Phytotoxicity of PFOS and PFOA to Brassica chinensis in different Chinese soils

PFOS and PFOA are potential persistent organic pollutants that have raised many concerns in recent years. Research focusing on phytotoxicity of PFOS and PFOA to higher plants is necessary for their risk assessments. However, few toxicity data exist for PFOS or PFOA and higher plants. Here we investigated phytotoxicity of PFOS and PFOA to Brassica chinensis root growth in six different Chinese soils varying widely in soil properties using a standardized root length assay. The effective concentrations of added PFOS and PFOA causing 50% inhibition (EC₅₀) ranged from 95 to >200 mg kg⁻¹ for PFOS and from 107 to 246 mg kg⁻¹ for PFOA, respectively, representing more than 2.1- and 2.3-fold variation among the tested soils. Regressions of soil PFOS and PFOA toxicity threshold values (EC_x and NOECs) with various soil properties showed that the amount of organic matter was the most significant factor affecting their toxicity to B. chinensis.     

Alterations in Differentially Expressed Genes After Repeated Exposure to Perfluorooctanoate and Perfluorooctanesulfonate in Liver of Oryzias latipes

Perfluorooctanoate (PFOA) and perfluorooctanesulfonate (PFOS) are considered biologically toxic due to their persistence in the environment. The effects of repeated exposure to these compounds on differentially expressed genes (DEGs) were investigated in liver of the medaka, Oryzias latipes. In this study, seven genes—except for cytochrome P450 3A (CYP450 3A)—were identified as DEGs that were downregulated in response to 15- and 30 days exposures to PFOA and/or PFOS. Four DEGs (c-type lysozyme, EF-1β, complement component C3-1, and NADH dehydrogenase subunit 1) returned to basal levels after 15 days of recovery after 30 days of exposure to the compounds. In contrast, three DEGs (transferrin, alcohol dehydrogenase class VI, and CYP450 3A) were still upregulated by PFOS after 15 days of recovery. In addition, the effect of PFOS showed more accumulation after 15 days of recovery than PFOA. These data suggest that PFOS accumulates more in tissue than PFOA and causes high cellular toxicity by way of suppression of the genes encoding transferrin and alcohol dehydrogenase class VI, whereas there is upregulation of cytochrome P450 3A.     

Toxicity of perfluorooctane sulfonic acid and perfluorooctanoic acid on freshwater macroinvertebrates (Daphnia magna and Moina macrocopa) and fish (Oryzias latipes)

Because of their global distribution, persistence, and tendency to bioaccumulate, concerns about perfluorooctane sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA) are growing. We determined the toxicity of PFOS and PFOA in several freshwater organisms, including two cladocerans, Daphnia magna and Moina macrocopa, and the teleost Oryzias latipes. In general, PFOS is approximately 10 times more toxic than PFOA in these organisms. In M. macrocopa, the median lethal concentration (LC50) was 17.95 mg/L for PFOS and 199.51 mg/L for PFOA. Moina macrocopa exhibited greater sensitivity than D. magna to both perfluorinated compounds in both acute and chronic exposures. In the 48-h acute toxicity test, M. macrocopa was approximately two times more sensitive than D. magna. In the 7-d chronic toxicity test, M. macrocopa showed significant reproductive changes at 0.31 mg/L for PFOS, which was approximately seven times lower than the effect concentrations observed over the 21-d exposure in D. magna. Two-generation fish toxicity tests showed that parental exposure to both compounds affected the performance of offspring. Unexposed progeny-generation (F1) fish exhibited elevated mortality and histopathological changes that were correlated with exposure in the parental generation (F0). Continuous exposure from F0 through F1 generations increased the extent of adverse effects. Considering the persistent nature of PFOS and PFOA, more research is required to determine potential consequences of long-term exposure to these compounds in aquatic ecosystems.     

Impacts of two perfluorinated compounds (PFOS and PFOA) on human hepatoma cells: cytotoxicity but no genotoxicity?

