ArticleEnvironmental health perspectives2009
Decreased PM10 exposure attenuates age-related lung function decline: genetic variants in p53, p21, and CCND1 modify this effect.
Article in Environmental health perspectives, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 30 citations in OpenAlex.
- Time to harmonize national ambient air quality standards.International journal of public health · 2017Article
- Particulate Matter and Respiratory Symptoms among Adults Living in Windhoek, Namibia: A Cross Sectional Descriptive Study.International journal of environmental research and public health · 2017Article
- Particulate air pollution and impaired lung function.F1000Research · 2016Review
- Investigation on the lung function of general population in Ilam, west of Iran, as a city exposed to dust storm.Global journal of health science · 2015Article
- Modification of the association between PM10 and lung function decline by cadherin 13 polymorphisms in the SAPALDIA cohort: a genome-wide interaction analysis.Environmental health perspectives · 2015Article
- A genetic variant of p53 restricts the mucous secretory phenotype by regulating SPDEF and Bcl-2 expression.Nature communications · 2014Article
- Improved air quality and attenuated lung function decline: modification by obesity in the SAPALDIA cohort.Environmental health perspectives · 2013Article
- A large scale gene-centric association study of lung function in newly-hired female cotton textile workers with endotoxin exposure.PloS one · 2013Article
- Article
- Update in environmental and occupational medicine 2009.American journal of respiratory and critical care medicine · 2010Review
- Significant Association of Cyclin D1 Promoter Genotypes With Asthma Susceptibility in Taiwan.In vivo (Athens, Greece)Article
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDecreasing 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.
objectiveWe 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 (FEF(25-75)) associated with improved air quality.
methodsSubjects 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 < or = 10 microm (PM(10)) to each participant's residential history 12 months before the baseline and follow-up assessments.
resultsThe effect of diminishing PM(10) exposure on FEF(25-75) decline appeared to be modified by p53 R72P, CCND1 P242P, and CCND1 rs667515. For example, a 10-microg/m(3) decline in average PM(10) exposure over an 11-year period attenuated the average annual decline in FEF(25-75) 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.
conclusionsOur results suggest that cell cycle control genes may modify the degree to which improved air quality may benefit respiratory function in adults.
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