Spatiotemporal analysis and human exposure assessment on polycyclic aromatic hydrocarbons in indoor air,settled house dust,and diet: A review

This review summarizes the published literature on the presence of polycyclic aromatic hydrocarbons (PAH) in indoor air, settled house dust, and food, and highlights geographical and temporal trends in indoor PAH contamination. In both indoor air and dust, ΣPAH concentrations in North America have decreased over the past 30 years with a halving time of 6.7 ± 1.9 years in indoor air and 5.0 ± 2.3 years in indoor dust. In contrast, indoor PAH concentrations in Asia have remained steady. Concentrations of ΣPAH in indoor air are significantly (p < 0.01) higher in Asia than North America. In studies recording both vapor and particulate phases, the global average concentration in indoor air of ΣPAH excluding naphthalene is between 7 and 14,300 ng/m³. Over a similar period, the average ΣPAH concentration in house dust ranges between 127 to 115,817 ng/g. Indoor/outdoor ratios of atmospheric concentrations of ΣPAH have declined globally with a half-life of 6.3 ± 2.3 years. While indoor/outdoor ratios for benzo[a]pyrene toxicity equivalents (BaP_eq) declined in North America with a half-life of 12.2 ± 3.2 years, no significant decline was observed when data from all regions were considered. Comparison of the global database, revealed that I/O ratios for ΣPAH (average = 4.3 ± 1.3), exceeded significantly those of BaP_eq (average = 1.7 ± 0.4) in the same samples. The significant decline in global I/O ratios suggests that indoor sources of PAH have been controlled more effectively than outdoor sources. Moreover, the significantly higher I/O ratios for ΣPAH compared to BaP_eq, imply that indoor sources of PAH emit proportionally more of the less carcinogenic PAH than outdoor sources. Dietary exposure to PAH ranges from 137 to 55,000 ng/day. Definitive spatiotemporal trends in dietary exposure were precluded due to relatively small number of relevant studies. However, although reported in only one study, PAH concentrations in Chinese diets exceeded those in diet from other parts of the world, a pattern consistent with the spatial trends observed for concentrations of PAH in indoor air. Evaluation of human exposure to ΣPAH via inhalation, dust and diet ingestion, suggests that while intake via diet and inhalation exceeds that via dust ingestion; all three pathways contribute and merit continued assessment.     

Dietary exposure to cadmium and risk of breast cancer in postmenopausal women: A systematic review and meta-analysis

BackgroundWith tobacco smoking, diet is the main source of cadmium (Cd) exposure in the general population. The carcinogenic and estrogenic activities of Cd make it a contaminant of potential concern for hormone-dependent cancers including breast cancer. Postmenopausal women represent the most appropriate population to investigate the possible impact of exogenous factors with potential estrogenic activity on breast cancer as, after menopause, their estrogenic influence is predominant.ObjectivesWe systematically reviewed available studies on the association between dietary exposure to Cd and breast cancer focusing on postmenopausal women. A meta-analysis combining the risk estimators was performed and potential sources of between studies heterogeneity were traced.MethodsStudies were searched from MEDLINE through 31 January 2015 and from the reference lists of relevant publications. Six eligible studies published between 2012 and 2014 were identified and relative risk estimates were extracted. Meta-rate ratio estimates (mRR) were calculated according to fixed and random-effect models. Meta-analyses were performed on the whole set of data and separate analyses were conducted after stratification for study design, geographic location, use of hormone replacement therapy (HRT), tumor estrogen receptor status (ER + or ER −), progesterone receptor status (PGR + or PGR −), body mass index (BMI), smoker status, zinc or iron intake.ResultsNo statistically significant increased risk of breast cancer was observed when all studies were combined (mRR = 1.03; 95% confidence interval [CI]: 0.89–1.19). Several sources of heterogeneity and inconsistency were identified, including smoker status, HRT use, BMI, zinc and iron intake. Inconsistency was also strongly reduced when only considering ER −, PGR −, tumors subgroups from USA and from Japan. The risks were, however, not substantially modified after stratifications. No evidence of publication bias was found.ConclusionThe present study does not provide support for the hypothesis that dietary exposure to Cd increases the risk of breast cancer in postmenopausal women. Misclassification in dietary Cd assessment in primary studies could have biased the results towards a finding of no association.     