Perfluorinated compounds (PFCs) and particularly two of them, perfluoroctanoate (PFOA) and perfluorooctanesulfonate (PFOS), have been widely produced and used since 1950. They both persist in the environment and accumulate in wildlife and humans. The toxicity of PFOS and PFOA has been studied extensively in rodents with several adverse effects mainly a hepatocarcinogenic potential. Carcinogenic effects are not highlighted in humans' studies. In this study, we investigated the cytotoxic and genotoxic effects of PFOA and PFOS using human HepG2 cells after 1 or 24h of exposure. The cytotoxic and genotoxic potential was evaluated by MTT assay, single cell gel electrophoresis (SCGE) assay and micronucleus assay respectively. We measured the intracellular generation of reactive oxygen species (ROS) using dichlorofluorescein diacetate to identify a potential mechanism of toxicity. We observed a cytotoxic effect of PFOA and PFOS after 24h of exposure starting from a concentration of 200 μM (MTT: -14.6%) and 300 μM (MTT: -51.2%) respectively. We did not observe an increase of DNA damage with the comet assay or micronucleus with the micronucleus assay after exposure to the two PFCs. After 24h of exposure, both PFOA and PFOS highlight a decrease of ROS generation (-5.9% to -23%). We did not find an effect after an hour of exposure. Our findings show that PFOA and PFOS exert a cytotoxic effect on the human cells line HepG2 but nor PFOA or PFOS could induce an increase of DNA damage (DNA strand breaks and micronucleus) or reactive oxygen species at the range concentration tested. Our results do not support that oxidative stress and DNA damage are relevant for potential adverse effects of PFOA and PFOS. These results tend to support epidemiological studies that do not show evidence of carcinogenicity.     

Relationships of perfluorooctanoate and perfluorooctane sulfonate serum concentrations between mother-child pairs in a population with perfluorooctanoate exposure from drinking water

Background: There are limited data on the associations between maternal or newborn and child exposure to perfluoroalkyl acids (PFAAs), including perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS). This study provides an opportunity to assess the association between PFAA concentrations in mother–child pairs in a population exposed to PFOA via drinking water.Objectives: We aimed to determine the relationship between mother–child PFAA serum concentrations and to examine how the child:mother ratio varies with child’s age, child’s sex, drinking-water PFOA concentration, reported bottled water use, and mother’s breast-feeding intention.Methods: We studied 4,943 mother–child pairs (children, 1–19 years of age). The child:mother PFAA ratio was stratified by possible determinants. Results are summarized as geometric mean ratios and correlation coefficients between mother–child pairs, overall and within strata.Results: Child and mother PFOA and PFOS concentrations were correlated (r = 0.82 and 0.26, respectively). Up to about 12 years of age, children had higher serum PFOA concentrations than did their mothers. The highest child:mother PFOA ratio was found among children ≤ 5 years (44% higher than their mothers), which we attribute to in utero exposure and to exposure via breast milk and drinking water. Higher PFOS concentrations in children persisted until at least 19 years of age (42% higher than their mothers). Boys > 5 years of age had significantly higher PFOA and PFOS child:mother ratios than did girls.Conclusion: Concentrations of both PFOA and PFOS tended to be higher in children than in their mothers. This difference persisted until they were about 12 years of age for PFOA and at least 19 years of age for PFOS.     

Per- and polyfluoroalkyl substances impact human spermatogenesis in a stem-cell-derived model

Per- and polyfluoroalkyl substances (PFASs) represent a highly ubiquitous group of synthetic chemicals used in products ranging from water and oil repellents and lubricants to firefighting foam. These substances can enter and accumulate in multiple tissue matrices in up to 100% of people assessed. Though animal models strongly identify these compounds as male reproductive toxicants, with exposed rodents experiencing declines in sperm count, alterations in hormones, and DNA damage in spermatids, among other adverse outcomes, human studies report conflicting conclusions as to the reproductive toxicity of these chemicals. Using an innovative, human stem-cell-based model of spermatogenesis, we assessed the effects of the PFASs perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), and a mixture of PFOS, PFOA, and PFNA for their impacts on human spermatogenesis in vitro under conditions relevant to the general and occupationally exposed populations. Here, we show that PFOS, PFOA, PFNA, and a mixture of PFOS, PFOA, and PFNA do not decrease in vitro germ cell viability, consistent with reports from human studies. These compounds do not affect mitochondrial membrane potential or increase reactive oxygen species generation, and they do not decrease cell viability of spermatogonia, primary spermatocytes, secondary spermatocytes, or spermatids in vitro under the conditions examined. However, exposure to PFOS, PFOA, and PFNA reduces expression of markers for spermatogonia and primary spermatocytes. While not having direct effects on germ cell viability, these effects suggest the potential for long-term impacts on male fertility through the exhaustion of the spermatogonial stem cell pool and abnormalities in primary spermatocytes.

