Altered fine motor function at school age in Inuit children exposed to PCBs, methylmercury, and lead

Boucher, Olivier; Muckle, Gina; Ayotte, Pierre; Dewailly, Éric; Jacobson, Sandra W.; Jacobson, Joseph L.

doi:10.1016/j.envint.2016.08.010

Cited by 41 publications

(14 citation statements)

References 67 publications

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“…53,64 The motor development of children at school age and adolescence was not found to be negatively associated with prenatal PCB exposure in all three recent published studies investigating motor development. 54,60,66 Regarding behavioral problems at school age, both recent published cohort studies reporting on behavioral problems did not find significant associations with prenatal PCB exposure, 61,62 but a case-control study in the USA found that higher prenatal PCB exposure was associated with an increased risk for autism spectrum disorder. 67 Main findings Dutch cohort-Prenatal exposure to (OH-)PCBs and neurodevelopment…”

Section: Resultsmentioning

confidence: 97%

“…65 In the latter mentioned study group, cord PCB-153 levels were non-significantly negatively associated with performances on a fine motor task. 66 A population-based case-control study in the USA including 1144 children studied whether higher prenatal exposure to PCBs was associated with an increased risk for autism spectrum disorder (ASD) or intellectual disability. 67 They found that higher maternal serum levels of PCBs, particularly PCBs 138/158 and PCB-153 were found to be associated with an increased risk of autism spectrum disorder, and that higher PCB 138/158 was also found to be associated with an increased risk for intellectual disability.…”

Section: Resultsmentioning

confidence: 99%

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Prenatal exposure to PCBs and neurological and sexual/pubertal development from birth to adolescence

Berghuis

Roze

2019

Current Problems in Pediatric and Adolescent Health Care

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Several chemical compounds are resistant to degradation and end up in the food chain. One group of these chemicals is polychlorinated biphenyls (PCBs) which are used as flame retardants and plasticizers. Although PCBs were banned several decades ago, PCBs are still found in environmental media, including in the body of humans. PCBs are transferred from mother to fetus via the placenta during pregnancy. Considering that the prenatal period is a sensitive period during which essential developmental processes take place, exposure to environmental chemicals might have considerable and permanent consequences for outcomes in later life. The aim of this review is to provide an update on the latest insights on the effects of prenatal exposure to PCBs on neurological, sexual and pubertal development in children. We give an overview of recent literature, and discuss it in the light of the findings in a unique Dutch birth cohort, with data on both neurological and pubertal development into adolescence. The findings in the studies included in this review, together with the findings in the Dutch cohort, demonstrate that prenatal exposure to PCBs can interfere with normal child development, not only during the perinatal period, but up to and including adolescence. Higher prenatal exposure to PCBs was found to be both negatively and positively associated with neurodevelopmental outcomes. Regarding pubertal development, higher prenatal PCB exposure was found to be associated with more advanced pubertal development, also in the Dutch cohort, whereas other studies also found delayed pubertal development. These findings raise concern regarding the effects of man-made chemical compounds on child development. They further contribute to the awareness of how environmental chemical compounds can interfere with child development and negatively influence healthy ageing.

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Section: Resultsmentioning

confidence: 97%

Section: Resultsmentioning

confidence: 99%

Prenatal exposure to PCBs and neurological and sexual/pubertal development from birth to adolescence

Berghuis

Roze

2019

Current Problems in Pediatric and Adolescent Health Care

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“…Significant association of neurodevelopmental delays with cord-blood-Hg was seen in few studies (Yorifuji et al 2011;Boucher et al 2012aBoucher et al , 2016Tratnik et al 2017). Prenatal exposure showed distinct domain-specific adverse effects for PCBs (impaired visual recognition memory), Hg (work memory), and Pb (slower speed of information processing) measured by the Fagan Test of Infant Intelligence and the A-not-B tests (Boucher et al 2014).…”

Section: Hg and Other Neurotoxicants: Additive Effect?-as Reviewed Inmentioning

confidence: 99%

“…Prenatal exposure showed distinct domain-specific adverse effects for PCBs (impaired visual recognition memory), Hg (work memory), and Pb (slower speed of information processing) measured by the Fagan Test of Infant Intelligence and the A-not-B tests (Boucher et al 2014). Altered fine-motor function in school children that were prenatally exposed to these neurotoxicants in traditional diets showed distinct neurological outcomes: higher current PCB levels were associated with poor Santa Ana Form Board and Finger Tapping performances; higher current Hg levels were independently associated with poor Finger Tapping (Boucher et al 2016). Recently, Kalia et al (2017) reported a beneficial effect on Gesell Development Scores in Chinese children by reducing Policycle Aromatic Hydrocarbon exposure but no significant association with Hg.…”