Non-specific physical symptoms and electromagnetic field exposure in the general population: Can we get more specific? A systematic review

ObjectiveA systematic review of observational studies was performed to address the strength of evidence for an association between actual and perceived exposure to electromagnetic fields (EMF) and non-specific physical symptoms (NSPS) in the general population. To gain more insight into the magnitude of a possible association, meta-analyses were conducted.MethodsLiterature databases Medline, Embase, SciSearch, PsychInfo, Psyndex and Biosis and additional bibliographic sources such as reference sections of key publications were searched for the detection of studies published between January 2000 and April 2011.ResultsTwenty-two studies met our inclusion criteria. Qualitative assessment of the epidemiological evidence showed either no association between symptoms and higher EMF exposure or contradictory results. To strengthen our conclusions, random effects meta-analyses were performed, which produced the following results for the association with actual EMF; for symptom severity: Headache odds ratio (OR) = 1.65; 95% confidence interval (CI) = 0.88–3.08, concentration problems OR = 1.28; 95% CI = 0.56–2.94, fatigue-related problems OR = 1.15; 95% CI = 0.59–2.27, dizziness-related problems OR = 1.38; 95% CI = 0.92–2.07. For symptom frequency: headache OR = 1.01; 95% CI = 0.66–1.53, fatigue OR = 1.12; 95% CI = 0.60–2.07 and sleep problems OR = 1.18; 95% CI = 0.80–1.74. Associations between perceived exposure and NSPS were more consistently observed but a meta-analysis was not performed due to considerable heterogeneity between the studies.ConclusionsThis systematic review and meta-analysis finds no evidence for a direct association between frequency and severity of NSPS and higher levels of EMF exposure. An association with perceived exposure seems to exist, but evidence is still limited because of differences in conceptualization and assessment methods.     

Biomonitoring Human Exposure to Household Air Pollution and Association with Self-reported Health Symptoms – A Stove Intervention Study in Peru

BackgroundHousehold air pollution (HAP) from indoor biomass stoves contains harmful pollutants, such as polycyclic aromatic hydrocarbons (PAHs), and is a leading risk factor for global disease burden. We used biomonitoring to assess HAP exposure and association with self-reported symptoms in 334 non-smoking Peruvian women to evaluate the efficacy of a stove intervention program.MethodsWe conducted a cross-sectional study within the framework of a community randomized control trial. Using urinary PAH metabolites (OH-PAHs) as the exposure biomarkers, we investigated whether the intervention group (n = 155, with new chimney-equipped stoves) were less exposed to HAP compared to the control group (n = 179, with mostly open-fire stoves). We also estimated associations between the exposure biomarkers, risk factors, and self-reported health symptoms, such as recent eye conditions, respiratory conditions, and headache.ResultsWe observed reduced headache and ocular symptoms in the intervention group than the control group. Urinary 2-naphthol, a suggested biomarker for inhalation PAH exposure, was significantly lower in the intervention group (GM with 95% CI: 13.4 [12.3, 14.6] μg/g creatinine) compared to control group (16.5 [15.0, 18.0] μg/g creatinine). Stove type and/or 2-naphthol was associated with a number of self-reported symptoms, such as red eye (adjusted OR with 95% CI: 3.80 [1.32, 10.9]) in the past 48 h.ConclusionsEven with the improved stoves, the biomarker concentrations in this study far exceeded those of the general populations and were higher than a no-observed-genotoxic-effect-level, indicating high exposure and a potential for increased cancer risk in the population.     

Dietary benzo(a)pyrene intake during pregnancy and birth weight: Associations modified by vitamin C intakes in the Norwegian Mother and Child Cohort Study (MoBa)

