Associations between serum perfluoroalkyl acid (PFAA) concentrations and health related biomarkers in firefighters.

OBJECTIVES: Firefighters who used aqueous film forming foam in the past have experienced elevated exposures to perfluoroalkyl acids (PFAAs). The objective of this study was to examine the associations between clinical chemistry endpoints and serum concentrations of perfluorooctanoic acid (PFOA), perfluorohexane sulfonate (PFHxS), perfluoroheptane sulfonate (PFHpS) and perfluorooctane sulfonate (PFOS) in firefighters. Multiple linear regression was used to assess relationships between PFAA serum concentrations and biochemical markers for cardiovascular disease, kidney-, liver- and thyroid function, in a cross-sectional survey of 783 firefighters with elevated levels of PFHxS, PFHpS and PFOS in relation to the most recently reported levels in the general Australian population. Linear logistic regression was used to assess the odds ratios for selected self-reported health outcomes. Repeated measures linear mixed models were further used to assess relationships between PFAAs and biomarkers for cardiovascular disease and kidney function longitudinally in a subset of the firefighters (n = 130) where serum measurements were available from two timepoints, five years apart. In the cross-sectional analysis, higher levels of all PFAAs were significantly associated with higher levels of biomarkers for cardiovascular disease (total-cholesterol, and LDL-cholesterol). For example, doubling in PFOS serum concentration were associated with increases in total cholesterol (ß:0.111, 95% confidence interval (95%CI): 0.026, 0.195 mmol/L) and LDL-cholesterol (ß: 0.104, 95%CI:0.03, 0.178 mmol/L). Doubling in PFOA concentration, despite not being elevated in the study population, were additionally positively associated with kidney function marker urate (e.g., ß: 0.010, 95%CI; 0.004, 0.016 mmol/L) and thyroid function marker TSH (e.g., ß: 0.087, 95%CI: 0.014, 0.161 mIU/L). PFAAs were not associated with any assessed self-reported health conditions. No significant relationships were observed in the longitudinal analysis. Findings support previous studies, particularly on the association between PFAAs and serum lipids.

Pesticide exposure in New Zealand school-aged children: Urinary concentrations of biomarkers and assessment of determinants.

This study aimed to assess pesticide exposure and its determinants in children aged 5-14 years. Urine samples (n = 953) were collected from 501 participating children living in urban areas (participant n = 300), rural areas but not on a farm (n = 76), and living on a farm (n = 125). The majority provided two samples, one in the high and one in the low spraying season. Information on diet, lifestyle, and demographic factors was collected by questionnaire. Urine was analysed for 20 pesticide biomarkers by GC-MS/MS and LC-MS/MS. Nine analytes were detected in > 80% of samples, including six organophosphate insecticide metabolites (DMP, DMTP, DEP, DETP, TCPy, PNP), two pyrethroid insecticide metabolites (3-PBA, trans-DCCA), and one herbicide (2,4-D). The highest concentration was measured for TCPy (median 13 µg/g creatinine), a metabolite of chlorpyrifos and triclopyr, followed by DMP (11 µg/g) and DMTP (3.7 µg/g). Urine metabolite levels were generally similar or low compared to those reported for other countries, while relatively high for TCPy and pyrethroid metabolites. Living on a farm was associated with higher TCPy levels during the high spray season. Living in rural areas, dog ownership and in-home pest control were associated with higher levels of pyrethroid metabolites. Urinary concentrations of several pesticide metabolites were higher during the low spraying season, possibly due to consumption of imported fruits and vegetables. Organic fruit consumption was not associated with lower urine concentrations, but consumption of organic food other than fruit or vegetables was associated with lower concentrations of TCPy in the high spray season. In conclusion, compared to other countries such as the U.S., New Zealand children had relatively high exposures to chlorpyrifos/triclopyr and pyrethroids. Factors associated with exposure included age, season, area of residence, diet, in-home pest control, and pets.

Biomonitoring of per- and polyfluoroalkyl substances (PFAS) exposure in firefighters: Study design and lessons learned from stakeholder and participant engagement.

