ACETALDEHYDE
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INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY
ENVIRONMENTAL HEALTH CRITERIA 167
ACETALDEHYDE
This report contains the collective views of an international group of experts and does not necessarily represent the decisions or the stated policy of the United Nations Environment Programme, the International Labour Organisation, or the World Health Organization.
First draft prepared by Mrs. J. de Fouw, National Institute of Public Health and Enviromental Protection, Bilthoven, Netherlands
Published under the joint sponsorship of the United Nations
Environment Programme, the International Labour Organisation, and the World Health Organization
World Health Organization Geneva, 1995
The International Programme on Chemical Safety (IPCS) is a joint venture of the United Nations Environment Programme, the International Labour Organisation, and the World Health Organization. The main
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epidemiological studies, and promotion of research on the mechanisms of the biological action of chemicals.
WHO Library Cataloguing in Publication Data Acetaldehyde.
(Environmental health criteria ; 167)
1.Acetadehyde - adverse effects 2.Enviromental exposure I.Series
ISBN 92 4 157167 5 (NLM Classification: QU 99) ISSN 0250-863X
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CONTENTS
ENVIRONMENTAL HEALTH CRITERIA FOR ACETALDEHYDE Preamble
Introduction 1. SUMMARY
1.1 Identity, physical and chemical properties, and analytical methods
1.2 Sources of human and environmental exposure 1.3 Environmental transport, distribution, and transformation
1.4 Environmental levels and human exposure 1.5 Kinetics and metabolism
1.5.1 Absorption, distribution, and elimination 1.5.2 Metabolism
1.5.3 Reaction with other components 1.6 Effects on organisms in the environment 1.6.1 Aquatic organisms
1.6.2 Terrestrial organisms
1.7 Effects on experimental animals and in vitro test systems
1.7.1 Single exposure
1.7.2 Short- and long-term exposures 1.7.3 Reproduction, embryotoxicity, and teratogenicity
1.7.4 Mutagenicity and related end-points 1.7.5 Carcinogenicity
1.7.6 Special studies 1.8 Effects on humans
1.9 Evaluation of human health risks and effects on the environment
2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL METHODS
2.1 Identity
2.2 Physical and chemical properties 2.3 Conversion factors
2.4 Analytical methods
3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE 3.1 Natural occurrence
3.2 Anthropogenic sources 3.2.1 Production
3.2.1.1 Production levels and processes 3.2.1.2 Emissions
3.2.2 Uses
3.2.3 Waste disposal 3.2.4 Other sources
4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION 4.1 Transport and distribution between media
4.2 Abiotic degradation 4.3 Biodegradation
5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE 5.1 Environmental levels
5.1.1 Air 5.1.2 Water 5.1.3 Soil 5.1.4 Food
5.1.5 Cigarette smoke 5.2 General population exposure 5.3 Occupational exposure
6. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND HUMANS 6.1 Absorption
6.2 Distribution
6.2.1 Animal studies
6.2.1.1 Distribution after inhalation exposure
6.2.1.2 Distribution to the embryo and fetus
6.2.1.3 Distribution to the brain 6.2.2 Human studies
6.3 Metabolism
6.3.1 Animal studies 6.3.1.1 Liver
6.3.1.2 Respiratory tract 6.3.1.3 Kidneys
6.3.1.4 Testes and ovaries 6.3.1.5 Embryonic tissue
6.3.1.6 Metabolism during pregnancy 6.3.2 Human studies
6.4 Elimination
6.5 Reaction with cellular macromolecules 6.5.1 Proteins
6.5.2 Nucleic acids
7. EFFECTS ON ORGANISMS IN THE ENVIRONMENT 7.1 Aquatic organisms
7.2 Terrestrial organisms
8. EFFECTS ON EXPERIMENTAL ANIMALS AND IN VITRO TEST SYSTEMS 8.1 Single exposure
8.1.1 LD50 and LC50 values 8.2 Short-term exposure
8.2.1 Oral
8.2.2 Inhalation 8.2.3 Dermal 8.2.4 Parenteral
8.3 Skin and eye irritation; sensitization 8.4 Long-term exposure
8.4.1 Oral
8.4.2 Inhalation
8.5 Reproductive and developmental toxicity 8.6 Mutagenicity and related end-points 8.6.1 Bacteria
8.6.2 Non-mammalian eukaryotic systems 8.6.2.1 Gene mutation assays 8.6.2.2 Chromosome alterations 8.6.3 Cultured mammalian cells
8.6.3.1 Gene mutation assays
8.6.3.2 Chromosome alterations and sister chromatid exchange
8.6.4 In vivo assays
8.6.4.1 Somatic cells 8.6.4.2 Germ cells 8.6.5 Other assays
8.6.5.1 DNA single-strand breaks 8.6.5.2 DNA cross-linking
8.6.6 Cell transformation 8.7 Carcinogenicity bioassays 8.7.1 Inhalation exposure
8.7.2 Co-carcinogenicity and promotion studies 8.8 Neurological effects
8.9 Immunological effects
8.9.1 Direct effects on immune cells
8.9.2 Generation of antibodies reacting with acetaldehyde-modified proteins
8.9.3 Related immunological effects 8.10 Biochemical effects
9. EFFECTS ON HUMANS
9.1 General population exposure 9.2 Occupational exposure
9.2.1 General observations 9.2.2 Clinical studies
9.2.3 Epidemiological studies 9.3 Effects of endogenous acetaldehyde
9.3.1 Effects of ethanol possibly attributable to acetaldehyde or acetaldehyde metabolism 10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE ENVIRONMENT
10.1 Evaluation of human health risks 10.1.1 Exposure
10.1.2 Health effects
10.1.3 Approaches to risk assessment 10.2 Evaluation of effects on the environment 11. RECOMMENDATIONS FOR RESEARCH
REFERENCES RESUME RESUMEN
NOTE TO READERS OF THE CRITERIA MONOGRAPHS
Every effort has been made to present information in the criteria monographs as accurately as possible without unduly delaying their publication. In the interest of all users of the Environmental Health Criteria monographs, readers are kindly requested to communicate any errors that may have occurred to the Director of the International Programme on Chemical Safety, World Health Organization, Geneva, Switzerland, in order that they may be included in corrigenda.
