Perfluorinated compounds (PFCs) have taken worldwide attention in recent years. Several PFCs are being used in manufacturing food contact materials, including non-stick coatings (polytetrafluoroethylene (PTFE) or Teflon) for cookware and also their use in paper coatings for oil- and moisture-resistant. PFCs are suggested as a new class of Persistent organic pollutant (POP), where they are chemical stability and do not degrade well naturally hence may accumulate in the body and poses problems for human safety. Thus, it is necessary to assess the migration of PFCs from food contact articles to food under typical cooking conditions. The main objective of this investigation was to study the effect of cooking at prolonged use (repeating for ten times) in household Tefal utensils on leaching PFOA and PFOS compounds from the Teflon layer which coats the inner surface of utensils to food-contact such as tomatoes fruit as the acidic food and white dry beans as the non-acidic food without and with adding of table salt. Also, measurement the surface morphology of Tefal layer before and after cooking by using small shapes as a pattern of Tefal cookware which analyzed by X-ray Diffraction (XRD) and X-ray Microanalysis (EDX), as well Environmental Scanning Electron Microscopy (ESEM). The obtained results indicated that, when the repeat of cooking increased from 1 up to 10 times, the amounts of Perfluorinated compounds (PFOS and PFOA, especially PFOS) were progressively increased in the food contact (tomatoes paste or white dry beans) from the Tefal cookware. On the other side, the addition of table salt to the tested samples at all repeats of cooking (1, 5 and 10 times) caused a highly leaching of perfluorinated compounds from the Teflon layer to food-contact more than the same tested samples at the same conditions without salt. Therefore, the acidic food such as tomatoes paste was more effect on the amounts of both PFOS and PFOA in the food-contact than the non-acidic food. Before that, the ESEM images of coating surface of Tefal layer after repeat of cooking exhibited some damage.
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Family members have a certain period sharing similar environmental conditions, including indoor dust, contact with consumer products containing PFCs, as well as die- tary intake of foods and drinking water, leading to simi- lar exposure to PFOS and PFOA. Hence, significant cor- relations of exposure to PFOS and PFOA among family members were observed. However, lack of correlation of serum PFOS concentrations between father and mother, son, or daughter, suggested more unidentified factors affecting the body load of PFOS than PFOA, possibly relating to both the exposure routes and accumulation and elimination in human bodies of PFOS. Larger vari- ability in serum PFOS levels of fathers than the mothers and offspring support the hypothesis (Figure 2). Further, the results illustrated that potential sources of PFOS might exist in some working environment and make a larger difference of exposure of the fathers with different occupation, although the subjects in the present study were recruited from those without known occupational exposure to fluorine chemicals. Therefore, exposure to PFOS from different working environment need to be further studied.
Results: We found no association between serum levels of PFOA and PFOS and hypertension in either unadjusted or multivariable-adjusted analyses controlling for age, sex, race-ethnicity, body mass index, annual household income, moderate activity, total serum cholesterol, and serum cotinine. Compared with the lowest quartile, the multivariable-adjusted odds ratio (95% confidence interval) of hypertension in the highest quartile of exposure was 0.69 (0.41–1.17) for PFOA and 0.77 (0.37–1.61) for PFOS (all P-trend values .0.30).
A likely mechanism for development of such a high- level research strategy was included in proposed amendments to the 2018 U.S. Defense authorization bill. The intent of these amendments was to authorize a five-year national study of PFOA and PFOS exposures resulting from military use of PFAS- containing firefighting foam. While the passage of these amendments is a step in the right direction, this study, as described, is likely insufficient. If and when the study is carried out, its scope should be expanded to include a wider range of PFASs than
There are limited numbers of reports regarding airborne and indoor levels of PFOA and PFOS. Harada et al.  showed that the concentrations of PFOA detected within urban atmospheric particles were 50-fold higher than those of PFOS. The amounts of PFOA and PFOS in the respi- rable fraction (1.1–11.4 lm) ranged from 58.3 to 89.8% of the total amounts . The levels of PFOS and PFOA were significantly higher in the urban atmosphere of Oyamazaki than in the suburban atmospheres of Morioka and Fuku- chiyama [30, 32]. Across Japan, there was a tendency for PFOA to be the predominant contaminant of outdoor air, particularly in Osaka . Boulanger et al.  reported that the mean concentration of PFOS in particulate-phase air samples was 6.4 pg/m 3 (SD 3.3) in the Great Lakes. In Manchester, PFOA and PFOS were both detected at rela- tively high concentrations (341 and 46 pg/m 3 , respectively) .
