studies, owing to the presence of diesel engine exhaust in ambient air for non-occupational settings; ossible confounders (smoking and asbestos exposure) that could contribute to the observed lung cancer risk in occupational studies of DE if the control for these confounders is not adequate; whether or not an exposure-response relationship for occupational lung cancer risk can be estimated for DE: the use of DPM (expressed as g/m3) as a surrogate dosimeter for DE exposure, given that the relative roles of various constituents in mediating carcinogenic effects and the carcinogenic mode of action are still not known, and the representativeness of occupational populations for the general population and vulnerable subgroups, including infants and children and individuals with preexisting diseases, particularly respiratory conditions. Use of animal data to develop dose-response based unit cancer risk values was judged inappropriate, since the only animal model with direct inhalation exposure and lung tumor responses was the rat, and the rat results were discounted because of mode-of-action information showing that the high exposure rat responses would not be a suitable basis for human dose-response analysis at environmental levels of exposure. __II.D.1. EPA Documentation Source Document -- U.S. EPA, 2002 The Health Assessment Document (HAD) (U.S. EPA, 2002) on which this IRIS Summary is based was peer reviewed by EPA's Clean Air Science Advisory Committee (CASAC) in October 2000. Written comments from CASAC were received in December 2000. Their comments were evaluated carefully and incorporated in finalization of the HAD. A record of these comments is available