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Objective: To evaluate whether higher omega-6:omega-3 (n-6:n-3) long-chain polyunsaturated fatty acid ratio in cord plasma is associated with more symptoms of attention deficit and hyperactivity disorder (ADHD) at 4 and 7 years of age.Study Design: This study was based on a population-based birth cohort in Spain. N-6 arachidonic acid and n-3 eicosapentaenoic and docosahexaenoic acid concentrations were measured in cord plasma. At 4 years old, ADHD symptoms were reported by teachers through the ADHD Diagnostic and Statistical Manual of Mental Disorders, 4th ed checklist (n = 580). At 7 years old, ADHD symptoms were reported by parents through the Conners' Rating Scale-Revised (short form; n = 642). The ADHD variable was treated as continuous (score) and as dichotomous (symptom diagnostic criteria). Child and family general characteristics were prospectively collected through questionnaires. We applied pooled zero-inflated negative binomial and logistic regressions adjusted for covariates.Results: A higher omega-6:omega-3 long-chain polyunsaturated fatty acid ratio in cord plasma was associated with a higher ADHD index (incidence rate ratio, 1.13; 95% CI, 1.03, 1.23) at 7 years old. The association was not observed at 4 years old (incidence rate ratio, 1.04; 95% CI, 0.92-1.18). No associations were found using ADHD symptom diagnostic criteria.Conclusions: High prenatal omega-6:omega-3 long-chain polyunsaturated fatty acid ratio preceded the appearance of subclinical ADHD symptoms during mid-childhood. Our findings suggest that maternal diet during pregnancy may modulate the risk to develop long-term ADHD symptoms in the offspring. [ABSTRACT FROM AUTHOR]

Objective We sought to assess the association between prenatal head growth and child neuropsychological development in the general population. Study Design We evaluated 2104 children at the age of 14 months from a population-based birth cohort in Spain. Head circumference (HC) was measured by ultrasound examinations at weeks 12, 20, and 34 of gestation and by a nurse at birth. Head growth was assessed using conditional SD scores between weeks 12-20 and 20-34. Trained psychologists assessed neuropsychological functioning using the Bayley Scales of Infant Development. Head size measurements at birth were transformed into a 3-category variable: microcephalic (<10th percentile), normocephalic (≥10th and <90th percentile), and macrocephalic (≥90th percentile) based on the cohort distribution. P values < .05 were considered statistically significant. Results No overall associations were observed between HC or head growth and mental and psychomotor scores. In particular, no associations were found between HC at birth and mental scores (coefficient, 0.04; 95% confidence interval, –0.02 to 0.09) and between interval head growth (20-34 weeks) and mental scores (0.31; 95% confidence interval, –0.36 to 0.99). Upon stratification by microcephalic, normocephalic, or macrocephalic head size, results were imprecise, although there were some significant associations in the microcephalic and macrocephalic groups. Adjustment by various child and maternal cofactors did not affect results. The minimum sample size required for present study was 883 patients (β = 2, α = 0.05, power = 0.80). Conclusion Overall prenatal and perinatal HC was not associated with 14-month-old neuropsychological development. Findings suggest HC growth during uterine life among healthy infants may not be an important marker of early-life neurodevelopment but may be marginally useful with specific populations. [ABSTRACT FROM AUTHOR]

• In utero exposure to BPA was prevalent from 1999 to 2010. • In utero exposure to BPA may increase the risk of asthma and wheeze among school-age girls. • No evidence of an association with lung function at school-age nor wheezing patterns across childhood. In utero exposure to bisphenols, widely used in consumer products, may alter lung development and increase the risk of respiratory morbidity in the offspring. However, evidence is scarce and mostly focused on bisphenol A (BPA) only. To examine the associations of in utero exposure to BPA, bisphenol F (BPF), and bisphenol S (BPS) with asthma, wheeze, and lung function in school-age children, and whether these associations differ by sex. We included 3,007 mother–child pairs from eight European birth cohorts. Bisphenol concentrations were determined in maternal urine samples collected during pregnancy (1999–2010). Between 7 and 11 years of age, current asthma and wheeze were assessed from questionnaires and lung function by spirometry. Wheezing patterns were constructed from questionnaires from early to mid-childhood. We performed adjusted random-effects meta -analysis on individual participant data. Exposure to BPA was prevalent with 90% of maternal samples containing concentrations above detection limits. BPF and BPS were found in 27% and 49% of samples. In utero exposure to BPA was associated with higher odds of current asthma (OR = 1.13, 95% CI = 1.01, 1.27) and wheeze (OR = 1.14, 95% CI = 1.01, 1.30) (p-interaction sex = 0.01) among girls, but not with wheezing patterns nor lung function neither in overall nor among boys. We observed inconsistent associations of BPF and BPS with the respiratory outcomes assessed in overall and sex-stratified analyses. This study suggests that in utero BPA exposure may be associated with higher odds of asthma and wheeze among school-age girls. [ABSTRACT FROM AUTHOR]

