Mangelsdorf, I.I.MangelsdorfVoß, J.-U.J.-U.VoßHeinrich, U.U.Heinrich2022-03-072022-03-072004https://publica.fraunhofer.de/handle/publica/292339The aim of this report was to review the pulmonary effects of diesel exhaust (DE) and diesel exhaust particles (DEP). Subjects reviewed were: - controlled short-term human toxicity studies in healthy and asthmatic subjects, - animal toxicity studies, - contribution of gas-phase and particles to the effects of DE, - relationships between particle properties and effects, - suitable metrics to describe dose-response relationships. The major findings and conclusions drawn from the data reviewed were: - In healthy human volunteers, exposure to DE or DEP led to increased airway resistance but had little effect on standard pulmonary functional parameters. Similar effects were observed in persons with asthma. Exposure to DE and DEP caused signs of inflammation in the lung of healthy humans. In persons with asthma, DE caused an enhanced reaction to allergic stimuli but no marked aggravation of inflammation. - In animal studies, DE and DEP led to an inflammatory reaction and (at high dose levels) to immunomodulating effects. - In short-term studies with humans, the inflammatory reaction in the lung following exposure to DE was slightly diminished by inclusion of a particle trap. The weak effect may have been due to the special exposure situation (engine under idling conditions) and limited effectiveness of the particle trap. However, animal studies with DE, filtered DE, and DEP or similar particles clearly indicate that particles are important contributors to the health effects caused by DE. Several comparative studies clearly show, that for the same particle weight the toxicity of particles is inversely related to particle size: ultrafine particles have higher toxicity than larger particles. - Studies correlating mass and surface area of DEP and other particles of low specific toxicity with pulmonary toxicity indicate that particle surface area is a much better dosimeter than particle mass. - When standardized by particle mass, the exhausts from high emitting gasoline and diesel engines were considerably mor toxic in animal experiments than those from low emitting engines. Generation of the exhausts at low temperature did not influence the toxicity of the emissions. - Soluble metals from ambient particles have been shown to lead to inflammatory reactions in the lung, by generating reactive oxygen species. Of these metals, zinc is the only metal present in DEP in amounts comparable to ambient particles. - Organic matter, especially aromatic hydrocarbons, may be involved in particle induced oxidative stress via formation of reactive quinones. - Particles with negligible content of metals or reactive organic matter, e.g. carbon blac and pjolystyrene, still induce inflammatory reactions in the lung, especially as ultrafine particles. - In conclusion, DE and DEP cause pulmonary effects. Particle size as well as particle and exhaust composition seem to play a role in these effects.enPulmonary effectsdiesel exhaust particleDiesel motor exhaust gasLungsRespiratory organsAir pollutionParticlesDiesel soot615610620report