Asbestos exposure and asbestos-related pleural and parenchymal disease. Associations with immune imbalance

Our plain-English summary of Asbestos exposure and asbestos-related pleural and parenchymal disease. Associations with immune imbalance, by N.L. Sprince, L.C. Oliver, T.C. McLoud, et al (The American Review of Respiratory Disease, 1991).

The study

• Authors: N.L. Sprince, L.C. Oliver, T.C. McLoud, E.A. Eisen, D.C. Christiani, L.C. Ginns
• Journal: The American Review of Respiratory Disease
• Published: 1991;143(4 Pt 1):822-8
• Cited by: 22 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. 004109).

Abstract

The study hypothesis was that asbestos exposure and asbestos-related pleural plaques and interstitial disease are associated with (1) immune imbalances favoring helper-inducer T-cell subsets in blood and bronchoalveolar lavage (BAL) and (2) T-lymphocyte accumulation in BAL. One hundred twenty-two asbestos-exposed subsets (AES), including 27 nonsmokers (NS), were evaluated and compared with 10 unexposed normal subjects. Data were collected on medical, smoking, and occupational histories, physical examination, spirometry, lung volumes, single-breath DLCO, chest films read by a "B" reader, and T-lymphocyte characterization in blood and BAL using flow cytometry analysis of monoclonal-antibody-treated cells. On average, AES were 47 yr of age and had 23 yr of asbestos exposure. Fifty-eight (48%) had pleural thickening, and seven (6%) had profusion greater than or equal to 1/0. In blood, asbestos-exposed NS had lower total and percent CD8 and lower total CD3 than did normal subjects. In BAL, asbestos-exposed NS had higher total CD3 than did normal subjects. Among AES, increased asbestos exposure was associated with increased percent CD8 in BAL and decreases in both percent lymphocytes and total CD8 in blood. Increase in CD4/CD8 ratio in BAL were associated with pleural thickening. In those seven with profusion greater than or equal to 1/0, there was increased percent CD4 in blood and decreased percent CD8 in BAL. These results suggest immune imbalance favoring helper-inducer T-cell subsets in association with asbestos exposure systemically and with pleural plaques in BAL.(ABSTRACT TRUNCATED AT 250 WORDS)

In plain English

This study measured immune cells in blood and lung-wash fluid (bronchoalveolar lavage) from 122 volunteers exposed to asbestos in New England building construction trades, comparing the 27 nonsmokers among them with 10 unexposed healthy nonsmokers. Exposed workers averaged 23 years of exposure. Of them, 58 (48%) had pleural thickening on chest films and seven (6%) had profusion of 1/0 or more. After adjusting for age, exposed nonsmokers had lower percent and total CD8 and lower total CD3 T-cells in blood than unexposed subjects. They also had higher "total" CD3 in lavage fluid. Among all exposed workers, higher exposure was associated with lower blood lymphocyte percentages and total CD8, and a higher lavage CD8 percentage. Exposed workers whose lavage CD4/CD8 ratio was in the top quarter had an odds ratio of 8.1 for pleural thickening versus the lower three quarters, adjusted for age, smoking and exposure index. No air measurements were available. Given many comparisons, the authors urged caution with p values. The authors concluded that immune imbalances may be associated with asbestos exposure and pleural thickening, and called for longitudinal studies.