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All women in the study gave birth to a live born child. Couples with unresolved infertility, spontaneous abortions, or stillbirths are therefore not studied. We were unable to include women with missing TTP, who were most likely to have conceived unexpectedly, but we found that their con- centrations of both PFOA and PFOS were approximately 10 % lower compared to those included. Exclusion of this particular group could underestimate the association if their TTP was short, and vice versa if it was long. However, inclusion of these women in the lowest TTP category did not strengthen the associations (Additional file 1 Table 4). Adding them to the highest TTP category removed the ob- served associations, which may be explained by the lower PFAA concentrations in these women. Recall of TTP during pregnancy may be imperfect, but the recall time period was short, and differential misclassification concern- ing TTP is unlikely since participants were unaware of exposure concentrations.
the Thomsen et al. study and the present study (94% vs. 34%) may be explained by relatively high PFOA exposures in our study population compared with the Norwegian mothers (Thomsen et al. 2010). Our data for mothers living in nonexposed areas are more comparable to the Thomsen et al. study; we estimated a 7% decrease in serum PFOA per month of breastfeeding, equivalent to a 60% decrease in PFOA concentrations after 12 months of breastfeeding. Recently, a 2–3% reduction in serum PFAA concentra tions per month of breastfeeding (with PFOA having the highest estimated decline of 2.4%) was reported in a study of 487 Norwegian mothers enrolled in the MoBa (Mother and Child Cohort Study) cohort (Brantsater et al. 2013) based on measured concentrations dur ing gestation and the total number of months of breastfeeding reported for all previous children. The estimated loss from lactation is in addition to loss from normal metabo lism and net excretion, which has been esti mated to be approximately 22–13% per year in adults following cessation of exposure, given a halflife of 2.3–3.8 years (Bartell et al. 2010; Olsen et al. 2007). Fei et al. (2010) reported that the duration of breastfeeding was negatively associated with serum PFOA and PFOS concentrations measured during pregnancy among 1,400 women enrolled in the Danish national birth cohort, but only among multiparous women. The authors sug gested that their findings could be explained if women who breastfed previous children for a relatively long time were also more likely to breastfeed the child included in the cohort study for a long period, and if their previous lactation also resulted in lower concentra tions of PFOA and PFOS during the index pregnancy. If so, their findings also would be consistent with those of the present study.
The mechanism of the effect of PFASs on neurobehav- ioral development remains unclear. In animal studies, some PFASs may affect the cholinergic or dopaminergic system, resulting in altered responses to nicotine or im- balanced expression of the acetylcholine/dopamine phenotype . PFASs also affect synaptogenesis and functional protein levels during neuron growth . PFOA and PFOS significantly increased the levels of synaptophysin and tau in the cerebral cortex and hippo- campus. Because these proteins are important for normal brain development, altered levels during a critical period of brain growth spurts could be one of the mechanisms of behavioral defects . Other possible mechanisms in- clude the endocrine-disrupting properties of PFASs in glucocorticoid, sex hormone  and thyroid hormone balance [35, 36]. Prenatal and postnatal exposure to PFASs interferes with thyroid hormone balance in humans, resulting in higher thyroid-stimulating hormone, de- creased total/free triiodothyronine, and decreased total/ Table 2 Maternal PFASs concentrations (ng/mL) at 12 – 16
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Up to thirteen PFASs were measured in plasma using high-performance liquid chromatography/tandem mass spectrometry at the Norwegian Institute of Public Health; these were PFOS, PFOA, perfluoroheptanoic acid (PFHpA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluoroundecanoic acid (PFUnDA), perfluoro- dodecanoic acid (PFDoDA), perfluorotridecanoic acid (PFTrDA), perfluorotetradecanoic acid (PFTeDA), per- fluorobutanoic acid (PFBA), perfluorohexane sulfonic acid (PFHxS), perfluoroheptane sulfonic acid (PFHpS), and perfluorooctane sulfonamide (PFOSA). A detailed description of the analytic method has been published . Among the substances measured, PFOA, PFOS, PFDA, PFHpS, PFHxS, PFNA, and PFUnDA were detected in more than 69% of samples; the six other PFASs were detected in less than 25% of the samples and were not included in the subsequent analysis. The limit of quanti- fication (LOQ) was 0.1 ng/ml for PFBA and 0.05 ng/ml for all others. For the seven most frequently detected PFASs, values below the LOQ were replaced by the LOQ divided by the square root of 2. The intra-assay coefficients of variation (CVs) of all seven PFASs were < 10% except PFUnDA (13.1%), and the inter-assay CVs of all seven PFASs were < 15% except PFUnDA (18.7%) and PFHpS (25.2%).