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A detailed data profile and a legal file can be obtained from the International Register of Potentially Toxic Chemicals, Case postale 356, 1219 Châtelaine, Geneva, Switzerland (Telephone No. 9799111).
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This publication was made possible by grant number
5 U01 ES02617-15 from the National Institute of Environmental Health Sciences, National Institutes of Health, USA, and by financial support from the European Commission.
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Objectives
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The first Environmental Health Criteria (EHC) monograph, on mercury, was published in 1976 and since that time an everincreasing number of assessments of chemicals and of physical effects have been produced. In addition, many EHC monographs have been devoted to evaluating toxicological methodology, e.g., for genetic, neurotoxic, teratogenic and nephrotoxic effects. Other publications have been concerned with epidemiological guidelines, evaluation of short-term tests for carcinogens, biomarkers, effects on the elderly and so forth.
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* Effects on other organisms in the laboratory and field
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WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR ACETALDEHYDE Members
Mrs I. Arts, Department of Biological Toxicology, TNO Nutrition and Food Research, Zeist, The Netherlands
Dr R.E. Barry, Faculty of Medicine, University of Bristol, Bristol Royal Infirmary, Bristol, United Kingdom
Professor D. Beritic-Stahuljak, Andrija œtampar School of Public Health, Faculty of Medicine, University of Zagreb, Zagreb, Croatia Dr Sai Mei Hou, Karolinska Institute, Huddinge, Sweden
Dr M.E. Meek, Environmental Health Directorate, Priority Substances Section, Health & Welfare Canada, Tunney's Pasture, Ottawa, Canada
(Chairperson)
Professor M.H. Noweir, Industrial Engineering Department, College of
Engineering, King Abdul Aziz University, Jeddah, Saudi Arabia Professor G. Obe, University of Essen, Essen, Germany
Professor T.V.N. Persaud, Department of Anatomy, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada
Mr D. Renshaw, Department of Health, Elephant & Castle, London, United Kingdom
Dr A. Smith, Health and Safety Executive, Toxicology Unit, Bootle, Merseyside, United Kingdom (Co-rapporteur)
Professor A. Watanabe, Toyama Medical and Pharmaceutical University, Faculty of Medicine, Toyama, Japan
Dr S. Worrall, Department of Biochemistry, University of Queensland, Brisbane, Queensland, Australia
Representatives from other organizations
Dr V. Krutovskikh, Programme of Multistage Carcinogenesis, International Agency for Research on Cancer, Lyon, France
Secretariat
Mrs J. de Fouw, National Institute of Public Health and Environmental Protection, Bilthoven, The Netherlands
(Co-rapporteur)
Professor F. Valic, IPCS Consultant, World Health Organization, Geneva, Switzerland, also Vice-Rector, University of Zagreb, Zagreb, Croatia (Responsible Officer and Secretary)
ENVIRONMENTAL HEALTH CRITERIA FOR ACETALDEHYDE
A WHO Task Group on Environmental Health Criteria for
Acetaldehyde met in Geneva from 6 to 10 December 1993. Professor F.
Valic opened the meeting on behalf of the three cooperating
organizations of the IPCS (UNEP/ILO/WHO). The Task Group reviewed and revised the draft monograph and made an evaluation of the risks for human health and the environment from exposure to acetaldehyde.
The first draft of this monograph was prepared by Mrs J. de Fouw, National Institute of Public Health and Environmental Protection, Bilthoven, The Netherlands.
Professor F. Valic was responsible for the overall scientific content of the monograph and for the organization of the meeting, and Mrs M.O. Head of Oxford for the technical editing of the monograph.
The efforts of all who helped in the preparation and finalization of this publication are gratefully acknowledged.
INTRODUCTION
This monograph will deal mainly with the effects of direct exposure to acetaldehyde. However, it should be borne in mind that for most people exposure to acetaldehyde will occur through the consumption of alcoholic beverages (IARC, 1988). These beverages contain ethanol, which is metabolized to acetaldehyde by alcohol dehydrogenase (ADH). ADH activity has been detected in nearly every tissue including liver, kidney, muscle, intestine, ovary, and testes (Buehler et al., 1983; Agarwal & Goedde, 1990).
However, data concerning metabolically formed acetaldehyde will only be considered when no data are available on direct exposure.
The accurate determination of acetaldehyde in body fluid and tissue samples is relatively difficult. Only the most recent techniques take into account artifactual acetaldehyde formation in biological samples, especially those containing ethanol (Eriksson &
Fukunaga 1993). As values for concentrations of acetaldehyde given in older references may well have been overestimates, absolute values are only given when necessary.
1. SUMMARY
1.1 Identity, physical and chemical properties, and analytical methods
Acetaldehyde is a colourless, volatile liquid with a pungent suffocating odour. The reported odour threshold is 0.09 mg/m3. Acetaldehyde is a highly flammable and reactive compound that is miscible in water and most common solvents.
Analytical methods are available for the detection of
acetaldehyde in air (including breath) and water. The principal method is based on the reaction of acetaldehyde with
2,4-dinitrophenylhydrazine and subsequent analysis of the hydrazone derivatives by high pressure liquid chromatography or gas
chromatography.
1.2 Sources of human and environmental exposure
Acetaldehyde is a metabolic intermediate in humans and higher plants and a product of alcohol fermentation. It has been identified in food, beverages, and cigarette smoke. It is also present in
vehicle exhaust and in wastes from various industries. Degradation of hydrocarbons, sewage, and solid biological wastes produces
acetaldehyde, as well as the open burning and incineration of gas, fuel oil, and coal.
