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Residual oil ashes with differing composition elicit pro-inflammatory chemokines in the lung and heart.

Authors
Clarke-RW; Al-Mutairi-E; Love-J; Rice-T; Antonini-JM; Paulauskis-JD; Godleski-JJ
Source
Toxicologist 1999 Mar; 48(1-S):259
NIOSHTIC No.
20027918
Abstract
Residual oil ash (ROA) is a significant environmental hazard and contributes to airborne particulate matter. In the present study, toxicity profiles for two ROAs differing in composition were examined. Residual oil ash 1 (ROA1) had a lower carbonaceous component and high vanadium content; ROA2 was rich in carbon and included high amounts of nickel and manganese. HYPOTHESIS: The greater presence of vanadium in ROA1 will result in more severe pulmonary injury. METHODS: Rats were lightly anesthetized and intratracheally instilled with 2.5 mg/kg ROA 1 or ROA2 or PBS. Animals were sacrificed at 4, 24, and 48 hours (hr) post-instillation (PI). Bronchoalveolar lavage (BAL) was performed and BAL cells as welt as lung and heart tissues were retained for RNA isolation and Northern analysis. RESULTS: Significant ROA induced pulmonary inflammation was observed in BAL samples at all time points with neutrophil and eosinophil influx and increased biochemical markers of inflammation (p < 0.05). These changes were significantly more severe in the ROA1 group for several parameters, particularly at 4 hr. Macrophage inflammatory protein (MIP)-1 alpha and MIP-2 mRNA levels were marked1y increased in ROA-exposed BAL cells at 4hr; expression was present but declining at later timepoints. Lung and cardiac tissue exhibited very low MIP-1 alpha and -2 mRNA levels at 4 hr PI only. There was no difference in the level of mRNA expression of these chemokines between the two ROA groups. CONCLUSION: ROA 1 appears to be a more toxic pro-inflammatory particle indicating that composition is an important determinant of pulmonary response. The presence of vanadium or lack of carbon content may playa role in this differing response. Secondly, these data indicate that ROA induces pulmonary inflammation by induction of pro-inflammatory chemokines.
Keywords
Analytical-methods; Analytical-chemistry; Environmental-hazards; Environmental-exposure; Environmental-pollution; Environmental-contamination; Airborne-dusts; Airborne-particles; Particulate-dust; Particulates; Laboratory-animals; Animal-studies; Pulmonary-system-disorders; Pulmonary-disorders; Respiratory-system-disorders; Lung-disorders; Lung-irritants; Lung; Lung-tissue; Heart; Cardiac-function
CAS No.
7440-62-2; 7440-02-0; 7439-96-5
Publication Date
19990301
Document Type
Abstract
Fiscal Year
1999
NTIS Accession No.
NTIS Price
Issue of Publication
1
ISSN
1096-6080
NIOSH Division
HELD
Source Name
The Toxicologist. Society of Toxicology 38th Annual Meeting, March 14-18, 1999, New Orleans, Louisiana
State
LA; WV; MA
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