Evidence map›Paper›PMID 35952751›Full record

ArticleEnvironmental research2022

Physical activity modifies the relation between gestational perfluorooctanoic acid exposure and adolescent cardiometabolic risk.

Joseph M Braun, George D Papandonatos, Nan Li, Clara G Sears, Jessie P Buckley, Kim M Cecil, Aimin Chen, Charles B Eaton, Heidi J Kalkwarf, Karl T Kelsey and 2 more

Open access · greenAbstract read
In one paragraph

Article in Environmental research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 7 institutions in 2 countries.

Joseph M BraunDepartment of Epidemiology, Brown University, Providence, RI, 02912, Box G-S121, United States. Electronic address: joseph_braun_1@brown.edu.
George D PapandonatosDepartment of Biostatistics, School of Public Health, Brown University, Providence, RI, United States.
Nan LiDepartment of Epidemiology, Brown University, Providence, RI, 02912, Box G-S121, United States.
Clara G SearsDivision of Environmental Medicine, Department of Medicine, University of Louisville, Louisville, KY, United States.
Jessie P BuckleyDepartment of Environmental Health and Engineering, Johns Hopkins University School of Public Health, Baltimore, MD, United States.
Kim M CecilDepartment of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, United States; Department of Radiology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH, United States.
Aimin ChenDepartment of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.
Charles B EatonDepartment of Epidemiology, Brown University, Providence, RI, 02912, Box G-S121, United States; Department of Family Medicine, Warren Alpert Medical School of Brown University, Providence, RI, United States; Kent Memorial Hospital, Warwick, RI, United States.
Heidi J KalkwarfDepartment of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, United States; Division of Gastroenterology, Hepatology and Nutrition, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, United States.
Karl T KelseyDepartment of Epidemiology, Brown University, Providence, RI, 02912, Box G-S121, United States; Department of Pathology and Laboratory Medicine, Brown University, Providence, RI, United States.
Bruce P LanphearFaculty of Health Sciences, Simon Fraser University, Burnaby, British Columbia, Canada.
Kimberly YoltonDepartment of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, United States.
Brown University · USCincinnati Children's Hospital Medical Center · USJohns Hopkins University · USSimon Fraser University · CAUniversity of Cincinnati Medical Center · USUniversity of Louisville · USUniversity of Pennsylvania · US

Funding

LCenter for Clinical and Translational Science and TrainingUL1TR001425 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., KISSELA, BRETT M · 2015 to 2024
$37.5M
UNC-CH CENTER FOR ENVIRONMENTAL HEALTH &SUSCEPTIBILITYP30ES010126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Stephanie Engel · 2001 to 2026
$36.3M
REPRODUCTIVE AND DEVELOPMENTAL TOXICOLOGY RESEARCHP30ES006096 · NIEHS · UNIVERSITY OF CINCINNATI · PI PINNEY, SUSAN MENGEL · 1992 to 2022
$35.4M
Study of Prevalent Neurotoxicants in ChildrenP01ES011261 · NIEHS · CINCINNATI CHILDRENS HOSP MED CTR · PI LANPHEAR, BRUCE P · 2001 to 2006
$6.4M
Developmental neurotoxicity of organophosphate and novel brominated flame retardants in childrenR01ES028277 · NIEHS · UNIVERSITY OF PENNSYLVANIA · PI CHEN, AIMIN · 2017 to 2022
$3.4M
Impact of pre- and postnatal chemical mixture exposures on child neurobehavior and neuroimagingR01ES033054 · NIEHS · UNIVERSITY OF PENNSYLVANIA · PI CHEN, AIMIN · 2021 to 2025
$3.3M
Early life perfluoroalkyl substance exposure & obesity: Mechanisms & phenotypingR01ES025214 · NIEHS · BROWN UNIVERSITY · PI BRAUN, JOSEPH M · 2016 to 2020
$3.1M
Endocrine disrupting chemical mixtures and bone health in adolescenceR01ES033252 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BUCKLEY, JESSIE P · 2021 to 2025
$3.0M
Internalizing Behaviors and Neuroimaging Outcomes: Impact of PBDE and PFC ExposuresR01ES027224 · NIEHS · CINCINNATI CHILDRENS HOSP MED CTR · PI CECIL, KIM M, YOLTON, KIMBERLY · 2016 to 2020
$3.0M
A Community-Based Trial to Prevent Lead Poisoning and InjuriesR01ES014575 · NIEHS · CINCINNATI CHILDRENS HOSP MED CTR · PI YOLTON, KIMBERLY · 2007 to 2011
$2.9M
Longitudinal study of exposure to PBDEs and PFCs and child neurobehaviorR01ES020349 · NIEHS · UNIVERSITY OF CINCINNATI · PI CHEN, AIMIN, LANPHEAR, BRUCE P · 2011 to 2015
$2.9M
Gestational PFAS Mixture Exposures, Longitudinal Metabolomic Profiles, and Adolescent Cardiometabolic HealthR01ES032836 · NIEHS · BROWN UNIVERSITY · PI BRAUN, JOSEPH M · 2021 to 2024
$2.4M
NCATS NIH HHS UL1 TR001425NIEHS NIH HHS L40 ES032257NIEHS NIH HHS P01 ES011261NIEHS NIH HHS P30 ES010126NIEHS NIH HHS R01 ES014575NIEHS NIH HHS R01 ES020349NIEHS NIH HHS R01 ES023826NIEHS NIH HHS R01 ES025214NIEHS NIH HHS R01 ES027224NIEHS NIH HHS R01 ES028277NIEHS NIH HHS R01 ES030078NIEHS NIH HHS R01 ES032836NIEHS NIH HHS R01 ES033054NIEHS NIH HHS R01 ES033252
6 · The paper itself

