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The occurrence of mesothelioma in man has been shown to be associated with exposure to asbestos fibres (Wagner et al., 1960) while in unexposed populations these tumours are rare. A doseresponse relationship for mesothelioma has been shown in several different groups of asbestos workers (Newhouse & Berry, 1976; McDonald & McDonald, 1980) and data from the Devonport Dockyard population at Plymouth tends to support this (Sheers & Coles, 1980). These workers have been extensively studied and their exposure to asbestos carefully documented (Harries, 1976, 1977). Terasaki et al. (1977) have pointed out that there is no strong abnormality in overall HLA antigen frequency among solid cancers, and they only demonstrated a weak negative association between HLA-A1 and B8 and carcinoma of the prostate. In studies of lung cancer significant positive HLA associations have been reported with good prognosis although at diagnosis these associations have not been found. (Weis et al., 1980; Ford et al., 1981). Lung cancer is associated with smoking and in asbestos workers there is a multiplicative effect (Berry et al., 1972). Smoking, however, has no effect on mesothelioma rate (McDonald & McDonald, 1980). Studies of genetic markers in mesotheliomas are of interest, therefore, because it is the response to asbestos dust by itself which might be shown to be influenced by genetic constitution. An investigation of the HLA-A and B antigen frequencies in relation to asbestos-induced pulmonary fibrosis and various pleural changes has been undertaken in the Devonport Dockyard population (Darke et al., 1979). We now report a further study of this population with respect to mesothelioma, where comparisons have been made with other groups of asbestos-exposed workers as well as to an unexposed control population. In addition to the mesotheliomas occurring in this area (12p.a.-R.M. Coles, Personal Communication) we have also HLA typed mesothelioma patients from other parts of Britain. Subjects were chosen who were suspected of having mesothelioma from their occupational history and on clinical and radiological examination. Diagnosis was finally confirmed in 54 cases using post-mortem histological material and in 11 cases using biopsy material. Accurate histological diagnosis of this tumour is well recognised as being difficult, therefore the examination was carried out and agreement required between at least two of the following pathologists: Drs. R.M.E. Seal, J.C. Wagner and F.C. Whitwell. In the remaining 6 mesothelioma cases only material from pleural effusions was available (cytological examination was performed by Dr E.B. Butler). Patient samples were obtained from 7 centres in the United Kingdom (Belfast, Cardiff, Carlisle, Derby, Liverpool, London and Plymouth). The HLA antigen frequencies of random populations from each area were pooled to provide a control group from the total patient catchment area (see footnote to Table I). These frequencies were first scrutinised for differences but no significant heterogeneity was found. The level of exposure to asbestos was graded using an exposure rating (exposure code x years in job-R.M. Coles, manuscript in preparation). The 8 categories of exposure code ranged from 1 (dockyard office work) to 25 (asbestos sprayer, lagger afloat). Exposure rating was used to divide the patients into 3 categories: (1) 0-100-light or no exposure; (2) 100-399-intermittent occupational and (3) 400 +-heavy occupational exposure. HLA antigen frequencies of the 27 mesothelioma patients from Plymouth were compared with 5 other asbestos-exposed groups from that area: (i) a case control study of 135 individuals which consisted of 5 men matched for age (±5 years),

HLA-A and B antigen frequencies and mesothelioma in relation to asbestos exposure