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    Published under the joint sponsorship of
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    and the World Health Organization

    World Health Orgnization
    Geneva, 1984

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    1.1. Summary
         1.1.1. Identity, properties and analytical methods
         1.1.2. Uses and sources of exposure
         1.1.3. Environmental concentrations and exposure
         1.1.4. Kinetics and metabolism
         1.1.5. Studies on experimental animals
         1.1.6. Effects on man
    1.2. Recommendations


    2.1. Identity
    2.2. Physical and chemical properties
    2.3. Analytical methods


    3.1. Production and uses
    3.2. Transport and distribution
         3.2.1. Air
         3.2.2. Water
         3.2.3. Soil
         3.2.4. Abiotic degradation


    4.1. Environmental levels
         4.1.1. Air
         4.1.2. Water
         4.1.3. Food
         4.1.4. Miscellaneous sources
         4.1.5. Wildlife
    4.2. General population exposure
    4.3. Occupational exposure


    5.1. Human studies
    5.2. Animal studies


    6.1. Single exposures
    6.2. Short-term exposures
    6.3. Long-term exposures.
    6.4. Dermal toxicity
    6.5. Reproduction studies
    6.6. Mutagenicity
    6.7. Teratogenicity

    6.8. Carcinogenicity
    6.9. Other studies


    7.1. Poisoning incidents
    7.2. Occupational exposure
    7.3. Controlled human studies


    8.1. Aquatic organisms
         8.1.1. Aquatic invertebrates
         8.1.2. Fish
    8.2. Terrestrial organisms
         8.2.1. Insects
         8.2.2. Birds
         8.2.3. Wild animals
         8.2.4. Plants
    8.3. Microorganisms
    8.4. Bioaccumulation and biomagnification
    8.5. Population and community effects
    8.6. Effects on the abiotic environment



    10.1. Camphechlor toxicity
    10.2. Exposure to camphechlor
    10.3. Effects on the environment
    10.4. Conclusions



    While every effort has been made to present information in 
the criteria documents as accurately as possible without unduly 
delaying their publication, mistakes might have occurred and are 
likely to occur in the future.  In the interest of all users of 
the environmental health criteria documents, readers are kindly 
requested to communicate any errors found 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. 

    In addition, experts in any particular field dealt with in 
the criteria documents are kindly requested to make available to 
the WHO Secretariat any important published information that may 
have inadvertently been omitted and which may change the 
evaluation of health risks from exposure to the environmental 
agent under examination, so that the information may be 
considered in the event of updating and re-evaluation of the 
conclusions contained in the criteria documents. 

                        *     *     *

    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 - 985850).



Dr Z. Adamis, National Institute of Occupational Health,
   Budapest, Hungary

Dr D.A. Akintonwa, Department of Biochemistry, Faculty of
   Medicine, University of Calabar, Calabar, Nigeriaa

Dr R. Goulding, Chairman of the Scientific Sub-committee, UK
   Pesticides Safety Precautions Scheme, Ministry of
   Agriculture, Fisheries & Food, London, England  (Chairman)

Dr S.K. Kashyap, National Institute of Occupational Health
   (Indian Council of Medical Research), Meghaninager,
   Ahmedabad, India

Dr D.C. Villeneuve, Environmental Contaminants Section,
   Environmental Health Centre, Tunney's Pasture, Ottawa,
   Ontario, Canada  (Rapporteur)

Dr D. Wassermann, Department of Occupational Health, The
   Hebrew University, Haddassah Medical School, Jerusalem,
   Israel  (Vice-Chairman)

 Representatives of Other Organizations

Dr C.J. Calo, European Chemical Industry Ecology and
   Toxicology Centre (ECETOC)

Mrs M.Th. van der Venne, Commission of the European
Communities, Health and Safety Directorate, Luxembourg

Dr D.M. Whitacre, International Group of National Associations
   of Agrochemical Manufacturers (GIFAP)


Dr M. Gilbert, International Register for Potentially Toxic
   Chemicals, United Nations Environment Programme, Geneva,

Mrs B. Goelzer, Division of Noncommunicable Diseases, Office
   of Occupational Health, World Health Organization, Geneva,

Dr Y. Hasegawa, Division of Environmental Health,
   Environmental Hazards and Food Protection, World Health
   Organization, Geneva, Switzerland

a   Unable to attend.

 Secretariat (contd.)

Dr K.W. Jager, Division of Environmental Health,
   Internationational Programme on Chemical Safety, World
   Health Organization, Geneva, Switzerland  (Secretary)

Mr B. Labarthe, International Register for Potentially Toxic
   Chemicals, United Nations Environment Programme, Geneva,

Dr I.M. Lindquist, International Labour Organisation, Geneva,

Dr M. Vandekar, Division of Vector Biology and Control,
   Pesticides Development and Safe Use Unit, World Health
   Organization, Geneva, Switzerland

Mr J.D. Wilbourn, Unit of Carcinogen Identification and
   Evaluation, International Agency for Research on Cancer,
   Lyons, France


    Following the recommendations of the United Nations 
Conference on the Human Environment held in Stockholm in 1972, 
and in response to a number of World Health Assembly Resolutions 
(WHA23.60, WHA24.47, WHA25.58, WHA26.68), and the recommendation 
of the Governing Council of the United Nations Environment 
Programme, (UNEP/GC/10, 3 July 1973), a programme on the 
integrated assessment of the health effects of environmental 
pollution was initiated in 1973.  The programme, known as the WHO 
Environmental Health Criteria Programme, has been implemented 
with the support of the Environment Fund of the United Nations 
Environment Programme.  In 1980, the Environmental Health 
Criteria Programme was incorporated into the International 
Programme on Chemical Safety (IPCS).  The result of the 
Environmental Health Criteria Programme is a series of criteria 

    A WHO Task Group on Environmental Health Criteria for 
Organochlorine Pesticides other than DDT met in Geneva from 28 
November to 2 December 1983.  Dr K.W. Jager opened the meeting on 
behalf of the Director-General.  The Task Group reviewed and 
revised the draft criteria document and made an evaluation of the 
health risks of exposure to camphechlor. 

    This document is a combination of drafts prepared by Dr D.C. 
Villeneuve of Canada and Dr S. Dobson of the United Kingdom. 

    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. 


1.1.  Summary

1.1.1.  Identity, properties and analytical methods

    Camphechlor (toxaphene) (C10H10Cl8 approx.) is an amber,
waxy solid consisting of a complex mixture of polychlorinated 
bicyclic terpenes. 

    Gas chromatography with electron capture detection is the
method of choice for the determination of camphechlor.

1.1.2.  Use and sources of exposure

    Camphechlor is a non-systemic contact and stomach insecticide 
with some acaricidal action.  It is often used in combination 
with other pesticides. 

    The main source of exposure for the general population is the 
residues of camphechlor in food, but these are generally very 

1.1.3.  Environmental concentrations and exposure

    Camphechlor is broken down in the environment by sunlight 
(ultraviolet radiation), high temperature, and by biodegradation.  
There are no details on the relative breakdown of the components 
of the mixture.  Camphechlor is readily lost from the soil by 
evaporation, but once it penetrates the soil it is tightly bound 
to soil particles and very resistent to leaching.  Its half-life 
in soil has been reported to vary from 70 days to 12 years, 
depending on the type and condition of the soil.  In some waters 
it has been shown to  persist for years at concentrations that 
are toxic for fish. 

    Camphechlor is rapidly removed from crops by weathering and 

    It is toxic for aquatic species and some terrestrial species 
and has been shown to bioaccumulate, mainly in aquatic species.  
It may present a major hazard for aquatic organisms.  It also 
poses a threat to birds. 

1.1.4.  Kinetics and metabolism

    Camphechlor is absorbed following ingestion and inhalation, 
as well as through the skin.  Detailed information is lacking on 
its metabolism, probably because of its complex composition.  
Both hydroxylation and dechlorination products have been found as 
metabolites.  Excretion takes place via both urine and faeces. 

1.1.5.  Studies on experimental animals

    Camphechlor is moderately toxic, i.e., the oral LD50 values 
in the rat range from 60 to 120 mg/kg body weight and can on acute 
oral over-exposure give rise to salivation, vomiting, hyper-
excitability, convulsions, and death.  The lethal dose for man is 
estimated to be 2 - 7 g.  It is an irritant for the skin.  

    In short-term and long-term studies on animals, hypertrophy 
of the liver with increased microsomal enzyme activity and 
histological changes in the liver cells occurs at high dose 
levels (1000 mg/kg diet), depending on the test conditions and 
the species tested.  Induction of microsomal enzyme activity in 
the rat has been found at levels of 5 mg or more/kg diet.  
Hypertrophy of the thyroid and adrenals and degeneration of the 
tubular epithelium of the kidney have also been reported.  At 
near lethal dosages, excitation of the CNS may occur. 

    Camphechlor has been shown not to have any effects on 
reproduction and was not found to be teratogenic.  It was mutagenic 
in  Salmonella typhimurium but results of a dominant lethal test 
on mice were negative.  It is carcinogenic for both rats and mice.

1.1.6.  Effects on man

    Several cases of poisoning have been described in man due to 
contamination of food with camphechlor or to accidental ingestion 
of camphechlor formulations.  Symptomatology consists of 
gastrointestinal complaints, followed by motor seizures.  Some 
incidents in children were lethal. 

    Although a survey of a population of workers in a plant 
manufacturing camphechlor did not reveal any cases of ill-health 
referable to their employment, some illness has been reported in 
a few people coming into contact with this chemical.  A group of 
8 women exposed to camphechlor were reported to have a higher 
incidence of chromosome abnormalities than the controls.  
Available epidemiological studies are not adequate to evaluate 
the carcinogenicity of camphechlor for human beings. 

1.2.  Recommendations

1.  Careful surveillance should be maintained over the future 
    production of camphechlor and the nature and extent of its 

2.  Levels in the environment should continue to be 
    comprehensively monitored. 


2.1.  Identity

Chemical Structure

Molecular formula:         C10H10Cl8 (approximately)

CAS chemical name:         Toxaphene (a mixture of poly-
                           chlorinated bicyclic terpenes with
                           chlorinated camphenes predominating)

Trade names:               Altox, Chem-Phene M5055, Chlor Chem
                           T-590, Crestoxo, Estonox, Fasco-
                           Terpene, Geniphene, Gy-Phene,
                           Hercules 3956, Huilex, Penphene,
                           Phenacide, Phenatox, Polychlor-
                           camphen, Strobane-T, Toxakil,
                           Toxaphene, Toxon 63

CAS registry number:       8001-35-2

Relative molecular mass:   413.8 (average)

2.2.  Physical and Chemical Properties

    Camphechlor is an amber, waxy solid (Canada, Department of
National Health and Welfare, 1978) with a melting range of
65 - 90 C.  Its vapour pressure is 3.3 x 10-5 mm Hg at 20 -
25 C.  Camphechlor may dechlorinate in the presence of
alkali, sunlight (UV radiation) or at temperatures above
120 C (Canada, Department of National Health and Welfare,
1978; IARC, 1979).  It is soluble in common organic solvents
but practically insoluble in water (0.4 - 3.0 mg/litre)
(Metcalf, 1976).

