The contribution of the diet to potentially toxic trace element exposure in pregnancy has been rarely addressed. The objective of the present study was to determine the association between the ...maternal diet during pregnancy and biomarkers of exposure for arsenic (As), mercury (Hg) and lead (Pb) at delivery. As was assessed in maternal urine, Hg in maternal hair, and Pb in cord blood, as a proxy for in utero exposure. Based on 2995 women from the ELFE nationwide birth cohort, higher scores for dietary patterns considered healthy were associated with higher concentrations of As and Hg in maternal matrices. Levels of cord blood Pb were inconsistently associated with dietary patterns considered healthy, and lower with a dietary pattern driven by milk and breakfast cereals. Lower levels of Hg were associated with higher Western dietary pattern scores. In conclusion, higher levels of maternal urinary As and hair Hg are associated with diets considered as “Healthy”, while cord blood Pb was not strongly correlated with dietary exposure.
•Arsenic, mercury and lead were measured at birth as a proxy for prenatal exposure.•Levels of arsenic and mercury were positively associated with “healthy” diets.•The association is likely driven by intakes of fish and seafood in healthy diets.•The less toxic species of both elements may be driving the positive association.•Cord blood lead concentrations were not strongly associated with dietary exposure.
Dietary guidelines available to pregnant women are made to improve maternal health and fetal development. But their adequacy to sustain offspring neurodevelopment has remained understudied.
We ...assessed the association between compliance with nutritional guidelines during pregnancy and neurodevelopment in preschool children.
The analyses were based on data for 6780 to 11,278 children from the Étude Longitudinale Française depuis l’Enfance (ELFE) study, a nationwide birth cohort. Maternal diet during the last 3 mo of pregnancy was evaluated at delivery by using a validated 125-item FFQ. From this FFQ, food group consumption, a diet quality score (adapted National Health and Nutrition Program Guideline Score), and a nutrient intake score (Probability of Adequate Nutrient intake based Diet quality index) were calculated and dietary patterns were derived by principal component analysis. Child neurodevelopment was reported by parents at 1 and 3.5 y with the Child Development Inventory (CDI-1, CDI-3.5) and at 2 y with the MacArthur–Bates Communicative Development Inventories (MB-2), and assessed by a trained investigator at 3.5 y with the Picture Similarities test (British Ability Scales, PS-3.5). Associations between maternal diet and child neurodevelopment were assessed by multivariable linear regression models on standardized variables.
Higher nutrient intake score was associated with higher neurodevelopmental scores from 1 to 3.5 y (β = 0.04; 95% CI: 0.02, 0.06 for CDI-1; β = 0.03; 95% CI: 0.01, 0.05 for MB-2; and β = 0.03; 95% CI: 0.01, 0.05 for CDI-3.5). Higher fruit and vegetables or fish intake and lower pork-meat products intake were related to higher CDI-3.5 scores (β = 0.03; 95% CI: 0.01, 0.05 for fruit and vegetables; β = 0.03; 95% CI: 0.01, 0.05 for fish; and β = −0.02; 95% CI: −0.04, 0.00 for pork-meat products). A higher score on the processed food pattern was associated with poorer neurodevelopmental score at 1 y (β = −0.05; 95% CI: −0.06, −0.03).
Higher diet quality during pregnancy was associated with higher parent-reported neurodevelopmental scores in early childhood. The negative association of pork-meat products consumption with early neurodevelopmental scores needs to be further confirmed.
Prenatal acrylamide exposure has been negatively associated with fetal growth but the association with child growth is unknown.
We studied the association between prenatal acrylamide exposure and ...child postnatal growth up to 8 years in the Norwegian Mother and Child Cohort Study (MoBa).
