Mercury and docosahexaenoic acid levels in maternal and cord blood in relation to segmental maternal hair mercury concentrations at parturition

Fish is a major source of harmful methylmercury (MeHg) and beneficial docosahexaenoic acid (DHA) in the developing brain. In this study, we investigated the correlations among maternal and umbilical cord (cord) MeHg and DHA levels at parturition, and mercury (Hg) concentration in 1-cm incremental segments hair samples which grew during gestation representing monthly MeHg exposure levels throughout the period. Whole blood Hg and plasma DHA levels were measured in blood sample pairs collected from 54 mothers at early gestation and parturition, and in cord blood. Maternal hair samples were collected at parturition, and Hg concentrations were measured in 1-cm incremental segments. Hg level in mothers at parturition was slightly lower than that at early gestation and the level in cord blood were approximately 1.9 times higher than that in mothers at parturition. On the other hand, DHA level in mothers at parturition was approximately 2.3 and 1.6 times higher than those in mothers at early gestation and in cord plasma, respectively. These results indicate that kinetics of these chemicals in mothers during gestation and placental transfer are completely different. However, Hg and DHA levels had significant positive correlation in fetal circulation. The cord blood Hg showed the strongest correlation with maternal hair Hg in the first 1-cm segment from the scalp at parturition (r = 0.87), indicating that fetal MeHg level reflects maternal MeHg burden at late gestation. In contrast, maternal and cord plasma DHA concentrations at parturition showed the highest correlation coefficients with Hg in the fifth (r = 0.43) and fourth (r = 0.38) 1-cm hair segments, suggesting that maternal and fetal DHA levels reflects maternal fish intake during mid-gestation.     

Associations between PBDEs in office air,dust, and surface wipes

Increased use of flame-retardants in office furniture may increase exposure to PBDEs in the office environment. However, partitioning of PBDEs within the office environment is not well understood. Our objectives were to examine relationships between concurrent measures of PBDEs in office air, floor dust, and surface wipes.We collected air, dust, and surface wipe samples from 31 offices in Boston, MA. Correlation and linear regression were used to evaluate associations between variables. Geometric mean (GM) concentrations of individual BDE congeners in air and congener specific octanol–air partition coefficients (K_oa) were used to predict GM concentrations in dust and surface wipes and compared to the measured concentrations.GM concentrations of PentaBDEs in office air, dust, and surface wipes were 472 pg/m³, 2411 ng/g, and 77 pg/cm², respectively. BDE209 was detected in 100% of dust samples (GM = 4202 ng/g), 93% of surface wipes (GM = 125 pg/cm²), and 39% of air samples. PentaBDEs in dust and air were moderately correlated with each other (r = 0.60, p = 0.0003), as well as with PentaBDEs in surface wipes (r = 0.51, p = 0.003 for both dust and air). BDE209 in dust was correlated with BDE209 in surface wipes (r = 0.69, p = 0.007). Building (three categories) and PentaBDEs in dust were independent predictors of PentaBDEs in both air and surface wipes, together explaining 50% (p = 0.0009) and 48% (p = 0.001) of the variation respectively. Predicted and measured concentrations of individual BDE congeners were highly correlated in dust (r = 0.98, p < 0.0001) and surface wipes (r = 0.94, p = 002). BDE209 provided an interesting test of this equilibrium partitioning model as it is a low volatility compound.Associations between PentaBDEs in multiple sampling media suggest that collecting dust or surface wipes may be a convenient method of characterizing exposure in the indoor environment. The volatility of individual congeners, as well as physical characteristics of the indoor environment, influence relationships between PBDEs in air, dust, and surface wipes.     

Levels and profiles of PCDD/Fs,PCBs in mothers' milk in Shenzhen of China: Estimation of breast-fed infants’ intakes

