be more sensitive to lung injury than humans to poorly soluble particles (ILSI, 2000), it is not clear that this is the case specifically for diesel exhaust particulates and the resulting inflammation effects. Since DE is a mixture of not just carbon particles but also various organics, both on the particles and in gases, there is some concern that the full impact of DE has not been assessed. In addition, differences in particle deposition, retention, and clearance mechanisms have been largely but perhaps not completely addressed by the use of the rat-to-human dosimetry model. In terms of the potential for other critical health effects, there is growing evidence suggesting that DE can exacerbate allergenic effects to known sensitizers, while also evoking production of biochemical markers typically associated with asthma. While some work in this area indicates that humans may be as sensitive as rats and mice to the immunologic effects (U.S. EPA, 2002; Chapter 6.3.4), this database is currently lacking key exposure-response data. It also should be noted that the ambient PM health effects data show a broader array of adverse human health concerns (e.g., cardiovascular effects, as well as acute exposure effects). __I.B.6. EPA Documentation and Review of the Inhalation RfC Source Document -- U.S. EPA, 2002 The Health Assessment Document (HAD) 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