable.
ns = Not specified.
f = Female.
m = Male.

Table 22.  Levels of PCP in the serum or urine of individuals without known exposure
Number Comments                Sample    Indoor    Serum       Urine (mg/litre)    Reference
of                             size      air       (mg/litre)  mean (range)
study                          (number)  (g/m3)   mean 
(1)    ns                      6         na        na          0.005               Cranmer & Freal
                                                               (0.002 - 0.011)a    (1970)

(2)    Control group for       ns        na        0.06b       ns                  Gossler & Schaller
       Number 8 in Table 20                        (0.03 -     (0.001 - 0.057)c    (1978)

(3)    US National Human       418       na        na          0.0063              Kutz et al. (1978)
       Monitoring Program for                                  (nd - 0.193)

(4)    Control group for       12        na        na          0.0135              Zimmerli et al.
       Number 2 in Table 21                                    (0.006 - 0.023)     (1979)

(5)    Control groups for      42        na        ns          ns                  Hernandez &
       Number 3 in Table 21;                       (0.004 -    (0.0007 - 0.011)    Strassmann-Sundy
       January 1980 "conven-                       0.068)                          (1980)
       tional" homes

       March 1980; untreated   2         na        0.051       0.0014
       log homes                                   (0.034 -    (0.001 - 0.002)

       March 1980;             11        na        0.048       0.0025
       "conventional"                              (0.015 -    (0.001 - 0.007)
       homes                                       0.055)

Table 22.  (contd.)
Number Comments                Sample    Indoor    Serum       Urine (mg/litre)    Reference
of                             size      air       (mg/litre)  mean (range)
study                          (number)  (g/m3)   mean 

(6)    Control group for       207       ndd       na          0.0127              Krause &
       Number 5 in Table 21                                    0.0102b             Englert (1980)
                                                               (0.0038 - 0.0214)

(7)    ns                      10        na        na          0.009               Lores et al. (1981)
                                                               (0.003 - 0.016)

(8)    Dutch draftees;         99        na        0.128       na                  Sangster et al.
       control group for                           (< 0.05 -                       (1982)
       Number 6 in Table 21                        1.10)       

(9)    Control group for       12        na        ns          0.0009              Janssens &
       Number 7 in Table 21                                    (0.0002 - 0.002)    Schepens (1984)

(10)   Non-specifically        12        na        0.025       0.014               Uhl et al.
       exposed persons         30                  (0.019 -    (0.007 - 0.034)c    (1986)
a   Range of replicate analysis of single urine samples.
b   Median (2/3 range).
c   Assuming a daily urine volume of 1.4 litre.
d   Below detection limit of 0.1 g/m3.
na = Not analysed.
nd = Not detectable.
ns = Not specified.
    Samples of human milk were found to contain between 0.03 and 
2.8 g PCP/kg (mean, 0.68  0.05 g/kg), which is considerably less 
than the PCP levels usually found in other body fluids or tissues 
(Gebefuegi & Korte, 1983). 

    In investigating the apparent decrease in sperm density in US 
males over the last 30 years, Dougherty et al. (1980) and Kuehl & 
Dougherty (1980) detected PCP (100 - 200 ppb) in all 50 samples of 
human seminal plasma analysed.  They also observed that PCP was 
selectively concentrated by the cellular material. 

    Only few monitoring data are available on the human body burden 
of microcontaminants as a result of exposure to PCP. Rappe et al. 
(1982) analysed urine and blood samples of 9 workers exposed to PCP 
or L-PCP.  In the case of 5 workers in the textile industry, 
urinary levels of PCDDs (total PCDDs, 3 - 365 ng/kg) and PCDFs 
(total PCDFs, < 1 - 45 ng/kg) paralleled the urinary-PCP levels 
(< 0.01 - 3.12 mg/litre).  Similar levels of these impurities were 
found in the blood of 4 tannery workers 8 months after last 
exposure, but these could not be compared with urinary-PCP levels.  
However, in both groups, the concentration pattern of the different 
isomers reflected the different proportions of contaminants in 
commercial PCP products. 

    Because of their high fat-solubility and slow metabolic 
degradation and elimination, impurities of PCP such as HCB, PCDDs, 
and PCDFs are expected to accumulate in body fat.  No data are 
available concerning the accumulation behaviour of these 
microcontaminants as a result of human PCP uptake.  However, levels 
of dioxins in the milk- or body-fat of cows orally treated with 
technical-grade PCP (10 mg/kg body weight per day) were about 1000 
times higher than those in blood, indicating a substantial 
accumulation (Firestone et al., 1979).  In addition, the three 
dioxins detected (1,2,3,6,7,8-H6CDD, 1,2,3,4,6,7,8 H7CDD, and OCDD) 
declined comparatively slowly from about 20, 40, and 25 g/kg 
composite milk-fat to 4.3, 6.9, and 3 g/kg, respectively, 100 days 
after PCP feeding was stopped.  For comparison, the steady-state 
PCP level of about 40 mg/kg in blood or 4 mg/kg in composite milk 
dropped to basal levels (0.02 - 0.08 mg/kg) within less than 10 
days.  Firestone et al. (1979) concluded from their results that 
"the absence of PCP in milk or biological tissue affords no 
guarantee of the absence of biologically active dioxins". 


6.1  Absorption

6.1.1  Animal studies

    PCP is readily absorbed through the skin as well as through the 
respiratory and gastrointestinal tracts.  Braun & Sauerhoff (1976) 
administered a single oral dose of 10 mg PCP/kg body weight in corn 
oil to 3 male and 3 female rhesus monkeys and calculated the half-
life for absorption to be 3.6 h in males and 1.8 h in females.  
After 12 - 24 h, plasma levels peaked in the range of 10 - 30 mg 

    In rats given a single oral dose of 10 mg of 14C-PCP/kg body 
weight, the peak plasma concentration (50 mg/litre) was attained 
much earlier, after 4 - 6 h.  The absorption rate constants were 
1.95 and 1.52/h for males and females, respectively (Braun et al., 
1977); assuming first order kinetics, the half-life for absorption 
can be calculated to be 0.36 and 0.46 h, respectively. 

    Rapid absorption of PCP was also observed in rats during 20-min 
inhalation of approximately 5.7 mg PCP/kg body weight (Hoben et 
al., 1976d) and in mice following intraperitoneal and subcutaneous 
injections of 14C-PCP (Jakobson & Yllner, 1971). 

    The same holds true for fish.  Goldfish exposed to PCP medium 
(0.4 mg/litre) absorbed PCP rapidly, until a lethal level of 
approximately 100 mg/kg body weight was reached after about 5 h 
(Kobayashi & Akitake, 1975a).  The apparent route of PCP uptake was 
via the gills and the skin.  Similarly, PCP was rapidly taken up 
from the water by rainbow trout and assimilated into various 
tissues (Glickman et al., 1977). 

6.1.2  Human studies

    Braun et al. (1979) studied 4 healthy male volunteers of normal 
weight, between 21 and 55 years of age, who ingested a dose of 0.1 
mg Na-PCP (> 99% purity)/kg body weight.  The observed half-life 
for absorption was about 1.3 h.  The peak plasma level of 0.245 mg 
PCP/litre occurred 4 h after ingestion of PCP.  In the study of Uhl 
et al. (1986), the PCP level in the plasma of a male volunteer was 
approximately 0.185 mg/litre, 2 days after a single oral dose of 
0.016 mg 13C-PCP/kg body weight in 40% ethanol.  This implies that 
absorption of PCP, when dissolved in alcohol, is much greater than 
when it is dissolved in water. 

    For the general population, the uptake of PCP by the oral route 
is thought to be more significant than that via other routes of 
exposure.  For individuals exposed to high airborne concentrations 
of PCP in the work-place or in PCP-treated dwellings, the major 
routes of exposure are probably via the skin and lungs.  No 
experimental data are available concerning these routes.  However, 
the cases of acute intoxication reported were almost exclusively 

due to extensive skin contact with PCP or to the inhalation of high 
doses of PCP, which subsequently led to high PCP levels in the 
human body. 

    Bevenue et al. (1967a) reported a case of PCP absorption 
through the skin.  A male individual had skin contact with PCP for 
10 min while cleaning a paint brush in a can containing a solution 
of 4% PCP.  Two days later, a urinary-PCP level of 236 g/litre was 

    One case of oral uptake has been reported (Haley, 1977).  A 
71-year-old Japanese male had intentionally ingested an amount 
estimated at between 113 and 226 g of weed killer containing 12% 
PCP.  Although the patient was treated with gastric aspiration and 
lavage within the next hour, a substantial amount of PCP must have 
already been absorbed as indicated by the high serum level of 150 
mg PCP/litre, 5 h after the incident. 

6.2  Distribution

6.2.1  Animal studies

    Available information indicates that usually the highest PCP 
levels can be found in the urine immediately after exposure, and 
consequently, the PCP concentrations in the tissues account for 
only a small fraction of the dose applied.  This is reflected by 
the data on excretion and recovery of radioactivity from groups of 
rats, 9 and 10 days after oral administration of 10 and 100 mg 
PCP/kg body weight, respectively (Table 23).  It should be noted 
that the percentages of the dose recovered are to be considered as 
cumulative over the period of 9 days (10 mg/kg dose) or 8 days (100 
mg/kg dose) in the case of the excreta, while the PCP contents of 
the organs were only analysed 9 days after administration of 10 
mg/kg body weight.  Thus, PCP is apparently eliminated much more 
rapidly from the kidney than from the liver (section 6.5.1). 

    The results of early studies did not show a uniform 
distribution pattern of PCP in experimental animals but indicated 
that very high levels of PCP could be found in liver and kidneys 
(Truhaut et al., 1952b).  However, following long-term exposure, 
most PCP was absorbed by the central nervous system. 

    Several recent studies on the distribution and elimination of 
PCP were performed using 14C-labelled PCP, thus making the results 
more reliable.  Larsen et al. (1972) studied the tissue distribution 
in rats after administering oral doses between 31 and 40 mg 14C-
PCP/kg body weight.  The body component containing the highest 
level appeared to be the liver, followed by the kidney and blood.  
Low levels of PCP were found in fat, brain, and muscle tissue.  
More than 99% of the total radioactivity in the blood was contained 
in the serum, indicating that PCP and/or its metabolites in the 
blood are not bound to the cellular constituents. 

Table 23.  Recovery of radioactivity from rats given a 
single oral dose of 10 or 100 mg of 14C-PCP/kg body weighta
                     Percentage of radioactivity (mean  SD)
                     dose: 10 mg/kg         dose: 100 mg/kg
  urine              79.8  2.9             64.0  14.9
  faeces             18.6  3.7             33.6  13.7
  expired 14CO2      0.2  0.1              -b

  liver              0.315  0.137          -b
  kidneys            0.045  0.014          -b

Total body           0.437  0.142          -b

Cage rinse           1.4  1.9              -b

Total recovery       99.8  4.4             97.6  2
a   From: Braun et al. (1977).
b   Samples were not analysed.
c   Other organs analysed were the stomach, lungs, testes, 
    ovaries, brain, heart, spleen, and adrenals.  Each of 
    these organs contained 0.005% of the dose or less and 
    were included with the liver and kidneys in the total 
    body figure.

    Jakobson & Yllner (1971) examined the distribution of PCP in 
the mouse after the subcutaneous or intraperitoneal injection of 
14C-PCP (15 - 37 mg/kg body weight).  Autoradiographic studies 
showed that the highest specific activity was in the liver, the 
gall bladder and its contents, the wall of the stomach fundus, the 
kidney, and the contents of the gastrointestinal tract, while the 
lung, heart, and brain contained only negligible amounts of PCP. 

    PCP concentrations were highest in the plasma of rats 
immediately after a 20-min inhalation exposure to an aerosol of Na-
PCP, resulting in a calculated dose of about 5.7 mg/kg body weight 
(Hoben et al., 1976d).  About 35% of the dose was found in the 
plasma, while the liver contained about 25% and the lung a little 
less than 2% at time 0.  After 24 h, the liver showed the highest 
PCP level followed by the plasma and the lung.  Other organs were 
not examined. 

    Zenzen (1979) administered a daily dose of 15 mg 14C-PCP/kg 
body weight intraperitoneally to rats for 15 days.  On day 1, the 
highest PCP levels in the organs examined were found in the liver 
and kidney of male rats, comprising 14.1 and 14.3 %, respectively, 
of the total activity on a dry weight basis.  Similar 
concentrations were measured in the testicle.  However, on a fresh 
weight basis, the levels in this organ were similar to those in the 
other endocrine organs. 

    Preliminary data obtained from a single sheep (Wilson et al., 
1982) indicated that PCP is absorbed into the lymphatic system; 47% 
of the PCP dose (10 mg/kg in corn oil, given by intraruminal 
injection) remained in the digestive tract 36 h after dosing.  Of 
the absorbed PCP (53% of total dose), approximately 17% was found 
in the lymph collected through a thoracic duct canula.  The 
remainder was probably absorbed from the digestive tract directly 
into the blood. 

    To study the placental transfer of PCP in rats, 60 mg 14C-
PCP/kg body weight was orally administered to pregnant rats on day 
15 of gestation.  The amount of specific radioactivity in the 
maternal blood-serum was greatest at 8 h (about 1.1% of the 
administered dose per gram of tissue), but, in the placentas and 
fetuses, it never exceeded 0.3% and 0.1%, respectively (Larsen et 
al., 1975).  Thus, the amount of PCP that crosses the placental 
barrier is very low.  Contrasting data have been obtained in a 
preliminary observation of a single pregnant monkey, but no full 
report has been published (Mller, 1981). 

    Kobayashi (1979) observed an accumulation of 14C in various 
organs of goldfish exposed to 0.1 mg 14C-PCP/litre water.  The gall 
bladder contained the highest 14C level after a 24-h exposure.  The 
biliary concentration increased, even after fish had been 
transferred to clean, running water for 24 h, whereas a decrease 
was observed in the levels in all other organs examined (Kobayashi 
& Akitake, 1975b).  This characteristic accumulation indicates that 
conjugated PCP is transferred to the gall bladder and bile due to 
an enterohepatic circulation (section 6.5.1). 

6.2.2  Human studies

    Human data concerning tissue distribution following PCP uptake 
are derived mainly from autopsy results on victims of fatal 
intoxications (Table 24).  No exact conclusions can be drawn from 
these data with regard to PCP accumulation, though PCP levels in 
the liver, kidney, and lungs are often elevated. The high levels in 
the lungs reported in some cases might be related to inhalation 
uptake of PCP.  Similarly, the stomach of the individual who 
committed suicide by ingesting PCP contained 750 mg PCP/kg, which 
highly exceeded the concentrations found in the other body parts 
examined (Cretney, 1976).  An unusually high kidney-PCP level of 
639 mg/kg, reported by Wood et al. (1983), might have been due to 
kidney malfunction.  In general, PCP levels in the various tissues 
do not indicate a clear accumulation of PCP, since blood-PCP levels 
are often similar to the corresponding tissue concentrations.  
Levels in urine can vary depending on the actual urine volume in 
the bladder at the time of poisoning and the pH value.  From the 
data in Table 24, liver and kidney residues associated with acute 
lethal intoxications can be estimated to be 10 - 225 mg PCP/kg and 
5 - 145 mg PCP/kg, respectively. 

Table 24.  PCP levels found in human tissues and body fluids
after PCP intoxication resulting in death
Reference        Case    Urine   Blood  Liver  Kidney   Lung     Brain    Supposed
                 number  (mg/    (mg/   (mg/   (mg/kg)  (mg/kg)  (mg/kg)  routes of uptake
                         litre)  litre) kg)
Truhaut et al.   1       55      5      10     5        1.5      na       dermala
(1952b)          2       96      6      52     21       38       6.5      dermala

Gordon (1956)    1       70      50     65     95       145      20       inhalation, dermala

Menon (1958)     1       160     na     na     na       na       na       inhalation, dermala

Blair (1961)     1       na      na     59     41       na       na       dermal, orala
                 2       na      na     62     84       76       na       inhalationa
                 3       na      na     59     63       na       na       oralb

Mason et al.     1       na      79     66     na       na       10       inhalationa
(1965)           2       365     110    89     86       na       25       inhalationa

Burger (1966)    1       na      39     na     na       na       na       orald

Barthel et al.   1       na      na     na     27.6     na       na       dermalc

Cretney (1976)   1       75      173    225    116      na       na       oral(?)d

Wood et al.      1       29      16     52     639      116      na       inhalation,
(1983)                                                                    dermala
a   Occupational exposure.
b   Accidentally contaminated food.
c   Accidentally contaminated diapers.
d   Suicide.
na = Not analysed.

    There is a paucity of data on the distribution of PCP in the 
tissues and body fluids in the general population.  In 2 
investigations (Table 25), autopsy samples were collected from 
human subjects in Northern Bavaria (Federal Republic of Germany) 
with no known history of PCP exposure.  Grimm et al. (1981) 
concluded from the data that there was only a slight tendency for 
PCP to accumulate in both liver and kidney.  The relatively high 
level observed in the brain samples was attributed to the fact that 
most of the persons with high brain-PCP levels had bled to death.  
In such cases, a cerebral hypoxia preceding the death might have 
led to the breakdown of the blood-brain barrier and accumulation of 
PCP in the brain.  Lwer (1982) found much lower brain-PCP levels, 
in conjunction with liver and kidney levels similar to those 
reported by Grimm et al. (1981).  There was no correlation between 
PCP levels in tissues and the age of the person examined (Lwer, 
1982).  Moreover, PCP levels in the body fluids were of the same 
order of magnitude as those in the tissues (Grimm et al., 1981). 

6.3  Metabolic Transformation

6.3.1  Animal studies

    The first studies on the fate of PCP in the body were conducted 
by Deichmann et al. (1942), who obtained evidence of metabolic 
transformation in the rabbit after oral administration and in the 
rat after intraperitoneal dosing with Na-PCP. The authors did not 
identify any metabolites. 

    Later studies using more advanced analytical methods have shown 
that PCP is metabolized, either to tetrachlorohydroquinone through 
oxidation or conjugated to PCP glucuronide.  Tetrachlorohydroquinone 
was found in its free form in the urine of mice and rats (Jakobson 
& Yllner, 1971; Ahlborg et al., 1974); in the rat, it is also 
conjugated with glucuronic acid (Ahlborg et al., 1978).  Traces of 
trichlorohydroquinone formed by the reductive dechlorination of 
tetrachlorohydroquinone were found in the urine of rats.  The 
formation of tetra- and trichlorohydroquinone as well as total 
elimination during the first 24 h can be enhanced through 
pretreatment with 3-methylcholanthrene or 2,3,7,8-T4CDD.  
Phenobarbital only increases the metabolism to tetrachlorohydro-
quinone. These observations were confirmed by  in vitro tests on rat 
liver microsomes (Ahlborg & Thunberg, 1978).  Glucuronidation rates 
were not significantly altered by pretreatment with phenobarbital 
or 3-methylcholanthrene (Lilienblum, 1985). 
Table 25.  Medians, means, and ranges of PCP concentrations in tissues
and body fluids at autopsy from people without known exposure
                 Number   Urine    Blood   Liver    Kidney   Brain    Body fat  Spleen
                 of       (mg/     (mg/    (mg/kg)  (mg/kg)  (mg/kg)  (mg/kg)   (mg/kg)
                 cases    litre)   litre)              
Median           21a      0.0044   0.0233  0.0670   0.0430   0.0470   0.0127    0.0190
5. Percentile             dlb      dl      0.0017   0.0240   0.0190   0.0100    0.0070
95. Percentile            0.1603   0.0679  0.1735   0.0950   0.0725   0.0225    0.0325
Mean                      0.0297   0.0260  0.0860   0.0641   0.0491   0.0145    0.0208

Median           51c      nad      na      0.0720   0.0223   0.0180   na        na
Lowest value              na       na      0.0140   nde      nd       na        na
Highest value             na       na      0.4190   0.1040   0.0560   na        na
a   From: Grimm et al. (1981).
b   dl = detection limit = 0.001 mg PCP/litre urine; 0.005 mg PCP/litre blood.
c   From: Lwer (1982).
d   na = not analysed.
e   nd = not detected (detection limit = 0.010 mg PCP/kg wet tissue).

    In contrast to these rodent species, the rhesus monkey 
eliminates PCP unchanged in the urine (Braun & Sauerhoff, 1976).  
This is the only recent study that failed to detect any metabolites 
of PCP. 

    Detoxication of PCP has also been observed in fish.  While no 
dechlorination processes have been reported, conjugation and 
subsequent excretion of the PCP conjugates occurs: PCP glucuronide 
is formed and excreted into the bile of both goldfish (Kobayashi & 
Nakamura, 1979b) and rainbow trout (Glickman et al., 1977), while 
pentachlorophenylsulfate is excreted into the surrounding water 
through the gills and in the urine of goldfish (Kobayashi & 
Nakamura, 1979a,b). 

6.3.2  Human studies

    Most of the human data available consist of analyses of urine 
samples from people exposed to different uncontrolled PCP regimes. 

    In the studies of Braun et al. (1979) and Uhl et al. (1986) on 
male volunteers (section 6.1.2), PCP was eliminated as both the 
parent compound and glucuronide.  No other metabolites could be 
detected.  Ahlborg et al. (1974) found tetrachlorohydroquinone in 
the urine of 2 occupationally exposed spray operators, who were 
also exposed to other chlorophenolic compounds. 

    Recently, the metabolic transformation of PCP to 
tetrachlorohydroquinone was substantiated by Juhl et al. (1985); 
human and rat liver homogenates showed similar metabolizing 
activities.  The rate of PCP metabolism dependedon the PCP 
concentration and was 1000 times lower at 1 mmol/litre (266 
mg/litre) than at 0.01 mmol/litre (2.66 mg/litre). 

6.4  Elimination and Excretion

6.4.1  Animal studies

    PCP has been rapidly eliminated by most of the animals 
examined.  It is cleared from the plasma by its distribution to the 
tissues and by excretion via the urine and the faeces; the 
metabolites, when produced, are also rapidly excreted. 

    The uptake of PCP by the tissues accounts for only a small 
amount of the total PCP dose taken up by the body (section 6.2.1).  
Most of it leaves the body immediately after uptake, mainly through 
the urinary excretion of PCP and its metabolites.  The proportions 
of PCP excreted via the two major excretion routes in the rat, 
mouse, and monkey are summarized in Table 26.  Although the species 
and the test conditions differed, the excretion patterns were very 
similar: renal excretion amounted to between 45 and 83% of the 
total dose applied, while most of the remaining activity appeared 
in the faeces.  Thus, excretion of PCP and its metabolites mainly 
occurs via the kidneys, and to a lesser extent by the processes of 
gastric and biliary secretion. 

