title: TRP channels and traffic-related environmental pollution-induced pulmonary disease.
abstract: Environmental pollutant exposures are major risk factors for adverse health outcomes, with increased morbidity and mortality in humans. Diesel exhaust (DE) is one of the major harmful components of traffic-related air pollution. Exposure to DE affects several physiological systems, including the airways, and pulmonary diseases are increased in highly populated urban areas. Hence, there are urgent needs to (1) create newer and lesser polluting fuels, (2) improve exhaust aftertreatments and reduce emissions, and (3) understand mechanisms of actions for toxic effects of both conventional and cleaner diesel fuels on the lungs. These steps could aid the development of diagnostics and interventions to prevent the negative impact of traffic-related air pollution on the pulmonary system. Exhaust from conventional, and to a lesser extent, clean fuels, contains particulate matter (PM) and more than 400 additional chemical constituents. The major toxic constituents are nitrogen oxides (NOx) and polycyclic aromatic hydrocarbons (PAHs). PM and PAHs could potentially act via transient receptor potential (TRP) channels. In this review, we will first discuss the associations between DE from conventional as well as clean fuel technologies and acute and chronic airway inflammation. We will then review possible activation and/or potentiation of TRP vanilloid type 1 (TRPV1) and ankyrin 1 (TRPA1) channels by PM and PAHs. Finally, we will discuss and summarize recent findings on the mechanisms whereby TRPs could control the link between DE and airway inflammation, which is a primary determinant leading to pulmonary disease.
authors.affiliation: Department of Endodontics, School of Dentistry, UT Health Science Center at San Antonio, San Antonio, TX, 78229, USA.
authors.forename: Armen N
authors.initials: AN
authors.lastname: Akopian
authors.affiliation: Office of Automotive Engineering, Southwest Research Institute, San Antonio, TX, 78228, USA.
authors.forename: E Robert
authors.initials: ER
authors.lastname: Fanick
authors.affiliation: Department of Pediatrics, Division of Immunology and Infectious Disease, School of Medicine, UT Health Science Center at San Antonio, San Antonio, TX, 78229, USA. brookse@uthscsa.edu.|Center for Airway Inflammation Research, UT Health Science Center at San Antonio, 8403 Floyd Curl Drive, STRF Microbiology MC 8259, San Antonio, TX, 78229, USA. brookse@uthscsa.edu.
authors.forename: Edward G
authors.initials: EG
authors.lastname: Brooks
mesh_terms: D000397:Air Pollution / Q000009:adverse effects; D000818:Animals; D002118:Calcium / Q000378:metabolism; D004781:Environmental Exposure / Q000009:adverse effects*; D004787:Environmental Pollution / Q000009:adverse effects*; D015870:Gene Expression; D006801:Humans; D008171:Lung Diseases / Q000453:epidemiology / Q000209:etiology* / Q000378:metabolism*; D052638:Particulate Matter / Q000009:adverse effects; D017382:Reactive Oxygen Species; D050051:Transient Receptor Potential Channels / Q000235:genetics* / Q000378:metabolism*; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D052638:Particulate Matter; D017382:Reactive Oxygen Species; D050051:Transient Receptor Potential Channels; D001335:Vehicle Emissions; D002118:Calcium
keywords: Acute lung injury; Asthma; Clean diesel; Diesel exhaust particles (DEP); Polycyclic aromatic hydrocarbons (PAHs); TRPA1; TRPV1
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