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.     

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.     

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.     

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.     

Baseline blood trihalomethanes,semen parameters and serum total testosterone: A cross-sectional study in China

Toxicological studies showed that trihalomethanes (THMs), the most abundant classes of disinfection by-products (DBPs) in drinking water, impaired male reproductive health, but epidemiological evidence is limited and inconsistent. This study aimed to examine the associations of baseline blood THMs with semen parameters and serum total testosterone in a Chinese population. We recruited 401 men seeking semen examination from the Reproductive Center of Tongji Hospital in Wuhan, China between April 2011 and May 2012. Baseline blood concentrations of THMs, including chloroform (TCM), bromodichloromethane (BDCM), dibromochloromethane (DBCM), and bromoform (TBM) were measured using SPME-GC/ECD method. Semen quality and serum total testosterone were analyzed. Multivariable linear regressions were used to assess the associations of baseline blood THM concentrations with semen parameters and serum total testosterone levels. We found that baseline blood THM concentrations were not associated with decrements in sperm motility, sperm straight-line and curvilinear velocity. However, moderate levels of BDCM (β = − 0.13 million; 95% CI: − 0.22, − 0.03) and DBCM (β = − 4.74%; 95% CI: − 8.07, − 1.42) were associated with decreased sperm count and declined sperm linearity compared with low levels, respectively. Suggestive dose–response relationships were also observed between elevated blood TCM or ∑ THMs (sum of TCM, BDCM, DBCM and TBM) concentration and decreased sperm concentration (both p for trend = 0.07), and between elevated blood DBCM concentration and decreased serum total testosterone (p for trend = 0.07). Our results indicate that elevated THM exposure may lead to decreased sperm concentration and serum total testosterone. However, the effects of THM exposure on male reproductive health still warrant further studies in humans.     

Farm residence and reproductive health among boys in rural South Africa

BackgroundFew studies have investigated reproductive health effects of contemporary agricultural pesticides in boys.ObjectivesTo determine the association between pesticide exposure and reproductive health of boys.MethodsWe conducted a cross-sectional study in rural South Africa of boys living on and off farms. The study included a questionnaire (demographics, general and reproductive health, phyto-estrogen intake, residential history, pesticide exposures, exposures during pregnancy); and a physical examination that included sexual maturity development ratings; testicular volume; height, weight, body mass index; and sex hormone concentrations.ResultsAmong the 269 boys recruited into the study, 177 (65.8%) were categorized as farm (high pesticide exposures) and 98 (34.2%) as non-farm residents (lower pesticide exposures). Median ages of the two groups were 11.3 vs 12.0 years, respectively (p < 0.05). After controlling for confounders that included socioeconomic status, farm boys were shorter (regression coefficient (RC) = − 3.42 cm; 95% confidence interval (CI): − 6.38 to − 0.45 cm) and weighed less (RC = − 2.26 kg; CI: − 4.44 to − 0.75 kg). The farm boys also had lower serum lutenizing hormone (RC = − 0.28 IU/L; CI: − 0.48 to − 0.08 IU/L), but higher serum oestradiol (RC = 8.07 pmol/L; CI: 2.34–13.81 pmol/L) and follicle stimulating hormone (RC = 0.63 IU/L; CI: 0.19–1.08 U/L).ConclusionsOur study provides evidence that farm residence is associated with adverse growth and reproductive health of pubertal boys which may be due to environmental exposures to hormonally active contemporary agricultural pesticides.     

Reduced birth weight in relation to pesticide mixtures detected in cord blood of full-term infants

Previous research has shown that prenatal exposure to pesticides may be associated with decreased fetal growth. The specific pesticides investigated and results reported across studies have been inconsistent, and there is a mounting need for the consideration of mixtures rather than individual agents in studies of health outcomes in relation to environmental exposures. There are also many individual pesticides that have not been investigated in human health studies to date. We conducted a pilot study in rural Zhejiang province, China, measuring 20 non-persistent pesticides (10 insecticides, 6 herbicides, 3 fungicides, and 1 repellant) in umbilical cord blood of 112 full term (> 37 weeks) infants. The pesticides detected with the greatest frequency were diethyltoluamide (DEET) (73%), a repellant, and vinclozolin (49%), a fungicide. The samples had detectable concentrations for a mean of 4.6 pesticides (SD = 1.9) with a maximum of 10. Adjusting for potential confounders, newborn birth weight was inversely associated with the number of pesticides detected in cord blood (p = 0.04); birth weight decreased by a mean of 37.1 g (95% CI, − 72.5 to − 1.8) for each detected pesticide. When assessing relationships by pesticide type, detection of fungicides was also associated with decreased birth weight (adjusted β = − 116 g [95% CI, − 212 to − 19.2]). For individual pesticides analyzed as dichotomous (detect vs. non-detect) variables, only vinclozolin (adjusted β = − 174 g [95% CI, − 312 to − 36.3]) and acetochlor (adjusted β = − 165 g [95% CI, − 325 to − 5.7]) were significantly associated with reduced birth weight. No significant associations were seen between birth weight and individual pesticides assessed as continuous or 3-level ordinal variables. Our findings from this pilot investigation suggest that exposure to fungicides may adversely impact fetal growth. Exposure to mixtures of multiple pesticides is also of concern and should be explored in addition to individual pesticides. Additional research is needed to establish causality and to understand the function and impact of fungicides and pesticide mixtures on fetal development.     

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.     

