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    and the World Health Organization

    World Health Organization
    Geneva, 1990

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    WHO Library Cataloguing in Publication Data


        (Environmental health criteria ; 103)


        ISBN 92 4 157103 9        (NLM Classification: QD 305.A4)
        ISSN 0250-863X

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


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

     3.1. Natural occurrence 
     3.2. Man-made sources 
           3.2.1. Production levels and processes
            Production levels 
            Production processes 
           3.2.2. Uses 
           3.2.3. Waste disposal 


     4.1. Transport and distribution between media 
     4.2. Abiotic degradation 
     4.3. Biotransformation 
           4.3.1. Biodegradation  
           4.3.2. Bioaccumulation 


     5.1. Environmental levels 
     5.2. General population exposure 
           5.2.1. Exposure via food 
           5.2.2. Exposure via other consumer products
     5.3. Occupational exposure 


     6.1. Absorption 
           6.1.1. Animals 
           6.1.2. Human beings 
     6.2. Distribution  
           6.2.1. Animals 
           6.2.2. Human beings 
     6.3. Metabolism 
           6.3.1. Animals 
           6.3.2. Human beings 
     6.4. Elimination and excretion 
           6.4.1. Animals 
           6.4.2. Human beings 


     7.1. Aquatic organisms
     7.2. Terrestrial organisms 
           7.2.1. Microorganisms 
           7.2.2. Insects 
           7.2.3. Plants 


     8.1. Single exposures
           8.1.1. Mortality 
           8.1.2. Signs of intoxication 
           8.1.3. Skin, eye, and respiratory tract irritation
     8.2. Continuous or repeated exposures  
     8.3. Neurotoxicity and behavioural effects 
     8.4. Biochemical effects  
           8.4.1. Effects on lipids in liver and blood 
           8.4.2. Effects on microsomal enzymes 
           8.4.3. Other biochemical findings 
     8.5. Immunological effects  
     8.6. Reproduction, embryotoxicity, and teratogenicity 
     8.7. Mutagenicity 
     8.8. Carcinogenicity  
     8.9. Factors modifying toxicity  


     9.1. General population exposure 
           9.1.1. Poisoning incidents 
           9.1.2. Controlled exposures  
           9.1.3. Skin irritation; sensitization 
     9.2. Occupational exposure 
           9.2.1. Epidemiology studies  
           9.2.2. Interacting agents 


     10.1. Evaluation of human health risks 
           10.1.1. Exposure 
           10.1.2. Health effects 
     10.2. Evaluation of effects on the environment 






Dr R. Drew, Department of Clinical Pharmacology, Flinders   
   University of South Australia, Bedford Park, South Australia, 

Dr B. Gilbert, Company for Development of Technology Transfer 
   (CODETEC), City University, Campinas, Brazil  (Rapporteur) 

Dr B. Hardin, Document Development Branch, Division of Standards  
   Development and Technology Transfer, National Institute for  
   Occupational Safety and Health, Cincinnati, Ohio, USA  (Chairman) 

Dr S.K. Kashyap, National Institute of Occupational Health, 
   Ahmedabad, India 

Professor M. Noweir, Occupational Health Research Centre, High 
   Institute of Public Health, University of Alexandria, 
   Alexandria, Egypt 

Dr L. Rosenstein, Office of Toxic Substances, US Environmental 
   Protection Agency, Washington, DC, USA 

Professor I.V. Sanotsky, Chief, Department of Toxicology, Institute 
   of Industrial Hygiene and Occupational Diseases, Moscow, USSR 

Dr J. Sokal, Division of Industrial Toxicology, Institute of 
   Occupational Medicine, Lodz, Poland 

Dr H.J. Wiegand, Toxicology Department, Huls AG, Marl, Federal 
   Republic of Germany 

Dr K. Woodward, Department of Health, Medical Toxicology and 
   Environmental Health Division, London, United Kingdom 


Dr K. Miller (Representing International Commission on Occupational 
   Health (ICOH)), British Industrial Biological Research 
   Association, Carshalton, Surrey, United Kingdom 


Professor F. Valic , Consultant, IPCS, World Health Organization, 
   Geneva, Switzerland,  also Vice-Rector, University of Zagreb, 
   Zagreb, Yugoslavia  (Secretary) 

Dr T. Vermeire, National Institute of Public Health and 
   Environmental Hygiene, Bilthoven, Holland 

 Host Organization

Dr S.D. Gangolli, British Industrial Biological Research 
   Association, Carshalton, Surrey, United Kingdom 

Dr D. Anderson, British Industrial Biological Research Association, 
   Carshalton, Surrey, United Kingdom 


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

                             *   *   *

    A detailed data profile and a legal file can be obtained from 
the International Register of Potentially Toxic Chemicals, Palais 
des Nations, 1211 Geneva 10, Switzerland (Telephone no. 7988400/ 


    A WHO Task Group on Environmental Health Criteria for 
2-Propanol met at the British Industrial Biological Research 
Association (BIBRA), Carshalton, Surrey, United Kingdom, from 10 to 
14 April 1989.  Dr S.D. Gangolli, who opened the meeting, welcomed 
the participants on behalf of the Department of Health, and  
Dr D. Anderson on behalf of BIBRA, the host institution. 
Dr F. Valic greeted the participants on behalf of the heads of the 
three IPCS cooperating organizations (UNEP/ILO/WHO).  The Task 
Group reviewed and revised the draft criteria document and made an 
evaluation of the human health risks and effects on the environment  
of exposure to 1-propanol. 

    The drafts of this document were prepared by Dr T. VERMEIRE, 
National Institute of Public Health and Environmental Hygiene, 
Bilthoven, Netherlands.  Dr F. VALIC was responsible for the 
overall scientific content of the document and Mrs M.O. HEAD of 
Oxford, England, for the editing. 

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

                             *   *   *

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

1.1  Identity, Physical and Chemical Properties, Analytical Methods

    2-Propanol is a colourless highly flammable liquid with an 
odour resembling that of a mixture of ethanol and acetone.  The 
compound is completely miscible with water, ethanol, acetone, 
chloroform, and benzene.  Analytical methods are available for the 
detection of 2-propanol in various media (air, water, blood, serum, 
and urine) with detection limits for air, water, and blood of 
2 x 10-5 mg/m3, 0.04 mg/litre, and 1 mg/litre, respectively.  Gas 
chromatographic methods (primarily using flame ionization 
detection) as well as paper electrophoresis and photoionization ion 
mobility spectrometry methods are available for the determination 
of 2-propanol in the various media. 

1.2  Sources of Human and Environmental Exposure

    World production of 2-propanol in 1975 was estimated to be more 
than 1100 kilotonnes and the global production capacity in 1984 was 
estimated to be more than 2000 kilotonnes.  2-Propanol is commonly 
manufactured from propene.  The previously used strong acid and 
weak acid processes, which involved potentially  hazardous 
intermediates and by-products, have now largely been replaced by 
the catalytic hydration process.  The catalytic reduction of 
acetone is an alternative process. 

    2-Propanol has been identified as a metabolic product of a 
variety of microorganisms. 

    The compound has widespread solvent applications, and is used 
as a component of household and personal products including aerosol 
sprays, topically applied pharmaceutical products, and cosmetics.  
2-Propanol is also used in the production of acetone and other 
chemicals, as a de-icing agent, as a preservative, in windscreen 
wiper concentrates, and as a flavour volatile in foodstuffs. 

    2-Propanol may enter the atmosphere, water, or soil following 
waste disposal and has been identified in the air and leachates 
from hazardous waste sites and landfills.  It is emitted in waste 
gases and waste water from industrial sources, and may be removed 
from the latter by biological oxidation or reverse osmosis.  
Disperse airborne emissions will occur during the use of 2-propanol 
in consumer products. 

1.3  Environmental Transport, Distribution, and Transformation

    The main pathway of entry of 2-propanol into the environment is 
through its emission into the atmosphere during production, 
processing, storage, transport, use, and disposal.  Emissions into 
soil and water also occur.  The emissions to each environmental 
compartment are difficult to estimate.  However, in 1976, the total 
release of this compound into the atmosphere was estimated to 
exceed 50% of the 2-propanol produced. 
    2-Propanol is rapidly removed from the atmosphere by reaction 
with hydroxyl radicals and by rain-out.  The latter is responsible 
for the transport of 2-propanol from the atmosphere to soil or 
water.  Once in the soil, it is likely to be very mobile and it 
increases soil permeability to some aromatic hydrocarbons.  
2-Propanol is readily biodegradable, both aerobically and 

    It is not expected to bioaccumulate because it is biodegradable 
and is completely miscible in water, with a log  n-octanol/water 
partition coefficient of 0.14 and a bioconcentration factor of 0.5. 
1.4  Environmental Levels and Human Exposure

    Exposure of the general population occurs through accidental or 
intentional ingestion, through the ingestion of food containing 
2-propanol as a natural or added flavour volatile or as a solvent 
residue, and through inhalation during use.  Concentrations have 
been found of between 0.2 and 325 mg/litre in non-alcoholic  
beverages and 50 - 3000 mg/kg in foods following the use of  
2-propanol as a solvent in their production.  Exposure of the 
general population through inhalation of ambient air is low, 
because of its rapid removal and degradation.  Various sites have 
been monitored and time-weighted average concentrations of up to 
35 mg/m3 have been measured for urban sites. 

    Workers are exposed to 2-propanol during the production of the 
compound itself, and of acetone and other derivatives, and also 
during  its use as a solvent.  In the USA, it was estimated by the 
National Occupational Exposure Survey (1980 - 83) that over 1.8 
million workers were potentially exposed.  Concentrations of up to 
1350 mg/m3 have been measured at work-places, with time-weighted 
averages of up to about 500 mg/m3. 
1.5  Kinetics and Metabolism

    2-Propanol is rapidly absorbed and distributed throughout 
the body after inhalation or ingestion.  At high doses, 
gastrointestinal absorption is delayed.  Blood levels of 2-propanol 
(detectable when ethanol is ingested simultaneously) or of its 
metabolite, acetone, are related to the exposure levels.  Human 
volunteers who ingested a dose of 3.75 mg/kg (with 1200 mg 
ethanol/kg) in orange juice exhibited a peak level of 0.8 ± 0.3 mg 
free 2-propanol/litre in the blood, and 2.3 ± 1.4 mg/litre after 
incubation with aryl sulfatase, suggesting sulfation.  Workers 
exposed to vapour (8 - 647 mg/m3) showed concentrations of 3 - 270 
mg/m3 in the alveolar air but, in this case, acetone, not 
2-propanol, was found in the blood and urine.  In treated 
laboratory animals, 2-propanol was detected not only in the blood 
but also in the spinal fluid, liver, kidneys, and brain.  It passes 
the blood-brain barrier twice as effectively as ethanol. 
    2-Propanol is excreted partly unchanged and partly as acetone, 
mainly via the lungs, but also via saliva and gastric juice.  
Reabsorption may follow excretion via the last 2 routes.  The 

metabolism to acetone via liver alcohol dehydrogenase (ADH) is 
rather slow since the relative affinity of ADH for 2-propanol is 
lower than it is for ethanol.   In vitro, human ADH with 2-propanol 
showed 9 - 10% of the activity of the enzyme with ethanol as 
substrate.   In vitro, rat liver microsomal oxidases are also 
capable of oxidizing 2-propanol.  In human beings, acetone is 
excreted unchanged, primarily via the lungs, and minimally by the 
kidneys.  Acetone levels in alveolar air, blood, and urine increase 
with the extent and the duration of exposure to 2-propanol.  The 
elimination of 2-propanol and acetone from the body is first order, 
and half-lives in human beings are 2.5 - 6.4 h and 22 h, 
1.6  Effects on Organisms in the Environment

    The toxicity of 2-propanol for aquatic organisms, insects, and 
plants is low.  The inhibitory threshold for cell multiplication of 
a sensitive protozoan species ranged from 104 to 4930 mg/litre 
under various experimental conditions.  Progressing higher through 
the phylogenetic chain, various species of crustacea, including 
 Daphnia magna, showed EC50s at levels ranging from 2285 to 9714 
mg/litre.  LC50s (96-h) for freshwater fish ranged from 4200 to 
11 130 mg/litre.  Data obtained for fruit fly species showed LC50s 
ranging between 10 200 and 13 340 mg/litre of nutrient media.  
The LC50 for third instar mosquito larvae  (Aedes aegypti) was 
25 - 120 mg/litre in a 4-h static test. 

    The effects on plants of exposure to 2-propanol at 
concentrations between 2100 mg/litre and more than 36 000 mg/litre 
ranged from no effect to complete inhibition of germination. 
1.7  Effects on Experimental Animals and  In Vitro Test Systems

    The acute toxicity of 2-propanol for mammals, based on 
mortality, is low, whether exposure is via the oral, dermal, or 
respiratory route.  The LD50 values for several animal species  
after oral administration varied between 4475 and 7990 mg/kg body 
weight; the inhalation 8-h LC50s for rats ranged from 46 000 to 
55 000 mg/m3 air.  At these lethal levels, rats showed severe 
irritation of the mucous membranes and severe depression of the 
central nervous system.  Death was caused by respiratory or cardiac 
arrest.  Histopathological lesions included congestion and oedema 
of the lungs, and cell degeneration in the liver. 

    Single oral doses of 3000 or 6000 mg 2-propanol/kg body weight 
resulted in a reversible accumulation of triglycerides in the liver 
of rats.  Microsomal enzyme induction was observed in rats at an 
oral dose level of 390 mg/kg. 

    Undiluted 2-propanol appeared non-irritant when applied to the 
clipped or abraded skin of rabbits for 4 h.  However, 2-propanol 
caused irritation when 0.1 ml of undiluted compound was applied to 
the rabbit eye.  High vapour concentrations of 2-propanol caused 

irritation of the respiratory tract in mice, and the respiratory 
rate was decreased by 50% at concentrations of 12 300 - 43 525 
mg/m3 of air. 
    Repeated exposure studies on the effects of 2-propanol in 
animals are rather limited.  After inhalation of 500 mg 
2-propanol/m3 for 5 days/week and 4 h/day over 4 months, irritation 
of the respiratory tract, haematological changes, and 
histopathological alterations in the liver and spleen were seen in 
rats.  In another study group, 5 rats of each sex received 
drinking-water containing 2-propanol for 27 weeks.  Comparison of 
animals receiving approximately 600 or 2300 mg/kg per day (males) 
and 1000 or 3900 mg/kg per day (females) with untreated controls 
showed growth retardation only in both exposed female groups.  No 
further adverse effects were found. 
    The available evidence suggests that the effects of 2-propanol 
on the central nervous system (CNS) are similar to those of 
ethanol.  The oral ED50 for narcosis in rabbits is 2280 mg/kg, the 
intraperitoneal ED50 for loss of righting reflex in mice is 165 
mg/kg, and the intraperitoneal threshold for induction of ataxia in 
rats is 1106 mg/kg.  These values are approximately two times lower 
than those for ethanol.  Inhalation of 2-propanol at 739 mg/m3 for 
6 h/day, 5 days/week for 15 weeks did not result in any adverse 
effects in an open field test. 
    2-Propanol was evaluated in a 2-generation study on rats by the 
administration of 1290, 1380, or 1470 mg/kg per day in the 
drinking-water to both generations.  The only adverse effect noted 
was a transient reduction in growth rate in the F0 generation.  In 
contrast, other research workers observed an increase in 
malformations in a teratology study after pregnant rats were dosed 
orally with 252 or 1008 mg 2-propanol/kg per day (maternal 
toxicity was not discussed).  Both of these doses, administered in 
the drinking-water for 45 days, were also reported to increase the 
estrous cycle to 5 days (versus 4 days in controls).  Increased 
total embryonic mortality was seen when female rats received 
drinking-water doses of 1800 mg/kg per day for 6 months prior to 
breeding; various effects on intrauterine and postnatal survival 
were reported at a dose as low as 0.18 mg/kg per day, but no 
consistent pattern was apparent.  Pregnant rats were exposed to 
airborne 2-propanol at concentrations of 9001, 18 327, or 23 210 
mg/m3 (3659, 7450, or 9435 ppm).  The two higher concentrations 
were toxic to the maternal animals, but 9001 mg/m3 was not.  
Developmental toxicity was seen at all three concentrations. 

    2-Propanol gave negative results in a test at 0.18 mg per plate 
for point mutations in  S. typhimurium and a test for sister 
chromatid exchange in Chinese hamster lung fibroblasts.  It induced 
mitotic abnormalities in rat bone marrow cells and in onion root 
tip cells  in vitro.  No other mutagenicity data were available. 

    2-Propanol was tested in several limited carcinogenicity 
studies in the mouse using the dermal (3 times weekly for 1 year), 
inhalation (7700 mg/m3 for 3 - 7 h/day, 5 days/week, over 5 - 8 

months) and subcutaneous (20 mg undiluted, weekly for 20 - 40 
weeks) routes of exposure.  The occurrence of tumours was 
investigated in the three studies in the skin, lung, and at the 
injection site, respectively.  There was no evidence of any 
carcinogenic effects.  There are no adequate epidemiology data with 
which to assess the carcinogenicity of 2-propanol for human beings.  
The available data suggest that di-2-propyl sulfate, an 
intermediate in the strong and weak acid processes for the 
production of 2-propanol, may be causally associated with the 
induction of paranasal sinus cancer in human beings. 

1.8  Health Effects in Human Beings

    Several cases of intoxication have been reported after oral 
ingestion and also in febrile children who were sponged with 
2-propanol preparations.  In cases of poisoning, the major signs 
are those of alcoholic intoxication including nausea, vomiting, 
abdominal pain, gastritis, hypotension, and hypothermia.  
2-Propanol depresses the central nervous system about twice as much 
as ethanol, causing unconsciousness, ending in deep coma; death may 
follow due to respiratory depression.  Other compound-related 
effects are hyperglycaemia, elevated protein levels in 
cerebrospinal fluid, and atelectasis.  Although skin absorption has 
been deemed insignificant, a case report on a child intoxicated 
after being sponged with 2-propanol suggested that dermal 
absorption should not be underestimated, particularly in children.  
No adverse effects were observed in healthy volunteers who drank 
syrup containing 2.6 or 6.4 mg 2-propanol/kg, daily, for 6 weeks.  
A group of male volunteers, when exposed to 2-propanol vapours at 
concentrations of 490, 980, or 1970 mg/m3 air for 3 - 5 min, judged 
irritation to be "mild" at 980 mg/m3 and to be "satisfactory" for 
their own 8-h occupational exposure. 

    Skin irritation in the form of erythema, 2nd and 3rd degree 
burns, and blisters was reported in premature infants following 
prolonged contact with 2-propanol.  Occasionally, cases of allergic 
contact dermatitis have also been reported. 

    Few epidemiological studies were available on mortality from 
cancer or from other causes.  In a group of 71 workers employed for 
over 5 years in a plant manufacturing 2-propanol by the strong acid 
process, 7 cancer cases were reported including 4 cases of 
paranasal sinus cancer.  In a cohort study on 779 workers at a 
similar plant, the age- and sex-adjusted incidences of sinus and 
laryngeal cancer were 21 times higher than expected.  The minimum 
latency period was 10 years.  In another retrospective cohort study 
at another plant using the strong acid process, there were more 
than 4000 person-years at risk.  The results showed that mortality 
rates due to all causes and due to neoplasms were not significantly 
higher than expected.  A retrospective cohort study was undertaken 
in a plant manufacturing 2-propanol by the weak acid process.  More 
than 11 000 person-years were at risk.  The mortality rate due to 
all causes was lower than expected.  No excess mortality due to all 
cancers was observed.  However, the incidence of buccal and 
pharyngeal cancer was 4 times higher than expected.  The cohort 

studies collectively suggest a cancer hazard related to the strong 
acid manufacturing process but, in two small case-control studies, 
no evidence of an association between exposure to 2-propanol and 
the incidence of gliomas or lymphatic leukaemia was reported. 

    There are reports suggesting that combined exposure to carbon 
tetrachloride and 2-propanol in workers results in potentiation of 
the toxicity of the former. 

1.9  Summary of Evaluation

    Exposure of human beings to 2-propanol may occur through 
inhalation during manufacture, processing, and both occupational 
and household use.  Exposure to a potentially lethal level in the 
general population may result from accidental or intentional 
ingestion and children may be exposed when sponged with 2-propanol 
preparations (rubbing alcohol). 
    2-Propanol is rapidly absorbed and distributed throughout the 
body, partly as acetone.  Exposure-effect data on human beings 
under conditions of acute overexposure are scarce and show great 
variation.  The major effects are gastritis, depression of the 
central nervous system with hypothermia and respiratory depression, 
and hypotension.  The acute mortality data on experimental animals 
indicate that the toxicity of 2-propanol is low, the oral LD50 
values in various species ranging between 4475 and 7990 mg/kg, and 
the inhalation LC50 values for rats being around 50 000 mg/m3.  In 
rabbits 2-propanol did not irritate the skin, but the application 
of 0.1 ml undiluted 2-propanol irritated the eyes. 
    In man, the most likely acute effects of exposure to high 
levels of 2-propanol through ingestion or inhalation are alcoholic 
intoxication and narcosis. 
    No adequate animal studies are available from which an 
evaluation can be made of the human health risks associated with 
repeated exposure to 2-propanol.  However, the results of two 
short-term studies on rats, including inhalation exposure (500 
mg/m3 for 4 h/day, 5 days per week, for 4 months) and oral exposure 
(600 - 3900 mg/kg in the drinking-water), suggest that exposure to 
2-propanol at some of the very high occupational exposure levels 
reported should be avoided. 
    Inhalation exposure of pregnant rats to 2-propanol provided a 
lowest-observed-effect level (LOEL) of 18 327 mg/m3 (7450 ppm) and 
a no-observed-effect level (NOEL) of 9001 mg/m3 (3659 ppm) for 
maternal toxicity.  In the same study, 9001 mg/m3 (3659 ppm) was a 
LOEL for developmental toxicity, with no demonstration of a NOEL.  
These concentrations are higher than those likely to be encountered 
under conditions of human exposure. 

