Perfluoroalkyl chemicals and elevated serum uric acid in US adults

Abstract

Background:Perfluoroalkyl chemicals, including perfluorooctanoic acid and perfluorooctane sulfonate, are man-made chemicals that have been detected in the blood of over 98% of the US population. Serum uric acid is a novel biomarker, even mild elevations of which has been implicated in the development of hypertension, diabetes mellitus, cardiovascular disease, and chronic kidney disease. We examined the relationship of serum perfluoroalkyl chemicals, including perfluorooctanoic acid and perfluorooctane sulfonate, and elevated uric acid levels in a representative sample of US adults.Methods:We examined 3883 participants from the 1999–2000 and 2003–2006 National Health and Nutritional Examination Surveys, a representative, multiethnic population-based survey of noninstitutionalized US adults. Serum perfluorooctanoic acid and perfluorooctane sulfonate were analyzed as quartiles. The main outcome was hyperuricemia.Results:We found that serum levels of perfluoroalkyl chemicals, including perfluorooctanoic acid and perfluorooctane sulfonate, were positively associated with hyperuricemia. This association appeared to be independent of confounders such as age, gender, race-ethnicity, body mass index, diabetes, hypertension, and serum cholesterol. Compared with subjects in quartile 1 (referent), the multivariate odds ratio for hyperuricemia among subjects in quartile 4 was 1.97 (95% confidence interval 1.44–2.70, P < 0.0001) for perfluorooctanoic acid and 1.48% (95% confidence interval 0.99–2.22, P = 0.0433) for perfluorooctane sulfonate. This observed association persisted in subgroup analysis by gender and body mass index.Conclusion:Our results demonstrate that elevated levels of perfluoroalkyl chemicals are associated with hyperuricemia even at low perfluoroalkyl chemical exposure levels as seen in the US general population.

Per- and polyfluorinated substances (PFASs): Environmental challenges

“…Another study found, however, a positive association with PFHxS [309]. PFOA and/or PFOS have been associated with serum uric acid [310,311], chronic kidney disease [312], abnormal liver enzyme increases, especially in obese individuals [313], cardiovascular disease [314] and thyroid disease [315]. Different PFAAs showed different, sex and ethnicity-dependent effects on thyroid [316].…”

Per- and polyfluoroalkyl substances in human serum and urine samples from a residentially exposed community

“…Human studies of people exposed to PFOA and PFOS occupationally, residentially, and at background levels have found associations with changes in lipid and cholesterol concentrations (Frisbee et al, 2010; Nelson et al, 2010; Fletcher et al, 2011; Steenland et al, 2015), increased uric acid levels (Costa et al, 2009; Steenland et al, 2010; Shankar et al, 2011; Geiger et al, 2013; Gleason et al, 2015), changes in the concentrations of thyroid and sex hormones (Olsen and Zobel, 2007; Knox et al, 2011; Jain, 2013; Wen et al, 2013; Winquist and Steenland, 2014), changes in liver enzymes (Olsen et al, 2000; Sakr et al, 2007; Lin et al, 2010; Gallo et al, 2012; Gleason et al, 2015), immune effects (Grandjean et al, 2012; Granum et al, 2013; Dalsager et al, 2016), reduced birth weight (Apelberg et al, 2007; Fei et al, 2007; Chen et al, 2012; Darrow et al, 2013), reproductive effects (Joensen et al, 2013; Kristensen et al, 2013; Crawford et al, 2017), and some cancers (Alexander and Olsen, 2007; Barry et al, 2013; Bonefeld-Jorgensen et al, 2014; Hardell et al, 2014; Steenland et al, 2015). Other studies have demonstrated no association between PFAS exposure and these health effects (Inoue et al, 2004; Alexander and Olsen, 2007; Fisher et al, 2013; Chang et al, 2014).…”

Associations between serum perfluoroalkyl acids and LINE-1 DNA methylation

“…Although PFAA exposure has not yet been directly linked to cardiovascular disease (CVD), epidemiological studies do suggest that exposure to PFOA and PFOS may be associated with CVD risk factors such as hyperuricemia (Costa et al, 2009; Shankar et al, 2011; Steenland et al, 2010) and increased total and low density lipoprotein cholesterol (LDL-C) (Costa et al, 2009; Eriksen et al, 2013; Fitz-Simon et al, 2013, Frisbee et al, 2010; Nelson et al, 2010; Olsen et al, 2003; Sakr et al, 2007; Steenland et al, 2009), although studies have not been entirely consistent (e.g. Fisher et al 2013; Olsen et al 2012), and have been predominantly cross-sectional, limiting causal inference.…”