A major challenge of non-invasive human biomonitoring using hair is to assess whether it can be used as an indicator of exposure to Flame Retardants, such as Organophosphate Flame Retardants (PFRs), since the contribution of atmospheric deposition (air and/or dust) cannot be neglected. Therefore, the aim of this study was to evaluate the suitability of using human hair more thoroughly by comparison of (i) levels of PFRs in human hair (from 48 mothers and 54 children), with levels measured in dust and air in their respective households; and (ii) levels of selected PFRs in hair with the levels of corresponding PFR metabolites in matching urine samples collected simultaneously. Most PFRs (tri-n-butyl phosphate (TNBP), 2-ethyl-hexyldiphenyl phosphate (EHDPHP), tri-phenyl phosphate (TPHP), tri-iso-butyl phosphate (TIBP), and tris(2-butoxyethyl) phosphate (TBOEP)) were detected in all human hair samples, tris(2-ethylhexyl) phosphate (TEHP) and tris(1,3-dichloro-iso-propyl) phosphate (TDCIPP) in 93%, tri-cresyl-phosphate (TCP) in 69% and tris(2-chloroethyl) phosphate (TCEP) in 21% of the samples. Levels of individual PFRs ranged between
Perfluoroalkyl substances (PFASs) are a group of highly persistent chemicals that are widespread contaminants in wildlife and humans. Exposure to PFAS affects thyroid homeostasis in experimental animals and possibly in humans. The objective of this study was to examine the association between plasma concentrations of PFASs and thyroid stimulating hormone (TSH) among pregnant women.
A total of 903 pregnant women who enrolled in the Norwegian Mother and Child Cohort Study from 2003 to 2004 were studied. Concentrations of thirteen PFASs and TSH were measured in plasma samples collected around the 18th week of gestation. Linear regression models were used to evaluate associations between PFASs and TSH.
Among the thirteen PFASs, seven were detected in more than 60% of samples and perfluorooctane sulfonate (PFOS) had the highest concentrations (median, 12.8 ng/mL; inter-quartile range [IQR], 10.1 -16.5 ng/mL). The median TSH concentration was 3.5 (IQR, 2.4 - 4.8) µIU/mL. Pregnant women with higher PFOS had higher TSH levels. After adjustment, with each 1 ng/mL increase in PFOS concentration, there was a 0.8% (95% confidence interval: 0.1%, 1.6%) rise in TSH. The odds ratio of having an abnormally high TSH, however, was not increased, and other PFASs were unrelated to TSH.
Our results suggest an association between PFOS and TSH in pregnant women that is small and may be of no clinical significance.
Brominated flame retardants (BFRs) have been in widespread use in a vast array of consumer products since the 1970s. The metabolites of some BFRs show a structural similarity to thyroid hormones and experimental animal studies have confirmed that they may interfere with thyroid hormone homeostasis. A major concern has been whether intrauterine exposure to BFRs may disturb thyroid homeostasis since the fetal brain is particularly susceptible to alterations in thyroid hormones. However, few reports on newborns have been published to date.
To evaluate the association between BFRs and neonatal thyroid-stimulating hormone (TSH).
We studied six polybrominated diphenyl ethers (PBDEs) measured in milk samples from 239 women who were part of the "Norwegian Human Milk Study" (HUMIS), 2003-2006. Hexabromocyclododecane (HBCD) and BDE-209 were measured in a subset of the women (193 and 46 milk samples, respectively). The milk was sampled at a median of 33 days after delivery. TSH was measured in babies three days after delivery as part of the routine national screening program for early detection of congenital hypothyroidism. Additional information was obtained through the Medical Birth Registry and questionnaires to the mothers.
The PBDE concentrations in human milk in Norway were comparable to concentrations reported from other European countries and Asia, but not the US and Canada where levels are approximately one order of higher magnitude. We observed no statistically significant associations between BDE-47, 99, 153, 154, 209 and HBCD in human milk and TSH in models adjusted for possible confounders and other environmental toxicants including polychlorinated biphenyls (PCBs).
We did not observe an association between TSH and exposure to HBCD and PBDEs within the exposure levels observed.
Perfluorinated alkyl acids (PFAAs), persistent chemicals with unique water-, dirt-, and oil-repellent properties, are suspected of having endocrine-disrupting activity. The PFAA compounds perfluorooctanoic acid (PFOA) and perfluorooctane sulfonic acid (PFOS) are found globally in humans; because they readily cross the placental barrier, in utero exposure may be a cause for concern.
We investigated whether in utero exposure to PFOA and PFOS affects semen quality, testicular volume, and reproductive hormone levels.
