Diet and particularly seafood are major sources of perfluorinated compounds in humans
Introduction
Perfluorinated compounds (PFCs) have been used in a multitude of industrial applications and consumer products for more than 50 years due to their unique physico-chemical characteristics (Kissa, 2001). As a consequence, PFCs are widespread in the environment and in humans (Houde et al., 2006, Lau et al., 2007). Perfluorooctane sulfonic acid (PFOS) was recently included as a persistent organic pollutant (POP) in Annex B of the Stockholm Convention (Stockholm Convention on Persistent Organic Pollutants, 2010). Several PFCs have long elimination half-lives (e.g. 5.4 years for PFOS) in humans (Olsen et al., 2007) and animal studies have shown hepatotoxicity, developmental toxicity, immunotoxicity as well as effects on thyroid hormones (Lau et al., 2007). A number of studies have been conducted in recent years to investigate possible associations between exposure to PFC and human health effects. However, even in occupationally and presumably highly exposed workers, no consistent associations between PFC concentrations in blood and adverse health effects have been found (Lau et al., 2007). In studies on the general population, developmental- and hormonal effects have been examined. The results have been divergent, with some studies showing effects on birth outcome, thyroid function and subfecundity (Apelberg et al., 2007, Dallaire et al., 2009a, Fei et al., 2007, Fei et al., 2009, Stein et al., 2009, Washino et al., 2009), while others do not (Bloom et al., 2009, Emmett et al., 2006, Fei et al., 2008, Hamm et al., 2009, Inoue et al., 2004, Monroy et al., 2008, Nolan et al., 2009). Although information on human exposure pathways to PFCs is important for identification of high risk population sub groups and for the development of efficient control strategies to minimize human exposure of PFCs, these routes are currently insufficiently characterized.
Dietary exposure has been suggested as the main exposure route of PFCs in general populations (Fromme et al., 2009, Tittlemier et al., 2007, Trudel et al., 2008, Vestergren and Cousins, 2009), but the relative impact of different foods is not clear. Consumption of fish and marine mammals has in some studies been associated with increased concentrations of PFCs in human blood (Dallaire et al., 2009b, Falandysz et al., 2006, Rylander et al., 2009, Weihe et al., 2008), while results from Denmark showed positive associations between PFOS concentrations in serum and consumption of red meat, animal fat and snacks, and none with fish consumption (Halldorsson et al., 2008). In another study, a significant association, relying on one participant, was found between concentrations of perfluoroheptane sulfonic acid (PFHpS) and perfluorooctane sulfonic acid (PFOS) in plasma and consumption of fatty fish (Rylander et al., 2009). In the few studies, in which estimated individual dietary intakes of PFCs have been compared with corresponding serum concentrations, no significant relationship has been found (Fromme et al., 2007, Kärrman et al., 2009). So far, the only knowledge we have about the diet as a source of exposure to PFCs in Norwegians is a rough dietary intake estimate of the general Norwegian population, based on concentrations in 21 samples of Norwegian foods and beverages (Haug et al., in press). The highest concentrations in the food samples were found in cod liver, cod, beef, salmon and canned mackerel. This is in accordance with what has been observed in other studies world-wide (Ericson et al., 2008, Tittlemier et al., 2007), demonstrating that PFC concentrations generally are higher in fish than in other food groups. Compared to most other European populations, Norwegians consume much fish (EFSA, 2004), and fish might therefore be an important source of PFC exposure for Norwegians.
The main objectives of this study were: a) to investigate relationships between reported consumption of habitual food intakes with particular focus on fish and shellfish, and serum PFC concentrations in Norwegian adult men and women, b) to estimate individual dietary intakes of PFCs and identify food groups of main influence, c) to explore correlations between individual total dietary intakes of PFCs and measured concentrations of the corresponding PFCs in the subjects' blood and d) to investigate possible relationships between concentrations of chlorinated or brominated contaminants and PFCs in serum.
Section snippets
Study subjects and data collection
The participants in this study, The Norwegian Fish and Game Study part C (NFG study part C), were recruited from a previous study (NFG study part B) and are described in detail elsewhere (Knutsen et al., 2008, Kvalem et al., 2009). In brief, the NFG study part B included 5502 participants from coastal and inland areas in Norway who answered a semi-quantitative four page food frequency questionnaire (FFQ) with questions specifically related to habitual consumption of seafood and game (Bergsten,
Serum PFC concentrations
All serum samples contained PFOA, perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), PFUnDA, perfluorohexane sulfonic acid (PFHxS) and PFOS. PFHpS was detected in all but one sample. Perfluorooctane sulfonamide (PFOSA) was found in 92% of the samples, perfluorotridecanoic acid (PFTrDA) in 75%, perfluorododecanoic acid (PFDoDA) in 59% and PFHpA was found in 37% of the samples (Table 1). The remaining eight PFCs were not detected above LOQ in any of the samples. The median
Conclusions
For the first time, significant relationships between estimated dietary intakes and measured serum concentrations of PFOA, PFUnDA and PFOS were found, showing that dietary exposure might be an important source of PFCs in humans. Further, consumption of fish and shellfish was observed to be significantly associated with an increase in the concentrations of PFCs in serum. Seafood was also the largest contributor to the estimated total dietary intakes of PFOA, PFUnDA and PFOS. PFOS was recently
Acknowledgement
We greatly acknowledge all the donors who voluntarily contributed the blood samples and made an effort to fill in the extensive questionnaires, the contribution of Bryndis Eva Birgisdottir to intake calculations, as well as the Norwegian Food Control Authority and the Research Council of Norway for financial support.
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