Fleisch Abby F, Aris Izzuddin M, Rifas-Shiman Sheryl L, Coull Brent A, Luttmann-Gibson Heike, Koutrakis Petros, Schwartz Joel D, Kloog Itai, Gold Diane R, Oken Emily
Pediatric Endocrinology and Diabetes, Maine Medical Center, Portland, ME, United States.
Center for Outcomes Research and Evaluation, Maine Medical Center Research Institute, Portland, ME, United States.
Front Endocrinol (Lausanne). 2019 Jan 7;9:771. doi: 10.3389/fendo.2018.00771. eCollection 2018.
Limited evidence suggests an association between prenatal exposure to traffic pollution and greater adiposity in childhood, but the time window during which growth may be most affected is not known. We studied 1,649 children in Project Viva, a Boston-area pre-birth cohort. We used spatiotemporal models to estimate prenatal residential air pollution exposures and geographic information systems to estimate neighborhood traffic density and roadway proximity. We used weight and stature measurements at clinical and research visits to estimate a BMI trajectory for each child with mixed-effects natural cubic spline models. In primary analyses, we examined associations of residential PM and black carbon (BC) exposures during the third trimester and neighborhood traffic density and home roadway proximity at birth address with (1) estimated BMI at 6 month intervals through 10 years of age, (2) magnitude and timing of BMI peak and rebound, and (3) overall BMI trajectory. In secondary analyses, we examined associations of residential PM and BC exposures during the first and second trimesters with BMI outcomes. Median (interquartile range; IQR) concentration of residential air pollution during the third trimester was 11.4 (1.7) μg/m for PM and 0.7 (0.3) μg/m for BC. Participants had a median (IQR) of 13 (7) clinical or research BMI measures from 0 to 10 years of age. None of the traffic pollution exposures were significantly associated with any of the BMI outcomes in covariate-adjusted models, although effect estimates were in the hypothesized direction for neighborhood traffic density and home roadway proximity. For example, greater neighborhood traffic density [median (IQR) 857 (1,452) vehicles/day x km of road within 100 m of residential address at delivery] was associated with a higher BMI throughout childhood, with the strongest associations in early childhood [e.g., per IQR increment natural log-transformed neighborhood traffic density, BMI at 12 months of age was 0.05 (-0.03, 0.13) kg/m higher and infancy peak BMI was 0.05 (-0.03, 0.14) kg/m higher]. We found no evidence for a persistent effect of prenatal exposure to traffic pollution on BMI trajectory from birth through mid-childhood in a population exposed to modest levels of air pollution.
有限的证据表明，产前暴露于交通污染与儿童期更高的肥胖程度之间存在关联，但生长可能受影响最大的时间窗尚不清楚。我们在“活力计划”中研究了1649名儿童，该计划是波士顿地区的一个出生前队列研究。我们使用时空模型来估计产前居住空气污染暴露，并使用地理信息系统来估计邻里交通密度和道路接近度。我们在临床和研究访视时使用体重和身高测量值，通过混合效应自然立方样条模型为每个儿童估计BMI轨迹。在主要分析中，我们研究了孕晚期居住的PM和黑碳（BC）暴露以及出生地址处的邻里交通密度和家庭道路接近度与以下方面的关联：（1）至10岁时每隔6个月的估计BMI；（2）BMI峰值和反弹的幅度及时间；（3）总体BMI轨迹。在次要分析中，我们研究了孕早期和孕中期居住的PM和BC暴露与BMI结果的关联。孕晚期居住空气污染的中位数（四分位间距；IQR）浓度，PM为11.4（1.7）μg/m，BC为0.7（0.3）μg/m。参与者从0至10岁有中位数（IQR）为13（7）次临床或研究BMI测量值。在协变量调整模型中，没有任何交通污染暴露与任何BMI结果显著相关，尽管邻里交通密度和家庭道路接近度的效应估计值符合假设方向。例如，更高的邻里交通密度[分娩时居住地址100米内道路的中位数（IQR）857（1452）辆/天·公里]与整个儿童期更高的BMI相关，在幼儿期关联最强[例如，每IQR增量自然对数转换后的邻里交通密度，12个月龄时的BMI高0.05（-0.03，0.13）kg/m，婴儿期BMI峰值高0.05（-0.03，0.14）kg/m]。在暴露于适度空气污染水平的人群中，我们没有发现产前暴露于交通污染对从出生到儿童中期的BMI轨迹有持续影响的证据。