Abbreviations: CDC: Centers for Disease Control; DMSO: dimethyl sulfoxide; GHR: growth hormone receptor; hESCs: human embryonic stem cells; PFASs: per- and polyfluoroalkyl substances; PFCs: perfluorinated compounds; PFNA: perfluorononanoic acid; PFOS: perfluorooctanesulfonic acid; PFOA: perfluorooctanoic acid; PLZF: promyelocytic leukemia zinc finger; ROS: reactive oxygen species; HILI: RNA-mediated gene silencing 2; SSC: spermatogonial stem cell     

Transplacental exposure of neonates to perfluorooctanesulfonate and perfluorooctanoate: a pilot study

Objectives Perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) can be released of perfluorinated compounds by biotic and/or metabolic decomposition. Due to their ubiquitous occurrence, persistence and bioaccumulative properties they can be found in blood of the general population all over the world. In animal studies PFOS and PFOA provoked cancer and showed developmental toxic potential besides other adverse health effects. On the basis of the comparison of maternal and umbilical cord plasma sample pairs we wanted to examine whether infants are exposed to PFOS and PFOA via their mothers’ blood. Methods We determined PFOS and PFOA in 11 plasma samples of mothers and the 11 corresponding cord plasma samples of neonates. An analytical method based on plasma protein precipitation followed by HPLC with MS/MS-detection was employed. As internal standards we used 1,2,3,4-¹³C₄-PFOS and 1,2-¹³C₂-PFOA. Results We found PFOS and PFOA in every plasma sample analysed. In maternal plasma samples PFOS concentrations were consistently higher compared to those of the related cord plasma samples (median: 13.0 μg/l vs. 7.3 μg/l). In the case of PFOA we observed only minor differences between PFOA concentrations within the analysed sample pairs (median: 2.6 μg/l vs. 3.4 μg/l for maternal and cord plasma samples, respectively). Discussion For both substances a crossing of the placental barrier could be shown. For PFOS we observed a decrease from maternal to cord plasma concentrations by a factor of 0.41–0.80. To the contrary, PFOA crosses the placental barrier obviously unhindered. These findings show that neonates are exposed to PFOS and PFOA via their mothers’ blood. Given the current situation that only little is known about the consequences of PFOS and PFOA exposure in the early state of development of humans and the fact that in animal studies both substances showed developmental toxic effects further research regarding human health effects is indispensable.     

Association of Perfluorooctanoic Acid (PFOA) and Perfluorooctane Sulfonate (PFOS) with Uric Acid among Adults with Elevated Community Exposure to PFOA

Background

Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) are compounds that do not occur in nature, have been widely used since World War II, and persist indefinitely in most environments. Median serum levels in the United States are 4 ng/mL for PFOA and 21 ng/mL for PFOS. PFOA has been associated with elevated uric acid in two studies of chemical workers. Uric acid is a risk factor for hypertension and possibly other cardiovascular outcomes.

Methods

We conducted a cross-sectional study of PFOA and PFOS and uric acid among 54,951 adult community residents in Ohio and West Virginia, who lived or worked in six water districts contaminated with PFOA from a chemical plant. Analyses were conducted by linear and logistic regression, adjusted for confounders.

Results

Both PFOA and PFOS were significantly associated with uric acid. An increase of 0.2–0.3 mg/dL uric acid was associated with an increase from the lowest to highest decile of either PFOA or PFOS. Hyperuricemia risk increased modestly with increasing PFOA; the odds ratios by quintile of PFOA were 1.00, 1.33 [95% confidence interval (CI), 1.24–1.43], 1.35 (95% CI, 1.26–1.45), 1.47 (95% CI, 1.37–1.58), and 1.47 (95% CI, 1.37–1.58; test for trend, p < 0.0001). We saw a less steep trend for PFOS. Inclusion of both correlated fluorocarbons in the model indicated PFOA was a more important predictor than was PFOS.

