Mesothelioma Cancer Info

Just before the United States entered World War II, an amosite asbestos factory was established in Paterson, New Jersey, to supply the Navy with asbestos insulation for the pipes, boilers and turbines of its ships. Amosite asbestos was used almost exclusively, with very small amounts of chrysotile.

Amosite asbestos is mined only in theTransvaal in South Africa, and it had not been studied as much as other fibre types. Thus data concerning its carcinogenic potential were unclear. Since there was no evidencethat amosite was carcinogenic, increasing amounts were used to substitute forcrocidolite. Before 1930, no amosite was imported into the United States. From 1935to 1965 imports rose from less than 500 tons to 21 400 tons. Therefore the full effectsof exposure to amosite may only be apparent now. From 1941 through 1945, 933 men worked in the Paterson plant, which continuedto operate until 1954. The employees tended to be older, and most worked for onlya short time. No dust counts were taken at the factory, but the ventilation system was extremely poor and asbestos fibre concentrations were probably very high. Many ofthe workers therefore were likely to have had short, intense exposure.

These workers were investigated by Selikoff and colleagues beginning in 1972.49–51 By 1977 they found significantly more deaths than expected, and 14 cases of mesothelioma – 7 pleuraland 7 peritoneal. Even those who were employed for short periods were at increased risk of asbestos-related disease. Longer term follow-up studies for the same factory were published in 1986 and1988. By 1988, of 820 men employed at the Paterson plant for some period between1941 and 1945, 740 were known to be dead. Mesothelioma was identified in 17 cases (8pleural, 9 peritoneal), or 2.2 per cent of deaths. The latency period was 20–41 years. The authors noted a rise in incidence until 35 years after exposure, and then a decrease.

Those with peritoneal disease tended to have worked longer in the factory. Mortality rate correlated with degree of exposure – both length and intensity. When the Paterson plant was closed in 1954, the company opened its successor in Tyler, Texas, which remained in operation until 1971. Like the Paterson plant, this factory was one of the few that used only amosite. In this plant, industrial hygiene data areavailable. Average fibre concentrations ranged from 15.9 to 19.4 f/mL, well above thestandard of 5 f/cm3 then in effect. However, even these levels may not reflect the highlevels of dust that existed intermittently. This plant was reported to be one of the dirtiest. In 1971, the National Institute of Occupational Safety and Health inspected the plant and found that thick layers of asbestos dust coated the floors and the ventilation was poor. The dust collection system consisted of canvas bags beneath the roof, which were periodically emptied by shaking, raining huge amounts of asbestos dust inside theplant. Some areas were too dusty to allow accurate fibre counts. The factory was shutdown. Employees were followed prospectively to determine adverse effects. Levin and colleagues found that as of 1993 there were 315 deaths among 1130 former worker from this plant. Six were due to mesothelioma, a rate of 3 per cent, significantly more than in the general population, but less than the rate found in somegroups, like Selikoff ’s insulators.

The experiences at these factories lend support to the concept that the amphiboleshave greater ability than chrysotile to cause mesothelioma. But they also indicate that the intensity of exposure is important. Fibre burden analyses have also confirmed the strong association between amosite exposure and mesothelioma. Roggli and colleagues identified amosite asbestos in 81 per cent of 90 cases of mesothelioma. The amosite fibres accounted for 58 per cent of all fibres 5 mm or greater in length.