Table 26.  Urinary and faecal excretion of 14C activity as a 
percentage of a single dose of 14C-PCP
Species   Dose      Time   % recovery in:   Reference
          (mg/kg    (h)    urine  faeces
 male     10a       168    75     12        Braun & Sauerhoff
 female   10a       360    70     17        (1976)

Monkey    30a       144    51.7   4.3       Ballhorn et al.
 male     50a       144    44.9   11.3      (1981)

Rat       10a       216    80     19        Braun et al. (1977)
          100a      192    64     34

Mouse     14.8b     96     83     8         Jakobson & Yllner
          18.2b     96     62     5         (1971)
          37.2b     96     73     4
          35.2b     168    82     10
          36.8b     168    80     12
a   Oral (corn oil solutions).
b   Intraperitoneal.

    Only trace amounts of radioisotopes from the metabolism of 
labelled compounds are expired.  Although this route is of minor 
importance, it could indicate other metabolic processes, provided 
that analytical errors can be excluded.  However, Larsen et al. 
(1972) questioned whether expired 14C originated from PCP 
metabolism, attributing it, instead, to impurities in the 
radiolabelled PCP. 

    Ahlborg et al. (1974) found that the radioactivity from 
labelled PCP excreted in the urine of mice treated intra-
peritoneally (10 mg/kg body weight) consisted of about 41% 
unchanged PCP, 13% conjugated PCP, 24% unconjugated, and 22% 
conjugated tetrachlorohydroquinone.  For rats, the corresponding 
values were 60%, 9 - 16%, 7%, and 16 - 22%, respectively (Ahlborg 
et al., 1978). 

    Following an oral dose of 100 mg/kg body weight, the urinary 
metabolites of 14C-PCP in rats accounted for 75% unchanged PCP, 9% 
PCP glucuronide, and 16% tetrachlorohydroquinone.  Levels of the 
last compound were below detectable values in the blood-plasma 
(Braun et al., 1977).  The authors concluded that the rate-limiting 
step for the elimination of the metabolites of PCP is the rate of 
metabolism rather than that of urinary excretion and therefore, PCP 
metabolites were unlikely to accumulate in the body. 

    The proportions of PCP glucuronide in urine may have been 
underestimated to date; this metabolite has recently been shown to 
undergo a partial hydrolysis under weakly acidic conditions in 
urine (Lilienblum, 1985). 

    In contrast to the rodents, rhesus monkeys excreted all of the 
14C activity in urine as unmetabolized PCP (Braun & Sauerhoff, 

    Goldfish, in addition to free PCP, mainly excrete sulfate and 
glucuronide conjugates via 3 pathways of elimination: the amounts 
of PCP lost by the branchial, renal, and biliary routes were 52, 
24, and 22% of the total amount of PCP excreted by the fish in the 
24 h following a 24-h exposure to 0.1 mg PCP/litre water.  The 
excretion of PCP from the body surface was minor.  About 30% of the 
PCP excreted via the gills was in the unchanged form, whereas 
almost all the PCP excreted in both the bile and urine was 
conjugated.  PCP sulfate was the major conjugate in the branchial 
and renal routes, while PCP glucuronide was the primary biliary 
conjugate (Kobayashi & Nakamura, 1979b). 

6.4.2  Human studies

    The PCP concentration in human urine has been widely used as an 
indicator of the PCP body burden (section 5.4), based on the fact 
that renal excretion of PCP is the major elimination route in man.  
In the study of Braun et al. (1979) (section 6.3.2), within 168 h 
of ingesting 0.1 mg Na-PCP/kg body weight, volunteers excreted 74% 
of the total dose in urine as PCP and 12% as PCP glucuronide.  
About 4% of the total dose was eliminated in the faeces; this 
amount consisted of equal parts of both free PCP and PCP 
glucuronide.  The fate of the remaining 10% of the dose was not 

    Uhl et al. (1986) found that about 30% of PCP was excreted as 
glucuronide in the urine of a volunteer, up to 4 days after a 
single dose of 0.31 mg PCP/kg body weight (section 6.5.2).  However, 
in contrast to the study of Braun et al. (1979), the percentage of 
PCP glucuronide gradually increased to reach about the normal range 
determined for people not specifically exposed (65  5% PCP 
glucuronide) after about 14 days.  The findings of Zimmerli et al. 
(1979) and Janssens & Schepens (1984) also indicated that long-term 
exposure result in a higher proportion of conjugated PCP than that 
reported by Braun et al. (1979).  On the average, two thirds of the 
PCP detected in the urine samples of non-occupationally exposed 
people was conjugated. 

6.5  Retention and Turnover

6.5.1  Animal studies

    Pharmacokinetic data on the retention and half-life of PCP in 
the compartments also indicate that most of the PCP absorbed is 
rapidly eliminated from the body. 

    The dynamics of elimination of PCP and its metabolites depend 
on the species and the sex of the test animal.  As summarized in 
Table 27, the monkey differs from other animal species in showing a 
much slower elimination rate as expressed by the half-life for the 
clearance from urine and plasma, perhaps because monkeys do not 
metabolize PCP. 

    An extensive enterohepatic circulation of PCP is also suggested 
by the slow but steady elimination of 14C activity in the faeces of 
the monkeys (Braun & Sauerhoff, 1976).  On treating rhesus monkeys 
with cholestyramine, this enterohepatic circulation was 
interrupted as the cholestyramine bound the PCP and/or its 
metabolites and bile acids, thus preventing their reabsorption 
(Ballhorn et al., 1981).  However, the results were derived from 
only 4 monkeys in single studies. 

    Apart from the monkey studies, pronounced differences in PCP 
kinetics that are only in part related to the species or type of 
application have been observed in different single-dose studies 
(Table 27).  Braun & Sauerhoff (1976) and Braun et al. (1977) 
observed a monophasic elimination of PCP in monkey, while, in rats, 
2 phases could be distinguished (Fig. 4): an alpha-phase with a 
rapid elimination rate (elimination half-lives, 13 - 17 h) followed 
by a beta-phase (elimination half-lives for male rats, 40 h (10 
mg/kg body weight), 121 h (100 mg/kg body weight)) with a 
comparatively slow elimination rate.  However, the beta-phase, is 
not well defined, as it does not remain constant. 

    Braun et al. (1977) found that, at a higher dose (100 mg/kg 
body weight), the female rats followed the monophasic scheme 
(elimination half-life, 27 h) (Fig. 4).  Hoben et al. (1976d) also 
reported a monophasic elimination in rats, while Larsen et al. 
(1972) and Zenzen (1979) described a distinct biphasic model.  The 
accuracy of the unusually slow beta-phase (102 days = 2448 h) 
reported by Larsen et al. (1972) has been questioned by Braun et 
al.  (1977), since this value was obtained by subtracting the 
cumulative amount excreted in the urine from the total dose, 
without knowing the total recovery.  On the other hand, the 
monophasic scheme claimed by Braun et al.  (1977) for female rats 
dosed with 100 mg/kg body weight is not as distinct as it seems to 
be; for, on omitting the last sample measured at 192 h, a biphasic 
scheme could be fitted to the points as well (Fig. 4). 

    The amount of the PCP or 14C activity remaining in the body 
several days after dosing differs markedly between test species.  
According to Braun et al. (1977), in each case, 90% or more of the 
radioactivity had been excreted by rats 3 days after dosing; 
detectable levels of PCP remained only in liver and kidney, 9 days 
after the 10 mg/kg dose (see also Table 23).  As a result of a 
slower elimination rate, about 11% of the administered 14C activity 
remained in the body of rhesus monkeys 15 days after oral 
application of 10 mg/kg body weight; approximately 80% of this 
remaining activity was identified in the large and small intestines 
and liver.  Braun & Sauerhoff (1976) calculated that a steady-state 
concentration of PCP in plasma would be reached by the 10th 
repeated daily dose; the approximate plasma concentration at this 
time was estimated to be 50 mg PCP/litre. 


Table 27.  Comparison of PCP elimination kinetics in mammals after administration of 
single doses
Species    Dose      Elimina-    Sex       Elimination         Kinetics       Reference
           (mg/kg    tion via              half-life (h)
           body                            of phase        
           weight)                         alpha       beta
Mousea,b   15 - 37   urine       female    approxi-    -       not reported   Jakobson &
                                           mately 24                          Yllner (1971)

Ratc       37 - 41   urine       female    approxi-    2448    biphasic       Larsen et al.
                                           mately 10                          (1972)

Ratd       5.7       urine       male      approxi-    -       monophasic     Hoben et al.
                                           mately 24                          (1976d)

Ratc       10        urine and   female    13          33      biphasic       Braun et al.
                     faeces      male      17          40      biphasic       (1977)
           100       urine and   female    27          -       monophasic
                     faeces      male      13          121     biphasic

Rata       15        all         female    6.3 - 9.9   33-     biphasic       Zenzen (1979)
                     routes                            374

Monkeyc    10        urine       female    92.4        -       monophasic     Braun &
                                 male      40.8        -       monophasic     Sauerhoff
a   Intraperitoneal.  b   Subcutaneous.
c   Oral.             d   Inhalation.

    When comparing the turnover of PCP in rats after single and 
after repeated inhalation exposure, Hoben et al. (1976d) did not 
find any evidence of accumulation.  The clearance rates for urine, 
plasma, liver, and lung were fairly parallel.  After repeated 
inhalation exposures to about 5.9 mg/kg body weight, the PCP body 
burden did not increase as expected from the 24-h half-life 
following a single exposure.  On the basis of the increased urinary 
excretion, the authors concluded that the biotransformation was 
accelerated and possibly induced by prior exposure to PCP. 

6.5.2  Human studies

    Braun et al. (1979) observed a time lag in the urinary 
excretion rate following a single oral dose of 0.1 mg Na-PCP/kg 
body weight given to 4 volunteers (section 6.1.2). Maximum urinary 
excretion was reached 40 h after ingestion and 36 h after the 
maximum plasma level of 0.245 mg PCP/litre. The authors ascribed 
this delay to a strong enterohepatic circulation similar to that 
reported in rats and monkeys.  The elimination half-life for PCP in 
plasma was about 30 h.  The elimination half-life for PCP and PCP 
glucuronide in urine was 33 and 13 h, respectively.  The 
elimination of PCP from plasma in these human subjects followed 
linear kinetics and was monophasic, and resembled the elimination 
kinetics reported for the monkey.  Elimination kinetics in the rat 
are biphasic; however, the rate constants and half-lives for the 
absorption and elimination of PCP from rat plasma are more similar 
to those for men than those for monkeys. 

    Using the kinetic parameters determined in their single-
exposure studies, Braun et al. (1979) calculated that men ingesting 
0.1 mg PCP/kg body weight daily (based on 100% uptake of 0.5 mg 
PCP/m3 by a man carrying out light work) would attain a steady-
state plasma concentration of 0.491 mg/litre, after 8.4 days.  This 
suggests that there is no cumulative effect, even with repeated 
daily low-level exposure.  This conclusion is based on a simulation 
model for the daily ingestion of PCP using data derived from 
single-dose studies. 

    Uhl et al. (1986) studied 3 healthy male volunteers aged 29, 
24, and 47 years, exposed to single oral doses of PCP (purity > 
99%) in 40% ethanol in 6 different studies.  The doses varied from 
0.016 to 0.31 mg PCP/kg body weight.  Their results are in contrast 
to those of Braun et al. (1979).  Uhl et al. (1986) determined PCP 
elimination half-lives of 16 days (plasma) and 18 - 20 days 
(urine), elimination rates being about 13 times slower than those 
reported by Braun et al. (1979).  Uhl et al. (1986) did not find 
any evidence for an enterohepatic accumulation mechanism.  They 
ascribed the low elimination rate to the high protein-binding 
tendency of PCP and the concomitantly low PCP clearance observed 
(0.07 ml/min).  At normal urinary pH (5 - 6), PCP exists in its 
phenolic form and therefore more than 99% of the filtered PCP is 
believed to be reabsorbed in the renal tubules.  In one study, 
alkalinization of the urine by administration of sodium bicarbonate 
considerably enhanced the elimination rate of PCP in urine.  Over 
the pH range 5.4 - 7.8, the rate of PCP elimination varied by a 

factor of 8; urinary excretion was approximately 2 g PCP/h at pH 
5.4 and about 16 g PCP/h at pH 7.4. 

    The differences in the pharmacokinetic profile established in 
the 2 studies may be explained by the different experimental 
regimes.  Uhl et al. (1986) administered the PCP in ethanol; Braun 
et al. (1979) administered the sodium salt of PCP in water.  The 
role of the dietary status of the volunteers before and after the 
PCP ingestion or of any other factors is unknown.  According to Uhl 
et al. (1986), the time lag necessary to attain a steady state 
after a change in the exposure, as calculated from the elimination 
half-life, is about 3 months.  These authors estimated that the 
human body burden of PCP at steady state is 10 - 20 times higher 
than that estimated by Braun et al. (1979). 

    Reported cases of accidental PCP exposure as well as data from 
occupationally exposed people seem to confirm the results of Uhl et 
al. (1986).  In the case of an accidental uptake of PCP through the 
skin (section 6.1.2), the urinary-PCP concentration decreased from 
236 g/litre, 2 days after the accident to 17 g/litre, 51 days 
later (Bevenue et al., 1967a).  From these data, an elimination 
half-life of about 15 days can be derived. 

    In the case of intentional ingestion of PCP (solvent: 82% 
aromatic petroleums) discussed in section 6.1.2, despite forced 
diuresis with furosemide and mannitol, the serum-PCP level of the 
patient decreased from the highest level on day 2 (155 mg 
PCP/litre) to 12 mg PCP/litre on day 37 (Haley, 1977), suggesting 
an elimination half-life of approximately 10 days. 

    Begley et al. (1977) surveyed PCP concentrations in the blood 
and urine of 18 workers in a wood-treatment factory before and 
during a 20-day vacation.  The blood and urine levels of PCP 
decreased from an average of 5.14 mg/litre to 2.19 mg/litre and 
from 1.31 mg/litre to 0.59 mg/litre, respectively, during vacation.  
Elimination half-lives of about 9 days for both urine and plasma 
can be derived. 

    Casarett et al. (1969) calculated an excretion half-life of 
about 10 h, based on measurements made one day after a single 
inhalation exposure in 2 wood-treatment workers. Despite this rapid 
elimination rate, the PCP concentrations in the urine of workers 
following a long-term high level exposure (PCP in urine, 1.6 - 2.6 
mg/litre) did not decrease by more than 60 - 80% "even after a long 
absence from exposure" (Casarett et al., 1969).  In a comparable 
survey with a group of woodworkers exposed long-term to Permatox 
100 (3% PCP, 21% tetrachlorophenol), no clear elimination pattern 
could be found during a 16-day vacation (Kalman & Horstman, 1983); 
half-times for urinary elimination varied from 4 to 72 days, as 
estimated from the urinary-PCP levels at day 0 and day 16.  A number 
of pre-exposed workers showed an increase in urinary-PCP during the 
vacation, either as a result of storage of PCP in tissues (section 
6.6), additional exposure to PCP independent of work-place 
exposure, or a continuous biotransformation of hexachlorobenzene 
and similar compounds to PCP (section 5.2.2).  However, the latter 

can hardly explain an increase in urinary-PCP levels of 53 - 88 
g/litre, as observed by Kalman & Horstman (1983); urinary-PCP 
levels range around 10 g/litre for the general population and 
around 40 g/litre for people exposed non-occupationally (section 

    Since all controlled studies on the metabolism of PCP in 
mammals have been performed using pure PCP, a judgement of the 
influence of impurities in commercial PCP on the metabolism of PCP 
is not possible.  In fish, Huckins & Petty (1983) observed a 
greater conjugation of PCP to its glucoronide with exposure to 
purified PCP compared with exposure to commercial PCP.  Conjugation 
may be a rate-limiting step in its elimination, in which case the 
toxic impurities in industrial PCP formulations could alter the 
turnover pattern. 

6.6  Reaction With Body Components

    Braun et al. (1977) found that 99% of the PCP in rat plasma was 
bound to protein.  Heterogenous binding has been demonstrated, 
indicating that, at very low plasma concentrations of PCP, the 
protein binding becomes even stronger, because of preferential 
binding to more limited but higher affinity sites.  Braun et al. 
(1977) and Uhl et al. (1986) suggested that this heterogenous 
plasma-protein binding might be the cause of long-term urinary 
excretion of PCP.  Hoben et al. (1976e) found that human plasma had 
a much higher capacity for binding to PCP than rat plasma; this 
could explain the longer retention times observed in human beings 
compared with that in the rat.  The difference in binding capacity 
could not be accounted for by albumin fraction. 

    PCP is conjugated  in vitro to palmitic acid in rat liver 
incubated with a coenzyme A-fortified microsomal system (Leighty & 
Fentiman, 1982).  Presumably, the binding of PCP to fatty acids 
could contribute to PCP retention in lipid-containing tissues. 

    Weinbach & Garbus (1965) had already discovered the strong 
affinity of PCP for rat liver mitochondrial protein.  In more 
recent studies of Arrhenius et al. (1977a,b) on the sub-cellular 
distribution of PCP, PCP accumulation in microsomes or in the 
cytosol was approximately 6 and 3 times, respectively, higher than 
in the mitochondria.  On this basis, the authors suggested that the 
microsomal functions, though 4 times less sensitive than 
mitochondrial oxidative phosphorylation, were disturbed by PCP 
concentrated in these organelles, possibly increasing the toxic 
and carcinogenic action of other xenobiotics. 


    The toxic effects of chlorophenols have been studied in a 
number of organisms.  The degree of oil solubility governs the 
toxicity of phenolic compounds by controlling their binding to 
lipoid cellular structures, e.g., biological membranes, which 
probably are the loci of action of PCP.  Blackman et al. (1955a,b) 
showed that, with the duckweed  Lemna minor and the mould 
 Trichoderma viride, the lipophilic behaviour and, hence, the 
toxicity of chlorophenols increased with the degree of chlorination 
of the aromatic ring, PCP being the most effective chlorophenol.  
Similar results have been reported from studies on fish (Ingols & 
Gaffney, 1965), bacteria (Liu et al., 1982), and algae (Huang & 
Gloyna, 1968; Rowe et al., 1982). 

    Although there have been some studies on the effects of PCP on 
ecosystems, most of the toxicity data have been derived from single 
species trials.  Moreover, most bioassays deal with acute rather 
than long-term toxic effects. 

7.1  Microorganisms

    The microbiocidal effectiveness of PCP has been the basis of 
its widespread use as a bactericide and fungicide (section 3.3).  
For instance, PCP at a concentration of 0.25% and 0.125% (v/v) was 
used to control the sapstain fungi  Trichoderma harzianum and 
 Phialophora sp., respectively (Cserjesi & Roff, 1975).  Conkey & 
Carlson (1963) screened PCP-containing pesticides against 2 
bacterial species and 2 species of fungi that are common in pulp 
and paper mill systems.  Depending on the PCP formulation and the 
microbial species, complete inhibition occurred on agar plates at 
4 - 250 ppm. 

    Ishizawa et al. (1961) found bacterial und fungal growth in 
soil to be depressed by PCP at 2 g Na-PCP/kg dry soil. Similarly, 
oxidative phosphorylation and ATPase activity in  Micrococcus 
 denitrificans cultures were strongly inhibited by PCP at a 
concentration of about 130 mg/litre (Imai et al., 1967). 

    In anaerobic soil containing 10 mg PCP/kg, Murthy et al. (1979) 
observed reduced soil respiration as PCP directly or indirectly 
inhibited cellulose degradation.  The degradation of PCP itself may 
also be affected by the toxicity of this compound for degrading 

    Godsy et al. (1986) studied the effects of PCP on the 
methanogenic fermentation of phenol in anaerobic laboratory 
digestors.  With PCP concentrations of 0.1 mg/litre or less, PCP 
was dechlorinated to non-toxic levels allowing for complete 
bioconversion of phenol (200 mg/litre) and PCP, presumably to 
methane and carbon dioxide (CO2).  Higher PCP levels inhibited the 
methanogenic fermentation; at 5 mg PCP/litre, complete inhibition 

    Tam & Trevors (1981a,b) studied the effects of PCP on 
asymbiotic nitrogen fixation in soil.  The EC50 values for the 
inhibition of nitrogenase activity in non-sterile soil, incubated 
aerobically and anaerobically, and in sterilized soil inoculated 
with  Azotobacter sp. were 49.8 mg Na-PCP/kg, 186.8 mg Na-PCP/kg, 
and 660.8 mg Na-PCP/kg, respectively.  The inhibition of both CO2 
evolution and oxygen uptake by  Azotobacter vinelandii was found to 
be similar to that of nitrogen fixation activity (Tam & Trevors, 
1981a).  The high concentrations required for inhibition suggest 
that, at normal field application rates, no adverse effects on 
nitrogenase activity would be expected. 

    Na-PCP at 50 and 100 mg/kg had a stimulating effect on soil 
microbial electron transport activity, while 200 mg Na-PCP/kg 
caused 5.8% inhibition (Trevors, 1982c).  Inhibition by Na-PCP was 
greater in soil enriched with glucose and yeast extract than in 
non-amended soil.  Concentrations of 25 - 50 mg PCP/litre of 
nutrient broth delayed the growth of the bacterium  Pseudomonas 
 fluorescens, which does not degrade PCP.  A 1-h exposure to 75 mg 
PCP/litre inhibited growth completely.  Higher concentrations of 
PCP were required to produce inhibition of respiration.  Oxygen 
consumption was reduced by 21% at a concentration of 25 mg 
PCP/litre, while CO2 evolution was not inhibited (Trevors et al., 
1981a; Trevors, 1982b). 

    Pre-exposure to PCP lowered the sensitivity of  Pseudomonas 
 fluorescens to PCP (Trevors et al., 1982).  In addition, non-toxic 
concentrations of the antioxidants butylated hydroxyanisole (BHA) 
and butylated hydroxytoluene (BHT), which have also been used as 
food additives, enhanced the toxicity of PCP for this bacterial 
species (Trevors et al., 1981b). 

    Izaki et al. (1981) found gram-negative bacteria to be more 
resistant to PCP than gram-positive bacteria.  Some very resistent 
 Pseudomonas strains tolerated over 500 mg PCP/litre.  Studies on 
various mutants, in which the lipopolysaccharide layers were more 
or less defective, supported the hypothesis that these layers act 
as a barrier for PCP and impart resistance to gram-negative 

7.2  Aquatic Organisms

    PCP has been used in aquatic environments as a molluscicide 
and an algicide.  The potential hazard of PCP was recognized early, 
leading to a number of toxicological studies on aquatic organisms; 
these have been reviewed by US EPA (1978) and Buikema et al. 
(1979).  In general, PCP is extremely toxic for aquatic organisms.  
Apart from very sensitive or resistant species, there is apparently 
no significant difference in sensitivity to PCP between the 
different taxonomic groups (Adema & Vink, 1981). 

7.2.1.  Plants

    Most toxicity tests on aquatic plants have been performed on 
algae, particularly the microscopic, free-floating forms.  A 
selection of these tests is summarized in Table 28.  One of the 

more striking features evident from the Table is the extreme 
variability in the PCP levels that result in toxic effects.  For 
example, Adema & Vink (1981) determined that a nominal 
concentration of 7 mg/litre inhibited the growth of  Chlorella 
 pyrenoidosa by 50%.  In contrast, Huang & Gloyna (1968) found that 
as little as 7.5 g/litre caused complete destruction of chlorophyll 
in the same species. 

