Manzano-Salgado, Cyntia BCasas, MaribelLopez-Espinosa, Maria-JoseBallester, FerranIniguez, CarmenMartinez, DavidRomaguera, DoraFernandez-Barres, SilviaSanta-Marina, LoretoBasterretxea, MikelSchettgen, ThomasValvi, DamaskiniSunyer, JordiVrijheid, Martine2024-07-112024-07-112017-09Manzano-Salgado CB, Casas M, Lopez-Espinosa MJ, Ballester F, Iniguez C, Martinez D, et al. Prenatal Exposure to Perfluoroalkyl Substances and Cardiometabolic Risk in Children from the Spanish INMA Birth Cohort Study. Environ Health Perspect. 2017 Sep;125(9):97018.0091-6765http://hdl.handle.net/20.500.13003/9689http://hdl.handle.net/20.500.12105/20451BACKGROUND: Perfluoroalkyl substances (PFAS) may affect body mass index (BMI) and other components of cardiometabolic (CM) risk during childhood, hut evidence is scarce and inconsistent. OBJECTIVES: We estimated associations between prenatal PFAS exposures and outcomes relevant to cardiometabolic risk, including a composite CM risk score. METHODS: We measured perfluorohexanesulfonic acid (PFHxS), perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), and perfluorononanoic acid (PFNA) in maternal plasma (first trimester). We assessed weight gain from birth until 6 mo. At 4 and 7 y, we calculated the age- and sex-specific z-scores for BMI, waist circumference (WC), and blood pressure (BP) (n approximate to 1,000). At age 4, we calculated the age-, sex-, and region specific z-scores for cholesterol, triglycerides (TGs), high-density (HDL-C), and low-density lipoprotein cholesterol (LDL-C) (n = 627). At age 4, we calculated a CM-risk score (n = 386) as the sum of the individual age-, sex-, and region-specific z-scores for WC, BP, HDL-C, and TGs. We used the average between the negative of HDE-C z-score and TGs z-score to give similar weight to lipids and the other components in the score. A higher score indicates a higher cardiometaholic risk at age 4. RESULTS: PFOS and PFOA were the most abundant PFAS (geometric mean: 5.80 and 2.32 ng/mL respectively). In general, prenatal PFAS concentrations were not associated with individual outcomes or the combined CM-risk score. Exceptions were positive associations between prenatal PFHxS and TGs z-score [for a doubling of exposure, beta = 0.11; 95% confidence interval (CI): 0.01, 0.21], and between PFNA and the CM-risk score (beta=0.60; 95% CI: 0.04, 1.16). There was not clear or consistent evidence of modification by sex. CONCLUSIONS: We observed little or no evidence of associations between low prenatal PFAS exposures and outcomes related to cardiometabolic risk in a cohort of Spanish children followed from birth until 7 y.enghttp://creativecommons.org/licenses/by/4.0/ChildSpainAdultEnvironmental PollutantsHumansEnvironmental ExposureFluorocarbonsCaprylatesPregnancyMaleAlkanesulfonic AcidsFemaleMaternal ExposurePrenatal Exposure Delayed Effectsresearch articleAttribution 4.0 International2893472012599701810.1289/EHP13301552-9924Environmental Health Perspectivesopen accessExposición MaternaFemeninoÁcidos AlcanesulfónicosExposición a Riesgos AmbientalesMasculinoContaminantes AmbientalesFluorocarburosCaprilatosHumanosEmbarazoNiñoAdultoEfectos Tardíos de la Exposición PrenatalEspaña2-s2.0-85031786350413792800028L619529577