Introduction Indoor air pollution and maternal smoking during pregnancy are associated with respiratory symptoms in infants, but little is known about the direct association with lung function or interactions with genetic risk factors. We examined associations of exposure to indoor particulate matter with a 50% cut-off aerodynamic diameter of 10 µm (PM10) and maternal smoking with infant lung function and the role of gene–environment interactions. Methods Data from the Drakenstein Child Health Study, a South African birth cohort, were analysed (n=270). Lung function was measured at 6 weeks and 1 year of age, and lower respiratory tract infection episodes were documented. We measured pre- and postnatal PM10 exposures using devices placed in homes, and prenatal tobacco smoke exposure using maternal urine cotinine levels. Genetic risk scores determined from associations with childhood-onset asthma in the UK Biobank were used to investigate effect modifications. Results Pre- and postnatal exposure to PM10 as well as maternal smoking during pregnancy were associated with reduced lung function at 6 weeks and 1 year as well as with lower respiratory tract infection in the first year. Due to a significant interaction between the genetic risk score and prenatal exposure to PM10, infants carrying more asthma-related risk alleles were more susceptible to PM10-associated reduced lung function (pinteraction=0.007). This interaction was stronger in infants with Black African ancestry (pinteraction=0.001) and nonexistent in children with mixed ancestry (pinteraction=0.876). Conclusions PM10 and maternal smoking exposures were associated with reduced lung function, with a higher susceptibility for infants with an adverse genetic predisposition for asthma that also depended on the infant's ancestry. Our findings from a South African birth cohort study show an association of indoor air pollution with reduced lung function at 6 weeks and 1 year of age, with a higher susceptibility in children with a genetic predisposition for asthma http://bit.ly/2NpkGRr

中文翻译：

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哮喘的遗传易感性增加了室内空气污染的脆弱性

引言 室内空气污染和孕期母亲吸烟与婴儿的呼吸道症状有关，但对与肺功能的直接关系或与遗传风险因素的相互作用知之甚少。我们研究了暴露于空气动力学直径 50% 为 10 µm (PM10) 的室内颗粒物暴露与母亲吸烟与婴儿肺功能的关联以及基因-环境相互作用的作用。方法 分析了来自南非出生队列 Drakenstein 儿童健康研究的数据（n=270）。在 6 周和 1 岁时测量肺功能，并记录下呼吸道感染事件。我们使用放置在家里的设备测量产前和产后 PM10 暴露，并使用母亲尿液可替宁水平测量产前烟草烟雾暴露。在英国生物库中，根据与儿童期哮喘相关性确定的遗传风险评分被用于研究效果改变。结果 产前和产后暴露于 PM10 以及孕期吸烟与 6 周和 1 年的肺功能降低以及第一年的下呼吸道感染有关。由于遗传风险评分与产前 PM10 暴露之间存在显着的相互作用，携带更多哮喘相关风险等位基因的婴儿更容易受到 PM10 相关肺功能下降的影响（pinteraction=0.007）。这种相互作用在具有非洲黑人血统的婴儿中更强 (pinteraction=0.001)，而在具有混合血统的儿童中不存在 (pinteraction=0.876)。结论 PM10 和母亲吸烟暴露与肺功能降低有关，对具有哮喘不良遗传倾向的婴儿具有更高的易感性，这也取决于婴儿的血统。我们在南非出生队列研究中的发现表明，室内空气污染与 6 周龄和 1 岁时的肺功能降低有关，具有哮喘遗传易感性的儿童的易感性更高 http://bit.ly/2NpkGRr