Sixty breast milk samples were collected in Shenzhen, China from July to November in 2007. The samples were analyzed of the concentrations of polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs) and polychlorinated biphenyls (PCBs). The range of upper-bound for ∑ TEQ-(PCDD/Fs + PCBs) in the samples was 4.10–35.3 pg TEQ g^− 1 lipid (median: 10.6 pg TEQ g^− 1 lipid; mean: 11.9 pg TEQ g^− 1 lipid). The levels of the measured contaminants in the breast milk had significant correlations with the length of inhabitation period in Shenzhen (r = 0.487, p < 0.05 for PCDD/Fs, r = 0.431, p < 0.05 for PCBs and r = 0.478, p < 0.05 for ∑ TEQ-(PCDD/Fs + PCBs)), and the consumption rate of fish (r = 0.366, p < 0.05 for PCDD/Fs, r = 0.486, p < 0.05 for PCBs and r = 0.416, p < 0.05 for ∑ TEQ-(PCDD/Fs + PCBs)), respectively. Moreover, significant positive correlations were also detected between the participant's age (r = 0.305, p < 0.05 for ∑ TEQ-PCBs and r = 0.275, p < 0.05 for ∑ TEQ-(PCDD/Fs + PCBs)) and the body burdens of these contaminants respectively. It is estimated that the daily intake (EDI) of the sum of PCDD/Fs and DL-PCBs by the breast-fed infants was 5.60–161 pg TEQ kg^− 1 bw per day (mean: 48.2 pg TEQ kg^− 1 bw per day; median: 42.2 pg TEQ kg^− 1 bw per day). The result showed that both the body burdens of PCDD/Fs and PCBs of the recruit population and the calculated EDI of the breast-fed infants were higher than those in the non-exposed areas in mainland China. This suggests that continuous surveillance on PCDD/Fs and PCBs levels in human milk is critical to more precisely evaluate the human health risk posed by the negative environmental impact in Shenzhen in the future.     

The ‘take home’ burden of workplace sensitizers: Flour contamination in bakers' families

BackgroundExposure to flour/flour constituents is a leading cause of occupational asthma. Paternal occupational exposure to flour has been associated with increased likelihood of childhood asthma, raising the possibility of para-occupational exposure whereby family members are exposed to sensitizers ‘taken home’ on contaminated skin/clothing.ObjectiveTo establish whether workplace contamination of skin/clothing with wheat flour allergen (WFA) and fungal α-amylase (FAA) is associated with increased levels of these allergens in bakers' homes.MethodsBakeries in north-east Scotland were invited to participate. Control subjects were recruited from University of Aberdeen staff and students. Exposure assessment was carried out in bakeries, bakers' cars and the homes of bakers and controls using surface wipe and vacuum sampling; samples were analyzed for total protein, FAA and WFA.Results164 wipe samples and 49 vacuum samples were collected from 38 bakers (from 5 bakeries) and 10 controls.Compared to non-bakers, bakers had higher median levels of WFA and FAA in house vacuum samples; the difference was statistically significant for WFA/total protein (515.8 × 10^− 6 vs. 163.7 × 10^− 6, p = 0.031), FAA/total protein ratios (1.45 × 10^− 6 vs. 0.04 × 10^− 6, p < 0.001) and FAA loading (median 1.2 pg/cm² vs. 0.1 pg/cm², p < 0.001) with workplace exposure–home contamination relationships between bakers with higher and lower workplace contamination.We found positive correlations between WFA contamination of the bakers' foreheads and cars (r_s0.57, p = 0.028), foreheads and houses (r_s0.46, p = 0.025), shoes and houses (r_s0.45, p = 0.029); and between FAA contamination of shoes and houses (r_s0.46, p = 0.023), and cars and houses (r_s0.70, p = 0.008). There was no evidence of bakers using work-sourced flour for domestic baking.ConclusionsThis work demonstrates pathways for ‘take home’ exposure of occupationally sourced flour. Taken with our previous work, showing that bakers' children are more likely to have asthma, this supports the need for further investigation to establish whether ‘take home’ of occupationally sourced flour is widespread with health consequences.     

Estimation of exposure to atmospheric pollutants during pregnancy integrating space–time activity and indoor air levels: Does it make a difference?

