Porphyrin Status in Aluminum Foundry Workers Exposed to Hexachlorobenzene and Octachlorostyrene

Abstract

The possible interference of hexachlorobenzene and octachlorostyrene (i.e., thermal byproducts from hexachloroethane in aluminum degassing) with porphyrin metabolism was investigated in exposed workers. Urine specimens from 9 male aluminum foundry workers (i.e., smelters) at 6 different companies and from 18 controls—matched for sex, age, residence, and socioeconomic status—were analyzed for total porphyrins and porphyrin isomers. Workers exposed to hexachlorobenzene and octachlorostyrene had a statistically significant increase in urinary total porphyrins, compared with controls (mean ± standard deviation: 13.63 ± 11.13 μmol/mol creatinine and 6.24 ± 3.84 μmol/mol creatinine, respectively; p = .02). The authors attributed the results mainly to differences in excretion of coproporphyrins—notably coproporphyrin III. Erythrocyte uroporphyrinogen decarboxylase activity was similar in both groups. There was a high correlation between levels of hexachlorobenzene and octachlorostyrene, respectively, in plasma and urinary excretion of porphyrins; these findings, however, relied heavily on 1 subject for whom extreme values were obtained. The results indicated that occupational exposure to hexachlorobenzene and octachlorostyrene in aluminum degassing with hexachloroethane may affect porphyrin metabolism in a manner consistent with early secondary coproporphyrinuria—the first recognized step in the development of chronic hepatic porphyria. It was also noted that changes remained detectable some years after exposure ceased.