Association between perfluoroalkyl acids and kidney function in a cross-sectional study of adolescents

Abstract

BackgroundPerfluoroalkyl acids are synthetic compounds widely used in industrial and commercial applications. Laboratory studies suggest that these persistent and bioaccumulative chemicals produce oxidant stress and damage glomerular endothelial cells, raising concern regarding the impact of these compounds on renal function.MethodsWe performed cross-sectional analyses of data 1960 participants aged 12–19 years of the 2003–2010 National Health and Nutrition Examination Surveys. PFAA exposure was assessed using levels of perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid, and perfluorohexane sulfonic acid. Primary study outcomes were estimated glomerular filtration rate (eGFR) and serum uric acid.ResultsWhile adjusting for demographics, cotinine, prehypertension, insulin resistance, body mass index, and hypercholesterolemia, adolescents in the highest PFOA and PFOS quartile had a lower eGFR, 6.84 mL/min/1.73 m2 (95 % CI: 2.19 to 11.48) and 9.69 mL/min/1.73 m2 (95 % CI: -4.59 to 14.78), respectively, compared to the lowest quartile. Highest PFOA and PFOS quartiles were also associated with 0.21 mg/dL (95 % CI: 0.056 to 0.37) and 0.19 mg/dL (95 % CI: 0.032 to 0.34) increases in uric acid, respectively.ConclusionsPFAAs are associated with a reduction in kidney function and increased uric acid levels in otherwise healthy adolescents. Reverse causation and residual confounding could explain the results. Our study results confirm and amplify previous findings, though longitudinal studies examining prenatal and childhood biomarkers in relationship with robust measures of childhood renal function are needed.

Serum perfluoroalkyl substances in children exposed to the world trade center disaster

“…13 In adolescents, PFOA and PFOS have been found to be significantly associated with dyslipidemia. 14 PFOS and PFNA concentrations have also been shown to be associated with lower levels of insulin growth factor-1 (IGF-1) in children and, 15 among 12–19 year olds in NHANES 2003–2010, those with the highest quartile of serum PFC had significantly lower renal glomerular function compared to those in the lowest quartile, 16 although the possibility of reverse causation cannot be excluded in this cross-sectional study.…”

“…28 Furthermore, PFASs have been associated with increases in serum uric acid in children ages 12–19 years enrolled in NHANES, and have been linked to reduced kidney function in children. 16 In addition, it has been reported that PFOS and PFNA concentrations were associated with lower levels of IGF-1 in children, 15 which, in turn, have been associated with metabolic syndrome 29 and increased risk of cardiovascular events in later life. 30 …”

“…Caloric intake and serum PFASs were not normally distributed and therefore were compared between the two groups using the Wilcoxon Rank Sum test. PFAS concentrations were log-transformed to account for skewed distribution; following published practices, levels less than the LOD were imputed to be LOD/√2, 16 and we limited our statistical analyses to PFASs detected in ≥50% of the samples. Chi-square analyses also compared sociodemographic variables between WTCHR participants who were recruited for this study and WTCHR participants who were not.…”

Environmental exposures and pediatric kidney function and disease: A systematic review

“…One study used a dipstick to measure proteinuria (Factor-Litvak et al, 1999). Among the studies that examined estimated glomerular filtration rate (eGFR), seven studies used creatinine based estimating equations (Fadrowski et al, 2010, Farzan et al, 2016, Garcia-Esquinas et al, 2013, Kataria et al, 2015a, Kooijman et al, 2015, Loghman-Adham, 1998, Watkins et al, 2013). Four studies used Cystatin C based estimating equations to determine eGFR (Fadrowski et al, 2010, Skroder et al, 2015, Hawkesworth et al, 2013, Filler et al, 2012).…”

“…These include studies of fluoride levels(Xiong et al, 2007; Liu et al, 2005), aflatoxin (Hassan et al, 2006a) and ochratoxin (Hassan et al, 2006b), maternal smoking levels (Taal et al, 2011, Kooijman et al, 2015), secondhand smoking (Garcia-Esquinas et al, 2013), Bisphenol A, Triclosan, Benzophenone-3 (Trasande et al, 2013), PFOA (Geiger et al, 2013; Watkins et al, 2013; Kataria et al, 2015a), Bisphenol-A-glycidyl-dimethacrylate (bisGMA) (Trachtenberg et al, 2014), melamine exposure (Lam et al, 2008; Guan et al, 2009), polycyclic aromatic hydrocarbons (PAHs) (Farzan et al, 2016) and various phthalate compounds (Trasande et al, 2014, Tsai et al, 2016) (Table 3). The study designs included 12 cross-sectional, 1 case control, 2 prospective cohort, 1 retrospective cohort, and 1 randomized clinical trial.…”