BackgroundMaternal exposure to polycyclic aromatic hydrocarbons (PAH) during pregnancy has been associated with reduced fetal growth. However, the role of diet, the main source of PAH exposure among non-smokers, remains uncertain.ObjectiveTo assess associations between maternal exposure to dietary intake of the genotoxic PAH benzo(a)pyrene [B(a)P] during pregnancy and birth weight, exploring potential effect modification by dietary intakes of vitamins C, E and A, hypothesized to influence PAH metabolism.MethodsThis study included 50,651 women in the Norwegian Mother and Child Cohort Study (MoBa). Dietary B(a)P and nutrient intakes were estimated based on total consumption obtained from a food frequency questionnaire (FFQ) and estimated based on food composition data. Data on infant birth weight were obtained from the Medical Birth Registry of Norway (MBRN). Multivariate regression was used to assess associations between dietary B(a)P and birth weight, evaluating potential interactions with candidate nutrients.ResultsThe multivariate-adjusted coefficient (95%CI) for birth weight associated with maternal energy-adjusted B(a)P intake was − 20.5 g (− 31.1, − 10.0) in women in the third compared with the first tertile of B(a)P intake. Results were similar after excluding smokers. Significant interactions were found between elevated intakes of vitamin C (> 85 mg/day) and dietary B(a)P during pregnancy for birth weight (P < 0.05), but no interactions were found with other vitamins. The multivariate-adjusted coefficients (95%CI) for birth weight in women in the third compared with the first tertile of B(a)P intake were − 44.4 g (− 76.5, − 12.3) in the group with low vitamin C intakes vs. − 17.6 g (− 29.0, − 6.1) in the high vitamin C intake group.ConclusionThe results suggest that higher prenatal exposure to dietary B(a)P may reduce birth weight. Lowering maternal intake of B(a)P and increasing dietary vitamin C intake during pregnancy may help to reduce any adverse effects of B(a)P on birth weight.     

Tobacco smoke increases the risk of otitis media among Greenlandic Inuit children while exposure to organochlorines remain insignificant

BackgroundPrenatal exposure to environmental levels of organochlorines (OCs) has been demonstrated to have immunotoxic effects in humans. We investigated the relationship between prenatal exposure to OCs and the occurrence of otitis media (OM) among Inuit children in Greenland.MethodsWe estimated the concentration of 14 PCB congeners and 11 pesticides in maternal and cord blood samples and in breast milk in a population-based cohort of 400 mother–child pairs. At follow-up, we examined the children's ears and used their medical records to assess the OM occurrence and severity. Multivariate regression analyses were used with adjustments for passive smoking, crowding, dietary habits, parent's educational level, breast feeding and the use of child-care.ResultsThe children were 4–10 years of age at follow-up and 223 (85%) participated. We found no association between prenatal OC exposure and the development of OM. Factors associated with the child's hazard of OM during the first 4 years of life were: mother's history of OM (HR 1.70, 95% CI 1.11–2.59, p = 0.01); mother's smoking habits: current (HR 2.47, 95% CI 1.45–4.21, p < 0.01) and previous (HR 2.00, 95% CI 1.19–3.36, p < 0.01); number of smokers in the home (HR 1.17, 95% CI 1.05–1.31, p < 0.01). After adjustment mothers' smoking habits remained significant.ConclusionWe found no relationship between high levels of prenatal exposure of OCs and occurrence of OM. Passive smoking was found as the strongest environmental risk factor for the development of OM.Interventions to reduce passive smoke in children's environment are needed.     

Saharan dust,particulate matter and cause-specific mortality: A case–crossover study in Barcelona (Spain)

BackgroundStudies measuring health effects of Saharan dust based on large particulate matter (PM) fraction groups may be masking some effects. Long distant transport reduces the amount of heavier and larger particles in the Saharan air masses increasing the relative contribution of smaller particles that may be more innocuous. This study investigates the association between different PM fractions and daily mortality during Saharan and non-Saharan days in Barcelona, Spain.MethodsWe collected daily PM₁, PM_2.5–1 and PM_10–2.5 fractions, and cause-specific mortality (cardiovascular, respiratory and cerebrovascular) between March 2003 and December 2007. Changes of effects between Saharan and non-Saharan dust days were assessed using a time-stratified case–crossover design.ResultsDuring non-Saharan dust days we found statistically significant (p < 0.05) effects of PM_10–2.5 for cardiovascular (odds ratio for increase of an interquartile range, OR = 1.033, 95% confidence interval: 1.006–1.060) and respiratory mortality (OR = 1.044, 95% CI: 1.001–1.089). During Saharan dust days strongest cardiovascular effects were found for the same fraction (OR = 1.085, 95% CI: 1.017–1.158) with an indication of effect modification (p = 0.111). Effects of PM_2.5–1 during Saharan dust days were about the double than in non-dust days for cardiovascular and respiratory mortality, but these differences were not statistically significant.ConclusionOur results using independent fractions of PMs provide further evidence that the effects of short-term exposure to PM during Saharan dust days are associated with both cardiovascular and respiratory mortality. A better understanding of which of the different PM size fractions brought by Saharan dust is more likely to accelerate adverse effects may help better understand mechanisms of toxicity.     

