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Vanadium-induced chemokine mRNA expression and pulmonary inflammation
L M Pierce1, F Alessandrini, J J Godleski
1Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02115, USA.
Toxicology and Applied Pharmacology
|May 1, 1996
Summary
Occupational vanadium exposure causes respiratory inflammation. Soluble vanadium compounds like sodium metavanadate and vanadyl sulfate induce rapid and intense pulmonary inflammation and cytokine mRNA expression in rats.
Area of Science:
- Toxicology
- Environmental Health
- Occupational Medicine
Background:
- Occupational exposure to vanadium is prevalent in industries like petrochemical and mining.
- Vanadium exposure is linked to respiratory tract inflammation and altered pulmonary function.
- The specific mechanisms by which vanadium compounds induce pulmonary inflammation require further investigation.
Purpose of the Study:
- To investigate the ability of different vanadium compounds to induce pulmonary inflammation.
- To examine the effect of vanadium compounds on cytokine mRNA levels in bronchoalveolar lavage (BAL) cells.
- To compare the inflammatory potential of soluble (sodium metavanadate, vanadyl sulfate) and less soluble (vanadium pentoxide) vanadium forms.
Main Methods:
- Rats were intratracheally instilled with sodium metavanadate, vanadyl sulfate, or vanadium pentoxide at various concentrations.
- Pulmonary inflammation was assessed via cytologic analysis of respiratory tract cells from 1 hour to 10 days post-exposure.
- Cytokine mRNA expression (MIP-2, KC) in BAL cells was analyzed using RT-PCR and in situ hybridization.
Main Results:
- All three vanadium compounds induced dose-dependent pulmonary inflammation, characterized by neutrophil influx.
- Vanadyl sulfate induced the greatest neutrophil influx, followed by sodium metavanadate, and then vanadium pentoxide.
- Soluble vanadium compounds (NaVO3, VOSO4) induced inflammation and cytokine mRNA expression more rapidly and intensely than V2O5.
- Rapid induction of MIP-2 and KC mRNA in BAL cells preceded neutrophilia, suggesting their role in initiating inflammation.
- Alveolar macrophages showed the highest expression of KC mRNA.
Conclusions:
- Vanadium compounds, particularly soluble forms, are potent inducers of pulmonary inflammation and cytokine mRNA expression.
- The rapid upregulation of MIP-2 and KC mRNA by BAL cells is a key early event in vanadium-induced lung inflammation.
- These findings highlight the importance of understanding vanadium compound properties in assessing occupational respiratory risks.