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Survey and environmental/health assessment of fluorinated substances in impregnated consumer products and impregnating agents 7 Human exposure
The pathways leading to general human exposure to polyfluorinated chemicals, including PFOS, PFOA and telomers are not well-known (Butenhoff et al. 2006). 7.1 Consumer productsThe contribution from consumer products containing these chemicals may be significant. PFOA and other polyfluorinated chemicals can be part of products either - because the product is treated with fluorinated compounds due to intentional application, or - in form of an unintended impurity, or - due to degradation of precursor compounds such as FTOHs. It is not always possible to distinguish between these cases, since recipes of technical applications are mostly confidential or the actual composition of the used mixture of active compounds confidential. Impregnation of all-weather-clothes, textiles, tents, footwear, furniture and carpets are among the most important uses of polyfluorinated chemicals. Direct skin exposure from product use or inhalation of aerosols from impregnation spray cans may occasionally be an important route of exposure but it is difficult to quantify, however, high concentrations of perfluorinated compounds have been measured in indoor air and dust. A study performed by Dinglasan-Panlilio and Mabury (2006), indicates the potential for a significant amount of fluorinated alcohols to be released as residuals from a suite of fluorinated materials that are industrially applied and commercially available and hence contribute substantially to the atmospheric burden of FTOHs. It was determined that the examined fluorinated materials contained 0.04-3.8% residual polyfluorinated telomer alcohol (dry mass basis). The seven materials were:
This study also suggests that direct exposure of the general population to these compounds is plausible, if these materials are applied in homes and are out gassing after treatment of surfaces, including carpet, textiles, or paper products. Metabolism of these volatile precursors could then lead to the perfluorinated acids detected in human blood samples worldwide. 7.2 Air exposureThe daily intake of PFOS from air exposure in Japan was calculated to 10-100 pg/day, which would result in 1.2-12 ng/L excess of plasma PFOS levels (Sasaki et al. 2003). The potential exposure of humans from indoor air of these chemicals was calculated in the study of Shoeib et al. (2005b); see Table 7: Table 7: Calculated intake (ng/d) of PFOS derivatives via inhalation and intake of dust (Shoeib et al. 2005b).
The results show that adults will inhale more PFOS, and children had a higher intake with dust. Based on body weight, children had a 5-10 times higher PFOS intake than adults. Concerning telomer alcohols the child intakes were estimated to 4.9, 8.0 and 4.6 ng/d for 6:2, 8:2 and 10:2 FTOH, respectively. 7.3 Non-stick cookwareThe chemical resistance, non-stick properties and thermal stability of fluoropolymers (polytetrafluoroethylene, PTFE, Teflon) have lead to several applications in dental practice and consumer products. The most publicly well-known occurrence of perfluorinated chemicals is probably PFOA as impurity in the non-stick surface layer of fluoropolymer treated cookware, such as frying pans. DuPont, the producer of the polymer, has detected PFOA content of 4–75 µg/kg in PTFE cookware (Begley et al. 2005). However, another study by DuPont of fluoropolymer treated cookware could, however, not at all detect PFOA under simulated cooking conditions (Powley et al. 2005). In a recent study by Sinclair et al. (2007) gas-phase release of PFOA, 6:2 FTOH, and 8:2 FTOH were measured from heating new nonstick frying pans. PFOA was reported to vaporize at 189 °C and decompose at >234 °C. PFOA, 6:2 FTOH and 8:2 FTOH were released into the gas phase at 7-337 ng (11-503 pg/cm²), <10-97 ng (<15-204 pg/cm²) and 40-298 ng (42-625 pg/cm²), respectively, per pan from four brands of nonstick frying pans during first use. This suggests that residual PFAS is released from the PTFE coating to the gas phase under the normal cooking temperatures. Gas-phase concentration of PFAS varied depending on the frying pan brand, which suggests that the sintering conditions (temperature, pressure, and duration) used in the coating of fluoropolymers may have an influence on the release of PFAS. In addition, PFOA was detected in water boiled for 10 minutes in nonstick pan brands. A pan in stainless steel did not release any PFAS at even higher temperature. Larsen et al. (2005) detected small amounts of PFOA (up to 140 ppb) in extracts of PTFE, obtained after applying pressure and increased temperatures to the material. A later study by The Norwegian Institute of Public Health (2007) goes in further detail about these findings. In a worst case scenario, the new study showed that an adult human would be exposed to 66 ng PFOA/kg bw, when drinking 100 ml water cooked in a Teflon coated pan. It was, however, surprisingly concluded that even at an assumption of 100% uptake of PFOA that being no essential intake route for humans. 