Thyroid and growth hormone concentrations in 8-year-old children exposed <i>in utero</i> to dioxins and polychlorinated biphenyls

Abstract

-The objective of this study was to examine the effects of in utero exposure to polychlorinated biphenyls (PCBs) and dioxins (polychlorinated dibenzo-p-dioxins, dibenzofurans (PCDD/F) on thyroid and growth hormone concentrations and growth in 8-year-old children. A total of 56 children (23 boys, 33 girls) were included in the study. All were stratified into high and low PCDD/F + PCB exposure groups based on maternal median indicator PCB and PCDD/F + PCB concentrations during pregnancy. Height, weight, body mass index, and thyroid and growth hormone concentrations were assessed and compared among the different exposure groups. There were no significant effects of indicator PCB or PCDD/F + PCB exposure levels on growth (height, weight, and bone age) among 8-year-old boys or girls. Boys exposed to high PCDD/F + PCB levels had significantly higher thyroxine-binding globulin (TBG) concentrations than boys exposed to low levels (P = 0.027). Girls exposed to high PCB levels had significantly lower IGF-binding protein-3 (IGFBP-3) concentrations than girls exposed to low levels (P = 0.038). Low levels of in utero exposure to PCDD/F+PCB and high indicator PCB levels were significantly associated with reduced serum concentrations of IGFBP-3. High levels of in utero exposure to PCDD/F+PCB plus either high or low indicator PCB levels were significantly associated with increased serum concentrations of growth hormone, T3, T4, and TBG. These findings suggest that the level of in utero exposure to PCBs and dioxins may affect serum concentrations of growth hormone, thyroid hormones, TBG, and IGFBP-3 in 8-year-old children.

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

“…Su et al. () compared levels of thyroid hormones (TSH, T4, free T4, T3) in 56 eight‐year old children with PCDD/F‐PCB‐TEQs above or below the median, which was 14.8 pg/g fat. No adjustment for potential confounders was applied and no significant differences were found.…”

Associations of peri-pubertal serum dioxins and polychlorinated biphenyls with growth and body composition among Russian boys in a longitudinal cohort

“…The majority of longitudinal studies have not observed associations between prenatal nor lactational NDL-PCB concentrations and childhood BMI or other measures of adiposity (Criswell et al 2017;Dallaire et al 2014;de Cock et al 2014;Hertz-Picciotto et al 2005;Jackson et al 2010;Karlsen et al 2017;Lauritzen et al 2018;Mendez et al 2011;Pan et al 2010;Patandin et al 1998;Su et al 2015;Vafeiadi et al 2015;Valvi et al 2014). Prenatal NDL-PCBs, however, were associated with higher BMI among both boys and girls in Belgium (Verhulst et al 2009) and Spain (Agay-Shay et al 2015;Valvi et al 2012) at ages 3 and 6.5-7 years, respectively, although the association was attenuated in the Belgian study by age 7-9 years (Delvaux et al 2014).…”

Perspective on prenatal polychlorinated biphenyl exposure and the development of the progeny nervous system (Review)

“…In early pregnancy, the fetal thyroid hormone is completely dependent on transport from the mother prior to fetal self-synthesis (113). An increasing number of epidemiological studies have confirmed that gestational PcB exposure was associated with disturbances in the thyroid function of neonates (114)(115)(116). This destruction has long-lasting effects in the offspring, potentially lasting until the child is 8 years old (116).…”

“…An increasing number of epidemiological studies have confirmed that gestational PcB exposure was associated with disturbances in the thyroid function of neonates (114)(115)(116). This destruction has long-lasting effects in the offspring, potentially lasting until the child is 8 years old (116). The effects of PcBs and OH-PcBs on thyroid function may involve the following mechanisms: i) PcBs may competitively bind to transthyretin, particularly OH-PcBs, which have stronger binding affinity compared with that in their parent compounds; ii) PcBs may interact with thyroxine receptors or suppress dNA transcription and iii) OH-PcBs inhibit thyroid hormone sulfation, affecting the peripheral metabolism of thyroid hormones (114,117).…”