    The exact chemical structure has not yet been elucidated
(von Rumker et al., 1974).  The technical product is a complex
mixture of chlorinated bicyclic terpenes containing 67 - 69%
chlorine by weight (Canada, Department of National Health and
Welfare, 1978), which result from the chlorination of pine
resins.  Camphechlor has been separated into at least 177
C10-polychloro compounds, including Cl6, Cl7, Cl8, Cl9, and
Cl10 derivatives, using absorption and gas-liquid
chromatography (Casida et al., 1974, Holmstead et al., 1974).

2.3.  Analytical Methods

    Much difficulty has been encountered in the determination of 
camphechlor residues due to the fact that camphechlor is not a 
single compound, but a mixture of over 177 compounds.  In addition, 
it is often used in conjunction with other pesticides, which may 
cause interference in analytical procedures for camphechlor 

    Several analytical methods used for the determination of 
camphechlor in air, water, soil, food, and animal tissues are 
summarized in Table 1 (IARC, 1979). 

Table 1.  Methods for the determination of camphechlor
Sample type  Sampling method                Analytical  Limit of     Reference
             extraction/clean-up            method      detection

 workplace   trap on cellulose membrane,    GC/ECD      0.225 -      NIOSH (1977b)
             extract (petroleum ether)                  1.155 mg/m3


 fish-tank   extract (acetone-petroleum     GC/ECD      10 g/litre  Stalling &
             ether) in a special                                     Huckins       
             syphon system, wash                                     (1976)
             resulting water-acetone layer
             (petroleum ether), bulk      
             petroleum ether fractions, CC

             moisten (water), extract       GC/ECD      0.05 -       Carey et al. 
             (hexane-isopropanol), wash                 0.1 mg/kg    (1976)


 molasses    dilute (water), extract        GC/ECD      0.03 mg/kg   Yang et al.  
             (hexane-isopropanol)                                    (1976)

 fruits and  extract (acetone) in blender,  GC/ECD                   Luke et al.
 vegetables  filter, extract (petroleum                              (1975)       
             ether-dichloromethane), wash
             aqueous phase
             (dichloromethane), bulk       
             solvent extracts, evaporate   
             to small bulk, add acetone,      
             reduce volume and repeat, CC  
tissues      macerate, add anhydrous        TLC         1 g       Tewari &    
             sodium sulfate, extract                               Sharma (1977)
             (acetone), add water,                          
             extract (chloroform)          
             wash (potassium
             hydroxide solution)
CC = column chromatography; 
GC = gas chromatography; 
ECD = electron capture detection; 
TLC = thin-layer chromatography.


3.1.  Production and Uses

    Camphechlor does not occur naturally in the environment 
(Canada, Department of National Health and Welfare, 1978). 
Camphechlor has been in use since 1949 and, in 1975, it was the 
most heavily-used insecticide in the USA (Pollock & Kilgore, 
1980).  In 1969, 168 uses for camphechlor were registered in the 

    Production in the USA has been estimated to range from 22 700 
- 40 800 tonnes per year (Canada, Department of National Health  
and Welfare, 1978).  Von Rumker et al. (1974) gave the following 
annual figures for the USA:  total production 34 200 tonnes, of 
which 8000 tonnes was exported and 26 500 tonnes was used in the 
USA:  450 tonnes for industrial application and 25 650 tonnes for 
agricultural use.  Estimated consumption in the USA was 9360 
tonnes in 1980 and 5400 tonnes in 1982.  Since late 1982, use in 
the USA has been limited to scabies control on cattle and sheep, 
insect control on pineapples and bananas in the Virgin Islands 
and Puerto Rico, and for emergency use against army worms and 
grasshoppers on cotton, corn, and grain.  These uses are 
restricted to certified spray operators wearing protective 
clothing (IRPTC, 1983a).  Registered uses in Canada are minimal 
and are decreasing. 

    Camphechlor is a non-systemic contact and stomach insecticide 
with some acaricidal action.  The primary crops on which camphechlor
is used are cotton, cereal grains, fruits, nuts, oil seeds, and 
vegetables.  Use on livestock is primarily for the control of ticks 
and mites.  The use of camphechlor on crops has not been a serious 
problem for bees fertilizing the treated crops (WHO, 1975).  
Camphechlor is often mixed with other pesticides and appears to act 
as a solubilizer for insecticides with low solubility.  The 
synergistic properties of camphechlor when used with some other 
insecticides have been reported (von Rumker et al., 1974).  
Camphechlor is often applied together with DDT or methyl or ethyl 
parathion (WHO, 1975). 

3.2.  Transport and Distribution

3.2.1.  Air

    The major route of removal of camphechlor from the soil is 
through evaporation (von Rumker et al., 1974).  Although there is 
little information on the atmospheric transport of camphechlor, 
it is likely that it may cover hundreds of miles.  Camphechlor 
levels in 75 out of 880 air samples from different parts of the 
USA ranged between 68 and 2520 ng/m3 (Stanley et al., 1971).  
Five out of 8 rainwater samples taken in Maryland, USA, contained 
camphechlor (Munson, 1976). 

3.2.2.  Water

    Accumulation of camphechlor occurs in water in areas where the
insecticide is in use and it may be quite persistent.  It has been 
found in water in some lakes, in toxic concentrations, for up to 5 
years after fish have been killed (Canada, Department of National 
Health and Welfare, 1978).  Camphechlor was not found in drinking-
water supplies in Canada above a detection level of 0.01 mg/litre 
(Canada, Department of National Health and Welfare, 1978).  In the 
USA, camphechlor concentrations were usually less than 0.001 
mg/litre; nevertheless, concentrations as high as 0.065 mg/litre 
were found in some areas where cotton had been sprayed several 
months earlier (Bradley et al., 1972).  Camphechlor concentrations 
of up to about 2 g/kg were found in the sediment of a stream that 
received the effluent of a camphechlor-manufacturing plant (Durant 
& Reimold, 1972).  Camphechlor residues in the range of 7 - 410 
ng/litre were also present in all water samples taken before and 
after treatment by a water treatment plant (Nicholson et al., 1964). 

    Although the majority of the residues are volatilized, levels 
in runoff from soil surfaces or treated plants may be substantial 
(von Rumker et al., 1974). 

3.2.3.  Soil

    As camphechlor is applied topically to livestock and 
agricultural crops, very little of the pesticide gets mixed into 
the soil.  However, that which penetrates into the soil becomes 
tightly bound to soil particles and is then highly resistant to 
leaching (von Rumker et al., 1974).  Residues adsorbed on soil 
particles may be transported via soil erosion and sediment 
transport.  The downward migration of camphechlor in soil is not 
significant.  The results of a study assessing the vertical 
distribution of camphechlor indicated that, after 3 years, 85 - 
90% of the remaining pesticide was in the top 23 cm of the soil 
(WHO, 1975). 

    The half-life of camphechlor in soil has been found to vary 
from 70 days (in moist, sandy soil) to 179 days (in moist clay 
soil).  The half-life in these same soils, if dried, became 136 
and 705 days, respectively (WHO, 1975).  In another study, 
involving the mixing of camphechlor with soil, 45% of the 
original application remained after 14 years (Nash & Woolson, 
1967).  Other authors have determined that the half-life of 
camphechlor in soil ranges from 100 days (LaFleur et al., 1973) 
up to 6 and 12 years (Alexander, 1965; Nash & Woolson, 1967; 
Menzie, 1972).  The disparity among these findings may be 
explained by variations in soil type and climates. 

    No evidence has been found to suggest the existence of 
conversion products of camphechlor in weathered crop residues 
(WHO, 1975).  However, camphechlor is rapidly removed from crops 
by weathering and volatilization. 

    In the USA, the average level of camphechlor in cropland soil 
is 0.07 mg/kg.  A study on 969 soil samples from cropland soils 
from 43 states and on non-cropland soils from 11 states showed 
camphechlor residues in only 4.2% of the sites examined, despite 
the fact that all the major camphechlor-using areas were included 
in the cropland states surveyed.  In the 199 non-cropland soil 
samples, camphechlor occurred only once (Wiersma et al., 

3.2.4.  Abiotic degradation

    Camphechlor is broken down by sunlight (ultraviolet radiation) 
and high temperatures.  It is also biologically degraded by soil 
bacteria and fungi, the bacteria utilizing it as a source of carbon 
(WHO/FAO, 1975).  No definitive data have been published on the 
degradation found in camphechlor (Metcalf, 1976). 


4.1.  Environmental Levels

4.1.1.  Air

    Because the concentrations of camphechlor in ambient air
in unsprayed areas are in the ng/m3 range (IARC, 1979), it
seems unlikely that it would cause any health hazard.

4.1.2.  Water

    Only bodies of water that have been treated with camphechlor 
for fish control or receive runoff from manufacturing sites or 
cropland areas treated with camphechlor have been found to 
contain significant amounts of camphechlor. 

    The lower limit of detection of camphechlor by taste is 
approximately 5 g/litre.  Water treated with activated carbon (a 
method used to clear water bodies of accidental camphechlor 
spills) is effectively free of camphechlor (WHO, 1975).  No 
damage to man resulting from camphechlor residues in water has 
been reported. 

4.1.3.  Food

    Camphechlor bioaccumulates and builds up in food chains, but 
not to the same extent as some other highly persistent chlorinated 
hydrocarbons (von Rumker et al., 1974).  For the most part, 
camphechlor levels in food seem to be below the national tolerances 
(WHO, 1975), which range from 2 - 7 mg/kg in Australia, Canada, and 
the USA, and are as low as 0.4 mg/kg in the Federal Republic of 
Germany and the Netherlands (WHO, 1975). 

    Camphechlor was evaluated by the Joint Meeting on Pesticide 
Residues (JMPR) in 1968 and 1973 (FAO/WHO, 1969, 1974).  In 1968, 
no recommendations were made because of the many unresolved 
questions.  In 1973, the meeting concluded that it could not 
establish an ADI for a material that varied in composition 
according to the method of manufacture. 

    Because camphechlor is not a systemic insecticide, the 
residues are more or less confined to the plant surfaces (WHO, 
1975).  Camphechlor residues generally occur in agricultural 
crops as well as in meat from domestic livestock and fish. 
Thirty-one days following an application of camphechlor to 
alfalfa, 72.9% of the compound had been lost.  Long-term losses 
depended on the quantity applied, the formulation, and the 
application route.  The greatest residue was left from oily 
solutions, followed by water emulsion, and by dusts (Pollock & 
Kilgore, 1978).  Camphechlor residues on growing leafy crops have 
a half-life of 5 - 10 days.  On alfalfa and clover, the half-life 
is in the range of 9 - 13 days.  The residue level is controlled 
by time of application, dosage rate, and appropriate pre-slaughter 
or pre-harvest intervals (WHO, 1975). 

    Fruits and vegetables have been found to contain camphechlor 
residues; the highest concentrations were found in spinach 
(FAO/WHO, 1969).  In studies conducted during 1964-67, the average 
levels of camphechlor residues found in leaf and stem vegetables 
was 0.18 mg/kg and that in processed foods 0.45 mg/kg.  Generally, 
levels of camphechlor in all foods were low.  In 1964-66, 
camphechlor residues were detected in 30, 8, and 2% of the cotton-
seed, soybean, and peanut oil samples listed, respectively (Pollock 
& Kilgore, 1978).  Heat processing of fruits and vegetables was 
found to reduce levels of camphechlor residues (WHO, 1975).  Sugar 
beet, sampled in the USA in the autumn of 1970, showed camphechlor 
residues of 0 - 0.34 mg/kg (Yang et al., 1976).  It has been 
demonstrated that peeling, abrasive peeling, and washing removes 
most of the camphechlor residues present on fruits and vegetables.  
The addition of 0.1% synthetic detergent or 1.0% neutral soap to 
the washing water increases the amount of the pesticide removed 
(WHO, 1975). 