Studies of air pollution effects during pregnancy generally only consider exposure in the outdoor air at the home address. We aimed to compare exposure models differing in their ability to account for the spatial resolution of pollutants, space–time activity and indoor air pollution levels. We recruited 40 pregnant women in the Grenoble urban area, France, who carried a Global Positioning System (GPS) during up to 3 weeks; in a subgroup, indoor measurements of fine particles (PM_2.5) were conducted at home (n = 9) and personal exposure to nitrogen dioxide (NO₂) was assessed using passive air samplers (n = 10). Outdoor concentrations of NO₂, and PM_2.5 were estimated from a dispersion model with a fine spatial resolution. Women spent on average 16 h per day at home. Considering only outdoor levels, for estimates at the home address, the correlation between the estimate using the nearest background air monitoring station and the estimate from the dispersion model was high (r = 0.93) for PM_2.5 and moderate (r = 0.67) for NO₂. The model incorporating clean GPS data was less correlated with the estimate relying on raw GPS data (r = 0.77) than the model ignoring space–time activity (r = 0.93). PM_2.5 outdoor levels were not to moderately correlated with estimates from the model incorporating indoor measurements and space–time activity (r = − 0.10 to 0.47), while NO₂ personal levels were not correlated with outdoor levels (r = − 0.42 to 0.03). In this urban area, accounting for space–time activity little influenced exposure estimates; in a subgroup of subjects (n = 9), incorporating indoor pollution levels seemed to strongly modify them.     

Exposure to organochlorines and mercury through fish and marine mammal consumption: Associations with growth and duration of gestation among Inuit newborns

BackgroundSeveral studies have reported negative associations of polychlorinated biphenyls (PCBs), hexachlorobenzene (HCB) and mercury (Hg) with duration of gestation and fetal growth in fish eating populations. Docosahexaenoic acid (DHA) from fish, seafood and marine mammal intake has been reported to be positively related with pregnancy duration and fetal growth. So far, it remains unclear, however, if the associations of environmental contaminants (ECs) with growth are direct or mediated through their relation with the duration of gestation and the degree to which DHA intake during pregnancy attenuates the negative association of ECs with fetal growth.ObjectivesTo investigate direct and indirect associations of in utero exposure to ECs with fetal growth and pregnancy duration while taking into account the possible positive effects of DHA.MethodsPregnant Inuit women (N = 248) from Arctic Quebec were recruited and cord blood samples were analyzed for PCBs, HCB, Hg and DHA. Anthropometric measurements were assessed at birth. Path models were used to evaluate direct and indirect associations.ResultsCord concentrations of PCB 153, HCB and Hg were significantly associated with shorter duration of pregnancy (β varying from − 0.17 to − 0.20, p < 0.05). Path models indicated that the associations of PCBs, HCB and Hg with reduced fetal growth (β varying from − 0.09 to − 0.13, p < 0.05) were mediated through their relations with shorter gestation duration. Cord DHA was indirectly related to greater growth parameters (β varying from 0.17 to 0.20, p < 0.05) through its positive association with gestation duration.ConclusionPrenatal exposure to ECs was associated with reduced gestation duration, which is a recognized determinant of fetal growth. DHA intake during pregnancy appeared to have independent positive association with fetal growth by prolonging gestation. Whether these associations are causal remains to be elucidated.     

Relative effect potency estimates of dioxin-like activity for dioxins,furans, and dioxin-like PCBs in adults based on cytochrome P450 1A1 and 1B1 gene expression in blood

BackgroundIn the risk assessment of PCDDs, PCDFs, and dioxin-like (DL) PCBs, regulatory authorities support the use of the toxic equivalency factor (TEF)-scheme derived from a heterogeneous data set of the relative effect potency (REPs) estimates.ObjectivesWe sought to determine REPs for dioxin-like compounds (DLCs) using expression of cytochrome P450 (CYP) 1A1 and 1B1 mRNA in human peripheral blood mononuclear cells representing two different pathways.MethodsWe used a sex and age adjusted regression-based approach comparing the strength of association between each DLC and the cytochrome P450 (CYP) 1A1 and 1B1 mRNA expression in 320 adults residing in an organochlorine-polluted area of eastern Slovakia.ResultsWe calculated REPs based on CYP1A1 expression for 4 PCDDs, 8 PCDFs, and 1 PCB congener, and based on CYP1B1 expression for 5 PCDFs and 11 PCB congeners. REPs from CYP1A1 correlated with REPs previously derived from thyroid volume (ρ = 0.85; p < 0.001) and serum FT4 (ρ = 0.77; p = 0.009). The 13 log REPs from CYP1A1 correlated with log WHO-TEFs (r = 0.63; p = 0.015) and 11 log PCB REPs with PCB consensus toxicity factors (CTFs) for compounds with WHO-TEFs (r = 0.80; p = 0.003). The complete set of derived 56 log REPs correlated with the log CTFs (r = 0.77; p = 0.001) and log WHO-TEFs (r = 0.81; p < 0.001).ConclusionsREPs calculated from thyroid and cytochrome P450 endpoints realistically reflect human exposure scenarios because they are based on human chronic and low-dose exposures. While the CYP 1A1 seems more suitable for toxicity evaluation of PCDD/Fs, the CYP 1B1 is more apt for PCDFs and PCBs and reflects different pathways.     

