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        (Environmental health criteria ; 102)


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1. SUMMARY    

    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 exposures  
    1.5. Kinetics and metabolism  
    1.6. Effects on organisms in the environment  
    1.7. Effects on experimental animals and  in vitro test systems 
    1.8. Health effects on 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  
          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  
    5.3. 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. Metabolic transformation  
          6.3.1. Animals   

    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. Insects   
          7.2.2. 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. Repeated exposures  
    8.3. Neurotoxic and behavioural effects  
    8.4. Biochemical effects   
          8.4.1. Effects on lipids in the liver and blood 
          8.4.2. Effects on microsomal enzymes  
          8.4.3. Other biochemical findings  
    8.5. Reproduction, embryotoxicity, and teratogenicity  
    8.6. Mutagenicity   
          8.6.1. Bacteria  
          8.6.2. Mammalian cells  in vitro  
    8.7. Carcinogenicity  
    9.1. General population exposure  
          9.1.1. Poisoning incidents  
          9.1.2. Controlled human studies  
    9.2. Occupational exposure  

    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 
1-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

    1-Propanol is a colourless, highly flammable liquid that is 
volatile at room temperature and normal atmospheric pressure.  It 
is miscible with water and organic solvents.  Analytical methods 
for propanol include gas chromatography, which can detect 
5 x 10-5 mg/m3 in air, 1 x 10-4 mg/litre in water, and 0.002 
mg/litre in blood, serum, or urine, when suitable extraction or 
concentration procedures are used with the sample. 

1.2  Sources of Human and Environmental Exposure

    The annual world production capacity in 1979 exceeded 130 000 
tonnes.  It is produced in nature by the decomposition of organic 
materials by a variety of microorganisms, and occurs in plants and 
fuel oil.  1-Propanol is produced from ethene by reaction with 
carbon monoxide and hydrogen to give propionaldehyde, which is then 
hydrogenated.  It is also a by-product of methanol manufacture and 
may be produced from propane directly or from acrolein.  The major 
use of 1-propanol is as a multi-purpose solvent in industry and in 
the home.  It is used in flexographic printing ink and textile 
applications, products for personal use, such as cosmetics and 
lotions, and in window cleaning, polishing, and antiseptic 
formulations.  Second in importance is its use as an intermediate 
in the manufacture of a variety of chemical compounds. 

1.3  Environmental Transport, Distribution and Transformation

    The main pathway of entry of 1-propanol into the environment is 
through its emission into the atmosphere during production, 
processing, storage, transport, use, and waste disposal.  Emissions 
into water and soil also occur.  Because the main use of 1-propanol 
is as a volatile solvent, much of the production volume is 
eventually released into the environment. 

    1-Propanol rapidly disappears from the atmosphere by reaction 
with hydroxyl radicals and through rain-out.  It is readily 
biodegradable, both aerobically and anaerobically, and, because of 
these chemical and biological removal mechanisms, measurable levels 
are not normally encountered in the environment.  However, the 
compound has been detected in urban air, at waste-disposal sites, 
and also in water leaching from a landfill.  Soil permeability for 
1-propanol is probably high and the compound enhances permeability 
for some aromatic solvents.  

    1-Propanol has a log  n-octanol/water partition coefficient of 
0.34 and a bioconcentration factor of 0.7, which render 
bioaccumulation highly unlikely. 
1.4   Environmental Levels and Human Exposures

    Exposure of the general population may occur through accidental 
ingestion, through inhalation during use, and through ingestion via 
food (containing 1-propanol as a natural or added flavour volatile 

or as a solvent residue) and non-alcoholic as well as alcoholic 
beverages.  For example, beer contains up to 195 mg/litre, wine up 
to 116 mg/litre, and various types of spirit up to 3520 mg/litre.  
Exposure of the general population to 1-propanol via inhalation and 
drinking-water is low (in the USA the average concentration in 
urban air samples was 0.00005 mg/m3 and that in drinking-water, 
0.001 mg/litre).  Workers are potentially exposed through 
inhalation during manufacture, processing, and use.  However, no 
data are available to quantify such exposures. 

1.5  Kinetics and Metabolism

    1-Propanol is rapidly absorbed and distributed throughout the 
body following ingestion.  Data on the absorption rate following 
inhalation and dermal exposures are lacking.  1-Propanol is 
metabolized by alcohol dehydrogenase (ADH) to propionic acid via 
the aldehyde and may enter the tricarboxylic acid cycle.  This 
oxidation is a rate-limiting step of 1-propanol metabolism.  In 
vitro, rat and rabbit microsomal oxidases are also capable of 
oxidizing 1-propanol to propionic aldehyde.  The relative affinity 
of ADH and the microsomal oxidizing systems for 1-propanol is much 
higher than that of ethanol; therefore 1-propanol is rapidly 
eliminated from the organism.  In the rat, the half-life after an 
oral dose of 1000 mg/kg was 45 min. 

    In both animals and man, 1-propanol may be eliminated from the 
body in the expired air or in urine.  In human beings administered 
an oral dose of 1-propanol of 3.75 mg/kg body weight and 1200 mg 
ethanol/kg body weight, the total urinary excretion of 1-propanol 
was 2.1% of the dose.  The urinary levels of 1-propanol were lower 
the lower the amount of simultaneously ingested ethanol, showing 
competition for ADH between 1-propanol and the ethanol overdose. 
1.6   Effects on Organisms in the Environment

    At concentrations normally encountered in the environment, 
1-propanol is not toxic for aquatic organisms, insects, or plants.  
The inhibitory threshold for cell multiplication of three of the 
more sensitive aquatic species (3 protozoa) was 38 - 568 mg/litre.  
For the higher organisms, the lethal concentration was about 5000 
mg/litre, varying remarkably little from one phylum to another and 
exhibiting a very steep dose-response curve.  Some bacteria and 
microorganisms in waste-water and activated sludge are able to 
adapt to concentrations greater than 17 000 mg/litre.  

    Seed germination may be inhibited or stimulated by 1-propanol 
depending on the concentration in water used and conditions of 
exposure.  The compound increases nitrite accumulation in maize, 
peas, and wheat. 

1.7  Effects on Experimental Animals and  In Vitro Test Systems

    The acute toxicity of 1-propanol for mammals (based on 
mortality) is low, whether exposure is via the dermal, oral, or the 
respiratory route.  Oral LD50 values for several animal species 

have been reported to range between 1870 and 6800 mg/kg body 
weight. However, an oral LD50 of 560 - 660 mg/kg body weight was 
reported for very young rats.  The principal toxic effect of 
1-propanol following a single exposure is depression of the central 
nervous system.  The available evidence for 1-propanol suggests 
that its effects on the central nervous system are similar to those 
of ethanol; however, 1-propanol appears to be more neurotoxic.  The 
ED50 values for narcosis in rabbits and loss of righting reflex in 
mice were, respectively, 1440 mg/kg body weight orally, and 
1478 mg/kg body weight intraperitoneally; these are approximately 
four times lower than those for ethanol.  In the tilted plane test, 
1-propanol was 2.5 times as potent as ethanol in rats. 
    Single oral doses of 3000 or 6000 mg/kg body weight resulted in 
a reversible accumulation of triglycerides in the liver of rats.  
High vapour concentrations caused irritation of the respiratory 
tract in mice.  The respiratory rate in mice was decreased by 50% 
at concentrations of approximately 30 000 mg/m3. 

    Data on eye and skin irritation are not available.  No 
sensitization was observed in one reported skin sensitization test 
on CF1 mice. 

    There was limited evidence, in male rats exposed for 6 weeks to 
15 220 mg/m3, that 1-propanol impairs reproductive function.  No 
effect was noted after a similar exposure to 8610 mg/m3.  When 
pregnant rats were exposed to 1-propanol, maternal and 
developmental toxicity were evident at 23 968 and 14 893 mg/m3 
(9743 and 6054 ppm); there was no toxicity at 9001 mg/m3 
(3659 ppm).  No evidence was seen of behavioural defects in the 
offspring of male rats exposed for 6 weeks to 8610 or 15 220 mg 
1-propanol/m3, or in offspring of rats exposed during pregnancy to 
the same concentrations.  However, when 5 to 8-day-old rats were 
orally dosed with 3000 - 7800 mg 1-propanol/kg, per day, there was 
evidence of CNS depression during dosing and signs of withdrawal 
when dosing ended.  The brains of these rats were examined when 
they were 18 days old; reductions were found in the absolute and 
relative brain weights and in the contents of DNA as well as 
regional decreases in cholesterol and protein levels. 

    1-Propanol gave negative results in 2 assays for point 
mutations using  Salmonella typhimurium and in a reverse mutation 
test with  Escherichia coli CA-274.  Negative results were obtained 
in tests for the induction of sister chromatid exchange or 
micronuclei in mammalian cells  in vitro.  No other mutagenicity 
data were available. 

    In a carcinogenicity study on small groups of Wistar rats 
exposed throughout their lifetime to oral doses of 240 mg/kg or to 
subcutaneous doses of 48 mg/kg, a significant increase in the 
incidence of liver sarcoma was noted in the group dosed 
subcutaneously.  However, the study was inadequate for the 
assessment of carcinogenicity for a number of reasons including 
lack of experimental detail, too few animals, and the use of a high 
single dose inducing liver toxicity. 

1.8  Health Effects on Human Beings

    There are no reports of adverse health effects in the general 
population or in occupational groups.  In the only fatal poisoning 
case reported, it was recorded that a woman was found unconscious 
and died 4 - 5 h after ingestion.  Autopsy revealed a "swollen 
brain" and lung oedema.  In a study on skin irritation and 
sensitization, allergic reactions were reported in a laboratory 
worker.  In another group of 12 volunteers, erythema lasting for at 
least 60 min was observed in 9 individuals following a 5-min 
application of filter papers containing 0.025 ml of a 75% solution 
of 1-propanol in water on the forearms.  No other reports on 
adverse health effects following occupational exposure to 
1-propanol are available. 

    No epidemiological studies are available to assess the long-
term effects, including the carcinogenicity, of 1-propanol in human 

1.9  Summary of Evaluation

    Exposure of human beings to 1-propanol may occur through the 
ingestion of food or beverages containing 1-propanol.  Inhalation 
exposure may occur during household use and occupationally during 
manufacture, processing, and use.  The very limited data on the 
level of 1-propanol in the ambient air and water suggest that 
concentrations are very low. 

    1-Propanol is rapidly absorbed and distributed throughout the 
body following ingestion.  Absorption following inhalation is 
expected to be rapid and dermal absorption is expected to be slow. 

    The acute toxicity of 1-Propanol for animals is low whether 
exposed via the dermal, oral, or the respiratory route.  Exposure 
of members of the general population to potentially lethal levels 
may occur through accidental or intentional ingestion.  However, 
only one case of lethal poisoning by 1-propanol has been reported.  
The most likely acute effects of 1-propanol in man are alcoholic 
intoxication and narcosis.  The results of animal studies indicate 
that 1-propanol is 2 - 4 times as intoxicating as ethanol. 

    1-Propanol may be irritating to hydrated skin.

    Animal toxicity data are not adequate to make an evaluation of 
the human health risks associated with repeated or long-term 
exposure to 1-propanol.  However, limited short-term rat studies 
suggest that oral exposure to 1-propanol is unlikely to pose a 
serious health hazard under the usual conditions of human exposure. 

    Inhalation exposure to a concentration of 15 220 mg/m3 caused 
impaired reproductive performance in male rats, but exposure to 
8610 mg/m3 did not.  In pregnant rats, 9001 mg/m3 (3659 ppm) was a 
no-observed-effect level (NOEL) and 14 893 mg/m3 (6054 ppm) was a 
lowest-observed-effect level (LOEL) for both maternal and 
developmental toxicity.  Thus, inhalation exposure to high 

concentrations of 1-propanol produced reproductive and 
developmental toxicity in male and female rats in the presence of 
overt toxicity in the exposed animals.  The concentrations required 
to produce these effects in rats were higher than those likely to 
be encountered under normal conditions of human exposure. 

    1-Propanol was negative in assays for point mutations in 
bacteria.  Although these findings suggest that the substance does 
not have any genotoxic potential, an adequate assessment of 
mutagenicity cannot be made on the basis of the limited data 
available.  The available study is inadequate to evaluate the 
carcinogenicity of 1-propanol in experimental animals.  No data are 
available on the long-term exposure of human populations to 
1-propanol.  Hence the carcinogenicity of 1-propanol for human 
beings cannot be evaluated. 

    Apart from one case of fatal poisoning following ingestion of 
half a litre of 1-propanol, there are practically no reports on the 
adverse health effects from exposure to 1-propanol, either in the 
general population or in occupational groups.  The Task Group 
considers it unlikely that 1-propanol will pose a serious health 
risk for the general population under normal exposure conditions. 

    1-Propanol can be released into the environment during 
production, processing, storage, transport, use, and waste 
disposal.  Because of its primary use as a volatile solvent, most 
of the production volume is eventually released into the 
atmosphere.  However, by reacting with hydroxyl radicals and 
through rain-out, 1-propanol will disappear rapidly from the 
atmosphere, with a residence time of less than 3 days.  Removal of 
1-propanol from water and soil also occurs rapidly so that 
measurable levels are rarely found in any of the three 
compartments.  Adsorption of 1-propanol on soil particles is poor, 
but it is 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 1-propanol,  
bioaccumulation is unlikely and, except in the case of accident or 
inappropriate disposal, 1-propanol does not present a risk for 
aquatic organisms, insects, and plants at concentrations that 
usually occur in the environment. 


2.1  Identity

Chemical  formula:   C3H8O

Chemical structure:      H   H   H
                         |   |   |
                     H - C - C - C - OH
                         |   |   |
                         H   H   H

Common name:          n-propyl alcohol
Abbreviation:        NPA
Common synonyms:     ethyl carbinol, 1-hydroxypropane, propanol, 
                      n-propanol (IUPAC name), 1-propanol (CAS 
                     name), propan-1-ol
Common trade names:  Albacol, Optal, Osmosol extra, UN 1274
CAS registry number: 71-23-8

Specifications:      commercial 1-propanol contains typically 
                     99.85% of the compound and, as main 
                     impurities, water (< 0.1% by weight), 
                     aldehydes (< 0.2% by weight), ethanol 
                     (< 10 mg/kg), and methanol (< 100 mg/kg) 
                     [35, 104-84].
Conversion factors:  1 ppm 1-propanol = 2.46 mg/m3 air; and
                     1 mg 1-propanol/m3 air = 0.41 ppm, at 25 °C 
                     and 101.3 kPa (760 mmHg).

