Neurobehavioural and cognitive effects of prenatal exposure to organochlorine compounds in three year old children

Abstract

Background We report data of a Belgian observational prospective cohort study regarding cognitive and behavioural development until the age of 36 months in relation to internal exposure to organochlorine pollutants [sum of polychlorinated biphenyls (sum PCB), dioxin-like activity, PCB118, PCB170, hexachlorobenzene (HCB) and p,p’-dichlorodiphenyldichloroethylene (DDE)] measured in cord blood. Methods Participants were recruited as part of an Flemish Environmental Health Survey (2002–2006). Two hundred and six mother-child pairs were recruited. Hundred twenty five toddlers [Reynell Taal Ontwikkelings Schalen (language development, RTOS), Snijders-Oomen Niet-verbale intelligentietest (non-verbal intelligence, SON), Bayley Scales, milestones, Infant Behaviour Questionnaire (IBQ), gender specific play behaviour, Neurobehavioral Evaluation System (NES)-attentional task] and their mothers [Home Observation Measurement of the Environment (HOME), Wechsler Abbreviated Scale of Intelligence (WASI), State-Trait Anxiety Inventory (STAI), general questionnaires] were tested. Statistical analysis was performed with the SPSS program. Much attention was paid to confounding factors. Results In the first years of development, higher organochlorine pollutants were associated with less active children (delayed crawling: sum PCB*HCB (p < 0.05), sumPCB*DDE (p < 0.1); delayed first steps alone: sum PCB (p < 0.5), PCB118 (p < 0.01), PCB170 (p < 0.01), HCB (p < 0.01); less switching between toys: sum PCB (p < 0.01); less switching between toys in boys: PCB118 (p < 0.01), sum PCB(p < 0.01)). At 12 months children with higher dioxin-like activity tended to show less fear responses(p < 0.1) (IBQ 12 months). At 36 months, a slower development of language comprehension (RTOS) was related to all organochlorine exposure parameters(p < 0.1 or p < 0.05) except DDE. Lower nonverbal IQ scores (SON) were related to PCB118 in boys only(p < 0.05 or p < 0.01). Less masculine and more non-gender specific play behaviour was associated with sum PCB in boys and girls at 36 months(p < 0.1). Moreover, PCB118 (p < 0.05), PCB170 (p < 0.1), HCB(p < 0.05) and DDE(p < 0.05) were associated with diminished masculine play behaviour in boys. Conclusion Our data confirm the observations that neurobehavioral development of young children is adversely influenced by environmental concentrations of PCBs, especially in boys. In this context, observation of play behaviour seems to be a reliable, easy to perform and sensitive test to detect neurotoxic effects of chemicals like PCB’s and dioxin-like compounds in very young children. On the basis of our results, we hypothesize that an underarrousal pattern may play a role in the spectrum of effects measured in toddlers prenatally exposed to PCBs and dioxin-like compounds.

Transgenerational Effects of Prenatal Endocrine Disruption on Reproductive and Sociosexual Behaviors in Sprague Dawley Male and Female Rats

“…All animal protocols were conducted in accordance with NIH and USDA guidelines and were approved by the Institutional Animal Care and Use Committee (IACUC) at The University of Texas at Austin. Sprague Dawley rats were obtained from Harlan Laboratories (Houston, TX, USA), switched to the low-phytoestrogen Harlan-Teklad 2019 Global Diet ad libitum, and housed in same-sex groups (2-3 per cage) under constant humidity and temperature (21)(22) • C) and a partially reversed 12:12 L:D cycle (lights on at 2400 h). Virgin females were impregnated in house.…”

“…Known as the Developmental Origins of Health and Disease or DOHaD [3], this phenomenon has been well studied for a variety of health outcomes in individuals who experienced direct exposure early in life (F1 generation). Regarding neuroendocrine functions and hormonedependent behaviors, the focus of this study, exposures to EDCs including bisphenol A (BPA), phthalates, and persistent organic pollutants such as polychlorinated biphenyls (PCBs) induce adverse phenotypic outcomes in animal studies [4][5][6][7][8][9][10][11][12][13][14][15][16][17], and are associated with increased prevalence of neurobehavioral disorders in epidemiological studies in humans [18][19][20][21][22].…”

Evaluating the association between placenta DNA methylation and cognitive functions in the offspring

“…One of the most heritable behavioural traits is intelligence or cognitive ability (often measured by general psychometric scale indexes or scores), with a heritability that rises from 20% in childhood to 70% in older adulthood [9]. However, previous research has revealed that a child's cognitive capacity is not just in uenced by genetics and that there are a number of other factors associated, such as socioeconomic status [10], the mother's gestational age [11], the mother's intelligence [12], family context [13], and, most importantly for this study, prenatal exposure to detrimental environmental factors such as cigarette smoke, organochlorine pollutants, maternal malnutrition, obesity, or stress, among others [14][15][16][17][18]. Thus, it is thought that placental function, and in particular placenta DNAm, could be a plausible mechanism contributing to this prenatal environmental in uence on cognitive functions later in life.…”

Prenatal Exposure to an EDC Mixture, NeuroMix: Effects on Brain, Behavior, and Stress Responsiveness in Rats

“…Animal models of the “developmental origins of health and disease” (DOHaD) hypothesis show cause-and-effect relationships between early life exposures to individual EDCs and abnormalities in cognitive, affective, and social behaviors later in life [ 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 ]. Epidemiological evidence in humans suggests that those with higher body burdens of EDCs may have a greater propensity for aberrations in these same behaviors [ 10 , 11 , 12 , 13 , 14 ]. Specific to anxiety-like disorders, these relationships have been shown, to date, for bisphenol A (BPA) [ 15 , 16 , 17 , 18 ], phthalates such as DEHP [ 19 , 20 ], and persistent organic pollutants such as polychlorinated biphenyls (PCBs) [ 21 , 22 ] in both rodent and human studies.…”