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

Abstract

The developmental origins of health and disease concept illustrates that exposure in early life to various factors may affect the offspring's long-term susceptibility to disease. during development, the nervous system is sensitive and vulnerable to the environmental insults. Polychlorinated biphenyls (PcBs), which are divided into dioxin-like (dL-PcBs) and non-dioxin-like PcBs (NdL-PcBs), are synthetic persistent environmental endocrine-disrupting chemicals. The toxicological mechanisms of dL-PcBs have been associated with the activation of the aryl hydrocarbon receptor and NdL-PcBs have been associated with ryanodine receptor-mediated calcium ion channels, which affect neuronal migration, promote dendritic growth and alter neuronal connectivity. In addition, PcB accumulation in the placenta destroys the fetal placental unit and affects endocrine function, particularly thyroid hormones and the dopaminergic system, leading to neuroendocrine disorders. However, epidemiological investigations have not achieved a consistent result in different study cohorts. The present review summarizes the epidemiological differences and possible mechanisms of the effects of intrauterine PcB exposure on neurological development.

Iodine Deficiency, Maternal Hypothyroxinemia and Endocrine Disrupters Affecting Fetal Brain Development: A Scoping Review

“…Another mechanism for the decrease in serumT4 concentrations in both adults and neonates may be the ability of PCBs to induce hepatic microsomal enzymes leading to biliary excretion and elimination of the thyroid hormones. Such changes could be particularly adverse during early pregnancy and even have long-term effects on the brain, as demonstrated in Table 2 [ 3 , 153 , 154 , 155 , 156 , 157 , 169 , 170 ].…”

“…From observational studies, there is strong evidence that TDCs are disturbing the thyroid hormone metabolism (s. Table 2 ). This is reported for several classes of TDCs, for mother-child pairs, in case controls, smaller cohorts or larger epidemiological studies [ 6 , 102 , 135 , 136 , 137 , 138 , 139 , 140 , 141 , 142 , 143 , 144 , 145 , 146 , 147 , 148 , 149 , 150 , 151 , 152 , 153 , 154 , 155 , 156 , 157 , 158 , 159 , 160 , 161 , 162 , 163 , 164 , 165 , 166 , 167 , 168 , 169 , 170 , 171 , 172 , 173 , 174 , 175 , 176 , 177 , 178 , 179 , 180 , 18...…”

The Impact of Oxidative Stress of Environmental Origin on the Onset of Placental Diseases

“…While maybe less understood at the molecular level, it is worth mentioning given its historical importance the case of dioxins for which a wide literature exists following the Seveso catastrophe, when in 1976, a chemical plant accidentally released a dioxin derivative, the TCDD (2, 3, 7, 8-tetrachlorodibenzo-p-dioxin), triggering the death of tenths of thousands of farm animals, either by the emanations or by slaughtering, while 193 children suffered from chloracne induced by the chemical. Several papers indicated that dioxin influences the development of the nervous system, as recently reviewed [ 129 ]. As an interface to the fetal organs, the placenta is particularly interesting to understand how fetal organs might be touched by the molecule.…”