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.
Exposure to phthalates has been associated with reproductive and developmental toxicity. Data on levels of these compounds in the Norwegian population is limited. In this study, urine samples were collected from 48 mothers and their children in two counties in Norway. Eleven different phthalate metabolites originating from six commonly used phthalates in consumer products were determined. Concentrations of phthalate metabolites were significantly higher in children compared to mothers except for mono-ethyl phthalate (MEP). The mothers provided several urine samples during 24hours (h) and diurnal variation showed that the concentrations in the morning urine samples (24-8h) were significantly higher than at other time-periods for most of the phthalate metabolites. Intraclass correlation coefficients (ICCs) for 24-hour time-period were in the range of 0.49-0.81. These moderate to high ICCs indicate that one spot urine sample can be used to estimate the exposure to phthalates. Since a significant effect of time of day was observed, it is still advisable to standardize the collection time point to reduce the variation. For the mothers, the use of personal care products (PCPs) were less associated with morning urine samples than early day (8-12h) and evening (16-24h) urine samples. The use of perfume and hair products were positively associated with the urinary concentrations of low molecular weight phthalates. Use of shower soap and shampoo were positively associated with urinary concentration of di(2-ethylhexyl) phthalate (DEHP) metabolites. For children, face cream use was positively associated with phthalate metabolites in the morning samples, and hand soap use was negatively associated with concentration of urinary DEHP metabolites in afternoon/evening samples. Since different PCPs were associated with the urinary phthalate metabolites in different time-periods during a day, more than one spot urine sample might be required to study associations between urinary phthalate metabolites and the use of PCPs.
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.
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.
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.
Perfluoroalkyl substances (PFAS) are suggested to have immunosuppressive effects; exposure in utero and in the first years of life is of special concern as fetuses and small children are highly vulnerable to toxicant exposure. The objective of this study was to investigate the effect of pre-natal exposure to PFAS on responses to pediatric vaccines and immune-related health outcomes in children up to 3 years of age. In the prospective birth-cohort BraMat, a sub-cohort of the Norwegian Mother and Child Cohort Study (MoBa), pregnant women from Oslo and Akershus, Norway, were recruited during 2007-2008. Three annual questionnaire-based follow-ups were performed. Blood samples were collected from the mothers at the time of delivery and from the children at the age of 3 years. As a measure of pre-natal exposure to PFAS, the concentrations of perfluorooctanoate (PFOA), perfluorononanoate (PFNA), perfluorohexane sulfonate (PFHxS), and perfluorooctane sulfonate (PFOS) were determined in maternal blood from 99 BraMat participants. Main outcome measures were anti-vaccine antibody levels, common infectious diseases and allergy- and asthma-related health outcomes in the children up to the age of 3 years. There was an inverse association between the level of anti-rubella antibodies in the children's serum at age 3 years and the concentrations of the four PFAS. Furthermore, there was a positive association between the maternal concentrations of PFOA and PFNA and the number of episodes of common cold for the children, and between PFOA and PFHxS and the number of episodes of gastroenteritis. No associations were found between maternal PFAS concentrations and the allergy- and asthma-related health outcomes investigated. The results indicate that pre-natal exposure to PFAS may be associated with immunosuppression in early childhood.
Perfluorinated compounds (PFCs) have been determined in 21 samples of selected food and beverages such as meat, fish, bread, vegetables, milk, drinking water and tea from the Norwegian marked. Up to 12 different PFCs were detected in the samples. Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonic acid (PFOS) were found in concentrations similar to or lower than what has been observed in other studies world-wide. Differences in the relative proportion of PFOA and PFOS between samples of animal origin and samples of non-animal origin were observed and support findings that PFOS has a higher bioaccumulation potential in animals than PFOA. Based on these 21 measurements and consumption data for the general Norwegian population, a rough estimate of the total dietary intake of PFCs was found to be around 100ngd(-1). PFOA and PFOS contributed to about 50% of the total intake. When dividing the population in gender and age groups, estimated intakes were decreasing with increasing age and were higher in males than females. The estimated intakes of PFOS and PFOA in the present study are lower than what has been reported in studies from Spain, Germany, United Kingdom, Canada and Japan. This study illustrates that by improving the analytical methods for determination of PFC in food samples, a broad range of compounds can be detected, which is important when assessing dietary exposure.