Assessment of human hair as an indicator of exposure to organophosphate flame retardants. Case study on a Norwegian mother–child cohort

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 < 1 and 3744 ng/g hair and were lower than in indoor dust from the participants' homes. Several statistically significant associations between PFR levels in human hair and PFR levels in house dust and/or air were found, e.g. Spearman correlation (r_S = 0.561, p < 0.05) between TBOEP in children's hair and in indoor air. Also, associations were found between TDCIPP in hair and its metabolite bis(1,3-dichloro-iso-propyl) phosphate (BDCIPP) in urine; they were stronger for children (e.g. Pearson correlation r_P = 0.475; p = 0.001) than for mothers (r_P = 0.395, p = 0.01). Levels of diphenyl phosphate (DPHP) in mothers' and children's urine were slightly correlated (r_S = 0.409, p = 0.008), suggesting similar sources of exposure. To the best of our knowledge, this is the first study with such design and our findings might help to understand human exposure to and body burdens of PFRs.     

Distribution of persistent organic pollutants in two different fat compartments from obese individuals

There are only few studies defining persistent organic pollutant (POP) concentrations in various fat compartments from living obese individuals. The present study has therefore determined the concentrations of various classes of organohalogenated compounds, such as dichlorodiphenyltrichloroethane and its metabolites (DDTs), chlordane compounds (CHLs), hexachlorocyclohexanes (HCHs), hexachlorobenzene (HCB), polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs) and hexabromocyclododecanes (HBCDs) in visceral fat (VF: n = 52) and subcutaneous abdominal fat (SF: n = 52) samples collected in 2010–2012 from obese individuals in Belgium. Organohalogen compounds were detected in all fat samples in the decreasing order of their concentrations: PCBs > DDTs > HCHs > CHLs > HCB > HBCDs > PBDEs, suggesting that Belgians have been widely exposed to these contaminants. The levels and the patterns of POP distribution in VF and SF tissue depots were not significantly different. Concentrations of PCBs (VF/SF; median: 285/275 ng/g lw) and DDTs (VF/SF; median: 150/155 ng/g lw) were the major POPs in all fat samples. Concerning PCBs, PCB 153 (VF/SF: 27/26%) was the most dominant congener, followed by PCB 180 (VF/SF: 17/18%), PCB 138 (VF/SF: 15/14.5%) and PCB 170 (VF/SF: 8.1/8.4%) to the sum PCBs, respectively. Levels of HBCDs (VF/SF; median: 4.0/3.7 ng/g lw) and PBDEs (VF/SF; median: 2.6/2.7 ng/g lw) were 1–2 orders of magnitude lower than those of PCBs and DDTs. Among PBDEs, BDE 153 (VF/SF: 31/34%) was the dominant congener, followed by BDE 47 (VF/SF: 26/23%), BDE 154 (VF/SF: 16/16%), BDE 100 (VF/SF: 10/11%) and BDE 99 (VF/SF: 9/9%). To our knowledge, this is the first report on HBCD concentrations in Belgian human fat tissues. Total PBDE and HBCD levels in human fat samples could not be correlated with age. In agreement with the literature, a significant correlation (p < 0.05) between age and the concentration of PCBs (r = 0.828), DDTs (r = 0.640), HCHs (r = 0.666), CHLs (r = 0.534) and HCB (r = 0.754), was observed in the present study. Levels of DDTs, HCHs, HCB and CHLs were also significantly correlated to each other, suggesting that they share similar exposure routes. Correlation with computed tomography (CT) scan data revealed that VF and VF/SF ratios are positive for most of the POPs, such as PCBs, PBDEs, p,p′DDE, CHLs, β-HCH, and HCB. To our knowledge, this study is the first to assess the relationship between POP levels in adipose tissue and markers of abdominal adiposity, determined by CT.     

