Effects of low-level prenatal exposure to dioxins on cognitive development in Japanese children at 42 months

Ikeno, Taketo; Miyashita, Chihiro; Nakajima, Sachiko; Kobayashi, Sumitaka; Yamazaki, Keiko; Saijo, Yasuaki; Kita, Toshiko; Sasaki, Seiko; Konishi, Kooichi; Kajiwara, Junboku; Hori, Tsuguhide; Kishi, Reiko

doi:10.1016/j.scitotenv.2017.09.267

Cited by 24 publications

(11 citation statements)

References 29 publications

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“…57 In Japanese children at the age of 42 months, higher maternal serum levels of PCBs were found to be positively associated with cognitive development. 52 Sex-specific effects have been reported in the Japanese study. In girls, higher prenatal PCB exposure was associated with higher achievement scores on a cognitive test, whereas in boys higher prenatal PCB exposure was associated with less optimal scores on the mental processing scale of the test (this scale intends to measure total intelligence).…”

Section: Resultsmentioning

confidence: 88%

“…In girls, higher prenatal PCB exposure was associated with higher achievement scores on a cognitive test, whereas in boys higher prenatal PCB exposure was associated with less optimal scores on the mental processing scale of the test (this scale intends to measure total intelligence). 52 The negative effects of prenatal PCB exposure on cognitive development found in the Japanese cohort at the age of 6 months, as described in the beginning of this paragraph, 51 were not observed at the age of 42 months. In 4-year-old children in Greece, higher prenatal PCB exposure was found to be associated with less optimal working memory.…”

Section: Resultsmentioning

confidence: 89%

“…55 In contrast, more optimal performance on cognitive tasks was found after higher prenatal PCB exposure in 1.5-and 3.5-year-old girls (not in boys) in two studies in a Japanese cohort. 51,52 At school age, higher prenatal PCB exposure has not been linked to less optimal performance on cognitive tasks in all four recent published cohort studies assessing cognitive tasks, 54,62,63,65 but a case-control study in the USA found that higher prenatal exposure to PCB-138/158 was associated with an increased risk for intellectual disability. 67 Regarding the effects of prenatal PCB exposure on attention at school age, both positive and negative associations were found with ADHDrelated behavior.…”

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: 88%

Section: Resultsmentioning

confidence: 89%

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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“…This conclusion of no association was confirmed with a larger sample size from the same cohort at 6 and 18 months (Nakajima et al., ). No associations with cognitive development were found at 42 months as well (Ikeno et al., ).…”

Section: Assessmentmentioning

confidence: 99%

Risk for animal and human health related to the presence of dioxins and dioxin‐like PCBs in feed and food

Knutsen¹,

Alexander²,

Barregård³

et al. 2018

EFS2

143

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The European Commission asked EFSA for a scientific opinion on the risks for animal and human health related to the presence of dioxins (PCDD/Fs) and DL‐PCBs in feed and food. The data from experimental animal and epidemiological studies were reviewed and it was decided to base the human risk assessment on effects observed in humans and to use animal data as supportive evidence. The critical effect was on semen quality, following pre‐ and postnatal exposure. The critical study showed a NOAEL of 7.0 pg WHO2005‐TEQ/g fat in blood sampled at age 9 years based on PCDD/F‐TEQs. No association was observed when including DL‐PCB‐TEQs. Using toxicokinetic modelling and taking into account the exposure from breastfeeding and a twofold higher intake during childhood, it was estimated that daily exposure in adolescents and adults should be below 0.25 pg TEQ/kg bw/day. The CONTAM Panel established a TWI of 2 pg TEQ/kg bw/week. With occurrence and consumption data from European countries, the mean and P95 intake of total TEQ by Adolescents, Adults, Elderly and Very Elderly varied between, respectively, 2.1 to 10.5, and 5.3 to 30.4 pg TEQ/kg bw/week, implying a considerable exceedance of the TWI. Toddlers and Other Children showed a higher exposure than older age groups, but this was accounted for when deriving the TWI. Exposure to PCDD/F‐TEQ only was on average 2.4‐ and 2.7‐fold lower for mean and P95 exposure than for total TEQ. PCDD/Fs and DL‐PCBs are transferred to milk and eggs, and accumulate in fatty tissues and liver. Transfer rates and bioconcentration factors were identified for various species. The CONTAM Panel was not able to identify reference values in most farm and companion animals with the exception of NOAELs for mink, chicken and some fish species. The estimated exposure from feed for these species does not imply a risk.

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“…Importantly, NDL PCBs represent a significantly greater percentage of the PCBs detected in human serum, adipose tissue, breast milk, and brain tissue from children diagnosed with a NDD [19,[54][55][56]. Although environmentally relevant exposures to dioxin and DL PCBs are associated with adverse outcomes in several organ systems, especially skin, liver and the immune system [57][58][59], and some are probably carcinogenic [60], there is little data demonstrating that DL PCBs are direct developmental neurotoxicants (but see [29,61,62]). In contrast, human, animal and mechanistic studies confirm the developmental neurotoxicity of legacy NDL PCBs [14,19,21,26,31,[63][64][65][66], and emerging evidence suggests that non-legacy LC-PCBs also pose a risk to the developing brain [67].…”

Section: Introductionmentioning

confidence: 99%

Evidence Implicating Non-Dioxin-Like Congeners as the Key Mediators of Polychlorinated Biphenyl (PCB) Developmental Neurotoxicity

Klocke

Lein

2020

IJMS

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Despite being banned from production for decades, polychlorinated biphenyls (PCBs) continue to pose a significant risk to human health. This is due to not only the continued release of legacy PCBs from PCB-containing equipment and materials manufactured prior to the ban on PCB production, but also the inadvertent production of PCBs as byproducts of contemporary pigment and dye production. Evidence from human and animal studies clearly identifies developmental neurotoxicity as a primary endpoint of concern associated with PCB exposures. However, the relative role(s) of specific PCB congeners in mediating the adverse effects of PCBs on the developing nervous system, and the mechanism(s) by which PCBs disrupt typical neurodevelopment remain outstanding questions. New questions are also emerging regarding the potential developmental neurotoxicity of lower chlorinated PCBs that were not present in the legacy commercial PCB mixtures, but constitute a significant proportion of contemporary human PCB exposures. Here, we review behavioral and mechanistic data obtained from experimental models as well as recent epidemiological studies that suggest the non-dioxin-like (NDL) PCBs are primarily responsible for the developmental neurotoxicity associated with PCBs. We also discuss emerging data demonstrating the potential for non-legacy, lower chlorinated PCBs to cause adverse neurodevelopmental outcomes. Molecular targets, the relevance of PCB interactions with these targets to neurodevelopmental disorders, and critical data gaps are addressed as well.

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Effects of low-level prenatal exposure to dioxins on cognitive development in Japanese children at 42 months

Cited by 24 publications

References 29 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

Risk for animal and human health related to the presence of dioxins and dioxin‐like PCBs in feed and food

Evidence Implicating Non-Dioxin-Like Congeners as the Key Mediators of Polychlorinated Biphenyl (PCB) Developmental Neurotoxicity

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