Per- and polyfluorinated compounds (PFCs) have been found to be ubiquitously distributed in human populations, however the sources of human exposure are not fully characterized. A wide range of PFCs were determined in paired samples of indoor air and dust from 41 Norwegian households. Up to 18 ionic and 9 neutral PFCs were detected. The concentrations found are comparable to or lower than what has previously been reported in North America, Europe, and Asia. The highest median concentrations in dust were observed for perfluorohexanoic acid (28 ng/g), perfluorononanoic acid (23 ng/g), perfluorododecanoic acid (19 ng/g), and perfluorooctanoic acid (18 ng/g). However, perfluoroalkyl sulfonic acids (PFSAs) were also frequently detected. Fluortelomer alcohols were the most prominent compounds found in indoor air, with median concentrations for 8:2 fluortelomer alcohol, 10:2 fluortelomer alcohol, and 6:2 fluortelomer alcohol of 5173, 2822, and 933 pg/m(3) air, respectively. All perfluoroalkyl sulfonamides and sulfonamidoethanols (FOSA/FOSEs) were detected in more than 40% of the air samples. For the first time, significant positive correlations (p
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.
Perfluorinated compounds (PFCs) comprise a large group of man-made fluorinated chemicals used in a number of consumer products and industrial applications. PFCs have shown to be persistent, bio-accumulative and widespread in the environment. Animal studies have demonstrated hepatotoxicity, immunotoxicity, developmental toxicity as well as hormonal effects. We investigated prenatal exposure to several PFCs and detected up to seven different PFCs in 123 paired samples of human maternal and cord blood, from a subcohort of the Norwegian Mother and Child Cohort Study (MoBa). The maternal and foetal levels were significantly correlated for all PFCs tested with median PFC concentrations in cord blood ranging between 30 and 79% of the maternal concentrations, demonstrating placental passage. The composition of the different PFCs varied between cord and maternal blood, with a higher proportion of shorter chained PFCs together with a higher amount of the branched isomers of perfluorooctane sulfonate (PFOS) in cord blood. Additionally, the sulfonate group seems to impede transfer efficiency. This indicates a selective placental passage of the different PFCs and hence a specific foetal exposure.
Brominated flame retardants (BFRs), in particular the polybrominated diphenyl ethers (PBDEs), have been used in consumer products for many years to increase fire resistance. Recently, developmental neurotoxicity at very low levels has increased the concern about these compounds. The major objectives of this study were to investigate the maternal and fetal exposure to PBDEs on the basis of maternal and umbilical cord plasma samples and to study the extent of placental transfer for different PBDE congeners. The findings were also compared with previously observed PBDE levels and patterns determined in placental tissue from the same individuals, and the relationship with the external exposure from house dust from the participants' homes was explored. Samples of maternal and umbilical cord plasma from a cohort of 51 pregnant women from the Copenhagen area were collected. Paired maternal and umbilical cord plasma were analysed for BDE-28, 37, 47, 85, 99, 100, 119, 138, 153, 154, 183, 209 and the brominated biphenyl BB-153 using automated SPE extraction and GC-HRMS for the tri- to hepta-BDEs and GC-LRMS (ECNI) for BDE-209. PBDEs were detected in all maternal and umbilical cord plasma samples. The sum of tri- to hexa-BDEs (SigmaPBDE) in maternal plasma varied between 640 and 51,946 pg/g lipid weight (lw) with a median level of 1765 pg/g lw. In the umbilical cord samples SigmaPBDE varied between 213 and 54,346 pg/g lw with a median of 958 pg/g lw. The levels observed in fetal and maternal plasma were highly correlated, but the placental transport of PBDE congeners was found to decrease with increasing diphenyl ether bromination. Maternal concentrations were significantly correlated (p
