Lower placental telomere length may be attributed to maternal residential traffic exposure; a twin study

BackgroundHigh variation in telomere length between individuals is already present before birth and is as wide among newborns as in adults. Environmental exposures likely have an impact on this observation, but remain largely unidentified. We hypothesize that placental telomere length in twins is associated with residential traffic exposure, an important environmental source of free radicals that might accelerate aging. Next, we intend to unravel the nature-nurture contribution to placental telomere length by estimating the heritability of placental telomere length.MethodsWe measured the telomere length in placental tissues of 211 twins in the East Flanders Prospective Twin Survey. Maternal traffic exposure was determined using a geographic information system. Additionally, we estimated the relative importance of genetic and environmental sources of variance.ResultsIn this twin study, a variation in telomere length in the placental tissue was mainly determined by the common environment. Maternal residential proximity to a major road was associated with placental telomere length: a doubling in the distance to the nearest major road was associated with a 5.32% (95% CI: 1.90 to 8.86%; p = 0.003) longer placental telomere length at birth. In addition, an interquartile increase (22%) in maternal residential surrounding greenness (5 km buffer) was associated with an increase of 3.62% (95% CI: 0.20 to 7.15%; p = 0.04) in placental telomere length.ConclusionsIn conclusion, we showed that maternal residential proximity to traffic and lower residential surrounding greenness is associated with shorter placental telomere length at birth. This may explain a significant proportion of air pollution-related adverse health outcomes starting from early life, since shortened telomeres accelerate the progression of many diseases.     

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.     

Associations between short/medium-term variations in black smoke air pollution and mortality in the Glasgow conurbation,UK

ObjectivesTo examine associations between short/medium-term variations in black smoke air pollution and mortality in the population of Glasgow and the adjacent towns of Renfrew and Paisley over a 25-year period at different time lags (0–30 days).MethodsGeneralised linear (Poisson) models were used to investigate the relationship between lagged black smoke concentrations and daily mortality, with allowance for confounding by cold temperature, between 1974 and 1998.ResultsWhen a range of lag periods were investigated significant associations were noted between temperature-adjusted black smoke exposure and all-cause mortality at lag periods of 13–18 and 19–24 days, and respiratory mortality at lag periods of 1–6, 7–12, and 13–18 days. Significant associations between cardiovascular mortality and temperature-adjusted black smoke were not observed. After adjusting for the effects of temperature a 10 μg m^− 3 increase in black smoke concentration on a given day was associated with a 0.9% [95% Confidence Interval (CI): 0.3–1.5%] increase in all cause mortality and a 3.1% [95% CI: 1.4–4.9%] increase in respiratory mortality over the ensuing 30-day period. In contrast for a 10 μg m^− 3 increase in black smoke concentration over 0–3 day lag period, the temperature adjusted exposure mortality associations were substantially lower (0.2% [95% CI: − 0.0–0.4%] and 0.3% [95% CI: − 0.2–0.8%] increases for all-cause and respiratory mortality respectively).ConclusionsThis study has provided evidence of association between black smoke exposure and mortality at longer lag periods than have been investigated in the majority of time series analyses.     

Occupational exposure to asthmagens and adult onset wheeze and lung function in people who did not have childhood wheeze: A 50-year cohort study

BackgroundThere are few prospective studies that relate the development of adult respiratory disease with exposure to occupational asthmagens.ObjectiveTo evaluate the risk of adult onset wheeze (AOW) and obstructive lung function associated with occupational exposures over 50 years.MethodsA population-based randomly selected cohort of children who had not had asthma or wheezing illness, recruited in 1964 at age 10–15 years, was followed-up in 1989, 1995, 2001 and 2014 by spirometry and respiratory questionnaire. Occupational histories were obtained in 2014 and occupational exposures determined with an asthma-specific job exposure matrix. The risk of AOW and lung function impairment was analysed in subjects without childhood wheeze using logistic regression and linear mixed effects models.ResultsAll 237 subjects (mean age: 61 years, 47% male, 52% ever smoked) who took part in the 2014 follow-up had completed spirometry. Among those who did not have childhood wheeze, spirometry was measured in 93 subjects in 1989, in 312 in 1995 and in 270 subjects in 2001 follow-up. For longitudinal analysis of changes in FEV₁ between 1989 and 2014 spirometry records were available on 191 subjects at three time points and on 45 subjects at two time points, with a total number of 663 records. AOW and FEV₁ < LLN were associated with occupational exposure to food-related asthmagens (adjusted odds ratios (adjORs) 95% CI: 2.7 [1.4, 5.1] and 2.9 [1.1, 7.7]) and biocides/fungicides (adjOR 95% CI: 1.8 [1.1, 3.1] and 3.4 [1.1, 10.8]), with evident dose-response effect (p-trends < 0.05). Exposure to food-related asthmagens was also associated with reduced FEV₁, FVC and FEF_25–75% (adjusted regression coefficients 95% CI: − 7.2 [− 12.0, − 2.4], − 6.2 [− 10.9, − 1.4], and − 13.3[− 23.4, − 3.3]). Exposure to wood dust was independently associated with AOW, obstructive lung function and reduced FEF_25–75%. Excess FEV₁ decline of 6-8ml/year was observed with occupational exposure to any asthmagen, biocides/fungicides and food-related asthmagens (p < 0.05).ConclusionsThis longitudinal study confirmed previous findings of increased risks of adult onset wheezing illness with occupational exposure to specific asthmagens. A novel finding was the identification of food-related asthmagens and biocides/fungicides as potential new occupational risk factors for lung function impairment in adults without childhood wheeze.     

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.     

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.     

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.     

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.     

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.     

Fibrin clot structure is affected by levels of particulate air pollution exposure in patients with venous thrombosis

BackgroundParticulate air pollution is a risk factor for cardiovascular diseases and thrombosis. Long-term exposure to particulate matter with a diameter < 10 μm (PM₁₀) has been associated with an increased risk of venous thrombosis.ObjectivesThe aim of this study was to investigate whether or not particulate air pollution alters fibrin clot structure and thus modulates thrombosis risk.MethodsWe investigated fibrin polymerization by turbidity (maximum absorbance mOD), clot structure by confocal microscopy (fibre number per μm) and fibrin pore size by permeability (Ks × 10^− 10 cm²) in 103 patients with deep vein thrombosis and 121 healthy controls, for whom levels of air pollution exposure had been recorded. Exposure groups were defined by mean PM₁₀ concentrations over the 730 days before the event.ResultsWe found a higher average number of fibres per clot area in patients than controls, but no difference in Ks or fibre thickness. When the two groups were divided into high or low exposure to PM₁₀, a significantly denser fibrin clot network structure with thicker fibres (higher maximum absorbance, p < 0.05), decreased permeability (lower Ks value, p < 0.05) and higher average fibre numbers per clot area (p < 0.05) was observed in patients in the high exposure group compared to those with low exposure. There were no significant differences in fibrin clot structure between the two exposure levels in healthy subjects.ConclusionsPM₁₀ levels are associated with altered fibrin clot structure in patients with deep vein thrombosis but not in controls, suggesting that air pollution may trigger differences in fibrin clot structure only in patients predisposed to thrombotic disease.     

Traffic-related air pollution and hyperactivity/inattention,dyslexia and dyscalculia in adolescents of the German GINIplus and LISAplus birth cohorts