Firefighters may be occupationally exposed to per- and polyfluoroalkyl substances (PFASs) through Aqueous Film-Forming Foam (AFFF), smoke, dust and turnout gear, in addition to other background exposure sources. Epidemiological assessment of PFAS exposure in an occupational cohort of firefighting staff commenced in 2013-2014, following cessation of PFAS-based AFFF in Australian aviation. Here we present the study design and methodology of a follow-up study conducted in 2018-2019. We focus on our experiences engaging with stakeholders and participants with the establishment of an inclusive study group and highlight the key lessons learned from implementing a co-design process in the study. The study included a cross-sectional assessment of blood serum concentrations of 40 PFASs, including perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS) and perfluorohexane sulfonate (PFHxS), and 14 health-related biomarkers in 799 current and former Aviation Rescue Firefighting Services employees. A large proportion (87%) of the participants from the preliminary exposure study in 2013-2014 were re-recruited in the follow-up study. This enabled further longitudinal analyses in this subset of 130 participants. Participants included employees from different work roles and timeframes, reflecting the periods when three different firefighting foams were utilised in Australia. Establishment of a collaborative and inclusive study group (including stakeholders and participants) contributed to several components of the study design, including the expansion of robust analytical quality assurance and control measurements, and tailoring of communication and dissemination strategies. These outcomes were key factors that improved transparency of the research design, methods and results. Additionally, implementing elements of co-design helped build trust between researchers and participants, which is an important consideration for studies funded by stakeholders related to the exposure source.

Phthalate esters in face masks and associated inhalation exposure risk.

This study assessed the composition of single-use face mask materials, quantified the concentration of phthalate esters in masks and evaluated associated inhalation exposure risk. All the mask samples, including 12 surgical and four N95/P1/P2 masks, were identified to be made of polypropylene, with polyethylene terephthalate present in the N95/P1/P2 masks. Di-methyl phthalate, di-n-butyl phthalate, di-ethyl phthalate, di-isobutyl phthalate and di(2-ethylhexyl) phthalate were frequently detected and their concentration summed up 55 ± 35 ~ 1700 ± 140 ng per surgical mask and 2300 ± 150 ~ 5200 ± 800 ng per N95/P1/P2 mask. Our simulation experiment suggested a mean loss of 13 - 71% of phthalate mass depending on compounds, during 5-hour wearing of these masks. This resulted in an estimated daily intake of individual compounds no higher than 20 ng/kg/day for adults and 120 ng/kg/day for toddlers, which were at least 80 times lower compared to relevant tolerable daily intake values. Two interventional trials were conducted where a volunteer wore a mask for four hours and urine samples were collected before and after the mask wearing. No obvious increase was observed for the urinary concentration of any phthalate metabolite, indicating minimal contribution to overall exposure to phthalate esters.

Comparison of lipid-normalised concentrations of persistent organic pollutants (POPs) between serum and adipose tissue.

Human biomonitoring of persistent organic pollutants (POPs) is typically based on serum analysis and for comparison and modelling purposes, data are often normalised to the lipid content of the serum. Such approach assumes a steady state of the compound between the serum lipids and for example lipid-rich adipose tissue. Few published data are available to assess the validity of this assumption. The aim of this study was to measure concentrations of POPs in both serum and adipose tissue samples from 32 volunteers and compare the lipid-normalised concentrations between serum and adipose tissue. For p,p'-DDE, PCB-138, PCB-153 and PCB-180, lipid-normalised adipose tissue concentrations were positively correlated to the respective serum concentrations but generally were more highly concentrated in adipose tissue. These results suggest that the investigated legacy POPs that were consistently found in paired samples may often not be in a steady state between the lipid compartments of the human body. Consequently, the analysis of serum lipids as a surrogate for adipose tissue exposure may more often than not underestimate total body burden of POPs. Further research is warranted to confirm the findings of this study.