Abstract

objectiveExposure to per- and polyfluoroalkyl substances (PFAS) - endocrine disrupting chemicals - may increase cardiometabolic risk. We evaluated whether adolescent lifestyle factors modified associations between gestational PFAS exposure and cardiometabolic risk using a prospective cohort study.

methodsIn 166 mother-child pairs (HOME Study), we measured concentrations of four PFAS in maternal serum collected during pregnancy. When children were age 12 years, we calculated cardiometabolic risk scores from visceral adiposity area, blood pressure, and fasting serum biomarkers. We assessed adolescent physical activity and Healthy Eating Index scores using the Physical Activity Questionnaire for Older Children (PAQ-C), actigraphy, and 24-h diet recalls. Using multivariable linear regression and weighted quantile sum regression, we examined whether physical activity or diet modified covariate-adjusted associations of PFAS and their mixture with cardiometabolic risk scores.

resultsPhysical activity modified associations between perfluorooctanoic acid (PFOA) and cardiometabolic risk scores. Each doubling of PFOA was associated with worse cardiometabolic risk scores among children with PAQ-C scores < median (β:1.4; 95% CI:0.5, 2.2, n = 82), but not among those with PAQ-C scores ≥ median (β: 0.2; 95% CI: 1.2, 0.7, n = 84) (interaction p-value = 0.01). Associations were most prominent for insulin resistance, leptin-adiponectin ratio, and visceral fat area. We observed results suggesting that physical activity modified the association of PFAS mixture with cardiometabolic risk scores, insulin resistance, and visceral fat area (interaction p-values = 0.17, 0.07, and 0.10, respectively); however, the 95% CIs of the interaction terms included the null value. We observed similar, but attenuated patterns for PFOA and actigraphy-based measures of physical activity. Diet did not modify any associations. Physical activity or diet did not modify associations for other PFAS.

conclusionsChildhood physical activity modified associations of prenatal serum PFOA concentrations with children's cardiometabolic risk in this cohort, indicating that lifestyle interventions may ameliorate the adverse effects of PFOA exposure.

Indexed as

Alkanesulfonic AcidsCardiovascular DiseasesEnvironmental PollutantsFluorocarbonsInsulin ResistanceAdolescentCaprylatesChildExerciseFemaleHumansPregnancyProspective StudiesAlkanesulfonic AcidsCaprylatesEnvironmental PollutantsFluorocarbonsperfluorooctanoic acidAdolescentEndocrine disruptorsEpidemiologyPerfluoroalkyl substances

Identifiers

PMID35952751
PMCPMC9637371
OpenAlexW4291674549

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.