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Background: Exposures to perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA), environmentally persistent chemicals detectable in the blood of most Americans, have been associated with several health outcomes. To offer insight into their possible biologic effects, we evaluated the metabolomic correlates of circulating PFOS and PFOA among 3,647 participants in eight nested case-control serum metabolomic profiling studies from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Methods: Metabolomic profiling was conducted by Metabolon Inc., using ultra high-performance liquid chromatography/tandem accurate mass spectrometry. We conducted study-specific multivariable linear regression analyses estimating the associations of metabolite levels with levels of PFOS or PFOA. For metabolites measured in at least 3 of 8 nested case-control studies, random effects meta-analysis was used to summarize study-specific results (1,038 metabolites in PFOS analyses and 1,100 in PFOA analyses). Results: The meta-analysis identified 51 and 38 metabolites associated with PFOS and PFOA, respectively, at a Bonferroni-corrected significance level (4.8x10-5 and 4.6x10-5, respectively). For both PFOS and PFOA, the most common types of associated metabolites were lipids (sphingolipids, fatty acid metabolites) and xenobiotics (xanthine metabolites, chemicals). Positive associations were commonly observed with lipid metabolites sphingomyelin (d18:1/18:0) (P = 2.0x10-10 and 2.0x10-8, respectively), 3-carboxy-4-methyl-5-pentyl-2-furanpropionate (P = 2.7x10-15, 1.1x10-17), and lignoceroylcarnitine (C24) (P = 2.6x10-8, 6.2x10-6). The strongest positive associations were observed for chemicals 3,5-dichloro-2,6-dihydroxybenzoic acid (P = 3.0x10-112 and 6.8x10-13, respectively) and 3-bromo-5-chloro-2,6-dihydroxybenzoic acid (P = 1.6x10-14, 2.3x10-6). Other metabolites positively associated with PFOS included D-glucose (carbohydrate), carotene diol (vitamin A metabolism), and L-alpha-aminobutyric acid (glutathione metabolism), while uric acid (purine metabolite) was positively associated with PFOA. PFOS associations were consistent even after adjusting for PFOA as a covariate, while PFOA associations were greatly attenuated with PFOS adjustment. Conclusions: In this large metabolomic study, we observed robust positive associations with PFOS for several molecules. Further investigation of these metabolites may offer insight into PFOS-related biologic effects.

Many epidemiology studies have investigated associations of perfluorooctanoate (PFOA) exposures with a variety of adverse health outcomes for participants in the C8 Health Project. The exposure concentrations (i.e., air and groundwater) used in these studies were determined primarily based on participant's residential locations. However, for residential addresses that could not be geocoded to the street level, the exposure concentrations were assigned based on population-weighted ZIP code centroid, which may result in exposure mischaracterization. The aim of this current study is to evaluate the potential impact of mischaracterized exposure concentrations due to geocoding uncertainty on the predicted serum PFOA concentrations and the epidemiological association between PFOA exposure and preeclampsia. For both workplace addresses and incompletely geocoded residential addresses, we used Monte Carlo (MC) simulation to assign alternate geographic locations within the reported ZIP code (instead of population-weighted ZIP code centroids) and the corresponding exposure concentrations. We found that mischaracterization of residential exposure due to population-weighted ZIP code centroid assignment had no significant impact on the serum PFOA concentration predictions and the epidemiological association of PFOA exposure with preeclampsia. In contrast, the uncertainty in workplace exposure moderately impacted the rank exposure among the participants. We observed a 41% increase in the average adjusted odds ratio of preeclampsia occurrence that may be due to differing proportions of cases (64.3%) and controls (54.5%) with workplace address geocodes during pregnancy. This finding suggests that differential exposure mischaracterization can be reduced by obtaining accurate exposure information such as street addresses and tap water consumption, for both workplaces and residences. The analysis we present is one approach for estimating the potential impacts of positional errors in a geocoding-based exposure assessment on exposure estimates and epidemiological study results.

We recently utilized a suite of environmental fate and transport models and an integrated exposure and pharmacokinetic model to estimate individual perfluorooctanoate (PFOA) serum concentrations, and also assessed the association of those concentrations with preeclampsia for participants in the C8 Health Project (a cross-sectional study of over 69,000 people who were environmentally exposed to PFOA near a major U.S. fluoropolymer production facility located in West Virginia). However, the exposure estimates from this integrated model relied on default values for key independent exposure parameters including water ingestion rates, the serum PFOA half-life, and the volume of distribution for PFOA. The aim of the present study is to assess the impact of inter-individual variability and epistemic uncertainty in these parameters on the exposure estimates and subsequently, the epidemiological association between PFOA exposure and preeclampsia. We used Monte Carlo simulation to propagate inter-individual variability/epistemic uncertainty in the exposure assessment and reanalyzed the epidemiological association. Inter-individual variability in these parameters mildly impacted the serum PFOA concentration predictions (the lowest mean rank correlation between the estimated serum concentrations in our study and the original predicted serum concentrations was 0.95) and there was a negligible impact on the epidemiological association with preeclampsia (no change in the mean adjusted odds ratio (AOR) and the contribution of exposure uncertainty to the total uncertainty including sampling variability was 7%). However, when epistemic uncertainty was added along with the inter-individual variability, serum PFOA concentration predictions and their association with preeclampsia were moderately impacted (the mean AOR of preeclampsia occurrence was reduced from 1.12 to 1.09, and the contribution of exposure uncertainty to the total uncertainty was increased up to 33%). In conclusion, our study shows that the change of the rank exposure among the study participants due to variability and epistemic uncertainty in the independent exposure parameters was large enough to cause a 25% bias towards the null. This suggests that the true AOR of the association between PFOA and preeclampsia in this population might be higher than the originally reported AOR and has more uncertainty than indicated by the originally reported confidence interval.

Oily wastewater treatment is a global challenge due to the substantial amount of effluent resulted from many industrial and domestic activities. To overcome the challenge of using existing treatment approach and fouling, superoleophobic coatings were fabricated. In this study, a superoleophobic membrane surface was obtained using the sol-gel technique with perfluorooctanoate (PFO), poly (diallyl dimethylammonium chloride) (PDADMAC), and nanoparticles as complex-polymer nanocomposites. The effects of coating cycles on the surface structure, chemical properties, surface chemistry, and oleophobicity of the surface were examined using field emission scanning electron microscopy (FESEM), Fourier transform infrared spectroscopy (FTIR), X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS) and oil contact angle measurement. The results showed that the coated layer successfully adhered to the substrate surface. However, the chemical stability with respect to oil contact angle (OCA) revealed a decline at pH 7 and pH 9 and maintained stability at pH 3. Besides, oil flux at 63.0 L/m2. h was achieved for PDADMAC-Al 2 O 3 /44 wt% PFO and the highest separation efficiency of 98% was obtained. Furthermore, the oil rejection decreases as the oil concentration increases from 1 to 3 g/L. OCA of 155° was obtained after 5 coating cycles. Apart from mitigating substrate fouling, the superoleophobic and superhydrophilic coating can be applied to a ceramic-based hollow fibre membrane and efficiently used for the separation of oil from oily wastewater. [Display omitted] [ABSTRACT FROM AUTHOR]

Background: The presence of perfluoroalkyl acids (PFAAs) in breast milk has been documented, but their lactational transfer has been rarely studied. Determination of the elimination rates of, these chemicals during breastfeeding is important and critical for assessing exposure in mothers, and infants., O b jectives: We aimed to investigate the association between breastfeeding and maternal serum, concentrations of perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS), perfluorononanoic, acid (PFNA), and perfluorohexane sulfonate (PFHxS). For a subset of the population, for, whom we also have their infants' measurements, we investigated associations of breastfeeding with, infant serum PFAA concentrations., Methods: The present analysis included 633 women from the C8 Science Panel Study who had, a child < 3.5 years of age and who provided blood samples and reported detailed information on, breastfeeding at the time of survey. PFAA serum concentrations were available for all mothers and, 8% (n=49) of the infants. Maternal and infant serum concentrations were regressed on duration of, breastfeeding. R esults: Each month of breastfeeding was associated with lower maternal serum concentrations, of PFOA (-3%, 95% CI:-5, -2%), PFOS (-3%, 95% CI:-3, -2%), PFNA (-2%, 95% CI, -2, -1%), and PFHxS (-1%, 95% CI:-2, 0%). The infant PFOA and PFOS serum concentrations, were 6% (95% CI: 1, 10%) and 4% (95% CI: 1, 7%) higher per month of breastfeeding., C onclusions: Breast milk is the optimal food for infants, but is also a PFAA excretion route for, lactating mothers and exposure route for nursing infants.

