CONICET | Buscador de Institutos y Recursos Humanos

Elevated lead (Pb) exposure and high stress both target low socio-economic status populations. Both also act onthe hypothalamic?pituitary?adrenal (HPA) axis. Pb disrupts cognition through effects on the mesocorticolimbic dopaminepathway. Stress hormones act on this same pathway via the HPA axis. The fact that Pb and stress are likely interactive riskfactors served as the rationale for a series of studies in our laboratory. These demonstrate that stress can modify Pb effects,that Pb can modify stress responsivity, and, notably, that Pb + stress effects can occur in the absence of an effect of eitheralone in rats. Furthermore, maternal only Pb exposure can permanently alter basal corticosterone levels, stress responsivity(i.e. permanent modification of HPA axis function) and brain catecholamines in offspring of both genders. Interactiveeffects of Pb + stress are not limited to early development: even Pb exposures initiated post-weaning alter basal corticosteroneand stress responsivity. Outcomes differ in relation to gender, brain region, stressor and time of measurement, makingPb + stress interactions complex. Altered HPA axis function may serve as a mechanism for the behavioural and catecholaminergicneurotoxicity associated with Pb, as well as for the increased incidence of disease and dysfunctions associatedwith low socio-economic status. The permanent consequences of maternal only Pb exposure suggest that Pb screeningprogrammes should include pregnant women at risk for elevated Pb exposure, and that stress should be considered as anadditional risk factor. Pb + stress effects observed in the absence of either risk factor alone raise questions about the capacityof current hazard identification approaches to adequately identify human health risks posed by neurotoxicants.

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