Neurotoxicity of prenatal carbon monoxide exposure

Despite the very wide recognition that carbon monoxide (CO) is a significant neurotoxicant, the level at which subtle effects occur, and the existence of sensitive periods in development for such toxicity, has been undetermined. In terms of risk to the fetus, a potentially susceptible sub-population, there is concern, first, that the level of exposure at which neurotoxicity occurs may be different from the adult, and second, that the site of toxic action and subsequent neurotoxic effects of CO may be different in the immature and mature brain. The investigator studied the susceptibility of the developing brain to moderate levels of CO maintained chronically through the period of neuronal proliferation, and into the period of synapse formation. Carbon monoxide may be thought of as both a prototypical hypoxic agent, and a significant public health hazard in its own right. Carbon monoxide is a ubiquitous toxic agent that accounts for large numbers of deaths and significant morbidity in human populations. Subtle neurotoxic effects of this agent may be even more common, but they may go largely undetected, or fail to be associated with CO exposure. We have shown that prenatal CO exposure at moderate levels can produce significant neurotoxic effects in rats. The data obtained from the cerebellum and neostriatum, in particular, suggest that chronic, moderate perinatal CO exposure may disrupt neuronal proliferation and, perhaps, may disrupt certain markers for neurochemical transmission.