Prenatal and Childhood Per- and Polyfluoroalkyl Substance (PFAS) Exposures and Blood Pressure Trajectories From Birth to Late Adolescence in a Prospective US Prebirth Cohort

被引:7
作者
Zhang, Mingyu [1 ,2 ,6 ]
Aris, Izzuddin M. [1 ,2 ]
Lin, Pi-I Debby [1 ,2 ]
Rifas-Shiman, Sheryl L. [1 ,2 ]
Brady, Tammy M. [3 ]
James-Todd, Tamarra [4 ]
Oken, Emily [1 ,2 ,4 ]
Hivert, Marie-France [1 ,2 ,5 ]
机构
[1] Harvard Med Sch & Harvard Pilgrim Hlth Care Inst, Boston, MA USA
[2] Harvard Pilgrim Hlth Care Inst, Boston, MA USA
[3] Johns Hopkins Univ, Sch Med, Baltimore, MD USA
[4] Harvard TH Chan Sch Publ Hlth, Boston, MA USA
[5] Massachusetts Gen Hosp, Boston, MA USA
[6] Harvard Med Sch & Harvard Pilgrim Hlth Care Inst, Dept Populat Med, 401 Pk Dr,Suite 401 East, Boston, MA 02215 USA
来源
JOURNAL OF THE AMERICAN HEART ASSOCIATION | 2023年 / 12卷 / 17期
基金
美国国家卫生研究院;
关键词
blood pressure; environmental exposure; hypertension; pediatrics; per- and polyfluoroalkyl substance; PERFLUOROALKYL SUBSTANCES; SERUM; HYPERTENSION; CHEMICALS; CHILDREN; LIFE; ASSOCIATIONS; PREDICTORS; PREGNANCY; ADULTHOOD;
D O I
10.1161/JAHA.123.030760
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
BACKGROUND: Evidence is limited regarding the associations of prenatal and childhood per- and polyfluoroalkyl substance (PFAS) exposures with blood pressure (BP) trajectories in children. METHODS AND RESULTS: Participants are from Project Viva, a prospective prebirth cohort in eastern Massachusetts. We measured PFAS in early-pregnancy maternal (median, 9.6 weeks) and midchildhood (median, 7.7 years) plasma samples. We conducted standardized BP measurements at 6 research visits: birth, infancy (median, 6.3 months), early childhood (median, 3.2 years), midchildhood (median, 7.7 years), early adolescence (median, 12.9 years), and late adolescence (median, 17.5 years). We used linear regression to examine associations of individual PFASs with BP at each visit, linear spline mixed-effects regression to model BP trajectories, and a mixture approach to estimate PFAS exposure burden. We included 9036 BP measures from 1506 participants. We observed associations between particular individual prenatal PFASs and child BP at specific time points, for example, prenatal 2-(N- ethyl-perfluorooctane sulfonamido) acetate (EtFOSAA) and 2-(N-methyl- perfluorooctane sulfonamido) acetate (MeFOSAA) with higher systolic BP at birth; prenatal perfluorooctane sulfonate (PFOS) and EtFOSAA with lower diastolic BP in infancy; and prenatal PFOS, perfluorooctanoate (PFOA), and EtFOSAA with higher systolic BP at midchildhood. No prenatal or childhood PFAS was consistently associated with BP across all visits. Diastolic BP trajectories from 0 to 20 years differed slightly by prenatal PFOA, perfluorohexane sulfonate (PFHxS), and perfluorononanoate ( PFNA) (P values 0.01-0.09). Diastolic BP trajectories from 6 to 20 years differed slightly by midchildhood PFHxS and MeFOSAA (P-values 0.03-0.08). Prenatal or childhood PFAS mixture burden scores were not associated with BP. CONCLUSIONS: We found associations of prenatal and childhood PFAS exposures with BP at specific time points between birth and late adolescence but no consistent associations across all time points or PFAS types.
引用
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页数:13
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