Gasoline vapor exposures. Part I. Characterization of workplace exposures.

Monitoring surveys of gasoline vapor exposures were conducted on truck drivers and terminal operators from five terminal loading facilities, on dockmen and seamen at two tanker/barge loading facilities, and on attendants at a single expressway service plaza. Results revealed wide variations in total C6+ hydrocarbon exposures for each location, with overall 8-hr time-weighted averaged (TWA) geometric means of 5.7 mg/m3 (1.4 ppm) for the terminals, and 4.0 mg/m3 (1.0 ppm) for the service plaza, respectively. The exposures ranged from 0.8 to 120.8 mg/m3 (0.2-30.1 ppm) for the terminals, and from 1.1 to 130.3 mg/m3 (0.3-32.5 ppm) for the service plaza. For the terminals, exposures were not significantly different regardless of loading method or the presence or absence of vapor recovery systems. Comprehensive chemical analyses of terminal employee exposure samples revealed that the C4 and C5 hydrocarbon components constituted 74.8 +/- 9.2% of the total exposure sample on a microgram/sample basis. The C6, C7, and C8+ components constituted 13.0 +/- 1.9, 6.2 +/- 3.0, and 5.9 +/- 7.2% of the total samples, respectively. Comprehensive analyses of the marine employee exposure samples resulted in a similar distribution of components; that is, 66.6 +/- 7.9, 17.5 +/- 4.7, 9.2 +/- 3.1, and 6.4 +/- 1.9% for the C4/C5, C6, C7, and C8+ components, respectively. The composition of the exposures, however, was weighted more toward the C5, C6 and C7 components when compared to the bulk terminal employee exposures.(ABSTRACT TRUNCATED AT 250 WORDS)

Gasoline vapor exposures. Part II. Evaluation of the nephrotoxicity of the major C4/C5 hydrocarbon components.

Analysis of workplace exposures to gasoline vapors revealed that C4 and C5 hydrocarbons constitute anywhere from 67 to 74% by weight of a typical vapor. Furthermore, it was found that n-butane, isobutane, n-pentane, and isopentane together comprise greater than 90% of all the C4/C5 vapor components and approximately 61 to 67% by weight of the total vapor. Accordingly, a 21-day inhalation toxicity study of a blend consisting of 25% (w/w) each of these four hydrocarbons was conducted using rats to assess the potential for these major gasoline vapor components to induce kidney damage. No evidence of the kidney lesions typically associated with hydrocarbon-induced nephropathy was observed in rats exposed at up to 11 800 mg/m3 (4437 ppm) of the blend.

Carcinogenicity of petroleum lubricating oil distillates: effects of solvent refining, hydroprocessing, and blending.

Certain refining processes were investigated to determine their influence on the dermal carcinogenic activity of petroleum-derived lubricating oil distillates. Specifically, the effects of solvent refining, hydroprocessing, a combination of both processes, and the blending of oils processed using each technique were evaluated in standard mouse skin-painting bioassays. The refining process used as well as the level or severity of treatment greatly influenced the carcinogenic outcome of processed lubricating oils. Solvent refining at severities normally used appeared to eliminate carcinogenicity. In contrast, hydroprocessing alone at mild levels of treatment was successful only in reducing the carcinogenic potency; severe hydroprocessing conditions were necessary to eliminate carcinogenic activity without the use of additional refining processes. Carcinogenic activity could also be eliminated by following moderate solvent refining with mild hydroprocessing. Blending of hydroprocessed oils with solvent-refined oils resulted in a substantial reduction or even elimination of carcinogenic activity. However, the degree of protection obtained varied with the particular distillates used and appeared largely dependent on the inherent biological activity of the hydroprocessed oil.

Tumor initiation and promotion effects of petroleum streams in mouse skin.

A furnace oil, a dewaxed heavy paraffinic distillate, and a solvent-extracted lubricant base oil induced skin tumors in 9/43, 26/48, and 1/47 male C3H mice, respectively, during lifetime skin-painting bioassays. An initiation/promotion (I/P) bioassay was conducted to assess the I/P potential of these materials. During a 28-week initiation bioassay, groups of 30 male CD-1 mice were first treated dermally once daily for 5 days with 25 or 50 microliter of test materials or 50 microliter of acetone, rested for 2 weeks, then treated twice per week for 25 weeks with 50 microliter (0.1 mg/ml) phorbol-12-myristate-13-acetate (PMA). Only groups treated with the heavy paraffinic distillate had a significantly higher incidence of papillomas relative to the acetone control group. During a 28-week promotion bioassay, groups of 30 male CD-1 mice were treated once with 50 microliter of either DMBA (1.0 mg/ml) or acetone, rested for 2 weeks, and then treated twice per week with test material for the remaining 25 weeks. The furnace oil and dewaxed heavy paraffinic distillate showed significantly higher incidences of carcinomas and papillomas in DMBA-initiated mice relative to their acetone-initiated controls. Together these bioassay data suggest that only the dewaxed heavy paraffinic distillate is a complete carcinogen, having both initiating and promoting activity; furnace oil is a promoter only, while the solvent-extracted lubricating oil is noncarcinogenic. Overall, the I/P bioassay correlated well with the results of the lifetime skin-painting bioassay.