The Impact of A 12-Month Exposure to A Diurnal Pattern of Ozone on Pulmonary Function, Antioxidant Biochemistry and Immunology

Grose, Elaine C.; Stevens, M. Allen; Hatch, Gary E.; Jaskot, Richard H.; Selgrade, MaryJane K.; Stead, Andrew G.; Costa, Daniel L.; Graham, Judith A.

doi:10.1016/s0166-1116(08)70618-6

Cited by 13 publications

(15 citation statements)

References 22 publications

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“…These changes occurred without alterations in AM size, light-scattering properties, or expression of cell surface markers of differentiation (Figure 4), suggesting they were not the result of ozone-induced recruitment of less mature AM or changes in AM subpopulations. Similar findings have been observed in animals: Ozone exposure decreased the oxidative burst of alveolar macrophages obtained from mice (Ryer-Powder et al, 1988), rats (Grose et al, 1989), and rabbits (Schlesinger et al, 1992). Exposure of rabbits to 0.1 ppm ozone 3 h daily for 5 days enhanced the b -agonist-induced inhibition of ROS production by AM (McGovern et al, 1996).…”

Section: Discussionsupporting

confidence: 62%

Ozone Exposure and the Production of Reactive Oxygen Species by Bronchoalveolar Cells in Humans

Voter

Whitin

Torres

et al. 2001

Inhalation Toxicology

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Exposure to ozone injures respiratory epithelium, and the mechanisms may involve the generation of reactive oxygen species (ROS). This study tested the hypothesis that ozone exposure increases the airway burden of ROS to a greater degree in smokers than nonsmokers, and that this effect is independent of ozone-induced changes in spirometry. Healthy subjects were selected as either responders (decrement in FEV1 > 15%) or nonresponders (decrement in FEV1 < 5%) to ozone; each underwent 2 exposures to ozone and 1 to air, with bronchoalveolar lavage (BAL) performed 30 min (early) and 18 h (late) after exposure. Release of superoxide anion (O2(-)) was used as a measure of ROS release by all BAL cells, and flow cytometry was used to detect ROS production in alveolar macrophages (AM) only. Recovery of AM was approximately threefold greater in smokers than nonsmokers. Unstimulated, but not stimulated, cells obtained by BAL from smokers released approximately twofold greater amounts of O2(-) than cells from nonsmokers, both early and late after ozone exposure (p =.012 and p =.046, respectively). Stimulated, but not unstimulated, ROS generation by AM from smokers increased following ozone exposure, but the ozone effect was not significant. ROS production by AM decreased in nonsmokers (air vs. ozone late, p =.014). Total protein, albumin, and immunoglobulin M (IgM) increased in BAL fluid, consistent with an increase in epithelial permeability. In addition, the concentration of alpha2-macroglobulin increased approximately threefold 18 h after exposure in nonsmokers (p <.001). No relationship was found between measures of ROS production and lung function responsiveness to ozone. These studies suggest the airways of smokers experience a greater burden of ROS than those of nonsmokers following ozone exposure.

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Section: Discussionsupporting

confidence: 62%

Ozone Exposure and the Production of Reactive Oxygen Species by Bronchoalveolar Cells in Humans

Voter

Whitin

Torres

et al. 2001

Inhalation Toxicology

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“…An ongoing low-level inflammatory process with increased numbers of neutrophils was accompanied by increased numbers of type II alveolar cells, thickening of the basement membrane, and increased numbers of collagen fibers in the interstitium (7)(8)(9). Measurement of pulmonary function in these animals suggested very small changes in some variables, including total lung capacity and the diffusing capacity of carbon monoxide (10,11 ).…”

Section: Introductionmentioning

confidence: 99%

Identification of Subpopulations That Are Sensitive to Ozone Exposure: Use of End Points Currently Available and Potential Use of Laboratory-Based End Points under Development