    Honey produced by bees exposed to 36Cl-camphechlor
contained less than 0.01 mg camphechlor/kg (WHO, 1975).

    Because livestock is treated with camphechlor to remove 
external insects and because some feeds are contaminated with 
camphechlor, camphechlor residues are found in meat and poultry.  
The residues in meat can be significantly reduced by trimming 
excess fat (the primary storage site for camphechlor) and also by 
cooking at temperatures sufficient to render out the fat (WHO, 
1975).  In animals, the level of storage of camphechlor is lower 
and its elimination more rapid than with most other chlorinated 
hydrocarbons (FAO/WHO, 1974), hence residues in poultry and meat 
are very low (WHO, 1975).  In general, the level stored in the 
fat of sheep and cattle is 25 - 50% of the level in the feed.  
This concentration is less in hogs, probably because of a greater 
fat content (FAO/WHO, 1969). 

    Camphechlor has been detected in the milk from cows sprayed or 
fed this insecticide (Clayborn et al., 1963; Canada, Department of 
National Health and Welfare, 1978).  The ratio of camphechlor 
concentration in feed to that in milk is approximately 100:1.  
Build-up in milk quickly fades when exposure to camphechlor is 
discontinued (WHO, 1975).  Residues of camphechlor in milk, due to 
feed containing 5 - 20 mg camphechlor/kg, plateaued after 28 days.  
Residues in milk, due to feed containing 2.5 mg camphechlor/kg, 
plateaued by the 9th day.  Milk contained 0.11 and 0.18 mg 
camphechlor residues/litre when feed containing 10 and 20 mg/kg, 
respectively.  The residues in milk fell off sharply, 4 days after 
camphechlor was absent from the diet and were negligible by the 
14th day (Zweig et al., 1963).  In the USA, camphechlor was 
detected in only 5 out of 7265 meat samples and 2 out of 5504 
poultry samples (Guyer et al., 1971). 

    In a study carried out by the Department of National Health 
and Welfare, Canada, between 1969 and 1971, no detectable levels 
(at the ppb level) of camphechlor were found in any of the 
several hundred food items analysed (Smith, 1971; Smith et al., 
1972, 1973), while, in another study carried out by the 
Department of National Health and Welfare, Canada, between 1974 
and 1975, unspecified amounts of camphechlor were found in 0.6% 
of the food items tested (Coffin & McLeod, 1975); thus, the 
incidence was very low. 

    In the USA, between 1971 and 1972, among a total of 420 
samples of food analysed, only one was found to contain 
camphechlor (Manske & Johnson, 1975).  In a study conducted in 
the USA during the period of 1964-69, residues of camphechlor 
were found to be the 6th most frequent in occurrence of all 
pesticides in processed foods.  However, levels were so low that 
few, if any, exceeded the 7 mg/kg tolerance level (WHO, 1975). 

4.1.4.  Miscellaneous sources

    Camphechlor residues have also been found in non-food items.  
Camphechlor residues in chewing tobacco, smoking tobacco, snuff, 
cigarettes, and cigars in the USA were found to have decreased 
over the period 1971-73.  The average concentration in cigarettes 
decreased from 3.3 to 1.4 mg/kg (Domanski et al., 1974).  In 
1972, examinations showed that 6 brands of cigars purchased in 5 
cities in the USA contained camphechlor residues ranging from 0.5 
to 3.42 mg/kg (Domanski & Guthrie, 1974), while results of a 
study conducted in 1970 (Domanski & Sheets, 1973), showed 
camphechlor residues in tobacco in the USA to be as high as 12 

4.1.5.  Wildlife

    Residues of camphechlor were found in 53% of samples of fish 
and invertebrates taken from waters near cotton-producing areas 
along the Guatemalan Pacific Coast (Keiser et al., 1973).  No 
changes in camphechlor levels were observed when fish containing 
5 - 10 mg/kg camphechlor were boiled or fried (Terriere & 
Ingalsbe, 1953). 

    Residues have been found infrequently and at low levels in 
non-aquatic wildlife (Pollock & Kilgore, 1978). 

4.2.  General Population Exposure

    Camphechlor exposure of the general population can result 
from residues in food. 

4.3.  Occupational Exposure

    Results of a study conducted in camphechlor-manufacturing
plants in the USSR showed camphechlor levels 5 - 6 times the
permissible limit of 0.2 mg/m3.  After a work shift, levels of
30 - 1000 mg/m2 were found on the uncovered skin of workers,
while levels on covered areas ranged up to 40 mg/m2 (Ashirova,
1971).  However, no adverse effects of this occupational exposure 
have been reported.  Although camphechlor was used extensively 
during the 1960s in agricultural and public health programmes in 
Alberta, analyses of human tissue from 50 autopsies at the 
University Hospital in Edmonton in 1967-68 did not reveal 
camphechlor in any of the 217 tissues examined (Kadis et al., 


5.1.  Human Studies

    In a 9-month-old child, poisoned with a 2:1 mixture of 
camphechlor and DDT, death occurred after convulsions and 
respiratory failure.  Ratios of camphechlor:DDT in the brain and 
liver were 10:1 and, in the kidney, 3:1 (Haun & Cueto, 1967).  No 
significant levels of camphechlor were found in the skin and 
subcutaneous tissue taken from 68 children, who died in the 
perinatal period, in 13 cities in the USA (Zavon et al., 1969). 

5.2.  Animal Studies

    The metabolism of camphechlor has been an area of little 
research, because of difficulties in detecting a complex and 
multicomponent substance.  However, a few such studies have been 

    About 37% of a single oral dose of technical grade
36Cl-camphechlor, administered to rats at 20 mg/kg body
weight, was eliminated in the faeces; 15% was excreted in the
urine in 9 days during the same period (Crowder & Dindal,
1974).  Rats were dosed orally with solutions containing
either 36Cl-camphechlor, 36Cl-camphechlor fractions, or
14C-camphechlor.  Urine and faeces samples were collected for
14 days (Ohsawa et al., 1975).  The rats excreted (combined
urine and methanol extract of faeces) 76% of the 36Cl-camphechlor, 
57% of the 14C-camphechlor, and 69 - 94% of the 36Cl-camphechlor 
fractions.  Very little of the material was excreted unmetabolized 
and the camphechlor had undergone dechlorination.

    A dose-related increase in the excretion of camphechlor in 
the milk of cows, fed diets containing camphechlor at 2.5 - 20 
mg/kg, was reported (Zweig et al., 1963).  Results of  in vitro 
studies, using rat liver homogenates, showed that isolated 
camphechlor fractions were metabolized to hydroxylated compounds, 
in addition to dechlorinated products (Chandurkar & Matsumura, 
1979).  However, the precise chemical structures of these 
metabolites were not unequivocally identified.  Pollack & Kilgore 
(1976) dosed rats orally with 14C-camphechlor and reported a 
cumulative elimination of 58% of the dose in the urine and 
faeces.  Increased amounts of polar "activity" and a small 
increase in non-polar fractions were found in the fat. 


6.1.  Single Exposures

    Camphechlor is absorbed through the skin, respiratory tract, 
and the intestinal tract (FAO/WHO, 1969; Gleason et al., 1969; 
Gosselin et al., 1976). 

    The principal toxic manifestations noted in animals exposed 
to a single dose of camphechlor consist of salivation, vomiting, 
reflex excitability, and convulsions terminating in respiratory 
failure (Taylor et al., 1979).  Typical LD50 values for a variety 
of animals are given in Table 2.  The influence of the solvent on 
camphechlor uptake can be seen from the wide range of LD50s in 
this table. 
Table 2.  The acute toxicity of camphechlor in several animal studies 
Species      Route     Vehicle                LD50 (mg/kg)    References 
Rat          oral      peanut oil             80 - 90         Gaines (1969) 

Rat          dermal    xylene                 780 - 1075      Gaines (1969)

Rat          oral      corn oil               60              US EPA (1976a)

Rat          oral      kerosene               120             US EPA (1976a)

Mouse        oral      corn oil               112             US EPA (1976a)

Dog          oral      corn oil               49              US EPA (1976a)

Dog          oral      kerosene               over 250        US EPA (1976a)

Guinea-pig   oral      kerosene               365             US EPA (1976a)

Cat          oral      peanut oil             25 - 40         US EPA (1976a)

Rabbit       oral      peanut oil             75 - 100        US EPA (1976a)

Rabbit       oral      kerosene               250 - 500       US EPA (1976a)

Rabbit       dermal    dust                   over 4000       US EPA (1976a)

Rabbit       dermal    peanut oil             over 250        US EPA (1976a)

Rabbit       dermal    wettable powder        1025 - 1075     Johnston &
                       (suspension in water)                  Eden (1953)

Cattle       oral      grain                  144             US EPA (1976a)

Goat         oral      xylene                 200             US EPA (1976a)

Sheep        oral      xylene                 200             US EPA (1976a)
    The acute toxicity of camphechlor in rats is increased at least 
3-fold by protein deficiency (Gleason et al., 1969).  The lethal 
oral dose for an adult man is estimated to be 2 -7 g (Conley, 1952). 

6.2.  Short-Term Exposures 

    Rats were fed camphechlor at levels of 0.2 - 50 mg/kg diet, 
for up to 13 weeks (Kinoshita et al., 1966).  Camphechlor was 
observed to induce microsomal enzyme activity at levels of 5.0 
mg/kg and higher. 

    Camphechlor did not induce any effects on the physical 
appearance, gross pathology, weight gain, or liver cell histology 
of albino rats fed 2.33 - 189 mg/kg diet, for up to 12 weeks 
(Clapp et al., 1971). 

    Camphechlor, when fed to rats for 7 days at 25 mg/kg diet, 
caused an increase in the metabolism of estrone and inhibited the 
increase in uterine weight produced by this compound (Welch et 
al., 1971). 

    Studies on pregnant albino rats showed that daily oral 
administration of camphechlor for up to 20 days resulted in 
interconnected structural and enzymic changes in the cerebral 
cortex (Badaeva, 1976). 

    Rats were dosed once, orally, with 120 mg camphechlor/kg body 
weight and monitored for up to 15 days (Peakall, 1976). Liver 
weight and microsomal enzyme activity were increased after 5 and 
15 days, respectively.  In another study in the same report, rats 
were administered camphechlor at 2.4 mg/kg body weight per day 
and killed at 1, 3, and 6 months.  Liver weight and microsomal 
enzyme activity increased at all time intervals, but plasma 
testosterone levels were not affected. 

    Administration to rats of a single oral dose of 120 mg/kg 
body weight, as well as a daily dose of 2.4 mg/kg body weight, 
for 1 or 3 months, produced a disturbance in catecholamine 
metabolism (Kuzminskaya & Ivanitski, 1979). 

    Adult male rats were fed diets containing 0, 50, 100, 150, 
and 200 mg camphechlor/kg for 14 days (Trottman & Desaiah, 1980).  
No changes were observed in body weight gain, food consumption, 
brain, kidney, heart, or testes weights; liver weight was 
increased at 200 mg/kg and thymus weight decreased at 150 and 200 
mg/kg.  Increased hydroxylation of aniline was observed at all 
dose levels. 