2.2  Physical and Chemical Properties

    1-Propanol is a highly flammable, volatile, colourless liquid 
at room temperature and standard atmospheric pressure.  Its odour 
is described as alcohol-like, sweet, and pleasant [83].  Continuous 
exposure can result in loss of sensitivity to the odour (olfactory 
adaptation) [182].  The compound is completely miscible with water 
and with most organic solvents.  It undergoes all chemical 
reactions typical of primary alcohols.  1-Propanol reacts violently 
with oxidizing agents. 

    Some physical and chemical data on 1-propanol are given in 
Table 1. 

2.3  Analytical Methods

    A summary of methods for the determination of 1-propanol in 
air, water, and biological media is presented in Table 2. 

    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 [109]. 

Table 1.  Some physical and chemical properties of 1-propanol
Physical state                       liquid
Colour                               colourless
Relative molecular mass:             60.09 
Odour perception threshold           <0.07-100 mg/m3a  
Odour recognition threshold          0.32-150 mg/m3b
Melting point (°C)                   -127
Boiling point (°C)                   97
Water solubility                     infinite
Log  n-octanol/water partition        0.34c
Specific density (20 °C)             0.804
Relative vapour density              2.07
Vapour pressure (20 °C)              1.9 kPa (14.5 mmHg)
Flash point 
 (open cup)                          25 °C
 (closed cup)                        15 °C
Flammability limits                  2.1-13.5% by volume
a From:  May [122]; Corbit & Engen [42]; Oelert & Florian 
  [138]; Stone et al. [182]; Dravnieks [50]; Hellman & Small 
  [83]; Laing [111]; and Punter [151].
b From:  May [122] and Hellman & Small [83].
c Experimentally derived by Hansch & Anderson [80].

    Ramsey & Flanagan [154] reported a method for the detection and 
identification of 1-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 
desirable.  After preincubation of the samples with a proteolytic 
enzyme, the method can be used for the analysis of tissues. 

    Gas chromatographic methods, using flame ionization detection, 
are available for the determination of 1-propanol in milk and milk 
products [142], in alcoholic beverages [91, 71, 64, 148], in 
foodstuffs [148], in food packaging [54], in digestive contents, 
silage juices, and microorganism growth cultures [98], and in drug 
raw materials [121].  Methods for the identification of 1-propanol 
as flavour volatile have also been described (see Table 4, section 

Table 2.  Sampling and analysis of 1-propanol
Medium  Sampling method       Analytical             Detection  Sample  Comments            Reference
                              method                 limit      size                                 
Air     sampling on           gas chromatography     0.01 mg/   1-10    suitable for        [195]    
        charcoal, desorption  with flame ionization  sample     litre   personal and                 
        by carbon disulfide   detection                                 area monitoring;             
                                                                        working range, 
                                                                        50-900 mg/m3
Air     sampling on           gas chromatography     0.25       24      suitable for        [112]    
        charcoal, desorption  with flame ionization  mg/m3      litre   area monitoring,             
        by a 1:1 mixture of   detection, packed                         applicable mixtures          
        carbon disulfide and  with Oronite NIW on                       of both polar and            
        water                 Carbopack B                               non-polar solvents           
Air     condensation, pre-    gas chromatography     5 x 10-5           suitable for        [174]    
        concentration by      with flame ionization  mg/m3              analysis of                  
        microdistillation,    detection, packed                         oxygenated                   
        purging by nitrogen,  with Poropack QS                          organic compounds
        trapping on porous    and S                                     in ambient air               
        polymer, desorption                                             
        by heating                                                                                   

Water   concentration by      gas chromatography     0.0001     60 ml   suitable for        [174]    
        microdistillation,    with flame ionization  mg/litre           analysis of                  
        purging by nitrogen,  detection, packed                         oxygenated                   
        trapping on porous    with Poropack QS                          organic compounds            
        polymer, desorption   and S                                     in water                     
        by heating                                                      
Water   direct injection      gas chromatography     1 mg/      0.001   suitable for        [106]    
                              with flame ionization  litre      ml      analysis of a                
                              detection, packed                         mixture of a                 
                              with porous polymer                       wide variety                 
                              Tenax GC                                  of compounds                 

Table 2.  (contd.)                                                                                   
Medium  Sampling method       Analytical             Detection  Sample  Comments            Reference
                              method                 limit      size                                 
Water   direct injection      gas chromatography     0.04 mg/   0.002   suitable for        [194]    
                              with steam as          litre      ml      analysis of                  
                              carrier and flame                         a mixture of                 
                              ionization detection,                     aliphatic                    
                              packed with Chromosorb                    compounds                    
                              PAW modified with                                                      
                              phosphoric acid                                                        
Water   derivatization by     paper electrophoresis  40 mg/     0.1 ml  suitable for        [8]      
        2-fluoro-1-methyl-    with detection by      litre              analysis of                  
        pyridinium  p-toluene  Dragendorff's reagent                     mixtures of                  
        sulfonate in                                                    primary and                  
        presence of                                                     secondary                    
        tridodecylamine                                                 alcohols, such as            
                                                                        in alcoholic                 
Water   derivatization with   TLC (silica gel G)     0.05 mg/   0.005                       [208]    
        4-(6-methylbenzo-     or HPTLC (RP-18) or    litre      ml                                   
        thiazol-2-yl)phenyl   HPLC (Silicagel Si 60  (TLC)                                           
        iso-cyanate in        or Li-Chrosorb RP-18)                                                  
        presence of           with fluorimetric                                                      
        triethylene-diamine   detection                                                              
        in xylene                                                                                    

Water   direct application    spot test detection    2.5 x              a qualitative       [162]    
                              using 0.1% vanadium    10-2 mg/           method with                  
                              (V)- N-phenylbenzo-     drop               interference                 
                              hydroxamate in                            by other alcohols,           
                              alcohol free                              phenols, cresols,            
                              chloroform                                dioxane, methyliso-          
                                                                        butyl ketone,                
                                                                        acetone, reaction 
                                                                        is immediate                 

Table 2.  (contd.)                                                                                   
Medium  Sampling method       Analytical             Detection  Sample  Comments            Reference
                              method                 limit      size                                 
Serum,  extraction by         gas chromatography     0.002      1 ml    suitable for        [114]    
urine   dichloromethane       with mass              mg/litre           determination                
                              spectrometric                             of aliphatic                 
                              detection, column                         alcohols                     
                              was coated with                                                        
                              Emulphor ON-870                                                        
Blood,  addition of           gas chromatography     0.01 mg/   1.1 ml  whole blood is      [21, 13, 
urine,  potassium carbonate;  with flame ionization  litre              pretreated with     110]     
tissue  headspace sampling    detection; split                          sodium fluoride              
                              columns packed with                       or perchloric acid;          
                              polypropylene glycol                      the method is                
                              on Chromosorb W NAW                       applicable to                
                              and SP1000 on                             tissue after                 
                              Carbopack,                                equilibration with           
                              respectively                              water                        
Blood   addition of sodium    gas chromatography     0.01 mg/   0.1 ml                      [209]    
        sulfate; headspace    with flame ionization  litre                                    
        sampling              detection, split fused
                              silica columns: DB 
                              1701 and CP Sil 8 CB


3.1  Natural Occurrence

    1-propanol occurs in fuel oils.  It has been identified as a 
metabolic product of microorganisms and as a flavour volatile in 
foodstuffs (section 5) [104].  Other potential sources of 
atmospheric alcohols are photochemical reactions of hydrocarbons, 
combustion, and, perhaps, oceans [174]. 

3.2  Man-Made Sources

3.2.1  Production levels and processes

    The global capacity for the production of 1-propanol in 1979 
exceeded 130 000 tonnes with most of this capacity in the USA 
[104].  In 1975, the total USA production amounted to 57 000 
tonnes, and 6600 tonnes were exported [176].  In 1979, 85 000 
tonnes were produced [104].  The production in the countries of the 
European Economic Community was estimated at 5100 tonnes in 1979 
and 3300 tonnes over the first 9 months of 1983.  The imports from 
the USA rose from 4000 tonnes in 1979 to 8700 tonnes over the first 
9 months of 1983 [5].  1-Propanol was not manufactured in eastern 
Europe or in the Far East in 1979, but one company in Japan was 
reported to produce this compound by Kirk & Othmer [104]. 

    1-Propanol is manufactured by the hydroformylation of ethene 
(reaction with carbon monoxide and hydrogen) to propionaldehyde, 
which is subsequently hydrogenated to 1-propanol [104].  The 
compound can also be recovered commercially as a by-product of the 
high pressure synthesis of methanol from carbon monoxide and 
hydrogen [35].  It has been produced by the vapour-phase oxidation 
of propane [104] and during the reduction of propene-derived 
acrolein [4, 35].  Earlier, 1-propanol was fractionally distilled 
from the fuel oils that form in the yeast fermentation process for 
the manufacture of ethanol [35]. 

3.2.2   Uses

    The major use of 1-propanol is as a solvent.  It is used as 
carrier and extraction solvent for natural products, such as 
flavourings, vegetable oils, resins, waxes, and gums, and as a 
solvent for synthetic polymers, such as polyvinyl butyral, 
cellulose esters, lacquers, and PVC adhesives.  Other solvent 
applications include the use of 1-propanol in the polymerization 
and spinning of acrylonitrile, in flexographic printing inks, and 
in the dyeing of wool.  1-Propanol is used for both its solvent and 
antiseptic properties in drugs and cosmetics, such as lotions, 
soaps, and nail polishes.  It is also used as a chemical 
intermediate, e.g., in the manufacture of propanal, 1-bromopropane, 
 O,O-dipropylphosphoro-dithioic acid,  n-propyl amines, esters 
(propyl acetate, propyl carbamate), alcoholates, and xanthates. 

    Miscellaneous uses include the application of 1-propanol in 
degreasing agents, polishing compounds (window cleaners, floor 
polishes), and brake fluid, as coupling and dispersing agents, and 
as a ruminant feed supplement.  It improves the water tolerance of 
motor fuels [82, 104, 35, 198]. 

3.2.3  Waste disposal

    1-Propanol may enter the atmosphere, water, and/or soil 
following waste disposal (section 4.1).  At landfill sites, 
1-propanol has been identified in the air and leachates (section 
5.1).  Emission of 1-propanol via waste gases and waste water 
occurs in industry, and diffuse airborne emissions occur during the 
use of the compound (section 4.1). 
    1-Propanol can be removed from waste water by biodegradation 
(section 4.3.1).  Activated carbon adsorption is not feasible, 
because the compound is poorly adsorbed [69].  Removal of the 
compound from waste water by reverse osmosis (hyperfiltration) may 
be successful, depending on the type of membrane.  Cellulose 
acetate membranes yielded an average of 40% separation of 
1-propanol [53], while cross-linked polyethyleneimine membranes 
yielded 60 - 85% separation for a primary alcohol, such as 
ethanol [55].  Ozonization of 1-propanol appears to be too slow a 
process to be of any significance for water treatment [90]. 

4.1  Transport and Distribution Between Media

    In view of the physical properties and the use pattern of 
1-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 is its 
emission into water and soil.  In the USA, industrial losses into 
the environment were estimated at 1.5% of the production in 1976, 
and 75% of the 1-propanol produced was estimated to be eventually 
released into the atmosphere [49]. 

    Intercompartmental transfer of 1-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.  Transport of 1-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 1-propanol in 
soil are scarce.  With respect to adsorption, there is one study 
showing that the compound is poorly adsorbed on activated carbon 
[198].  Since 1-propanol is completely miscible with water, it can 
be expected to be mobile in the soil.  It has also been shown to 
increase the permeability of soil to aromatic hydrocarbons [57]. 

4.2  Abiotic Degradation

    Once in the atmosphere, 1-propanol is mainly degraded 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, photodegradation 
is not expected [34].  Experimentally determined rate constants  
for the reaction between 1-propanol and hydroxyl radicals are 
0.43 x 10-11 cm3/molecule per second at 19 °C [32], and 0.53 x 
10-11 cm3/molecule per second at 23 °C [141].  Atmospheric 
residence times of 2.7 and 2.2 days, respectively, can be calculated 
on the basis of these rate constants [44].  These short lifetimes 
will prevent migration of the chemical to the stratosphere. 

    The initial reaction product of 1-propanol with a hydroxyl 
radical is an alpha-hydroxypropyl.  By analogy with the irradiation 
of ethanol in an NOx-air atmosphere, these radicals are expected to 
react with oxygen, almost exclusively with hydrogen abstraction 
from the hydroxyl group to produce propionaldehyde [34]. 

    Hydrolysis or light-induced degradation of 1-propanol in water 
cannot be expected.  No data are available on abiotic degradation 
in soil. 

4.3  Biotransformation

4.3.1  Biodegradation

    The results of the determination of the biological oxygen 
demand (BOD) of 1-propanol in various sources at 20 °C, using 
dilution methods, are summarized in Table 3.  Unless otherwise 
stated, they are expressed as a percentage of the theoretical 
oxygen demand (ThOD), which is 2.40 g oxygen/g 1-propanol.  The 
chemical oxygen demand (COD) was reported to be 91% of the ThOD 
Table 3.  BOD of 1-propanol
Dilution water  Source or seed material  Adaptation  BODxa  Value     Reference
                                         (+/-)              (% ThOD)
Fresh           domestic waste water                 BOD5   64        [149]
                                                     BOD20  75  
                domestic waste water                 BOD5   93        [202]
                synthetic waste water                BOD5   97        [202]
                activated sludge         +           BOD5   99b       [144]

Salt            domestic waste water                 BOD5   43        [149]
                                         -           BOD20  73  
a BODx = biological oxygen demand after x days of incubation.
b Expressed as percentage of the COD.
    Gerhold & Malaney [66] added 1-propanol to undiluted activated 
sludge and found an oxygen uptake of 37% of the ThOD in 24 h. 

    There are two reports on anaerobic biodegradation.  Typical 
1-propanol removal efficiencies for an anaerobic lagoon treatment 
facility with a retention time of 15 days were 77% and 81% after 
loading with concentrated wastes [92].  In closed bottle studies, 
1-propanol was completely degraded anaerobically by an acetate- 
enriched culture, derived from a seed of domestic sludge.  The 
culture started to utilize cross-fed, 1-propanol after 4 days, at a 
rate of 110 mg/litre per day.  In a mixed reactor with a 20-day 
retention time, seeded by the same culture, 41% removal was 
achieved in the 20 days following 70 days of acclimation to give a 
final 1-propanol concentration of 10 000 mg/litre [38]. 

