Perfluorinated Substances in Human Food and Other Sources of Human Exposure
Laboratory for Ecophysiology, Biochemistry and Toxicology, Department of Biology, University of Antwerp, 2020 Antwerp, Belgium.Reviews of environmental contamination and toxicology (Impact Factor: 3.74). 09/2010; 208:179-215. DOI: 10.1007/978-1-4419-6880-7_4
Perfluorinated compounds (PFCs) are ubiquitous environmental contaminants, which persist and may bioaccumulate through the food chain (Haukås et al. 2007; Martin et al. 2004b; Taniyasu et al. 2003). As a consequence, several PFCs have been detected in different biota worldwide. In recent years, an increasing number of papers report high levels of PFCs in blood, tissues, and breast milk from both occupationally and non-occupationally exposed human populations (Kannan et al. 2004; Kärrman et al. 2007; Olsen et al. 2007). The most important exposure pathways of perfluorinated compounds for humans are thought to be intake of drinking water and food and inhalation of dust (Björklund et al. 2009; Ericson et al. 2008a). Due to the widespread distribution, environmental degradation, and metabolism of the PFCs released into the environment, a very complex exposure situation exists (Fromme et al. 2007a). As a result, the relative contribution to human exposure from different routes or from a single source (e.g., diet) is not yet known. More specifically, it is currently unknown as to what extent exposure to drinking water, food, or dust contributes to the PFCs measured in human breast milk and blood. Moreover, data on levels of PFCs in the human diet are rather scarce (Kärrman et al. 2009; Tittlemier et al. 2006, 2007). Only PFC levels in fish appear to be well documented (Houde et al. 2006). Few studies, however, report the levels of PFCs in drinking water or human food such as vegetables, meat, and eggs (FSA 2006; US EPA 2001). Food processing such as cooking (boiling, baking, or grilling) could alter the concentration of PFCs in food and as a consequence affect the risk for humans.
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- "Despite consistent results from these two Danish studies, results from studies examining dietary habits in relation to serum PFAA concentrations have been relatively conflicting (Domingo, 2012) with the exception of seafood being in some studies reported as potential source of exposure (Berg et al., 2014; Falandysz et al., 2006; Haug et al., 2010b). Trace levels of PFAAs, particularly PFOS, have also consistently been found in seafood (D'Hollander et al., 2010), while results for other food items have been less consistent (Haug et al., 2010a; Vestergren et al., 2012). It is however well established that PFAAs can enter the food chain trough indirect contamination via leakage from food packaging material (D'eon and Mabury, 2011; Zafeiraki et al., 2014) and this may potentially account for the association we observe for meat and meat products in our study. "
ABSTRACT: Background: Perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) have consistently been associated with higher cholesterol levels in cross sectional studies. Concerns have, however, been raised about potential confounding by diet and clinical relevance. Objective: To examine the association between concentrations of PFOS and PFOA and total cholesterol in serum during pregnancy taking into considerations confounding by diet. Methods: 854 Danish women who gave birth in 1988-89 and provided a blood sample and reported their diet in week 30 of gestation. Results: Mean serum PFOS, PFOA and total cholesterol concentrations were 22.3ng/mL, 4.1ng/mL and 7.3mmol/L, respectively. Maternal diet was a significant predictor of serum PFOS and PFOA concentrations. In particular intake of meat and meat products was positively associated while intake of vegetables was inversely associated (P for trend <0.01) with relative difference between the highest and lowest quartile in PFOS and PFOA concentrations ranging between 6% and 25% of mean values. After adjustment for dietary factors both PFOA and PFOS were positively and similarly associated with serum cholesterol (P for trend ≤0.01). For example, the mean increase in serum cholesterol was 0.39mmol/L (95%CI: 0.09, 0.68) when comparing women in the highest to lowest quintile of PFOA concentrations. In comparison the mean increase in serum cholesterol was 0.61mmol/L (95%CI: 0.17, 1.05) when comparing women in the highest to lowest quintile of saturated fat intake. Conclusion: In this study associations between PFOS and PFOA with serum cholesterol appeared unrelated to dietary intake and were similar in magnitude as the associations between saturated fat intake and serum cholesterol.Environmental Research 11/2015; 143(Pt A):33-38. DOI:10.1016/j.envres.2015.09.001 · 4.37 Impact Factor