    Administration of 5, 50, or 500 mg camphechlor/kg diet to 
quail for up to 4 months produced hypertrophy of the thyroid with 
increased uptake of 131I and adrenal hypertrophy (Hurst et al., 

    Feeding of camphechlor in the diet at 5, 50, or 100 mg/kg to 
chickens for 31 weeks induced sternal deformation and nephrosis 
(Bush et al., 1977).  Occasional keel deformation, involving 
cartilaginous tissue as well as an apparent increase in the 
growth of cartilage, was found in birds fed 0.50 mg camphechlor/kg. 

    Camphechlor was administered in capsules at a daily dose of 4 
mg/kg body weight to 2 dogs for 44 days and to 2 other dogs for 106 
days.  Occasional manifestations of acute toxicity (CNS stimulation) 
occurred for a short time after administration.  There were no 
significant changes in body weight, blood picture, or gross 
appearance of organs. Histological examination of many organs 
revealed some damage to the kidney (degeneration of the tubular 
epithelium) and to the liver (generalized hydropic degenerative 
changes, but no destruction of the cells).  Liver glycogen levels 
were normal (Lackey, 1949). 

6.3.  Long-Term Exposures

    Four groups each of 40 rats (20 males and 20 females), were 
fed camphechlor in the diet at 10, 100, 1000, and 1500 mg/kg.  
Effects were determined through gross observation, mortality 
rates, body weight, blood tests, liver weight, liver to body-
weight ratio, gross autopsy, and histological examination of the 
tissues.  After 7 1/2 - 10 months of feeding, some of the rats 
fed 1500 mg/kg and a few of the rats fed 1000 mg/kg suffered 
occasional convulsions.  The body weight gain of the rats fed the 
highest feeding level (1500 mg/kg) for the first 20 weeks was 
less than that in the controls, probably because of decreased 
food intake through unpalatability of the diet.  As the rats 
became accustomed to the diet, growth rate was essentially the 
same as that of the controls.  There were no significant effects 
on mortality rate or on the haematopoietic system.  The liver 
weight and liver to body weight ratio was significantly increased 
only in the 1000 and 1500 mg/kg groups.  Liver changes consisted 
of swelling, cellular hypertrophy, and proliferation of smooth 
endoplasmic reticulum with cytoplasmic margination in the 
centrilobular hepatic cells.  These changes occurred to a 
moderate extent in the 1500 mg/kg group and to a slight extent in 
the 1000 mg/kg group (Treon et al., unpublished data, 1952). 

    Six male and 6 female rats per group were fed 50 or 200 mg 
camphechlor/kg diet for up to 9 months (Ortega et al., 1957). 
There were no clinical signs of toxicity and no effects on body 
weight gain, food intake, or liver weights.  No histological 
changes were seen in the kidney or spleen.  Three out of 12 rats 
fed 50 mg/kg diet for 9 months showed histological changes in the 
liver consisting of centrilobular cell hypertrophy, peripheral 
migration of basophilic granulation, and the presence of 
liposphere inclusion bodies. Six of the 12 rats fed 200 mg/kg 
showed liver changes. 

    Groups of rats were fed camphechlor in the diet at 25,
100, and 400 mg/kg for their lifetime (Fitzhugh & Nelson,
1951).  The only organ that showed significant histological

changes was the liver and these occurred at the 100 mg/kg and 400 
mg/kg levels.  There was centrilobular hepatic cell enlargement 
with increased oxyphilia and peripheral margination of basophilic 
granules.  The effects at the various feeding levels were summarized 
by Lehman (1952b), as follows:  400 mg/kg, liver enlargement; 100 
mg/kg, no gross effects, but tissue damage occurred; and 25 mg/kg, 
no tissue damage. 

    Camphechlor dissolved in maize oil, in gelatin capsules, was 
administered daily, for 5 days per week, to dogs.  A dose of 25 
mg/kg body weight was fatal.  Two dogs were administered 10 mg/kg 
(equivalent to 400 mg/kg diet); one dog died after 33 days, but 
the other lived and was sacrificed after 3 1/2 years.  Four dogs 
were administered 5 mg/kg; all survived and were sacrificed after 
almost 4 years.  No information on the pathological findings was 
reported (Lehman, 1952b). 

    Camphechlor was fed daily (6 days per week) for 2 years to
3 male and 5 female dogs, beginning when the animals were
approximately 4 months old.  Camphechlor was added to the
diet, including their drinking liquids, at levels of 10 and
50 mg/kg.  The dogs received a daily dose of 0.60 - 1.47 mg/kg
or 3.12 - 6.56 mg/kg (equivalent to approximately 40 or
200 mg/kg on a dry diet basis).  Gross behaviour, body weight,
mortality, peripheral circulating blood elements, gross
pathology, organ to body weight ratios, and histopathology
were recorded (Treon et al., unpublished data, 1952).  There
were no effects on behaviour, body weight, mortality, or blood
elements, but there were increases in the liver weights, liver
to body weight ratios, and moderate liver degeneration at the
higher dose level (200 mg/kg).  At the lower dose level
(40 mg/kg), 1 out of 3 dogs was reported to have slight liver
enlargement and slight granularity and vacuolization of the
cytoplasm.  Re-examination of the sections of these animals
failed to confirm any difference from control animals.  All
other tissues were normal at both feeding levels (Brock &
Calandra, 1964).a

    Groups of dogs, comprising 6 male and 6 females, were fed 
camphechlor at dietary levels of 5, 10, or 20 mg/kg together with 
control groups.  Two male and 2 female animals were sacrificed 
after 6, 12, and 24 months.  None of the feeding levels produced 
any changes in organ weights, gross or histological examination, 
or any of the clinical or organ function tests, at any time 
(Industrial Bio-Test Laboratories Inc., unpublished data, 1965)b.

a   Brock, D. & Calandra, J.C. (1964)   Re-evaluation of
     microscopic sections from chronic oral toxaphene study,
    Industrial Bio-Test Laboratories, Inc., unpublished report.

b   Industrial Bio-Test Laboratories Inc. (1965)   Two-year
     chronic oral toxicity of toxaphene in beagle dogs
    (Unpublished report).

    Two adult female monkeys were given camphechlor in their 
food, 6 days per week, at a daily dose of 0.64 - 0.78 mg/kg for 2 
years.  A third animal served as a control.  There were no signs 
of intoxication and no evidence of tissue or organ damage as 
evaluated by growth rate, ratios of liver to body weight, spleen 
to body weight, or histological examination of the tissues (Treon 
et al, unpublished data, 1952). 

6.4.  Dermal Toxicity

    The acute LD50 for rabbits exposed dermally to camphechlor
in the dry form was > 4000 mg/kg body weight (Lehman, 1952a).
The animals showed only moderate skin irritation and systemic
effects were characterized by hyperexcitability but no deaths
occurred.  The animals recovered in 5 or 6 days.  The 90-day
dermal LD50 has been estimated to be approximately 40 mg/kg
body weight for rabbits (Lehman, 1952a).

    A review of the effects of camphechlor on livestock
revealed that cattle, sheep, and hogs can tolerate repeated
applications of solutions containing less than 2% camphechlor
(Penumarthy et al., 1976).  However, dips containing 2.5%
camphechlor emulsion caused toxicosis in cattle.

6.5.  Reproduction Studies

    A 3-generation, 6-litter reproduction study was conducted with 
camphechlor.  Groups of weanling rats were fed 25 mg/kg diet and 
100 mg/kg diet for 79 days before mating.  All the animals continued 
on their respective dietary concentration of camphechlor during 
mating, gestation, and weaning during 2 generations, or for a 
period of 36 - 39 weeks.  Weanlings from the second litter were 
selected as parents for the second generation and continued on 
their respective diets until after weaning of a second litter.  A 
third generation was selected in the same manner.  Complete gross 
and histological examination was performed on all three parental 
generations after 36 weeks of camphechlor administration.  The only 
pathological changes found were slight alterations in the livers of 
the 100 mg/kg group, similar to the changes seen in long-term 
studies.  Reproductive performance, fertility, and lactation were 
normal.  The progeny was viable and normal in size and anatomical 
structure.  Findings among all test animals, 3 parental generations 
and 6 litters of progeny, were comparable to those in control 
animals for all variables (Kennedy et al., 1973). 

    Groups of mice (4 males and 14 females per group) were fed 
camphechlor in the diet at levels of 0 and 25 mg/kg in a 5-
generation, 2 litter-per-generation, reproduction study.  No 
effects were noted on any of the reproduction parameters measured 
(Keplinger et al., 1970). 

    Camphechlor in a corn-oil carrier was injected into fertile 
hen eggs.  It did not cause any reduction in hatchability, even 
at the highest dose used, 1.5 mg/egg (Smith et al., 1970).  In 

another study, white leghorn hens were fed camphechlor at 0, 10, 
and 100 mg/kg diet (Arscott et al., 1976).  Except for a slight 
decrease in egg production, no adverse effects were observed on 
fertility, hatchability, or survival of progeny. 

6.6.  Mutagenicity

    Camphechlor did not induce dominant lethal mutations in mice 
(Epstein et al., 1972).  When males were injected with 36 and 180 
mg/kg body weight ip and bred with untreated females during 8 
weeks, the frequencies of early fetal deaths and preimplantation 
losses were normal.  Negative results were also obtained in animals 
treated orally for 5 successive days with 40 or 80 mg/kg body 
weight.  In an  in vitro test to determine breakage of DNA in 
bacteria, camphechlor did not induce breaks at a significantly 
higher rate than that occurring in controls (Griffin & Hill, 1978).  
Camphechlor was mutagenic in a test using  Salmonella typhimurium  
without requiring activation by liver homogenate (Hooper et al., 

6.7.  Teratogenicity

    Camphechlor was administered to mice and rats on days 7 -
16 of gestation by oral intubation at levels of 15 - 35 mg/kg
body weight per day (Chernoff & Carver, 1976).  The highest
dose produced marked maternal mortality in rats and mice and
an increase in encephaloceles among offspring of mice.  Fetal
mortality was slightly increased in mice at all dose levels.
Small decreases in fetal body weight and in the number of
sternal and caudal ossification centres were observed in rats,
mostly in the 25 mg/kg dosage group (Chernoff & Carver, 1976).

6.8.  Carcinogenicity 

    A bioassay of technical grade camphechlor was conducted in 
mice and rats by administering the test chemical in the feed 
(NCI, 1979b).  Groups of 50 mice of each sex were given time-
weighted average doses of 99 or 198 mg/kg diet for 90 - 91 weeks.  
There was a dose-related decrease in survival in male mice and a 
decrease in survival in high-dose females.  The incidence of 
hepatocellular carcinomas was dose-related in both males and 
females.  The statistical significance was maintained when the 
incidence of hepatocellular carcinomas was combined with that of 
hyperplastic nodules of the liver.  It was concluded that, under 
the conditions of the assay, camphechlor was carcinogenic in male 
and female B6C3F1 mice. 