Concentrations of polybrominated diphenyl ethers (PBDEs) and 2,4,6-tribromophenol in human placental tissues

Legacy environmental contaminants such as polybrominated diphenyl ethers (PBDEs) are widely detected in human tissues. However, few studies have measured PBDEs in placental tissues, and there are no reported measurements of 2,4,6-tribromophenol (2,4,6-TBP) in placental tissues. Measurements of these contaminants are important for understanding potential fetal exposures, as these compounds have been shown to alter thyroid hormone regulation in vitro and in vivo. In this study, we measured a suite of PBDEs and 2,4,6-TBP in 102 human placental tissues collected between 2010 and 2011 in Durham County, North Carolina, USA. The most abundant PBDE congener detected was BDE-47, with a mean concentration of 5.09 ng/g lipid (range: 0.12–141 ng/g lipid; detection frequency 91%); however, 2,4,6-TBP was ubiquitously detected and present at higher concentrations with a mean concentration of 15.4 ng/g lipid (range:1.31–316 ng/g lipid; detection frequency 100%). BDE-209 was also detected in more than 50% of the samples, and was significantly associated with 2,4,6-TBP in placental tissues, suggesting they may have a similar source, or that 2,4,6-TBP may be a degradation product of BDE-209. Interestingly, BDE-209 and 2,4,6-TBP were negatively associated with age (r_s = − 0.16; p = 0.10 and r_s = − 0.17; p = 0.08, respectively). The results of this work indicate that PBDEs and 2,4,6-TBP bioaccumulate in human placenta tissue and likely contribute to prenatal exposures to these environmental contaminants. Future studies are needed to determine if these joint exposures are associated with any adverse health measures in infants and children.     

Perfluoroalkyl substances in soft tissues and tail feathers of Belgian barn owls (Tyto alba) using statistical methods for left-censored data to handle non-detects

Perfluoroalkyl substances (PFASs) were investigated in tail feathers and soft tissues (liver, muscle, preen gland and adipose tissue) of barn owl (Tyto alba) road-kill victims (n = 15) collected in the province of Antwerp (Belgium). A major PFAS producing facility is located in the Antwerp area and levels of PFASs in biota from that region have been found to be very high in previous studies. We aimed to investigate for the first time the main sources of PFASs in feathers of a terrestrial bird species. Throughout this study, we have used statistical methods for left-censored data to cope with levels below the limit of detection (LOD), instead of traditional, potentially biased, substitution methods.Perfluorooctane sulfonate (PFOS) was detected in all tissues (range: 11 ng/g ww in muscle–1208 ng/g ww in preen oil) and in tail feathers (< 2.2–56.6 ng/g ww). Perfluorooctanoate (PFOA) was measured at high levels in feathers (< 14–670 ng/g ww), but not in tissues (more than 50% < LOD). Perfluorohexane sulfonate (PFHxS) could only be quantified in liver and preen oil, while other PFASs were sporadically detected in liver. PFOS levels in feathers and liver were highly correlated (r = 0.78, p < 0.01), in contrast to PFOA (r = − 0.11, p = 0.78). Combined with high PFOA levels in feathers this suggests that PFOA may be present on the external surface of feathers, due to external contamination originating from the air in the vicinity of point sources. Therefore the possibility of using feathers as a passive air sampler for high PFOA levels should be investigated in the future.     

Gene-gene and gene-environment interactions on risk of male infertility: Focus on the metabolites

Infertility affects about 17% couples, and males contribute to half of the cases. Compared with independent effects of genetic and environmental factors, interactions between them help in the understanding of the susceptibility to male infertility. Thus, we genotyped 25 polymorphisms, measured 16 urinary chemical concentrations and explored interactions between gene-gene and gene-environment in 1039 Han Chinese using metabolomic analysis. We first observed that GSTT1 might interact with GSTM1 (P_inter = 6.33 × 10^− 8). Furthermore, an interaction between GSTM1 and 4-n-octylphenol (4-n-OP) was identified (P_inter = 7.00 × 10^− 3), as well as a 2-order interaction among GSTT1, GSTM1 and 4-n-OP (P_inter = 0.04). Subjects with GSTT1-present and GSTM1-null genotypes were susceptible to male infertility when exposed to 4-n-OP (OR = 14.05, 95% CI = 4.78–60.20, P = 2.34 × 10^− 5). Most metabolites identified were involved in the tricarboxylic acid cycle. In conclusion, it is a novel study of the interaction on male infertility from the aspect of metabolomics.     