In 51,952 mother-child pairs from MoBa, acrylamide intake during pregnancy was estimated by combining maternal food intake with food concentrations of acrylamide. Mothers reported their child's weight and length/height up to 11 times between 6 weeks and 8 years. Weight and height growth trajectories were modelled using Jenss-Bayley's growth model. Logistic regression models were used to study the association with overweight/obese status at 3, 5 and 8 years, as identified using the International Obesity Task Force cut-offs. Linear mixed-effect models were used to explore associations with overall growth.
At 3 years, the adjusted odds ratios (95% Confidence Intervals (CI)) of being overweight/obese were 1.10 (1.02, 1.20), 1.12 (1.04, 1.22) and 1.21 (1.11, 1.31) by increasing prenatal acrylamide exposure quartile. Similar dose-response associations were found at 5 and 8 years. Acrylamide intake during pregnancy was associated with higher weight growth velocity in childhood. Children exposed at the highest level had 22 g (95% CI: 8, 37), 57 g (95% CI: 32, 81), and 194 g (95% CI: 110, 278) higher weight at 0.5, 2, and 8 years, respectively, compared to their low exposed peers.
Children prenatally exposed to acrylamide in the highest quartile experienced a moderate increase in weight growth velocity during early childhood that resulted in a moderately increased prevalence of overweight/obesity compared to peers in the lowest quartile. Our study is the first to link prenatal acrylamide exposure and postnatal growth.
•Prenatal dietary acrylamide exposure was assessed combining FFQ and contamination data.•Prenatally exposed children were more likely to be overweight or obese.•Prenatally exposed children were more likely to have higher weight growth velocity.•First study on prenatal dietary exposure and postnatal growth that need replication
Telomere length (TL) and mitochondrial function expressed as mitochondrial DNA copy number (mtDNAcn) are biomarkers of aging and oxidative stress and inflammation, respectively. Methylmercury (MeHg), ...a common pollutant in fish, induces oxidative stress. We hypothesized that elevated oxidative stress from exposure to MeHg decreases mtDNAcn and shortens TL.
Study participants are 6–11-year-old children from the HELIX multi-center birth cohort study, comprising six European countries. Prenatal and postnatal total mercury (THg) concentrations were measured in blood samples, TL and mtDNAcn were determined in child DNA. Covariates and confounders were obtained by questionnaires. Robust regression models were run, considering sociodemographic and lifestyle covariates, as well as fish consumption. Sex, ethnicity, and fish consumption interaction models were also run.
We found longer TL with higher pre- and postnatal THg blood concentrations, even at low-level THg exposure according to the RfD proposed by the US EPA. The prenatal association showed a significant linear relationship with a 3.46 % increase in TL for each unit increased THg. The postnatal association followed an inverted U-shaped marginal non-linear relationship with 1.38 % an increase in TL for each unit increased THg until reaching a cut-point at 0.96 μg/L blood THg, from which TL attrition was observed. Higher pre- and postnatal blood THg concentrations were consistently related to longer TL among cohorts and no modification effect of fish consumption nor children's sex was observed. No association between THg exposure and mtDNAcn was found.
We found evidence that THg is associated with TL but the associations seem to be time- and concentration-dependent. Further studies are needed to clarify the mechanism behind the telomere changes of THg and related health effects.
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•Higher mercury concentrations were related to longer telomere length in children.•Mercury exposures were associated with telomere length even at low exposure levels.•Postnatal mercury and telomere length showed a non-linear relationship.•Fish consumption did not affect the association between mercury and telomere length.•No association between mercury exposure and mitochondrial DNA was found.
Pregnant women and their unborn child are exposed to a large number of substances during pregnancy. Some of these substances may cross the placenta, resulting in exposure of the foetus. There is ...growing evidence that certain substances could interact to produce a mixture effect. It is therefore essential to identify the main mixtures mothers are exposed to.
This study aimed to identify the major mixtures French pregnant women included in EDEN and ELFE cohorts were exposed to, on the basis of the 441 substances analysed in the second French total diet study. Exposure systems and the composition of substances were identified from co-exposures using sparse non-negative matrix under-approximation to generate the main mixtures. Individuals were clustered to define clusters with similar co-exposure profiles.