BackgroundFew studies have examined the link between air pollution exposure and behavioural problems and learning disorders during late childhood and adolescence.ObjectivesTo determine whether traffic-related air pollution exposure is associated with hyperactivity/inattention, dyslexia and dyscalculia up to age 15 years using the German GINIplus and LISAplus birth cohorts (recruitment 1995–1999).MethodsHyperactivity/inattention was assessed using the German parent-completed (10 years) and self-completed (15 years) Strengths and Difficulties Questionnaire. Responses were categorized into normal versus borderline/abnormal. Parent-reported dyslexia and dyscalculia (yes/no) at age 10 and 15 years were defined using parent-completed questionnaires. Individual-level annual average estimates of nitrogen dioxide (NO₂), particulate matter (PM)₁₀ mass, PM_2.5 mass and PM_2.5 absorbance concentrations were assigned to each participant's birth, 10 year and 15 year home address. Longitudinal associations between the air pollutants and the neurodevelopmental outcomes were assessed using generalized estimation equations, separately for both study areas, and combined in a random-effects meta-analysis. Odds ratios and 95% confidence intervals are given per interquartile range increase in pollutant concentration.ResultsThe prevalence of abnormal/borderline hyperactivity/inattention scores and parental-reported dyslexia and dyscalculia at 15 years of age was 12.9%, 10.5% and 3.4%, respectively, in the combined population (N = 4745). In the meta- analysis, hyperactivity/inattention was associated with PM_2.5 mass estimated to the 10 and 15 year addresses (1.12 [1.01, 1.23] and 1.11 [1.01, 1.22]) and PM_2.5 absorbance estimated to the 10 and 15 year addresses (1.14 [1.05, 1.25] and 1.13 [1.04, 1.23], respectively).ConclusionsWe report associations suggesting a potential link between air pollution exposure and hyperactivity/inattention scores, although these findings require replication.     

Predictors of exposure to organophosphate pesticides in schoolchildren in the Province of Talca,Chile

BackgroundFew data exist in Latin America concerning the association between organophosphate (OP) urinary metabolites and the consumption of fruits and vegetables and other exposure risk variables in schoolchildren.MethodsWe collected samples of urine from 190 Chilean children aged 6–12 years, fruits and vegetables, water and soil from schools and homes, and sociodemographic data through a questionnaire. We measured urinary dialkylphosphate (DAP) OP metabolites and OP pesticide residues in food consumed by these 190 children during two seasons: December 2010 (summer) and May 2011 (fall). We analyzed the relationship between urinary DAP concentrations and pesticide residues in food, home pesticide use, and residential location.ResultsDiethylalkylphosphates (DEAP) and dimethylalkylphosphates (DMAP) were detected in urine in 76% and 27% of the samples, respectively. Factors associated with urinary DEAP included chlorpyrifos in consumed fruits (p < 0.0001), urinary creatinine (p < 0.0001), rural residence (p = 0.02) and age less than 9 years (p = 0.004). Factors associated with urinary DMAP included the presence of phosmet residues in fruits (p < 0.0001), close proximity to a farm (p = 0.002), home fenitrothion use (p = 0.009), and season (p < 0.0001).ConclusionsUrinary DAP levels in Chilean school children were high compared to previously reported studies. The presence of chlorpyrifos and phosmet residues in fruits was the major factor predicting urinary DAP metabolite concentrations in children.     

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.     

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.     

Neighborhood deprivation,race/ethnicity,and urinary metal concentrations among young girls in California

BackgroundAlthough metals can adversely impact children's health, the distribution of exposures to many metals, particularly among vulnerable subpopulations, is not well characterized.ObjectivesWe sought to determine whether neighborhood deprivation was associated with urinary concentrations of thirteen metals and whether observed relationships varied by race/ethnicity.MethodsWe obtained neighborhood characteristics from the 2005–2009 American Community Survey. Demographic information and urine samples from 400 healthy young girls in Northern California were obtained during a clinical visit. Urine samples were analyzed for metals using inductively-coupled plasma-mass spectrometry and levels were corrected for creatinine. We ran analysis of variance and generalized linear regression models to estimate associations of urinary metal concentrations with neighborhood deprivation and race/ethnicity and stratified multivariable models to evaluate possible interactions among predictors on metals concentrations.ResultsUrinary concentrations of three metals (barium, lead, antimony) varied significantly across neighborhood deprivation quartiles, and four (barium, lead, antimony, tin) varied across race/ethnicity groups. In models adjusted for family income and cotinine, both race/ethnicity (F_3,224 = 4.34, p = 0.01) and neighborhood deprivation (F_3,224 = 4.32, p = 0.01) were associated with antimony concentrations, but neither were associated with lead, barium, or tin, concentrations. Examining neighborhood deprivation within race/ethnicity groups, barium levels (p_interaction < 0.01) decreased with neighborhood deprivation among Hispanic girls (p_trend < 0.001) and lead levels (p_interaction = 0.06) increased with neighborhood deprivation among Asian girls (p_trend = 0.04).ConclusionsOur results indicate that children's vulnerability to some metals varies by neighborhood deprivation quartile and race/ethnicity. These differential distributions of exposures may contribute to environmental health disparities later in life.     

