The effect of oxidative stress polymorphisms on the association between long-term black carbon exposure and lung function among elderly men
Black carbon (BC) is a pro-oxidant, traffic-related pollutant linked with lung function decline. We evaluated the influence of genetic variation in the oxidative stress pathway on the association between long-term BC exposure and lung function decline. Lung function parameters (FVC and FEV1) were measured during one or more study visits between 1995 and 2011 (n=651 participants) among an elderly cohort: the Normative Aging Study. Residential BC exposure levels were estimated using a spatiotemporal land use regression model. We evaluated whether oxidative stress variants, combined into a genetic score, modify the association between 1-year and 5-year moving averages of BC exposure and lung function levels and rates of decline, using linear mixed models. We report stronger associations between long-term BC exposure and increased rate of lung function decline, but not baseline lung function level, among participants with higher oxidative stress allelic risk profiles compared with participants with lower risk profiles. Associations were strongest when evaluating 5-year moving averages of BC exposure. A 0.5 µg/m(3) increase in 5-year BC exposure was associated with a 0.1% yearly increase in FVC (95% CI -0.5 to 0.7) among participants with low genetic risk scores and a 1.3% yearly decrease (95% CI -1.8 to -0.8) among those with high scores (p-interaction=0.0003). Our results suggest that elderly men with high oxidative stress genetic scores may be more susceptible to the effects of BC on lung function decline. The results, if confirmed, should inform air-quality recommendations in light of a potentially susceptible subgroup..
| Medienart: |
Artikel |
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| Erscheinungsjahr: |
2015 |
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| Erschienen: |
2015 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:70 |
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| Enthalten in: |
Thorax - 70(2015), 2, Seite 133-137 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Mordukhovich, Irina [VerfasserIn] |
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| Links: |
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| doi: |
10.1136/thoraxjnl-2014-206179 |
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| Förderinstitution / Projekttitel: |
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| 245 | 1 | 4 | |a The effect of oxidative stress polymorphisms on the association between long-term black carbon exposure and lung function among elderly men |
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| 520 | |a Black carbon (BC) is a pro-oxidant, traffic-related pollutant linked with lung function decline. We evaluated the influence of genetic variation in the oxidative stress pathway on the association between long-term BC exposure and lung function decline. Lung function parameters (FVC and FEV1) were measured during one or more study visits between 1995 and 2011 (n=651 participants) among an elderly cohort: the Normative Aging Study. Residential BC exposure levels were estimated using a spatiotemporal land use regression model. We evaluated whether oxidative stress variants, combined into a genetic score, modify the association between 1-year and 5-year moving averages of BC exposure and lung function levels and rates of decline, using linear mixed models. We report stronger associations between long-term BC exposure and increased rate of lung function decline, but not baseline lung function level, among participants with higher oxidative stress allelic risk profiles compared with participants with lower risk profiles. Associations were strongest when evaluating 5-year moving averages of BC exposure. A 0.5 µg/m(3) increase in 5-year BC exposure was associated with a 0.1% yearly increase in FVC (95% CI -0.5 to 0.7) among participants with low genetic risk scores and a 1.3% yearly decrease (95% CI -1.8 to -0.8) among those with high scores (p-interaction=0.0003). Our results suggest that elderly men with high oxidative stress genetic scores may be more susceptible to the effects of BC on lung function decline. The results, if confirmed, should inform air-quality recommendations in light of a potentially susceptible subgroup. | ||
| 540 | |a Nutzungsrecht: © Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions. | ||
| 650 | 4 | |a Glutathione Transferase - genetics | |
| 650 | 4 | |a Forced Expiratory Volume - genetics | |
| 650 | 4 | |a Lung - physiopathology | |
| 650 | 4 | |a Glutathione S-Transferase pi - genetics | |
| 650 | 4 | |a Glutamate-Cysteine Ligase - genetics | |
| 650 | 4 | |a Oxidative Stress - genetics | |
| 650 | 4 | |a NAD(P)H Dehydrogenase (Quinone) - genetics | |
| 650 | 4 | |a Vital Capacity - genetics | |
| 650 | 4 | |a Occupational Exposure - adverse effects | |
| 650 | 4 | |a Heme Oxygenase-1 - genetics | |
| 650 | 4 | |a Soot - toxicity | |
| 650 | 4 | |a Catalase - genetics | |
| 650 | 4 | |a Care and treatment | |
| 650 | 4 | |a Aged | |
| 650 | 4 | |a Oxidative stress | |
| 650 | 4 | |a Analysis | |
| 650 | 4 | |a Genetic polymorphisms | |
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| 700 | 1 | |a Vokonas, Pantel |4 oth | |
| 700 | 1 | |a Schwartz, Joel |4 oth | |
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