Residual Oil Ashes With Differing Composition Elicit Pro-Inflammatory Chemokines in the Lung and Heart

Details

• Personal Author:
  Al-Mutairi E ; Antonini JM ; Clarke RW ; Godleski JJ ; Love J ; Paulauskis JD ; Rice T
• Description:
  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. [Description provided by NIOSH]
• Subjects:
  Air Pollutants, Occupational Animals Cardiovascular System Chemistry Chemistry, Analytic Dust Environmental Exposure Environmental Pollution Laboratories Lung Lung Diseases Occupational Health Particulate Matter Respiratory System Respiratory Tract Diseases Safety

  More +
• Keywords:
  Airborne-dusts Airborne-particles Analytical-chemistry Analytical-methods Animal-studies Cardiac-function Environmental-contamination Environmental-exposure Environmental-hazards Environmental-pollution Heart Laboratory-animals Lung-disorders Lung-irritants Lung-tissue Particulate-dust Particulates Pulmonary-disorders Pulmonary-system-disorders Respiratory-system-disorders

  More +
• ISSN:
  1096-6080
• Document Type:
  Text
• Genre:
  Abstract or Summary
• Place as Subject:
  Louisiana ; Massachusetts ; OSHA Region 1 ; OSHA Region 3 ; OSHA Region 6 ; West Virginia
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Division:
  HELD - Health Effects Laboratory Division
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Volume:
  48
• Issue:
  1
• NIOSHTIC Number:
  nn:20027918
• Citation:
  Toxicologist 1999 Mar; 48(1-S):259
• CAS Registry Number:
  Manganese (CAS RN 7439-96-5) ; Nickel (CAS RN 7440-02-0) ; Vanadium (CAS RN 7440-62-2)
• Federal Fiscal Year:
  1999
• Peer Reviewed:
  False
• Source Full Name:
  The Toxicologist. Society of Toxicology 38th Annual Meeting, March 14-18, 1999, New Orleans, Louisiana
• Supplement:
  1-S
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:3c4690cc8942edfaa98d33e270edbcea18d3fb000df83c72bbd58bed3f6e12159cbccf1cd0e94b97990fbe8cf54349a312aa9b17ccca47fa2f14e4911489d982
• Download URL:
  https://stacks.cdc.gov/view/cdc/189674/cdc_189674_DS1.pdf
• File Type:
  [PDF - 141.02 KB ]