Among many short-term, subchronic, and chronic toxicology studies with ammonium perfluorooctanoate (PFOA), the gastrointestinal tract has not been identified as a target organ for PFOA-related toxicity in laboratory animals where the corresponding serum PFOA concentrations typically approach several orders of magnitude higher than the general human population. These lack of gastrointestinal tract-related findings were in direct contrast to an epidemiological observation where a positive trend was observed for ulcerative colitis, an idiopathic chronic inflammatory condition of the gut, in a Mid-Ohio River community whose drinking water contained higher levels of PFOA. This study was conducted to perform a histological reevaluation of large intestine sections in laboratory animals from 2 long-term toxicological studies: one was with Sprague Dawley rats that received ammonium PFOA in their diet for 2 years and the other one was with cynomolgus macaques that received daily capsules of ammonium PFOA for 6 months. In both studies, there was a lack of histological evidence of treatment-related inflammatory lesions that was suggestive of the occurrence of ulcerative colitis in these laboratory animals even under the most rigorous treatment schedules. These findings do not offer support for the biological plausibility of the epidemiological associations reported. [ABSTRACT FROM AUTHOR]

BACKGROUND: Drinking water in multiple water districts in the Mid-Ohio Valley has been contaminated with perfluorooctanoic acid (PFOA), which was released by a nearby DuPont chemical plant. Two highly contaminated water districts began granular activated carbon filtration in 2007. OBJECTIVES: To determine the rate of decline in serum PFOA, and its corresponding half-life, during the first year after filtration. METHODS: Up to six blood samples were collected from each of 200 participants from May 2007 until August 2008. The primary Source of drinking water varied over time for some participants; Our analyses were grouped according to water source at baseline in May-June 2007. RESULTS: For Lubeck Public Service District customers, the average decrease in serum PFOA concentrations between May-June 2007 and May-August 2008 was 32 ng/mL (26%) for those primarily consuming public water at home (n = 130), and 16 ng/mL (28%) for those primarily consuming bottled water at home (n = 17). For Little Hocking Water Association customers, the average decrease in serum PFOA concentrations between November-December 2007 and May-June 2008 was 39 ng/mL (11%) for consumers of public water (n = 39) and 28 ng/mL (20%) for consumers of bottled water (n = 11). The covariate-adjusted average rate of decrease in serum PFOA concentration after water filtration was 26% per year (95% confidence interval, 25-28% per year). CONCLUSIONS: The observed data are consistent with first-order elimination and a median serum PFOA half-life of 2.3 years. Ongoing follow-up will lead to improved half-life estimation.

Per- and polyfluoroalkyl substances (PFAS) are a class of chemicals that were widely used in manufacturing and are now present in the environment throughout the world. It is known that various PFAS are quantifiable in human in blood, but potential adverse health outcomes remain unclear. Sentinel and non-traditional model species are useful to study potential toxicity of PFAS in order to understand the relationship between environmental and human health. Here, we present a critical review of studies on the neurotoxicity of PFAS in sentinel and non-traditional laboratory model systems, including Caenorhabditis elegans (nematode), Dugesia japonica (planarian), Rana pipiens (frogs), Danio rerio and Oryzias melastigma (fish), and Ursus maritimus (polar bears). PFAS have been implicated in developmental neurotoxicity in non-traditional and traditional model systems as well as sentinel species, including effects on neurotransmitter levels, especially acetylcholine and its metabolism. However, further research on the mechanisms of toxicity needs to be conducted to determine if these chemicals are affecting organisms in a similar manner. Overall, findings tend to be similar among the various species, but bioaccumulation may vary, which needs to be taken into account in future studies by quantifying target organ concentrations of PFAS to better compare different species. Furthermore, data on the majority of PFAS is lacking in neurotoxicity testing, and additional studies are needed to corroborate findings thus far.

Graphical abstract Highlights • Gamma and electron beam irradiation effective under reductive conditions. • Strong effect of dose-rate observed in electron beam (EB) irradiation. • Support of radiolytic decomposition by formate or nitrate in treated PFOA solutions. • EB irradiation decomposes PFOA in seconds at initial ppm level. • A successful kinetic modeling can be carried out based on known rate constants. Abstract It has been demonstrated through the use of both gamma-rays and beam of accelerated electrons (EB) for the radiolytic decomposition of PFOA in diluted aqueous solutions that the most reactive species among the products of water radiolysis are hydrated electrons e aq. The reaction of PFOA with the hydrated electrons takes place with the largest yield in strongly alkaline deaerated solutions. The PFOA decomposition performed at an initial concentration level of 1 mg/L by γ-irradiation requires the use of absorbed doses below 10 kGy, which, depending on the activity of employed 60Co source, requires 2–3 h irradiation time. Similar results were obtained at pH 12 in the presence and also in the absence of t -butanol in the treated solutions. In the case of EB irradiation in a wide range of the absorbed doses (up to 100 kGy), a very pronounced effect of the dose-rate was observed, which can be attributed to various recombination reactions of the products of water radiolysis. A significant improvement in the yield of the PFOA decomposition by EB irradiation can be observed in the presence of trace amounts of nitrate or 100 mM of a formate in the treated solutions. In optimized conditions, about 70–80% decomposition of the initial level of 1 ppm of PFOA can be obtained with an irradiation using 100 kGy absorbed dose, which corresponds to about 5 s treatment with the use of an employed electron accelerator. The acute toxicity measurements and a kinetic modeling are presented, together with a suggestion of the mechanism of radiolytic decomposition of PFOA. [ABSTRACT FROM AUTHOR]

Perfluorooctanoate (PFOA) is a fully fluorinated eight-carbon fatty acid analog with exceptional stability toward degradation that has been used as an industrial surfactant and has been detected in environmental and biological matrices. Exposures to PFOA in the workplace and in the environment have continuously stimulated investigations into its potential human health hazards. In this article, the results of fifteen unpublished genotoxicity assays conducted with perfluorooctanoate (as either the linear or linear/branched ammonium salt (APFO) or the linear/branched sodium salt) are reported and include: seven mutation assays (three in vitro reverse mutation assays with histidine auxotrophic strains of Salmonella typhimurium, two in vitro reverse mutation assays with the tryptophan auxotrophic Escherichia coli WP2uvr strain, one in vitro mitotic recombination (gene conversion) assay with Saccharomyces cerevisiae D4, and an in vitro Chinese hamster ovary (CHO) HGPRT forward mutation assay); seven studies to assess potential for chromosomal damage (three in vitro CHO chromosomal aberration studies, an in vitro human whole blood lymphocyte chromosomal aberration study, and three in vivo mouse micronucleus assays); and an in vitro C3H 10T1/2 cell transformation assay. Although PFOA has not been demonstrated to be metabolized, all in vitro assays were conducted both in the presence and in the absence of a mammalian hepatic microsomal activation system. These assays were originally described in twelve contract laboratory reports which have been available via the United States Environmental Protection Agency public docket (Administrative Record 226) for over a decade; however, the details of these assays have not been published previously in the open scientific literature. With the exception of limited positive findings at high and cytotoxic concentrations in some assay trials which reflected the likely consequence of cytotoxic disruption of normal cellular processes and not a specific genotoxic effect, the results of the studies presented in this paper and other published results clearly demonstrate the absence of direct mutagenic or genotoxic risk associated with PFOA. This finding is consistent with the physical/chemical characteristics of PFOA and is supported by other published genotoxicity studies.