Development and validation of prediction models for blood concentrations of dioxins and PCBs using dietary intakes

BackgroundDioxins and PCBs accumulate in the food chain and might exert toxic effects in animals and humans. In large epidemiologic studies, exposure estimates of these compounds based on analyses of biological material might not be available or affordable.ObjectivesTo develop and then validate models for predicting concentrations of dioxins and PCBs in blood using a comprehensive food frequency questionnaire and blood concentrations.MethodsPrediction models were built on data from one study (n = 195), and validated in an independent study group (n = 66). We used linear regression to develop predictive models for dioxins and PCBs, both sums of congeners and 33 single congeners (7 and 10 polychlorinated dibenzo-p-dioxins and furans (PCDDs/PCDFs), 12 dioxin-like polychlorinated biphenyls (PCBs: 4 non-ortho and 8 mono-ortho), sum of all the 29 dioxin-like compounds (total TEQ) and sum of 4 non dioxin-like PCBs (∑ CB-101, 138, 153, 183 = PCB₄). We used the blood concentration and dietary intake of each of the above as dependent and independent variables, while sex, parity, age, place of living, smoking status, energy intake and education were covariates. We validated the models in a new study population comparing the predicted blood concentrations with the measured blood concentrations using correlation coefficients and Weighted Kappa (К_W) as measures of agreement, considering К_W > 0.40 as successful prediction.ResultsThe models explained 78% (sum dioxin-like compounds), 76% (PCDDs), 76% (PCDFs), 74% (no-PCBs), 69% (mo-PCBs), 68% (PCB₄) and 63% (CB-153) of the variance. In addition to dietary intake, age and sex were the most important covariates.The predicted blood concentrations were highly correlated with the measured values, with r = 0.75 for dl-compounds 0.70 for PCB₄, (p < 0.001) and 0.66 (p < 0.001) for CB-153. К_W was 0.68 for sum dl-compounds 0.65 for both PCB₄ and CB-153. Out of 33 congeners 16 (13 dl-compounds and 3 ndl PCBs) had К_W > 0.40.ConclusionsThe models developed had high power to predict blood levels of dioxins and PCBs and to correctly rank subjects according to high or low exposure based on dietary intake and demographic information. These models underline the value of dietary intake data for use in investigations of associations between dioxin and PCB exposure and health outcomes in large epidemiological studies with limited biomaterial for chemical analysis.     

Selenium exposure in subjects living in areas with high selenium concentrated drinking water: Results of a French integrated exposure assessment survey

BackgroundSelenium is an essential element which can be toxic if ingested in excessive quantities. The main human exposure is food. In addition, intake may be boosted by consumption drinking water containing unusual high selenium concentration.ObjectiveWe measured the individual selenium level of people exposed to selenium concentration in drinking water greater than the maximum recommended limit which is 10 μg/L.MethodsWe carried out a prospective cohort study on 80 adults (40 exposed subjects i.e. living in the involved area and 40 non-exposed ones i.e. living elsewhere) in western France. We used three different approaches: (1) direct measurement of ingested selenium by the duplicate portion method, (2) dietary reconstitution with a food frequency questionnaire (FFQ) and (3) evaluation of the individual selenium status by measuring the selenium content in toenail clippings. Analyses were performed by inductively coupled plasma-mass spectrometry. The association between toenail selenium concentration and area of residence was analyzed using linear regression with repeated measurements.ResultsWe estimated selenium intake from FFQ at 64 ± 14 μg/day for exposed subjects as opposed to 52 ± 14 μg/day for the non-exposed ones. On the basis of 305 duplicate diet samples, average intake was estimated at 64 ± 26 μg/day for exposed subjects. Area of residence (p = 0.0030) and smoking (p = 0.0054) were independently associated with toenail selenium concentration.ConclusionWhatever method used for estimating selenium intake, the selenium level in this studied area with high selenium concentrated drinking water is much lower than in seleniferous areas.     