More than 80% of the acetaldehyde used commercially is produced by the liquid-phase oxidation of ethylene with a catalytic solution of palladium and copper chlorides. Production in Japan was 323 thousand tonnes in 1981. In the USA, production was 281 thousand tonnes in 1982 while in Western Europe it was 706 thousand tonnes in 1983. Most acetaldehyde produced commercially is used in the production of acetic acid. It is also used in flavourings and foods.
The annual emission of acetaldehyde from all sources in the USA is estimated to be 12.2 million kg.
1.3 Environmental transport, distribution, and transformation
Because of its high reactivity, intercompartmental transport of acetaldehyde is expected to be limited. Some transfer of acetaldehyde to air from water and soil is expected because of the high vapour pressure and low sorption coefficient.
It is suggested that the photo-induced atmospheric removal of acetaldehyde occurs predominantly via radical formation. Photolysis is expected to contribute another substantial fraction to the removal process. Both processes cause a reported daily loss of about 80% of atmospheric acetaldehyde emissions. Reported half-lives of
acetaldehyde in water and air are 1.9 h and 10-60 h, respectively.
Acetaldehyde is readily biodegradable.
1.4 Environmental levels and human exposure
Levels of acetaldehyde in ambient air generally average 5 µg/m3. Concentrations in water are generally less than 0.1 µg/litre. Analysis of a wide range of foodstuffs in the
Netherlands showed that concentrations, generally less than 1 mg/kg, occasionally ranged up to several 100 mg/kg, particularly in some fruit juices and vinegar.
By far, the main source of exposure to acetaldehyde for the majority of the general population is through the metabolism of alcohol. Cigarette smoke is also a significant source of exposure.
With respect to other media, the general population is exposed to acetaldehyde principally from food and beverages, and, to a lesser extent, from air. The contribution from drinking-water is negligible.
Available data are inadequate to determine the extent of exposure to acetaldehyde in the workplace. Workers may be exposed in some manufacturing industries and during alcohol fermentation, where the principal route of exposure is most likely inhalation with possible dermal contact.
1.5 Kinetics and metabolism
1.5.1 Absorption, distribution, and elimination
Available studies on toxicity indicate that acetaldehyde is absorbed through the lungs and gastrointestinal tract; however, no adequate quantitative studies have been identified. Absorption through the skin is probable.
Following inhalation by rats, acetaldehyde is distributed to the blood, liver, kidney, spleen, heart, and other muscle tissues. Low levels were detected in embryos after maternal intraperitoneal (ip) injection of acetaldehyde (mouse) and following maternal exposure to ethanol (mouse and rat). Potential production of acetaldehyde has also been observed in rat fetuses and in the human placenta,
in vitro.
Distribution of acetaldehyde to brain interstitial fluid, but not to brain cells, has been demonstrated following ip injection of
ethanol. A high affinity, low Km ALDHa may be important in maintaining low levels of acetaldehyde in the brain during the metabolism of ethanol.
Acetaldehyde is taken up by red blood cells and, following ethanol consumption in humans and in baboons, in vivo,
intracellular levels can be 10 times higher than plasma levels.
Following oral administration, virtually no unchanged acetaldehyde is excreted in the urine.
1.5.2 Metabolism
The major pathway for the metabolism of acetaldehyde is by oxidation to acetate under the influence of NADb-dependent ALDH.
Acetate enters the citric acid cycle as acetyl-CoA. There are several isoenzymes of ALDH with different kinetic and binding parameters that influence acetaldehyde oxidation rates.
ALDH activity has been localized in the respiratory tract epithelium (excluding olfactory epithelium) in rats, in the renal
cortex and tubules in the dog, rat, guinea-pig, and baboon, and, in the testes in the mouse.
Acetaldehyde is metabolized by mouse and rat embryonic tissue in vitro. Acetaldehyde crosses the rat placenta, in spite of placental metabolism.
Though there is some metabolism of acetaldehyde in human renal tubules, the liver is the most important metabolic site.
Several isoenzymic forms of ALDH have been identified in the human liver and other tissues. There is polymorphism for the
mitochondrial ALDH. Subjects who are homozygous or heterozygous for a point mutation in the mitochondrial ALDH corresponding gene have low activity of this enzyme, metabolize acetaldehyde slowly, and are intolerant of ethanol.
The metabolism of acetaldehyde can be inhibited by
crotonaldehyde, dimethylmaleate, phorone, disulfiram, and calcium carbamide.
a ALDH = acetaldehyde dehydrogenase.
b NAD = nicotinamide adenine dinocleotide.
1.5.3 Reaction with other components
Acetaldehyde forms stable and unstable adducts with proteins.
This can impair protein function, as evidenced by inhibition of enzyme activity, impaired histone-DNA binding, and inhibition of
polymerization of tubulin.
Unstable adducts of acetaldehyde of undetermined significance occur in vitro with nucleic acids.
Acetaldehyde can react with various macromolecules in the body, preferentially those containing lysine residues, which can lead to marked alterations in the biological function of these molecules.
1.6 Effects on organisms in the environment
1.6.1 Aquatic organisms
LC50s in fish ranged from 35 (guppy) to 140 mg/litre (species not specified). An EC5 of 82 mg/litre and an EC50 of 42 mg/litre were reported for algae and Daphnia magna, respectively.
1.6.2 Terrestrial organisms
Acetaldehyde in air appears to be toxic for some microorganisms at relatively low concentrations.
Aphids were killed when exposed to acetaldehyde at a concentration of 0.36 µg/m3 for 3 or 4 h.
Median lethal values were 8.91 mg/litre per h and 7.69 mg/litre per h for the slug species, Arion hortensis and Agriolimax
reticulatus, respectively.
Inhibition of seed germination in the onion, carrot, and tomato by acetaldehyde (up to 1.52 mg/litre) was reversible, whereas
inhibition of Amaranthus palmeri, similarly exposed, was
irreversible. Acetaldehyde at 0.54 µg/m3 damaged lettuce.