Abstract: Polychlorinated biphenyls (PCB) are synthetic organochlorine compounds with potential neurotoxic effects. Although negative effects on neuropsychological development have been observed in previous studies on PCB exposure, there are inconsistencies in these effects at current exposure levels of these compounds which are much lower than for previous generations. This study aimed to disentangle the effects of prenatal and postnatal PCB exposure on neuropsychological development at 4years of age. This study is based on a population-based birth cohort design established in Menorca (Spain) as part of the INMA [Environment and Childhood] Project. We assessed general neuropsychological development using the McCarthy Scales of Children''s Abilities (MCSA). A total of 422 4-year old children were assessed with the MCSA. Levels of PCBs were measured in cord blood (n=405) and in blood samples taken at 4years (n=285). We found no statistically significant effects of the sum of prenatal PCBs on MCSA scores. Nevertheless, individual congener analyses yielded significant detrimental effects of prenatal PCB153 on the majority of MCSA scores, while no effects were reported for other congeners. The levels of PCBs at 4years of age were not associated with neuropsychological development. Thus, prenatal exposure to low-level concentrations of PCBs, particularly PCB153, was associated with an overall deleterious effect on neuropsychological development at 4years of age, including negative effects on executive function, verbal functions and visuospatial abilities, but not on motor development. [Copyright &y& Elsevier]

• We assessed cardiometabolic (CM) effects of prenatal POP exposure into adolescence. • Prenatal exposure to POPs (particularly HCB) was positively associated with BMI. • p,p'-DDT and HCB were positively associated with other CM markers in adolescence. • Prenatal POP exposure may increase the risk of metabolic disorders in adolescence and adult life. Prenatal exposure to persistent organic pollutants (POPs) has been linked to cardiometabolic (CM) risk factors in childhood, but there are no studies evaluating the persistence of these associations into adolescence, a period of relevant changes in endocrine-dependent organ systems and rapid increases in lean and fat mass. We examined the associations of prenatal POP exposures with body mass index (BMI) from age 4 to 18 years, and with other CM risk markers in adolescence. We analysed 379 children from the Spanish INMA-Menorca birth cohort study with measured cord blood POP concentrations. We calculated BMI z-scores at ages 4, 6, 11, 14 and 18 years using the WHO growth reference. Body fat % was measured at 11 and 18 years and waist-to-height ratio (WHtR) and blood pressure (BP) at 11, 14 and 18 years. We measured CM biomarkers in fasting blood collected at age 14 years and calculated a CM-risk score as the sum of the sex-, and age-specific z-scores for waist circumference, mean arterial BP, homeostatic model assessment of insulin resistance, fasting blood triglycerides, and high-density lipoprotein cholesterol (HDL-C) (n = 217). Generalised estimating equations and multivariate linear regression models assessed the associations with repeated and single time-point measures, respectively. Hexachlorobenzene (HCB) exposure in the third tertile, compared to the first tertile, was associated with higher BMI (β = 0.24; 95% CI: 0.01, 0.47) and WHtR z-score (β = 0.27; 95% CI: 0.04, 0.51). A continuous increase in HCB was associated with an elevated body fat % (β per 10-fold increase = 4.21; 95% CI: 0.51, 7.92), systolic BP (β = 0.32; 95% CI: 0.02, 0.64) and diastolic BP z-score (β = 0.32; 95% CI: 0.02, 0.62) across all ages, and with higher CM-risk score (β = 1.59; 95% CI: 0.02, 3.18) and lipid biomarkers (total cholesterol, triglycerides and low-density lipoprotein cholesterol (LDL-C)) at 14 years. Dichlorodiphenyltrichloroethane (p,p'-DDT) exposure was non-monotonically associated with BMI and systolic BP. p,p'-DDE and Σ-polychlorinated biphenyls (PCBs) (sum of congeners 118, 138, 153, 180) were not associated with adiposity or BP. p,p'-DDT exposure was associated with an increased CM-risk score, and ΣPCBs concentrations with LDL-C in all adolescents and with total cholesterol only in girls (p -sex interaction = 0.05). This first longitudinal study from 4 to 18 years suggests that the previously reported POP associations with child BMI persist later in adolescence and that prenatal POP exposures are associated with major risk factors for adult CM syndrome. [ABSTRACT FROM AUTHOR]

