You are here:
Differential pulmonary and cardiac effects of pulmonary exposure to a panel of PM-associated metals
Citation:
WALLENBORN, G., M. SCHLADWEILER, J. E. RICHARDS, AND U. P. KODAVANTI. Differential pulmonary and cardiac effects of pulmonary exposure to a panel of PM-associated metals. TOXICOLOGY AND APPLIED PHARMACOLOGY. Academic Press Incorporated, Orlando, FL, 241(1):71-80, (2009).
Impact/Purpose:
This manuscript provides evidance or comparative pulmonary and cardiac toxiccity of soluable metals adn are associated with particulate matter. the data show that nickle and zinc are the most cardiotoxic metals and produce systemic response in the liver.
Description:
Biological mechanisms underlying the epidemiological association between exposure to particulate matter (PM) and increased risk of cardiovascular health effects are under investigation. Water soluble metals reaching systemic circulation following pulmonary exposure are likely exerting a direct effect. However, it is unclear whether specific PM-associated metals may be driving this. We hypothesized that exposure to equimolar amounts of five individual PM-associated metals would cause differential pulmonary and cardiac effects. To test this, we exposed male WKY rats (14 wks old) via a single intratracheal instillation (IT) to saline or 1 umol/kg body weight of zinc, nickel, vanadium, copper or iron in sulfate form. Responses were analyzed 4, 24, 48 or 96 h after exposure. Pulmonary effects were assessed by increases in bronchoalveolar lavage fluid levels of total cells, macrophages, neutrophils, protein, albumin, and activities of lactate dehydrogenase, y-glutamyl transferase, and n-acetyl glucosaminidase. Copper induced earlier effects while zinc and nickel produced later effects. Vanadium or iron exposure induced minimal pulmonary injury/inflammation. Zinc, nickel or copper induced increases in serum cholesterol, red blood cells and white blood cells at different time points. IT ofnickel andcopperinducedincreasesinexpression ofmetallothionein-I (MT-I)inthelung. Zinc, nickel, vanadium and iron exposure induced increases in hepatic MT-I expression. No significant changes in zinc transporter-I (ZnT-I) expression were noted in the lung or liver; however zinc IT caused an increase in cardiac ZnT-I at 24 h, indicating a possible zinc specific cardiac effect. Nickel exposure induced an increase in cardiac ferritin 96 h post IT. This data set demonstrating metal-specific cardiotoxicity is important for the practice of source apportionment, to eventually link certain PM sources with adverse health effects. Disclaimer: The research described in this article has been reviewed by the National Health and Environmental Effects Research Laboratory, US Environmental Protection Agency and NIEHS, and approved for publication. Approval does not signify that the contents necessarily reflect the views and the policies of the agencies nor does mention of trade names or commercial products \ constitute endorsement or recommendation for use. Disclaimer: The research described in this article has been reviewed by the National Health and Environmental Effects Research Laboratory, US Environmental Protection Agency and NIEHS, and approved for publication. Approval does not signify that the contents necessarily reflect the views and the policies of the agencies nor does mention of trade names or commercial products \ constitute endorsement or recommendation for use.
