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

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.

Bayesian hierarchical distributed lag models for summer ozone exposure and cardio‐respiratory mortality

“…Epidemiological studies have found associations between low ozone levels and: 1) decline in pulmonary functions (Galizia and Kinney, 1999;Folinbee et al, 1988;Kinney et al, 1996;Devlin et al, 1991); 2) increase in hospital admissions for asthma, especially among children (Stern et al, 1994;Galizia and Kinney, 1999); and 3) congestive heart failure among the elderly (Burnett et al, 1997b). Positive associations between short-term 1-hour max ozone levels and mortality, adjusted for the potential confounding effects of other pollutants and weather, have been found in Los Angeles and New York (Kinney and Ozkaynak, 1991;Kinney et al, 1996).…”

“…The health effects associated with short-term exposure to ambient ozone are well documented in air pollution studies (Galizia and Kinney, 1999;Devlin et al, 1991;Folinbee et al, 1988;Kinney et al, 1996;Stern et al, 1994;Levy et al, 2001;Kelsall et al, 1997;Moolgavkar, 2000;Thurston and Ito, 2001;Glodberg et al, 2001). Exposure to ozone levels less than 100ppb can irritate the respiratory tract, particularly for sensitive populations, concentrations above 300ppb can cause nose and throat irritation, and levels above 1000ppb (typical levels in very smoggy air) can cause breathing problems and headaches.…”

Air pollution, aeroallergens and cardiorespiratory emergency department visits in Saint John, Canada

“…Some investigators have found that ozone was significantly associated with cardiac hospital admissions (Burnett et al, 1997a;Ponka and Virtanen, 1996 ), whereas several others have found no association or a borderline significant association ( Burnett et al, , 1997b( Burnett et al, , 1999Morris et al, 1995;Poloniecki et al, 1997;Schwartz, 1997;Schwartz and Morris, 1995 ). Although the respiratory pathophysiology of ozone is relatively well understood (Crapo et al, 1992;Devlin et al, 1991;Vincent et al, 1997 ) , effects on the cardiovascular system are not. Cardiovascular effects may occur by way of a nonspecific insult, perhaps mediated through the respiratory system ( Bouthillier et al, 1998) .…”

Introduction to working group on tropospheric ozone, Health Effects Institute environmental epidemiology planning project.

“…Moreover, the link between current measures of acute symptomatic and/or functional responses to ozone (6,7) and the occurrence of chronic effects has not been established in humans, nor has it been established that the mechanisms that underlie acute effects [e.g., airways hyperreactivity (8), reflex neural alterations of measured vital capacity (9), inflammatory changes (10)] are the same as those that underlie chronic effects (e.g., loss of lung elastic recoil, deposition of excess collagen).…”