1.7 Effects on experimental animals and in vitro test systems
1.7.1 Single exposure
LD50s in rats and mice and LC50s in rats and Syrian hamsters showed that the acute toxicity of acetaldehyde is low. Acute dermal studies were not identified.
1.7.2 Short- and long-term exposures
In repeated dose studies, by both the oral and inhalation routes, toxic effects at relatively low concentrations were limited
principally to the sites of initial contact. In a 28-day study in which acetaldehyde at 675 mg/kg body weight (no-observedeffect level (NOEL): 125 mg/kg body weight) was administered in the drinking-water to rats, effects were limited to slight focal hyperkeratosis of the forestomach. Following administration of a single dose level (0.05%
in the drinking-water) for 6 months (estimated by the Task Group to be approximately 40 mg/kg body weight) in a biochemical study,
acetaldehyde induced synthesis of rat liver collagen, an observation that was supported by in vitro data.
Following inhalation, NOELs for respiratory effects were 275 mg/m3 in rats exposed for 4 weeks and 700 mg/m3 in hamsters
exposed for 13 weeks. At lowest-observed-effect levels, degenerative changes were observed in the olfactory epithelium in rats
(437 mg/m3) and the trachea (2400 mg/m3) in hamsters.
Degenerative changes in the respiratory epithelium and larynx were observed at higher concentrations. No repeated dose dermal studies were identified.
1.7.3 Reproduction, embryotoxicity, and teratogenicity
In several studies, parenteral exposure of pregnant rats and mice to acetaldehyde induced fetal malformations. In the majority of these studies, maternal toxicity was not evaluated. No data on reproductive toxicity were identified.
1.7.4 Mutagenicity and related end-points
Acetaldehyde is genotoxic in vitro, inducing gene mutations, clastogenic effects, and sister-chromatid exchanges (SCEs) in mammalian cells in the absence of exogenous metabolic activation.
However, negative results were reported in adequate tests on
Salmonella. Following intraperitoneal injection, acetaldehyde induced SCEs in the bone marrow of Chinese hamsters and mice. However,
acetaldehyde administered intraperitoneally did not increase the
frequency of micronuclei in early mouse spermatids. There is indirect evidence from in vitro and in vivo studies to suggest that
acetaldehyde can induce protein-DNA and DNA-DNA cross-links.
1.7.5 Carcinogenicity
Increased incidences of tumours have been observed in inhalation studies on rats and hamsters exposed to acetaldehyde. In rats, there were dose-related increases in nasal adenocarcinomas and squamous cell carcinomas (significant at all doses). However, in hamsters,
increases in nasal and laryngeal carcinomas were non-significant. All concentrations of acetaldehyde administered in the studies induced chronic tissue damage in the respiratory tract.
1.7.6 Special studies
Adequate studies on the potential neuro- and immunotoxicity of acetaldehyde were not identified.
1.8 Effects on humans
In limited studies on human volunteers, acetaldehyde was mildly irritating to the eyes and upper respiratory tract following exposure for very short periods to concentrations exceeding approximately 90 and 240 mg/m3, respectively. Cutaneous erythema was observed in patch testing with acetaldehyde, in twelve subjects of "Oriental ancestry".
One limited investigation in which the incidence of cancer was examined in workers exposed to acetaldehyde and other compounds has been reported.
On the basis of indirect evidence, acetaldehyde has been implicated as the putatively toxic metabolite in the induction of alcohol-associated liver damage, facial flushing, and developmental effects.
1.9 Evaluation of human health risks and effects on the environment The acute toxicity of acetaldehyde by the inhalation or oral route in studies conducted on animals was low. According to studies on humans and animals, acetaldehyde is mildly irritating to the eyes and the upper respiratory tract. In limited studies on human
volunteers, acetaldehyde was mildly irritating to the eyes and upper respiratory tract (section 1.8). Cutaneous erythema has also been observed in the patch testing of humans. Although a possible mechanism has been identified, available data are inadequate to assess the
potential of acetaldehyde to induce sensitization.
Available data on the effects of acetaldehyde following ingestion are limited. Following oral administration of 675 mg/kg body weight per day to rats, a borderline increase in hyper-keratosis of the forestomach was observed (NOEL: 125 mg/kg body weight). In rats exposed to a dose level of approximately 40 mg acetaldehyde/kg body weight in the drinking-water for 6 months, there was an increase in collagen synthesis in the liver, the significance of which is unclear.
On the basis of studies on rats and hamsters, the target tissue in inhalation studies is the upper respiratory tract. In available studies, the lowest concentration at which effects were observed was 437 mg/m3 following administration for 5 weeks. The NOELs
identified for respiratory effects were 275 mg/m3 in rats exposed for 4 weeks and 700 mg/m3 in hamsters exposed for 13 weeks.
At concentrations that induced tissue damage in the respiratory tract, increased incidences were observed of nasal adenocarcinomas and squamous cell carcinomas in the rat and laryngeal and nasal carcinomas in the hamster.
There is evidence to suggest that acetaldehyde causes genetic damage to somatic cells in vivo.
Available data are inadequate for the assessment of the potential reproductive, developmental, neurological, or immunological effects associated with exposure to acetaldehyde in the general, or
occupationally exposed, populations.
On the basis of data on irritancy in humans, a tolerable concentration of 2 mg/m3 has been derived. Since the mechanism of
induction of tumours by acetaldehyde has not been well studied, two approaches were adopted for the provision of guidance with respect to this end-point, i.e., the development of a tolerable concentration based on division of an effect level for irritancy in the respiratory tract of rodents by an uncertainty factor, and, estimation of lifetime cancer risk based on linear extrapolation. The tolerable
concentration is 0.3 mg/m3. The concentrations associated with a 10-5 excess lifetime risk are 11-65 µg/m3.
The limited available data preclude definitive conclusions concerning the potential risks of acetaldehyde for environmental biota. However, on the basis of the short half-lives of acetaldehyde in air and water and the fact that it is readily biodegradable, the impact of acetaldehyde on organisms in the aquatic and terrestrial environments is expected to be low, except, possibly, during
industrial discharges or spills.