Intake of phthalate-tainted foods and microalbuminuria in children: The 2011 Taiwan food scandal

BackgroundA major threat to public health involving phthalate-tainted foodstuffs occurred in Taiwan in 2011. Phthalates, mainly di-(2-ethylhexyl) phthalate (DEHP), were intentionally added to several categories of food commonly consumed by children. This study investigated the relationship between intake of the phthalate-tainted foods and renal function in children.MethodsChildren aged ≤ 10 years with possible phthalate exposure were enrolled in this study between August 2012 and January 2013. Questionnaires were used to collect details of exposure to phthalate-tainted foodstuffs, and blood and urine samples were collected for clinical biochemical workup. The clinical biomarkers of renal injury, including urinary microalbumin, N-acetyl-beta-d-glucosaminidase (NAG), and β2-microglobulin were measured. Exposure was categorized based on recommended tolerable daily intake level defined by the U.S. Environmental Protection Agency (0.02 mg/kg/day) and the European Food Safety Authority (0.05 mg/kg/day).ResultsWe analyzed intake and renal function of 184 children whose intake of DEHP-tainted foods was known. Higher DEHP exposure to DEHP-tainted foods was significantly associated with increase of urine albumin/creatinine ratio (ACR). Children in the high-exposed group (daily DEHP intake (DDI) > 0.05 mg/kg/day) had 10.395 times the risk of microalbuminuria than the low-exposed group (DDI ≤ 0.02 and > 0 mg/kg/day) and no-exposed group combined after adjustment (95% CI = 1.096–98.580, P = 0.04).ConclusionIntake of DEHP from phthalate-tainted foods may be a potential risk factor for microalbuminuria, a marker of glomerular injury in children.     

Male specific association between xenoestrogen levels in placenta and birthweight

BackgroundFetal exposure to endocrine disrupting chemicals may increase the risk for adverse health effects at birth or later in life.ObjectivesThe objective of this study is to analyze the combined effect of xenoestrogens on reproductive and perinatal growth outcomes (child birthweight, early rapid growth and body mass index (BMI) at 14 months) using the biomarker total effective xenoestrogen burden (TEXB).Methods490 placentas were randomly collected in the Spanish prospective birth cohort Environment and Childhood (INMA) project. TEXB was used to assess the estrogenicity of placental samples in two fractions: that largely attributable to environmental organohalogenated xenoestrogens (TEXB-alpha), and that mostly due to endogenous estrogens (TEXB-beta), both expressed in estrogen equivalent units (Eeq) per gram of tissue. Linear or logistic regression models were performed adjusting for cohort and confounders. Sex interactions were investigated.ResultsThe median TEXB-alpha level was 0.76 pM Eeq/g (interquartile range (iqr): 1.14). In multivariate models, higher TEXB-alpha levels (third tertile, > 1.22 pM Eeq/g; iqr: 1.73) were associated with increased birthweight in boys but not in girls (β = 148.2 g, 95% CI: 14.01, 282.53, p_int = 0.057). Additionally, higher TEXB-alpha values in boys were related with a lower risk of early rapid growth (OR = 0.37; 95% CI: 0.15, 0.88) and with a non significant association with larger BMI z-scores at 14 months of age (β = 0.29; 95% CI: − 0.11, 0.69).ConclusionsThese findings suggest that prenatal exposure to xenoestrogens may increase birthweight in boys, which might have an impact on child obesity and other later health outcomes.     

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.     

Dietary benzo(a)pyrene and fetal growth: Effect modification by vitamin C intake and glutathione S-transferase P1 polymorphism