Six clusters associated with eight mixtures were identified. For example in ELFE, cluster 2 comprising 10% of the population was characterised by mixtures “Pest-1” mainly contains pesticides and ”TE-F-PAH″ contains trace elements, furans and polycyclic aromatic hydrocarbons. Five other clusters were also described with their associated mixtures. Similar results were observed for EDEN.
This study helps to prioritise mixtures for which it is crucial to investigate possible toxicological effects and to recommend epidemiological studies concerning health effects.
•Exposures to 200 substances were assessed for French women before and during their pregnancy.•Co-exposure data was reduced into two matrices using SNMU method: exposure systems and individuals' coefficients.•Eight main mixtures were defined from exposure systems and six of them were common.•Six clusters of mothers with similar pattern of contaminant intake were identified.
There is limited epidemiological evidence on the association of prenatal exposure to phthalates and synthetic phenols with altered pubertal timing.
To examine the association of prenatal exposure to ...phthalates, bisphenol A (BPA), parabens, benzophenone 3 (BP-3), and triclosan (TCS) with pubertal development in girls and boys from three European cohorts.
Urinary metabolites of six different phthalate diesters (DEP, DiBP, DnBP, BBzP, DEHP, and DiNP), BPA, methyl- (MePB), ethyl- (EtPB), propyl- (PrPB), and butyl-paraben (BuPB), BP-3, and TCS were quantified in one or two (1st and 3rd trimester) urine samples collected during pregnancy (1999–2008) from mothers in three birth cohorts: INMA (Spain), EDEN (France), and MoBa (Norway). Pubertal development of their children was assessed at a single visit at age 7–12 years (579 girls, 644 boys) using the parent-reported Pubertal Development Scale (PDS). Mixed-effect Poisson and g-computation and Bayesian Kernel Machine Regression (BKMR) were employed to examine associations of individual and combined prenatal chemical exposure, respectively, with the probability of overall pubertal onset, adrenarche, and gonadarche (stage 2+) in girls and boys. Effect modification by child body mass index (BMI) was also assessed.
Maternal concentrations of the molar sum of DEHP and of DiNP metabolites were associated with a slightly higher probability of having started puberty in boys (relative risk, RR 95% CI = 1.13 0.98–1.30 and 1.20 1.06–1.34, respectively, for a two-fold increase in concentrations), with a stronger association for DiNP in boys with overweight or obesity. In contrast, BPA, BuPB, EtPB, and PrPB were associated with a lower probability of pubertal onset, adrenarche, and/or gonadarche in all boys (e.g. overall puberty, BPA: RR 95% CI = 0.93 0.85–1.01 and BuPB: 0.95 0.90–1.00, respectively), and the association with BPA was stronger in boys with underweight/normal weight. In girls, MEHP and BPA were associated with delayed gonadarche in those with underweight/normal weight (RR 95% CI = 0.86 0.77–0.95 and 0.90 0.84–0.97, respectively). Most of these associations were trimester specific. However, the chemical mixture was not associated with any pubertal outcome in boys or girls.
Prenatal exposure to certain phthalates and synthetic phenols such as BPA may impact the pubertal development of boys, and weight status may modify this effect. BPA may also alter the pubertal development of girls.
•Prenatal exposure to DEHP and DiNP was associated with earlier puberty in boys.•Exposure to BPA and parabens was associated with delayed puberty in boys.•Prenatal BPA exposure was also associated with delayed puberty in girls.•The chemical mixture was not associated with pubertal development in boys or girls.
Acrylamide is a contaminant formed in a wide variety of carbohydrate-containing foods during frying or baking at high temperatures. Recent studies have suggested reduced foetal growth after exposure ...to high levels of acrylamide during pregnancy.
To study the relationship between maternal dietary acrylamide intake during pregnancy and their offspring’s anthropometry at birth.
