[ RadSafe ] Indoor Radon

[Susan Gawarecki]

Baratta, Edmond J wrote:

> I agree with Susan, except that acetone is not benign. 

Compared to most other solvents and many other household products, it is 
relatively benign.  By the way, it's found in the nail polish remover, 
not the nail polish, from what I can find.  EPA took acetone off the 
Toxic Release Inventory list a few years ago.  The following info is 
from the Hazardous Substances Data Bank at 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/r?dbs+hsdb:@term+@rn+67-64-1

ACETONE
CASRN: 67-64-1

Human Health Effects:

Toxicity Summary:

Exposure to acetone results from both natural and anthropogenic sources. 
Acetone also occurs as a metabolic component in blood, urine and human 
breath. ... Acetone is one of three ketone bodies that occur naturally 
throughout the body. It can be formed endogenously in the mammalian body 
from fatty acid oxidation. Fasting, diabetes mellitus and strenuous 
exercise increase endogenous generation of acetone. Under normal 
conditions, the production of ketone bodies occurs almost entirely 
within the liver and to a smaller extent in the lung and kidney. ... 
Products are excreted in the blood and transported to all tissues and 
organs of the body where they can be used as a source of energy. Two of 
these ketone bodies, acetoacetate and beta-hydroxybutyrate, are organic 
acids that can cause metabolic acidosis when produced in large amounts, 
as in diabetes mellitus. ... Endogenous acetone is eliminated from the 
body either by excretion in urine and exhaled air or by enzymatic 
metabolism. ... Acetone is rapidly absorbed via the respiratory and 
gastrointestinal tracts of human and laboratory animals, as indicated by 
the detection of acetone in blood within 30 min of inhalation exposure 
and 20 min of oral administration. ... The nasal cavities of human and 
laboratory animals appear to have a limited ability to absorb and 
excrete acetone vapor, compared with the remainder of the respiratory 
tract. Acetone is uniformly distributed among non-adipose tissues and 
does not accumulate in adipose tissue. ... Acetone is rapidly cleared 
from the body by metabolism and excretion. ... Exhalation is the major 
route of elimination for acetone and its terminal metabolite (carbon 
dioxide), and the fraction of administered acetone that is exhaled as 
unchanged acetone is dose-related. Urinary excretion of acetone and its 
metabolites occurs but this route of elimination is minor ... 
Exogenously supplied acetone enters into many metabolic reactions in 
tissues throughout the body, but the liver appears to be the site of 
most extensive metabolism. Carbon from orally administered acetone has 
been detected in cholesterol, amino acids, fatty acids and glycogen in 
rat tissues, urea in urine and unchanged acetone and CO2 in exhaled 
breath. Metabolically, acetone is degraded to acetate and formate ... 
Oral LD50 values in adult rats are in the range of 5800-7138 mg/kg. ... 
Experimental animal data characterizing the effects of long term oral or 
inhalation exposure to acetone are not available, due probably to its 
low toxicity and its endogenous characteristics. ... Pretreatment of 
rodents with acetone enhances the hepatotoxic effects of a number of 
compounds, notably halogenated alkanes. ... Acetone is not considered to 
be genotoxic or mutagenic. ... In a study of pregnant rats and mice 
exposed to acetone vapor during days 6-19 of gestation, slight 
developmental toxicity was observed ... Reports of other reproductive 
effects of acetone include observations of testicular effects and 
changes of sperm quality in rats ... Acetone has been used extensively 
as a solvent vehicle in skin carcinogenicity studies and is not 
considered carcinogenic when applied to the skin. Acetone is relatively 
less toxic than many other industrial solvents; however, at high 
concentrations, acetone vapor can cause CNS depression, 
cardiorespiratory failure and death. Acute exposures of humans to 
atmospheric concentrations ... have been reported to produce either no 
gross toxic effects or minor transient effects, such as eye irritation. 
More severe transient effects (including vomiting and fainting) were 
reported for workers exposed to acetone vapor concentrations ... for 
about 4 hr. Acute exposures to acetone have also been reported to alter 
performances in neurobehavioral tests in humans. ... Females ... were 
reported to suffer menstrual irregularities.
[Environmental Health Criteria 207: Acetone. pp. 1-7 (1998) by the 
International Programme on Chemical Safety (IPCS) under the joint 
sponsorship of the United Nations Environment Programme, the 
International Labour Organisation and the World Health 
Organization.]**QC REVIEWED**

