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

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

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.     

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.     

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.     

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.     

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

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

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.     

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.     

Environmental exposure to lithium during pregnancy and fetal size: A longitudinal study in the Argentinean Andes

BackgroundLithium, used for treating bipolar disease, crosses freely the placenta and is classified as teratogenic. It is unclear to what extent environmental lithium exposure may affect fetal growth and development.ObjectivesTo elucidate potential effects of lithium exposure through drinking water during pregnancy on fetal size.MethodsWe developed a prospective population-based mother–child cohort (N = 194) in an area with highly varying drinking water lithium concentrations (5-1600 μg/L) in northern Argentinean Andes. Blood and urinary lithium concentrations (sampled repeatedly during pregnancy) were measured using inductively coupled plasma mass spectrometry. We measured fetal size by ultrasound in second and third trimesters, and weight, length and head circumference at birth. Multivariable models were used to examine associations between lithium exposure (continuous and in tertiles) and fetal size measures.ResultsLithium in maternal blood (median 25; range 1.9–145 μg/L) and urine (1645; 105–4600 μg/L) was inversely associated (apparently linearly) with all fetal measures (body, head and femur) in the second trimester, and with birth length (β − 0.53 cm per 25 μg/L increase in blood lithium, 95%CI − 1.0; − 0.052). An increase of 100 μg/L in blood was associated with 2 cm shorter newborns (about one standard deviation).ConclusionsLithium exposure through drinking water was associated with impaired fetal size and this seemed to be initiated in early gestation. Further studies are warranted to confirm causality and to understand the mechanisms. If confirmed, these findings have public health relevance and emphasize the need for more data on lithium concentrations in drinking water, including bottled water.     

Boron exposure through drinking water during pregnancy and birth size

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

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

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

The influence of maternal dietary exposure to dioxins and PCBs during pregnancy on ADHD symptoms and cognitive functions in Norwegian preschool children

BackgroundPolychlorinated dibenzo-p-dioxins/dibenzofurans (dioxins) and polychlorinated biphenyls (PCBs) are persistent organic pollutants (POPs) with potentially adverse impact on child neurodevelopment. Whether the potential detrimental effects of dioxins and PCBs on neurodevelopment are of specific or unspecific character is not clear.ObjectivesThe purpose of the current study was to examine the influence of maternal dietary exposure to dioxins and PCBs on ADHD symptoms and cognitive functioning in preschoolers. We aimed to investigate a range of functions, in particular IQ, expressive language, and executive functions.Material and methodsThis study includes n = 1024 children enrolled in a longitudinal prospective study of ADHD (the ADHD Study), with participants recruited from The Norwegian Mother and Child Cohort Study (MoBa). Boys and girls aged 3.5 years participated in extensive clinical assessments using well-validated tools; The Preschool Age Psychiatric Assessment interview (PAPA), Stanford-Binet 5th revision (SB-5), Child Development Inventory (CDI), and Behavior Rating Inventory of Executive Function, Preschool version (BRIEF-P). Maternal dietary exposure to dioxins and PCBs was estimated based on a validated food frequency questionnaire (FFQ) answered mid-pregnancy and a database of dioxin and PCB concentrations in Norwegian foods. Exposure to dioxins and dioxin-like PCBs (dl-compounds) was expressed in total toxic equivalents (TEQ), and PCB-153 was used as marker for non-dioxin-like PCBs (ndl-PCBs). Generalized linear and additive models adjusted for confounders were used to examine exposure-outcome associations.ResultsExposure to PCB-153 or dl-compound was not significantly associated with any of the outcome measures when analyses were performed for boys and girls together. After stratifying by sex, adjusted analyses indicated a small inverse association with language in girls. An increase in the exposure variables of 1 SD was associated with a reduction in language score of − 0.2 [CI − 0.4, − 0.1] for PCB-153 and − 0.2 [CI − 0.5, − 0.1] for dl-compounds in girls. For boys, exposure to PCB-153 or dl-compounds was not associated with language skills. The difference between sex-specific associations was not statistically significant (p-value = 0.13). No sex-specific effects were observed for ADHD-symptoms, IQ scores, or executive functions.ConclusionsWe found no indications that variation in current low-level exposure to PCB-153 or dl-compounds in Norway is associated with variation ADHD-symptoms, verbal/non-verbal IQ, or executive functions including working memory in preschoolers. However, our findings indicated that maternal dietary exposure to PCB-153 or dl-compounds during pregnancy was significantly associated with poorer expressive language skills in preschool girls, although the sex-specific associations were not significantly different.     