Two chronic dietary studies, conducted years apart, with ammonium perfluorooctanoate (APFO) in Sprague Dawley rats have been previously reported. Although both included male 300 ppm dietary dose groups, only the later study, conducted in 1990–1992 by Biegel et al., reported an increase in proliferative lesions (hyperplasia and adenoma) of the acinar pancreas. An assessment of the significance of the differences between both studies requires careful consideration of: the diagnostic criteria for proliferative acinar cell lesions of the rat pancreas (for example, the diagnosis of pancreatic acinar cell hyperplasia versus adenoma is based on the two-dimensional size of the lesion rather than distinct morphological differences); the basis for those criteria in light of their relevance to biological behavior; and the potential diagnostic variability between individual pathologists for difficult-to-classify lesions. A pathology peer review of male exocrine pancreatic tissues from the earlier study, conducted in 1981–1983 by Butenhoff et al., was undertaken. This review identified an increase in acinar cell hyperplasia but not adenoma or carcinoma in the earlier study. Both studies observed a proliferative response in the acinar pancreas which was more pronounced in the study by Biegel et al. Definitive reasons for the greater incidence of proliferative lesions in the later study were not identified, but some possible explanations are presented herein. The relevance of this finding to human risk assessment, in the face of differences in the biological behavior of human and rat pancreatic proliferative lesions and the proposed mechanism of formation of these lesions, are questionable.

Understanding sorption of PFOA on soil particles is crucial to evaluate its environmental risk. Here, sorption of PFOA onto ten agricultural soils was examined. The influence of soil physico-chemical properties on PFOA sorption was investigated. The sorption rate of PFOA followed a pseudo-second-order kinetics. Isotherm data of PFOA sorption was fitted with both Freundlich and linear models and the latter fitted better. The sorption-desorption of PFOA onto ten soil samples depended on soil organic carbon content and composition of soil minerals. The sorption and desorption isotherms of PFOA on ten soils were linear, except for the sorption of PFOA onto a few soils, which was described by the Freundlich equation with the parameter N >1. The main sorption mechanism of PFOA was hydrophobic interaction between the perfluorinated carbon chain and the organic matter of soil, as evidenced by the correlation between the solid-liquid distribution coefficient and the fraction of soil organic carbon. The sorption of PFOA in soils was highly irreversible. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Perfluorooctanoate (PFOA) has been associated with impaired lactation in mice. We examined whether maternal perfluorooctanesulfonate (PFOS) and PFOA concentrations correlated with duration of breastfeeding among women. METHODS: We randomly selected 1400 pregnant women from the Danish national birth cohort (1996–2002) and measured PFOS and PFOA concentrations in early pregnancy by using high performance liquid chromatography/tandem mass spectrometry. Self-reported data on the duration of any and exclusive breastfeeding were collected twice during telephone interviews around 6 and 18 months after the birth of the child. RESULTS: The duration of breastfeeding decreased with increasing concentrations of pregnancy PFOS and PFOA among multiparous women, for whom the adjusted odds ratios (OR) for weaning before 6 months of age were 1.20 (95% CI 1.06–1.37) per 10 ng/ml increase in PFOS concentrations and 1.23 (95% CI 1.13–1.33) per 1 ng/ml increase in PFOA concentrations. No consistent association was found for primiparous women. CONCLUSIONS: These findings suggest that PFOA and PFOS may reduce the ability to lactate, but could equally reflect reverse causation since no association was seen in primiparous women.

Objectives: Perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) have been widely used as industrial products, and are persistent organic pollutants due to their chemical stability. Previous studies suggested that PFOS and PFOA might disrupt thyroid hormone (TH) status. Although TH plays an important role in fetal growth during pregnancy, little attention has been paid to the relationships between maternal exposure to perfluorocarbons and TH statuses of mothers and fetuses. We investigated the effects of low levels of environmental PFOS and PFOA on thyroid function of mothers and infants. Methods: Of the eligible subjects in a prospective cohort, 392 mother-infant pairs were selected. Concentration of maternal serum PFOS and PFOA was measured in samples taken during the second and third trimesters or within 1 week of delivery. Blood samples for measuring thyroid stimulating hormone (TSH) and free thyroxine (FT4) levels were obtained from mothers at early gestational stage (median 11.1 weeks), and from infants between 4 and 7 days of age, respectively. Results: Median concentrations of PFOS and PFOA were 5.2 [95 % confidence interval (CI) 1.6-12.3] and 1.2 (95 % CI limitation of detection-3.4) ng/mL, respectively. Maternal PFOS levels were inversely correlated with maternal serum TSH and positively associated with infant serum TSH, whereas maternal PFOA showed no significant relationship with TSH or FT4 among mothers and infants. Conclusions: These findings suggest that PFOS may independently affect the secretion and balances of maternal and infant TSH even at low levels of environmental exposure. [ABSTRACT FROM AUTHOR]

The consumption of lactic acid bacteria capable of binding or degrading food-borne carcinogens may reduce human exposure to these deleterious compounds. In this study, 25 Lactobacillus strains isolated from human, plant, or dairy environments were investigated for their potential probiotic capacity against perfluorooctanoate (PFOA) toxicity. The PFOA binding, tolerance ability, and acid and bile salt tolerance were investigated and assessed by principal component analysis. Additionally, the effect of different pH levels and binding times was assessed. These strains exhibited different degrees of PFOA binding; the strain with the highest PFOA binding capability was Lactobacillus plantarum CCFM738, which bound to 49.40 ± 1.5 % of available PFOA. This strain also exhibited relatively good cellular antioxidative properties, acid and bile salt tolerance, and adhesion to Caco-2 cells. This study suggests that L. plantarum CCFM738 could be used as a potential probiotic in food applications against PFOA toxicity. [ABSTRACT FROM AUTHOR]

Background Previous studies on the exposure to perfluoroalkyl acids (PFAAs) and female fertility have provided conflicting results. We aimed to investigate the association between several PFAAs and time to pregnancy among nulliparous women. Methods From 2008 to 2013, we included 1372 women from the Aarhus Birth Cohort, Aarhus University Hospital, Denmark, who provided data on time to pregnancy and a blood sample before 20 gestational weeks. We measured the levels of 16 PFAAs in maternal serum and report data for seven compounds with quantifiable values in at least 50% of samples. Fecundability ratios according to PFAA levels (quartiles or continuous levels) were estimated by discrete-time survival analyses, adjusted for potential confounders. We further investigated the association between PFAAs and infertility (time to pregnancy>12 months or infertility treatment prior to the studied pregnancy) by multivariable logistic regression. Results Median levels of perfluorooctane sulfonate and perfluorooctanoate were 8.3 and 2.0 ng/mL. Overall, no obvious associations were found between any PFAAs and fecundability or infertility. Adjusted fecundability ratios (95% confidence intervals) were 1.09 (0.92–1.29) for perfluorooctane sulfonate and 1.10 (0.93–1.30) for perfluorooctanoate (highest versus lowest quartile). Conclusions We found no evidence of an association between present serum levels of PFAAs and longer time to pregnancy or infertility in nulliparous women. This study further adds to the sparse knowledge on PFAAs besides perfluorooctane sulfonate and perfluorooctanoate. [ABSTRACT FROM AUTHOR]

