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Dear Colleagues,

We live in a world in which we are exposed to man-made chemicals daily. Nearly 1000 of these chemicals are known or suspected to interfere with the endocrine system, such as altered gene expression, which may affect hormone synthesis, hormone receptor binding, which may mimick or block hormonal activity, or hormone conversion. These compounds are therefore referred to as endocrine disrupting chemicals (EDCs). They also may interfere with developmental processes in the embryonic and fetal period. Therefore, the health of all age groups may encounter adverse effects of exposure to EDCs: children, pregnant women, fertile populations, the elderly, the poor, workers, and other vulnerable groups. Some of these chemicals are persistent in our environment, such as dioxins, polychlorinated biphenyls, organochlorine pesticides, while others do have a shorter half life, such as perfluorinated alkyl acids, phthalates, polybrominated diphenyl ethers, and bisphenol. Studies reveal that exposure to EDCs is linked to the development of, e.g., certain cancers, brain development disorders, asthma, allergies, immune deficiencies, obesity, and low sperm count. Thus, exposure to EDCs creats a great concern for public health. However, significant knowledge gaps still exist about the manner in which EDCs accumulate in the human body and the effect (mixtures of) chemicals could have on human health.

We invite investigators to contribute original research papers as well as review articles that will provide new insights into the role of EDCs on the development of disorders/diseases in humans (e.g., endocrine, immune, atopic, metabolic, reproductive, brain). In particular, studies addressing the developmental origins of health and disease (DOHaD) concept are very welcome. In addition, research that aims to clarify the molecular mechanisms of action by specific EDCs on structure and function of organs, as well as studies documenting the interaction between genes and EDCs are desirable. Research presented may cover in vitro, in vivo and human cohort studies with the intention to unravel the role of EDCs on the development of disease. Clinical trials must have been registered with a known database.

Prof. Dr. Margot Van de Bor
Guest Editor

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Keywords

Reproduction
Adverse pregnancy outcome
Developmental Origins of Health and Disease
Genital malformations
Puberty
Thyroid (hormone)
Brain development
Neurobehavioral development
Attention deficit/hyperactivity disorder
Obesity
Type 2 diabetes
Metabolic syndrome
Allergy
Asthma
Immune deficiency
Endocrine related cancers

Published Papers (2 papers)

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Research

281 KiB

Open AccessArticle

First Trimester Phthalate Exposure and Infant Birth Weight in the Infant Development and Environment Study

by Sheela Sathyanarayana, Emily Barrett, Ruby Nguyen, Bruce Redmon, Wren Haaland and Shanna H. Swan

Int. J. Environ. Res. Public Health 2016, 13(10), 945; https://doi.org/10.3390/ijerph13100945 - 23 Sep 2016

Cited by 25 | Viewed by 5550

Abstract

Phthalate exposure is widespread among pregnant women but whether it is related to fetal growth and birth weight remains to be determined. We examined whether first trimester prenatal phthalate exposure was associated with birth weight in a pregnancy cohort study. We recruited first trimester pregnant women from 2010–2012 from four centers and analyzed mother/infant dyads who had complete urinary phthalate and birth record data (N = 753). We conducted multiple linear regression to examine if prenatal log specific gravity adjusted urinary phthalate exposure was related to birthweight in term and preterm (≤37 weeks) infants, stratified by sex. We observed a significant association between mono carboxy-isononyl phthalate (MCOP) exposure and increased birthweight in term males, 0.13 kg (95% CI 0.03, 0.23). In preterm infants, we observed a 0.49 kg (95% CI 0.09, 0.89) increase in birthweight in relation to a one log unit change in the sum of di-ethylhexyl phthalate (DEHP) metabolite concentrations in females (N = 33). In summary, we observed few associations between prenatal phthalate exposure and birthweight. Positive associations may be attributable to unresolved confounding in term infants and limited sample size in preterm infants. Full article

(This article belongs to the Special Issue Early exposure to endocrine disrupting chemicals)

740 KiB

Open AccessArticle

Prenatal Exposure to Perfluoroalkyl Substances and Behavioral Development in Children

by Ilona Quaak, Marijke De Cock, Michiel De Boer, Marja Lamoree, Pim Leonards and Margot Van de Bor

Int. J. Environ. Res. Public Health 2016, 13(5), 511; https://doi.org/10.3390/ijerph13050511 - 19 May 2016

Cited by 55 | Viewed by 6734

Abstract

Background: In recent years, prevalence rates of behavioral disorders in children have increased. One factor possibly implied in the etiology of behavioral disorders is exposure to perfluoroalkyl substances (PFASs). The use of PFASs is highly integrated into everyday life, and exposure is ubiquitous. Exposure to PFASs during early life may be particularly harmful, as it represents a critical time window for brain development. However, research in the area is limited, especially among preschool children. The objective of the current study was to explore the relationship between prenatal exposure to several PFASs and behavioral development at the age of 18 months. Methods: Data from the Dutch cohort LINC (Linking Maternal Nutrition to Child Health) were used. Perfluorooctanesulfonic acid (PFOS) and perfluorooctanoic acid (PFOA) were measured in cord plasma. The total exposure of PFASs was also calculated (ΣPFASs). Behavioral development was assessed with the Child Behavior Checklist 1.5–5 (CBCL 1.5–5). The CBCL scales “Attention Deficit Hyperactivity Disorder” (ADHD) and “Externalizing problems” were used for further analysis. Separate regression models were composed for each combination, in which exposure levels were classified in tertiles. Both whole population and sex-stratified analyses were performed. A family history of ADHD, the educational level, smoking or using alcohol or illicit drugs during pregnancy were considered as confounders. In total, data from 76 mother-child pairs was included. Results: No significant associations were found between prenatal PFAS exposure and ADHD scores in the whole population and in the sex-stratified analyses. With regard to externalizing behavior, a significant negative association was found between the highest levels of ΣPFAS exposure and externalizing problem behavior in the whole population, but only in the crude model. After stratifying for sex, boys in the second and third tertile of exposure to PFOA presented significantly lower scores on the Externalizing Problem Scale than boys with the lowest exposure levels in the adjusted model. Girls exposed to higher levels of ΣPFAS exposure (T2) showed significantly lower scores on the Externalizing Problem Scale, in both crude and adjusted models. No significant associations with PFOS were found. Conclusions: Results from the current study show that prenatal exposure to PFOA was negatively related to externalizing behavior in boys. Results were different for boys and girls, emphasizing that mechanisms at work might be sex-dependent. However, results should be interpreted with caution as the sample size was small. Full article

(This article belongs to the Special Issue Early exposure to endocrine disrupting chemicals)

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