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dc.contributor.authorWilker, Elissaen_US
dc.contributor.authorMittleman, Murray A.en_US
dc.contributor.authorLitonjua, Augusto A.en_US
dc.contributor.authorPoon, Audreyen_US
dc.contributor.authorBaccarelli, Andreaen_US
dc.contributor.authorSuh, Helenen_US
dc.contributor.authorWright, Robert O.en_US
dc.contributor.authorSparrow, Daviden_US
dc.contributor.authorVokonas, Pantelen_US
dc.contributor.authorSchwartz, Joelen_US
dc.date.accessioned2012-01-09T14:19:59Z
dc.date.available2012-01-09T14:19:59Z
dc.date.issued2009-06en_US
dc.identifier.citationWilker, Elissa, Murray A. Mittleman, Augusto A. Litonjua, Audrey Poon, Andrea Baccarelli, Helen Suh, Robert O. Wright, David Sparrow, Pantel Vokonas, Joel Schwartz. "Postural Changes in Blood Pressure Associated with Interactions between Candidate Genes for Chronic Respiratory Diseases and Exposure to Particulate Matter" Environmental Health Perspectives 117(6): 935-940. (2009)en_US
dc.identifier.issn1552-9924en_US
dc.identifier.urihttp://hdl.handle.net/2144/2750
dc.description.abstractBACKGROUND. Fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM2.5)] has been associated with autonomic dysregulation. OBJECTIVE. We hypothesized that PM2.5 influences postural changes in systolic blood pressure (ΔSBP) and in diastolic blood pressure (ΔDBP) and that this effect is modified by genes thought to be related to chronic lung disease. METHODS. We measured blood pressure in participants every 3-5 years. ΔSBP and ΔDBP were calculated as sitting minus standing SBP and DBP. We averaged PM2.5 over 48 hr before study visits and analyzed 202 single nucleotide polymorphisms (SNPs) in 25 genes. To address multiple comparisons, data were stratified into a split sample. In the discovery cohort, the effects of SNP x PM2.5 interactions on ΔSBP and ΔDBP were analyzed using mixed models with subject-specific random intercepts. We defined positive outcomes as p < 0.1 for the interaction; we analyzed only these SNPs in the replicate cohort and confirmed them if p < 0.025 with the same sign. Confirmed associations were analyzed within the full cohort in models adjusted for anthropometric and lifestyle factors. RESULTS. Nine hundred forty-five participants were included in our analysis. One interaction with rs9568232 in PHD finger protein 11 (PHF11) was associated with greater ΔDBP. Interactions with rs1144393 in matrix metalloprotease 1 (MMP1) and rs16930692, rs7955200, and rs10771283 in inositol 1,4,5-triphosphate receptor, type 2 (ITPR2) were associated with significantly greater ΔSBP. Because SNPs associated with ΔSBP in our analysis are in genes along the renin-angiotensin pathway, we then examined medications affecting that pathway and observed significant interactions for angiotensin receptor blockers but not angiotensin-converting enzyme inhibitors with PM2.5. CONCLUSIONS. PM2.5 influences blood pressure and autonomic function. This effect is modified by genes and drugs that also act along this pathway.en_US
dc.description.sponsorshipNational Institute of Environmental Health Sciences (T32 ES07069, ES0002, ES015172-01, ES014663, P01 ES09825); United States Environmental Protection Agency (R827353, R832416); National Institutes of Health/National Institute of Aging (AG027014); United States Department of Veterans Affairs; Massachusetts Veterans Epidemiology Research and Information Centeren_US
dc.language.isoenen_US
dc.publisherNational Institute of Environmental Health Sciencesen_US
dc.rightsThis is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.en_US
dc.subjectAging and susceptible populationsen_US
dc.subjectBlood pressureen_US
dc.subjectEnvironmental epidemiologyen_US
dc.subjectGene-environment interactionen_US
dc.subjectParticulate matteren_US
dc.titlePostural Changes in Blood Pressure Associated with Interactions between Candidate Genes for Chronic Respiratory Diseases and Exposure to Particulate Matteren_US
dc.typearticleen_US
dc.identifier.doi10.1289/ehp.0800279en_US
dc.identifier.pubmedid19590686en_US
dc.identifier.pmcid2702409en_US


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