Abstract 37: Associations of Prenatal Per- and Polyfluoroalkyl Substances (PFAS) Exposures and Childhood Blood Pressure in the Environmental influences on Child Health Outcomes (ECHO) Cohort

F Frances Wang (Beth Israel Deaconess Med Center, Diamond Bar, California, United States) P Pi-i Lin (Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, Massachusetts, United States) I Izzuddin Aris (Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, Massachusetts, United States) T Theresa Bastain (University of Southern California, Los Angeles, California, United States) C Courtney Carignan (Michigan State University, East Lansing, Michigan, United States) A Andrea Cassidy-Bushrow (Henry Ford Health, Detroit, Michigan, United States) W Whitney Cowell (NYU Grossman School of Medicine, New York, New York, United States) L Lisa Croen (Kaiser Permanente Northern California, Pleasanton, California, United States) D Dana Dabelea A Anne Dunlop A Assiamira Ferrara (Kaiser Permanente Northern California, Pleasanton, California, United States) S Shohreh Farzan (University of Southern California, Los Angeles, California, United States) S Sarah Geiger (University of Illinois, Urbana, Illinois, United States) R Rachel Kelly (Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, United States) M Margaret Karagas (Dartmouth College, Lebanon, New Hampshire, United States) M MICHELE LEVINE (University Of Pittsburgh, Pittsburgh, Pennsylvania, United States) Z Zeyu Li (Beijing National Laboratory for Molecular Sciences) D Donghai Liang Z Zhongzheng Niu T Thomas OConnor (University of Rochester Medical Center, Rochester, New York, United States) J Jiwon Oh (St. Michael’s Hospital, University of Toronto, Toronto) A Alicia Peterson (Kaiser Permanente Northern California, Pleasanton, California, United States) C Christina Porucznik (University of Utah, Salt Lake City, Utah, United States) M Megan Romano (Dartmouth College, Lebanon, New Hampshire, United States) A Anne Starling (University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States) J Julia Varshavsky (Northeastern University, Boston, Massachusetts, United States) Q Qi Zhao M Marie-France Hivert E Emily Oken M Mingyu Zhang (Hubei Key Laboratory of Electrochemical Power Sources, College of Chemistry and Molecular Sciences)

Abstract

Background: PFAS are widespread, persistent chemicals that cross the placenta and may affect fetal development. Animal studies suggest prenatal PFAS exposure increases offspring blood pressure (BP); however, epidemiologic evidence is limited and inconsistent. Hypothesis: We hypothesized that prenatal PFAS exposure is associated with higher childhood BP. Methods: We included children aged 3-13 years in the U.S. ECHO Cohort with data on gestational plasma or serum concentrations of PFOA, PFOS, PFHxS, PFNA, PFDA, and MeFOSAA. Children’s BP was obtained from study visits or medical records. We derived age-, sex-, and height-specific BP percentiles according to the 2017 American Academy of Pediatrics Guidelines and defined elevated BP as systolic BP (SBP) or diastolic BP (DBP) ≥90 th percentile. We used multivariable linear and modified Poisson models with generalized estimating equations and repeated BP measures clustered by participant (adjustment variables shown in Figure 1 footnotes ) and addressed missing data using multiple imputation by chained equations. We conducted subgroup analyses by child sex, ethnicity, and race, and we examined trimester-specific associations. Results: Among 2,435 children (50% female, 21% Hispanic, 25% Black), 22% had elevated BP at their last visit at a median age of 7.3 years ( Table 1 ). In adjusted analyses ( Figure 1 ), each doubling of PFOA was associated with a 1.23 (95% CI: 0.02, 2.45) higher SBP percentile, a 0.95 (0.10, 1.79) higher DBP percentile, and 1.07 (1.00, 1.15) times the risk of elevated BP. Each doubling of PFOS and PFNA was associated with a 1.14 (0.01, 2.27) and 0.85 (0.09, 1.61) higher DBP percentile, respectively. The PFOA-SBP association was stronger in males, and associations of PFOA, PFOS, and PFNA with DBP were stronger in females and non-Hispanic children. In trimester-specific analyses ( Figure 2 ), first-trimester PFOA, PFOS, and PFDA were associated with elevated BP; second-trimester PFOA and PFNA were associated with higher SBP percentiles; and third-trimester PFOS and MeFOSAA were associated with higher DBP percentiles. Conclusions: Prenatal exposure to PFOA, PFOS, and PFNA was associated with higher childhood BP. The trimester-specific associations should be interpreted with caution as they may also reflect cohort differences in PFAS profiles. PFAS may contribute to early-life programming of elevated lifelong cardiovascular risk, reinforcing the importance of population-level prevention.

Article Details

Journal Circulation
Volume / Issue Vol. 153, Issue Suppl_1
Published March 24, 2026
ISSN 0009-7322
Publisher Lippincott Williams & Wilkins

Journal Info

Circulation

Lippincott Williams & Wilkins

ISSN: 0009-7322 Health Sciences

Authors (30)

F

Frances Wang

Beth Israel Deaconess Med Center, Diamond Bar, California, United States

P

Pi-i Lin

Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, Massachusetts, United States

I

Izzuddin Aris

Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, Massachusetts, United States

T

Theresa Bastain

University of Southern California, Los Angeles, California, United States

C

Courtney Carignan

Michigan State University, East Lansing, Michigan, United States

A

Andrea Cassidy-Bushrow

Henry Ford Health, Detroit, Michigan, United States

W

Whitney Cowell

NYU Grossman School of Medicine, New York, New York, United States

L

Lisa Croen

Kaiser Permanente Northern California, Pleasanton, California, United States

D

Dana Dabelea

A

Anne Dunlop

A

Assiamira Ferrara

Kaiser Permanente Northern California, Pleasanton, California, United States

S

Shohreh Farzan

University of Southern California, Los Angeles, California, United States

S

Sarah Geiger

University of Illinois, Urbana, Illinois, United States

R

Rachel Kelly

Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, United States

M

Margaret Karagas

Dartmouth College, Lebanon, New Hampshire, United States

M

MICHELE LEVINE

University Of Pittsburgh, Pittsburgh, Pennsylvania, United States

Z

Zeyu Li

Beijing National Laboratory for Molecular Sciences

D

Donghai Liang

Z

Zhongzheng Niu

T

Thomas OConnor

University of Rochester Medical Center, Rochester, New York, United States

J

Jiwon Oh

St. Michael’s Hospital, University of Toronto, Toronto

A

Alicia Peterson

Kaiser Permanente Northern California, Pleasanton, California, United States

C

Christina Porucznik

University of Utah, Salt Lake City, Utah, United States

M

Megan Romano

Dartmouth College, Lebanon, New Hampshire, United States

A

Anne Starling

University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States

J

Julia Varshavsky

Northeastern University, Boston, Massachusetts, United States

Q

Qi Zhao

M

Marie-France Hivert

E

Emily Oken

M

Mingyu Zhang

Hubei Key Laboratory of Electrochemical Power Sources, College of Chemistry and Molecular Sciences