Different Genes Interact with Particulate Matter and Tobacco Smoke Exposure in Affecting Lung Function Decline in the General Population
Identifieur interne : 001156 ( Main/Exploration ); précédent : 001155; suivant : 001157Different Genes Interact with Particulate Matter and Tobacco Smoke Exposure in Affecting Lung Function Decline in the General Population
Auteurs : Ivan Curjuric [Suisse] ; Medea Imboden [Suisse] ; Rachel Nadif [France] ; Ashish Kumar [Suisse, Royaume-Uni] ; Christian Schindler [Suisse] ; Margot Haun [Autriche] ; Florian Kronenberg [Autriche] ; Nino Künzli [Suisse] ; Harish Phuleria [Suisse] ; Dirkje S. Postma [Pays-Bas] ; Erich W. Russi [Suisse] ; Thierry Rochat [Suisse] ; Florence Demenais [France] ; Nicole M. Probst-Hensch [Suisse]Source :
- PLoS ONE [ 1932-6203 ] ; 2012.
Abstract
Oxidative stress related genes modify the effects of ambient air pollution or tobacco smoking on lung function decline. The impact of interactions might be substantial, but previous studies mostly focused on main effects of single genes.
We studied the interaction of both exposures with a broad set of oxidative-stress related candidate genes and pathways on lung function decline and contrasted interactions between exposures.
For 12679 single nucleotide polymorphisms (SNPs), change in forced expiratory volume in one second (FEV1), FEV1 over forced vital capacity (FEV1/FVC), and mean forced expiratory flow between 25 and 75% of the FVC (FEF25-75) was regressed on interval exposure to particulate matter <10 µm in diameter (PM10) or packyears smoked (a), additive SNP effects (b), and interaction terms between (a) and (b) in 669 adults with GWAS data. Interaction p-values for 152 genes and 14 pathways were calculated by the adaptive rank truncation product (ARTP) method, and compared between exposures. Interaction effect sizes were contrasted for the strongest SNPs of nominally significant genes (pinteraction<0.05). Replication was attempted for SNPs with MAF>10% in 3320 SAPALDIA participants without GWAS.
On the SNP-level, rs2035268 in gene SNCA accelerated FEV1/FVC decline by 3.8% (pinteraction = 2.5×10−6), and rs12190800 in PARK2 attenuated FEV1 decline by 95.1 ml pinteraction = 9.7×10−8) over 11 years, while interacting with PM10. Genes and pathways nominally interacting with PM10 and packyears exposure differed substantially. Gene CRISP2 presented a significant interaction with PM10 (pinteraction = 3.0×10−4) on FEV1/FVC decline. Pathway interactions were weak. Replications for the strongest SNPs in PARK2 and CRISP2 were not successful.
Consistent with a stratified response to increasing oxidative stress, different genes and pathways potentially mediate PM10 and tobacco smoke effects on lung function decline. Ignoring environmental exposures would miss these patterns, but achieving sufficient sample size and comparability across study samples is challenging.
