Exposure of Humans to Ambient Levels of Ozone for 6.6 Hours Causes Cellular and Biochemical Changes in the Lung

TLDR

A 2‑hour exposure to 0.4 ppm ozone triggers lung biochemical changes that drive inflammation and potential long‑term damage, yet most people are exposed to lower concentrations for several hours. This study aimed to assess whether a prolonged, low‑level ozone exposure can also provoke cellular and biochemical lung alterations. Nonsmoking men were randomly exposed to filtered air or 0.10/0.08 ppm ozone for 6.6 h while exercising at 40 L/min, and bronchoalveolar lavage was performed 18 h later to analyze cells and fluid. Exposure to 0.10 ppm ozone markedly increased neutrophils, protein, PGE2, fibronectin, IL‑6, LDH, and impaired macrophage phagocytosis, while 0.08 ppm ozone raised neutrophils, PGE2, LDH, IL‑6, alpha‑1‑antitrypsin, and reduced phagocytosis but did not elevate protein or fibronectin, demonstrating that 0.08 ppm for 6.6 h initiates a lung inflammatory response.

Abstract

An acute (2 h) exposure of humans to 0.4 ppm ozone initiates biochemical changes in the lung that result in the production of components mediating inflammation and acute lung damage as well as components having the potential to lead to long-term effects such as fibrosis. However, many people are exposed to lower levels of ozone than this, but for periods of several hours. Therefore, it is important to determine if a prolonged exposure to low levels of ozone is also capable of causing cellular and biochemical changes in the lung. Nonsmoking males were randomly exposed to filtered air and either 0.10 ppm ozone or 0.08 ppm ozone for 6.6 h with moderate exercise (40 liters/min). Bronchoalveolar lavage (BAL) was performed 18 h after each exposure, and cells and fluid were analyzed. The BAL fluid of volunteers exposed to 0.10 ppm ozone had significant increases in neutrophils (PMNs), protein, prostaglandin E2 (PGE2), fibronectin, interleukin-6 (IL-6), and lactate dehydrogenase (LDH) compared with BAL fluid from the same volunteers exposed to filtered air. In addition, there was a decrease in the ability of alveolar macrophages to phagocytize yeast via the complement receptor. Exposure to 0.08 ppm ozone resulted in significant increases in PMNs, PGE2, LDH, IL-6, alpha 1-antitrypsin, and decreased phagocytosis via the complement receptor. However, BAL fluid protein and fibronectin were no longer significantly elevated. We conclude that exposure of humans to as low a level as 0.08 ppm for 6.6 h is sufficient to initiate an inflammatory reaction in the lung.