    At least part of this variability reflects different 
sensitivities to PCP between algal species.  Adema & Vink (1981) 
found that the green alga  Scenedesmus quadricauda had an EC50 for 
growth that was 87.5 times lower than that for  Chlorella 
 pyrenoidosa.  The most sensitive algae were  Ankistrodesmus falcatus 
and  Microcystis sp., for which as little as 0.001 mg PCP/litre 
inhibited photosynthesis by an average of 21%, in semi-continuous 

    However, the tremendous variability in susceptibility to PCP 
presented in the Table cannot be accounted for solely by species-
specific differences in sensitivity.  They probably also reflect 
differences in the experimental conditions under which the tests 
were run, such as the ambient pH, which affects PCP toxicity for 
invertebrates (section 7.2.2), and presumably algae. 

    Some aquatic vascular plants have also been used for toxicity 
studies.  The water hyacinth  (Crassipes eichhornia) is relatively 
tolerant to Na-PCP; a concentration of 5 mg/litre was required to 
affect its appearance, and 80 mg/litre to kill the plant (Hirsch, 
1942).  Only 7.1 x 10-7 mol PCP/litre (approximately 0.19 mg/litre) 
were required to induce 50% chlorosis in the fronds of the duckweed 
 (Lemna minor) (Blackman et al., 1955a).  In contrast, Huber et al. 
(1982) noted a 50% decrease in the chlorophyll content of this 
aquatic macrophyte on exposure to 3 - 4 mg PCP/litre.  
Photosynthesis as well as the activity of glutamate dehydrogenase 
and alanine aminotransferase were similarly inhibited, but there 
was no pronounced effect on dark respiration. 

7.2.2  Invertebrates

    As shown in Table 29, the toxicity of PCP or Na-PCP for 
invertebrates varies with concentrations ranging from 0.068 
mg/litre to 10.39 mg/litre.  Most of the reported 50% lethal or 
effective concentrations are below 1 mg/litre. 

    In general, developing embryos and larvae are more affected by 
PCP than the adults (Table 29).  The most striking difference was 
reported by van Dijk et al. (1977), who found that, at the same Na-
PCP concentration, the larvae of the marine decapod  Palaemon 
 elegans were inhibited (in terms of the 96-h LC50) about 130 times 
more than the adults.

Table 28.  The toxicity of PCP and Na-PCP for algae
Test species     Aquatic     Test type        Test      Concent-    Effects            Reference
                 system                       duration  ration
                                              (h)       (mg/litre)
 Chlorella        freshwater  static           72        0.008       complete           Huang & Gloyna
  pyrenoidosa                                                        destruction of     (1968)

 Chlorella        freshwater  static and flow  96        7a          EC50, growth       Adema & Vink
  pyrenoidosa                                                                           (1981)

 Scenedesmus      freshwater  static and flow  96        0.08a       EC50, growth       Adema & Vink
  quadricauda                                                                           (1981)

 Microcystis      freshwater  static           96        1           NOEC, growth       Sloof & Canton
  aeruginosa                                                                            (1983)

 Scenedesmus      freshwater  static           96        0.1         NOEC, growth       Sloof & Canton
  pannonicus                                                                            (1983)

 Cylindrospermum  freshwater  static           72        2           no growth          Palmer & Maloney
  licheniformeb                                                                         (1955)

 Microcystis      freshwater  static           72        2           no growth          Palmer & Maloney
  aeruginosab                                                                           (1955)

 Scenedesmus      freshwater  static           72 - 168  2           growth inhibition  Palmer & Maloney
  obliquusb                                                                             (1955)

 Chlorella        freshwater  static           72 - 504  2           no inhibition      Palmer & Maloney
  variegatab                                                                            (1955)

 Monochrysis sp.  marine      static and flow  96        0.2a        EC50, growth       Adema & Vink

Table 28.  (contd.)
Test species     Aquatic     Test type        Test      Concent-    Effects            Reference
                 system                       duration  ration
                                              (h)       (mg/litre)
 Chlamydomonas    marine      static and flow  96        1.4a        EC50, growth       Adema & Vink
  sp.                                                                                  (1981)

 Phaeodactylum    marine      static and flow  96        3a          EC50, growth       Adema & Vink
  tricornutum                                                                           (1981)

 Dunaliella sp.   marine      static and flow  96        3.6a        EC50, growth       Adema & Vink

 Chlorella ovalis marine      static and flow  96        5.5a        EC50, growth       Adema & Vink

 Ankistrodesmus   marine      semi-continuous  216 -     0.001       inhibition of      Gotham & Rhee
  falcatus                    flow             264                   photosynthesis     (1982)

 Microcystis sp.  marine      semi-continuous  216 -     0.001       inhibition of      Gotham & Rhee
                             flow             264                   photosynthesis     (1982)

 Melosira sp.     marine      semi-continuous  216 -     0.001       inhibition of      Gotham & Rhee
                             flow             264                   photosynthesis     (1982)
                                                                    and growth

 Selenastrum      marine      static           2         0.05 -      beginning inhibi-  Jayaweera et al.
  capricornutum                                          0.1         tion of carbon     (1982)
                                                                    assimilation rate

 Selenastrum      marine      static           2         2.66        complete inhibi-   Jayaweera et al.
  capricornutum                                                      tion               (1982)
a   Average results of static and flow-through tests.
b   Na-PCP.
    Dragonfly nymphs ( Epicordulia sp.), damsel fly nymphs ( Ischnura
sp.), isopods ( Asellus communis Say), and amphipods ( Hyalella 
 knickerbockeri Bate) were resistant to Na-PCP compared with other 
invertebrate species, and easily survived exposure to 5 mg/litre 
(Goodnight, 1942).  Turner et al. (1948) found that 0.1 mg Na-
PCP/litre was ineffective against mussels  (Mytilus edulis), 
anemones, and barnacles, while a concentration of 1 mg/litre 
prevented attachment and growth in sea water. 

    The results of more recent studies, mainly conducted on 
annelids, molluscs, and crustaceans, are mostly based on median 
lethal or effective concentrations (LC50, EC50, TLm).  However, a 
comparison of acute toxicity data established within equal test 
duration may only be appropriate if the various organisms have 
similar life cycles.  It is arbitrary to compare, for instance, the 
96-h LC50 of copepods, crayfish, and trout.  On a basis of the 
median life span, a 96-h toxicity test with the cladoceran  Daphnia 
would correspond to a test with trout or carp lasting as long as 
one year. 

    Very few studies have been carried out to assess chronic or 
sublethal effects, or the influence of various environmental 
conditions on the toxicity of PCP.  Examining the effect of Na-PCP 
on the burrowing activity of a lugworm  (Arenicola cristata), 
Rubinstein (1978) noted a significant adverse effect at 
concentrations of 80 and 156 g Na-PCP/litre.  At both 
concentrations, no mortality was observed.  The reduced lugworm 
activity could affect the sediment turnover. 

    At sublethal concentrations (120 g PCP/litre), coelomic fluid 
glucose in the marine sandworm  Neanthes virens increased to about 
twice the control levels after 24 h and then gradually decreased 
(Carr & Neff, 1981; Thomas et al., 1981).  Ascorbic acid levels 
became elevated during exposure, indicating sublethal stress.  
During the acute lethal exposure (above 365 g/litre), a 
significant hypoglycaemic response and ascorbic acid depletion were 

    The acute toxicity of PCP has been found to be pH dependent 
(Table 29).  The data of Whitley (1968) indicate that the toxicity 
of PCP for tubificid worms increased up to almost 5-fold, when the 
pH value decreased from 9.5 to 7.5. This is consistent with the 
sensitivity pattern of various oligochaete species (Chapman et al., 
1982).  Similarly, lowering the pH from 7.5 to 6.5 increased the 
toxicity of PCP for the crayfish  (Astacus fluviatilis) by a factor 
of 5.9 (Kaila & Saarikoski, 1977).  The non-ionized form of a 
compound penetrates biological membranes much more easily than the 
ionized form, which accounts for the effects of pH on PCP toxicity. 

Table 29.  The toxicity of PCP and Na-PCP for invertebrates
Test species            Life    Aquatic     Test    Test      Test  Concen-  Effects      Reference
                        stage   system      type    modifier  dura- tration
                                                              tion  (mg/
                                                              (h)   litre)  
Tubificid wormsa,b              freshwater  static  pH 7.5    24    0.31     LC50         Whitley (1968)

Tubificid wormsa,b              freshwater  static  pH 8.5    24    0.67     LC50         Whitley (1968)

Tubificid wormsa,b              freshwater  static  pH 9.5    24    1.40     LC50         Whitley (1968)

Water flea                      freshwater  static            24    0.8      EC50         Bringmann &
 (Daphnia magna)                                                                           Khn (1982)

Fresh-water snail               freshwater  static            96    0.16     LC50         Gupta & Rao
 (Lymnaea acuminata)                                                                       (1982)

Fresh-water snail               freshwater  static            96    0.19b    LC50         Gupta & Rao
 (Lymnaea acuminata)                                                                       (1982)

Eastern oyster                  marine      static            48    < 0.25   LC50, egg    Davis & Hidu
 (Crassostrea virginica)                                                      development  (1969)

Eastern oyster                  marine      static            336   0.07     LC50,        Davis & Hidu
 (Crassostrea virginica)                                                      survival     (1969)
                                                                             of larvae

Pacific oysterb                 marine      static            48    0.027    4.3%         Woelke (1972)
 (Crassostrea gigas)                                                          abnormal

Pacific oyster                  marine      static            48    0.069    72.4%        Woelke (1972)
 (Crassostrea gigas)                                                          abnormal

Table 29.  (contd.)
Test species            Life    Aquatic     Test    Test      Test  Concen-   Effects     Reference
                        stage   system      type    modifier  dura- tration
                                                              tion  (mg/
                                                              (h)   litre)  
Pacific oyster                  marine      static            48    0.11     100%         Woelke (1972)
 (Crassostrea gigas)                                                          abnormal

Eastern oyster                  marine      static            48    0.04     EC50,        Borthwick &
 (Crassostrea virginica)                                                      embryo       Schimmel (1978)

European brown shrimp   adult   marine      static            96    1.79     LC50         van Dijk et
 (Crangon crangon)b                                                                        al. (1977)

European brown shrimp   larvae  marine      static            96    0.11     LC50         van Dijk et
 (Crangon crangon)b                                                                        al. (1977)

Marine decapod          adult   marine      static            96    10.39    LC50         van Dijk et
 (Palaemon elegans)b                                                                       al. (1977)

Marine decapod          larvae  marine      static            96    0.08     LC50         van Dijk et
 (Palaemon elegans)b                                                                       al. (1977)

Brackish water decapod  adult   marine      static            96    5.09     LC50         van Dijk et 
 (Palaemonetes varians)b                                                                   al. (1977)

Brackish water decapod  larvae  marine      static            96    0.36     LC50         van Dijk et
 (Palaemonetes varians)b                                                                   al. (1977)

Table 29.  (contd.)
Test species            Life    Aquatic     Test    Test      Test  Concen-  Effects      Reference
                        stage   system      type    modifier  dura- tration
                                                              tion  (mg/
                                                              (h)   litre)  
Grass shrimp            inter-  marine      static            96    2.63     LC50         Conklin & Rao
 (Palaemonetes pugio)b   molt                                                              (1978)

Grass shrimp            early   marine      static            96    2.74     LC50         Conklin & Rao
 (Palaemonetes pugio)b   premolt                                                           (1978)

Grass shrimp            late    marine      static            96    0.44     LC50         Conklin & Rao
 (Palaemonetes pugio)b   premolt                                                           (1978)

Brown shrimp                    marine      flow              96    > 0.195  LC50         Schimmel et
 (Penaeus aztecus)b                                                                        al. (1978)

Copepod  (Pseudodiap-            marine      static            96    0.068    LC50         Hauch et al.
 tomus coronatus)b                                                                         (1980)

Crayfish                        marine      semi-   pH 7.5    192   53       LC50         Kaila &
 (Astacus fluviatilis)                       contin-                                       Saarikoski
                                            uous                                          (1977)

Crayfish                        marine      semi-   pH 6.5    192   9        LC50         Kaila &
 (Astacus fluviatilis)                       contin-                                       Saarikoski
                                            uous                                          (1977)
a   Mixed population of  Tubifex tubifex and  Limnodrilus hoffmeisteri.
b   Na-PCP.
7.2.3  Vertebrates

    Most studies on vertebrates have been performed with fish.  In 
short-term studies, the LC50 values for PCP or Na-PCP are generally 
less than 1 mg PCP/litre, and, in many cases, even less than 0.1 mg 
PCP/litre (Table 30). 

    The effectiveness of purified PCP and Na-PCP as well as of 
commercial products has been investigated under comparable 
conditions in only a few cases.  Borthwick & Schimmel (1978) 
determined that the 96-h LC50 for 14-day-old sheepshead minnow fry 
exposed to analytical grade PCP was similar to that of the 
commercial formulation Dowicide G (0.392 and 0.516 mg/litre, 
respectively, corresponding to 1.47 and 1.41 mol). Similarly, the 
prolarval pinfish was, on a molar basis, about equally affected by 
analytical grade Na-PCP (LC50, 0.038 mg/litre = 0.14 mol) and 
Dowicide G (LC50, 0.066 mg/litre = 0.18 mol). 

    Differences in the toxicity of PCP and Na-PCP for fish have 
been observed under various test conditions.  For example, both the 
goldfish  (Carassius auratus) and the sheepshead minnow  (Cyprinodon 
 variegatus) were more affected by PCP in static than in continuous-
flow bioassays (Table 30).  Ruesinck & Smith (1975) noted that the 
fathead minnow  (Pimephales promelas) was more resistant to Na-PCP 
at 25 C than at 15 C.  In contrast, Crandall & Goodnight (1959) 
observed that higher temperatures increased the toxicity of Na-PCP 
for the fathead minnow  (Pimephales promelas), i.e., the LD50 at 
10 C, 18 C, and 26 C was 260, 81, and 46 mg/litre, respectively.  
Temperature was also found to control PCP toxicity for rainbow 
trout  (Salmo gairdneri) (Hodson & Blunt, 1981).  Eggs of trout 
exposed to PCP at 0.01 - 0.1 mg/litre) showed elevated mortality 
between fertilization and hatch and reduced weight at hatch.  The 
effects on hatch weight were greater at 6 C than at 10 C, while 
growth rates were reduced more at 20 C than at 12 C. 

    Saarikoski & Viluksela (1981) also demonstrated that the 
ambient pH influences the toxicity of PCP for fish. The 96-h LC50 
values for the guppy  (Poecilia reticulata) were about 0.04 mg/litre 
at pH 5, 0.12 mg/litre at pH 6, 0.44 mg/litre at pH 7, and 0.91 
mg/litre at pH 8.  At pH 5, 33.39% of PCP is in the molecular form, 
while, at pH 8, more than 99% exists as phenate ion.  Since the 
change in toxicity was substantially smaller than it would be if 
only the molecular PCP were toxic, the authors concluded that the 
phenate ion also contributes to the toxic effect. 

    Dissolved oxygen also plays an important role in modifying the 
toxicity of PCP for fish.  Dissolved oxygen levels of 7.8, 6.5, or 
5 mg/litre resulted in 96-h LC50 values of 0.107, 0.083, and 0.026 
mg PCP/litre, respectively (Gupta et al., 1983a).  The increase in 
toxicity at low levels of dissolved oxygen may be due to enhanced 
absorption of PCP via gills, as the ventilation rate speeds up 
under low oxygen regimes. 

Table 30.  The toxicity of PCP and Na-PCP for various fish species
Test species             Life      Aquatic Test     Test      Test      Concen-   Effect  Reference
                         stage     system  type     modifier  duration  tration
                                                              (h)       (mg/litre)
Brown trout                        fresh-  static             24        0.2       LC50    Hattula et al.
 (Salmo trutta)                     water                                                  (1981)

Bluegill sunfish                   fresh-  static   hardness  48        0.03 -    LC50    Inglis & Davis
 (Lepomis macrochirus)              water                                0.04              (1972)

Goldfish                           fresh-  static   hardness  48        0.08 -    LC50    Inglis & Davis
 (Carassius auratus)                water                                0.17              (1972)

Fathead minnow           juvenile  fresh-  flow               48        0.21      LC50    Ruesinck & Smith
 (Pimephales promelas)              water                                                  (1975)

Rainbow trouta                     fresh-  static   labora-   96        0.05 -    LC50    Davis & Hoos
 (Salmo gairdneri)                  water            toryb               0.10              (1975)

Coho salmona                       fresh-  static   labora-   96        0.03 -    LC50    Davis & Hoos
 (Oncorhynchus kisutch)             water            toryb               0.09              (1975)

Goldfish                           fresh-  flow               96        0.22      LC50    Adelmann & Smith
 (Carassius auratus)                water                                                  (1976)

Fathead minnow           juvenile  fresh-  static             96        0.6       LC50    Mattson et al.
 (Pimephales promelas)              water                                                  (1976)

Common carpa             larvae    fresh-  static             96        0.01      LC50    Verma et al.
 (Cyprinus carpio)                  water                                                  (1981b)

Table 30.  (contd.)
Test species             Life      Aquatic Test     Test      Test      Concen-   Effect  Reference
                         stage     system  type     modifier  duration  tration
                                                              (h)       (mg/litre)
Guppy                              fresh-  static             96        0.97      LC50    Gupta et al.
 (Lebistes reticulatus)             water                                                  (1982)

Sheepshead minnow                  marine  flow               96        0.44      LC50    Parrish et al.
 (Cyprinodon variegatus)                                                                   (1978)

Sheepshead minnow        1-day-    marine  static             96        0.329     LC50    Borthwick &
 (Cyprinodon variegatus)  old fry                                                          Schimmel (1978)

Sheepshead minnow        14-day-   marine  static             96        0.392     LC50    Borthwick &
 (Cyprinodon variegatus)  old fry                                                          Schimmel (1978)

Sheepshead minnow        28-day-   marine  static             96        0.240     LC50    Borthwick &
 (Cyprinodon variegatus)  old fry                                                          Schimmel (1978)

Sheepshead minnow        42-day-   marine  static             96        0.223     LC50    Borthwick &
 (Cyprinodon variegatus)  old fry                                                          Schimmel (1978)

Pin percha               adult     marine  flow               96        0.053     LC50    Schimmel et al.
 (Lagodon rhomboides)                                                                      (1978)

Pin percha               48-h      marine  static             96        0.038     LC50    Borthwick &
 (Lagodon rhomboides)     pro-                                                             Schimmel (1978)
a   Na-PCP.
b   Results of an inter-laboratory bioassay standardization exercise.
    The size of fresh-water fish may also influence the toxicity of 
PCP.  The toxicity of PCP for  Notopterus notopterus decreased with 
increasing fish length up to 14.5 cm, though larger fish were again 
more susceptible (Gupta et al., 1982).  Similarly, slight 
differences in sensitivity were observed when  Cyprinodon variegatus
fry of different ages were exposed to PCP (Borthwick & Schimmel, 

    As with invertebrates, larvae of fish seem to be more 
vulnerable to PCP than adult fish.  The lowest value in Table 30 in 
terms of LC50 is based on tests with the larvae of the fresh-water 
carp  (Cyprinus carpio). 

    Data derived from acute toxicity tests are of limited value in 
estimating the long-term effects of PCP on fish. Studies dealing 
with sublethal concentrations of PCP may provide more valuable 
information, since they involve PCP concentrations approaching 
ambient levels.  Since responses to sublethal concentrations 
require prolonged periods of time, the continuous-flow method is 
usually chosen to keep test conditions, particularly the 
concentration of the toxicant, constant. 

    In underyearling sockeye salmon  (Oncorhynchus nerka) exposed to 
sublethal concentrations of Na-PCP, Webb & Brett (1973) observed 
significant reductions in growth rate and food conversion 
efficiency.  The EC50 for these processes is about 1.80 g Na-
PCP/litre (approximately 2.8% of the 96-h LC50 of 0.063 mg/litre). 

    Similarly, low concentrations of PCP (13.6 - 60.2 g/litre) 
were used to induce physiological stress in the fresh-water fish 
 Notopterus notopterus, as measured by the activity of hepatic acid 
and alkaline phosphatases and succinic dehydrogenase (Dalela et 
al., 1980a). The activity of these 3 enzymes was reduced after 10, 
20, and 30 days of exposure. The greatest effect was observed in 
acid phosphatase after 30 days at a concentration of 60.2 g 
PCP/litre caused a 71.09% inhibition of enzyme activity. 

     In vivo blood variables of  Notopterus notopterus (Verma et al., 
1981c) were sensitive to PCP concentrations as low as 1/10th, 
1/15th, and 1/20th of the 96-h LC50 of 0.083 mg PCP/litre.  
Generally, red and white blood cell counts and packed cell volume 
were increased after 30 days of exposure, while clotting time, 
erythrocyte sedimentation rate, levels of haemoglobin and mean 
corpuscular haemoglobin, and mean cell volume were decreased.  In 
addition, there were significant increases in the activity of 
transaminases in the blood-serum (Verma et al., 1981a) and in the 
brain, liver, kidney, and gills (Gupta et al., 1983b).  Succinic 
dehydrogenase and pyruvic dehydrogenase were inhibited, while the 
activity of lactic dehydrogenase was stimulated, thus indicating 
the development of anaerobic conditions at the cellular level at 
these sublethal concentrations (Verma et al., 1982). 

    Other biochemical responses were observed in juvenile striped 
mullet  (Mugil cephalus), a marine fish (Thomas et al., 1981); 
environmental stress was indicated by a rapid rise in plasma-
cortisol concentrations at 200 g PCP/litre, accompanied by a 
marked hyperglycaemia and a depletion of hepatic glycogen reserves. 

    Cleveland et al. (1982) evaluated the chronic toxicities of 
commercial PCP, purified PCP, and Dowicide EC-7 in 90-day partial 
life-cycle studies with fathead minnows  (Pimephales promelas).  The 
commercial grade PCP used contained relatively large quantities of 
hexachlorobenzene, chlorophenoxyphenols, chlorodiphenyloxides, 
chlorodibenzodioxins, and chlorodibenzofurans.  The purified PCP 
included relatively high amounts of chlorinated phenoxyphenols, and 
the Dowicide EC-7 contained a broad spectrum of impurities, 
generally at lower concentrations than the other 2 formulations.  
The commercial composite PCP formulation was the most toxic 
preparation; a concentration of 13 g/litre reduced growth of the 
fish, and 27 g/litre also reduced survival.  Growth, but not 
survival, was affected by the purified PCP at concentrations equal 
to, or greater than, 85 g/litre.  Dowicide EC-7 was the least 
toxic of the PCPs tested, and at the maximum level tested (139 
g/litre), did not adversely affect growth or survival of fathead 
minnows.  Thus, impurities present in PCP were found clearly to 
increase toxicity under long-term exposure conditions.  Moreover, 
degeneration of the fins and opercula, as well as malfunction of 
the anterior regions of the skull were also noted in fathead minnows 
exposed to the commercial composite of PCP mixture. 