    2-Propanol was negative in genotoxicity tests but induced 
mitotic aberrations in the bone marrow of rats.  Although these 
findings suggest that the substance does not have any genotoxic 
potential, no adequate assessment of mutagenicity can be made on 
the basis of the limited data. 

    The available data are inadequate to assess the carcinogenicity 
of 2-propanol in experimental animals.  There are no data to assess 
the carcinogenicity of 2-propanol in human beings.  

    It is unlikely that 2-propanol will pose a serious health risk 
for the general population under exposure conditions likely to be 
normally encountered. 

    2-Propanol disappears rapidly (half-time <2.5 days) from the 
atmosphere and removal of 2-propanol from water and soil occurs 
rapidly by aerobic and anaerobic biodegradation, especially after 
adaptation of initially seeded microorganisms.  In view of the 
physical properties of 2-propanol, its potential for 
bioaccumulation is low.  It does not present a risk to naturally 
occurring organisms at concentrations that usually occur in the 

2.1  Identity

Chemical formula:    C3H8O
Chemical structure:      H   H   H
                         |   |   |
                     H - C - C - C - H
                         |   |   |
                         H  OH   H
Common name:         isopropyl alcohol
Common synonyms:     dimethylcarbinol, isopropanol, 2-propanol 
                     (IUPAC and CAS name), propanol-2, propan-2-ol, 
Common trade names:  Alcojel, Alcosolve 2, Avantin(e), Chromar, 
                     Combi-Schutz, E 501, Hartosol, Imsol A, IPS-1, 
                     Isohol, Lutosol, Perspirit, Petrohol, PRO, 
                     Propol, Spectrar, Takineocol, UN 1219 

Abbreviation:        IPA 

CAS registry number: 67-63-0 

Specifications:      three commercial grades with different water 
                     contents are available in the USA: 91% and 95% 
                     by volume, and anhydrous 2-propanol (IARC, 
                     1977); the anhydrous grade typically contains 
                     99.5% or more of 2-propanol, and water (0.5% 
                     by weight) and aldehydes and ketones (0.1% by 
                     weight as acetone) as the main impurities [47]. 

Conversion factors:  1 mg 2-propanol/m3 air = 0.41 ppm at 25 °C and 
                     101.3 kPa (760 mmHg); 1 ppm = 2.46 mg/m3 air. 

2.2  Physical and Chemical Properties

    2-Propanol is a highly flammable liquid at room temperature and 
standard atmospheric pressure.  Its odour resembles that of a 
mixture of ethanol and acetone, and its taste is slightly bitter.  
The compound is completely miscible with water, ethanol, acetone, 
chloroform, and benzene.  2-Propanol and water form a constant 
boiling mixture that contains 88% by weight (91% by volume) of 
2-propanol and boils at 80 - 81 °C.  2-Propanol undergoes all 
chemical reactions typical of secondary alcohols.  It reacts 
violently with strong oxidizing agents.  In a fire, it may 
decompose to form toxic gases, such as carbon monoxide.  Physical 
and chemical data on 2-propanol are given in Table 1. 

Table 1.  Some physical and chemical properties of 2-propanol
Physical state                             liquid
Colour                                     colourless
Relative molecular mass                    60.09
Odour perception threshold                 7.990 mg/m3a
Odour recognition threshold                18.4-120 mg/m3a
Boiling point (°C)                         82
Water solubility                           infinite
log  n-octanol/water partition coefficient  0.14b
Specific density (20 °C)                   0.785
Relative vapour density                    2.07
Vapour pressure (20 °C)                    4.4 kPa (33 mmHg)
Flash point (°C)                           12 (closed cup)
                                           17 (open cup)c
Flammability limits                        2-12% by volume
a From:  May [185], Oelert & Florian [196], and Hellman & Small 
b Experimentally derived by Veith et al. [262].
c From:  Kirk & Othmer [137].

2.3  Analytical Methods

    A summary of methods for the determination of 2-propanol in 
air, water, and biological media is presented in Table 2. 
    Kring et al. [144] evaluated the US NIOSH charcoal tube 
sampling method after having identified several shortcomings in the 
NIOSH validation procedure, including dry air dilution and small 
sample sizes, because of short sampling periods (15 min).  The 
overall accuracy for the determination of 2-propanol was 30.4% at 
concentrations of 128 and 428 mg/m3, 80% relative humidity, and 
sampling periods of 6 h. 
    The sensitivity of the gas chromatographic determination of 
alcohols with electron capture or photoionization detection can be 
greatly improved by prior derivatization with pentafluorophenyl- 
dimethylsilyl chloride [145]. 

    Ramsey & Flanagan [211] reported a method for the detection and 
identification of 2-propanol and other volatile organic compounds 
in the headspace of blood, plasma, or serum, using gas chromatography 
with flame-ionization and electron-capture detection.  The method is 
applicable to samples obtained from victims of poisoning, for which a 
high sensitivity is not required.  After preincubation of the samples 
with a proteolytic enzyme, the method can be used for the analysis 
of tissues. 

Table 2.  Sampling, preparation, and determination of 2-propanol
Medium  Sampling method              Analytical method              Detection limit  Sample size      Comments                    Reference
Air     sampling on charcoal,        gas chromatography with flame  0.01 mg/sample   0.0002-0.003 m3  suitable for personal and   [259]
        desorption by carbon         ionization detection, packing                                    area monitoring validated
        disulfide containing 1%      by FFAP on Chromosorb W                                          over the range of       
        butanol                                                                                       165-3300 mg/m3

Air     sampling on charcoal,        gas chromatography with flame  0.25 mg/m3       0.024 m3         suitable for area           [152]
        desorption by a 1:1 mixture  ionization detection, packing                                    monitoring, applicable to
        of carbon disulfide and      by Oronite NIW on Carbopack B                                    mixtures of both polar and
        water                                                                                         non-polar solvents

Air     sampling on porous polymer,  gas chromatography with mass   0.0012 mg/m3     0.002 m3         suitable for area           [123]
        based on 2,6-diphenyl- p-     spectrometric detection and                                      monitoring, designed for
        phenylene oxide, desorption  OV-101, SE-30, or SP-1000                                        the analysis of ambient 
        by heating                   capillary columns                                                and indoor air

Air     cryogenic sampling on        two-dimensional gas            2 x 10-5 mg/m3   0.002-0.003 m3   suitable for area           [126]
        chromosorb WAW coated with   chromatography with                                              monitoring, identification
        trifluoropropylmethyl-       photoionization and flame                                        of unknown compounds by 
        silicone, desorption by      ionization detection, column                                     mass spectometry; designed 
        heating                      1: 1,2,3-tris(2-cyanoethoxy)-                                    for the analysis of a wide
                                     propane on Chromosorb WAW,                                       range of low-molecular mass
                                     column 2: OV-101 packed                                          compounds; oxygenates in
                                     capillary                                                        ambient air

Air     direct injection             photoionization-ion mobility   0.025 mg/m3                       working range, 25-2500      [154]
                                     spectrometry                                                     mg/m3

Water   direct injection             gas chromatography with flame  1 mg/litre       0.001 ml         applicable to a mixture     [139]
                                     ionization detection, packing                                    of a wide variety of
                                     by porous polymer Tenax GC                                       compounds

Water   direct injection             gas chromatography with steam  0.04 mg/litre    0.002 ml         applicable to a mixture of  [256]
                                     as a carrier and flame                                           aliphatic compounds        
                                     ionization detection, packing
                                     by Chromosorb PAW modified 
                                     with phosphoric acid

Table 2.  (contd.)
Medium  Sampling method              Analytical method              Detection limit  Sample size      Comments                    Reference
Water   extraction by micro steam    gas chromatography with flame  0.2 mg/litre     50 ml            applicable to the analysis  [260]
        distillation with ethyl      ionization detection, packing                                    of soft drinks
        ether                        by Carbowax 20M; confirmation
                                     by mass spectrometry

Water   derivatization by 2-fluoro-  paper electrophoresis with     39 mg/litre      0.2 ml           applicable to the analysis  [20]
        1-methyl-pyridinium  p-       detection by Dragendorff's                                       of mixtures of primary and
        toluene, sulfonate in        reagent                                                          secondary alcohols, such 
        presence of tridodecylamine                                                                   as in alcoholic beverages

Blood   sampled blood placed in      gas chromatography with flame  1 mg/litre       0.0005 ml        headspace method            [150]
        aluminium capsule, capsule   ionization, detection packing 
        heated in GC injector and    with Carbowax 20M on 
        and pierced                  Chromosorb WAW-DMCS

Serum   direct injection of          gas chromatography with flame  60 mg/litre      0.2 ml           applicable to a mixture of  [236]
        deproteinized sample with    ionization detection, bonded                                     aliphatic alcohols and
         n-propanol added as          methyl-silicone-coated                                           acetone
        internal standard column     capillary

Blood,  headspace sampling, 1%       gas chromatography with flame  not reported     0.2 ml           applicable to a mixture of  [180]
urine   dioxane in water added to    ionization detection, packing                                    aliphatic alcohols,
        samples as internal          with Carbowax 20M on                                             acetone, and acetaldehyde
        standard                     Carbopack B
    Gas chromatographic methods, using flame-ionization detection, 
are available for the determination of 2-propanol in milk and milk 
products [201], in fruits [45], in oilseed meals and flours [84], 
in solid fish protein [3, 237], in drugs [115], and in drug raw 
materials [183].  The determination of C1 - C4 alcohols in gasoline 
can be done by direct injection into a gas chromatograph with an 
ion-trap detector [231].  Another direct method for the 
determination of C1 - C3 alcohols and water in gasoline is size-
exclusion liquid chromatography and detection by a differential 
refractometry [292].  One gas chromatographic method, using thermal 
conductivity detection, is described for the determination of 
2-propanol in aerosol products [142].  Methods for the 
identification of 2-propanol as flavour volatile are also described 
[115] (Table 6; section 5.2). 

    On the basis of the correlation found between alveolar and 
blood acetone levels in rats and human beings and 2-propanol 
exposure levels (section 6.3), it can be concluded that these 
acetone levels can be used for biological monitoring.  Acetone 
concentrations in the saliva of human beings have also been shown 
to be well correlated with 2-propanol exposure levels [250].  
Although 2-propanol levels in the breath and saliva are equally 
well correlated with environmental 2-propanol concentrations, the 
half-life of 2-propanol is much shorter than that of acetone 
(section 6.4). 

3.1  Natural Occurrence

    2-Propanol has been identified as a metabolic product of a 
variety of microorganisms and as a flavour volatile in foodstuffs, 
primarily plant products (section 5). 

3.2  Man-Made Sources

3.2.1  Production levels and processes  Production levels

    Estimated production capacities for 2-propanol in 1984 in the 
USA and western Europe were 1129 and nearly 1000 kilotonnes, 
respectively [72, 223], although current production may be lower.  
The major producers in western Europe are the Federal Republic of 
Germany, France, the Netherlands, and the United Kingdom, with 
estimated production capacities of 29, 13, 29, and 24% of the total 
western European capacity in 1981, respectively [137].  In the USA, 
real production gradually declined from 878 kilotonnes in 1976 to 
550 kilotonnes in 1983 [223, 275].  Japan was reported to produce 
58 kilotonnes in 1975 [120] and 96 kilotonnes in 1982 [199].  On 
the basis of data from Japan, western Europe, and the USA [120, 
223], world production in 1975 can be estimated to have exceeded 
1100 kilotonnes.  Production processes

    2-Propanol can be produced from propene by 2 different 
processes, i.e., indirect hydration and direct catalytic hydration.  
The former process is believed to have been replaced by the direct 
hydration process in Japan, the USA, and in western Europe.  
2-Propanol is also produced by the catalytic hydrogenation of 
acetone [120, 223].  Initially, indirect hydration involved the 
feeding of 88 - 93% sulfuric acid and propene gas into a reactor to 
produce a mixture of isopropyl and diisopropyl sulfates, which were 
hydrolysed with water to 2-propanol.  Principal by-products were 
diisopropyl ether and isopropyl oils consisting mainly of 
polypropylenes of high relative molecular mass [257].  Acetone and 
other by-products of low molecular mass, as well as sulfur dioxide 
were formed and these gave rise to further condensation products.  
This so-called strong-acid process has been causally related with 
an excess risk of cancer of the paranasal sinuses [120] (section 
9.2.1).  It has gradually been replaced by the weak-acid process, 
in which propene gas is absorbed in, and reacted with, 60% sulfuric 
acid and the resulting sulfates hydrolysed in a single-step 
process.  2-Propanol is stripped and refined from the condensate, 
which also contains diisopropyl ether, acetone, and polymer oils of 
low relative molecular mass [257].  The current major process, 
catalytic hydration of propene with water, has three variants:  
gas-phase hydration using a fixed-bed supported phosphoric acid 
catalyst, a mixed-phase reaction using a cation-exchange resin 
catalyst, and a liquid phase reaction in the presence of a 

dissolved tungsten catalyst [137].  Catalytic hydration largely 
avoids the corrosion and effluent problems associated with the 
sulfuric acid processes. 

3.2.2  Uses

    2-Propanol is mainly used as a solvent, and in pharmaceutical, 
household, and personal products [14, 120, 137, 223].  It is a low-
cost solvent with many consumer and industrial applications (Table 
3) and it has been estimated that, in 1975, between 35 and 45% of 
the total consumption of 2-propanol in Japan, western Europe, and 
the USA, was used in this way [120].  Apart from its solvent 
properties, 2-propanol also possesses cooling, antipyretic, 
rubefacient, cleansing, and antiseptic properties [202]. 
Table 3.  Solvent application of 2-propanola
Function             Application
1. Process solvent   - extraction and purification of natural products, such as vegetable
                       and animal oils and fats, gums resins, waxes, colours, flavourings,
                       alkaloids, vitamins, kelp and alginates
                     - carrier in the manufacture of food products
                     - purification, crystallization and precipitation of organic 

2. Coating and dye   - in synthetic polymers, such as phenolic varnishes and 
   solvent             nitrocellulose lacquers
                     - in cements, primers, paints, and inks

3. Cleaning and      - in the manufacture of electronic parts, for metals and photographic 
   drying agent        films and papers, in glass cleaners, liquid soaps and detergents,
                       and in aerosols (see 5)

4. Solvent in        - in pharmaceutical products: embrocations, massage solutions, such 
   topically           as rubbing alcohol (70% 2-propanol aerosols (see 5))
   applied           - in cosmetics: hair tonics, perfumes, skin lotions, hair dye rinses 
   preparations        and permanent wave lotions, skin cleaners and deodorants, nail 
                       polishes, shampoos

5. Aerosol solvent   - cleaners, waxes, polishes, paints, de-icers, shoe and sock sprays,
                       insect repellants, hair sprays, deodorants, air-fresheners
                     - medical and veterinary products: antiseptics, foot fungicides, 
                       first aid and medical vapour sprays, skin soothers, veterinary pink
                       eye, wound, and dehorning sprays, house and garden type 
a From:  Anon. [14], CEC [47], Kirk & Othmer [137], Zakhari [291].
    2-Propanol is used in the production of acetone and its 
derivatives and in the manufacture of other chemicals, such as 
isopropyl acetate, isopropylamine, diisopropyl ether, isopropyl 
xanthate, fatty acid esters of 2-propanol, herbicidal esters, and 
aluminium isopropoxide [47, 137].  

    Other uses include the application of 2-propanol as:  a 
denaturant in industrial solvents, a coolant in beer manufacture, a 
coupling agent, a dehydrating agent, a polymerization modifier in 
the production of polyvinyl fluoride, a foam inhibitor, a de-icing 
agent, a preservative, a heat-exchange medium, and in windscreen 
wiper concentrates [47, 137, 291].  It is also used as a flavouring 
agent in, for example, tea and beer [47, 242]. 

3.2.3  Waste disposal

    2-Propanol may enter the atmosphere, water, and soil following 
waste disposal (section 4.1).  At hazardous waste sites and 
landfills, 2-propanol was identified in the air and in leachate 
(section 5.1).  Emissions of 2-propanol via waste gases and waste 
water occur in industry and diffuse airborne emissions will occur 
during the use of the compound in consumer products (section 4.1). 

    Air emissions can be controlled by incineration, gas stripping, 
or biological oxidation in biofiltration systems [72].  2-Propanol 
can be removed from waste water by biodegradation (section 4.3.1).  
Activated carbon adsorption is not feasible as adsorption on this 
compound is poor [97].  Removal of the compound from waste water by 
reverse osmosis (hyperfiltration) can be successful, depending on 
the type of membrane used.  Cellulose acetate membranes yielded 
40 - 60% separation of 2-propanol, while cross-linked 
polyethyleneimine and aromatic polyamine membranes yielded 80 - 90% 
separation [76, 80]. 

    Ozonization of 2-propanol appears to be too slow a process to 
be of any significance for water treatment [114]. 


4.1  Transport and Distribution Between Media

    In view of the physical properties and the use pattern of 
2-propanol, it can be concluded that the main pathway of entry of 
this compound into the environment is through its emission into the 
atmosphere during production, handling, storage, transport, and 
use, and following waste disposal.  Second in importance will be 
its emission to water and soil.  In the USA, it was estimated that 
1.5% of the production in 1976 was lost to the environment [74].  
Emission registration data from the Netherlands over the years 
1974 - 79 indicated that industrial airborne emissions amounted to 
3.3% of the 1975 production volume, and emissions into water to 
0.2%.  From more recent data, a total industrial release into the 
environment of approximately 0.6% of the 1985 production capacity 
was estimated [72].  However, this figure is hardly significant, 
because of the wide use of 2-propanol in a considerable range of 
consumer products; disposal of wastes will also account for large 
emissions.  For example, in the Netherlands, an emission factor for 
the domestic use of 2-propanol in aerosol sprays was estimated to 
be 430 mg per inhabitant per day [212].  This source alone would  
result in an annual emission into the air of 2.1% of the 1975 
production volume [72].  In 1976 in the USA, 50% of the 2-propanol 
produced was estimated to be released into the atmosphere [74]. 
    Intercompartmental transfer of 2-propanol can occur between 
water, soil or waste and air, and between soil or waste and water.  
Volatilization of the compound will be considerable in view of its 
rather high vapour pressure.  Jones & McGugan [125] measured the 
evaporation rate of 2-propanol, undiluted or as a 1:1 (v/v) mixture 
with water, from a shallow pool or from pulverized domestic waste, 
under controlled conditions.  The rate of evaporation of undiluted 
2-propanol from a pool was 1.1 kg/m2 per h at a wind speed of 
0.5 m/second, an ambient air temperature of 12 °C, and a pool 
temperature of 13 °C.  The evaporation rate of diluted 2-propanol 
was 1.5 kg/m2 per hour at a wind speed of 4.5 m/second, a pool 
temperature of 20 °C, and an ambient air temperature of 22 °C.  
Addition of domestic waste to both the diluted and the undiluted 
2-propanol initially increased the evaporation rate, but strongly 
attenuated the release of vapour within 2 h. 
    Transport of 2-propanol from the atmosphere to soil or water 
will occur via rain-out, as it is highly soluble in water. Data on 
the behaviour of 2-propanol in soil are scarce.  With respect to 
adsorption, there is one study showing that the compound is poorly 
adsorbed on activated carbon [97].  Since 2-propanol is completely 
miscible with water, it can be expected to be very mobile in the 
soil [72] and it has been shown to increase the permeability of 
soil to aromatic hydrocarbons [81]. 

4.2  Abiotic Degradation

    Once in the atmosphere, 2-propanol will be degraded mainly by 
hydroxyl radicals.  It is not expected to react at appreciable 
rates with other reactive species, such as ozone, and hydroperoxy-, 

alkyl-, and alkoxy-radicals.  Since the compound does not absorb 
ultraviolet radiation within the solar spectrum, photolysis is not 
expected [46].  Experimentally determined rate constants for the 
reaction between 2-propanol and hydroxyl radicals are 0.71 x 10-11 
ml/molecule per second at 32 °C [164], and 0.54 x 10-11 ml/molecule 
per second at 23 °C [200].  On the basis of these rate constants, 
atmospheric residence times of 1.4 and 2.3 days, respectively, can 
be calculated [61].  These short lifetimes will prevent migration 
of the chemical into the stratosphere. 
    The initial reaction product of 2-propanol with a hydroxy 
radical is an alpha-hydroxy-2-propyl radical.  By analogy with the 
irradiation of 2-butanol in an NOx--air atmosphere, these radicals 
are expected to react with oxygen almost exclusively with hydrogen 
abstraction from the hydroxyl-group to produce acetone, or with 
loss of methyl to give acetaldehyde.  Follow-up reactions will 
produce small quantities of peroxyacetyl nitrate, formaldehyde, 
methyl nitrate, and formic acid [46]. 

    Hydrolysis or light-induced degradation of 2-propanol in water 
cannot be expected. No data are available on abiotic degradation in 

4.3  Biotransformation

4.3.1  Biodegradation

    The results of the determination of the biological oxygen 
demand (BOD) by dilution methods at 20 °C are summarized in Table 
4.  Unless otherwise stated, the results are expressed as a 
percentage of the theoretical oxygen demand (ThOD), which is 2.40 g 
oxygen/g 2-propanol.  The chemical oxygen demand (COD) was reported 
to be 96 and 93% of the ThOD by Price et al. [208] and Bridie et 
al. [33], respectively. 

    Adaptation of the seed material to the chemical enhances the 
rate of biodegradation considerably.  Gerhold & Malaney [95] added 
2-propanol to undiluted activated sludge and found an oxygen uptake 
of 10% of the ThOD in 24 h.  Mack [175] measured total degradation 
of 2-propanol within 96 h and total degradation of the initial 
product acetone within 120 - 144 h following incubation in a 
standard medium that had been inoculated by effluent from a water 
purification plant.  In another study, 2-propanol (50 mg/litre) was 
added as the sole source of carbon to a mineral medium in a 
continuous flow reactor, seeded by a culture isolated from 
activated sludge using methanol, phenol, acetone, and 2-propanol as 
substrates.  Growth was extremely poor.  However, when acetone (100 
mg/litre) was added as well, almost 100% degradation of the 2 
chemicals was achieved within a minimum of 2.9 h.  The authors 
concluded that, in this case, the oxidation of 2-propanol was 
dependent on the simultaneous oxidation of acetone.  When 2-propanol 
was added to the same medium, seeded by a culture isolated using 
2-propanol as the sole substrate, almost 100% degradation was 
achieved within a minimum of 4.3 h [281]. 

