Biomonitoring of the general population living near a modern solid waste incinerator: A pilot study in Modena,Italy

Background and goalsAs part of the authorization process for the solid waste incinerator (SWI) in Modena, Italy, a human biomonitoring cross-sectional pilot study was conducted to investigate the degree to which people living and working in the proximity of the plant were exposed to SWI emissions.MethodsBetween May and June 2010, 65 subjects living and working within 4 km of the incinerator (exposed) and 103 subjects living and working outside this area (unexposed) were enrolled in the study. Blood, serum and urinary metals (Pb, Cd, Cu, Zn, Hg, Mn, Ni), urinary benzene, toluene, xylene (BTEX), S-phenylmercapturic acid (SPMA), and urinary polycyclic aromatic hydrocarbons (PAHs) were analysed. Information about lifestyle, anthropometric characteristics, residence, and health status was collected by a self-administered questionnaire. Exposure to particulate matter (PM) emitted from the SWI was estimated using fall-out maps from a quasi-Gaussian dispersion model. A multiple linear regression analysis investigated the relationship between biomarkers and the distance of a subject's place of residence from the SWI plant or the exposure to PM.ResultsUrinary BTEX and SPMA and blood, serum and urinary metals showed no differences between exposed and unexposed subjects. PAHs were higher in exposed than in unexposed subjects for phenanthrene, anthracene, and pyrene (median levels: 9.5 vs. 7.2 ng/L, 0.8 vs. < 0.5 ng/L and 1.6 vs. 1.3 ng/L, respectively, p < 0.05). Multiple linear regression analysis showed that blood Cd and Hg and urinary Mn, fluorene, phenanthrene, anthracene and pyrene were inversely correlated to the distance of a subject's residence from the SWI. Urinary Mn, fluorene and phenanthrene were directly correlated to PM exposure.ConclusionsThis study, although not representative of the general population, suggests that specific biomarkers may provide information about the degree of exposure the subjects working and living in the proximity of the SWI plant may have to emissions from that facility.     

Dietary exposure to polychlorinated biphenyls and risk of myocardial infarction in men — A population-based prospective cohort study

BackgroundMajor food contaminants such as polychlorinated biphenyls (PCBs) are proposed to play a role in the etiology of cardiovascular disease (CVD), but to date the impact of PCBs on cardiovascular health need to be explored.Methods and resultsWe assessed the association between validated food frequency questionnaire-based estimates of dietary PCB exposure and risk of myocardial infarction, ascertained through register-linkage, among 36,759 men from the population-based Swedish Cohort of Men, free of cardiovascular disease, diabetes and cancer at baseline (1997). Relative risks were adjusted for known cardiovascular risk factors, long-chain omega-3 fatty acids (eicosapentaenoic and docosahexaenoic acids) and methyl mercury exposure. During 12 years of follow-up (433,243 person-years), we ascertained 3005 incident cases of myocardial infarction (654 fatal). Compared with the lowest quintile of dietary PCB exposure (median 113 ng/day), men in the highest quintile (median 436 ng/day) had multivariable-adjusted relative risks of 1.74 (95% confidence interval [CI], 1.30–2.33; p-trend < 0.001) for total and 1.97 (95% CI 1.42–2.75; p-trend < 0.001) for non-fatal myocardial infarction. In mutually adjusted models, dietary PCB exposure was associated with an increased risk of myocardial infarction, while the intake of long-chain omega-3 fish fatty acids was associated with a decreased risk. We also observed an effect modification by adiposity on the association between of dietary PCB exposure and myocardial infarction, with higher risk among lean men (p value for interaction = 0.03).ConclusionsExposure to PCBs via diet was associated with increased risk of myocardial infarction in men.     