The distribution and fate of perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) were investigated in the water and sediment of Bohai Bay, China, during 2011–2013. A total of 360 water samples and 60 sediment samples were collected from 20 locations. The median concentrations of PFOS and PFOA were 4.8 and 12.15 ng/L in the water, and 2.65 and 0.62 ng/g-dry in the sediment, respectively. Significant enrichment were observed for PFOS and PFOA in water of sea surface microlayer. The concentrations of these two compounds showed an apparent gradient from nearshore to offshore stations. The correlation analysis and the distribution tendencies indicated that freshwater inflowing to the bay was the main source of PFOS and PFOA. The salinity of seawater and the total organic carbon (TOC) content of sediment heavily affected the spatial distribution and the partitioning of PFOS and PFOA in the sediment-water system. [ABSTRACT FROM AUTHOR]

While selected perfluoroalkyl acids/substances (PFAAs) like perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS) have been detected and measured in laboratory, a method to estimate the total concentration of PFAAs (∑PFAA) in serum has not been developed. Because of the health concerns associated with PFAAs and because of the inability of every laboratory to measure every PFAA as well as because of the non-availability of sensitive enough equipment to be able to detect very small amounts of certain PFAAs, it is of interest to know ∑PFAA. We used data from the National Health and Nutrition Examination Survey for the years 2005–2012 to develop regression models to estimate ∑PFAA by using the levels of PFOA and PFOS only. While data for 2005–2008 were used to develop regression models, data for 2009–2012 were used to evaluate the accuracy of the developed models. Over 63% of observed values for evaluation data were found to be within 10% of the predicted values. The model so developed can be used with just the knowledge of the age, gender, and concentrations of PFOA and PFOS. While the data used to develop the model were generated in U.S., the model can be used to estimate ∑PFAA for data collected in North America and Europe and probably elsewhere in the world. [ABSTRACT FROM AUTHOR]

Background: We previously demonstrated an association between plasma perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) and longer time to pregnancy (TTP) in a sample from the Danish National Birth Cohort (DNBC, 1996-2002). In this study we investigated this association in a new sample from the same cohort. Methods: Sample 1 consisted of 440 women, and Sample 2 consisted of 1161 women from whom we previously published the associations between PFOS or PFOA and TTP. We performed sample-specific and pooled analyses using discrete-time survival analyses to estimate fecundability ratios according to PFOS and PFOA quartiles, adjusted for potential confounders chosen guided by a directed acyclic graph. We also estimated odds ratios for infertility (TTP > 12 months or infertility treatment) according to PFOS and PFOA by multivariable logistic regression. Results: In Sample 1 PFOS was not associated with lower fecundability ratios or infertility, and there was a tendency towards longer TTP with increasing PFOA only in parous women. In Sample 2 previously reported associations were again seen. In the pooled analyses including both parous and nulliparous women fecundability ratios were 13-22 % lower for the three higher quartiles of PFOS or PFOA compared to the reference quartile. Conclusions: The pooled analyses were driven by the larger old sample, but we did not corroborate our previous finding of an association between high PFOS and longer TTP in the new sample. The tendency towards an association for PFOA and TTP in parous women may be due to reverse causation. Results from the new sample are more in line with the recent literature. [ABSTRACT FROM AUTHOR]

Rainbow trout ( Oncorhynchus mykiss ) confined to respirometer-metabolism chambers were dosed with perfluorooctanoate (PFOA) by intra-arterial (i.a.) injection and sampled to obtain concentration time-course data for plasma, urine, and expired water. The data were then analyzed by compartmental modeling to estimate rates of renal and branchial clearance. Averaged across all animals, the renal clearance rate (1.35 mL/h/kg) was more than ten times greater than the branchial clearance rate (0.12 mL/h/kg). The average whole-body elimination half-life was 12.6 d, which is somewhat longer than values obtained in previous studies with smaller trout. The tissue distribution of PFOA was assessed by collecting tissues at the end of chambered exposures and in a separate tissue time-course experiment. From the time-course study it appeared that an internal steady-state was established within 24 h of i.a. injection. Consistent with previous studies, the rank order of PFOA concentration in tissues at steady state was: plasma > liver > kidney > muscle. In a second set of chambered experiments, fish were exposed to PFOA in water to determine the rate of branchial uptake. Branchial uptake rates were too low to assess directly by measuring PFOA concentrations in inspired and expired water. Uptake rate constants (mean 0.19 L/d/kg; 0.1% uptake efficiency) were therefore estimated by compartmental modeling using plasma concentration time-course data and model parameters derived from the elimination experiments. It is clear from this effort that elimination of PFOA by trout occurs primarily via the renal route. This finding is consistent with numerous studies of mammals and suggests that trout possess membrane transporters that facilitate the movement of PFOA from plasma to urine. [ABSTRACT FROM AUTHOR]

Abstract: We examined whether perfluorooctanoate (PFOA) or perfluorooctane sulfonate (PFOS) had obesogenic effects and if they increased spontaneous intestinal tumorigenesis in the mouse model C57BL/6J-Min/+ (multiple intestinal neoplasia) after in utero exposure. The dams were exposed to PFOA or PFOS (0.01, 0.1 or 3.0mg/kg bw/day) by po gavage on GD1–17. The Min/+ and wild-type offspring were terminated at week 11 for examination of intestinal tumorigenesis or at week 20 for obesogenic effect, respectively. Body weights of the dams and pups were recorded throughout life. Food intake was determined at week 6 and 10. Blood glucose (non-fasted) was measured at week 6 and 11. No obesogenic effect of PFOA or PFOS was observed up to 20 weeks of age. PFOA or PFOS did not increase the incidence or number of tumors in the small intestine or colon of the Min/+ mice or affect their location along the intestines. Feed intake was not affected. There were some indications of toxicity of PFOA, but not of PFOS. There was lower survival of pups after 3.0mg/kg PFOA, lower body weight in pups after 3.0 and possibly 0.1mg/kg PFOA, and increased relative liver weight after 0.01 and possibly 0.1mg/kg PFOA. Plasma glucose was lower after 0.01 and 0.1mg/kg PFOA. In conclusion, exposure to PFOA and PFOS in utero with the doses used did not have obesogenic effect on either Min/+ or wild-type mice, at least not up to 11 or 20 weeks of age, nor increased intestinal tumorigenesis in Min/+ mice. [Copyright &y& Elsevier]

Highlights: [•] Perfluorooctanoate in methanol solutions decreased with length of storage. [•] Methyl perfluorooctanoate and methyl formate increased with length of storage. [•] Methyl perfluorooctanoate increased with increase in methyl formate. [•] Methyl perfluorooctanoate increased when perfluorooctanoate decreased. [•] Variation in the solutions stored around 5°C was smaller than that at room temp. [ABSTRACT FROM AUTHOR]

Fetal exposure to the perfluoroalkyl acids, perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA), has been associated with lower birth weight and lower weight and body mass index (weight (kg)/height (m)²) in early infancy. It is, however, unclear if exposure to prenatal PFOS and PFOA has a lasting influence on growth. We estimated the associations between the maternal plasma level of PFOS or PFOA and the children's body mass index, waist circumference, and risk of overweight at 7 years of age. A total of 1,400 women were randomly selected from the Danish National Birth Cohort among those who provided blood samples early in pregnancy and gave birth to liveborn singletons in 1996-2002. Weight and height information at 7 years was available for 811 children. Multiple linear and logistic regression models were used for analyses. Maternal PFOS and PFOA concentrations were overall inversely but nonsignificantly associated with the children's body mass index, waist circumference, and risk of overweight at 7 years of age. In conclusion, plasma levels of PFOS and PFOA in pregnant women did not seem to have any appreciable influence on their children's anthropometry at this point in childhood. [ABSTRACT FROM AUTHOR]

