Rosa Maria José, Just Allan C, Kloog Itai, Pantic Ivan, Schnaas Lourdes, Lee Alison, Bose Sonali, Chiu Yueh-Hsiu Mathilda, Hsu Hsiao-Hsien Leon, Coull Brent, Schwartz Joel, Cohen Sheldon, Téllez Rojo Martha María, Wright Robert O, Wright Rosalind J
Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, New York.
Department of Geography and Environmental Development, Ben-Gurion University of the Negev, Beer Sheva, Israel.
Ann Allergy Asthma Immunol. 2017 Sep;119(3):232-237.e1. doi: 10.1016/j.anai.2017.06.016. Epub 2017 Jul 27.
Air pollution exposure in childhood is associated with greater incidence and exacerbation of asthma, particularly in children whose parents report high levels of psychological stress. However, this interaction has not been completely elucidated in pregnancy.
To examine whether the association between prenatal exposure to particulate matter no larger than 2.5 μm in diameter (PM) and wheeze in children is modified by prenatal stress.
Mexican women were recruited during pregnancy (N = 552). Residential prenatal daily exposure to PM was estimated using a satellite-based spatiotemporally resolved prediction model and averaged over trimesters. Maternal stress was indexed by maternal negative life events (NLE) score (range 0-11) ascertained during mid to late pregnancy. NLE scores were dichotomized at the median as low (NLE score ≤ 3) and high (NLE score > 3) stress. Reports of ever wheeze and wheeze in the past 12 months (current wheeze) for children were obtained using the International Study of Asthma and Allergies in Childhood survey at 48 months. The association between prenatal PM and wheeze was analyzed using a modified Poisson regression and stratified by low vs high stress.
Greater PM exposure during the first trimester was associated with increased risk of current wheeze among children with mothers reporting high prenatal stress (relative risk 1.35, 95% confidence interval 1.00-1.83, per interquartile range increase 3.8 μg/m) but not among those reporting low stress (relative risk 0.84, 95% confidence interval 0.61-1.16, per interquartile range increase 3.8 μg/m; P for interaction = .04).
Increased prenatal stress enhanced the association between PM exposure in early pregnancy, and child wheeze at 48 months of age. It is important to consider chemical and nonchemical stressors together to more comprehensively characterize children's environmental risk.
儿童期暴露于空气污染与哮喘发病率增加及病情加重相关,尤其是父母报告心理压力水平高的儿童。然而,这种相互作用在孕期尚未完全阐明。
研究孕期压力是否会改变产前暴露于直径不超过2.5微米的颗粒物(PM)与儿童喘息之间的关联。
招募了孕期的墨西哥女性(N = 552)。使用基于卫星的时空分辨预测模型估算孕期每日住宅PM暴露量,并按孕期进行平均。通过孕中期至晚期确定的母亲负面生活事件(NLE)得分(范围0 - 11)来衡量母亲压力。NLE得分以中位数分为低压力(NLE得分≤3)和高压力(NLE得分> 3)。在48个月时使用儿童哮喘和过敏国际研究调查获取儿童曾喘息及过去12个月内喘息(当前喘息)的报告。使用修正的泊松回归分析产前PM与喘息之间的关联,并按低压力与高压力分层。
在母亲报告产前压力高的儿童中,孕早期较高的PM暴露与当前喘息风险增加相关(相对风险1.35,95%置信区间1.00 - 1.83,每四分位间距增加3.8μg/m),而在报告低压力的儿童中则不然(相对风险0.84,95%置信区间0.61 - 1.16,每四分位间距增加3.8μg/m;交互作用P = 0.04)。
产前压力增加增强了孕早期PM暴露与48月龄儿童喘息之间的关联。综合考虑化学和非化学应激源对于更全面地描述儿童的环境风险很重要。