title: Diesel exhaust and asthma: hypotheses and molecular mechanisms of action.
abstract: Several components of air pollution have been linked to asthma. In addition to the well-studied critera air pollutants, such as nitrogen dioxide, sulfur dioxide, and ozone, diesel exhaust and diesel exhaust particles (DEPs) also appear to play a role in respiratory and allergic diseases. Diesel exhaust is composed of vapors, gases, and fine particles emitted by diesel-fueled compression-ignition engines. DEPs can act as nonspecific airway irritants at relatively high levels. At lower levels, DEPs promote release of specific cytokines, chemokines, immunoglobulins, and oxidants in the upper and lower airway. Release of these mediators of the allergic and inflammatory response initiates a cascade that can culminate in airway inflammation, mucus secretion, serum leakage into the airways, and bronchial smooth muscle contraction. DEPs also may promote expression of the T(subscript)H(/subscript)2 immunologic response phenotype that has been associated with asthma and allergic disease. DEPs appear to have greater immunologic effects in the presence of environmental allergens than they do alone. This immunologic evidence may help explain the epidemiologic studies indicating that children living along major trucking thoroughfares are at increased risk for asthmatic and allergic symptoms and are more likely to have objective evidence of respiratory dysfunction.
authors.affiliation: Division of Occupational and Environmental Medicine, University of California at San Francisco and San Francisco General Hospital, San Francisco, California 94143-0843, USA.
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Pandya
authors.forename: Gina
authors.initials: G
authors.lastname: Solomon
authors.forename: Amy
authors.initials: A
authors.lastname: Kinner
authors.forename: John R
authors.initials: JR
authors.lastname: Balmes
mesh_terms: D000393:Air Pollutants / Q000009:adverse effects*; D001249:Asthma / Q000209:etiology* / Q000503:physiopathology; D018925:Chemokines / Q000494:pharmacology; D002648:Child; D016207:Cytokines / Q000494:pharmacology; D016021:Epidemiologic Studies; D005740:Gases; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology; D007249:Inflammation; D019570:Inhalation Exposure; D008168:Lung / Q000187:drug effects / Q000473:pathology; D009119:Muscle Contraction; D009130:Muscle, Smooth / Q000502:physiology; D010316:Particle Size; D010641:Phenotype; D012307:Risk Factors; D014186:Transportation; D001335:Vehicle Emissions / Q000009:adverse effects*; D014835:Volatilization
chemical_list: D000393:Air Pollutants; D018925:Chemokines; D016207:Cytokines; D005740:Gases; D001335:Vehicle Emissions