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Neurotoxicity of diesel exhaust.

Exposure to air pollution as been linked to alterations in the central nervous system, but the mechanism for these effects is poorly understood. Levesque et al. (p. 1149) examined the association between exposure to diesel exhaust (DE) and brain region--specific changes in microglia activation, neuroinflammation, and dopaminergic (DA) systems in vivo and in vitro. They report that DE caused oxidative stress, activated microglia in vivo, and up-regulated pattern recognition receptors, neurotoxic cytokines, and chemokines in the rat brain, particularly in the midbrain. Intratracheal administration of DE resulted in elevated serum and brain tumor necrosis factor-OC, suggesting a key role for systemic inflammation. Mechanistic studies suggested that DE interacts with ongoing inflammation to amplify the proinflammatory response, which may be neurotoxic. No significant loss of DA neurons was detected in vivo, but results suggest that fractalkine, which was elevated after DE exposure in vivo, may be responsible for adaptation by inhibiting DE-induced DA neurotoxicity, at least temporarily. Together, these findings reveal complex, interacting mechanisms that may be responsible for the association of air pollution with neuroinflammation and toxicity to DA systems.
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Title Annotation:Research
Publication:Environmental Health Perspectives
Article Type:Brief article
Geographic Code:1USA
Date:Aug 1, 2011
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