Exposure and Toxicity Characterization of Chemical Emissions and Chemicals in Products: Global Recommendations and Implementation in USEtox.

PURPOSE: Reducing chemical pressure on human and environmental health is an integral part of the global sustainability agenda. Guidelines for deriving globally applicable, life cycle based indicators are required to consistently quantify toxicity impacts from chemical emissions as well as from chemicals in consumer products. In response, we elaborate the methodological framework and present recommendations for advancing near-field/far-field exposure and toxicity characterization, and for implementing these recommendations in the scientific consensus model USEtox. METHODS: An expert taskforce was convened by the Life Cycle Initiative hosted by UN Environment to expand existing guidance for evaluating human toxicity impacts from exposure to chemical substances. This taskforce evaluated advances since the original release of USEtox. Based on these advances, the taskforce identified two major aspects that required refinement, namely integrating near-field and far-field exposure and improving human dose-response modeling. Dedicated efforts have led to a set of recommendations to address these aspects in an update of USEtox, while ensuring consistency with the boundary conditions for characterizing life cycle toxicity impacts and being aligned with recommendations from agencies that regulate chemical exposure. The proposed framework was finally tested in an illustrative rice production and consumption case study. RESULTS AND DISCUSSION: On the exposure side, a matrix system is proposed and recommended to integrate far-field exposure from environmental emissions with near-field exposure from chemicals in various consumer product types. Consumer exposure is addressed via submodels for each product type to account for product characteristics and exposure settings. Case study results illustrate that product-use related exposure dominates overall life cycle exposure. On the effect side, a probabilistic dose-response approach combined with a decision tree for identifying reliable points of departure is proposed for non-cancer effects, following recent guidance from the World Health Organization. This approach allows for explicitly considering both uncertainty and human variability in effect factors. Factors reflecting disease severity are proposed to distinguish cancer from non-cancer effects, and within the latter discriminate reproductive/developmental and other non-cancer effects. All proposed aspects have been consistently implemented into the original USEtox framework. CONCLUSIONS: The recommended methodological advancements address several key limitations in earlier approaches. Next steps are to test the new characterization framework in additional case studies and to close remaining research gaps. Our framework is applicable for evaluating chemical emissions and product-related exposure in life cycle assessment, chemical alternatives assessment and chemical substitution, consumer exposure and risk screening, and high-throughput chemical prioritization.

How Many Urine Samples Are Needed to Accurately Assess Exposure to Non-Persistent Chemicals? The Biomarker Reliability Assessment Tool (BRAT) for Scientists, Research Sponsors, and Risk Managers.

In epidemiologic and exposure research, biomonitoring is often used as the basis for assessing human exposure to environmental chemicals. Studies frequently rely on a single urinary measurement per participant to assess exposure to non-persistent chemicals. However, there is a growing consensus that single urine samples may be insufficient for adequately estimating exposure. The question then arises: how many samples would be needed for optimal characterization of exposure? To help researchers answer this question, we developed a tool called the Biomarker Reliability Assessment Tool (BRAT). The BRAT is based on pharmacokinetic modeling simulations, is freely available, and is designed to help researchers determine the approximate number of urine samples needed to optimize exposure assessment. The BRAT performs Monte Carlo simulations of exposure to estimate internal levels and resulting urinary concentrations in individuals from a population based on user-specified inputs (e.g., biological half-life, within- and between-person variability in exposure). The BRAT evaluates-through linear regression and quantile classification-the precision/accuracy of the estimation of internal levels depending on the number of urine samples. This tool should guide researchers towards more robust biomonitoring and improved exposure classification in epidemiologic and exposure research, which should in turn improve the translation of that research into decision-making.

Association of endocrine active environmental compounds with body mass index and weight loss following bariatric surgery.

