Prenatal particulate air pollution and neurodevelopment in urban children: Examining sensitive windows and sex-specific associations

BackgroundBrain growth and structural organization occurs in stages beginning prenatally. Toxicants may impact neurodevelopment differently dependent upon exposure timing and fetal sex.ObjectivesWe implemented innovative methodology to identify sensitive windows for the associations between prenatal particulate matter with diameter ≤ 2.5 μm (PM_2.5) and children's neurodevelopment.MethodsWe assessed 267 full-term urban children's prenatal daily PM_2.5 exposure using a validated satellite-based spatio-temporally resolved prediction model. Outcomes included IQ (WISC-IV), attention (omission errors [OEs], commission errors [CEs], hit reaction time [HRT], and HRT standard error [HRT-SE] on the Conners' CPT-II), and memory (general memory [GM] index and its components — verbal [VEM] and visual [VIM] memory, and attention-concentration [AC] indices on the WRAML-2) assessed at age 6.5 ± 0.98 years. To identify the role of exposure timing, we used distributed lag models to examine associations between weekly prenatal PM_2.5 exposure and neurodevelopment. Sex-specific associations were also examined.ResultsMothers were primarily minorities (60% Hispanic, 25% black); 69% had ≤ 12 years of education. Adjusting for maternal age, education, race, and smoking, we found associations between higher PM_2.5 levels at 31–38 weeks with lower IQ, at 20–26 weeks gestation with increased OEs, at 32–36 weeks with slower HRT, and at 22–40 weeks with increased HRT-SE among boys, while significant associations were found in memory domains in girls (higher PM_2.5 exposure at 18–26 weeks with reduced VIM, at 12–20 weeks with reduced GM).ConclusionsIncreased PM_2.5 exposure in specific prenatal windows may be associated with poorer function across memory and attention domains with variable associations based on sex. Refined determination of time window- and sex-specific associations may enhance insight into underlying mechanisms and identification of vulnerable subgroups.     

Pre- and postnatal exposures to pesticides and neurodevelopmental effects in children living in agricultural communities from South-Eastern Spain

BackgroundChildrens exposure to neurotoxic compounds poses a major problem to public health because of their actively developing brain that makes them highly vulnerable. However, limited information is available on neuropsychological effects in children associated with pre- and postnatal exposures to pesticides.ObjectiveTo evaluate the association between current and pre- and postnatal exposures to pesticides and their effects on neurodevelopment in children aged 6–11 years living in agricultural communities from South-Eastern Spain.MethodsAn ambispective study was conducted on 305 children aged 6–11 years randomly selected from public schools of the study area. Current exposure to organophosphate pesticides was assessed measuring children's urinary levels of dialkylphosphates (DAPs). Both prenatal and postnatal residential exposure to pesticides was estimated by developing a geographical information system (GIS) technology-based index that integrated distance-weighted measure of agricultural surface, time-series of crop areas per municipality and year, and land-use maps. Neuropsychological performance was evaluated with the Wechsler Intelligence Scale for Children-Fourth Edition (WISC-IV). The association of pre- and postnatal and current pesticide exposure with WISC-IV scale scores was assessed using multivariate linear regression models and generalized estimating equation (GEE) models, respectively.ResultsGreater urinary DAP levels were associated with a poorer performance on intelligence quotient and verbal comprehension domain, with effects being more prominent in boys than in girls. The influence of an increase in 10 ha per year in crop surface around the child's residence during the postnatal period was associated with decreased intelligence quotient, processing speed and verbal comprehension scores. As regards prenatal exposure to pesticides, a poor processing speed performance was observed. These effects were also more prominent in boys than in girls.ConclusionsOur results suggest that postnatal exposure to pesticides can negatively affect children's neuropsychological performance. Prenatal exposure was weakly associated to neurodevelopment impairment.     

