Developing brain as a target of toxicity.

Abstract

The human brain forms over an unusually long period compared to other organs. While most of the basic structure is laid down before birth, neuron proliferation and migration continue in the postnatal period. The blood-brain barrier is not fully developed until the middle of the first year of life. The number of synaptic connections between neurons reaches a peak around age two and is then trimmed back by about half. Similarly, there is great postnatal activity in the development of receptors and transmitter systems as well as in the production of myelin. Many of the toxic agents known to damage the developing brain interfere with one or more of these developmental processes. Those with antimitotic action, such as X-ray and methyl mercury, have distinctly different effects on structure depending on which neurons are forming at the time of exposure. Vulnerability to agents that interfere with cell production decreases rapidly over the early postnatal period. Other toxic substances, such as psychoactive drugs and agents that alter hormone levels, are especially hazardous during synaptogenesis and the development of transmitter systems, and thus continue to be damaging for years after birth. Still other toxic substances such as lead, seem to have their greatest effects during even later stages of brain development, perhaps by interfering with the trimming back of connections. Guidelines designed to protect human populations from developmental neurotoxicity need to take into account the changing sensitivity of the brain as it passes through different developmental stages, as well as the fundamental differences in the effects of toxicants on the mature and the developing brain. -Environ Health Perspect 1 03(Suppl 6): 73-76 (1995)

Public Health and Economic Consequences of Methyl Mercury Toxicity to the Developing Brain

“…Our analysis also omits the cost of the cardiovascular impacts of mercury exposure (Grandjean et al 2004) or the costs of mercury exposure to children in the first 2 years of postnatal life, when myelination is still continuing and the blood–brain barrier remains vulnerable to penetration by methyl mercury (Rodier 1995). We chose not to include these aspects of methyl mercury toxicity in our range of estimates at this time because there do not exist sufficient quantitative data to permit construction of a reliable model.…”

“…The vulnerability of the developing brain to methyl mercury reflects the ability of lipophilic methyl mercury to cross the placenta and concentrate in the central nervous system (Campbell et al 1992). Moreover, the blood–brain barrier is not fully developed until after the first year of life, and methyl mercury can cross this incomplete barrier (Rodier 1995). …”

Anthropogenic flank attack on polar bears: interacting consequences of climate warming and pollutant exposure

“…The relative high concentrations of several POPs reported in polar bear brains may cause adverse effects, with a possible heightened susceptibility during the more sensitive fetal and neonatal stages of brain development (Rodier, 1995;Grandjean and Landrigan, 2006). Similarly to humans, this could alter behavioral traits and reduce cognitive abilities related to memory and learning in offspring.…”

Dioxin exposure in breast milk and infant neurodevelopment in Vietnam

“…Brain development during the fetal and infant periods is highly sensitive to environmental neurotoxicants, often at levels far below those that are known to harm adults 1 2. Polychlorinated biphenyls (PCBs) and dioxins including polychlorinated dibenzo-p-dioxins/furans (PCDDs/Fs) are of particular concern due to their adverse impact on infant neurodevelopment.…”