No abstract

No abstract

A cohort of 820 men in a Paterson, New Jersey, amosite asbestos factory which began work during 1941-1945 was observed from 5 to 40 years after start of work. Most of the cohort had limited duration of work experience (days, weeks, months), though some men worked for several years until the factory closed in 1954. With white males of New Jersey as the control population, Standardized Mortality Ratios (SMRs) of 500 are evident for the cohort for lung cancer and for noninfectious pulmonary diseases (including asbestosis), while being almost 300 for total cancer and about 170 for all causes of death. A statistically significant SMR of almost 200 is seen for colon-rectum cancer. Mesothelioma incidence initially shows a strong relationship with advancing time since onset of exposure and then tails off. The main concern of the study is with dose-response patterns. Response is measured by the mortality for relevant causes of death, while the direct asbestos dosage was measured in two ways. One way was the length of time worked in the factory and the other was the individual's accumulated fiber exposure, calculated by multiplying the aforementioned length of time worked by the estimated fiber exposures associated with the particular job that the worker had in the factory. Whichever measure of dosage is used, it was found that, in general, the lower the dose, the longer it took for adverse mortality to become evident and, also, the smaller the magnitude of that adverse mortality.

A cohort of 1,117 asbestos insulation workers was established in 1963 and has been prospectively followed since then. Chest X-ray abnormalities detected at the initial medical examination, and interpreted according to the International Labour Office Classification of Radiographs of Pneumoconioses are reported in this paper. The prevalence of all radiographic abnormalities (pleural and pulmonary) increased with duration from onset of asbestos exposure. A positive smoking history was associated with a significantly higher prevalence of small irregular opacities indicating interstitial pulmonary fibrosis. Such an association was not found for pleural fibrosis. The possible mechanisms which underlie the effect of smoking on asbestos-induced interstitial fibrosis seem to be of much less importance in the development of pleural fibrosis. Progression of radiographic changes over the 20-year interval 1963-1983 will be separately reported as will the predictive significance of these changes.