Prenatal DDT and DDE exposure and child IQ in the CHAMACOS cohort

Although banned in most countries, dichlorodiphenyl-trichloroethane (DDT) continues to be used for vector control in some malaria endemic areas. Previous findings from the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) cohort study found increased prenatal levels of DDT and its breakdown product dichlorodiphenyl-dichloroethylene (DDE) to be associated with altered neurodevelopment in children at 1 and 2 years of age. In this study, we combined the measured maternal DDT/E concentrations during pregnancy obtained for the prospective birth cohort with predicted prenatal DDT and DDE levels estimated for a retrospective birth cohort. Using generalized estimating equation (GEE) and linear regression models, we evaluated the relationship of prenatal maternal DDT and DDE serum concentrations with children's cognition at ages 7 and 10.5 years as assessed using the Full Scale Intelligence Quotient (IQ) and 4 subtest scores (Working Memory, Perceptual Reasoning, Verbal Comprehension, and Processing Speed) of the Wechsler Intelligence Scale for Children (WISC). In GEE analyses incorporating both age 7 and 10.5 scores (n = 619), we found prenatal DDT and DDE levels were not associated with Full Scale IQ or any of the WISC subscales (p-value > 0.05). In linear regression analyses assessing each time point separately, prenatal DDT levels were inversely associated with Processing Speed at age 7 years (n = 316), but prenatal DDT and DDE levels were not associated with Full Scale IQ or any of the WISC subscales at age 10.5 years (n = 595). We found evidence for effect modification by sex. In girls, but not boys, prenatal DDE levels were inversely associated with Full Scale IQ and Processing Speed at age 7 years. We conclude that prenatal DDT levels may be associated with delayed Processing Speed in children at age 7 years and the relationship between prenatal DDE levels and children's cognitive development may be modified by sex, with girls being more adversely affected.     

Prenatal and early-life polychlorinated biphenyl (PCB) levels and behavior in Inuit preschoolers

BackgroundWhereas it is well established that prenatal exposure to polychlorinated biphenyls (PCBs) can disrupt children's behavior, early postnatal exposure has received relatively little attention in environmental epidemiology.ObjectivesTo evaluate prenatal and postnatal exposures to PCB-153, a proxy of total PCB exposure, and their relation to inattention and activity in 5-year-old Inuits from the Cord Blood Monitoring Program.MethodsPrenatal exposure to PCBs was informed by cord plasma PCB-153 levels. We used a validated pharmacokinetic model to estimate monthly infants' levels across the first year of life. Inattention and activity were assessed by coding of video recordings of children undergoing fine motor testing. We used multivariable linear regression to evaluate the association between prenatal and postnatal PCB-153 levels and inattention (n = 97) and activity (n = 98) at 5 years of age.ResultsCord plasma PCB-153 was not associated with inattention and activity. Each interquartile range (IQR) increase in estimated infant PCB-153 levels at 2 months was associated with a 1.02% increase in the duration of inattention (95% CI: 0.04, 2.00). Statistical adjustment for the duration of breastfeeding slightly increased regression coefficients for postnatal level estimates, some of which became statistically significant for inattention (months: 2–4) and activity (months: 2–5).ConclusionsOur study adds to the growing evidence of postnatal windows of development during which children are more susceptible to neurotoxicants like PCBs.     

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.     

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.     

Polymorphisms in ATP-binding cassette transporters associated with maternal methylmercury disposition and infant neurodevelopment in mother-infant pairs in the Seychelles Child Development Study

BackgroundATP-binding cassette (ABC) transporters have been associated with methylmercury (MeHg) toxicity in experimental animal models.AimsTo evaluate the association of single nucleotide polymorphisms (SNPs) in maternal ABC transporter genes with 1) maternal hair MeHg concentrations during pregnancy and 2) child neurodevelopmental outcomes.Materials and methodsNutrition Cohort 2 (NC2) is an observational mother-child cohort recruited in the Republic of Seychelles from 2008–2011. Total mercury (Hg) was measured in maternal hair growing during pregnancy as a biomarker for prenatal MeHg exposure (N = 1313) (mean 3.9 ppm). Infants completed developmental assessments by Bayley Scales of Infant Development II (BSID-II) at 20 months of age (N = 1331). Genotyping for fifteen SNPs in ABCC1, ABCC2 and ABCB1 was performed for the mothers.ResultsSeven of fifteen ABC SNPs (ABCC1 rs11075290, rs212093, and rs215088; ABCC2 rs717620; ABCB1 rs10276499, rs1202169, and rs2032582) were associated with concentrations of maternal hair Hg (p < 0.001 to 0.013). One SNP (ABCC1 rs11075290) was also significantly associated with neurodevelopment; children born to mothers with rs11075290 CC genotype (mean hair Hg 3.6 ppm) scored on average 2 points lower on the Mental Development Index (MDI) and 3 points lower on the Psychomotor Development Index (PDI) than children born to mothers with TT genotype (mean hair Hg 4.7 ppm) while children with the CT genotype (mean hair Hg 4.0 ppm) had intermediate BSID scores.DiscussionGenetic variation in ABC transporter genes was associated with maternal hair Hg concentrations. The implications for MeHg dose in the developing child and neurodevelopmental outcomes need to be further investigated.     

