Skip directly to search Skip directly to A to Z list Skip directly to page options Skip directly to site content

NIOSHTIC-2 Publications Search

Search Results

Differential ability of transitional metals to induce pulmonary inflammation.

Authors
Rice-TM; Clarke-RW; Hauser-R; Antonini-JM; Godleski-JJ; Paulauskis-JD
Source
Toxicologist 2000 Mar; 54(1):36
NIOSHTIC No.
20021053
Abstract
Transition metals are components of airborne particles and have been implicated in adverse health effects. Relative toxicity and inflammatory potential of these metals are usually inferred from separate studies since little directly comparable data are available. The objective of this study was to compare the pulmonary effects of intratracheally-instilled, equimolar. soluble forms of six metal sulfates. Rats received either phosphate-buffered saline. 0.1 umol/kg, or 1.0 umol/kg of vanadium. nickel, iron (II), copper, manganese, or zinc. Bronchoalveolar lavage was performed at 0, 4, 16, or 48 hrs post-installation. At the 0.1 umol/kg dose, only Cu induced significant neutrophil influx at 16 and 48 hrs (p<0.05). For the 1.0 umol/kg dose at 4 hrs, Cu and Fe(II)-exposed animals had a significant increase in percent neutrophils compared to saline controls, and Cu had a significantly higher percentage than all other metals. After 16 hrs, each metal tested induced significant neutrophilia compared to controls, and Cu and Mn induced significantly higher neutrophilia than the other metals. At 48 hrs, neutrophilia was still increased in all metal exposures except Fe(II). Interestingly, Mn was the only metal to induce a significant increase in eosinophils (16 hr post-instillation, p<0.05). Additionally, Cu and Ni-exposed rats had significantly higher levels of lactate dehydrogenase in lavage supernatant compared to the other metals and controls. These results indicate that transition metals differ in their ability to induce pulmonary inflammation and toxicity. Cu appears to be the most pro-inflammatory metal, followed by Mn and Ni, while V, Fe(II), and Zn induced similar levels of neutrophilia. We conclude that the extent and cellular nature of metal-induced pulmonary inflammation depends on the individual metal.
Keywords
Metals; Pulmonary-system-disorders; Respiratory-system-disorders; Airborne-particles; Health-hazards; Toxic-effects; Laboratory-animals; Animals; Animal-studies; Exposure-levels; Metal-compounds
CAS No.
7440-62-2; 7440-02-0; 7439-89-6; 7440-50-8; 7439-96-5; 7440-66-6
Publication Date
20000301
Document Type
Abstract
Fiscal Year
2000
NTIS Accession No.
NTIS Price
Issue of Publication
1
ISSN
1096-6080
NIOSH Division
HELD
Source Name
The Toxicologist. Society of Toxicology 39th Annual Meeting, March 19-23, 2000, Philadelphia, Pennsylvania
State
WV; MA
TOP