Biological Effects of Atmospheres Contaminated by Auto Exhaust

Hueter, F. Gordon; Contner, G.L.; Busch, Kenneth A.; Hinners, R.G.

doi:10.1097/00043764-196702000-00035

Cited by 7 publications

(9 citation statements)

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“…The cancer study by Brightwell et al (9) of rats and hamsters exposed to GE, mentioned above, also included limited evaluations of respiratory function (24), but no significant alterations were observed. In 1966, Hueter et al (25) reported limited measurements of the respiratory function of guinea pigs during 20 months of exposure to GE at 100 ppm CO, but found no significant effects. In 1979, Pepelko et al (26) reported exposing rats 16 hr/day for 90 days to GE at a dilution of 1:10.…”

Section: Lung Cancer From Engine Exhaustmentioning

confidence: 99%

Toxicological and epidemiological evidence for health risks from inhaled engine emissions.

Mauderly

1994

Environ Health Perspect

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Information from toxicological and epidemiological studies of the cancer and noncancer health risks from inhaled diesel engine exhaust (DE) and gasoline engine exhaust (GE) was reviewed. The toxicological database is more extensive for DE than for GE. Animal studies have shown that heavy, chronic exposures to both DE and GE can cause lung pathology and associated physiological effects. Inhaled GE has not been shown to be carcinogenic in animals. Chronically inhaled DE at high concentrations is a pulmonary carcinogen in rats, but the response is questionable in mice and negative in Syrian hamsters. The response in rats is probably not attributable to the DE soot-associated organic compounds, as previously assumed, and the usefulness of the rat data for predicting risk in humans is uncertain. Experimental human exposures to DE show that lung inflammatory and other cellular effects can occur after single exposures, and sparse data suggest that occupational exposures might affect respiratory function and symptoms. Epidemiology suggests that heavy occupational exposures to exhaust probably increase the risks for mortality from both lung cancer and noncancer pulmonary disease. The small magnitudes of the increases in these risks make the studies very sensitive to confounding factors and uncertainties of exposure; thus, it may not be possible to resolve exposure-response relationships conclusively by epidemiology. Our present knowledge suggests that heavy occupational exposures to DE and GE are hazardous but does not allow quantitative estimates of risk with a high degree of certainty. -Environ Health Perspect 102(Suppl 4): 165-171 (1994).

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Section: Lung Cancer From Engine Exhaustmentioning

confidence: 99%

Toxicological and epidemiological evidence for health risks from inhaled engine emissions.

Mauderly

1994

Environ Health Perspect

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“…In the past, a number of investigators had reported that during chronic inhalation studies there was a significant increase in spontaneous pneumonia in the animals being exposed to gaseous test substances (26,27 In addition to testing of pure compounds, this system has also been used to evaluate "real world" industrial particulates collected from copper smelter and from a fluidized-bed coal fired power plant (25). Mice were exposed for 5, 10, or 20 daily 3-hr (5 days per week) exposures prior to receiving the streptococcal infection.…”

Section: Effects Of Gaseous Pollutantsmentioning

confidence: 99%

Use of Experimental Airborne Infections for Monitoring Altered Host Defenses

Gardner¹

1982

Environmental Health Perspectives

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“…23 Similar exposures on a long-term basis have produced an increase in neonatal mortality in mice at 0.01 to 1.5 ppm oxidant. 24 Exposure of rats for 3 hr to ambient air containing more than 0.4 ppm oxidant produced changes in the fine structure of the lung with the severity of the damage increasing with age and becoming irreversible at age 21 months. 25 Guinea pigs exposed continuously to ambient air showed a significant increase in flow resistance when the oxidant exceeded 0.5 ppm.…”

Section: Oxidantsmentioning

confidence: 99%