Epichlorohydrin (ECH) is one of the more commercially important aliphatic epoxides, widely used as epichlorohydrin industrial intermediates, laboratory reagents, and pesticides. It is a volatile, colorless liquid with a faint odour. It acts as an alkylating agent. It has been reported to cause respiratory and dermal toxicity in animals and humans. It has been reported to be carcinogenic in experimental models. Therefore, the widespread use of such aliphatic epoxides has drawn great concern for human health issues. The purpose of this article is to critically review and update the mutagenic and mutagenic effects of ECH in light of the existing literature.
Epichlorohydrin (ECH, CAS No. 106-89-8) is an aliphatic epoxide synthesized commercially from allyl chloride, allyl alcohol, dichlorohydrin, glycerol, or propylene. Colorless liquid, soluble in ethanol, ether, slightly soluble in water. Vapors of ECH form explosive mixtures with air. It emits phosgene, hydrogen chloride and carbon monoxide during combustion. Acids, caustic solutions and halide salts initiate polymerization. This compound is highly reactive with metals such as zinc and aluminum, anhydrous metal halides, strong acids and bases, and materials containing alcohol. In the presence of moisture, ECH will attack steel. It is widely used in the manufacture of epoxy resin, synthetic glycerol, glycidyl ether, etc. in industry. It is also used as an insecticide and rodenticide, and in the manufacture of paper, textiles and pharmaceuticals (IARC, 1976). Total world production of ECH is not available. In the United States, production of ECH has grown steadily, with 276, 330, and 640 million pounds produced in 1977, 1982, and 1990, respectively (US EPA, 1984; SRI, 1990).

ECH is rapidly absorbed through the skin, gastrointestinal tract, and through the lungs as a vapor. Rats develop acute respiratory irritation with hemorrhage and severe edema after inhalation or oral administration (Kremneva and Tolgskaja, 1961; Laskin et al., 1980). Subacute and subchronic inhalational exposure to ECH can cause liver and kidney defects (Gage, 1956). Adult male and female rats exposed to 100 ppm ECH exhibit increased relative kidney weight, tubular dilation, and tubular epithelial cell swelling (Quast et al., 1976).