The role of particulate matter in exacerbation of atopic asthma.
Increasing evidence shows that elevated levels of particulate matter (PM) can exacerbate existing asthma, while evidence that PM can promote the induction of asthma is limited. PM in ambient air has been associated with increased emergency room visits and medication use by asthmatics. Controlled human exposure studies of acid aerosols suggest increased responses among adolescent asthmatics. Increased ambient and indoor levels of bioaerosols (e.g., house dust mite, fungal spores, endotoxin) have been associated with exacerbation of asthma. Environmental Protection Agency (EPA) studies focus on the effects of exposing humans and animal models to a combination of various PM samples (e.g., diesel exhaust particles, oil fly ash) and allergens (e.g., house dust mite, ovalbumin). These research efforts to understand the mechanisms by which PM exposure can promote allergic sensitization and exacerbate existing asthma concentrate on the role of transition metals. Exposure of animal models to combined PM and allergen promotes allergic sensitization and increases allergic inflammation and airway hyperresponsiveness. Exposure of healthy human volunteers to emission source PM samples promotes inflammation and increased indices of oxidant formation correlating with the quantity of transition metals in the samples. Results of these studies suggest that transition metals in ambient PM promote the formation of reactive oxygen species and subsequent lung injury, inflammation, and airway hyperresponsiveness leading to airflow limitation and symptoms of asthma.
Gavett
S H
SH
National Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Research Triangle Park, NC 27711, USA.
Koren
H S
HS
D000397:Air Pollution / Q000009:adverse effects*; D000485:Allergens / Q000276:immunology; D000818:Animals; D001249:Asthma / Q000453:epidemiology* / Q000276:immunology; D016535:Bronchial Hyperreactivity / Q000276:immunology; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D016207:Cytokines / Q000096:biosynthesis; D005742:Gasoline / Q000009:adverse effects; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000453:epidemiology* / Q000276:immunology; D019216:Metals, Heavy / Q000009:adverse effects; D051379:Mice; D008925:Mites / Q000276:immunology; D018448:Models, Immunological; D010047:Ovalbumin / Q000276:immunology; D051381:Rats; D018418:Th2 Cells / Q000276:immunology
D000485:Allergens; D016207:Cytokines; D005742:Gasoline; D019216:Metals, Heavy; D010047:Ovalbumin