In our population of 1471 mother-child pairs from two French cities, Nancy and Poitiers, dietary acrylamide intake during pregnancy was assessed by combining maternal food frequency questionnaires with data on food contamination at the national level, provided by the second “French Total Diet Study”. Newborns weighing less than the 10th percentile, according to a customised definition, were defined as small for gestational age (SGA). Linear and logistic regression models were used to study continuous and binary outcomes respectively, adjusting for the study centre, maternal age at delivery, height, education, parity, smoking during pregnancy, the newborn’s gestational age at birth and sex.
The median and interquartile range of dietary acrylamide intake were 19.2μg/day (IQR, 11.8;30.3). Each 10μg/day increase in acrylamide intake was associated with an odds-ratio for SGA of 1.11 (95% Confidence Interval: 1.03,1.21), birth length change of −0.05cm (95% CI: −0.11,0.00) and birth weight change of −9.8g (95% CI: −21.3,1.7).
Our results, consistent with both experimental and epidemiological studies, add to the evidence of an effect of acrylamide exposure on the risk of SGA and suggest an effect on foetal growth, for both weight and length.
•Acrylamide arises in carbohydrate-containing foods during cooking at high temperatures.•Food frequency questionnaire and Total Diet Study were linked to estimate exposure.•Dietary acrylamide increased the risk of being small for gestational age (SGA).•Results pointed out to a global effect affecting both birth weight and length.•Animal studies and two epidemiological studies have shown consistent results.
Abstract According to the “environmental obesogen hypothesis”, early-life (including in utero ) exposure to endocrine disrupting chemicals (EDCs) may disturb the mechanisms involved in adipogenesis ...or energy storage, and thus may increase the susceptibility to overweight and obesity. Animal models have shown that exposure to several of these chemicals could induce adipogenesis and mechanisms have been described. Epidemiological studies are crucial to know whether this effect could also be observed in humans. We aimed at summarizing the literature in epidemiology on the relationship between EDCs exposure and child's growth. Overall, epidemiological studies suggest that pre- and/or early postnatal exposure to some EDCs may increase the risk of overweight or obesity during childhood. In that review, we present some limitations of these studies, mainly in exposure assessment, that currently prevent to conclude about causality. Recent advances in epidemiology should bring further knowledge.
Introduction Des études épidémiologiques ont montré qu'une restriction nutritionnelle pendant la grossesse pouvait conduire à une réponse adaptative du fœtus conduisant à une altération durable du ...métabolisme. Ainsi, les enfants nés avec un petit poids de naissance sont plus à risque de développer des maladies cardiovasculaires à l'âge adulte. L'exposition à des contaminants obésogènes pourrait également jouer un rôle dans l'augmentation du risque d'obésité. L’alimentation est une des principales voies d'exposition à ces contaminants. Après une description de la qualité de l’alimentation pendant la grossesse, l’objectif était d'étudier l'association entre l'exposition prénatale aux contaminants alimentaires et la croissance des enfants.MéthodesLes données de trois cohortes de naissance ont été utilisées : deux études françaises (EDEN et ELFE), et une étude norvégienne (MoBa). Les femmes de ces cohortes, ont rempli un questionnaire de fréquence alimentaire (QFA) portant sur l’alimentation pendant la grossesse. L'évaluation des contaminants a été réalisée en combinant le QFA et des bases de données de contamination, la deuxième Etude de l’Alimentation Total (EAT2) française pour EDEN et plusieurs bases de données de contamination pour MoBa. Premièrement dans ELFE, nous avons créé un score de qualité de l'alimentation et un score spécifique à la grossesse, puis nous avons étudié les facteurs associés à une meilleure qualité alimentaire. Ensuite, nous avons examiné l’association entre la qualité de l'alimentation et la croissance prénatale. Deuxièmement, nous avons étudié la relation entre un contaminant alimentaire : l'acrylamide (AA), et la croissance prénatale, dans EDEN, et la croissance postnatale, dans MoBa. Troisièmement, nous avons étendu nos analyses à tous les contaminants alimentaires de