The results of epidemiological studies examining the neurodevelopmental effects of PFAS are few and incon- clusive. Fei et al. reported no associations between high pregnancy levels of PFOA (median (inter-quartile-range): 5.4 (4.0-7.1 ng/ml)) and PFOS (34.4 (26.6-44.5 ng/ml)) and developmental coordination disorder (assessed by DCDQ’07) at 7 years among a sub-sample of 537 partici- pants from the Danish National Birth Cohort , which is in accordance with our results. In the same study, no associations were observed between PFOS and PFOA and SDQ-total or any of the SDQ sub-scales, using top 10 percentile cut-offs . This is in accordance with our sensitivity analysis using top 10 percentile cut-off, whereas we observed associations between PFOA and Table 1 Characteristics of mothers and their children according to country (Continued)
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Perfluoroalkyl acids (PFAAs) are ubiquitous in the environment due to their extensive applications as industrial surfactants, surface coating agents, firefighting foams, additives, and several other products. Because of the prevalence, bioaccumulation and toxicity concern; certain agencies and governments has been considering regulating the PFAAs. For example European Commission has prohibited the use of perfluorooctane sulfonate (PFOS) as a constituent chemical in most consumer products  while U.S. has banned the manufacture of PFOS . The Stockholm convention has labeled PFOS as a persistent organic pollutant (POP). Recently, perfluoroocanoic acid (PFOA) has been enlisted in Contaminant Candidate List-3 by US EPA .
In recent years, numerous publications have appeared in which biological properties of PFCs are described; however, these are generally limited to PFOA and PFOS. These two substances are, to the best of our knowledge, the only PFCs that have been toxicologically examined in animal studies that would allow conclusions to be drawn about potential human toxicity. Data on short-chain PFCs that are apparently being substituted for longer chain molecules in indus- trial processes are, if available at all, only of a fragmen- tary nature. Because of their solubility in water and the increasingly wide spectrum and volume of their use, these short-chain PFCs deserve considerable study. This is particularly evident since they appear to be ubi- quitously distributed throughout the water pathway and can thus lead to an increased background contam- ination of the environment. Additionally, PFCs are being used in mixtures with varying compositions, making toxicological evaluations much more difficult. For this reason, standardized in vitro and in vivo meth- ods should be used and further developed in order to allow reliable conclusions to be drawn concerning the toxicity of the individual substances as well as of var- ious PFC mixtures. Consequently, an adequate toxico- logical evaluation of the total situation is presently not possible.
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Um eine gleichmäßige Verteilung dieser geringen Mengen an PFT zu erreichen, wurde die für 50 Kilogramm Futter benötigte Menge von PFOS und PFOA zunächst in Wasser gelöst und mit einer Komponente des Futters vermischt. Die Futtermischung enthält zu 37,34% Mais in Mehlform (siehe Tabelle 4). Das stärkereiche Maismehl weist günstige Wasserbindungseigenschaften auf und wurde deshalb als Trägerstoff gewählt. Um eine möglichst einheitliche Partikelgröße zu gewährleisten, wurden 500 Gramm Maismehl gesiebt und anschließend mit der PFT-Lösung vermischt. Das so behandelte Maismehl wurde in flachen Metallwannen über drei Tage unter einem Abzug getrocknet. In einem Futtermischer mit einer Kapazität von einem Kilogramm wurde das präparierte Maismehl auf ein Kilogramm hochgemischt, wobei zusätzlich bei der Trocknung verklumptes Mehl wieder fein zerkleinert wurde. Daraufhin konnte das Maismehl zu den übrigen Komponenten für 50 Kilogramm Futter in einen 100-Kilogramm- Mischer gegeben werden. Diese Prozedur wurde in aufsteigender Dosishöhe für die vier vorgesehenen Dosierungen in gleicher Weise wiederholt.