4.3.2  Bioaccumulation

    1-Propanol is completely miscible with water.  Its log 
 n-octanol/water partition coefficient is 0.34 [80].  A 
bioconcentration factor of 0.7 can be calculated using the formula 
of Veith & Kosian [197].  In addition, the compound is 
biodegradable.  In view of these data, no bioaccumulation is 


5.1  Environmental Levels

    The rapid chemical and physical removal of 1-propanol from air 
and water is reflected in the few reports indicating its presence 
in these compartments.  No data are available on the occurrence of 
the compound in soil. 

    In 11 samples of air from a city in the USA in 1982, the 
average concentration of 1-propanol was 0.00005 mg/m3, while the 
compound was not detected in 18 rural samples [174]. 

    1-Propanol at a concentration of 73 mg/m3 was detected in the 
air beneath the surface of 1 out of 6 landfill sites sampled in the 
United Kingdom.  This particular site was used for the disposal of 
domestic waste [216].  1-Propanol was also detected in the leachate 
from two sanitary landfill sites in the USA.  This would, at least 
partly, have originated from the anaerobic degradation of organic 
compounds by microorganisms [30, 102].  1-Propanol was identified 
as a product of the bacterial fermentation of dead blue-green algae 
[214], fish spoilage bacteria [3], and Kluyveromyces lactis yeast 
[78].  The compound was measured in fresh swine manure [215]. 
5.2  General Population Exposure

    1-Propanol was detected in drinking-water samples in the USA at 
a concentration of 0.001 mg/litre [165]. 

    Alcoholic beverages nearly always contain 1-propanol as a 
product  of fermentation.  Beer contains up to 195 mg/litre [17], 
wine up to 116 mg/litre [18], various types of spirit up to 
3520 mg/litre [130], and neat ethanol up to 2910 mg/litre [9, 19, 
146, 140, 186, 148]. 

    Studies summarized in Table 4 show the presence of low levels 
of 1-propanol as a flavour volatile in a variety of foodstuffs and 
non-alcoholic drinks.  According to Stofberg & Grundschober [179], 
most of the 1-propanol that they found in the foodstuffs and drinks 
was of natural origin, not added. 

5.3  Occupational Exposure

    Workers are potentially exposed to 1-propanol during the 
production of the compound itself or its derivatives, or during its 
use in solvent-type applications.  No data are available on levels 
of exposure. 

Table 4.  1-Propanol as a flavour volatile in foodstuffs and 
non-alcoholic drinksa
           Foodstuff/drink                             Reference
Common name                Scientific name
Kefir culture                                          [142]      
Cream culture                                          [142]      
Filberts (roasted)          Corylus avellana            [103]      
Raw milk                                               [97]       
Heat-treated milk                                      [97]       
Kumazasa Sasa                                          [134]      
Heated trioleinb                                       [123]      
Boiled buckwheat flour      Fagopyrum esculentum        [211]      
Ripe tomato, tomato         Lycopersicon esculentum     [39]       
 juice, puree, and paste                                 
Kogyoku apple                                          [212]      
Apple and apple juice                                  [179]      
Tomato                      Lycopersicon esculentum     [179]      
White bread                                            [179]      
Butter                                                 [179]      
Cheddar/Swiss cheese                                   [179]      
Swiss Gruyere cheese                                   [22]       
Soy sauce (Shoyu)                                      [135]      
Fish sauce (Patis)                                     [163]      
Pigweed                     Amaranthus retroflexus      [58]       
Winged bean (raw/roasted)   Psophocarpus tetragonalobus [47]       
Soybean (raw, roasted)      Glycine max                 [47]       
Potato tuber                Solanum tuberosum           [205, 206] 
Roasted watermelon seeds    Citrullus colocynthis       [175]
Babaco fruit                Carica pentagona            [168]
Tilsit cheese                                          [133]
Endive                      Cichorium endivia           [73]
Valancia orange juice                                  [127]
a Detected by GC/FI, GC/FP, or GC/MS.
b The triolein was heated at 185 °C with periodic injection of 
  steam, during 75 h.                                        


6.1  Absorption

6.1.1  Animals

    Data on absorption following inhalation or dermal exposure are 
not available. 

    Oral exposure of Wistar rats to one dose of 3004 mg 1-propanol/kg 
body weight in water resulted in a maximum blood concentration of 
1860 mg 1-propanol/litre, 1.5 h after exposure [11]. 

    In rabbits receiving single intraperitoneal doses of 800, 1200, 
or 1600 mg 1-propanol/kg body weight in saline, maximum blood 
concentrations, attained within 0.5 h, were proportional to the 
dose [139]. 

    Blood levels of 1-propanol were determined in groups of 3 adult 
(200 - 300 g) Sprague-Dawley rats following 1, 10, or 19 consecutive 
7-h daily exposures to measured concentrations of 9001 or 14 893 mg/m3 
(3659 or 6054 ppm), and after a single exposure to 23 968 mg/m3 
(9743 ppm).  Immature (110 - 120 g) females of the same strain were 
also evaluated following a single 7-h exposure to 23 968 mg/m3 
(9743 ppm).  In the immature females, the blood level of 1-propanol 
was 1640 mg/litre.  The blood levels in adult rats following a single 
exposure were 26 mg/litre (9001 mg/m3), 42 mg/litre (14 893 mg/m3), 
and 66 mg/litre (23 968 mg/m3).  Blood levels in adults were not 
detected following 10 and 19 exposures to 9001 mg/m3 (3659 ppm), and 
were 49 and 43 mg/litre after exposure to 14 893 mg/m3 (6054 ppm) [132]. 

6.1.2  Human beings

    Ten human volunteers drank 1-propanol in ethanolic orange juice 
at doses of 3.75 mg 1-propanol 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 1-propanol was 0.85 ± 0.17 mg/litre (mean ± 
standard deviation).  When the blood samples taken at comparable 
times were analysed after incubation with aryl sulfatase (EC, an average peak concentration of 0.92 ± 0.19 mg/litre was 
measured, just after exposure [19].  These data suggest that 
1-propanol is not extensively sulfate conjugated. 

6.2  Distribution

6.2.1  Animals

    1-Propanol, a compound that is infinitely soluble in water, is 
rapidly distributed throughout the body of various species [1, 157].  
When 14C-1-propanol was administered intraperitoneally to rats 
in a single dose of 450 mg/kg body weight, the concentrations of 
1-propanol and/or its metabolites in the blood, liver, and brain 
were similar 5 min after administration.  Radioactivity was 

detected in the nuclear and mitochondrial fractions of liver and 
brain homogenates.  Maximum levels were reached later in these 
subcellular fractions than in the whole organs [125]. 

6.2.2  Human beings

    In the presence of other aliphatic alcohols, after oral 
ingestion of an alcoholic beverage, 1-propanol appears to be widely 
distributed throughout the human body [14, 15]. 

    1-Propanol was shown  in vitro to bind to human alpha-fetoprotein 
with a higher affinity than either methanol or ethanol, which is in 
accordance with its higher hydrophobicity [87]. 

6.3  Metabolic Transformation

6.3.1  Animals

    The metabolic fate of 1-propanol is shown in Fig. 1.  
1-Propanol is primarily oxidized to propionaldehyde by the non-
specific cytosolic enzyme alcohol dehydrogenase (ADH) (EC 
followed by conversion to propionic acid  [139].   ADH activity is 
known to be the rate-limiting factor in the elimination of 
aliphatic alcohols.  The Michaelis-Menten  constant (Km) of ADH 
purified from rat, dog, horse, or human liver with 1-propanol as 
substrate, is lower than the Km for ethanol or 2-propanol [45, 7, 
72].  Hence, 1-propanol is a better substrate for ADH than ethanol 
or 2-propanol and retards the elimination of the latter compounds.  
It has been shown  in vitro that rat and rabbit liver microsomal 
oxidases (EC are also capable of oxidizing 1-propanol to 
propionaldehyde [188, 126].  The relative affinity of the 
microsomal ethanol oxidizing system (MEOS) for 1-propanol is about 
three times higher than for ethanol and is in accordance with their 
relative hydrophobicities.  In rabbits, cytochrome P-450 isozyme 3a 
is responsible for the microsomal metabolism of alcohols [126], in 
rats, it is isozyme P-450j, and in human liver, isozyme P-450 HLj 
[160].  These forms of cytochrome P-450 are inducible by ethanol 
[126, 160], it may therefore be expected that in individuals who 
regularly consume ethanol, the MEOS will contribute to the overall 
oxidation of 1-propanol.  The metabolism of  N-nitrosodimethylamine 
and 1-propanol is mediated by the same isozyme of cytochrome P-450 
[160].  Tomera et al., [191] showed that 1-propanol inhibited the 
metabolism of  N-nitrodimethylamine in isolated perfused rat livers. 

    As in the case of propionic acid formed from the catabolism of 
odd chain fatty acids, propionic acid arising from the oxidation of 
1-propanol can form a coenzyme A (CoA) conjugate [157] catalysed by 
acyl CoA synthetase (EC  A number of different pathways 
for the further metabolism of propionyl-CoA (Fig. 1) are discussed.  
However, the relative contribution of each of these to the overall 
elimination of 1-propanol is not known. 


(i) In the methylmalonyl pathway, propionyl-CoA is carboxylated to 
methylmalonyl-CoA, this is followed by trans-carboxylation to 
succinyl-CoA, which subsequently enters the tricarboxcylic acid 
cycle to be metabolized to carbon dioxide and water. 

(ii) In the lactate pathway, the propionyl-CoA is dehydrogentated 
to acrylolyl-CoA, alpha-hydration gives L-lactoyl-CoA, which is 
hydrolysed to lactate. 

(iii) In another pathway the acrylolyl-CoA is hydrated to 
3-hydroxypropionyl-CoA, deacylation and oxidation result in the 
formation of malonic acid semialdehyde, which is converted to 
acetyl-CoA.  These reactions, which constitute the major pathways 
for propionic acid metabolism in plant mitochondria, also occur in 

(iv) The propionyl CoA may also participate in triglyceride 

(v) The obligatory formation of propionyl carnitine required for 
the transport of propionic acid into mitochrondria may also be an 
excretory pathway under conditions of high carnitine and propionic 
acid concentrations [158, 153].  

    Propionic acid and/or propionyl-CoA are potent inhibitors of 
several mitochondrial enzymes required for fatty acid oxidation, 
gluconeogenesis, and ureagenesis; their inhibitory effects can be 
reversed with carnitine [24, 23].  The formation of propionyl-CoA, 
its metabolism and effects on oxidative metabolism provide an 
explanation for the hepatic effects observed in rats after high 
oral exposure to 1-propanol (section 8.2) and for the biochemical 
effects seen in some studies (section 8.3.1).  Indeed the 
accumulation of acyl-CoA esters, including propionyl-CoA, is 
implicated in the pathogenesis of Reye syndrome [43]. 

6.4  Elimination and Excretion

    Aliphatic alcohols may be eliminated from the body via expired 
air or the urine.  Theoretically, urinary metabolites may arise 
from oxidation or from conjugation with glucuronic acid or sulfate.  
There are no reports of the excretion of unchanged 1-propanol in 
expired air or urine and, following an oral dose to rabbits of 
800 mg/kg, only 0.9% was found in the urine as propyl-glucuronide 
and none as a sulfate conjugate [100]. 

6.4.1  Animals

    Available  in vivo data, reviewed by Rietbrock & Abshagen [157], 
showed that the elimination of 1-propanol was dose independent 
above a single oral dose of 1000 mg/kg body weight in rats and 
above a single intraperitoneal dose of 1200 mg/kg body weight in 
rabbits [139, 1, 11].  The rate of the zero-order elimination of 
the compound from the blood of rats that had received a single oral  
dose of 3000 mg/kg body weight was found to be 510 mg/kg body 
weight per hour [11].  At lower doses, the elimination rate was 
first order.  When rats were given a single oral dose of 1000 mg/kg 
body weight, the half-life of 1-propanol was 45 min [1].  The 
overall metabolism and elimination of 1-propanol are described in 
section 6.3.1.  In mice, a half-life of 57 min was estimated for 
the exponential elimination phase following a single oral exposure 
[1].  This should be considered an approximation because there were 
only 2 or 3 time points per dose. 

     In vitro, the elimination of 1-propanol from the perfusate of 
rat liver was also shown to be saturable, a zero-order phase being 
succeeded below a concentration of 78 mg/litre by an exponential 
phase with a half-life of 14 min [7]. 

6.4.2  Human beings

    No data were available describing the elimination kinetics of 
1-propanol in human beings. 

    When 10 volunteers drank 1-propanol in ethanolic orange juice 
at doses of 3.75 mg 1-propanol and 1200 mg ethanol/kg body weight 
over a period of 2 h, the compound was detected in the blood and in 
the urine, partly as glucuronide.  The total urinary excretion of 
1-propanol was 2.1% of the dose.  The urinary levels of 1-propanol 
were lower when the amount of simultaneously ingested ethanol was 
less, showing competition for ADH between 1-propanol and the 
ethanol overdose [19, 20]. 


7.1  Aquatic Organisms

    A summary of acute aquatic toxicity data is presented in Table 
5.  In none of these studies was the concentration of 1-propanol 
reported to have been measured.  In view of the volatility of the 
compound, it can be expected that the toxic effects observed in the 
open-system studies occurred at lower concentrations than the 
nominal ones.  

    Several short-term studies have also been conducted.  Seiler et 
al. [167] determined the breakpoint of bioinhibition for a total 
of 20 strains of several 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 
1-propanol in an open system at 30 °C, 100% growth inhibition 
occurred at concentrations of 10 000 - 30 000 mg/litre of medium.  
No analysis for the compound was reported. 

    Inhibition of cell multiplication of blue algae  (Microcystis 
 aeruginosa) and green algae  (Scenedesmus quadricauda) reached 100% 
after 8 days of static exposure to 255 and 3100 mg 1-propanol/litre 
water, respectively, in a closed system at 27 °C and a pH of 7 
[25, 27]. 

7.2  Terrestrial Organisms

7.2.1  Insects

      The toxicity of 1-propanol for insect larvae is summarized in 
Table 5.  In static tests, the 48-h LC50 values for adults of the 
fruit fly strains of  Drosophila melanogaster and  Drosophila 
 simulans were between 18 490 and 24 120 mg/litre of nutrient medium 
and 11 260 and 12 860 mg/litre of nutrient medium, respectively [46]. 

