A Mechanistic Approach to Assessing the Lung Cancer Risk of Diesel Exhaust and Carbon Black

Abstract

Diesel exhaust soot particles, consisting principally of a carbonaceous core and absorbed organic compounds, are ubiquitous contaminants of the environment because of the widespread use of diesel engines. Carbon black is produced in large quantities and has many commercial uses around the world. Because the particle size of both materials is small, they are readily inhaled and deposited in the lung, giving rise to concern for induction of lung cancer in humans. Concern that exposure to diesel exhaust or carbon black may cause human lung cancer has been heightened by the finding that long-term exposure of rats to high concentrations of either diesel exhaust or carbon black causes an increased incidence of lung cancer. In this article, the available data are reviewed on diesel exhaust and carbon as agents that cause lung cancer in humans and laboratory animals from the perspective of using the data to assess human lung cancer risk. Current mechanistic data on the pathogenesis of lung cancer induced in rats by diesel soot and carbon black are reviewed. The mechanism of lung tumor induction in rats is apparently unique to high-level exposures, and a threshold relationship exists between exposure and lung tumor induction. Furthermore, mice and Syrian hamsters do not respond with increased lung tumors when exposed to high levels of diesel exhaust, suggesting that the lung tumor response may be unique to the rat, even at high levels of exposure. Thus, in my opinion, the rat lung tumor data from high level exposures to either diesel soot or carbon black should not be used in assessing the human lung cancer risk of exposure to either material. The available human data indicate that the human lung cancer risk will not be increased if exposures to these agents are controlled to low levels.