Devlin¹

1993

Environmental Health Perspectives

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A number of epidemiological studies have attempted to assess the effect of recurrent ozone exposure in humans. For the most part, they have failed to document convincingly an association between chronic ozone exposure and differences in lung function performance or respiratory symptoms. This is not surprising given the small respiratory effects observed in animals chronically exposed to ozone and assuming that people with abnormal respiratory function resulting from other occupational or environmental exposures, such as tobacco smoke, would make up a much larger percentage of the population than people with respiratory effects attributable to ozone. Therefore, either more sensitive end points must be developed to detect subtle changes due to chronic ozone exposure, or ways of selecting subpopulations that are especially sensitive to ozone must be devised. It has been well documented that there are large and reproducible differences in the acute response of individuals to ozone as measured by pulmonary function tests. Recently, it has also been shown that there are large differences in the acute response of individuals to ozone as measured by inflammatory and other biochemical parameters. This paper discusses the problems of selecting individuals who are sensitive to ozone depending on the end point chosen. It also describes potential new sensitive end points that might be available for ozone epidemiology studies in the near future. -Environ Health Perspect 101 (Suppl 4): 225-230 (1993).

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“…It i s likely that the focal tissue stiffening induced by ozone exposure in this study was not sufficiently severe or widespread to influence total lung elastic recoil measurably, or that the effect was manifested at a lung volume that was not examined by the assays used. The only previous assessments of the pulmonary function of rats exposed to ozone for 12 mo or longer were those conducted at General Motors (Gross & White, 1987) and at the EPA (Grose et al, 1989;Tepper et al, 1991 ), and described earlier in the introduction. Because the exposure patterns, concentrations, and times used in these studies differed from those of the present study, neither of the previous studies provides a good direct comparison.…”

Section: Discussionmentioning

confidence: 99%

“…In a study at the U.S. Environmental Protection Agency (EPA), male F344 rats were exposed to a simulated urban ozone profile for up to 18 mo (Grose et al, 1989;Tepper et al, 1991 ). The rats were exposed 13 h/day, 7 days/wk to 0.06 ppm.…”

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confidence: 99%

Pulmonary Function Alterations in F344 Rats Following Chronic Ozone Inhalation

Harkema

Mauderly

Griffith

1996

Inhalation Toxicology

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The impact of a 20-mo exposure to ozone on the pulmonary function o f rats was assessed by performing a single series of measurements after exposures were completed. Four to 10 male and female F344 rats per group were exposed 6 hlday, 5 dayslwk for 20 m o to ozone at 0.72, 0.5, or 1.0 ppm, or to clean air as controls. One to 3 days after the last exposure, the rats were anesthetized using halothane, fitted with oral endotracheal and esophageal catheters, and measured using plethysmographic techniques. The significances of differences between mean values for control and treated rats were tested by multiple comparisons. The values and intersubject variability for over 30 measured and calculated parameters were similar to those reported previously for similarly aged rats. The only consistent exposure-related effect was a small reduction of residual volume measured during slow lung deflation. This trend was observed in most exposed groups, but was most significant in females at the 0.5 ppm level. Fibrosis and epithelial changes were observed in the terminal bronchiole-alveolar duct region in parallel studies of different rats from the same exposure groups. It was hypothesized that these changes stiffened airspace walls and acted to maintain the patency of the air pathway to a lower than normal lung volume during deflation. Overall, the exposures had little impact on the integrated pulmonary function of the lung as measured in anesthetized rats.

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The Impact of A 12-Month Exposure to A Diurnal Pattern of Ozone on Pulmonary Function, Antioxidant Biochemistry and Immunology

Cited by 13 publications

References 22 publications

Ozone Exposure and the Production of Reactive Oxygen Species by Bronchoalveolar Cells in Humans

Ozone Exposure and the Production of Reactive Oxygen Species by Bronchoalveolar Cells in Humans

Identification of Subpopulations That Are Sensitive to Ozone Exposure: Use of End Points Currently Available and Potential Use of Laboratory-Based End Points under Development

Pulmonary Function Alterations in F344 Rats Following Chronic Ozone Inhalation

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