Genotoxic and Carcinogenic Activity of Oil Refinery Effluents

Abstract

<p>Concentrated extracts were prepared from particulate, dissolved, and volatile components of effluents from three low-temperature cracking refineries. Extracts were tested for genotoxic activity using the Ames bacterial mutagenicity assay, and an in vitro assay for sister chromatid exchange. The dissolved and volatile components of effluents showed little genotoxic activity, but particulate extracts from two of three refineries sampled were significantly mutagenic. One particulate sample gave a positive response in the sister chromatid exchange (SCE) assay. All samples required exogenous activation with rat-liver microsomes (S-9) for expression of genotoxic activity. Subfractionation of particulate extracts indicated that mutagenic activity was concentrated in neutral, polar fractions.</p> <p>The mutagenic/carcinogenic hazard associated with the chlorination of water contaminated with oil refinery effluents was also investigated. Non-volatile agents with mutagenic (Ames test) and clastogenic (SCE) activity were formed by chlorination of dilute refinery effluents. These compounds were direct-acting, in that the addition of S-9 was not required for genotoxic activity. Contact time with chlorine, chlorine concentration, effluent concentration, and the pH of the reaction mixture were found to vary the mutagenicity of the extracts.</p> <p>The effluent extracts were tested for carcinogenicity using an in vivo embryo assay developed for these studies. Microlitre volumes of extracts were injected into eyed rainbow trout embryos, and the fish raised for 12 months before necropsy. Refinery extracts were not directly carcinogenic. Coinjection of aflatoxin B₁ with extracts from both the particulate and dissolved components of effluents significantly increased the incidence of hepatic carcinomas. This co-carcinogenic effect was most pronounced when the extracts and aflatoxin B₁ were preincubated with rat S-9 before embryo injection. Effluent extracts coinjected with a direct-acting carcinogen, N-methyl -N'-nitro-N-nitrosoguanidine (MNNG), did not increase the incidence of hepatic carcinomas.</p>