Url:
DOI: 10.1371/journal.pone.0040175
PubMed: 22792237
PubMed Central: 3391223
Affiliations:
- Autriche, France, Pays-Bas, Royaume-Uni, Suisse
- Angleterre, Canton de Zurich, Groningue (province), Oxfordshire, Île-de-France
- Groningue, Oxford, Paris, Zurich
- Université d'Oxford
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Le document en format XML
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</affiliation>
</author>
<author><name sortKey="Kunzli, Nino" sort="Kunzli, Nino" uniqKey="Kunzli N" first="Nino" last="Künzli">Nino Künzli</name>
<affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Epidemiology and Public Health, Swiss Tropical and Public Health Institute SwissTPH, Basel, Switzerland</addr-line>
</nlm:aff>
<country xml:lang="fr">Suisse</country>
<wicri:regionArea>Department of Epidemiology and Public Health, Swiss Tropical and Public Health Institute SwissTPH, Basel</wicri:regionArea>
<wicri:noRegion>Basel</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="aff2"><addr-line>University of Basel, Basel, Switzerland</addr-line>
</nlm:aff>
<country xml:lang="fr">Suisse</country>
<wicri:regionArea>University of Basel, Basel</wicri:regionArea>
<wicri:noRegion>Basel</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Phuleria, Harish" sort="Phuleria, Harish" uniqKey="Phuleria H" first="Harish" last="Phuleria">Harish Phuleria</name>
<affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Epidemiology and Public Health, Swiss Tropical and Public Health Institute SwissTPH, Basel, Switzerland</addr-line>
</nlm:aff>
<country xml:lang="fr">Suisse</country>
<wicri:regionArea>Department of Epidemiology and Public Health, Swiss Tropical and Public Health Institute SwissTPH, Basel</wicri:regionArea>
<wicri:noRegion>Basel</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="aff2"><addr-line>University of Basel, Basel, Switzerland</addr-line>
</nlm:aff>
<country xml:lang="fr">Suisse</country>
<wicri:regionArea>University of Basel, Basel</wicri:regionArea>
<wicri:noRegion>Basel</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Postma, Dirkje S" sort="Postma, Dirkje S" uniqKey="Postma D" first="Dirkje S." last="Postma">Dirkje S. Postma</name>
<affiliation wicri:level="3"><nlm:aff id="aff7"><addr-line>Department of Pulmonary Medicine and Tuberculosis, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands</addr-line>
</nlm:aff>
<country xml:lang="fr">Pays-Bas</country>
<wicri:regionArea>Department of Pulmonary Medicine and Tuberculosis, University Medical Center Groningen, University of Groningen, Groningen</wicri:regionArea>
<placeName><settlement type="city">Groningue</settlement>
<region nuts="2" type="province">Groningue (province)</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Russi, Erich W" sort="Russi, Erich W" uniqKey="Russi E" first="Erich W." last="Russi">Erich W. Russi</name>
<affiliation wicri:level="3"><nlm:aff id="aff8"><addr-line>Division of Pulmonary Medicine, University Hospital Zürich, Zürich, Switzerland</addr-line>
</nlm:aff>
<country xml:lang="fr">Suisse</country>
<wicri:regionArea>Division of Pulmonary Medicine, University Hospital Zürich, Zürich</wicri:regionArea>
<placeName><settlement type="city">Zurich</settlement>
<region nuts="3" type="region">Canton de Zurich</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Rochat, Thierry" sort="Rochat, Thierry" uniqKey="Rochat T" first="Thierry" last="Rochat">Thierry Rochat</name>
<affiliation wicri:level="1"><nlm:aff id="aff9"><addr-line>Division of Pulmonary Medicine, Geneva University Hospitals, Geneva, Switzerland</addr-line>
</nlm:aff>
<country xml:lang="fr">Suisse</country>
<wicri:regionArea>Division of Pulmonary Medicine, Geneva University Hospitals, Geneva</wicri:regionArea>
<wicri:noRegion>Geneva</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Demenais, Florence" sort="Demenais, Florence" uniqKey="Demenais F" first="Florence" last="Demenais">Florence Demenais</name>
<affiliation wicri:level="3"><nlm:aff id="aff10"><addr-line>INSERM, U946, Genetic Variation and Human Diseases Unit, Paris, France</addr-line>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>INSERM, U946, Genetic Variation and Human Diseases Unit, Paris</wicri:regionArea>
<placeName><region type="region">Île-de-France</region>
<region type="old region">Île-de-France</region>
<settlement type="city">Paris</settlement>
</placeName>
</affiliation>