Fate,distribution, and contrasting temporal trends of perfluoroalkyl substances (PFASs) in Lake Ontario,Canada

Lake Ontario water and sediment collected from tributary, nearshore, and open lake sites were analyzed for perfluoroalkyl substances (PFASs), namely perfluoroalkyl carboxylic acids (PFCAs, F(CF₂)_nCO₂⁻; n = 6-11,13) and perfluoroalkane sulfonic acids (PFSAs, F(CF₂)_nSO₃⁻; n = 6,8,10). Survey results of surface sediment and water indicated that shorter chained PFASs were predominant in and near urban/industrial area watersheds, while longer chained PFASs were predominant in fine-grained sediment from major depositional basins. Niagara River suspended solids (1981–2006) demonstrated temporal trends that may have been influenced by recent changes in North American production and use of PFASs. Perfluorooctane sulfonate (PFOS) reached a peak concentration in 2001 of 1.1 ng/g, followed by a decrease from 2001 to 2006 (half-life = 9 years). Perfluorooctanoic acid (PFOA) increased from 2001 to 2006 (doubling time = 2 years) reaching a peak concentration of 0.80 ng/g. In contrast, three sediment cores from western, central, and eastern Lake Ontario showed increasing temporal trends to surface sediment for all PFASs. PFOA and PFOS concentrations increased from 1988 to 2004 (doubling time = ~ 4 years) in the western Lake Ontario core. The observed variations in temporal trends from different environmental compartments may be a result of the physico-chemical properties of PFASs, ongoing emissions, and the environmental transformation and degradation of PFAS precursor compounds.     

Recreational swimmers' exposure to Vibrio vulnificus and Vibrio parahaemolyticus in the Chesapeake Bay,Maryland, USA

Vibrio vulnificus and Vibrio parahaemolyticus are ubiquitous in the marine–estuarine environment, but the magnitude of human non-ingestion exposure to these waterborne pathogens is largely unknown. We evaluated the magnitude of dermal exposure to V. vulnificus and V. parahaemolyticus among swimmers recreating in Vibrio-populated waters by conducting swim studies at four swimming locations in the Chesapeake Bay in 2009 and 2011. Volunteers (n = 31) swam for set time periods, and surface water (n = 25) and handwash (n = 250) samples were collected. Samples were analyzed for Vibrio concentrations using quantitative PCR. Linear and logistic regressions were used to evaluate factors associated with recreational exposures. Mean surface water V. vulnificus and V. parahaemolyticus concentrations were 1128 CFU mL^− 1 (95% confidence interval (CI): 665.6, 1591.4) and 18 CFU mL^− 1 (95% CI: 9.8, 26.1), respectively, across all sampling locations. Mean Vibrio concentrations in handwash samples (V. vulnificus, 180 CFU cm^− 2 (95% CI: 136.6, 222.5); V. parahaemolyticus, 3 CFU cm^− 2 (95% CI: 2.4, 3.7)) were significantly associated with Vibrio concentrations in surface water (V. vulnificus, p < 0.01; V. parahaemolyticus, p < 0.01), but not with salinity or temperature (V. vulnificus, p = 0.52, p = 0.17; V. parahaemolyticus, p = 0.82, p = 0.06). Handwashing reduced V. vulnificus and V. parahaemolyticus on subjects' hands by approximately one log (93.9%, 89.4%, respectively). It can be concluded that when Chesapeake Bay surface waters are characterized by elevated concentrations of Vibrio, swimmers and individuals working in those waters could experience significant dermal exposures to V. vulnificus and V. parahaemolyticus, increasing their risk of infection.     

Perinatal exposure to dioxins and dioxin-like compounds and infant growth and body mass index at seven years: A pooled analysis of three European birth cohorts

