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Modification of the Interleukin-6 Response to Air Pollution by Interleukin-6 and Fibrinogen Polymorphisms.

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Title: Modification of the Interleukin-6 Response to Air Pollution by Interleukin-6 and Fibrinogen Polymorphisms.
Authors: Ljungman, Petter1,2 petter.ljungman@ki.se, Bellander, Tom2, Schneider, Alexandra3, Breitner, Susanne3, Forastiere, Francesco4, Hampel, Regina3, Illig, Thomas3, Jacquemin, Bénédicte5,6, Katsouyanni, Klea7, von Klot, Stephanie3,8, Koenig, Wolfgang9, Lanki, Timo10, Nyberg, Fredrik2,11, Pekkanen, Juha10, Pistelli, Riccardo12, Pitsavos, Christos13, Rosenqvist, Mårten1, Sunyer, Jordi5,14,15,16, Peters, Annette3
Source: Environmental Health Perspectives. Sep2009, Vol. 117 Issue 9, p1373-1379. 7p. 4 Charts, 3 Graphs.
Subject Terms: *Physiological effects of air pollution, *Genotype-environment interaction, *Carbon monoxide, *Nitrogen dioxide, Interleukin-6, Patients, Cardiovascular diseases, Fibrinogen polymorphisms, Gene expression, Myocardial infarction, Anti-inflammatory agents, Meta-analysis
Abstract: Background: Evidence suggests that cardiovascular effects of air pollution are mediated by inflammation and that air pollution can induce genetic expression of the interleukin-6 gene (IL6). Objectives: We investigated whether IL6 and fibrinogen gene variants can affect plasma IL-6 responses to air pollution in patients with cardiovascular disease. Methods: We repeatedly determined plasma IL-6 in 955 myocardial infarction survivors from six European cities (n = 5,539). We conducted city-specific analyses using additive mixed models adjusting for patient characteristics, time trend, and weather to assess the impact of air pollutants on plasma IL-6. We pooled city-specific estimates using meta-analysis methodology. We selected three IL6 single-nucleotide polymorphisms (SNPs) and one SNP each from the fibrinogen α-chain gene (FGA) and β-chain gene (FGB) for gene-environment analyses. Results: We found the most consistent modifications for variants in IL6 rs2069832 and FBG rs1800790 after exposure to carbon monoxide (CO; 24-hr average; p-values for interaction, 0.034 and 0.019, respectively). Nitrogen dioxide effects were consistently modified, but p-values for interaction were larger (0.09 and 0.19, respectively). The strongest effects were seen 6-11 hr after exposure, when, for example, the overall effect of a 2.2% increase in IL-6 per 0.64 mg/m3 CO was modified to a 10% (95% confidence interval, 4.6-16%) increase in IL-6 (p-value for interaction = 0.002) for minor homozygotes of FGB rs1800790. Conclusions: The effect of gaseous traffic-related air pollution on inflammation may be stronger in genetic subpopulations with ischemic heart disease. This information could offer an opportunity to identify postinfarction patients who would benefit more than others from a cleaner environment and antiinflammatory treatment. [ABSTRACT FROM AUTHOR]
Copyright of Environmental Health Perspectives is the property of National Institute of Environmental Health Sciences and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Modification of the Interleukin-6 Response to Air Pollution by Interleukin-6 and Fibrinogen Polymorphisms.
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  Data: <searchLink fieldCode="AR" term="%22Ljungman%2C+Petter%22">Ljungman, Petter</searchLink><relatesTo>1,2</relatesTo><i> petter.ljungman@ki.se</i><br /><searchLink fieldCode="AR" term="%22Bellander%2C+Tom%22">Bellander, Tom</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Schneider%2C+Alexandra%22">Schneider, Alexandra</searchLink><relatesTo>3</relatesTo><br /><searchLink fieldCode="AR" term="%22Breitner%2C+Susanne%22">Breitner, Susanne</searchLink><relatesTo>3</relatesTo><br /><searchLink fieldCode="AR" term="%22Forastiere%2C+Francesco%22">Forastiere, Francesco</searchLink><relatesTo>4</relatesTo><br /><searchLink fieldCode="AR" term="%22Hampel%2C+Regina%22">Hampel, Regina</searchLink><relatesTo>3</relatesTo><br /><searchLink fieldCode="AR" term="%22Illig%2C+Thomas%22">Illig, Thomas</searchLink><relatesTo>3</relatesTo><br /><searchLink fieldCode="AR" term="%22Jacquemin%2C+Bénédicte%22">Jacquemin, Bénédicte</searchLink><relatesTo>5,6</relatesTo><br /><searchLink fieldCode="AR" term="%22Katsouyanni%2C+Klea%22">Katsouyanni, Klea</searchLink><relatesTo>7</relatesTo><br /><searchLink fieldCode="AR" term="%22von+Klot%2C+Stephanie%22">von Klot, Stephanie</searchLink><relatesTo>3,8</relatesTo><br /><searchLink fieldCode="AR" term="%22Koenig%2C+Wolfgang%22">Koenig, Wolfgang</searchLink><relatesTo>9</relatesTo><br /><searchLink fieldCode="AR" term="%22Lanki%2C+Timo%22">Lanki, Timo</searchLink><relatesTo>10</relatesTo><br /><searchLink fieldCode="AR" term="%22Nyberg%2C+Fredrik%22">Nyberg, Fredrik</searchLink><relatesTo>2,11</relatesTo><br /><searchLink fieldCode="AR" term="%22Pekkanen%2C+Juha%22">Pekkanen, Juha</searchLink><relatesTo>10</relatesTo><br /><searchLink fieldCode="AR" term="%22Pistelli%2C+Riccardo%22">Pistelli, Riccardo</searchLink><relatesTo>12</relatesTo><br /><searchLink fieldCode="AR" term="%22Pitsavos%2C+Christos%22">Pitsavos, Christos</searchLink><relatesTo>13</relatesTo><br /><searchLink fieldCode="AR" term="%22Rosenqvist%2C+Mårten%22">Rosenqvist, Mårten</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Sunyer%2C+Jordi%22">Sunyer, Jordi</searchLink><relatesTo>5,14,15,16</relatesTo><br /><searchLink fieldCode="AR" term="%22Peters%2C+Annette%22">Peters, Annette</searchLink><relatesTo>3</relatesTo>
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  Data: <searchLink fieldCode="JN" term="%22Environmental+Health+Perspectives%22">Environmental Health Perspectives</searchLink>. Sep2009, Vol. 117 Issue 9, p1373-1379. 7p. 4 Charts, 3 Graphs.
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  Data: *<searchLink fieldCode="DE" term="%22Physiological+effects+of+air+pollution%22">Physiological effects of air pollution</searchLink><br />*<searchLink fieldCode="DE" term="%22Genotype-environment+interaction%22">Genotype-environment interaction</searchLink><br />*<searchLink fieldCode="DE" term="%22Carbon+monoxide%22">Carbon monoxide</searchLink><br />*<searchLink fieldCode="DE" term="%22Nitrogen+dioxide%22">Nitrogen dioxide</searchLink><br /><searchLink fieldCode="DE" term="%22Interleukin-6%22">Interleukin-6</searchLink><br /><searchLink fieldCode="DE" term="%22Patients%22">Patients</searchLink><br /><searchLink fieldCode="DE" term="%22Cardiovascular+diseases%22">Cardiovascular diseases</searchLink><br /><searchLink fieldCode="DE" term="%22Fibrinogen+polymorphisms%22">Fibrinogen polymorphisms</searchLink><br /><searchLink fieldCode="DE" term="%22Gene+expression%22">Gene expression</searchLink><br /><searchLink fieldCode="DE" term="%22Myocardial+infarction%22">Myocardial infarction</searchLink><br /><searchLink fieldCode="DE" term="%22Anti-inflammatory+agents%22">Anti-inflammatory agents</searchLink><br /><searchLink fieldCode="DE" term="%22Meta-analysis%22">Meta-analysis</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Background: Evidence suggests that cardiovascular effects of air pollution are mediated by inflammation and that air pollution can induce genetic expression of the interleukin-6 gene (IL6). Objectives: We investigated whether IL6 and fibrinogen gene variants can affect plasma IL-6 responses to air pollution in patients with cardiovascular disease. Methods: We repeatedly determined plasma IL-6 in 955 myocardial infarction survivors from six European cities (n = 5,539). We conducted city-specific analyses using additive mixed models adjusting for patient characteristics, time trend, and weather to assess the impact of air pollutants on plasma IL-6. We pooled city-specific estimates using meta-analysis methodology. We selected three IL6 single-nucleotide polymorphisms (SNPs) and one SNP each from the fibrinogen α-chain gene (FGA) and β-chain gene (FGB) for gene-environment analyses. Results: We found the most consistent modifications for variants in IL6 rs2069832 and FBG rs1800790 after exposure to carbon monoxide (CO; 24-hr average; p-values for interaction, 0.034 and 0.019, respectively). Nitrogen dioxide effects were consistently modified, but p-values for interaction were larger (0.09 and 0.19, respectively). The strongest effects were seen 6-11 hr after exposure, when, for example, the overall effect of a 2.2% increase in IL-6 per 0.64 mg/m3 CO was modified to a 10% (95% confidence interval, 4.6-16%) increase in IL-6 (p-value for interaction = 0.002) for minor homozygotes of FGB rs1800790. Conclusions: The effect of gaseous traffic-related air pollution on inflammation may be stronger in genetic subpopulations with ischemic heart disease. This information could offer an opportunity to identify postinfarction patients who would benefit more than others from a cleaner environment and antiinflammatory treatment. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Environmental Health Perspectives is the property of National Institute of Environmental Health Sciences and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1289/ehp.0800370
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