Decreased PM10 Exposure Attenuates Age-Related Lung Function Decline: Genetic Variants in p53, p21, and CCND1 Modify This Effect

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Decreased PM10 Exposure Attenuates Age-Related Lung Function Decline: Genetic Variants in p53, p21, and CCND1 Modify This Effect

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dc.contributor.author Imboden, Medea
dc.contributor.author Schindler, Christian
dc.contributor.author Curjuric, Ivan
dc.contributor.author Berger, Wolfgang
dc.contributor.author Liu, Sally L.J.
dc.contributor.author Russi, Erich W.
dc.contributor.author Ackermann-Liebrich, Ursula
dc.contributor.author Rochat, Thierry
dc.contributor.author Probst-Hensch, Nicole M.
dc.contributor.author Schwartz, Joel David
dc.date.accessioned 2011-05-11T01:51:19Z
dc.date.issued 2009
dc.identifier.citation Imboden, Medea, Joel Schwartz, Christian Schindler, Ivan Curjuric, Wolfgang Berger, Sally L. J. Liu, Erich W. Russi, Ursula Ackermann-Liebrich, Thierry Rochat, and Nicole M. Probst-Hensch. 2009. Decreased PM10 Exposure Attenuates Age-Related Lung Function Decline: Genetic Variants in p53, p21, and CCND1 Modify This Effect. Environmental Health Perspectives 117(9): 1420-1427. en_US
dc.identifier.issn 0091-6765 en_US
dc.identifier.uri http://nrs.harvard.edu/urn-3:HUL.InstRepos:4887108
dc.description.abstract Background: Decreasing exposure to airborne particulates was previously associated with reduced age-related decline in lung function. However, whether the benefit from improved air quality depends on genetic background is not known. Recent evidence points to the involvement of the genes p53 and p21 and of the cell cycle control gene cyclin D1 (CCND1) in the response of bronchial cells to air pollution. Objective: We determined in 4,326 participants of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA) whether four single-nucleotide polymorphisms in three genes [CCND1 (rs9344 [P242P], rs667515), p53 (rs1042522 [R72P]), and p21 (rs1801270 [S31R])] modified the previously observed attenuation of the decline in the forced expiratory flow between 25% and 75% of the forced vital capacity (FEF25–75) associated with improved air quality. Methods: Subjects of the prospective population-based SAPALDIA cohort were assessed in 1991 and 2002 by spirometry, questionnaires, and biological sample collection for genotyping. We assigned spatially resolved concentrations of particulate matter with aerodynamic diameter ≤ 10 μm (PM10) to each participant’s residential history 12 months before the baseline and follow-up assessments. Results: The effect of diminishing PM10 exposure on FEF25–75 decline appeared to be modified by p53 R72P, CCND1 P242P, and CCND1 rs667515. For example, a 10-μg/m3 decline in aver-age PM10 exposure over an 11-year period attenuated the average annual decline in FEF25–75 by 21.33 mL/year (95% confidence interval, 10.57–32.08) among participants homozygous for the CCND1 (P242P) GG genotype, by 13.72 mL/year (5.38–22.06) among GA genotypes, and by 6.00 mL/year (−4.54 to 16.54) among AA genotypes. Conclusions: Our results suggest that cell cycle control genes may modify the degree to which improved air quality may benefit respiratory function in adults. en_US
dc.language.iso en_US en_US
dc.publisher National Institute of Environmental Health Sciences en_US
dc.relation.isversionof doi:10.1289/ehp.0800430 en_US
dc.relation.hasversion http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737020/pdf/ en_US
dash.license LAA
dc.subject air pollution en_US
dc.subject cell cycle en_US
dc.subject cohort study en_US
dc.subject genes en_US
dc.subject respiratory function tests en_US
dc.title Decreased PM10 Exposure Attenuates Age-Related Lung Function Decline: Genetic Variants in p53, p21, and CCND1 Modify This Effect en_US
dc.type Journal Article en_US
dc.description.version Version of Record en_US
dc.relation.journal Environmental Health Perspectives en_US
dash.depositing.author Schwartz, Joel David
dc.date.available 2011-05-11T01:51:19Z
dash.affiliation.other HMS^Medicine-Brigham and Women's Hospital en_US
dash.affiliation.other SPH^Exposure Epidemiology and Risk Program en_US

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