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Acetone is believed to exhibit only slight toxicity in normal use, and there is no strong evidence of chronic health effects if basic precautions are followed.[13]
At very high vapor concentrations, acetone is irritating and, like many other solvents, may depress the central nervous system. It is also a severe irritant on contact with eyes, and a potential pulmonary aspiration risk. In one documented case, ingestion of a substantial amount of acetone led to systemic toxicity, although the patient eventually fully recovered.[14] Some sources estimate LD50 for human ingestion at 1.159 g/kg; LD50 inhalation by mice is given as 44 g/m3, over 4 hours.[15]
Acetone has been shown to have anticonvulsant effects in animal models of epilepsy, in the absence of toxicity, when administered in millimolar concentrations.[16] It has been hypothesized that the high-fat low-carbohydrate ketogenic diet used clinically to control drug-resistant epilepsy in children works by elevating acetone in the brain.[16]
EPA EPCRA Delisting (1995). EPA removed acetone from the list of “toxic chemicals” maintained under Section 313 of the Emergency Planning and Community Right to Know Act (EPCRA). In making that decision, EPA conducted an extensive review of the available toxicity data on acetone and found that acetone “exhibits acute toxicity only at levels that greatly exceed releases and resultant exposures,” and further that acetone “exhibits low toxicity in chronic studies.”
Genotoxicity. Acetone has been tested in more than two dozen in vitro and in vivo assays.
These studies indicate that acetone is not genotoxic.
Carcinogenicity. EPA in 1995 concluded, “There is currently no evidence to suggest a concern for carcinogenicity.”(EPCRA Review, described in Section 3.3). NTP scientists have recommended against chronic toxicity/carcinogenicity testing of acetone because “the prechronic studies only demonstrated a very mild toxic response at very high doses in rodents.”
Neurotoxicity and Developmental Neurotoxicity. The neurotoxic potential of both acetone and isopropanol, the metabolic precursor of acetone, have been extensively studied. These studies demonstrate that although exposure to high doses of acetone may cause transient central nervous system effects, acetone is not a neurotoxicant. A guideline developmental neurotoxicity study has been conducted with isopropanol, and no developmental neurotoxic effects were identified, even at the highest dose tested. (SIAR, pp. 1, 25, 31).
Environmental. When the EPA exempted acetone from regulation as a volatile organic compound (VOC) in 1995, EPA stated that this exemption would “contribute to the achievement of several important environmental goals and would support EPA’s pollution prevention efforts.” 60 Fed. Reg. 31,634 (June 16, 1995). 60 Fed. Reg. 31,634 (June 16, 1995). EPA noted that acetone could be used “as a substitute for several compounds that are listed as hazardous air pollutants (HAP) under section 112 of the [Clean Air] Act.
[edit] Environmental effects
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