Two cohort studies of mortality made previously by our group (McDonald et al., 1983; McDonald et al., 1980) using similar methods showed that the risk of respiratory cancer appeared much higher in chrysotile textile workers (plant in Charleston) than in Quebec chrysotile production workers (mine and mills at Thetford Mines and Asbestos). Most of the chrysotile processed in Charleston came from Thetford Mines. In both cohorts, cumulative exposure was estimated from each employee individually from work histories and all available measurements of past dust concentrations. Although the accumulated exposures in Charleston were reported to be one tenth of those in Quebec, the Charleston workers experienced a 5 times higher risk of respiratory cancer. Two explanatory hypotheses were considered: 1) exposure had not been correctly measured; 2) cocarcinogens were present in the Charleston textile plant. In support of hypothesis 1 was the fact that cumulative exposure estimates were mainly based upon air measurements made in the past with the midget impinger and gave the concentration in millions of dust particles per cubic foot (mpcf). The use of oil sprays to reduce dust at the Charleston plant could support hypothesis 2. In order to test hypothesis 1, other information on past exposure was obtained by measuring fibres retained in lung tissue from autopsied cases from both cohorts. Autopsied cases were traced through death certificates and pathologists were contacted in the USA and Quebec. Specimens of lung tissue in formalin or paraffin block were obtained for 75 subjects from Charleston and 228 from Quebec. Fibre content of the lung was measured using a combination of optical microscopy (OM) and analytical transmission electron microscopy (ATEM). We report here preliminary data for 70 subjects from Charleston and 37 from Thetford Mines. Chrysotile and tremolite were the principal mineralogical types encountered by ATEM. Tremolite, which accounts for about only 1% of airborne asbestos in Thetford Mines, was found in the lung in higher concentrations than those of chrysotile. Length distributions of fibres in the lung were similar in the two locations, although fibres were slightly longer in the Charleston textile plant. ]n each location, a clear relationship was found between cumulative exposure and lung concentrations of tremolite and asbestos bodies. The pattern was less dear with chrysotile. Overall, in relation to cumulative exposure expressed in mpcfy, the numerical concentrations of chrysotile fibres in lung were also somewhat higher for Quebec subjects. These preliminary findings indicate that the employees in Quebec and Charleston were exposed to the same type of asbestos materials but in higher concentrations, certainly of tremolite, in Quebec. This suggests that some factor other than fibre exposure per se was responsible, at least in part, for the higher lung cancer SMR in the textile plant.