We compared the human exposure to organophosphate flame retardants (PFRs) via inhalation, dust ingestion, and dermal absorption using different sampling and assessment strategies. Air (indoor ...stationary air and personal ambient air), dust (floor dust and surface dust), and hand wipes were sampled from 61 participants and their houses. We found that stationary air contains higher levels of ΣPFRs (median = 163 ng/m3, IQR = 161 ng/m3) than personal air (median = 44 ng/m3, IQR = 55 ng/m3), suggesting that the stationary air sample could generate a larger bias for inhalation exposure assessment. Tris(chloropropyl) phosphate isomers (ΣTCPP) accounted for over 80% of ΣPFRs in both stationary and personal air. PFRs were frequently detected in both surface dust (ΣPFRs median = 33 100 ng/g, IQR = 62 300 ng/g) and floor dust (ΣPFRs median = 20 500 ng/g, IQR = 30 300 ng/g). Tris(2-butoxylethyl) phosphate (TBOEP) accounted for 40% and 60% of ΣPFRs in surface and floor dust, respectively, followed by ΣTCPP (30% and 20%, respectively). TBOEP (median = 46 ng, IQR = 69 ng) and ΣTCPP (median = 37 ng, IQR = 49 ng) were also frequently detected in hand wipe samples. For the first time, a comprehensive assessment of human exposure to PFRs via inhalation, dust ingestion, and dermal absorption was conducted with individual personal data rather than reference factors of the general population. Inhalation seems to be the major exposure pathway for ΣTCPP and tris(2-chloroethyl) phosphate (TCEP), while participants had higher exposure to TBOEP and triphenyl phosphate (TPHP) via dust ingestion. Estimated exposure to ΣPFRs was the highest with stationary air inhalation (median =34 ng·kg bw–1·day–1, IQR = 38 ng·kg bw–1·day–1), followed by surface dust ingestion (median = 13 ng·kg bw–1·day–1, IQR = 28 ng·kg bw–1·day–1), floor dust ingestion and personal air inhalation. The median dermal exposure on hand wipes was 0.32 ng·kg bw–1·day–1 (IQR = 0.58 ng·kg bw–1·day–1) for ΣTCPP. The selection of sampling and assessment strategies could significantly affect the results of exposure assessment.
•This study contributed to the field of human exposure to poly- and perfluoroalkyl substances.•Dietary exposure from the ingestion of food and drinks was the predominant exposure pathway.•Measured ...and modelled serum concentrations were in the same order of magnitude.•The estimated daily intakes of PFASs in this study were lower than the health-based guidance values.
Exposure to PFASs may result in adverse health effects. This study aimed to characterise the exposure to PFASs from diet, house dust, indoor air, and dermal contact and the relative contribution from different external exposure pathways to human serum concentrations. Daily intakes of 18 perfluoroalkyl acids (PFAAs) and 12 PFAA precursors from diet, dust ingestion, inhalation of indoor air and dermal absorption were estimated using a comprehensive dataset comprising 61 adults from the Oslo area, Norway. Concentrations of PFAAs and PFAA precursors in house dust, indoor air, hand wipes, foods and drinks were utilised to estimate the daily intakes. Perfluorooctanesulfonate (PFOS) was the predominant PFAS in serum for this study group. On a median level, perfluorooctanoate (PFOA) contributed most to the total estimated daily intake of PFAAs, with a median intake of 280 (range: 72–1810) pg·kg bw−1·day−1, covering both direct and indirect (precursors) exposure. Out of this, only 3% (range: <1–48%) of the total PFOA intake came from indirect exposure. Dietary exposure from ingestion of food and drinks was in general the predominant exposure pathway, followed by exposure from ingestion of house dust, inhalation of indoor air, and dermal absorption, but considerable variations were observed among individuals. House dust ingestion and indoor air inhalation contributed most to the total intakes for some participants, for which most of them were among the 20% participants with the highest total estimated intakes. Some statistical significant associations between concentrations of PFASs measured in serum and estimated intakes were observed. Measured serum concentrations and modelled serum concentrations based on external exposure estimates were in the same order of magnitude for PFOS, PFHxS, PFOA, and PFNA, but only PFOA concentrations were comparable, 1.9 and 2.0 ng mL−1 for observed and modelled serum concentrations, respectively. The estimated daily intakes of PFASs in this study were lower than the health-based guidance values, e.g. the tolerable weekly intakes derived by EFSA. This study underlines the importance of performing studies considering multiple exposure pathways on an individual basis.