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.     

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.     

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

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

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.     

Tobacco smoke increases the risk of otitis media among Greenlandic Inuit children while exposure to organochlorines remain insignificant

BackgroundPrenatal exposure to environmental levels of organochlorines (OCs) has been demonstrated to have immunotoxic effects in humans. We investigated the relationship between prenatal exposure to OCs and the occurrence of otitis media (OM) among Inuit children in Greenland.MethodsWe estimated the concentration of 14 PCB congeners and 11 pesticides in maternal and cord blood samples and in breast milk in a population-based cohort of 400 mother–child pairs. At follow-up, we examined the children's ears and used their medical records to assess the OM occurrence and severity. Multivariate regression analyses were used with adjustments for passive smoking, crowding, dietary habits, parent's educational level, breast feeding and the use of child-care.ResultsThe children were 4–10 years of age at follow-up and 223 (85%) participated. We found no association between prenatal OC exposure and the development of OM. Factors associated with the child's hazard of OM during the first 4 years of life were: mother's history of OM (HR 1.70, 95% CI 1.11–2.59, p = 0.01); mother's smoking habits: current (HR 2.47, 95% CI 1.45–4.21, p < 0.01) and previous (HR 2.00, 95% CI 1.19–3.36, p < 0.01); number of smokers in the home (HR 1.17, 95% CI 1.05–1.31, p < 0.01). After adjustment mothers' smoking habits remained significant.ConclusionWe found no relationship between high levels of prenatal exposure of OCs and occurrence of OM. Passive smoking was found as the strongest environmental risk factor for the development of OM.Interventions to reduce passive smoke in children's environment are needed.     

Prenatal exposure to multiple pesticides is associated with auditory brainstem response at 9 months in a cohort study of Chinese infants

BackgroundPesticides are associated with poorer neurodevelopmental outcomes, but little is known about the effects on sensory functioning.MethodsAuditory brainstem response (ABR) and pesticide data were available for 27 healthy, full-term 9-month-old infants participating in a larger study of early iron deficiency and neurodevelopment. Cord blood was analyzed by gas chromatography–mass spectrometry for levels of 20 common pesticides. The ABR forward-masking condition consisted of a click stimulus (masker) delivered via ear canal transducers followed by an identical stimulus delayed by 8, 16, or 64 milliseconds (ms). ABR peak latencies were evaluated as a function of masker-stimulus time interval. Shorter wave latencies reflect faster neural conduction, more mature auditory pathways, and greater degree of myelination. Linear regression models were used to evaluate associations between total number of pesticides detected and ABR outcomes. We considered an additive or synergistic effect of poor iron status by stratifying our analysis by newborn ferritin (based on median split).ResultsInfants in the sample were highly exposed to pesticides; a mean of 4.1 pesticides were detected (range 0–9). ABR Wave V latency and central conduction time (CCT) were associated with the number of pesticides detected in cord blood for the 64 ms and non-masker conditions. A similar pattern seen for CCT from the 8 ms and 16 ms conditions, although statistical significance was not reached. Increased pesticide exposure was associated with longer latency. The relation between number of pesticides detected in cord blood and CCT depended on the infant's cord blood ferritin level. Specifically, the relation was present in the lower cord blood ferritin group but not the higher cord blood ferritin group.ConclusionsABR processing was slower in infants with greater prenatal pesticide exposure, indicating impaired neuromaturation. Infants with lower cord blood ferritin appeared to be more sensitive to the effects of prenatal pesticide exposure on ABR latency delay, suggesting an additive or multiplicative effect.     

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.     

