Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-12-25
pubmed:abstractText
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.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1096-6080
pubmed:author
pubmed:issnType
Print
pubmed:volume
65
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
99-106
pubmed:dateRevised
2010-9-17
pubmed:meshHeading
pubmed-meshheading:11752689-Air Pollutants, pubmed-meshheading:11752689-Animals, pubmed-meshheading:11752689-Bronchoalveolar Lavage, pubmed-meshheading:11752689-Cell Division, pubmed-meshheading:11752689-Drug Interactions, pubmed-meshheading:11752689-Immunohistochemistry, pubmed-meshheading:11752689-Inflammation, pubmed-meshheading:11752689-Inhalation Exposure, pubmed-meshheading:11752689-Interleukin-6, pubmed-meshheading:11752689-Lung, pubmed-meshheading:11752689-Macrophages, Alveolar, pubmed-meshheading:11752689-Male, pubmed-meshheading:11752689-Mice, pubmed-meshheading:11752689-Mice, Inbred Strains, pubmed-meshheading:11752689-Multiple Chemical Sensitivity, pubmed-meshheading:11752689-Ozone, pubmed-meshheading:11752689-Time Factors, pubmed-meshheading:11752689-Tobacco Smoke Pollution, pubmed-meshheading:11752689-Tumor Necrosis Factor-alpha
pubmed:year
2002
pubmed:articleTitle
Short-term exposure to aged and diluted sidestream cigarette smoke enhances ozone-induced lung injury in B6C3F1 mice.
pubmed:affiliation
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.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't