Determining the major human exposure pathways is a prerequisite for the development of effective management strategies for environmental pollutants such as chlorinated paraffins (CPs). As a first ...step, the internal and external exposure to CPs were quantified for a well-defined human cohort. CPs in participants’ plasma and diet samples were analyzed in the present study, and previous results on paired air, dust, and hand wipe samples were used for the total exposure assessment. Both one compartment pharmacokinetic modeling and forensic fingerprinting indicate that dietary intake contributed the most to body burden of CPs in this cohort, contributing a median of 60–88% of the total daily intakes. The contribution from dust ingestion and dermal exposure was greater for the intake of long-chain CPs (LCCPs) than short-chain CPs (SCCPs), while the contribution from inhalation was greater for the intake of SCCPs than medium-chain CPs (MCCPs) and LCCPs. Significantly higher concentrations of SCCPs and MCCPs were observed in diets containing butter and eggs, respectively (p < 0.05). Additionally, other exposure sources were correlated to plasma levels of CPs, including residence construction parameters such as the construction year (p < 0.05). This human exposure to CPs is not a local case. From a global perspective, there are major knowledge gaps in biomonitoring and exposure data for CPs from regions other than China and European countries.
Currently, there is limited knowledge on the distribution of poly- and perfluoroalkyl substances (PFASs) in different blood matrices, particularly for novel PFASs such as polyfluoroalkyl phosphate ...esters (PAPs) and perfluoroalkyl phosphonates (PFPAs). To explore this, serum, plasma, and whole blood from 61 adults in Oslo, Norway were collected. The largest number of PFASs were detected in whole blood. For PAPs and PFPAs, the highest frequencies of detection and concentrations were observed in plasma. PAPs contributed to 8% of total PFASs in plasma (median, 0.81 ng mL–1). Perfluorohexylphosphonate (PFHxPA) was the dominant PFPA, regardless of blood matrix. The relative composition profiles of PFASs in blood matrices differed. For some specific PFASs such as perfluorooctanesulfonamide (PFOSA) and perfluorohexanoate (PFHxA), the highest concentrations were observed in whole blood. The PFAS concentration ratios varied between blood matrices, depending on the compounds. However, similar ratios were observed for 6:2 polyfluoroalkyl phosphate diester (6:2diPAP) as well as well-known PFASs such as perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA). Besides the determination of 25 PFASs in human blood, this study also lead to better understanding of biomonitoring data from different blood matrices, which is key knowledge for performing both exposure assessments and epidemiological studies.
Indoor dust has been acknowledged as a major source of flame retardants (FRs) and dust ingestion is considered a major route of exposure for humans. In the present study, we investigated the presence ...of PBDEs and alternative FRs such as emerging halogenated FRs (EHFRs) and organophosphate flame retardants (PFRs) in indoor dust samples from British and Norwegian houses as well as British stores and offices. BDE209 was the most abundant PBDE congener with median concentrations of 4700ngg−1 and 3400ngg−1 in UK occupational and house dust, respectively, 30 and 20 fold higher than in Norwegian house dust. Monomeric PFRs (m-PFRs), including triphenyl phosphate (TPHP), tris(chloropropyl) phosphate (TCPP) and tris(2-chloroethyl) phosphate (TCEP) dominated all the studied environments. To the best of our knowledge, this is the first report of isodecyldiphenyl phosphate (iDPP) and trixylenyl phosphate (TXP) in indoor environments. iDPP was the most abundant oligomeric PFR (o-PFR) in all dust samples, with median concentrations one order of magnitude higher than TXP and bisphenol A bis(diphenyl phosphate (BDP). iDPP and TXP worst-case scenario exposures for British workers during an 8h exposure in the occupational environment were equal to 34 and 1.4ngkgbw−1day−1, respectively. The worst-case scenario for BDE209 estimated exposure for British toddlers (820ngkgbw−1day−1) did not exceeded the proposed reference dose (RfD) (7000ngkgbw−1day−1), while exposures for sum of m-PFRs (Σm-PFRs) in British toddlers and adults (17,900 and 785ngkgbw−1day−1 respectively) were an order of magnitude higher than for Norwegian toddlers and adults (1600 and 70ngkgbw−1day−1).
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•PBDEs, EHFRs and PFRs were analysed in Norwegian and UK house, store & office dust.•First report of iDPP and TXP in indoor dust with several o-PFRs also detected.•m-PFRs dominated all indoor environments, followed by EHFRs, PBDEs, and o-PFRs.•BDE209 levels were significantly higher in British than Norwegian house dust.•iDPP is commonly added in toys and culinary products, while TXP is used in IT products.