Could exposure to phthalates speed up or delay pubertal onset and development? A 1.5-year follow-up of a school-based population

PurposePhthalates may interfere with the timing of pubertal development in adolescence and existing studies have shown inconsistent results. This study aims to assess the associations of pubertal onset and progression with urinary concentrations of phthalate metabolites in school-aged boys and girls.MethodsUsing isotope-dilution liquid chromatography tandem mass spectrometry, we analyzed 6 phthalate metabolites in urine samples of 430 children (222 boys and 208 girls) aged 9.7 ± 2.2 years (age range 6.1 to 13.8 years) at baseline and 18 months of follow-up. The associations of exposures to phthalates with pubertal development such as the testis, breast and pubic hair were evaluated using ordered logistic regression models, adjusting for baseline development stage, current chronological age, current body fat composition, and parental education.ResultsUrinary mono-n-butyl phthalate (MnBP) was associated with a 39% increase in the odds of presenting lower pubic hair development stages in boys, and mono (2-ethylhexyl) phthalate (MEHP) (p < 0.10), mono (2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) and mono (2-ethyl-5-oxohexyl) phthalate (MEOHP) were associated with 54%–65% increase in the odds of presenting higher breast development stages in girls (p < 0.05), while MEHHP and MEOHP were also associated with a 70% increase in the odds of menarche onset (p < 0.05). After adjusting for potential confounding variables, the associations of girls' pubertal onset with MnBP, MMP, MEP and MEHP were significant. The odds of girls' breast onset were 4 to 10 times higher in high MnBP, MMP, MEP or MEHP exposure group than in low exposure group.ConclusionsOur findings suggest subtle effects of phthalate metabolites associated with pubertal onset and progression. MnBP exposure may be associated with delayed pubic hair development in boys, while MnBP, MMP, MEP, and MEHP exposures may be associated with breast onset, and MEHP metabolites associated with speedup in breast development progression and earlier menarche onset in girls.     

Human exposure pathways to organophosphate triesters — A biomonitoring study of mother–child pairs

The worldwide ban of several formulations of brominated flame retardants has caused an increase in the production of organophosphorus flame retardants (PFRs) to meet the existing fire regulations for a wide range of household products. This biomonitoring study surveys the occurrence of the metabolites from PFRs and related plasticizers (dialkyl and diaryl phosphates; DAPs) in urine from a Norwegian mother–child cohort (48 mothers and 54 children). Concentrations of DAPs were higher in the children than in their mothers (Wilcoxon signed-rank test p = 0.001). Median urinary concentrations of diphenyl phosphate (DPHP) were 1.1 and 0.51 ng/mL in children and mothers, respectively, followed by bis(1,3-dichloro-2-propyl) phosphate (BDCIPP) with medians of 0.23 and 0.12 ng/mL, respectively. Detection frequencies for bis(2-butoxyethyl) phosphate (BBOEP) in urine from children and mothers were 32 and 1%, respectively (median < 0.18 ng/mL), and for di-n-butyl phosphate (DNBP) 15 and 8%, respectively (median < 0.12 ng/mL). The concentrations of DPHP and BDCIPP in urine from children were significantly correlated with those found for their parent compounds in air and dust from the households (Spearman's rank correlations 0.30 < R_s < 0.36; p < 0.05). For mothers, only the urinary concentration of BDCIPP was correlated to its precursor in dust from the households (R_s = 0.40; p < 0.01), which might indicate higher impact of the household environment on children than mothers. A diurnal variability study of the mothers' urinary concentrations of DPHP and BDCIPP showed lower concentrations at time periods when women were likely to be outside the household. In contrast, no relevant associations between organophosphate metabolites in urine and food consumption data obtained through a 24 hour recall were seen. This suggests that the residential environment is a more important exposure pathway to PFRs than the diet.     