Respiratory medication sales and urban air pollution in Brussels (2005 to 2011)

BackgroundWe investigated the associations between daily sales of respiratory medication and air pollutants in the Brussels-Capital Region between 2005 and 2011.MethodsWe used over-dispersed Poisson Generalized Linear Models to regress daily individual reimbursement data of prescribed asthma and COPD medication from the social security database against each subject's residential exposure to outdoor particulate matter (PM₁₀) or NO₂ estimated, by interpolation from monitoring stations. We calculated cumulative risk ratios (RR) and their 95% confidence intervals (CI) for interquartile ranges (IQR) of exposure for different windows of past exposure for the entire population and for seven age groups.ResultsMedian daily concentrations of PM₁₀ and NO₂ were 25 μg/m³ (IQR = 17.1) and 38 μg/m³ (IQR = 20.5), respectively. PM₁₀ was associated with daily medication sales among individuals aged 13 to 64 y. For NO₂, significant associations were observed among all age groups except > 84 y. The highest RR were observed for NO₂, among adolescents, including three weeks lags (RR = 1.187 95%CI: 1.097–1.285).ConclusionThe associations found between temporal changes in exposure to air pollutants and daily sales of respiratory medication in Brussels indicate that urban air pollution contributes to asthma and COPD morbidity in the general population.     

Persistent organic pollutants exposure during pregnancy,maternal gestational weight gain,and birth outcomes in the mother–child cohort in Crete,Greece (RHEA study)

BackgroundPersistent organic pollutants (POPs), including polychlorinated biphenyls (PCBs) and pesticides bioaccumulate through the food chain and cross the placenta. POPs are developmental toxicants in animals but the epidemiological evidence on pregnancy outcomes is inconsistent. Maternal gestational weight gain has been recently suggested as a key factor explaining the association between PCBs with lower birth weight.AimsWe examined whether in utero exposure to current low levels of different POPs is associated with fetal growth and gestational age in a mother–child cohort in Crete, Greece (Rhea study), and evaluated specifically whether maternal gestational weight gain may affect this association.MethodsWe included 1117 mothers and their newborns from the Rhea study. Mothers were interviewed and blood samples collected during the first trimester of pregnancy. Information on birth outcomes was retrieved from medical records. Concentrations of several PCBs, other organochlorine compounds (dichlorodiphenyl dichloroethene [DDE], dichlorodiphenyl trichloroethane [DDT] and hexachlorobenzene [HCB]) and one polybrominated diphenyl ether congener (tetra-bromodiphenyl ether [BDE-47]), were determined in maternal serum by triple quadrupole mass spectrometry. Multiple linear regression models were used to investigate the associations of birth weight, gestational age, and head circumference with each compound individually on the log₁₀ scale, and with combined exposures through the development of an exposure score.ResultsIn multivariate models, birth weight was negatively associated with increasing levels of HCB (β = − 161.1 g; 95% CI: − 296.6, − 25.7) and PCBs (β = − 174.1 g; 95% CI: − 332.4, − 15.9); after further adjustment for gestational weight gain these estimates were slightly reduced (β = − 154.3 g; 95% CI: − 300.8, − 7.9 for HCB and β = − 135.7 g; 95% CI: − 315.4, 43.9 for PCBs). Furthermore, in stratified analysis, the association between POPs and birth weight was only observed in women with inadequate or excessive gestational weight gain. Small, negative associations were observed with head circumference while no association was observed with gestational age.ConclusionsThe findings suggest that prenatal exposure to PCBs and HCB impairs fetal growth and adds to the growing literature that demonstrates an association between low-level environmental pollutant exposure and fetal growth. Furthermore our results suggest that the association of POPs, maternal gestational weight gain and birth weight is probably more complex than that previously hypothesized.     

