TY - JOUR
T1 - No association between prenatal lead exposure and neurodevelopment during early childhood in the Japan Environment and Children’s Study
AU - The Japan Environment and Children’s Study Group
AU - Inoue, Hirosuke
AU - Sanefuji, Masafumi
AU - Sonoda, Yuri
AU - Ogawa, Masanobu
AU - Hamada, Norio
AU - Shimono, Masayuki
AU - Suga, Reiko
AU - Nakayama, Shoji F.
AU - Taniguchi, Yu
AU - Kusuhara, Koichi
AU - Ohga, Shouichi
AU - Kamijima, Michihiro
AU - Kamijima, Michihiro
AU - Yamazaki, Shin
AU - Ohya, Yukihiro
AU - Kishi, Reiko
AU - Yaegashi, Nobuo
AU - Hashimoto, Koichi
AU - Mori, Chisato
AU - Ito, Shuichi
AU - Yamagata, Zentaro
AU - Inadera, Hidekuni
AU - Nakayama, Takeo
AU - Iso, Hiroyasu
AU - Shima, Masayuki
AU - Nakamura, Hiroshige
AU - Suganuma, Narufumi
AU - Kusuhara, Koichi
AU - Katoh, Takahiko
N1 - Funding Information:
We thank all participants of the JECS and all staff members involved in data collection. This study was funded by the Ministry of the Environment, Japan. The findings and conclusions of this article are the sole responsibility of the authors and do not represent the official views of the Japanese government.
Funding Information:
We thank all participants of the JECS and all staff members involved in data collection. This study was funded by the Ministry of the Environment, Japan. The findings and conclusions of this article are the sole responsibility of the authors and do not represent the official views of the Japanese government.
Publisher Copyright:
© 2022, The Author(s).
PY - 2022/12
Y1 - 2022/12
N2 - Compared with the relatively well-investigated effects of childhood exposure to lead on neurocognitive deficits, those of prenatal exposure remain relatively inconclusive. We aimed to investigate the association between prenatal blood lead levels and neurodevelopmental delay during the first three years of life. From a prospective cohort of the Japan Environment and Children’s Study, we analyzed a total of 80,759 children. The exposure factors were prenatal lead concentrations measured from maternal whole blood in the second/third trimesters and umbilical cord blood at birth. Neurodevelopment was assessed at 6, 12, 18, 24, 30, and 36 months old using a screening tool, the Ages and Stages Questionnaires, third edition (ASQ). The outcome measures were any suspected neurodevelopmental delay (sNDD) identified via the ASQ during the first (sNDD-1Y), second (sNDD-2Y), and third (sNDD-3Y) years of life. sNDD-1Y, 2Y, and 3Y were identified in 18.0%, 16.2%, and 17.2% of children, respectively. The geometric means of blood lead concentration in this study were much lower (0.62 μg/dL in maternal blood and 0.50 μg/dL in cord blood) than previously investigated levels. Multivariable regression models revealed that there were no associations between maternal blood lead and sNDD-1Y and 2Y and between cord blood lead and sNDD-1Y, 2Y, and 3Y. Although a higher maternal blood lead was associated with a reduced risk of sNDD-3Y (adjusted relative risk: 0.84, 95% confidence interval 0.75–0.94, per 1 increase in common logarithm of lead concentration), there were no dose–response relationships in the analysis using quintiles of lead concentrations. Using a large-scale data set, the present study demonstrated no convincing evidence for an inverse association between levels of prenatal blood lead and neurodevelopment in early childhood. Longitudinal measurements of prenatal and postnatal lead levels are needed to understand the relationship between lead exposure and neurocognitive development.
AB - Compared with the relatively well-investigated effects of childhood exposure to lead on neurocognitive deficits, those of prenatal exposure remain relatively inconclusive. We aimed to investigate the association between prenatal blood lead levels and neurodevelopmental delay during the first three years of life. From a prospective cohort of the Japan Environment and Children’s Study, we analyzed a total of 80,759 children. The exposure factors were prenatal lead concentrations measured from maternal whole blood in the second/third trimesters and umbilical cord blood at birth. Neurodevelopment was assessed at 6, 12, 18, 24, 30, and 36 months old using a screening tool, the Ages and Stages Questionnaires, third edition (ASQ). The outcome measures were any suspected neurodevelopmental delay (sNDD) identified via the ASQ during the first (sNDD-1Y), second (sNDD-2Y), and third (sNDD-3Y) years of life. sNDD-1Y, 2Y, and 3Y were identified in 18.0%, 16.2%, and 17.2% of children, respectively. The geometric means of blood lead concentration in this study were much lower (0.62 μg/dL in maternal blood and 0.50 μg/dL in cord blood) than previously investigated levels. Multivariable regression models revealed that there were no associations between maternal blood lead and sNDD-1Y and 2Y and between cord blood lead and sNDD-1Y, 2Y, and 3Y. Although a higher maternal blood lead was associated with a reduced risk of sNDD-3Y (adjusted relative risk: 0.84, 95% confidence interval 0.75–0.94, per 1 increase in common logarithm of lead concentration), there were no dose–response relationships in the analysis using quintiles of lead concentrations. Using a large-scale data set, the present study demonstrated no convincing evidence for an inverse association between levels of prenatal blood lead and neurodevelopment in early childhood. Longitudinal measurements of prenatal and postnatal lead levels are needed to understand the relationship between lead exposure and neurocognitive development.
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U2 - 10.1038/s41598-022-19509-6
DO - 10.1038/s41598-022-19509-6
M3 - Article
C2 - 36097036
AN - SCOPUS:85137686880
SN - 2045-2322
VL - 12
JO - Scientific reports
JF - Scientific reports
IS - 1
M1 - 15305
ER -