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CAS: Chemical Abstracts Service (system for identification of chemicals); DPSIR: drivers, pressure, status, impact and response; a causal framework for describing the interactions between society and the environment, adopted by the European Environment Agency; EC50: effect concentration causing 50% effect; MEC: measured environmental concentration; msPAF: multi-substance potentially affected fraction of species; NOEC: no effect concentration; PEC: predicted environmental concentration; PFOS: perfluorooctanesulfonate; PFOA: perfluorooctanoic acid; REACH: registration, evaluation, authorisation and restriction of chemicals; SSD: species sensitivity distribution; SVHC: sub- stances of very high concern; WFD: Water Framework Directive.
Laboratory analyses of serum PFAS were conducted by a commercial laboratory (Exygen Research). Samples collected at survey were analyzed for 10 PFAS including PFHxS, PFOA, PFOS, and PFNA. The analytical methods and quality control procedures employed by the laboratory have been described elsewhere (Flaherty et al. 2005; Frisbee et al. 2009). Briefly, the technique used solid-phase extraction followed by reverse-phase high-performance liquid chromatography/mass spectrometry. Over a range of 0.5-40 ng/mL, the coefficient of variation (CV) for PFOA was generally less than 10% for multiple samples measured in different batches. CV for PFHxS, PFOS, and PFNA were similar to those for PFOA. The LOD was 0.5 ng/mL for all of them. A quality assurance program was carried out by analysis of duplicate samples at AXYS Analytical Service Ltd. Details on the interlab reliability have been extensively reported in Frisbee et al. (2009).
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and PFOA in the samples of livers and muscles from two groups: (i) benthonic fish (Conger conger, Scyliorhinus canicula, Mullus surmuletus, Pagel- lus erythrinus and Scorpaena scrofa), (ii) pelagic fish (Mugil cephalus, Dentex dentex, Trachurus mediterraneus, Lamna nasus, Mustelus mustelus, Xiphias gladius, and Thunnus thynnus) originated in the Mediterranean Sea. Thus the results obtained were not specified by the individual species but, on an average, by the tissues of each group. The target analytes concentrations were comparable in the case of the muscle samples – PFOS/PFOA levels reached up to 14/12 µg/kg and 43/40 µg/kg in pelagic and benthonic groups, respectively. Un- like, with the muscle samples, higher PFOS levels in the livers of those – 40 µg/kg and 83 µg/kg were found, respectively. PFOA followed PFOS also in the liver samples at lower concentration levels – 13 µg/kg and 37 µg/kg in pelagic and benthonic groups, respectively. The results of the researches realised within Europe show the same or slightly higher levels in fish depending on the localities. Voogt et al. (2008) detected perfluorocarboxy- lated acids (PFNA, PFDA, PFUnA, PFDoA and PFTrDA) in cod which had been bought in the local supermarket in Flanders, the concentrations did not exceed 0.5 µg/kg. PFOS was found in this sample at the level of 2.6 µg/kg, PFOA was not detected. Llorca et al. (2009) investigated the livers and muscles of swordfish, stripped mullet, young hake, including hake roe, and anchovy ob- tained from retail fish markets and supermarkets in Spain. The highest concentration of PFOS, 23 µg/kg, was determined in the hake rRoe, but in term of fillets, a high content, 8.2 µg/kg, was found in the swordfish. Surprisingly, the measured levels of PFOS in the other samples were lower than those of PFOA and did not exceed levels of 1.3 µg/kg in the muscles and of 3.5 µg/kg in the livers (young hake), PFOA was found at maximum levels of 3.3 µg/kg and 5.2 µg/kg (young hake). In the sample of the stripped mullet, PFOS was not detected (Llorca et al. 2009).
