title: Responses to subchronic inhalation of low concentrations of diesel exhaust and hardwood smoke measured in rat bronchoalveolar lavage fluid.
abstract: Air pollution exposure is associated with adverse health effects, but the causal components and mechanisms are unclear. We compared effects of daily exposure for 6 mo to diesel exhaust (DE) or hardwood smoke (HWS) at 4 concentrations between 30 and 1000 microg/(3) of total particulate matter, or filtered air, in male and female rats. Lung lavage fluid was assayed for toxicity indicators, cytokines, and glutathione. Statistical analyses included pairwise comparisons with control and exposure-related trends, modeled using techniques that facilitated evaluation of nonlinear exposure effects. Lactate dehydrogenase increased with exposure concentration in DE-exposed females, but in other groups, low exposure concentrations caused increases while higher concentrations had less effect. Total protein in the HWS-exposed males and females followed similar patterns. Alkaline phosphatase increased in DE-exposed females, but decreased in HWS-exposed males and females. Beta-Glucuronidase decreased in HWS- and DE-exposed males, but HWS-exposed females showed decreases at low exposure concentrations and weak increases at higher exposure concentrations. Macrophage inflammatory protein-2 decreased in HWS-exposed males and females and DE-exposed females. Tumor necrosis factor-alpha levels decreased in DE-exposed females and males, but HWS-exposed males showed small increases. DE did not affect total glutathione in either gender, but HWS decreased glutathione in females, while in males, increases at low exposure concentrations but not at higher exposure levels were observed. Thus, these two combustion emissions differentially affect lung responses, with gender affecting response patterns. Furthermore, effects may be nonmonotonic functions of exposure levels, with maximal responses in environmentally or occupationally relevant exposure ranges.
authors.affiliation: Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA. jseagrav@LRRI.opg
authors.forename: JeanClare
authors.initials: J
authors.lastname: Seagrave
authors.forename: Jacob D
authors.initials: JD
authors.lastname: McDonald
authors.forename: Matthew D
authors.initials: MD
authors.lastname: Reed
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*; D000395:Air Pollutants, Occupational / Q000633:toxicity*; D000469:Alkaline Phosphatase / Q000032:analysis; D000818:Animals; D001273:Atmosphere Exposure Chambers; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry* / Q000166:cytology; D054426:Chemokine CXCL2; D019743:Chemokines, CXC / Q000032:analysis; D004305:Dose-Response Relationship, Drug; D005260:Female; D019570:Inhalation Exposure; D036341:Intercellular Signaling Peptides and Proteins / Q000032:analysis; D007770:L-Lactate Dehydrogenase / Q000032:analysis; D008297:Male; D051381:Rats; D011916:Rats, Inbred F344; D012737:Sex Factors; D012906:Smoke / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D001335:Vehicle Emissions / Q000032:analysis / Q000633:toxicity*; D014934:Wood
chemical_list: D000393:Air Pollutants; D000395:Air Pollutants, Occupational; D054426:Chemokine CXCL2; D019743:Chemokines, CXC; C513296:Cxcl2 protein, rat; D036341:Intercellular Signaling Peptides and Proteins; D012906:Smoke; D014409:Tumor Necrosis Factor-alpha; D001335:Vehicle Emissions; D007770:L-Lactate Dehydrogenase; D000469:Alkaline Phosphatase