<affiliation wicri:level="3"><nlm:aff id="aff11"><addr-line>Fondation Jean Dausset - Centre d’Etude du Polymorphisme Humain (CEPH), Paris, France</addr-line>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>Fondation Jean Dausset - Centre d’Etude du Polymorphisme Humain (CEPH), Paris</wicri:regionArea>
<placeName><region type="region">Île-de-France</region>
<region type="old region">Île-de-France</region>
<settlement type="city">Paris</settlement>
</placeName>
</affiliation>
<affiliation wicri:level="3"><nlm:aff id="aff12"><addr-line>Université Paris Diderot, Sorbonne Paris Cité, Institut Universitaire d’Hématologie, Paris, France</addr-line>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>Université Paris Diderot, Sorbonne Paris Cité, Institut Universitaire d’Hématologie, Paris</wicri:regionArea>
<placeName><region type="region">Île-de-France</region>
<region type="old region">Île-de-France</region>
<settlement type="city">Paris</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Probst Hensch, Nicole M" sort="Probst Hensch, Nicole M" uniqKey="Probst Hensch N" first="Nicole M." last="Probst-Hensch">Nicole M. Probst-Hensch</name>
<affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Epidemiology and Public Health, Swiss Tropical and Public Health Institute SwissTPH, Basel, Switzerland</addr-line>
</nlm:aff>
<country xml:lang="fr">Suisse</country>
<wicri:regionArea>Department of Epidemiology and Public Health, Swiss Tropical and Public Health Institute SwissTPH, Basel</wicri:regionArea>
<wicri:noRegion>Basel</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="aff2"><addr-line>University of Basel, Basel, Switzerland</addr-line>
</nlm:aff>
<country xml:lang="fr">Suisse</country>
<wicri:regionArea>University of Basel, Basel</wicri:regionArea>
<wicri:noRegion>Basel</wicri:noRegion>
</affiliation>
</author>
</analytic>
<series><title level="j">PLoS ONE</title>
<idno type="eISSN">1932-6203</idno>
<imprint><date when="2012">2012</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p>Oxidative stress related genes modify the effects of ambient air pollution or tobacco smoking on lung function decline. The impact of interactions might be substantial, but previous studies mostly focused on main effects of single genes.</p>
</sec>
<sec><title>Objectives</title>
<p>We studied the interaction of both exposures with a broad set of oxidative-stress related candidate genes and pathways on lung function decline and contrasted interactions between exposures.</p>
</sec>
<sec><title>Methods</title>
<p>For 12679 single nucleotide polymorphisms (SNPs), change in forced expiratory volume in one second (FEV<sub>1</sub>
), FEV<sub>1</sub>
over forced vital capacity (FEV<sub>1</sub>
/FVC), and mean forced expiratory flow between 25 and 75% of the FVC (FEF<sub>25-75</sub>
) was regressed on interval exposure to particulate matter <10 µm in diameter (PM10) or packyears smoked (a), additive SNP effects (b), and interaction terms between (a) and (b) in 669 adults with GWAS data. Interaction p-values for 152 genes and 14 pathways were calculated by the adaptive rank truncation product (ARTP) method, and compared between exposures. Interaction effect sizes were contrasted for the strongest SNPs of nominally significant genes (p<sub>interaction</sub>
<0.05). Replication was attempted for SNPs with MAF>10% in 3320 SAPALDIA participants without GWAS.</p>
</sec>
<sec><title>Results</title>
<p>On the SNP-level, rs2035268 in gene SNCA accelerated FEV<sub>1</sub>
/FVC decline by 3.8% (p<sub>interaction</sub>
= 2.5×10<sup>−6</sup>
), and rs12190800 in PARK2 attenuated FEV1 decline by 95.1 ml p<sub>interaction</sub>
= 9.7×10<sup>−8</sup>
) over 11 years, while interacting with PM10. Genes and pathways nominally interacting with PM10 and packyears exposure differed substantially. Gene CRISP2 presented a significant interaction with PM10 (p<sub>interaction</sub>
= 3.0×10<sup>−4</sup>
) on FEV<sub>1</sub>
/FVC decline. Pathway interactions were weak. Replications for the strongest SNPs in PARK2 and CRISP2 were not successful.</p>
</sec>
<sec><title>Conclusions</title>
<p>Consistent with a stratified response to increasing oxidative stress, different genes and pathways potentially mediate PM10 and tobacco smoke effects on lung function decline. Ignoring environmental exposures would miss these patterns, but achieving sufficient sample size and comparability across study samples is challenging.</p>
</sec>
</div>
</front>
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