Modifying effect of a common polymorphism in the interleukin-6 promoter on the relationship between long-term exposure to traffic-related particulate matter and heart rate variability

Exposure to particulate matter (PM) has been associated with an increase in many inflammatory markers, including interleukin 6 (IL6). Air pollution exposure has also been suggested to induce an imbalance in the autonomic nervous system (ANS), such as a decrease in heart rate variability (HRV). In th...

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Veröffentlicht in:PloS one 2014-08, Vol.9 (8), p.e104978
Hauptverfasser: Adam, Martin, Imboden, Medea, Boes, Eva, Schaffner, Emmanuel, Künzli, Nino, Phuleria, Harish Chandra, Kronenberg, Florian, Gaspoz, Jean-Michel, Carballo, David, Probst-Hensch, Nicole
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container_issue 8
container_start_page e104978
container_title PloS one
container_volume 9
creator Adam, Martin
Imboden, Medea
Boes, Eva
Schaffner, Emmanuel
Künzli, Nino
Phuleria, Harish Chandra
Kronenberg, Florian
Gaspoz, Jean-Michel
Carballo, David
Probst-Hensch, Nicole
description Exposure to particulate matter (PM) has been associated with an increase in many inflammatory markers, including interleukin 6 (IL6). Air pollution exposure has also been suggested to induce an imbalance in the autonomic nervous system (ANS), such as a decrease in heart rate variability (HRV). In this study we aimed to investigate the modifying effect of polymorphisms in a major proinflammatory marker gene, interleukin 6 (IL6), on the relationship between long-term exposure to traffic-related PM10 (TPM10) and HRV. For this cross-sectional study we analysed 1552 participants of the SAPALDIA cohort aged 50 years and older. Included were persons with valid genotype data, who underwent ambulatory 24-hr electrocardiogram monitoring, and reported on medical history and lifestyle. Main effects of annual average TPM10 and IL6 gene variants (rs1800795; rs2069827; rs2069840; rs10242595) on HRV indices and their interaction with average annual exposure to TPM10 were tested, applying a multivariable mixed linear model. No overall association of TPM10 on HRV was found. Carriers of two proinflammatory G-alleles of the functional IL6 -174 G/C (rs1800795) polymorphism exhibited lower HRV. An inverse association between a 1 µg/m3 increment in yearly averaged TPM10 and HRV was restricted to GG genotypes at this locus with a standard deviation of normal-to-normal intervals (SDNN) (GG-carriers: -1.8%; 95% confidence interval -3.5 to 0.01; pinteraction(additive) = 0.028); and low frequency power (LF) (GG-carriers: -5.7%; 95%CI: -10.4 to -0.8; pinteraction(dominant) = 0.049). Our results are consistent with the hypothesis that traffic-related air pollution decreases heart rate variability through inflammatory mechanisms.
doi_str_mv 10.1371/journal.pone.0104978
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Air pollution exposure has also been suggested to induce an imbalance in the autonomic nervous system (ANS), such as a decrease in heart rate variability (HRV). In this study we aimed to investigate the modifying effect of polymorphisms in a major proinflammatory marker gene, interleukin 6 (IL6), on the relationship between long-term exposure to traffic-related PM10 (TPM10) and HRV. For this cross-sectional study we analysed 1552 participants of the SAPALDIA cohort aged 50 years and older. Included were persons with valid genotype data, who underwent ambulatory 24-hr electrocardiogram monitoring, and reported on medical history and lifestyle. Main effects of annual average TPM10 and IL6 gene variants (rs1800795; rs2069827; rs2069840; rs10242595) on HRV indices and their interaction with average annual exposure to TPM10 were tested, applying a multivariable mixed linear model. No overall association of TPM10 on HRV was found. Carriers of two proinflammatory G-alleles of the functional IL6 -174 G/C (rs1800795) polymorphism exhibited lower HRV. An inverse association between a 1 µg/m3 increment in yearly averaged TPM10 and HRV was restricted to GG genotypes at this locus with a standard deviation of normal-to-normal intervals (SDNN) (GG-carriers: -1.8%; 95% confidence interval -3.5 to 0.01; pinteraction(additive) = 0.028); and low frequency power (LF) (GG-carriers: -5.7%; 95%CI: -10.4 to -0.8; pinteraction(dominant) = 0.049). Our results are consistent with the hypothesis that traffic-related air pollution decreases heart rate variability through inflammatory mechanisms.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0104978</identifier><identifier>PMID: 25133672</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Aged ; Air pollution ; Analysis ; Atherosclerosis ; Atmospheric pollution ; Autonomic nervous system ; Autonomic Nervous System - drug effects ; Autonomic Nervous System - metabolism ; Biology and Life Sciences ; Cardiology ; Cardiovascular disease ; Carriers ; Confidence intervals ; Cross-Sectional Studies ; Cytokines ; Diabetes ; Ecology and Environmental Sciences ; EKG ; Electrocardiography ; Epidemiology ; Ethics ; Exposure ; Female ; Gene polymorphism ; Genetic aspects ; Genetic polymorphisms ; Genotype ; Genotypes ; Health care ; Health risk assessment ; Heart attacks ; Heart rate ; Heart Rate - drug effects ; Humans ; Inflammation ; Interleukin ; Interleukin 6 ; Interleukin-6 - genetics ; Interleukins ; Male ; Medicine ; Medicine and Health Sciences ; Middle Aged ; Mortality ; Outdoor air quality ; Particulate emissions ; Particulate matter ; Particulate Matter - toxicity ; Particulates ; Pollution ; Pollution control ; Polymorphism ; Polymorphism, Genetic - genetics ; Population ; Promoter Regions, Genetic - genetics ; Public health ; Studies ; Traffic ; Variability</subject><ispartof>PloS one, 2014-08, Vol.9 (8), p.e104978</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Adam et al. 