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historically, PFOS is usually found to be the most abun- dant PFSA. PFSAs are stronger acids than PFCAs with pKa’s < 0 and are thus fully dissociated anions in envir- onmental media . Although properties vary with chain-length, the environmental fate and bioaccumu- lation behavior of PFSAs is broadly similar to that of PFCAs; PFSAs are persistent, are mostly distributed to surface waters , bind weakly to organic phases  compared to other persistent organic substances, are shown to bioaccumulate in the laboratory [71,72] and biomagnify in food webs [73,74]. Also similar to PFCAs, the global distribution of PFSAs is governed by a combination of direct release and transport as well as release and transport of precursors that subse- quently degrade to PFSAs . One difference in behavior is that PFSAs with perfluoroalkyl chains of the same length tend to sorb  and bioaccumulate [31,75,76] more strongly than PFCAs, [31,75,77] which is an effect of the different anionic head groups. Con- sequently, PFSAs with perfluoroalkyl chain lengths of C6 (i.e. perfluorohexane sulfonate) and higher are consid- ered to be long-chain (http://www.oecd.org/ehs/pfc/), whereas for PFCAs those with perfluoroalkyl chain lengths of C8 (i.e. PFOA) and higher are considered to be long-chain.
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The mode of action through which prenatal exposures to the PFAAs could alter testosterone concentrations remains to be explained, but may involve several pathways. One mode of action could involve alterations in choles- terol metabolism through PPARα activation. Alterations in the expression of genes associated with lipid transport, lipoprotein metabolism, and cholesterol biosynthesis in fetal livers of mice prenatally exposed to PFOA, consistent with PPARα activation, suggest opportunities of fetal programming of PFOA (Rosen et al. 2007). Another mode of action could involve activation of the PPARγ subtype. PPARγ is believed to regulate energy homeostasis and appears to be involved in fertility (Froment et al. 2006). PPARγ is expressed in adipose tissue, which is where conversion of about half of the body’s circulating testosterone occurs. Neither PFOS nor PFOA appears to increase mouse or human liver PPARγ activity in a cell assay study (Takacs and Abbott 2007). To our knowledge, it is unclear whether prenatal exposure to PFAA could alter adipose tissue PPARγ activity. Exposure to the PFAAs was not associated with menarche timing in our study population (Christensen et al. 2011), but it was inversely associated with birth weight (Maisonet et al. 2012), and birth weight could be regulated by PPAR activation. Last, other modes of action could include increased levels of gonadotropins (Vested et al. 2013) or reduced conversion to estrogens.
Potentially plausible mechanisms linking AKP to PFOA include shared biomechanical risk factors, such as malalignment and muscular dysfunction. These are acknowledged risk factors for AKP that are also thought to be important in the pathogenesis of PFOA [8-10]. Other potential mechanisms include cumulative mechanical loading and micro-trauma and propriocep- tive deficits. These remain relatively speculative. Our aim was not to test causal hypotheses but simply to systematically review the literature to describe the strength of evidence for a temporal association between AKP in younger adults and the subsequent development of PFOA. A clearly demonstrable association would provide impetus for further research on the underlying mechanisms with possible implications for the routine management of AKP problems and more widespread use of potential preventive strategies.
After 6 weeks, both groups showed a high level of ad- herence, with those in the foot orthoses group reporting slightly higher adherence compared to the flat insert group. These high adherence levels are similar to those reported in a previous study of foot orthoses for PFP, where participants reported wearing their foot orthoses for ≥ 60% of the study duration . Furthermore, the high adherence levels may also explain the low dropout rate (3.8%) in this study, which again has been reported in previous foot orthoses for PFP research [15, 16, 18]. In spite of the small loss to follow-up, we have allowed for a 20% dropout rate in our sample size calculation in order to account for the longitudinal study design, which is in line with previously published trial protocol papers investi- gating shoe inserts in PFP  and PFOA  populations. Despite successful recruitment, adherence to the inter- vention, and study completion, it should be highlighted
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