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: Comparison of asbestos-exposed workers with unexposed volunteers, using blood and bronchoalveolar lavage tests, lung function and chest films taken at one point in time. The authors do not give a design label.
• Who was studied: 122 asbestos-exposed volunteers (27 nonsmokers, 43 current smokers, 52 ex-smokers) from New England building construction trades, recruited through local unions and the Massachusetts General Hospital Occupational Medicine Clinic. Mean age was 47 years. Immune-cell comparisons with the 10 unexposed healthy nonsmoking volunteers, recruited at the hospital, used only the 27 exposed nonsmokers. Analyses of exposure level and chest-film findings used the whole exposed group. The last year of data collection on exposed subjects was 1986.
• Exposure: Workplace asbestos exposure in building construction trades: pipecoverer, plumber and pipefitter, boilermaker, sheetmetal worker, and cement mason. Exposure was estimated with a weighted-duration index (each year worked before 1965 weighted 4, 1965 through 1972 weighted 2, after 1972 weighted 1) and split into high and low at a cutoff of 14. Mean length of exposure was 23 years. No air samples were available. Citing another source, the authors stated that more than 95% of asbestos used in buildings was chrysotile; fiber type was not measured in these workers.
• Main results:
  • Among all 122 exposed subjects, 58 (48%) had pleural thickening and seven (6%) had profusion of 1/0 or more on chest films. Unexposed volunteers did not have chest radiographs.
  • Lung function showed no significant differences between the total exposed group and the unexposed subjects.
  • In blood, after adjusting for age, exposed nonsmokers had lower percent and total CD8 and lower total CD3 than unexposed subjects.
  • In blood, exposed nonsmokers showed a trend toward a higher CD4/CD8 ratio than unexposed subjects, but it was not statistically significant (p = 0.053).
  • In lavage fluid, exposed nonsmokers had higher "total" CD3 than unexposed subjects, both including and excluding one outlier (Subject x). Their higher "total" CD2 lost significance when Subject x was excluded (P = 0.10).
  • Among exposed subjects only, after adjusting for age and smoking, high exposure was associated with increased neutrophil percentages, decreased lymphocyte percentages and decreased total CD8 in blood, and with increased CD8 percentages in lavage.
  • Among exposed subjects, increases in the lavage CD4/CD8 ratio, treated as a continuous measure, were associated with pleural thickening (P = 0.029), after adjusting for age, smoking and exposure index.
  • Among exposed subjects, those whose lavage CD4/CD8 ratio was in the upper quartile had an odds ratio of 8.1 (p = 0.0025) for pleural thickening compared with those in the lower three quartiles. The model also included current smoking, ex-smoking, age and exposure index.
  • The seven subjects with profusion of 1/0 or more (six current smokers, one nonsmoker) were compared with 60 exposed subjects who had normal radiographs. Blood percent CD4 was higher in the seven (49 versus 45, p = 0.013), and lavage percent CD8 was lower (18 versus 32, p = 0.017).
• The authors' conclusion: The authors concluded that immunologic imbalances may be associated with asbestos exposure and with pleural thickening. They stated that longitudinal studies would be useful to confirm this and to see whether these imbalances signal later asbestosis, lung cancer or mesothelioma.
• Limitations the authors state:
  • Neither air concentrations of asbestos nor asbestos body counts in lavage fluid were available.
  • The authors could not rule out effects of slight differences in lung function on the results.
  • Many comparisons were made without correction for multiple comparisons, so the authors asked that p values be interpreted cautiously.

Topics

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

Medical terms in this study, explained in our Lexicon: Asbestos Exposure, Pleural Plaques, Interstitial, Bronchoalveolar Lavage (BAL), Spirometry, Diffusing Capacity (DLCO), Chest X-Ray, Monoclonal.

Related studies

• Asbestos-related disease: progression of parenchymal abnormalities on high-resolution CT — C.I. Silva, N.L. Müller, et al. (2008)
• Asbestos-related disease in railroad workers. A cross-sectional study — L.C. Oliver, E.A. Eisen, et al. (1985)
• T-cell alveolitis in lung lavage of asbestos-exposed subjects — N.L. Sprince, L.C. Oliver, et al. (1992)
• Asbestos-related pleural and parenchymal fibrosis: detection with high-resolution CT — T.C. McLoud (1989)
• Development of radiological and clinical evidence of parenchymal fibrosis in men with non-malignant asbestos-related pleural lesions — G.H. McMillan, C.E. Rossiter (1982)
• Chest pain in asbestos-exposed individuals with benign pleural and parenchymal disease — S. Mukherjee, N. de Klerk, et al. (2000)

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