These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: The role of inflammatory mediators in the synergistic toxicity of ozone and 1-nitronaphthalene in rat airways.
    Author: Schmelzer KR, Wheelock AM, Dettmer K, Morin D, Hammock BD.
    Journal: Environ Health Perspect; 2006 Sep; 114(9):1354-60. PubMed ID: 16966088.
    Abstract:
    Ambient air is polluted with a mixture of pulmonary toxicants. Previous studies indicate that prior exposure to atmospheric oxidant pollutants such as ozone may significantly alter the response to other pollutants, such as 1-nitronaphthalene (1-NN) . 1-NN, a component of the particulate exhaust from diesel engines, has been found at low concentrations in ambient air. Using a metabolomic approach, we investigated inflammatory responses in arachidonic and linoleic acid biochemical cascades (35 metabolites) and the expression of 19 cytokines/chemokines at three time points (2, 6, and 24 hr) following exposure to 1-NN with and without prior long-term O3 exposure. Long-term O3 exposure is associated with biochemical changes that have been shown to render the lung resistant to further O3 exposure. This study indicates that airways of O3-tolerant rats exhibited a low level of chronic inflammation, rendering the lungs more susceptible to other environmental pollutants such as 1-NN. Specifically, a 12.5-mg/kg dose of 1-NN to O3-tolerant rats produced significantly higher levels of cysteinyl-leukotrienes in bronchiolar lavage fluid even when compared to a 50-mg/kg dose of 1-NN in rats exposed to filtered air. Collectively, these results indicate that the combination of exposures as encountered in polluted ambient air are considerably more injurious to the lung than would be anticipated from previous studies employing single exposures. The observed synergism between O3 and 1-NN may be causally related to a shift in a T-helper 1 to T-helper 2 immune response in the airways.
    [Abstract] [Full Text] [Related] [New Search]