BackgroundMunicipal drinking water contaminated with perfluorinated alkyl acids had been distributed to one-third of households in Ronneby, Sweden. The source was firefighting foam used in a nearby ...airfield since the mid-1980s. Clean water was provided from 16 December 2013.ObjectiveTo determine the rates of decline in serum perfluorohexane sulfonate (PFHxS), perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA), and their corresponding half-lives.MethodsUp to seven blood samples were collected between June 2014 and September 2016 from 106 participants (age 4–84 years, 53% female).ResultsMedian initial serum concentrations were PFHxS, 277 ng/mL (range 12–1660); PFOS, 345 ng/mL (range 24–1500); and PFOA, 18 ng/mL (range 2.4–92). The covariate-adjusted average rates of decrease in serum were PFHxS, 13% per year (95% CI 12% to 15%); PFOS, 20% per year (95% CI 19% to 22%); and PFOA, 26% per year (95% CI 24% to 28%). The observed data are consistent with a first-order elimination model. The mean estimated half-life was 5.3 years (95% CI 4.6 to 6.0) for PFHxS, 3.4 years (95% CI 3.1 to 3.7) for PFOS and 2.7 years (95% CI 2.5 to 2.9) for PFOA. The interindividual variation of half-life was around threefold when comparing the 5th and 95th percentiles. There was a marked sex difference with more rapid elimination in women for PFHxS and PFOS, but only marginally for PFOA.ConclusionsThe estimated half-life for PFHxS was considerably longer than for PFOS and PFOA. For PFHxS and PFOS, the average half-life is shorter than the previously published estimates. For PFOA the half-life is in line with the range of published estimates.
The persistent environmental contaminants perfluoroalkyl substances (PFASs) have gained attention due to their potential adverse health effects, in particular following early life exposure. ...Information on human fetal exposure to PFASs is currently limited to one report on first trimester samples. There is no data available on PFAS concentrations in fetal organs throughout all three trimesters of pregnancy.
We measured the concentrations of perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluoroundecanoic acid (PFUnA), and perfluorohexane sulfonic acid (PFHxS) in human embryos and fetuses with corresponding placentas and maternal serum samples derived from elective pregnancy terminations and cases of intrauterine fetal death. A total of 78 embryos and fetuses aged 7–42 gestational weeks were included and a total of 225 fetal organs covering liver, lung, heart, central nervous system (CNS), and adipose tissue were analyzed, together with 71 placentas and 63 maternal serum samples. PFAS concentrations were assayed by liquid chromatography/triple quadrupole mass spectrometry.
All evaluated PFASs were detected and quantified in maternal sera, placentas and embryos/fetuses. In maternal serum samples, PFOS was detected in highest concentrations, followed by PFOA > PFNA > PFDA = PFUnA = PFHxS. Similarly, PFOS was detected in highest concentrations in embryo/fetal tissues, followed by PFOA > PFNA = PFDA = PFUnA. PFHxS was detected in very few fetuses. In general, PFAS concentrations in embryo/fetal tissue (ng/g) were lower than maternal serum (ng/ml) but similar to placenta concentrations. The total PFAS burden (i.e. the sum of all PFASs) was highest in lung tissue in first trimester samples and in liver in second and third trimester samples. The burden was lowest in CNS samples irrespective of fetal age. The placenta:maternal serum ratios of PFOS, PFOA and PFNA increased across gestation suggesting bioaccumulation in the placenta. Further, we observed that the ratios were higher in pregnancies with male fetuses compared to female fetuses.
Human fetuses were intrinsically exposed to a mixture of PFASs throughout gestation. The compounds were detected in all analyzed tissues, suggesting that PFASs reach and may affect many types of organs. Collectively, our results demonstrate that PFASs pass the placenta and deposit to embryo and fetal tissues, calling for risk assessment of gestational exposures.
