Department of Integrative Physiology, University of Colorado Boulder, Boulder, CO, USA.
Department of Pediatrics, The Saban Research Institute, Children's Hospital of Los Angeles, University of Southern California, Los Angeles, CA, USA.
Environ Health. 2021 Jun 5;20(1):67. doi: 10.1186/s12940-021-00753-8.
Prior epidemiological and animal work has linked in utero exposure to ambient air pollutants (AAP) with accelerated postnatal weight gain, which is predictive of increased cardiometabolic risk factors in childhood and adolescence. However, few studies have assessed changes in infant body composition or multiple pollutant exposures. Therefore, the objective of this study was to examine relationships between prenatal residential AAP exposure with infant growth and adiposity.
Residential exposure to AAP (particulate matter < 2.5 and 10 microns in aerodynamic diameter [PM, PM]; nitrogen dioxide [NO]; ozone [O]; oxidative capacity [O: redox-weighted oxidative potential of O and NO]) was modeled by spatial interpolation of monitoring stations via an inverse distance-squared weighting (IDW2) algorithm for 123 participants from the longitudinal Mother's Milk Study, an ongoing cohort of Hispanic mother-infant dyads from Southern California. Outcomes included changes in infant growth (weight, length), total subcutaneous fat (TSF; calculated via infant skinfold thickness measures) and fat distribution (umbilical circumference, central to total subcutaneous fat [CTSF]) and were calculated by subtracting 1-month measures from 6-month measures. Multivariable linear regression was performed to examine relationships between prenatal AAP exposure and infant outcomes. Models adjusted for maternal age, pre-pregnancy body mass index, socioeconomic status, infant age, sex, and breastfeeding frequency. Sex interactions were tested, and effects are reported for each standard deviation increase in exposure.
NO was associated with greater infant weight gain (β = 0.14, p = 0.02) and TSF (β = 1.69, p = 0.02). PM and PM were associated with change in umbilical circumference (β = 0.73, p = 0.003) and TSF (β = 1.53, p = 0.04), respectively. Associations of O (p < 0.10) with infant length change, umbilical circumference, and CTSF were modified by infant sex. O was associated with attenuated infant length change among males (β = -0.60, p = 0.01), but not females (β = 0.16, p = 0.49); umbilical circumference among females (β = 0.92, p = 0.009), but not males (β = -0.00, p = 0.99); and CTSF among males (β = 0.01, p = 0.03), but not females (β = 0.00, p = 0.51).
Prenatal AAP exposure was associated with increased weight gain and anthropometric measures from 1-to-6 months of life among Hispanic infants. Sex-specific associations suggest differential consequences of in utero oxidative stress. These results indicate that prenatal AAP exposure may alter infant growth, which has potential to increase childhood obesity risk.
先前的流行病学和动物研究将子宫内暴露于环境空气污染物（AAP）与出生后体重加速增加联系起来，而出生后体重加速增加是儿童和青少年代谢危险因素增加的预测因素。然而，很少有研究评估婴儿身体成分或多种污染物暴露的变化。因此，本研究的目的是研究产前住宅 AAP 暴露与婴儿生长和肥胖之间的关系。
通过空间插值监测站，使用距离平方反比加权（IDW2）算法对 123 名来自南加州的西班牙裔母婴对正在进行的纵向母乳研究的参与者的住宅 AAP（空气动力学直径 < 2.5 和 10 微米的颗粒物[PM、PM]；二氧化氮[NO]；臭氧[O]；氧化能力[O：O 和 NO 的氧化还原加权氧化电势]）进行建模。结果包括婴儿生长（体重、长度）、总皮下脂肪（TSF；通过婴儿皮褶厚度测量计算）和脂肪分布（脐周长、中央到总皮下脂肪[CTSF]）的变化，通过从 6 个月的测量值中减去 1 个月的测量值来计算。使用多变量线性回归来检查产前 AAP 暴露与婴儿结果之间的关系。模型调整了母亲的年龄、孕前体重指数、社会经济地位、婴儿年龄、性别和母乳喂养频率。测试了性别交互作用，并报告了每个标准偏差增加暴露的影响。
NO 与婴儿体重增加（β=0.14，p=0.02）和 TSF（β=1.69，p=0.02）有关。PM 和 PM 分别与脐周长（β=0.73，p=0.003）和 TSF（β=1.53，p=0.04）的变化有关。O（p<0.10）与婴儿长度变化、脐周长和 CTSF 的关系受到婴儿性别的修饰。O 与男性婴儿的长度变化减弱有关（β=-0.60，p=0.01），但与女性无关（β=0.16，p=0.49）；O 与女性的脐周长有关（β=0.92，p=0.009），但与男性无关（β=-0.00，p=0.99）；O 与男性的 CTSF 有关（β=0.01，p=0.03），但与女性无关（β=0.00，p=0.51）。
在西班牙裔婴儿中，产前 AAP 暴露与 1 至 6 个月的体重增加和人体测量结果有关。性别特异性关联表明，子宫内氧化应激的后果不同。这些结果表明，产前 AAP 暴露可能会改变婴儿的生长，这有可能增加儿童肥胖的风险。