7.2.2  Plants

      The effects of 1-propanol on the rate of seed germination 
have been 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 8050 
mg 1-propanol/litre water [40].  The germination of white amaranth 
 (Amaranthus albus) seeds was stimulated in a dose-related manner 
after 5 h incubation at 25 °C on filter papers moistened with a 
solution containing 3600 - 36 050 mg 1-propanol/litre water [36].  
Reynolds [36] measured 50% inhibition of germination of lettuce 
 (Lactuca sativa) seeds after incubation for 3 days at 30 °C on agar 
containing 3065 mg 1-propanol/litre.  The percentage germination 
and the axis length of soya bean  (Glycine max) seeds, with the 
testa removed, were not reduced after exposure to pure 1-propanol 
for 2 h.  After treatment with a 50% (v/v) 1-propanol/water mixture 
for 2 min, germination was almost completely inhibited and axis 
length was reduced [150]. 

Table 5.  Acute aquatic toxicity of 1-propanol
Organism                   Temper-  pH       Dissolved   Hardness    Systema  Exposure  Parameter       Nominal         Reference
                           ature             oxygen      (mg/CaCO3/           period                    concentration            
                           (°C)              (mg/litre)  litre)                                         (mg/litre)               
Pseudomonas putida         25       7                                closed   16 h      TTb             2 700           [27]      
Activated sludge           21       7.4-8                            closed   3 h       50% inhibition  1 000           [105]     
                                                                                        of respiration                            
Acclimated mixed           30       6.8                              closed   1.2 h     50% inhibition  19 085          [196]     
waste-water culture                                                                     of respiration                            
 Entosiphon sulcatum        25       6.9                              closed   72 h      TTb             38              [26]      
 Chilomonas paramecium      20       6.9                              closed   48 h      TTb             175             [29]      
 Uronema parduczi           25       6.9                              closed   20 h      TTb             568             [28]      
 Selenastrum capricornutum  25-26                                     closed   96 h      NOAECc          2 000           [172]     
 Scenedesmus pannonicus     25-26                                     closed   48 h      NOAECc          2 900           [172]     
 Chlorella pyrenoidosa      25-26                                     closed   48 h      NOAECc          1 150           [172]     
Hydra oligactis            17       8.2-8.4  >5                      closed   48 h      LC50            6 800           [170]    
Flatworm  (Dugesia)         20       8.2-8.4  >5                      closed   48 h      LC50            4 700           [170]    
Tubificid worm             20       8.2-8.4  >5                      closed   48 h      LC50            9 200           [170]    

Giant pond snail           20       8.2-8.4  >5                      closed   48 h      LC50            6 500           [170]    
 (Lymnea stagnalis)                                                                                                                

Table 5.  (contd.)                                                                                                                
Organism                   Temper-  pH       Dissolved   Hardness    Systema  Exposure  Parameter       Nominal         Reference
                           ature             oxygen      (mg/CaCO3/           period                    concentration            
                           (°C)              (mg/litre)  litre)                                         (mg/litre)               
Water flea                 20       8        >2          250         open     24 h      EC50d           4 415           [27]     
 (Daphnia magna)e                                                                        EC0             3 336                     
                                                                                        EC100           5 909                     
                           19                                        open     48 h      LC50            7 080           [33]      
Water flea                 19                                        open     48 h      LC50            3 025           [33]      
 (Daphnia pulex)e                                                                                                                  
Water flea                 19                                        open     48 h      LC50            5 820           [33]      
 (Daphnia cucullata)e                                                                                                              
Isopod                     20       8.2-8.4  >5          209         closed   48 h      LC50            2 500           [170]    
 (Asellus aquaticus)                                                                                                               
Scud  (Gammarus pulex)      20       8.2-8.4  >5          209         closed   48 h      LC50            1 000           [170]    
Mosquito larvae            22-24                                     open     4 h       LC50            10 450          [107]     
 (Aedes aegypti)                                                                                                                   
Mosquito larvae  (Aedes     26       8.2-8.4  >5          209         open     48 h      LC50            4 400, 4 800    [172]    
 aegypti, Culex pipiens)                                                                 LC0             3 200, 3 600              
Midge larvae               20       8.2-8.4  >5          209         closed   48 h      LC50            2 350           [170]    
 (Chironomus gr. thummi)                                                                                                           
Leech larvae               20       8.2-8.4  >5          209         closed   48 h      LC50            1 400           [170]    
 (Eropdella octoculata)                                                                                                            
Dragon fly larvae          20       8.2-8.4  >5          209         closed   48 h      LC50            4 200           [170]    
 (Ischnura elegans)                                                                                                                
Stonefly larvae            20       8.2-8.4  >5          209         closed   48 h      LC50            1 520           [170]    
 (Nemoura cinerea)                                                                                                                 
Mayfly larvae              20       8.2-8.4  >5          209         closed   48 h      LC50            3 110           [170]    
 (Cloeon dipterum)                                                                                                                 
 Corixa punctata (larvae)   20       8.2-8.4  >5          209         closed   48 h      LC50            2 000           [170]    

Table 5.  (contd.)                                                                                                                
Organism                   Temper-  pH       Dissolved   Hardness    Systema  Exposure  Parameter       Nominal         Reference
                           ature             oxygen      (mg/CaCO3/           period                    concentration            
                           (°C)              (mg/litre)  litre)                                         (mg/litre)               
Creek chub                 15-21    8.3                  98          open     24 h      LC0             200             [68]      
 (Semotitus atromaculatus)                                                                                                         
Golden orfe                20       7-8      >5          200-300              48 h      LC50            4 320, 4 560    [99]     
 (Leuciscus idus melanotus)                                                              LC0             3 600, 4 000              
Fathead minnow             20       8.2-8.4  >5          209        open      48 h      LC50            5 000           [172]    
 (Pimephales promelas)                                                                   LC0             2 600                     
Rainbow trout              15       7-8      >5          98         open      48 h      LC50            3 200           [172]    
 (Salmo gairdneri)                                                                       LC0             2 000                     
Paddy fish                 24       8.2-8.4  >5          209        open      48 h      LC50            5 900           [172]    
 (Oryzias latipes)                                                                       LC0             4 400                     
South African clawed toad  20       8.2-8.4  >5          209        open      48 h      LC50            4 000           [171]    
 (Xenopus laevis)                                                                                                                  
Mexican axolotl            20       8.2-8.4  >5          209        open      48 h      LC50            4 000           [171]    
 (Ambystoma mexicanum)                                                                                                             
SEA WATER                                                                                                                         
 Photobacterium             15                                                  15 min   50% light       8 686           [84]      
 phosphorerum                                                        closed              reduction                                 
                           5                                                   5 min    50% light       17 700          [48]      
                                                                    closed     15 min   reduction       18 400                    
Brine shrimp               24                                                 24 h      LC50            4 200           [149]f    
 (Artemia salina)                                                    open                                                          
Harpacticoid copepod       21       7.9      >5                               96 h      LC50            2 300           [12]g    
 (Nitocra spinipes)                                                                                                                

Table 5.  (contd.)                                                                                                                
Organism                   Temper-  pH       Dissolved   Hardness    Systema  Exposure  Parameter       Nominal         Reference
                           ature             oxygen      (mg/CaCO3/           period                    concentration            
                           (°C)              (mg/litre)  litre)                                         (mg/litre)               
Bleak  (Alburnus alburnus)  10       7.9      >5                     open      96 h      LC50            3 800           [12]g    
a  Static systems used in all experiments reported.
b  TT = toxic threshold for inhibition of cell multiplication.
c  NOAEC = no-observed-adverse-effect-concentration; effect is growth inhibition.
d  Effect is complete immobilization.
e  Age of  Daphnia was 24 h for  Daphnia magna and  Daphnia pulex, and 11 ± 1 day for  Daphnia cucullata.
f  Salinity was 2.8%.
g  Salinity was 0.7%.
    1-Propanol was marginally effective in breaking the dormancy of 
seeds of genetically pure dormant lines of wild oat  (Avena fatua) 
after 5 days of exposure to solutions containing up to 1202 mg/litre.  
Seed viability was affected at higher concentrations [2]. 

    When excised seedling roots of maize  (Zea mays) were treated by 
vacuum infiltration in a 5% solution of 1-propanol in water, 3 
times for 60 seconds, and then incubated anaerobically at 28 °C, 
nitrite accumulation increased by 10 times or more, the utilization 
of nitrate increased, and the utilization of exogenous nitrite was 
inhibited.  These effects were enhanced under aerobic conditions 
[75].  Dry et al. [51] observed that stimulation of nitrite 
accumulation in pea and wheat roots under aerobic conditions was 
accompanied by a decline in the cellular levels of glucose-6-
phosphate.  It was suggested by Gray & Cresswell [75] that an 
increase in the utilization of nitrate was related to increased 
access of nitrate to the site of nitrate metabolism as a result of 
an increase in membrane permeability. 


8.1  Single Exposures

8.1.1  Mortality

    The available LD50s for various animal species are summarized 
in Table 6.  Based on mortality estimates, 1-propanol exhibits low 
toxicity, except in very young rats.  Oral LD50 values for several 
animal species range between 1870 and 6800 mg/kg body weight.  For 
very young rats, oral LD50s of 560 - 660 mg/kg body weight have 
been reported [152]. 

    An intraperitoneal dose of 785 mg 1-propanol/kg was lethal to 10 
out of 10 C57B/6J and 10 out of 10 DBa/2J mice, but a dose of 392 mg/
kg did not cause any deaths in either strain [183].  An LD16 of 
450 mg/kg was reported in rats after intraperitoneal administration. 

    When rats were exposed to 1-propanol vapour for 4 h at a 
concentration of approximately 9840 mg/m3, 2 out of 6  died within 
14 days [173]. 

8.1.2  Signs of intoxication

    Osborne-Mendel or Sherman rats of both sexes receiving a lethal 
oral dose of undiluted 1-propanol became comatose within a few 
minutes [187].  Deep narcosis occurred in mice exposed through 
inhalation of 1-propanol at a concentration of 50 mg/litre for 2 h. 

    Very young rats (60 - 100 g) of an unspecified strain and of 
both sexes, received a single oral dose of between 150 and 3000 mg 
undiluted 1-propanol/kg body weight.  Animals that died showed 
hyperaemia, vacuolation, and dilated sinusoids in the liver, and 
hyperaemia, tubular cloudy swelling, and tubular necrosis in the 
kidneys [152]. 

    When anaesthetized Sprague-Dawley rats were made to inspire 
160 mg of the undiluted compound, all 9 exposed rats died within 
165 min, 6 of them dying immediately from respiratory arrest.  All 
controls survived and were killed 24 h later.  It was not reported 
whether the latter were sham-exposed or not.  The average absolute 
lung weight of the exposed rats was increased by 92%.  The lungs 
showed oedema and small areas of focal haemorrhage [65]. 

    Special studies on neurotoxic and behavioural effects, and on 
biochemical effects are described in sections 8.3 and 8.4. 

Table 6.  LD50s for 1-propanol
Species            Sex       Route of         Observation  LD50 (mg/kg   Comments         Reference
                             exposure         period       body weight)
Wistar rat (non-   male      oral             14 days      1870          vehicle: water   [173]
Osborne-Mendel     male,     oral             until        6500          undiluted        [187]
or Sherman rat     female                     recovery
CD mouse           not       oral             3 days       6800          undiluted        [164]

Rabbit             male,     oral             1 day        2820                           [130]

Wistar rat         male      intravenous      5 days       590           vehicle: water   [190]
H mouse            male      intravenous      5 days       697           vehicle: water   [190]
                   female    intravenous      not          1090          vehicle: water   [40]

Chinchilla rabbit  male,     intravenous      5 days       483           vehicle: water   [190]
Wistar rat         male      intraperitoneal  5 days       2247          vehicle: water   [190]
H mouse            male      intraperitoneal  5 days       3695          vehicle: water   [190]
Syrian hamster     male      intraperitoneal  5 days       2337          vehicle: water   [190]
Guinea-pig                   intraperitoneal  5 days       1208          vehicle: water   [190]
New Zealand        male      dermal           14 days      4050          1/10 of body     [173]
rabbit                                                                   surface exposed 
                                                                         under cover for 
                                                                         24 h
8.1.3  Skin, eye, and respiratory tract irritation; sensitization 

    Data for skin and eye irritation were not available.  One skin 
sensitization test has been reported concerning an ear-swelling 
test on CF1 mice.  No sensitization was observed [61].  Although 
the test requires further validation, it correctly discriminated 
between a number of known positive and negative human sensitizing 
agents.  The authors claim it to be an accurate, sensitive, and 
efficient method for evaluating delayed contact sensitization. 

    The sensory irritation of 1-propanol was investigated using a 
50% reflex decrease in the respiratory rate of mice (RD50) as an 
index.  Only the heads of the mice were exposed.  An exposure-
related effect was found with RD50 values for the first 10 min of 
exposure of 31 252 mg/m3 for Swiss Webster mice [101] and 
33 604 mg/m3 for CF-1 mice [108].  The potential of 1-propanol as 
a respiratory irritant is therefore low. 

8.2  Repeated Exposures

    Only a few data are available concerning the oral exposure of 

    When 3 male and 3 female rats of unspecified strain were 
exposed to 4 daily oral doses of 2160 mg undiluted 1-propanol, no 
deaths occurred and no gross pathological signs were seen in the 
liver [187]. 

    In a group of 6 male rats of unspecified strain, receiving 
drinking-water containing 1-propanol at a concentration of 60 090 
mg/litre for 4 months, food consumption, body weight gain, and 
liver histopathology were comparable to those of the control group. 
It should be noted that the authors reported a dose rate of 3 mg/kg 
body weight per day, while a dose rate of approximately 3000 mg/kg 
body weight per day seems more appropriate, assuming a water 
consumption of 20 ml/day and a body weight of 400 g [85]. 

    Groups of 10 Wistar rats were exposed to 1-propanol in the 
drinking-water at a concentration of 320 000 mg/litre (calculated 
by the Task Group to be equivalent to approximately 16 000 mg/kg 
body weight per day, on the basis of the assumptions made above) 
for 5, 9, or 13 weeks.  Control groups comprised 10 rats each.  The 
exposed rats gradually became weak, losing their appetites and 
showing a decreased body weight gain.  Electron microscopic studies 
of the liver showed irregularly shaped megamitochondria with few 
cristae, and normally sized but irregularly shaped mitochondria 
with a decreased number of cristae.  Biochemical changes included a 
decreased state 3 respiration using glutamate as a substrate and 
decreased specific activities of cytochrome c oxidase (EC  
and monoamine oxidase (EC [203]. 

