Previous subchronic and/or chronic inhalation studies of unleaded gasoline and a variety of petroleum naphthas, solvents, and distillates have shown that these complex materials are capable of inducing a distinctive nephropathy which appears limited to male rats. Therefore a series of gavage screening studies using male F-344 rats was conducted on components of gasoline to more clearly identify the major contributors to this nephrotoxicity. The dosing regimen consisted of 20 doses administered once daily, 5 days per wk for 4 wk. Tested were 15 pure hydrocarbon compounds typically found in unleaded gasoline boiling range, 4 naphtha streams representative of those commonly used to blend gasolines and 3 distillation fractions covering the less volatile portions of gasoline. The results revealed that the alkane (paraffin) components were primarily responsible for the nephrotoxic activity seen in unleaded gasoline, with a positive structure-activity response relating the degree of alkane branching to the potency of the nephrotoxic response. In addition, the nephrotoxic activity observed with the naphtha streams and distillation fraction correlated well with the proportion of branched alkanes contained in each.
Sprague-Dawley rats and Cynomolgus monkeys were exposed to dust aerosol concentrations (0, 10.2, and 30.7 mg/m3) of micronized delayed process petroleum coke for 6 hr/day, 5 days/week over 2 years. With the exception of pulmonary effects, particularly in the rats, no significant adverse treatment-related effects were observed. Both dust-exposed groups of both species exhibited a gray to black discoloration of the lung, an observation consistent with pulmonary deposition of the coke dust, as well as increased absolute and/or relative lung weight values. The pulmonary histopathology in the monkeys was limited to the deposition and phagocytosis of the test material by pulmonary macrophages. The rats also exhibited these responses, but with concomitant signs of chronic inflammation and focal areas of fibrosis, bronchiolization, sclerosis, squamous alveolar metaplasia, and keratin cyst formation. No difference in the mortality rate was observed between the control and exposed groups of rats. Lastly, no significant increases in chromosomal aberrations were observed in rodents of the 10.2 or 30.7 mg/m3 exposure groups when examined after 5 days, 12 months, and 22 months of exposure.
Ninety-day inhalation studies were conducted on 50:50 weight percent (wt %) mixtures of n-butane:n-pentane and isobutane:isopentane, respectively, and on a distillation cut boiling below 145 degrees F of a reference unleaded gasoline blend to assess the nephrotoxicity of these volatile mixtures. The mixtures of butanes and pentanes were selected because these four hydrocarbons are the most prevalent components of gasoline vapors encountered under typical occupational exposures. The 0-145 degrees F gasoline distillation fraction was tested because it reasonably approximates the composition of gasoline vapors measured under occupational settings. Male and female F-344 rats were exposed to 2 levels of each mixture, 6 hours per day, 5 days per week, for 13 weeks. The target concentrations for the butane:pentane mixtures were 4500 and 1000 parts per million (ppm), while 5200 and 1200 ppm were set for the gasoline distillation fraction. An interim sacrifice was conducted after 28 days. The rats were not significantly affected by the exposures, and there was no evidence of hydrocarbon-induced nephropathy in either sex at the termination of each study. However, at the 28-day interim sacrifice period for both butane:pentane mixtures, mild, transient treatment-related but not exposure-related kidney effects were observed in the male rats. These perturbations were absent at the interim sacrifice period for the gasoline distillation fraction.
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.
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)
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