VOL.: 35 (1985) (p. 161)
Workers involved in oil-shale mining and processing may be exposed to complex mixtures of dusts, gases and vapours. The dusts may contain significant levels of crystalline silica. Inorganic gases and vapours to which workers may be exposed include carbon monoxide and hydrogen sulphide. Workers may also be exposed to gases and vapours containing organic compounds, including low levels of polynuclear aromatic compounds. The composition of spent oil shale can vary widely in respect to the remaining tar material, depending on the variation of retorting methods. Skin contact with crude shale-oil may occur, but is limited primarily to maintenance workers in modern oil-shale processing facilities.
Contact with shale-oil liquids occurred extensively in the past in the Scottish shale-oil industry, and in the British cotton-textile industry where lubricants derived from shale-oils were used.
Crude shale-oils from low-temperature retorting from different sources were tested for carcinogenicity in various experiments by skin application in different strains of mice. Samples from Jurassic Chuvash (USSR), Estonia (USSR), the Green River Formation (USA) and Fushun (China) all resulted in the induction of benign and malignant skin tumours. A sample from Estonia was also tested by skin application in rabbits and induced benign and malignant skin tumours. Lung tumours were produced in mice following intratracheal administration of a crude shale-oil from the Green River Formation.
Three samples of crude shale-oils from high-temperature retorting from Estonia were tested for carcinogenicity by skin application in mice, and one sample was also tested in rabbits. All the samples resulted in the induction of benign and malignant skin tumours; these samples were more carcinogenic than crude shale-oils from low-temperature retorting from the same source.
An extract of spent oil shale from the Green River Formation resulted in the induction of skin tumours in mice after topical application. Dusts prepared from this sample induced lung tumours in rats after inhalation exposure. No lung tumour occurred in rats or hamsters exposed by intratracheal administration to a suspension of the spent oil-shale dusts.
Various fractions of low- and high-temperature shale-oils were tested by skin application in mice and rabbits and by intramuscular application in mice; their carcinogenic activities did not necessarily parallel the benzo[a]pyrene content of the fractions.
Various crude shale-oil distillation fractions from Scotland were tested by skin application in mice; the less refined shale-oils were more highly carcinogenic to the skin than the more refined products. Heavy fractions of shale-oil from Estonia were more carcinogenic than the light fractions or the total oil when tested in mice by skin application; in contrast, in a study from Scotland, light distillation fractions of a lubricating oil induced more tumours than heavier fractions.
Comparative carcinogenicity studies in mice by skin application indicate that residual shale-oil bitumen (Estonia) was more active in inducing skin tumours than blown (oxidized) bitumen.
Commercial samples representing blends of shale-oils from Estonia induced skin tumours in mice after topical application; the carcinogenic effect increased with increasing content of crude shale-oil from high-temperature retorting. In similar experiments, commercial products containing low-temperature retorting oils did not induce skin tumours.
A pot residue of shale-oil distillation ('shale-oil coke') from the Green River Formation was carcinogenic to mouse skin after topical application in benzene; however, the same sample did not induce respiratory tumours in hamsters after intratracheal instillation.
No relevant data were available to the Working Group on the carcinogenicity in experimental animals of oil-shale retort process-waters.
All the shale-derived materials tested in short-term tests came from sources in the USA, and were therefore all from low-temperature processes.
Chromosomal aberrations were induced in bone-marrow cells of rats following administration by gavage of a suspension of raw oil shale. In-vitro tests of extracts of raw oil shale in bacteria, yeast and cultured mammalian cells gave negative results.
Preparations of spent oil shale yielded contradictory results in bacterial mutation assays and were negative in mutation assays with eukaryotic cells in vitro and in a chromosomal assay in vivo.
Preparations of shale-derived crude oils from various sources and retort processes were mutagenic in bacteria, yeast and cultured mammalian cells following metabolic or photo-induced activation. Three crude shale-oil preparations did not induce mitotic gene conversion in yeast; two others induced sister chromatid exchanges in cultured mammalian cells. Both positive and negative results were obtained in mammalian in-vivo assays for chromosomal effects.
As compared with the corresponding crude shale-oils, preparations of hydrotreated oils showed decreased activity or were negative in various short-term tests.
A preparation of refined shale-oil was not mutagenic in bacteria.
Oil-shale retort process-waters elicited DNA damage and mutations in bacteria and in cultured mammalian cells following metabolic activation or photoactivation. They induced chromosomal aberrations in cultured mammalian cells; and induced chromosomal aberrations but not sister chromatid exchanges in mouse cells in vivo.
Extracts of oil-shale ash were mutagenic in bacteria both in reversion and forward mutation assays in the absence of a metabolic system. Tests with eukaryotic systems gave negative results.
There is limited evidence for the carcinogenicity in experimental animals of raw oil shale, spent oil shale and a residue of shale-oil distillation.
There is sufficient evidence that shale-oils are carcinogenic in humans.
For definition of the italicized terms, see Preamble Evaluation.
Subsequent evaluation: Suppl. 7 (1987)
See Also: Toxicological Abbreviations Shale-Oils (IARC Summary & Evaluation, Supplement7, 1987)