Technology Transfer Network - Air Toxics Web Site
Acetaldehyde is mainly used as an intermediate in the synthesis of other chemicals. It is ubiquitous in the environment and may be formed in the body from the breakdown of ethanol. Acute (short-term) exposure to acetaldehyde results in effects including irritation of the eyes, skin, and respiratory tract. Symptoms of chronic (long-term) intoxication of acetaldehyde resemble those of alcoholism. Acetaldehyde is considered a probable human carcinogen (Group B2) based on inadequate human cancer studies and animal studies that have shown nasal tumors in rats and laryngeal tumors in hamsters.
Please Note: The main sources of information for this fact sheet are EPA's Health Assessment Document for Acetaldehyde and the Integrated Risk Information System (IRIS), which contains information on inhalation chronic toxicity of acetaldehyde and the RfC. Other secondary sources include the International Agency for Research on Cancer (IARC) Monographs on Chemicals Carcinogenic to Humans.
- The predominant use of acetaldehyde is as an intermediate in the synthesis of other chemicals. (1)
- Acetaldehyde is used in the production of perfumes, polyester resins, and basic dyes. Acetaldehyde is also used as a fruit and fish preservative, as a flavoring agent, and as a denaturant for alcohol, in fuel compositions, for hardening gelatin, and as a solvent in the rubber, tanning, and paper industries. (1,2)
Sources and Potential Exposure
- Acetaldehyde is ubiquitous in the ambient environment. It is an intermediate product of higher plant respiration and formed as a product of incomplete wood combustion in fireplaces and woodstoves, coffee roasting, burning of tobacco, vehicle exhaust fumes, and coal refining and waste processing. Hence, many individuals are exposed to acetaldehyde by breathing ambient air. It should be noted that residential fireplaces and woodstoves are the two highest sources of emissions, followed by various industrial emissions. (1)
- In Los Angeles, California, levels of acetaldehyde up to 32 parts per billion (ppb) have been measured in the ambient environment. (1)
- Exposure may also occur in individuals occupationally exposed to acetaldehyde during its manufacture and use. (1,2)
- In addition, acetaldehyde is formed in the body from the breakdown of ethanol; this would be a source of acetaldehyde among those who consume alcoholic beverages. (1)
Assessing Personal Exposure
- Acetaldehyde can be detected in the blood and breath to determine whether or not exposure has occurred. (12)
Health Hazard InformationAcute Effects:
- The primary acute effect of inhalation exposure to acetaldehyde is irritation of the eyes, skin, and respiratory tract in humans. At higher exposure levels, erythema, coughing, pulmonary edema, and necrosis may also occur. (1)
- Acute inhalation of acetaldehyde resulted in a depressed respiratory rate and elevated blood pressure in experimental animals. (1)
- Tests involving acute exposure of rats, rabbits, and hamsters have demonstrated acetaldehyde to have low acute toxicity from inhalation and moderate acute toxicity from oral or dermal exposure. (3)
- Symptoms of chronic intoxication of acetaldehyde in humans resemble those of alcoholism. (5)
- In hamsters, chronic inhalation exposure to acetaldehyde has produced changes in the nasal mucosa and trachea, growth retardation, slight anemia, and increased kidney weight. (1,4)
- The Reference Concentration (RfC) for acetaldehyde is 0.009 milligrams per cubic meter (mg/m3) based on degeneration of olfactory epithelium in rats. The RfC is an estimate (with uncertainty spanning perhaps an order of magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups), that is likely to be without appreciable risk of deleterious noncancer effects during a lifetime. It is not a direct esimator of risk but rather a reference point to gauge the potential effects. At exposures increasingly greater than the RfC, the potential for adverse health effects increases. Lifetime exposure above the RfC does not imply that an adverse health effect would necessarily occur. (4)
- EPA has medium confidence in the principal studies because appropriate histopathology was performed on an adequate number of animals and a no-observed-adverse-effect level (NOAEL) and a lowest-observed-adverse-effect level (LOAEL) were identified, but the duration was short and only one species was tested; low confidence in the database due to the lack of chronic data establishing NOAELs and due to the lack of reproductive and developmental toxicity data; and, consequently, low confidence in the RfC. (4)
- EPA has not established a Reference Dose (RfD) for acetaldehyde. (4)
- No information is available on the reproductive or developmental effects of acetaldehyde in humans.