Associations between blood persistent organic pollutants and 25-hydroxyvitamin D3 in pregnancy

Persistent organic pollutants (POPs) are suggested to contribute to lower vitamin D levels; however, studies in humans are scarce and have never focused on pregnancy, a susceptibility period for vitamin D deficiency. We investigated whether serum levels of POPs were associated with circulating 25-hydroxyvitamin D3 [25(OH)D3] concentration in pregnancy. Cross-sectional associations of serum concentrations of eight POPs with plasma 25(OH)D3 concentration were analyzed in 2031 pregnant women participating in the Spanish population-based cohort INfancia y Medio Ambiente (INMA) Project. Serum concentrations of POPs were measured by gas chromatography and plasma 25(OH)D3 concentration was measured by high-performance liquid chromatography in pregnancy (mean 13.3 ± 1.5 weeks of gestation). Multivariable regression models were performed to assess the relationship between blood concentrations of POPs and 25(OH)D3. An inverse linear relationship was found between serum concentration of PCB180 and circulating 25(OH)D3. Multivariate linear regression models showed higher PCB180 levels to be associated with lower 25(OH)D3 concentration: quartile Q4 vs. quartile Q1, coefficient = − 1.59, 95% CI − 3.27, 0.08, p trend = 0.060. A non-monotonic inverse relationship was found between the sum of predominant PCB congeners (PCB 180, 153 and 138) and 25(OH)D3 concentration: coefficient (95% CI) for quartile Q2 vs. Q1 [− 0.50 (− 1.94, 0.94)], quartile Q3 vs. Q1 [− 1.56 (− 3.11, − 0.02)] and quartile Q4 vs. Q1 [− 1.21 (− 2.80, 0.38)], p trend = 0.081. No significant associations were found between circulating 25(OH)D3 and serum levels of p,p′-DDE, p,p′-DDT, HCB, and ß-HCH. Our results suggest that the background exposure to PCBs may result in lower 25(OH)D3 concentration in pregnant women.     

Dietary and sociodemographic determinants of bisphenol A urine concentrations in pregnant women and children

Bisphenol A (BPA) exposure during early life may have endocrine-disrupting effects, but the dietary and sociodemographic predictors of BPA exposure during pregnancy and childhood remain unclear. Our aim was to evaluate the correlations between, and sociodemographic and dietary predictors of, serial urinary BPA concentrations measured during pregnancy and childhood in a Spanish birth cohort study. BPA was measured in two spot urine samples collected from 479 women during the first and third trimester of pregnancy and in one urine sample from their 4-year old children (n = 130). Average dietary intakes were reported in food frequency questionnaires during the first and third pregnancy trimester and at age 4 years. Multivariate mixed models and linear regression models were used to estimate associations between sociodemographic and dietary factors and BPA concentrations. A small, but statistically significant correlation was found between serial maternal BPA concentrations measured during pregnancy (r = 0.17). Pregnant women who were younger, less-educated, smoked, and who were exposed to second-hand tobacco smoke (SHS) had higher BPA concentrations than others. BPA concentrations were also higher in children exposed to SHS. High consumption of canned fish during pregnancy was associated with 21% [GM ratio = 1.21; 95%CI 1.02, 1.44] and 25% [GM ratio = 1.25; 95%CI 1.05, 1.49] higher urinary BPA concentrations in the first and third pregnancy trimester, respectively, compared to the lowest consumption group. This study suggests that canned fish may be a major source of BPA during pregnancy in Spain, a country of high canned fish consumption. Further evaluation of specific BPA exposure sources in the sociodemographic group of younger women who smoke, are exposed to SHS, and have a low educational level is needed. Studies identifying sources of exposure would benefit from repeat BPA measurements and questionnaires specifically focused on dietary and packaging sources.     

Long-term exposure to traffic-related PM10 and decreased heart rate variability: Is the association restricted to subjects taking ACE inhibitors?