Prenatal DDT and DDE exposure and child IQ in the CHAMACOS cohort

Although banned in most countries, dichlorodiphenyl-trichloroethane (DDT) continues to be used for vector control in some malaria endemic areas. Previous findings from the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) cohort study found increased prenatal levels of DDT and its breakdown product dichlorodiphenyl-dichloroethylene (DDE) to be associated with altered neurodevelopment in children at 1 and 2 years of age. In this study, we combined the measured maternal DDT/E concentrations during pregnancy obtained for the prospective birth cohort with predicted prenatal DDT and DDE levels estimated for a retrospective birth cohort. Using generalized estimating equation (GEE) and linear regression models, we evaluated the relationship of prenatal maternal DDT and DDE serum concentrations with children's cognition at ages 7 and 10.5 years as assessed using the Full Scale Intelligence Quotient (IQ) and 4 subtest scores (Working Memory, Perceptual Reasoning, Verbal Comprehension, and Processing Speed) of the Wechsler Intelligence Scale for Children (WISC). In GEE analyses incorporating both age 7 and 10.5 scores (n = 619), we found prenatal DDT and DDE levels were not associated with Full Scale IQ or any of the WISC subscales (p-value > 0.05). In linear regression analyses assessing each time point separately, prenatal DDT levels were inversely associated with Processing Speed at age 7 years (n = 316), but prenatal DDT and DDE levels were not associated with Full Scale IQ or any of the WISC subscales at age 10.5 years (n = 595). We found evidence for effect modification by sex. In girls, but not boys, prenatal DDE levels were inversely associated with Full Scale IQ and Processing Speed at age 7 years. We conclude that prenatal DDT levels may be associated with delayed Processing Speed in children at age 7 years and the relationship between prenatal DDE levels and children's cognitive development may be modified by sex, with girls being more adversely affected.     

Umbilical cord blood PBDEs concentrations are associated with placental DNA methylation

BackgroundIn utero polybrominated diphenyl ethers (PBDEs) exposure has been associated with adverse fetal growth. Alterations in placental DNA methylation might mediate those adverse effects.ObjectivesTo examine the associations between in utero PBDEs exposure and DNA methylation in human placenta.MethodsEighty apparently healthy mother-newborn pairs delivering at the Second Affiliated Hospital of Wenzhou Medical College were enrolled in this study. Placental DNA methylation of LINE1, NR3C1 and IGF2 was measured by quantitative polymerase chain reaction-pyrosequencing. In utero PBDEs exposure was assessed by measuring umbilical cord blood PBDEs concentrations.ResultsFor LINE-1, higher levels of BDE-66 exposure were associated with decreased DNA methylation (β = − 0.9, 95% CI, − 1.8 to − 0.1); For NR3C1, BDE-153 concentrations was significantly inversely associated with DNA methylation (β = − 2.0, 95% CI, − 3.7 to − 0.2); For IGF2, elevated concentrations of both BDE-153 (β = − 1.7; 95% CI, − 3.0 to − 0.4) and BDE-209 (β = − 1.0; 95% CI, − 1. 9 to − 0.1) were significantly associated with decreased DNA methylation.ConclusionsWe found that placental DNA methylation is associated with in utero PBDEs exposure. Changes in placental DNA methylation might be part of the underlying biological pathway between in utero PBDEs exposure and adverse fetal growth.     

Exposure to endocrine disrupting chemicals among residents of a rural vegetarian/vegan community

Background & AimsEndocrine-disrupting chemicals (EDCs) are increasingly thought to be involved in the rising prevalence of disorders such as obesity, diabetes, and some hormone-dependent cancers. Several lines of evidence have indicated that vegetarian and vegan diets may offer some protection from such diseases. We hypothesized that exposure to selected EDCs among residents of the unique vegetarian/vegan community of Amirim would be lower than what has recently been reported for the omnivorous population in the first Israel Biomonitoring Study (IBMS).MethodsWe studied 42 Amirim residents (29 vegetarians/13 vegans; 24 women/18men, aged 50.7 ± 13.7 y). Subjects answered detailed lifestyle, and multipass, memory-based 24-hr dietary recall questionnaires. Concentrations of bisphenol A (BPA), 11 phthalate metabolites, and the isoflavone phytoestrogens (genistein and daidzein) were determined by GC or LC tandem mass-spectrometry on a spot urine sample. The results were compared to those obtained following the same methodology in the Jewish subgroup of the IBMS (n = 184).ResultsWhile a vegetarian/vegan nutritional pattern had no effect on exposure to BPA, it seemed to confer a modest protection (~ 21%) from exposure to high molecular weight phthalates. Furthermore, the summed metabolites of the high molecular weight phthalate DiNP were 36% lower in vegans compared to vegetarians (P < 0.05). In contrast, Amirim residents exhibited a level of exposure to isoflavone phytoestrogens about an order of magnitude higher than in the IBMS (P < 0.001).ConclusionsIn Israel, a country whose inhabitants demonstrate exposure to EDCs comparable to that of the US and Canada, a voluntary lifestyle of vegetarianism and preference for organic food has a modest, but possibly valuable, impact on exposure to phthalates, while it is associated with a very steep increase in the exposure to phytoestrogens. Major reduction in exposure to EDCs will require regulatory actions.     