•PFASs were detected in maternal serum, placenta and fetal organs throughout pregnancy.•PFASs concentrations in fetal tissues were similar to placenta levels.•Fetal PFAS levels were highest in liver and lung and lowest in central nervous system.•PFOS, PFOA, and PFNA accumulated in placenta across gestation.•PFOA accumulated more in placentas with male fetuses compared to female fetuses.
Chemicals such as phthalates, parabens, bisphenol A (BPA) and triclosan (TCS), used in a wide variety of consumer products, are suspected endocrine disrupters although their level of toxicity is ...thought to be low. Combined exposure may occur through ingestion, inhalation and dermal exposure, and their toxic as well as combined effects are poorly understood.
The objective of the study was to estimate the exposure to these chemicals in Swedish mothers and their children (6–11years old) and investigate potential predictors of the exposure. Urine samples from 98 mother–child couples living in either a rural or an urban area were analyzed for the concentrations of four metabolites of di-(2-ethylhexyl) phthalate (DEHP), three metabolites of di-iso-nonyl phthalate (DiNP), mono-ethyl phthalate (MEP), mono-benzyl phthalate (MBzP) and mono-n-butyl phthalate (MnBP), methylparaben (MetP), ethylparaben (EthP), propylparaben (ProP), butylparaben, benzylparaben, BPA, and TCS. Information on sociodemographics, food consumption habits and use of personal care products, obtained via a questionnaire, was used to investigate the associations between the urinary levels of chemicals and potential exposure factors.
There were fairly good correlations of biomarker levels between the mothers and their children. The children had generally higher levels of phthalates (geometric mean ΣDEHP 65.5μg/L; ΣDiNP 37.8μg/L; MBzP 19.9μg/L; MnBP 76.9μg/L) than the mothers (ΣDEHP 38.4μg/L; ΣDiNP 33.8μg/L; MBzP 12.8μg/L; MnBP 63.0μg/L). Conversely, the mother's levels of parabens (MetP 37.8μg/L; ProP 13.9μg/L) and MEP (43.4μg/L) were higher than the children's levels of parabens (MetP 6.8μg/L; ProP 2.1μg/L) and MEP (28.8μg/L). The urinary levels of low molecular weight phthalates were higher among mothers and children in the rural area (MBzP p=<0.001; MnBP p=0.001–0.002), which is probably due to higher presence of PVC in floorings and wall coverings in this area, whereas the levels of parabens were higher among the children in the urban area (MetP p=0.003; ProP p=0.004) than in the rural area. The levels of high molecular weight phthalates were associated with consumption of certain foods (i.e. chocolate and ice cream) whereas the levels of parabens were associated with use of cosmetics and personal care products.
•We quantified the levels of phthalates, BPA, parabens and triclosan in urine.•The levels were significantly correlated to certain foods and hygiene products.•Mothers had higher levels of parabens and a phthalate used in hygiene products.•Children had generally higher levels of phthalates present in food.
Perfluoroalkyl substances (PFAS) are used in numerous consumer products. They are persistent, bioaccumulating, and suspected to be endocrine disrupting chemicals (EDCs). A growing body of research ...has reported the association between PFAS exposure and adverse health effects. Concerns have been raised with special focus in childhood development.
Perfluoroheptanoic acid (PFHpA), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluoroundecanoic acid (PFUnDA), perfluorododecanoic acid (PFDoDA), perfluorohexane sulfonate (PFHxS) and perfluorooctane sulfonate (PFOS) were analyzed by LC/MS/MS in serum from 1,616 pregnant women in the Swedish SELMA study. The serum samples were collected in the first trimester (median week 10). Least square geometric means (LSGM) of PFAS were estimated for each year period for, adjusted for potential determinants including parity, fish intake in the family, and mother's age.