    Fifty rats of each sex were administered camphechlor in their 
diets at time-weighted average doses of 556 and 1112 mg/kg for 
male rats, and 540 and 1080 mg/kg for females; the study lasted 
for 108 - 110 weeks.  There were no dose-related effects on 
survival rates; clinical signs of toxicity in rats included 
generalized body tremors at week 53 in the high-dose males and 
females and later, leg paralysis, ataxia, epistaxis, haematuria, 
and vaginal bleeding.  Abdominal distention, diarrhoea, dyspnoea, 

and rough haircoats were common to both dose groups.  At the high 
dose, 26% (9/35) and at the low-dose, 17% (7/41) of male rats 
developed follicular-cell carcinoma or adenoma of the thyroid.  
In the high-dose, female rat group, 17% (7/42) developed thyroid 
tumours and in the low-dose group only 2%.  On the basis of the 
findings in the above study, it was concluded that the results 
"suggest carcinogenicity of camphechlor for the thyroid of male 
and female Osborne-Mendel rats" (NCI, 1979b). 

6.9.  Other Studies

    Camphechlor has also been shown to increase the activity of 
gluconeogenic enzymes in the rat (Desaiah et al., 1979), alter 
mitochondrial electron transport  in vitro (Pardino et al., 1971), 
and inhibit ATPase activity  in vitro (Yap et al., 1975) and  in 
 vivo (Fattah & Crowder, 1980).

    Protein deficiency was shown to increase the acute toxicity 
of camphechlor, 3 to 4-fold (Boyd, 1972b). 


7.1.  Poisoning Incidents

    McGee et al. (1952) described 10 cases of poisoning with 3 
deaths; the victims ranged in age from 17 months to 49 years.  All 
ingested camphechlor accidentally either in the form of the 
insecticide, as in the case of the children, or as camphechlor-
polluted food, in the adults.  Four of the cases were children 
aged 17 months to 4 years, of whom three died.  All the adults 
survived.  The onset of illness in all but one was characterized by 
a major motor seizure; the latter had only gastrointestinal 
complaints.  The 3 deaths occurred within a matter of several hours 
and those who recovered did so in 24 h. 

    Another poisoning incident involved a 16-month-old child who 
ingested a material presumed to be camphechlor (Pollock, 1953).  
Death was preceded by respiratory depression and convulsions. 

    Another child's death due to camphechlor poisoning was 
reported in 1967 (Haun & Cueto, 1967).  In this case, a 9-month-
old girl had been playing with a dust containing 13.8% 
camphechlor and 7.04% DDT, which was found on her skin and in her 
mouth.  Convulsions, respiratory arrest, and death followed.  
Cerebral oedema was found at autopsy. 

7.2.  Occupational Exposure

    Two workers involved in harvesting cotton that had been 
sprayed with camphechlor developed dyspnoea and reduced pulmonary 
function and were found to have miliary opacities distributed 
over their lung fields (Warraki, 1963). 

    Eight women working in an area that had been sprayed with 
camphechlor at the rate of 2 kg/ha were reported to have a higher 
incidence of chromosome aberrations (acentric fragments and 
chromatid exchanges) in cultured lymphocytes (13.1%) than control 
individuals (1.6%) (Samosh, 1974). 

    In a review of the chronic toxicity of organochlorine 
pesticides in man (Deichmann, 1973), a survey of 137 workers 
involved in the manufacture of camphechlor was reported.  The 
average length of exposure was 3.7 years, but some workers were 
exposed for as long as 18 years.  Physical examinations conducted 
annually on these people failed to reveal any "adverse effects 
that could be associated with camphechlor exposure". 

    An instance was reported where a rancher, who dusted his 
sheep with a mixture of 5% camphechlor and 1% lindane, 
demonstrated resistance to the hypothrombinemic effect of 
warfarin (Jeffery et al., 1976).  This effect was attributed to 
the enzyme-inducing properties of camphechlor, which led to 
increased metabolism of warfarin. 

    Two cases of acute aplastic anaemia associated with dermal 
exposure to camphechlor-lindane mixtures, have been reported. One 
of these cases terminated in death due to acute myelomonocytic 
leukaemia (US EPA, 1976a). 

    In a survey of 199 employees, who worked or had worked with 
camphechlor between 1949 and 1977, with exposures ranging from 6 
months to 26 years (mean 5.23 years), 20 employees died, 1 with 
cancer of colon; none of these deaths appeared to be related to 
exposure to camphechlor (US EPA, 1978). 

7.3.  Controlled Human Studies

    Twenty-five human volunteers were exposed to an aerosol of 
camphechlor in a closed chamber, for 30 min per day, on 10 
consecutive days (Shelanski, unpublished data, 1947).  After 3 
weeks, they received the same exposure on 3 consecutive days. 
Assuming a retention of 50% of the inhaled camphechlor, each 
individual absorbed 75 mg camphechlor per day or approximately 1 
mg/kg body weight per day.  Physical examinations and blood and 
urine tests did not reveal any abnormalities. 


8.1.  Aquatic Organisms

8.1.1.  Aquatic invertebrates

    The toxicity of camphechlor for aquatic invertebrates is very 
variable (Tables 3 and 4).  Needham (1966) measured levels of 
mortality at different concentrations of camphechlor for 14 genera 
of invertebrates and determined the level that each could tolerate 
for 24 h without any deaths.  These are tabulated in Table 5.  
Tolerance varied from 1 mg/litre for a leech to 10 g/litre for 
 Haliplus sp.  Values for molluscs ranged from 20 g/litre for the 
oyster to 460 mg/litre for the mactrid clam in 96-h tests, and for 
crustacea from 54 ng/litre for a stage I zoeal larva of  Sesarma to 
290 g/litre for a stage III zoeal larva of  Rhithropanopeus, also 
in 96-h tests.  Resistance to camphechlor may develop.  The 24-h 
LD50 for fresh water shrimp taken from an area that had been 
regularly treated for cotton pests was 10 times that of shrimp 
taken from a wildlife reserve (Naqvi & Ferguson, 1970).  Similarly,
cyclopoid copepods from a pesticide-contaminated area had a higher 
tolerance for camphechlor than cyclopoids from a pesticide-free 
area (Naqvi & Ferguson, 1968). 

    The only well-documented sublethal effects on invertebrates 
are found in oysters.  Yearling oysters showed a marked 
inhibition in shell deposition after a 24-h exposure to 60% 
camphechlor at 100 g/litre (Butler et al., 1962).  Mature 
oysters showed reduced activity, as measured by shell opening 
movements, during 4 weeks exposure to camphechlor at 100 

8.1.2.  Fish

    A series of studies on fathead minnows, brook trout, and 
channel catfish (Mayer et al., 1975; Mehrle & Mayer, 1975a,b; 
Mayer & Mehrle, 1976) document the "broken-back syndrome" in 
response to camphechlor concentrations ranging from 55 to 621 
g/litre.  Fish showed increased levels of calcium but decreased 
levels of collagen in the backbone; phosphorus levels were 
unaffected.  The backbone became more brittle and sub-lethal 
electric shock led to multiple fracture at all dose levels.  In 
addition to changes in the calcium/collagen ratio, there was a 
reduction in the amino acids: alanine, valine, leucine, 
isoleucine, lysine, phenylalanine, and hydroxyproline in bone 
collagen.  Hydroxyproline was also reduced in skin. Because of 
the importance of this particular amino acid in collagen 
formation, it is postulated that camphechlor may reduce the 
wound-healing capacity in fish.  Camphechlor, at concentrations 
as low as 68 g/litre, inhibited collagen synthesis (monitored by 
hydroxyproline measurement) in brook trout fry, 7 days after 
hatching.  None of these effects were dose related and only at 
the highest dose were any deaths observed.  More recently, Mayer 
& Mehrle (1976) showed that vitamin C levels in fish backbone 

also decreased after camphechlor exposure, but levels in the liver 
were unchanged.  The authors postulated that detoxification of 
camphechlor required vitamin C, which moved from storage in bone to 
the liver.  Vitamin C is involved in the conversion of proline to 
hydroxyproline.  Competition for available vitamin C was put 
forward as a credible explanation for collagen synthesis effects.  
Camphechlor inhibited ATPase activity in trout gill microsomes at 
concentrations in incubates of 4 mg or more/litre (Davis et al., 
1972).  In channel catfish, brain and gill ATPases were more 
severely affected than kidney ATPase (Desaiah & Koch, 1975).  Non-
mitochondrial Mg-ATPase was most severely inhibited. 

Table 3.  Toxicity of camphechlor for aquatic invertebratesa
Organism         Temperature  Size   End point        Parameter   Concentration  Reference
                 (C)         (mm)                                (g/litre)
American oyster  27-29               shell growth     96-h EC50   16             Schimmel et al.
 (Crassostrea                                                                     (1977)

crayfish         from clean   11.8-  no response to   48-h EC50   60.7           Albaugh (1972)
 (Procambarus      area        14.6    stimuli
 acutus)          from cotton  11.8-  no response to   48-h EC50   90.2           Albaugh (1972)
                  field       14.6    stimuli

 Daphnia pulex    15.5                immobilisation   48-h EC50   15             Sanders & Cope
first instar                                                                     (1966)

pink shrimp,                                          96-h LC50   2.2            Courtenay &
nauplius                                                                           Roberts (1973)

pink shrimp,     24.5-26                              96-h LC50   1.4            Schimmel et al.
adult                                                             (1.1-1.8)      (1977)

drift line crab  25                                   96-h LC50   0.054          Courtenay &
 (Sesarma                                                                         Roberts (1973)
stage I zoeal
a  A more comprehensive table listing different conditions and exposure times is available on 
   request from IRPTC, Geneva.

Table 4.  Toxicity of camphechlor for aquatic organisms
Organism           Stat  Temp  pH   Size       Alk   End     Parameter  Concen-       Reference
                   /flow (C)                  (mg/  point              tration   
                                               litre)                   (g/litre)
Goldfish           stat  25    7.4  1-2 g      18            96-h LC50  5.6           Henderson et al.
 (Carassius                          38-64 mm                                          (1959)

Bluegill           stat  18    7.1  0.6-1.7 g  35            96-h LC50  21 (14-30)    Macek &
 (Lepomis                                                                              McAllister (1970)

Fathead minnow     stat  12.7  7.1  0.6-1.5 g  35            96-h LC50  3.2 (2.8-3.7) Macek et al. (1969)
 (Pimephales        stat  18    7.1  0.6-1.7 g  35            96-h LC50  14 (9-22)     Macek &
 promelas)                                                                             McAllister (1970)
Sheepshead minnow  flow  27-                   21a           96-h LC50  1.1 (0.9-1.4) Schimmel et al.
 (Cyprinodon              29.5                  25.5                                   (1977)

Mosquito fish      flow  25-   7.8  0.28 g     28a   sensi-  36-h LC50  1             Burke & Ferguson
 (Gambusia                26                          tive                             (1969)
 affinis)           flow  25-   7.8  0.28 g     28a   insen-  36-h LC50  200           Burke & Ferguson
                         26                          sitive                           (1969)

Spot, 1 month      flow  11-        20 mm      21b           144-h      0.5           Lowe (1964)
 (Leiostomus              28                    28b           LC50

Rainbow trout            7.2                                 96-h LC50  5.4           Cope (1965)
 (Salmo                   18.3                                96-h LC50  1.8           Cope (1965)

Longnose           flow  28.5-      32-51 mm   10b           28-day     0.9           Schimmel et al.
killifish, juv.          31.5                  20b           LC50                     (1977)

Toad                                                         48-h LC50  290           Guyer et al. (1971)
 (Bufo woodhousi) 
a  Hardness mg/litre.
b  Salinity o/oo.
Table 5.  Concentrations of camphechlor tolerated by invertebratesa
Organism               Concentration for    Next higherb
                       zero mortality       concentration
                       (g/litre)           tested (g/litre)
 Hirudinea              1000

 Gammarus sp.           100                  200 (61%)

 Hydracarina            1000

 Callibaetis sp.        150                  300 (29%)

 Aeshna sp.             200                  275 (16%)

 Lestes sp.             450                  500 (19%)

 Notonecta sp.          275                  300 (29%)

 Signara sp.            50                   75 (40%)

 Limephilus sp.         500                  550 (51%)

 Haliplus sp.           10                   40 (55%)

 Hydroporus sp.         60                   100 (27%)

 Dytiscus sp.           15                   50 (24%)

 Eyrinus sp.            65                   100 (22%)

 Lymnara sp.            700
a  From:  Needham (1966).
b  Value in parentheses is percentage mortality found at the next 
   higher concentration tested above that giving zero mortality.