Abstract: A novel SnO2-Sb/CA electrode, possessing high surface area, strong adsorption capacity, good electrical conductivity and electrocatalytic activity, was firstly proposed for ultrasonic electrochemical oxidation (US-EC) of persistent high concentration perfluorooctanoate (PFOA) in this study. The optimal calcination temperature for sinking micro-sized SnO2-Sb particles existed on the surface of CA into the structure of CA as nanoparticles was 600°C. Its application on degrading PFOA (60mL of 100mgL−1) exhibited efficient electrocatalytic performance. After 5h electrolysis, over 91% of PFOA was degraded with a first-order kinetic constant of 0.52h−1 and over 86% TOC removal was achieved, while 47% PFOA removal and 33% TOC removal were obtained in traditional electrochemical (EC) process. The main role of determining the decomposition efficiency, i.e., the mass transport, hydroxyl radical (·OH) generation and electrode surface reaction, were greatly enhanced in US-EC system. Additionally, the generated intermediates existing on electrode surface and in solution were separately detected after different electrolysis time and the proper mechanism for efficient removing PFOA in US-EC process was investigated in detail. At early reaction stage (<0.5h), the intermediate products on SnO2-Sb/CA surface were C5F11COO−, C4F9COO−, C3F7COO−, C2F5COO−, CF3COO−, while in solution were C5F11COO−, C4F9COO−, C3F7COO−. At late reaction stage (>5h), the intermediates either on electrode surface or in solution became the same including C5F11COO−, C4F9COO−, C3F7COO−. [Copyright &y& Elsevier]

Background: Perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS) are persistent, synthetic industrial chemicals. Perfluorinated compounds are linked to health impacts that may be relevant to osteoarthritis, cartilage repair, and inflammatory responses. Objectives: We investigated whether PFOA and PFOS exposures are associated with prevalence of osteoarthritis, and whether associations differ between men and women. Methods: We used multiple logistic regression to estimate associations between serum PFOA and PFOS concentrations and self-reported diagnosis of osteoarthritis in persons 20-84 years of age who participated in NHANES during 2003-2008. We adjusted for potential confounders including age, income, and race/ethnicity. Effects by sex were estimated using stratified models and interaction terms. Results: Those in the highest exposure quartile had higher odds of osteoarthritis compared with those in the lowest quartile [odds ratio (OR) for PFOA = 1.55; 95% CI: 0.99, 2.43; OR for PFOS = 1.77; 95% CI: 1.05, 2.96]. When stratifying by sex, we found positive associations for women, but not men. Women in the highest quartiles of PFOA and PFOS exposure had higher odds of osteoarthritis compared with those in the lowest quartiles (OR for PFOA = 1.98; 95% CI: 1.24, 3.19 and OR for PFOS = 1.73; 95% CI: 0.97, 3.10). Conclusions: Higher concentrations of serum PFOA were associated with osteoarthritis in women, but not men. PFOS was also associated with osteoarthritis in women only, though effect estimates for women were not significant. More research is needed to clarify potential differences in susceptibility between women and men with regard to possible effects of these and other endocrine-disrupting chemicals. [ABSTRACT FROM AUTHOR]

Abstract: The sources and pathways of human exposure to perfluoroalkyl acids (PFAAs) are not well characterized, particularly in China where many perfluorinated substances are now manufactured. Here, isomer-specific PFAA analysis was used for the first time to evaluate exposure sources for Chinese people, by applying the method to 129 serum samples collected in two typical cities (Shijiazhuang and Handan) in North China. Among all samples, total perfluorooctanesulfonate (∑PFOS, mean 33.3ng/ml) was the predominant PFAA followed by perfluorohexanesulfonate (2.95ng/ml), total perfluorooctanoate (∑PFOA, 2.38ng/ml), and perfluorononanoate (0.51ng/ml). The level of ∑PFOS was higher than in people from North America in recent years. The mean concentrations of ΣPFAAs in the participants living in urban Shijiazhuang (59.0ng/ml) and urban Handan (35.6ng/ml) were significantly higher (p<0.001 and p=0.041, respectively) than those living in the rural district of Shijiazhuang (24.3ng/ml). The young female sub-population had the lowest ΣPFAA concentrations compared with older females and all males. On average, the proportion of linear PFOS (n-PFOS) was only 48.1% of ∑PFOS, which is much lower than what was present in technical PFOS from the major historical manufacturer (ca. 70% linear), and which is also lower than data reported from any other countries. Moreover, the proportion of n-PFOS decreased significantly with increasing ∑PFOS concentration in the serum samples (r=−0.694, p<0.001). Taken together, the data lend weight to previous suggestions that i) high branched PFOS content in serum is a biomarker of exposure to PFOS-precursors, and ii) that people with the highest ∑PFOS concentrations are exposed disproportionately to high concentrations of PFOS-precursors. On average, linear PFOA (n-PFOA) contributed 96.1% of ∑PFOA, significantly higher than in technical PFOA (ca. 75–80% linear), but lower than in Americans, suggesting higher exposure to electrochemically fluorinated PFOA than in other countries, including the United States. [Copyright &y& Elsevier]

Abstract: It is well established that exposure of mice to perfluorooctanoate (PFOA) or perfluorooctane sulfonate (PFOS) exerts adverse effects on the thymus and spleen. Here, we characterize the effects of a 10-day dietary treatment with these compounds (0.001–0.02%, w/w) on the bone marrow (BM) of mice. At a dose of 0.02%, both compounds reduced food consumption and caused atrophy of the thymus and spleen. At this same dose, histopathological and flow cytometric analysis revealed that (i) the total numbers of BM as well as the numbers of myeloid, pro/pre B, immature B and early mature B cells were all reduced significantly; and (ii) these adverse effects were reversed either partially or completely 10days after withdrawal of these compounds. At the lower dose of 0.002%, only PFOA reduced the B-lymphoid cell population. Finally, mice fed an amount of diet equivalent to that consumed by the animals exposed to 0.02% PFOA also exhibited atrophy of the thymus and spleen, and a reduction in the number of B-lymphoid population, without affecting myeloid cells. Thus, in mice, immunotoxic doses of PFOA or PFOS induce adverse effects on the myeloid and B-lymphoid cells in the BM, in part as a consequence of reduced food consumption. [Copyright &y& Elsevier]

Sorption of perfluorinated compounds (PFCs) on carbon nanotubes (CNTs) is critical for understanding their subsequent transport and fate in aqueous environments, but the sorption mechanisms remain largely unknown. In this study, the sorption of six PFCs on CNTs increased with increasing C-F chain length when they had a same functional group, and the CNTs with hydroxyl and carboxyl groups had much lower adsorbed amount than the pristine CNTs, indicating that hydrophobic interaction dominated the sorption of PFCs on the CNTs. Electrostatic repulsion suppressed the sorption of PFCs on the CNTs, resulting in the lower sorption with increasing pH. Hydrogen bonding interaction was negligible. The hydrophobic C-F chains can be closely adsorbed on the CNTs surface in parallel to the axis or along the curvature, making it impossible to form micelles on the CNT surface, leading to the lower sorption than other adsorbents. [Copyright &y& Elsevier]

Background: Recent studies have shown effects of prenatal exposure to perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) on infants in the general environmental levels. Laboratory animal studies have shown that exposure to PFOS and PFOA is associated with immunotoxic effects. Objectives: To investigate the relationship between maternal PFOS and PFOA levels and infant allergies and infectious diseases during the first 18 months of life. Cord blood immunoglobulin (Ig) E levels were also evaluated. Methods: We conducted a prospective cohort study of pregnant women from 2002 to 2005 in Sapporo, Japan. Maternal PFOS and PFOA levels were measured in relation to cord blood IgE concentrations (n=231) and infant allergies and infectious diseases (n=343). Characteristics of mothers and their infants were obtained from self-administered questionnaires and medical records. Development of infant allergies and infectious diseases was determined from self-administered questionnaires at 18 months of age. Concentrations of PFOS and PFOA in maternal serum and concentrations of IgE in umbilical cord serum at birth were measured. Results: Cord blood IgE levels decreased significantly with high maternal PFOA concentration among female infants. However, there were no significant associations among maternal PFOS and PFOA levels and food allergy, eczema, wheezing, or otitis media in the 18 month-old infants (adjusted for confounders). Conclusions: Although cord blood IgE level decreased significantly with high maternal PFOA levels among female infants, no relationship was found between maternal PFOS and PFOA levels and infant allergies and infectious diseases at age in 18 months. [Copyright &y& Elsevier]

