Acetone

Direct observations: clinical cases, poisoning incidents and other

Administrative data

Endpoint:

direct observations: clinical cases, poisoning incidents and other

Type of information:

other: clinical data from cases of acute human intoxication

Adequacy of study:

weight of evidence

Reliability:

2 (reliable with restrictions)

Rationale for reliability incl. deficiencies:

other: Information from handbook with comprehensive summary of data, from collections of data for asessment of health effects and from original publication; information acceptable for weight of evidence approach

Data source

Reference

Reference 1

Reference Type:

review article or handbook

Title:

Acetone

Author:

Morgott DA

Year:

2001

Bibliographic source:

Binggham E (Ed) Patty's toxicology: hydrocarbons, organic nitrogen compounds. Volume 6, Chapter 74. John Wiley & Sons Inc., New York, 5th edition; pages 1-116

Reference 2

Reference Type:

other: Collection of data for toxicological assessment

Title:

Environmental Health Criteria for Acetone

Author:

WHO

Year:

1998

Bibliographic source:

Environmental Health Criteria 207: 1-159

Reference 3

Reference Type:

other: assessment of health effects

Title:

Acetone (CAS No: 67-64-1)

Author:

OECD

Year:

1999

Bibliographic source:

SIDS International Assessment Report (SIAR) for the 9th SIAM, pages 1-118

Reference 4

Reference Type:

other: assessment of health effects

Title:

Acetone (CAS No. 67-64-1). VCCEP Submission

Author:

American Chemistry Council Acetone Panel

Year:

2003

Materials and methods

Study type:

other: accidental or intentional overexposure

Endpoint addressed:

acute toxicity: oral

acute toxicity: inhalation

acute toxicity: dermal

Test material

Test material information

Constituent 1

Reference substance name:

Acetone

EC Number:

200-662-2

EC Name:

Acetone

Cas Number:

67-64-1

Molecular formula:

C3H6O

IUPAC Name:

propan-2-one

Method

Type of population:

general

Route of exposure:

dermal

inhalation

oral

Details on exposure:

For the development of any overt signs of acetone-induced toxicity accidental exposures to extremely large amounts of acetone are necessary:
Iatrogenic cases: Patients fitted with a synthetic cast material experienced acute acetone intoxication via inhalational or dermal uptake.
Occupational accidents with inhalational exposures up to 12,000 ppm, and in the range of 330-496 ppm ( with concomittant exposure to 398-561 ppm methylethylketone)
Most severe cases occurred after ingestion of acetone due to attempted suicide (e.g. 200 ml of pure acetone) or accidental ingestion of e.g. nail polish remover by children. Extremely high blood acetone levels of up to 3,900 mg/L and 4,500 mg/L were found in adults and a child, respectively.

Results and discussion

Clinical signs:

Unspecific symptoms: unconsciousness, coma, drowsiness, vomiting, hematemesis, acetonuria, glycosuria, tachycardia, labored breathing, seizures, throat irritation.
No fatalities have ever been documented.

Results of examinations:

Among 1000 to 1500 cases of poisoning per year (United States from 1988 to 1997), mainly with ingestion of pure acetone, no fatalities occurred, occasional minor organ damage, as e.g. mild functional renal insufficiency, low potential for causing chronic or delayed health effects; nonspecific local and systemic effects with respiratory tract irritation as most sensitive indicator of acetone overexposure, most noticeable systemic effect generalized central nervous system depression ranging from light-headedness to narcosis

Any other information on results incl. tables

About 1000 to 1500 incidents of human acetone poisoning per year were listed throughout the United States in the years 1988 to 1997 which were mainly due to ingestion of pure acetone. About 30 % of the cases required treatment in a health-care facility. No fatalities occurred.

Minor organ damage, as e.g. mild functional renal insufficiency, was occasionally reported in cases of acetone-induced narcosis, and was likely to oxygen deprivation and tissue hypoxia. Acetone has a low potential for causing chronic or delayed health effects following an acute exposure.

Hyperglycemia is characteristically observed in severe acetone intoxication, as a portion of the absorbed dose is metabolized to glucose.

Applicant's summary and conclusion

Conclusions:

Following acute overexposure acetone toxicity is characterized by nonspecific local and systemic effects. No cases of fatality are known and acetone has a low potential for causing chronic or delayed health effects.

Executive summary:

The experience with human cases of acetone intoxication has been compiled in several health assessments and reviews (American Chemistry Council Acetone Panel, 2003; Morgott, 2001; OECD, 1999; WHO, 1998).

For the development of any overt signs of acetone-induced toxicity accidental exposures to extremely large amounts of acetone by inhalation of vapour or ingestion of liquid are necessary (e.g. several thousand ppm of acetone vapour, or ingestion resulting in acetone blood levels up to several thousand mg/L). Acetone toxicity in humans is characterized by nonspecific local and systemic effects. Respiratory tract irritation is the most sensitive indicator of acetone overexposure. The most noticeable systemic effect is a generalized central nervous system depression, which can range from light-headedness to narcosis, depending on the magnitude and length of the exposure, and the ability of acetone to disrupt normal intermediary metabolism. Due to its lack of specifity the clinical picture of acetone intoxication in humans can be easily confused with other medical conditions, such as diabetes and nonspecific mixed-solvent-induced narcosis, including symptoms as unconsciousness, coma, drowsiness, vomiting, hematemesis, hyperglycemia, acetonuria, glycosuria, tachycardia, labored breathing, seizures, and throat irritation. Based on an extensive experience with cases of acetone poisoning (e.g. 1000 to 1500 incidents per year listed throughout the United States in1988-1997), no cases of fatality are known and acetone has a low potential for causing chronic or delayed health effects. Minor organ damage, as e.g. mild functional renal insufficiency, was occasionally reported in cases of acetone-induced narcosis, and was likely to oxygen deprivation and tissue hypoxia.