Pentachlorophenol and the lower chlorinated phenols, tetra- and trichlorophenols, have gained an increasing use as fungicides, herbicides, insecticides, and precursors in the synthesis of other pesticides since the early 1930s. World-wide production totals about 200,000 tons. Production and use of chlorinated phenols have caused industrial hygiene problems but, otherwise, have not been recognized to create more than limited environmental problems. The introduction of modern analytical techniques, however, has revealed the ubiquitous occurrence of chlorophenols in the environment, and the discovery of chlorinated dimers, such as dibenzo-p-dioxins and dibenzofurans, as impurities in commercial chlorophenol formulations, has made a reevaluation of the chlorinated phenols necessary. The present article reviews recent studies on the toxicity and metabolism in mammals and aquatic organisms and the degradation of the chlorophenols under various conditions in the environment. Finally, the hazards of burning of chlorophenol wastes are discussed, as well as health considerations with regard to humans and the environment.

Pentachlorophenol has earlier been shown to be metabolized in mammals to tetrachloro-p-hydroquinone. The metabolite possesses pronounced inhibitory activity on bacterial beta-glucuronidase but not on beta-glucuronidase from liver. Indirect evidence for the occurrence of both pentachlorophenol and tetrachloro-p-hydroquinone as conjugates with glucuronic acid in the urine from pentachlorophenol-treated rats is now presented. Bovine liver beta-glucuronidase has been utlizied to split the conjugates present. The in vivo metabolism of pentachlorophenol has also been studied in rats treated with phenobarbital and beta-diethylaminoethylidiphenyl propylacetate (SKF 525-A). In vitro metabolism has been studied using liver microsomes from rats pretreated with pehnobarbital. Quantitative analysis of the compounds occurring in extracts of urine or extracts from the microsomal incubates was performed by means of mass fragmentography. Pretreatment with phenobarbital increased the metabolism of pentachlorophenol to tetrachloro-p-hydroquinone both in vivo and in vitro. SKF 525-A, however, inhibited the metabolism in vitro but enhanced the metabolism in vivo when given less frequently than every 6th h. Dechlorination of pentachlorophenol is mediated by microsomal enzymes that can be induced by phenobarbital. SKF 525-A does not inhibit the dechlorination in vivo but does so in vitro.

The effect of various dietary sources of vitamin A on liver storage of retinol has been investigated in Sprague-Dawley rats treated with single oral doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD): 0,0.1,1.0, or 10 microgram.kg-1. Each dose group consisted of 3 subgroups, each comprising 10 rats which received a diet with normal, low or high retinol content. The animals were killed 4 weeks after TCDD administration. Analyses of retinol were performed by high pressure liquid chromatography and glucuronosyltransferase activities were determined spectrophotometrically. A dose-dependent decrease in hepatic storage of retinol was evident. The high retinol diet did not fully compensate for the reduction caused by the highest TCDD-dose. Glucuronosyltransferase activity increased directly in relation to the TCDD-dose but in inverse proportion to the retinol content of the diet.