Abstract: Objectives: To examine whether prenatal exposure to perfluorooctanesulfonate (PFOS) or perfluorooctanoate (PFOA) is associated with the occurrence of hospitalization for infectious diseases during early childhood. Methods: We randomly selected 1400 pregnant women and their offspring from the Danish National Birth Cohort (1996–2002) and measured PFOS and PFOA levels in maternal blood during early pregnancy. Hospitalizations for infection of the offspring were identified by the linkage to the National Hospital Discharge Register through 2008. Results: Hospitalizations due to infections were not associated with prenatal exposure to PFOA and PFOS. On the contrary, the relative risks of hospitalizations ranged from 0.71 to 0.84 for the three higher quartiles of maternal PFOA levels compared with the lowest, but no dose-response pattern was found. No clear pattern was observed when results were stratified by child’s age at infection, with the exception of an inverse association between maternal PFC levels and risk of hospitalization during the child’s first year of life. Conclusions: These findings suggest that prenatal exposure to PFOA or PFOS is not associated with increased risk of infectious diseases leading to hospitalization in early childhood. [ABSTRACT FROM AUTHOR]

BACKGROUND: Perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) are man-made, ubiquitous, and persistent contaminants in the environment, wildlife, and humans. Although recent studies have shown that these chemicals interfere with fetal growth in humans, the results are inconsistent. OBJECTIVES: Our goal was to investigate the correlation between relatively low levels of PFOS and PFOA in maternal serum and birth weight and birth size. METHODS: We conducted a hospital-based prospective cohort study between July 2002 and October 2005 in Sapporo, Japan. A total of 428 women and their infants were involved in the study. We obtained characteristics of the mothers and infants from self-administered questionnaire surveys and from medical records. We analyzed maternal serum samples for PFOS and PFOA by liquid chromatography--tandem mass spectrometry (LC/MS/MS). RESULTS: After adjusting for confounding factors, PFOS levels negatively correlated with birth weight [per log10 unit: β = --148.8 g; 95% confidence interval (CI), --297.0 to --0.5 g]. In addition, analyses stratified by sex revealed that PFOS levels negatively correlated with birth weight only in female infants (per log10 unit: β = --269.4 g; 95% CI, --465.7 to --73.0 g). However, we observed no correlation between PFOA levels and birth weight. CONCLUSION: Our results indicate that in utero exposure to relatively low levels of PFOS was negatively correlated with birth weight. [ABSTRACT FROM AUTHOR]

BACKGROUND: Perfluoroalkanoates, [e.g., perfluorooctanoate (PFOA)], are known peroxisome proliferators that induce hepatomegaly and hepatocarcinogenesis in rodents, and are classic nongenotoxic carcinogens that inhibit in vitro gap-junctional intercellular communication (GJIC). This inhibition of GJIC is known to be a function of perfluorinated carbon lengths ranging from 7 to 10. OBJECTIVES: The aim of this study was to determine if the inhibition of GJIC by PFOA but not perfluoropentanoate (PFPeA) observed in F344 rat liver cells in vitro also occurs in F344 rats in vivo and to determine mechanisms of PFOA dysregulation of GJIC using in vitro assay systems. METHODS: We used an incision load/dye transfer technique to assess GJIC in livers of rats exposed to PFOA and PFPeA. We used in vitro assays with inhibitors of cell signaling enzymes and antioxidants known to regulate GJIC to identify which enzymes regulated PFOA-induced inhibition of GJIC. RESULTS: PFOA inhibited GJIC and induced hepatomegaly in rat livers, whereas PFPeA had no effect on either end point. Serum biochemistry of liver enzymes indicated no cytotoxic response to these compounds. In vitro analysis of mitogen-activated protein kinase (MAPK) indicated that PFOA, but not PFPeA, can activate the extracellular receptor kinase (ERK). Inhibition of GJIC, in vitro, by PFOA depended on the activation of both ERK and phosphatidylcholine-specific phospholipase C (PC-PLC) in the dysregulation of GJIC in an oxidative-dependent mechanism. CONCLUSIONS: The in vitro analysis of GJIC, an epigenetic marker of tumor promoters, can also predict the in vivo activity of PFOA, which dysregulated GJIC via ERK and PC-PLC. [ABSTRACT FROM AUTHOR]

Abstract: Recent concerns have been raised concerning the widespread distribution of perfluorinated compounds in environmental matrices and biota. The compounds of interest include ammonium perfluorooctanoate (APFO, the ammonium salt of perfluorooctanoic acid, PFOA). APFO is used primarily as a processing aid in the production of fluoropolymers and fluoroelastomers. The environmental presence of perfluorooctanoate (PFO−, the anion of APFO) and its entry into the environment as APFO make quality aquatic toxicity data necessary to assess the aquatic hazard and risk of APFO. We conducted acute and chronic freshwater aquatic toxicity studies with algae, Pseudokirchneriella subcapitata, the water flea, Daphnia magna, and embryo-larval rainbow trout, Oncorhynchus mykiss, using OECD test guidelines and a single, well-characterized sample of APFO. Acute 48–96h LC/EC50 values were greater than 400mg/l APFO and the lowest chronic NOEC was 12.5mg/l for inhibition of the growth rate and biomass of the freshwater alga. Un-ionized ammonia was calculated to be a potential significant contributor to the observed toxicity of APFO. Based on environmental concentrations of PFO− from various aquatic ecosystems, the PNEC value from this study, and unionized ammonia contributions to observed toxicity, APFO demonstrates little or no risk for acute or chronic toxicity to freshwater and marine aquatic organisms at relevant environmental concentrations. [Copyright &y& Elsevier]

BACKGROUND: The widespread detection of perfluoroalkyl acids and their derivatives in wildlife and humans, and their entry into the immature brain, raise increasing concern about whether these agents might be developmental neurotoxicants. OBJECTIVES: We evaluated perfluorooctane sulfonate (PFOS), perfluorooctanoic acid (PFOA), perfluorooctane sulfonamide (PFOSA), and perfluorobutane sulfonate (PFBS) in undifferentiated and differentiating PC12 cells, a neuronotypic line used to characterize neurotoxicity. METHODS: We assessed inhibition of DNA synthesis, deficits in cell numbers and growth, oxidative stress, reduced cell viability, and shifts in differentiation toward or away from the dopamine (DA) and acetylcholine (ACh) neurotransmitter phenotypes. RESULTS: In general, the rank order of adverse effects was PFOSA > PFOS > PFBS ≈ PFOA. However, superimposed on this scheme, the various agents differed in their underlying mechanisms and specific outcomes. Notably, PFOS promoted differentiation into the ACh phenotype at the expense of the DA phenotype, PFBS suppressed differentiation of both phenotypes, PFOSA enhanced differentiation of both, and PFOA had little or no effect on phenotypic specification. CONCLUSIONS: These findings indicate that all perfluorinated chemicals are not the same in their impact on neurodevelopment and that it is unlikely that there is one simple, shared mechanism by which they all produce their effects. Our results reinforce the potential for in vitro models to aid in the rapid and cost-effective screening for comparative effects among different chemicals in the same class and in relation to known developmental neurotoxicants. [ABSTRACT FROM AUTHOR]