7.3  Terrestrial Organisms

7.3.1  Plants

    Previously, PCP was widely used as a herbicide, defoliant, and 
preharvest desiccant.  However, as PCP is not a very specific 
herbicide in terms of inhibiting special target species (Kozak et 
al., 1979), non-target crop and wildlife species can also be 
adversely affected, though no data are available in this respect. 

    Plants may be damaged by contact with the PCP in treated wooden 
material as, for example, when fruit trees in the vicinity of 
freshly-treated wooden support posts or stakes suffered bark 
lesions and chlorosis (Ferree, 1974).  Golden delicious trees 
 (Malus domesticus) were the most sensitive, some even died. 

7.3.2  Animals

    Data on the toxicity of PCP for terrestrial animals have been 
obtained almost exclusively from laboratory studies.  The results 
of toxicity tests on experimental animals are presented in section 
8.  Some fatal cases have been reported in which farm animals were 
incidentally exposed to PCP.  Blevins (1965), for example, described 
a case of acute and lethal poisoning of baby pigs by PCP.  The 
owners of a newly constructed farrowing house had exceeded the 
manufacturer's recommendation in treating the floor with a solution 

of PCP in used crankcase oil.  All piglets died within one day 
after they had been moved into the farrowing house.  The sow was 
moved outside where she recovered.  No information was given 
concerning the PCP levels in the air or in the swine. 

    A recent case, in Canada, of the mortality of young pigs kept 
on a PCP-treated wooden floor was reported by Ryan (1983).  
Although PCP residues of 310 g/litre were found in sow's milk 
samples, no PCP could be detected in the liver and stomach of the 
young pigs.  However, g/kg concentrations of the higher 
chlorinated dioxins were found in the skin and liver of the young 
pigs, and Ryan (1983) concluded from these findings that these 
impurities were responsible for their deaths. 

    Pesticide poisonings of livestock in the United Kingdom have 
been reviewed by Quick (1982) for the period 1977-80.  Of 38 
suspected PCP poisoning incidents, only 9 were confirmed as PCP 
intoxications.  High PCP levels found in wood shavings and sawdust, 
used as bedding or litter for cats and poultry, apparently caused 
the death of animals.  Quick (1982) suspected that impurities 
present in the commercial PCP products could have been partly 
responsible for the deaths. 

    Hill et al. (1975) reported a study in which the toxicity of 
PCP was determined in young birds of 4 species after 5 days of 
feeding PCP in the diet; the relatively high LC50 values 
(3400 - 5204 mg/kg body weight) do not indicate that PCP is highly 
toxic for birds.  However, Vermeer et al. (1974) found 50 dead 
snail kites after extensive application of Na-PCP as a molluscicide 
in the rice fields of Surinam (section 5.1.4). 

7.4  Population and Ecosystem Effects

    Very few studies have addressed the effects of PCP on aquatic 
or terrestrial communities.  Field studies on pesticides have 
usually been carried out when their accidental release resulted in 
visible kills of fish, birds, or other organisms.  For instance, 
Pierce et al. (1977) and Pierce & Victor (1978) investigated the 
fate of PCP in a fresh-water lake after an overflow from a pole 
treatment waste pond caused extensive fish kills (section 7.5). 

    More valuable information about the effects of PCP on 
communities can be obtained from model ecosystem studies, in which 
the response of portions of the environment placed in a laboratory 
was observed.  Tagatz et al. (1977) designed a test system 
consisting of constant-flow aquaria containing a layer of sand, and 
seawater with its plankton as well as animals representing 
estuarine macrobenthic communities.  The averages and ranges of the 
PCP concentrations in the exposed aquaria were 7 g/litre (3 - 13 
g/litre), 76 g/litre (47 - 112 g/litre), and 622 g/litre (330 - 
964 g/litre).  After the 9-week exposure period, a dose-related 
decrease was found in the numerically dominant groups.  Molluscs in 
particular were markedly reduced at 7 g PCP/litre, and annelids 
and arthropods at 76 g/litre.  Almost no animals occurred at 622 
g PCP/litre, while the total numbers of individuals and species 

were significantly less in aquaria exposed to 76 g PCP/litre than 
in controls or those exposed to 7 g PCP/litre.  These striking 
changes in the relative abundance and diversity of species are 
evidence of substantial alterations in the community structure 
induced by PCP.  In nature, the stability of macrobenthic 
communities could be disrupted. 

    In a second study conducted with Dowicide G-ST (79% Na-PCP), 
molluscs were also the most sensitive organisms tested.  Levels of 
15.8 and 161 g PCP/litre caused similar reductions in the numbers 
of individuals and species (Tagatz et al., 1978). 

    Using the same test procedure, Cantelmo & Rao (1978) studied 
the effects of PCP on meiobenthic communities. Meiofauna comprise 
organisms that pass through a 0.5 mm sieve but are retained on a 
sieve with mesh widths smaller than 0.1 mm.  The  Nematoda are 
generally the most common taxon in marine sediments (83% in this 
study).  PCP at 76 g/litre caused an increase in the biomass and 
density of nematodes compared with those in control aquaria, while 
higher concentrations of PCP (161 and 622 g/litre) caused a 
decrease.  One of the major effects of PCP on nematodes was a shift 
from epistrate feeders to deposit feeders at concentrations of 161 
and 622 g PCP/litre.  Part of this alteration may have been due to 
the reduction of algae serving as a food supply. 

    Tagatz et al. (1981) reported the effects of PCP on field and 
laboratory estuarine benthic communities.  In principle, test 
apparata were the same as those used in earlier studies, except 
that already established communities were exposed to PCP.  
Community structure was significantly altered at a PCP 
concentration of about 140 g/litre in both field and laboratory 
aquaria; the populations of several invertebrate species were 
significantly reduced.  There were slight differences in the 
effects of PCP on numbers of individuals and species between the 
field and laboratory systems. 

    Cook et al. (1980) examined the effects of PCP on the 
microfungal succession of an estuarine benthic microcosm. 
 Trichoderma sp. was initially the most common fungus isolated from 
the sediment.  The addition of PCP (140 g/litre) resulted in an 
alteration in the pattern of species; a different species, probably 
 Penicillium canescens, assumed dominance. 

    Considerable effects of PCP on the population dynamics of 
several species were noted by Schauerte et al. (1982) during an 
outdoor study on a natural pond divided into 6 compartments of 
about 100 litres each.  PCP was applied in the water of 2 
compartments at a concentration of 1 mg/litre.  Three days after 
application, the population of  Daphnia pulex pulex was eliminated 
from the treated enclosures.  The phytoplankton species showed 
marked alterations in population dynamics: the autotrophic blue-
green alga  Chroococcus limneticus decreased, while the mixotrophic 
flagellate  Euglena acus significantly increased.  This increase was 
attributed to the reduced grazing pressure by  Daphnia; 
interspecific competition was also discussed as possible cause.  As 

a further secondary effect, the oxygen concentration significantly 
decreased, because of the "changed balance between autotrophic and 
heterotrophic populations" (Schauerte et al., 1982). 

    The US Environmental Protection Agency examined the effects of 
PCP on a periphyton community in outdoor experimental streams.  
Even at the low PCP level corresponding to the water quality 
criterion (48 g/litre) (US EPA, 1980), adverse effects were noted 
in terms of community alterations and suppressed community 
metabolism (Yount & Richter, 1986). PCP at this concentration also 
caused adverse effects on fish growth, larval drift, and larval 
yield (Zischke et al., 1985). 

7.5  Biotransformation, Bioaccumulation, and Biomagnification

7.5.1.  Aquatic organisms

    Most research on the bioaccumulation of PCP has been carried 
out in aquatic situations.  This presents difficulties in that the 
bioconcentration factors, which are generally directly related to 
the partition coefficients, could vary by several orders of 
magnitude, depending on the pH and, at high pH values, on the ionic 
strength, the two factors governing the partition coefficient of 
PCP (Kaiser & Valdmanis, 1982).  In addition, exposure time must 
also be taken into account when interpreting PCP residues in 
organisms.  These influences may, in part, explain the wide range 
in bioconcentration factors that has been found. 

    In general, substances with the solubility properties of PCP 
are predominantly taken up by the surrounding water (Niimi & 
McFadden, 1982).  However, PCP accumulation along the food chains 
contributes to its overall bioaccumulation as well. 

    Table 31 shows the bioconcentration factors derived for several 
fish species along with the ambient levels in water. Fresh-water 
species seem to accumulate PCP to a much greater extent than marine 
fish, possibly because the relevant enzyme systems in marine 
species respond faster than those in fresh-water fish (Trujillo et 
al., 1982). 

    Since the ambient concentrations of PCP in the water of natural 
aquatic environments are usually less than 1 g/litre (section 
5.1.2), the studies of Niimi & McFadden (1982) are of particular 
importance.  The authors applied realistic concentrations in 
exposing rainbow trout  (Salmo gairdneri) to < 10 (control), 35, 
and 660 ng Na-PCP/litre, and distinguished between PCP content in 
liver and gall bladder, the remaining tissues, and whole fish.  As 
shown in Table 32, rainbow trout accumulated PCP, even when exposed 
to concentrations as low as 35 ng Na-PCP/litre over prolonged 
periods.  The percentage of PCP stored was highest in the liver and 
gall bladder.  On the basis of this high bioconcentration at the 
low waterborne toxicant concentrations, the authors suggested that 
rainbow trout may be less efficient in eliminating PCP than other 

    On removal from PCP-containing water, fish eliminate previously 
accumulated PCP.  However, a portion of the PCP incorporated is 
more persistent: residues of 0.32 mg/kg (Trujillo et al., 1982) and 
0.03 in the muscle to 0.6 mg/kg in the liver (Pruitt et al., 1977) 
were still detectable after 18 and 16 days of depuration, 
respectively.  Elimination half-lives during depuration phases were 
4.7 days in killifish (Trujillo et al., 1982) and 6 - 24 days in 
rainbow trout (Glickman et al., 1977). 
Table 31.  Measured bioconcentration factors for PCP for several
fish species
Species                Time    Concentration  Bioconcen-  Reference
                       (days)  in water       tration
                               (g/litre)     factor
 Fresh-water fish
   Carassius auratus    5       100            1000        Kobayashi &
                                                          Akitake (1975a)

   Lepomis macro-       1       100            320         Pruitt et al.
   chirus (various      4       100            5 - 350     (1977)
  tissues)             16      100            4 - 230

   Salmo trutta         1       200            100         Hattula et al.
  (whole body)                                            (1981)

   Salmo gairdneri      20      0.035          200         Niimi &
  (whole body)                 0.660          130         McFadden (1982)
                       65      0.035          600
                               0.660          232

   Leuciscus idus       3       42             1050        Freitag et al.
   melanotus (whole                                        (1982)

 Marine fish
   Fundulus similis     4       36 - 306       30          Schimmel et al.
  (unspecified                                            (1978)

   Mugil cephalus       4       26 - 308       38          Schimmel et al.
  (unspecified                                            (1978)

   Mugil cephalus       4       46             6           Faas & Moore
  (edible tissues)     4       85             79          (1979)
                       4       157            56

   Fundulus similus     1       57 - 610       8           Trujillo et al.
  (whole body)         1                      49          (1982)
                       7                      64
                       7                      47
    In an ecotoxicological profile analysis, Freitag et al. (1982) 
determined the bioconcentration of PCP not only in fish (Table 31) 
but also in the green alga  Chlorella fusca var. vacuolata and in 
activated sludge.  The bioaccumulation factor in the 24-h algal 
test was 1250; in a 5-day activated sludge assay it was 1100 at a 
waterborne concentration of 0.05 mg PCP/litre. 

Table 32.  PCP levels in tissues, organs, and 
whole body of rainbow trout  (Salmo gairdneri) 
exposed to < 10 (control), 35, and 660 ng 
       Na-PCP      PCP concentrations (g/kg) in: 
Days   in water    liver and      remaining  whole 
       (ng/litre)  gall bladder   tissue     body
0      < 10        2.3            1.1        1.1
20     < 10        1.2            1.5        1.5
       35          28             7          7
       660         674            77         86

65     < 10        3.9            3.7        3.6
       35          135            20         21
       660         1984           135        153

115    < 10        3.1            1.9        1.9
       35          63             6          7
       660         2204           128        160
a   Adapted from: Niimi & McFadden (1982).

    Ernst (1979) measured PCP residues in water and benthic 
invertebrates at steady state in a static marine system.  For the 
common mussel  (Mytilus edulis) and the polychaete  (Lanice 
 conchilega), bioconcentration factors averaged 390 and 3820 on a
wet weight basis, respectively, at an initial PCP concentration in 
sea water of 0.002 - 0.005 mg/litre.  The species studied and the 
lipid contents of the animals had pronounced effects on the 
bioconcentration factor, while temperature and metabolic activity 
did not show any remarkable effects on the bioaccumulation.  In a 
similar study, the polychaete  (Neanthes virens) was exposed to 0.1 
mg 14C-PCP/litre in sea water (Carr & Neff, 1981).  The 
bioconcentration factor of 280 was 10 times lower than that 
reported by Ernst (1979) for  Lanice conchilega. 

    Clams from the Jadebusen, a North Sea bight, sampled near the 
end of a waste-water pipe, accumulated 100 - 1000 times more PCP 
than the sediments (Butte et al., 1985). 

    The studies of Pierce et al. (1977) and Pierce & Victor (1978) 
are some of the few field studies concerning the biotransformation 
of PCP.  The authors followed an accidental discharge into a fresh-
water lake near Hattiesburg, Mississippi, USA.  Within two months, 
the initially lethal levels of PCP, which had resulted in an 

extensive fish kill, decreased to between 6 and 19 g/litre in the 
water and remained near this level throughout the studies, 
apparently because of the continuous influx of contaminated water 
from other areas.  In a control pond with a low background 
concentration of 0.5 g PCP/litre, fish contained only 50 g 
PCP/litre, whereas much higher levels were found in fish in the 
contaminated pond.  Two months following the spill, levels in fish 
averaged 2500 g PCP/kg dry weight but dropped to 130 g/kg after 
6 months; background levels were achieved within about 10 months. 

    In a Finnish lake area contaminated through pulp bleaching and 
with wood preservative wastes, PCP residues in fish and plankton 
did not indicate a strong accumulation via the food chain, 
plankton > roach >> pike.  However, tetrachlorocatechol, a 
possible biodegradation product of PCP, was found to be strongly 
absorbed in plankton (Paasivirta et al., 1980). 

    In littoral microcosms, 14C-PCP was linearly accumulated by 
aquatic plants, mainly  Potamogeton foliosus and  Najos 
 guadalupensis, during the first 35 days, levelling off to 
concentrations over 700 times the initial concentration in water 
(41 g/litre).  After 8 weeks, PCP concentration in the macrophytes 
rapidly decreased (Knowlton & Huckins, 1983). 

    In an aquatic model ecosystem, the ecological magnification 
value for PCP in fish was 296, the parent compound representing 74% 
of the total extractable 14C.  The other members had lower 
bioconcentration factors: algae, 1.5; mosquito larvae, 16; snail, 
121; and  Daphnia, 165.  In a terrestrial-aquatic model ecosystem, 
the bioconcentration factors were: algae, 5;  Daphnia, 205; snail, 
21; mosquito, 26; and fish, 132 (Lu et al., 1978).  These data 
indicate that bioaccumulation takes place not only through the 
surrounding water but also along the food chains. 

7.5.2  Terrestrial organisms

    The terrestrial model ecosystem established by Lu et al. (1978) 
simulated a crop-soil interaction and included the following 
organisms: earthworm  (Lumbricus terrestris), slug  (Limax maximus), 
pillbug  (Armadillidium vulgare), saltmarsh caterpillar  (Estigmene 
 acrea), prairie vole  (Microtus ochregaster), and corn  (Zea mays). 
Corn plants grown on the soil of the model system rapidly 
accumulated radioactivity.  After 14 days, they contained 6.3 mg/kg 
of which 16% was intact PCP, 40% were unknown compounds, and 44% 
were conjugates.  The prairie vole, at the top of the food chain, 
consumed virtually all the plant and animal material in the system 
within the 5-day exposure time, and then was found to contain 0.5% 
of the total dosage applied (25 g). 

    Gruttke et al. (1986) investigated the fate of Na-PCP in two 
different  model food chains representing important groups of 
organisms commonly present in soils.  In food chain 1, contaminated 
bakers-yeast (0.87 g 14C-Na-PCP/mg dry weight) was fed to 
springtails  (Folsomia candida), which accumulated up to 0.37 g 

PCP/mg fresh weight after 10 days.  Carabid beetles  (Nebria 
 brevicollis) preying on the contaminated springtails showed a body 
burden of approximately 4.5 mg PCP/kg fresh weight in the steady 
state, from day 4 to 12.  Four days after offering uncontaminated 
prey, the PCP content in the beetles dropped to 0.4 mg/kg fresh 
weight.  Similar results were obtained in food chain 2, which 
consisted of contaminated leaves of poplar (700 mg Na-PCP/kg dry 
weight), with isopods  (Oniscus asellus) as primary consumers, and 
staphylinid beetles  (Ocypus olens) as predators.  Because of the 
low accumulation tendency, a lasting effect on the predators would 
only be expected in case of long-term contamination. 

    Apart from these model ecosystem studies, little information is 
available on the biotransformation of PCP in terrestrial systems.  
Miller & Aboul-Ela (1969) observed that cottonseed kernels of bolls 
that were closed during spraying accumulated PCP or its metabolites 
in quantities of up to 2 mg/kg.  No PCP was detected when the bolls 
were open during spraying. 

    PCP, applied in nutrient solution to the roots of growing corn 
plants, was taken up by the roots (Schuppener, 1974).  At 
concentrations of up to 20 mg/litre, roots of sterile hydro-ponic 
cultures accumulated as much as 151 mg PCP/kg.  Apparently, PCP did 
not translocate in the corn plants as it was not detected in the 
upper parts of the plants.  The root system of sugarcane treated 
with 5 mg PCP/litre nutrient solution accumulated 14C-PCP within 4 
weeks, retaining over 99% of the total PCP taken up from solution 
(Hilton et al., 1970): no measurable translocation into stalks or 
leaves occurred.  These findings contrast with the translocation 
within corn plants described by Lu et al. (1978). 


    Toxicology data on both purified and commercial PCP are 
provided in this review because both are relevant for a health 
assessment. The mode of action of chlorophenol can only be 
determined using purified chemicals.  Furthermore, any decision to 
remove or reduce the levels of microcontaminants in PCP would have 
to be based on a clear understanding of the toxicity of these 
purified products. 

8.1.  Acute Toxicity

    PCP, regardless of the route of administration, is the most 
acutely toxic of the chlorophenols tested in laboratory animal 
species.  Oral LD50 values range between 27 and 205 mg/kg body 
weight for a variety of species, regardless of the vehicle of 
administration and the grade of PCP (Table 33).  Acute oral exposure 
of mice and rats to lethal doses of PCP (Deichmann, 1943; 
Farquharson et al., 1958; Borzelleca et al., 1985; Renner et al., 
1986) results in an increase in respiratory rate, a marked rise in 
temperature (4 - 4.5 C), tremors or possibly convulsions, and a 
loss of the righting reflex.  Asphyxial spasms and cessation of 
breathing usually occurs 0.5 - 2 min before cardiac arrest.  A 
rapid and intense rigor mortis is observed within 3 - 5 min of 
death and approximately 45 min sooner than the onset of rigor 
mortis in rats given ether.  Similar signs are observed with lethal 
exposure to PCP and its sodium salt, regardless of the route of 

    In addition to its systemic effects, PCP also induces more 
localized effects in test organisms.  Both dermal and subcutaneous 
applications have produced swelling, skin damage, and occasionally 
hair loss in a variety of animals (Kehoe et al., 1939; Baader & 
Bauer, 1951; Johnson et al., 1973). Localized effects on blood 
vessels may result in hyperaemia or erythema (Kehoe et al., 1939; 
Baader & Bauer, 1951).  Contact with PCP causes irritation of the 
eye, skin, or respiratory mucosae in man (section 9).  Skin 
bioassay techniques have shown that technical PCP, but not purified 
PCP, is acnegenic for rabbits, and that the acnegenic effects are 
caused by the microcontaminants, particularly H6CDD (Johnson et 
al., 1973). 

    There are far fewer published data on the effects of acute 
exposure of animals to PCP and Na-PCP via the dermal and pulmonary 
exposure routes compared with oral exposure, which is surprising 
considering that the primary exposures in the work-place are via 
the skin and lung.  Kozak et al. (1979) reported that PCP was 
readily absorbed when applied to the skin of experimental animals.  
The effects of acute dermal exposure have been examined only in the 
rat and rabbit.  For rats, but not rabbits, PCP is much more toxic 
when given orally than when applied dermally (Table 33).  However, 
with Na-PCP, toxicity via the 2 routes appears to be similar (Table 
34).  The only acute inhalation toxicity value reported for Na-PCP 
is for rats; Na-PCP is at least 10 times more toxic via inhalation 
than by oral ingestion (Hoben et al., 1976c). 