2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL METHODS 2.1 Identity
Chemical formula: C2H4O Chemical structure: CH3-CHO Common name: acetaldehyde
Common synonyms: ethanal; acetic aldehyde; acetylaldehyde;
ethylaldehyde; diethylacetal;
1,1-diethyoxy ethane CAS chemical name: acetaldehyde
CAS registry number: 75-07-0 RTECS registry number: AB 1925000
2.2 Physical and chemical properties
The most important physical and chemical properties of acetaldehyde are given in Table 1.
Acetaldehyde is a volatile liquid with a pungent, suffocating odour that is fruity in dilute concentrations. The odour threshold for acetaldehyde is reported to be 0.09 mg/m3 (0.05 ppm). This was a geometric average of all available literature data (Amoore & Hautala, 1983). In the case of carbon dioxide solutions in acetaldehyde, the acetaldehyde odour is weakened by the carbon dioxide (Hagemeyer, 1978).
Acetaldehyde is a highly reactive compound that undergoes numerous condensation, addition, and polymerization reactions. It decomposes at temperatures above 400°C, forming principally methane and carbon monoxide. Acetaldehyde is highly flammable when exposed to heat or flame, and, in air, it can be explosive. Acetaldehyde can react violently with acid anhydrides, alcohols, ketones, phenols, NH3, HCN, H2S, P, halogens, isocyanates, strong alkalies, and
amines. It is miscible in all proportions with water and the most common organic solvents. In aqueous solutions, acetaldehyde exists in equilibrium with the hydrate, CH3 CH(OH)2. The enol form, vinyl
alcohol (CH2=CHOH) exists in equilibrium with acetaldehyde to the extent of approximately one molecule per 30 000 (Hagemeyer, 1978).
Table 1. Physical and chemical properties of acetaldehydea
Colour colourless Relative molecular mass 44.1
Boiling point at 101.3 kPa 20.2°C Melting point -123.5°C Octanol/water partition coefficient as 0.63 log Pow
Flash point, closed cup -38°C Autoignition temperature 185-193°C
Explosion limits of mixtures with air 4.5-60.5 vol % acetaldehyde Vapour pressure at -50°C 2.5 kPa
0°C 44.0 kPa 20.16°C 101.3 kPa Specific gravity (20/4) 0.778 Relative vapour density 1.52 Refractive index 20/D 1.33113 Dissociation constant at 0°C, Ka 0.7 × 10-14
Solubility miscible in water and most common solvents
a From: Hagemeyer (1978); IPCS/CEC (1990).
Commercial acetaldehyde should have the following typical
specifications: purity, 99% min; acidity (as acetic acid), 0.1% max, and a specific gravity of 0.804-0.811 (0°/20°C) (US NRC, 1981).
2.3 Conversion factors
1 mg acetaldehyde/m3 air = 0.56 ppm at 25°C and 101.3 kPa (760 mmHg).
1 ppm = 1.8 mg acetaldehyde/m3 air.
2.4 Analytical methods
Several analytical procedures used for the sampling and determination of acetaldehyde in various media are summarized in Table 2.
Table 2. Sampling, preparation, and determination of acetaldehydea
Medium Sampling method Analytical method Detection limit
Air collection in a midget HPLC with 18 µg/m3 impinger containing 2,4-DNPH spectrophotometric in acetonitrile with detection
perchloric acid as catalyst
Air collection in a tube containing HPLC with 0.9 µg/m3 a thermal stable organic polymer spectrophotometric based on 2,6-diphenyl-p- detection
phenylene oxide
Air adsorption on a silica gel GC-FTD 0.09-0.45 treated with 2,4-DNPH µg/m3 exhaust
Air collection in a 2,4-DNPH HPLC with < 18 µg/m3 coated Sep-PAK cartridge, spectrophotometric acidified with HCl detection
Table 2 (contd).
Medium Sampling method Analytical method Detection
Air collection in annular denuders HPLC with UV 0.36 µg/m3 coated with 2,4-DNPH absorbance or detection voltametric
pollution
Air collection and derivatization HPLC with UV 90 µg/m3 on 2,4-DNPH coated detection Chromosorb P
Air collection on DNPH-coated C18 HPLC with UV 12 ng per cartridge detection cartridge Air collection and derivatization HPLC with UV 32 mg/m3b in midget bubblers containing detection Girard T solution
Table 2 (contd).
Medium Sampling method Analytical method Detection limit
Air collection in a Chromosorb 104 GC-FID 0.1 µg/lit tube installed in an automated sampler Air collection on a XAD-2 sorbent GC-FID 1.3 mg/m3c coated with 2-(hydroxymethyl)- piperidine Water derivatization in a two-phase HPLC with 21 µg system by addition of 2,4-DNPH electrochemical and isooctane detection
Water purging with nitrogen gas and sweeping by rapid 200 µg/
collection on a Tenax GC heating of trap litre sorbent and silica gel trap into GC-MS
Water derivatization with 2,4-DNPH HPLC; the reaction < 10 µg pe (in acetonitrile) mixture is analysed sample directly, without and mist samples
prior separation of the DNPH-derivatives
Table 2 (contd).
Medium Sampling method Analytical method Detecti limit
Water collection in a PTFE-cartridge HPLC with UV 0.3 µg/li packed with sulfonated cation detection exchange resin charged with 2,4-DNPH
Water collection of aqueous solution HS-GC-FID 25 µg/lit in vials, no special treatments released from plastics into aqueous foods
Water collection on cyanogen bromide spectrophotometric 0.6 mg/
activated Sepharose 4B detection litre containing aldehyde dehydrogenase; soluble aldehyde dehydrogenase injected in the
sampler flow stream using a double injection technique
Beverage collection of the 2,6- HPLC with 0.01 µg p dimethylpyridine derivative spectrophotometric sample on a 3-aminopropyl- detection
triethoxysiloxane or a
Nucleosil 5NH2 treated silica gel with propionaldehyde as internal standard
Table 2 (contd).