Six PFAS (PFNA, PFDA, PFUnDA, PFHxS, PFOA, and PFOS) were detected above levels of detection (LOD) in more than 99% of the SELMA women, while PFHpA, and PFDoDA were detected above LOD in 73.4% and 46.7% respectively. Parity, maternal age, maternal smoking, and fish intake during pregnancy were found to be significantly associated (p<0.05) with serum PFAS levels in the pregnant women. Finally, serum concentration of six PFAS (PFNA, PFDA, PFHxS, PFHpA, PFOA and PFOS) were significantly decreasing (range 14-31%) during the period of 30 months from 2007-2010.
Our analysis shows that six out of eight PFAS could be identified in serum of more than 99% of SELMA subjects with a significant slightly decreasing trend for five of these compounds. Furthermore, parity, higher fish intake and mothers age are determinants for serum levels of PFAS in pregnant women.
Bisphenols and triclosan are considered as potential thyroid disruptors. While mild alterations in maternal thyroid function can result in adverse pregnancy and child developmental outcomes, there is ...still uncertainty whether bisphenols or triclosan can interfere with thyroid function during pregnancy.
We aimed to investigate the association of urinary bisphenol A (BPA), bisphenol S (BPS), bisphenol F (BPF) and triclosan with early pregnancy thyroid function.
This study was embedded in the Swedish Environmental Longitudinal, Mother and child, Asthma and allergy study (SELMA), a population-based prospective pregnancy cohort. In total, 1996 participants were included in the current study. Maternal urinary concentrations of three bisphenols and triclosan, collected at median (95% range) 10 (6–14) weeks of pregnancy as well as serum concentrations of thyroid stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3), total thyroxine (TT4), and total triiodothyronine (TT3) were measured.
Higher BPA levels were associated with lower TT4 concentrations (non-monotonic, P = 0.03), a lower FT4/FT3 ratio (β SE -0.02 0.01, P = 0.03) and a lower TT4/TT3 ratio (β SE -0.73 0.27, P = 0.008). Higher BPF levels were associated with a higher FT3 (β SE 0.01 0.007, P = 0.04). There were no associations between other bisphenols or triclosan and absolute TSH, (F)T4 or (F)T3 concentrations. The association of BPA with thyroid function differed with gestational age. The negative association of BPA with FT4/FT3 and TT4/TT3 ratios was only apparent in early but not late gestation (P for interaction: 0.003, 0.008, respectively).
These human data during pregnancy substantiate experimental findings suggesting that BPA could potentially affect thyroid function and deiodinase activities in early gestation.
•Bisphenol A (BPA) had a non-monotonic association with total T4 in pregnant women.•Higher BPA was associated with lower (F)T4/(F)T3 ratio in very early pregnancy.•Bisphenol F had a positive association with FT3.•Bisphenol S and triclosan were not associated with thyroid function.
Phthalates are used as plasticizers in soft polyvinyl chloride (PVC) and in a large number of consumer products. Because of reported health risks, diisononyl phthalate (DiNP) has been introduced as a ...replacement for di(2-ethylhexyl) phthalate (DEHP) in soft PVC. This raises concerns because animal data suggest that DiNP may have antiandrogenic properties similar to those of DEHP. The anogenital distance (AGD)--the distance from the anus to the genitals--has been used to assess reproductive toxicity.
The objective of this study was to examine the associations between prenatal phthalate exposure and AGD in Swedish infants.
AGD was measured in 196 boys at 21 months of age, and first-trimester urine was analyzed for 10 phthalate metabolites of DEP (diethyl phthalate), DBP (dibutyl phthalate), DEHP, BBzP (benzylbutyl phthalate), as well as DiNP and creatinine. Data on covariates were collected by questionnaires.
The most significant associations were found between the shorter of two AGD measures (anoscrotal distance; AGDas) and DiNP metabolites and strongest for oh-MMeOP mono-(4-methyl-7-hydroxyloctyl) phthalate and oxo-MMeOP mono-(2-ethyl-5-oxohexyl) phthalate. However, the AGDas reduction was small (4%) in relation to more than an interquartile range increase in DiNP exposure.
These findings call into question the safety of substituting DiNP for DEHP in soft PVC, particularly because a shorter male AGD has been shown to relate to male genital birth defects in children and impaired reproductive function in adult males and the fact that human levels of DiNP are increasing globally.