Table 33.  Acute toxicity of PCP
Species  Para-   Sex  Doseb  Route            Purity/carrier                 Reference
Mouse    LD50    F    74     oral             PCP in 40% ETOH                Ahlborg & Larsson (1978)
         LD50    M    36     oral             PCP in 40% ETOH                Ahlborg & Larsson (1978)
         LD50    F    150    oral             PCP in polypropylene glycol    Ahlborg & Larsson (1978)
         LD50    M    177    oral             PCP in 10% Emulphor            Borzelleca et al. (1985)
         LD50    F    117    oral             PCP in 10% Emulphor            Borzelleca et al. (1985)
         LD50    M    129    oral             PCP in corn oil                Renner et al. (1986)
         LD50    F    134    oral             PCP in corn oil                Renner et al. (1986)
         LD50    F    32     intraperitoneal  PCP in 40% ETOH                Ahlborg & Larsson (1978)
         LD50    M    59     intraperitoneal  PCP in polypropylene glycol    Ahlborg & Larsson (1978)
         LD50    M    59     intraperitoneal  PCP in corn oil                Renner et al. (1986)
         LD50    F    61     intraperitoneal  PCP in corn oil                Renner et al. (1986)
         LD50    M/F  82     subcutaneous                                    Ning et al. (1984)
Rat      LD50         150    oral                                            Schwetz et al. (1978)
         LD50    F    135    oral             commercial PCP                 Schwetz et al. (1974)
         LD50    M    205    oral             commercial PCP                 Schwetz et al. (1974)
         LD50         78     oral             1% in olive oil                Deichmann et al. (1942)
         LD50         65     oral                                            Schwetz et al. (1978)
         (3- to
         LD50         27     oral             0.5% in Stanolex fuel oil      Deichmann et al. (1942)
         LD50    M/F  83     oral             reagent grade                  Ning et al. (1984)
         LD50    M    146    oral             peanut oil                     Gaines (1969)
         LD50    F    175    oral             peanut oil                     Gaines (1969)
         MLD     M/F  160    oral             peanut oil                     Gaines (1969)
         LD50    F    149    cutaneous        PCP technical 40% w/v          Noakes & Sanderson (1969)
                                              solution in glycerol formal
         LD50         320    cutaneous        xylene                         Gaines (1969)
         LD50         330    cutaneous        xylene                         Gaines (1969)
         MLD     M/F  300    cutaneous        xylene                         Gaines (1969)
Rat      MDLD    M    56     intraperitoneal  olive oil                      Farquharson et al. (1958)
         LD50         100    subcutaneous     4% in fuel oil                 Deichmann (1943)
         LD50         90     subcutaneous     4% in fuel oil                 Deichmann & Mergard (1948)
         LD50    M/F  40     subcutaneous     reagent grade                  Ning et al. (1984)

Table 33.  (contd.)
Species  Para-   Sex  Doseb  Route            Purity/carrier                 Reference
Rabbit   MLD          100 -  oral             11% PCP in olive oil           Kehoe et al. (1939)
         MLD          70 -   oral             5% in Stanolex fuel oil No. 1  Deichmann et al. (1942)
         MLD          40 -   cutaneous        various carriers               Deichmann et al. (1942)
         MLD          350    cutaneous        11% in olive oil               Kehoe et al. (1939)
         MLD          39     cutaneous        1.8% in pine oil               Kehoe et al. (1939)
         MLD          60     cutaneous        5% in Stanoflex fuel oil No.1  Kehoe et al. (1939)
         MLD          110    cutaneous        5% in Shell Dione oil          Kehoe et al. (1939)
         MLD          70 -   subcutaneous     5% in Olive Oil                Kehoe et al. (1939)

Hamster  LD50         168    oral                                            Cabral et al. (1979)
         LD50         70 -   subcutaneous     5% in olive oil                Kehoe et al. (1939)

Sheep    MLD          120    oral             aqueous suspension of sawdust  Harrison (1959)
                                              treated at 20 lb technical
                                              PCP/cu. ft
Calf     MLD          140    oral             aqueous suspension of sawdust  Harrison (1959)
                                              treated at 20 lb technical
                                              PCP/cu. ft
a   MLD = Minimum lethal dose.
    MDLD = Median lethal dose.
    LD50 = Estimated dosage capable of causing 50% mortality of a test population.
    LC50 = Estimated concentration capable of causing 50% mortality of a test population.
b   LD50 or MLD in mg/kg body weight; LC50 in mg/m3 air.
    The limited data on other routes of administration (intra-
peritoneal, intravenous, perhaps subcutaneous), which introduce 
PCP or Na-PCP directly into the body indicate that these exposures 
result in a stronger toxic effect on rats, hamsters, and mice than 
either oral or dermal exposure (Tables 33, 34). These differences 
probably result from incomplete uptake of the compound via the 
oral, dermal, and perhaps subcutaneous routes. 

    PCP is considerably more toxic than its sodium salt when 
administered orally to rats or rabbits, or dermally to rabbits 
(Tables 33, 34).  However, subcutaneous or intravenous injections 
of PCP and Na-PCP are almost equally toxic.  These patterns may 
reflect differences in the rate of absorption of the parent 
compounds when applied to the skin of rats, but this does not 
appear to be true of PCP. 

    One sex is not consistently more strongly affected by PCP than 
the other.  For a given combination of organism (rats and mice), 
vehicle, and exposure route (mostly oral), males are sometimes 
more, sometimes equally, and sometimes less sensitive than females 
(Table 33).  However, technical PCP is more toxic for female rats 
than for males (Schwetz et al., 1974) and more toxic for young rats 
than for adults (Schwetz et al., 1978).  This differential toxicity 
between the sexes is apparent in both short- and long-term studies 
with technical PCP and with one of its contaminants, hexachloro-
dibenzo- p-dioxin (H6CDD). 

    Although the influence of exposure route, the form of the PCP 
(sodium salt or parent molecule), and the sex of the experimental 
animal are evident within a given study, such patterns may be 
masked by a number of factors.  Unfortunately, the type and extent 
of contamination of PCP tested under acute exposure conditions is 
rarely described, despite the fact that some of the 
microcontaminants, especially some congeners of polychlorinated 
dibenzo- p-dioxin (PCDD) and polychlorinated dibenzofuran (PCDF), 
are extremely toxic.  Furthermore, a variety of solvents is used to 
administer chemicals tested for acute toxicity, and some of these 
solvents can enhance or decrease absorption of PCP, thus affecting 
toxicity.  Hence, the variations in the LD50, LDLO and TDLO values 
reported in Kozak et al. (1979), Ahlborg & Thunberg (1980), Jones 
(1981), NRCC (1981), and NIOSH (1983) for each animal species and 
route of exposure may result, in part, from the use of a variety of 
purified and commercial products containing several different 
solvents, as well as possible differences in animal strains, or 
test design (in this regard, note that some of the earlier studies 
involved only a small number of animals, sometimes as few as two).  
Acute toxic effects, other than chloracne, which are due 
exclusively to the presence of PCDDs or PCDFs, are difficult to 
identify. PCDDs, in particular, have a delayed toxic effect that is 
masked by the rapid onset of signs of acute exposure to the PCP 

Table 34.  Acute toxicity of Na-PCP
Species  Parametera  Doseb      Route            Purity/carrier                 Reference
Mouse    LD50        83         subcutaneous     reagent grade                  Ning et al. (1984)

Rat      LD50        210.6      oral             2% aqueous                     Deichmann et al. (1942)
         LD50 (F)    125 - 200  oral             commercial (79%); aqueous      Stohlman (1951)
         LD50        71         oral             reagent grade                  Ning et al. (1984)
         LD50        104        dermal           reagent grade                  Ning et al. (1984)
         LD50        66         subcutaneous     2% aqueous                     Deichmann et al. (1942)
         LD50        38         subcutaneous     reagent grade                  Ning et al. (1984)
         LC50        294        inhalation       reagent grade; 2-h inhalation  Ning et al. (1984
         LD50c       11.7       inhalation       aqueous aerosol                Hoben et al. (1976c)
         LD50        34         intraperitoneal  aqueous                        Hoben et al. (1976c)

Rabbit   MLD         218        oral             1% NaCl                        Kehoe et al. (1939)
         MLD         250 - 300  oral             5% aqueous                     Deichmann et al. (1942)
         MLD         450 - 700  oral             aqueous                        McGavack et al. (1941)
         MLD         250        cutaneous        10% aqueous                    Deichmann et al. (1942)
         MLD         257        cutaneous        2% aqueous                     Kehoe et al. (1939)
         MLD         450 - 600  cutaneous        aqueous                        McGavack et al. (1941)
         MLD         100        subcutaneous     10% aqueous                    Deichmann et al. (1942)
         MLD         250 - 300  subcutaneous     aqueous                        McGavack et al. (1941)
         MLD         50 - 150   intraperitoneal  aqueous                        McGavack et al. (1941)
         MLD         22 - 23    intravenous      2% aqueous                     Deichmann et al. (1942)
         MLD         22         intravenous      1% aqueous                     Kehoe et al. (1939)

Guinea-  MLD         266        cutaneous        aqueous                        Kehoe et al. (1939)

Dog      MLD         135        subcutaneous     aqueous                        McGavack et al. (1941)
a   MLD = Minimum lethal dose.
    LD50 = Estimated dosage capable of causing 50% mortality of a test population.
    LC50 = Estimated concentration capable of causing 50% mortality of a test population.
b   LD50 or MLD in mg/kg body weight; LC50 in mg/m3 air.
c   Inhalation toxicity value expressed by author as LD50, not LC50.
8.2.  Short-Term Toxicity

    As discussed in the previous section, some of the acute effects 
of exposure to commercial PCP are attributable to microcontaminants 
present in the technical preparation.  In addition, signs of 
exposure to some of these microcontaminants, notably PCDDs, may 
not appear for weeks.  As a consequence, it is particularly 
important to consider the possible confounding effects of these 
impurities in reviewing the long-term toxicity of chlorophenols.  
In this section, studies on the toxicity of purified PCP, technical 
grade PCP, and comparative studies are discussed separately. 

8.2.1.  Pure or purified PCP

    Debets et al. (1980) studied the effect of 99% pure PCP fed to 
female rats for 5 weeks.  The PCP concentration used was 500 mg/kg 
feed, which corresponds to an approximate dose of 40 - 50 mg/kg 
body weight per day.  Of several liver microsomal enzymes tested, 
only ethoxyresorufin  O-de-ethylase (20-fold) and glucuronyl 
transferase (3-fold) increased in activity with exposure.  Body 
weight gain, urine and liver porphyrin concentrations, and liver 
weights were unaffected by PCP.  Interestingly, PCP accelerated the 
onset of hexachlorobenzene (HCB) porphyria, suggesting that it is 
the PCP metabolized from HCB that causes the porphyria. 

    In 6-week-old pigs, Greichus et al. (1979) found no overt signs 
of toxicosis associated with the oral administration of purified 
PCP (at 5, 10, and 15 mg/kg body weight per day in capsules) for 30 
days.  However, at 10 and 15 mg/kg per day, hepatocyte size 
increased and enlarged livers were observed. 

8.2.2.  Technical grade PCP

    Knudsen et al. (1974) fed rats diets containing 0, 25, 50 and 
200 mg commercial PCP/kg for 12 weeks.  The 50 mg/kg exposure 
(corresponding to about 2.3 mg/kg body weight per day) increased 
liver weights in both sexes, while haemoglobin concentrations, 
haematocrit, and glucose concentrations in serum were elevated in 
the 2 highest dosage groups.  The no-observed-adverse-effect level 
of 25 mg/kg corresponded to an ingested dose of about 1.2 mg/kg 
body weight per day. 

    Post-mortem examination of dairy cattle fed 0.2 mg/kg body 
weight per day, for 75 - 84 days, and 2 mg/kg body weight per day 
for another 56 - 60 days during lactation, revealed enlargement of 
the liver, lungs, kidneys, and adrenals, thickening of the urinary 
bladder walls, chronic interstitial nephritis, and subacute 
urocystitis in exposed animals (Kinzell et al., 1981).   In vitro 
testing identified a significant loss of renal function associated 
with exposure. 

8.2.3.  Comparative studies

    Recent studies of between 2 and 8 months duration are useful in 
discerning differences in the effects of purified and technical 

grade pentachlorophenol (Table 35).  These studies on rats and mice 
have been summarized by Fielder et al. (1982) and NRCC (1982). 

    Rats receiving 500 mg technical PCP (Table 1, section 2.2) per 
kg feed for 8 months had slower growth rates, hepatomegaly, 
porphyria, and increased hepatic enzyme activities (aryl 
hydrocarbon hydroxylase, glucoronyl transferase, and cytochrome 
P-450) (Goldstein et al., 1977).  When rats were fed purified PCP 
under similar conditions, i.e., 500 mg/kg feed for 8 months, only 
retardation of growth rate and an increase in liver glucoronyl 
transferase activity were observed.  Rats fed 20 mg technical 
PCP/kg feed for 8 months had elevated liver enzyme activities, 
while rats fed purified PCP at the same concentrations did not. 

    These findings have been confirmed by Kimbrough & Linder (1978) 
using rats exposed to 0, 20, 100, and 500 mg/kg of the same 
technical and purified PCP and the same protocol as was employed by 
Goldstein et al. (1977).  Male and female rats exposed to either 
purified or technical PCP gained less weight than controls.  
Exposure to purified PCP in the diet at 500 mg/kg resulted in 
slightly enlarged liver cells and caused occasional cytoplasmic 
inclusions.  These effects were not observed in rats fed lower 
doses.  In contrast, exposure of rats to diets containing 500 mg 
technical PCP/kg increased liver weights and thickened the walls of 
the hepatic central veins in both sexes, and also caused 
pleiomorphic hepatocytes with foamy or vacuolar cytoplasm in male 
rats.  The livers of females exposed to 500 mg/kg were 
characterized by vacuolation and degeneration of hepatocytes and 
mitotic anomalies. Similar, but less severe, effects were noted in 
rats exposed to diets containing 100 mg and 20 mg technical PCP/kg. 

    Wainstok de Calmanovici & San Martin de Viale (1980) determined 
that technical PCP is more toxic for porphyrin metabolism in rats 
than the purified compound.  Dosing with 45 - 90 mg technical 
PCP/kg body weight per day (the amount given by stomach tube for 18 
weeks varied) enhanced the excretion of porphyrins and their 
precursors, increased the deposition of porphyrins in the spleen, 
liver, and kidney, and altered the activity of enzymes involved in 
porphyrin metabolism.  Larger doses of purified PCP (100 - 195 
mg/kg body weight per day) had similar effects. 

Table 35. No-observed-adverse-effect-levels (NOAELs) established in rats 
exposed orally to pure, technical, and purified technical grades of PCP
PCP                 Sex           NOAEL (mg/kg   Reference
                                  body weight
                                  per day)
 Short-term toxicity

    Pure                          3              Johnson et al. (1973)
    Purified                      3              Johnson et al. (1973)
    Technical                     < 3            Johnson et al. (1973)
    Technical                     approximately  Knudsen et al. (1974)


    Technical       male, female  5              Schwetz et al. (1974)
    Purified        male, female  < 5            Schwetz et al. (1974)
     technical      (progeny)


    Purified        male, female  3              Schwetz et al. (1978)

 Long-term toxicity

    Pure                          approximately  Goldstein et al. (1977)
    Technical                     < 1            Kimbrough & Linder (1978)
    Purified        female        < 3            Schwetz et al. (1978)
     technical      male          < 10           Schwetz et al. (1978)
a   Studies involved exposure of females during days 6 - 15 of gestation
    and evaluation of progeny.
b   Studies involved exposure of both sexes for 62 days before mating, for
    15 days during mating, and, subsequently, throughout gestation and
    lactation for females.

    In a similar comparative study by Johnson et al. (1973), 99% 
pure PCP and purified technical PCP (H6CDD reduced to 1 mg/kg) at 
10 and 30 mg/kg body weight per day increased liver weight, but did 
not affect other variables monitored.  In contrast, unpurified PCP 
increased liver and kidney weights, enhanced serum-alkaline 
phosphatase activity, and reduced serum-albumin, numbers of 
erythrocytes, total haemoglobin, and haematocrit. 

    The toxicity of different grades of PCP has also been studied 
in cattle (McConnell et al., 1980; Parker et al., 1980; Hughes et 
al., 1985).  These studies have confirmed that effects such as 

reduced weight gain, anaemia, liver pathology, and a decrease in 
thymus weight were induced by microcontaminants in the technical 
PCP. Reductions in serum-thyroid hormones (triiodo-thyronine T3 and 
thyroxine - T4) observed in cows fed either purified or technical 
PCP were probably due to the chlorophenol itself.  Significant 
levels of octa-, hepta-, and hexachlorodioxins were found in liver, 
fat, and milk at the conclusion of 160 days of exposure (Parker et 
al., 1980).  Firestone et al. (1979) also reported residues of PCP 
and related chemicals in cows' milk, body fat, and blood following 
short-term exposures.  Only 3 out of 7 PCDD congeners identified in 
the technical PCP used were found in tissue and body fluids, i.e., 
1,2,3,6,7,8-H6CDD, 1,2,3,4,6,7,8-H6CDD, and OCDD.  
Hexachlorobenzene (HCB) and PCP were also detected.  Levels of PCP, 
HCB, and PCDD in pooled milk fat from 3 cows reached 4 mg/kg, 200 
g/kg, and 85 g/kg, respectively.  PCP levels fell to 100 g/kg a 
few days after the cessation of dosing and levels of HCB and total 
dioxin declined by 50% in 50 days. 

8.3.  Long-Term Toxicity

    The 8-month PCP feeding studies on rats by Goldstein et al. 
(1977) and Kimbrough & Linder (1978) might be considered by some to 
be long-term.  The results of these studies (section 8.2) indicate 
that the toxicity of technical PCP preparations is primarily 
attributable to microcontaminants. 

    Schwetz et al. (1978) reported a 2-year exposure of rats to 
purified PCP (Table 35).  In females, no toxic effects were 
observed at levels below 3 mg/kg body weight per day; pigment 
accumulation was observed at 10 mg/kg body weight per day, and 
decreased body weight gain, increased serum-glutamic pyruvic 
transaminase (GPT) activity, and pigment accumulation were observed 
at 30 mg/kg body weight per day.  Fewer changes were observed in 
male rats; no effects were observed at levels below 10 mg/kg body 
weight per day, and pigment accumulation and increased GPT activity 
were reported at 30 mg/kg body weight per day.  It is interesting 
to note that Schwetz et al. (1978) did not observe any absolute or 
relative weight increase in kidney and liver at 30 mg/kg body 
weight per day.  In contrast, Johnson et al. (1973) reported 
increased weights of these tissues in male and female rats after a 
90-day exposure to the same purified PCP used by Schwetz et al. 
(1978) at 30 mg/kg body weight per day (section 8.2).  An earlier 
90-day rat study with purified PCP containing < 0.5 mg PCDD or 
PCDF/kg also demonstrated changes in liver and kidney weight at the 
30 mg/kg body weight per day dose level (Kociba et al., 1971). 

    Ning et al. (1984) reported test results for laboratory animals 
exposed to airborne Na-PCP.  Both weanling rats (males) and rabbits 
(males and females) were exposed to reagent grade Na-PCP at 21.4 
mg/m3 or 3.1 mg/m3 for 4 h per day, 6 days per week, for 4 months.  
Rabbits (6 pooled males and females) in the high-dose group showed 
a statistically significant increase in serum-gamma-globulin but 
not in alpha- or beta-globulin or serum-albumin.  Lung weight 
increased significantly in the high-dose group and liver weight 

increased significantly in both dose groups compared with controls.  
In rats, the lung, kidney, liver, and adrenal gland all increased 
significantly in weight in the high-dose group compared with the 
same organs in control animals.  Blood-glucose levels in rats from 
the group exposed to 21.4 mg/m3 remained higher than those in 
controls, throughout the study. 

    These results are consistent with previous observations 
reported by Demidenko (1969).  Rats and rabbits exposed to 28.9 or 
2.97 mg PCP/m3 for 4 h per day and 4 months were significantly 
adversely affected at the high dose (anaemia, leukocytosis, 
eosinophilia, hyperglycaemia, dystrophic processes in the liver).  
At the low dose, only minor effects on liver function, 
cholinesterase activity, and blood sugar were registered, which 
returned to normal one month after completion of exposure. 

    Although the results of these 2 inhalation toxicity studies are 
only preliminary, they give an indication that short-term 
inhalation of Na-PCP or PCP at concentrations as low as about 3 
mg/m3 can cause biochemical and gross pathological effects in 
laboratory mammals.  Assessing the data of Demidenko (1969), Kunde 
& Bhme (1978) calculated from the 3 mg/m3 concentration a daily 
dose of 0.3 mg/kg body weight per day for rats, assuming 100% 
pulmonary uptake and absorption.  This dose would indicate that 
PCP is at least 10 times more toxic with inhalation exposure than 
with oral exposure. This finding is corroborated by the results of 
studies comparing acute inhalation and acute oral exposure 
(section 8.1). 

    Other long-term studies on animals have been designed 
specifically to evaluate the carcinogenic properties of PCP and are 
reported in section 8.6. 

8.4.  Effects on Reproduction and Fetal Development

    There is good agreement that PCP is a fetotoxic agent; however, 
it does not appear to be teratogenic (Kozak et al., 1979; Ahlborg & 
Thunberg, 1980; Fielder et al., 1982; NRCC, 1982).  These 
conclusions are based primarily on the studies of Schwetz et al. 
(1974, 1978) on rats. 

    Technical grade PCP administered to pregnant female rats from 
day 6 to day 15 of gestation did not have any effects on the mother 
or fetus at 5 mg/kg body weight per day (Schwetz et al., 1974).  
Fetal resorptions and delayed development of fetuses were observed 
at 15 mg/kg body weight per day, and signs of maternal toxicity, 
based on weight loss, were observed at 35 mg/kg body weight per 
day.  Reports of delayed ossification of the skull, supernumerary, 
fused, or missing vertebrae and lumbar spurs are usually considered 
indicative of delayed development rather than teratogenicity, and 
are responsible for the differences of opinion between the early 
position of US EPA, that PCP is teratogenic (Cirelli, 1978b), and 
most other reviews.  Purified PCP induced effects similar to those 
of technical PCP; however, maternal toxicity and decreased fetal 
weights occurred at 30 mg/kg body weight per day, and delayed fetal 

development was observed at the 5 mg/kg body weight per day dose 
level, which had previously been found to be the no-observed-
adverse-effect-level for technical grade PCP.  More limited 
fetotoxic effects were observed in rats exposed to PCP by Courtney 
et al. (1976). 

    Na-PCP (> 98% pure) fed to female Wistar rats at 10, 30, or 60 
mg/kg body weight during days 8 - 19 of gestation led to 
statistically significant reductions in body weight in females, 
decreased litter weights, and dramatic increases in fetal 
resorption and fetal death in the 2 highest dose groups (Anon, 
1981).  No birth defects were observed in the control group or in 
the group fed 10 mg/kg body weight; however, 3/31 pups examined 
from females in the 30 mg/kg body weight group had major 
malformations (hare lip, umbilican hernia, exocephalus) and 60% 
had spine and rib malformations (supernumerary, fused, bifurcated, 
or short ribs).  In addition, retardation of ossification and 
increased breadth of sagittal fissure were extensive in this group.  
No pups were born to females in the 60 mg/kg body weight group.  
The authors concluded that 10 mg/kg body weight was the no-
observed-adverse-effect level for teratogenicity, fetotoxicity, and 
embryotoxicity in rats administered Na-PCP.  Considering the 
linearity of the dose-response curve and the fact that 10 mg/kg 
body weight was the lowest dose administered, the no-observed-
adverse-effect level reported in this study is not substantially 
different from that determined for PCP. 

    It is probable that the reduced fetotoxicity of technical PCP 
relative to the purified material, if not artifactual, is a result 
of the presence of microcontaminants (NRCC, 1982). Liver enzymes 
that accelerate the rate of PCP metabolism are known to be 
activated by phenobarbital, 3-methylcholanthrene, and 2,3,7,8-T4CDD 
(Ahlborg & Thunberg, 1978).  Other PCDD and PCDF microcontaminants 
in technical PCP may also activate microsomes and reduce the amount 
of fetal exposure to PCP, causing a concomitant decrease in 
toxicity.  Indeed, the induction of liver enzymes by technical PCP 
has been demonstrated in the rat by Goldstein et al. (1977).  
Purified PCP did not increase the activity of liver enzymes.  
Technical grade PCP was contaminated with 8 - 1380 mg PCDDs/kg and 
4 -1500 mg PCDFs/kg, while purified PCP contained less than 0.1 mg 
of these contaminants per kg. 

