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Comparison of inducible nitric oxide synthase gene expression and lung inflammation following intratracheal instillation of silica, coal, carbonyl iron, or titanium dioxide in rats.

Authors
Blackford-JA; Jones-W; Dey-RD; Castranova-V
Source
J Toxicol Environ Health, A 1997 Jun; 51(3):203-218
NIOSHTIC No.
20033963
Abstract
The pulmonary toxicity of the respirable dusts silica, coal, carbonyl iron, and titanium dioxide on alveolar macrophage (AM) and neutrophil (PMN) inducible nitric oxide syn thase (iNOS) gene expression and nitric oxide (NO) production was investigated. Rats were intratracheal instilled with 5 mg/100 g body weight of silica, coal, carbonyl iron, or titanium dioxide. The dust particles averaged less than 5 pm in diameter. Bronchoalveolar lavage was performed 24 h later. Bronchoalveolar lavage cell (BALC) differentials, iNOS gene expression and NO production by BALC (measured indirectly as NO-dependent chemiluminescence), and lavageable lung protein levels were measured. Analyzed on an equal mass basis, silica, coal, and titanium dioxide dusts increased the production of iNOS-dependent NO by AM. Silica and titanium dioxide both increased the levels of iNOS mRNA while carbonyl iron and coal did not. Each dust caused an increase in PMN, indicating an inflammatory response. Carbonyl iron and titanium dioxide decreased the numbers of AM. Levels of acellular lavageable lung protein were increased by silica, car bonyl iron, and titanium dioxide. When exposure was normalized for an equal number of particles, the pneumotoxic dusts, silica and coal, caused more inflammation and NO pro duction than the nuisance dusts, carbonyl iron and titanium dioxide. Therefore, it appears that particle number is a more appropriate metric of exposure than mass when comparing the relative pathogenicity of dusts of different sizes. Furthermore, since the potency of these dusts (on a particle number basis) to increase iNOS gene expression reflects their inflammatory and pathogenic potential, it is proposed that NO may contribute to the early inflammatory damage observed in the lung following dust exposure.
Keywords
Genotoxic-effects; Genetic-factors; Heavy-metals; Metallic-dusts; Metallic-compounds; Metal-dusts; Metal-compounds; Particulate-dust; Dust-particles; Dust-exposure; Dust-inhalation; Aerosol-particles; Respirable-dust; Respiratory-irritants; Respiratory-system-disorders; Pulmonary-system-disorders; Quartz-dust; Silica-dusts; Neutrophils; Coal-dust; Lung-irritants; Lung-disease; Lung-disorders
Contact
Vincent Castranova, PhD, Chief, Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, 1095 Willowdale Road, Mail Stop 2015, Morgantown, WV 26505
CODEN
JTEHD6
CAS No.
14808-60-7; 13463-67-7; 10102-43-9; 13463-40-6
Publication Date
19970601
Document Type
Journal Article
Email Address
VIC1@NIORDS1.EM.CDC.GOV
Fiscal Year
1997
NTIS Accession No.
NTIS Price
Issue of Publication
3
ISSN
1528-7394
NIOSH Division
HELD; DRDS
Source Name
Journal of Toxicology and Environmental Health, Part A: Current Issues
State
WV
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