Evidence for Carcinogenicity:

CLASSIFICATION: D; not classifiable as to human carcinogenicity. BASIS 
FOR CLASSIFICATION: Based on lack of data concerning carcinogenicity in 
humans or animals. HUMAN CARCINOGENICITY DATA: None. ANIMAL 
CARCINOGENICITY DATA: None.
[U.S. Environmental Protection Agency's Integrated Risk Information 
System (IRIS) on Acetone (67-64-1) Available from: 
http://www.epa.gov/ngispgm3/iris on the Substance File List as of March 
15, 2000]**PEER REVIEWED**

A4; Not classifiable as a human carcinogen.
[American Conference of Governmental Industrial Hygienists. TLVs & BEIs: 
Threshold limit Values for Chemical Substances and Physical Agents and 
Biological Exposure Indices for 2002. Cincinnati, OH. 2002., p. 13]**QC 
REVIEWED**

Human Toxicity Excerpts:

EFFECTS SIMILAR TO ETHYL ALCOHOL ... BUT ANESTHETIC POTENCY IS GREATER. 
10-20 ML TAKEN BY MOUTH WITHOUT ILL EFFECT. IN ACUTE CASES A LATENT 
PERIOD MAY BE FOLLOWED BY RESTLESSNESS AND VOMITING LEADING TO 
HEMATEMESIS AND PROGRESSIVE COLLAPSE WITH STUPOR.
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of 
Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. 
III-168]**PEER REVIEWED**

WORKERS HAVING BEEN EXPOSED TO 1000 PPM, 3 HR/DAY FOR 7-15 YEARS, ALSO 
COMPLAINED OF CHRONIC INFLAMMATION OF AIRWAYS, STOMACH AND DUODENUM; 
SOME OF THEM COMPLAINED OF DIZZINESS & ASTHENIA. SIMILAR COMPLAINTS WERE 
REPORTED AFTER EXPOSURE ... TO 700 PPM.
[International Labour Office. Encyclopedia of Occupational Health and 
Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 
1983., p. 38]**PEER REVIEWED**

PROLONGED OR REPEATED SKIN CONTACT MAY DEFAT THE SKIN & PRODUCE DERMATITIS.
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and 
Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley 
Sons, 1981-1982., p. 4720]**PEER REVIEWED**

... Onset of hepatorenal lesions in two men & two women acutely exposed 
to acetone /is described/. One person had inhaled acetone vapors whereas 
the others had ingested acetone. Clinical manifestation of liver injury 
was observed in all four workers & renal lesions were detected in two.
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and 
Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley 
Sons, 1981-1982., p. 4725]**PEER REVIEWED**

Repeated exposure to 25-920 ppm: chronic conjunctivitis, pharyngitis, 
bronchitis, gastritis, and gastroduodenitis. /Route not specified/
[Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 
2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983., p. 150]**PEER 
REVIEWED**

SYMPTOMATOLOGY (acute intoxication): 1. Early emotional lability: 
exhilariation, boastfulness, talkativeness, remorse, and belligerency. 
2. Impaired motor coordination: slowed reaction time, slurred speech, 
ataxia. 3. Sensory disturbances: diplopia, vertigo. 4. Flushing of face, 
rapid pulse, sweating. 5. Nausea and vomiting. Eventual incontinence of 
urine and feces. 6. Drowsiness, stupor and finally coma, with impaired 
or absent tendon reflexes. Convulsive episodes may indicate 
hypoglycemia. /Ethyl alcohol/
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of 
Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. 
III-169]**PEER REVIEWED**

SYMPTOMATOLOGY (acute intoxication): 7. Pupils dilated or normal. 8. 
Peripheral vascular collapse (shock): hypotension, tachycardia, cold 
pale skin, hypothermia. 9. Slow stertorous respirations. 10. Death from 
respiratory or circulatory failure or from aspiration pneumonitis. 11. 
During convalescence: postalcoholic headache and gastritis; infections 
(for example, pneumonia, septicemia); alcoholic psychoses (for example, 
delirium tremens). /Ethyl alcohol/
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of 
Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. 
III-169]**PEER REVIEWED**