    Larsen et al. (1975) reported single instances of dwarfism, 
exencephaly, macrophthalmia, and taillessness in fetuses after 
pregnant rats were fed single doses of 60 mg purified PCP per kg 
body weight per day on days 8, 9, or 10 of gestation.  However, 
these findings were attributed to maternal hyperthermia, which is 
known to cause teratogenic effects in rats (Edwards, 1968).  
Hyperthermia is a common outcome of exposure to large, single doses 
of chlorophenol. 

    Exon & Koller (1983a) investigated the effects of PCP on rats 
exposed pre- and postnatally.  Females were exposed to technical 
PCP (95% pure) in the feed from 21 days of age, throughout breeding 
(at 90 days), gestation, and up to weaning of the pups, 21 days 

after parturition.  Exposure doses were 0, 5, 50, and 500 mg/kg 
body weight per day.  The progeny were exposed to the same levels 
of PCP in feed as their mothers for a total exposure period of 12 
1/2 months.  No significant decreases in mean litter size or 
percentage of still-born pups were recorded in the groups given 
PCP.  There was a significant decrease in survival to weaning in 
the group fed 5 mg/kg body weight but not in the 2 higher dose 

    A level of purified technical PCP of 30 mg/kg body weight per 
day (Schwetz et al., 1978) as well as pure Na-PCP at 26 mg/kg body 
weight per day (Kunde & Bhme, 1978) fed to male and female rats 
for 62 days before mating, 15 days during mating, and to females 
during gestation and lactation, caused reductions in the numbers of 
offspring, neonatal body weight, neonatal survival, and growth of 
weanlings.  The no-observed-adverse-effect level was 3 mg/kg body 
weight per day (Table 35).  Male fertility did not appear to be 
affected in this study. 

8.5.  Mutagenicity

    Williams (1982) reviewed the literature and concluded that, 
although there are deficiencies in the data, the Ames  Salmonella 
 typhimurium test (Andersen et al., 1972), a sex-linked lethal test 
with  Drosophila melanogaster (Vogel & Chandler, 1974), and a host-
mediated assay (Schwetz et al., 1978) all indicate that PCP 
probably does not cause point mutations.  On the basis of negative 
findings in an  in vivo mammalian dominant lethal test (Buselmaier 
et al., 1973), PCP does not seem to cause chromosomal aberrations.  
However, an  in vitro study to show primary damage using
 Saccharomyces cerevisiae demonstrated an increase in mitotic gene 
conversion (Fahrig, 1974; Fahrig et al., 1978).  A mammalian spot-
test pointed to weak mutagenic activity (Fahrig et al., 1978).  PCP 
did not cause single-strand breaks in human fibroblast DNA, while 
its metabolite tetrachlorohydroquinone did (Witte et al., 1985).  
Lymphocytes taken from workers at a PCP factory showed a small, but 
significantly higher, incidence of dicentric and acentric mitoses 
(Bauchinger et al., 1982).  Sodium pentachlorophenate (20 mmol) 
reportedly increased the frequency of both auxotrophic and 
morphological variations in the fungus  Aspergillus niger strain 350 
(Roy et al., 1981).  However, because of shortcomings in these 
studies, the information available is still insufficient to assess 
the mutagenicity of PCP.  The host-mediated assay with bacteria 
(Schwetz et al., 1978) and the sex-linked recessive lethal assay 
(Vogel & Chandler, 1974) have only been carried with single dose 
levels.  In the Ames test (Andersen et al., 1972), no metabolic 
activation system was used.  The increase in the incidence of 
offspring with coat discoloration in the mouse spot test (Fahrig et 
al., 1978) was not statistically significant.  The mutagenicity 
test of sodium pentachlorophenate on  Aspergillus niger 350 (Roy et 
al., 1981) did not include a control group. 

8.6.  Carcinogenicity

    The carcinogenicity of chlorophenols in mammals is a 
contentious issue.  In 1979, the International Agency for Research 
on Cancer reviewed the data available on the carcinogenic 
properties of PCP (IARC, 1979a) and concluded that the information 
was inadequate for a meaningful assessment of carcinogenicity. 

    Two carcinogenicity bioassays have been carried out using PCP.  
Innes et al. (1969) exposed 2 hybrid strains of mice to roughly the 
maximum tolerated dose of PCP for a total of 78 weeks, and did not 
find any significant increases in tumour incidence in males or 
females of either strain.  Schwetz et al. (1978) report similar 
findings in rats exposed to a maximum of 30 mg technical PCP/kg 
body weight per day, for 24 months.  Using these data, the 
Carcinogenic Assessment Group of the US EPA concluded that PCP was 
negative with respect to oncogenic effects (Williams, 1982). 

    PCP (technical and commercial grade) is currently being tested 
by the National Toxicology Program of the US EPA (NRC, 1986), 
however, data from this study were not available to the Task Group 
for evaluation. 

NOTE: The results of these studies have now been published 
(US NTP (1989) Toxicology and carcinogenesis studies of two 
pentachlorophenol technical-grade mixtures (CAS No. 87-86-5) in 
B6C3F1 mice (feed studies), Research Triangle Park, 
North Carolina, US National Toxicology Program, Technical Report 
No. 349, p. 98).  The conclusions were as follows:

     "Under the conditions of these 2-year feed studies, there 
     was clear evidence of carcinogenic activity for male 
     B6C3F1 mice fed diets containing technical-grade 
     pentachlorophenol, as shown by increased incidences of adrenal 
     medullary and hepatocellular neoplasms. There was some 
     evidence of carcinogenic activity for female B6C3F1 
     mice exposed to technical-grade pentachlorophenol, as shown by 
     increased incidences of hemangiosarcomas and hepatocellular 
     neoplasms.  There was clear evidence of carcinogenic 
     activity for male B6C3F1 mice exposed to 
     pentachlorophenol, EC-7, as shown by increased incidences of 
     adrenal medullary and hepatocellular neoplasms.  There was 
     clear evidence of carcinogenic activity for female 
     B6C3F1 mice exposed to pentachlorophenol, EC-7, as 
     shown by increased incidences of adrenal medullary and 
     hepatocellular neoplasms and hemangiosarcomas."
    Exon & Koller (1983a) investigated the potential for PCP to act 
as a co-carcinogen by administering ethylnitrosourea (ENU) to 
female rats exposed pre- and/or postnatally to 0, 5, 50, or 500 mg 
PCP/kg body weight per day.  ENU was administered as ethylurea in 
drinking-water and nitrite in feed during days 14 - 21 of 
gestation.  The progeny were exposed to the same levels of PCP in 
feed as their mothers for a total exposure period of 12.5 months.  
High incidences of tumours in progeny exposed to PCP + ENU could 
not be separated from those observed in progeny exposed to ENU 

    Tumour promotion studies on phenol and chlorophenol using 
dimethylbenzanthracene (DMBA) as the initiator on mouse skin 
indicated that phenol, 2-MCP, 2,4-DCP, and 2,4,5-T3CP were probable 
tumour promoters, but that 2,4,6-T3CP and higher chlorophenols, 
including PCP, were not (Boutwell & Bosch, 1959).  None of the 
chlorophenols tested were tumorigenic, when applied alone. 

    Carcinogenicity bioassays involving oral exposure have been 
conducted on one other chlorophenol, 2,4,6-trichorophenol (NCI, 
1979) and on a mixture of 2 hexachlorodibenzo- p-dioxin isomers 
(NCI, 1980a).  2,4,6-T3CP caused a significant increase in cancer 
in a variety of tissues in both male and mice and in male rats. 

    A mixture of two H6CDD isomers known to contaminate technical 
PCP caused a significant increase in cancer in the livers of female 
rats and mice (Table 36). 

    Thus, animal data indicate that, when PCP is ingested, it does 
not cause cancer in mice or rats, and that, when applied to the 
skin or administered orally, it does not act as a tumorigen or a 
tumour promoter.  Nevertheless, there is evidence that one other 

chlorophenol is an animal carcinogen, the lower chlorinated phenols 
are tumorigens, and that H6CDD found in PCP is carcinogenic, when 
ingested by rodents.  In addition, Arrhenius et al. (1977b) 
suggested that PCP may be able to act as a co-carcinogen, on the 
basis of its effects on liver microsomes. 

8.7.  Other Studies

    The immunotoxic effects of PCP have been investigated in a 
variety of animal species.  Cows fed technical PCP have shown 
thymic hypoplasia in one study (McConnell et al., 1980) but no 
overt differences in immunological function in another (Forsell et 
al., 1981).  Mice exposed to technical grade PCP have shown reduced 
humoral immunity and an  in vitro impairment of T-cell cytolytic 
activity (Kerkvliet et al., 1982a,b).  Analytical grade PCP did not 
have any effect.  In the rat, a decrease in humoral immunity and an 
increase in cell-mediated immunity was demonstrated following 
exposure to technical PCP (97% pure) (Exon & Koller, 1983b).  
Hillam & Greichus (1983) reported a suppression of total leukocyte 
counts, gamma globulins, and IgG in young pigs exposed to technical 
PCP (95% pure) at dose levels of 5 and 10 mg/kg body weight per day 
for 30 days.  Chickens ingesting 2400 g/g feed of purified PCP 
exhibited significantly reduced humoral responses to injections of 
bovine serum-albumin and lymphoproliferative responses to the 
mitogens concanavalin and phytohaemaglutinin and lower white blood 
cell counts (Prescott et al., 1982). Thus, some immunotoxic effects 
are observed when PCP (pure and technical) is administered to 
experimental animals.  In studies carried out with technical PCP, 
it is likely that the non-phenolic contaminants such as PCDD are 
responsible for most of the observed immunotoxic effects. 

    A neurotoxic effect of PCP (grade not specified) has been 
reported by Walum & Peterson (1984) on the basis of an  in vitro 
assay with cultured mice neuroblastoma cells in which an increase 
in cell detachments with exposure to PCP was observed.  Also, a 
transient alteration in brain tissue enzyme activity was found in 
rats given 20 mg technical PCP per litre drinking-water over a 
period of 3 - 18 weeks (Savolainen & Pekari, 1979).  The 
significance of these findings is unclear. 

8.8.  Contaminants Affecting Toxicity

    The toxicological evaluation of pentachlorophenol is 
complicated by the presence of several impurities in technical 
grade formulations of this chemical.  Some of these impurities are 
extremely toxic in their own right.  On the other hand, some 
microcontaminants are capable of inducing liver microsomal 
enzymes, and in so doing, affect the rates of metabolism and 
excretion and the fetotoxicity of PCP (Ahlborg & Thunberg, 1978) 
(section 8.4).  Thus, meaningful assessments of toxicological 
studies on the effects of pentachlorophenol are impossible without 
an accurate knowledge of the type and extent of contamination of 
the PCP under investigation. 

    Concern for the toxic effects of microcontaminants has focused 
on the dioxins, because of the extreme toxicity of the intensely 
studied congener 2,3,7,8-T4CDD.  However, it is necessary to 
emphasize that this congener has not been found frequently in PCP.  
A brief summary of the toxic properties of the microcontaminants of 
chlorophenols is provided in section 2.2.  Extensive reviews of the 
toxicology and residue levels of PCDDs and PCDFs are available in 
Hutzinger et al. (1982), Jones (1981), NRCC (1981), Fielder et al. 
(1982), Kociba & Schwetz (1982), Umweltbundesamt (1985), and in 
several articles published in Boddington et al. (1985). 

8.8.1.  Octachlorodibenzodioxin (OCDD)

    Only one congener exists of this fully substituted isomer.  It 
was not acutely toxic for rats, when administered orally at 1 mg/kg 
body weight or acnegenic for rabbits, when applied to the ear as a 
10% solution in chloroform (Fielder et al., 1982).  Exposures of 
approximately 1 mg/kg body weight per day for 3 weeks did not cause 
any toxic signs.  Livers were nominally enlarged, but appeared 
normal under the light microscope.  OCDD does not appear to be 
mutagenic in the Ames test and has not undergone a carcinogenicity 
bioassay.  Studies of the effects of OCDD on reproduction and fetal 
development indicate that it is not teratogenic at 500 g/kg body 
weight per day or fetotoxic at 100 g/kg body weight per day, when 
administered to females on days 6 - 15 of gestation. 

8.8.2.  Heptachlorodibenzodioxin (H7CDD)

    Few data available on H7CDD.  The LD50 value has not been 
determined accurately for either the 1,2,3,4,6,7,8- or 

    An  in vitro assessment of the induction of aryl hydrocarbon 
hydroxylase (AHH) in rat hepatoma cell cultures was used to 
calculate the biological potency of both H7CDD isomers relative to 
2,3,7,8-T4CDD.  The relative potencies of 1,2,3,4,6,7,8-H7CDD and 
1,2,3,4,6,7,9-H7CDD were 0.3 - 0.5% and 0.011 - 0.025% respectively 
(Bradlaw et al., 1980). 

Table 36.  Summary of toxicology data for hexachlorodibenzo- p-dioxin (H6CDD)
Species  Toxic for:  Vehiclea    Isomerb   Route         Toxicity    Observations             Reference
         (sex)                                           (g/kg body
                                                         body weight
                                                         per exposure
 Acute toxicity
Lethality (LD50)

Rat      females     CO:acetone  B/C mix   oral          800         Observations in all      NCI (1980a)
         males                                           1800        studies included:

Mouse    females     CO:acetone  B/C mix   oral          500         weight loss, skin        NCI (1980a)
         males                                           750         eruptions, delayed
                                                                     death; Tissues
         females,    CO          A         oral          825         affected: liver,         McConnell 
         males       CO          B         oral          1250        thymus, spleen,          et al.
                     CO          C         oral          1440        kidney, testes           (1978)

Guinea-  females,    CO          A         oral          73                                   McConnell 
pig      males       CO          B         oral          70 - 100                             et al.
                     CO          C         oral          60 - 100                             (1978)

 Short-term toxicity

Rat      female,     CO:acetone  B/C mix   oral          < 2.5       thymic atrophy, splenic  NCI (1980a)
         male                                            (per week)  hypertrophy, and liver
                                                                     lesions at 10 - 50 g/kg
                                                                     body weight per week

Mouse    female,     CO:acetone  B/C mix   oral          1.2         only liver damage at     NCI (1980a)
         male                                            (per week)  higher levels (10 - 50
                                                                     g/kg body weight
         female,     acetone               dermal        << 1.5      per week                 NCI (1980b)
         male                                            (per week)

Table 36.  (contd.)
Species  Toxic for:  Vehiclea    Isomerb   Route         Toxicity    Observations             Reference
         (sex)                                           (g/kg body
                                                         body weight
                                                         per exposure
 Fetal toxicity

Rat      females,    CO:acetone            oral          0.1 (per    fetal oedema at 1 g/kg  Schwetz 
         males                                           day during  body weight; resorptions et al.      
                                                         gestation)  at 10 g/kg body         (1973)
                                                                     weight; teratogenic and
                                                                     maternal toxicty at
                                                                     100 g/kg body weight

 Long-term toxicity

Rat      females     CO:acetone  B/C mix   oral          carcinogen  Loss of body weight      NCI (1980a)
                                                         > 1.5       (male and female);
                                                         (per week)  hepatocellular 
                                                                     carcinomas and 
                                                                     neoplastic nodules 
                                                                     in females only

Mouse    females     CO:acetone  B/C mix   oral          carcinogen  hepatocellular carcin-   NCI (1980a)
         (incon-                                         > 2.5       omas and adenomas in
         clusive                                         (per week)  females only; 
         in males)                                                   incidence in males
                                                                     not significant

         incon-      acetone     B/C mix   dermal        inconclu-   fibrosarcomas observed   NCI (1980b)
         clusive                                         sive        in females; incidence
                                                                     not significant
a   CO = corn oil; CO:acetone = 9:1 mixture of corn oil and acetone.
b   A = 1,2,3,4,7,8-H6CDD; B = 1,2,3,6,7,8-H6CDD; C = 1,2,3,7,8,9-H6CDD.
8.8.3.  Hexachlorodibenzodioxin (H6CDD)

    Commercial PCP and Na-PCP have been found to contain 4 out of 
10 possible H6CDD isomers; however, the 1,2,3,6,8,9- and 
1,2,3,6,7,8-isomers predominate (Fielder et al., 1982). Levels have 
been in the 5 - 10 mg/kg range in recent commercial samples of PCP 
and Na-PCP.  The acute oral toxicity (LD50) of 1,2,3,6,7,8-H6CDD in 
the mouse is 1250 g/kg (Table 36). H6CDD is more toxic for female 
rats and mice than for males.  Signs of toxicity include weight 
loss and deterioration of the skin.  The onset of mortality is 
often delayed for up to 3 weeks.  Thymus, liver, spleen, kidney, 
and testes are affected by H6CDD.  This isomer is also known to be 

    Oral exposure of rats to H6CDD isomers indicated that no-
observed-adverse-effect levels for the rat were < 2.5 g/kg body 
weight per week and, for the mouse, < 1.25 g/kg body weight per 
week (NCI, 1980a).  Above these levels, weight loss and liver 
damage were observed.  Dermal exposure of mice to H6CDD also 
resulted in liver damage and mortality, even at the lowest dose of 
1.5 g/kg body weight per week (NCI, 1980b). Thus, H6CDD is readily 
absorbed through the skin and extremely toxic.  A mixture of 
1,2,3,6,7,8- and 1,2,3,7,8,9-H6CDD has been shown to be 
carcinogenic for female mice and rats; however, males did not 
develop hepatocellular carcinomas or adenomas in excess of the 
control rate in the same study (NCI, 1980a).  Carcinogenicity 
assays using dermal exposures were inconclusive (NCI, 1980b). 

    On the basis of the results of exposure of pregnant rats to an 
unidentified mixture of H6CDD isomers, this homologue is considered 
fetotoxic and teratogenic (Schwetz et al., 1973).  The no-observed-
adverse-effect-level was 0.1 g/kg body weight.  Cleft palate, 
vertebrae with split or unfused centra, and split sternebrae were 
observed in the fetuses of females fed 100 g/kg body weight on 
days 6 - 15 of gestation.  Fetal resorptions were observed at 
maternal doses of 10 g/kg body weight and fetal subcutaneous 
oedema at doses of > 1 g/kg body weight. 

8.8.4.  Polychlorinated dibenzofurans (PCDFs)

    Little is known of the toxicity of the PCDFs, despite their 
relatively common occurrence in chlorophenol formulations at 
concentrations of 1 - 500 mg/kg.  Some have considerable acute oral 
toxicity.  For example, the LD50 of 2,3,7,8-T4CDF in guinea-pigs 
and monkeys is 5 - 10 g/kg body weight and 1000 g/kg body weight, 
respectively (Jones, 1981).  Rappe et al. (1982) indicated that 
1,2,3,7,8-P5CDF, 2,3,4,7,8P5CDF, and 2,3,4,6,7,8-H6CDF all had LD50 
values in the 1 - 100 g/kg body weight range for the most 
sensitive species tested.  As with PCDD, the toxicity of PCDF 
isomers appears related to the extent of symmetrical positioning of 
chlorine atoms in the 2, 3, 7, and 8 positions of the molecule.  
2,3,7,8-T4CDF and 2,3,4,7,8-P5CDF appear to have the longest half-
lives of the PCDFs studied (Masuda & Kuroki, 1982).  Furthermore, 
these authors have suggested that PCDFs, especially the tetra- and 
penta-isomers, may have been largely responsible for the signs of 

Yusho disease reported in the Japanese who ingested rice oil 
contaminated with PCBs, PCDF, and polychlorinated quarterphenyls 
(PCQs).  PCDFs have acnegenic properties, but may not be 

8.8.5.  Polychlorodiphenyl ethers (PCDPEs)

    PCDPEs are common contaminants of chlorophenols and are found 
almost exclusively in T4CP and PCP (Jones, 1981).  Little is known 
of their toxicity. 

8.8.6.  Other microcontaminants

    Less common impurities of chlorophenols include polychlorinated 
phenoxyphenols (PCPP) ("predioxins" or "isopredioxins"), 
polychlorinated biphenyls (PCBs), and polychlorinated benzenes 
(Jones, 1981).  Extensive toxicology data exist on the effects of 
PCBs (WHO, 1976) and some members of the chlorinated benzene group, 
i.e., hexachlorobenzene (IARC, 1979b).  Although these 2 groups of 
chemicals are not acutely toxic, they can affect reproduction and 
are considered carcinogenic.  The levels found in technical 
formulations of PCP are not likely to increase their toxicity or 

8.9.  Mechanism of Toxicity

    PCP is known to be cytotoxic for mammalian cells (Packham et 
al., 1982).  All chlorophenols, especially PCP, are uncouplers of 
oxidative phosphorylation (Kozak et al., 1979).  However, the 
molecular basis for the uncoupling action is not clear (NRCC, 
1981).  PCP binds to mitochondrial protein and inhibits 
mitochondrial ATPase activity.  PCP may have 2 independent effects 
on mitochondria; uncoupling oxidative phosphorylation and also 
inhibiting mitochondrial ATPase (Stockdale & Selwyn, 1971a,b).  
Thus, both the formation of ATP and the release of energy to the 
cell from the breakdown of ATP to ADP are prevented.  Electron 
transport is not inhibited by PCP, though reactions dependent on 
available high-energy bonds, such as oxidative and glycolytic 
phosphorylation, are affected.  Binding to enzymic protein has 
been reported and may lead to the observed inhibition of other 
cellular enzymes (Kozak et al., 1979).  An increase in cellular 
oxygen demand during the uncoupling of oxidative phosphorylation 
has also been observed, which gives rise to the initial increase in 
respiration rate reported for individuals poisoned by PCP 
(Weinbach, 1957; Mitsuda et al., 1963; Wood et al., 1983). 


    There are no studies or case reports of the effects of pure or 
purified PCP on human beings.  Human exposure is nearly always to 
technical grades of PCP or Na-PCP in a variety of formulations.  
Reference to "PCP" in this section is to the technical grade. 

9.1.  Acute Toxicity - Poisoning Incidents

    In man, the minimum lethal oral dose (LDLO) of PCP has been 
estimated to be 29 mg/kg body weight (Ahlborg & Thunberg, 1980).  
Kozak et al. (1979) report that this value depends on the ambient 
temperature at the time of exposure, and the general health and 
renal competence of the individual.  PCP is approximately 5 times 
more toxic than phenol (estimated oral LDLO is 140 mg/kg body 
weight).  The proportional lethality of these 2 chemicals (LDLO 
phenol:LDLO pentachlorophenol) in man is almost identical to the 
proportional lethality of the LD50 values for these substances in 

    Numerous accidental or suicidal poisonings with commercial 
chlorinated phenols have been reported (Nomura, 1954; Menon, 1958; 
Blair, 1961; Bergner et al., 1965; Mason et al., 1965; Armstrong et 
al., 1969; Robson et al., 1969; Watanabe & Watanabe, 1970; Haley, 
1977; Stevens & Richardson, 1979; Gjovik et al., 1981; Wood et al., 
1983), and nearly 60% of these acute exposures have resulted in 
death.  These cases together with the results of animal studies 
provide a relatively clear picture of the signs and symptoms of 
acute exposure to technical pentachlorophenol in man. 