Table 4.  BOD and COD of 2-propanol
Dilution  Source or seed         Adaptation  BODxa  Value  Reference
water                            (+/-)              (% of
Fresh     municipal waste water  -           BOD5   7      [289]
                                 -           BOD20  70

          domestic waste water   -           BOD5   28     [208]
                                 -           BOD20  78

          domestic waste water   -           BOD5   66     [268]

          domestic waste water   -           BOD5   74     [269]

          activated sludge       +           BOD5   99b    [203]

          effluent from a        +           BOD5   72     [33]
          biological waste       -           BOD5   49
          treatment plant

Salt      domestic waste water   -           BOD5   13     [208]
                                 -           BOD20  72
a BODx = biological oxygen demand after x days of incubation.
b Expressed as percentage of the COD.
    In a water treatment facility of a plant manufacturing organic 
chemicals, a typical removal efficiency for 2-propanol was 76%, 
using an aerated, non-flocculent, biological stabilization process 
[25].  After conversion to an activated sludge facility, the 
removal efficiency increased to 96% [147]. 

    There are two reports on anaerobic biodegradation.  Typical 
2-propanol removal efficiencies for an anaerobic lagoon treatment 
facility, with a retention time of 15 days, were 50% after loading 
with dilute waste, and 69 and 74% after loading with concentrated 
wastes [118].  In closed bottle studies, 2-propanol was completely 
degraded anaerobically by an acetate-enriched culture, derived from 
a seed of domestic sludge.  The culture started to use cross-fed 
2-propanol, after 4 days, at a rate of 200 mg/litre per day.  In a 
mixed reactor with a 20-day retention time, seeded by the same 
culture, 56% removal was achieved in the 20 days following 70 days 
of acclimation to a final 2-propanol concentration of 10 000 
mg/litre [55]. 

4.3.2  Bioaccumulation

    2-Propanol is completely miscible with water.  Its log 
 n-octanol/water partition coefficient is 0.14 [263].  A 
bioconcentration factor of 0.5 can be calculated using the formula 
of Veith & Kosian [262].  In addition, the compound is 
biodegradable.  In view of these data, no bioaccumulation is 

5.1  Environmental Levels

    The rapid removal of 2-propanol from air and water is reflected 
in the few reports indicating its presence in these compartments 
(sections 4.2 and 4.3).  No data are available on the occurrence of 
the compound in soil. 
    2-Propanol was detected, at a level of 95 mg/m3 air, at the 
outlet of the main chimney of a paint-manufacturing plant in France 
in 1980.  The compound was not detected at a distance of 10 - 30 m 
from this chimney [51].  In 1970, Gorlova [98] reported that 
average atmospheric levels of 2-propanol at distances of 500 and 
5000 m from a plant producing 2-propanol by indirect hydration, 
were 1.7 and 0.2 mg/m3 air, with maxima of 3 and 0.5 mg/m3 air, 
respectively.  In 260 1-h samples of air from 4 sites in Stockholm, 
Sweden, in 1983, 2-propanol concentrations ranging between 0.61 and 
108 mg/m3 were measured with averages of between 1.52 and 35.2 
mg/m3.  In 56 air samples from a monitoring site near dense traffic 
12 km outside central Stockholm, concentrations of between 0.12 and 
2.93 mg/m3 were measured, the average being 0.74 mg/m3.  The 
2-propanol levels were not correlated with typical vehicle exhaust 
compound levels.  However, a correlation was found between 
2-propanol levels and the use of anti-freezing agents for 
windscreen washers at a similar site [126]. 
    2-Propanol was detected in the air beneath the surface of 2 out 
of 6 landfill sites sampled in the United Kingdom.  At these 2 
sites, used for the disposal of domestic waste, the 2-propanol 
concentrations were 17 mg/m3 and more than 46 mg/m3, respectively 
[288].  Analysis of a total of 82 air samples at 5 hazardous waste 
sites in New Jersey, USA, revealed the presence of 2-propanol at 4 
sites [151].  Leaching from landfills may result in ground water 
pollution.  In 1982-83, 2-propanol concentrations of up to 8.8 
mg/litre water were measured in 6 out of 7 samples of leachate, 
obtained from test wells in 1 of 5 landfills sampled in the United 
Kingdom [225]. 

    2-Propanol has been identified as a metabolic product in 
microorganisms, as shown in Table 5. 
Table 5.  2-Propanol production by microorganisms
Type                            Species                                      Reference
Aerobic fish spoilage bacteria   Pseudomonas spp.,  Moraxella-like,            [7]
                                 Flavobacterium, Micrococcus, Coryneforms, 

Aerobic beef spoilage bacteria   Pseudomonas spp.                             [63]

Aerobic potato tuber soft rot    Erwinia carotovora                           [273]

Table 5.  (contd.)
Type                            Species                                      Reference
Anaerobic bacteria               Clostridium beijerinckii                     [92]
                                 Clostridium aurantibutyricum

Anaerobic methylotrophic,                                                    [181]
propane fed bacteria

Fungi, mushroom                  Leucocoprinus elaedis                        [93]

Yeast                            Kluyveromyces lactis                         [107]
5.2  General Population Exposure

5.2.1  Exposure via food

    When 2-propanol is used as an extraction or carrier solvent for 
food constituents, the compound may be found in the final product.  
It was detected in 8 out of 17 samples of lemonade, prepared with 
natural essence extracted with 2-propanol.  Concentrations of 
between 0.2 and 82 mg/litre were measured in 7 samples and 325 
mg/litre in one sample [260].  The compound was also identified in 
fish protein concentrate, extracted by 2-propanol [237].  The 
Scientific Committee for Food of the Commission of the European 
Communities has published industry-derived residue levels in 
foodstuffs following the use of 2-propanol as an extraction and/or 
carrier solvent.  Typical levels are:  250 mg/kg of dry fish 
protein concentrate, 50 mg/kg of meat product as consumed, 750 
mg/kg of meat after use of 2-propanol as a smoke flavour carrier 
and before drying, 1200 mg/kg of jam, and 3000 mg/kg of jelly [47]. 

    Studies showing the presence of 2-propanol as a flavour 
volatile in a variety of foodstuffs are summarized in Table 6. 

Table 6.  2-Propanol as a flavour volatile in foodstuffs
               Foodstuff                                Reference
Common name                Scientific name
Reunion geranium oil        Pelargonium roseum Bourbon   [249]

Rooibos tea                 Asphalathus linearis         [104]

Winged bean (raw/roasted)   Psophocarpus tetragonalobus  [70]
Soybean (raw/roasted)       Glycine max  

Virginia peanut (raw)                                   [166]

Peanut (raw/roasted)        Arachis hypogaea             [156]

Filbert (roasted)           Corylus avellana             [136]

Table 6.  (contd.)
               Foodstuff                                Reference
Common name                Scientific name
Babaco fruit                Carica pentagona             [229]

Apple                       Malus                        [242]
Tomato                      Lycopersicum

Endive                      Cichorium endivia            [99]

Lime essence                Citrus arantifolia           [189]

Grapefruit essence          Citrus paradisi              [58]
Grapefruit aroma oil

Mushroom (fresh/edible)     Leucocoprinus elaedis        [93]

Kefir culture                                           [201]
Yoghurt culture

Swiss Gruyere cheese                                    [31]

Feta cheese                                             [116]
    Microbial metabolism may be responsible for the presence of 
2-propanol in certain foodstuffs, such as cheese, as suggested by 
Bosset & Liardon [31].  Approximately 25% of the 2-propanol found 
in beer is added as a flavouring agent during its manufacture [242].
5.2.2  Exposure via other consumer products

    The general population is potentially exposed to a wide variety 
of consumer products containing 2-propanol (section 3.2.2).  In a 
1980 survey in Japan, commercial heterogeneous solvent products 
were collected throughout the country.  Of 102 products, 12 out of 
59 samples of paint, 6 out of 18 samples of ink, 1 out of 12 
samples of adhesives, and 3 out of 13 samples of other products 
contained 2-propanol [146].  Not surprisingly, 2-propanol was one 
of over 250 compounds found in the indoor air of homes in 2 urban 
areas of the USA, where the levels were all less than 0.25 mg/m3 
    Intentional or accidental poisoning by 2-propanol in consumer 
products has been reported frequently.  Several cases will be 
discussed in section 9.1.  The subject of non-beverage alcohol use 
has been reviewed recently by Egbert et al. [77], who reported that 
10 - 15% of a specified group of alcoholics in the USA (admitted to 
a Veteran Administration detoxication unit) were found to have 
consumed non-beverage alcohols.  Addiction to a disinfectant 
containing 2-propanol was reported in one case [133].  In Canada, 
the incidence of cases of exposure to 2-propanol in rubbing alcohol 

reported to the Poison Control Centres increased from 254 in 1973 
to 338 in 1976 [151].  Rubbing alcohol is also the single most 
frequent source of 2-propanol intoxication in small children.  This 
can occur from accidental ingestion, or via inhalation following 
sponging for fever reduction [163]. 

5.3  Occupational Exposure

    Workers are potentially exposed to 2-propanol during production 
of the compound itself or of acetone and other derivatives, or 
during its use in solvent type applications.  In the USA, NIOSH 
estimated, on the basis of the 1980 - 83 National Occupational 
Exposure Survey, that over 1.8 million workers, of whom over 1.1 
million were females, were potentially exposed to this compound 
[259].  Inhalation exposure of workers in various industries where 
2-propanol or 2-propanol-containing products are used, is 
summarized in Table 7.  In most cases, these workers were also 
exposed to other chemicals.  No data are available on the exposure 
of workers in 2-propanol- or acetone-producing industries, except 
for the report of Guseinov [103] pertaining to a plant in the USSR 
producing 2-propanol by indirect hydration. 
Table 7.  Occupational inhalation exposure to 2-propanol
Job description        Country  Sampling  Concentration (mg/m3)                 Reference
(number of workers)
Car painting (40)      Finland  personal  7.1 (average)                         [148]
                                          209 (maximum)

Printing (12)          Italy    area      8-647                                 [41]
                                          15-493 (time-weighted average)

Ink production (41)    Italy    area      6.3-32.8                              [42]

Paint manufacture (3)  Sweden   personal  6-258 (time-weighted average)         [168]
                                          129 (time-weighted average-average)

Work in hospital       United   area      8.8 (average)                         [106]
operating theatre      Kingdom            30 (maximum)

Tractor painting (28)  USA      personal  NDa-697                               [102]
                                area      33-332

Higher aromatic booth  USA      personal  4.7 (time-weighted average-average)   [279]
spray painting (14)                       32 (time-weighted average-maximum)
                                          54 (maximum)

Lower aromatic booth   USA      personal  10.6 (time-weighted average-average)  [279]
spray painting (16)                       125 (time-weighted average-maximum)
                                          605 (maximum)

Solvent wiping (11)    USA      personal  2.5 (time-weighted average-average)   [279]
                                          13 (maximum)

Table 7.  (contd.)
Job description        Country  Sampling  Concentration (mg/m3)                 Reference
(number of workers)
Paint mixing (3)       USA      personal  4.2 (time-weighted average-average)   [276]
                                          10 (maximum)

Spraying paint,        USA      personal  <2.5 (time-weighted average-average)  [177]

Printing (26)          USA      personal  396 (time-weighted average-average)   [177]

Printing (2)           USA      personal  33-67                                 [140]

Printing (7)           USA      personal  85-293                                [101]
                                area      236

Printing (4)           USA      personal  0.5-3.7                               [152]
                                area      2.2-16.5

Printing (8)           USA      personal  NDa-519                               [282]
                                area      15-307

Printed circuit        USA      personal  5.8-23                                [280]
boards manufacture 

Furniture stripping    USA      personal  42-160                                [179]

Degreasing metal (14)  USA      personal  2.2-10.6                              [271]

Manufacture of rubber  USA      personal  NDa-34                                [278]
weather strips (67)             area      6.5-140

Chemicals packaging    USA      area      150-1350                              [83]

2-Propanol production  USSR     area      92 (average)b                         [103]
                                area      165 (average)c

Chloramphenicol        USSR     area      10-36 (average)d                      [173]
production                                NDa-120

Sulfite additive       USSR     area      7.1-14.6 (average)                    [17]
a ND = not detected.
b Wintertime.
c Summertime.
d Average of positive samples.
6.1  Absorption

6.1.1  Animals

    Exposure of dogs, rabbits, and rats via various routes resulted 
in detectable levels of 2-propanol in the blood within 0.5 h of the 
start of the exposure [1, 121, 150, 151, 158, 181, 195]. 

    Maximum blood concentrations of 2-propanol of up to 2950 
µg/litre were attained in dogs within 0.5 - 2 h following single 
oral doses of the compound in water of up to 2940 mg/kg body 
weight.  The blood concentration was directly related to the dose 
level [158].  Following single oral dosing of rats with 2-propanol 
in water at 2000 mg/kg body weight [121] or 6000 mg/kg body weight 
[195], peak blood concentrations were 1080 µg/litre after 1 h and 
4800 - 6000 µg/litre after 8 h, respectively.  Apparently, 
gastrointestinal absorption is delayed at high doses. 
    Blood levels of 2-propanol were determined in groups of 3 adult 
(200 - 300 g) female Sprague-Dawley rats following 1, 10, or 19 
consecutive 7-h daily exposures to measured concentrations of 7636, 
18 327, or 23 210 mg/m3 (3104, 7450, or 9435 ppm).  Immature 
(approximately 90 g) females of the same strain were also evaluated 
following a single 7-h exposure to 23 210 mg/m3 (9435 ppm).  In the 
immature females, the blood level of 2-propanol averaged 9600 µg/ 
litre.  The blood levels in adult rats following a single exposure 
were not detectable at 7636 mg/m3 (3104 ppm), 6800 µg/litre at 
18 327 mg/m3 (7450 ppm), and 7900 µg/litre at 23 210 mg/m3 (9435 
ppm).  Following 10 and 19 consecutive daily exposures, blood 
levels in adult rats were consistently not detected at 7636 mg/m3 
(3104 ppm); 5800 and 5700 µg/litre at 18 327 mg/m3 (7450 ppm), and 
7000 and 6400 µg/litre at 23 210 (9435 ppm) [193], respectively.  
The Task Group noted that these blood 2-propanol levels appeared to 
be exceptionally high. 

    When rats inhaled 2-propanol at concentrations of between 1230 
and 19 680 mg/m3 for 4 or 8 h, maximum blood concentrations 
attained at the end of the exposure period at the highest exposure 
level were 235 and 760 µg/litre, respectively [151]. 

    Wax et al. [274] injected equal volumes of 2-propanol in saline 
into each of several ligated loops of the intestines and into the 
stomach loop of anaesthetized dogs.  The concentration of the 
solutions varied, the total dose always being 980 mg/kg body 
weight.  Absorption from the intestines was 67 - 91% of the dose 
within 30 min and 99% within 2 h.  Absorption from the stomach loop 
was 41% within 30 min. 
    Rats exposed intraperitoneally to 1000 mg 2-propanol/kg body 
weight in saline showed peak blood concentrations of 1020 - 1300 
µg/litre within 1 h [1, 195]. 
    Groups of 3 rabbits received 2-propanol in water orally at 2 or 
4 mg/kg body weight or were exposed to 2-propanol in towels, one 
applied to the chest and others on the floor of the inhalation 
chamber, with or without a plastic layer to prevent skin contact.  
The highest blood levels of 2-propanol were produced by the oral 
exposures, followed by the combined dermal and inhalation exposure 

6.1.2  Human beings

    Ten human volunteers drank orange juice containing doses of 
3.75 mg 2-propanol/kg and 1200 mg ethanol/kg body weight over a 
period of 2 h.  At the end of this period, the average peak blood 
concentration of 2-propanol was 0.83 ± 0.34 (mean ± standard 
deviation) mg/litre.  When the blood was analysed after incubation 
with aryl sulfatase (EC, an average peak concentration of 
2.27 ± 1.43 mg/litre was measured 1 h after exposure [27].  These 
data provide limited evidence for the sulfation of 2-propanol. 

    Brugnone et al. [41] analysed the alveolar air, blood, and 
urine of 12 printing workers, exposed to 2-propanol at 
concentrations of between 8 and 647 mg/m3 air.  The alveolar 
2-propanol concentration was highly correlated with the exposure 
level at any time of exposure, the ratio of the two concentrations 
being 0.418.  The alveolar uptake (0.03 - 6.6 mg/min) showed a 
linear increase with exposure levels. 

6.2  Distribution

6.2.1  Animals

    2-Propanol, a compound with infinite water solubility, is 
rapidly distributed throughout the body [1]. 

    Wax et al. [274] recovered 2-propanol from the blood, spinal 
fluid, liver, kidneys, and brain of dogs, 30 min after exposure via 
injection into ligated loops of the gastrointestinal tract.  Three 
hours after a single oral exposure of rats, the compound was found 
in the blood, liver, kidneys, and brain [121].  No other tissues 
were analysed in either study. 

    The permeability of the blood-brain barrier for 2-propanol 
was investigated in monkeys and rabbits.  Anaesthetized monkeys 
received a single injection of 0.2 ml of an 11C-labelled alcohol in 
the carotid artery, followed by an injection of 15O-labelled water.  
At a cerebral blood flow of 50 ml/100 g per min, about 99% of 
2-propanol, 97% of ethanol, and 93% of labelled water exchanged 
freely with the brain during a single capillary transit.  On the 
basis of these data, the blood-brain barrier permeabilities for 
these three compounds were estimated to be 5, 2.5, and 1.8 x 10-4 
cm/second, respectively [209]. 

6.2.2  Human beings

    Following ingestion of an unknown amount of rubbing alcohol, 
2-propanol as well as its metabolite acetone were found in the 
spinal fluid of 2 persons at levels similar to those in the serum 
[5, 191]. 

6.3  Metabolism

6.3.1  Animals

    The metabolism and elimination of 2-propanol in mammals is 
summarized in Fig. 1.  It has been well established that 2-propanol 
is metabolized to acetone in the rat, dog, and rabbit [1, 121, 150, 
151, 195, 224, 232].  Oral (0.2, 1.0 ml) and inhalation exposure 
(1230 - 19 680 mg/m3, for 4 h) (500 - 8000 ppm) of rats produced 
dose-related increases in blood levels of 2-propanol and its 
metabolite acetone.  Following inhalation, the acetone/2-propanol 
ratio in blood decreased with increasing 2-propanol concentrations 
indicating saturation of the oxidative metabolic pathway above 
concentrations of approximately 9840 mg/m3 (4000 ppm) [150, 151]. 


    Since adequate balance studies have not been conducted, the 
extent of this metabolism to acetone is not known.  Siebert et al. 
[232] injected 750 or 1300 mg/kg body weight intravenously in 
rabbits and estimated that 64 - 84% of the dose was oxidized to 
acetone, confirming the earlier findings of Pohl [204]. 

    Evidence of another metabolic pathway was found in rabbits 
given an oral dose of 2-propanol of 3000 mg/kg body weight, 10.2% 
of the dose was found in the urine as beta-isopropyl-glucuronide 

    Sufficient evidence is available to show that 2-propanol is 
oxidized to acetone mainly by the non-specific cytosolic enzyme 
alcohol dehydrogenase (ADH) (EC  When either pyrazole or 
4-methylpyrazole (inhibitors of ADH) was administered to rats prior 
to exposure to 2-propanol, both the elimination of 2-propanol and 
the production of acetone were retarded [121, 193].  The 
elimination of 2-propanol by rats was retarded when it was given in 
combination with ethanol; both compounds are substrates for ADH [2, 
121].  Enzyme kinetic data show that 2-propanol is a poorer 
substrate of ADH than ethanol.   In vitro, the Michaelis-Menten 
constant (Km) for horse liver ADH was 0.0126 mol/litre, using 
2-propanol as a substrate, and 0.00018 mol/litre, using ethanol as 
a substrate [64].  For rat liver ADH  in vivo, Km was 0.034 
mol/litre, using 2-propanol as a substrate, and 0.00192 mol/litre, 
using ethanol as a substrate.  The maximum initial velocity (Vmax) 
of rat liver ADH and the substrate 2-propanol  in vivo was 1.7 times 
less than that with the substrate ethanol.  It was further shown 
that the ratio of the relative rates of oxidation of 2-propanol and 
deuterated 2-propanol-d7 were about the same  in vitro and  in vivo.  
From this, it can be concluded that ADH activity is the rate-
limiting factor in 2-propanol metabolism [54]. 

    It has been shown that rat liver microsomal oxidases are also 
capable of oxidizing 2-propanol, but that the compound is not an 
effective substrate for the peroxidative activity of catalase 
(EC [48, 193]. 
6.3.2  Human beings

    Acetone has also been found in the blood of human beings after 
exposure to 2-propanol [e.g., 11, 41, 65, 131].  Furthermore, 
acetone was detected in the spinal fluid, at levels similar to 
those in serum, in 2 persons after ingestion of 2-propanol [5, 191]. 

    In the investigations of Brugnone et al. [41] (section 6.1.2), 
elevated acetone levels were measured in the blood, alveolar air, 
and urine of 12 printing workers.  2-Propanol was not detected in 
the blood or urine.  The concentrations of acetone ranged between 
0.76 and 15.6 mg/litre in the blood and between 3 and 93 mg/m3 in 
the alveolar air.  The acetone levels in alveolar air and blood 
increased with the increasing exposure period and were linearly  
related to the alveolar 2-propanol levels.  Urinary acetone levels  
ranged from 0.85 to 53.7 mg/litre in overnight pooled urine samples 
and were highly correlated with the alveolar 2-propanol uptake and 
with blood acetone levels.  Pulmonary and renal clearance of 
acetone were 41 - 97 and 0.1 - 3 ml/min, respectively, for 8 of the 
workers, showing that acetone is mainly excreted via the lungs.  
Pulmonary acetone excretion varied from 10.7 to 39.8% of the  
uptake and was inversely related to the exposure level [41].  It  
is known that the metabolic capacity of the human liver for acetone 
is limited [161]. 
    2-Propanol and acetone have also been found in the returns of 
gastric lavage [5] and in saliva [250].  Reabsorption may follow 
excretion via these routes. 