    The acute toxicity of camphechlor for fish species is
summarized in Table 4.  Although the range of LC50 values is
not great, some species differences are clear.  However, the
pattern of camphechlor toxicity is unrelated to fish families 
(Macek & McAllister, 1970).  Several of the studies in Table 4 
illustrate the temperature dependence of camphechlor toxicity 
(Hooper & Grzenda, 1955; Cope, 1965; Mahdi, 1966; Macek et al., 
1969); camphechlor being more toxic at higher temperatures.  No 
other test-condition variables showed such a clear relationship, 
but there was a suggestion of increased toxicity with increased 
alkalinity (Hooper & Grzenda, 1955; Henderson et al., 1959). 

    Various symptoms of camphechlor poisoning have been
described for fish (Gruber, 1959; Henderson et al., 1959;
Ludemann & Neumann, 1960; Workman & Neuhold, 1963; Schaper &
Crowder, 1976).  Initial hyperactivity is followed by muscular

spasms.  Later, fish show loss of equilibrium with short, jerky 
movements.  Mosquito fish also show respiratory distress.  These 
symptoms are similar to those caused by most chlorinated hydro-
carbon insecticides.  The mechanism of the toxic action of 
camphechlor is assumed to be mainly nervous. 

    There are few long-term studies on fish.  Mehrle & Mayer 
(1975b) showed a 46% reduction in the weight of brook trout fry 
after 90 days' exposure to camphechlor at 0.039 g/litre; which 
was the lowest concentration tested.  When brook trout fry, 
hatched from unexposed eggs, were held in camphechlor solutions 
for 90 days, the mortality rate was higher than that in unexposed 
fry at 30 days and thereafter (Mayer et al., 1975).  All fry 
exposed to 0.288 g/litre died before 60 days.  Yearling brook 
trout were less sensitive to camphechlor, showing a reduction in 
weight at 0.288 g/litre and a 40% reduction at 0.502 g/litre 
after exposure for 180 days.  At these concentrations, length was 
also reduced. During 150 days of exposure to camphechlor, at 
concentrations ranging from 0.055 to 0.621 g/litre, fathead 
minnows showed weight reductions ranging from 10.9% to 21.1%, but 
this was not dose-related (Mehrle & Mayer, 1975a). 

    Egg viability in female trout was significantly reduced when 
they had been exposed to camphechlor at nominal concentrations of 
0.075 g or more per litre since they were yearlings (Mayer et 
al., 1975).  At a long-term exposure of 0.5 g/ litre, egg 
viability was reduced to zero.  When eggs from unexposed females 
were incubated in camphechlor solutions of between 0.039 to 0.502 
g/litre for 22 days, prior to hatching, they did not show any 
reduction in hatchability (Mayer et al., 1975; Mehrle & Mayer, 

    Adaptation or resistance to camphechlor may develop, since 
natural populations of mosquito fish, which had either received 
run-off from pesticide-treated fields or been sprayed directly, 
were from 6 to 48 times more resistant to camphechlor than newly-
exposed fish (Boyd & Ferguson, 1964). 

8.2.  Terrestrial Organisms

8.2.1.  Insects

    Several studies of the effects of technical camphechlor on
honey bees gave a wide variety of results.  Graves & Mackensen
(1965) determined a 24-h LD50 at 19.08 g/bee, whereas Torchio
(1973) measured a 48-h LD50 as 0.144 g/bee.  In both these
studies, camphechlor was applied in acetone to the dorsal
thorax.  Anderson & Atkins (1968) list camphechlor as
"relatively non-toxic" with an LD50 greater than 11.0 g/bee.
Torchio (1973) looked at 3 bee species over different time
periods.  For honey bees and alkali bees, the numbers of
deaths increased 24 - 48 h after application, but no further
deaths occurred between 48 and 72 h.  All bees surviving up to
72 h also survived up to 96 h.  For the leaf cutting bee,
there were more deaths between 48 and 72 h, but none between

72 and 96 h.  Exposure of western yellowjacket wasps to the 
topical application of 1 liltre drops of camphechlor resulted in 
mortality rates in 48 h of:  13% with exposure to 1 g/litre, 40% 
with exposure to 5 g/litre, and 65% with exposure to 10 g/litre 
(Johansen & Davis, 1972).  Extensive research has been carried out
on target and non-target insects.  This has been reviewed by the US 
EPA (1979), who concluded that technical camphechlor was roughly 
equally toxic for both pest and beneficial insects.  Lepidopterans 
were more resistant, possibly reflecting the long usage of 
camphechlor to control lepidopteran pests and the consequent 
development of resistance. 

8.2.2.  Birds

    The acute toxicity of technical camphechlor for birds is
summarized in Table 6.  There is some species variability; sharp-
tailed grouse, the most sensitive species, having an LD50 of 10 - 
20 mg/kg body weight, and mourning dove, the least sensitive 
species, having an LD50 of 200 - 250 mg/kg body weight.  Dahlen & 
Haugen (1954) reported a lack of motor coordination preceding death 
in bobwhite quail.  There was a clear age effect in the toxicity of 
camphechlor for the mallard (Hudson et al., 1972), with young birds 
(36 h after hatching) being the least sensitive.  No satisfactory 
explanation of this phenomenon is available.  Two major field 
studies showed that spraying with technical camphechlor could cause 
death in birds.  Eyer et al. (1953) applied insecticide at 2.2, 4.4, 
5.5, and 6.6 kg/ha and examined domestic geese of 3 varieties.  No 
deaths resulted at the lowest application rate.  Birds of 2 varieties 
were killed within 3 h of direct contact with 4.4 kg/ha spray but 
only 1 variety was killed at 5.5 kg/ha.  No birds died at the 
highest dose rate.  The inconsistency of these results was not 
explained, but it is clear that the compound killed birds.  McEwen 
et al. (1972) counted wild birds on control and sprayed areas of 
rangeland.  Spraying at 884 g/ha reduced the number of birds 
relative to that in the control areas and to pre-spray observations.  
Dead birds (5 larks, a cowbird, a killdeer, and a dove), found on 
the sprayed area, contained between 9.6 and 0.1 mg camphechlor 
residues/kg body weight.  No deaths or decrease in numbers from 
emigration occurred until more than a week after spraying. 

Table 6.  Toxicity of camphechlor for birds
Species       Age         Sex   Routea  Parameter   Concentrationb    Reference
Mallard       36                oral    LD50        130 (80.4-210)    Hudson et al. (1972)

Mallard       7 days            oral    LD50        30.8 (23.3-40.6)  Hudson et al. (1972)

Mallard       3-5 months        oral    LD50        70.7 (37.6-133)   Hudson et al. (1972)

Mallard       3-5 months  F     oral    LD50        70.7              Tucker & Crabtree (1970)

Bobwhite      8 weeks           oral    LD50        80-100            Dahlen & Haugen (1954)

Bobwhite      3 months    M     oral    LD50        85.4              Tucker & Crabtree (1970)

Mourning                        oral    LD50        200-250           Dahlen & Haugen (1954)

Sharp-tailed  1-4 years   M     oral    LD50        10-20             Tucker & Crabtree (1970)

Fulvous       3-6 months  M     oral    LD50        99.0              Tucker & Crabtree (1970)
tree duck

Lesser sand-              F     oral    LD50        100-316           Tucker & Crabtree (1970)
bill crane    

Pheasant      2 weeks           diet    5-day LC50  500-550           Heath et al., (1970)c

Coturnix      2 weeks           diet    5-day LC50  600-650           Heath et al., (1970)c

Bobwhite      chick             diet    5-day LC50  834               Heath & Stickel (1965)

Mallard       duckling          diet    5-day LC50  563               Heath & Stickel (1965)
a  Oral dosing - a single dose by gelatin capsule; dietary dosing for 5 days then 3 days 
   of uncontaminated food.
b  Concentrations - in mg/kg body weight for oral dosing; in mg/kg diet for dietary dosing.
c  Unpublished data.
    Long-term toxicity of camphechlor for birds is not well 
documented.  Keith (1966) fed sardines injected with camphechlor 
to white pelicans, giving the birds a daily dose of 10 or 50 mg/kg 
diet for 3 months.  The mortality rate was high in all groups, but 
only the higher dose resulted in definite symptoms of poisoning 
prior to death.  At death, birds on insecticide diets had little 
subcutaneous and mesentery fat.  Dietary dosing of 6-month-old 
female, ring-necked pheasants for up to 3 months at 25, 100, 200, 
or 300 mg/kg diet did not cause death (Genelly & Rudd, 1956a).  The 
initial depression in body weight observed was attributed to reduced 
feeding.  Autopsy of mature birds dosed for 74 days with 100 or 300 
mg/kg diet showed vacuolation in the livers. 

    Two studies on various parameters related to reproductive 
success in birds did not show any effects at doses up to 100 
mg/kg diet.  Bush et al. (1977) dosed female domestic chickens 
from 1 day of age up to maturity with one of 4 dose levels of 
camphechlor, ranging from 0.5 to 100 mg/kg diet.  No significant 
effects were found on egg production, hatchability, or fertility.  
Genelly & Rudd (1956b) dosed female, ring-necked pheasants with 
camphechlor at either 100 or 300 mg/kg diet.  Significant effects 
were only noticed at the higher dose rate, with reductions in egg 
laying and hatchability.  "Relative reproductive success rate", 
calculated on the basis of several reproductive parameters, was 
70% for controls, 62% for birds given camphechlor at 100 mg/kg 
diet, and 46% for birds given 300 mg/kg diet.  In two studies on 
egg hatchability (Dunachie & Fletcher, 1969; Smith et al., 1970); 
camphechlor was injected into hens' eggs with no consistent 
effects.  Maximum doses given were 500 mg/kg egg weight in one 
study and 1.5 mg/egg in the other.  Haegele & Tucker (1974) 
showed that a single oral dose of technical camphechlor at 10 
mg/kg body weight did not significantly alter egg shell thickness 
in Japanese quail.  When bobwhite quail were given technical 
grade camphechlor at 5, 50, or 500 mg/kg in their feed for 4 
months, thyroid growth was stimulated and adrenal hypertrophy 
occurred at all dose levels (Hurst et al., 1974).  However, only 
the highest dose increased uptake of I131.  This dose also 
decreased body weight.  It is difficult to attribute these 
effects to a direct thyroid lesion. 