BackgroundDioxins and dioxin-like compounds are endocrine disrupting chemicals (EDCs). Experimental studies suggest perinatal exposure to EDCs results in later obesity. However, the few epidemiological investigations on dioxins are inconclusive. We investigated perinatal exposure to dioxins and dioxin-like compounds, infant growth and body mass index (BMI) in childhood.MethodsWe pooled data from 3 European birth cohorts (Belgian, Norwegian, Slovak) with exposure assessment in cord blood or breast milk. Two cohorts had dioxin-like toxicity assessed using dioxin-responsive chemical-activated luciferase expression (DR-CALUX) bioassay and one cohort had measured concentrations of dioxins, furans and dioxin-like polychlorinated biphenols with CALUX relative potency values applied. Growth was cohort- and sex-specific change in weight-for-age z-score between birth and 24 months (N = 367). BMI was calculated at around 7 years (median 7.17, interquartile range [IQR] 7.00–7.37 years, N = 251), and overweight defined according to international standards for children equivalent to adult BMI > 25 kg/m² (Cole and Lobstein, 2012). We fitted multivariate models using generalized estimating equations, and tested effect modification by sex, breastfeeding and cohort. Results per 10 pg CALUX TEQ/g lipid increase in exposure.ResultsDioxin exposure was highest in the Belgian and lowest in the Norwegian cohort; median (IQR) of the pooled sample 13 (12.0) pg CALUX TEQ/g lipid. Perinatal exposure to dioxins and dioxin-like compounds appeared associated with increased growth between 0 and 24 months (adjusted estimate for change in z-score: β = 0.07, 95% CI: − 0.01, 0.14). At 7 years, dioxins exposure was associated with a statistically significant increase in BMI in girls (adjusted estimate for BMI units β = 0.49, 95% CI: 0.07, 0.91) but not in boys (β = − 0.03, 95% CI: − 0.55, 0.49) (p-interaction = 0.044). Furthermore, girls had a 54% (− 6%, 151%) increased risk of overweight at 7 years (p-interaction = 0.023).ConclusionPerinatal exposure to dioxin and dioxin-like compounds was associated with increased early infant growth, and increased BMI in school age girls. Studies in larger sample sizes are required to confirm these sex-specific effects.     

Blood pressure changes in association with black carbon exposure in a panel of healthy adults are independent of retinal microcirculation

Exposure to ambient particulate matter and elevated blood pressure are risk factors for cardiovascular morbidity and mortality. Microvascular changes might be an important pathway in explaining the association between air pollution and blood pressure. The objective of the study was to evaluate the role of the retinal microcirculation in the association between black carbon (BC) exposure and blood pressure.We estimated subchronic BC exposure based on 1-week personal measurements (μ-Aethalometer, AethLabs) in 55 healthy nurses. Blood pressure and retinal microvasculature were measured on four different days (range: 2–4) during this week.Subchronic BC exposure averaged (± SD) 1334 ± 631 ng/m³ and ranged from 338 ng/m³ to 3889 ng/m³. An increased exposure of 631 ng/m³ BC was associated with a 2.77 mm Hg (95% CI: 0.39 to 5.15, p = 0.027) increase in systolic blood pressure, a 2.35 mm Hg (95% CI: 0.52 to 4.19, p = 0.016) increase in diastolic blood pressure and with 5.65 μm (95% CI: 1.33 to 9.96, p = 0.014) increase in central retinal venular equivalent. Mediation analysis failed to reveal an effect of retinal microvasculature in the association between blood pressure and subchronic BC exposure.In conclusion, we found a positive association between blood pressure and subchronic black carbon exposure in healthy adults. This finding adds evidence to the association between black carbon exposure and cardiovascular health effects, with elevated blood pressure as a plausible intermediate effector. Our results suggest that the changes in a person's blood pressure as a result of subchronic black carbon exposure operate independently of the retinal microcirculation.     

Back-extrapolated and year-specific NO2 land use regression models for Great Britain - Do they yield different exposure assessment?

Robust methods to estimate historic population air pollution exposures are important tools for epidemiological studies evaluating long-term health effects. We developed land use regression (LUR) models for NO₂ exposure in Great Britain for 1991 and explored whether the choice of year-specific or back-extrapolated LUR yields 1) similar LUR variables and model performance, and 2) similar national and regional address-level and small-area concentrations. We constructed two LUR models for 1991using NO₂ concentrations from the diffusion tube monitoring network, one using 75% of all available measurement sites (that over-represent industrial areas), and the other using 75% of a subset of sites proportionate to population by region to study the effects of monitoring site selection bias. We compared, using the remaining (hold-out) 25% of monitoring sites, the performance of the two 1991 models with back-extrapolation of a previously published 2009 model, developed using NO₂ concentrations from automatic chemiluminescence monitoring sites and predictor variables from 2006/2007. The 2009 model was back-extrapolated to 1991 using the same predictors (1990 & 1995) used to develop 1991 models. The 1991 models included industrial land use variables, not present for 2009. The hold-out performance of 1991 models (mean-squared-error-based-R²: 0.62–0.64) was up to 8% higher and ~ 1 μg/m³ lower in root mean squared error than the back-extrapolated 2009 model, with best performance from the subset of sites representing population exposures. Year-specific and back-extrapolated exposures for residential addresses (n = 1.338,399) and small areas (n = 10.518) were very highly linearly correlated for Great Britain (r > 0.83). This study suggests that year-specific model for 1991 and back-extrapolation of the 2009 LUR yield similar exposure assessment.     