Children are exposed to a wide range of chemicals in their everyday environments, including the preschool. In this study, we evaluated the levels of phthalates, non-phthalate plasticizers and ...bisphenols in dust from 100 Swedish preschools and identified important exposure factors in the indoor environment. In addition, children's total exposure to these chemicals was determined by urine analysis to investigate their relation with dust exposure, and to explore the time trends by comparing with children who provided urine fifteen years earlier. The most abundant plasticizers in preschool dust were the phthalates di-isononyl phthalate (DiNP) and di-(2-ethylhexyl) phthalate (DEHP) with geometric mean levels of 450 and 266μg/g dust, respectively, and the non-phthalate plasticizers bis(2-ethylhexyl) terephthalate (DEHT) and diisononylcyclohexane-1,2-dicarboxylate (DiNCH) found at 105 and 73μg/g dust, respectively. The levels of several substitute plasticizers were higher in newer preschools, whereas the levels of the strictly regulated phthalate di-n-butyl phthalate (DnBP) were higher in older preschools. The presence of foam mattresses and PVC flooring in the sampling room were associated with higher levels of DiNP in dust. Children's exposure from preschool dust ingestion was below established health based reference values and the estimated exposure to different phthalates and BPA via preschool dust ingestion accounted for 2–27% of the total exposure. We found significantly lower urinary levels of BPA and metabolites of strictly regulated phthalates, but higher levels of DiNP metabolites, in urine from the children in this study compared to the children who provided urine samples fifteen years earlier.
•Phthalates, non-phthalate plasticizers and bisphenols analyzed in preschool dust•Building year of the preschool is important for plasticizer concentrations in dust.•Foam mattresses and PVC flooring associated with higher levels of DiNP in dust•Negative time trends for children's urinary levels of now banned phthalates and BPA
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•This study provides refined estimates of the half-life of eight PFAS, especially including the branched PFOS-isomers.•The determinants leading to shorter half-life were young age; ...better kidney function; female gender in fertile age; and possibly gut inflammation and lower gut permeability.•The result also suggested a time-dependent PFAS elimination process, with more rapid elimination in the first year after the end of exposure, than later.
Per- and polyfluoroalkyl substances (PFAS) are persistent substances with surfactant and repellent properties. Municipal drinking water contaminated with PFAS had been distributed for decades to one third of households in Ronneby, Sweden. The source was firefighting foam used in a nearby airfield since the mid-1980s. Clean water was provided from December 16, 2013.
The purpose was to estimate serum half-lives and their determinants in the study population for different PFAS.
Up to ten blood samples were collected between 2014 and 2018 from 114 participants (age 4–84 years at entry, 53% female). 19 PFAS were analysed. Linear mixed models were used to estimate the half-lives.
Eight PFAS were increased in Ronneby: perfluorooctanoic acid (PFOA), perfluoropentane sulfonate (PFPeS), perfluorohexane sulfonate (PFHxS), perfluoroheptane sulfonate (PFHpS), linear perfluorooctane sulfonate (L-PFOS) and three branched perfluorooctane sulfonates (1 m-PFOS, 3/4/5m-PFOS and 2/6m-PFOS). The mean estimated half-lives (in years) were 0.94 (95 %CI 0.86–1.02) for PFPeS, 2.47 (2.27–2.7) for PFOA, 2.67 (2.51–2.85) for 2/6m-PFOS, 2.73 (2.55–2.92) for L-PFOS, 3.43 (3.19–3.71) for 3/4/5m-PFOS, 4.52 (4.14–4.99) for PFHxS, 4.55 (4.14–5.06) for PFHpS, and 5.01 (4.56–5.55) for 1 m-PFOS.
