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.
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.
Brominated and phosphorous flame retardants (BFRs, PFRs) are added to household and consumer products to reduce their flammability. Some FRs are persistent in the environment and may have adverse health effects. As exposure indoors contributes significantly to total exposure, we wanted to estimate the exposure of children (3 years of age) through dust ingestion, inhalation, and dermal absorption. We measured 17 BFRs and 10 PFRs in indoor dust, predicted their respective concentrations in the indoor air and assessed children's exposure. Among the BFRs, decabromodiphenyl ether (BDE-209) had highest median level in the dust (411?ng/g) followed by decabromodiphenyl ethane (DBDPE, 119?ng/g) and bis-ethylhexyl tetrabromophthalate (BEH-TEBP, 106?ng/g). Among the PFRs, trisbutoxyethyl phosphate (TBOEP) had the highest concentration (11100?ng/g) followed by tris(2-chloroisopropyl) phosphate (TCIPP, 1870?ng/g) and triphenyl phosphate (TPHP, 773?ng/g). FR concentration in air predicted from dust concentrations were within the interquartile range of experimental data for 10/13 of BFRs and 4/8 of PFRs compared. Dust ingestion was the major route of exposure (75-99%) for higher molecular weight BFRs, TBOEP and phenyl based PFRs (73-77%). Inhalation was important for volatile BFRs like pentabromobenzene (PBB 71%) and pentabromotoluene (PBT 52%) and dermal exposure for volatile chlorinated PFRs (TCEP 84%, TCIPP 77%). Margins of Exposure (MoE) were calculated as the ratio of total exposure to oral Reference Dose (RfD). MoEs were lowest for TCEP (220), TBOEP (240) and TCIPP (830), and > 1000 for all other FRs. These MoEs imply no risk for Finnish children by the studied FRs.
Phthalates and bisphenol A (BPA) are ubiquitous in our environment. These chemicals have been characterized as endocrine disruptors that can cause functional impairment of development and reproduction. Processed and packaged foods are among the major sources of human exposure to these chemicals. No previous report showing the levels of these chemicals in food items purchased in Norway is available. The aim of the present study was to determine the concentration of ten different phthalates and BPA in foods and beverages purchased on the Norwegian market and estimate the daily dietary exposure in the Norwegian adult population. Commonly consumed foods and beverages in Norway were purchased in a grocery store and analysed using gas- and liquid chromatography coupled with mass spectrometry. Daily dietary exposures to these chemicals in the Norwegian adult population were estimated using the latest National dietary survey, Norkost 3 (2010-2011). This study showed that phthalates and BPA are found in all foods and beverages that are common to consume in Norway. The detection frequency of phthalates in the food items varied from 11% for dicyclohexyl phthalate (DCHP) to 84% for di-iso-nonyl phthalate (DiNP), one of the substitutes for bis(2-ethylhexyl) phthalate (DEHP). BPA was found in 54% of the food items analysed. Among the different phthalates, the highest concentrations were found for DEHP and DiNP in the food items. Estimated dietary exposures were also equally high and dominated by DEHP and DiNP (400-500 ng/kg body weight (bw)/day), followed by di-iso-butyl phthalate (DiBP), di-n-butyl phthalate (DnBP), di-n-octyl phthalate (DnOP) and di-iso-decyl phthalate (DiDP) (30-40 ng/kg bw/day). Dimethyl phthalate (DMP), diethylphthalate (DEP) and DCHP had the lowest concentrations and the exposures were around 10-20 ng/kg bw/day. Estimated dietary exposure to BPA was 5 ng/kg bw/day. In general, levels of phthalates and BPA in foods and beverages from the Norwegian market are comparable to other countries worldwide. Grain and meat products were the major contributors of exposure to these chemicals in the Norwegian adult population. The estimated dietary exposures to these chemicals were considerably lower than their respective tolerable daily intake (TDI) values established by the European Food Safety Authority (EFSA).
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.
Exposure to persistent organic pollutants (POPs) during prenatal and postnatal life has been extensively studied in relation to adverse health effects in children.
The aim was to identify determinants of the concentrations of polychlorinated biphenyls (PCBs), brominated flame retardants (polybrominated diphenyl ethers, PBDEs; polybrominated biphenyl, PBB), and organochlorine pesticides (OCPs) in blood samples from pregnant women and children in The Norwegian Mother and Child Cohort Study (MoBa).
Blood samples were collected from two independent subsamples within MoBa; a group of women (n=96) enrolled in mid-pregnancy during the years 2002-2008 and a group of 3 year old children (n=99) participating during 2010-2011. PCB congeners (74, 99, 138, 153, 180, 170, 194, 209, 105, 114, 118, 156, 157, 167, and 189), brominated flame retardants (PBDE-28, 47, 99, 100, 153, 154, and PBB-153), as well as the OCPs hexachlorobenzene (HCB), oxychlordane, 4,4'dichlorodiphenyltrichloroethane (DDT), and 4,4'dichlorodiphenyldichloroethylene (DDE) were measured in both pregnant women and children.
Age, low parity, and low pre-pregnant BMI were the most important determinants of increased plasma concentrations of POPs in pregnant women. In 3 year old children, prolonged breastfeeding duration was a major determinant of increased POP concentrations. Estimated dietary exposure to PCBs during pregnancy was positively associated with plasma concentrations in 3 year old children, but not in pregnant women. Plasma concentrations were approximately 40% higher in children compared to pregnant women.
Several factors associated with exposure and toxicokinetics, i.e. accumulation, excretion and transfer via breastmilk of POPs were the main predictors of POP levels in pregnant women and children. Diet, which is the main exposure source for these compounds in the general population, was found to predict PCB levels only among children. For the PBDEs, for which non-dietary sources are more important, toxicokinetic factors appeared to have less predictive impact.