INTRODUCTION: The objective of this study was to study associations of a wide range of halogenated biphenyls, dibenzo-p-dioxins, dibenzofurans and diphenylethers with body mass index (BMI) and evaluate changes in their concentration following bariatric surgery. METHODS: Subcutaneous fat, visceral fat and liver tissue samples were collected from 106 patients undergoing Roux-en-Y gastric bypass surgery for weight loss or patients who were undergoing abdominal surgery for nonbariatric reasons. We measured concentrations of an extensive panel of chlorinated and brominated biphenyls, dioxins, and furans, and brominated diphenylethers in the samples. We conducted linear regression to examine associations with BMI, adjusting for age and gender. Changes in concentration for indicator chemicals were evaluated in samples collected following bariatric surgery in a small subpopulation. RESULTS: After adjustments for age and gender and correction for multiple testing, seven ortho-chlorinated biphenyls, one nonortho-chlorinated biphenyl, four PCDD/Fs and one ortho-brominated biphenyl were associated with BMI. The strongest associations between BMI and lipid-adjusted concentrations were seen with PCB-105 in subcutaneous fat (beta = 16.838 P-val = 1.45E-06) PCB-126 in visceral fat (beta = 15.067 P-val = 7.72E-06) and PCB-118 (beta = 14.101 P-val = 2.66E-05) in liver. The concentrations of sum PCBs, chlorinated toxic equivalent quantity (TEQ's) and brominated compounds increased significantly with weight loss in subcutaneous fat in a group of ten individuals resampled up to five years after bariatric surgery and substantial weight loss. CONCLUSION: We show that selected polychlorinated biphenyls PCBs and structurally related polychlorinated dibenzo-p-dioxins dibenzofurans (PCDD/Fs) were associated with BMI. Concentrations of these lipophilic compounds in subcutaneous fat increased following bariatric surgery.

Exposure to selected preservatives in personal care products: case study comparison of exposure models and observational biomonitoring data.

Exposure models provide critical information for risk assessment of personal care product ingredients, but there have been limited opportunities to compare exposure model predictions to observational exposure data. Urinary excretion data from a biomonitoring study in eight individuals were used to estimate minimum absorbed doses for triclosan and methyl-, ethyl-, and n-propyl- parabens (TCS, MP, EP, PP). Three screening exposure models (European Commission Scientific Commission on Consumer Safety [SCCS] algorithms, ConsExpo in deterministic mode, and RAIDAR-ICE) and two higher-tier probabilistic models (SHEDS-HT, and Creme Care & Cosmetics) were used to model participant exposures. Average urinary excretion rates of TCS, MP, EP, and PP for participants using products with those ingredients were 16.9, 3.32, 1.9, and 0.91 µg/kg-d, respectively. The SCCS default aggregate and RAIDAR-ICE screening models generally resulted in the highest predictions compared to other models. Approximately 60-90% of the model predictions for most of the models were within a factor of 10 of the observed exposures; ~30-40% of the predictions were within a factor of 3. Estimated exposures from urinary data tended to fall in the upper range of predictions from the probabilistic models. This analysis indicates that currently available exposure models provide estimates that are generally realistic. Uncertainties in preservative product concentrations and dermal absorption parameters as well as degree of metabolism following dermal absorption influence interpretation of the modeled vs. measured exposures. Use of multiple models may help characterize potential exposures more fully than reliance on a single model.

Evaluation of human biomonitoring data in a health risk based context: An updated analysis of population level data from the Canadian Health Measures Survey.