Background: Perfluoroalkyl adds are persistent compounds used in various industrial applications. Of these compounds, perfluorooctanoate (PFOA) is currently detected in humans worldwide. A recent ...study on low-dose developmental exposure to PFOA in mice reported increased weight and elevated biomarkers of adiposity in postpubertal female offspring. Objective: We examined whether the findings of increased weight in postpubertal female mice could be replicated in humans. Methods: A prospective cohort of 665 Danish pregnant women was recruited in 1988-1989 with offspring follow-up at 20 years. PFOA was measured in serum from gestational week 30. Offspring body mass index (BMI) and waist circumference were recorded at follow-up (n = 665), and bio-markers of adiposity were quantified in a subset (n = 422) of participants. Results: After adjusting for covariates, including maternal prepregnancy BMI, smoking, education, and birth weight, in utero exposure to PFOA was positively associated with anthropometry at 20 years in female but not male offspring. Adjusted relative risks comparing the highest with lowest quartile (median: 5.8 vs. 2.3 ng/mL) of maternal PFOA concentration were 3.1 95% confidence interval (CI): 1.4, 6.9 for overweight or obese (BMI ≥ 25 kg/m²) and 3.0 (95% CI: 1.3, 6.8) for waist circumference > 88 cm among female offspring. This corresponded to estimated increases of 1.6 kg/m² (95% CI: 0.6, 2.6) and 4.3 cm (95% CI: 1.4, 7.3) in average BMI and waist circumference, respectively. In addition, maternal PFOA concentrations were positively associated with serum insulin and leptin levels and inversely associated with adiponectin levels in female offspring. Similar associations were observed for males, although point estimates were less precise because of fewer observations. Maternal perfluorooctane sulfonate (PFOS), perfluorooctane sulfonamide (PFOSA), and perfluorononanoate (PFNA) concentrations were not independently associated with offspring anthropometry at 20 years. Conclusions: Our findings on the effects of low-dose developmental exposures to PFOA are in line with experimental results suggesting obesogenic effects in female offspring at 20 years of age.
The European Commission asked EFSA for a scientific evaluation on the risks to human health related to the presence of perfluoroalkyl substances (PFASs) in food. Based on several similar effects in ...animals, toxicokinetics and observed concentrations in human blood, the CONTAM Panel decided to perform the assessment for the sum of four PFASs: PFOA, PFNA, PFHxS and PFOS. These made up half of the lower bound (LB) exposure to those PFASs with available occurrence data, the remaining contribution being primarily from PFASs with short half‐lives. Equal potencies were assumed for the four PFASs included in the assessment. The mean LB exposure in adolescents and adult age groups ranged from 3 to 22, the 95th percentile from 9 to 70 ng/kg body weight (bw) per week. Toddlers and ‘other children’ showed a twofold higher exposure. Upper bound exposure was 4‐ to 49‐fold higher than LB levels, but the latter were considered more reliable. ‘Fish meat’, ‘Fruit and fruit products’ and ‘Eggs and egg products’ contributed most to the exposure. Based on available studies in animals and humans, effects on the immune system were considered the most critical for the risk assessment. From a human study, a lowest BMDL10 of 17.5 ng/mL for the sum of the four PFASs in serum was identified for 1‐year‐old children. Using PBPK modelling, this serum level of 17.5 ng/mL in children was estimated to correspond to long‐term maternal exposure of 0.63 ng/kg bw per day. Since accumulation over time is important, a tolerable weekly intake (TWI) of 4.4 ng/kg bw per week was established. This TWI also protects against other potential adverse effects observed in humans. Based on the estimated LB exposure, but also reported serum levels, the CONTAM Panel concluded that parts of the European population exceed this TWI, which is of concern.
This publication is linked to the following EFSA Supporting Publications article: http://onlinelibrary.wiley.com/doi/10.2903/sp.efsa.2020.EN-1931/full
Organophosphate flame retardants (PFRs) have largely replaced the market of polybrominated diphenyl ethers (PBDEs). Concerns about PFR contamination and its impact on human health have consequently ...increased. A comprehensive investigation on the human exposure pathways to PFRs is to be endeavoured. This study investigated the occurrence of PFR metabolites in human urine, serum and hair, correlating them with external exposure data that was presented in our previous studies. Participants from Oslo (n = 61) provided a set of samples, including dust, air, handwipes, food, urine, serum and hair. Associations between PFR metabolites analyzed in the biological samples and the PFRs in environmental samples were explored. Different sampling strategies for dosimeters (e.g. floor/surface dust, personal/stationary air) were also compared to understand which is better for predicting human exposure to PFRs. Seven out of the eleven target PFR metabolites, including diphenyl phosphate (DPHP) and bis(1-chloro-2-propyl)-1-hydroxy-2-propyl phosphate (BCIPHIPP), were frequently detected (DF > 30%) in urine. DPHP was the most frequently detected metabolite in both serum and hair. Several PFR metabolites had higher levels in morning urine than in afternoon urine. Floor dust appeared to be a better proxy for estimating PFR internal exposure than surface dust, air, and handwipes. Some PFRs in handwipes and air were also correlated with their metabolites in urine and hair. Age, beverage consumption and food consumption were negatively associated with DPHP levels in urine. Discrepancies observed between the external and internal exposure for some PFRs call for further investigation on PFR bioaccessibility and clearance.
