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How Exposure to Environmental Tobacco Smoke, Outdoor Air Pollutants, and Increased Pollen Burdens Influences the Incidence of Asthma

Asthma is a multifactorial airway disease that arises from a relatively common genetic background interphased with exposures to allergens and airborne irritants. The rapid rise in asthma over the past three decades in Western societies has been attributed to numerous diverse factors, including incre...

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Detalles Bibliográficos
Autores principales: Gilmour, M. Ian, Jaakkola, Maritta S., London, Stephanie J., Nel, Andre E., Rogers, Christine A.
Formato: Texto
Lenguaje:English
Publicado: National Institute of Environmental Health Sciences 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1440792/
https://www.ncbi.nlm.nih.gov/pubmed/16581557
http://dx.doi.org/10.1289/ehp.8380
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author Gilmour, M. Ian
Jaakkola, Maritta S.
London, Stephanie J.
Nel, Andre E.
Rogers, Christine A.
author_facet Gilmour, M. Ian
Jaakkola, Maritta S.
London, Stephanie J.
Nel, Andre E.
Rogers, Christine A.
author_sort Gilmour, M. Ian
collection PubMed
description Asthma is a multifactorial airway disease that arises from a relatively common genetic background interphased with exposures to allergens and airborne irritants. The rapid rise in asthma over the past three decades in Western societies has been attributed to numerous diverse factors, including increased awareness of the disease, altered lifestyle and activity patterns, and ill-defined changes in environmental exposures. It is well accepted that persons with asthma are more sensitive than persons without asthma to air pollutants such as cigarette smoke, traffic emissions, and photochemical smog components. It has also been demonstrated that exposure to a mix of allergens and irritants can at times promote the development phase (induction) of the disease. Experimental evidence suggests that complex organic molecules from diesel exhaust may act as allergic adjuvants through the production of oxidative stress in airway cells. It also seems that climate change is increasing the abundance of aeroallergens such as pollen, which may result in greater incidence or severity of allergic diseases. In this review we illustrate how environmental tobacco smoke, outdoor air pollution, and climate change may act as environmental risk factors for the development of asthma and provide mechanistic explanations for how some of these effects can occur.
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spelling pubmed-14407922006-05-02 How Exposure to Environmental Tobacco Smoke, Outdoor Air Pollutants, and Increased Pollen Burdens Influences the Incidence of Asthma Gilmour, M. Ian Jaakkola, Maritta S. London, Stephanie J. Nel, Andre E. Rogers, Christine A. Environ Health Perspect Research Asthma is a multifactorial airway disease that arises from a relatively common genetic background interphased with exposures to allergens and airborne irritants. The rapid rise in asthma over the past three decades in Western societies has been attributed to numerous diverse factors, including increased awareness of the disease, altered lifestyle and activity patterns, and ill-defined changes in environmental exposures. It is well accepted that persons with asthma are more sensitive than persons without asthma to air pollutants such as cigarette smoke, traffic emissions, and photochemical smog components. It has also been demonstrated that exposure to a mix of allergens and irritants can at times promote the development phase (induction) of the disease. Experimental evidence suggests that complex organic molecules from diesel exhaust may act as allergic adjuvants through the production of oxidative stress in airway cells. It also seems that climate change is increasing the abundance of aeroallergens such as pollen, which may result in greater incidence or severity of allergic diseases. In this review we illustrate how environmental tobacco smoke, outdoor air pollution, and climate change may act as environmental risk factors for the development of asthma and provide mechanistic explanations for how some of these effects can occur. National Institute of Environmental Health Sciences 2006-04 2006-01-26 /pmc/articles/PMC1440792/ /pubmed/16581557 http://dx.doi.org/10.1289/ehp.8380 Text en http://creativecommons.org/publicdomain/mark/1.0/ Publication of EHP lies in the public domain and is therefore without copyright. All text from EHP may be reprinted freely. Use of materials published in EHP should be acknowledged (for example, ?Reproduced with permission from Environmental Health Perspectives?); pertinent reference information should be provided for the article from which the material was reproduced. Articles from EHP, especially the News section, may contain photographs or illustrations copyrighted by other commercial organizations or individuals that may not be used without obtaining prior approval from the holder of the copyright.
spellingShingle Research
Gilmour, M. Ian
Jaakkola, Maritta S.
London, Stephanie J.
Nel, Andre E.
Rogers, Christine A.
How Exposure to Environmental Tobacco Smoke, Outdoor Air Pollutants, and Increased Pollen Burdens Influences the Incidence of Asthma
title How Exposure to Environmental Tobacco Smoke, Outdoor Air Pollutants, and Increased Pollen Burdens Influences the Incidence of Asthma
title_full How Exposure to Environmental Tobacco Smoke, Outdoor Air Pollutants, and Increased Pollen Burdens Influences the Incidence of Asthma
title_fullStr How Exposure to Environmental Tobacco Smoke, Outdoor Air Pollutants, and Increased Pollen Burdens Influences the Incidence of Asthma
title_full_unstemmed How Exposure to Environmental Tobacco Smoke, Outdoor Air Pollutants, and Increased Pollen Burdens Influences the Incidence of Asthma
title_short How Exposure to Environmental Tobacco Smoke, Outdoor Air Pollutants, and Increased Pollen Burdens Influences the Incidence of Asthma
title_sort how exposure to environmental tobacco smoke, outdoor air pollutants, and increased pollen burdens influences the incidence of asthma
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1440792/
https://www.ncbi.nlm.nih.gov/pubmed/16581557
http://dx.doi.org/10.1289/ehp.8380
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