Associations of air pollution exposure with blood pressure and heart rate variability are modified by oxidative stress genes: A repeated-measures panel among elderly urban residents

Oxidative stress has been suggested as a major cause of elevated blood pressure (BP) and reduced heart rate variability (HRV) due to air pollution. We hypothesized that the associations of air pollution exposure with BP and HRV are modified by oxidative stress gene polymorphisms. Between 2008 and 20...

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Veröffentlicht in:Environmental health 2016-03, Vol.15 (1), p.47-47, Article 47
Hauptverfasser: Kim, Kyoung-Nam, Kim, Jin Hee, Jung, Kweon, Hong, Yun-Chul
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container_title Environmental health
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creator Kim, Kyoung-Nam
Kim, Jin Hee
Jung, Kweon
Hong, Yun-Chul
description Oxidative stress has been suggested as a major cause of elevated blood pressure (BP) and reduced heart rate variability (HRV) due to air pollution. We hypothesized that the associations of air pollution exposure with BP and HRV are modified by oxidative stress gene polymorphisms. Between 2008 and 2010, we conducted up to 5 surveys of 547 elderly participants, measured their BP and HRV, and genotyped 47 single nucleotide polymorphisms (SNPs) in 18 oxidative stress genes. Linear mixed models were constructed to evaluate the associations of particulate matter ≤10 μm, nitrogen dioxide, and sulfur dioxide with BP and HRV, as well as the modifications of these associations by the genotyped SNPs. Single-SNP analyses revealed interactions between air pollution and 15 SNPs (for BP) and 33 SNPs (for HRV) (all, P for interaction 
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We hypothesized that the associations of air pollution exposure with BP and HRV are modified by oxidative stress gene polymorphisms. Between 2008 and 2010, we conducted up to 5 surveys of 547 elderly participants, measured their BP and HRV, and genotyped 47 single nucleotide polymorphisms (SNPs) in 18 oxidative stress genes. Linear mixed models were constructed to evaluate the associations of particulate matter ≤10 μm, nitrogen dioxide, and sulfur dioxide with BP and HRV, as well as the modifications of these associations by the genotyped SNPs. Single-SNP analyses revealed interactions between air pollution and 15 SNPs (for BP) and 33 SNPs (for HRV) (all, P for interaction &lt; 0.05). When we generated genetic risk scores for BP and HRV, using the SNPs with interactions in the single-SNP models, we found that associations of air pollution exposure with BP and HRV were modified by the genetic risk scores (P for interaction &lt; 0.05). These results strongly suggest that the associations of air pollution with BP and HRV are mediated by oxidative stress pathways.</description><identifier>ISSN: 1476-069X</identifier><identifier>EISSN: 1476-069X</identifier><identifier>DOI: 10.1186/s12940-016-0130-3</identifier><identifier>PMID: 27015811</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Aged ; Air Pollutants - toxicity ; Air pollution ; Air Pollution - adverse effects ; Analysis ; Blood Pressure - drug effects ; Cities ; Environmental Exposure - adverse effects ; Environmental health ; Female ; Genetic aspects ; Health aspects ; Heart beat ; Heart Rate - drug effects ; Humans ; Korea ; Male ; Nitrogen Dioxide - toxicity ; Oxidative stress ; Oxidative Stress - genetics ; Particulate Matter - toxicity ; Polymorphism, Single Nucleotide ; Risk factors ; Single nucleotide polymorphisms ; Sulfur Dioxide - toxicity</subject><ispartof>Environmental health, 2016-03, Vol.15 (1), p.47-47, Article 47</ispartof><rights>COPYRIGHT 2016 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2016</rights><rights>Kim et al. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c494t-884a1532bac0563fc4a561560f682fc4ab6b442bded1d9f1412aa8a8e643ec093</citedby><cites>FETCH-LOGICAL-c494t-884a1532bac0563fc4a561560f682fc4ab6b442bded1d9f1412aa8a8e643ec093</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4807581/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4807581/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27015811$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Kyoung-Nam</creatorcontrib><creatorcontrib>Kim, Jin Hee</creatorcontrib><creatorcontrib>Jung, Kweon</creatorcontrib><creatorcontrib>Hong, Yun-Chul</creatorcontrib><title>Associations of air pollution exposure with blood pressure and heart rate variability are modified by oxidative stress genes: A repeated-measures panel among elderly urban residents</title><title>Environmental health</title><addtitle>Environ Health</addtitle><description>Oxidative stress has been suggested as a major cause of elevated blood pressure (BP) and reduced heart rate variability (HRV) due to air pollution. We hypothesized that the associations of air pollution exposure with BP and HRV are modified by oxidative stress gene polymorphisms. Between 2008 and 2010, we conducted up to 5 surveys of 547 elderly participants, measured their BP and HRV, and genotyped 47 single nucleotide polymorphisms (SNPs) in 18 oxidative stress genes. Linear mixed models were constructed to evaluate the associations of particulate matter ≤10 μm, nitrogen dioxide, and sulfur dioxide with BP and HRV, as well as the modifications of these associations by the genotyped SNPs. Single-SNP analyses revealed interactions between air pollution and 15 SNPs (for BP) and 33 SNPs (for HRV) (all, P for interaction &lt; 0.05). When we generated genetic risk scores for BP and HRV, using the SNPs with interactions in the single-SNP models, we found that associations of air pollution exposure with BP and HRV were modified by the genetic risk scores (P for interaction &lt; 0.05). 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We hypothesized that the associations of air pollution exposure with BP and HRV are modified by oxidative stress gene polymorphisms. Between 2008 and 2010, we conducted up to 5 surveys of 547 elderly participants, measured their BP and HRV, and genotyped 47 single nucleotide polymorphisms (SNPs) in 18 oxidative stress genes. Linear mixed models were constructed to evaluate the associations of particulate matter ≤10 μm, nitrogen dioxide, and sulfur dioxide with BP and HRV, as well as the modifications of these associations by the genotyped SNPs. Single-SNP analyses revealed interactions between air pollution and 15 SNPs (for BP) and 33 SNPs (for HRV) (all, P for interaction &lt; 0.05). When we generated genetic risk scores for BP and HRV, using the SNPs with interactions in the single-SNP models, we found that associations of air pollution exposure with BP and HRV were modified by the genetic risk scores (P for interaction &lt; 0.05). These results strongly suggest that the associations of air pollution with BP and HRV are mediated by oxidative stress pathways.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>27015811</pmid><doi>10.1186/s12940-016-0130-3</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record>
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subjects Aged
Air Pollutants - toxicity
Air pollution
Air Pollution - adverse effects
Analysis
Blood Pressure - drug effects
Cities
Environmental Exposure - adverse effects
Environmental health
Female
Genetic aspects
Health aspects
Heart beat
Heart Rate - drug effects
Humans
Korea
Male
Nitrogen Dioxide - toxicity
Oxidative stress
Oxidative Stress - genetics
Particulate Matter - toxicity
Polymorphism, Single Nucleotide
Risk factors
Single nucleotide polymorphisms
Sulfur Dioxide - toxicity
title Associations of air pollution exposure with blood pressure and heart rate variability are modified by oxidative stress genes: A repeated-measures panel among elderly urban residents
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