    When 10 volunteers drank orange juice containing doses that 
gave 3.75 mg 2-propanol and 1200 mg ethanol/kg body weight over 
2 h, 2-propanol was detected in the blood, partly as sulfate 
(section 6.1.2), and in the urine, partly as glucuronide.  The 
total urinary excretion of 2-propanol was 1.9% of the dose [27, 28]. 
    Human data support the importance of the ADH pathway for the 
oxidation of 2-propanol as observed in experimental animals.  In 
the studies of Bonte et al. [27, 28] described above, 2-propanol 
was only detected in the blood when ethanol was ingested 
simultaneously, indicating a retarded elimination.  Among 74 
persons intoxicated by 2-propanol, significantly lower acetone 
values were found in the blood of those who had also been exposed 
to ethanol [11, 131].  In  in vitro studies, the activity of human 
ADH with 2-propanol was 9 - 10% of the activity of the enzyme with 
ethanol as substrate [121]. 
    Endogenous formation of 2-propanol has been revealed at 
autopsies of individuals not previously exposed to this compound.  
This observation and the results of additional studies on rats show 
that 2-propanol can result from the reduction of acetone by liver 
ADH, especially when high levels of acetone and high NADH/NAD+ 
ratios occur.  Such conditions are found in diabetes mellitus, 
starvation, high fat feeding, chronic alcoholism, and dehydration 
[68, 161, 248]. 

6.4  Elimination and Excretion

6.4.1  Animals

    In a review article, Rietbrock & Abshagen [218] concluded that 
urinary excretion of both 2-propanol and its metabolite acetone is 
limited and in each case does not exceed 4% of the dose in the rat, 
rabbit, and dog.  The major route of excretion is via the lungs.  
2-Propanol is excreted via the gastric juice and saliva in the dog 
[158] and through breast milk in the rat, as shown by tissue levels 
in the newborn [159]. 
    The disappearance of 2-propanol from the blood of experimental 
animals was found to be a first-order process at doses <1500 mg/kg 
[1, 232].  In rats, the half-life of 2-propanol was 1.5 h at an 
intraperitoneal dose of 500 mg/kg body weight and increased to 
2.5 h at a dose of 1500 mg/kg body weight.  This can be explained 
by a limited metabolic capacity as suggested in section 6.3.1 
[218].  Simultaneous administration of ethanol to rats increased 
the half-life of 2-propanol in the blood approximately 5-fold 
following acute exposure [2].  A half-life of 4 h was determined in 
dogs administered 1000 mg 2-propanol/kg body weight intravenously [1]. 
    The biotransformation of 2-propanol and the elimination of the 
acetone produced are both slow processes.  Peak acetone levels in 
the blood of various species, following single exposures via 
different routes, were only reached several hours after exposure, 
though acetone was already detectable shortly after the start of 
exposure [1, 121, 150, 151, 193, 232].  The elimination of acetone 
in the dog and the rat was found to be a first-order process with 
half-lives of 11 and 5 h, respectively [1]. 

    After prolonged administration of 2-propanol to dogs [159] and 
rats [224], the elimination rate of 2-propanol was increased.  
Simultaneous exposure of rats to ethanol in the drinking-water (5%) 
and atmospheric 2-propanol at 738 mg/m3 (300 ppm) for 5 - 21 weeks 
significantly increased the rates of elimination of 2-propanol and 
acetone [224]. 

6.4.2  Human beings

    The elimination of 2-propanol in human beings also appears to 
follow first-order kinetics.  In two alcoholics who had ingested 
rubbing alcohol, 2-propanol was eliminated from the blood with 
half-lives of 2.5 and 3 h, respectively.  Acetone levels declined 
slowly over the next 30 h;  no ethanol was detected [65].  A half-
life of 2-propanol of 6.4 h was determined in a non-alcoholic, who 
also had ingested rubbing alcohol.  The acetone level in the blood 
reached a maximum 30 h after admission to hospital.  The half-life 
of acetone was 22 h.  Ethanol was also found in the blood.  The 
differences in the half-lives in these three cases may reflect 
metabolic adaptation in the alcoholics, or genetic variations in 
ADH [191]. 

    When 4 volunteers ingested an artificial liquor containing 40% 
2-propanol, acetone was detectable in exhaled air from 15 min after 
exposure and in the urine from 1 h after exposure [132]. 

7.1  Aquatic Organisms

    A summary of acute aquatic toxicity data is presented in Table 8.  
The concentration of 2-propanol was reported to have been measured 
in only 3 of the studies [34, 111, 263] and in no case were 
potential metabolites considered.  In view of the volatility of the 
compound, it can be expected that the toxic effects observed in the 
other open systems studied occurred at lower concentrations than 
the nominal ones. 

    Several short- and long-term studies have also been conducted.  
Seiler et al. [227] determined the breakpoint of bioinhibition for 
a total of 20 strains of bacterial groups prevalent in a waste-
water treatment plant in the chemical industry, i.e.,  Zoogloea, 
 Alcaligenes, and  Pseudomonas.  After one week of static exposure to 
2-propanol in an open system at 30 °C, 100% growth inhibition 
occurred at concentrations of 80 000 - 100 000 mg/litre of medium.  
No analysis for the compound was reported.  The cell multiplication 
of blue algae  (Microcystis aeruginosa) and green algae  (Scenedesmus 
 quadricauda) was just inhibited after 8 days of static exposure to 
1000 and 1800 mg/litre water, respectively, in a closed system at 
27 °C and a pH of 7 [35, 37].  When water fleas  (Daphnia magna) 
were exposed to 2-propanol for 16 days in a semi-static test at 
19 °C and a water hardness of 100 mg CaCO3/litre, the highest 
concentration that did not result in a significant reduction in 
growth was 141 mg/litre water.  The water was analysed for the 
compound just before and after each renewal of test solution [111].  
A 7-day LC50 of 7060 mg 2-propanol/litre water was determined for 
2 - 3-month-old guppies  (Poecilia reticulata) in a semi-static 
test.  No analysis for 2-propanol was reported for this open system 

7.2  Terrestrial Organisms

7.2.1  Microorganisms

    The sensitivity of 4 soil fungi, i.e.,  Chrysosporium 
 crassitunicatum, Nannizzia fulva(+),  Nannizzia fulva(-), and 
 Trichophyton equinum, to saturated 2-propanol vapour was  
determined at 28 °C and a pH of 7.  Mycelial growth of 
 Chrysosporium was stimulated after 14 days of exposure, while that  
of the other strains was inhibited.  Sporulation was poor in 
 Chrysosporium and in  Trichophyton, and fair or good in the other 
strains [233]. 

Table 8.  Acute aquatic toxicity of 2-propanol
Organism   Description     Temperature  pH     Dissolved   Hardness    Stat/flow     Exposure  Parameter       Nominal        Reference
                           (°C)                oxygen      (mg CaCO3/  open/closeda  period                    concentration
                                               (mg/litre)  litre)                                              (mg/litre)

Bacteria    Pseudomonas     25           7                              stat, closed  16 h      TTb             1 050          [37]
Micro-     activated       21           7.4-8                          stat, closed  3 h       50% inhibition  1 000          [138]
organisms  sludge                                                                              of respiration

Protozoa    Entosiphon      25           6.9                            stat, closed  72 h      TTb             4 930          [36]

Protozoa    Chilomonas      20           6.9                            stat, closed  48 h      TTb             104            [40]

Protozoa    Uronema         25           6.9                            stat, closed  20 h      TTb             3 425          [38]

Crustacea  water flea      20           8      2           250         stat, open    24 h      EC50c           9 714          [39]
            (Daphnia                                                                            EC0             5 102
            magna)                                                                              EC100           10 000

Crustacea  water flea      22                              100         stat          44 h      EC50c,d         2 285          [110]

Amphibia   frog tadpole    20                                          stat                    threshold       22 530         [190]
            (Rana pipiens)                                                                      narcotic

Fish       fathead minnow  18-22               4                       stat, open    96 h      LC50            11 130         [184]
            (Pimephales                                                               24 h      LC50            11 160

Fish       fathead minnow  25           7.5    5           45          flow, open    96 h      LC50            9 640-10 400f  [262]
Table 8.  (contd.)
Organism   Description     Temperature  pH     Dissolved   Hardness    Stat/flow     Exposure  Parameter       Nominal        Reference
                           (°C)                oxygen      (mg CaCO3/  open/closeda  period                    concentration
                                               (mg/litre)  litre)                                              (mg/litre)
Fish       goldfish        20           6-8    4           280         stat, open    24 h      LC50            5 000f         [34]

Fish       golden orfe     20           7-8    5           200-300     stat          48 h      LC50            8 970          [127]
            idus melanotus) 

Fish       harlequin fish  20           8.1                20          flow, open    96 h      LC50            4 200          [251]
            (Rasbora                                                                  96 h      LC10            1 500

Fish       Creek chub      15-21        8.3                98          stat, open    24 h      LC0             900            [96]


Bacteria    Photobacterium  15           7                              stat, closed  2 min     TTh             15 000         [43]
            phosphoreum     15                                          stat, closed  5 min     50% light       35 000         [44, 62]
                                                                                               reduction       42 000

Worm        Tubifex         20                                          stat          2 min     EC100c          51 080         [56]

Crustacea  Brine shrimp    24                                          stat, open    24 h      LC50            10 000         [208]

Crustacea  Brown shrimp                                                semi-stat,    96 h      LC50            1 150          [26]
            (Crangon                                                    open
a Static or flow-through test; open or closed system.                   e Concentration at which touching the tadpoles failed to cause
b TT = toxic threshold for inhibition of cell multiplication.             motion; exposure period and conditions; and the method of 
c Effect is complete immobilization.                                      calculation of the threshold not specified.
d Calculated value based on a quantitative structure-activity           f Analysis for 2-propanol reported.
  relationship between the  n-octanol/water partition coefficient of     g Test compound was Imsol A (90% 2-propanol, remainder unknown)
  a group of 19 organic chemicals and their anaesthetic potency.        h TT = toxic threshold for light reduction.
7.2.2  Insects

    The 4-h LC50 for third instar mosquito larvae  (Aedes aegypti) 
was 25 120 mg/litre water in a static test at 22 - 24 °C [143].  
The 48-h LC50 values for the fruit fly strains  Drosophila 
 melanogaster and  Drosophila simulans were between 10 200 and 13 340 
mg/litre of nutrient medium in static tests [66].  Exposure of 
 Drosophila melanogaster eggs and larvae to 7850 mg 2-propanol/litre 
of nutrient medium caused an 87% decrease in the activity of the 
non-specific enzyme alcohol dehydrogenase (EC in the 14-
day-old larvae.  At the same time, viability was decreased by 74%.  
The development of  Drosophila simulans was completely inhibited at 
the same concentration.  Gas chromatographic analysis revealed 
that, after 4 days of exposure, acetone appeared as the 2-propanol 
concentration decreased.  The appearance of acetone was associated 
with an observed decrease in enzyme activity [265].  Anderson & 
McDonald [13] also found a decrease in the specific activity of 
alcohol dehydrogenase in  Drosophila melanogaster after 1 - 4 days 
of exposure to 2-propanol.  On the other hand, they found that the 
stability and concentration of the enzyme increased.  The authors 
explained the findings as an adaptation of the fruit fly to its 

7.2.3  Plants

    The effects of 2-propanol on the rate of seed germination were 
investigated on several occasions.  Total inhibition of the 
germination of barley grains was reached after incubation for 4 
days at 18 °C on filter papers, absorbing a solution containing 
39 420 mg 2-propanol/litre water [56].  The germination of white 
amaranth  (Amaranthus albus) seeds was not affected after 5 h of 
incubation at 25 °C on filter papers moistened with a solution 
containing 36 050 mg 2-propanol/litre of water [49].  Reynolds 
[216] measured 50% inhibition of germination in lettuce  (Lactuca 
 sativa) seeds after incubation for 3 days at 30 °C on agar 
containing 2100 mg 2-propanol/litre.  At 6000 mg/litre, no 
germination at all was observed.  However, above 18 030 mg/litre, 
germination was again observed and reached a maximum of 62% at 
26 440 mg/litre.  Inhibition of the growth of hypocotyls and 
rootlets after 6 days of incubation gradually increased with 
concentration.  ED50 values were above 36 000 mg/litre. 

    In a 28-day study on cell suspensions of root sections of 
soybean,  (Glycine max), at 26 °C and a pH of 5.6, onset of growth 
was delayed for 1 and 2 weeks at 2-propanol concentrations of 
10 000 and 20 000 mg/litre of nutrient medium, respectively [67]. 


8.1  Single Exposures

8.1.1   Mortality

    Available acute mortality data are summarized in Table 9.  
Except where otherwise indicated, the vehicle was water or saline 
solution.  LD50 values for several animal species after oral 
administration vary between 4475 and 7990 mg/kg body weight.  Using 
14-day-old rats of both sexes, Kimura et al. [134] established an 
oral LD50 of 4396 mg/kg body weight for undiluted 2-propanol; this 
was not significantly different from that obtained for young male 
adults (4710 mg/kg body weight) or older male adults (5338 mg/kg 
body weight). 

8.1.2  Signs of intoxication

    Sprague-Dawley rats of both sexes, inhaling 2-propanol for 8 h 
at concentrations between 19 680 and 64 206 mg/m3, showed severe 
irritation of the mucous membranes and depression of the central 
nervous system indicated by subsequent ataxia, prostration, and 
narcosis.  These effects were concentration- and time-dependent.  
Rats surviving the narcosis recovered.  Transient paralysis of the 
hind limbs was observed at levels between 49 200 and 54 120 mg/m3.  
The rats died at and above 44 280 mg/m3, usually within 2 days, 
with females dying earlier than males.  All rats were autopsied, 
including survivors, 15 days after exposure.  At non-lethal levels, 
congestion of the liver, lung, and spleen were observed, especially 
in males.  At lethal levels, vacuolation of the liver, acute 
pneumonitis, and spleen oedema were found.  These effects were most 
pronounced in survivors.  At 51 660 mg/m3, severe cytoplasmic 
degeneration of the liver and oedema of the lung and brain occurred 
in all rats [151].  Deep narcosis occurred in rats exposed through 
inhalation to 40 mg/litre for 2 h.  Significant and lasting 
hypothermia was induced in Sprague-Dawley rats exposed for 4 h to 
vapour concentrations of 19 680 mg/m3 or more [151]. 

    Rats and mice of unknown strains, exposed orally or through 
inhalation to lethal levels of 2-propanol, showed unspecified signs 
of irritation and died through respiratory arrest while under 
narcosis, usually within 24 h following exposure.  Necropsy 
revealed oedema, haemorrhage, inflammation, and dystrophy in the 
interstitial tissues of parenchymal organs.  In the lung, 
infiltration, oedema, and thinning of the alveolar walls were 
observed [103]. 

Table 9.  Lethality of 2-propanol
Species/strain      Sex           Route of exposure  Observation   LD50          LC50     Reference     
                                                     period        (mg/kg body   (mg/m3)           
Rat                 not reported  oral               3 days        5 280         -        [157]         
Sherman rat         not reported  oral               14 days       5 480         -        [239]         
Sprague-Dawley rat  male          oral               7 days        4 710         -        [134]         
Rat                 not reported  oral               14 days       5 500         -        [103]         
Mouse               not reported  oral               14 days       4 475         -        [103]         
Rabbit              not reported  oral               3 days        5 030         -        [157]         
Rabbit              male          oral               1 day         7 990                  [190]         
Dog                 not reported  oral               3 days        4 830         -        [157]         
Wistar rat          male          intravenous        5 days        1 088         -        [247]         
H mouse             male          intravenous        5 days        1 580         -        [247]         
H mouse             female        intravenous        not reported  1 860         -        [56]          
Chinchilla rabbit   male, female  intravenous        5 days        1 184         -        [247]         
Wistar rat          male          intraperitoneal    5 days        2 830         -        [247]         
H mouse             male          intraperitoneal    5 days        4 868         -        [247]         
Syrian hamster      male          intraperitoneal    5 days        3 467         -        [247]         
Rabbit              not reported  dermal             not reported  12 870        -        [239]         
Rat                 not reported  inhalation (4 h)   14 days       -             72 600   [103]         
Sprague-Dawley rat  male          inhalation (8 h)   15 days       -             46 740   [150]         
Sprague-Dawley rat  female        inhalation (8 h)   15 days       -             55 350   [150]         
Mouse               not reported  inhalation (2 h)   14 days       -             53 000   [103]         
    The effects of 2-propanol on the mucociliary system of the 
trachea [197] and the middle ear [198] were investigated in two 
separate studies.  Groups of 20 or 24 Hartley guinea-pigs were 
exposed to 2-propanol vapour at measured concentrations of 0, 969, 
or 13 382 mg/m3 for 24 consecutive hours.  Four animals from each 
of the 3 groups were killed by decapitation at 12 h, 24 h, and 3, 
7, and 14 days after the exposure period.  A concentration-related 
deterioration of ciliary activity and mucosal degeneration were 
observed in both the trachea and in the middle ear.  At the lower 
exposure level, the effects completely reversed within 2 weeks of 
exposure, but, at the higher exposure level, they did not. 
    2-Propanol can enter the trachea and deeper lung structures by 
aspiration through the oral and nasal cavities.  Anaesthetized rats 
were made to inspire 110 or 140 mg of the compound in water, or 160 
mg of the undiluted compound.  Survivors were sacrificed 24 h later 
for lung examination.  At the lower doses, 1 out of 10 rats in each 
group died.  At the highest dose, 6 out of 10 rats died of cardiac 
or respiratory arrest.  All controls survived.  It was not reported 
whether the latter were sham-exposed or not.  The average absolute 
lung weight in the high-dose group was increased by 75% [94]. 

8.1.3  Skin, eye and respiratory tract irritation

    In primary irritation patch tests on groups of 6 rabbits and 6 
Hartley guinea-pigs, 0.5 ml of undiluted 2-propanol was applied to 
areas of clipped or abraded skin.  No irritation was observed for 
up to 48 h after a 4-h exposure [194].  Erythema and changes in 
vascular permeability did not occur when the clipped skin of 
guinea-pigs was exposed for 2 min to discs of filter paper soaked 
in undiluted 2-propanol [240]. 

    Marzulli & Ruggles [182] reported on an interlaboratory 
evaluation of the ocular irritancy of 2-propanol, according to 
Draize scores, in groups of 6 rabbits, 1 - 7 days after application 
of 0.1 ml of a 70% solution on the cornea.  One day after exposure, 
mean Draize scores were approximately 0.6 for corneal opacity, 0.3 
for iritis, 1.5 for conjunctival redness, and 1.3 for chemosis.  
The maximum total Draize score was 10.1.  In each laboratory, 
67 - 97% of the rabbits met the criteria for eye irritation, which 
decreased over time.  In another Draize test, groups of 6 - 9 New 
Zealand rabbits received doses of 70% 2-propanol at levels of 0.01, 
0.03, or 0.10 ml per eye.  Maximum total Draize scores were 21, 36, 
and 37, respectively, the maximum on the Draize scale being 110.  
Using irritation categories based on the number of days required 
for the effects to disappear, the compound was substantially 
irritating (clearing within 14 days) at the higher doses and 
moderately irritating (clearing within 7 days) at the lowest dose 

    The eye irritancy of 2-propanol was evaluated using Stauffland 
albino rabbits, each of which received 0.1 ml of undiluted propanol 
in one eye.  Eye irritation was scored according to Draize up to 21 
days after application.  The exact scores were not reported, but 
2-propanol was found to be corrosive according to the US EPA 

criteria used in 1981, implying corneal involvement and irritation 
or eye damage that persisted for more than 21 days after treatment 

    2-Propanol was tested on several occasions in  in vitro 
cytotoxicity assays and the results showed good agreement with 
those  in vivo [29, 30, 213]. 

    The potency of 2-propanol as a sensory irritant was evaluated, 
using a 50% reflex decrease in the respiratory rate of mice (RD50) 
as an index.  The mice were exposed by their heads only.  An 
exposure-related effect was found with RD50 values of 12 300 mg/m3 
for Swiss OF1 mice and 43 525 mg/m3 for Swiss Webster mice [61, 130]. 

8.2  Continuous or Repeated Exposures

    Groups of rats were exposed to 2-propanol vapour at 
concentrations of 0, 100, or 500 mg/m3 air for 5 days/week and 
4 h/day over 4 months [103].  Strain, sex, and group size were not 
given, but were presumably in accordance with CMEA standards.  No 
deaths were reported.  At the end of 4 months of exposure to 500 
mg/m3 air, growth was reduced significantly by 10% and the 
respiratory rate was increased by 22%.  The white blood cell count 
was decreased at both exposure levels in an exposure-related 
manner.  At 500 mg/m3, this was attributed to a decreased absolute 
and relative number of lymphocytes.  Decreases in hippuric acid 
excretion and in total serum protein, and an increase in blood 
acetylcholine were found at both exposure levels.  The decrease in 
total serum protein was exposure-related and could partly be 
accounted for by the observed decrease in alpha1- and alpha2-
globulins and in albumin at 500 mg/m3.  Blood glucose levels were 
decreased at 500 mg/m3.  Macroscopic and microscopic changes, 
observed at 500 mg/m3, included irritant effects on the respiratory 
system, such as thinning of the alveolar walls, perivascular 
infiltration, pneumonia, and bronchitis.  Dystrophic changes and 
perivascular cell reactions were seen in the liver.  Follicular 
hyperplasia was observed in the spleen [103]. 