We recruited 169 male offspring (19-21 years of age) from a pregnancy cohort established in Aarhus, Denmark, in 1988-1989, corresponding to 37.6% of the eligible sons. Each man provided a semen sample and a blood sample. Semen samples were analyzed for sperm concentration, total sperm count, motility, and morphology, and blood samples were used to measure reproductive hormones. As a proxy for in utero exposure, PFOA and PFOS were measured in maternal blood samples from pregnancy week 30.
Multivariable linear regression analysis suggested that in utero exposure to PFOA was associated with lower adjusted sperm concentration (ptrend = 0.01) and total sperm count (ptrend = 0.001) and with higher adjusted levels of luteinizing hormone (ptrend = 0.03) and follicle-stimulating hormone (ptrend = 0.01). PFOS did not appear to be associated with any of the outcomes assessed, before or after adjustment.
The results suggest that in utero exposure to PFOA may affect adult human male semen quality and reproductive hormone levels.
Cites: Environ Sci Technol. 2004 Sep 1;38(17):4489-9515461154
Cites: Environ Health Perspect. 2004 Aug;112(11):1204-715289168
The temporal trends and influence of age and gender on levels of selected brominated flame retardants (BFRs) in human serum have been assessed by analyzing archived samples from Norway. Serum from 40 to 50 year old men collected at six time periods during 1977 to 1999 and from eight groups of differing age and gender sampled in 1998 were pooled into six and eight samples, respectively. The BFRs were isolated using solid-phase extraction (SPE) and the serum lipids decomposed bytreatmentwith concentrated sulfuric acid directly on the polystyrene-divinylbenzene SPE column, prior to elution of the BFRs. Following diazomethane derivatization, the samples were analyzed by gas chromatography-electron capture mass spectrometry. Eight BFRs were quantified in the serum samples: 2,4,4'-tribromodiphenyl ether (BDE-28), 2,2',4,4'-tetrabromodiphenyl ether (BDE-47), 2,2',4,4',5-pentabromodiphenyl ether (BDE-99), 2,2',4,4',6-pentabromodiphenyl ether (BDE-100), 2,2',4,4',5,5'-hexabromodiphenyl ether (BDE-153), 2,2',4,4',5,6'-hexabromodiphenyl ether (BDE-154), 2,4,6-tribromophenol (TriBP), and tetrabromobisphenol A (TBBP-A). The serum concentrations of all the BFRs, increased during the entire period with the exception of TriBP, and the sum of the six polybrominated diphenyl ethers increased from 0.44 ng/g lipids in 1977 to 3.3 ng/g lipids in 1999. The BFR concentrations in the serum from the different age groups were relatively similar, except for the age group 0-4 years, which had 1.6-3.5 times higher serum concentrations. Women older than 25 years had lower serum concentrations of BFRs compared to the corresponding group of men. No trend related to age or gender, nor time during the period 1977 to 1999 was observed for TriBP. The present study indicates an ongoing increase in human exposure to BFRs, and the current body burden appears to be independent of age, except for infants (0-4 years old), who seem to experience elevated exposure.
Comment In: Environ Sci Technol. 2002 May 1;36(9):188A-192A12026967
At present, scientific knowledge on depuration rates of persistent organic pollutants (POPs) is limited and the previous assumptions of considerable reduction of body burdens through breast-feeding have recently been challenged. We therefore studied elimination rates of important POPs in nine Norwegian primiparous mothers and one mother breast-feeding her second child by collecting breast-milk samples (n = 70) monthly from about two weeks to up to twelve months after birth. Perfluorinated compounds (PFCs), polybrominated diphenyl ethers (PBDEs), hexabromocyclododecane (HBCD), and polychlorinated biphenyls (PCBs) were determined in the breast-milk samples. Linear mixed effect models were established for selected compounds, and significant decreases in the range of 1.2-4.7% in breast-milk concentrations per month were observed for a wide range of PCBs and PBDEs. For the first time, depuration rates for perfluorooctylsulfonate (PFOS) and perfluorooctanoic acid (PFOA) are presented, being 3.8 and 7.8% per month, respectively (p
Erratum In: Environ Sci Technol. 2011 Apr 1;45(7):3192
Commercially used per- and polyfluorinated compounds (PFCs) have been widely detected in humans, but the sources of human exposure are not fully characterized. The objectives of this study were to assess the relative importance of different exposure pathways of PFCs in a group of Norwegians and compare estimated intakes with internal doses obtained through biomonitoring. Individual PFC intakes from multiple exposure sources for a study group of 41 Norwegian women were estimated using measured PFC concentrations in indoor air and house dust as well as information from food frequency questionnaires and PFC concentrations in Norwegian food. Food was generally the major exposure source, representing 67-84% of the median total intake for PFOA and 88-99% for PFOS using different dust ingestion rates and biotransformation factors of 'precursor' compounds. However, on an individual basis, the indoor environment accounted for up to around 50% of the total intake for several women. Significant positive associations between concentrations of PFCs in house dust and the corresponding serum concentrations underline the importance of indoor environment as an exposure pathway for PFCs. For breast-fed infants, breast milk was calculated to be the single most important source to PFCs by far. The estimated intakes were confirmed by comparing serum concentrations of PFOA and PFOS calculated using PK models, with the corresponding concentrations measured in serum. Even though food in general is the major source of exposure for PFCs, the indoor environment may be an important contributor to human exposure. This study provides valuable knowledge for risk assessment of PFCs and control strategies.