BackgroundPrevious studies have reported maternal exposure to airborne polycyclic aromatic hydrocarbons (PAH), as well as DNA adducts reflecting total PAH exposure, to be associated with reduced fetal growth. The role of diet, the main source of PAH exposure among non-smokers, remains uncertain.ObjectiveTo assess associations between birth weight, length and small size for gestational age (SGA) with maternal intakes of the genotoxic PAH benzo(a)pyrene [B(a)P] during pregnancy, exploring potential effect modification by dietary intakes of vitamin C, vitamin E, alpha- and beta-carotene, as well as glutathione S-transferase P1 (GSTP1) polymorphisms, hypothesized to influence PAH metabolism.Methods657 women in the INMA (Environment and Childhood) Project from Sabadell (Barcelona) were recruited during the first trimester of pregnancy. Dietary B(a)P and nutrient intakes were estimated from food consumption data. Genotyping was conducted for the Ile105Val variant of GSTP1. Multivariable models were used to assess associations between size at birth and dietary B(a)P, evaluating potential interactions with candidate nutrients and GSTP1 variants.ResultsThere were significant interactions between elevated intakes of vitamin C (above the mean of 189.41 mg/day) and dietary B(a)P during the first trimester of pregnancy in models for birth weight and length (P < 0.05), but no interactions were found with other nutrients. B(a)P intakes were associated with significant reductions in birth weight and length (coefficient ± SE for a 1-SD increase in B(a)P: − 101.63 ± 34.62 g and − 0.38 ± 0.16 cm, respectively) among women with low, but not high, vitamin C intakes. Elevated dietary B(a)P was also associated with increased risk of SGA births among women with low dietary vitamin C. Among these women, associations were strongest in those carrying the GSTP1 Val allele, associated with lower contaminant detoxification activity.ConclusionResults suggest that dietary B(a)P exposure may impair fetal growth, particularly in genetically susceptible populations, and that increasing maternal intakes of vitamin C may help to reduce any adverse effects.     

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.     

Maternal urinary bisphenol A levels and infant low birth weight: A nested case–control study of the Health Baby Cohort in China

BackgroundExposure to bisphenol A (BPA), a known endocrine disruptor, has been demonstrated to affect fetal development in animal studies, but findings in human studies have been inconsistent.ObjectivesWe investigated whether maternal exposure to BPA during pregnancy is associated with an increased risk of infant low birth weight (LBW).MethodsA total 452 mother-infant pairs (113 LBW cases and 339 matched controls) were selected from the participants enrolled in the prospective Health Baby Cohort (HBC) in Wuhan city, China, during 2012–2014. BPA concentrations were measured in maternal urine samples collected at delivery, and the information of birth outcomes was retrieved from the medical records. A conditional logistic regression was used to evaluate the relationship between urinary BPA levels and LBW.ResultsMothers with LBW infants had significantly higher urinary BPA levels (median: 4.70 μg/L) than the control mothers (median: 2.25 μg/L) (p < 0.05). Increased risk of LBW was associated with higher maternal urinary levels of BPA [adjusted odds ratio (OR) = 3.13 for the medium tertile, 95% confidence interval (CI): 1.21, 8.08; adjusted OR = 2.49 for the highest tertile, 95% CI: 0.98, 6.36]. The association was more pronounced among female infants than among male infants, with a statistical evidence of heterogeneity in risk (p = 0.03).ConclusionsPrenatal exposure to higher levels of BPA may potentially increase the risk of delivering LBW infants, especially for female infants. This is the first case–control study to examine the association in China.     

Novel exposure biomarkers of N,N-diethyl-m-toluamide (DEET): Data from the 2007–2010 National Health and Nutrition Examination Survey

BackgroundN,N-diethyl-m-toluamide (DEET) is a widely used insect repellent in the United States.ObjectivesTo assess exposure to DEET in a representative sample of persons 6 years and older in the U.S. general population from the 2007–2010 National Health and Nutrition Examination Survey.MethodsWe analyzed 5348 urine samples by using online solid-phase extraction coupled to isotope dilution-high-performance liquid chromatography-tandem mass spectrometry. We used regression models to examine associations of various demographic parameters with urinary concentrations of DEET biomarkers.ResultsWe detected DEET in ~ 3% of samples and at concentration ranges (> 0.08 μg/L–45.1 μg/L) much lower than those of 3-(diethylcarbamoyl)benzoic acid (DCBA) (> 0.48 μg/L–30,400 μg/L) and N,N-diethyl-3-hydroxymethylbenzamide (DHMB) (> 0.09 μg/L–332 μg/L). DCBA was the most frequently detected metabolite (~ 84%). Regardless of survey cycle and the person's race/ethnicity or income, adjusted geometric mean concentrations of DCBA were higher in May–Sep than in Oct–Apr. Furthermore, non-Hispanic whites in the warm season were more likely than in the colder months [adjusted odds ratio (OR) = 10.83; 95% confidence interval (CI), 3.28–35.79] and more likely than non-Hispanic blacks (OR = 3.45; 95% CI, 1.51–7.87) to have DCBA concentrations above the 95th percentile.ConclusionsThe general U.S. population, including school-age children, is exposed to DEET. However, reliance on DEET as the sole urinary biomarker would likely underestimate the prevalence of exposure. Instead, oxidative metabolites of DEET are the most adequate exposure biomarkers. Differences by season of the year based on demographic variables including race/ethnicity likely reflect different lifestyle uses of DEET-containing products.     