    Another report described the continuous exposure of groups of 
15 rats of unknown strain and sex to 2-propanol vapour at 
concentrations of 0, 0.6, 2.5, or 20 mg/m3 air for 86 days.  The 
data were not statistically analysed.  No deaths were reported.  At 
the highest exposure level, changes in the latency period of 
unconditional reaction and an increase in the number of fluorescent 
leukocytes were found.  Effects reported at this exposure level 
included an increase in sulfobromophthalein retention and decreased 
blood levels of nucleic acids.  Microscopy only revealed adverse 
effects at 20 mg/m3 with liver dystrophy, degenerative changes in 
the cerebral cortex, and spleen hyperplasia [19]. 

    These studies [19, 103] lack a number of essential details 
concerning the protocol, the effects observed, the incidence of 
these effects, and the statistical analysis. 

    A "coefficient of accumulation" (the ratio between cumulative 
LD50 and single dose LD50) reported for repeated oral exposure to 
2-propanol was 4.0 in rats and 4.9 in mice [10]. 

    Groups of 5 white rats of each sex and of unknown strain 
received drinking-water containing 2-propanol for 27 weeks.  
Average daily intakes were 0, 600, or 2300 mg/kg body weight for 
males and 0, 1000, or 3900 mg/kg body weight for females.  Only 
males died:  2 at the lower dose and 3 at the higher dose.  It was 
reported that extensive postmortem changes prevented an accurate 
diagnosis of the cause of death.  At the end of the exposure 
period, all exposed females showed growth retardation.  Males 
showed a slight decrease in growth initially but overtook the 
controls in body weight towards the end of the exposure period.  No 
adverse effects were found on food intake, behaviour, and 
histopathology [157]. 
8.3  Neurotoxicity and Behavioural Effects

    2-Propanol passes the blood-brain barrier twice as effectively 
as ethanol (section 6.2.1).  The oral ED50 for narcosis in rabbits 
exposed to 2-propanol was 2280 mg/kg body weight, i.e., 2.5 times 
lower than that for ethanol [190].  The threshold of an acute 
effect on the CNS was observed in rats after a 4-h exposure at 1450 
mg/m3 using the method of flexor reflexes, the "summation threshold 
method" [10].  The intraperitoneal ED50 for loss of righting reflex 
in Swiss Webster mice, which was 164 mg/kg body weight, was 1.8 
times lower than that for ethanol [169].  The threshold for the 
induction of ataxia in Sprague-Dawley rats following intraperitoneal 
exposure was 1106 mg/kg body weight [171].  In 2 tilted plane 
tests, the performance of rats decreased by an average of 30 - 40% 
after oral or intraperitoneal exposure to 2000 and 1800 mg/kg body 
weight, respectively [178, 270].  On a molar basis, 2-propanol was 
2.7 times as intoxicating as ethanol [270].  When C57BL/6J or 
DBA/2J mice were exposed intraperitoneally to a single dose of 2-
propanol at 3 dose levels, the former strain showed increased 
activity in the open field test at 392 mg/kg body weight, no effect 
on activity at 785 mg/kg body weight, and narcosis at 1570 mg/kg 
body weight.  DBA/2J mice showed increased activity at the middle 
dose level and narcosis at the high dose level [243].  Wistar rats, 
inhaling 2-propanol at a concentration of 739 mg/m3 for 6 h/day, 5 
days/week, for up to 15 weeks, did not show any adverse effects in 
the open field test [224]. 

    The depressive action of 2-propanol on the central nervous 
system was related by several investigators to interactions with  
neuronal membranes  in vitro and  in vivo.  Lyon et al. [169] 
observed a high correlation between the narcotic potencies of 
aliphatic alcohols in mice and their ability to disorder brain 
synaptosomal plasma membrane  in vitro, as measured by electron 
paramagnetic resonance, which was, in turn, related to membrane 
solubility.  In Sprague-Dawley rats, no change in synaptosomal 
membrane fluidity was measured via  in vitro registration of the 
fluorescence polarization of 1,6-diphenyl-1,3,5-hexatriene, 20 h 
after a single oral dose of 3000 mg/kg body weight.  When 

2-propanol was added subsequently, a change in membrane fluidity 
was observed.  This effect was related to membrane solubility.  
The activity of synaptosomal Na+/K+-transporting 
adenosinetriphosphatase (EC was increased both  in vitro 
and  in vivo [24]. 
    Functional loss due to disruption of membrane integrity by 
2-propanol was also observed  in vitro by the blocking of the action 
potentials of sciatic nerves in the toad,  Bufo marinus [214], and 
by the inhibition of membrane-bound guanylate cyclase (EC 
in intact murine neuroblastoma N1E-115 cells [241].  It was also 
indicated by the interference of 2-propanol with the transport of 
Ca2+ ions across biological membranes, as shown,  in vitro, by the 
inhibition of Ca2+ ion-induced contractions of guinea-pig ileum 
(Yashuda et al., 1976), and,  in vivo, in rats by a decrease in 
regional brain Ca2+ ion levels, 30 min after one intraperitoneal 
dose of 2000 mg/kg body weight [221]. 
    Several neurochemical parameters were measured in the brain or 
spinal cord axon of Wistar rats, inhaling 2-propanol at a 
concentration of 739 mg/m3 air for 6 h/day, 5 days/week, over 5, 
10, 16, or 21 weeks.  In cerebellar homogenates, the activities of 
superoxide dismutase (EC and azoreductase (EC 
were decreased at weeks 16 and 21, but no effects were found on the 
activity of dihydrolipoamide dehydrogenase (EC  In 
cerebellar glial cells, the activity of acid proteinase (EC was stimulated at weeks 5 and 10, while the glutathione 
concentration was unaffected at all times.  In the spinal cord 
axon, the phosphate/cholesterol ratio of lipid was reduced by 25% 

8.4  Biochemical Effects

8.4.1  Effects on lipids in liver and blood

    Oral administration of single doses of 3000 or 6000 mg 
2-propanol/kg body weight to Wistar rats caused a reversible 
accumulation of triglycerides in the liver [21, 22, 23, 90].  At 
the 6000 mg/kg body weight dose, a slight fatty infiltration was 
observed histologically [90].  Observations that could explain this 
effect were increased hepatic uptake of palmitate [23], increased 
incorporation of palmitate into hepatic triglycerides, decreased 
hepatic palmitate oxidation, and, at a later stage of intoxication, 
interference with the synthesis and excretion of very dense 
lipoproteins [21, 22, 23]. 
    Decreased palmitate oxidation was related to the observed 
increase in the hepatic b-hydroxybutyrate/acetoacetate ratio, 
implying a decrease in the intramitochondrial NAD+/NADH ratio [21, 
23, 195].  Excess extramitochondrial reducing equivalents, 
indicated by an increased lactate/pyruvate ratio, was also observed 
 in vivo [21] and  in vitro [85].  However, all these changes in the 
redox state of the liver were very modest and therefore were not 
thought to be fully responsible for the fatty livers induced. 
    More significant seemed to be the observation that the 
incorporation of palmitate and glycerol into serum triglycerides 
and the incorporation of palmitate into serum and hepatic 
phospholipids were inhibited.  This indicates an impaired secretion 
of lipo-proteins, partly explained by the observed disturbance of 
the biosynthesis of phospholipids, and partly by the observed 
inhibition of hepatic protein synthesis [21, 22, 23].  Inhibition 
of hepatic protein synthesis, as shown by the synthesis of the 
marker enzymes ornithine decarboxylase (EC and tyrosine 
amino-transferase (EC, was observed in hepatectomized rats 
following oral exposure to 2300 mg 2-propanol/kg body weight [205]. 

    Acetone administration to rats up to a blood level comparable 
to that in 2-propanol-dosed rats only slightly increased the level 
of liver triglycerides; therefore acetone does not seem to play a 
major role in the induction of fatty liver by 2-propanol [22]. 

8.4.2  Effects on microsomal enzymes

    Oral exposure of Sprague-Dawley rats to 390 mg 2-propanol/kg 
body weight, once or on 4 subsequent days, caused a slight but 
significant increase in the hepatic cytochrome P-450 content and a 
2 - 3-fold increase in the activities of the microsomal liver 
enzymes (EC aniline hydroxylase and 7-ethoxycoumarin 
O-deethylase, 18 h after exposure [255].  Direct activation of these 
enzymes does not offer a satisfactory explanation, as it was shown 
 in vitro that 2-propanol is an inhibitor of several microsomal 
enzymes via an interaction with cytochrome P-450, which causes a 
change in the reverse Type I spectrum [8, 57, 222, 246, 254, 285].  
It was therefore concluded that, as acetone also does not appear to 
be involved in aniline hydroxylase induction  in vivo, 2-propanol 
induces one or more forms of cytochrome P-450 [255].  In young 
Sprague-Dawley rats, receiving 2-propanol once at a level of 1960 
or 3140 mg/kg body weight and sacrificed 22 - 24 h later, the 
hepatic cytochrome P-450 content increased, as well as the 
activities of several nitrosamine  N-demethylases, benzphetamine 
demethylase, ethylmorphine demethylase,  p-nitroanisole demethylase, 
and 7-ethoxycoumarin- O-deethylase.  A slight increase was observed 
in the activity of NADPH cytochrome c reductase (EC  
Acetone appeared to play a role in this induction.  From several 
lines of observations, it was concluded that the enhanced activity 
of nitrosodimethylamine  N-demethylase was due to the induction of 
specific forms of P-450 isozymes and P-450-dependent enzymes [255]. 

    In several earlier studies on rats, at comparable or higher 
oral doses, induction of microsomal liver enzymes was observed, 
including a slight induction of NADPH cytochrome c reductase, but 
no increase in hepatic cytochrome P-450 content [206, 207, 234].  
Ueng et al. [255] explained the latter observation by suggesting 
that the species of cytochrome P-450 induced must be normally 
present in low concentrations, so that a several-fold increase in 
catalytic activity could be induced without markedly increasing the 
total content of the haemoprotein. 

    Sprague-Dawley rats were also exposed by inhalation to 
2-propanol at concentrations of 490, 4920, or 19 680 mg/m3 air for 
6 days/week, 6 h/day over 2 weeks.  In the liver and kidneys, the 
contents of cytochrome P-450 and cytochrome b5 were increased as 
well as the activity of NADPH cytochrome c reductase at 4920 and 
19 680 mg/m3.  These effects were completely reversible in the 
liver of rats exposed at 19 680 mg/m3 for 2 weeks and allowed to 
recover for 4 weeks.  However, they persisted in the kidneys [290]. 

8.4.3  Other biochemical findings

    Differential effects have been observed on the glutathione 
status of the liver following exposure of rats to 2-propanol.  In 
Sprague-Dawley rats inhaling 2-propanol at a concentration of 4920 
or 19 680 mg/m3 for 6 days/week, 6 h/day, over 2 weeks, the reduced 
glutathione concentration in the liver and kidneys increased 
slightly while, at 19 680 mg/m3, the activity of glutathione 
 S-transferase (EC increased by 13% in the liver only 
[290].  The glutathione level in the liver of Wistar rats that had 
received a single oral dose of 3110 mg 2-propanol/kg body weight 
was reduced 6 h following exposure, while there was a 10% increase 
in lipid peroxidation, as indicated by the formation of diene 
conjugates [264].  A homogenate of normal or regenerating rat liver 
did not show any increase in malondialdehyde production after 
incubation with 2-propanol [6]. 

    The activity of hepatic and kidney alanine aminotransferase (EC in rats was unchanged 18 h after exposure to 1 or 4 daily 
doses of 392 mg 2-propanol/kg body weight [255] or 4 h after 
exposure to a single dose of 2300 mg/kg body weight  [205].  Liver 
damage was not observed in guinea-pigs histopathologically or by 
any increase in serum ornithine carbamoyltransferase (EC, 
24 h after receiving intraperitoneal doses of up to 1000 mg 
2-propanol/kg body weight [73]. 

    In Charles River rats, 2-propanol (785 mg/kg body weight ip) 
induced hepatic metallothionein and caused low blood zinc levels 
[244].  These changes were not prevented by adrenalectomy. 

8.5  Immunological Effects

    2-Propanol and acetone both enhanced the incorporation of 
labelled thymidine into concanavalin A-stimulated murine spleen 
cells  in vitro [210].  2-Propanol inhibited the killing of YAC-1 
tumour cells by natural killer effector cells from mouse or rat 
spleens [219].  Inhibition of the synthesis and/or the secretion 
and/or function of at least one monocyte-derived substance that 
inhibited cell proliferation was suggested as an explanation of 
these findings [210]. 
8.6  Reproduction, Embryotoxicity, and Teratogenicity

    Groups of 13 - 15 pregnant Sprague-Dawley rats were exposed to 
2-propanol for 7 h/day on gestation days 1 - 19 at measured 
concentrations of 9001, 18 327, or 23 210 mg/m3 (3659, 7450, or 

9435 ppm).  At the highest concentration, rats were completely 
narcotized at the end of the first exposures, but by the end of the 
19 days the effect was slight.  Initial exposures to 18 327 mg/m3 
(7450 ppm) caused an unsteady gait, but this was not noticeable by 
the end of 19 days of exposure.  Food consumption and maternal body 
weight gain were significantly reduced by exposure to 18 327 and 
23 210 mg/m3 (7450 and 9435 ppm).  In the group exposed to 23 210 
mg/m3 (9435 ppm):  6 out of 15 mated rats were not pregnant at 
term, which was attributed to an exposure-induced failure of 
implantation; 4 out of 9 pregnancies were totally resorbed; and 
resorptions per litter were significantly increased.  Fetal body 
weights were significantly reduced, in a concentration-related 
pattern, at all 3 concentrations.  The incidence of cervical ribs 
was significantly increased in the 23 210 mg/m3 (9435 ppm) group 
    A group of 6 female and 3 male rats (38 - 40 days old), of 
unspecified strain, received drinking-water containing 2-propanol.  
They were mated after approximately 2 months of exposure.  This 
schedule was repeated through 2 further generations.  Average daily 
intakes for the 3 generations were 1470, 1380, and 1290 mg/kg body 
weight, respectively.  The growth of the first generation was 
retarded initially, but returned to normal by the 13th week.  
Otherwise, no effects were found on growth and reproductive 
functions [159]. 

    When female hybrid rats received oral doses of 252 or 1008 mg 
2-propanol/kg body weight per day for 45 days, the length of the 
estrus cycle was increased by 23 - 24% [15].  Five female hybrid 
rats also received daily doses of 1800 mg/kg body weight for 3 
months before mating.  Together with 6 controls they were 
sacrificed on day 21 of pregnancy.  The total embryonic mortality 
rate was increased 2-fold, which was statistically significant [15]. 
    In a 6-month drinking-water study, 2-propanol was administered 
to hybrid rats of both sexes, at daily doses of 0.018, 0.18, 1.8, 
or 18 mg/kg body weight.  Mating of males with 5 - 7 females per 
group occurred after the exposure period.  When both sexes were 
exposed to 18 mg/kg body weight, the litter size was increased.  
The neonatal mortality rate was increased at 0.18 and 1.8 mg/kg, 
when females only were exposed, at 18 mg/kg body weight, when males 
only were exposed, and at the 2 highest exposure levels, when both 
sexes were exposed.  Neonates from the last group showed a dose-
related decrease in the rate of reaction to electric stimuli 
(unconditioned defence reaction), but no other effects on their 
development [15]. 

    Groups of 10 - 13 female hybrid rats received 252 or 1008 mg 
2-propanol/kg body weight from day 1 to day 20 of pregnancy.  They 
were sacrificed on day 21 of pregnancy together with 11 controls.  
Litter size was reduced at both exposure levels.  General embryonic 
toxicity was 18 and 31%, respectively (10% in controls).  At 1008 
mg/kg body weight, total embryonic mortality rate was trebled and 
10 out of 70 fetuses showed developmental anomalies compared with 

none out of 90 controls.  The anomalies found were brain damage in 
3 fetuses, kidney damage in 5 fetuses, and gastrointestinal damage 
in 2 fetuses.  The lesions were not specified further.  Data on 
maternal toxicity were not reported [15]. 
8.7  Mutagenicity

    A reverse mutation spot test with the  Salmonella typhimurium 
strains TA 98, TA 100, TA 1525, and TA 1537 was negative at 0.18 mg 
per plate, with and without metabolic activation by S9 rat liver 
    Rat bone marrow cells were examined after 4 months of exposure 
of rats to 2-propanol vapour at concentrations of 0, 1.03, or 10.2 
mg/m3 air for 4 h/day.  Statistically significant increases were 
counted in the percentage of mitotic aberrations [18].  However, 
the authors did not report the number of rats exposed, their sex, 
or strain. 

    Root tip cells of onion  (Allium cepa) exposed to 2-propanol 
showed a 2.8-fold increase in the mitotic aberration rate [230]. 

    2-Propanol did not increase sister chromatid exchange 
frequencies  in vitro in V79 Chinese hamster lung fibroblasts, with 
or without S9 mix, when tested at concentrations of 3.3, 10, 33.3, 
and 100 mmol/litre [267]. 

    A dose-related increase in the inhibition of metabolic 
cooperation in hamster V79 cells, a phenomenon believed to reflect 
carcinogenic promotion ability and not to be indicative of 
genotoxic potential, was observed by Chen et al. [53].  This may be 
due to the membrane effects of 2-propanol. 
8.8  Carcinogenicity

    Several limited carcinogenicity studies on the mouse have been 
conducted with 2-propanol, using the inhalation, dermal, and 
subcutaneous routes of exposure. 

    Groups of 3 month-old, male C3H, ABC, and C57/BL mice were 
exposed to 2-propanol vapour at a concentration of 7700 mg/m3 air 
for 3 - 7 h/day, 5 days/week, over 5 - 8 months.  The sizes of the 
experimental and control groups were not reported.  The occurrence 
of lung tumours was examined microscopically in mice that had 
survived until killed at the age of 8 months (36 exposed and 69 
control C3H mice, 49 exposed and 120 control ABC mice), or 12 
months (47 exposed and 52 control C57/BL mice) and showed 
macroscopic lesions.  The mice were not examined for the occurrence 
of sinus tumours as occurred in workers engaged in the manufacture 
of 2-propanol (section 9.2.1).  No excess of lung tumours was 
observed [276]. 

    2-Propanol was painted on the clipped backs of 30 Rockland 
mice, 3 times/week for 1 year.  Sex, dose, and observation period 
were not specified.  Skin papillomas developed in 3 control mice, 

one of which also had a skin carcinoma, while there was no response 
in treated mice (Weil, C.S., written communication to US NIOSH [257]). 

    Groups of 3-month-old male C3H, ABC, and C57/BL mice received 
20 mg undiluted 2-propanol subcutaneously once a week, for 
20 - 40 weeks.  The sizes of the treated and untreated control 
groups were not reported.  Surviving mice that showed macroscopic 
lung lesions were examined microscopically for lung tumours.  No 
excess of lung tumours was observed.  Lung tumour incidence in the 
control group was high [276]. 

    Doses of 20 mg undiluted 2-propanol were injected 
subcutaneously in 40 C3H mice, once a week, over a period of 20 
weeks.  Controls were untreated.  The occurrence of lung tumours 
was examined in mice that survived until killed 5 months after the 
first injection (22 exposed and 33 control mice).  No excess of 
lung tumours was observed (Weil, C.S., written communication to US  
NIOSH [257]). 

    In these studies, only lung tumours and, in the case of dermal 
exposure, skin tumours were investigated.  Moreover, the exposure 
periods, where given, were too short to allow for tumour induction.  
Experimental details including size of experimental and control 
groups, sex ratio, and observation periods were not quoted for some 
of the studies.  Because of these shortcomings, the studies are 
inadequate for the assessment of carcinogenic potential. 

8.9  Factors Modifying Toxicity

    As a result of the induction of specific isozymes of cytochrome 
P-450 (section 8.4.2) by 2-propanol and/or acetone, the 
hepatotoxicity of carbon tetrachloride, 1,1,2-trichloroethane, 
chloroform (CHCl3), trichloroethylene, and dimethylnitrosamine in 
rodents is enhanced [60, 165, 234, 252, 253, 254].  The metabolic 
activation of  n-hexane by liver and kidney microsomes is also 
increased by 2-propanol pretreatment [290]. 


9.1  General Population Exposure

9.1.1  Poisoning incidents
    The subject of non-beverage alcohol use has already been 
addressed in section 5.2.2.  The clinical literature has been 
reviewed [149, 176, 245, 163].  A brief summary of cases of 
intoxication and major symptoms is presented in Table 10. 

Table 10.  Acute intoxications by 2-propanola
No. of  No. of      Observationsb                 Reference
cases   alcoholics  1    2   3   4    5   6   7

57      46          +57                           [11]
5       2           +5   +5  +4  +2   +4  +2      [4]
1c      0           -    +   +   +    +   +   +   [186]
3       3           -    +3  -   +2   +2  +1  +2  [170]
1       0           -    +   +   +    +   +   -   [191]
2       0           -    +2  +2       +2      +1  [149]
1       1           -    +   +   -    +   -   +   [245]
17      14          -    +2  +3  +10  -   -       [131]
1                   -    +   +   +            -   [88]
1       1           -    +   +        +           [135]
1c      0           -    +   +   -    +   -   -   [266]
1       1           -    +   +   -        -   +   [261]
1       0           -    +                +       [75]
1       0           -    +       -        -   -   [220]
2       1           -    -   +   +2   -   +2  +1  [5]
1       1           -    -   -   +    -   +   -   [128]
1       1           -    -   -   +        +       [108]


1c      -           -    +   +   +    +   +       [228]
1c      -           -    +   +   +    -   -   +   [160]
1c      -           -    +       +        +       [91]
1c      -           -    +       +    -   -   +   [172]
1c      -           -    +                        [181]
1c      -           -    +   +   +    +   -   +   [16]
a +N = observed in N cases; - = not observed; no sign = not 
b 1 = death; 2 = coma; 3 = hypotension, meaning < 100 mm Hg systolic
  pressure and/or < 60 mmHg diastolic pressure; 4 = tachycardia, 
  meaning > 100 beats per min; 5 = hypothermia, meaning < 36.5 °C;
  6 = gastritis, characterized by nausea, vomiting, abdominal pain;
  and/or gastric haemorrhage; 7 = elevated blood glucose, meaning
  > 1500 mg/litre.
c Child below 2.5 years of age.