    In contrast to the lower chlorinated phenols, PCP does not 
cause convulsions.  Ataxia, mental and physical fatigue, headaches, 
dizziness, disorientation, anorexia, nausea, vomiting, dyspnoea, 
hyperpyrexia, tachycardia, and a rise in metabolic rate are common 
signs and symptoms of PCP poisoning. Most prominent are extreme 
weakness, elevated body temperature, and profuse sweating.  Death 
is due to cardiac arrest and poison victims usually show a marked 
rigor mortis (Truhaut et al., 1952a,b; Nomura, 1954; Mason et al., 
1965; Robson et al., 1969; Watanabe & Watanabe, 1970). 

    The gross pathology and histological lesions associated with 
acute exposures to PCP are generally consistent between laboratory 
animals and man.  Oral exposures result in gastric and intestinal 
inflammation; however, the severity can depend on the carrier 
solvent and the presence of other chemicals (Menon, 1958; Stevens & 
Richardson, 1979).  Pulmonary oedema and congestion have been 
reported after inhalation exposure, and occasionally oral exposure, 
if aspiration of ingested PCP has occurred.  Splenomegaly, 
cardiomegaly, renal congestion, hepatomegaly, and hepatic 
congestion are also frequently observed at autopsy.  
Histologically, fatty degeneration, and necrosis in the 
centrilobular region of the liver have been reported, together with 
degenerative lesions in renal tubules (Gordon, 1956; Menon, 1958; 
Blair, 1961; Bergner et al., 1965; Mason et al., 1965; Robson et 
al., 1969). 

    It is generally agreed that the signs and symptoms of acute 
toxicity observed in animals and human beings exposed to 
chlorophenols result from the effects of the chlorophenol molecule 
itself rather than the microcontaminants, with hyperthermia, 
profuse sweating, and the rapid onset of morbidity and early death 
associated with acute chlorophenol exposures. These signs are not 
observed in animals exposed only to PCDD and PCDF; death is delayed 
by up to 3 weeks in acute exposure studies with these 

9.2.  Effects of Short- and Long-Term Exposures

    Most data on the effects of non-acute exposures to 
chlorophenols in man come from occupational studies.  The clinical 
outcome of repeated exposure to PCP has been reviewed by Fielder et 
al. (1982), Williams (1982), and Exon (1984). The high rate of 
employee turnover and variation in the level and duration of 
exposure make it difficult to distinguish between subacute, short- 
and long-term exposures.  For this reason, the following studies 
concerning occupational PCP toxicity in man are not separated on 
the basis of duration of exposure.  Interpretation of these studies 
is frequently confounded by factors such as age, alcohol 
consumption, tobacco smoking, and other aspects of life style. 

9.2.1.  Occupational exposure

    Clinical studies have identified a number of toxic effects of 
short-term PCP exposure in man, some of which are also 
characteristic of acute intoxication (section 9.1).  Symptoms 
include irritation of the skin, mucous membranes, and respiratory 
tract, signs of chloracne, neurasthesia, depression, headaches, 
porphyria cutanea tarda, and liver and kidney functional changes 
(Fielder et al., 1982).  These effects are discussed in greater 
detail in the following sections.  Among workers employed in 
pressure-treating wood with PCP, insomnia and vertigo have also 
been reported (Arsenault, 1976).  Skin and mucous membranes

    Workers exposed to airborne concentrations of 1 mg PCP/m3 or 
more have reported painful nasal irritation (Deichmann & Keplinger, 
1981).  Variations in the effect level are associated with the 
historical exposure of the individual to inhaled PCP.  Workers 
accustomed to exposure may have a higher threshold for irritating 
effects and may tolerate up to 2.4 mg PCP/m3 air. 

    As in the case of experimental animals (section 8), persons 
exposed to large amounts of technical PCP develop chloracne.  
Fielder et al. (1982) summarized published cases of chloracne in 
workers at PCP-manufacturing sites in Czechoslovakia, the Federal 
Republic of Germany, the United Kingdom, and the USSR.  Kozak et 
al. (1979) reported other cases in Japan and the USA.  The use of 
Na-PCP and Na-tetra-chlorophenol has also resulted in chloracne in 
woodworkers (Behrbohm, 1959).  Baxter (1984) reported chloracne and 
minor disturbances of the lipid metabolism among 40 workers from a 

PCP-manufacturing plant over a 3-year study period.  However, the 
author concluded that the abnormalities observed were due to the 
PCDD contaminants and could not be attributed to the PCP 

    A survey of sawmill workers in British Columbia, Canada, 
carried out using self-administered questionnaires, indicated that 
dermatological and respiratory symptoms were significantly higher 
in a PCP/T4CP exposed group than in the control group (Sterling et 
al., 1982).  However, no reliable estimates of exposure were 

    A more detailed study carried out in the same geographical area 
made use of personal monitors carried by individual workers to 
determine exposure levels of PCP and T4CP (Embree et al., 1984).  
Blood and urine samples were collected and analysed, and health and 
employment histories were recorded by a trained interiewer.  The 
workers were divided into 3 groups: a high exposure group handling 
wet-treated lumber; a medium exposure group with no manual contact 
with treated lumber; and a control group with no exposure to PCP, 
T4CP, or related chemicals.  Exposure concentrations for PCP are 
shown in Table 20.  The authors reported a correlation between 
exposure levels and serum- and urine-chlorophenol concentrations. 
However, they were unable to substantiate the findings of Sterling 
et al. (1982) of increased incidences of respiratory and 
dermatological health problems in workers exposed to PCP/T4CP. 

    A study on 113 employees at a wood-treatment facility found 
that workers were in good health overall, but with a greater than 
expected prevalence of skin pustular eruptions (Flickinger & 
Lawrence, 1982).  Airborne exposures were less than 0.03 mg/m3. 

    Klemmer et al. (1980) reported the results of a 7-year study on 
400 Hawaiians, many of whom had long-term, high-level exposure to 
PCP.  Concentrations of PCP in blood-serum far exceeded the 1.05 
mg/litre reported in Arsenault's (1976) study; workers treating 
wood in open-vats had a mean level of 3.78 mg PCP/litre, pressure-
tank workers 1.72 mg/litre, and farmers and controls 0.25 and 0.32, 
mg/litre, repectively.  After considering data on 189 individuals of 
the total of 400, Klemmer et al. (1980) concluded ... "despite high 
chronic exposures to PCP, individuals in the wood treatment group 
of workers had not undergone any serious health effects from this 
exposure.  The only evidence of tangible health effects, part of 
which could have been caused by exposures to chemicals other than 
PCP, were the low-grade infections or inflammations of the skin and 
subcutaneous tissue, of the protective membrane of the eye, and of 
the mucous membrane of the upper respiratory tract.  No specific 
long-term effects could be elicited in the exposed group".  Liver and kidney

    Indications of significant liver damage have not been found.  
Elevations in circulating levels of some hepatic enzymes have been 
reported; however, they are usually transitory and do not suggest 
severe functional impairment (Kozak et al., 1979; Fielder et al., 

1982).  These findings are consistent with those reported in 
studies on rats with short-term exposure to technical PCP (section 

    Kidney functional changes resulting in reductions in creatinine 
clearance and resorption of phosphorus have been reported by Begley 
et al. (1977).  The spontaneous normalization in kidney function 
during a 3-week non-exposure period indicated that this effect on 
kidney is largely reversible. 

    Jirasek et al. (1974) reported the clinical signs exhibited by 
workers who suffered intoxication during the manufacture of Na-
2,4,5-T3CP and Na-PCP.  These workers displayed abnormal porphyrin 
metabolism (increased uroporphyrin and delta-aminolevulinic acid 
in urine, UV fluorescence of liver), and indications of 
hepatotoxicity (liver enlargement, mild steatosis or fibrosis of 
liver tissue, elevated levels/activities of bilirubin, serum-
glutamic-oxaloacetic transaminase and serum-glutamic-pyruvic 

    Mild dysfunction of the liver has been reported among Soviet 
workers engaged in the production of Na-PCP (Vinogradova et al., 
1973) including, for example, a reduced ability to synthesize 

    Zober et al. (1981) reported a study on a small group of 
woodworkers involved in the application of PCP.  The average 
concentration of PCP in the air at the time of the study was 2.4 
g/m3, the average exposure period for the cohort was 3 years and 
the average levels in urine and serum were 46 g PCP/g creatinine 
and 1 g/ml, respectively.  Elevations in serum-aminotransferases 
and alpha-glutamyl transpeptidase were observed; however, 
confounding factors of sample size and alcohol consumption 
prevented the formation of any conclusions concerning the effects 
of PCP on liver function. 

    As part of a similar study (Embree et al., 1984) (section, Enarson et al. (1986) found that serum levels of 
creatinine, bilirubin, glutamic oxaloacetic transaminase, and 
alkaline phosphatase in sawmill workers exposed to a mixture of Na-
PCP and Na-tetrachloropenate did not differ from those measured in 
the controls.  Blood and the haematopoietic system

    Aplastic anaemia has been associated with PCP use (Roberts, 
1981); however, sample sizes were small and exposures were not 
quantified.  Incidental references to haematological changes in 
isolated workers in a German chemical plant manufacturing PCP and 
HCB were made by Baader & Bauer (1951).  Effects on the 
haematopoetic systems of animals have been reported in studies with 
PCDD contaminated PCP (Johnson et al., 1973; Knudsen et al., 1974; 
McConnell et al., 1980) and 2,3,7,8-T4CDD (Allen & van Miller, 
1978).  Wood (1980) examined the relationship between anaemias 
(with no established cause) in 128 Canadian woodworkers and 

exposure to PCP.  No significant differences between the 
haematology values of exposed and unexposed workers were found.  
Wood (1980) concluded that PCP exposure did not appear to have any 
significant effects on the prevalence of anaemias in these 

    In a companion report to that of Embree et al. (1984) (section, Enarson et al. (1986) found few exposure effects in 
sawmill workers exposed to Na-PCP and Na-tetra-chlorophenate.  Most 
blood variables monitored were within normal ranges and did not 
differ between exposed and unexposed workers.  A significant 
decrease in haematocrit and an increase in haematuria were reported 
in workers handling treated lumber, but not in workers exposed 
solely through inhalation. 

    Urinary-PCP values (2.2 mg/litre) reported by Shirakawa et al. 
(1959) in primarily female workers at several rubber manufacturing 
factories indicated that these workers were exposed to high levels 
of Na-PCP (presumably technical grade).  Increased blood sugar 
levels, decreased blood pressure, and dermatoses were reported, but 
no worker was reported to have missed work through the effects of 
PCP exposure.  Nervous system

    Investigation of clinical reports of neuropathy did not 
indicate any overt significant signs of peripheral neuropathy in a 
recent study on PCP workers (Triebig et al., 1981). Sensory nerve 
conduction velocity was significantly reduced in exposed workers, 
but was not correlated with urinary levels of PCP. 

    Skin, blood, and neurological disorders have been reported 
among workers at a Na-PCP manufacturing factory in the USSR 
(Vinogradova et al., 1973).  The workers were exposed to air levels 
of PCP and Na-PCP ranging between 0.03 and 1 mg/m3.  Readings for 
21% of the air samples ranged from 0.21 to 1 mg/m3, exceeding the 
maximum permissible concentration in the USSR of 0.1 mg/m3.  
Washings taken from clothing and exposed skin yielded PCP and Na-
PCP values of 21 - 212 mg/dm2 and 7.6 - 75 mg/dm2, respectively.  
However, concentrations of hexachlorobenzene were also 2 - 3 times 
higher than the maximum permissible concentration (0.9 mg/m3) set 
in the USSR and may have had an influence on the disorders 
reported.  Immunological system

    McGovern (1982) suggested that man may suffer an immunotoxic 
response to phenolic compounds, including chlorinated phenolic 
compounds.  Marked T-cell suppression has been observed in several 
patients exposed to phenols.  Zober et al. (1981) reported that 
some woodworkers exposed to PCP displayed increased concentrations 
of immunoglobulins, though this increase was not correlated with 
exposure.  Ning (1984) reported that workers exposed to PCP showed 
significant decreases in IgG and IgA immunoglobulins.  The results 

of animal studies, while indicating that PCP is not strongly 
immunotoxic, confirm that PCP exposure can lead to immunological 
changes (section 8.7).  Reproduction

    There are few published data on the effects on male or female 
reproductive capacity of short- or long-term exposure to 
chlorophenols.  Schrag & Dixon (1985) classified PCP as "agents 
with inconclusive effects" on male reproduction.  Corddry (1981) 
investigated pregnancy outcomes in women married to sawmill workers 
in Canada.  Analysis of data from 43 women, with a total of 100 
pregnancies, did not reveal any significant differences in the 
pregnancy outcomes of women living with "exposed" compared with 
"unexposed" men.  There was a slight trend towards more adverse 
pregnancy outcomes in the exposed group, but this trend disappeared 
when the alcohol consumption was considered as a confounding 
factor.  Male fertility was not studied.  Cytogenetic effects

    There is no evidence to indicate that PCP or other 
chlorophenols exert cytogenetic effects on human cells.  A study of 
circulating lymphocytes in a small group of workers in Idaho, USA, 
indicated that individuals exposed to PCP had a slightly higher 
rate of chromosome breakage than controls, but the increase was not 
statistically significant (Wyllie et al., 1975).  Bauchinger et al. 
(1982) reported that lymphocytes from 22 workers in a PCP-
manufacturing factory had a significantly elevated number of 
chromosomal aberrations (dicentrics and acentrics).  These data are 
not adequate for assessing the cytogenetic effects of PCP in man.  Carcinogenicity

    Only 2 reports associating exposure to PCP specifically with 
human cancer are available.  Greene et al. (1978) suggested that 
there was an association between exposure to wood treatment 
chemicals (PCP) and the incidence of Hodgkin's disease, on the 
basis of a family case history (2 of 4 siblings contracting the 
disease were occupationally exposed to PCP) and a relative risk 
(RR) of 4.2 (from death certificates, in the USA) for persons 
employed in carpentry and lumbering.  Bishop & Jones (1981) 
reported 2 cases of non-Hodgkin's lymphoma in PCP workers in the 
United Kingdom; both cases were associated with chloracne.  These 
data are not adequate for the identification of a positive and 
statistically sound correlation between lymphomas and PCP. 

    However, there is some epidemiological evidence that exposure 
of workers to mixtures of chlorophenols, but not specifically PCP, 
increases their risk of developing soft-tissue sarcomas and 
lymphomas.  Considerable debate has ensued since the initial report 
of chlorophenol-related cancer by Hardell (1977) and the subsequent 
reports of Hardell and his co-workers in Sweden.  Case control 
studies of soft-tissue sarcoma patients in Sweden indicated a 
relative risk (RR) of 6.6 for those "exposed" to chlorophenols 

compared to those who did not appear to have been exposed (Hardell 
& Sandstrm, 1979).  Individuals exposed to 2,4,5-T had an RR of 
5.8.  A follow-up study in another area of Sweden involving 330 
subjects tended to confirm the overall risk of soft-tissue sarcomas 
in individuals exposed to phenoxyacetic acids and chlorophenols 
(Erickson et al., 1981).  The authors reported RR values of 6.8 for 
all phenoxyacetic acid exposures and 3.3 for chlorophenol 
exposures.  Exposures to phenoxyacetic acids, assumed by the 
authors to be free of PCDD and PCDF impurities resulted in an RR of 
4.2.  Hence, Erickson et al. (1981) concluded that impurities in 
these chlorinated phenols and phenoxyacids were probably not the 
sole cause of the elevated cancer rates reported, though they might 
have played a role in this apparent carcinogenicity. 

    The validity of the assumption that 2,4-D is free of PCDD and 
PCDF "impurities" is questionable inasmuch as 2,4-D has been found 
to be contaminated, in one case, with H6CDD (IARC, 1977) and, in 
another, with T4CDF (Norstrm et al., 1979).  However, it is 
reasonable to assume that the contamination of the phenoxy-acid 
herbicides 2,4-D, MCPA, necoprop, and dichlorprop with PCDDs and 
PCDFs is very low. 

    Hardell et al. (1981) have also applied their case-referent 
technique to malignant lymphoma patients (both Hodgkin's disease 
and non-Hodgkin's lymphomas) in Sweden. They reported RR values in 
individuals exposed to phenoxy acids, chlorophenols, and other 
organic solvents to be 4.8, 4.3, and 2.4, respectively.  The RR 
value for high-level exposure to chlorophenols was as high as 8.4.  
A possible explanation for the lymphomas may rest with the 
immunological effects (in animals) of the PCDD contaminant, 
2,3,7,8-T4CDD.  Some immunosuppressive chemicals have been shown to 
cause an increase in histiocytic lymphomas in man (Hardell, 1979). 

    In response to criticisms that recall bias was a significant 
factor in his studies, Hardell (1981a) applied his case-control 
method to study colon cancer, a disease that correlates positively 
with asbestos exposure, but not with chlorophenol exposure.  His 
findings indicated that recall and observer bias were negligible in 
his earlier studies, since colon cancers correlated significantly 
only with asbestos exposure, and not with phenoxy acids or 
chlorophenols exposure.  Hardell et al. (1982) also used their 
technique to demonstrate an increased risk of nasal/nasopharyngeal 
cancer (RR = 7) among workers exposed to chlorophenols. 

    Others have not found associations between cancer and human 
exposure to chlorophenols.  In contrast to Hardell et al. (1982), 
Tola et al. (1980) did not find any relationship between nasal 
cancer and chlorophenol exposure in Finnish workers.  A case-
control study in New Zealand (Smith et al., 1984) did not reveal a 
higher incidence of soft-tissue sarcoma in workers exposed to 
chlorophenols.  Gilbert et al. (1983) conducted a cohort study in 
Hawaii with workers employed in the wood-treatment industry, in 
which chromated copper-arsenate, tributyl tin oxide, and PCP were 
used.  They did not find any adverse health effects, but urinary-
PCP levels were higher in the exposed group. 

    In a recent Swedish study on the risks of soft-tissue sarcoma, 
a cohort of 354 620 men employed in agriculture or forestry was 
compared to a reference cohort of 1 725 845 men employed in other 
industries during the period 1961-79 (Wiklund & Holm, 1986).  A 
relative risk of 0.9 (95% confidence interval 0.8 - 1) was found.  
When the cohort was divided into 6 subgroups, based on assumed 
exposure to phenoxy acid herbicides, no significant differences in 
relative risks were found.  Despite the increased use of phenoxy 
acid herbicides in Sweden between 1947 and 1970, no time-related 
increase in the relative risk of soft-tissue sarcomas was found.  
The authors concluded that their study did not confirm the results 
of Hardell (1981b).  However, they pointed out that only a small 
percentage of their total cohort of agricultural and forestry 
workers in Sweden were possibly exposed to phenoxy acid herbicides 
(15%) and chlorophenols (2%).  Hence, a relative risk of 1.5 
observed for sarcomas in these groups, as defined in their study, 
would be equivalent to an actual 6-fold risk from exposure to these 
compounds.  Thus, it is unlikely that their study would have 
detected a true increased risk from such exposures, if the risk 
were less than 6-fold. 

    Pearce et al. (1986) studied 82 cases of non-Hodgkin's lymphoma 
in New Zealand with 168 cancer controls and 228 general population 
controls.  They obtained statistically significant odds ratios (OR) 
of 2.7 and 2, respectively, for workers in the pelt department of 
meat works with potential exposure to 2,4,6-trichlorophenol and for 
workers who carried out fencing with potential exposure to both 
2,4,6-trichlorophenol and pentachlorophenol.  Further examination 
of the data revealed that: 2 of the 4 lymphoma cases who worked in 
the pelt department were possibly not exposed to TCP; that a 
significant proportion of the fencing workers also worked in the 
meat works; and that no significant risk was found for exposure to 
chlorophenols as a group.  Pearce et al. (1986) concluded that the 
excess risk observed in these 2 groups of workers might not be due 
to chlorophenol exposure.  In a second study, Pearce et al. (in 
press) added other lymphoma cases to their previous study sample 
and found similar relationships.  They concluded that, though an 
association with chlorophenol exposure was unlikely, it could not 
be ruled out.  They proposed that alternative hypotheses, such as 
exposure to oncogenic zoonotic viruses should be considered to 
explain their findings. 

    While there is some evidence that chlorophenols, and in 
particular trichlorophenols, are associated with elevations in the 
rates of certain cancers in exposed individuals, there is no clear-
cut dose-effect relationship.  "Exposure" has been loosely defined 
in most studies and no quantitative assessments have been 
published.  In addition, it has been suggested that, since other 
environmental chemicals such as hexachlorobenzene, 
pentachlorobenzene, and pentachloronitrobenzene, are metabolized to 
PCP in animals and man, there is no necessary relationship between 
PCP concentrations in body fluids and exposure to PCP (Renner & 
Mcke, 1986).  Other factors that could have a bearing on the 
conflicting reports of chlorophenol exposure and cancer incidence 

include differences in study methods and the diagnosis of soft-
tissue sarcoma cases, and inadequacies in death-certificate data.  
The results of epidemiological studies, currently underway in 
several countries, could confirm or refute the association between 
chlorophenol exposure and human cancer (Fingerhut et al., 1984).  Other systems

    It is not unusual to find few or no signs of toxicity in 
workers with long-term exposure to low levels of PCP or Na-PCP.  
Arsenault (1976) reported a prospective clinical evaluation of 21 
PCP workers involved in the pressure-treatment of wood, who had 
been exposed for an average of 9 years and had elevated blood-serum 
levels of PCP (on average, 1.05 mg/litre, versus 0.1 mg/litre in 
controls).  The only significant clinical findings in the pressure-
treatment workers were vertigo and insomnia.  Arsenault (1976) also 
provides information obtained from the health records of 1330 
workers in a large wood-processing company.  From 1961 to 1971, 
only 26 cases of health problems related to PCP use and exposure 
were identified; however, it is probable that this is an 
underestimate because of under-reporting. 

    Similarly, in a cohort study comparing 88 wood-treatment 
workers with 61 controls (Gilbert et al., 1983), no significant 
effects of exposure (by history or physical examination) to wood 
preservatives, including PCP, were reported on: skin or mucous 
membranes of the eyes or upper respiratory tract; mental status; 
cardiovascular, gastrointestinal, genitourinary, or neuromuscular 
systems; or reproduction.  In the accompanying historical 
perspective study, calculations of age-specific deaths rates from 
all causes for 125 workers, over 21 years, showed that observed 
rates were similar to, or lower than, those expected. 