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

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

Metal exposures in an inner-city neonatal population

ObjectivesWe measured concentrations of lead (Pb), manganese (Mn), chromium (Cr), and copper (Cu) in umbilical cord whole blood and examined sources of environmental Pb exposures in a predominantly African-American population.MethodsBetween April and July 2006, we collected reproductive histories, questionnaires, and blood samples from 102 women, aged 16–45 years, who delivered at a Memphis, TN hospital.ResultsThe prevalence of preeclampsia and low birth weight infancy in the study population was 11% and 10%, respectively. Twenty-eight percent of mothers reported living near a potential Pb-contaminated area, while 43% lived in a residence built before 1978. Geometric mean (GM) concentrations for umbilical cord blood in the study population were 1.3, 3.5, 9.0, and 52.0 µg/dL for Pb, Mn, Cr, and Cu, respectively. Six neonates had cord blood Pb (CBL) concentrations above 10 µg/dL, while 20 had CBL concentrations ≥ 2 µg/dL. GM umbilical CBL levels were higher in neonates born to women living near a potential Pb-contaminated area (2.2 vs. 1.1 µg/dL) and those with friends, family or household members exposed to lead products (1.6 vs. 1.1 μg/dL). Some evidence of an exposure–response relationship was also detected between all four metal concentrations and an increasing number of maternal lead exposures. After adjustment for confounding, proximity to a Pb-contaminated area was the strongest environmental determinant of CBL levels among neonates with CBL concentrations of ≥ 2 µg/dL (odds ratio = 5.1; 95% CI = 1.6, 16.7).ConclusionsMetal concentrations were elevated in this population, and CBL levels were associated with proximity to Pb-contaminated areas.     

Prenatal and postnatal insecticide use and infant neuropsychological development in a multicenter birth cohort study

There is little evidence about exposure to currently used insecticides during early life periods and adverse effects on child neuropsychological development. The aim of this study is to examine the association between residential insecticide use during pregnancy and infancy, and the development of children.Study subjects were participants in the INMA (Environment and Childhood) Project, a Spanish multicenter birth cohort study. Prenatal and postnatal use of indoor insecticides and other variables were obtained from personal interview during pregnancy and infancy. Mental and psychomotor development was assessed around 14 months using the Bayley Scales of Infant Development. The associations were analyzed by linear regression models.54% of women used indoor insecticides at home during pregnancy and 47% postnatally. 34% of women used insecticide sprays and 33% used plug-in devices during pregnancy. During infancy, the percentage of women who used insecticide sprays decreased (22%), but the use of plug-in devices was similar to the prenatal period (32%). The use of insecticide sprays during pregnancy was associated with a decrement in psychomotor development (β = − 1.9; 95%CI: − 3.4, − 0.5) but postnatal use did not associate with mental and psychomotor development. The negative effect was enhanced according to some modifying factors, such as being female, higher levels of prenatal exposure to PCB and mercury and belonging to the lowest social class.We found certain evidence about the adverse effect of using insecticide sprays during pregnancy on the psychomotor development of children. Some socio-demographic factors and other exposures could enhance that effect.     

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.     

Associations of birth outcomes with maternal polybrominated diphenyl ethers and thyroid hormones during pregnancy

BackgroundPrevious research has linked polybrominated diphenyl ether (PBDE) exposure to poor birth outcomes and altered thyroid hormone levels.ObjectivesWe examined whether maternal PBDE serum levels were associated with infant birth weight (g), head circumference (cm), birth length (cm), and birth weight percentile for gestational age. We explored the potential for a mediating role of thyroid hormone levels.MethodsDuring 2008–2010, we recruited 140 pregnant women in their third trimester as part of a larger clinical obstetrics study known as Healthy Pregnancy, Healthy Baby. Blood samples were collected during a routine prenatal clinic visit. Serum was analyzed for PBDEs, phenolic metabolites, and thyroid hormones. Birth outcome information was abstracted from medical records.ResultsIn unadjusted models, a two-fold increase in maternal BDE 153 was associated with an average decrease in head circumference of 0.32 cm (95% CI: − 0.53, − 0.12); however, this association was attenuated after control for maternal risk factors. BDE 47 and 99 were similarly negatively associated but with 95% confidence intervals crossing the null. Associations were unchanged in the presence of thyroid hormones.ConclusionsOur data suggest a potential deleterious association between maternal PBDE levels and infant head circumference; however, confirmatory studies are needed in larger sample sizes. A mediating role of thyroid hormones was not apparent.     

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.