In order to characterize exposure of the Canadian population to environmental chemicals, a human biomonitoring component has been included in the Canadian Health Measures Survey (CHMS). This nationally-representative survey, launched in 2007 by the Government of Canada, has measured over 250 chemicals in approximately 30,000 Canadians during the last decade. The capacity to interpret these data at the population level in a health risk context is gradually improving with the development of biomonitoring screening values, such as biomonitoring equivalents (BE) and human biomonitoring (HBM) values. This study evaluates recent population level biomonitoring data from the CHMS in a health risk context using biomonitoring screening values. Nationally representative biomonitoring data for fluoride, selenium, molybdenum, arsenic, silver, thallium, cyfluthrin, 2,4-dichlorophenoxyacetic acid (2,4-D), 3-phenoxybenzoic acid (3-PBA), chlorpyrifos, deltamethrin, bisphenol A, triclosan, acrylamide, cadmium, perfluorooctane sulfonate (PFOS), perfluorooctanoic acid (PFOA), bromoform, chloroform, benzene, toluene, xylene, ethylbenzene, styrene and tetrachloroethylene were screened as part as this study. For non-cancer endpoints, hazard quotients (HQs) were calculated as the ratio of population level concentrations of a specific chemical at the geometric mean and 95th percentile to the corresponding biomonitoring screening value. Cancer risks were calculated at the 5th, 25th, 50th, 75th and 95th percentiles of the population concentration using BEs based on a risk specific dose. Most of the chemicals analyzed had HQs below 1 suggesting that levels of exposure to these chemicals are not a concern at the population level. However, HQs exceeded 1 in smokers for cadmium, acrylamide and benzene, as well as in the general population for inorganic arsenic, PFOS and PFOA, 3-PBA and fluoride. Furthermore, cancer risks for inorganic arsenic, acrylamide, and benzene at most population percentiles of exposure were elevated (>10-5). Specifically, for inorganic arsenic in the general population, the HQ was 3.13 at the 95th percentile concentration and the cancer risk was 3.4 × 10-4 at the 50th percentile of population concentrations. These results suggest that the levels of exposure in the Canadian population to some of the environmental chemicals assessed might be of concern. The results of this screening exercise support the findings of previous risk assessments and ongoing efforts to reduce risks from exposure to chemicals evaluated as part of this study. Although paucity of biomonitoring screening values for several environmental contaminants may be a limitation to this approach, our assessment contributes to the prioritization of a number of chemicals measured as part of CHMS for follow-up activities such as more detailed characterization of exposure sources.

Serum measures of hexabromocyclododecane (HBCDD) and polybrominated diphenyl ethers (PBDEs) in reproductive-aged women in the United Kingdom.

We investigated the serum concentrations of two brominated flame retardants (BFRs) - polybrominated diphenyl ethers (PBDEs) and hexabromocyclododecane (HBCDD) -in 59 women aged between 23 and 42 from the United Kingdom. We also collected demographic data, including age, bodyweight and height in order to test for associations with BFR levels. Temporal and global differences were also assessed using previously published data. HBCDD was detected in 68% of samples with a mean concentration of 2.2 ng/g lipid (range = <0.3-13 ng/g lipid). The dominant stereoisomer was α-HBCDD with an average contribution of 82% (0-100%) towards ΣHBCDD, was followed by γ-HBCDD (average contribution = 17%). PBDEs were detected in 95% of samples with a mean ∑PBDE (sum of BDEs -28, -47, -99, -100, -153, -154 and -183) concentration of 2.4 ng/g lipid (range = <0.4-15 ng/g lipid). BDEs -153 and -47 were the dominant congeners, contributing an average of 40% and 37% respectively, to the average ΣPBDE congener profile. Data from this study suggests that HBCDD levels decrease with age, it also suggests a positive association between bodyweight and HBCDD levels, which likewise requires a large-scale study to confirm this. The data also show that 10 years after their European ban, PBDE body burden has begun to decrease in the UK. Whilst it is too early to draw any firm conclusions for HBCDDs, they appear to be following a similar pattern to PBDEs, with levels decreasing by a factor of >2.5 since 2010. Whilst the human body burden appear to be decreasing, both PBDEs and HBCDD are still consistently detected in human serum, despite legislative action limiting their production and use. This highlights the need to continuously assess human exposure and the effectiveness of policy aimed at reducing exposure.

Pesticide metabolite concentrations in Queensland pre-schoolers - Exposure trends related to age and sex using urinary biomarkers.