Conclusion

Higher serum levels of PFOA were associated with a higher prevalence of hyperuricemia, but the limitations of cross-sectional data and the possibility of noncausal mechanisms prohibit conclusions regarding causality.     

Pilot study on the perfluorooctanesulfonate and perfluorooctanoate exposure of the German general population

Perfluorinated chemicals (PFCs) are used in a wide variety of consumer products. Major fields of application include surfactants, surface protection (e.g., for textiles, carpets, and upholstery), paper treatment (e.g., for food packages), and lubricants. Perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) are raw materials or manufacturing aids for some PFCs and can be released of those by biotic and/or metabolic decomposition. Due to their widespread use, persistence and bioaccumulative properties they are taken up by the general population from different sources. This might be a problem for environmental medicine because in animal studies PFOS and PFOA provoked various types of cancer and showed developmental toxic potential besides other adverse health effects.

We determined the PFOS and PFOA plasma concentrations of 105 non-smokers out of the German general population as a first estimate of the exposure situation in Germany. We employed an analytical method based on serum protein precipitation followed by HPLC with MS/MS-detection. The median plasma concentrations of all participants were 22.3 and 6.8 μg/l, the 95th percentiles 54.3 and 14.6 μg/l for PFOS and PFOA, respectively. These values are comparable with those of other biomonitoring studies. In our study, men were higher burdened both with PFOS (median: 27.1 vs. 19.9 μg/l) and PFOA (median: 8.3 vs. 5.8 μg/l) than women. No significant influence of age on PFOS and PFOA plasma concentrations could be observed. A strong correlation (r=0.82) between PFOS and PFOA plasma levels indicates the same exposure sources. The ubiquitous internal exposure of the general population to PFOS and PFOA must lead to further activities primarily regarding clarification of sources, metabolism, pharmacokinetics, and health effects.     

全氟丁酸毒性研究进展

全氟丁酸（perfluorobutanoic acid, PFBA）作为全氟辛酸（Perfluorooctanoic acid, PFOA）和全氟辛烷磺酸（perfluorooctane sulfonate, PFOS）的替代物，应用于工业和日用品的生产中，导致近年来在环境中广泛检出PFBA。本文对PFBA的毒理学研究进行了系统综述，目前研究结果提示PFBA肝脏毒性小于PFOA和PFOS，就安全性而言可能是PFOA和PFOS的良好替代物，但仍需更规范完整的毒性数据以评估潜在不良健康效应。     

Isomer profiles of perfluorochemicals in matched maternal, cord, and house dust samples: manufacturing sources and transplacental transfer

Background: Perfluorochemicals (PFCs) are detectable in the general population and in the human environment, including house dust. Sources are not well characterized, but isomer patterns should enable differentiation of historical and contemporary manufacturing sources. Isomer-specific maternal–fetal transfer of PFCs has not been examined despite known developmental toxicity of perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) in rodents.Objectives: We elucidated relative contributions of electrochemical (phased out in 2001) and telomer (contemporary) PFCs in dust and measured how transplacental transfer efficiency (TTE; based on a comparison of maternal and cord sera concentrations) is affected by perfluorinated chain length and isomer branching pattern.Methods: We analyzed matching samples of house dust (n = 18), maternal sera (n = 20), and umbilical cord sera (n = 20) by isomer-specific high-performance liquid chromatography tandem mass spectrometry.Results: PFOA isomer signatures revealed that telomer sources accounted for 0–95% of total PFOA in house dust (median, 31%). This may partly explain why serum PFOA concentrations are not declining in some countries despite the phase-out of electrochemical PFOA. TTE data indicate that total branched isomers crossed the placenta more efficiently than did linear isomers for both PFOS (p < 0.01) and PFOA (p = 0.02) and that placental transfer of branched isomers of PFOS increased as the branching point moved closer to the sulfonate (SO₃^–) end of the molecule.Conclusions: Results suggest that humans are exposed to telomer PFOA, but larger studies that also account for dietary sources should be conducted. The exposure profile of PFOS and PFOA isomers can differ between the mother and fetus—an important consideration for perinatal epidemiology studies of PFCs.     