BACKGROUND: Recent studies have reported developmental toxicity among rodents dosed with perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA). OBJECTIVES: We examined the relationship between concentrations of PFOS and PFOA in cord serum (surrogates for in utero exposures) and gestational age, birth weight, and birth size in humans. METHODS: We conducted a hospital-based cross-sectional epidemiologic study of singleton deliveries in Baltimore, Maryland. Cord serum samples (n = 293) were analyzed for PFOS and PFOA by online solid-phase extraction, coupled with reversed-phase high-performance liquid chromatography-isotope dilution tandem mass spectrometry. Maternal characteristics and anthropometric measures were obtained from medical charts. RESULTS: After adjusting for potential confounders, both PFOS and PFOA were negatively associated with birth weight [per In-unit: β = -69 g, 95% confidence interval (CI), -149 to 10 for PFOS; β = -104 g, 95% CI, -213 to 5 for PFOA], ponderal index (per In-unit: β = -0.074 g/cm³ × 100, 95% CI, -0.123 to -0.025 for PFOS; β = -0.070 g/cm³ × 100, 95% CI, -0.138 to -0.001 for PFOA), and head circumference (per In-unit: β = -0.32 cm, 95% CI, -0.56 to -0.07 for PFOS; β = -0.41 cm, 95% CI, -0.76 to -0.07 for PFOA). No associations were observed between either PFOS or PFOA concentrations and newborn length or gestational age. All associations were independent of cord serum lipid concentrations. CONCLUSIONS: Despite relatively low cord serum concentrations, we observed small negative associations between both PFOS and PFOA concentrations and birth weight and size. Future studies should attempt to replicate these findings in other populations. [ABSTRACT FROM AUTHOR]

BACKGROUND: The presence of perfluorooctanesulfonate (PFOS), perfluorohexanesulfonate (PFHS), and perfluorooctanoate (PFOA) has been reported in humans and wildlife. Pharmacokinetic differences have been observed in laboratory animals. OBJECTIVE: The purpose of this observational study was to estimate the elimination half-life of PFOS, PFHS, and PFOA from human serum. METHODS: Twenty-six (24 male, 2 female) retired fluorochemical production workers, with no additional occupational exposure, had periodic blood samples collected over 5 years, with serum stored in plastic vials at -80°C. At the end of the study, we used HPLC-mass spectrometry to analyze the samples, with quantification based on the ion ratios for PFOS and PFHS and the internal standard 18O2-PFOS. For PFOA, quantitation was based on the internal standard 13C2-PFOA. RESULTS: The arithmetic mean initial serum concentrations were as follows: PFOS, 799 ng/mL (range, 145-3,490); PFHS, 290 ng/mL (range, 16-1,295); and PFOA, 691 ng/mL (range, 72-5,100). For each of the 26 subjects, the elimination appeared linear on a semi-log plot of concentration versus time; therefore, we used a first-order model for estimation. The arithmetic and geometric mean half-lives of serum elimination, respectively, were 5.4 years [95% confidence interval (CI), 3.9-6.9] and 4.8 years (95% CI, 4.0-5.8) for PFOS; 8.5 years (95% CI, 6.4-10.6) and 7.3 years (95% CI, 5.8-9.2) for PFHS; and 3.8 years (95% CI, 3.1-4.4) and 3.5 years (95% CI, 3.0-4.1) for PFOA. CONCLUSIONS: Based on these data, humans appear to have a long half-life of serum elimination of PFOS, PFHS, and PFOA. Differences in species-specific pharmacokinetics may be due, in part, to a saturable renal resorption process. [ABSTRACT FROM AUTHOR]

Perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) are detected in the environment and, more specifically, in wildlife and humans. The large variation in the reported biological half-lives for PFOA and PFOS has remained unexplored. In this study, we aimed to evaluate their partition from serum to bile and cerebrospinal fluid (CSF) in humans. Four pairs of serum and bile, and 7 pairs of serum and CSF were donated by patients. In considering biliary excretion, the median concentrations of PFOA and PFOS in serum samples were 3.8 and 23.2ng/mL, respectively, whereas those in bile samples were 1.0 and 27.9ng/mL, respectively. The median ratio of PFOS concentrations (bile/serum: 0.60) was significantly higher than that for PFOA, 0.21 (p <0.01). Biliary excretion rates for PFOA and PFOS in the present study subjects were estimated as 1.06 and 2.98mL/kg/day, respectively, which is significantly higher than serum clearances via urine in humans and might represent a major excretion route. Biliary reabsorption rates of PFOA and PFOS were estimated to be 0.89 and 0.97, respectively. In considering partition into the cerebrospinal fluid, the median concentrations of PFOA and PFOS in serum samples were 2.6 and 18.4ng/mL, respectively, whereas those in CSF samples were 0.06 and 0.10ng/mL, respectively. The median ratio of PFOS concentrations (CSF/serum: 9.1 (×10−3)) was comparable to that of PFOA, 17.6 (×10−3), suggesting that PFOA and PFOS cannot pass through the blood–brain barrier freely. In conclusion, the biliary excretion of these compounds was comparable in both rats and humans and the long half-lives in humans might be attributable to low levels of excretion in urine and high biliary reabsorption rates. [Copyright &y& Elsevier]

The purpose of this pilot study was to determine whether perfluorooctanesulfonate () and perfluorooctanoate () concentrations in American Red Cross blood donors from Minneapolis-St. Paul, Minnesota have declined after the 2000–2002 phase-out of perfluorooctanesulfonyl-fluoride (POSF, C8F17SO2F)-based materials by the primary global manufacturer, 3M Company. Forty donor plasma samples, categorized by age and sex, were collected in 2005, and PFOS and PFOA concentrations were compared to 100 (non-paired) donor serum samples collected in 2000 from the same general population that were analyzed at the time using ion-pair extraction methods with tetrahydroperfluorooctanesulfonate as an internal standard. Eleven of the 100 samples originally collected were reanalyzed with present study methods that involved 13C-labeled PFOA spiked into the donor samples, original samples, control human plasma, and the calibration curve prior to extraction, and was used as a surrogate to monitor extraction efficiency. Quantification was performed by high performance liquid chromatography tandem mass spectrometry methods. Among the 100 serum samples analyzed for PFOS, the geometric mean was 33. 1ngml−1 (95% CI 29. 8–36. 7) in 2000 compared to 15. 1ngml−1 (95% CI 13. 3–17. 1) in 2005 (p <0. 0001) for the 40 donor plasma samples. The geometric mean concentration for PFOA was 4. 5ngml−1 (95% CI 4. 1–5. 0) in 2000 compared to 2. 2ngml−1 (95% CI 1. 9–2. 6) in 2005 (p <0. 0001). The decrease was consistent across donors’ age and sex. To confirm these preliminary findings, additional sub-sets of year 2000 samples will be analyzed, and a much larger biomonitoring study of other locations is planned. [Copyright &y& Elsevier]

In order to understand better the pathways for transport of ammonium perfluorooctanoate (APFO) from a point source, a focused investigation of environmental media (water and soil) near a fluoropolymer manufacturing facility (Site) was undertaken. Methods were developed and validated at 2μgkg−1 [the limit of quantitation (LOQ)] in soil, and at 50ngl−1 in water. Environmental media were sampled from a public water supply well field located north of the Site, across a river. The data suggest that APFO air emissions from the Site are transported to the well field, deposited onto the soil, and then migrate downward with precipitation into the underlying aquifer. [Copyright &y& Elsevier]

Perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) are widespread contaminants in the environment, as well as in wildlife and in humans. The PFOS and PFOA concentrations were determined in historical human serum samples collected in Shenyang, China, in 1987 (n = 15), 1990 (n = 33), 1999 (n = 68) and 2002 (n = 119). The serum donors were students, faculty members and university workers. Since the serum PFOA and PFOS levels did not follow a normal or log-normal distribution, a nonparametric method was applied to analyze the historical trends. For the total male and female subjects, the median level of serum PFOA increased significantly from 0.08 μg/l in 1987 to 4.3 μg/l in 2002 (p < 0.05), while the median level of serum PFOS also increased significantly from 0.03 μg/l in 1987 to 22.4 μg/l in 2002 (p < 0.05). Both the serum PFOA and PFOS levels continued to increase from 1999 to 2002, with remarkable increases observed in females: 6.3-fold increase for PFOA and 13-fold increase for PFOS. In 2002, serum PFOA and PFOS concentrations of female subjects have increased to 4.9 μg/l and 22.4 μg/l in median, respectively, which are comparable to those in U.S.A. and Japan. For male subjects, serum PFOA and PFOS concentrations (1.6 μg/l and 8.3 μg/l in median, respectively) are comparable to those in Italy. The data from this study indicate that females are likely to experience higher exposure to these chemicals. [ABSTRACT FROM AUTHOR]

Interest in human exposure to perfluorinated acids, including perfluorobutanesulfonate (PFBS), perfluorohexanesulfonate (PFHS), perfluorooctanesulfonate (PFOS), and perfluorooctanoate (PFOA) has led to their measurement in whole blood, plasma and serum. Comparison of measurements in these different blood-based matrices, however, has not been rigorously investigated to allow for across-matrix comparisons. This research evaluated concentrations of PFBS, PFHS, PFOS, and PFOA in whole blood collected in heparin (lithium) and ethylenediamine tetraacetic acid (EDTA), plasma samples collected in heparin and EDTA, and serum (from whole blood allowed to clot). Blood samples were collected from 18 voluntary participants employed at 3M Company. Solid phase extraction methods were used for all analytical sample preparations, and analyses were completed using high-pressure liquid chromatography/tandem mass spectrometry methods. Serum concentrations ranged from: limit of quantitation (LOQ, 5ng/mL) to 25ng/mL for PFBS; LOQ (5ng/mL) to 75ng/mL for PFHS; LOQ (5ng/mL) to 880ng/mL for PFOS; and LOQ (5 or 10ng/mL) to 7320ng/mL for PFOA. Values less than the LOQ were not included in the statistical analyses of the mean of the ratios of individual values for the matrices. PFBS was not quantifiable in most samples. Serum to plasma ratios for PFHS, PFOS, and PFOA were 1:1 and this ratio was independent of the level of concentrations measured. Serum or plasma to whole blood ratios, regardless of the anticoagulant used, approximated 2:1. The difference between plasma and serum and whole blood corresponded to volume displacement by red blood cells, suggesting that the fluorochemicals are not found intracellularly or attached to the red blood cells. [Copyright &y& Elsevier]

Abstract: Perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) have recently received attention due to their widespread contamination in the environment, as well as in wildlife and humans. We measured the PFOS and PFOA concentrations in historically recorded human serum samples at an age range between 20 and 59 years collected in Kyoto, 20 persons per each time point (n =100), and also the PFOS and PFOA concentrations in human serum samples at an age range between 20 and 59 years from 10 locations throughout Japan (n =200). The historical samples collected from 1983 to 1999 demonstrated that the PFOA concentrations in males and females from Kyoto have increased 4.4-fold and 4.3-fold at a rate of increase of 0.49ng/ml/year and 0.42ng/ml/year, respectively. In contrast, serum concentrations of PFOS reached a plateau in the late 1980s. There are also regional differences in both the PFOS and PFOA serum concentrations. The concentrations in serum [geometric mean (geometric standard deviation)] (ng/ml) in 2003–2004 ranged from 7.6(1.6) in the town of Matsuoka in Fukui prefecture to 27.8(1.6) in Kyoto city, and ranged from 2.3(1.5) in Matsuoka to 14.5(1.3) in Osaka city for PFOS and PFOA, respectively. [Copyright &y& Elsevier]

Abstract: Turtles rank high in the river food chain, and are suitable for predicting the bioconcentrations of chemicals through the food chain. Trachemys scripta elegans () and Chinemys reevesii () were captured in a river in Japan, from September to October 2003 and April to June 2004. Surface water samples were collected simultaneously from the same sites at which the turtles were caught. Serum perfluorooctane sulfonate (PFOS) ranged from 2.4 to 486μg/L, while water PFOS levels ranged from 2.9 to 37ng/L. The geometric mean (GM) (geometric standard deviation, GSD) of the bioconcentration factor (BCF) of PFOS was 10,964 (2.5). In contrast, the perfluorooctanoate (PFOA) level in water ranged from 16.7–87,100ng/L, and serum PFOA ranged from <0.2 to 870μg/L. The GM (GSD) of the BCF of PFOA was 3.2 (7.9). Furthermore, the BCF of PFOA decreased as the PFOA level in the surface water increased. PFOS could be preferentially bioconcentrated in biota, and PFOA, slightly bioconcentrated. [Copyright &y& Elsevier]

Abstract: Perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) are detected in the environment, as well as more specifically in wildlife and humans. However, the toxicokinetic aspects of perfluorochemicals in humans are unclear. In this study, we measured concentrations of PFOA and PFOS in subjects who had lived in Kyoto city for more than 10 years. The serum concentrations of PFOA and PFOS were higher in females who menstruated than those who did not menstruation (), but in males this did not change by age; the levels in females reached those in males at an age of ⩾60 years. We then determined the renal clearances of PFOA and PFOS in young (20–40 years old, for each sex) and old (⩾60 years old, for each sex) subjects of both sexes. All young females were menstruating, while all old females were not. The renal clearances were 10−5-fold smaller than the glomerular filtration rate in humans, suggesting the absence of active excretion in human kidneys. The renal clearances of PFOA and PFOS were approximately one-fifth of the total clearance based on their serum half-lives, assuming a one-compartment model. The sex differences in renal clearance that have been reported in rats and Japanese macaques were not found in our human subjects. We tried to build a one-compartment pharmacokinetic model using the reported half-lives in human. The model was simple but could predict the serum concentrations in both males and females fairly well. We therefore suggest that an internal dose approach using a pharmacokinetic model should be taken because of the large species differences in kinetics that exist for PFOA and PFOS. [Copyright &y& Elsevier]

The purpose of this investigation was to determine whether there has been a change in the human blood concentration of perfluorooctanesulfonate (PFOS), perfluorooctanoate (PFOA), and five other fluorochemicals since 1974. Blood samples were collected in 1974 (serum) and 1989 (plasma) from volunteer participants of a large community health study. The study included a total of 356 samples (178 from each time period). These samples were analyzed by high-pressure liquid chromatography/tandem mass spectrometry methods. The median 1974 and 1989 fluorochemical concentrations, respectively, were as follows: PFOS, 29.5 ng/mL vs. 34.7 ng/mL; PFOA, 2.3 ng/mL vs. 5.6 ng/mL; perfluorohexanesulfonate (PFHS), 1.6 ng/mL vs. 2.4 ng/mL; and N-ethyl perfluorooctanesulfonamidoacetate (PFOSAA), less than the lower limit of quantitation (LLOQ; 1.6 ng/mL, vs. 3.4 ng/mL). For N-methyl perfluorooctanesulfonamidoacetate (M570), perfluorooctanesulfonamide, and perfluorooctanesulfonamidoacetate, median serum concentrations in both years were less than the LLOQ values (1.0, 1.0, and 2.5 ng/mL, respectively). Statistical analysis of 58 paired samples indicated that serum concentrations of PFOS, PFOSAA, PFOA, PFHS, and M570 were significantly (p < 0.001) higher in 1989 than in 1974. The data from 1989 were then compared with geometric mean fluorochemical concentrations of serum samples collected in 2001 from 108 American Red Cross adult blood donors from the same region. Except for M570, there were no statistically significant (p < 0.05) geometric mean fluorochemical concentration differences between the 1989 and 2001 samples. In conclusion, based on this study population, PFOS and other serum fluorochemical concentrations have increased between 1974 and 1989. Comparison with other regional data collected in 2001 did not suggest a continued increase in concentrations since 1989. [ABSTRACT FROM AUTHOR]