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.     

Shorter sperm telomere length in association with exposure to polycyclic aromatic hydrocarbons: Results from the MARHCS cohort study in Chongqing,China and in vivo animal experiments

It has been well demonstrated that polycyclic aromatic hydrocarbons (PAHs) can cause reproductive toxicity, and shorter telomere length in sperm may be one of the factors causing male infertility. However, whether exposure to PAHs is associated with sperm telomere length (STL) has never been evaluated. The present study aimed to assess the potential association between PAHs exposure and STL, and to explore potential biomarkers that may predict the effects of low-level exposure to PAHs on human sperm. Questionnaires and biological samples were collected from 666 volunteers participating in the Male Reproductive Health in Chongqing College Students (MARHCS) cohort study in 2014. Semen parameters were measured for 656 participants, while urinary PAH metabolites, STL and sperm apoptosis were successfully measured for 492, 444 and 628 participants, respectively. The linear regression analysis revealed that increased levels of urinary 1-hydroxypyrene (1-OHPyr) and 1-hydroxynapthalene (1-OHNap) were associated with decreased STL (− 0.385; 95% CI, − 0.749, − 0.021 for 1-OHPyr; and − 0.079; 95% CI, − 0.146, − 0.011 for 1-OHNap). The significant negative associations remained after adjusting for potential confounders. However, no significant associations were observed between urinary PAH metabolites and semen quality or sperm apoptosis. We also administrated rats with benzo[a]pyrene (B[a]P; 0, 1, 5, and 10 mg/kg) for 4 weeks and found shorter STL and decreased telomerase expression in germ cells in a dose-dependent manner. In conclusion, environmental exposure to some PAHs may be associated with decreased human STL, and the in vivo animal results also demonstrate the adverse effects of B[a]P on telomere of male germ cells.     

Associations of gestational and early life exposures to ambient air pollution with childhood respiratory diseases in Shanghai,China: A retrospective cohort study

BackgroundAssociations of ambient air pollutants with respiratory health are inconsistent.ObjectivesWe analyzed the associations of gestational and early life exposures to air pollutants with doctor-diagnosed asthma, allergic rhinitis, and pneumonia in children.MethodsWe selected 3358 preschool children who did not alter residences after birth from a cross-sectional study in 2011–2012 in Shanghai, China. Parents reported children's respiratory health history, home environment, and family lifestyle behaviors. We collected daily concentrations of sulphur dioxide (SO₂), nitrogen dioxide (NO₂), and particulate matter with an aerodynamic diameter ≤ 10 μm (PM₁₀) during the child's total lifetime (2006–2012) for each district where the children lived. We analyzed the associations using logistic regression models.ResultsAfter adjusting for covariates and the other studied pollutants, we found that exposure to NO₂ (increment of 20 μg/m³) during the first year of life was significantly associated with asthma [odds ratio (OR) = 1.77; 95% confidence interval (CI): 1.29–2.43] and allergic rhinitis (OR = 1.67; 95% CI: 1.07–2.61). Exposure to NO₂ during gestation, the first two and three years, and over total lifetimewas all consistently associated with increased odds of allergic rhinitis. Quartiles of NO₂ concentration during different exposure periods showed a slight dose–response relationship with the studied diseases. These diseases had significant associations with pollutant mixtures that included NO₂, but had no significant association with exposures to SO₂ and PM₁₀ individually or in mixtures.ConclusionsGestational and early life exposures to ambient NO₂ are risk factors for childhood respiratory diseases.