Background:Over 10 epidemiological studies have investigated air pollutants' association with thyroid hormone levels in pregnant women, but none have used personal air pollutant exposure data or included benzene, toluene, ethylbenzene, and xylene (BTEX). We assessed the relationship between personal exposure to nitrogen dioxide (NO2), particulate matter ≤2.5 µm (PM2.5), and BTEX with maternal thyroid hormones during pregnancy. Methods:The study relied on 437 pregnant women from the SEPAGES cohort (Grenoble, France, 2014-2017). Personal exposure to NO2, PM2.5, and BTEX was measured 1 week before blood sampling (mean: 19th gestational week), where thyroid hormones (free and total triiodothyronine (FT3, TT3), thyroxine (FT4, TT4), thyroid-stimulating hormone, and the TT3/TT4 ratio) were assessed. We linearly regressed air pollutants against individual thyroid hormone concentrations, adjusting for covariates, including urinary iodine concentration. Ambient NO2 and PM2.5 exposures were also analyzed for comparison. Results:Personal PM2.5 was positively associated with TT4 (β = 2.3%; 95% confidence interval [CI] = 0.4%, 4.2%, per doubling of exposure) and FT4 (β = 1.9%; 95% CI = -0.3%, 4.2%). On the contrary, negative associations between doubling the ethylbenzene exposure and TT4 (β = -1.2%; 95% CI = -2.4%, 0.1%) and FT4 levels (β = -1.3%; 95% CI = -2.7%, 0.1%) were observed. The association between ambient PM2.5 1 week before hormone measurement and FT4 was consistent with the association observed for personal exposure. Associations between ambient PM2.5 and TT4 were positive but attenuated across all examined time windows. Conclusions:Personal short-term exposure estimates provide evidence of a potential association between PM2.5, ethylbenzene, and altered thyroxine (TT4 and FT4) levels in pregnant women, warranting replication in other populations and larger samples.

Abstract Early life is a vulnerable period to environmental exposures that may be associated with autism spectrum disorder (ASD). We investigated associations between prenatal and postnatal exposure to weekly averages of temperature and air pollutants (PM2.5, PM10, NO2) with autism screening scores (based on the Modified Checklist for Autism in Toddlers, Revised version) in 12,139 2-year-olds from the French ELFE birth cohort. Exposures were based on daily outdoor predictions at 1 km resolution (200 m in large urban areas for temperature and NO2). Relationships were modeled with confounder-adjusted distributed lag nonlinear models and generalized linear models. Autism screening scores significantly increased following exposure to night-time heat throughout the beginning of the third trimester and possibly toward the end of pregnancy, even after adjusting for PM2.5 and PM10. During the postnatal period, night-time heat (months 2–7.5) and increased PM2.5 and PM10 exposures (months 7–11.5) led to higher scores in males compared to females. Conversely, night-time heat (months 17–20) led to higher scores in females. Our findings suggest that prenatal exposure to heat, but not air pollution, may be associated with early ASD risk indicators, while sex-specific effects of heat and PM exposure were observed in the postnatal period.

BACKGROUND:Rising global temperatures affect maternal and neonatal health, yet the effects on maternal cardiovascular physiology and potential windows of vulnerability remain largely unexplored. METHODS:We investigated subacute (0-28 days) heat and cold exposure, estimated using a high-resolution spatiotemporal temperature model, in relation to heart rate, hematocrit levels, and repeated systolic and diastolic blood pressure measurements (transformed into gestational age-specific Z-scores, zSBP, zDBP) among 1854 pregnant women from the French EDEN cohort. Distributed lag non-linear models were used to model both cumulative and lagged effects of heat (95th percentile; 20 °C compared to 11 °C) and cold (5th percentile; 4 °C compared to 11 °C). Models accounted for air pollution, vegetation and humidity and were stratified by gestational age and fetal sex. RESULTS:Heat was associated with a sharp decrease in zSBP for up to 10 days after exposure (-0.14 SD [-0.20; -0.08] 95%-CI). Cold was associated with higher hematocrit (0.28% [0.04; 0.51]) and a modest increase in zSBP (0.06 SD [0.02; 0.09]) over 2-6 days after exposure, with zSBP associations observed only in pregnancies with female fetuses. Subacute effects of heat were not modified by gestational age, nor by air pollution and vegetation. CONCLUSION:This study underscores the role of short-term heat exposure in shaping maternal cardiovascular responses during pregnancy, while suggesting more limited effects of cold exposure, with variations by fetal sex. These results provide insights into the biological plausibility of temperature extremes effects on pregnancy complications.

