Acute, Subchronic, and Chronic Exposure to a Simulated Urban Profile of Ozone: Effects on Extrapulmonary Natural Killer Cell Activity and Lymphocyte Mitogenic Responses

Selgrade, MaryJane K.; Daniels, Mary J.; Grose, Elaine C.

doi:10.3109/08958379009145264

Cited by 5 publications

(3 citation statements)

References 27 publications

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“…Indeed, most experimental animal studies have had to use 03 exposures in excess of the ambient and spike urban 03 concentrations to demonstrate an immunotoxic effect. In this regard, the study of Selgrade et al (18) found no effect on multiple immune parameters when rats were chronically exposed to 03 in a way that simulated an urban profile. Finally, in addition to the 03 concentrations, the inferences that can be drawn between human health effects and the battery of immune tests recommended in the National Toxicology Program guidelines for immunotoxicity evaluation in mice (113) need to be clarified.…”

Section: Discussionmentioning

confidence: 96%

“…The above-mentioned studies on the effects of 03 exposure on mitogen responses and NK cell activity used exposures to 03 in great excess of that found in ambient air. To investigate the effects of acute and chronic exposure to 03 at near ambient concentrations, Selgrade et al (18) used an experimental protocol designed to mimic diurnal urban 03 exposure patterns. Rats were exposed to a background level of 0.06 ppm for a period of 13 hr, a broad exposure spike rising from 0.06 ppm to 0.25 ppm and returning to 0.06 ppm over 9 hr, and a 2-hr downtime.…”

Section: Effect Of Ozone On Immune Function In the Absence Of Antigenmentioning

confidence: 99%

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The effects of ozone on immune function.

Jakab

Spannhake

Canning

et al. 1995

Environ Health Perspect

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A review of the literature reveals that ozone (O3) exposure can either suppress or enhance immune responsiveness. These disparate effects elicited by O3 exposure depend, in large part, on the experimental design used, the immune parameters examined as well as the animal species studied. Despite the apparent contradictions, a general pattern of response to O3 exposure can be recognized. Most studies indicate that continuous O3 exposure leads to an early (days 0-3) impairment of immune responsiveness followed, with continued exposures, by a form of adaptation to O3 that results in a re-establishment of the immune response. The effects of O3 exposure on the response to antigenic stimulation also depend on the time at which O3 exposure occurred. Whereas O3 exposure prior to immunization is without effect on the response to antigen, O3 exposure subsequent to immunization suppresses the response to antigen. Although most studies have focused on immune responses in the lung, numerous investigators have provided functional and anatomical evidence to support the hypothesis that O3 exposure can have profound effects on systemic immunity.

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Section: Discussionmentioning

confidence: 96%

Section: Effect Of Ozone On Immune Function In the Absence Of Antigenmentioning

confidence: 99%

The effects of ozone on immune function.

Jakab

Spannhake

Canning

et al. 1995

Environ Health Perspect

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“…Small but significant decreases in lung volume and enhanced nitrogen washout kinetics were also found (Costa, personal communication) that are consistent with the fibrotic lesions reported herein. Local and systemic immune functions were apparently unaffected by the chronic Oj exposure (Selgrade et al, 1990). Pinkerton et al (1989) reported that rats exposed to the same simulated ambient pattern of O3 for 6 weeks followed by a 5-hr exposure to asbestos fibers retained three times as much fibers in their lungs as did control rats exposed only to the asbestos fibers.…”

Section: Discussionmentioning

confidence: 99%

Epithelial injury and interstitial fibrosis in the proximal alveolar regions of rats chronically exposed to a simulated pattern of urban ambient ozone

Chang

Huang

Stockstill

et al. 1992

Toxicology and Applied Pharmacology

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Electron microscopic morphometry was used to study the development of lung injury during and after chronic (78 weeks) exposure to a pattern of ozone (O3) designed to simulate high urban ambient concentrations that occur in some environments. The daily exposure regimen consisted of a 13-hr background of 0.06 ppm, an exposure peak that rose from 0.06 to 0.25 ppm, and returned to the background level over a 9-hr period, and 2-hr downtime for maintenance. Rats were exposed for 1, 3, 13, and 78 weeks. Additional groups of rats exposed for 13 or 78 weeks were allowed to recover in filtered clean air for 6 or 17 weeks, respectively. Rats exposed to filtered air for the same lengths of time were used as controls. Samples from proximal alveolar regions and terminal bronchioles were obtained by microdissection. Analysis of the proximal alveolar region revealed a biphasic response. Acute tissue reactions after 1 week of exposure included epithelial inflammation, interstitial edema, interstitial cell hypertrophy, and influx of macrophages. These responses subsided after 3 weeks of exposure. Progressive epithelial and interstitial tissue responses developed with prolonged exposure and included epithelial hyperplasia, fibroblast proliferation, and interstitial matrix accumulation. The epithelial responses involved both type I and type II epithelial cells. Alveolar type I cells increased in number, became thicker, and covered a smaller average surface area. These changes persisted throughout the entire exposure and did not change during the recovery period, indicating the sensitivity of these cells to injury. The main response of type II epithelial cells was cell proliferation. The accumulation of interstitial matrix after chronic exposure consisted of deposition of both increased amounts of basement membrane and collagen fibers. Interstitial matrix accumulation underwent partial recovery during follow-up periods in air; however, the thickening of the basement membrane did not resolve. Analysis of terminal bronchioles showed that short-term exposure to O3 caused a loss of ciliated cells and differentiation of preciliated and Clara cells. The bronchiolar cell population stabilized on continued exposure; however, chronic exposure resulted in structural changes, suggesting injury to both ciliated and Clara cells. We conclude that chronic exposure to low levels of O3 causes epithelial inflammation and interstitial fibrosis in the proximal alveolar region and bronchiolar epithelial cell injury.

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