Dataset Information

Different genes interact with particulate matter and tobacco smoke exposure in affecting lung function decline in the general population.

ABSTRACT: BACKGROUND: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. OBJECTIVES: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. METHODS:For 12679 single nucleotide polymorphisms (SNPs), change in forced expiratory volume in one second (FEV(1)), FEV(1) over forced vital capacity (FEV(1)/FVC), and mean forced expiratory flow between 25 and 75% of the FVC (FEF(25-75)) 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 (p(interaction)<0.05). Replication was attempted for SNPs with MAF>10% in 3320 SAPALDIA participants without GWAS. RESULTS:On the SNP-level, rs2035268 in gene SNCA accelerated FEV(1)/FVC decline by 3.8% (p(interaction)?=?2.5×10(-6)), and rs12190800 in PARK2 attenuated FEV1 decline by 95.1 ml p(interaction)?=?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 (p(interaction)?=?3.0×10(-4)) on FEV(1)/FVC decline. Pathway interactions were weak. Replications for the strongest SNPs in PARK2 and CRISP2 were not successful. CONCLUSIONS: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.

SUBMITTER: Curjuric I

PROVIDER: S-EPMC3391223 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Different genes interact with particulate matter and tobacco smoke exposure in affecting lung function decline in the general population.

Curjuric Ivan I Imboden Medea M Nadif Rachel R Kumar Ashish A Schindler Christian C Haun Margot M Kronenberg Florian F Künzli Nino N Phuleria Harish H Postma Dirkje S DS Russi Erich W EW Rochat Thierry T Demenais Florence F Probst-Hensch Nicole M NM

PloS one 20120706 7

<h4>Background</h4>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.<h4>Objectives</h4>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.<h4>Methods</h4>For 12679 single nu ...[more]

PMID: 22792237

Similar Datasets

Project description:BackgroundExposure to particulate matter <2.5 μm in diameter (PM2.5) and environmental tobacco smoke (ETS) are associated with respiratory morbidity starting in utero. However, their potential synergistic effects have not been completely elucidated. Here, we examined the joint effects of prenatal and early life PM2.5 and prenatal ETS exposure on respiratory outcomes in children.Material and methodsWe studied 536 mother-child dyads in the Programming Research in Obesity, Growth, Environment and Social Stressors (PROGRESS) study in Mexico City. Exposure to PM2.5 was estimated using residence in pregnancy and child's first year of life with a satellite-based spatio-temporal model. ETS exposure was assessed by caregiver's report of any smoker in the household during the second or third trimester. Outcomes included report of ever wheeze and wheeze in the past 12 months (current wheeze) assessed when children were 6-8 years old considered in separate models. Associations were modeled using distributed lag models (DLM) with daily PM2.5 averages for pregnancy and the first year of life, adjusting for child's sex, birth weight z-score, mother's age and education at enrollment, maternal asthma, season of conception and stratified by prenatal ETS exposure (yes/no).ResultsWe identified a sensitive window from gestational week 14 through postnatal week 18 during which PM2.5 was associated with higher risk of ever wheeze at age 6-8 years. We also observed a critical window of PM2.5 exposure between postnatal weeks 6-39 and higher risk of current wheeze. We found significant associations between higher prenatal and early life PM2.5 exposure and higher cumulative risk ratios of ever wheeze (RR:3.76, 95%CI [1.41, 10.0] per 5 μg/m3) and current wheeze in the past year (RR:7.91, 95%CI [1.5, 41.6] per 5 μg/m3) only among children born to mothers exposed to ETS in pregnancy when compared to mothers who were not exposed.ConclusionsExposure to prenatal ETS modified the association between prenatal and early life PM2.5 exposure and respiratory outcomes at age 6-8 years. It is important to consider concurrent chemical exposures to more comprehensively characterize children's environmental risk. Interventions aimed at decreasing passive smoking might mitigate the effects of ambient air pollution.

Project description:BackgroundAirports may represent significant sources of secondhand smoke (SHS) exposure for both travelers and employees. While previously common smoking rooms have largely disappeared from US airports, smoking continues to occur outdoors at terminal entrances. SHS may be especially high at arrival areas, since they oftentimes are partially enclosed by overhead departures, creating stagnant microenvironments. This study assessed particulate matter <2.5 microns in diameter (PM2.5), a common surrogate for SHS, at airport terminal locations to evaluate both outdoor exposure risk and possible indoor drift of SHS from outdoor sources.MethodsA convenience sample of nine airport terminal arrival areas in the US state of Florida was surveyed between February and July 2018. PM2.5 levels were assessed outdoors and indoors at terminal entrances and at control areas far into terminal interiors. We also examined the impact of smoking location on SHS exposure by correlating cigarette and passing vehicle counts with PM2.5 levels at terminals with contrasting proximity of designated smoking locations to terminal entrances.ResultsAlthough outdoor PM2.5 levels (mean 17.9, SD 6.1 µg/m3) were significantly higher than indoors (p < 0.001), there was no difference between indoor areas directly inside terminal entrances and areas much further interior (mean 8.8, SD 2.6 vs mean 8.5, SD 3.0 µg/m3, p=0.49). However, when smoking areas were in close proximity to terminal entrances, the number of lit cigarettes and vehicular traffic per minute predicted 70% of the variance of PM2.5 levels (p < 0.001), which was attributable mostly to the cigarette number (β = 0.83; 95% CI (0.55 to 1.11); p < 0.001). This effect was not observed at smoking areas further away.ConclusionPM2.5 data did not suggest indoor drift from outside smoking. Nevertheless, absolute exposure outdoors was high and correlated with the location of designated smoking areas. Further studies are needed to examine the effect of microclimate formation on exposure risk.

Dataset Information

Different genes interact with particulate matter and tobacco smoke exposure in affecting lung function decline in the general population.

Publications

Different genes interact with particulate matter and tobacco smoke exposure in affecting lung function decline in the general population.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets