Environmental tobacco smoke: overview of chemical composition and genotoxic components

Löfroth, Göran

doi:10.1016/0165-1218(89)90021-9

Cited by 131 publications

(64 citation statements)

References 34 publications

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“…Passive smoke consists of a complex mixture of Ͼ4000 different chemicals (34) and thus the specific chemical ingredient(s) in ETS responsible for interacting with allergen to induce increased airway remodeling are currently unknown. Interestingly, recent studies suggest that specific genes may exist that increase the susceptibility to develop asthma in the presence of exposure to tobacco smoke (35,36).…”

Section: Discussionmentioning

confidence: 99%

Coexposure to Environmental Tobacco Smoke Increases Levels of Allergen-Induced Airway Remodeling in Mice

Min

Song

Miller

et al. 2007

The Journal of Immunology

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Environmental tobacco smoke (ETS) can increase asthma symptoms and the frequency of asthma attacks. However, the contribution of ETS to airway remodeling in asthma is at present unknown. In this study, we have used a mouse model of allergen-induced airway remodeling to determine whether the combination of chronic exposure to ETS and chronic exposure to OVA allergen induces greater levels of airway remodeling than exposure to either chronic ETS or chronic OVA allergen alone. Mice exposed to chronic ETS alone did not develop significant eosinophilic airway inflammation, airway remodeling, or increased airway hyperreactivity to methacholine. In contrast, mice exposed to chronic OVA allergen had significantly increased levels of peribronchial fibrosis, increased thickening of the smooth muscle layer, increased mucus, and increased airway hyperreactivity which was significantly enhanced by coexposure to the combination of chronic ETS and chronic OVA allergen. Mice coexposed to chronic ETS and chronic OVA allergen had significantly increased levels of eotaxin-1 expression in airway epithelium which was associated with increased numbers of peribronchial eosinophils, as well as increased numbers of peribronchial cells expressing TGF-β1. These studies suggest that chronic coexposure to ETS significantly increases levels of allergen-induced airway remodeling (in particular smooth muscle thickness) and airway responsiveness by up-regulating expression of chemokines such as eotaxin-1 in airway epithelium with resultant recruitment of cells expressing TGF-β1 to the airway and enhanced airway remodeling.

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Section: Discussionmentioning

confidence: 99%

Coexposure to Environmental Tobacco Smoke Increases Levels of Allergen-Induced Airway Remodeling in Mice

Min

Song

Miller

et al. 2007

The Journal of Immunology

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“…More than 4000 compounds have been identified in laboratory-based studies, including many known human toxins and carcinogens such as carbon monoxide, ammonia, formaldehyde, nicotine, tobacco-specific nitrosamines, benzo(a)pyrene, benzene, cadmium, nickel, and aromatic amines. 29,30 Many of these toxic constituents are more concentrated in sidestream than in mainstream smoke. 31 In studies conducted in residences and office buildings with tobacco smoking, ETS was a substantial source of many gas and particulate polycyclic aromatic compounds.…”

Section: Environmental Tobacco Smokementioning

confidence: 99%

Health hazard evaluation report: HETA-93-0351-2413, Goodwill Industries of America, Inc., Bethesda, Maryland.

1994

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“…More than 4000 compounds have been identified in laboratory-based studies, including many known human toxins and carcinogens such as CO, ammonia, formaldehyde, nicotine, tobacco-specific nitrosamines, benzo(a)pyrene, benzene, cadmium, nickel, and aromatic amines. 24,25 Many of these toxic constituents are more concentrated in sidestream than in mainstream smoke. 26 In studies conducted in residences and office buildings with tobacco smoking, ETS was a substantial source of many gas and particulate polycyclic aromatic compounds.…”

Section: Recommendationsmentioning

confidence: 99%

Health hazard evaluation report: HETA-93-1000-2406, Ithaca City School District, Transportation Department, Ithaca, New York.

1994

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This Health Hazard Evaluation (HHE) report and any recommendations made herein are for the specific facility evaluated and may not be universally applicable. Any recommendations made are not to be considered as final statements of NIOSH policy or of any agency or individual involved.Additional HHE reports are available at http://www.cdc.gov/niosh/hhe/reports This Health Hazard Evaluation (HHE) report and any recommendations made herein are for the specific facility evaluated and may not be universally applicable. Any recommendations made are not to be considered as final statements of NIOSH policy or of any agency or individual involved.Additional HHE reports are available at http://www.cdc.gov/niosh/hhe/reports This Health Hazard Evaluation (HHE) report and any recommendations made herein are for the specific facility evaluated and may not be universally applicable. Any recommendations made are not to be considered as final statements of NIOSH policy or of any agency or individual involved. applicable. Any recommendations made are not to be considered as final statements of NIOSH policy or of any agency or individual involved.Additional HHE reports are available at http://www.cdc.gov/niosh/hhe/reports

show abstract

Environmental tobacco smoke: overview of chemical composition and genotoxic components

Cited by 131 publications

References 34 publications

Coexposure to Environmental Tobacco Smoke Increases Levels of Allergen-Induced Airway Remodeling in Mice

Coexposure to Environmental Tobacco Smoke Increases Levels of Allergen-Induced Airway Remodeling in Mice

Health hazard evaluation report: HETA-93-0351-2413, Goodwill Industries of America, Inc., Bethesda, Maryland.

Health hazard evaluation report: HETA-93-1000-2406, Ithaca City School District, Transportation Department, Ithaca, New York.

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