Perfluoroalkyl acids in children and their mothers: Association with drinking water and time trends of inner exposures—Results of the Duisburg birth cohort and Bochum cohort studies

BackgroundPerfluoroalkyl acids (PFAAs) are widely distributed in the environment and humans are globally exposed with them. Contaminated drinking water can considerably contribute to the inner exposure levels.ObjectivesWe report the results of a human biomonitoring study with mother–child pairs living in two German cities, one city with PFAA contaminated drinking water in the sub μg/l-range (Bochum) and the other one without contamination (Duisburg). Furthermore, we studied time trends of exposure levels within the Duisburg cohort study.MethodsWe measured seven PFAAs (PFOS, PFOA, PFHxS, PFNA, PFBS, PFDeA, PFDoA) in blood samples by high performance liquid chromatography and tandem mass spectrometry. Samples were taken during pregnancy, from umbilical cord blood (2000–2002), 6–7 years (5th follow-up) and 8–10 years after birth (7th follow-up). The consumption of drinking water was recorded by a standardized questionnaire. Statistical analyses were calculated with multiple linear regression models.ResultsChildren and mothers from Bochum showed higher PFOS and PFOA plasma concentrations than from Duisburg. The median concentrations (μg/l) for children were: PFOS 4.7 vs. 3.3; PFOA 6.0 vs. 3.6 μg/l (p ≤ 0.05). Consumption of >0.7 l (children) and >0.9 l (mothers) drinking water/day was associated with 13–18% higher PFOS, PFOA and PFHxS concentrations in children (p ≤ 0.01), and 22% higher PFOA in mothers (p ≤ 0.05). Within the Duisburg cohort, PFAA levels in children peaked in the 5th follow-up study (medians (μg/l): cord plasma: 2.7 (PFOS); 1.9 (PFOA); 5th follow-up: 3.6 (PFOS); 4.6 (PFOA); 7th follow-up: 3.3 (PFOS); 3.6 (PFOA)). PFOS concentrations in mothers declined from pregnancy to the 5th follow-up (medians: 8.7 vs. 4.0 μg/l).ConclusionResidents exposed to PFOS and PFOA through drinking water showed significantly higher PFOS and PFOA concentrations in blood plasma. Although PFAA concentrations in the children slightly decreased from the 5th to the 7th follow-up, we detected increasing exposure trends with increasing age in the 7th follow-up.     

Perfluorinated chemicals and fetal growth: a study within the Danish National Birth Cohort

Background

Perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) are man-made, persistent organic pollutants widely spread throughout the environment and human populations. They have been found to interfere with fetal growth in some animal models, but whether a similar effect is seen in humans is uncertain.

Objectives

We investigated the association between plasma levels of PFOS and PFOA in pregnant women and their infants’ birth weight and length of gestation.

Methods

We randomly selected 1,400 women and their infants from the Danish National Birth Cohort among those who completed all four computer-assisted telephone interviews, provided the first blood samples between gestational weeks 4 and 14, and who gave birth to a single live-born child without congenital malformation. PFOS and PFOA were measured by high performance liquid chromatography–tandem mass spectrometer.

Results

PFOS and PFOA levels in maternal plasma were on average 35.3 and 5.6 ng/mL, respectively. Only PFOA levels were inversely associated with birth weight (adjusted β = −10.63 g; 95% confidence interval, −20.79 to −0.47 g). Neither maternal PFOS nor PFOA levels were consistently associated with the risk for preterm birth or low birth weight. We observed no adverse effects for maternal PFOS or PFOA levels on small for gestational age.

Conclusion

Our nationwide cohort data suggest an inverse association between maternal plasma PFOA levels and birth weight. Because of widespread exposure to these chemicals, our findings may be of potential public health concern.     

