Mutagenicity of ethylene chlorohydrin. Degradation product present in foods exposed to ethylene oxide

Abstract

causes a decrease in the phosphorylation product-ATP. This reduction in available free phosphate would be directly proportional to the reduction in total ATP produced.The amount of inhibition present in the cloacal bladder and intestinal mucosa of all species indicates that DDT may have a pronounced effect upon absorption of metabolites due to a lack of energy required for active transport across the cellular membrane. In this study there was marked inhibition of intestinal mucosa and cloacal bladder ATPase after in vitro treatment with 53 p M DDT. It is possible that treatment with equal concentrations of DDT in vivo would cause a serious inability to effectively utilize metabolites.The action of the lowest concentration (0.53 FLM) of DDT in the kidney of all species studied except Pseude m y s scripta resulted in low remaining (Na+ ,K+)-dependent ATPase activity. Assuming that the (Na-,K+)-dependent ATPase activity in the turtle kidney is similar in function to that of other vertebrates, the inability to reabsorb electrolytes from the glomerular filtrate due to enzyme inhibition by DDT may cause serious electrolyte imbalances.The observed action of DDT in all tissues assayed might be related to the i3bility of the compound to alter the cellular membrane configuration by binding with the fat por-tion of the membrane. Since ATPase is a structural part of the membrane, the active site of the enzyme would be altered. Movement of substances by active transport would be blocked. If the uptake of DDT by turtles in a natural environment reaches tissue concentrations equal to those found in this study, the resulting ATPase inhibition may be sufficient to impair organ function.Ethylene chlorohydrin (2-chloroethanol) is muta-ability to react with the DNA of living cells. In genic for Salmonella t y p h i m u r i u m in which mi-view of the possible presence of ethylene chlorcroorganism it induces mutations of the base-ohydrin in foodstuffs exposed to ethylene oxide, substitution type. This chemical also preferen-the potential hazard of human exposure to this tially inhibits the growth of DNA polymerase de-chemical requires examination. ficient bacteria which is taken to indicate an Ethylene oxide (EO) is widely used as a fumigant to sterilize foodstuffs,, textiles, medical instruments, and a variety of other objects (Merck Index, 1968; Fishbein, 1969). EO has wide applications in agriculture as a pesticide (Merck Index, 1968; Fishbein, 1969; Fishbein e t al., 1970) and in the tobacco industry to shorten the aging process and to reduce the nicotine content of tobacco leaves (see Fishbein, 1969; Fishbein e t al., 1970). The toxicity and mutagenic potential of EO are well recognized (Fishbein e t al., 1!370); however, because of its volatile nature, it has generally been assumed that EO was safe, not leaving a residue (see, however, Fishbein, 1969; Fishbein e t al., 1970). It has been found, however, that under conditions for effective fumigation, EO reacted with moisture and chloride ions to form ethylene chlorohydrin (...

Potential carcinogenic and mutagenic industrial chemicals. I. Alkylating agents

“…A dose-related increase in mutation rate in 5. typhimurium strains TA1530 and TA1535 (but not TA1538) was found on exposure to ethylene chlorohydrin, indicating that this agent induced base-pair substitutions but not frameshift mutations (Rosenkranz and Wlodkowski, 1974). Ethylene chlorohydrin was shown to be a weaker mutagen than ETO in Salmonella TA1535 (Rannug et al, 1976).…”

2‐Chloroethanol [MAK Value Documentation, 1993]

“…2-Chloroethanol was mutagenic in a mutant strain of Klebsiella pneumoniae [37,38]. Weak mutagenic activity was also detected in the Salmonella/microsome test [39][40][41][42].…”

Mutagenicity of halogenated olefins and their derivatives

“…2-Chloroethanol is a residue present in foodstuffs sterilized with ethylene oxide (5,6). It has also been implicated as a metabolite of 1,2-dichloroethane (19), and of vinyl chloride (29-33) and as an intermediate in the chemical degradation of the therapeutically promising compounds 1-(2chloroethyl)-3-cyclohexyl-1 -nitrosourea (CCN U) and 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-l-nitrourea) (methyl-CCNU) (34).…”