To evaluate the relationship between human leukocyte antigen (HLA) and
both asbestos-induced pulmonary fibrosis and pleural fibrosis, we obt
ained HLA-A, B, C, DQ, and DR phenotypes in 42 long-term asbestos-expo
sed workers. Among these exposed workers, 15 had asbestosis (ILO great
er-than-or-equal-to 1/0) on the chest radiograph and 18 had asbestos i
nduced pleural fibrosis. We found that there was an increased percenta
ge of HLA-A29. HLA-B44, and HLA-Bw4 in the subjects with asbestosis. I
n addition, we observed a marginally positive relationship between HLA
-A29 and the severity of pulmonary fibrosis. Similarly, there was a hi
gher prevalence of HLA-DRw53 and DQ2 in the subjects with asbestos-ind
uced pleural fibrosis. The presence of HLA-DQ2 was significantly relat
ed to the extent and type of asbestos-induced pleural fibrosis while H
LA-DRw53 was not consistently related to the type of 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 la
tency of asbestos exposure. Moreover, none of the HLA haplotypes (A29,
B44, Bw4, DRw53, and DQ2) that we found to be associated with radiogr
aphic manifestations of asbestos-induced lung disease were associated
with the physiologic abnormalities that have been traditionally associ
ated with asbestos-induced lung disease. The only exception was an iso
lated decrease in the residual volume associated with the presence of
HLA-A29. These results suggest that the HLA-A29 phenotype may be assoc
iated with the development of asbestosis and the HLA-DQ2 phenotype may
be associated with the development of asbestos-induced pleural fibros
is. However. these associations are not particularly strong, physiolog
ic correlation lacking, and previous studies do not support our findin
gs.