Cold Stress Provokes Lung Injury in Rats Co-Exposed to Fine Particulate Matter and Lipopolysaccharide

Details

• Personal Author:
  Hammond SK ; Liu S ; Luo B ; Niu J ; Shi H ; Wang J ; Wei Q ; Zhang K
• Description:
  Cold exposure aggravates respiratory diseases, which are also influenced by the exposures to particulate matter and endotoxin in the air. The aim of this study was to investigate the potential interactions among cold stress, fine particulate matter (PM2.5, particles with aerodynamic diameter of 2.5um or less) and lipopolysaccharide (LPS, pure chemical form of endotoxin) on rat lung and to explore the related possible mechanisms of the interactions. Wistar rats were randomly grouped to be exposed to, 1) normal saline (0.9% NaCl), 2) PM2.5, 3) LPS, and 4) PM2.5 and LPS (PM2.5 + LPS) through intratracheal instillation under cold stress (0 degrees C) and normal temperature (20 degrees C). Lung function, lung tissue histology, inflammatory response and oxidative stress levels were measured to examine the lung injury and to investigate the potential mechanisms. Exposure to PM2.5 or LPS substantially changed pulmonary function [indicated by peak inspiratory flow (PIF) and peak expiratory flow (PEF)], inflammatory cytokine levels [indicated by interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-a)] and lung histology, compared to the non-exposed groups. Exposure to PM2.5 + LPS under cold stress induced the most significant changes, including the increases of IL-6, TNF-a and thiobarbituric acid-reactive substances (TBARS), the decreases of PIF and PEF and more severe lung injury, among all exposure scenarios. Glutathione peroxidase activity and, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were found to be suppressed under cold stress, whereas Nrf2 and HO-1 levels were observed to be upregulated by exposure to PM2.5 or LPS under normal temperature. In conclusion, cold stress may aggravate the lung injury in rats induced by simultaneous exposure to PM2.5 and LPS. The progress may involve the suppressing of Nrf2/HO-1 signal pathway. [Description provided by NIOSH]
• Subjects:
  Animals Cold Temperature Endotoxins Lipids Lung Occupational Health Particulate Matter Respiratory System Safety Temperature
• Keywords:
  Animal Studies Author Keywords: Cold Stress Cold Environments Fine Particulate Matter Lipopolysaccharide Lung Function Nrf2/HO-1 Particulates Respiratory Function Temperature Effects
• ISSN:
  0147-6513
• Document Type:
  Text
• Funding:
  Grant
• Genre:
  Journal Article
• Place as Subject:
  California ; Indiana ; OSHA Region 5 ; OSHA Region 9
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Pages in Document:
  9-16
• Volume:
  168
• NIOSHTIC Number:
  nn:20055600
• Citation:
  Ecotoxicol Environ Saf 2019 Jan; 168:9-16
• Contact Point Address:
  Bin Luo, Institute of Occupational and Environmental Health, School of Public Health, Lanzhou University, DongGang West Road Chengguan District, Lanzhou 730000 China
• Email:
  luob@lzu.edu.cn
• Federal Fiscal Year:
  2019
• Performing Organization:
  University of California, Berkeley
• Peer Reviewed:
  True
• Start Date:
  20050701
• Source Full Name:
  Ecotoxicology and Environmental Safety
• End Date:
  20250630
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:3ef4eb65cc7e8476b112d0ca93b7ad5f59afb5bd660e17ffbe2d30f7d8edacfd092803f7ce4d98b5026c74f1aae8859c4cd4baf63e0e4ac41a4ef920b67f9c0c
• Download URL:
  https://stacks.cdc.gov/view/cdc/213417/cdc_213417_DS1.pdf
• File Type:
  [PDF - 1.31 MB ]