9.2.2.  General population exposure

    References to non-occupational exposure to chlorophenols, for 
example from wood in homes, confirm that pulmonary, and, to a 
lesser extent, dermal exposure to PCP can produce symptoms of 
poisoning similar to those documented in occupational settings.  
These studies (section 5.2) may be of significance in as much as 
they identify new sources of exposure; however, they add little to 
the toxicology data base for PCP.  Concentrations of PCP in the 
indoor air of homes and in the urine and serum of their residents 
are elevated relative to those in the general population (Table 
21).  The limited effects of this exposure are considered briefly 

    In cases where individuals display symptoms of PCP 
intoxication, usually as a result of the application of PCP in the 
interior of houses, typical acute symptoms are observed, but other 
parameters (haematological, biochemical) may be normal.  Sangster 
et al. (1982) outlined case histories of 3 families in PCP-treated 
houses who reported experiencing one or more of the following signs 
or symptoms: generalized itching or burning dermatosis, nausea, 
vomiting, decreased appetite, headache, dizziness, and fatigue.  

Haematological, urinary, and biochemical parameters were unaffected 
by exposure.  Similarly, a young girl poisoned by bathwater stored 
in a PCP-contaminated tank displayed fever, intermittent delirium, 
rigors, acidosis, and elevated urine levels of ketones and amino 
acids, but her respiratory rate and other clinical symptoms were 
normal (Chapman & Robson, 1965).  However, longer-term exposure may 
have more profound effects.  Brandt et al. (1977) reported that 
exposure to PCP for several years in the air of a treated wooden 
house resulted in liver damage and elevated activities of several 
liver enzymes in a German woman (Ahlborg & Thunberg, 1980). 

    A Sacramento woman lost weight, and complained of weakness and 
tightness in the chest after the interior of her house was treated 
with PCP (Anon, 1970). 

    Krause & Englert (1980) examined several medical and laboratory 
parameters in 250 persons with elevated PCP exposure (section 
5.3).  No clear relationship could be found between elevated 
concentrations of PCP in the urine and biochemical parameters 
related to the liver, kidney, and blood.  However, significantly 
more complaints of headache, fatigue, tonsillitis, hair loss, and 
bronchitis were reported in persons with PCP exposure.  Because the 
signs and symptoms usually reported in connection with indoor PCP 
exposure are relatively non-specific, thye cannot be definitively 
ascribed to PCP.  However, the observation that many symptoms 
disappeared when exposure was reduced (by improving ventilation, 
sealing wood surfaces, or leaving the premises) is indicative that 
PCP or the substances included in the formulated product might well 
be the causative agents.  The persistence of some biochemical and 
dermatological signs, similar to those reported in the work-place, 
is a further indication that PCP may induce subacute effects in 
these exposed persons. 

    In general, however, no adverse effects can be ascribed to the 
low ambient concentrations of PCP resulting from the diffuse 
sources to which most people are exposed. 


10.1.  Evaluation of Human Health Risks

    In this subsection, PCP and Na-PCP are referred to as PCP.

10.1.1.  Occupational exposure  Exposure levels and routes

    Occupational exposure to technical PCP mainly occurs through 
inhalation and dermal contact.  Virtually all workers exposed to 
airborne concentrations take up PCP through the lungs and skin.  In 
addition, workers handling treated lumber or maintaining PCP-
contaminated equipment would be exposed dermally to PCP in 
solution, and may take up from one-half (based on urinary-PCP 
concentrations) to two-thirds (using serum levels) of their total 
PCP burden through the skin. 

    The actual concentrations to which workers have been exposed 
are seldom measured but, where they have been monitored, they are 
predictably high.  Airborne levels at PCP-production and wood-
preservation facilities have ranged from several g/m3 to more than 
500 g/m3 in some work areas.  The outer layer of treated wood can 
contain up to several hundred mg/kg, though levels are usually less 
than 100 mg/kg. 

    These exposures result in concentrations of PCP in the serum 
and urine that are 1 - 2 orders of magnitude higher than those in 
the general population without known exposure. Mean/median urinary-
PCP concentrations of approximately 1 mg/litre are typical for 
workers in contact with PCP, compared with urinary concentrations 
of approximately 0.01 mg/litre for the general population (section 

    Automated processes and the use of closed systems have greatly 
reduced worker exposure in large-scale manufacturing and modern 
wood-treatment factories and sawmills.  Other improvements in 
industrial hygiene can significantly reduce exposure, as measured 
by lower urinary-PCP concentrations.  Toxic effects

    Past use of PCP has affected workers producing or using this 
chemical.  Chloracne, skin irritation and rashes, respiratory 
disorders, neurological changes, headaches, nausea, weakness, 
irritability, and drowsiness have been documented in exposed 
workers.  Work-place exposures are to technical PCP, which usually 
contains mg/kg quantities of microcontaminants, particularly H6CDD.  
Subacute effects such as chloracne and potential subchronic and 
chronic effects such as hepatotoxicity, fetotoxicity, and 
immunotoxicity (as reported in animal studies) are probably mainly 
caused by microcontaminants.  However, the PCP molecule itself 
appears to play a role in the pathology of the last 3 effects and 
is likely to be wholly responsible for the reports of skin and 

mucous membrane irritiation, hyperpyrexia and, in severe cases, 
coma and death.  The toxicity of pure or purified PCP has not been 
evaluated for human beings, because human exposure has usually been 
to technical PCP. 

    Investigations of biochemical changes in woodworkers with long-
term exposure to PCP have failed to detect consistently significant 
effects on major organs, nerves, blood, reproduction, or the 
immune system.  However, the statistical power of these studies has 
been limited as a result of the small sample sizes used.  Overall, 
the body of research suggests that long-term exposure to levels of 
PCP encountered in the work-place is likely to cause borderline 
effects on some organ systems and biochemical processes. 

    Some epidemiological studies from Sweden and the USA have 
revealed an association between exposure to mixtures of 
chlorophenols, especially 2,4,5-T3CP, and the incidences of soft-
tissue sarcomas, lymphomas, and nasal and nasopharyngeal cancers.  
Other studies have failed to detect such a relationship.  None of 
these studies has managed to address the effects of exposure to PCP 

    Animal studies designed to assess the carcinogenicity of PCP 
and reported to date have been negative.  Carcinogenicity bioassays 
with one other chlorophenol (2,4,6-T3CP) and a mixture of two H6CDD 
congeners found in PCP have been positive.  Hence, the carcinogenic 
effects of long-term exposure of animals to technical PCP are not 
clear.  Risk evaluation

    It is clear that the levels of PCP found in work-places have 
adversely affected some aspects of the health of exposed workers.  
Potentially the most deleterious effect of technical PCP is on the 
fetus, and pregnant women should avoid exposure, whenever possible.  
There is limited evidence that PCP may cause hepatotoxicity, 
neurological disorders, and effects on the immune system.  No 
convincing data for or against a carcinogenic link exists. 

Note: Since the publication of this monograph in 1987, however, the 
results of adequate carcinogenicity studies with commercial-grade 
pentachlorophenol have been published. The conclusions of these studies 
are indicated in the addendum to 8.6 Carcinogenicity.

    The National Academy of Sciences (1977) calculated an 
acceptable daily intake (ADI) for PCP of 3 g/kg body weight per 
day.  This ADI is based on data from a feeding study on rats and a 
1000-fold safety factor.  The results of long-term studies indicate 
that the no-observed-adverse-effect level for rats is below 3 mg/kg 
body weight per day (section 8.2).  A recent human study has shown 
that the steady-state body burden is 10 - 20 times higher than the 
value extrapolated from rat pharmacokinetic data, suggesting that 
caution should be applied when extrapolating directly from the rat 
model to man.  Furthermore, the US ADI was not based on an 
inhalation study, and does not account for the possibly greater 
toxicity of PCP via inhalation, as indicated by animal studies 
(sections 8.1 and 8.3).  Hence, the safety factor of 1000 used to 
derive this ADI value is by no means too conservative.  The intake 
for a 60-kg adult exposed to concentrations of PCP at the ADI level 
would be 180 g/person per day. 

    A rough estimate of occupational exposure alone can be 
calculated, assuming a moderate breathing rate of 1.8 m3/h for a 
60-kg worker, 100% uptake of all inhaled PCP (which takes some 
account of the often significant dermal uptake), and an 8-h working 
shift per day, 5 days per week.  Hence, an exposure to 500 g 
PCP/m3 per shift (section 5.2) would result in an average daily PCP 
intake of approximately 5000 g/person per day, averaged over the 
entire week.  Under these circumstances, the ADI level proposed by 
the National Academy of Sciences is significantly exceeded, even 
when consideration is given to the effects of intermittant 
exposures during the working week and the high health status 
assumed for workers. 

    There is a clear need for a reduction in occupational exposure 
to PCP.  Emphasis must be placed on reducing airborne 
concentrations at production and wood-treatment facilities, as well 
as dermal contact with solutions containing PCP.  In addition, 
reductions in the concentrations of microcontaminants in technical 
PCP, particularly PCDDs and PCDFs, would reduce the potential for 
expression of several effects and would better protect the health 
of workers in these industries. 

10.1.2.  Non-occupational exposure  Exposure levels and routes

    Domestic use of products containing technical PCP, especially 
the indoor application of wood preservatives and paints based on 
PCP, has led to elevated concentrations of PCP in indoor air.  
Indoor exposures have been well documented in houses constructed 
with PCP-treated wood, or in which interior wood panels or boards 
have been treated with PCP.  PCP concentrations in indoor air can 
be expected to reach 30 g/m3 during the first month after 
treatment.  Considerably higher levels, up to 160 g/m3, have been 
reported in houses with concomitant poor indoor ventilation.  Even 
higher concentrations can be encountered immediately after do-it-
yourself applications of PCP-containing wood preservatives. 

    In the long term, values of between 1 and 10 g/m3 are typical, 
though higher levels, up to 25 g/m3, have been found in rooms 
treated one to several years earlier.  Indoor air concentrations 
are influenced by a variety of factors, e.g., intensity of 
treatment, solvents and additives involved, species of wood 
treated, environmental conditions, and time elapsed since 

    In many cases, levels of PCP in the serum and urine of people 
exposed in the home overlap those for occupationally exposed 
persons; but, on average, urine-PCP levels are approximately 0.04 
mg/litre for non-occupationally exposed persons. 

    In the long term, exposure to PCP in treated buildings 
continuously decreases, because of the high volatility of PCP.  
Because of their lower vapour pressure, the volatilization of 
PCDDs and PCDFs from the wood surface is much slower than that of 

PCP.  Hence, these microcontaminants are emitted at a low rate, but 
over a longer period of time. Long-term exposure to these 
lipophilic contaminants is likely to lead to accumulation of PCDDs 
and PCDFs in fatty body tissues. 

    As a result of regulations restricting the use of PCP, and also 
changing use patterns, indoor exposure to PCP is probably declining 
in most developed countries.  Risk evaluation

    Assuming a daily respiratory volume of 20 m3/adult and 100% 
uptake of all inhaled PCP (a worst case that takes some account of 
dermal uptake), the exposure of persons living in PCP-treated 
buildings, shortly after treatment, or, in some cases, after a long 
period of time, could be expected to range between 600 and 3200 
g/person per day.  Long-term exposure to concentrations of 1 - 25 
g PCP/m3 could result in a daily PCP intake of 20 500 g/person 
per day.  The median value of 5 g/m3 reported from a survey of 104 
homes (section 5.3) corresponds to a daily PCP uptake of 100 g/
person per day. Other potential sources of exposure to PCP 
including food, drinking-water, and consumer products contribute 
further to PCP uptake (section 

    The indoor air data suggest that, at least during the first 
weeks following indoor treatment, and occasionally for quite 
prolonged periods of time, the ADI level of 180 g/person per day 
is significantly exceeded.  Under these circumstances, there is a 
potential health risk.  This conclusion is supported, in part, by 
reports of signs and symptoms similar to those in persons 
occupationally exposed to PCP (dermatosis, nausea, headache, 
dizziness, fatigue).  These signs and symptoms are most likely 
associated with the effects of the PCP molecule and, in some cases, 
the solvents associated with the wood treatment chemicals used.  
The long-term significance of exposure to low levels of PCDDs and 
PCDFs and their accumulation in human tissues is not entirely 
clear; however, at least 2 isomeric groups of the PCDDs family are 
carcinogenic for animals.  Animal data indicate that low 
concentrations of PCP in biological tissues or body fluids do not 
signify an absence of biologically active PCDDs and PCDFs. 

    It is worth noting that exposure in the home is frequently for 
longer periods of time than exposures in the work-place and can 
affect subpopulations potentially at greater risk than workers, for 
example, children, the elderly, pregnant women, or those with an 
existing adverse health condition. 

10.1.3.  General population exposure    Exposure levels and routes

    Exposure of the general population to low levels of PCP is 
common.  PCP has been found in air, food, water, and other consumer 
products.  Biotransformation of some chlorinated hydrocarbons 
(e.g., lindane, hexachlorobenzene) to PCP also contribute to the 
human body burden. 

    The ambient air in urban areas typically contains several 
ng/m3, while concentrations in less developed areas are roughly an 
order of magnitude lower (section 5.1.1). 

    Drinking-water concentrations of PCP rarely exceed several 
g/litre, even in highly industrialized regions, and most are less 
than 1 g/litre (section 5.1.5). 

    Fruits, vegetables, and other produce usually contain much less 
than 10 g/kg, but may on occasion exceed this level. Most meats 
contain similar concentrations of PCP (< 10 g/kg) but, a few 
samples, particularly liver, can contain over 100 g/kg.  Fish 
skeletal muscle typically contains PCP levels of 4 g/kg or less.  
Overall estimates of PCP intake from all foods, based on total diet 
samples in the USA and the Federal Republic of Germany, are 
remarkably similar, i.e., up to 6 g/person per day (section 

    PCP is also present in a wide variety of consumer products, 
including veterinary supplies, disinfectants, photographic 
solutions, fabrics, home-care products, and pharmaceutical 
products. No calculated estimates of the contribution made by 
consumer products to overall exposure to PCP are available.  Risk evaluation

    On the basis of the PCP levels in the various compartments, 
the overall exposure of an average person without known specific 
exposure can be estimated to be approximately 6 g/person per day 
from food, 2 g/person per day from drinking-water, and 2 g/person 
per day from the ambient air. Thus, the total exposure of the 
general population could be approximately 10 g/person per day 
(exclusive of exposure to consumer products), which is far below 
the intake based on the ADI proposed by the US National Academy of 
Science of 180 g/person per day.  On the basis of available data, 
this exposure is not likely to constitute a health hazard. 

    However, the diffuse contamination of the environment with 
technical PCP must be considered as an important source of 
environmental PCDDs and PCDFs. 

10.2.  Evaluation of Effects on the Environment

    The widespread use of technical PCP and its physical and 
chemical properties (water solubility,  n-octanol/water partition 
coefficient, volatility) lead to ubiquitous contamination of air, 
soil, water, sediments, and environmental organisms. 

    Depending on the soil type, PCP can be very mobile, potentially 
leading to contamination of groundwater and hence, of drinking-
water.  Because applications in agriculture have been reduced, soil 
contamination will, for the most part, be confined to treatment 

    Photodecomposition and biodegradation processes may not be 
adequate to eliminate PCP from the different compartments. 
Unfavourable temperature, pH, and other environmental conditions 
may retard degradation of PCP allowing it to persist in the 
environment.  Biological decomposition may also be limited in 
waste-treatment factories resulting in high concentrations in the 
final effluents.  PCP has also been used in aquatic environments as 
a molluscicide and an algicide. 

    PCP concentrations in surface waters are usually in the range 
of 0.1 - 1 g/litre, though much higher levels can be found near 
point sources or after accidental spills (section 5.1.2). 

    PCP is highly toxic for aquatic organisms.  Apart from very 
sensitive or resistant species, there is apparently no difference 
in the sensitivity to PCP of the different taxonomic groups 
(section 7.2).  Invertebrates (annelids, molluscs, crustaceans) and 
fish are adversely affected by PCP concentrations below 1 mg/litre 
in acute toxicity tests. Sublethal concentrations are in the low 
g/litre range. 

    As little as 1 g PCP/litre can have adverse effects on very 
sensitive algal species.  Moreover, low concentrations (g/litre) 
may lead to substantial alterations in community structures, as 
seen in model ecosystem studies. 

10.3.  Conclusions

    In this subsection, PCP and Na-PCP are referred to as PCP.

1.  Human exposure to PCP is usually from technical products that 
contain several toxic microcontaminants, including PCDDs and PCDFs. 

2.  The acute health effects of exposure to high concentrations of 
technical PCP are generally the result of the biological action of 
the PCP molecule itself.  Sub-chronic effects and the effects of 
long-term exposure to technical PCP are most probably largely 
related to the biological action of the PCDDs and PCDFs. 

3.  A dose-effect relationship for the acute or chronic toxicity of 
technical PCP for human beings cannot be derived from available 
data.  Derivation of this relationship is confounded by variations 
in individual susceptibility, social and environmental influences, 
concomitant exposure to other chemical substances, a lack of 
accurate exposure estimates, and inadequate toxicity data. 

4.  Occupational exposure to technical PCP can lead to adverse 
health effects. 

5.  Non-occupationally exposed persons (using products containing 
technical PCP and/or those living in buildings treated with wood 
preservatives or paints containing PCP) can be exposed to 
concentrations of PCP in air that can have adverse health effects. 

6.  The exposure of the general population to diffuse sources of 
PCP (via food, drinking-water, ambient air, consumer products, 
chlorinated compounds that can be metabolized to PCP) is very low 
and, on the basis of available data, it is not likely to constitute 
a health hazard. 

7.  Epidemiological investigations and animal studies, conducted to 
date, are insufficient for an evaluation of the carcinogenicity of 
technical PCP.  Uncertainties also exist over the genotoxic and 
fetotoxic effects of technical PCP. 

8.  PCP is rather persistent, quite mobile, and found in all 
environmental compartments.  At the higher concentrations found in 
the surface water near point sources or discharges (mg/litre), 
aquatic life is adversely affected.  Ambient concentrations of PCP 
commonly found in surface waters (0.1 -1 g/litre) may adversely 
affect very sensitive organisms and may lead to alterations in the 

9.  Use of technical PCP and its improper disposal (landfill and 
low-temperature combustion) can contribute significantly to the 
contamination of the environment with PCP, PCDDs, and PCDFs. 


    In this section, PCP and Na-PCP are referred to as PCP.

11.1.  Environmental Contamination and Human Exposure

(a) Concentrations of microcontaminants in technical PCP, 
    especially PCDDs and PCDFs, must be reduced by improving the 
    quality in production processes. 

(b) There is a need for specification of a technical PCP. 

(c) Disposal of technical PCP and associated waste should 
    preferably involve high-temperature combustion or, where this 
    is not possible, the use of secure land-fill sites. 

(d) In order to reduce contamination of surface waters and the 
    hazards for the aquatic ecosystem, manufacturers and users of 
    technical PCP should prevent releases into the environment. 

(e) Protective measures should be provided for non-target aquatic 
    organisms in cases where PCP is used as molluscicide or 

(f) Occupational exposure to technical PCP must be reduced to a 
    minimum.  Reduction in exposure can be achieved by: 

    -   explicit product labelling;

    -   employee instruction on product handling;

    -   lowering airborne concentrations; and

    -   use of effective protective equipment.

(g) Industries handling technical PCP should ensure adequate 
    routine monitoring and health surveillance of all potentially 
    exposed employees. 

(h) The indoor application of PCP-based wood preservatives and wood 
    stains and the use of PCP-treated wood products in the interior 
    of buildings should cease. 

(i) The availability and use of consumer products containing PCP 
    should be reduced and controlled. 

(k) The following commercial uses of PCP-based products should be 
    eliminated, in order to reduce contamination of food and the 

    -   application as wood preservatives on wooden food
        containers, horticultural lumber, wood and tools in
        mushroom houses, and above-ground interior wood of
        farm buildings;

    -   application during the curing of hides;

    -   application as a herbicide or soil sterilant;

    -   application as a slimicide in wood pulp and paper
        operations; and

    -   application as a molluscicide in surface water if
        another control chemical or measure is available that
        is less toxic for man and the aquatic ecosystem.
11.2.  Future Research

11.2.1.  Human exposure and effects

(a) Reliable estimates of human absorption of airborne PCP via the 
    lung and skin are required. 

(b) The importance of the biotransformation of hexachlorobenzene 
    and related compounds as contributors to human body burdens of 
    PCP needs to be quantified. 

(c) It is necessary to determine the intake and accumulation by 
    human beings of the lipophilic microcontaminants (especially 
    the PCDDs and PCDFs) resulting from exposure to technical PCP. 

(d) Development of reliable estimates of biochemical and 
    reproductive no-observed-adverse-effect levels is desirable. 

(e) Studies on persons occupationally exposed to technical PCP 
    should be conducted using a large enough cohort or sufficient 
    numbers of cases to provide the statistical power necessary to 
    determine the relationships between exposure to PCP and 
    morbidity, mortality in general, and cancer.  Such studies 
    should include quantitative estimates of concentrations and 
    duration of exposure to PCP, wherever possible. 

11.2.2.  Effects on experimental animals and  in vitro test systems

(a) New data on the carcinogenicity of technical and pure PCP in 
    both sexes of 2 mammalian species are required. 

(b) There is a need for a long-term inhalation study on the effects 
    of both technical and pure PCP. 

(c) Studies should be undertaken to clearly determine the 
    teratogenic effects of pure and technical PCP.  The potential 
    effects of PCP induced maternal hyperthermia on embryological 
    development and fetal growth warrant investigation. 

(d) More research on the genotoxic and mutagenic activity of pure 
    and technical PCP is required. 

11.2.3.  Effects on the ecosystem

(a) Studies are needed to clarify the fate of sediment-bound PCP 
    and its effects on the environment. 

(b) Studies of the effects of long-term, low-level exposure on 
    fresh-water aquatic communities are required to establish no-
    observed-adverse-effect levels. 


    "The WHO Recommended Classification of Pesticides by Hazard" 
(WHO, 1984) distinguishes between the four hazard classes Ia, Ib, 
II, and III, based on the toxicity of technical products.  In this 
report, PCP is classified in class Ib, being highly hazardous. 

    The WHO manual "Prevention, Diagnosis and Treatment of 
Insecticide Poisoning" (Plestina, 1981) provides practical advice 
that generally applies to nitro- and chlorophenols. 

    In the  Guidelines for Drinking-Water Quality (WHO, 1985), a 
guideline value of 10 g/litre is recommended for PCP. 

    No evaluation of the carcinogenicity of PCP was made by the 
International Agency for Research on Cancer (IARC, 1979a), because 
the available data on the carcinogenic and mutagenic effects of PCP 
were considered inadequate for a sound evaluation. 

    Regulatory standards established by national bodies in 
different countries and the EEC are summarized in the data profile 
of the International Register of Potentially Toxic Chemicals 
(IRPTC, 1983). 

    IRPTC (1984), in its series "Scientific reviews of Soviet 
literature on toxicity and hazard of chemicals", issued a review on 


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    See Also:
       Toxicological Abbreviations
       Pentachlorophenol (HSG 19, 1989)
       Pentachlorophenol (ICSC)
       Pentachlorophenol (PIM 405)
       Pentachlorophenol (IARC Summary & Evaluation, Volume 53, 1991)