Cord serum concentrations of perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) in relation to weight and size at birth

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 ln-unit: beta = -69 g, 95% confidence interval (CI), -149 to 10 for PFOS; beta = -104 g, 95% CI, -213 to 5 for PFOA], ponderal index (per ln-unit: beta = -0.074 g/cm(3) x 100, 95% CI, -0.123 to -0.025 for PFOS; beta = -0.070 g/cm(3) x 100, 95% CI, -0.138 to -0.001 for PFOA), and head circumference (per ln-unit: beta = -0.32 cm, 95% CI, -0.56 to -0.07 for PFOS; beta = -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.     

全氟辛烷磺酸和全氟辛酸毒理学研究进展

全氟有机化合物,尤其是其代表性化合物全氟辛烷磺酸(PFOS)和全氟辛酸(PFOA)以及它们的盐类作为持久性有机环境污染物新成员,其所造成的全球性生态系统污染已成事实。本文以近年来国内外学者对PFOS和PFOA毒理学研究资料为依据,系统地阐述了PFOS和PFOA在实验动物和人体内的吸收、分布、排泄、代谢和毒物代谢动力学,以及它们对实验动物及人类可能造成的一般毒性、肝脏毒性、神经毒性、心血管毒性、胚胎发育与生殖毒性、遗传毒性与致癌性、免疫毒性等。同时指出,由于种属差异以及一些研究资料的尚不确定性,根据现有资料对PFOA和PFOS进行安全性评价的科学性值得商榷,进一步深入对PFOA和PFOS毒作用敏感指标及毒作用机制的探讨与研究,将成为今后环境科学和预防医学领域的研究重点。     

Studies on the Toxicological Effects of PFOA and PFOS on Rats Using Histological Observation and Chemical Analysis

As an emerging class of environmentally persistent and bioaccumulative contaminants, perfluorinated compounds (PFCs), especially perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS), have been ubiquitously found in the environment. Increasing evidence shows that the accumulated levels of PFCs in animals and the human body might cause potential impairment to their health. In the present study, toxicological effects of PFOA and PFOS on male Sprague–Dawley rats were examined after 28 days of subchronic exposure. Abnormal behavior and sharp weight loss were observed in the high-dose PFOS group. Marked hepatomegaly, renal hypertrophy, and orchioncus in treated groups were in accordance with the viscera–somatic indexes of the liver, kidney, and gonad. Histopathological observation showed that relatively serious damage occurred in the liver and lung, mainly including hepatocytic hypertrophy and cytoplasmic vacuolation in the livers and congestion and thickened epithelial walls in the lungs. PFOA concentrations in main target organs were in the order of kidney > liver > lung > (heart, whole blood) > testicle > (spleen, brain), whereas the bioaccumulation order for PFOS was liver > heart > kidney > (whole blood) > lung > (testicle, spleen, brain). The highest concentration of PFOA detected in the kidney exposed to 5 mg/kg/day was 228 ± 37 μg/g and PFOS in the liver exposed to 20 mg/kg/day reached the highest level of 648 ± 17 μg/g, indicating that the liver, lung, and kidney might serve as the main target organs for PFCs. Furthermore, a dose-dependent accumulation of PFOS in various tissues was found. The accumulation levels of PFOS were universally higher than PFOA, which might explain the relative high toxicity of PFOS. The definite toxicity and high accumulation of the tested PFCs might pose a great threat to biota and human beings due to their widespread application in various fields.     

Co-exposure of Freshwater Microalgae to Tetrabromobisphenol A and Sulfadiazine: Oxidative Stress Biomarker Responses and Joint Toxicity Prediction

Combined toxicity and oxidative stress biomarker responses were determined for tetrabromobisphenol A (TBBPA) and sulfadiazine (SDZ) to the unicellular green alga Scenedesmus obliquus. Concentration–response analyses were performed for single toxicants and for mixtures containing TBBPA and SDZ with two different mixture ratios. The effect concentrations and the observed effects of the mixtures were compared to the predictions of the joint toxicity by the concentration addition (CA) model and independent action (IA) model. Results showed that the observed joint toxicity was within the scope of the highest (TBBPA) and lowest (SDZ) toxicity observed for the individual components. Furthermore, co-exposure of S. obliquus to TBBPA and SDZ provided preliminary evidence that the mixtures induced oxidative stress leading to cell damage. The CA and IA models proved to be valid for the prediction of the joint toxicity of TBBPA and SDZ. This study highlights a combined environmental risk assessment for two emerging pollutants.     

