title: Early life exposure to environmental tobacco smoke alters immune response to asbestos via a shift in inflammatory phenotype resulting in increased disease development.
abstract: Asbestos in combination with tobacco smoke exposure reportedly leads to more severe physiological consequences than asbestos alone; limited data also show an increased disease risk due to environmental tobacco smoke (ETS) exposure. Environmental influences during gestation and early lung development can result in physiological changes that alter risk for disease development throughout an individual's lifetime. Therefore, maternal lifestyle may impact the ability of offspring to subsequently respond to environmental insults and alter overall disease susceptibility. In this study, we examined the effects of exposure to ETS in utero and during early postnatal development on asbestos-related inflammation and disease in adulthood. ETS exposure in utero appeared to shift inflammation towards a Th2 phenotype, via suppression of Th1 inflammatory cytokine production. This effect was further pronounced in mice exposed to ETS in utero and during early postnatal development. In utero ETS exposure led to increased collagen deposition, a marker of fibrotic disease, when the offspring was later exposed to asbestos, which was further increased with additional ETS exposure during early postnatal development. These data suggest that ETS exposure in utero alters the immune responses and leads to greater disease development after asbestos exposure, which is further exacerbated when exposure to ETS continues during early postnatal development.
authors.affiliation: a Center for Environmental Health Sciences, Biomedical and Pharmaceutical Sciences, University of Montana , Missoula , MT , USA and.
authors.forename: Traci Ann
authors.initials: TA
authors.lastname: Brown
authors.affiliation: a Center for Environmental Health Sciences, Biomedical and Pharmaceutical Sciences, University of Montana , Missoula , MT , USA and.
authors.forename: Andrij
authors.initials: A
authors.lastname: Holian
authors.affiliation: b Center for Health and the Environment, University of California , Davis , CA , USA.
authors.forename: Kent E
authors.initials: KE
authors.lastname: Pinkerton
authors.affiliation: a Center for Environmental Health Sciences, Biomedical and Pharmaceutical Sciences, University of Montana , Missoula , MT , USA and.
authors.forename: Joong Won
authors.initials: JW
authors.lastname: Lee
authors.affiliation: a Center for Environmental Health Sciences, Biomedical and Pharmaceutical Sciences, University of Montana , Missoula , MT , USA and.
authors.forename: Yoon Hee
authors.initials: YH
authors.lastname: Cho
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D001194:Asbestos / Q000633:toxicity*; D003094:Collagen / Q000378:metabolism; D016207:Cytokines / Q000276:immunology; D005260:Female; D007249:Inflammation / Q000139:chemically induced* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008168:Lung / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008810:Mice, Inbred C57BL; D010641:Phenotype; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*
chemical_list: D000393:Air Pollutants; D016207:Cytokines; D014028:Tobacco Smoke Pollution; D001194:Asbestos; D003094:Collagen
keywords: Asbestos; environmental tobacco smoke; fibrosis; inflammation