- Acetaldehyde has been shown, in animals, to cross the placenta to the fetus. (1,4)
- Data from animal studies suggest that acetaldehyde may be a potential developmental toxin. In one study, a high incidence of embryonic resorptions was observed in mice injected with acetaldehyde. In rats exposed to acetaldehyde by injection, skeletal malformations, reduced birth weight, and increased postnatal mortality have been reported. (1,6)
- Human data regarding the carcinogenic effects of acetaldehyde are inadequate. Only one epidemiology study is available that has several limitations including short duration, small number of subjects, and concurrent exposure to other chemicals and cigarettes. (1,4,6)
- An increased incidence of nasal tumors in rats and laryngeal tumors in hamsters has been observed following inhalation exposure to acetaldehyde. (1,4,6)
- EPA has classified acetaldehyde as a Group B2, probable human carcinogen. (1,4)
- EPA uses mathematical models, based on human and animal studies, to estimate the probability of a person developing cancer from breathing air containing a specified concentration of a chemical. EPA calculated an inhalation unit risk of 2.2 x 10-6 (µg/m3)-1. EPA estimates that, if an individual were to continuously breathe air containing acetaldehyde at an average of 0.5 µg/m3 (5 x 10-4 mg/m3) over his or her entire lifetime, that person would theoretically have no more than a one-in-a-million increased chance of developing cancer as a direct result of breathing air containing this chemical. Similarly, EPA estimates that breathing air containing 5.0 µg/m3 (5 x 10-3 mg/m3) would result in not greater than a one-in-a-hundred thousand increased chance of developing cancer, and air containing 50.0 µg/m3 (5 x 10-2 mg/m3) would result in not greater than a one-in-ten thousand increased chance of developing cancer. For a detailed discussion of confidence in the potency estimates, please see IRIS. (4)
- The chemical formula for acetaldehyde is CH3CHO, and it has a molecular weight of 44.06 g/mol. (1)
- Acetaldehyde is a colorless mobile liquid that is flammable and miscible with water. (1,6)
- Acetaldehyde has a pungent suffocating odor, but at dilute concentrations it has a fruity and pleasant odor. The odor threshold of acetaldehyde is 0.05 parts per million (ppm) (0.09 mg/m3). (1,7)
- The vapor pressure for acetaldehyde is 740 mm Hg at 20 °C, and it has a log octanol/water partition coefficient (log Kow) of 0.43. (1)
Conversion Factors (only for the gaseous form):
To convert concentrations in air (at 25°C) from ppm to mg/m3: mg/m3 = (ppm) × (molecular weight of the compound)/(24.45). For acetaldehyde: 1 ppm = 1.8 mg/m3. To convert concentrations in air from µg/m3 to mg/m3: mg/m3 = (µg/m3) × (1 mg/1,000 µg).
Health Data from Inhalation Exposure
AIHA ERPG--American Industrial Hygiene Association's emergency
response planning guidelines. ERPG 1 is the maximum airborne concentration
below which it is believed nearly all individuals could be exposed up
to one hour without experiencing other than mild transient adverse health
effects or perceiving a clearly defined objectionable odor; ERPG 2 is
the maximum airborne concentration below which it is believed nearly all
individuals could be exposed up to one hour without experiencing or developing
irreversible or other serious health effects that could impair their abilities
to take protective action.
ACGIH ceiling--American Conference of Governmental and Industrial Hygienists' threshold limit value ceiling; the concentration of a substance that should not be exceeded during any part of the working exposure.
LC50 (Lethal Concentration50)--A calculated concentration of a chemical in air to which exposure for a specific length of time is expected to cause death in 50% of a defined experimental animal population.
NIOSH IDLH--National Institute of Occupational Safety and Health's immediately dangerous to life or health limit; NIOSH recommended exposure limit to ensure that a worker can escape from an exposure condition that is likely to cause death or immediate or delayed permanent adverse health effects or prevent escape from the environment.
OSHA PEL--Occupational Safety and Health Administration's permissible exposure limit expressed as a time-weighted average; the concentration of a substance to which most workers can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
The health and regulatory values cited in this factsheet were obtained
in December 1999.
a Health Numbers are toxicological numbers from animal testing or risk assessment values developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while advisory numbers are nonregulatory values provided by the Government or other groups as advice. OSHA numbers are regulatory, whereas NIOSH, ACGIH, and AIHA numbers are advisory.
c The LOAEL and NOAEL are from the critical study used as the basis for the EPA RfC.
- U.S. Environmental Protection Agency. Health Assessment Document for Acetaldehyde. EPA/600/8-86-015A. Environmental Criteria and Assessment Office, Office of Health and Environmental Assessment, Office of Research and Development, Research Triangle Park, NC. 1987.
- M. Sittig. Handbook of Toxic and Hazardous Chemicals and Carcinogens. 2nd ed. Noyes Publications, Park Ridge, NJ. 1985.
- U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical Substances (RTECS, online database). National Toxicology Information Program, National Library of Medicine, Bethesda, MD. 1993.
- U.S. Environmental Protection Agency. Integrated Risk Information System (IRIS) on Acetaldehyde. National Center for Environmental Assessment, Office of Research and Development, Washington, D.C. 1999.
- The Merck Index. An Encyclopedia of Chemicals, Drugs, and Biologicals. 11th ed. Ed. S. Budavari. Merck and Co. Inc., Rahway, NJ. 1989.
- International Agency for Research on Cancer (IARC). IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans: Allyl Compounds, Aldehydes, Epoxides and Peroxides. Volume 36. World Health Organization, Lyon. 1985.
- J.E. Amoore and E. Hautala. Odor as an aid to chemical safety: Odor thresholds compared with threshold limit values and volatilities for 214 industrial chemicals in air and water dilution. Journal of Applied Toxicology, 3(6):272-290. 1983.
- American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological Exposure Indices. Cincinnati, OH. 1999.
- Occupational Safety and Health Administration (OSHA). Occupational Safety and Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29 CFR 1910.1000. 1998.
- National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to Chemical Hazards. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
- American Industrial Hygiene Association (AIHA). The AIHA 1998 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook. 1998.
- U.S. Department of Health and Human Services. Hazardous Substances Data Bank (HSDB, online database). National Toxicology Information Program, National Library of Medicine, Bethesda, MD. 1993.
Created in April 1992; Revised in January 2000