    Intoxications have been reported after oral ingestion (Table 
10), rectal administration [59], and inhalation by children who 
have been sponged for several hours with 2-propanol preparations 
for fever reduction (Table 10).  Skin absorption in 2-propanol 
sponging has been deemed insignificant [e.g., 149, 176].  However, 
a case report on a child with an almost lethal blood level of 
2-propanol after sponge bathing for fever reduction, and 
questionable ingestion, suggested to the authors that the 
importance of dermal absorption, compared with inhalation, should 
not be underestimated [181]. 

    2-Propanol depresses the central nervous system.  At comparable 
doses, 2-propanol is thought to be approximately twice as active as 
ethanol in this respect with a longer duration of the coma due to 
slower metabolism and to the contribution of acetone to the 
depression of the central nervous system [149, 163, 176, 245].  As 
with ethanol, excessive intoxication with 2-propanol causes 
unconsciousness, usually, but not always ending in a deep coma [5, 
59, 108, 128]; death may follow due to respiratory depression [4].  
In most cases, decreased or absent reflexes are reported.  Pupil 
size is variable, but most often miotic [16, 88, 149, 220, 228, 
266].  Early gastrointestinal problems and hypothermia frequently 
occur.  Cardiovascular effects include severe hypotension, shock 
[4, 266], and even cardiac arrest [176, 266].  Tachycardia is found 
as a secondary effect.  Other possible compound-related effects are 
hyperglycaemia, elevated protein levels in cerebrospinal fluid [5, 
170, 266], and atelectasis [191, 220].  Lung congestion was 
observed in fatal cases [4, 11]. 
    In cases of 2-propanol intoxication, hypotension can be a grave 
prognostic sign [4], which some authors suggest requires immediate 
action by gastric lavage, haemodialysis [5, 22, 88, 135, 176], or 
peritoneal dialysis [75, 186, 245].  Following treatment, recovery 
is usually complete, unless the hypotension is severe and persistent.  
In such cases, renal injury and death may occur [4, 128]. 
    Acetone can be detected in the blood, urine, and breath.  
Because other ketone bodies are not found in significant quantities, 
early acidosis does not usually occur, serum bicarbonate, anion 
gap, and blood pH remaining normal.  Sometimes, a mild metabolic 
acidosis and anion gap may develop as a result of lactic acid 
accumulation.  Acetonaemia and/or acetonuria without metabolic 
acidosis and with normal or slightly elevated blood glucose levels 
differentiate 2-propanol poisoning from diabetic ketoacidosis and 
poisoning by other alcohols [16, 163, 176].  In addition, a 
significant osmolality gap may be observed [16, 261]. 
    None of the biochemical findings could be related to blood 
levels of 2-propanol or acetone.  2-Propanol levels, measured at 
different times after exposure, varied between undetectable 
concentrations and 5600 mg/litre [176].  Acetone levels varied 
between undetectable concentrations and 18 780 mg/litre [75].  

Alexander et al. [11] suggested that combined levels of 2-propanol 
and acetone may allow greater accuracy in predicting the clinical 
course of the condition of a patient. 

    Adults have been reported to survive ingestion of 700 ml of 
2-propanol [88] and to die after ingestion of 400 ml of 2-propanol 
[4].  The lowest dose reported to be life-threatening was in an 
18-month-old child who ingested approximately 170 ml of 2-propanol 
9.1.2  Controlled exposures

    No adverse effects were observed in groups of 8 healthy male 
volunteers (24 - 57 years of age) who drank a daily dose of 2.6 or 
6.4 mg 2-propanol/kg body weight in diluted syrup for 6 weeks.  
Investigations included haematology, blood chemistry, urinalysis, 
and ophthalmoscopy [283]. 

    Another group of 10 healthy male volunteers (age not stated) 
was exposed to 2-propanol vapour at nominal concentrations of 490, 
980, or 1970 mg/m3 air for 3 - 5 min.  After each exposure, the 
participants were asked to classify the effects of the vapour on 
the eyes, nose, and throat.  The volunteers judged irritation to be 
"mild" at 980 mg/m3 and "not severe" at 1970 mg/m3.  They also 
judged 490 mg/m3 to be "satisfactory" for their own 8-h 
occupational exposure [192].  The validity of these results is 
doubtful, for various reasons including the subjective criteria 
used, the lack of control exposures, and the unreliability of the 
exposure levels. 

9.1.3  Skin irritation; sensitization

    No skin irritation was observed in 6 human volunteers when 0.5 
ml of undiluted 2-propanol was applied to a 4 cm square area on the 
back and evaluated after 4 h, 24 h and 48 h [194].  Closed patch 
tests with 10-min applications of 0.1 - 0.3 ml undiluted 2-propanol 
on the dry skin of 10 healthy volunteers and 12 persons receiving 
disulfiram therapy for the treatment of chronic alcoholism did not 
result in any reaction.  After immersion of the skin in tepid water 
for 10 min, a transient erythema rapidly appeared on the site of 
application in 19 subjects [105]. 

    Skin irritation was also reported in a total of 6 premature 
infants with a gestational age of less than 27 weeks.  They were 
exposed via swabs used for conduction in ECG recording or by the 
application of 2-propanol on the umbilical area with subsequent 
soaking of the diaper.  Erythema and second or third degree burns 
or blisters were observed in areas of prolonged contact with 
2-propanol.  Hypoperfusion of the skin was suggested to be a 
contributing factor [226, 277]. 

    In 1968, Wasilewski [272] reported a case of alleged allergic 
contact dermatitis following skin disinfection with a 70% 
2-propanol swab.  The patient was treated for allergic rhinitis.  
Patch tests were positive for 2-propanol.  However, controls were 

not tested and there was no information on the purity of the 
alcohol.  This report was followed by several others concerning a 
total of 8 persons who showed dermatitis after contact with medi-
swabs containing 2-propanol.  Patch testing revealed that another 
volatile agent, presumably propylene oxide, caused the effect [174, 
124, 217].  Only one of these 8 persons was also hypersensitive to 
2-propanol of unknown purity [124]. 

    Itching eczematous lesions developed in a laboratory worker, in 
a company manufacturing hair cosmetics, in patch tests with 
chemically pure 2-propanol solutions (2.5 - 99.7% by volume).  This 
person also reacted to 1-propanol, 1-butanol, 2-butanol, and 
formaldehyde, but not to ethanol and methanol.  Controls were not 
tested [167].  Two out of 4 confirmed cases of hypersensitivity to 
primary alcohols were also found to be hypersensitive to secondary 
alcohols.  Both cases had a history of contact allergies.  
Recurrent exposures to 2-propanol and/or other alcohols occurred 
through consumption of alcoholic beverages, pre-injection 
disinfection, via a hair lotion in one case and occupationally in 
the other case. Patch tests were positive for pure undiluted 
2-propanol and 2-butanol.  Twenty controls did not show any 
reactions to secondary alcohols [86, 87].  The mechanism of alcohol 
hypersensitivity is not clear.  Fregert et al. [87] pointed out 
that it is difficult to understand how alcohols can act as haptens. 
9.2  Occupational Exposure

9.2.1  Epidemiology studies

    A retrospective cohort study was reported among 182 workers at 
a plant, in the USA, manufacturing 2-propanol by the strong acid 
process over the period 1928 - 50.  In a subgroup of 71 men, who 
had been employed for more than 5 years, 7 cases of cancer were 
observed:  4 cancers of the paranasal sinuses, 1 lung carcinoma, 1 
laryngeal carcinoma, and 1 laryngeal papilloma.  The minimum 
latency period was 6 years [276].  According to USA vital 
statistics for 1948, 0.0014 paranasal sinus cancers would have been 
expected for the total cohort [286]. 

    Two cases of paranasal sinus cancer and 2 cases of laryngeal 
cancer were reported in 1966 in a cohort of 779 workers in a 
similar plant in the USA that had been in operation since 1927.  
The minimum latency period was 10 years.  The age- and sex-adjusted 
incidence of sinus and laryngeal cancer in this group was 21 times 
higher than expected [119]. 

    Another retrospective cohort study was undertaken among 262 men 
who had worked for at least one year in a 2-propanol-manufacturing 
plant in the United Kingdom using the strong acid procedure over 
the period 1949 - 76.  There were more than 4000 person-years at 
risk.  No person was lost to follow-up, which was over an average 
of 15.5 years.  The mortality rates due to all causes and due to 
neoplasms were not significantly higher than expected according to 
national vital statistics.  One person died from nasal cancer 

against 0.02 expected.  Other significant findings were 2 "kidney 
and adrenal malignancies" and 2 cancers of "the brain and the 
central nervous system" [9]. 
    A fourth retrospective cohort study was conducted over the 
years 1966 - 78 among 433 workers in a 2-propanol manufacturing 
plant, in the USA, who were exposed for at least 3 months during 
the period 1941 - 65.  The strong acid process used in 1941 had 
been gradually changed to the weak acid process by 1965.  More than 
11 000 person-years were at risk.  The mortality rate due to all 
causes was lower than expected on the basis of state vital 
statistics.  No excess mortality due to all cancers was observed, 
but the incidence of buccal and pharyngeal cancer was 4 times 
higher than expected (2 versus 0.5).  There was a slight excess of 
lung cancer (7 versus 5.94) [79]. 
    These cohort studies collectively suggest a cancer hazard 
related to the strong acid manufacturing process.  The excess in 
respiratory cancers was initially attributed to isopropyl oils 
[119, 276].  However, the experimental basis for this assumption is 
weak (section 8.8) and more recently diisopropyl sulfate, an 
intermediate produced in the strong acid process, has been proposed 
as a more likely causative agent.  The concentration of this 
chemical is high in the strong acid process and low in the weak 
acid process [79, 286]. 
    Two small case-control studies were conducted in the USA:  one 
to consider the risk of lymphocytic leukaemia associated with 24 
solvents among rubber industry workers [52], and the other to 
consider the risk of brain gliomas associated with exposure 
conditions during work at a chemical plant [155].  Although there 
was no evidence of an association between exposure to 2-propanol 
and the incidence of gliomas or lymphocytic leukaemia, the small 
number of subjects and multiple exposures mean that no conclusions 
can be drawn from these studies. 

9.2.2  Interacting agents

    Fourteen out of 43 workers in a 2-propanol-packaging plant 
became ill when carbon tetrachloride was used for cleaning 
equipment.  The incidence and the severity of the effects increased 
where exposure to carbon tetrachloride was the highest, and where, 
on another occasion, the mean concentration of 2-propanol in air 
was also highest, i.e., 1010 mg/m3.  In 4 cases, renal failure or 
hepatitis developed [83].  Another similar incident was reported in 
a colour printing factory, 17 workers had abnormal liver function 
and 3 developed acute hepatitis following combined exposure to 
carbon tetrachloride and 2-propanol [71].  These reports suggest 
potentiation of the toxicity of carbon tetrachloride by 2-propanol, 
which was also found in experimental animals (section 8.9). 

    Some shaving lotions containing 2-propanol and other ingredients 
(e.g., menthol, camphor, methyl salicylate, naphthalene) have been 
reported to produce central stimulation with motor restlessness, 
extreme apprehension, hallucinations, and general disorientation 
[89, 238].  

10.1  Evaluation of Human Health Risks

10.1.1  Exposure

    Exposure of human beings to 2-propanol may occur through 
inhalation during manufacture, processing, and both occupational 
and household use.  Average concentrations of up to 35 mg/m3 in the 
ambient urban air and up to 500 mg/m3 in the occupational 
environment have been measured.  Concentrations between 0.2 and 325 
mg/litre have been found in non-alcoholic beverages, and between 50 
and 3000 mg/kg in foods (section 5). 

    Exposure of the general public to a potentially lethal level 
may result from accidental or intentional ingestion and children 
may be exposed when sponged with 2-propanol preparations (rubbing 
alcohol) (sections 6 and 9). 

10.1.2  Health effects

    2-Propanol is rapidly absorbed after inhalation or ingestion 
and distributed throughout the body as such, sulfated, or as its 
metabolite, acetone (section 6).  The possibility of dermal 
absorption should not be neglected. 

    The acute toxicity of 2-propanol for animals is low (based on 
lethality estimates) whether exposure occurs via the dermal, oral, 
or respiratory route. 

    In man, the most likely acute effects of exposure to high 
levels of 2-propanol by ingestion or inhalation are alcoholic 
intoxication and narcosis.  The results of animal studies indicate 
that 2-propanol is approximately twice as intoxicating as ethanol 
with an oral ED50 for rabbits of 2280 mg/kg and a threshold for 
ataxia in rats of 1106 mg/kg intraperitoneally (section 8.3).  Oral 
LD50 values in various species vary between 4475 and 7990 mg/kg and 
inhalation LC50 values between 50 000 and 70 000 mg/m3 (section 

    Because ethanol retards the elimination of 2-propanol and is 
also a CNS depressant, interaction between ethanol and propanol may 
be expected to increase the CNS effects of either agent.  The 
majority of acute intoxication cases involved ingestion by known 
alcoholics.  Febrile children have experienced life-threatening 
intoxications when treated by skin sponging with 2-propanol. In 
these cases, skin absorption may also be an important route of 
exposure in addition to inhalation (section 9.1.1). 
    Exposure-effect data on human beings in an acute overexposure 
situation are scarce and show great variation.  The major effects 
are gastritis, depression of the central nervous system with 
hypothermia and respiratory depression, and hypotension (section 
    In rabbits, 2-propanol did not irritate the skin but did 
irritate the eyes when 0.1 ml undiluted compound was applied 
(section 8.1.3).  Care is required in the use of 2-propanol as a 
disinfectant on premature babies as it may cause severe skin 
irritation following prolonged contact. 
    No adequate animal studies are available to make an evaluation 
of the human health risks associated with repeated exposure to 
2-propanol.  However, 2 studies in rats with inhalation (500 mg/m3, 
4 h/day, 5 days per week, for 4 months) or oral (600 - 3900 mg/kg 
in drinking-water) exposure suggest that exposure to 2-propanol at 
some of the very high occupational exposures reported should be 
avoided (section 8.2). 
    2-Propanol administered in the drinking-water has been tested 
for reproductive effects in a number of studies with conflicting 
results.  In one study, impaired neonatal survival was reported 
after 6 months exposure of female rats to 0.18 mg/kg per day.  In a 
multi-generation study there were no adverse effects at drinking-
water doses as high as 1470 mg/kg per day.  In a teratology study, 
drinking-water doses of 252 and 1008 mg/kg per day produced 
developmental toxicity, but this was not related to maternal 
toxicity.  Inhalation exposure of pregnant rats to 2-propanol 
provided a LOEL of 18 327 mg/m3 (7450 ppm) and a NOEL of 9001 mg/m3 
(3659 ppm) for maternal toxicity.  In the same study, 9001 mg/m3 
(3659 ppm) was a LOEL for developmental toxicity, with no 
demonstration of a NOEL (section 8.6).  These concentrations are 
higher than those likely to be encountered under conditions of 
human exposure. 
    2-Propanol was negative in a bacterial spot test and in a test 
for sister chromatid exchange in mammalian cells  in vitro.  It 
induced mitotic aberrations in the bone marrow of rats.  Although 
these findings suggest that the substance has no genotoxic 
potential, no adequate assessment of mutagenicity can be made on 
the basis of the limited data available.  An  in vitro test said to 
predict promotional activity was negative (section 8.7). 
    The data available are inadequate to assess the carcinogenicity 
of 2-propanol in experimental animals (section 8.8).  There are no 
data to assess the carcinogenicity of 2-propanol itself in human 
beings.  There are adequate data to indicate that the strong acid 
process for the production of 2-propanol is causally associated 
with the induction of paranasal sinus cancer in human beings, 
probably due to exposure to the intermediate, di-2-propyl sulfate, 
an alkylating agent and not to 2-propanol itself (section 9.2.1). 

    2-Propanol is shown to potentiate the hepatic toxicity of 
halocarbons, such as carbon tetrachloride.  Therefore simultaneous 
exposure to 2-propanol and halocarbons should be avoided (section 

    The Task Group considers it unlikely that 2-propanol will pose 
a serious health risk to the general population under exposure 
conditions likely to be encountered. 
10.2  Evaluation of Effects on the Environment

    By reacting with hydroxyl radicals and through rain-out, 
2-propanol will disappear rapidly from the atmosphere, with a 
residence time of less than 2.5 days (section 4.2).  Hydrolysis and 
photolysis are not important in the removal of 2-propanol from 
water and soil but removal occurs quite rapidly by aerobic and 
anaerobic biodegradation, especially after adaptation of initially 
seeded microorganisms (section 4.3.1).  Adsorption of 2-propanol on 
soil particles is poor but it should be mobile in soil and it has 
been shown to increase the permeability of soil to some aromatic 
hydrocarbons.  In view of the physical properties of 2-propanol, 
its potential for bioaccumulation is low (section 4.3.2). 

    Toxicity in aquatic organisms was observed at levels ranging 
from 104 mg/litre for one protozoan to over 50 000 mg/litre for 
Tubifex worms.  Insects and plant seeds were only affected at 
concentrations above 2000 mg/litre (section 7). 

    On the basis of these data, it can be concluded that, except in 
cases of accident and inappropriate disposal, 2-propanol does not 
present a risk to naturally occurring organisms at concentrations 
that usually occur in the environment. 

1.  2-Propanol has not shown mutagenic potential in the small number 
    of assays performed.  A full array of modern genotoxicity tests 
    should be completed. 

2.  Several studies of the carcinogenic activity of 2-propanol have 
    been published but all are seriously flawed and cannot be used 
    to evaluate the potential carcinogenicity of 2-propanol.  The 
    desirability of a carcinogenesis bioassay of 2-propanol should 
    be considered based on the outcome of genotoxicity tests. 

3.  Inhalation exposure to overtly toxic concentrations of 
    2-propanol produced reproductive and developmental toxicity.  
    Additionally, the data available from drinking-water studies 
    are conflicting.  In view of the potential for environmental 
    and drinking-water contamination, reproductive and 
    developmental toxicity should be conducted using oral dosing. 

4.  Epidemiological studies including precise exposure data would 
    assist in an assessment of the occupational hazards from 


    An evaluation of the carcinogenicity of 2-Propanol by the 
International Agency for Research on Cancera was reported as 

    "A. Evidence for carcinogenicity to humans  (sufficient for the 
     manufacture of isopropyl alcohol by the strong-acid process; 
     inadequate for isopropyl alcohol and isopropyl oils). 

    An increased incidence of cancer of the paranasal sinuses was 
    observed in workers at factories where isopropyl alcohol was 
    manufactured by the strong-acid process.  The risk for 
    laryngeal cancer may also have been elevated in these workers.  
    It is unclear whether the cancer risk is due to the presence of 
    diisopropyl sulfate, which is an intermediate in the process, 
    to isopropyl oils, which are formed as by-products, or to other 
    factors, such as sulfuric acid.  Epidemiological data 
    concerning the manufacture of isopropyl alcohol by the weak-
    acid process are insufficient for an evaluation of 

    "B. Evidence for carcinogenicity to animals  (inadequate for 
     isopropyl alcohol and isopropyl oils). 

    Isopropyl oils, formed during the manufacture of isopropyl 
    alcohol by both the strong-acid and weak-acid processes, were 
    tested inadequately in mice by inhalation, skin application and 
    subcutaneous administration.  Isopropyl oils formed during the 
    strong-acid process were also tested inadequately in dogs by 
    inhalation and instillation into the sinuses. 

    The available data on isopropyl alcohol were inadequate for 

    "C. Other relevant data 

    No data were available to the Working Group."
a International Agency for Research on Cancer,  Overall Evaluations 
   of Carcinogenicity: An updating of IARC Monographs volumes 1 to 
   42.  Lyon, France, 1987 (IARC Monographs on the Evaluation of 
  Carcinogenic Risks to Humans, Supplement 7) 


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      chromatography.  Anal. Chem., 56: 244-247. 

1.  Identité, propriétés physiques et chimiques, méthodes d'analyse

    Le propanol-2 est un liquide incolore, très inflammable dont 
l'odeur rappelle celle d'un mélange d'éthanol et d'acétone.  Il est 
entièrement miscible à l'eau, à l'éthanol, à l'acétone, au 
chloroforme et au benzène.  Il existe des méthodes d'analyse pour 
la recherche du propanol-2 dans divers milieux (air, eau, sang, 
sérum et urine), avec des limites de détection dans l'air, l'eau et 
le sang respectivement égales à 2 x 10-5 mg/m3, 0,04 mg/litre et 1 
mg/litre.  La chromatographie en phase gazeuse (essentiellement 
avec détection par ionisation de flamme) ainsi que l'électrophorèse 
sur papier et la spectrométrie de mobilité ionique par 
photoionisation permettent de doser le propanol-2 dans divers 

2.  Sources d'exposition humaine et environnementale

    On estime qu'en 1975, la production mondiale de propanol-2 
dépassait 1100 kilotonnes, la capacité mondiale de production étant 
supérieure à 2000 kilotonnes en 1984.  Le propanol-2 est couramment 
produit à partir du propène.  Les procédés antérieurs de 
fabrication qui reposaient sur l'utilisation d'acides forts ou 
d'acides faibles, et donnaient naissance à des produits 
intermédiaires et à des sous-produits potentiellement dangereux, 
sont désormais largement supplantés par le procédé d'hydratation 
catalytique.  On peut également procéder par réduction catalytique 
de l'acétone. 

    Le propanol-2 est un produit du métabolisme de divers micro- 

    Il a de nombreuses applications comme solvant et il entre dans 
la composition de différents produits ménagers et produits de soins 
personnels, sous forme d'aérosols et d'excipients pour produits 
pharmaceutiques à usage externe et pour cosmétiques.  Le propanol-2 
est également utilisé pour la production de l'acétone et autres 
produits chimiques, comme agent de dégivrage, comme conservateur et 
il entre dans la composition des concentrés pour le nettoyage des 
pare-brise et de certains aromatisants alimentaires. 