Serum Perfluorooctanoic Acid and Perfluorooctane Sulfonate Concentrations in Relation to Birth Outcomes in the Mid-Ohio Valley, 2005–2010

Background: Previous research suggests perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) may be associated with adverse pregnancy outcomes.Objective: We conducted a population-based study of PFOA and PFOS and birth outcomes from 2005 through 2010 in a Mid-Ohio Valley community exposed to high levels of PFOA through drinking-water contamination.Methods: Women provided serum for PFOA and PFOS measurement in 2005–2006 and reported reproductive histories in subsequent follow-up interviews. Reported singleton live births among 1,330 women after 1 January 2005 were linked to birth records (n = 1,630) to identify the outcomes of preterm birth (< 37 weeks gestation), pregnancy-induced hypertension, low birth weight (< 2,500 g), and birth weight (grams) among full-term infants.Results: We observed little or no evidence of association between maternal serum PFOA or PFOS and preterm birth (n = 158) or low birth weight (n = 88). Serum PFOA and PFOS were both positively associated with pregnancy-induced hypertension (n = 106), with adjusted odds ratios (ORs) per log unit increase in PFOA and PFOS of 1.27 (95% CI: 1.05, 1.55) and 1.47 (95% CI: 1.06, 2.04), respectively, but associations did not increase monotonically when categorized by quintiles. Results of subanalyses restricted to pregnancies conceived after blood collection were consistent with the main analyses. There was suggestion of a modest negative association between PFOS and birth weight in full-term infants (–29 g per log unit increase; 95% CI: –66, 7), which became stronger when restricted to births conceived after the blood sample collection (–49 g per log unit increase; 95% CI: –90, –8).Conclusion: Results provide some evidence of positive associations between measured serum perfluorinated compounds and pregnancy-induced hypertension and a negative association between PFOS and birth weight among full-term infants.Citation: Darrow LA, Stein CR, Steenland K. 2013. Serum perfluorooctanoic acid and perfluorooctane sulfonate concentrations in relation to birth outcomes in the Mid-Ohio Valley, 2005–2010. Environ Health Perspect 121:1207–1213; http://dx.doi.org/10.1289/ehp.1206372     

Thyroid function and perfluoroalkyl acids in children living near a chemical plant

Background: Animal studies suggest that some perfluoroalkyl acids (PFAAs), including perfluorooctanoate (PFOA), perfluorooctane sulfonate (PFOS), and perfluorononanoic acid (PFNA) may impair thyroid function. Epidemiological findings, mostly related to adults, are inconsistent.Objectives: We investigated whether concentrations of PFAAs were associated with thyroid function among 10,725 children (1–17 years of age) living near a Teflon manufacturing facility in the Mid-Ohio Valley (USA).Methods: Serum levels of thyroid-stimulating hormone (TSH), total thyroxine (TT₄), and PFAAs were measured during 2005–2006, and information on diagnosed thyroid disease was collected by questionnaire. Modeled in utero PFOA concentrations were based on historical information on PFOA releases, environmental distribution, pharmacokinetic modeling, and residential histories. We performed multivariate regression analyses.Results: Median concentrations of modeled in utero PFOA and measured serum PFOA, PFOS, and PFNA were 12, 29, 20, and 1.5 ng/mL, respectively. The odds ratio for hypothyroidism (n = 39) was 1.54 [95% confidence interval (CI): 1.00, 2.37] for an interquartile range (IQR) contrast of 13 to 68 ng/mL in serum PFOA measured in 2005–2006. However, an IQR shift in serum PFOA was not associated with TSH or TT₄ levels in all children combined. IQR shifts in serum PFOS (15 to 28 ng/mL) and serum PFNA (1.2 to 2.0 ng/mL) were both associated with a 1.1% increase in TT₄ in children 1–17 years old (95% CIs: 0.6, 1.5 and 0.7, 1.5 respectively).Conclusions: This is the first large-scale report in children suggesting associations of serum PFOS and PFNA with thyroid hormone levels and of serum PFOA and hypothyroidism.