8.3  Neurotoxic and Behavioural Effects

    In one study on anaesthetized mongrel dogs, it was shown that 
1-propanol, as well as other primary alcohols, could increase the 
permeability of the blood-brain barrier.  The dogs received a 
sodium fluorescein solution and 0.578 mg 1-propanol in saline, 

intravenously.  The concentration of sodium fluorescein in the 
cerebrospinal fluid rose to a maximum within 10 min and returned to 
control levels, 3 h after exposure [78]. 

    The oral ED50 (1440 mg/kg body weight) for narcosis in rabbits 
exposed to 1-propanol was 4 times lower than that for ethanol 
[129].  Deep narcosis occurred in mice exposed through inhalation 
to 50 mg 1-propanol/litre for 2 h, and a 40-min exposure to 2.3 mg/
litre reduced the unconditioned flexor response in rabbits.  When 
rabbits were intravenously infused with 1-propanol at a rate of 9 - 
30 mg/min per kg body weight, positional nystagmus with an 
inhibited rotatory response was observed at and above a blood 
concentration of 900 mg/litre [137]. 

    The intraperitoneal ED50 for loss of righting reflex in Swiss 
Webster mice administered 1478 mg 1-propanol/kg body weight was 2.8 
times lower than that for ethanol [117].  When C57BL/6J or DBA/2J 
mice were given a single dose of 1-propanol intraperitoneally, both 
strains showed decreased activity in the open field test at 
392 mg/kg body weight, but the decrease was not significant.  All 
mice given 785 and 1570 mg/kg body weight died [183].  The rotarod 
performance of Swiss-Cox mice decreased in a dose-related manner 
after single oral doses of 1-propanol of 2000 or 4000 mg/kg body 
weight.  A dose of 1000 mg/kg body weight did not cause behavioural 
impairment.  When the study was repeated on days 4, 6, 7, and 8 
after the first trial, tolerance did not develop [1].  
    The threshold for the induction of ataxia in Sprague-Dawley 
rats following intraperitoneal exposure was 799 mg/kg body weight 
[119].  In a tilted plane test, the performance of rats decreased 
by an average of 71% after oral exposure to 2000 mg/kg body weight.  
On a molar basis, 1-propanol was 2.5 times as intoxicating as 
ethanol [204]. 

    According to several investigators, depression of the central 
nervous system by 1-propanol was related to interactions with 
neuronal membranes.  Lyon et al. [117] observed a high correlation 
between the narcotic potencies of the aliphatic alcohols, including 
1-propanol, in mice and their ability to disorder the brain 
synaptosomal plasma membrane  in vitro, as measured by electron 
paramagnetic resonance, which was in turn related to membrane 
solubility.  A change in membrane fluidity was shown to occur in 
isolated synaptosomal plasma membranes of rat cortex  in vitro by a 
decrease in 1,6-diphenyl-1,3,5-hexatriene fluorescence polarization 

    Functional loss due to disruption of membrane integrity by 
1-propanol was observed  in vitro.  The action potentials of the 
sciatic nerves of the toad  (Bufo marinus) [155] and of giant axons 
of the squid  (Loligo forbesi) [143] were decreased by 1-propanol. 
In isolated rat phrenic nerve-diaphragm, 1-propanol increased the 
amplitudes of end-plate and miniature end-plate potentials and the 
number of quanta of acetylcholine of end-plate potentials [62].  
The compound also affected the rate of decay of postsynaptic 

currents in the neuromuscular junction of the crayfish  (Cherax 
 destructor) [200], and in the phrenic nerve-diaphragm of the rat 

    Effects on the ionic currents underlying the changes in 
excitability described above were also investigated  in vitro.  
1-Propanol inhibited both the K+-stimulated and the Na+-dependent 
influx of Ca2+ ions into isolated rat brain synaptosomes [80, 81, 
124], and the influx of Na+ ions into rat brain synaptosomes [128].  
It decreased the Na+ and K+ currents in the giant axons of the 
squid  (Loligo forbesi) [143], and in sciatic nerve fibres of the 
clawed toad  (Xenopus laevis) [6].  The interference of 1-propanol 
with the transport of Ca2+ ions across biological membranes was 
also shown  in vitro by the inhibition of Ca2+ ion-induced 
contractions of guinea-pig ileum [213], 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 [159]. 

    The disruption of neuronal membranes by 1-propanol was also 
thought to explain its inhibitory action on the binding of 
dihydromorphine to isolated mouse brain caudate membranes [185] and 
on membrane-bound guanylate cyclase (EC in intact murine 
neuroblastoma N1E-115 cells [172].  The activation by 1-propanol of 
membrane-bound adenylate cyclase (EC  from isolated mouse 
striatal membranes, in the presence of guanine nucleotides, was 
also suggested to be the result of membrane perturbation [116]. 

8.4  Biochemical Effects 

8.4.1  Effects on lipids in the liver and blood

    Oral administration of single doses of 3000 or 6000 mg 
1-propanol/kg body weight to Wistar rats caused a transient 
increase in hepatic triglycerides, which was related to the  
duration of an elevated blood-1-propanol concentration [10, 11].  
Gaillard & Derache [63] did not observe an increase in hepatic 
triglycerides in Wistar rats, 17 h after a single dose of 6000 mg 
1-propanol/kg body weight. 

    Factors possibly responsible for hepatic triglyceride 
accumulation include:  an increase in hepatic uptake of labelled 
palmitate [11], an increased esterification of palmitate to form 
liver triglycerides [10, 11], and decreased palmitate oxidation 
[11].  The decrease in palmitate oxidation was related to an 
increase in the hepatic alpha-hydroxybutyrate/acetoacetate ratio, 
implying a decrease in the intramitochondrial NAD+/NADH ratio [11].  
An increase in extramitochondrial reducing equivalents, indicated 
by an increased lactate/pyruvate ratio, was observed  in vitro by 
Forsander [60], but not  in vivo by Beaugé et al. [11]. 

    The effects of 1-propanol on palmitate incorporation into 
triglycerides appear to depend on the dose, high doses causing 
inhibition and lower ones leading to an increase.  The 
incorporation of palmitate into serum triglycerides and serum and 
liver phospholipids, 4.5 h after a single oral dose of 6000 mg 

1-propanol/kg body weight to rats, was found to be inhibited, while 
an increase in hepatic triglyceride accumulation was only observed 
8 h after dosing [10].  Three hours after a dose of 3000 mg/kg body 
weight, the incorporation of palmitate in blood triglycerides was 
increased concomitantly with an increase in hepatic triglycerides 
while levels of phospholipids in the liver and blood were unaffected 
[11].  Similar effects have been noted with ethanol [11]. 

8.4.2  Effects on microsomal enzymes

    The effects of 1-propanol on microsomal enzymes (EC 
 in vivo was investigated by Powis [147], who administered a single 
oral dose of 960 mg/kg body weight to Wistar rats.  Twenty four 
hours after exposure, no effects were observed on the activities of 
aniline hydroxylase and aminopyrine demethylase in liver 
microsomes.  This study is inadequate to demonstrate an inductive 
effect of 1-propanol on the microsomal mixed function oxidase 
system.   In vitro, 1-propanol inhibited aldrin epoxidase and 
 p-aniline hydroxylase in isolated rat liver microsomes via an 
interaction with cytochrome P-450, which causes a reverse Type I 
spectral change [41, 210, 189, 161].  At high concentrations, the 
inhibition of the mixed function monoxygenase system by aliphatic 
alcohols correlates directly with the lipophilicity of the 
alcohols, and is probably the result of unspecific effects on the 
membrane (see section 8.3).  The compound did not affect the levels 
of hepatic microsomal cytochrome P-450, haem, cytochrome b5, and 
NADPH-cytochrome c reductase (EC in phenobarbital-induced 
rats [96].  1-Propanol increased the levels of cytochrome P-450 in 
cultured chick embryo hepatocytes.  The activities of benzphetamine 
demethylase and UDP-glucuronosyl transferase (EC were 
also increased [169].

8.4.3  Other biochemical findings

    The glutathione level in the liver of Wistar rats administered 
a single dose of 1660 mg 1-propanol/kg body weight, orally, had 
decreased by 20%, 6 h after exposure.  Lipid peroxidation, as 
indicated by diene conjugates formation, was increased; ethanol in 
equivalent doses produced similar effects [199]. 

    The activities of liver ornithine decarboxylase (EC 
and liver tyrosine aminotransferase (EC increased in 
partially hepatectomized rats 4 h after one oral dose of 2300 mg 
1-propanol/kg body weight or an equivalent dose of ethanol.  No 
effects were observed on levels of alanine aminotransferase 
(EC in the liver and kidneys, and on levels of ornithine 
decarboxylase in the kidneys and brain [145]. 

    The effects of 1-propanol on neuronal membrane-bound adenylate 
cyclase (EC and guanylate cyclase (EC  in vitro 
are discussed in section 8.3.  1-Propanol and ethanol, can have 
different effects on the activity of adenylate cyclase, depending 
on the concentration of alcohol and the biological system being 
investigated [178, 192, 93]. 

    When Sprague-Dawley rats inhaled 1-propanol for 6 h at a 
concentration of 490 mg/m3, the serum level of testosterone was 
decreased by 42% immediately after exposure, but not 18 h after 
exposure.  When this exposure regimen was repeated daily over one 
week, no effects on serum testosterone levels were observed.  Serum 
levels of luteinizing hormone and corticosterone were unchanged at 
all times [31]. 

    When a crude homogenate of dispersed acinar cells, prepared 
from guinea-pig pancreas, was incubated with 1-propanol and 
secretin, the secretin-stimulated activities of adenylate cyclase 
(EC and cellular cyclic adenosine 3',5'-monophosphate were 
potentiated at low concentrations of 1-propanol, but the 
potentiation was reversible.  Irreversible inhibition occurred at 
higher concentrations [192]. 

8.5  Reproduction, Embryotoxicity, and Teratogenicity

    Groups of 15 male Sprague-Dawley rats were exposed to 
1-propanol at measured concentrations of 8610 or 15 220 mg/m3 for 
7 h/day over 6 weeks.  Beginning on the third day after the last 
exposure, males were mated for a maximum of 5 days with unexposed 
females.  There was no apparent effect of exposure to 8610 mg/m3 on 
mating performance or fertility.  After exposure to 15 220 mg/m3, 
17 out of 18 males copulated (as evidenced by the presence of a 
vaginal plug), but only 2 of 17 mated females became pregnant.  The 
offspring of the exposed males were evaluated postnatally in a 
battery of behavioural tests.  There was no evidence of any 
exposure-related effect [132]. 

    These investigators also exposed groups of 15 pregnant Sprague- 
Dawley rats to the same concentrations of 1-propanol on gestation 
days 1 - 20.  Pregnant females exposed to 15 220 mg/m3 showed 
significantly reduced weight gain and food consumption.  Their 
female offspring also showed reduced weight gain up to 3 weeks of 
age, but there was no consistent effect on male offspring.  Litter 
sizes were not affected.  "Several" of the offspring from dams 
exposed to 15 220 mg/m3 had crooked tails.  Behavioural testing of 
offspring did not reveal any evidence of an exposure-related 
effect, though there was an increase in total external, visceral, 
and skeletal malformations at 23 968 mg/m3 (9743 ppm) and in total 
skeletal malformation at 14 893 mg/m3 (6054 ppm) [132]. 

    The effects of 1-propanol on brain development in the neonatal 
rat were also studied.  A group of 21, 5-day-old Long-Evans rats 
was exposed to 1-propanol via an artificial milk formula, which was 
administered through an intragastric catheter for 4 consecutive 
days.  The rats received 12 feeds daily, each lasting 20 min.  
Doses were 3800, 7500, 3000, or 7800 mg/kg body weight on day 
5 - 8, respectively.  Controls received the milk formula only.  
During the exposure, the exposed pups frequently showed an impaired 
righting response.  After the last exposure, withdrawal symptoms 
were displayed.  Pups were killed at 18 days of age, at which time 
there was no effect on body weight or on absolute weight of 
kidneys, heart, or liver.  However, the absolute and relative brain 

weights were decreased in the exposed pups.  Biochemical analysis 
showed that the exposed pups had a decreased amount of DNA in all 
brain areas examined.  Cholesterol levels were decreased in the 
forebrain and cerebellar samples, while protein levels were 
decreased only in the forebrain samples [74]. 

8.6  Mutagenicity

8.6.1  Bacteria

    1-Propanol was tested for mutagenic activity using Ames test 
without S9; up to 100-µmol/plate was negative with  Salmonella 
 typhimurium TA-100 [181].  Negative results were also reported in 
TA-100 and TA-98 with or without metabolic activation, following 
standard Ames test protocol [94]. 

    In a reverse mutation assay with  Escherchia coli CA-274 
following a pre-incubation protocol, a 5-fold increase in the 
number of revertants was observed at a concentration of 4.5% 
1-propanol.  No metabolic activation system was used [86]. 

8.6.2  Mammalian cells  in vitro

    1-Propanol (100 mg/litre once a day for 7 days) did not 
increase the number of sister chromatid exchanges in Chinese 
hamster ovary cells [136], or in V79 Chinese hamster lung 
fibroblasts at 6000 mg/litre for 3 h (with activation) and 28 h 
(without activation) [200].  It did not increase the number of 
micronuclei in V79 Chinese hamster lung fibroblasts at 40 200 mg/
litre for 1 h [113]. 

    A dose-related increase in the inhibition of metabolic 
cooperation between hamster V79 cells, a phenomenon believed to 
reflect carcinogenic promotion ability and not be indicative of 
genotoxic potential, was observed by Chen et al. [37].  This may be 
due to the membrane effects of 2-propanol. 

8.7  Carcinogenicity

    A group of 18 Wistar rats of both sexes received doses of 
240 mg 1-propanol/kg body weight, by gavage, twice a week, for 
their lifetime.  Another group of 31 Wistar rats of both sexes 
received subcutaneous injections of 48 mg compound/kg body weight, 
twice a week, for their lifetime.  Control groups, comprising 25 
rats for each route, received saline.  It was not reported whether 
the analytical grade, double-distilled test compound was analysed 
for the presence of impurities.  The average survival time was 570 
days for the orally exposed rats, 666 days for the subcutaneously 
exposed rats, and 643 days for both control groups.  The tumour 
incidence is reported in Table 7.  The data were not statistically 
analysed.  It was reported that "nearly all rats" showed liver 
damage including congestion, steatosis, necrosis, fibrosis, and 
metaplasia and hyperplasia of the haematopoietic bone marrow 
parenchyma.  However, the incidence of these lesions were not 
reported [67]. 