Medium Sampling method Analytical method Detection limit
Beverage steam distillation followed by HPLC with UV ± 5 µg/
liquid liquid extraction, detection litre derivatization with p-nitrobenzyl-
oxyamine-hydrochloride with T-2 undecenal as internal standard
Beverage conversion of acetaldehyde HS-GC-FID ± 1 mg/
acetals and bisulfite addition litre products to free acetaldehyde by a series of 1-min acid, base, and iodine treatments followed by a 10-min equilibration period Breast collection of volatile compounds thermal -- milk on a Tenax cartridge after desorption
warming milk and purging with into GC-MS helium
Blood precipitation of protein with GC headspace 4.4 µg per perchloric acid analysis sample artificial formation
of acetaldehyde
Blood derivatization with 2,4-DNPH HPLC with UV 4.4 ng per with butyraldehyde as internal detection sample standard and perchloric acid
(for protein precipitation)
Table 2 (contd).
Medium Sampling method Analytical method Detection limit
Blood rapid separation plasma: HPLC with > 0.9 ng plasma: deproteinization and spectrophotometric per sample derivatization with 2,4-DNPH detection haemolysate: deproteinization haemolysate:
and mixed with semicarbazide HS-GC-FID hydrochloride
Blood separation of plasma and HPLC with 11 µg per haemolysate plasma: fluorescence sample 1,3-cyclo-hexanedione and detection isooctane haemolysate:
1,3-cyclo-hexadione both in presence of ammonium ion
Blood reaction with 1,3-cyclo-hexanone HPLC with 4.4 µg per in the presence of ammonium ion fluorescence sample propionaldehyde used as internal detection standard
Blood collection in an organic solution HPLC with > 0.13 µg of 2-diphenylacetyl- spectrofluometric per sample 1,3-indandione-1-hydrazone, and detection forming fluorescent azine derivative-precipitation of proteins
Table 2 (contd).
Medium Sampling method Analytical method Detection limit
Blood reaction with methanolic solution HPLC; the 4.4 µg/lit and of 2,4-DNPH, with acetaldehyde adduct tissue dinitrophenyl-[14C]-formaldehyde was identified by as internal standard co-chromatography with the authentic derivative and by mass spectrometry
a 2,4-DNPH = 2,4-dinitrophenylhydrazine; HPLC = high pressure liquid chromat detection; GC-FTD = gas chromatography with flame thermionic detection; GC HS-GC-FID = head space gas chromatography with flame ionization detection.
b minimum working range (estimated LOD: 1.6 mg/m3).
c minimum working range (estimated LOD: 0.67 mg/m3).
The most specific and sensitive analytical method, widely used to date, is based on the reaction of acetaldehyde with
2,4-dinitro-phenylhydrazine (2,4-DNPH) and the subsequent analysis of the hydrazone derivatives by high pressure liquid chromatography (HPLC) or gas chromatography (GC). Methods mentioned by US NIOSH are based on derivatization with Girard T solution followed by HPLC
analysis with UV detection (US NIOSH, 1987), or, on derivatization with 2-(hydroxymethyl)piperidine followed by GC analysis with a flame ionization detector (FID) (US NIOSH, 1989). In the method based on Girard T derivation, other volatile aldehydes compete for the Girard T reagent. Chromatographic conditions may be adjusted to resolve
acetaldehyde from other aldehydes.
Spingarn et al. (1982) determined volatile organic compounds in aqueous solutions, including acetaldehyde, using a technique in which the compounds were purged from the solution by bubbling with an inert gas into a trap containing a Tenax sorbent and silica gel. The
analytes were separated by GC and detected with either specific ionization detection or MS. An improvement in detection limits, compared with those of the widely used spectrophotometric method of analysing carbonyls in aqueous solution, was obtained by Facchini et al. (1986) by means of an electrochemical detector.
In the determination of acetaldehyde in blood, two main
difficulties exist. The first is related to its disappearance from blood prior to measurement and the second is related to the formation of acetaldehyde in blood after collection. According to Pezzoli et al. (1984), the addition of butyraldehyde to blood, as an internal standard, immediately after withdrawal, obviates some of the
inconveniences in the determination of acetaldehyde in blood. The addition of butyric acid makes it possible to obtain results both for the interaction of the aldehyde group of the acetaldehyde with amino groups, and for the formation and extraction of the derivative
compound. However, Di Padova et al. (1986) stated that the addition of butyraldehyde was not specific for the determination of the
acetaldehyde but was related to the aldehyde group reactivity.
Therefore, they described an improved procedure for measuring acetaldehyde in plasma, based on rapid separation, 2,4-DNPH derivatization, and HPLC analysis, and a procedure for measuring acetaldehyde in red blood cells, based on the use of a semicarbazide solution and analysis by head space gas chromatography.
3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE 3.1 Natural occurrence
Acetaldehyde is a metabolic intermediate in humans and higher plants and it is a product of alcohol fermentation (IARC, 1985). It has been identified as a volatile component of mature cotton leaves and cotton blossoms (Berni & Stanley, 1982) and as a component in the essential oil of alfalfa at a concentration of about 0.2% (Kami, 1983). It occurs in food, various fruits, and several spices (see section 5.1.4) and in oak and tobacco leaves (Furia & Bellanca, 1975;
US NRC, 1985).
Acetaldehyde is formed in the atmosphere in a variety of ways.
It is generated by the oxidation of non-methane hydrocarbons both in the background troposphere and in photochemical smog (Grosjean, 1982).
3.2 Anthropogenic sources
3.2.1 Production
3.2.1.1 Production levels and processes
Until 1968, most acetaldehyde produced in the USA was made by the partial oxidation of ethanol over a silver catalyst; however,
currently less than 5% of US production is based on this process. The liquid-phase oxidation of ethylene using a catalytic solution of
palladium and copper chlorides was first used commercially in the USA in 1960 and more than 80% of the world production of acetaldehyde is made by this process. The remainder is produced by the oxidation of ethanol and the hydration of acetylene. Acetaldehyde is produced by a limited number of companies over the world. The total production of acetaldehyde in the USA in 1982 amounted to 281 thousand tonnes.