Acute acetone intoxication was reported in a 10-year old boy who wore a 
hip cast set with a mixture of 90% acetone, 9% pentane and 1% methyl 
salicylate. The following symptoms were described: restlessness, 
headache, vomiting (positive benzidine for blood), stupor, blood 
pressure 80/60, rapid and irregular respiration rate.
[American Conference of Governmental Industrial Hygienists, Inc. 
Documentation of the Threshold Limit Values and Biological Exposure 
Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 
10]**PEER REVIEWED**

A total of 659 males occupationally exposed to acetone and other 
solvents were divided into nine unrelated groups working in plastic 
boat, chemical, plastic button, paint, and shoe factories. Urine samples 
were collected at the beginning of the workshift and at the end of the 
first half of the shift. A close relationship (correlation coefficient 
always above 0.85) between the average environmental solvent 
concentration (mg/cu m) measured in the breathing zone and the urinary 
concentration of unchanged solvent (ug/l) was observed. A Biological 
Equivalent Exposure Limit (56 mg/l) corresponding to the environmental 
Threshold Limit Value (58 mg/l) was recommended for acetone. The 
biological exposure data for urine collected over 4 hr during random 
sampling for at least 1 yr could be used to evaluate long-term exposure 
and probability of non-compliance for individual or groups of workers.
[Ghittori S et al; Am Ind Hyg Assoc J 48 (9): 786-90 (1987)]**PEER 
REVIEWED**

Direct contact of acetone with the eyes may produce irritation and 
corneal injury.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. 
New York, NY: John Wiley and Sons, 1978-1984., p. 1(78) 186]**PEER 
REVIEWED**

High vapor concentrations will produce anesthesia.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. 
New York, NY: John Wiley and Sons, 1978-1984., p. 1(78) 186]**PEER 
REVIEWED**

Acetone can be placed among solvents of comparatively low acute and 
chronic toxicities. Acetone does not have sufficient warning properties 
to prevent repeated exposures to vapors which may have adverse effects. 
There has been no reports that prolonged inhalation of low vapor 
concentrations result in any serious chronic effects in humans.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. 
New York, NY: John Wiley and Sons, 1978-1984., p. 1(78) 186]**PEER 
REVIEWED**

Severe toxic effects: 4,000 ppm= 9,650 mg/cu m, 60 minutes; symptoms of 
illness: 800 ppm= 1,930 mg/cu m, 60 minutes.
[Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 
2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983., p. 150]**PEER 
REVIEWED**

Toxic concn in human blood: 200.0-300.0 ug/ml (20.0-30.0 mg %); lethal 
concn in human blood: 550.0 ug/ml (55.0 mg %)
[Winek, C.L. Drug and Chemical Blood-Level Data 1985. Pittsburgh, PA: 
Allied Fischer Scientific, 1985., p. 1]**PEER REVIEWED**

Symptoms following acute acetone ingestion include nausea, vomiting, 
gastric hemorrhage, sedation, respiratory depression, ataxia, and 
paresthesia. Depression resembles alcoholic stupor, but its onset is 
quicker than that with ethanol. Coughing and bronchial irritation may be 
the only clues to ingestion of quantities that are too small to produce 
sedation. Hyperglycemia and ketonemia with acidosis that resembles acute 
diabetic coma may be present.
[Gossel, T.A., J.D. Bricker. Principles of Clinical Toxicology. 3rd ed. 
New York, NY: Raven Press, Ltd., 1994., p. 89]**PEER REVIEWED**

EXPOSURE FOR 15 MINUTES TO 1660 PPM CAUSES IRRITATION OF EYES AND NOSE ...
[Thienes, C., and T.J. Haley. Clinical Toxicology. 5th ed. Philadelphia: 
Lea and Febiger, 1972., p. 137]**PEER REVIEWED**

Human Toxicity Values:

In children 2 to 3 ml/kg is considered to be toxic.
[Gossel, T.A., J.D. Bricker. Principles of Clinical Toxicology. 3rd ed. 
New York, NY: Raven Press, Ltd., 1994., p. 89]**PEER REVIEWED**