Perfluoroalkyl substances (PFAS) are persistent and ubiquitous environmental contaminants, and human exposure to these substances may be related to preeclampsia, a common pregnancy complication. Previous studies have found serum concentrations of PFAS to be positively associated with pregnancy-induced hypertension and preeclampsia in a population with high levels of exposure to perfluorooctanoate. Whether this association exists among pregnant women with background levels of PFAS exposure is unknown. Using data from the Norwegian Mother and Child Cohort Study conducted by the Norwegian Institute of Public Health, we carried out a study of nulliparous pregnant women enrolled in 2003-2007 (466 cases, 510 noncases) to estimate associations between PFAS concentrations and an independently validated diagnosis of preeclampsia. We measured levels of 9 PFAS in maternal plasma extracted midpregnancy; statistical analyses were restricted to 7 PFAS that were quantifiable in more than 50% of samples. In proportional hazards models adjusted for maternal age, prepregnancy body mass index (weight (kg)/height (m)(2)), educational level, and smoking status, we observed no strongly positive associations between PFAS levels and preeclampsia. We found an inverse association between preeclampsia and the highest quartile of perfluoroundecanoic acid concentration relative to the lowest quartile (hazard ratio = 0.55, 95% confidence interval: 0.38, 0.81). Overall, our findings do not support an increased risk of preeclampsia among nulliparous Norwegian women with background levels of PFAS exposure.
Perfluorinated compounds are ubiquitous pollutants; epidemiologic data suggest they may be associated with adverse health outcomes, including subfecundity. We examined subfecundity in relation to 2 perfluorinated compounds-perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA).
This case-control analysis included 910 women enrolled in the Norwegian Mother and Child Cohort Study in 2003 and 2004. Around gestational week 17, women reported their time to pregnancy and provided blood samples. Cases consisted of 416 women with a time to pregnancy greater than 12 months, considered subfecund. Plasma concentrations of perfluorinated compounds were analyzed using liquid chromatography-mass spectrometry. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated for each pollutant quartile using logistic regression. Estimates were further stratified by parity.
The median plasma concentration of PFOS was 13.0 ng/mL (interquartile range [IQR] = 10.3-16.6 ng/mL) and of PFOA was 2.2 ng/mL (IQR = 1.7-3.0 ng/mL). The relative odds of subfecundity among parous women was 2.1 (95% CI = 1.2-3.8) for the highest PFOS quartile and 2.1 (1.0-4.0) for the highest PFOA quartile. Among nulliparous women, the respective relative odds were 0.7 (0.4-1.3) and 0.5 (0.2-1.2).
Previous studies suggest that the body burden of perfluorinated compounds decreases during pregnancy and lactation through transfer to the fetus and to breast milk. Afterward, the body burden may increase again. Among parous women, increased body burden may be due to a long interpregnancy interval rather than the cause of a long time to pregnancy. Therefore, data from nulliparous women may be more informative regarding toxic effects of perfluorinated compounds. Our results among nulliparous women did not support an association with subfecundity.
This study investigates the occurrence of 37 organohalogen and organophosphate flame retardants (FRs) from Norwegian households (n = 48) and classrooms from two primary schools (n = 6). Around 80% of the targeted FRs were detected in air and dust from the sampling sites. The comparison of settled dust with floor dust revealed no statistical differences between median concentrations of the FRs (n = 12). Decabromodiphenyl ether and tris(2-butoxyethyl) phosphate showed the highest median floor dust concentrations in both environments. In the air samples, the highest concentrations were observed for 2,2',4,4'-tetrabromodiphenyl ether and tris(1-chloro-2-propyl) phosphate. Remarkably, the emerging FR, 4-(1,2-dibromoethyl)-1,2-dibromocyclohexane, abbreviated as TBECH or DBE-DBCH, showed the highest indoor air concentrations reported in the literature (households, 77.9 pg/m(3) and schools, 46.6 pg/m(3)). Good Spearman correlations between the FR concentrations in dust and air (0.36
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.
