Exposure to low levels of ozone results in enhanced pulmonary retention of inhaled asbestos fibers

Our plain-English summary of Exposure to low levels of ozone results in enhanced pulmonary retention of inhaled asbestos fibers, by K.E. Pinkerton, A.R. Brody, F.J. Miller, et al (The American Review of Respiratory Disease, 1989).

The study

• Authors: K.E. Pinkerton, A.R. Brody, F.J. Miller, J.D. Crapo
• Journal: The American Review of Respiratory Disease
• Published: 1989;140(4):1075-81
• Cited by: 15 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Health effects associated with exposure to ozone at environmentally relevant concentrations are subject to considerable controversy. Currently, no compelling evidence exists that exposure to low levels of ozone leads to lasting impairment of pulmonary structure or function. One adverse health effect of ozone may be to change lung uptake or clearance functions for other inhaled air pollutants. As a test of this hypothesis, Fischer 344 rats were continuously exposed to 0.06 ppm ozone 7 days a week with a slow rise in ozone to a peak of 0.25 ppm and subsequent decrease to 0.06 ppm over a 9-h period five times each week for 6 wk. Three days after the end of ozone exposure, animals-were exposed to aerosolized asbestos fibers for 5 h and examined immediately after or 30 days after exposure to asbestos. Filtered air control animals were simultaneously exposed to asbestos. Immediately after the end of fiber exposure, lung asbestos fiber burden was similar in both groups. However, 1 month after exposure, fiber mass and fiber number were significantly greater (p less than 0.05) in the lungs of animals exposed to ozone than in the lungs of those exposed to air. These findings suggest that ambient levels of ozone can impair clearance of fibrogenic and carcinogenic materials such as asbestos from the lungs and represent an important adverse effect of prolonged exposure to low levels of this oxidant gas.

In plain English

In this animal experiment, the authors exposed young male Fischer 344 rats to ozone for 6 weeks. The ozone level was held at a baseline of 0.06 ppm, and on weekdays, over a 9-hour period, it was gradually raised to 0.25 ppm, held there for 30 minutes, and lowered back to baseline. A comparison group breathed filtered air. Three days after the ozone exposure ended, rats from both groups inhaled chrysotile asbestos for 5 hours. Immediately afterwards, the two groups had similar amounts of asbestos in their lungs. After 30 days, more than 80% of the fibers had been cleared, but the ozone-exposed rats retained about twice as many fibers as the air-exposed rats (2,800 versus 1,200 fibers per cubic millimetre of fixed lung, averages for five rats per group). They also retained more than twice the fiber mass. The authors reported both differences as statistically significant (p less than 0.05). The authors concluded that ambient levels of ozone can impair fiber clearance from the lungs of animals. They noted that the groups were small, only one ozone exposure pattern was tested, and lung function was not measured.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Animal experiment in rats: inhaled ozone or filtered air, followed by a single inhalation exposure to chrysotile asbestos
• Who was studied: Male, specific pathogen-free Fischer 344 rats, 35 days old at the start. Sixty animals were randomly divided into 36 exposed to ozone and 24 exposed to filtered room air. Of these, 21 ozone-exposed and 19 air-exposed rats then inhaled asbestos. Exposures took place at US Environmental Protection Agency and National Institute of Environmental Health Sciences facilities in Research Triangle Park, North Carolina. Fiber burden groups had n = 5 each.
• Exposure: Ozone at a baseline of 0.06 ppm, with a 2-hour break each day for feeding and maintenance. On weekdays, over a 9-hour period, ozone was gradually raised to 0.25 ppm, held there for 30 minutes, and gradually lowered back to baseline. This was done five times a week for 6 weeks. The authors describe the cycle as equivalent to a constant exposure of about 0.19 ppm. Three days later, rats inhaled chrysotile asbestos for 5 hours at a chamber mass concentration of 8.7 mg per cubic metre.
• Main results:
  • Immediately after asbestos inhalation, the numbers of fibers on the first alveolar duct bifurcations were nearly identical in the ozone and air groups.
  • At 24 hours, fibers on the bifurcation surfaces were markedly reduced compared with 0 hours (p less than 0.05), and the reduction was similar in both groups.
  • More than 80% of the fibers initially deposited in the lungs were cleared by 1 month.
  • Fiber number per cubic millimetre of fixed lung (mean plus or minus SEM, n = 5 per group) was 16,900 plus or minus 3,200 (air) and 16,600 plus or minus 3,700 (ozone) at 0 hours. At 30 days it was 1,200 plus or minus 200 (air) and 2,800 plus or minus 600 (ozone).
  • Thirty days after asbestos exposure, ozone-exposed rats retained twice as many fibers as air-exposed rats (p less than 0.05, Duncan's multiple range test; gas-by-time interaction p = 0.044). Fiber counts in individual animals did not overlap between the groups.
  • At 30 days, ozone-exposed rats had more than twice the asbestos fiber mass in their lungs compared with air-exposed rats (p less than 0.05).
  • Mean fiber length rose from 2.7 and 2.6 microns at 0 hours to 6.5 and 7.1 microns at 30 days (air and ozone groups respectively), because fibers under 10 microns long were cleared more readily. Only the time effect was significant.
• The authors' conclusion: The authors concluded that ambient levels of ozone can impair the clearance of fibers from the lungs of animals, even when peak ozone exposures are brief. They speculated that prior ozone exposure could enhance the harmful effects of inhaled asbestos, which they said future studies need to address.
• Limitations the authors state:
  • Sample size for each group was small (n = 5).
  • Only one ozone exposure regimen was used, so the roles of ozone concentration versus duration could not be addressed.
  • Pulmonary function tests were not done on the animals.
  • Differences in fiber length distribution between groups were not statistically tested.
  • The number of macrophages in the alveoli and airways could not be accurately determined.
  • The mechanism of the enhanced retention was not completely clear.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis.

Medical terms in this study, explained in our Lexicon: Fiber Burden, Fibrogenic, Carcinogenic.

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• Reaction of rat lungs to inhaled chrysotile asbestos following acute and subchronic exposures — B.E. Barry, K.C. Wong, et al. (1983)
• Comparative pulmonary responses to inhaled inorganic fibers with asbestos and fiberglass — K.P. Lee, C.E. Barras, et al. (1981)
• Fiber localization and its relationship to lung reaction in rats after chronic inhalation of chrysotile asbestos — K.E. Pinkerton, P.C. Pratt, et al. (1984)

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