PCB-related neurodevelopmental deficit may be transient: follow-up of a cohort at 6 years of age

Developmental aspects of environmental neurotoxicology: Lessons from lead and polychlorinated biphenyls

“…This might reflect the extended effect of the quality of the child's environment or could also be due to an age-related increase of the precision of developmental testing. In contrast to the K-ABC at 42 months no PCB-related K-ABCdeficit was found upon follow-up at 72 months any more, which is suggestive of PCB-related developmental delay rather than deficit [30]. This is at variance with observations in 11-year-old children of the Michigan cohort [31] and with recently reported loss of IQ in 9-year-old children relative to prenatal PCB exposure in the Oswego cohort [32], but corresponds to those of the full Rotterdam cohort at school age [33].…”

Risk assessments of polychlorinated dibenzo‐ p‐dioxins, polychlorinated dibenzofurans, and dioxin‐like polychlorinated biphenyls in food

“…Transient differences in these parameters were reported when a high exposure group was compared with the low exposure group (below 63 ng total TEQ/kg fat in human milk). The observed differences were subtle, within the normal range and considered to be without clinical relevance [1].In another European study involving also a German cohort, PCB-related delay of mental development was found at 30 months, but upon reassessment between 72 and 77 months developmental delay was no longer observed [34].…”

Prenatal dioxin exposure and neurocognitive development in Hong Kong 11-year-old children

“…Second, it is still unclear whether PCB-related neurocognitive deficits, if any, observed in infancy persist or diminish in childhood. While poorer intellectual function and attention by prenatal PCB exposure was still detected at 9-11 years in the Dutch (Vreugdenhil et al, 2004b;Vreugdenhil et al, 2004a), Michigan and Oswego cohorts (Jacobson and Jacobson, 1996;Stewart et al, 2008), prenatal PCB exposurerelated deficits in neurocognitive function observed in infancy were no longer detected at older ages in the German Dusseldorf (Winneke et al, 2005) and North Carolina (Gladen and Rogan, 1991) cohorts. Third, although earlier studies concluded that the observed adverse effects of dioxins, including delays in psychomotor development (Koopman-Esseboom et al, 1996), neurodevelopment (Huisman et al, 1995) and intellectual function (Jacobson and Jacobson, 1996) have been associated with prenatal, rather than lactational, dioxin and/or dioxin-like PCB exposure, it is still inconclusive as to whether children who are breastfed longer are protected from the adverse neurocognitive consequence of prenatal dioxin exposure (Patandin et al, 1999;Jacobson and Jacobson 2002).…”

“…First the North Carolina (Gladen and Rogan, 1991) and the German Dusseldorf cohorts (Winneke et al, 2005) observed diminishing effects of PCBs on neurodevelopment from infancy to childhood, such that associations of prenatal PCB exposure with markers of neurocognitive function were no longer observed in older children being followed-up at 3-5 years and Adjusted for child's sex, mother's place of birth, mother's age at delivery, mother's habitual seafood consumption, parents' education, household income and children's age at assessments. a Comparing to children with maternal CALUX-TEQ of 1st to 3rd quartiles.…”