8.2.3.  Wild animals

    Tucker & Crabtree (1970) reported a 96-h LD50 for 16 to 17-
month-old male mule deer of 139 - 240 mg/kg body weight, when 
camphechlor was administered orally as a single dose in a gelatin 
capsule.  The effect on  in vitro fermentation of dry matter 
(alfalfa hay) by inocula of rumen fluid from mule deer was 
investigated by Schwartz & Nagy (1974).  Inhibition was found at a 
dose of 1000 mg camphechlor/kg dry matter.  Accidental poisoning 
occurred in a female Bengal tiger that ate a llama calf which had 
been dipped in a solution of camphechlor.  Symptoms included 
periodic convulsions and hyperreflexia to sudden auditory and 
visual but not to tactile stimuli (Peavy 1975). 

8.2.4.  Plants

    Effects of camphechlor on higher plants have only been reported 
for crop varieties.  In greenhouse studies on cotton, using a sandy 
or clay soil, Franco et al. (1960) found some toxicity at a dose 
equivalent to a field application of 72.3 kg/ha, but only with 
camphechlor applied as an emulsion.  When applied as a powder, the 
insecticide was not phytotoxic for cotton plants at a dose equivalent 
to 101.5 kg/ha.  Hagley (1965) studied the growth of seedlings of 3 
vegetables, including Chinese cabbage and tomatoes, treated with 
camphechlor at rates of 1.57 and 15.7 kg/ha, in the greenhouse.  
Both levels inhibited shoot growth in Chinese cabbage.  The higher 
dose rate affected average weekly growth in all 3 cultivars, with 
little root inhibition.  A level of 15.7 kg/ha was toxic for tomato 
seedlings, with 50% dying in the second, and a further 33% in the 
third week of growth.  Emergence, growth, yield, and chemical 
composition of soybeans were not affected by the application of 
camphechlor at 44.8 kg/ha, which was considerably higher than 
recommended usage level (Probst & Everly, 1957). 

8.3.  Microorganisms

    No effects were observed  on either soil bacteria or fungi  
when camphechlor was applied to the soil at 22.4 kg/ha, annually, 
for 5 years (Martin et al., 1959), or twice yearly for 3 years, 
at 16.8 kg/ha (Eno et al., 1964).  Bollen et al. (1954) showed 
that camphechlor stimulated mold numbers, 10 - 20 days after field 
application at 11.2 kg/ha.  A higher dosage of 22.4 kg/ha, after 
the same period, did not show any effects on fungi.  Bacteria were
not affected by either dosage. 

    In greenhouse studies on the effects of camphechlor on 
nodulation bacteria, doses equivalent to between 4.9 and 40.3 
kg/ha did not significantly affect bacterial growth or nodulation 
of legumes (Elfadl & Fahmy, 1958).  Treating soil with between 
12.5 and 100 mg camphechlor/kg and incubating for between 1 and 
16 months in a greenhouse, did not result in any measurable 
effects on numbers of soil bacteria or fungi, but did stimulate 
nitrification and carbon dioxide evolution after one month; after 
16 months, there were no effects (Eno & Everett, 1958). 

    The results of studies on marine and freshwater unicellular 
algae and protozoa are summarized in Table 7.  The single study 
on marine algae (Ukeles, 1962) showed species variability.  The 
dinoflagellate,  Monochrysis lutheri, is the most sensitive, 
showing total inhibition of growth at camphechlor concentrations 
of 0.00015 mg/litre.  The study by Stadnyk et al. (1971), whilst 
showing little effect on cell numbers or biomass, demonstrated 
marked stimulation of carbon fixation in the presence of 
camphechlor.  At a concentration of 0.1 mg/litre, there was an 
initial 48% increase in carbon dioxide fixation by the green alga, 
 Scenedesmus quadricaudata, but this became insignificant later

in the 10-day exposure period.  An initial increase of 450% had 
fallen to 30%, after 10 days' exposure to 1 mg camphechlor/litre.  
No explanation for this stimulation seems to be available.  The 
complex study by O'Kelley & Deason (1976) showed that camphechlor 
at 0.01 mg/litre could inhibit growth in a few strains of algae 
(which had been isolated from the Warrior River) and stimulate 
growth in others.  More strains showed inhibited growth at 0.1 
mg/litre, but 6 out of the 21 strains used were unaffected, even by 
the highest dose of 1.0 mg/litre. 

Table 7.  Toxicity of camphechlor for unicellular algae and protozoa
Organism     Temp   Sex  Sal.  Species            Expo-  Concen-   Effect             Reference             
             (C)        o/oo                     sure   tration                                     
                                                  (days) (mg/litre)                                  
Unicellular  19.5-  M    22-                      10     0.00015-  100% inhibition    Ukeles (1962)         
algae        21.5        28                              0.15      of growth                         
Blue-green   22     F           Cylindrospermum    21     2a        partially toxic,   Palmer &              
alga                            licheniforme                        reduced growth     Maloney (1955)        
Green alga   22     F           Scenedesmus        21     2a        partially toxic,   Palmer &                 
                                obliquus                            reduced growth     Maloney (1955)        
                                                                   up to 14 days                     
                                                                   no effect on                      
                                                                   growth after                      
                                                                   14 days                           
Diatom       22     F           Gomphonema         21     2a        partially toxic,   Palmer &                
                                parvulum                            reduced growth     Maloney (1955)        
Alga         20-    F           Selenastrum        0.38             EC50 inhibition    US EPA (1980)         
             22                 capricornutum                       of growth                         
Green alga          F           Scenedesmus        up to  1.0       19% decrease in    Stadnyk et al.        
                                quadricaudata      10               cell number,       (1971)                
                                                                   no significant                    
                                                                   effect on biomass                 
Protozoa            F          culture dominated  1      1.3       24-h LC50          Weber et al.          
                               by ciliates;                                           (1982)                
                               ( Eupoletes sp.)                                                      
                               and microflagellates                                                         
a  2 mg/litre of a 60% solution of camphechlor.
F = Freshwater.
M = Marine.
    The lowest concentrations of camphechlor inducing toxic 
effects in protozoa from a salt marsh, were comparable to 
concentrations found in the environment (Weber et al., 1982). 
When a lake was treated with camphechlor (60%) at 0.1 mg/litre, 
protozoan numbers were reduced almost to zero (Hoffman & Olive, 
1961).  Turbidity of the lake water decreased until the bottom 
(at a depth of 4.5 m) was clearly visible. 

8.4.  Bioaccumulation and Biomagnification

    Schoettger & Olive (1961), in a study to determine the
bioaccumulation of camphechlor, exposed planktonic alga  (Scenedesmus 
 incrassatulus) cultures to 10 mg camphechlor/litre for 384 h.  The 
alga did not accumulate enough camphechlor to kill fish fed on it.  
However, periphytons (various algae, diatoms, and ciliates), exposed 
to the same dose of camphechlor, accumulated enough to kill fish 
within 24 h.  Sanborn et al. (1976) reported a concentration factor 
of 6902 for an alga in a model ecosystem with a water concentration 
of 44.4 g/litre.  Concentration factors of 9600 for the snail and 
890 for the mosquito were also reported. 

    After applying camphechlor at 50 g/litre, to eradicate rough 
fish, Kallman et al. (1962) studied uptake by the rooted aquatic 
weed,  Potamogeton.  After 5 days and 9 days, mean concentrations 
in plants were 4.4 mg/kg and 14.6 mg/kg, respectively, which 
represents concentration factors of 4400 and 14600 over the water 
concentration of 1 g/litre. Terriere et al. (1966) also found 
accumulation of camphechlor by aquatic plants.  Plants absorbed up 
to 15.5 mg/kg from water containing 2 g/litre; roots contained the 
highest concentrations.  Salt marsh cord grass,  Spartina alterniflora, 
growing near the discharge point of a camphechlor manufacturing plant, 
was analysed for camphechlor residues by Reimold & Durant (1972).  
They found maximum levels of 72.8 mg/kg in the leaves and lower 
concentrations in other parts of the plant.  In contrast, Reimold 
(1974) using 36Cl-labelled camphechlor, found that plant roots 
and rhizomes absorbed the largest amounts.  The differences between 
uptake in these studies may be because of differences between sea 
water and marsh soil. 

    Oysters exposed to 1 g/litre for 36 weeks bioaccumulated
camphechlor throughout the pre-spawning period (Lowe et al., 1971).  
Concentrations in oyster tissues at 12, 24, and 36 weeks were 20 
mg/kg, 23 mg/kg, and 8 mg/kg, respectively.  Johnson (1966) 
measured camphechlor residues in plankton from Big Bear Lake, 
California, following 2 treatments with camphechlor at rates of 
0.03 and 0.1 mg/litre, applied 2 weeks apart.  Camphechlor 
concentrations increased to a peak of 97 mg/kg, 114 days after the 
final application.  Concentrations decreased with time but, even 
265 days after application, were still higher (at 2.0 mg/kg) than 
the original treatment level.  Tubificid worms may accumulate 
camphechlor since worms collected in the Mississippi River delta 
contained trace amounts of camphechlor.  

However, worms exposed experimentally to camphechlor did not 
accumulate enough to kill the fish to which they were fed (Naqvi, 

    Fish are able to absorb and bioconcentrate significant amounts 
of camphechlor, a large proportion being complexed with the lipid 
stores.  Schaper & Crowder (1976) found that exposing mosquito fish 
to a fatally-toxic level of 2 mg camphechlor/litre for 8 h did not 
result in bioconcentration, the average concentration in whole fish 
being 0.586 mg/kg.  Thus, exposure for 8 h is not sufficient for 
bioaccumulation to occur in fish.  When 14C-labelled camphechlor 
was added to a terrestrial-aquatic model ecosystem at 44.4 g/litre 
in the water, mosquito fish concentrated camphechlor by a factor of 
4247 (Sanborn et al., 1976).  Hughes (1970) exposed bluegills to 
17.3 g/litre or 70.3 g/litre, and achieved camphechlor 
concentrations in the fish of 9.4 mg/kg and 7.7 mg/kg, respectively, 
after 96 h.  Mayer et al. (1975) carried out several studies on 
brook trout.  Brook trout fry, when exposed to camphechlor 
concentrations of 0.041 - 0.5 g/litre, concentrated the chemical 
between 4900 and 76 000 times.  Large CF values, recorded after 15 
days, were partially attributed to the presence of a yolk sac, 
which contains large quantities of lipid.  Falling values, 
occurring after 60 days, were due to the disappearance of the yolk 
sac, and the rise after 90 days to the increasing lipid content of 
maturing fry.  Yearling brook trout bioconcentrated less camphechlor 
than fry during the 161-day exposure, achieving bioconcentration 
factors of between 3200 and 16000. 

    Residues of camphechlor found in fish from camphechlor-treated 
lakes are usually similar to levels measured in the laboratory, 
indicating that free-living fish can bioconcentrate camphechlor by 
a factor of several thousand.  Kallman et al. (1962) studied the 
uptake of camphechlor by rainbow trout and bullhead in Clayton 
Lake, New Mexico, following an application of the pesticide.  
Seventy-two hours after treatment, the average concentration of 
camphechlor in the water was 2 g/litre, and the concentration 
factors were 1700 for trout and 2100 for bullheads.  After 5 days, 
the average water concentration of camphechlor was 11.5 g/litre 
and, at this concentration, bullheads contained mean body residues 
of 13 mg/kg and were severely affected.  After the water 
concentration stabilized at 1 g/litre, trout exposed to this water 
had concentration factors ranging from 800 to 2500 after 7 days, 
and factors of between 1300 and 3500 after 17 days.  After 108 to 
170 days exposure, trout showed body residues of 0.3 mg/kg, but the 
water concentration had fallen to non-detectable levels. 

