title: Engine-operating load influences diesel exhaust composition and cardiopulmonary and immune responses.
abstract: BACKGROUND
  The composition of diesel engine exhaust (DEE) varies by engine type and condition, fuel, engine operation, and exhaust after treatment such as particle traps. DEE has been shown to increase inflammation, susceptibility to infection, and cardiovascular responses in experimentally exposed rodents and humans. Engines used in these studies have been operated at idle, at different steady-state loads, or on variable-load cycles, but exposures are often reported only as the mass concentration of particulate matter (PM), and the effects of different engine loads and the resulting differences in DEE composition are unknown.
  
  
  OBJECTIVE
  We assessed the impacts of load-related differences in DEE composition on models of inflammation, susceptibility to infection, and cardiovascular toxicity.
  
  
  METHODS
  We assessed inflammation and susceptibility to viral infection in C57BL/6 mice and cardiovascular toxicity in APOE-/- mice after being exposed to DEE generated from a single-cylinder diesel generator operated at partial or full load.
  
  
  RESULTS
  At the same PM mass concentration, partial load resulted in higher proportions of particle organic carbon content and a smaller particle size than did high load. Vapor-phase hydrocarbon content was greater at partial load. Compared with high-load DEE, partial-load DEE caused greater responses in heart rate and T-wave morphology, in terms of both magnitude and rapidity of onset of effects, consistent with previous findings that systemic effects may be driven largely by the gas phase of the exposure atmospheres. However, high-load DEE caused more lung inflammation and greater susceptibility to viral infection than did partial load.
  
  
  CONCLUSIONS
  Differences in engine load, as well as other operating variables, are important determinants of the type and magnitude of responses to inhaled DEE. PM mass concentration alone is not a sufficient basis for comparing or combining results from studies using DEE generated under different conditions.
authors.affiliation: Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA. jmcdonal@lrri.org
authors.forename: Jacob D
authors.initials: JD
authors.lastname: McDonald
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: Campen
authors.forename: Kevin S
authors.initials: KS
authors.lastname: Harrod
authors.forename: Jeanclare
authors.initials: J
authors.lastname: Seagrave
authors.forename: Steven K
authors.initials: SK
authors.lastname: Seilkop
authors.forename: Joe L
authors.initials: JL
authors.lastname: Mauderly
mesh_terms: D000393:Air Pollutants / Q000633:toxicity; D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D002319:Cardiovascular System / Q000187:drug effects; D007249:Inflammation / Q000139:chemically induced*; D008168:Lung / Q000187:drug effects / Q000276:immunology / Q000821:virology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D052638:Particulate Matter / Q000633:toxicity; D012136:Respiratory Syncytial Viruses; D001335:Vehicle Emissions / Q000633:toxicity
chemical_list: D000393:Air Pollutants; D001057:Apolipoproteins E; D052638:Particulate Matter; D001335:Vehicle Emissions