Increased ambient heat exposure poses a health risk to pregnant women, which may be amplified by environmental and social determinants, but these interactions have been insufficiently characterized. We examined critical windows for the associations between heat exposure during pregnancy and fetal growth and investigated the role of air pollution, vegetation, and social stressors in these associations. Weekly exposure to ambient temperature and air pollutants (PM2.5, NO2, O3) from highly resolved spatiotemporal models, vegetation, and contextual deprivation were estimated for 20,904 French women (2002-2017). Distributed lag nonlinear models evaluated associations between heat and term birth weight (tBW), tBW Z-score, and small-for-gestational-age. We further adjusted our models for air pollutants and stratified on vegetation and social determinants. Heat exposure during the first two trimesters was associated with reduced fetal growth. A mean temperature of 21.6 °C (95th percentile vs median 13.6 °C) during weeks 2-15 was associated with a reduced tBW (-199 g [95% CI: -268; -131]). These associations differed after adjusting for O3 exposure. Trends for stronger associations were observed in women with low vegetation exposure, low social position, and high contextual deprivation. This study highlights how heat stress during early pregnancy could reduce birth weight.

An increasing number of epigenome-wide association studies report tobacco smoking-associated DNA methylation levels. However, comprehensive replication studies remain scarce, particularly in placenta, despite their crucial interest in such a large-scale context. Using DNA methylation data from the EPIC array of 341 new placentas (85 smokers, 219 non-smokers, and 37 former smokers) from the EDEN cohort, we used a candidate approach to replicate maternal smoking-associated CpGs and regions previously identified using the 450K array, and an exploratory approach to discover new associations within EPIC-specific CpGs. Smoking-associated changes in DNA methylation in CpGs and regions were classified as either transient or persistent (indicating epigenetic memory), depending on the stability of their association with smoking status. Among candidate loci, 38% of probes and 9% of regions were replicated, providing robust evidence of effects of prenatal smoke exposure on methylation patterns of these loci. LEKR1 was the top hit in both the initial and replication studies. Most of the replicated loci were transient CpGs (i.e. current smokers), while persistent CpGs (i.e. former smokers) remained scarce and somewhat inconsistent with previous findings. The additional exploratory analysis identified 733 novel probes and 75 novel regions, including 18% and 30% of transient loci, respectively. Results suggested that most of the effects were related to in utero exposure only, supporting pregnant women's efforts to quit smoking. This replication study also evidences the importance of reproducible work in omic investigations to provide a more in-depth and robust understanding of the effects of environmental exposures on health biomarkers..

Heat exposure in pregnancy has been associated with mother-child health. However, characterization of exposure to heat in pregnant women and its associated factors, such as air pollution, vegetation or social stressors, is lacking. We aimed to describe heat exposure according to air pollution and vegetation co-exposures, individual social position and socio-economic context of residence among French pregnant women. We studied 12,235 pregnant women from four mother-child cohorts. Exposure to heat (intensity, duration, severity), particulate matter, nitrogen dioxide (NO2), ozone (O3), and vegetation during summer were estimated at the women's residences. Socio-economic context of residence was assessed using the European Deprivation Index (EDI). Cumulative overexposure to heat, air pollution and vegetation were estimated according to reference values. Three profiles of heat exposure, multi-exposure and individual social position, were created using multivariate analysis and unsupervised clustering. Associations of the profiles of heat exposure and multi-exposure with air pollution, vegetation, individual social position and EDI were described using Wilcoxon tests and polytomous regressions. About one-third of pregnant women had a high heat exposure profile combining intense, severe and durable exposure. Depending on the location and year of pregnancy, 27-88% of women were overexposed to heat, air pollution and lack of vegetation. The relationships between profiles of heat and multi-exposure with air pollution, vegetation and individual social position and socioeconomic context of residence depended on the geographical and temporal context. No clear differential exposure pattern across social strata was found. Co-exposure to heat, air pollution and lack of vegetation is common among French pregnant women. Protective measures against summer heat would apply to all pregnant women, as heat exposure represents a universal risk, regardless of socioeconomic status. This research supports future epidemiological studies on combined effects of heat and co-exposures on pregnancy outcomes.