Skin, Eye and Respiratory Irritations:

EXPOSURE FOR 15 MINUTES TO 1660 PPM CAUSES IRRITATION OF EYES AND NOSE ...
[Thienes, C., and T.J. Haley. Clinical Toxicology. 5th ed. Philadelphia: 
Lea and Febiger, 1972., p. 137]**PEER REVIEWED**

Medical Surveillance:

Urinary glucaric acid and the ratio between 6-beta-OH-cortisol and 
17-OH-corticosteroids were determined in chemical workers exposed to 
styrene greater than or equal to 164 mg/cu m, and acetone greater than 
or equal to 571 mg/cu m, and in a control group. Exposed workers had 
significantly higher excretion of glucaric acid and a higher ratio. ... 
Urinary mercapturic acids were also increased. Simultaneous styrene and 
acetone exposure induces mono-oxygenases in humans. ...
[Dolara P et al: Annals of Occupat Hyg 27 (2): 183-8 (1983)]**PEER 
REVIEWED**

Probable Routes of Human Exposure:

NIOSH (NOES Survey 1981-1983) has statistically estimated that 1,510,107 
workers (466,677 of these are female) are potentially exposed to Acetone 
in the US(1). Occupational exposure may be through inhalation and dermal 
contact with this compound at workplaces where acetone is produced or 
used(SRC). The 8 hour TWA exposure to acetone was in the range of 
0-70,000 umols/cu m in a survey of 659 occupationally exposed male 
subjects working in shoe, plastics and chemical plants in Italy (2). 
Workers in a Japanese acetate fiber producing plant had detectable 
levels of acetone in urine samples between 1 and 160 mg/l(3). The 
average TWA exposure to acetone in 7 spray painting and glue spraying 
plants was 0.9, 3.2, 2.3 0.9 and 5.6 ppm for higher-aromatic paint 
spraying, lower-aromatic paint spraying, glue spraying, solvent wiping, 
and paint mixing respectively(4).
[(1) NIOSH; National Occupational Exposure Survey (NOES) (1983) (2) 
Ghittori S et al; Am Ind Hyg Assoc J 48: 786 (1987) (3) Fujino A et al; 
Br J Ind Med 49: 654-57 (1992) (4) Whitehead LW et al; Am Ind Hyg Assoc 
J 45: 767-72 (1984)]**PEER REVIEWED**

The general population may be exposed to acetone through the use of 
commercially available products containing this compound such as paints, 
adhesives, cosmetics, and rubber cements(SRC). Exposure will also arise 
from inhalation of ambient air, ingestion of drinking water, and food 
that contains acetone(SRC). The average blood concn of acetone in 600 
non-occupationally exposed persons in the US was 3,100 ppb(1).
[(1) Ashley DL et al; Clin Chem 40: 1401-04 (1994)]**PEER REVIEWED**

Body Burden:

Acetone was detected in the expired breath of 23 of 26 smokers and 42 of 
43 nonsmokers in the US(1). Acetone was ubiquitous in the expired air 
from a carefully selected urban population of 54 normal healthy 
non-smoking people (387 samples) with a geometric mean concn of 101.3 
ng/l(2). Acetone loss in the urine is generally 1 mg/24 hr for a normal 
adult but is about 50 mg in children(3,4). Acetone was detected in the 
expired breath of children in 2 classrooms in France at an average concn 
of 800 ng/l(5).
[(1) Gordon SM; J Chromatogr 511: 291-302 (1990) (2) Krotoszynski BK et 
al; J Anal Toxicol 3: 225-34 (1979) (3) Harper HA; Review of 
Physiological Chemistry 12th ed p. 303 (1969) (4) White WL et al; 
Chemistry for Medical Technologists 3rd ed Mosby Co St Louis, MO (1970) 
(5) Cailleux A et al; Chromatographia 37: 57-59 (1993)]**PEER REVIEWED**

Average Daily Intake:

AIR INTAKE (assume air concn of 0.05-20 ppb): 24-960 mg; WATER INTAKE - 
insufficient data; FOOD INTAKE - insufficient data. (SRC)
**PEER REVIEWED**