The most important determinants of a shorter half-life were young age, and better kidney function measured by estimated glomerular filtration rate and ratio of paired urine and serum PFAS levels, followed by female sex during their fertile period aged 15–50. Markers of gut inflammation and reduced permeability i.e. zonulin and calprotectin were also possibly associated with shorter half-life. The results also suggested a time-dependent PFAS elimination process, with more rapid elimination in the first year after the end of exposure.
The half-life estimates are in line with past estimates for some PFAS such as PFOA, and the novel results for different PFOS isomers. These results provide observational support for elimination routes – renal, fecal and maternal.
•Exposure to phthalates disrupt the maternal thyroid system.•Metabolites of DEHP can disrupt the maternal hypothalamic-pituitary-thyroid axis.•Several phthalates can increase the maternal T4 ...metabolism.•Phthalate substitutes such as DINCH are also capable of thyroid system disruption.
The extent of thyroid disruptive effects of phthalates during pregnancy remains unclear.
To investigate the association of maternal urinary phthalates with markers of the thyroid system during early pregnancy.
Urinary concentrations of phthalate metabolites and serum concentrations of thyroid stimulating hormone (TSH), free and total thyroxine (FT4 and TT4) and free and total triiodothyronine (FT3 and TT3) were measured in pregnant women in early pregnancy in the Swedish Environmental Longitudinal, Mother and child, Asthma and allergy study (2007-ongoing), a population-based prospective cohort.
In the 1,996 included women, higher di-ethyl-hexyl phthalate (DEHP) metabolites were associated with a lower FT4 (β SE for the molar sum: −0.13 0.06, P = 0.03) and a higher TSH/FT4 ratio (0.003 0.001, P = 0.03). Higher concentrations of di-iso-nonyl phthalate (DINP) metabolites were associated with a lower TT4 (β SE for the molar sum: 0.93 0.44, P = 0.03) as well as with lower TT4/FT4 and TT4/TT3 ratios. Higher metabolites of both dibutyl and butyl-benzyl phthalate (DBP and BBzP) were associated with lower T4/T3 ratio (free and total) and higher FT4/TT4 and FT3/TT3 ratios. A higher diisononyl cyclohexane dicarboxylate (DINCH) metabolite concentration was associated with a higher TT3.
These results translate results from experimental studies suggesting that exposure to phthalates may interfere with the thyroid system during pregnancy. This is also true for compounds that have been introduced to replace known disruptive phthalates. Further experimental studies should take into account the human evidence to better investigate the potential underlying mechanisms of thyroid disruption by phthalates.
Exposures to perfluoroalkyl substances (PFAS) have shown positive associations with serum lipids in previous studies. While many studies on lipids investigated associations with perfluorooctane ...sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA), there are only a few studies regarding other PFAS, such as perfluorohexane sulfonic acid (PFHxS). The purpose of the current study is to investigate if associations with serum lipids were present, not only for serum PFOS and PFOA, but also for PFHxS, and if the associations with PFAS remained also in a comparison based only on residency in areas with contrasting exposure to PFAS.
1945 adults aged 20-60 were included from Ronneby, Sweden, a municipality where one out of two waterworks had been heavily contaminated from aqueous fire-fighting foams, and from a nearby control area. The exposure was categorized based on either been living in areas with contrasting PFAS exposure or based on the actual serum PFAS measurements. Regression analyses of serum lipids were fitted against serum PFAS levels, percentile groups, smooth splines and between exposed and reference areas, adjusting for age, sex and BMI.
Drinking water contamination caused high serum levels of PFOS (median 157 ng/ml) and PFHxS (median 136 ng/ml) and PFOA (median 8.6 ng/ml). These serum PFAS levels in the exposed groups were 5 to 100-fold higher than in the controls. In this population with mixed PFAS exposure, predominantly PFOS and PFHxS, PFAS exposure were positively associated with serum lipids. This was observed both when quantifying exposure as contrast between exposed and controls, and in terms of serum PFAS. Due to high correlations between each PFAS, we cannot separate them.
In conclusion, the present study provides further evidence of a causal association between PFAS and serum lipids, especially for PFHxS.