TY - JOUR
T1 - The joint effects of prenatal exposure to PM2.5 constituents and reduced fetal growth on children’s accelerated growth in the first 3 years
T2 - a birth cohort study
AU - Zhou, Shuang
AU - Li, Tiantian
AU - Han, Na
AU - Zhang, Kai
AU - Chen, Gongbo
AU - Zhang, Yi
AU - Li, Qin
AU - Ji, Yuelong
AU - Liu, Jue
AU - Wang, Hui
AU - Hu, Jianlin
AU - Liu, Ting
AU - Raat, Hein
AU - Guo, Yuming
AU - Wang, Haijun
N1 - Funding Information:
The present study was supported by the National Natural Science Foundation of China (Grant No. 81973053). SZ was supported by the China Scholarship Council at the Erasmus University Medical Centre, Rotterdam, The Netherlands (202106010220) as well as the Innovation Fund for Outstanding PhD Candidates of Peking University Health Science Centre.
Publisher Copyright:
© The Author(s), under exclusive licence to Springer Nature America, Inc. 2024.
PY - 2024
Y1 - 2024
N2 - Background: Prenatal fine particulate matter (PM2.5) constituents exposure and reduced fetal growth may be risk factors for accelerated growth in early childhood, an important indicator for lifelong health. Objective: The study investigated whether the joint effects are present between PM2.5 constituents and reduced fetal growth. Methods: The study was embedded in a birth cohort in China, including 5424 mother-child pairs. Prenatal PM2.5 and its constituents’ [organic carbon (OC), elementary carbon (EC), ammonium (NH4+), nitrate (NO3−), and sulfate (SO42−)] concentrations were estimated based on maternal residential addresses. Fetal growth was evaluated by fetal growth trajectory in utero and preterm birth (PTB), low birth weight (LBW), and small for gestational age (SGA). Children’s accelerated growth was defined as body mass index (BMI) Z-score change of >0.67 between birth and 3 years. Generalized logistic regression was used to analyze the effects of prenatal PM2.5 constituents exposure and fetal growth on children’s accelerated growth. Joint effect was tested on multiplicative scale and additive scale with the relative excess risk due to interaction (RERI). Results: Children with lower fetal growth trajectory, PTB, LBW, and SGA had increased odds of children’s accelerated growth, with odds ratios (ORs) ranging from 1.704 to 11.605. Compared with lower exposure (≤median), higher exposure (>median) of PM2.5, OC, and SO42− were significantly associated with increased odds of children’s accelerated growth, varying in ORs from 1.163 to 1.478. Prenatal exposure to OC had joint effects with lower fetal growth on children’s accelerated growth. We observed that the interaction was statistically significant on an additive scale in OC and lower fetal growth trajectory (RERI: 0.497, 95% CI: 0.033,0.962). Impact: Fine particulate matter (PM2.5) is a huge threat to human health worldwide, causing 6.7 million death globally in 2019. According to the theory of DOHaD, prenatal PM2.5 exposure could influence early childhood growth, which is important for lifelong health. We found that prenatal exposure to PM2.5, OC, and SO42− was associated with higher risk of accelerated childhood growth in the first 3 years. More importantly, reduced fetal growth moderated these associations. Our findings highlight the need for policies and interventions on PM2.5 constituents to improve lifelong health, especially for those vulnerable populations with reduced fetal growth.
AB - Background: Prenatal fine particulate matter (PM2.5) constituents exposure and reduced fetal growth may be risk factors for accelerated growth in early childhood, an important indicator for lifelong health. Objective: The study investigated whether the joint effects are present between PM2.5 constituents and reduced fetal growth. Methods: The study was embedded in a birth cohort in China, including 5424 mother-child pairs. Prenatal PM2.5 and its constituents’ [organic carbon (OC), elementary carbon (EC), ammonium (NH4+), nitrate (NO3−), and sulfate (SO42−)] concentrations were estimated based on maternal residential addresses. Fetal growth was evaluated by fetal growth trajectory in utero and preterm birth (PTB), low birth weight (LBW), and small for gestational age (SGA). Children’s accelerated growth was defined as body mass index (BMI) Z-score change of >0.67 between birth and 3 years. Generalized logistic regression was used to analyze the effects of prenatal PM2.5 constituents exposure and fetal growth on children’s accelerated growth. Joint effect was tested on multiplicative scale and additive scale with the relative excess risk due to interaction (RERI). Results: Children with lower fetal growth trajectory, PTB, LBW, and SGA had increased odds of children’s accelerated growth, with odds ratios (ORs) ranging from 1.704 to 11.605. Compared with lower exposure (≤median), higher exposure (>median) of PM2.5, OC, and SO42− were significantly associated with increased odds of children’s accelerated growth, varying in ORs from 1.163 to 1.478. Prenatal exposure to OC had joint effects with lower fetal growth on children’s accelerated growth. We observed that the interaction was statistically significant on an additive scale in OC and lower fetal growth trajectory (RERI: 0.497, 95% CI: 0.033,0.962). Impact: Fine particulate matter (PM2.5) is a huge threat to human health worldwide, causing 6.7 million death globally in 2019. According to the theory of DOHaD, prenatal PM2.5 exposure could influence early childhood growth, which is important for lifelong health. We found that prenatal exposure to PM2.5, OC, and SO42− was associated with higher risk of accelerated childhood growth in the first 3 years. More importantly, reduced fetal growth moderated these associations. Our findings highlight the need for policies and interventions on PM2.5 constituents to improve lifelong health, especially for those vulnerable populations with reduced fetal growth.
KW - Accelerated childhood growth
KW - Constituents
KW - Fetal growth
KW - Particulate matters
UR - http://www.scopus.com/inward/record.url?scp=85188601760&partnerID=8YFLogxK
U2 - 10.1038/s41370-024-00658-x
DO - 10.1038/s41370-024-00658-x
M3 - Article
C2 - 38532124
AN - SCOPUS:85188601760
SN - 1559-0631
JO - Journal of Exposure Science and Environmental Epidemiology
JF - Journal of Exposure Science and Environmental Epidemiology
ER -