A Chronic Inhalation Toxicity Study of Diesel Engine Emissions and Coal Dust, Alone and Combined

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Abstract
To evaluate the potential health hazards of diesel engine emissions in underground coal mines, inhalation studies were performed using three species of animals. A wide range of toxicological responses was measured. Exhaust was provided by a 425 in.3 displacement four-cycle, water-cooled, naturally aspirated diesel engine (Caterpillar Model 3304) equipped with a water scrubber. Exposures were 7 h/day, 5 days/week, for periods up to 24 months. Micronized coal dust was generated using a Wright dust feeder. Four exposures were evaluated: (1) filtered ambient air, (2) 2 mg/m3 diesel particulate, (3) 2 mg/m3 respirable coal dust, and (4) 1 mg/m3 each of 2 and 3. Gaseous and vapor concentrations were similar in both exposures employing diesel exhaust. Male cynomolgus monkeys, Fischer-344 male and female rats, and female CD-1 mice were the experimental subjects. Monkeys were sacrificed at 24 months, rats at 3, 6, 12, and 24 months, and mice at 1, 3, and 6 months. Gross morphology and histopathology demonstrated that both diesel and coal dust particles are deposited in the lungs and retained in alveolar tissue. Alveolar type II cell hyperplasia and pulmonary lipidosis occurred in rats, being most evident in rats exposed to diesel exhaust alone. There was, however, no evidence of emphysema or chronic bronchitis, and only minimal fibrosis was seen in association with the retained particulate. Both particulates affected the defense mechanisms of the lung. Exposure to coal dust activated responses associated with phagocytosis, whereas exposure to diesel exhaust depressed them. Severity of influenza challenge increased concomitantly with decreased interferon production in diesel-exposed mice. Exposure to diesel emissions did not result in genotoxic effects as measured by increases in sister chromatid exchange, chromosomal aberrations, micronucleus testing, and urine genotoxic assays. Pulmonary function studies in monkeys showed mild obstructive airway disease in coal dust, diesel exhaust, and the combined exposed animals. This effect was most pronounced in monkeys exposed to diesel exhaust. Evidence of restrictive lung disease was not seen in any group. Clearance of F3O4 particles appeared to be stimulated by exposure to diesel exhaust in the first 3 months, but long-term clearance of diesel particulate appeared to be inhibited. No evidence was found for increases in tumorogenicity (rats) or induction of xenobiotic metabolizing enzymes in the lung or liver (rats). Humoral and cellular immunities were not significantly affected by exposure (rats). No adverse seminal effects were observed in monkeys exposed for 2 years. There was no frank evidence of chronic toxicity as demonstrated by changes in mortality, body weight gains, organ-body weight ratios, or clinical parameters in rats or monkeys. Synergistic effects between diesel exhaust and coal dust were not demonstrated.