Environmental Health Perspectives 105, Supplement 5, September 1997

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In Vivo and in Vitro Proinflammatory Effects of Particulate Air Pollution (PM 10 )

X.Y. Li, 1 P.S. Gilmour, 2 K. Donaldson, 2 and W. MacNee 1

1 Unit of Respiratory Medicine, 2 Royal Infirmary and the Department of Biological Sciences, Napier University, Edinburgh, United Kingdom

Abstract
Epidemiologic studies have reported associations between fine particulate air pollution, especially particles less than 10 µm in diameter (PM 10 ), and the development of exacerbations of asthma and chronic obstructive pulmonary disease. However, the mechanism is unknown. We tested our hypothesis that PM 10 induces oxidant stress, causing inflammation and injury to airway epithelium. We assessed the effects of intratracheal instillation of PM 10 in rat lungs. The influx of inflammatory cells was measured in bronchoalveolar lavage (BAL). Airspace epithelial permeability was assessed as total protein in bronchoalveolar lavage fluid (BALF) in vivo . The oxidant properties of PM 10 were determined by their ability to cause changes in reduced glutathione (GSH) and oxidized glutathione (GSSG). We also compared the effects of PM 10 with those of fine (CB) and ultrafine (ufCB) carbon black particles. Six hours after intratracheal instillation of PM 10 , we noted an influx of neutrophils (up to 15% of total BAL cells) in the alveolar space, increased epithelial permeability, an increase in total protein in BALF from 0.39±0.01 to 0.62±0.01 mg/ml (mean±SEM) and increased lactate dehydrogenase concentrations in BALF. An even greater inflammatory response was observed after intratracheal instillation of ufCB, but not after CB instillation. PM 10 had oxidant activity in vivo , as shown by decreased GSH in BALF (from 0.36±0.05 to 0.25±0.01 nmol/ml) after instillation. BAL leukocytes from rats treated with PM 10 produced greater amounts of nitric oxide, measured as nitrite (control 3.07±0.33, treated 4.45±0.23 mM/1 Multiple 10 6 cells) and tumor necrosis factor alpha (control 21.0±3.1, treated 179.2±29.4 unit/1 Multiple 10 6 cells) in culture than BAL leukocytes obtained from control animals.These studies provide evidence that PM 10 has free radical activity and causes lung inflammation and epithelial injury. These data support our hypothesis concerning the mechanism for the adverse effects of particulate air pollution on patients with airway diseases. -- Environ Health Perspect 105(Suppl 5):1279-1283 (1997)

Key words : air pollution, reactive oxygen species, oxidant, antioxidant, glutathione, epithelial cells

This paper is based on a presentation at The Sixth International Meeting on the Toxicology of Natural and Man-Made Fibrous and Non-Fibrous Particles held 15-18 September 1996 in Lake Placid, New York. Manuscript received at EHP 26 March 1997; accepted 20 June 1997.

This research was supported by the British Lung Foundation and the Medical Research Council.

Address correspondence to Prof. W. MacNee, Respiratory Medicine Unit, Department of Medicine, Royal Infirmary, Lauriston Place, Edinburgh EH3 9YW, Scotland, UK. Telephone: 0131 536 3254. Fax: 0131 536 3255. E-mail: wmacnee@ed.ac.uk

Abbreviations used: BAL, bronchoalveolar lavage; BALF, bronchoalveolar lavage fluid; BSA, bovine serum albumin; CB, fine carbon black particles; DMEM, Dulbecco's minimum Eagle's medium; FFS, filter fiber suspension; GSH, reduced glutathione; GSSG, oxidized glutathione; LDH, lactate dehydrogenase; PBS, phosphate-buffered saline; PM 10 , particulate matter with anerodynamic diameter of < 10 µm; NO, nitric oxide; TNF, tumor necrosis factor; ufCB, ultrafine carbon black particles.

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Last Update: November 28, 1997