Residential proximity to traffic and female pubertal development

BackgroundTraffic-related air pollution (TRAP) has been linked with several adverse health outcomes, including preterm birth and low birth weight, which are both related to onset of puberty. No studies to date have investigated the association between TRAP and altered pubertal timing.ObjectiveDetermine the association between residential proximity to traffic, as a marker of long-term TRAP exposure, and age at pubertal onset in a longitudinal study of girls.MethodsWe analyzed data for 437 girls at the CYGNET study site of the Breast Cancer and Environment Research Program. TRAP exposure was assessed using several measures of residential proximity to traffic based on address at study entry. Using accelerated failure time models, we calculated time ratios (TRs) and their corresponding 95% confidence intervals (CIs) for specified traffic metrics and pubertal onset, defined as stage 2 or higher for breast or pubic hair development (respectively, B2 + and PH2 +). Models were adjusted for race/ethnicity, household income, and cotinine levels.ResultsAt baseline, 71% of girls lived within 150 m of a major road. The median age of onset was 10.3 years for B2 + and 10.9 years for PH2 +. Living within 150 m downwind of a major road was associated with earlier onset of PH2 + (TR 0.96, 95% CI 0.93, 0.99). Girls in the highest quintile of either distance-weighted traffic density, annual average daily traffic, and/or traffic density also reached PH2 + earlier than girls in the lowest quintiles.ConclusionsIn this first study to assess the association between residential proximity to traffic and pubertal onset we found girls with higher exposure reached one pubertal milestone several months earlier than low exposed girls, even after consideration of likely confounders. Results should be expanded in larger epidemiological studies, and with measured levels of air pollutants.     

Prenatal particulate air pollution and neurodevelopment in urban children: Examining sensitive windows and sex-specific associations

BackgroundBrain growth and structural organization occurs in stages beginning prenatally. Toxicants may impact neurodevelopment differently dependent upon exposure timing and fetal sex.ObjectivesWe implemented innovative methodology to identify sensitive windows for the associations between prenatal particulate matter with diameter ≤ 2.5 μm (PM_2.5) and children's neurodevelopment.MethodsWe assessed 267 full-term urban children's prenatal daily PM_2.5 exposure using a validated satellite-based spatio-temporally resolved prediction model. Outcomes included IQ (WISC-IV), attention (omission errors [OEs], commission errors [CEs], hit reaction time [HRT], and HRT standard error [HRT-SE] on the Conners' CPT-II), and memory (general memory [GM] index and its components — verbal [VEM] and visual [VIM] memory, and attention-concentration [AC] indices on the WRAML-2) assessed at age 6.5 ± 0.98 years. To identify the role of exposure timing, we used distributed lag models to examine associations between weekly prenatal PM_2.5 exposure and neurodevelopment. Sex-specific associations were also examined.ResultsMothers were primarily minorities (60% Hispanic, 25% black); 69% had ≤ 12 years of education. Adjusting for maternal age, education, race, and smoking, we found associations between higher PM_2.5 levels at 31–38 weeks with lower IQ, at 20–26 weeks gestation with increased OEs, at 32–36 weeks with slower HRT, and at 22–40 weeks with increased HRT-SE among boys, while significant associations were found in memory domains in girls (higher PM_2.5 exposure at 18–26 weeks with reduced VIM, at 12–20 weeks with reduced GM).ConclusionsIncreased PM_2.5 exposure in specific prenatal windows may be associated with poorer function across memory and attention domains with variable associations based on sex. Refined determination of time window- and sex-specific associations may enhance insight into underlying mechanisms and identification of vulnerable subgroups.     

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.     

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.     

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.     

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.     

