The acute effects of chrysotile asbestos exposure on lung function

Our plain-English summary of The acute effects of chrysotile asbestos exposure on lung function, by K.W. Harless, S. Watanabe, A.D. Renzetti (Environmental Research, 1978).

The study

• Authors: K.W. Harless, S. Watanabe, A.D. Renzetti
• Journal: Environmental Research
• Published: 1978;16(1-3):360-72
• Cited by: 35 articles, as counted by NIH iCite
• Read it: PubMed · Publisher
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 001076).

In plain English

This study tested 23 male construction workers who referred themselves after an intense five-month exposure (December 1975 to May 1976) while finishing a college building in Orem, Utah. Inside the closed building, concrete asbestos board containing 30% chrysotile was cut with an unventilated power saw. Airborne fiber levels were not measured during the work. The men were tested about 1.5 months after exposure ended; 16 were retested about seven months later. No man showed restrictive lung disease. Twelve of the 23 had airflow obstruction at the first test, and 17 of 23 at either test. In the retested men, average closing volume (a test of airway closure) rose significantly. Carbon monoxide diffusing capacity, measured only at follow-up, was normal in all men tested. Hours of exposure did not differ significantly between men with and without obstruction; the authors called their exposure estimates very crude. Four men, all smokers, had abnormal chest X-rays that the authors said could not be related to asbestos. The authors concluded that acute chrysotile exposure causes airflow obstruction as early as 1.5 months after exposure.

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: Clinical case series with follow-up: lung function testing of self-referred exposed workers about 1.5 months and about 8 months after exposure, with no control group
• Who was studied: 23 men, out of approximately 79 exposed construction workers, who referred themselves for pulmonary evaluation after work on the Automotive Trades Building at Utah Technical College, Orem, Utah. 16 of the 23 returned for follow-up about seven months after the first evaluation.
• Exposure: Chrysotile asbestos from concrete asbestos Flexboard (30% chrysotile) cut indoors with an unventilated portable power saw, December 1975 to May 1976. Floor dust samples contained 1 to 30% asbestos. Estimated exposure averaged 518 hours (range 6 to 896 hours). Men cutting the board were classed as heavily exposed.
• Main results:
  • At the first evaluation, no man had restrictive lung disease as measured by FVC, FRC or TLC.
  • At the first evaluation, 12 of the 23 men had airflow obstruction (printed as 50%).
  • Hours of exposure did not differ significantly between men with airflow obstruction (528, plus or minus 348 hours) and men without it (507, plus or minus 331 hours). No dose response was shown.
  • The 16 men who returned had higher average exposure (656, plus or minus 290 hours) than the seven who did not return (203, plus or minus 209 hours). The difference was significant (P less than 0.005).
  • In the 16 returning men, average closing volume rose from 17.11% (plus or minus 7.26%) to 21.89% (plus or minus 7.96%), P less than 0.05. Using the authors' threshold, seven men had significant individual increases.
  • Carbon monoxide diffusing capacity was measured only at follow-up, in the returning men. It was normal in all men in whom it was measured. At follow-up, all had normal static compliance and nine showed frequency dependence of compliance.
  • Across both evaluations, 17 of 23 men (74%) had airflow obstruction.
  • In 6 of the 17 men with obstruction (35%), the authors identified no possible cause other than asbestos exposure. Using a criterion that less than 20 pack-years of smoking rarely causes obstruction, the authors considered asbestos the probable major determinant in 12 (71%).
  • Ten men had low arterial oxygen at rest or a fall in arterial oxygen after exercise. All but one of these 10 had airflow obstruction.
  • Chest radiographs were abnormal in four men, all cigarette smokers. The authors stated these abnormalities could not be related to the asbestos exposure.
• The authors' conclusion: The authors concluded that acute exposure to chrysotile asbestos dust causes airflow obstruction as early as 1.5 months after exposure.
• Limitations the authors state:
  • Airborne asbestos concentration was not measured while the men were exposed.
  • Air samples were taken after the job closed, without board cutting or active work, so they probably underestimate the actual fiber levels the men encountered.
  • The estimates of exposure intensity were very crude.
  • Because exposure probably exceeded the OSHA standard, the authors could not predict the effects of an acute exposure below the standard.

Topics

Medical terms in this study, explained in our Lexicon: Chrysotile, Asbestos Exposure.

Related studies

• Early effects of asbestos exposure on lung function — G. Jodoin, G.W. Gibbs, et al. (1971)
• Airway function in lifetime-nonsmoking older asbestos workers — R. Bégin, A. Cantin, et al. (1983)
• Relation of airway responsiveness to duration of work in a dusty environment — P. Ernst, R.E. Dales, et al. (1989)
• Ethnic differences in lung function: evidence for proportional differences — C.E. Rossiter, H. Weill (1974)
• Asbestos-related pleural plaques and lung function — L.C. Oliver, E.A. Eisen, et al. (1988)
• Reaction of rat lungs to inhaled chrysotile asbestos following acute and subchronic exposures — B.E. Barry, K.C. Wong, et al. (1983)

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