    Le propanol-2 peut pénétrer dans l'atmosphère, dans l'eau et 
dans le sol lors du rejet de déchets et on en a trouvé dans l'air 
et dans les eaux de lessivage de décharges mal protégées.  Présent 
dans les gaz et eaux résiduaires industriels, on peut l'en éliminer 
par oxydation biologique ou osmose inverse.  Il peut être dissipé 
dans l'atmosphère lors de l'utilisation de produits de consommation 
qui en contiennent. 

3.  Transport et distribution dans l'environnement

    C'est principalement lors d'opérations telles que la 
production, la transformation, le stockage, le transport, 
l'utilisation et le rejet de déchets que le propanol-2 pénètre dans 

l'environnement atmosphérique.  Il peut être également déchargé 
dans le sol et l'eau.  Il est difficile d'évaluer la part qui 
revient à chaque compartiment du milieu.  Toutefois on estimait en 
1976 que plus de 50 % du propanol-2 produit finissait par être 
libéré dans l'atmosphère. 

    Le propanol-2 est rapidement éliminé de l'atmosphère par 
réaction sur les radicaux hydroxyles et entraînement par les 
précipitations.  Ce sont ces dernières qui sont responsables du 
transport de ce composé de l'atmosphère dans le sol ou l'eau.  Une 
fois dans le sol, il doit y être très mobile et augmente la 
perméabilité du sol à certains hydrocarbures aromatiques.  Le 
propanol-2 est facilement biodégradable par voie aérobie ou 

    Comme il est biodégradable et complètement miscible à l'eau, 
avec un coefficient de partition octanol/eau logarithmique de 0,14 
et un facteur de bioconcentration de 0,5, il est peu probable qu'il 
donne lieu à une bioaccumulation. 
4.  Niveaux dans l'environnement et exposition humaine

    L'exposition de la population en général peut se produire par 
ingestion accidentelle ou volontaire, par absorption de nourriture 
contenant du propanol-2 d'origine naturelle, ou sous forme 
d'aromatisant volatil ou de résidus de solvant, ou encore par 
inhalation lors de l'utilisation de produits qui en contiennent.  
On en a trouvé aux concentrations de 0,2 à 325 mg/litre dans des 
boissons non alcoolisées et aux concentrations de 50 à 3000 mg/kg 
dans des denrées alimentaires pour la production desquelles on 
l'avait utilisé comme solvant.  L'exposition de la population en 
général par inhalation de l'air ambiant est faible, du fait de 
l'élimination et de la dégradation rapides de ce produit.  En 
procédant à des contrôles en divers lieux et, en particulier, dans 
des sites urbains, on a obtenu des concentrations moyennes 
pondérées par rapport au temps allant jusqu'à 35 mg/m3. 

    Les travailleurs peuvent être exposés au propanol-2 au cours de 
la production du composé lui-même, lors de la fabrication de 
l'acétone ou d'autres dérivés et également lorsqu'on utilise ce 
produit comme solvant.  Aux Etats-Unis, une enquête (National 
Occupational Exposure Survey) effectuée en 1980-83 a montré que 
plus de 1,8 million de travailleurs pouvaient être exposés.  On a 
mesuré sur les lieux de travail des concentrations atteignant 1350 
mg/m3 avec des moyennes pondérées par rapport au temps allant 
jusqu'á 500 mg/m3. 
5.  Cinétique et métabolisme

    Le propanol-2 est rapidement absorbé et se répartit dans tout 
l'organisme par inhalation et ingestion.  A forte dose, 
l'absorption dans les voies digestives est retardée.  Les taux 
sanguins de propanol-2 (décelables lorsqu'il y a ingestion 
simultanée d'éthanol) ou de son métabolite, l'acétone, sont 
corrélés avec l'intensité de l'exposition.  Des volontaires qui 

avaient ingéré une dose de 3,75 mg/kg de propanol-2 (avec 1200 mg 
d'éthanol/kg) dans du jus d'orange, présentaient une concentration 
sanguine maximale de propanol-2 libre de 0,8 ± 0,3 mg/litre, et de  
2,3 ± 1,4 mg/litre après incubation en présence d'arylsulfatase, ce 
qui témoigne d'une sulfatation.  Chez les ouvriers exposés à des 
vapeurs de propanol-2 (8 - 647 mg/m3), on a observé des 
concentrations de 3 - 270 mg/m3 dans l'air alvéolaire, mais dans ce 
cas, c'est de l'acétone et non du propanol-2 que l'on a trouvé dans 
le sang et les urines.  Chez des animaux de laboratoire exposés au 
propanol-2, on a retrouvé celui-ci non seulement dans le sang mais 
également dans le liquide céphalo-rachidien, dans le foie, les 
reins et le cerveau.  Le propanol-2 traverse la barrière 
hémoméningée deux fois plus facilement que l'éthanol.  Le propanol-
2 est excrété en partie tel quel et en partie sous forme d'acétone, 
essentiellement au niveau des poumons mais également dans la salive 
et le suc gastrique.  Il peut y avoir réabsorption après excrétion 
par ces deux dernières voies.  La métabolisation en acétone en 
présence d'alcool-déshydrogénase (ADH) hépatique est assez lente, 
du fait que l'ADH a une moindre affinité pour le propanol-2 que 
pour l'éthanol.   In vitro, l'activité de l'ADH humaine vis-à-vis du 
propanol-2 correspond à 9 - 10 % de l'activité de cette enzyme 
lorsque le substrat est de l'éthanol.  Les oxydases microsomiques 
du foie de rat sont également capables d'oxyder le propanol-2 
 in vitro.  Chez l'homme, l'acétone est excrétée telle quelle, 
essentiellement au niveau des poumons et en quantité minime au 
niveau des reins.  Plus l'exposition au propanol-2 se prolonge, 
plus la concentration d'acétone dans l'air alvéolaire, dans le sang 
et dans les urines est élevée.  Le propanol-2 et l'acétone sont 
éliminés de l'organisme selon une cinétique du premier ordre et 
leur demi-vie  chez l'homme est de 2,5 - 6,4 heures et 22 heures, 
6.  Effets sur les êtres vivants dans leur milieu naturel

    Le propanol-2 est peu toxique pour la faune et la flore 
aquatiques, les insectes et les plantes.  Son seuil d'inhibition de 
la multiplication cellulaire, mesuré chez une espèce sensible de 
protozoaire, varie de 104 à 4930 mg/litre selon les conditions 
expérimentales.  Si l'on s'élève dans l'arbre phylogénétique, on 
constate que diverses espèces de crustacés, notamment  Daphnia 
 magna, présentent des CE50 allant de 2285 à 9714 mg/litre.  Pour 
des poissons d'eau douce, on a obtenu des CL50 à 96 heures allant 
de 4200 à 11 130 mg/litre.  Chez la drosophile, les CL50 vont de 
10 200 à 13 340 mg/litre de milieu nutritif.  Pour le troisième 
stade larvaire du moustique  Aedes aegypti, on a obtenu, lors d'une 
épreuve statique de 4 heures, des valeurs de la CL50 allant de 25 à 
120 mg/litre. 
    L'exposition de végétaux à du propanol-2 à des concentrations 
comprises entre 2100 mg/litre et plus de 36 000 mg/litre, a 
provoqué toute une gamme d'effets allant de l'absence totale 
d'anomalies à une inhibition complète de la germination. 

7.  Effets sur les animaux d'expérience et les systèmes d'épreuves 
 in vitro

    A en juger d'après la mortalité qu'il provoque, le propanol-2 
présente une faible toxicité aiguë pour les mammifères, que 
l'exposition ait lieu par voie orale, percutanée ou respiratoire.  
Chez plusieurs espèces animales on a obtenu, après administration 
par voie orale, des valeurs de la DL50 allant de 4475 à 7990 mg par 
kg de poids corporel; la CL50 pour une inhalation de 8 heures 
allait de 46 000 à 56 000 mg/m3 d'air chez le rat.  A ces doses 
mortelles, les rats présentaient une forte irritation des muqueuses 
et une grave dépression du système nerveux central.  La mort est 
survenue par arrêt cardiaque ou respiratoire.  Entre autres lésions 
histopathologiques, on notait une congestion et un oedème du poumon 
ainsi qu' une dégénérescence des hépatocytes. 

    Administré en dose unique par voie orale à des rats à raison de 
3000 ou 6000 mg par kg de poids corporel, le propanol-2 a provoqué 
une accumulation réversible de triglycérides dans le foie.  On a 
également observé chez ces rats une induction des enzymes 
microsomiques à la dose de 390 mg/kg. 
    Non dilué, le propanol-2 n'est pas irritant en applications de 
4 heures sur la peau, intacte ou abrasée, de lapins tondus.  
Toutefois, en instillations oculaires de 0,1 ml, le propanol-2 non 
dilué a provoqué une irritation chez le lapin.  De fortes 
concentrations de vapeurs de propanol-2 ont provoqué une irritation 
respiratoire chez la souris et l'on a noté une réduction de 50 % du 
rythme respiratoire à des concentrations allant de 12 300 à 43 525 
mg/m3 d'air. 

    Les études conscrées aux effets  sur l'animal d'exposition 
répétées  au propanol-2 sont plutôt limitées.  Après inhalation par 
des rats de 500 mg/m3 de propanol-2, cinq jours par semaine et 
quatre heures par jour pendant quatre mois, on a noté une 
irritation des voies respiratoires, des anomalies haématologiques 
et des altérations histopathologiques au niveau du foie et de la 
rate.  Un autre groupe expérimental composé de cinq rats de chaque 
sexe a reçu pendant 27 semaines du propanol-2 dans son eau de 
boisson.  En comparant les animaux qui recevaient environ 600 ou 
2300 mg/kg par jour (mâles) et 1000 ou 3900 mg/kg par jour 
(femelles) de propanol-2 à des témoins non traités, on a constaté 
un retard de croissance, mais uniquement chez les deux groupes de 
femelles traitées.  Aucun autre effet indésirable n'a été constaté. 
    Les données disponibles donnent à penser que le propanol-2 
produit sur le système nerveux central (SNC) des effets analogues à 
ceux de l'éthanol.  La DE50 d'anésthésie par voie orale est de 2280 
mg/kg chez le lapin, la DE50 par voie intrapéritonéale 
correspondant à la perte du réflexe de redressement chez la souris 
est égale à 165 mg/kg et le seuil d'induction de l'ataxie par voie 
intrapéritonéale est de 1106 mg/kg chez le rat.  Ces valeurs sont 
sont environ deux fois plus faibles que pour l'éthanol.  Lors d'une 
expérience menée à l'air libre, on a constaté que l'inhalation de 

propanol-2 à la dose de 739 mg/m3, dix heures par jour, et cinq 
jours par semaine pendant 15 semaines ne produisait aucun effet 
    Le propanol-2 a été soumis à une étude portant sur deux 
générations de rats qui ont reçu dans leur eau de boisson des doses 
quotidiennes de 1290, 1380 ou 1479 mg de ce produit par kg de poids 
corporel.  Les seuls effets indésirables qui ont été notés 
consistaient dans une réduction passagère du taux de croissance 
dans la génération F0.  En revanche, d'autres chercheurs ont 
constaté une augmentation des malformations lors d'une étude 
tératogènicité, au cours de laquelle on avait administré à des 
rates gravides, des doses orales quotidiennes de 252 ou 1008 mg de 
propanol-2 par kg de poids corporel (toxicité maternelle non 
étudiée).  On a également indiqué que ces deux doses, administrées 
pendant 45 jours dans l'eau de boisson, faisaient passer le cycle 
oestral à cinq jours (contre quatre chez les témoins).  Chez des 
rates ayant reçu pendant six mois dans leur eau de boisson, des 
doses quotidiennes de propanol-2 de 1800 mg/kg avant de mettre bas, 
on a constaté un accroissement de la mortalité embryonnaire totale;  
divers effets ont également été signalés concernant la survie 
intra-utérine et postnatale à des doses aussi basses que 0,8 mg/kg, 
sans qu'on puisse toutefois dégager une tendance précise.  Des 
rates gravides ont été exposées à de l'air contenant du propanol-2 
aux concentrations respectives de 9001, 18 327 et 23 210 mg/m3 
(3659, 7450 ou 9435 ppm).  Les deux concentrations les plus fortes 
se sont révélées toxiques pour les mères, la concentration de 9001 
mg/m3 ne produisant aucun effet.  A toutes les concentrations on a 
constaté un effet nocif sur le développement. 

    Une épreuve de recherche des mutations ponctuelles utilisant 
 S. typhimurium a donné des résultats négatifs avec du propanol-2 à 
la dose de 0,18 mg par boîte; la recherche d'échanges entre 
chromatides soeurs sur fibroblastes de hamster chinois a également 
été négative.  Le propanol-2 a provoqué des anomalies de la mitose 
dans des cellules médullaires de rat ainsi que des cellules de 
l'extrêmité radiculaire d'oignons  in vitro.  On ne dispose d'aucune 
autre donnée sur la mutagénicité de ce produit. 

    Un certain nombre d'études restreintes ont été consacrées au 
pouvoir cancérogène du propanol-2, au cours desquelles des souris 
ont été exposées à cette substance par voie percutanée (3 fois par 
semaine pendant un an), par voie respiratoire (7700 mg/m3, 3 à 7 
heures par jour, cinq jours par semaine pendant 5 à 8 mois) et par 
voie sous-cutanée (20 mg de propanol non dilué par semaine pendant 
20 à 40 semaines).  Au cours de ces trois études, on a recherché la 
présence de tumeurs sur la peau, dans les poumons et au point 
d'injection.  Aucun signe d'effets cancérogènes n'a été observé.  
On ne dispose pas de données épidémiologiques suffisantes pour 
évaluer la cancérogénicité du propanol-2 chez l'homme.  A la 
lumière des données disponibles, on peut penser que le sulfate de 
dipropyl-2, un produit intermédiaire de la fabrication du 
propanol-2 par le procédé aux acides forts et faibles, pourrait 
être à l'origine de cancers du sinus maxillaire chez l'homme. 
8.  Effets sur la santé de l'homme

    On a signalé plusieurs cas d'intoxication consécutifs à 
l'ingestion de propanol-2 ou à l'utilisation de lotions à base de 
ce produit pour rafraîchir des enfants fébriles.  Les principaux 
signes d'intoxication rappellent ceux de l'intoxication alcoolique:  
nausées, vomissements, douleurs abdominales, gastrite, hypotension 
et hypothermie.  La dépression du SNC par le propanol-2 est deux 
fois plus intense qu'avec l'éthanol et entraîne l'inconscience puis 
un coma profond; la mort peut survenir par dépression respiratoire.  
Parmi les autres effets on peut noter l'hyperglycémie, un taux 
élevé de protéines dans le liquide céphalorachidien et une 
atélectasie.  Il semblerait que l'absorption percutanée soit 
négligeable mais on connaît le cas d'un enfant qui a été intoxiqué 
après avoir été lotionné avec du propanol-2, ce qui donne à penser 
qu'il ne faut pas négliger l'absorption percutanée, notamment chez 
les enfants.  Aucun effet indésirable n'a été observé chez des 
volontaires en bonne santé qui avaient bu tous les jours pendant 
six semaines un sirop contenant du propanol-2 à des doses 
corrrespondant respectivement à 2,6 et 6,4 mg de propanol-2 par kg 
de poids corporel.  Des volontaires du sexe masculin, exposés 3 à 5 
minutes à des vapeurs de propanol-2 correspondant à des 
concentrations de 490, 980 ou 1970 mg/m3 d'air, ont estimé qu'ils 
ressentaient une irritation légère à 980 mg/m3 et que la situation 
était "satisfaisante" pendant les 8 heures correspondant à leur 
propre exposition professionnelle. 

    Des enfants prématurés ayant subi un contact prolongé avec du 
propanol-2 ont présenté une irritation cutanée prenant la forme 
d'érythèmes, voire de brûlures du 2ème et du 3ème degré et de 
phlyctènes.  On a également signalé ça et là des cas de dermatites 
allergiques de contact. 

    Il n'existe de peu d'études épidémiologiques consacrées à la 
mortalité par cancers ou autres maladies provoquées par le 
propanol-2.  Parmi un groupe de 61 travailleurs, employés pendant 
plus de cinq ans dans un atelier de fabrication de propanol-2 par 
le procédé à l'acide fort, on a observé sept cas de cancer dont 
quatre de cancer des sinus maxillaires.  Une étude portant sur une 
cohorte de 779 travailleurs d'un atelier analogue a révélé que 
l'incidence des cancers du sinus et du larynx, corrigée de 
l'influence de l'âge et du sexe, était 21 fois plus forte que 
prévue.  La période minimale de latence était de dix ans.  Dans une 
autre étude rétrospective de cohorte portant sur le personnel d'une 
autre usine où on utilisait le procédé à l'acide fort, on a 
constitué une cohorte représentant plus de 4000 années-hommes 
exposés au risque.  Les résultats de cette étude ont montré que les 
taux de mortalité pour toutes causes et les taux de mortalité par 
cancer n'étaient pas sensiblement plus élevés que les taux 
prévisibles.  Une autre étude rétrospective a été menée dans une 
usine qui fabriquait du propanol-2 par le procédé à l'acide faible.  
Cette fois, on comptait plus de 11 000 années-hommes exposés au 
risque.  Dans ce cas, le taux de mortalité pour toutes causes était 
inférieur aux prévisions et l'on ne constatait pas de surmortalité 
attribuable aux cancers en général.  Toutefois, l'incidence des 

cancers de la bouche et du pharynx était 4 fois supérieure à la 
normale.  Dans l'ensemble, ces études de cohorte donnent à penser 
qu'il existe un risque de cancer imputable au procédé à l'acide 
fort; toutefois lors de deux petites études castémoins, on n'a noté 
aucune association entre l'exposition au propanol-2 et l'incidence 
des gliomes ou de la leucémie lymphatique. 

    Certaines études font état d'une potentialisation de la 
toxicité du tétrachlorure de carbone chez des ouvriers 
simultanément exposés au propanol-2. 
9.  Résumé de l'évaluation

    L'homme peut être exposé au propanol-2 par inhalation lors de 
la fabrication, de la transformation ou de l'utilisation de cette 
substance dans le cadre professionnel ou domestique.  En ce qui 
concerne la population en général, l'exposition à des doses 
potentiellement mortelles peut se produire par suite d'ingestion 
accidentelle ou volontaire de cette substance et les enfants 
peuvent être exposés par application de lotions à base de propanol-

    Le propanol-2 est vite absorbé et se répartit rapidement dans 
l'ensemble de l'organisme, en partie sous forme d'acétone.  Les 
données relatives aux effets aigus consécutifs à l'exposition 
d'êtres humains à des doses excessives sont rares et contrastées.  
Les principaux effets consistent en gastrite, dépression du système 
nerveux central, hypothermie, dépression respiratoire et 
hypotension.  Les données de mortalité aiguë obtenues sur des 
animaux de laboratoire indiquent que le propanol-2 est peu toxique, 
les valeurs de la DL50 par voie orale chez diverses espèces vont de 
4475 à 7990 mg/kg, et les valeurs de la CL50 par inhalation se 
situent aux alentours de 50 000 mg/m3 chez le rat.  Chez le lapin, 
le propanol-2 ne provoque pas d'irritation cutanée, toutefois 
l'instillation de 0,1 ml de cette substance non diluée dans les 
yeux a provoqué une irritation. 

    Chez l'homme, les effets aigus les plus probables d'une 
exposition de fortes concentrations de propanol-2 par ingestion ou 
inhalation, consistent en une intoxication de type alcoolique 
aboutissant à la narcose. 

    Les études sur l'animal sont insuffisantes pour qu'on puisse 
évaluer les risques encourus par l'homme à la suite d'expositions 
répétées au propanol-2.  Toutefois les résultats de deux études à 
court terme chez le rat, au cours desquelles on a fait a) inhaler 
500 mg/m3 de cette substance, 4 heures par jour, 5 heures par 
semaine pendant 4 mois et b)  ingérer le même produit à raison de 
600 à 3900 mg/kg dans l'eau de boisson, donnent à penser qu'il 
serait préférable d'éviter de s'exposer aux fortes concentrations 
en propanol-2 signalées dans le cadre de certaines activités 
    En faisant inhaler du propanol-2 à des rattes gravides on a 
constaté que le seuil d'apparition d'un effet se situait à 18 327 
mg/m3 (7450 ppm), la dose sans effet observable était de 9001 mg/m3 
(3659 ppm), la toxicité maternelle étant prise comme critère.  Au 
cours de la même étude, le seuil d'apparition d'effets s'est situé 
à 9001 mg/m3 (3659 ppm) pour les anomalies du développement et 
aucune dose sans effet observable n'a pu être mise en évidence.  
Ces concentrations sont plus élevées que celles auxquelles l'homme 
est susceptible d'être exposé. 

    Les épreuves de génotoxicité ont donné des résultats négatifs 
dans le cas du propanol-2, cependant on a observé des anomalies de 
la mitose dans des cellules médullaires de rats.  Ces résultats 
indiquent que le propanol-2 n'est pas du tout génétoxique mais les 
données sont trop limitées pour qu'on puisse se prononcer 
véritablement sur le pouvoir mutagène de cette substance. 

    Les données existantes sont insuffisantes pour permettre une 
évaluation de la cancérogénicité du propanol-2 chez l'animal 
d'expérience.  On ne dispose pas de données permettant d'évaluer 
cette cancérogénicité chez l'homme. 

    Le propanol-2 ne fait probablement pas courir de risque 
important à la population dans son ensemble dans les conditions 
d'exposition qui sont susceptibles de se produire. 

    Le propanol-2 disparaît rapidement (demi-vie, 5 jours) de 
l'atmosphère et s'élimine à bref délai de l'eau et du sol par 
biodégradation aérobie ou anaérobie, en particulier une fois que 
les microorganismes préalablement ensemencés se sont adaptés.  
Compte tenu de ses propriétés physiques, le propanol-2 n'a qu'une 
faible tendance à la bioaccumulation.  Il ne présente pas de risque 
pour la faune et la flore aux concentrations auxquelles il est 
habituellement présent dans l'environnement. 


