or probable human carcinogens, and hence their distribution in the environment and possible exposure to humans have been the focus of much attention (1, 2). The eight PAHs that are typically considered as possible or probable carcinogens are: benzo[a]anthracene, chrysene, benzo dibenzo-[a,h]anthracene and benzo[g,h,i]perylene (1, 2).PAHs are introduced into the environment via natural and anthropogenic combustion processes. Volcanic eruptions and forest and prairie fires are among the major sources of naturally produced
Phenol, a monohydroxy derivative of benzene, occurs naturally in animal waste and by decomposition of organic wastes. It is also produced by man, originally by fractional distillation of coal tar, but more recently by cumene hydroperoxidation and toluene oxidation. As a result of large production volume and natural sources, occupational and environmental exposure to phenol is likely. Phenol poisoning can occur by skin absorption, vapor inhalation, or ingestion, and, regardless of route of exposure, can result in detrimental health effects. Acute toxicity has been observed in man and experimental animals, resulting in muscle weakness, convulsions, and coma. In addition, studies have shown that although teratogenic effects have not been associated with exposure to phenol by either inhalation or oral route, high doses of phenol are fetotoxic. This paper addresses these studies and others in an attempt to determine if human health is at risk to those levels of phenol present in the environment and workplace. However, because data are limited, further research is necessary to analyze the mutagenic and carcinogenic potential of this chemical.
The reported high mutagenic potency of 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)furanone against Salmonella typhimurium (TA100) was confirmed in the determined value of 6,300 net revertantshmol. Partial inactivation of the furanone by Arochlor 1254-induced rat liver homogenate fraction (S9) was observed. Inactivation by the nucleophiles hydroxide ion, S02, S20$-, pyrrolidine and glutathione, all in aqueous solutions, was determined and the results compared. Mutagenic reduction was observed for all of the nucleophiles but was most pronounced for glutathione. Inactivation by hydroxide ion was most sensitive in the pH range of 9 to 11, was associated with chloride ion formation and paralleled irreversible ultraviolet spectral change resulting in the loss of the 227 nm absorption maximum and the appearance of a new maximum at 255 nm. Neutral aqueous solutions of the furanone and glutathione were marked by two UV maxima, at 250 and 270 nm, and lacked the aldehydic 'H-NMR signal, which was observed in the spectrum of the neutral solution of the furanone alone and was attributed to the presence of its acyclic tautomeric form. Several other furanones were prepared. Their Ames mutagenicities and those of chlorine-substituted intermediates obtained in the synthesis of the furanone were determined and compared, and then related to the reported mutagenicities of some 2-chloropropenals.
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