•A detailed picture of human external and internal exposure to PFRs is presented.•Several PFR metabolites were found in Norwegian urine, blood and hair samples.•Urinary PFR metabolites were associated with parent PFRs in floor dust and personal air.•DPHP in hair could not be associated with DPHP in urine, but was correlated with TPHP in dust.
•Associations between early-life exposome and allergy-related outcomes were studied.•No childhood exposures were associated with the allergy-related health outcomes.•Prenatally, traffic variables, ...PMabs and phthalates were associated with rhinitis.•Prenatally, traffic variables and phthalates were associated with itchy rash.
Early onset and high prevalence of allergic diseases result in high individual and socio-economic burdens. Several studies provide evidence for possible effects of environmental factors on allergic diseases, but these are mainly single-exposure studies. The exposome provides a novel holistic approach by simultaneously studying a large set of exposures. The aim of the study was to evaluate the association between a broad range of prenatal and childhood environmental exposures and allergy-related outcomes in children.
Analyses of associations between 90 prenatal and 107 childhood exposures and allergy-related outcomes (last 12 months: rhinitis and itchy rash; ever: doctor-diagnosed eczema and food allergy) in 6–11 years old children (n = 1270) from the European Human Early-Life Exposome cohort were performed. Initially, we used an exposome-wide association study (ExWAS) considering the exposures independently, followed by a deletion-substitution-addition selection (DSA) algorithm considering all exposures simultaneously. All the exposure variables selected in the DSA were included in a final multi-exposure model using binomial general linear model (GLM).
In ExWAS, no exposures were associated with the outcomes after correction for multiple comparison. In multi-exposure models for prenatal exposures, lower distance of residence to nearest road and higher di-iso-nonyl phthalate level were associated with increased risk of rhinitis, and particulate matter absorbance (PMabs) was associated with a decreased risk. Furthermore, traffic density on nearest road was associated with increased risk of itchy rash and diethyl phthalate with a reduced risk. DSA selected no associations of childhood exposures, or between prenatal exposures and eczema or food allergy.
This first comprehensive and systematic analysis of many environmental exposures suggests that prenatal exposure to traffic-related variables, PMabs and phthalates are associated with rhinitis and itchy rash.
The European Commission asked EFSA for a scientific evaluation on the risks to human health related to the presence of perfluorooctane sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA) in food. ...Regarding PFOS and PFOA occurrence, the final data set available for dietary exposure assessment contained a total of 20,019 analytical results (PFOS n = 10,191 and PFOA n = 9,828). There were large differences between upper and lower bound exposure due to analytical methods with insufficient sensitivity. The CONTAM Panel considered the lower bound estimates to be closer to true exposure levels. Important contributors to the lower bound mean chronic exposure were ‘Fish and other seafood’, ‘Meat and meat products’ and ‘Eggs and egg products’, for PFOS, and ‘Milk and dairy products’, ‘Drinking water’ and ‘Fish and other seafood’ for PFOA. PFOS and PFOA are readily absorbed in the gastrointestinal tract, excreted in urine and faeces, and do not undergo metabolism. Estimated human half‐lives for PFOS and PFOA are about 5 years and 2–4 years, respectively. The derivation of a health‐based guidance value was based on human epidemiological studies. For PFOS, the increase in serum total cholesterol in adults, and the decrease in antibody response at vaccination in children were identified as the critical effects. For PFOA, the increase in serum total cholesterol was the critical effect. Also reduced birth weight (for both compounds) and increased prevalence of high serum levels of the liver enzyme alanine aminotransferase (ALT) (for PFOA) were considered. After benchmark modelling of serum levels of PFOS and PFOA, and estimating the corresponding daily intakes, the CONTAM Panel established a tolerable weekly intake (TWI) of 13 ng/kg body weight (bw) per week for PFOS and 6 ng/kg bw per week for PFOA. For both compounds, exposure of a considerable proportion of the population exceeds the proposed TWIs.
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