Background:Previous studies have demonstrated that in utero and early life heat exposure can influence neurodevelopment. However, to our knowledge, these investigations have not evaluated realistic counterfactual scenarios; instead, they have primarily relied on static, crude comparisons of extreme temperatures versus a reference temperature over an extended period. Methods:We employed the framework of longitudinal modified treatment policy to examine the impact of heat exposure during prenatal and postnatal periods on the linguistic development of two-year-old children in the Etude Longitudinale Française depuis l'Enfance birth cohort (N = 12,163). Heat exposure was defined as the number of periods when overall daytime and nighttime daily temperatures surpassed the 90th percentile (20.6, 27.5, and 15.3 °C, respectively) for at least two consecutive days. Context-specific counterfactual scenarios were constructed by increasing daily temperatures by 1, 2, or 3 °C, in line with projections from Intergovernmental Panel on Climate Change scenarios. Causal effects were estimated by comparing the population mean outcomes under hypothetical counterfactual scenarios vs. those actually observed in the data using a doubly robust estimation technique (targeted maximum likelihood estimation). A library of machine learning algorithms was employed to model the intricate relationships between covariates and both the exposure and outcome variables. Results:In counterfactual scenarios where daily temperature increases by one degree, mean differences in log-transformed population outcome did not reach statistical significance. A two-degree daily increase in nighttime temperature showed a decrease in linguistic development scores of 30% (P < 0.001). A three-degree increase in overall, daytime and nighttime daily temperatures showed a decrease in scores of at least 6% (P < 0.003). Conclusion:Our study revealed a negative impact of increased air temperatures on the linguistic development of 2-year-old children in counterfactual scenarios involving two- and three-degree temperature rises. The longitudinal modified treatment policy approach offers valuable new insights for causal inference in environmental epidemiology, particularly through its ability to directly assess the effects of anticipated, policy-relevant temperature changes.

A number of negative developmental outcomes in response to extreme temperature have been documented. Yet, to our knowledge, environmental research has left the question of the effect of temperature on human neurodevelopment largely unexplored. Here, we aimed to investigate the effect of ambient temperature on linguistic development at the age of 2 years-old. We used data from the prospective national French birth cohort ELFE (N = 12,163) and highly-resolved exposure models with daily temporal resolution and 200 m to 1 km spatial resolution. We investigated the effect of weekly averages of overall, daytime and night-time temperature in the prenatal (first 30 weeks of gestation) and postnatal (91 weeks after birth) period on vocabulary production scores from the MacArthur-Bates Communicative Development Inventories (MB-CDI) at 2 years-old. Exposure-response and lag-response relationships were modeled with confounder-adjusted distributed lag non-linear models. Scores at the MB-CDI decreased by 3.2

Early environmental exposures can have long-term effects on child's development and health. Epigenetic modifications may partly explain these effects, and studying them could lead to significant advances in our understanding of the underlying mechanisms. This review summarises recent data on epigenetic and environmental epidemiology during the first 1000 days of life for several common exposures, including tobacco, phenols and phthalates, air pollutants, ambient temperature and vegetation.

Les expositions environnementales précoces peuvent influencer le développement et la santé de l’enfant à long terme. Des modifications épigénétiques pourraient partiellement expliquer ces effets, et leur identification conduire à des progrès significatifs dans la compréhension des mécanismes impliqués. Dans cette revue, nous présentons les données récentes en épidémiologie épigénétique et environnementale pendant la période des 1 000 premiers jours de vie concernant plusieurs expositions très courantes, dont le tabac, les phénols et les phtalates, les polluants de l’air, la température ambiante et la végétation.

