ABSTRACT
Early concerns about the possible neurotoxicity of OP insecticides for humans derived from rodent studies showing that prenatal and early postnatal exposures to CPF were associated with neurodevelopmental defi - cits, and these effects have been seen at exposure levels well below the threshold for systemic toxicity caused by cholinesterase inhibition in the brain (e.g., Slotkin and Seidler 2005). Evidence has accumulated over the past decade showing that noncholinergic mechanisms may play a role in the neurotoxic effects of CPF exposure in rodents, involving disruption of neural cell development, neurotransmitter systems (Aldridge et al. 2005; Slotkin 2004), and synaptic formation in different brain regions (Qiao et al. 2003). Such developmental disruptions have been associated with later functional impairments in learning, short-term working memory, and long-term reference memory (Levin et al. 2002).