Both building materials and consumer products have been identified as possible sources for potentially hazardous substances like phthalates, polychlorinated biphenyls (PCBs), organophosphorous flame retardants (OPFRs), polybrominated diphenyl ethers (PBDEs) and short chain chlorinated paraffins (SCCPs) in indoor air. Thus, indoor air has been suggested to contribute significantly to human exposure to these chemicals. There is lack of data on the occurrence of several of the aforementioned chemicals in indoor air. Therefore, indoor air (gas and particulate phase) was collected from 48 households and 6 classrooms in two counties in Norway. In both the households and schools, median levels of low molecular weight phthalates (785?ng/m3), OPFRs (55?ng/m3) and SCCPs (128?ng/m3) were up to 1000 times higher than the levels of PCBs (829?pg/m3) and PBDEs (167?pg/m3). Median concentrations of dimethyl phthalate (DMP), diethyl phthalate (DEP), di-isobutyl phthalate (DiBP) and SCCPs were 3-6 times higher in households compared to schools. The levels of OPFRs, PCBs and PBDEs were similar in households and schools. In univariate analysis, the indoor concentrations of different environmental chemicals were significantly affected by location of households (OPFRs), airing of living room (some PCBs and PBDEs), presence of upholstered chair/couch (OPFRs), pet animal hold (some PBDEs) and presence of electrical heaters (selected PCBs and PBDEs). Significant correlations were also detected for the total size of households with OPFRs, frequency of vacuuming the living room with selected PCBs and PBDEs, frequency of washing the living room with selected PCBs and the total number of TVs in the households with selected phthalates and SCCPs. Finally, intake estimates indicated that indoor air contributed more or equally to low molecular weight phthalates and SCCPs exposure compared to food consumption, whereas the contribution from indoor air was smaller than the dietary intake for the other groups of chemicals.
This study investigates dietary exposure and serum levels of polybrominated diphenyl ethers (PBDEs) and hexabromocyclododecane (HBCD) in a group of Norwegians (n = 184) with a wide range of seafood consumption (4-455 g/day). Mean dietary exposure to Sum 5 PBDEs (1.5 ng/kg body weight/day) is among the highest reported. Since concentrations in foods were similar to those found elsewhere in Europe, this may be explained by high seafood consumption among Norwegians. Oily fish was the main dietary contributor both to Sum PBDEs and to the considerably lower HBCD intake (0.3 ng/kg body weight/day). Milk products appeared to contribute most to the BDE-209 intake (1.4 ng/kg body weight/day). BDE-209 and HBCD exposures are based on few food samples and need to be confirmed. Serum levels (mean Sum 7 PBDEs = 5.2 ng/g lipid) and congener patterns (BDE-47 > BDE-153 > BDE-99) were comparable with other European reports. Correlations between individual congeners were higher for the calculated dietary exposure than for serum levels. Further, significant but weak correlations were found between dietary exposure and serum levels for Sum PBDEs, BDE-47, and BDE-28 in males. This indicates that other sources in addition to diet need to be addressed.
The worldwide ban of several formulations of brominated flame retardants has caused an increase in the production of organophosphorus flame retardants (PFRs) to meet the existing fire regulations for a wide range of household products. This biomonitoring study surveys the occurrence of the metabolites from PFRs and related plasticizers (dialkyl and diaryl phosphates; DAPs) in urine from a Norwegian mother-child cohort (48 mothers and 54 children). Concentrations of DAPs were higher in the children than in their mothers (Wilcoxon signed-rank test p=0.001). Median urinary concentrations of diphenyl phosphate (DPHP) were 1.1 and 0.51ng/mL in children and mothers, respectively, followed by bis(1,3-dichloro-2-propyl) phosphate (BDCIPP) with medians of 0.23 and 0.12ng/mL, respectively. Detection frequencies for bis(2-butoxyethyl) phosphate (BBOEP) in urine from children and mothers were 32 and 1%, respectively (median