Seasonal variation in outdoor,indoor, and personal air pollution exposures of women using wood stoves in the Tibetan Plateau: Baseline assessment for an energy intervention study

Cooking and heating with coal and biomass is the main source of household air pollution in China and a leading contributor to disease burden. As part of a baseline assessment for a household energy intervention program, we enrolled 205 adult women cooking with biomass fuels in Sichuan, China and measured their 48-h personal exposure to fine particulate matter (PM_2.5) and carbon monoxide (CO) in winter and summer. We also measured the indoor 48-h PM_2.5 concentrations in their homes and conducted outdoor PM_2.5 measurements during 101 (74) days in summer (winter). Indoor concentrations of CO and nitrogen oxides (NO, NO₂) were measured over 48-h in a subset of ~ 80 homes. Women's geometric mean 48-h exposure to PM_2.5 was 80 μg/m³ (95% CI: 74, 87) in summer and twice as high in winter (169 μg/m³ (95% CI: 150, 190), with similar seasonal trends for indoor PM_2.5 concentrations (winter: 252 μg/m³; 95% CI: 215, 295; summer: 101 μg/m³; 95% CI: 91, 112). We found a moderately strong relationship between indoor PM_2.5 and CO (r = 0.60, 95% CI: 0.46, 0.72), and a weak correlation between personal PM_2.5 and CO (r = 0.41, 95% CI: − 0.02, 0.71). NO₂/NO ratios were higher in summer (range: 0.01 to 0.68) than in winter (range: 0 to 0.11), suggesting outdoor formation of NO₂ via reaction of NO with ozone is a more important source of NO₂ than biomass combustion indoors. The predictors of women's personal exposure to PM_2.5 differed by season. In winter, our results show that primary heating with a low-polluting fuel (i.e., electric stove or wood-charcoal) and more frequent kitchen ventilation could reduce personal PM_2.5 exposures. In summer, primary use of a gaseous fuel or electricity for cooking and reducing exposure to outdoor PM_2.5 would likely have the greatest impacts on personal PM_2.5 exposure.     

Sources and human exposure implications of concentrations of organophosphate flame retardants in dust from UK cars,classrooms, living rooms,and offices

Concentrations of a number of organophosphate flame retardants (PFRs) were measured in floor dust collected from UK living rooms (n = 32), cars (n = 21), school and child daycare centre classrooms (n = 28), and offices (n = 61). While concentrations were overall broadly within the range of those reported previously for North America, Japan, and other European countries, median concentrations of TCIPP in all UK microenvironments exceeded those reported elsewhere in the world. Moreover, concentrations of TCIPP and TDCIPP in 2 UK car dust samples were – at 370 μg g^− 1 and 740 μg g^− 1 respectively – amongst the highest reported globally in indoor dust to date. Consistent with this, concentrations of TDCIPP in dust from UK cars exceed significantly those detected in the other microenvironments studied. Concentrations of EHDPP were shown for the first time to be significantly higher in classroom dust than in samples from other microenvironments. When compared to concentrations of PBDEs determined previously in the classroom dust samples; concentrations of all target PFRs exceeded substantially those of those PBDEs that are the principal constituents of the Penta- and Octa-BDE formulations. Moreover, while mass-based concentrations of BDE-209 exceeded those of most of our target PFRs, they still fell below those of TCIPP and EHDPP. In line with a previous observation in Sweden that indoor air contamination with TNBP was significantly lower in newer buildings; concentrations of TNBP in classroom dust were significantly higher in older compared to more recently-constructed schools. Consistent with the reported extensive use of TCIPP and TDCIPP in polyurethane foam, the highest concentrations of both TCIPP and TDCIPP in the classrooms studied, were observed in rooms containing the highest numbers of foam chairs (n = 31 and 18 respectively). Exposure to PFRs of both adults and young children via ingestion of indoor dust was estimated. While even our high-end exposure estimate for young children was ~ 100 times lower than one previously reported health-based limit (HBLV) value for TCIPP; the margin of safety was only 5-fold when compared to another HBLV for this contaminant.