Short-term exposure to aged and diluted sidestream cigarette smoke enhances ozone-induced lung injury in B6C3F1 mice.
To determine the effects of aged and diluted sidestream cigarette smoke (ADSS) as a surrogate of environmental tobacco smoke (ETS) on ozone-induced lung injury, male B6C3F1 mice were exposed to (1) filtered air (FA), (2) ADSS, (3) ozone, or (4) ADSS followed by ozone (ADSS/ozone). Exposure to ADSS at 30 mg/m3 of total suspended particulates (TSP) for 6 h/day for 3 days, followed by exposure to ozone at 0.5 ppm for 24 h was associated with a significant increase in the number of cells recovered by bronchoalveolar lavage (BAL) compared with exposure to ADSS alone or ozone alone. The proportion of neutrophils and lymphocytes, as well as total protein level in BAL, was also significantly elevated following ADSS/ozone exposure, when compared with all other groups. Within the centriacinar regions of the lungs, the percentage of proliferating cells identified by bromodeoxyuridine (BrdU) labeling was unchanged from control, following exposure to ADSS alone, but was significantly elevated following exposure to ozone (280% of control) and further augmented in a statistically significant manner in mice exposed to ADSS/ozone (402% of control). Following exposure to ozone or ADSS/ozone, the ability of alveolar macrophages (AM) to release interleukin (IL)-6 under lipopolysaccharide (LPS) stimulation was significantly decreased, while exposure to ADSS or ADSS/ozone caused a significantly increased release of tumor necrosis factor alpha from AM under LPS stimulation. We conclude that ADSS exposure enhances the sensitivity of animals to ozone-induced lung injury.
Yu
Mang
M
Center for Comparative Respiratory Biology and Medicine, Institute of Toxicology and Environmental Health, and California Regional Primate Research Center, University of California, One Shields Avenue, Davis, California 95616, USA.
Pinkerton
Kent E
KE
Witschi
Hanspeter
H
D000393:Air Pollutants / Q000009:adverse effects* / Q000032:analysis; D000818:Animals; D018893:Bronchoalveolar Lavage; D002455:Cell Division; D004347:Drug Interactions; D007150:Immunohistochemistry; D007249:Inflammation / Q000139:chemically induced / Q000209:etiology; D019570:Inhalation Exposure / Q000009:adverse effects* / Q000032:analysis; D015850:Interleukin-6 / Q000378:metabolism; D008168:Lung / Q000737:chemistry / Q000187:drug effects* / Q000473:pathology; D016676:Macrophages, Alveolar / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D018777:Multiple Chemical Sensitivity / Q000209:etiology; D010126:Ozone / Q000633:toxicity*; D013997:Time Factors; D014028:Tobacco Smoke Pollution / Q000009:adverse effects* / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects / Q000378:metabolism
D000393:Air Pollutants; D015850:Interleukin-6; D014028:Tobacco Smoke Pollution; D014409:Tumor Necrosis Factor-alpha; D010126:Ozone