Exposure to multiple sources of polycyclic aromatic hydrocarbons and breast cancer incidence

BackgroundDespite studies having consistently linked exposure to single-source polycyclic aromatic hydrocarbons (PAHs) to breast cancer, it is unclear whether single sources or specific groups of PAH sources should be targeted for breast cancer risk reduction.ObjectivesThis study considers the impact on breast cancer incidence from multiple PAH exposure sources in a single model, which better reflects exposure to these complex mixtures.MethodsIn a population-based case-control study conducted on Long Island, New York (N = 1508 breast cancer cases/1556 controls), a Bayesian hierarchical regression approach was used to estimate adjusted posterior means and credible intervals (CrI) for the adjusted odds ratios (ORs) for PAH exposure sources, considered singly and as groups: active smoking; residential environmental tobacco smoke (ETS); indoor and outdoor air pollution; and grilled/smoked meat intake.ResultsMost women were exposed to PAHs from multiple sources, and the most common included active/passive smoking and grilled/smoked food intake. In multiple-PAH source models, breast cancer incidence was associated with residential ETS from a spouse (OR = 1.20, 95%CrI = 1.03, 1.40) and synthetic firelog burning (OR = 1.29, 95%CrI = 1.06, 1.57); these estimates are similar, but slightly attenuated, to those from single-source models. Additionally when we considered PAH exposure groups, the most pronounced significant associations included total indoor sources (active smoking, ETS from spouse, grilled/smoked meat intake, stove/fireplace use, OR = 1.45, 95%CrI = 1.02, 2.04).ConclusionsGroups of PAH sources, particularly indoor sources, were associated with a 30–50% increase in breast cancer incidence. PAH exposure is ubiquitous and a potentially modifiable breast cancer risk factor.     

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.     

A novel model to characterize postnatal exposure to lipophilic environmental toxicants and application in the study of hexachlorobenzene and infant growth

BackgroundInfants are exposed to persistent environmental contaminants through breast milk, yet studies assessing the health effects of postnatal exposure are lacking. Existing postnatal exposure assessment is either too simple (lactation exposure model, LEM) or requires complex physiologically-based pharmacokinetic (PBPK) models.ObjectivesWe present equations for postnatal exposure calculations. We applied these equations to study the effect of hexachlorobenzene (HCB) on infant growth in the two first years of life.MethodsHCB was measured in breast milk samples in 449 mother-child pairs participating in the Norwegian birth cohort study HUMIS. We used these concentrations, mother's weight, height and age, together with child's weight at 8 age points, and proportion of milk consumed each month, to calculate HCB concentrations in the infant over age. We then estimated the association between HCB and infant growth using a linear mixed model.ResultsChildren exposed to HCB via mother's milk reached concentrations 1–5 times higher than the mother. HCB was associated with lower weight gain in the first 2 years (− 33 g per unit HCB and month, 95% CI: − 38, − 27 at 6 months). Associations were stronger during the first 3 months (− 57 g per unit HCB and month, 95% CI: − 67, − 49 at 1 month), indicating a critical window of effect. Our equations gave more precise estimates than the LEM.ConclusionOur equations for postnatal exposure of lipophilic environmental toxicants give better results than the LEM and are easier to implement than the complex PBPK models. HCB exposure, especially during the first three months of life, has a negative effect on infant growth up to 2 years.     

Morphology,spatial distribution,and concentration of flame retardants in consumer products and environmental dusts using scanning electron microscopy and Raman micro-spectroscopy

We characterized flame retardant (FR) morphologies and spatial distributions in 7 consumer products and 7 environmental dusts to determine their implications for transfer mechanisms, human exposure, and the reproducibility of gas chromatography–mass spectrometry (GC–MS) dust measurements. We characterized individual particles using scanning electron microscopy/energy dispersive x-ray spectroscopy (SEM/EDS) and Raman micro-spectroscopy (RMS). Samples were screened for the presence of 3 FR constituents (bromine, phosphorous, non-salt chlorine) and 2 metal synergists (antimony and bismuth). Subsequent analyses of select samples by RMS enabled molecular identification of the FR compounds and matrix materials. The consumer products and dust samples possessed FR elemental weight percents of up to 36% and 31%, respectively. We identified 24 FR-containing particles in the dust samples and classified them into 9 types based on morphology and composition. We observed a broad range of morphologies for these FR-containing particles, suggesting FR transfer to dust via multiple mechanisms. We developed an equation to describe the heterogeneity of FR-containing particles in environmental dust samples. The number of individual FR-containing particles expected in a 1-mg dust sample with a FR concentration of 100 ppm ranged from < 1 to > 1000 particles. The presence of rare, high-concentration bromine particles was correlated with decabromodiphenyl ether concentrations obtained via GC–MS. When FRs are distributed heterogeneously in highly concentrated dust particles, human exposure to FRs may be characterized by high transient exposures interspersed by periods of low exposure, and GC–MS FR concentrations may exhibit large variability in replicate subsamples. Current limitations of this SEM/EDS technique include potential false negatives for volatile and chlorinated FRs and greater quantitation uncertainty for brominated FR in aluminum-rich matrices.     