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Air pollution exposure has also been suggested to induce an imbalance in the autonomic nervous system (ANS), such as a decrease in heart rate variability (HRV). In this study we aimed to investigate the modifying effect of polymorphisms in a major proinflammatory marker gene, interleukin 6 (IL6), on the relationship between long-term exposure to traffic-related PM10 (TPM10) and HRV. For this cross-sectional study we analysed 1552 participants of the SAPALDIA cohort aged 50 years and older. Included were persons with valid genotype data, who underwent ambulatory 24-hr electrocardiogram monitoring, and reported on medical history and lifestyle. Main effects of annual average TPM10 and IL6 gene variants (rs1800795; rs2069827; rs2069840; rs10242595) on HRV indices and their interaction with average annual exposure to TPM10 were tested, applying a multivariable mixed linear model. No overall association of TPM10 on HRV was found. 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing &amp; Allied Health Premium</collection><collection>Advanced Technologies &amp; Aerospace Database</collection><collection>ProQuest Advanced Technologies &amp; Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Adam, Martin</au><au>Imboden, Medea</au><au>Boes, Eva</au><au>Schaffner, Emmanuel</au><au>Künzli, Nino</au><au>Phuleria, Harish Chandra</au><au>Kronenberg, Florian</au><au>Gaspoz, Jean-Michel</au><au>Carballo, David</au><au>Probst-Hensch, Nicole</au><au>Coulombe, Roger A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modifying effect of a common polymorphism in the interleukin-6 promoter on the relationship between long-term exposure to traffic-related particulate matter and heart rate variability</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-08-18</date><risdate>2014</risdate><volume>9</volume><issue>8</issue><spage>e104978</spage><pages>e104978-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Exposure to particulate matter (PM) has been associated with an increase in many inflammatory markers, including interleukin 6 (IL6). Air pollution exposure has also been suggested to induce an imbalance in the autonomic nervous system (ANS), such as a decrease in heart rate variability (HRV). In this study we aimed to investigate the modifying effect of polymorphisms in a major proinflammatory marker gene, interleukin 6 (IL6), on the relationship between long-term exposure to traffic-related PM10 (TPM10) and HRV. For this cross-sectional study we analysed 1552 participants of the SAPALDIA cohort aged 50 years and older. Included were persons with valid genotype data, who underwent ambulatory 24-hr electrocardiogram monitoring, and reported on medical history and lifestyle. Main effects of annual average TPM10 and IL6 gene variants (rs1800795; rs2069827; rs2069840; rs10242595) on HRV indices and their interaction with average annual exposure to TPM10 were tested, applying a multivariable mixed linear model. No overall association of TPM10 on HRV was found. Carriers of two proinflammatory G-alleles of the functional IL6 -174 G/C (rs1800795) polymorphism exhibited lower HRV. An inverse association between a 1 µg/m3 increment in yearly averaged TPM10 and HRV was restricted to GG genotypes at this locus with a standard deviation of normal-to-normal intervals (SDNN) (GG-carriers: -1.8%; 95% confidence interval -3.5 to 0.01; pinteraction(additive) = 0.028); and low frequency power (LF) (GG-carriers: -5.7%; 95%CI: -10.4 to -0.8; pinteraction(dominant) = 0.049). Our results are consistent with the hypothesis that traffic-related air pollution decreases heart rate variability through inflammatory mechanisms.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25133672</pmid><doi>10.1371/journal.pone.0104978</doi><oa>free_for_read</oa></addata></record>
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subjects Aged
Air pollution
Analysis
Atherosclerosis
Atmospheric pollution
Autonomic nervous system
Autonomic Nervous System - drug effects
Autonomic Nervous System - metabolism
Biology and Life Sciences
Cardiology
Cardiovascular disease
Carriers
Confidence intervals
Cross-Sectional Studies
Cytokines
Diabetes
Ecology and Environmental Sciences
EKG
Electrocardiography
Epidemiology
Ethics
Exposure
Female
Gene polymorphism
Genetic aspects
Genetic polymorphisms
Genotype
Genotypes
Health care
Health risk assessment
Heart attacks
Heart rate
Heart Rate - drug effects
Humans
Inflammation
Interleukin
Interleukin 6
Interleukin-6 - genetics
Interleukins
Male
Medicine
Medicine and Health Sciences
Middle Aged
Mortality
Outdoor air quality
Particulate emissions
Particulate matter
Particulate Matter - toxicity
Particulates
Pollution
Pollution control
Polymorphism
Polymorphism, Genetic - genetics
Population
Promoter Regions, Genetic - genetics
Public health
Studies
Traffic
Variability
title Modifying effect of a common polymorphism in the interleukin-6 promoter on the relationship between long-term exposure to traffic-related particulate matter and heart rate variability
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