The relationship between HLA-A, B, DQ, and DR antigens and asbestos-induced lung disease

Our plain-English summary of The relationship between HLA-A, B, DQ, and DR antigens and asbestos-induced lung disease, by J.F. Shih, G.W. Hunninghake, N.E. Goeken, et al (Chest, 1993).

The study

• Authors: J.F. Shih, G.W. Hunninghake, N.E. Goeken, J.R. Galvin, J.A. Merchant, D.A. Schwartz
• Journal: Chest
• Published: 1993;104(1):26-31
• Cited by: 3 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

To evaluate the relationship between human leukocyte antigen (HLA) and both asbestos-induced pulmonary fibrosis and pleural fibrosis, we obtained HLA-A, B, C, DQ, and DR phenotypes in 42 long-term asbestos-exposed workers. Among these exposed workers, 15 had asbestosis (ILO > or = 1/0) on the chest radiograph and 18 had asbestos-induced pleural fibrosis. We found that there was an increased percentage of HLA-A29, HLA-B44, and HLA-Bw4 in the subjects with asbestosis. In addition, we observed a marginally positive relationship between HLA-A29 and the severity of pulmonary fibrosis. Similarly, there was a higher prevalence of HLA-DRw53 and DQ2 in the subjects with asbestos-induced pleural fibrosis. The presence of HLA-DQ2 was significantly related to the extent and type of asbestos-induced pleural fibrosis while HLA-DRw53 was not consistently related to the type or extent of pleural disease. Importantly, we observed that HLA-A29, HLA-B44, HLA-Bw4, HLA-DRw53, and HLA-DQ2 do not have a significantly shorter duration or latency of asbestos exposure. Moreover, none of the HLA haplotypes (A29, B44, Bw4, DRw53, and DQ2) that we found to be associated with radiographic manifestations of asbestos-induced lung disease were associated with the physiologic abnormalities that have been traditionally associated with asbestos-induced lung disease. The only exception was an isolated decrease in the residual volume associated with the presence of HLA-A29. These results suggest that the HLA-A29 phenotype may be associated with the development of asbestosis and the HLA-DQ2 phenotype may be associated with the development of asbestos-induced pleural fibrosis. However, these associations are not particularly strong, physiologic correlation is lacking, and previous studies do not support our findings.

In plain English

This study examined whether immune-system markers called HLA antigens were linked to asbestos-related lung disease. The authors tested HLA types in 42 white men with long-term occupational asbestos exposure. Nearly all were sheet metal workers exposed mainly to chrysotile, and 15 had asbestosis on chest X-ray. Comparisons included 2,104 bone marrow donors. HLA-A29 was found in 26.7 percent of men with asbestosis versus 3.7 percent of men with normal lung tissue on X-ray (p=0.05), and was more common than among the donors (p=0.01). HLA-B44 and Bw4 were more common in men with asbestosis than in men with neither asbestosis nor pleural fibrosis, but not more common than in the donors. Pleural fibrosis was marginally associated with DRw53 and DQ2 (each p=0.03). Men carrying these markers did not have significantly shorter exposure or latency. Apart from a lower residual volume with HLA-A29, the markers were not linked to lung function measures. The authors noted that no result would remain statistically significant after accounting for the many comparisons. They concluded that HLA probably does not play an important role in asbestos-induced lung disease.

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: Study of HLA antigen types in asbestos-exposed workers. Workers with and without asbestosis or pleural fibrosis were compared with each other and with a reference group of random bone marrow donors.
• Who was studied: 42 white men occupationally exposed to asbestos, identified through the Sheet Metal Workers 1986 screening program or the University of Iowa Occupational Medicine Clinic. All had at least one year of exposure in a high exposure setting and at least 20 years since first exposure. HLA frequencies were compared with 2,104 random bone marrow donors from the University of Iowa.
• Exposure: Occupational asbestos exposure, mainly chrysotile, among workers who were nearly all sheet metal workers.
• Main results:
  • 15 of the 42 men were classified as having asbestosis on chest X-ray (ILO profusion 1/0 or greater); the other 27 had normal lung parenchyma.
  • HLA-A29 was present in 3.7 percent of men with normal parenchyma on X-ray and 26.7 percent of men with asbestosis (p=0.05).
  • HLA-A29 was more common in men with asbestosis than in the bone marrow donor reference group (p=0.01).
  • HLA-B44 and Bw4 were more frequent in men with asbestosis than in men with neither asbestosis nor pleural fibrosis.
  • HLA-B44 and Bw4 were not more frequent in men with asbestosis than in the bone marrow donors.
  • HLA-B27 was only slightly more common among men with asbestosis, and the difference was not statistically significant.
  • There was a marginal relationship (p=0.05) between HLA-A29 and the severity of lung fibrosis by ILO profusion category.
  • Pleural fibrosis was only marginally associated with HLA-DRw53 (p=0.03) and HLA-DQ2 (p=0.03). No other HLA antigens were associated with pleural fibrosis.
  • HLA-DQ2 correlated with the extent of pleural abnormality (unilateral vs bilateral; p value garbled in the scan) and with its type (circumscribed vs diffuse, p=0.04).
  • Men with asbestosis who were HLA-A29, B44 or Bw4 positive did not have significantly shorter exposure duration or latency.
  • Men with pleural fibrosis who were HLA-DQ2 or DRw53 positive did not have significantly shorter exposure duration or latency.
  • HLA-A29 was associated with a decreased residual volume (p=0.03).
  • No other significant differences in lung function were linked to HLA-A29, B44, Bw4, DRw53 or DQ2.
• The authors' conclusion: The authors concluded that the marginal nature of these relationships, and their lack of consistency with earlier studies, suggest that the HLA complex does not play an important role in the development of asbestos-induced lung disease.
• Limitations the authors state:
  • The authors stated that none of their results would be statistically significant if the analysis were controlled for the number of comparisons made.
  • Only two subjects had a category 2 ILO profusion, which limits the analysis of asbestosis severity.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis, Pleural plaques and thickening.

Medical terms in this study, explained in our Lexicon: Pulmonary Fibrosis, Fibrosis, Chest X-Ray, Latency, Asbestos Exposure.

Related studies

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• Restrictive lung function and asbestos-induced pleural fibrosis. A quantitative approach — D.A. Schwartz, J.R. Galvin, et al. (1993)
• Human T cell responses to endogenously presented HLA-A*0201 restricted peptides of Simian virus 40 large T antigen — M.P. Velders, M.F. Macedo, et al. (2001)
• Asbestos-induced pleural fibrosis and impaired lung function — D.A. Schwartz, L.J. Fuortes, et al. (1990)
• Pleural disease during treatment with bromocriptine in patients previously exposed to asbestos — G. Hillerdal, J. Lee, et al. (1997)
• Asbestosis: interstitial pulmonary fibrosis and pleural fibrosis in a cohort of asbestos insulation workers: influence of cigarette smoking — R. Lilis, I.J. Selikoff, et al. (1986)

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