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Publication Information
Affiliation
Division of Chronic Disease Research Across the Lifecourse, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, MA, USA. Electronic address: p_lin@harvardpilgrim.org.; Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, Berkeley, CA, USA. Electronic address: andres.cardenas@berkeley.edu.; Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA. Electronic address: rhauser@hsph.harvard.edu.; Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA; Channing Division of Network Medicine, Brigham and women's Hospital, Boston, MA, USA. Electronic address: redrg@channing.harvard.edu.; Department of Biostatistics, School of Public Health and Human Sciences, University of Massachusetts Amherst, Amherst, MA, USA.; Division of Chronic Disease Research Across the Lifecourse, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, MA, USA; Diabetes Unit, Massachusetts General Hospital, Boston, MA, USA. Electronic address: mhivert@partners.org.; Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, GA, USA. Electronic address: aic7@cdc.gov.; Department of Environmental Health, Boston University School of Public Health, Boston, MA, USA. Electronic address: twebster@bu.edu.; Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA. Electronic address: edward.horton@joslin.harvard.edu.; Division of Chronic Disease Research Across the Lifecourse, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, MA, USA. Electronic address: emily_oken@harvardpilgrim.org.
Authors
Lin Pi-I D, Cardenas Andres, Hauser Russ, Gold Diane R, Kleinman Ken P, Hivert Marie-France, Calafat Antonia M, Webster Thomas F, Horton Edward S, Oken Emily
Studies
Abstract
Per- and polyfluoroalkyl substances (PFAS) are ubiquitously detected in populations worldwide and may hinder kidney function. The objective of the study was to determine longitudinal associations of plasma PFAS concentrations with estimated glomerular filtration rate (eGFR) and evaluate whether a lifestyle intervention modify the associations. We studied 875 participants initially randomized to the lifestyle or placebo arms in the Diabetes Prevention Program (DPP, 1996-2002) trial and Outcomes Study (DPPOS, 2002-2014). We ran generalized linear mixed models accounting a priori covariates to evaluate the associations between baseline PFAS concentrations and repeated measures of eGFR, separately, for six PFAS (PFOS, PFOA, PFHxS, EtFOSAA, MeFOSAA, PFNA); then used quantile-based g-computation to evaluate the effects of the six PFAS chemicals as a mixture. The cohort was 64.9% female; 73.4% 40-64 years-old; 29.4% with hypertension; 50.5% randomized to lifestyle intervention and 49.5% to placebo and had similar plasma PFAS concentrations as the general U.S. population in 1999-2000. Most participants had normal kidney function (eGFR > 90 mL/min/1.73 m2) over the approximately 14 years of follow-up. We found that plasma PFAS concentrations during DPP were inversely associated with eGFR during DPPOS follow-up. Each quartile increase in baseline plasma concentration of the 6 PFAS as a mixture was associated with 2.26 mL/min/1.73 m2 lower eGFR (95% CI: -4.12, -0.39) at DPPOS Year 5, approximately 9 years since DPP randomization and PFAS measurements. The lifestyle intervention did not modify associations, but inverse associations were stronger among participants with hypertension at baseline. Among prediabetic adults, we found inverse associations between baseline plasma PFAS concentrations and measures of eGFR throughout 14 years of follow-up. The lifestyle intervention of diet, exercise and behavioral changes did not modify the associations, but persons with hypertension may have heightened susceptibility.