In retrospect, it is now safe to conclude that short-term mutagenicity assays were not only useful but instrumental in: (1) indicating that diesel soot was potentially carcinogenic and should be evaluated in chronic animal cancer bioassays, (2) identifying NO2-PAHs as potential carcinogens in this very complex mixture, (3) providing initial evidence that the mutagens were bioavailable, and (4) estimating the relative importance of various sources and fuels and other factors which can influence human exposure to carcinogens. This is not to say that short-term bioassays used alone can accomplish all of this. However, used in combination with chemical/analytical methods and toxicological tools, short-term genetic bioassays have become a critical component of many environmental health studies. Although substantial advances in our knowledge of the toxicology of diesel emissions have been made since 1978 when the initial observation that the organics extracted from diesel soot were mutagenic, a number of important questions remain not only for diesel emissions but for other combustion sources as well.

Includes bibliographical references (p. 19-22). EPA/600/D-86/189." "August 1986." "PB86-240934."

In retrospect, it is now safe to conclude that short-term mutagenicity assays were not only useful but instrumental in: (1) indicating that diesel soot was potentially carcinogenic and should be evaluated in chronic animal cancer bioassays, (2) identifying NOb2s-PAHs as potential carcinogens in this very complex mixture, (3) providing initial evidence that the mutagens were bioavailable, and (4) estimating the relative importance of various sources and fuels and other factors which can influence human exposure to carcinogens. This is not to say that short-term bioassays used alone can accomplish all of this. However, used in combination with chemical/analytical methods and toxicological tools, short-term genetic bioassays have become a critical component of many environmental health studies. Although substantial advances in our knowledge of the toxicology of diesel emissions have been made since 1978 when the initial observation that the organics extracted from diesel soot were mutagenic, a number of important questions remain not only for diesel emissions but for other combustion sources as well. Are the chemicals which induce positive results in the short-term bioassays the same agents which cause tumors in chronic animal bioassays? Which phase of the diesel emissions (gaseous or particulate) is carcinogenic in the animal inhalation studies? With advances in our understanding of the molecular mechanisms involved in producing chronic effects such as cancer, it is possible that new genetic tools and short-term bioassays will continue to contribute to our ability to answer these and other questions as they arise.