The impact of maternal diet during pregnancy on child neurodevelopment is of public health and clinical relevance. We evaluated the associations of dietary quality based on the Dietary Approaches to Stop Hypertension (DASH) score and dietary inflammatory potential based on the energy-adjusted Dietary Inflammatory Index (E-DII) score during pregnancy with emotional and behavioral symptoms of offspring at 7 to 10 years of age. Individual participant data for 11,870 mother–child pairs from four European cohorts participating in the ALPHABET project were analyzed. Maternal antenatal DASH and E-DII scores were generated from self-completed food frequency questionnaires. Symptoms of depression and anxiety, aggressive behavior, and attention-deficit/hyperactivity disorder in children were assessed using mother-reported tests and classified within the normal or borderline/clinical ranges using validated cutoffs. Adjusted odds ratios were determined by multivariable logistic regression models and aggregated by the two-level individual participant data meta-analysis method. Higher maternal DASH scores (indicating better dietary quality) were associated with lower risk of depressive and anxiety symptoms, aggressive behavior symptoms, and attention-deficit/hyperactivity disorder symptoms within the borderline/clinical ranges: odds ratio [OR] 0.97, 95% confidence interval [CI], 0.95–0.99; OR 0.97, 95% CI, 0.94–0.99; OR 0.97, 95% CI, 0.95–0.98, per one-unit DASH score increase, respectively. For depression and anxiety, aggressive behavior, and attention-deficit/hyperactivity disorder symptoms, a one-unit increase in E-DII scores (a more proinflammatory diet) was associated with a 7% increased risk of all three analyzed emotional and behavioral symptoms: OR 1.07, 95% CI, 1.03–1.11; OR 1.07, 95% CI, 1.02–1.13; OR 1.07, 95% CI, 1.01–1.13, respectively. Our findings suggest that a maternal low-quality and proinflammatory diet may increase the risk of emotional and behavioral symptoms in children. [ABSTRACT FROM AUTHOR]

Prenatal exposure to organochlorine compounds (OCs) can increase the risk of reported respiratory symptoms in children. It remains unclear whether these compounds can also impact on lung function. We assessed the association between prenatal exposure to OCs and lung function during childhood. We included 1308 mother-child pairs enrolled in a prospective cohort study. Prenatal concentrations of p , p ′-dichlorodiphenyltrichloroethane [ p , p ′-DDT], p , p ′-dichlorodiphenyldichloroethylene [ p , p ′-DDE], hexachlorobenzene [HCB], and seven polychlorinated biphenyls [PCBs] were measured in cord blood. Spirometry was performed in the offspring at ages 4 (n = 636) and 7 years (n = 1192). More than 80% of samples presented quantifiable levels of p , p ′-DDE, HCB, PCB-138, PCB-153, and PCB-180; p , p ′-DDE was the compound with the highest median concentrations. At 4 years, prenatal p , p ′-DDE exposure was associated with a decrease in forced expiratory volume in 1 s (FEV 1) in all quartiles of exposure (e.g., third quartile [0.23–0.34 ng/mL]: β for FEV 1 −53.61 mL, 95% CI −89.87, −17.35, vs. the lowest). Prenatal p , p ′-DDE levels also decreased forced vital capacity (FVC) and FEV 1 /FVC, but associations did not reach statistical significance in most exposure quartiles. At 7 years, p , p ′-DDE was associated with a decrease in FVC and FEV 1 in only the second quartile of exposure (e.g. β for FEV 1 −36.96 mL, 95% CI −66.22, −7.70, vs. the lowest). Prenatal exposure to HCB was associated with decreased FVC and FEV 1 , but in only the second quartile and at 7 years (e.g. [0.07–0.14 ng/mL]: β for FEV 1 −25.79 mL, 95% CI −55.98, 4.39, vs. the lowest). PCBs were not consistently associated with lung function. Prenatal exposure to p , p ′-DDE may decrease lung function during childhood, especially FEV 1 and at medium levels of exposure. Further and deeper knowledge on the impact of environmental chemicals during pregnancy on lung development is needed. • Current low but widespread human exposure to banned organochlorine compounds • Prenatal exposure to organochlorine pesticides linked to lower lung function in childhood • Low levels found in current populations can be harmful for offspring respiratory health. [ABSTRACT FROM AUTHOR]