Table 7. Tumour incidence in Wistar rats exposed orally or 
subcutaneously to 1-propanol for lifetimea
Organ/    Tumour type       Incidence                           
tissue                      oral exposure      sc exposure      
affected                    exposed  controls  exposed  controls 
Blood     myeloid leukemia  2/18     0/25      4/31     0/25
Liver     carcinoma         1/18     0/25      0/31     0/25
Liver     sarcoma           2/18     0/25      5/31     0/25
Other     carcinoma         0/18     0/25      3/31b    0/25
          sarcoma           0/18     0/25      2/31c    0/25
          benign tumoursd   10/18    3/25      7/31     2/25
a  From:  Gibel et al. [67]. 
b  One carcinoma each in kidney, bladder, and uterus.
c  One sarcoma each in spleen and at injection site.
d  Mostly papillomas and mammary fibroadenomas.            
    Although there was an apparent increase in the incidence of 
liver sarcoma, the study is inadequate for the assessment of 
carcinogenicity.  The dosing schedule did not conform to standard 
protocol.  Too few animals were used in each dose group, the sex 
ratio of each group was unclear, no data were provided on the 
histological type of liver sarcoma, no statistical analysis was 
conducted, the maximum tolerated dose was exceeded, as evidenced by 
the reported liver damage, and only single dose levels were used.  
In the case of subcutaneous administration, the exposure route was 


9.1  General Population Exposure

9.1.1  Poisoning incidents

    One case of poisoning by 1-propanol has been reported.  It 
concerned a 46-year-old woman who was estimated to have consumed 
approximately half a litre of the compound as a solvent in a 
cosmetic preparation, probably a hair lotion.  It was pointed out 
that the woman could have ingested this preparation more than once 
in the past.  The woman was found unconscious.  She died 4 - 5 h 
after ingestion.  No other signs or symptoms were reported.  
Autopsy revealed a "swollen brain" and lung oedema [52]. 

9.1.2  Controlled human studies

    Filter papers moistened with 0.025 ml of a 75% solution of 
1-propanol in water were placed on the forearms of a group of 12 
volunteers following immersion of the forearms in water at 23 °C 
for 10 min.  The patches were covered for 5 min and then gently 
blotted.  Nine of the 12 persons showed erythema for at least 60 
min following exposure.  The cutaneous reaction was totally blocked 
in 4 out of 4 persons after pretreatment with 40% 4-methylpyrazole 
in hydrophilic ointment 1 h before the challenge, showing, 
according to the authors, that 1-propanol must be metabolized to 
propanal before vasoactivity occurs [207]. 

9.2  Occupational Exposure

    A laboratory worker in a company manufacturing hair cosmetics 
developed allergic reactions in patch tests with chemically pure 
1-propanol solutions in water (10 - 99.5% by volume).  This person 
also reacted to 2-propanol, 1-butanol, 2-butanol, and formaldehyde, 
but not to ethanol and methanol.  Controls were not tested [115]. 

10.1  Evaluation of Human Health Risks

10.1.1  Exposure

    Exposure of human beings to 1-propanol may occur through 
ingestion of food and alcoholic beverages containing 1-propanol 
(e.g., wine and beer 100 - 200 mg/litre, spirits up to 3500 
mg/litre).  Inhalation exposure may occur during household use and 
occupationally during manufacture and processing.  Exposure of the 
general population via inhalation and drinking-water is very low 
(average concentrations in urban air and drinking-water in the USA, 
0.00005 mg/m3 and drinking-water 0.001 mg/litre, respectively) 
(section 5). 

10.1.2  Health effects

    1-Propanol is rapidly absorbed and distributed throughout the 
body following ingestion.  Data on the absorption rate following 
inhalation are lacking but, in view of the physical properties of 
the compound, it is also expected to be rapid.  Dermal absorption 
is expected to be slow (section 6). 

    1-Propanol exhibits low acute toxicity for animals (based on 
lethality estimates), whether exposed via the dermal, oral, or 
respiratory route (section 8.1).  Exposure to potentially lethal 
levels may occur in the general population through accidental or 
intentional ingestion.  However, only one case of lethal poisoning 
by 1-propanol has been reported, which probably reflects its low 
toxicity and limited use by the public (section 9.1.1).  The 
principal toxic effect of 1-propanol following a single exposure is 
depression of the central nervous system.  Quantitative exposure-
effect data on human beings are not available.  The most likely 
acute effects of 1-propanol in man are alcoholic intoxication and 
narcosis.  Animal studies indicate that 1-propanol is 2 - 4 times 
as intoxicating as ethanol. 

    A controlled human study has indicated that 1-propanol may be 
irritating to hydrated skin.  However, the potential of 1-propanol 
as a respiratory irritant is low (section 8.1.3).  Data are 
inadequate for evaluation of the irritating properties of this 
compound for the skin, eye, and respiratory tract in human beings, 
or for evaluation of its sensitizing potential. 

    The results of limited drinking-water studies on animals 
suggest that oral exposure to 1-propanol is unlikely to pose a 
serious health hazard under the usual conditions of human exposure 
(section 8.2). 

    Inhalation exposure to a concentration of 15 220 mg/m3 caused 
impaired reproductive performance in male rats, but exposure to 
8610 mg/m3 did not.  In pregnant rats, 9001 mg/m3 (3659 ppm) was a 
NOEL and 14 893 mg/m3 (6054 ppm) was a LOEL for both maternal and 
developmental toxicity.  Behavioural effects were not detected in 

offspring whose mothers were exposed during pregnancy to 15 220 
mg/m3, but oral dosing of neonatal rats produced biochemical 
changes in the brain that were detected 10 days after the last 
treatment (section 8.5).  Inhalation exposure to high concentrations 
of 1-propanol produced reproductive and developmental toxic effects 
in male and female rats.  These effects occurred in the presence of 
other overt signs of toxicity in the exposed animals and 1-propanol 
does not appear to be selectively toxic to male or female 
reproductive processes.  The concentrations required to produce 
these effects in rats were higher than those likely to be 
encountered under normal conditions of human exposure. 

    1-Propanol was negative in assays for point mutations in 
bacteria.  It did not increase the incidence of sister chromatid 
exchange or micronuclei in mammalian cells  in vitro.  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 available.  The results of an 
 in vitro test said to predict promotional activity were negative 
(section 8.6).  The available study is inadequate to evaluate the 
carcinogenicity of 1-propanol in experimental animals (section 
8.7).  No data are available on the long-term exposure of human 
populations to 1-propanol.  Hence, the carcinogenicity of 
1-propanol in human beings cannot be evaluated.  Apart from one 
case of fatal poisoning following ingestion of half a litre of 
1-propanol, there are practically no reports on adverse health 
effects from exposure to 1-propanol either in the general 
population or in occupational groups (section 9). 

    The Task Group considers it unlikely that 1-propanol will pose 
a serious health risk for the general population under normal 
exposure conditions. 

10.2  Evaluation of Effects on the Environment

    1-Propanol can be released into the environment during 
production, processing, storage, transport, use, and waste disposal 
(section 3).  It is transferred from water, soil, and waste 
disposal sites to the atmosphere by volatilization, from the 
atmosphere to water and soil by rain-out, and from soil and waste 
disposal sites to ground water by leaching.  It is difficult to 
estimate its emission into each compartment.  Because of its 
primary use as a volatile solvent, most of the production volume is 
eventually released into the atmosphere (section 4.1). 

    By reacting with hydroxyl radicals and through rain-out, 
1-propanol will disappear rapidly from the atmosphere, with a 
residence time of less than 3 days (section 4.2).  Thus, measurable 
atmospheric levels of 1-propanol are not usually encountered. 

    Hydrolysis and photolysis are not expected to be important in 
the removal of 1-propanol from water and soil, but removal occurs 
rapidly by aerobic and anaerobic biodegradation (section 4.3.1) so 

that measurable levels are rarely found.  Adsorption of 1-propanol 
on soil particles is poor but it is likely to be mobile in soil and 
it has been shown to increase the permeability of soil to some 
aromatic hydrocarbons (section 4.1). 

    In view of the physical properties of 1-propanol, its potential 
for bioaccumulation is low (section 4.3.2).  Except in the case of 
accident or inappropriate disposal, 1-propanol does not present a 
risk for aquatic organisms, insects, or plants at concentrations 
that usually occur in the environment.  However, 1-propanol at 
concentrations of around 5000 mg/litre in water is lethal to 
oxygen-using aquatic organisms, indicating that its emission into 
surface water at this level may result in serious alteration of the 
local ecosystem (section 7). 


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

2.   A single published report suggests carcinogenic activity by 
     1-propanol, but this study is seriously flawed and cannot be 
     used to evaluate the potential carcinogenicity of 1-propanol.  
     The desirability of a carcinogenesis bioassay of 1-propanol 
     should be considered, on the basis of the outcome of 
     genotoxicity tests.

3.   Inhalation exposure to overtly toxic concentrations of 
     1-propanol produced reproductive and developmental toxicity in 
     experimental animals.  In view of the potential for 
     environmental and drinking-water contamination, reproductive 
     and developmental toxicity should be investigated using oral 

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

5.   The unusually uniform level of toxicity in diverse types of 
     aquatic organisms that consume gaseous oxygen, and the 
     exceptionally steep dose-effect curve observed, suggest a 
     nonspecific effect that may not be restricted to 1-propanol.  
     These effects merit investigation.


    1-Propanol was considered by the Joint FAO/WHO Expert 
Committee on Food Additives (JECFA) in its twenty-third report. 
Specifications were formulated, but no toxicological monograph was 
prepared, and the substance could not be evaluated on the basis of 
the data available.  Additional toxicological information was 
available to JECFA at a later meeting, including the results of a 
limited study in rats suggesting a carcinogenic potential for 
1-propanol.  In its twenty-fifth report,a JECFA noted that life-
time feeding studies in rodents were required to resolve the 
problem of carcinogenicity.  A toxicological monograph was 
prepared.  The existing specifications were revised and designated 
as "tentative", but no ADI was established. 

a WHO Technical Report Series, No. 669, 1981 ( Evaluation of 
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1.  Identité, propriétés physiques et chimiques, méthodes d'analyse

    Le propanol-1 est un liquide incolore, très inflammable, qui 
est volatil à la température ambiante et sous la pression 
atmosphérique normale.  Il est miscible à l'eau et aux solvants 
organiques.  Parmi les méthodes d'analyse, on peut citer la 
chromatographie en phase gazeuse, qui permet de déceler jusqu'à 
5 x 10-5 mg/m3 dans l'air, 1 x 10-4 mg/litre dans l'eau et 
0,002 mg/litre dans le sang, le sérum ou les urines lorsque 
l'échantillon a été extrait ou concentré de façon satisfaisante. 

2.  Sources d'exposition humaine et environnementale

    La capacité de production mondiale a dépassé 130 000 tonnes en 
1979.   Le  propanol-1 d'origine naturelle résulte de la 
décomposition de matériaux organiques par divers microorganismes et 
on le rencontre également dans les végétaux et le mazout.  
Industriellement, on le produit par réaction de l'éthylène sur 
l'oxyde de carbone et l'hydrogène qui donne du propionaldéhyde, 
celui-ci étant ensuite hydrogéné en propanol.  C'est également un 
sous-produit de la fabrication du méthanol et il peut être obtenu 
directement à partir du propane ou de l'acroléine.  Le propanol-1 
est essentiellement un solvant à tout faire, à usage industriel ou 
domestique.  Il entre dans la composition des encres d'imprimerie 
flexographiques et il est également utilisé dans l'industrie 
textile, dans des produits à usage personnel tels que les produits 
cosmétiques, les lotions ainsi que dans les produits pour le 
nettoyage des vitres, les encaustiques et les antiseptiques.  En 
second lieu par ordre d'importance, on peut citer son utilisation 
comme produit intermédiaire dans la fabrication de divers composés 

3.  Transport, distribution et transformation dans l'environnement

    La principale voie de pénétration de propanol-1 dans 
l'environnement est constituée par les émissions dans l'atmosphère 
qui se produisent au cours de la production, de la transformation, 
du stockage, du transport et de l'utilisation de ce composé ou du 
rejet de déchets qui en contiennent.  Il peut y avoir également des 
décharges dans l'eau et le sol.  Le propanol-1 étant principalement 
utilisé comme solvant volatil, il finit par se dissiper en grande 
partie dans l'environnement. 
    Le propanol-1 est rapidement éliminé de l'atmosphère par 
réaction sur les radicaux hydroxyles et par les précipitations.  Il 
est facilement biodégradable tant par voie aérobie que par voie 
anaérobie et du fait de l'existence de ces mécanismes d'élimination 
chimique et biologique, on ne le rencontre normalement pas en 
quantité mesurable dans l'environnement.  Toutefois on en a décelé 
la présence dans l'air des agglomérations urbaines, dans des 
décharges, ainsi que dans les eaux s'échappant de zones 
d'enfouissement de déchets. 

    Le logarithme du coefficient de partage n-octanol/eau du 
propanol-1 est de 0,34 et son facteur de bioconcentration a une 
valeur de 0,7, ce qui en rend la bioaccumulation très improbable. 

4.  Niveau dans l'environnement et exposition humaine

    La population en général peut être exposée au propanol par 
suite d'une ingestion accidentelle, par inhalation lors de 
l'utilisation du produit ou par absorption avec la nourriture 
(propanol d'origine naturelle, additif d'aromatisation ou reste de 
solvant) ou des boissons alcoolisées ou non.  Par exemple la bière 
en contient jusqu'à 195 mg/litre, le vin jusqu'à 116 mg/litre et 
certains spiritueux jusqu'à 3500 mg/litre.  L'exposition de la 
population par suite d'inhalation ou de la consommation d'eau de 
boisson est faible (aux Etats-Unis la concentration moyenne dans 
des échantillons d'air urbain se situait à 0,00005 mg/m3 et dans 
des échantillons d'eau de boisson, à 0,001 mg/litre).  Les 
travailleurs courent un risque d'exposition par inhalation lors de 
la production, de la transformation et de l'utilisation du produit.  
Toutefois, on ne dispose d'aucune donnée qui permettrait de 
chiffrer ce type d'exposition. 