1.  Identidad, propiedades físicas y químicas, métodos analíticos

    El 2-propanol es un líquido incoloro, sumamente inflamable, con 
un olor que recuerda al de la mezcla de etanol y acetona.  El 
compuesto es completamente miscible con agua, etanol, acetona, 
cloroformo y benceno.  Se dispone de métodos analíticos para 
detectar el 2-propanol en diversos medios (aire, agua, sangre, 
suero y orina) con límites de detección de 2 x 10-5 mg/m3, 0,04 
mg/litro y 1 mg/litro en el aire, el agua y la sangre, 
respectivamente.  Existen métodos de cromatografía de gases (que se 
sirven principalmente de la detección de ionización de llama) así 
como métodos de electroforesis en papel y de espectrometría de 
movilidad iónica inducida por fotoionización para determinar el 
2-propanol en los distintos medios. 
2.  Fuentes de exposición humana y ambiental

    La producción mundial estimada de 2-propanol en 1975 fue 
superior a 1100 kilotoneladas y la capacidad de producción mundial 
en 1984 se cifró en más de 2000 kilotoneladas.  El 2-propanol se 
fabrica comúnmente a partir del propeno.  Los antiguos procesos 
basados en ácidos fuertes y débiles, en los que se generaban 
productos intermedios y desechos potencialmente peligrosos, se han 
sustituido actualmente en gran medida por el proceso de hidratación 
catalítica.  La reducción catalítica de la acetona es otro proceso 

    El 2-propanol se ha identificado como producto metabólico de 
diversos microorganismos. 

    El compuesto tiene amplias aplicaciones como disolvente y se 
utiliza como componente de productos domésticos y personales, entre 
ellos vaporizadores de aerosoles, productos farmacéuticos de 
aplicación tópica y cosméticos.  El 2-propanol se utiliza también 
para producir acetona y otras sustancias químicas, como agente 
descongelante, como conservante, en concentrados para 
limpiaparabrisas y como aromatizante volátil en alimentos. 

    El 2-propanol puede ingresar en la atmósfera, el agua o el 
suelo por la evacuación de desechos y se ha aislado en el aire y en 
el líquido que rezuma de basureros y terraplenados.  Se encuentra 
en los gases y las aguas residuales que emiten algunas industrias, 
y puede extraerse de esas aguas por oxidación biológica o por 
ósmosis inversa.  Durante el uso de 2-propanol en productos de 
consumo se producen emisiones dispersas a la atmósfera. 

3. Transporte, distribución y transformación en el medio ambiente

    La vía principal de entrada del 2-propanol en el medio ambiente 
es su emisión a la atmósfera durante la producción, el tratamiento, 
el almacenamiento, el transporte, el uso y la evacuación.  También 
se producen emisiones al suelo y al agua.  Es difícil calcular el 

volumen que ingresa en cada compartimiento ambiental.  No obstante, 
se calculó que en 1976 la liberación total de este compuesto en la 
atmósfera fue superior al 50% del 2-propanol producido. 

    El 2-propanol desaparece rápidamente de la atmósfera por 
reacción con radicales hidroxilo y arrastrado por la lluvia.  A 
este último proceso se debe el transporte del 2-propanol desde la 
atmósfera hasta el suelo o el agua.  Una vez que está en el suelo, 
se cree que es muy móvil y que aumenta la permeabilidad del suelo a 
algunos hidrocarburos aromáticos.  El 2-propanol es fácilmente 
biodegradable, en condiciones tanto aerobias como anaerobias. 

    La bioacumulación del compuesto no es probable, dados su 
carácter biodegradable y su miscibilidad total con el agua; su 
coeficiente de reparto log  n-octanol/agua es de 0,14 y su factor de 
bioconcentración de 0,5. 

4.  Niveles ambientales y exposición humana

    La exposición de la población general se produce por ingestión 
accidental o intencionada, por la ingestión de alimentos que lo 
contengan como aromatizante volátil natural o añadido o como 
residuo de disolvente, y por inhalación durante su uso.  Se han 
encontrado concentraciones de 0,2 a 325 mg por litro en bebidas no 
alcohólicas y de 50 a 3000 mg por kg en alimentos tras el uso de 
2-propanol como disolvente en su producción.  La exposición de la 
población general por inhalación de aire ambiental es baja a causa 
de su rápida desaparición y degradación.  Se han estudiado diversas 
localizaciones y se han medido concentraciones medias ponderadas en 
función del tiempo de hasta 35 mg/m3 en emplazamientos urbanos. 

    Los trabajadores se ven expuestos al 2-propanol durante la 
producción del propio compuesto y de acetona y otros derivados, así 
como durante su uso como disolvente.  En la encuesta nacional de 
exposición ocupacional (1980 - 83) realizada en los Estados Unidos, 
se estimó que más de 1,8 millones de trabajadores estaban 
potencialmente expuestos.  En ciertos lugares de trabajo se han 
medido concentraciones de hasta 1350 mg/m3, con promedios 
ponderados en función del tiempo de hasta 500 mg/m3. 

5.  Cinética y metabolismo

    El 2-propanol se absorbe y distribuye rápidamente por todo el 
organismo tras su inhalación o ingestión.  A dosis elevadas se 
retrasa la absorción gastrointestinal.  Las concentraciones 
sanguíneas de 2-propanol (detectables cuando se ingiere etanol 
simultáneamente) o de su metabolito, la acetona, guardan relación 
con los niveles de exposición.  En voluntarios que ingirieron una 
dosis de 3,75 mg/kg (con 1200 mg de etanol/kg) en zumo de naranja, 
se observó un nivel máximo de 0,8 ± 0,3 mg de 2-propanol libre por 
litro en la sangre, y de 2,3 ± 1,4 mg por litro tras la incubación 
con arilsulfatasa, lo que es un signo de sulfatación.  Los 
trabajadores expuestos a vapores (8 - 647 mg/m3) mostraron 
concentraciones de 3 - 270 mg/m3 en el aire alveolar, pero en este 
caso se encontró acetona y no 2-propanol en la sangre y la orina.  

En animales de laboratorio tratados, el 2-propanol se detectó no 
sólo en la sangre sino también en el líquido espinal, el hígado, 
los riñones y el cerebro.  Atraviesa la barrera hematocerebral dos 
veces mejor que el etanol.  El 2-propanol se excreta en parte como 
tal y en parte como acetona, principalmente por vía pulmonar, pero 
también en la saliva y el jugo gástrico.  La reabsorción puede 
producirse después de la excreción por las últimas dos vías.  La 
transformación en acetona por medio de la deshidrogenasa alcohólica 
del hígado es más bien lenta, porque la afinidad relativa de la 
deshidrogenasa por el 2-propanol es más baja que por el etanol.  
 In vitro, la actividad enzimática de la deshidrogenasa humana con 
2-propanol fue del 9 - 10% de la actividad que exhibe cuando el 
sustrato es el etanol.   In vitro las oxidasas microsómicas de 
hígado de rata también son capaces de oxidar el 2-propanol.  En el 
hombre, la acetona se excreta sin cambios, principalmente por los 
pulmones y en cantidad mínima por los riñones.  La concentración de 
acetona en el aire alveolar, la sangre y la orina aumenta con la 
intensidad y la duración de la exposición al 2-propanol.  La 
eliminación de 2-propanol y de acetona del organismo es de primer 
orden, y los periodos de semieliminación en el hombre son de 
2,5 - 6,4 horas y 22 horas, respectivamente. 

6.  Efectos en los organismos en el medio ambiente

    La toxicidad del 2-propanol para organismos acuáticos, insectos 
y plantas es baja.  El umbral inhibitorio para la multiplicación 
celular de una especie de protozoo sensible varió de 104 a 4930 mg 
por litro en diversas condiciones experimentales.  Avanzando en la 
cadena filogenética, varias especies de crustáceos, incluida 
 Daphnia magna, mostraron CE50 a concentraciones que iban desde 2285 
hasta 9714 mg por litro.  Las CL50 (96 h) para peces de agua dulce 
variaron desde 4200 hasta 11 130 mg por litro.  Los datos obtenidos 
para especies de moscas de la fruta mostraron CL50 comprendidas 
entre 10 200 y 13 340 mg por litro de medio nutritivo.  La CL50 
para larvas de mosquito ( Aedes aegypti) en la tercera etapa de 
desarrollo fue de 25 - 120 mg/litro en un ensayo estático de 4 

    Los efectos que tiene en las plantas la exposición a 2-propanol 
en concentraciones entre 2100 mg/litro y más de 36 000 mg/litro 
variaron entre la ausencia de efecto y la inhibición total de la 

7.  Efectos en animales de experimentación y en sistemas de ensayo 
 in vitro

    La toxicidad aguda del 2-propanol para los mamíferos, a juzgar 
por la mortalidad, es baja, sea cual sea la vía de exposición oral, 
cutánea o respiratoria.  Los valores de la DL50 para varias 
especies animales tras la administración oral variaron entre 4475 y 
7990 mg por kg de peso corporal; La CL50 de inhalación durante 8 
horas en la rata varió de 46 000 a 55 000 mg por m3 de aire.  A 
estos niveles letales, las ratas mostraron grave irritación de las 
mucosas y depresión profunda del sistema nervioso central.  La 

muerte fue provocada por paro respiratorio o cardiaco.  Entre las 
lesiones histopatológicas figuraron la congestión y el edema 
pulmonar, así como la degeneración celular en el hígado. 

    Con dosis orales únicas de 3000 ó 6000 mg de 2-propanol por kg 
de peso corporal se produjo una acumulación reversible de 
triglicéridos en el hígado de la rata.  En la rata se observó 
inducción de enzimas microsómicas a dosis orales de 390 mg/kg. 

    El 2-propanol sin diluir no produjo irritaciones cuando se 
aplicó a la piel cortada o raspada del conejo durante 4 horas.  En 
cambio, se observó irritación cuando se aplicó 0,1 ml de compuesto 
sin diluir en el ojo del conejo.  Con concentraciones de vapor 
elevadas de 2-propanol se produjo irritación del tracto 
respiratorio en el ratón, y el ritmo respiratorio disminuyó en un 
50% a concentraciones de 12 300 - 43 525 mg/m3 de aire. 

    Se han hecho escasos estudios de exposición repetida sobre los 
efectos del 2-propanol en animales.  Tras la inhalación de 500 mg 
de 2-propanol/m3 durante 5 días a la semana y 4 horas al día 
durante más de 4 meses, se observaron irritación del tracto 
respiratorio, cambios hematológicos y alteraciones histopatológicas 
en el hígado y el bazo de la rata.  En otro grupo de estudio, se 
administró a 5 ratas de cada sexo agua de bebida que contenía 
2-propanol durante 27 semanas.  La comparación de animales que 
recibían aproximadamente 600 ó 2300 mg por kg al día (machos) y 
1000 ó 3900 mg por kg al día (hembras) con grupos de control no 
tratados reveló un retraso del crecimiento sólo en ambos grupos de 
hembras expuestas.  No se observaron otros efectos adversos. 

    Los datos disponibles indican que los efectos del 2-propanol en 
el sistema nervioso central son semejantes a los del etanol.  La 
DE50 por vía oral para la narcosis en conejos es de 2280 mg/kg; la 
DE50 intraperitoneal correspondiente a la pérdida del reflejo de 
enderezamiento en el ratón es de 165 mg/kg, y el umbral 
intraperitoneal de inducción de ataxia en la rata es de 1106 mg/kg.  
Estos valores son aproximadamente dos veces más bajos que los 
correspondientes al etanol.  La inhalación de 2-propanol a una 
concentración de 739 mg/m3 durante 6 horas al día y 5 días a la 
semana durante 15 semanas no originó ningún resultado adverso en un 
ensayo en campo abierto. 

    El 2-propanol se evaluó en un estudio de 2 generaciones de 
ratas mediante la administración de 1290, 1380 ó 1470 mg por kg al 
día en el agua de bebida a ambas generaciones.  El único efecto 
adverso observado fue una reducción transitoria del ritmo de 
crecimiento en la generación Fo.  En cambio, otros investigadores 
observaron un aumento de las malformaciones en un estudio de la 
teratogénesis después de administrar por vía oral a ratas gestantes 
252 ó 1008 mg de 2-propanol por kg al día (no se formularon 
observaciones sobre la toxicidad materna).  Ambas dosis, 
administradas en el agua de bebida durante 45 días, también 
aumentaron la duración del ciclo estrual hasta 5 días (frente a 4 
días en los sujetos de control).  Se observó una mortalidad 
embrionaria total mayor cuando se administraban a la rata hembra 

dosis de 1800 mg/kg en el agua de bebida al día durante 6 meses 
antes de criar; se notificaron diversos efectos en la supervivencia 
intrauterina y puerperal a dosis tan bajas como 0,18 mg/kg al día, 
pero no se observó ninguna pauta coherente.  Se expusieron ratas 
gestantes a 2-propanol atmosférico a concentraciones de 9001, 
18 327 ó 23 210 mg por m3 (3659, 7450 ó 9435 ppm).  Las dos 
concentraciones más elevadas fueron tóxicas para las madres, pero 
no así la de 9001 mg/m3.  Se observó toxicidad en el desarrollo con 
las tres concentraciones. 

    El 2-propanol dio resultados negativos en una prueba con 0,18 
mg por placa para detectar mutuaciones puntuales en  S. 
 typhimurium y en una prueba de intercambio de cromátidas hermanas 
en fibroblastos pulmonares de hámster chino.  Indujo anomalías 
mitóticas en células de médula ósea de rata y en células de ápice 
radicular de cebolla  in vitro.  No se dispone de otros datos sobre 

    El 2-propanol se ensayó en varios estudios limitados de 
carcinogenicidad en el ratón utilizando las vías de exposición 
cutánea (3 veces a la semana durante un año), inhalación (7700 
mg/m3 durante 3 - 7 h/día, 5 días/semana, durante 5 - 8 meses) y 
subcutánea (20 mg sin diluir, semanalmente durante 20 - 40 
semanas).  La aparición de tumores se investigó en los tres 
estudios en la piel, el pulmón y el lugar de inyección, 
respectivamente.  No se observaron efectos carcinogénicos.  No se 
dispone de datos epidemiológicos adecuados con los que evaluar la 
carcinogenicidad del 2-propanol para el ser humano.  Los datos 
disponibles indican que el di-2-propilsulfato, un producto 
intermedio en los procesos de ácidos fuertes y débiles para 
producir 2-propanol, puede estar asociado causalmente con la 
inducción de cáncer del seno paranasal en el ser humano. 
8.  Efectos en la salud humana

    Se han notificado varios casos de intoxicación tras la 
ingestión oral y también en niños con fiebre a los que se refrescó 
con esponjas impregnadas con preparaciones con 2-propanol.  En 
casos de envenenamiento, los principales signos son los de la 
intoxicación alcohólica, en particular náuseas, vómitos, dolores 
abdominales, gastritis, hipotensión e hipotermia.  El 2-propanol 
deprime el sistema nervioso central unas dos veces más que el 
etanol, provocando una inconsciencia que termina en coma profundo; 
puede sobrevenir la muerte por depresión respiratoria.  Otros 
efectos relacionados con el compuesto son la hiperglucemia, 
elevados niveles de proteínas en el líquido cefalorraquídeo y 
atelectasia.  Aunque se considera que la absorción por la piel es 
insignificante, en un informe sobre un caso de un niño intoxicado 
tras refrescársele con una esponja impregnada con 2-propanol, se 
indicaba que no conviene subestimar el riesgo de absorción dérmica, 
especialmente en los niños.  No se observaron efectos adversos en 
voluntarios sanos que bebieron diariamente durante 6 semanas un 
jarabe que contenía 2,6 ó 6,4 mg de 2-propanol/kg.  Un grupo de 
varones voluntarios, cuando se expusieron a vapores de 2-propanol 

en concentraciones de 490, 980 ó 1970 mg por m3 de aire durante 
3 - 5 minutos juzgaron que la irritación era "leve" a 980 mg/m3 y 
"satisactoria" para su propia exposición ocupacional de 8 horas. 

    Las irritaciones de la piel en forma de eritema, quemaduras de 
segundo y tercer grado y ampollas se notificaron en niños 
prematuros tras un contacto prolongado con 2-propanol.  En 
ocasiones también se han notificado casos de dermatitis alérgica 
por contacto. 

    Se dispone de pocos estudios epidemiológicos sobre mortalidad 
por cáncer o por otras causas.  En un grupo de 71 trabajadores 
empleados durante más de 5 años en una fábrica de 2-propanol por el 
proceso del ácido fuerte, se notificaron 7 casos de cáncer, entre 
ellos 4 de cáncer del seno paranasal.  En un estudio de cohortes 
realizado sobre 779 trabajadores en una fábrica similar, las 
incidencias reajustadas en función de la edad y del sexo de cáncer 
del seno y de la laringe fueron 21 veces mayores de lo esperado.  
El periodo mínimo de latencia fue de 10 años.  En otro estudio 
retrospectivo de cohortes realizado en otra fábrica que utilizaba 
el proceso del ácido fuerte, había más de 4000 personas-años 
expuestas.  Los resultados mostraron que las tasas de mortalidad 
por todas las causas y por neoplasmas no eran significativamente 
mayores de lo previsto.  Se llevó a cabo un estudio retrospectivo 
de cohortes en una planta que fabricaba 2-propanol por el proceso 
del ácido débil.  Había más de 11 000 personas-años expuestas.  La 
tasa de mortalidad debida a todas las causas fue más baja de lo 
esperado.  No se observó mortalidad excesiva por todos los 
cánceres.  Sin embargo, la incidencia del cáncer de la boca y de la 
faringe fue 4 veces más elevada de lo previsto.  Los estudios de 
cohortes indican en conjunto un riesgo de cáncer relacionado con el 
proceso de fabricación con ácido fuerte, pero, en dos pequeños 
estudios controlados de casos, no se observó correlación alguna 
entre la exposición a 2-propanol y la incidencia de gliomas o de 
leucemia linfática. 

    Algunos informes parecen indicar que la exposición combinada a 
tetracloruro de carbono y 2-propanol en los trabajadores potencia 
la toxicidad del primero. 

9.  Resumen de la evaluación

    La exposición del hombre al 2-propanol puede producirse por 
inhalación durante la fabricación, el tratamiento y el uso tanto 
ocupacional como doméstico.  La exposición a un nivel 
potencialmente letal en la población general puede producirse por 
ingestión accidental o intencionada y los niños pueden estar 
expuestos cuando se les refresca con esponjas impregnadas con 
preparaciones a base de 2-propanol (alcohol para friegas). 

    El 2-propanol se absorbe y distribuye rápidamente por todo el 
organismo, en parte en forma de acetona.  Los datos sobre 
exposición-efecto en el hombre en condiciones de sobreexposición 
aguda son escasos y muestran grandes variaciones.  Los principales 
efectos son la gastritis, la depresión del sistema nervioso central 

con hipotermia y depresión respiratoria, y la hipotensión.  Los 
datos de mortalidad aguda en animales de experimentación indican 
que la toxicidad del 2-propanol es baja, siendo los valores de DL50 
orales en diversas especies entre 4475 y 7990 mg/kg, y los valores 
de CL50 de inhalación en ratas alrededor de 50 000 mg/m3.  En el 
conejo, el 2-propanol no produjo irritaciones cutáneas, pero la 
aplicación de 0,1 ml de 2-propanol sin diluir produjo irritación en 
los ojos. 

    En el hombre, los efectos agudos más probables de la exposición 
a concentraciones elevadas de 2-propanol por ingestión o inhalación 
son la intoxicación alcohólica y la narcosis. 
    No se han hecho suficientes estudios en animales como para 
evaluar los riesgos que entraña para la salud humana la exposición 
repetida al 2-propanol.  No obstante, los resultados de dos 
estudios a corto plazo en la rata, incluida la exposición por 
inhalación (500 mg/m3 durante 4 horas al día y 5 días a la semana 
durante 4 meses) y la exposición oral (600 - 3900 mg/kg en el agua 
de bebida) indican que debe evitarse la exposición al 2-propanol en 
algunos de los muy elevados niveles de exposición ocupacional que 
se han notificado. 

    La exposición por inhalación de ratas gestantes a 2-propanol 
dio un nivel mínimo de observación de efectos de 18 327 mg/m3 (7450 
ppm) y un nivel sin efectos observados de 9001 mg/m3 (3659 ppm) 
respecto a la toxicidad materna.  En el mismo estudio, 9001 mg/m3 
(3659 ppm) fue el nivel más bajo de observación de efectos en lo 
que respecta a la toxicidad de desarrollo; no se indicó nivel sin 
efectos observados.  Estas concentraciones son más elevadas que las 
que normalmente se registran en condiciones de exposición humana. 

    El 2-propanol dio resultado negativo en las pruebas de 
genotoxicidad, pero indujo aberraciones mitóticas en la médula ósea 
de la rata.  Aunque estos resultados indican que la sustancia no 
tiene potencial genotóxico, no puede hacerse una evaluación 
correcta de la mutagenicidad basándose en datos tan limitados. 

    Los datos disponibles no bastan para evaluar la carcinogenicidad 
del 2-propanol en animales de experimentación.  No se dispone de 
datos para evaluar la carcinogenicidad del 2-propanol en el ser 

    Es poco probable que el 2-propanol plantee un riesgo grave para 
la salud de la población general en las condiciones de exposición 
que se producen normalmente. 

    El 2-propanol desaparece rápidamente (periodo de semieliminación 
2,5 días) de la atmósfera y su desaparición del agua y del suelo se 
produce rápidamente por biodegradación aerobia y anaerobia, 
especialmente tras la adaptación de microorganismos inicialmente 
sembrados.  En vista de las propiedades físicas del 2-propanol, su 
potencial de bioacumulación es bajo.  No representa un riesgo para 
los organismos naturales en las concentraciones en que suele 
encontrarse en el medio ambiente. 

    See Also:
       Toxicological Abbreviations