Total acetaldehyde production in Western Europe in 1982 was 706 thousand tonnes, and the production capacity was estimated to have been nearly 1 million tonnes. In Japan, the estimated production in 1981 was 323 thousand tonnes (Hagemeyer, 1978; IARC, 1985).
3.2.1.2 Emissions
Eimutis et al. (1978) estimated that the annual atmospheric emissions of acetaldehyde in the USA amounted to 12.2 thousand tonnes (Table 3). Emissions of acetaldehyde in the Netherlands in the year 1980 were reported to be 584 tonnes (Guicherit & Schulting, 1985).
Table 3. Emission and sources of acetaldehyde in the USA
Source Emissions (tonnes/year)
Residential external combustion of wood 5056.4 Coffee roasting 4411.4 Acetic acid manufacture 1460.9 Vinyl acetate manufacture from ethylene 1094.6 Ethanol manufacture 57.8 Acrylonitrile manufacture 51.6 Acetic acid manufacture from butane 20.8 Crotonaldehyde manufacture 4.5 Acetone and phenol manufacture from cumene 1.9 Acetaldehyde manufacture by hydration of ethylene 0.5 Polyvinyl chloride manufacture 0.2 Acetaldehyde manufacture by oxidation of ethanol 0.1
3.2.2 Uses
Acetaldehyde is an important intermediate in the production of acetic acid, ethyl acetate, peracetic acid, pentaerythritol, chloral, glyoxal, alkylamines, and pyridines (Hagemeyer, 1978). The use
pattern for the estimated 281 thousand tonnes of acetaldehyde produced in the USA in 1982 was as follows: acetic acid 61%, pyridine and
pyrine bases 9%, peracetic acid 8%, pentaerythritol 7%, 1,3-butylene glycol 2%, chloral 1%, and other applications (including use as a food additive and exports) 12%. The use pattern for the estimated 706 thousand tonnes of acetaldehyde produced in Western Europe was as follows: acetic acid 62%, ethyl acetate 19%, pentaerythritol 5%,
synthetic pyridines 3%, and all other uses 11% (IARC, 1985).
Acetaldehyde is used for the flavourings: berry, butter, chocolate, apple, apricot, banana, grape, peach, black walnut, and rum, and it is used in the following foods: beverages, ice cream and ices, candy, baked goods, gelatin desserts, and chewing gum (Furia &
Bellanca, 1975; US NRC, 1981, 1985). Acetaldehyde is also used in perfumes, aniline dyes, plastics, in the manufacture of synthetic rubber, in the silvering of mirrors, in the hardening of gelatin fibres, and in the laboratory (Verschueren, 1983).
3.2.3 Waste disposal
Degradation of hydrocarbons, sewage, and solid biological wastes produces acetaldehyde. It has been detected in effluents from
sewage-treatment plants and chemical plants (US EPA, 1975; Shackelford & Keith, 1976).
Acetaldehyde has been identified as a constituent in the wastes from petroleum refining, coal processing, the oxidation of alcohols, saturated hydrocarbons, or ethylene, and the hydration of acetylene (IARC, 1985).
3.2.4 Other sources
Acetaldehyde is detected as a combustion product of plastics and polycarbonate and polyurethane foams of western European origin
(Hagen, 1967; Boettner et al., 1973).
Acetaldehyde occurs in vehicle exhaust at levels of 1.4-8.8 mg/m3 in gasoline exhaust, about 5.8 mg/m3 in diesel
exhaust (Verschueren, 1983), and 51.6% acetaldehyde/ n-hexane GC peak area ratio in exhaust gas oxygenates (Hugues & Hum, 1960). It also occurs in the open burning and incineration of gas, fuel oil, and coal, and evaporation products of perfumes (Verschueren, 1983).
Acetaldehyde has been identified in fresh tobacco leaves and in tobacco smoke (concentrations ranging from 2.1 to 4.6 mg/litre smoke) (Buyske et al., 1956; Osborne et al., 1956; Mold & McRae, 1957).
When Lipari et al. (1984) measured aldehyde emissions from wood-burning fireplaces, they ranged from 0.08 to 0.20 g/kg of wood burned, based on tests with cedar, jack pine, red oak, and green ash.
Acetaldehyde emissions from wood-burning furnaces and
stoves were also measured in a Swedish study (Rudling et al., 1981) and in a Norwegian study (Ramdahl et al., 1982). In the Swedish study, the emissions ranged from 1-72 mg/kg wood in prechamber ovens to 9-710 mg/kg wood in fireplace stoves. In the Norwegian study, the reported emissions from stoves were 14.4 mg/kg dry wood under normal burning conditions and up to 992 mg/kg dry wood under low-efficiency combustion.
4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION 4.1 Transport and distribution between media
Acetaldehyde can enter the atmosphere during production of the compound itself, as a product of incomplete combustion, and also as a by-product of fermentation (Grosjean, 1982).
Photochemical oxidation of acetaldehyde has been shown to be an important process in the chemistry of photochemical smog (Bagnall &
Sidebottom, 1984; Leone & Seinfeld, 1984). Present theories ascribe
the importance of acetaldehyde to its being a precursor of
peroxyacetylnitrate (PAN) in polluted atmospheres (Kopczynski et al., 1974; Grosjean et al., 1983; Bagnall & Sidebottom, 1984; Moortgat &
McQuigg, 1984). Acetaldehyde is likely to be a precursor of acetic acid, which is a component of natural precipitation and contributes to its acidity (Moortgat & McQuigg, 1984).
Intercompartmental transport of acetaldehyde is expected to be limited, because of its high reactivity. However, because of the high vapour pressure of acetaldehyde, some transfer to air from water and soil can be expected.