Background and Aim: Exposure to endocrine-disrupting chemicals may increase cardiovascular risk from early life, but studies in children have shown inconsistent results, most focused on analysis of single chemicals, and none included measures of micro-vascularization as early preclinical markers. This study aimed to evaluate the association between prenatal exposure to phthalates and phenols and macro- and microvascular health during early adolescence.Methods: Using data from a Spanish birth cohort (n = 416), prenatal exposure to eight phthalate metabolites and seven phenols (bisphenol A, four parabens, benzophenone-3, triclosan) were assessed using first and/or third trimester spot-urine concentrations. Macrovascular health (systolic and diastolic blood pressure (SBP and DBP, mmHg), pulse wave velocity (PWV, m/s)) and microvascular health (central retinal artery/vein equivalent (CRAE/CRVE, μm)), were measured at 11 years old. Linear regression models assessed associations for individual chemicals and Bayesian weighted quantile sum regression (BWQS) evaluated the overall association of the phthalate and phenol mixture with cardiovascular health.Results: In single exposure models, bisphenol-A was associated with decreased PWV (β per doubling of exposure = -0.06; 95% CI: -0.10, -0.01). Mono-iso-butyl phthalate was associated with an increase in CRAE (β = 1.89; 95% CI: 0.34, 3.44). Methyl- and butyl-parabens were associated with a decrease in CRVE (β = -0.71; 95% CI: -1.41, -0.01) and (β = -0.96; 95% CI: -1.57, -0.35), respectively. No statistically significant associations were observed between any of the exposures and SBP or DBP. BWQS models showed no evidence of associations between the phthalate and phenol mixture and any of the outcomes.Conclusions: Our results provide little evidence to suggest that prenatal exposure to phthalates and phenols is associated with macro- or microvascular health during early adolescence, except a few associations with certain compounds. Errors in exposure measurement and reduced variability in cardiovascular measures at this early age limit our ability to draw strong conclusions. [ABSTRACT FROM AUTHOR]

Abstract: Background: Fetal exposure to endocrine disrupting chemicals may increase the risk for adverse health effects at birth or later in life. Objectives: The 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 14months) using the biomarker total effective xenoestrogen burden (TEXB). Methods: 490 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. Results: The median TEXB-alpha level was 0.76pMEeq/g (interquartile range (iqr): 1.14). In multivariate models, higher TEXB-alpha levels (third tertile, >1.22pMEeq/g; iqr: 1.73) were associated with increased birthweight in boys but not in girls (β=148.2g, 95% CI: 14.01, 282.53, pint =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 14months of age (β=0.29; 95% CI: −0.11, 0.69). Conclusions: These 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. [Copyright &y& Elsevier]

Abstract: Objective: Thyroid hormones play an important role in human brain development, and some organochlorine compounds (OCs) act as thyroid disruptors. The objective of the present study was to evaluate the association between prenatal exposure to organochlorine compounds and thyroid function in newborns from a general population birth cohort in Menorca, with an a-priori specific focus on β-HCH. Methods: Levels of polychlorinated biphenyls (PCB congeners 28, 52, 101, 118, 138, 153 and 180), hexachlorobenzene (HCB), beta-hexachlorocyclohexane (β-HCH), dichlorodiphenyl dichloroethylene (p′p′-DDE) and dichlorodiphenyl trichloroethane (p′p-DDT) in cord serum, and thyrotropin (TSH) concentration in plasma three days after birth were measured in 387 newborns from Menorca. The TSH concentration was categorized (high or low), except for 27 children whose TSH levels were quantified. Results: Levels of β-HCH and PCB-153 were positively related to TSH concentrations (gestational age-adjusted coefficient (p-value): 0.26 (p = 0.006) and 0.31 (p = 0.050), respectively). Conclusions: β-HCH is potentially a new thyroid disrupting compound, deserving special interest in future studies given its high body burden in humans. [Copyright &y& Elsevier]