    In a similar study, Terriere et al. (1966) monitored the 
relationship between camphechlor levels in 2 Oregon lakes (Davis 
Lake treated with 80 g camphechlor/litre and Miller Lake treated 
with 40 g/litre).  In Davis Lake, residues were measured in 
rainbow trout and Atlantic salmon; the trout consistently 
accumulated more camphechlor than the salmon.  As in experimental 
exposures (Mayer et al., 1975), these fish concentrated 

camphechlor by a factor of several thousand.  In Miller Lake, 
where the water concentration of camphechlor was 0.84 (0.70 - 
1.1) g/litre, brook trout, the only species monitored in this 
lake, concentrated camphechlor 14 800 times. 

    Hughes & Lee (1973) found that predator fish accumulated less 
camphechlor than prey fish.  Bluegills and suckers, both prey 
fish, accumulated whole body residues of 9.4 mg/kg and 10.6 
mg/kg, respectively, whereas predator fish, i.e., bass, northern 
pike, and walleyes, accumulated residues of only 2.2, 3.3, and 
1.2 mg/kg, respectively.  This suggests that the biomagnification 
of camphechlor in aquatic food chains may not be as great as 
might be indicated from bioconcentration factors. 

    Bioconcentration factors in a freshwater model ecosystem were 
shown by Metcalf (1976) to be 5 for plankton, 176 - 1152 for 
carp, 200 for insects, and 200 for crayfish. 

    There are no data on birds and mammals from which residue 
levels can be related to exposure levels. 

8.5.  Population and Community Effects

    The effects of the application of 0.1 mg camphechlor/litre to 
control rough fish on the macroscopic bottom fauna of a lake in 
Colorado were studied by Cushing & Olive (1956).  During the first 
3 weeks following treatment, treated and control lakes were sampled 
fairly frequently and, thereafter, samples were taken approximately 
every other week.  Tendipedes were killed immediately, and no 
larvae were found in the following 8 months.   Chaoborus were not 
immediately affected, but numbers began to decline 3 months later.  
None were found 6 months after treatment.  The authors speculated 
that the  Chaoborus, which prey on tendipedes, starved to death.  
The number of oligochaetes increased, probably due to the extra
organic matter available.  In the control lake, the numbers of
tendipedid,  Chaoborus, and oligochaete remained fairly constant 
throughout the sampling period.   Chaoborus numbers fell in late 
June/August when emergence was at its peak but, unlike the 
experimental lake, repopulation occurred in September.

    Needham (1966) studied plankton and aquatic invertebrates in 4 
North Dakota lakes.  The first lake (9.7 ha, depth 2.7 m) was 
treated with 35 g camphechlor/litre.  Samples were taken prior to 
treatment and 1 week, 1 month, and 1 year after treatment.  Plankton 
were monitored as numbers of organisms per litre.   Keratella 
decreased from 91 pre-treatment to 15, one week after treatment, 
and subsequently to very low numbers.   Asplanchna increased from 
73 to 106, 1 week after treatment, but none were present in samples 
taken 1 month or 1 year later.  Numbers of  Daphnia decreased from 
244 to 18, 1 week after treatment, increasing to 129 after 1 month 
but dropping to 28 after 1 year.   Bosmina increased from 98 to 130 

following treatment, but declined to 18 after 1 month and had only 
risen to 25, 1 year later.  Copepoda ( Diaptomus, Cyclops, and 
undetermined nauplii) declined in numbers after treatment, but the 
number of nauplii had begun to increase again, 1 year after 
treatment.  Five invertebrate genera that lived on water plants 
were found in significant numbers.   Gammarus varied throughout 
the study but remained abundant.   Callibaetis, Caenis, and  Ischnura 
decreased 1 week and 1 month after treatment, but were more abundant 
after 1 year.   Tendipes decreased from 44 (prior to treatment) to 
9, 1 week after treatment, increasing to 48, 1 month after treatment 
and falling back to 25, 1 year after treatment.  Gastropoda  (Physa
and  Gyraulus) increased from 771 before treatment to 1107, 1 week, 
1366, 1 month, and 1558, 1 year after treatment.  In the lake bottom 
fauna, only 2 genera were abundant;  Gammarus, which fluctuated 
greatly during the study and tendipedes, which decreased following 
treatment but, 1 year later, had increased again to original numbers 
in samples.  Comparison between plant-inhabiting organisms and 
bottom fauna did not reveal any shifting of populations, 1 year 
after treatment, apart from  Physa, which increased greatly.

    The second lake studied by Needham (1966) (having a surface 
area of 6 ha and a maximum depth of 5.5 m) was treated twice with 
camphechlor, first with 25 g/litre and then, 53 days later, with 
90 g/litre.  Samples were taken 1 day before, and 11, 33, and 371 
days after the initial treatment.  Plankton were monitored as 
numbers of organisms per litre.  A decline in population was 
recorded for all genera found in significant numbers.   Brachionus, 
which had decreased from 114 to 108 organisms/litre, 11 days after 
treatment, decreased to 15 after 33 days and to 3 after 371 days.  
The numbers of the other abundant rotifer,  Asplanchna increased 
from 24 to 194, 11 days after treament but dropped after 33 days to 
16; by 371 days, there was only one organism/litre.   Daphnia, 
 Ceriodaphnia, and  Bosmina were the most abundant zooplankton.  
Both  Daphnia and  Ceriodaphnia showed similar patterns, an 
increase in numbers, 11 days after treatment, and a subsequent 
decline.   Bosmina had declined from 314 to 283, 11 days after 
treatment, and continued to decline reaching 50 after 33 days; none 
were found in the 371-day sample.  Copepods also decreased in 
numbers during the study.  Although the number of  Cyclops had 
increased between 11 and 33 days, it decreased again after 371 

    The third lake studied by Needham (1966) (a glacial lake of 
370 ha and an average depth of 2.7 m) was treated with 10 g 
camphechlor/litre followed 2 days later by 5 g/litre, and a 
fourth lake (40.5 ha, maximum depth 4.9 m) was treated with 5 
g/litre.  Results from this lake were similar to those from the 
second; camphechlor failed to affect any of the organisms 

    When sediments containing camphechlor were disturbed by 
dredging, camphechlor was released into the water leading to 

higher concentrations in aquatic flora and fauna, but this did 
not appear to affect the biological balance in the area (Reimold 
& Durant, 1974). 

8.6.  Effects on the Abiotic Environment

    Five annual field applications of 22.4 kg camphechlor/ha did 
not have any effect on the moisture content, total infiltration, 
and aggregation of the soil (Martin et al., 1959). 


    Camphechlor was evaluated by the Joint Meeting on Pesticide 
Residues (JMPR) in 1968 and 1973 (FAO/WHO, 1969, 1974).  In 1968, 
no recommendations were made because of the many unresolved 
questions.  In 1973, the meeting concluded that it could not 
establish an ADI for a material that varied in composition 
according to the method of manufacture. 

    IARC (1979) evaluated the carcinogenic hazard resulting from 
exposure to camphechlor and concluded that "there is sufficient 
evidence that toxaphene is carcinogenic in mice and rats.  In the 
absence of adequate data in humans, it is reasonable, for 
practical purposes, to regard toxaphene as if it presented a 
carcinogenic risk to humans". 

    Practical advice has been issued by WHO/FAO (1975) in the 
"Data Sheets on Pesticides", No. 20, which deals with 
camphechlor, and includes information on labelling, safe-
handling, transport, storage, disposal, decontamination, 
selection, training and medical supervision of workers, first 
aid, and medical treatment. 

    Over recent years, a number of official registrations for the 
use of camphechlor have been drawn in several countries, for 
various reasons.  Further details may be obtained from IRPTC. 

    Regulatory standards established by national bodies in 12 
different countries (Argentina, Brazil, Czechoslovakia, the 
Federal Republic of Germany, India, Japan, Kenya, Mexico, Sweden, 
the United Kingdom, the USA, and the USSR) and the EEC can be 
obtained from the IRPTC (International Register of Potentially 
Toxic Chemicals) Legal File (IRPTC, 1983). 

    IPRTC (1983), in its series "Scientific reviews of Soviet 
literature on toxicity and hazards of chemicals", issued a review 
on camphechlor. 


10.1.  Camphechlor Toxicity

    The acute toxicity of camphechlor in the rat is moderate,
i.e., the oral LD50 ranges from 60 to 120 mg/kg body weight.
Camphechlor is readily absorbed via all routes of entry.  It is 
metabolized in the body, but a certain amount of accumulation in 
adipose tissue takes place on continuous exposure. 

    Signs and symptoms of poisoning are salivation and vomiting 
and, at higher exposures, excitation of the CNS with convulsions, 
respiratory failure, and death.  On prolonged exposure of 
animals, hypertrophy of the liver with induction of microsomal 
enzymes (5 mg/kg in the diet or 0.25 mg/kg body weight per day) 
are the major findings. 

    Camphechlor has been shown not to have an effect on reproduction 
and it is not teratogenic.  It is mutagenic in a bacterial test, but 
the results of a dominant lethal test in mice were negative.  There 
is sufficient evidence for its carcinogenicity for rats and mice.  
Epidemiological studies are inadequate to evaluate the carcinogenic 
potential of camphechlor for human beings. 

10.2.  Exposure to Camphechlor

    Exposure of the general population is mainly through residues 
in food.  However, these are normally below residue tolerances.  
Accidental over-exposure has occurred as a result of contamination 
of food with camphechlor. 

    In the past, occupational exposure to camphechlor may 
occasionally have been considerable.  Nevertheless, only a few 
cases of adverse effects have been reported.  Workplace exposures 
above the permissible level have been reported. 

10.3.  Effects on the Environment

    Movement of camphechlor through the environment is not 
clearly understood, but the dominant factor in the distribution 
of the chemical appears to be its high volatility.  Camphechlor 
is a widespread contaminant of aquatic ecosystems.  Residues have 
also been found in non-aquatic organisms. 

    Camphechlor has been used extensively as a fish poison to 
clear rough fish from lakes before introducing game fish.  The 
toxic effects have not only been directly on adult fish but also, 
via adult females, on the development of eggs and young.  Non-
target aquatic organisms have also been affected.  Some 
invertebrates showed long-term deleterious effects of camphechlor 
poisoning.  The environmental levels of camphechlor in waters 
where the chemical has not been deliberately applied can exceed 

laboratory concentrations that have caused death or sublethal 
lesions in experimental fauna. Thus, camphechlor presents a major 
hazard for aquatic organisms. 

    Available field data suggest that birds have been adversely 
affected by camphechlor. 

10.4.  Conclusions

1.  Although no serious adverse effects on workers resulting
    from occupational exposure to camphechlor have been reported,
    and epidemiological studies remain inadequate, this chemical
    should be considered for practical purposes as being
    potentially carcinogenic for human beings.

2.  For the same reason, and recognizing the limitations of
    residue analysis for camphechlor, as well as the reluctance of
    the JMPR to issue an ADI, reservations must remain about the
    safety of this chemical in food, despite the relatively low
    residues so far reported.

3.  Environmentally, camphechlor is a major hazard for aquatic
    and also some terrestrial species.

4.  Taking into account these considerations, it is felt that
    the use of this chemical should be discouraged, except where
    there is no adequate alternative.


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    See Also:
       Toxicological Abbreviations
       Camphechlor (HSG 40, 1990)
       Camphechlor (ICSC)