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PARTICULATE MATTER, OXIDATIVE STRESS AND NEUROTOXICITY
Citation:
VERONESI, B. PARTICULATE MATTER, OXIDATIVE STRESS AND NEUROTOXICITY. NEUROTOXICOLOGY. Intox Press, Inc, Little Rock, AR, 29(3):479-488, (2008).
Impact/Purpose:
Particulates are covered with biocontaminants (e.g., endotoxins, mold, pollen) which convey free radical activity that can damage the lipids, nucleic acids, and proteins of target cells on contact and stimulate inflammatory cytokine release. Although, the historical focus of PM toxicity has been cardiopulmonary targets, it is now appreciated that inhaled nano-size (<100 nm) particles quickly exit the lungs and enter the circulation where they distribute to various organ systems (l.e., liver, kidneys, testes, lymph nodes) (Takenaka et aI., 2001; Kreyling et aI., 2002; Oberdorster et aI., 2004). They damage these secondary targets though oxidative stress pathways (Samet et aI., 2004; Cordier etaI., 2004).
Description:
Particulate matter (PM), a component of air pollution has been epidemiologically associated with sudden deaths, cardiovascular and respiratory illnesses. The effects are more pronounced in patients with pre-existing conditions such as asthma, diabetes or obstructive pulmonary disorders. Clinical and experimental studies have historically focused on the cardiopulmonary effects of PM. However, since PM particles carry numerous biocontaminants that are capable of triggering free radical production and cytokine release, the possibility that PM may affect organs systems sensitive to oxidative stress must be considered. Four independent studies that summarize the neurochemical and neuropathological changes found in the brains of PM exposed animals are described here. These were recently presented at two 2007 symposia sponsored by the Society of Toxicology (Charlotte, NC) and the International Neurotoxicology Association (Monterey, CA).