Gene-air pollution interaction and cardiovascular disease: a review |
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Authors: | Zanobetti Antonella Baccarelli Andrea Schwartz Joel |
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Affiliation: | Department of Environmental Health, Exposure Epidemiology and Risk Program, Harvard School of Public Health, Boston, MA 02115 |
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Abstract: | Genetic susceptibility is likely to play a role in response to air pollution. Hence, gene-environment interaction studies can be a tool for exploring the mechanisms and the importance of the pathway in the association between air pollution and a cardiovascular outcome.In this article, we present a systematic review of the studies that have examined gene-environment interactions in relation to the cardiovascular health effects of air pollutants.We identified 16 articles meeting our search criteria. Of these studies, most have focused on individual functional polymorphisms or individual candidate genes. Moreover, they were all based on 3 study populations that have been extensively investigated in relation to air pollution effects: the Normative Aging Study, Air Pollution and Inflammatory Response in Myocardial Infarction Survivors: Gene-Environment Interaction in a High Risk Group, and Multiethnic Study of Atherosclerosis.In conclusions, the studies differed substantially in both the cardiovascular outcomes examined and the polymorphisms examined, so there is little confirmation of results across cohorts. Gene-environment interaction studies can help explore the mechanisms and the potential pathway in the association between air pollution and a cardiovascular outcome; replication of findings and studies involving multiple cohorts would be needed to draw stronger conclusions. |
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Keywords: | ACE, angiotensin-I converting enzyme ADRB2, β2-adrenergic receptor AGT, angiotensinogen AGTR1, type 1 angiotensin II receptor ALOX15, arachidonate 15-lipoxygenase APOE, apolipoprotein E BC, black carbon BP, blood pressure CRP, C-reactive protein cSHMT, cytoplasmic serine hydroxymethyltransferase CVD, cardiovascular disease DGCR8, DiGeorge critical region-8 EDN1, endothelin 1 GRK4, G protein-coupled receptor kinase 4 GSS, genetic susceptibility score GSTM1, glutathione S-transferase μ1 GSTP1, glutathione S-transferase π1 GSTT1, glutathione S-transferase θ1 GT, guanine thymine GWAS, genome-wide association study HFE, hemocromatosis HMOX-1, heme oxygenase 1 HRV, heart rate variability IL-6, interleukin 6 ITPR2, inositol 1,4,5-triphosphate receptor 2 LPL, lipoprotein lipase LVM, left ventricular mass MESA, Multiethnic Study of Atherosclerosis MI, myocardial infarction miRNA, microRNA MTHFR, methylenetetrahydrofolate reductase NAS, Normative Aging Study NQO1, NAD(P)H dehydrogenase, quinone 1 PM, particulate matter PTGS1, prostaglandin-endoperoxide synthase 1 PTGS2, prostaglandin-endoperoxide synthase 2 ROS, reactive oxygen species SNP, single-nucleotide polymorphism TLR4, toll-like receptor 4 VEGF, vascular endothelial growth factor |
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