l’EAT2, en analysant les composés pris individuellement, puis considérés en mélange.RésultatsPremièrement, nous avons montré que les recommandations générales et spécifiques étaient globalement bien suivies par les femmes enceintes. Certaines caractéristiques socioéconomiques ou démographiques étaient associées à la fois au score de qualité de l’alimentation et au score spécifique de la grossesse telles que l’âge à l’accouchement, niveau d’étude et revenu du foyer et le tabagisme. Un score élevé de qualité de l’alimentation était associé à un poids de naissance plus élevé et un risque plus faible d'avoir un enfant petit pour l’âge gestationnel (PAG).Deuxièmement, nous avons montré que plus l'exposition pendant la grossesse à l’AA est importante, plus la taille de naissance était faible et plus le risque de PAG est élevé. Dans MoBa, nous avons constaté que l'exposition prénatale à l'AA était associée à une prévalence accrue d'enfants en surpoids ou obèses et à une plus grande vitesse de croissance du poids durant l’enfance.Dans EDEN, sur les 99 composés chimiques sélectionnés, le poids de naissance était associé négativement à l’exposition à quatre contaminants alimentaires et positivement à l’exposition à quatre autres. L'IMC à 5 ans était associé négativement à un contaminant. Aucune de ces associations étaient statistiquement significative après prise en compte de la multiplicité des tests. Lorsque les composés chimiques étaient considérés en mélanges, un mélange de contaminants était positivement associé au poids de naissance et aucun mélange n’était associé à l'IMC à 5 ans.ConclusionUne qualité de l’alimentation élevée est associée à un poids de naissance plus élevé et une diminution du risque de PAG, alors que l'exposition alimentaire à l'AA est associée à une altération de la croissance fœtale. L’exposition prénatale aux contaminants alimentaires, évaluée à partir des données d’EAT, ne semble pas préoccupante vis-à-vis de la croissance prénatale et postnatale précoce car les effets retrouvés sont de faible amplitude et ne sont plus significatifs après prise en compte des tests multiples.
Introduction Maternal diet is the only prenatal source of nutrients and the major source for non-nutrients and can influence foetal growth and offspring’s long-term health. Chemicals known as “obesogens” might also play a role in increasing obesity risk and one of the main route of exposure to these chemicals is through foods. After a description of diet quality during pregnancy, the aim of this thesis was to study the association between prenatal exposure to food chemicals and prenatal and postnatal growth among children.MethodsWe used the data of three birth cohort studies: two French studies (EDEN and ELFE), and a Norwegian study (MoBa). We first described the compliance to dietary guidelines of French pregnant women and the impact of a better diet quality on birth outcomes using the data of the ELFE study. Secondly, we studied the relationship of a specific food contaminant, acrylamide, on birth size in the EDEN and postnatal growth in MoBa. Finally, we extended analyses to all available food chemicals in the second French Total Diet Study (TDS).ResultsThe nutritional guidelines for pregnant women were rather well followed in ELFE. The diet quality score was associated with higher birth weight and lower risk of having a small for gestational (SGA) baby. We showed that prenatal dietary exposure to acrylamide was associated with reduced birth size in EDEN, and to increased postnatal growth in MoBA. In EDEN, on the 99 selected food chemicals, birth weight was associated with eight chemicals (four negatively and four positively). BMI at 5 years was associated with one food chemical. These results were not significant after correction for multiple testing. When using the mixture approach, one mixture of chemical was positively associated with postnatal growth.ConclusionsThe diet quality score was associated with higher birth size. Whereas dietary exposure to acrylamide was associated with impaired foetal growth, when looking at a larger number of food chemicals, we did not find concerning association on child prenatal or postnatal growth. Exposure to food chemical assessed by TDS did not appear to be of major concern for growth but other windows of susceptibility, such as early childhood, and other outcomes, such as cognitive development, should be considered in future studies.
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