ArticlePloS one2012
Different genes interact with particulate matter and tobacco smoke exposure in affecting lung function decline in the general population.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
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- Gene-Smoking Interaction Analysis for the Identification of Novel Asthma-Associated Genetic Factors.International journal of molecular sciences · 2023Article
- NFκB1 Polymorphisms Are Associated with Severe Influenza A (H1N1) Virus Infection in a Canadian Population.Microorganisms · 2022Article
- Integrative analysis to explore the biological association between environmental skin diseases and ambient particulate matter.Scientific reports · 2022Article
- MAP2K2 Delays Recovery in Murine Models of Acute Lung Injury and Associates with Acute Respiratory Distress Syndrome Outcome.American journal of respiratory cell and molecular biology · 2022Article
- A large-scale genetic correlation scan between rheumatoid arthritis and human plasma protein.Bone & joint research · 2022Article
- Epidemiologic evidence linking oxidative stress and pulmonary function in healthy populations.Chronic diseases and translational medicine · 2021Review
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- Genetic underpinnings of lung function and COPD.Journal of genetics · 2019Review
- Genome-wide assessment of gene-by-smoking interactions in COPD.Scientific reports · 2018Article
- Multitissue Transcriptomics Delineates the Diversity of Airway T Cell Functions in Asthma.American journal of respiratory cell and molecular biology · 2018Article
- Genes and pathways underlying susceptibility to impaired lung function in the context of environmental tobacco smoke exposure.Respiratory research · 2017Article
- Identification of differentially methylated BRCA1 and CRISP2 DNA regions as blood surrogate markers for cardiovascular disease.Scientific reports · 2017Article
- Article
- Genes Interacting with Occupational Exposures to Low Molecular Weight Agents and Irritants on Adult-Onset Asthma in Three European Studies.Environmental health perspectives · 2017Article
- Article
- Adult onset asthma and interaction between genes and active tobacco smoking: The GABRIEL consortium.PloS one · 2017Article
- Multiple-level validation identifies PARK2 in the development of lung cancer and chronic obstructive pulmonary disease.Oncotarget · 2016Article
- Particulate air pollution and impaired lung function.F1000Research · 2016Review
- Article
Corrections and comments
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Authors and funding
14 authors at 8 institutions in 5 countries.
Funding
Abstract
backgroundOxidative stress related genes modify the effects of ambient air pollution or tobacco smoking on lung function decline. The impact of interactions might be substantial, but previous studies mostly focused on main effects of single genes.
objectivesWe studied the interaction of both exposures with a broad set of oxidative-stress related candidate genes and pathways on lung function decline and contrasted interactions between exposures.
methodsFor 12679 single nucleotide polymorphisms (SNPs), change in forced expiratory volume in one second (FEV(1)), FEV(1) over forced vital capacity (FEV(1)/FVC), and mean forced expiratory flow between 25 and 75% of the FVC (FEF(25-75)) was regressed on interval exposure to particulate matter <10 µm in diameter (PM10) or packyears smoked (a), additive SNP effects (b), and interaction terms between (a) and (b) in 669 adults with GWAS data. Interaction p-values for 152 genes and 14 pathways were calculated by the adaptive rank truncation product (ARTP) method, and compared between exposures. Interaction effect sizes were contrasted for the strongest SNPs of nominally significant genes (p(interaction)<0.05). Replication was attempted for SNPs with MAF>10% in 3320 SAPALDIA participants without GWAS.
resultsOn the SNP-level, rs2035268 in gene SNCA accelerated FEV(1)/FVC decline by 3.8% (p(interaction) = 2.5×10(-6)), and rs12190800 in PARK2 attenuated FEV1 decline by 95.1 ml p(interaction) = 9.7×10(-8)) over 11 years, while interacting with PM10. Genes and pathways nominally interacting with PM10 and packyears exposure differed substantially. Gene CRISP2 presented a significant interaction with PM10 (p(interaction) = 3.0×10(-4)) on FEV(1)/FVC decline. Pathway interactions were weak. Replications for the strongest SNPs in PARK2 and CRISP2 were not successful.
conclusionsConsistent with a stratified response to increasing oxidative stress, different genes and pathways potentially mediate PM10 and tobacco smoke effects on lung function decline. Ignoring environmental exposures would miss these patterns, but achieving sufficient sample size and comparability across study samples is challenging.
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