Associations between maternal exposure to air pollution and traffic noise and newborn's size at birth: A cohort study

BackgroundMaternal exposure to air pollution and traffic noise has been suggested to impair fetal growth, but studies have reported inconsistent findings.ObjectiveTo investigate associations between residential air pollution and traffic noise during pregnancy and newborn's size at birth.MethodsFrom a national birth cohort we identified 75,166 live-born singletons born at term with information on the children's size at birth. Residential address history from conception until birth was collected and air pollution (NO₂ and NO_x) and road traffic noise was modeled at all addresses. Associations between exposures and indicators of newborn's size at birth: birth weight, placental weight and head and abdominal circumference were analyzed by linear and logistic regression, and adjusted for potential confounders.ResultsIn mutually adjusted models we found a 10 μg/m³ higher time-weighted mean exposure to NO₂ during pregnancy to be associated with a 0.35 mm smaller head circumference (95% confidence interval (CI): 95% CI: − 0.57; − 0.12); a 0.50 mm smaller abdominal circumference (95% CI: − 0.80; − 0.20) and a 5.02 g higher placental weight (95% CI: 2.93; 7.11). No associations were found between air pollution and birth weight. Exposure to residential road traffic noise was weakly associated with reduced head circumference, whereas none of the other newborn's size indicators were associated with noise, neither before nor after adjustment for air pollution.ConclusionsThis study indicates that air pollution may result in a small reduction in offspring's birth head and abdominal circumference, but not birth weight, whereas traffic noise seems not to affect newborn's size at birth.     

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.     

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.     

Brominated and chlorinated flame retardants in San Francisco Bay sediments and wildlife

Restrictions on the use of polybrominated diphenyl ethers (PBDEs) have resulted in the use of alternative flame retardants in consumer products to comply with flammability standards. In contrast to PBDEs, information on the occurrence and fate of these alternative compounds in the environment is limited, particularly in the United States. In this study, a survey of flame retardants in San Francisco Bay was conducted to evaluate whether PBDE replacement chemicals and other current use flame retardants were accumulating in the Bay food web. In addition to PBDEs, brominated and chlorinated flame retardants (hexabromocyclododecane (HBCD) and Dechlorane Plus (DP)) were detected in Bay sediments and wildlife. Median concentrations of PBDEs, HBCD, and DP, respectively, were 4.3, 0.3, and 0.2 ng g^− 1 dry weight (dw) in sediments; 1670, < 6.0, and 0.5 ng g^− 1 lipid weight (lw) in white croaker (Genyonemus lineatus); 1860, 6.5, and 1.3 ng g^− 1 lw in shiner surfperch (Cymatogaster aggregata); 5500, 37.4, and 0.9 ng g^− 1 lw in eggs of double-crested cormorant (Phalacrocorax auritus); 770, 7.1, and 0.9 ng g^− 1 lw in harbor seal (Phoca vitulina) adults; and 330, 3.5, and < 0.1 ng g^− 1 lw in harbor seal (P. vitulina) pups. Two additional flame retardants, pentabromoethylbenzene (PBEB) and 1,2-bis(2,4,6 tribromophenoxy)ethane (BTBPE) were detected in sediments but with less frequency and at lower concentrations (median concentrations of 0.01 and 0.02 ng g^− 1 dw, respectively) compared to the other flame retardants. PBEB was also detected in each of the adult harbor seals and in 83% of the pups (median concentrations 0.2 and 0.07 ng g^− 1 lw, respectively). The flame retardants hexabromobenzene (HBB), decabromodiphenyl ethane (DBDPE), bis(2-ethylhexyl) tetrabromophthalate (TBPH), and 2-ethylhexyl 2,3,4,5-tetrabromobenzoate (TBB), were not detected in sediments and BTBPE, HBB and TBB were not detected in wildlife samples. Elevated concentrations of some flame retardants were likely associated with urbanization and Bay hydrodynamics. Compared to other locations, concentrations of PBDEs in Bay wildlife were comparable or higher, while concentrations of the alternatives were generally lower. This study is the first to determine concentrations of PBDE replacement products and other flame retardants in San Francisco Bay, providing some of the first data on the food web occurrence of these flame retardants in a North American urbanized estuary.     

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.     

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

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

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.     

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.     

Maternal dietary intake of dioxins and polychlorinated biphenyls and birth size in the Norwegian Mother and Child Cohort Study (MoBa)

Maternal diet not only provides essential nutrients to the developing fetus but is also a source of prenatal exposure to environmental contaminants. We investigated the association between dietary intake of dioxins and PCBs during pregnancy and birth size. The study included 50,651 women from the Norwegian Mother and Child Cohort Study (MoBa). Dietary information was collected by FFQs and intake estimates were calculated by combining food consumption and food concentration of dioxins, dioxin-like PCBs and non-dioxin-like PCBs. We used multivariable regression models to estimate the association between dietary intake of dioxins and PCBs and fetal growth. The contribution of fish and seafood intake during pregnancy was 41% for dietary dioxins and dioxin-like PCBs and 49% for dietary non-dioxin-like PCBs. Further stratified analysis by quartiles of seafood intake during pregnancy was conducted. We found an inverse dose–response association between dietary intake of dioxins and PCBs and fetal growth after adjustment for confounders. Newborns of mothers in the upper quartile of dioxin and dioxin-like PCBs intake had 62 g lower birth weight (95% CI: − 73, − 50), 0.26 cm shorter birth length (95% CI: − 0.31, − 0.20) and 0.10 cm shorter head circumference (95% CI: − 0.14, − 0.06) than newborns of mothers in the lowest quartile of intake. Similar negative associations for intake of dioxins and dioxin-like PCBs were found after excluding women with intakes above the tolerable weekly intake (TWI = 14 pg TEQ/kg bw/week). The negative association of dietary dioxins and PCBs with fetal growth was weaker as seafood intake was increasing. No association was found between dietary dioxin and PCB intake and the risk for small-for-gestational age neonate. In conclusion, dietary intakes of dioxins and PCBs during pregnancy were negatively associated with fetal growth, even at intakes below the TWI.     

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

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

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.     

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.