Perfluorinated Substances in Human Food and Other Sources of Human Exposure
ABSTRACT The widespread distribution and degradation of PFCs in the environment results in a very complex exposure pattern, which makes it difficult to define the relative contribution to human exposure from different exposure pathways. The present review is designed to provide an overview of the existing data on levels of PFCs measured in the human diet and in drinking water. Data on levels of PFCs in the human diet are rather scarce, but the level in the fish appear to be well documented. Among PFCs, PFOS and PFOA are the best studied compounds in fish from both experimental and monitoring studies. Recently, the number of publications that address other PFCs has increased, but the total number available is still limited. In general, we discovered that care should be exercised when using the reviewed data, because, in the majority of publications, quality control and/or details on analysis are, at least partly, lacking. It has been well documented that PFOA and PFOS have the potential to accumulate in fish and concentrations up to 7 and 170 ng/g wwt, respectively in edible fish species have been found. PFOS is the most crucial and prominent compound identified, followed by the PFOA. Also, in aquatic invertebrate such as shrimps, mussels, clams, and oysters, high PFOS levels have been reported (up to 387 ng/g wwt). However in most publications PFC level reported in molluscs were less than 1 ng/g wwt. Positive correlations were found between PFC body burden and self reported fish consumption. In recognition of the potential for human exposure to PFCs via fish consumption, the Minnesota Department of Health has recently issued fish consumption advisories for contaminated sections of the Mississippi River. It is interesting to note that 79% of the reviewed publications on PFCs in the whole fish homogenates exceed the that threshold. Moreover, five of the PFC concentration reported in muscles tissue exceeded the advisory level of 38 ng/g wwt. Even though several authors concluded that consumption of contaminated food and drinking water constitutes the major exposure pathway for humans, only a few reports on PFCs in composite food exist. Food can be contaminated in an indirect way, because PFCs are widely used in food-packaging coatings and cooking materials. On the other hand, PFCs can also enter food organisms via environmental routes such as inhalation or adsorption from air. In a few studies, composite samples, duplicate diet samples, or other food items were analyzed for several PFCs, PFOS and PFOA, PFHpA, PFHxA, and PFHxS were meAsured and displayed concentrations ranging from-detected up to 15 ng/g wwt. In one study, a very high PFOA concentration of 118 ng/g were reported, but overall, PFC levels are below 10 ng/g wwt. It is important to note that, among all studies reviewed, PFCs were found in a maximum of 50% of the analyzed samples and generally only in 10% or less of samples analyzed. In contrast to what is observed in fish and other food items PFOA levels in drinking water (ND - 50 ng/L) and other PFCs (1-3 ng/L). In one study, extremely high values (519 ng/L) were measured in drinking water of a contaminated area in the Ruhr region. In Spain, bottled water was analyzed and four PFCs (PFOA, PFNA,PFDA and PFHpA) were found at low levels (<1 ng/L). Because of higher levels found in drinking water at several locations, some provisional drinking water guideline values for PFOS and PFOA have already been established, e.g., in the UK, Bavaria, and Minnesota. Since PFCs are present both in food and drinking water, Tolerable Daily Intake values for PFOS and PFOA have also been proposed by several institutes in Europe and in the USA. The ingestion of dust through hand-to-mouth transfer from indoor house dust can also be a potential source of PFC exposure, especially for toddlers and children. In publications on PFCs in indoor dust, the mean PFOS and PFOA levels varied between 39 and 1,200 ng/g and between 11 and 220 ng/g, respectively. Overall, it is clear that there is still lack of PFC exposure data for food and beverages, which renders the assessment of the contribution of the diet to total human PFC exposure uncertain. It is, therefore, appropriate that several scientific projects have recently been launched that addresses the assessment of human exposure to PFCs and related compounds from dietary sources.
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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 · 1.92 Impact Factor
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ABSTRACT: Exposure to chemicals that cause rodent mammary gland tumors is common, but few studies have evaluated potential breast cancer risks in humans. The goal of this paper is to facilitate measurement of biomarkers of exposure to potential breast carcinogens in breast cancer studies and biomonitoring. We conducted a structured literature search to identify measurement methods for exposure biomarkers for 102 chemicals that cause rodent mammary tumors. To evaluate concordance, we compared human and animal evidence for agents identified as plausibly linked to breast cancer in major reviews. To facilitate future application of exposure biomarkers, we compiled information about relevant cohort studies. Exposure biomarkers have been developed for nearly three-quarters of these rodent mammary carcinogens. Methods have been published for 73 of the chemicals. Some of the others could be measured with modified versions of existing methods for related chemicals. Exposure to 62 has been measured in humans, 45 in a non-occupationally exposed population. US CDC has measured 23 in the US population. Seventy-five of the rodent mammary carcinogens fall into 17 groups, based on exposure potential, carcinogenicity, and structural similarity. Carcinogenicity in humans and rodents is generally consistent, although comparisons are limited because few agents have been studied in humans. We identified 44 cohort studies that have recorded breast cancer incidence and stored biological samples, with a total of over 3.5 million enrolled women. Exposure measurement methods and cohort study resources are available to expand biomonitoring and epidemiology related to breast cancer etiology and prevention.Environmental Health Perspectives 05/2014; 122(9). DOI:10.1289/ehp.1307455 · 7.03 Impact Factor
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ABSTRACT: A previously developed and validated methodology based on liquid chromatography coupled to high resolution mass spectrometry was used for determine the concentration levels of 14 perfluoroalkylated substances (PFASs) in a set of 48 breast milk samples collected from French women in the frame of the ELFE pilot study. In accordance with other similar studies conducted at european and international levels, PFOS, PFOA, and PFHxS were detected and quantified in most of the analyzed samples (90%, 98% and 100%, respectively), and appeared as major contributors to the total PFAS exposure (38%, 37%, 25%, respectively), whereas the other targeted PFAS were very rarely, if not, found at the limits of detection of the method. Also in agreement with other published data, the concentration levels measured for the detected substances varied from <0.05 to 0.33μg/L for PFOS (median=0.079), from <0.05 to 0.22μg/L for PFOA (median=0.075), and from 0.04 to 0.07μg/L for PFHxS (median=0.050). On the basis of this relatively limited data set, no statistically significant relation was observed between these exposure levels and developmental outcomes, in particular the weight at birth. Similarly, no relation was observed between the measured PFAS levels and various socio-demographical parameters including the consumption of seafood, alcohol, smoking, or socio-economical level. These results suggest a need for further research and better knowledge regarding the sources, pharmacokinetics, and factors of exposure for other substances belonging to this class of emerging contaminants.Chemosphere 03/2013; 91(6). DOI:10.1016/j.chemosphere.2013.01.088 · 3.50 Impact Factor