Concentrations of polybrominated diphenyl ethers (PBDEs) in matched samples of human milk,dust and indoor air

Polybrominated diphenyl ethers (PBDEs) are lipophilic, persistent pollutants found worldwide in environmental and human samples. Exposure pathways for PBDEs remain unclear but may include food, air and dust. The aim of this study was to conduct an integrated assessment of PBDE exposure and human body burden using 10 matched samples of human milk, indoor air and dust collected in 2007–2008 in Brisbane, Australia. In addition, temporal analysis was investigated comparing the results of the current study with PBDE concentrations in human milk collected in 2002–2003 from the same region.PBDEs were detected in all matrices and the median concentrations of BDEs -47 and -209 in human milk, air and dust were: 4.2 and 0.3 ng/g lipid; 25 and 7.8 pg/m³; and 56 and 291 ng/g dust, respectively. Significant correlations were observed between the concentrations of BDE-99 in air and human milk (r = 0.661, p = 0.038) and BDE-153 in dust and BDE-183 in human milk (r = 0.697, p = 0.025). These correlations do not suggest causal relationships — there is no hypothesis that can be offered to explain why BDE-153 in dust and BDE-183 in milk are correlated. The fact that so few correlations were found in the data could be a function of the small sample size, or because additional factors, such as sources of exposure not considered or measured in the study, might be important in explaining exposure to PBDEs. There was a slight decrease in PBDE concentrations from 2002–2003 to 2007–2008 but this may be due to sampling and analytical differences. Overall, average PBDE concentrations from these individual samples were similar to results from pooled human milk collected in Brisbane in 2002–2003 indicating that pooling may be an efficient, cost-effective strategy of assessing PBDE concentrations on a population basis.The results of this study were used to estimate an infant's daily PBDE intake via inhalation, dust ingestion and human milk consumption. Differences in PBDE intake of individual congeners from the different matrices were observed. Specifically, as the level of bromination increased, the contribution of PBDE intake decreased via human milk and increased via dust. As the impacts of the ban of the lower brominated (penta- and octa-BDE) products become evident, an increased use of the higher brominated deca-BDE product may result in dust making a greater contribution to infant exposure than it does currently.To better understand human body burden, further research is required into the sources and exposure pathways of PBDEs and metabolic differences influencing an individual's response to exposure. In addition, temporal trend analysis is necessary with continued monitoring of PBDEs in the human population as well as in the suggested exposure matrices of food, dust and air.     

Acute respiratory response to traffic-related air pollution during physical activity performance

BackgroundPhysical activity (PA) has beneficial, whereas exposure to traffic related air pollution (TRAP) has adverse, respiratory effects. Few studies, however, have examined if the acute effects of TRAP upon respiratory outcomes are modified depending on the level of PA.ObjectivesThe aim of our study was to disentangle acute effects of TRAP and PA upon respiratory outcomes and assess the impact of participants TRAP pre-exposure.MethodsWe conducted a real-world crossover study with repeated measures of 30 healthy adults. Participants completed four 2-h exposure scenarios that included either rest or intermittent exercise in high- and low-traffic environments. Measures of respiratory function were collected at three time points. Pre-exposure to TRAP was ascertained from land-use-modeled address-attributed values. Mixed-effects models were used to estimate the impact of TRAP and PA on respiratory measures as well as potential effect modifications.ResultsWe found that PA was associated with a statistically significant increases of FEV₁ (48.5 mL, p = 0.02), FEV₁/FVC (0.64%, p = 0.005) and FEF_25–75% (97.8 mL, p = 0.02). An increase in exposure to one unit (1 μg/m³) of PM_coarse was associated with a decrease in FEV₁ (− 1.31 mL, p = 0.02) and FVC (− 1.71 mL, p = 0.01), respectively. On the other hand, for an otherwise equivalent exposure an increase of PA by one unit (1%Heart rate max) was found to reduce the immediate negative effects of particulate matter (PM) upon PEF (PM_2.5, 0.02 L/min, p = 0.047; PM₁₀, 0.02 L/min p = 0.02; PM_coarse, 0.03 L/min, p = 0.02) and the several hours delayed negative effects of PM upon FVC (PM_coarse, 0.11 mL, p = 0.02). The negative impact of exposure to TRAP constituents on FEV₁/FVC and PEF was attenuated in those participants with higher TRAP pre-exposure levels.ConclusionsOur results suggest that associations between various pollutant exposures and respiratory measures are modified by the level of PA during exposure and TRAP pre-exposure of participants.     