This study aimed to assess pesticide concentration and composition trends associated with age and sex in Australian infants and toddlers. Individual urine samples (n = 400) were collected in 2014/5 from Queensland infants and toddlers aged 0-5 y and composited into 20 pools of 20 individual samples by age (of 5 strata) and sex. Nineteen biomarkers including organophosphate and pyrethroid pesticide metabolites, herbicides and metabolites, and an insect repellent, DEET, were measured. In total, seven organophosphate pesticide metabolites, three pyrethroid metabolites and one herbicide metabolite were detectable in >50% of the sample pools. A significant increase of concentrations of dimethyl phosphate, dimethyl dithiophosphate, diethyl thiophosphate (DETP), 3,5,6-trichloro-2-pyridinol (TCPY), 4-nitrophenol and 3-phenoxybenzoic acid with age was observed (with the p value of <0.0001 to 0.034). This suggested that exposure increases following weaning or as a result of increased dietary intake and mobility/activity. Significant age trends remained after adjustment for body weight and urine flow for DETP and TCPY (p = 0.029 and 0.016 respectively). The level of estimated "worst-case scenario" daily intake of chlorpyrifos from these pooled samples ranged from 0.40 to 1.8 µg/kg-day, which was below the Australian Acceptable Daily Intake guideline (3 µg/kg-day). This study presents the first dataset of age trends in concentrations of these pesticides for infants and toddlers and contributed to new understanding of exposure pathways and potential risks.

Advancements in Life Cycle Human Exposure and Toxicity Characterization.

BACKGROUND: The Life Cycle Initiative, hosted at the United Nations Environment Programme, selected human toxicity impacts from exposure to chemical substances as an impact category that requires global guidance to overcome current assessment challenges. The initiative leadership established the Human Toxicity Task Force to develop guidance on assessing human exposure and toxicity impacts. Based on input gathered at three workshops addressing the main current scientific challenges and questions, the task force built a roadmap for advancing human toxicity characterization, primarily for use in life cycle impact assessment (LCIA). OBJECTIVES: The present paper aims at reporting on the outcomes of the task force workshops along with interpretation of how these outcomes will impact the practice and reliability of toxicity characterization. The task force thereby focuses on two major issues that emerged from the workshops, namely considering near-field exposures and improving dose­response modeling. DISCUSSION: The task force recommended approaches to improve the assessment of human exposure, including capturing missing exposure settings and human receptor pathways by coupling additional fate and exposure processes in consumer and occupational environments (near field) with existing processes in outdoor environments (far field). To quantify overall aggregate exposure, the task force suggested that environments be coupled using a consistent set of quantified chemical mass fractions transferred among environmental compartments. With respect to dose­response, the task force was concerned about the way LCIA currently characterizes human toxicity effects, and discussed several potential solutions. A specific concern is the use of a (linear) dose­response extrapolation to zero. Another concern addresses the challenge of identifying a metric for human toxicity impacts that is aligned with the spatiotemporal resolution of present LCIA methodology, yet is adequate to indicate health impact potential. CONCLUSIONS: Further research efforts are required based on our proposed set of recommendations for improving the characterization of human exposure and toxicity impacts in LCIA and other comparative assessment frameworks. https://doi.org/10.1289/EHP3871.

Cohort study of workers at a New Zealand agrochemical plant to assess the effect of dioxin exposure on mortality.