7.4 Paper impregnation and migration into foodPerfluorochemicals are used to treat paper to improve its moisture and oil barrier properties. In particular, papers used in contact with high-fat content foods and feeds tend to be treated with fluorotelomer or fluorotelomer-based paper additives/coatings to prevent oil stains or oil soak through the paper. Food wrappers may be an important source of perfluorinated chemicals in humans (Renner 2007b). Typically, these fluorotelomer paper coatings/additives are either very low molecular weight fluorotelomers, which are mixtures of C6-, C8-, C10- and C12-perfluorinated chemicals, or high molecular weight polymers with fluorotelomer-based side chains (Begley et al. 2005; D’Eon and Mabury 2007). Fluorotelomer-based paper coating/additive formulations may before application onto paper have very high PFOA content (88-160 mg/kg), but during normal application rates this amount of PFOA will be diluted by about 300 times on the final paper product (Begley et al. 2005). Before 2000 for example, a Canadian study of fast food composites revealed that more than 55% of the composites contained N-ethyl perfluorooctane sulfonamide (EtFOSA). The highest level measured (23.5 mg/kg) was in a pizza. The degradation product or impurity PFOS was also detected in three samples. Most samples after 2000 were free of these contaminants, because fluorotelomers have since substituted PFOS (Tittlemier et al. 2003, 2006). A well-known occurrence of perfluorinated chemicals and telomers is as greaseproof additive (mg quantities) in microwave popcorn bags, from which the chemicals can be released gradually during microwave heating and leak into the food or found in the vapors (Sinclair et al. 2007). One of the three brands investigated did release 16 ng PFOA, 223 ng 6:2 FTOH and 258 ng 8:2 FTOH. Another did not release anything. In the highly contaminated brand the packaging paper contained seven PFCAs (PFPeA, PFHpA, PFOA, PFNA, PFDA, PFUnA and PFDoA) and the two telomers in concentrations from 0.4-4.7 ng/cm² before cooking. 7.5 Food intakeFood may also be polluted by PFCs via the environment. A study from Poland (Falandysz et al. 2006) reports high level of perfluorinated chemicals in cod and eider duck from the Baltic, and people from Gdansk, who eat much fish from the Baltic Sea had about three times higher levels of perfluorinated chemicals in their blood than a reference population. 7.6 Drinking waterA Japanese study has shown that consumption of drinking water obtained from a polluted river may lead to a significantly increased daily intake of 0.2-1 mg PFOS/day and may contribute 8-16 µg PFOS/L to blood serum levels and result in a 25-50% rise in normal levels (Harada et al. 2003). The New Jersey Department of Environmental Protection has recently recommended a drinking water guidance level of 0.04 µg/L (Renner 2007a). 7.7 Overall exposure scenariosIn a recent PhD thesis the total average internal exposures to PFOS and PFOA in humans were assessed by using a Scenario-Based Risk Assessment (SceBRA) (Horowitz 2007). The modelled average total internal exposure to PFOS was in the range of 17 ng/kg bw/day (adults) to 66 ng/kg bw/day (infants). The pathway contributing most to the internal exposure to PFOS in adults was ingestion of food (>98%). The modelled internal exposure to PFOA is in the range of 1 ng/kg bw/day (adults) to 4 ng/kg bw/day (infants). For PFOA the pathway ingestion of food is also the main contributor (>75%) to the total internal exposure. Oral exposure from hand-to-mouth contact with carpets and incidental ingestion of dust contribute to some extent to the exposure of infants, toddlers, and children. The study concludes that the exposures modelled with SceBRA and exposures deduced from measured blood serum levels correspond well for PFOS, but for PFOA the modelled exposures are one order of magnitude lower than the exposures deduced from the measured blood levels. Possible explanations are either overlooked exposure pathways or contribution from precursor compounds, which have not been included in the Horowitz study.
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