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- "cosmetics, plastics), individuals are routinely exposed to multiple phthalate metabolites simultaneously (Dodson et al., 2012). The concentrations of multiple perfluoroalkyl substances in household dust have been shown to be correlated (D'Hollander et al., 2010). We employed an analytical approach to account for the potential effects of correlated exposures. "
ABSTRACT: The fetal time period is a critical window of immune system development and resulting heightened susceptibility to the adverse effects of environmental exposures. Epidemiologists and toxicologists have hypothesized that phthalates, bisphenol A (BPA) and perfluoroalkyl substance have immunotoxic properties. Immunotoxic effects of chemicals may manifest in an altered immune system profile at birth. Immunoglobulin E, thymic stromal lymphopoietin (TSLP), and interleukin-33 (IL-33) are integral in the etiology of childhood allergy and detectable at birth. The objective of this study was to determine the association between maternal levels of phthalates, bisphenol A (BPA), and perfluoroalkyl substances and elevated umbilical cord blood levels of IgE, TSLP, and IL-33. This study utilized data collected in the Maternal-Infant Research on Environmental Chemicals (MIREC) Study, a trans-Canada cohort study of 2001 pregnant women. Of these women, 1258 had a singleton, term birth and cord blood sample. A Bayesian hierarchical model was employed to determine associations between log-transformed continuous variables and immune system biomarkers while adjusting for potential confounding from correlated environmental contaminants. Inverse, nonlinear associations were observed between maternal urinary MCPP levels and elevated levels of both IL-33/TSLP and IgE and between maternal urinary BPA levels and elevated levels of IL-33/TSLP. In this primarily urban Canadian population of pregnant women and their newborns, maternal urinary and plasma concentrations of phthalate metabolites, BPA, and perfluoroalkyl substances were not associated with immunotoxic effects that manifest as increased odds of elevated levels of IgE, TSLP or IL-33. Copyright © 2015. Published by Elsevier Inc.Environmental Research 07/2015; 140. DOI:10.1016/j.envres.2015.04.010 · 4.37 Impact Factor
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- "The extensive use and disposal of these perfluoroalkyl products have led to environmental contamination and have been detected in the air, water, soil, sediments, wildlife, food, human breast milk, and blood (Fromme et al. 2009; Mak et al. 2009; Naile et al. 2010; Nakata et al. 2006; Olsen et al. 2012; Pico et al. 2011; Sinclair et al. 2006; Tao et al. 2008; Zhang et al. 2011). Several studies have investigated the importance of the exposure routes including diet, drinking water, house dust, food packaging, nonstick cookware , indoor and outdoor air to perfluorinated compounds (D'Hollander et al. 2010; Fromme et al. 2009; Vestergren and Cousins 2009). Based on these investigations, the oral route of exposure has been considered the most important exposure pathway for perfluorinated compounds (Domingo 2012; Fromme et al. 2009). "
ABSTRACT: Perfluorohexanoic acid (PFHxA) a 6-carbon perfluoroalkyl (C6; CAS # 307-24-4), has been proposed as a replacement for the commonly used 8-carbon perfluoroalkyls: perfluorooctanoic acid and perfluorooctane sulfonate. PFHxA is not currently a commercial product but rather the ultimate degradation product of C6 fluorotelomer used to make C6 fluorotelomer acrylate polymers. It can be expected that, to a greater or lesser extent, the environmental loading of PFHxA will increase, as C6 fluorotelomer acrylate treatments are used and waste is generated. This article reports on a chronic study (duration 104 weeks) that was performed to evaluate the possible toxicologic and carcinogenic effects of PFHxA in gavage (daily gavage, 7 days per week) treated male and female Sprague-Dawley (SD) rats. In the current study, dosage levels of 0, 2.5, 15, and 100 mg/kg/day of PFHxA (males) and 5, 30, and 200 mg/kg/day of PFHxA (females) were selected based on a previous subchronic investigation. No effects on body weights, food consumption, a functional observational battery, or motor activity were observed after exposure to PFHxA. While no difference in survival rates in males was seen, a dose-dependent decrease in survival in PFHxA-treated female rats was observed. Hematology and serum chemistry were unaffected by PFHxA. PFHxA-related histologic changes were noted in the kidneys of the 200-mg/kg/day group females. Finally, there was no evidence that PFHxA was tumorigenic in male or female SD rats at any of the dosage levels examined.Toxicologic Pathology 05/2014; 43(2). DOI:10.1177/0192623314530532 · 2.14 Impact Factor
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