Occupational exposure to pesticides and Parkinson's disease: A systematic review and meta-analysis of cohort studies

ObjectivesTo systematically review available cohort studies and estimate quantitatively the association between occupational exposure to pesticides and Parkinson's disease (PD).MethodsStudies were identified from a MEDLINE search through 30 November 2011 and from the reference lists of identified publications. Relative risk (RR) estimates were extracted from 12 studies published between 1985 and 2011. Meta-rate ratio estimates (mRR) were calculated according to fixed and random-effect meta-analysis models. Meta-analyses were performed on the whole set of data and separate analyses were conducted after stratification for gender, exposure characterisation, PD cases identification, geographic location, reported risk estimator and cohort study design.ResultsA statistically significant increased risk of PD was observed when all studies were combined (mRR = 1.28; 95% confidence interval [CI]: 1.03–1.59) but there was a high heterogeneity and inconsistency among studies. The highest increased risks were observed for studies with the best design, i.e. reporting PD diagnosis confirmed by a neurologist (mRR = 2.56; CI: 1.46–4.48; n = 4), for cohort studies reporting incidence of PD (mRR = 1.95; CI: 1.29–2.97; n = 3) as well as for prospective cohorts (mRR = 1.39; CI: 1.09–1.78; n = 6). A significant increased risk was also seen for banana, sugarcane and pineapple plantation workers (mRR = 2.05; CI: 1.23–3.42; n = 2).ConclusionsThe present study provides some support for the hypothesis that occupational exposure to pesticides increases the risk of PD.     

Air pollution exposure and telomere length in highly exposed subjects in Beijing,China: A repeated-measure study

BackgroundAmbient particulate matter (PM) exposure has been associated with short- and long-term effects on cardiovascular disease (CVD). Telomere length (TL) is a biomarker of CVD risk that is modified by inflammation and oxidative stress, two key pathways for PM effects. Whether PM exposure modifies TL is largely unexplored.ObjectivesTo investigate effects of PM on blood TL in a highly-exposed population.MethodsWe measured blood TL in 120 blood samples from truck drivers and 120 blood samples from office workers in Beijing, China. We measured personal PM_2.5 and Elemental Carbon (EC, a tracer of traffic particles) using light-weight monitors. Ambient PM₁₀ was obtained from local monitoring stations. We used covariate-adjusted regression models to estimate percent changes in TL per an interquartile-range increase in exposure.ResultsCovariate-adjusted TL was higher in drivers (mean = 0.87, 95%CI: 0.74; 1.03) than in office workers (mean = 0.79, 95%CI: 0.67; 0.93; p = 0.001). In all participants combined, TL increased in association with personal PM_2.5 (+ 5.2%, 95%CI: 1.5; 9.1; p = 0.007), personal EC (+ 4.9%, 95%CI: 1.2; 8.8; p = 0.01), and ambient PM₁₀ (+ 7.7%, 95%CI: 3.7; 11.9; p < 0.001) on examination days. In contrast, average ambient PM₁₀ over the 14 days before the examinations was significantly associated with shorter TL (− 9.9%, 95%CI: − 17.6; − 1.5; p = 0.02).ConclusionsShort-term exposure to ambient PM is associated with increased blood TL, consistent with TL roles during acute inflammatory responses. Longer exposures may shorten TL as expected after prolonged pro-oxidant exposures. The observed TL alterations may participate in the biological pathways of short- and long-term PM effects.