The tendency of acetaldehyde to adsorb on soil particles can be expressed in terms of Koc, the ratio of the amount of chemical
adsorbed per unit weight of organic carbon to the concentration of the chemical in solution at equilibrium. On the basis of the available empirical relationships derived for estimating Koc, a low soil
adsorption potential is expected (Lyman et al., 1982). Koch & Nagel (1988) calculated a soil sorption coefficient of 0.90 for
acetaldehyde, and, therefore, acetaldehyde was classified as a compound with a very low sorption tendency.
4.2 Abiotic degradation
It is suggested that photo-induced atmospheric removal of
acetaldehyde occurs predominantly via radical formation. Singh et al.
(1982) reported that photolysis and reaction with hydroxyl radicals cause a daily loss rate of about 80% of atmospheric acetaldehyde emissions. Grosjean et al. (1983) reported that the reaction with hydroxyl radicals could remove 50-300 tonnes of carbonyls from the Los Angeles air over a 12-h daytime period and, thus, is considered to be a major removal process for all aldehydes. The absolute rate constant for the reaction of the hydroxyl radical with acetaldehyde was
determined over a temperature range of 26-153°C by Atkinson & Pitts (1978). At 26°C, they obtained a rate constant of (1.60 ± 0.16) × 10-11 cm3 per molecule per second. This results in a half-life for acetaldehyde of 10 h, using a 12-h daytime average hydroxyl radical concentration of 2 × 10-15 mol/litre (Lyman et al., 1982).
Hustert & Parlar (1981) reported that 49.5% acetaldehyde was
photochemically degraded (reaction with hydroxyl radicals) after a 2-h radiation (lambda > 230 nm) at 25°C, which, contrary to Atkinson &
Pitts (1978), shows a half-life of 2 h. Atkinson et al. (1984) obtained a rate constant of (1.34 ± 0.28) × 10-15 for the gas-phase reaction of nitrate radicals with acetaldehyde at 25°C. This results in a half-life for acetaldehyde of 59.6 h using a 12-h nighttime average nitrate radical concentration of 4.0 × 10-12 mol/litre (Atkinson et al., 1987).
There is a considerable amount of evidence that acetaldehyde in aqueous solution is in equilibrium with its hydrated form
CH3CH(OH)2. The degree of hydration decreases with increasing
temperature (e.g., at 0°C, the fraction of acetaldehyde hydrated is 0.73; at 25°C, it is 0.59) (Bell & Clunie, 1952).
Von Burg & Stout (1991) reported a half-life of 1.9 h for acetaldehyde in river water; no other details were provided.
4.3 Biodegradation
Several studies have revealed significant degradation of acetaldehyde by mixed cultures obtained from sludges and settled sewage. Hatfield (1957) reported the ability of acclimatized sludge to oxidize acetaldehyde (major portion of the biological and chemical
oxygen demand (BOD and COD) removed within a 4-h aeration period).
Ludzack & Ettinger (1960) determined the BOD for acetaldehyde in activated sludge at 20°C and found that 93% of the acetaldehyde was removed after an observation period of 1/3-5 days and an
acclimatization period of 30 days. Thom & Agg (1975) and Speece (1983) also reported that acetaldehyde was easily biodegradable by biological sewage treatment (additional information was not provided).
However, Gerhold & Malaney (1966) reported little degradation of
acetaldehyde by unacclimatized municipal sludge with a BOD of 27.6% as a percentage of the theoretical oxygen demand in 24 h.
Acetaldehyde is also degraded by anaerobic biological treatment with unacclimatized acetate-enriched cultures. A COD-removal of 97%
was obtained at the end of a 90-day acclimatization period in
completely mixed reactors with a 20-day hydraulic retention time, no solids recycle, and a final daily feed concentration of
10 000 mg/litre (Chou & Speece, 1978).
Acetaldehyde is reported to be readily biodegradable using the biodegradability MITI test, defined in OECD Guidelines for testing of chemicals (OECD, 1992).
5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE 5.1 Environmental levels
5.1.1 Air
The concentrations of acetaldehyde in uncontaminated Arctic air masses, determined over a 24-h period, ranged from not detected to 0.54 µg/m3 (Cavanagh et al., 1969).
In samples collected during April 1981, the levels of acetaldehyde in the air in Pittsburg (PA) and Chicago (Il) were 0.36-4.68 µg/m3 and 1.62-6.12 µg/m3, respectively (Singh et al., 1982). In samples collected at 7 other locations in the USA between 1975 and 1978, mean concentrations in ambient air were 5-124 µg/m3 (Brodzinsky & Singh, 1982).
Schulam et al.(1985) determined the levels of acetaldehyde in air (June-August 1983) in the urban location of Schenectady (NY) and the rural location of Whiteface Mountain (NY). Concentrations of
acetaldehyde were similar in the two locations (the levels of acetaldehyde varied from 0.36 to 1.44 µg/m3, detection limit:
0.29 µg/m3).
The average ambient atmospheric level of acetaldehyde, measured during the four seasons at Brookhaven National Laboratory (Upton, Long Island, NY) from July 1982 to May 1983, was 5.2 µg/m3, with a mean minimum concentration in winter of 1.8 µg/m3 and a mean maximum value in summer of 15.1 µg/m3 (Tanner & Meng, 1984). Concentrations of acetaldehyde in the air in Tulsa, OK (sampled in July 1978), Rio Blanco County, CO (sampled in July 1978), and the Great Smoky
Mountains, TN (sampled in September 1978), ranged up to 14.9, 16.9, and 23.9 µg/m3, respectively (Arntz & Meeks, 1981).
Mean concentrations of acetaldehyde in the air in Tokyo during four seasons in 1985-86 ranged from 2.2 to 7.3 µg/m3 (Watanabe, 1987). Seasonal trends were not noted. Concentrations of acetaldehyde in an environmental survey conducted by the Japan Environment Agency in 1987 ranged from 0.9 to 22 µg/m3 (number of sites sampled unspecified) (Japan Environment Agency, 1989).