5.  Cinétique et métabolisme

    Après ingestion, le propanol-1 est rapidement absorbé et 
distribué dans l'ensemble de l'organisme.  On manque de données sur 
la vitesse d'absorption après inhalation et exposition cutanée.  Le 
propanol-1 est métabolisé par l'alcool déshydrogénase (ADH) en 
aldéhyde puis acide propionique et peut entrer dans le cycle de 
Krebs.  Cette oxydation constitue l'étape limitante du métabolisme 
du propanol-1.   In vitro, les oxydases microsomiques du rat et du 
lapin sont également capables d'oxyder le propanol-1 en aldéhyde 
propionique.  L'ADH et des systèmes d'oxydation microsomiques ont 
une affinité beaucoup plus importante pour le propanol-1 que pour 
l'éthanol; aussi le propanol-1 est-il rapidement éliminé de 
l'organisme.  Chez le rat, sa demi-vie après administration par 
voie orale d'une dose de 1000 mg/kg est de 45 minutes. 

    Chez l'animal et chez l'homme, le propanol-1 peut être éliminé 
de l'organisme dans l'air expiré ou dans les urines.  Chez des 
êtres humains ayant reçu par voie orale une dose de 3,75 mg de 
propanol-1 par kg de poids corporel et de 1200 mg d'éthanol par kg 
de poids corporel, l'excrétion urinaire totale du propanol-1 a été 
de 2,1 % de la dose.  Les concentrations urinaires de propanol-1 
étaient d'autant plus basses que la quantité d'éthanol ingérée 
simultanément était basse, ce qui montre qu'il y avait compétition 
pour l'ADH entre le propanol-1 et la surdose d'éthanol.

6.  Effets sur les êtres vivant dans leur milieu naturel

    Aux concentrations normalement présentes dans l'environnement, 
le propanol-1 n'est pas toxique pour la vie aquatique, les insectes 
ou les végétaux.  Chez trois des espèces aquatiques les plus 
sensibles (trois protozoaires), le seuil l'inhibition de la 
multiplication cellulaire se situait entre 38 et 568 mg/litre.  

Dans le cas d'organismes plus évolués, la concentration létale 
était d'environ  5000 mg/litre, avec des variations remarquablement 
faibles d'un phylum à l'autre et une courbe dose-réponse de très 
forte pente.  Certaines bactéries et micro-organismes qui vivent 
dans les eaux résiduaires et les boues activées sont capables de 
s'adapter à des concentrations supérieures à 17 000 mg/litre. 

    Le propanol-1 peut inhiber ou au contraire stimuler la 
germination des semences selon sa concentration dans l'eau 
d'arrosage et les conditions d'exposition.  Le composé accroît 
l'accumulation de nitrites dans le maïs, les pois et le froment. 

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

    Le propanol-1 présente une faible toxicité aiguë pour les 
mammifères (mesurée d'après la mortalité), que l'exposition se 
fasse par voie percutanée, orale ou respiratoire.  On a fait état 
de valeurs allant de 1870 à 6800 mg par kg de poids corporel pour 
la DL50 par voie orale chez plusieurs espèces animales.  Toutefois 
pour de très jeunes rats, on donne une DL50 orale de 560 à 660 mg 
par kg de poids corporel.  Après une seule exposition, le principal 
effet toxique du propanol-1 consiste dans la dépression du système 
nerveux central.  Selon les données disponibles, le propanol-1 
exercerait sur le système nerveux central des effets analogues à 
ceux de l'éthanol; toutefois il semblerait que la neurotoxicité du 
propanol-1 soit plus importante.  Les DE50 pour l'anesthésie chez 
le lapin et la perte du réflexe de redressement chez la souris se 
situaient respectivement à 1440 mg par kg de poids corporel par 
voie orale et à 1478 mg par kg de poids corporel par voie intra- 
péritonéale; ces doses sont environ quatre fois plus faibles que 
dans le cas de l'éthanol.  Dans l'épreuve du plan incliné, le 
propanol-1 s'est révélé 2,5 fois plus actif que l'éthanol chez le 
    Des doses uniques de 3000 ou 6000 mg par kg de poids corporel 
administrées par voie orale à des rats ont provoqué une 
accumulation réversible de triglycérides dans le foie.  Les vapeurs 
fortement concentrées provoquent une irritation des voies 
respiratoires chez la souris.  Aux concentrations d'environ 30 000 
mg/m3 on note une réduction de 50 % du rythme respiratoire chez la 

    On ne dispose de données ni sur l'irritation oculaire ni sur 
l'irritation cutanée.  Aucun effet n'a été observé lors d'une 
épreuve de sensibilisation cutanée sur des souris CF1.  

    Chez des rats mâles exposés pendant six semaines à une dose de 
15 220 mg/m3 de propanol-1, on a relevé quelques signes d'une 
action nocive possible sur la fonction de reproduction.  En 
revanche aucun effet n'a été noté à la dose de 8610 mg/m3.  Après 
exposition de rattes gravides au propanol-1, on a observé des 
signes patents de toxicité pour les mères et les foetus aux doses 
de 23 968 et 14 893 mg/m3 (9743 et 6054 ppm respectivement); aucun 
signe de toxicité n'a été noté à 9001 mg/m3 (3659 ppm).  On n'a 
observé aucune anomalie comportementale parmi les descendants de 

rats mâles exposés pendant six semaines à 8610 ou 15 220 mg de 
propanol-1 par m3, ni dans la descendance de rattes exposées 
pendant leur gestation aux mêmes concentrations.  Toutefois, en 
administrant à des ratons de 5 à 8 jours des doses orales de 3000 à 
7800 mg de propanol-1 par kg et par jour, on constatait des signes 
de dépression du SNC pendant l'administration et un syndrome de 
sevrage à la cessation du traitement.  Le cerveau de ces rats a été 
examiné à l'âge de 18 jours; on a constaté une réduction du poids 
de cet organe tant en valeur absolue qu'en valeur relative, avec 
diminution de la teneur en ADN et  réduction localisée des taux de 
cholestérol et de protéine. 

    La recherche de mutations ponctuelles au moyen de 2 épreuves 
utilisant  Salmonella typhimurium n'a donné que des résultats 
négatifs, de même la recherche de mutations réverses sur 
 Escherichia coli CA-274.  Les résultats ont été également négatifs 
en ce qui concerne les échanges entre chromatides soeurs ou la 
présence de micro-noyaux dans les cellules mammaliennes  in vitro.  
Il n'existe pas d' autres données relatives à la mutagénicité. 

    Lors d'une étude de cancérogénicité portant sur de petits 
groupes de rats Wistar exposés tout au long de leur existence par 
voie orale à des doses de 240 mg/kg ou par voie sous cutanée à des 
doses de 48 mg/kg, on a constaté un accroissement sensible de 
l'incidence des sarcomes du foie dans le groupe recevant le produit 
par voie sous cutanée.  Toutefois cette étude ne permet pas 
d'apprécier la cancérogénicité du propanol-1, notamment à cause de 
l'absence de détails expérimentaux, du nombre trop restreint 
d'animaux et de l'utilisation d'une dose hépatotoxique unique très 

8.  Effets sur la santé humaine 

    On n'a pas signalé d'effets nocifs sur la santé humaine dans la 
population en général ou parmi des groupes professionnels.  Le seul 
cas d'intoxication mortelle qui ait été signalé est celui d'une 
femme, retrouvée inconsciente et qui est décédé 4 à 5 heures après 
l'ingestion de propanol.  L'autopsie a révélé un oedème cérébral et 
pulmonaire.  Lors d'une étude sur l'irritation et la sensibilisation 
cutanées, on a signalé des réactions allergiques chez un membre du 
personnel du laboratoire.  Chez neuf volontaires sur 12, on a 
observé un érythème qui a duré au moins 1 h après 5 minutes 
d'application sur les avant-bras de papiers filtres imprégnés de 
0,025 ml d'une solution aqueuse à 75 % de propanol-1.  On ne 
dispose d'aucun autre rapport concernant d'éventuels effets 
toxiques après exposition professionnelle au propanol-1. 

    Il n'existe pas d'études épidémiologiques qui permettent 
d'établir les effets à long terme, et notamment la cancérogénicité, 
du propanol-1 chez l'homme. 

9.  Résumé de l'évaluation

    Il peut y avoir exposition humaine au propanol-1 à la suite de 
l'absorption de nourriture ou de boissons qui en contiennent.  Une 
exposition par inhalation peut se produire lors de l'utilisation de 
ce produit à des fins ménagères, ou professionnelles, au cours de 
la fabrication, de la transformation et de l'utilisation de ce 
produit.  Les données très limitées dont on dispose sur la teneur 
de l'air ambiant et de l'eau en propanol-1 indiquent que ces 
teneurs sont très faibles. 

    Le propanol-1 est rapidement absorbé et se répartit dans tout 
l'organisme après ingestion.  Après inhalation, l'absorption est 
également rapide mais la résorption  percutanée devrait être lente. 

    Chez l'animal, la toxicité aiguë du propanol-1 est faible, que 
l'exposition ait lieu par voie percutanée, par voir orale ou par 
voie respiratoire.  L'exposition de personnes appartenant à la 
population générale à des teneurs potentiellement mortelles peut se 
produire à la suite d'une ingestion accidentelle ou volontaire.  
Toutefois, un seul cas d'intoxication mortelle par le propanol-1 a 
été signalé jusqu'ici.  Les effets aigus les plus probables chez 
l'homme sont une intoxication de type alcoolique pouvant entraîner 
une narcose.  L'expérimentation animale montre que le propanol-1 
est 2 à 4 fois plus toxique que l'éthanol.  

    Le propanol-1 peut être irritant pour la peau mouillée.  

    On ne dispose pas de données suffisantes sur la toxicité chez 
l'animal pour procéder à une évaluation des risques pour la santé 
humaine qui découleraient d'une exposition répétée ou prolongée au 
propanol-1.  Toutefois, un certain nombre d'études à court terme 
sur le rat, bien que limitées, indiquent que dans les conditions où 
se produit habituellement l'exposition humaine, il est peu probable 
que le risque encouru soit très grave. 

    Une exposition par inhalation à une concentration de 15 220 
mg/m3 a affecté la fonction de reproduction de rats mâles, ce qui 
n'a pas été le cas à la dose de 8610 mg/m3.  Chez des rattes 
gravides, la dose sans effet observable se situait à 9001 mg/3 
(3659 ppm); quant à la dose la plus faible donnant lieu à un effet 
observable, elle était de 14 893 mg/m3 (6054 ppm), en ce qui 
concerne la toxicité pour la mère et le foetus.  L'exposition par 
inhalation à de fortes concentrations de propanol-1 a donc des 
effets nocifs sur la reproduction et le développement des rats 
mâles et femelles lorsque les concentrations utilisées sont 
manifestement toxiques pour ces animaux.  Pour obtenir ces effets, 
il a fallu utiliser des concentrations plus élevées que celles 
auxquelles l'homme pourrait être normalement exposé.     

    Différentes épreuves ont montré que le propanol-1 ne provoquait 
pas de mutations ponctuelles chez les bactéries.  Toutefois, si ces 
résultats donnent à penser que le produit n'est pas génotoxique, 
les données disponibles sont trop limitées pour qu'on puisse en 
évaluer correctement le pouvoir mutagène.  La seule étude dont on 

possède les résultats ne permet pas d'évaluer convenablement la 
cancérogénicité du propanol-1 chez l'animal d'expérience.  On ne 
dispose d'aucune donnée sur l'exposition à long terme des 
populations humaines à ce produit, de sorte qu'on ne peut pas se 
prononcer sur son pouvoir cancérogène chez l'homme. 

    A part un cas d'intoxication mortelle consécutif à l'ingestion 
d'un demi-litre de propanol-1, il n'existe pratiquement aucun 
rapport concernant d'éventuels effets nocifs découlant d'une 
exposition au propanol-1, qu'il s'agisse de la population générale 
ou de groupes professionnels.  Le Groupe spécial estime qu'il est 
improbable que le propanol-1 presente des risques graves pour la 
population générale dans les conditions normales d'exposition. 

    Du propanol-1 peut être libéré dans l'environnement lors de la 
production, de la transformation, du stockage, du transport, de 
l'utilisation ou de rejet de ce produit.  Comme il est 
essentiellement utilisé comme solvant volatil, l'essentiel de la 
production finit par aboutir dans l'atmosphère.  Toutefois, par 
réaction avec les radicaux hydroxyles et entraînement par les 
précipitations, le propanol-1 est rapidement éliminé de 
l'atmosphère, d'où il disparaît en moins de trois jours.  Le 
propanol-1 s'élimine également rapidement de l'eau et du sol de 
sorte que l'on ne le rencontre que rarement en concentrations 
mesurables dans l'air, l'eau et la terre.  Le propanol-1 est peu 
absorbé par les particules du sol où il se révèle mobile et dont il 
accroît la perméabilité à certains hydrocarbures aromatiques. 

    Compte tenu des propriétés physiques du propanol-1, il est peu 
probable qu'il donne lieu à une bioaccumulation et sauf accident ou 
rejet négligent, le propanol-1 ne présente aucun risque pour la 
faune ou la flore aquatique aux concentrations où on le rencontre 
habituellement dans l'environnement. 


1.  Identidad, propiedades físicas y químicas, métodos analíticos

    El 1-propanol es un líquido incoloro y sumamente inflamable, 
volátil a temperatura ambiente y presión atmosférica normal.  Es 
miscible con el agua y los disolventes orgánicos.  Entre los 
métodos analíticos para el propanol figuran la cromatografía de 
gases, que puede detectar hasta 5 x 10-5 mg/m3 en el aire, 
1 x 10-4 mg/litro en el agua y 0,002 mg/litro en la sangre, el 
suero o la orina cuando se utilizan con la muestra procedimientos 
adecuados de extracción o concentración. 
2.  Fuentes de exposición humana y ambiental

    En 1979, la capacidad de producción mundial al año superó las 
130 000 toneladas.  En la naturaleza se produce por descomposición 
de material orgánico por diversos micro-organismos, y se halla en 
las plantas y en los aceites combustibles.  El 1-propanol se 
produce a partir del eteno por reacción con el monóxido de carbono 
y el hidrógeno para dar propionaldehído, que a continuación se 
hidrogena.  Aparece también como sub-producto en la fabricación del 
metanol y puede producirse a partir del propano directamente o a 
partir de la acroleína.  El uso principal del 1-propanol es como 
disolvente de uso múltiple en la industria y el hogar.  Se utiliza 
en las tintas de impresión flexográfica y en aplicaciones textiles, 
productos de uso personal como cosméticos y lociones, en productos 
para limpiar cristales, en abrillantadores y en fórmulas 
antisépticas.  Le sigue en importancia su uso como producto 
intermedio en la fabricación de diversos compuestos químicos. 
3.  Transporte, distribución y transformación en el medio ambiente

    La principal vía de entrada del 1-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 de 
desechos.  También se producen emisiones al agua y al suelo.  
Puesto que el uso principal del 1-propanol es como disolvente 
volátil, gran parte del volumen de producción acaba en el medio 

    El 1-propanol desaparece rápidamente de la atmósfera por 
reacción con radicales hidroxilo y por el lavado con la lluvia.  Es 
fácilmente biodegradable, tanto en condiciones aerobias como 
anaerobias y, a causa de estos mecanismos de eliminación química y 
biológica, no suelen encontrarse niveles medibles de la sustancia 
en el medio ambiente.  No obstante, se ha detectado en la atmósfera 
urbana, en vertederos de desechos y también en las aguas que se 
rezumaban de un terraplenado.  La permeabilidad del suelo al 
1-propanol es probablemente elevada y el compuesto aumenta la 
permeabilidad a ciertos disolventes aromáticos. 