OBJECTIVES: To describe how the exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) influenced mortality in a cohort of workers who were exposed more recently, and at lower levels, than other cohorts of trichlorophenol process workers. DESIGN: A cohort study. SETTING: An agrochemical plant in New Zealand PARTICIPANTS: 1,599 men and women working between 1 January 1969 and 1 November 1988 at a plant producing the herbicide 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) with TCDD as a contaminant. Cumulative TCDD exposure was estimated for each individual in the study by a toxicokinetic model. PRIMARY OUTCOME MEASURES: Calculation of cause-specific standardised mortality ratios (SMRs) and 95% confidence intervals (95% CI's) compared those never and ever exposed to TCDD. Dose-response trends were assessed firstly through SMRs stratified in quartiles of cumulative TCCD exposure, and secondly with a proportional hazards model. RESULTS: The model intercept of 5.1 ppt of TCDD was consistent with background TCDD concentrations in New Zealand among older members of the population. Exposed workers had non-significant increases in all-cancer deaths (SMR=1.08, 95% CI 0.86 to 1.34), non-Hodgkin lymphoma (SMR=1.57, 95% CI: 0.32 to 4.59), soft tissue sarcoma (one death) (SMR=2.38, 95% CI: 0.06 to 13.26), diabetes (SMR=1.27, 95% CI: 0.55 to 2.50) and ischaemic heart disease (SMR=1.21, 95% CI: 0.96 to 1.50). Lung cancer deaths (SMR=0.95, 95% CI: 0.56 to 1.53) were fewer than expected. Neither the stratified SMR nor the proportional hazard analysis showed a dose-response relationship. CONCLUSION: There was no evidence of an increase in risk for 'all cancers', any specific cancer and no systematic trend in cancer risk with TCDD exposure. This argues against the carcinogenicity of TCDD at lower levels of exposure.

Temporal trends in serum polybrominated diphenyl ether concentrations in the Australian population, 2002-2013.

In Australia, systematic biomonitoring of persistent organic pollutants (POPs) in pooled serum samples stratified by age and sex has occurred every two years between 2002/03 and 2012/13. Multiple regression modeling on log10-transformed serum pool concentrations of BDEs 47, 99, 100 and 153 and on the sum of these (Σ4PBDE) was conducted to examine trends by sex and time since baseline, stratified by age group. Temporal trends were age- and congener-specific, with the largest changes per year of observation in the 0-4 year old group, with ß (SE) = -0.098 (0.013) for log10BDE47; -0.119 (0.012) for log10BDE99; -0.084 (0.014) for log10BDE100, and -0.053 (0.013) for log10BDE153, all p < 0.001. Adults over age 16 showed much smaller decreasing temporal trends for BDE47 and BDE99, no significant changes in BDE100, and, for the oldest age groups, slight increases in BDE153. As a result, Σ4PBDE concentrations were stable over the entire time period in adults older than 16. Concentrations of each BDE in pools from females aged 31-60 were significantly lower compared to males. Relative proportions of BDE47 declined, while BDE153 accounted for a greater share of Σ4PBDE over time. Whereas previously we saw a large elevation in the youngest age groups compared to older children and adults, this is no longer the case. This may be due to a decline in infant and toddler exposures in the indoor environment as use of PBDEs in consumer products has been phased out, suggesting temporal changes in the relative sources of exposure for young children in Australia.

Biomonitoring Equivalents for interpretation of urinary iodine.

Iodine is an essential nutrient whose deficiency or excess exposure can cause adverse health effects. The primary sources of iodine exposure in the general population are iodized salt, dairy products, bread and sea food. Urinary iodine concentrations (UIC) have been measured by Canadian Health Measures Survey (CHMS) and US National Health and Nutrition Examination Survey (NHANES). The Institute of Medicine (IOM), the US Agency for Toxic Substances and Disease Registry (ATSDR) and World Health Organization (WHO) have established exposure guidance values for nutrition (IOM Estimated Average Requirement (EAR), Recommended Dietary Allowance (RDA), WHO Recommended Nutrient Intake (RNI)) and toxicity (IOM Tolerable Upper Intake Level (UL); ATSDR Minimal Risk Level (MRL), WHO International Programme on Chemical Safety (IPCS) Tolerable Daily Intake (TDI)). Using a urinary excretion fraction of 0.9, Biomonitoring Equivalents (BE) for the EAR, RDA, UL and MRL were derived for adults (60, 100, 730 and 450 µg/L, respectively) and children (50, 80, 580 and 360 µg/L, respectively). The population median UIC values from NHANES and CHMS for adults (140-181, 122-126 µg/L, respectively) and children (232, 189 µg/L, respectively) were above the criteria for assessing iodine nutrition, indicating that US and Canadian populations are likely to have adequate population iodine nutrition. The median UIC from NHANES and CHMS do not exceed BE values derived from exposure guidance values for toxicity.