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The effects of intermittent high asbestos exposure (peak dose levels) on the lungs of rats

Our plain-English summary of The effects of intermittent high asbestos exposure (peak dose levels) on the lungs of rats, by J.M. Davis, S.T. Beckett, R.E. Bolton, et al (British Journal of Experimental Pathology, 1980).

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The study

Abstract

Four groups of rats were treated by inhalation with the UICC preparations of amosite or chrysotile in order to explore the effects of intermittent high dust concentrations (peak dosing). For each of the 2 asbestos types one group of rats was treated for 5 days each week, 7 h a day, for 1 year. Two other groups were treated with amosite or chrysotile at 5 times the previous dose for 1 day each week for 1 year. Results showed that the lung dust levels of both chrysotile or amosite in the lungs of rats after the 12-month inhalation period were similar regardless of whether "peak" or "even" dosing had been used. During the following 6 months, asbestos was cleared from the "peak" chrysotile group more slowly than the "even" chrysotile group but clearance from the "peak" amosite group was faster than that found after "even" dosing with amosite. Levels of early peribronchial fibrosis were generally lower for the "peak" dosing groups than for "even" dosing although levels of interstitial fibrosis were slightly higher following "peak" dosing. The incidence of pulmonary neoplasms did not differ between the "peak"-dosing and "even"-dosing experiments. These findings therefore give no indication that short periods of high dust exposure in an asbestos factory would result in a significantly greater hazard than would be indicated by the raised overall dust counts for the day in question.

In plain English

This animal experiment tested whether short bursts of very high asbestos dust harm rat lungs more than the same amount breathed evenly. Rats inhaled UICC amosite or chrysotile for 12 months. 'Even' groups breathed dust 7 hours a day, 5 days a week. 'Peak' groups breathed five times that concentration 1 day a week. Peak chrysotile (10 mg/m3) was compared with earlier even-chrysotile data (2 mg/m3), and peak amosite (50 mg/m3) with even amosite (10 mg/m3). Seven days after dusting ended, chrysotile lung burdens were extremely close (526 and 501 micrograms). Peak-dosed amosite rats held more dust (11226 versus 9169 micrograms), but no lung-dust or clearance difference was statistically significant. Early fibrosis around the small airways was significantly lower after peak chrysotile. Later interstitial fibrosis was higher after peak dosing of both fibers, though not significantly. Lung tumour figures showed no significant differences, though peak amosite produced 2 bronchial carcinomas where even amosite produced none. The authors concluded the findings gave no indication that short high factory exposures carry a significantly greater hazard than that day's raised overall dust counts would indicate.

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 inhalation experiment comparing intermittent high ('peak') with constant ('even') asbestos dosing in rats
  • Who was studied: Groups of 48 male random-bred white SPF Wistar rats (AF/HAN strain) at the Institute of Occupational Medicine, Edinburgh. Groups of 4 were killed at 12 and 18 months after dusting began, and the experiment ended at 29 months. The even-dosing chrysotile comparison used previously obtained data. Study dates are not given.
  • Exposure: Inhalation of UICC amosite or chrysotile for 12 months. Even dosing was 7 h a day, 5 days a week. Peak dosing was 5 times that concentration for 1 day a week. For chrysotile, peak was 10 mg/m3 against even 2 mg/m3, because chrysotile could not be generated much above 20 mg/m3. For amosite, peak was 50 mg/m3 against even 10 mg/m3. Mean concentrations achieved were 2.0, 9.0, 10.0 and 49.2 mg/m3 respectively.
  • Main results:
    • Mean lung dust content (4 rats per group, measured 7 and 182 days after the end of exposure) was as follows. Even chrysotile: 526 then 180 micrograms. Peak chrysotile: 501 then 270 micrograms. Even amosite: 9169 then 7020 micrograms. Peak amosite: 11226 then 7331 micrograms.
    • The amount of chrysotile in the lungs at the end of the 12-month dusting period was extremely close for peak and even dosing.
    • Peak-dosed amosite rats appeared to retain more dust than even-dosed amosite rats, but with 4 animals per group the difference was not significant.
    • Over the 6 months after dusting, chrysotile clearance appeared slower after peak dosing and amosite clearance appeared faster after peak dosing. Statistical examination of the lung-dust figures showed no significant differences.
    • Early peribronchiolar fibrosis was significantly lower after peak than after even dosing with chrysotile (P less than 0.05).
    • With amosite, early peribronchiolar fibrosis showed no significant difference between the two dosing regimes.
    • In the later stages, interstitial fibrosis was higher after peak dosing of both amosite and chrysotile than after even dosing, but the differences were not statistically significant.
    • Lung tumour and mesothelioma figures showed no significant differences between peak and even dosing.
    • Peak amosite dosing produced 2 bronchial carcinomas where even amosite dosing produced none. Table IV lists 44 peak-dosed and 40 even-dosed amosite rats.
    • There were no overall differences in survival between rats given the different asbestos clouds.
  • The authors' conclusion: The authors concluded that the findings gave no indication that short periods of high dust exposure in an asbestos factory would result in a significantly greater hazard than the raised overall dust counts for that day would indicate. They suggested peak dosing may leave more dust in the alveoli rather than near the bronchioles.
  • Limitations the authors state:
    • Only 4 animals per group were used for lung dust measurements.
    • Chrysotile could not be generated at 50 mg/m3 because the fibres flocculated. The chrysotile comparison therefore used a peak of 10 mg/m3 against even dosing at 2 mg/m3.
    • The factory situation, with very low background levels and brief peaks, differs greatly from the experimental design, and that extreme difference could not be reproduced in the laboratory.

Topics

Medical terms in this study, explained in our Lexicon: Asbestos Exposure, UICC, Amosite, Chrysotile, Fibrosis, Interstitial Fibrosis, Neoplasm.

Browse more research in British Journal of Experimental Pathology, or return to medical research.

Cited on this site

How to cite it

Cite the study

J.M. Davis, S.T. Beckett, R.E. Bolton, K. Donaldson. The effects of intermittent high asbestos exposure (peak dose levels) on the lungs of rats. British Journal of Experimental Pathology 1980;61(3):272-80. PMID: 7426382.

Cite our summary

“The effects of intermittent high asbestos exposure (peak dose levels) on the lungs of rats.” AsbestosClaims.Law Library. https://asbestosclaims.law/library/research/the-effects-of-intermittent-high-asbestos-exposure-peak-dose-levels.

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