Boron exposure through drinking water during pregnancy and birth size

BackgroundBoron is a metalloid found at highly varying concentrations in soil and water. Experimental data indicate that boron is a developmental toxicant, but the few human toxicity data available concern mostly male reproduction.ObjectivesTo evaluate potential effects of boron exposure through drinking water on pregnancy outcomes.MethodsIn a mother-child cohort in northern Argentina (n = 194), 1–3 samples of serum, whole blood and urine were collected per woman during pregnancy and analyzed for boron and other elements to which exposure occurred, using inductively coupled plasma mass spectrometry. Infant weight, length and head circumference were measured at birth.ResultsDrinking water boron ranged 377–10,929 μg/L. The serum boron concentrations during pregnancy ranged 0.73–605 μg/L (median 133 μg/L) and correlated strongly with whole-blood and urinary boron, and, to a lesser extent, with water boron. In multivariable-adjusted linear spline regression analysis (non-linear association), we found that serum boron concentrations above 80 μg/L were inversely associated with birth length (B − 0.69 cm, 95% CI − 1.4; − 0.024, p = 0.043, per 100 μg/L increase in serum boron). The impact of boron appeared stronger when we restricted the exposure to the third trimester, when the serum boron concentrations were the highest (0.73–447 μg/L). An increase in serum boron of 100 μg/L in the third trimester corresponded to 0.9 cm shorter and 120 g lighter newborns (p = 0.001 and 0.021, respectively).ConclusionsConsidering that elevated boron concentrations in drinking water are common in many areas of the world, although more screening is warranted, our novel findings warrant additional research on early-life exposure in other populations.     

Exposure to fine particle matter,nitrogen dioxide and benzene during pregnancy and cognitive and psychomotor developments in children at 15 months of age

BackgroundPrenatal exposure to air pollutants has recently been identified as a potential risk factor for neuropsychological impairment.ObjectivesTo assess whether prenatal exposure to fine particulate matter (PM_2.5), nitrogen dioxide (NO₂) and benzene were associated with impaired development in infants during their second year of life.MethodsRegression analyses, based on 438 mother–child pairs, were performed to estimate the association between mother exposure to air pollutants during pregnancy and neurodevelopment of the child. The average exposure to PM_2.5, NO₂ and benzene over the whole pregnancy was calculated for each woman. During the second year of life, infant neuropsychological development was assessed using the Bayley Scales of Infant Development. Regression analyses were performed to estimate the association between exposure and outcomes, accounting for potential confounders.ResultsWe estimated that a 1 μg/m³ increase during pregnancy in the average levels of PM_2.5 was associated with a − 1.14 point decrease in motor score (90% CI: − 1.75; − 0.53) and that a 1 μg/m³ increase of NO₂ exposure was associated with a − 0.29 point decrease in mental score (90% CI: − 0.47; − 0.11). Benzene did not show any significant association with development. Considering women living closer (≤ 100 m) to metal processing activities, we found that motor scores decreased by − 3.20 (90% CI: − 5.18; − 1.21) for PM_2.5 and − 0.51 (− 0.89; − 0.13) for NO₂, while mental score decreased by − 2.71 (90% CI: − 4.69; − 0.74) for PM_2.5, and − 0.41 (9% CI: − 0.76; − 0.06) for NO₂.ConclusionsOur findings suggest that prenatal residential exposure to PM_2.5 and NO₂ adversely affects infant motor and cognitive developments. This negative effect could be higher in the proximity of metal processing plants.     

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.