Background Pregnancy air pollution exposure (PAPE) has been linked to a wide range of adverse birth and childhood outcomes, but there is a paucity of data on its influence on the placental epigenome, which can regulate the programming of physiological functions and affect child development. This study aimed to investigate the association between prenatal air pollutant exposure concentrations and changes in placental DNA methylation patterns, and to explore the potential windows of susceptibility and sex-specific alterations. Methods This multi-site study used three prospective population-based mother-child cohorts: EDEN, PELAGIE, and SEPAGES, originating from four French geographical regions (Nancy, Poitiers, Brittany, and Grenoble). Pregnant women were included between 2003 and 2006 for EDEN and PELAGIE, and between 2014 and 2017 for SEPAGES. The main eligibility criteria were: being older than 18 years, having a singleton pregnancy, and living and planning to deliver in one of the maternity clinics in one of the study areas. A total of 1539 mother-child pairs were analysed, measuring placental DNA methylation using Illumina BeadChips. We used validated spatiotemporally resolved models to estimate PM 25 , PM 10 , and NO 2 exposure over each trimester of pregnancy at the maternal residential address. We conducted a pooled adjusted epigenome-wide association study to identify differentially methylated 5'- C-phosphate-G-3' (CpG) sites and regions (assessed using the Infinium HumanMethylationEPIC BeadChip array, n=871), including sex-specific and sex-linked alterations, and independently validated our results (assessed using the Infinium HumanMethylation450 BeadChip array, n=668). Findings We identified four CpGs and 28 regions associated with PAPE in the total population, 469 CpGs and 87 regions in male infants, and 150 CpGs and 66 regions in female infants. We validated 35% of the CpGs available. More than 30% of the identified CpGs were related to one (or more) birth outcome and most significant alterations were enriched for neural development, immunity, and metabolism related genes. The 28 regions identified for both sexes overlapped with imprinted genes (four genes), and were associated with neurodevelopment (nine genes), immune system (seven genes), and metabolism (five genes). Most associations were observed for the third trimester for female infants (134 of 150 CpGs), and throughout pregnancy (281 of 469 CpGs) and the first trimester (237 of 469 CpGs) for male infants. Interpretation These findings highlight the molecular pathways through which PAPE might affect child health in a widespread and sex-specific manner, identifying the genes involved in the major physiological functions of a developing child. Further studies are needed to elucidate whether these epigenetic changes persist and affect health later in life.

ImportanceLittle is known about long-term associations of early-life exposure to extreme temperatures with child health and lung function.ObjectivesTo investigate the association of prenatal and postnatal heat or cold exposure with newborn lung function and identify windows of susceptibility.Design, Setting, and ParticipantsThis population-based cohort study (SEPAGES) recruited pregnant women in France between July 8, 2014, and July 24, 2017. Data on temperature exposure, lung function, and covariates were available from 343 mother-child dyads. Data analysis was performed from January 1, 2021, to December 31, 2021.ExposuresMean, SD, minimum, and maximum temperatures at the mother-child’s residence, estimated using a state-of-the-art spatiotemporally resolved model.Main Outcomes and MeasuresOutcome measures were tidal breathing analysis and nitrogen multiple-breath washout test measured at 2 months of age. Adjusted associations between both long-term (35 gestational weeks and first 4 weeks after delivery) and short-term (7 days before lung function test) exposure to ambient temperature and newborn lung function were analyzed using distributed lag nonlinear models.ResultsA total of 343 mother-child pairs were included in the analyses (median [IQR] maternal age at conception, 32 [30.0-35.2] years; 183 [53%] male newborns). A total of 246 mothers and/or fathers (72%) held at least a master’s degree. Among the 160 female newborns (47%), long-term heat exposure (95th vs 50th percentile of mean temperature) was associated with decreased functional residual capacity (−39.7 mL; 95% CI, −68.6 to −10.7 mL for 24 °C vs 12 °C at gestational weeks 20-35 and weeks 0-4 after delivery) and increased respiratory rate (28.0/min; 95% CI, 4.2-51.9/min for 24 °C vs 12 °C at gestational weeks 14-35 and weeks 0-1 after delivery). Long-term cold exposure (5th vs 50th percentile of mean temperature) was associated with lower functional residual capacity (−21.9 mL; 95% CI, −42.4 to −1.3 mL for 1 °C vs 12 °C at gestational weeks 15-29), lower tidal volume (−23.8 mL; 95% CI, −43.1 to −4.4 mL for 1 °C vs 12 °C at gestational weeks 14-35 and weeks 0-4 after delivery), and increased respiratory rate (45.5/min; 95% CI, 10.1-81.0/min for 1 °C vs 12 °C at gestational weeks 6-35 and weeks 0-1 after delivery) in female newborns as well. No consistent association was observed for male newborns or short-term exposure to cold or heat.Conclusions and RelevanceIn this cohort study, long-term heat and cold exposure from the second trimester until 4 weeks after birth was associated with newborn lung volumes, especially among female newborns.

