Association between maternal exposure to perfluorooctanoic acid (PFOA) from electronic waste recycling and neonatal health outcomes

ObjectivePerfluorooctanoic acid (PFOA) has applications in numerous industrial and consumer products. The widespread prevalence of PFOA in humans demonstrated in recent studies has drawn considerable interest from the public. We aimed to evaluate the exposure of mothers to PFOA and the potential hazards to neonates in a primitive electronic waste recycling area, Guiyu, China, and a control area, Chaonan, China.MethodsOur investigation included analyses of maternal serum samples, health effect examinations, and other relevant factors. Questionnaires were administered and maternal serum samples were collected for 167 pregnant women. Solid phase extraction method was used for all analytical sample preparation, and analyses were completed using high performance liquid chromatography tandem mass spectrometry method.ResultsThe PFOA concentration was higher in maternal serum samples from Guiyu than in samples from Chaonan (median 16.95, range 5.5–58.5 ng mL^− 1; vs. 8.7, range 4.4–30.0 ng mL^− 1; P < 0.001). Residence in Guiyu, involvement in e-waste recycling, husband's involvement in e-waste and use of the family residence as workshop were significant factors contributing to PFOA exposure. Maternal PFOA concentrations were significantly different between normal births and adverse birth outcomes including premature delivery, term low birth weight, and stillbirths. After adjusting for potential confounders, PFOA was negatively associated with gestational age [per lg-unit: β = − 15.99 days, 95% confidence interval (CI), − 27.72 to − 4.25], birth weight (per lg-unit: β = − 267.3 g, 95% CI, − 573.27 to − 37.18), birth length (per lg-unit: β = − 1.91 cm, 95% CI, − 3.31 to − 0.52), and Apgar scores (per lg-unit: β = − 1.37, 95% CI, − 2.42 to − 0.32), but not associated with ponderal index.ConclusionsMothers from Guiyu were exposed to higher levels of PFOA than those from control areas. Prenatal exposure to PFOA was associated with decreased neonatal physical development and adverse birth outcomes.     

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.     

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

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

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.     

Levels and congener profiles of polybrominated diphenyl ethers (PBDEs) in breast milk from Shanghai: Implication for exposure route of higher brominated BDEs

Breast milk has been widely used as a bioindicator to assess the extent of human exposure to PBDEs via various exposure routes. In this study, 48 breast milk samples were collected from primiparous women in Shanghai city, and 14 PBDEs congeners (BDE-28, − 47, − 99, − 100, − 153, − 154, − 183, − 196, − 197, − 203, − 206, − 207, − 208, and − 209) were quantified using gas chromatography-electron capture negative ionization-mass spectrometry. The mean concentration of total PBDEs was 8.6 ng/g lipid weight, and ranged from 1.8 to 26.7 ng/g lipid weight. These concentration levels were similar to those reported in Europe and Asia, but one order of magnitude lower than those in North America. The congener profiles in this study exhibited a specific pattern in human milk found worldwide, BDE-153 and BDE-28 accounted for a relatively higher proportion of lower brominated BDEs (from tri- to hepta-BDEs), whereas higher brominated BDEs (from octa- to deca-BDEs) contributed more than 70% of the total PBDEs. The Spearman's correlation coefficient among higher brominated BDEs showed a positive relationship, and concentration levels of higher brominated BDEs were statistically different between office workers and housewives. Due to relatively higher proportion of PBDEs from octa- to deca-BDEs were detected, air inhalation and dust ingestion might be the major exposure routes of higher brominated BDEs. Further research is needed to clarify the major exposure route of higher brominated BDEs to humans.     

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.     

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.     

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.     

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.     

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

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

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 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.     

Polybrominated diphenyl ethers (PBDEs) in human samples of mother–newborn pairs in South China and their placental transfer characteristics

There are limited data concerning the placenta transfer characteristics and accumulation of polybrominated diphenyl ethers (PBDEs) in infants. However, PBDEs received increasing health concerns due to their endocrine disrupt and neurodevelopment toxicity effects. The present study assessed the accumulation of PBDEs in 30 paired placenta, breast milk, fetal cord blood, and neonatal urine samples collected from five major cities of the South China. The age of mothers ranged from 21 to 39 (mean 27.6 ± 4.56). The ∑ PBDE concentrations were 15.8 ± 9.88 ng g^− 1 lipid in placenta, 13.2 ± 7.64 ng g^− 1 lipid in breast milk, 16.5 ± 19.5 ng g^− 1 lipid in fetal cord blood, and 1.80 ± 1.99 ng ml^− 1 in neonatal urine. BDE-47 was the predominant congener in all types of human sample. Octa-BDEs such as BDE-196/-197 were detected highly in placenta and cord blood while moderately in breast milk and neonatal urine. Significant (p < 0.01) correlations were observed for both total and most individual PBDEs in cord blood–maternal placenta and breast milk–urine paired individual samples. The extent of placental transfer of higher brominated BDEs such as BDE-196/-197 was greater than that of BDE-47. The estimated daily intake (EDI) analysis for breast-fed infants revealed that newborns in these areas were exposed to relatively high levels of PBDEs via breast milk. Our study not only provided systematic fundamental data for PBDE distribution but also revealed the placenta transfer characteristics of PBDE congeners in South China.     