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
Several studies have suggested that exposure to organophosphorus (OP) pesticides is detrimental for health, and in particular for children where moderate doses may have a negative impact on the neurodevelopment. This study surveys levels of the 6 non-specific urinary metabolites (dialkyl phosphates (DAPs)) of OP pesticides in Norwegian mothers (n=48) and their children (n=54), and examines the diurnal variation in concentrations as well as associations with consumption of specific food products. The highest median concentration measured in urine was found for dimethyl thiophosphate (5.3 and 5.5ng/mLSG; specific gravity corrected) for both children and mothers, respectively, followed by diethyl phosphate (3.8 and 5.3ng/mLSG, respectively). The intra-class correlation coefficients of DAPs among mothers were moderate (0.49-0.68), and consumption of fruit explained between 8% and 55% of the variations in the mothers' and their children's urinary DAP concentrations.
Perfluorooctane sulfonate and perfluorooctanoic acid are perfluorinated compounds (PFCs) widely distributed in the environment. Previous studies of PFCs and birth weight are equivocal. The authors examined this association in the Norwegian Mother and Child Cohort Study (MoBa), using data from 901 women enrolled from 2003 to 2004 and selected for a prior case-based study of PFCs and subfecundity. Maternal plasma samples were obtained around 17 weeks of gestation. Outcomes included birth weight z scores, preterm birth, small for gestational age, and large for gestational age. The adjusted birth weight z scores were slightly lower among infants born to mothers in the highest quartiles of PFCs compared with infants born to mothers in the lowest quartiles: for perfluorooctane sulfonate, ß = -0.18 (95% confidence interval: -0.41, 0.05) and, for perfluorooctanoic acid, ß = -0.21 (95% confidence interval: -0.45, 0.04). No clear evidence of an association with small for gestational age or large for gestational age was observed. Perfluorooctane sulfonate and perfluorooctanoic acid were each associated with decreased adjusted odds of preterm birth, although the cell counts were small. Whether some of the associations suggested by these findings may be due to a noncausal pharmacokinetic mechanism remains unclear.
Cites: Toxicol Sci. 2006 Apr;90(2):510-816415327
Cites: JAMA. 2006 Apr 19;295(15):1809-2316622143
Cites: Toxicology. 2006 Oct 3;227(1-2):156-6416978759
Cites: Int J Epidemiol. 2006 Oct;35(5):1146-5016926217
Cites: Epidemiology. 2007 Jul;18(4):441-517473707
Cites: J Occup Environ Med. 2007 Jul;49(7):722-917622844
Cites: Environ Health Perspect. 2007 Sep;115(9):1298-30517805419
Cites: Environ Health Perspect. 2007 Nov;115(11):1670-618008002
Cites: Environ Health Perspect. 2007 Nov;115(11):1677-8218008003
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
Dietary patterns were related to intake and blood concentrations of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/PCDFs), dioxin-like polychlorinated biphenyls (dl-PCBs) and selected non-dioxin-like-PCBs (ndl-PCBs). Intake calculations were based on an extensive food frequency questionnaire and a congener-specific database on concentrations in Norwegian foods. The study (2003) applied a two-step inclusion strategy recruiting representative (n=73) and high consumers (n=111) of seafood and game. Estimated median intakes of sum PCDD/PCDFs and dl-PCBs of the representative and high consumers were 0.78 and 1.25 pg toxic equivalents (TEQ)/kg bw/day, respectively. Estimated median intakes of ndl-PCBs (sum chlorinated biphenyl (CB)-28, 52, 101, 138, 153, 180) were 4.26 and 6.40 ng/kg bw/day. The median blood concentrations of PCDD/PCDFs/dl-PCBs were 28.7 and 35.1 pg TEQ/g lipid, and ndl-PCBs (sum of CB-101, 138, 153 and 180) 252 and 299 ng/g lipid. The Spearman correlations between dietary intake and serum concentration were r=0.34 (p=0.017) for dl-compounds and r=0.37 (p