BACKGROUND AND AIM: Exposure to air pollution during pregnancy may alter placental DNA methylation patterns and induce changes in placental and fetal development and later disease susceptibility. We investigated the association between prenatal NO2, PM10 and PM25 exposure levels and changes in placental DNA methylation (DNAm) patterns and further explored potential windows of susceptibility and sex-specific alterations. METHOD: DNAm levels were measured using the Infinium Methylation EPIC BeadChip in 871 placental samples from the three mother-child cohorts EDEN, PELAGIE and SEPAGES, recruited across four different French cities. Daily exposure levels of each pollutant were estimated based on maternal residential address, using validated spatiotemporally resolved exposure models. We conducted an epigenome-wide association study to identify differentially methylated positions (DMPs) and regions (DMRs). RESULTS: We found 4 CpG sites significantly associated with at least one air pollutant in the whole population after correction for multiple tests and more than 300 sex-specific associations. Top DMPs (p-value0.001) associated with PM exposure during the third trimester of pregnancy were significantly enriched (FDR0.05) in genes related to the calcium signaling pathway in girls and to the development of the hypothalamus in boys. The regional analyses identified 31 DMRs associated with air pollutant exposure in the whole population. Moreover, we detected sex-specific (34 in girls, 35 in boys) and pollutant-specific (5 for NO2, 4 for PM) DMRs. Our results were validated using an independent data set of 668 EDEN participants whose placenta DNAm levels were measured using the Illumina 450K BeadChip. CONCLUSIONS: These findings highlight global and sex-specific modifications of placental DNA methylation patterns associated with prenatal air pollutant levels which could provide clues about the molecular pathways through which air pollution may influence sex-specific response to oxidative stress and brain development.

Background: Combined effect of both prenatal and early postnatal exposure to ambient air pollution on child cognition has rarely been investigated and periods of sensitivity are unknown. This study explores the temporal relationship between pre- and postnatal exposure to PM10, PM2.5, NO2 and child cognitive function. Methods: Using validated spatiotemporally resolved exposure models, pre- and postnatal daily PM2.5, PM10 (satellite based, 1 km resolution) and NO2 (chemistry-transport model, 4 km resolution) concentrations at the mother's residence were estimated for 1271 mother-child pairs from the French EDEN and PELAGIE cohorts. Scores representative of children's General, Verbal and Non-Verbal abilities at 5-6 years were constructed based on subscale scores from the WPPSI-III, WISC-IV or NEPSY-II batteries, using confirmatory factor analysis (CFA). Associations of both prenatal (first 35 gestational weeks) and postnatal (60 months after birth) exposure to air pollutants with child cognition were explored using Distributed Lag Non-linear Models adjusted for confounders. Results: Increased maternal exposure to PM10, PM2.5 and NO2, during sensitive windows comprised between the 15th and the 33rd gestational weeks, was associated with lower males' General and Non-verbal abilities. Higher postnatal exposure to PM2.5 between the 35th and 52nd month of life was associated with lower males' General, Verbal and Non-verbal abilities. Some protective associations were punctually observed for the very first gestational weeks or months of life for both males and females and the different pollutants and cognitive scores. Discussion: These results suggest poorer cognitive function at 5-6 years among males following increased maternal exposure to PM10, PM2.5 and NO2 during mid-pregnancy and child exposure to PM2.5 around 3-4 years. Apparent protective associations observed are unlikely to be causal and might be due to live birth selection bias, chance finding or residual confounding.

BACKGROUND:Ambient temperature, particularly heat, is increasingly acknowledged as a trigger for preterm delivery but study designs have been limited and results mixed. We aimed to comprehensively evaluate the association between ambient temperature throughout pregnancy and preterm delivery.METHODS:We estimated daily temperature throughout pregnancy using a cutting-edge spatiotemporal model for 5347 live singleton births from three prospective cohorts in France, 2002-2018. We performed Cox regression (survival analysis) with distributed lags to evaluate time-varying associations with preterm birth simultaneously controlling for exposure during the first 26 weeks and last 30 days of pregnancy. We examined weekly mean, daytime, night-time and variability of temperature, and heatwaves accounting for adaptation to location and season.RESULTS:Preterm birth risk was higher following cold (5th vs 50th percentile of mean temperature) 7-9 weeks after conception [relative risk (RR): 1.3, 95% CI: 1.0-1.6 for 2°C vs 11.6°C] and 10-4 days before delivery (RR: 1.6, 95% CI: 1.1-2.1 for 1.2°C vs 12.1°C). Night-time heat (95th vs 50th percentile of minimum temperature; 15.7°C vs 7.4°C) increased risk when exposure occurred within 5 weeks of conception (RR: 2.0, 95% CI: 1.05-3.8) or 20-26 weeks after conception (RR: 2.9, 95% CI: 1.2-6.8). Overall and daytime heat (high mean and maximum temperature) showed consistent effects. We found no clear associations with temperature variability or heatwave indicators, suggesting they may be less relevant for preterm birth.CONCLUSIONS:In a temperate climate, night-time heat and chronic and acute cold exposures were associated with increased risk of preterm birth. These results suggest night-time heat as a relevant indicator. In the context of rising temperatures and more frequent weather hazards, these results should inform public health policies to reduce the growing burden of preterm births.