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.     

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.     

Serum and follicular fluid concentrations of polybrominated diphenyl ethers and in-vitro fertilization outcome

There is evidence of endocrine disruption and reproductive effects in animals following exposure to certain PBDEs, but human studies are limited. The goal of this study was to investigate the use of serum and follicular fluid as biomarkers of exposure to PBDEs and to explore whether a relationship between PBDE exposure and early pregnancy loss exists. We measured 8 PBDE congeners in archived serum and ovarian follicular fluid samples from 65 women undergoing in-vitro fertilization (IVF). Logistic regression models were used to predict the odds of failed embryo implantation associated with higher levels of PBDEs among the women in the study. There were moderate Kendall's Tau-beta correlations between serum and follicular fluid concentrations of BDE 28, 47, 100 and 154 (T_β = 0.29–0.38, all p-values < 0.005), but BDE 99 and 153 were not correlated between the two matrices (T_β < 0.2, p-values > 0.05). Women with detectable concentrations of BDE 153 (39% had detectable levels) in follicular fluid had elevated odds of failed implantation compared with women who had non-detectable concentrations (adjusted OR = 10.0; 95%CI: 1.9 to 52; p = 0.006; adjusted by age and body mass index). These findings suggest that exposure to BDE 153 may be associated with failed embryo implantation. Due to our observation of only moderate correlations between matrices, serum PBDE concentrations may not be a good indicator of follicular fluid concentrations when studying early pregnancy endpoints in women undergoing IVF.     

Personal exposure to fine particulate matter and blood pressure: A role of angiotensin converting enzyme and its DNA methylation

BackgroundThe underlying intermediate mechanisms about the association between fine particulate matter (PM_2.5) air pollution and blood pressure (BP) were unclear. Few epidemiological studies have explored the potential mediation effects of angiotensin-converting enzyme (ACE) and its DNA methylation.MethodsWe designed a longitudinal panel study with 4 follow-ups among 36 healthy college students in Shanghai, China from December 17, 2014 to July 11, 2015. We measured personal real-time exposure to PM_2.5, serum ACE level, and blood methylation of ACE gene and the repetitive elements. We applied linear mixed-effects models to examine the effects of PM_2.5 on ACE protein, DNA methylation and BP markers. Furthermore, we conducted mediation analyses to evaluate the potential pathways.ResultsAn interquartile range increase (26.78 μg/m³) in 24-h average exposure to PM_2.5 was significantly associated with 1.12 decreases in ACE average methylation (%5mC), 13.27% increase in ACE protein, and increments of 1.13 mmHg in systolic BP, 0.66 mmHg in diastolic BP and 0.82 mmHg in mean arterial pressure. ACE hypomethylation mediated 11.78% (P = 0.03) of the elevated ACE protein by PM_2.5. Increased ACE protein accounted for 3.90 ~ 13.44% (P = 0.35 ~ 0.68) of the elevated BP by PM_2.5. Repetitive-element methylation was also decreased but did not significantly mediate the association between PM_2.5 and BP.ConclusionsThis investigation provided strong evidence that short-term exposure to PM_2.5 was significantly associated with BP, ACE protein and ACE methylation. Our findings highlighted a possible involvement of ACE and ACE methylation in the effects of PM_2.5 on elevating BP.     

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.     

Memory performance,wireless communication and exposure to radiofrequency electromagnetic fields: A prospective cohort study in adolescents

BackgroundThe aim of this study is to investigate whether memory performance in adolescents is affected by radiofrequency electromagnetic fields (RF-EMF) from wireless device use or by the wireless device use itself due to non-radiation related factors in that context.MethodsWe conducted a prospective cohort study with 439 adolescents. Verbal and figural memory tasks at baseline and after one year were completed using a standardized, computerized cognitive test battery. Use of wireless devices was inquired by questionnaire and operator recorded mobile phone use data was obtained for a subgroup of 234 adolescents.RF-EMF dose measures considering various factors affecting RF-EMF exposure were computed for the brain and the whole body.Data were analysed using a longitudinal approach, to investigate whether cumulative exposure over one year was related to changes in memory performance. All analyses were adjusted for relevant confounders.ResultsThe kappa coefficients between cumulative mobile phone call duration and RF-EMF brain and whole body dose were 0.62 and 0.67, respectively for the whole sample and 0.48 and 0.28, respectively for the sample with operator data. In linear exposure–response models an interquartile increase in cumulative operator recorded mobile phone call duration was associated with a decrease in figural memory performance score by − 0.15 (95% CI: − 0.33, 0.03) units. For cumulative RF-EMF brain and whole body dose corresponding decreases in figural memory scores were − 0.26 (95% CI: − 0.42, − 0.10) and − 0.40 (95% CI: − 0.79, − 0.01), respectively. No exposure-response associations were observed for sending text messages and duration of gaming, which produces tiny RF-EMF emissions.ConclusionsA change in memory performance over one year was negatively associated with cumulative duration of wireless phone use and more strongly with RF-EMF dose. This may indicate that RF-EMF exposure affects memory performance.     

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.