    El 1-propanol tiene un coeficiente de reparto log 
 n-octanol/agua de 0,34 y un factor de bioconcentración de 0,7, lo 
que hace muy poco probable su bioacumulación. 

4.  Niveles ambientales y exposición humana

    La exposición de la población general puede producirse por 
ingestión accidental, por inhalación durante el uso y por ingestión 
junto con los alimentos (que contengan 1-propanol como aromatizante 
volátil natural o añadido o como residuo de disolvente) y bebidas 
alcohólicas y no alcohólicas.  Por ejemplo, la cerveza contiene 
hasta 195 mg/litro, el vino hasta 116 mg/litro y los diversos tipos 
de licores hasta 3520 mg/litro.  La exposición de la población 
general al 1-propanol por inhalación y en el agua de bebida es baja 
(en los Estados Unidos, la concentración media en muestras de aire 
urbano fue de 0,00005 mg/m3 y la correspondiente al agua de bebida 
0,001 mg/litro).  Aunque los trabajadores están potencialmente 
expuestos por la inhalación durante la fabricación, el tratamiento 
y la utilización, no se dispone de datos para cuantificar esas 

5.  Cinética y metabolismo

    El 1-propanol se absorbe y distribuye rápidamente por todo el 
organismo tras la ingestión.  Se carece de datos sobre la tasa de 
absorción tras la inhalación y la exposición dérmica.  El 
1-propanol es metabolizado por la deshidrogenasa alcohólica para 
dar ácido propiónico por intermedio del aldehído y puede entrar en 
el ciclo del ácido tricarboxílico.  Esta oxidación es una etapa 
limitativa de la velocidad del metabolismo del 1-propanol.   In 
 vitro, las oxidasas microsómicas de rata y conejo también son 
capaces de oxidar el 1-propanol a aldehído propiónico.  La afinidad 
relativa de la deshidrogenasa alcohólica y los sistemas de 
oxidación microsómicos por el 1-propanol es mucho más elevada que 
en el caso del etanol; así pues, el 1-propanol se elimina 
rápidamente del organismo.  En la rata, el periodo de 
semieliminación de una dosis oral de 1000 mg/kg fue de 45 minutos. 

    Tanto en animales como en el hombre, el 1-propanol puede ser 
eliminado del organismo en el aire exhalado o en la orina.  A 
sujetos a los que se administró una dosis de 1-propanol de 3,75 mg 
por kg de peso corporal y 1200 mg de etanol por kg de peso corporal 
por vía oral, la excreción urinaria total de 1-propanol fue del 
2,1% de la dosis.  Los niveles urinarios de 1-propanol fueron más 
bajos cuanto más baja era la cantidad de etanol ingerida 
simultáneamente, lo que demuestra la competencia por la 
deshidrogenasa alcohólica entre el 1-propanol y la sobredosis de 

6.  Efectos en los organismos en el medio ambiente

    A las concentraciones en que normalmente se encuentra en el 
medio ambiente, el 1-propanol no resulta tóxico para los organismos 
acuáticos, los insectos ni las plantas.  El umbral de inhibición 
para la multiplicación celular de tres de las especies acuáticas 
más sensibles (tres protozoos) fue de 38 - 568 mg/litro.  Para los 
organismos superiores, la concentración letal fue de unos 5000 
mg/litro, y variaba notablemente poco de un filum a otro y exhibía 
una curva dosis-respuesta sumamente pronunciada.  Algunas bacterias 

y microorganismos de aguas residuales y cienos activados son 
capaces de adaptarse a concentraciones superiores a 17 000 

    La germinación de semillas puede verse inhibida o estimulada 
por el 1-propanol según la concentración en el agua utilizada y las 
condiciones de exposición.  El compuesto aumenta la acumulación de 
nitritos en el maíz, los guisantes y el trigo. 

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

    La toxicidad aguda del 1-propanol para los mamíferos (a juzgar 
por la mortalidad) es baja, por cualquiera de las vías de 
exposición:  cutánea, oral o respiratoria.  Se ha comunicado que 
los valores de la DL50 por vía oral para varias especies animales 
varían entre 1870 y 6800 mg/kg de peso corporal.  No obstante, en 
ratas muy jóvenes se notificó una DL50 por vía oral de 560 - 660 
mg/kg de peso corporal.  El principal efecto tóxico del 1-propanol 
tras una exposición única es la depresión del sistema nervioso 
central.  Los datos de que se dispone sobre el 1-propanol parecen 
indicar que sus efectos sobre el sistema nervioso central son 
semejantes a los del etanol; no obstante, el 1-propanol parece ser 
más neurotóxico.  Los valores de la DE50 para la narcosis en el 
conejo y la pérdida del reflejo de enderezamiento en el ratón 
fueron, respectivamente, de 1440 mg/kg de peso corporal por vía 
oral, y de 1478 mg/kg de peso corporal por vía intraperitoneal; 
estos valores son unas cuatro veces más bajos que los 
correspondientes al etanol.  En el ensayo del plano inclinado, el 
1-propanol fue 2,5 veces más potente que el etanol en la rata. 

    La administración de dosis únicas por vía oral de 3000 ó 
6000 mg/kg de peso corporal tuvo como resultado una acumulación 
reversible de triglicéridos en el hígado de la rata.  Las 
concentraciones elevadas de vapor provocaron irritaciones en el 
tracto respiratorio del ratón.  El ritmo respiratorio del ratón se 
vio disminuido en un 50% a concentraciones de aproximadamente 
30 000 mg/m3.  

    No se dispone de datos sobre irritación ocular y cutánea.  No 
se observó sensibilización en una prueba de sensibilización cutánea 
en ratones CF1. 

    En machos de rata expuestos durante seis semanas a 15 220 
mg/m3, se obtuvieron pruebas limitadas de que el 1-propanol 
disminuye la capacidad reproductora.  No se observaron efectos tras 
una exposición similar a 8610 mg/m3.  Cuando se expusieron ratas 
gestantes al 1-propanol, se observó toxicidad materna y fetal a 
23 968 y 14 893 mg/m3 (9743 y 6054 ppm); no se observó toxicidad a 
9001 mg/m3 (3659 ppm).  No se observaron defectos de comportamiento 
en la progenie de machos de rata expuestos durante seis semanas a 
8610 ó 15 220 mg de 1-propanol/m3, ni en la de ratas expuestas 
durante la gestación a las mismas concentraciones.  No obstante, 
cuando se administró a ratas de 5 a 8 días de edad 3000 - 7800 mg 
de 1-propanol/kg por vía oral al día, se observó depresión del 
sistema nervioso central durante la dosificación y síntomas de 
privación cuando se retiraba la dosis.  Cuando las ratas cumplieron 

18 días se examinaron sus cerebros y se observaron reducciones en 
los pesos cerebrales absoluto y relativo y en el contenido de ADN, 
así como disminuciones regionales de los niveles de colesterol y de 

    El 1-propanol dio resultados negativos en dos ensayos de 
detección de mutaciones puntuales utilizando  Salmonella typhimurium 
y en un ensayo de mutación inversa realizado con  Escherichia coli 
CA-274.  Se obtuvieron resultados negativos en ensayos para inducir 
intercambio de cromátidas hermanas o micronúcleos en células de 
mamíferos  in vitro.  No se obtuvieron otros datos sobre 

    En un estudio de carcinogenicidad realizado en grupos reducidos 
de ratas Wistar expuestas durante toda su vida a dosis orales de 
240 mg/kg o a dosis subcutáneas de 48 mg/kg, se observó un aumento 
significativo de la incidencia de sarcoma hepático en el grupo en 
el que la dosis se administraba por vía subcutánea.  No obstante, 
el estudio resultó insuficiente para evaluar la carcino-genicidad 
por diversos motivos, entre ellos la falta de detalle experimental, 
el reducido número de animales y el empleo de una sola dosis 
elevada para inducir toxicidad hepática. 

8.  Efectos en la salud humana

    No se tiene noticia de efectos adversos para la salud en la 
población general o en grupos profesionales.  El único caso 
notificado de intoxicación mortal, fue el de una mujer que perdió 
el conocimiento y falleció a las 4 - 5 h de la ingestión.  La 
autopsia reveló "inflamación cerebral" y edema pulmonar.  En un 
estudio sobre irritación cutánea y sensibilización, se comunicó la 
aparición de reacciones alérgicas en un operario de laboratorio.  
En otro grupo de 12 voluntarios, se observó en 9 individuos un 
eritema que duró al menos 60 minutos tras la aplicación durante 5 
minutos de papeles de filtro impregnados con 0,025 ml de una 
solución al 75% de 1-propanol en agua aplicados sobre los 

    No se dispone de más informes sobre efectos adversos para la 
salud tras la exposición profesional al 1-propanol.  No se dispone 
de estudios epidemiológicos para evaluar los efectos a largo plazo, 
incluida la carcinogenicidad, del 1-propanol en el ser humano. 

9.  Resumen de la evaluación

    La exposición del ser humano al 1-propanol puede producirse por 
la ingestión de alimentos o bebidas que lo contengan.  La 
exposición por inhalación puede tener lugar durante el uso 
doméstico de la sustancia y en el ámbito laboral durante su 
fabricación, tratamiento y uso.  Los muy limitados datos de que se 
dispone sobre el nivel de 1-propanol en el aire y el agua parecen 
indicar que las concentraciones son muy reducidas. 

    El 1-propanol se absorbe y distribuye rápidamente por todo el 
organismo tras la ingestión.  Se cree que la absorción tras la 
inhalación es rápida y la absorción por vía cutánea lenta. 

    La  toxicidad aguda del 1-propanol para los animales es baja  
en toda exposición, ya sea por vía cutánea, oral o respiratoria.  
La exposición de miembros de la población general a niveles 
potencialmente letales puede producirse por ingestión accidental o 
intencionada.  No obstante, sólo se ha notificado un caso de 
envenenamiento mortal por 1-propanol.  Los efectos agudos más 
probables del 1-propanol en el hombre son la intoxicación 
alcohólica y la narcosis.  Los resultados de los estudios en 
animales indican que el 1-propanol es 2 - 4 veces más tóxico que 
el etanol. 

    El 1-propanol puede ser irritante para la piel hidratada. 

    Los datos sobre toxicidad animal no bastan para evaluar los 
riesgos para la salud humana asociados a la exposición repetida o 
duradera al 1-propanol.  No obstante, estudios limitados a corto 
plazo sobre la rata indican que la exposición por vía oral al 
1-propanol tiene pocas probabilidades de suponer un riesgo grave 
para la salud en las condiciones habituales de exposición humana. 

    En la rata la exposición por inhalación a una concentración de 
15 220 mg/m3 redujo la capacidad reproductiva del macho, pero no 
así la exposición a 8610 mg/m3.  En la rata gestante, 9001 mg/m3 
(3659 ppm) fue el nivel de efectos no observados y 14 893 mg/m3 
(6054 ppm) el nivel más bajo de observación de efectos tanto 
respecto a la toxicidad materna como a la fetal.  Así pues, la 
exposición por inhalación a concentraciones elevadas de 1-propanol 
produjo toxicidad reproductiva y embriológica en el macho y la 
hembra en presencia de toxicidad manifiesta en los animales 
expuestos.  Las concentraciones necesarias para producir esos 
efectos en la rata fueron más elevadas que las que probablemente  
se observen en condiciones normales de exposición humana. 

    El 1-propanol dio resultados negativos en los ensayos de 
detección de mutaciones puntuales en bacterias.  Aunque esto indica 
que la sustancia no tiene ningún potencial genotóxico, no puede 
evaluarse adecuadamente la mutagenicidad basándose en los limitados 
datos disponibles.  El estudio realizado no basta para evaluar la 
carcino-genicidad del 1-propanol en animales de experimentación.  
No se dispone de datos sobre la exposición a largo plazo de 
poblaciones humanas al 1-propanol.  Por todo ello, no puede 
evaluarse la carcinogenicidad del 1-propanol en el ser humano. 

    Aparte de un caso de intoxicación mortal tras la ingestión de 
medio litro de 1-propanol, no se tiene prácticamente noticia de 
efectos adversos para la salud producidos por la exposición al 
1-propanol, ni en la población general ni en grupos profesionales.  
El Grupo Especial de Trabajo considera poco probable que el 
1-propanol plantee un riesgo grave para la salud de la población 
general en condiciones normales de exposición. 

    El 1-propanol puede liberarse al medio ambiente durante la 
producción, el tratamiento, el almacenamiento, el transporte, el 
uso y la evacuación de desechos.  A causa de su uso principal como 
disolvente volátil, la mayoría del volumen de producción acaba por 

ser liberado a la atmósfera.  No obstante, por reacciones con 
radicales hidroxilo y por lavado pluvial, el 1-propanol 
desaparecerá rápidamente de la atmósfera, siendo su tiempo de 
presencia en ella inferior a 3 días.  La eliminación del 1-propanol 
del agua y del suelo también se produce rápidamente, de modo que 
raras veces se detectan niveles medibles en cualquiera de estos 
tres compartimientos.  La adsorción del 1-propanol en las 
partículas del suelo es escasa, pero la sustancia es móvil en el 
suelo y se ha demostrado que aumenta la permeabilidad del mismo a 
ciertos hidrocarburos aromáticos. 

    En vista de las propiedades físicas del 1-propanol, la bio- 
acumulación es poco probable y, salvo en el caso de evacuación 
accidental o inadecuada, el 1-propanol no constituye un riesgo para 
los organismos acuáticos, los insectos y las plantas en las 
concentraciones que por lo general se encuentran en el medio 

    See Also:
       Toxicological Abbreviations