BACKGROUND AND AIM: Despite recognition of climate change, little is known on how ambient temperature may affect fetal development and child respiratory health. This study investigated the effect of prenatal and early postnatal exposure to ambient temperature on newborn lung function in France. METHODS: Prenatal and early postnatal mean temperature and temperature variability at the mother's residence were estimated based on a validated spatiotemporally resolved exposure model in 343 mother–child pairs from the SEPAGES cohort. Newborn lung function was assessed at two months during unsedated sleep with tidal breathing and multiple breath washout test. Associations of ambient temperature with newborns lung function were analyzed using adjusted Distributed Lag Non-linear Models (DLNM) for the whole cohort and then stratified by sex. Both chronic (the first 35 gestational weeks and the 4 weeks after birth) and acute (the 7 days before the respiratory tests) exposures were investigated. RESULTS: Among girls, chronic exposure to severe cold (the 5th percentile vs the median temperature) was robustly related to lower Functional Residual Capacity (FRC), lower tidal volume and higher respiratory rate. Chronic exposure to severe heat (the 95th percentile vs the median temperature) in girls was related to lower FRC and higher respiratory rate. Most of the significant windows of vulnerability to ambient temperature occurred between the second trimester of pregnancy and the first weeks of life. CONCLUSIONS: Prenatal and early postnatal exposure to severe cold or heat may alter lung function among infants, especially in girls. Lung volumes appeared more specifically affected than airflows. Considering children and adults respiratory health are closely linked, long-term consequences may be substantial. KEYWORDS: Ambient temperature; Climate change; DLNM; Infants; Lung function; Prenatal/Postnatal exposure; Restrictive lung disease

Background: Synthetic phenols and phthalates can interfere with biological pathways involved in brain development. Despite the high within-subject temporal variability of urinary concentrations observed for their metabolites, studies investigating effects of phenols and phthalates on child behaviour often relied on a limited number of spot biospecimens to assess exposure. Besides, the majority did not consider mixture effects. Objectives: To study the combined effect of prenatal exposure to synthetic phenols and phthalates on child behaviour using repeated exposure measurements. Methods: We assessed concentrations of 12 phenols, 13 phthalate and 2 non-phthalate plasticizer metabolites in within-subject pools of multiple urine samples (median = 21 samples per individual pool) collected at two distinct time points during pregnancy in 416 mother-child pairs from the French SEPAGES cohort. Child behaviour was evaluated at two years using the Child Behaviour Checklist 1.5-5 (CBCL). Associations between a mixture of biomarkers of exposure and externalizing and internalizing behaviour scores were studied using adjusted Weighted Quantile Sum (WQS) regressions with a repeated holdout validation (100 repetitions). Results: The positive WQS indexes were associated with both the externalizing and internalizing behaviour scores in the whole population, indicating greater risk of behavioural problems. Stratification for child sex suggested stronger associations in girls than boys. On average, girls externalizing and internalizing scores increased by 3.67 points (95% CI: 1.24, 6.10) and 2.47 points (95 %CI: 0.60, 4.33) respectively, for an increase of one tertile in the WQS index, compared with 1.70 points (95 %CI:-0.42, 3.81) and 1.17 points (95 %CI:-0.50, 2.84) in boys. Main contributors for the associations observed in girls were bisphenol A (weight of 18%), triclosan (17%) and monoethyl phthalate (MEP, 15%) for the externalizing score and MEP (19%), mono-benzyl phthalate (MBzP, 19%) and mono-n-butyl phthalate (MnBP, 16%) for the internalizing score. Discussion: Our results suggest adverse associations between in utero exposure to a mixture of phenols and phthalates and child behaviour, mainly in girls. Public health consequences may be substantial due to the widespread exposure of the population to these compounds.