BackgroundAlterations in heart rate variability (HRV) are a potential link between exposure to traffic-related air pollution and cardiovascular mortality.ObjectivesWe investigated whether long-term exposure to traffic-related PM₁₀ (TPM₁₀) is associated with HRV in older subjects and/or in participants taking specific cardiovascular treatment or with self-reported heart disease.MethodsWe included 1607 subjects from the general population aged 50 to 72 years. These participants from the SAPALDIA cohort underwent ambulatory 24-hr electrocardiogram monitoring. Associations of average annual exposure to TPM₁₀ over 10 years with HRV parameters from time and frequency domains were estimated using multivariable mixed linear models. Effect estimates are expressed as percent changes in geometric means.ResultsHRV was only associated with TPM₁₀ in participants under ACE inhibitor therapy (N = 94). A 1 μg/m³ increment, approximately equivalent to an interquartile range, in 10 year average TPM₁₀ was associated with decrements of 14.5% (95% confidence interval (CI), − 25.9 to − 1.3) in high frequency (HF) power, of 4.5% (− 8.2 to − 0.5) in the standard deviation of all normal-to-normal RR intervals (SDNN), of 10.6% (− 18.5 to − 1.9) in total power (TP) and an increase of 9.2% (0.8 to 20.2) in the LF/HF power ratio.ConclusionsIn the absence of an overall effect our results suggest that alterations in HRV, a measure of autonomic control of the cardiac rhythm, may not be a central mechanism by which long-term exposure to TPM₁₀ increases cardiovascular mortality. Novel evidence on an effect in persons under ACE inhibitor treatment needs to be confirmed in future studies.     

Prenatal exposure to PCB-153, p,p′-DDE and birth outcomes in 9000 mother–child pairs: Exposure–response relationship and effect modifiers

Low-level exposure to polychlorinated biphenyl-153 (PCB-153) and dichlorodiphenyldichloroethylene (p-p′-DDE) can impair fetal growth; however, the exposure–response relationship and effect modifiers of such association are not well established. This study is an extension of an earlier European meta-analysis. Our aim was to explore exposure–response relationship between PCB-153 and p-p′-DDE and birth outcomes; to evaluate whether any no exposure–effect level and susceptible subgroups exist; and to assess the role of maternal gestational weight gain (GWG). We used a pooled dataset of 9377 mother–child pairs enrolled in 14 study populations from 11 European birth cohorts. General additive models were used to evaluate the shape of the relationships between organochlorine compounds and birth outcomes. We observed an inverse linear exposure–response relationship between prenatal exposure to PCB-153 and birth weight [decline of 194 g (95% CI − 314, − 74) per 1 μg/L increase in PCB-153]. We showed effects on birth weight over the entire exposure range, including at low levels. This reduction seems to be stronger among children of mothers who were non-Caucasian or had smoked during pregnancy. The most susceptible subgroup was girls whose mothers smoked during pregnancy. After adjusting for absolute GWG or estimated fat mass, a reduction in birth weight was still observed. This study suggests that the association between low-level exposure to PCB-153 and birth weight exists and follows an inverse linear exposure–response relationship with effects even at low levels, and that maternal smoking and ethnicity modify this association.     

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.     

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.     

Particulate matter and early childhood body weight

Concerns over adverse effects of air pollution on children's health have been rapidly rising. However, the effects of air pollution on childhood growth remain to be poorly studied. We investigated the association between prenatal and postnatal exposure to PM10 and children's weight from birth to 60 months of age. This birth cohort study evaluated 1129 mother-child pairs in South Korea. Children's weight was measured at birth and at six, 12, 24, 36, and 60 months. The average levels of children's exposure to particulate matter up to 10 μm in diameter (PM10) were estimated during pregnancy and during the period between each visit until 60 months of age. Exposure to PM10 during pregnancy lowered children's weight at 12 months. PM10 exposure from seven to 12 months negatively affected weight at 12, 36, and 60 months. Repeated measures of PM10 and weight from 12 to 60 months revealed a negative association between postnatal exposure to PM10 and children's weight. Children continuously exposed to a high level of PM10 (> 50 μg/m³) from pregnancy to 24 months of age had weight z-scores of 60 that were 0.44 times lower than in children constantly exposed to a lower level of PM10 (≤ 50 μg/m³) for the same period. Furthermore, growth was more vulnerable to PM10 exposure in children with birth weight < 3.3 kg than in children with birth weight > 3.3 kg. Air pollution may delay growth in early childhood and exposure to air pollution may be more harmful to children when their birth weight is low.