Section: Hg and Other Neurotoxicants: Additive Effect?-as Reviewed Inmentioning

confidence: 99%

Neurodevelopmental Effects of Mercury

Oliveira

Nogara

Ardisson-Araújo

et al. 2018

Advances in Neurotoxicology

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The toxicology of mercury (Hg) is of concern since this metal is ubiquitously distributed in the environment, and living organisms are routinely exposed to Hg at low to high levels. The toxic effects of Hg are well studied and it is known that they may differ depending on the Hg chemical species. In this chapter, we emphasize the neurotoxic effects of Hg during brain development. The immature brain is more susceptible to Hg exposure, since all the Hg chemical forms, not only the organic ones, can harm it. The possible consequences of Hg exposure during the early stages of development, the additive effects with other co-occurring neurotoxicants, and the known mechanisms of action and targets will be addressed in this chapter.

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“…Stewart et al (2000), Vreugdenhil et al (2002), and Boucher et al (2016) all reported motor deficits in children exposed to PCBs. In the most recent study, mean levels of PCBs in cord blood ranged were 22.4 μg/kg fat for PCB 118, 50.2 μg/kg fat for PCB 180, 81.6 μg/kg fat for PCB 138, and 124.3 μg/kg fat for PCB 153 (Boucher et al 2016) with levels up to 50% lower when the children were retested at 11 years of age. All four congeners were associated with decreased fine motor skills, and the strongest association was with blood levels at age 11.…”

Section: Introductionmentioning

confidence: 98%

Genetic differences in the aryl hydrocarbon receptor and CYP1A2 affect sensitivity to developmental polychlorinated biphenyl exposure in mice: relevance to studies of human neurological disorders

et al. 2017

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Polychlorinated biphenyls (PCBs) are persistent organic pollutants that remain a human health concern with newly discovered sources of contamination and ongoing bioaccumulation and biomagnification. Children exposed during early brain development are at highest risk of neurological deficits, but highly exposed adults reportedly have an increased risk of Parkinson's disease. Our previous studies found allelic differences in the aryl hydrocarbon receptor and cytochrome P450 1A2 (CYP1A2) affect sensitivity to developmental PCB exposure, resulting in cognitive deficits and motor dysfunction. High-affinity Ahr Cyp1a2(-/-) mice were most sensitive compared with poor-affinity Ahr Cyp1a2(-/-) and wild-type Ahr Cyp1a2(+/+) mice. Our follow-up studies assessed biochemical, histological, and gene expression changes to identify the brain regions and pathways affected. We also measured PCB and metabolite levels in tissues to determine if genotype altered toxicokinetics. We found evidence of AHR-mediated toxicity with reduced thymus and spleen weights and significantly reduced thyroxine at P14 in PCB-exposed pups. In the brain, the greatest changes were seen in the cerebellum where a foliation defect was over-represented in Cyp1a2(-/-) mice. In contrast, we found no difference in tyrosine hydroxylase immunostaining in the striatum. Gene expression patterns varied across the three genotypes, but there was clear evidence of AHR activation. Distribution of parent PCB congeners also varied by genotype with strikingly high levels of PCB 77 in poor-affinity Ahr Cyp1a2(-/-) while Ahr Cyp1a2(+/+) mice effectively sequestered coplanar PCBs in the liver. Together, our data suggest that the AHR pathway plays a role in developmental PCB neurotoxicity, but we found little evidence that developmental exposure is a risk factor for Parkinson's disease.

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Altered fine motor function at school age in Inuit children exposed to PCBs, methylmercury, and lead

Cited by 41 publications

References 67 publications

Prenatal exposure to PCBs and neurological and sexual/pubertal development from birth to adolescence

Prenatal exposure to PCBs and neurological and sexual/pubertal development from birth to adolescence

Neurodevelopmental Effects of Mercury

Genetic differences in the aryl hydrocarbon receptor and CYP1A2 affect sensitivity to developmental polychlorinated biphenyl exposure in mice: relevance to studies of human neurological disorders

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