The adverse effects of asbestos were first observed in the early 1900s and the relationship to mesothelioma was suggested in the 1940s. One of the earliest reports linking mesothelioma to occupational asbestos exposure came out of the medical clinic at anasbestos mine in Canada. At a scientific meeting in 1952 Cartier, then in charge of the industrial medical clinic at Thetford Mines, Quebec, reported eight cases of respiratory cancer, two of which he described as pleural tumors. He declared that two such rare cancers in a small series of only eight cases suggested an occupational origin.

By 1960 the scientific community generally recognised asbestos as a cause of mesothelioma. However, the issue was far from settled. In a national survey of mesothelioma in Canada from 1960 to 1968, McDonald and colleagues found a history of asbestos contact in a relatively small proportion of cases – mostly in insulation and allied trades rather than in the asbestos-producing industry. They surveyed pathologists across the country to find all cases of mesothelioma after 1959. They found 165 cases (111 pleural,47 peritoneal, 3 both and 4 pericardial). Updates in subsequent years showed aslightly increased association with asbestos exposure, but still lower than expected. When pathologists reviewed the cases the diagnosis was confirmed in only about 50 per cent of the cases, among whom the incidence of asbestos exposure was also higher.

A follow-up analysis added a chrysotile mining industry cohort and two small groups of employees in gas mask factories to the survey data. They found 254 fatal cases ofmesothelioma (181 men, 73 women) in Quebec from 1960 to 1978. They were able to obtain occupational and residential histories for the majority, and found that only about 40 per cent of the male cases and 5.4 per cent of the female cases were attributable to occupational asbestos exposure (asbestos manufacture, production, insulation, heating trades, shipyards, and construction). Six people probably had household exposure. The intervals between first employment and death from mesothelioma were longer for miners and millers than for manufacturing workers. All the miners and millers had pleural mesothelioma, while the factory workers included 8 with peritoneal mesothelioma. The incidence did not clearly increase over this time period. Subsequent studies showed an increased percentage of cases attributable to asbestos exposure. Ruffie and colleagues conducted a retrospective study of 332 patients diagnosed with pleural mesothelioma at several teaching hospitals in Ontario andQuebec between 1965 and 1984.  They found 396 patients with mesothelioma, including 332 of the pleura. Of the patients with pleural mesothelioma, 262 were menand 70 were women. Ages ranged from 22 to 85 years. About 60 per cent of those with history available had identifiable asbestos exposure. Only 3 were known to have had household exposure and 68 per cent of men and 17 per cent of women had identifiable occupational exposure.

With more detailed occupational histories, more exposures may have been found. In Sherbrooke and Quebec City, almost all of the exposed patients came from the asbestos mining areas of Asbestos and Thetford Mines – mostworking in asbestos processing, as opposed to mining. In Ontario, an important sourceof exposure was from asbestos-cement factories, where 21 cases were observed in acohort of 535. Twenty-five per cent of patients with mesothelioma in Ontario wereimmigrants who had asbestos exposure in their country of origin. In 1994 Spirtas and colleagues published a study aimed at defining the attributable risk of asbestos exposure in the United States. They used the Los Angeles County Cancer Surveillance Program, the New York State Cancer Registry (excluding New YorkCity), and 39 large Veterans Administration hospitals to identify people diagnosed with mesothelioma from 1975 to 1980. They identified 208 cases of pathologically confirmed mesothelioma. Controls were 533 people who had died of other causes. They interviewed immediate family members to obtain asbestos exposure history. Among men the attributable risk for asbestos exposure was 88 per cent, among women it was 23 per cent(although the confidence interval was very wide at 3–72%).

The increasing incidence of mesothelioma in the United States is primarily due to the increased incidence amongmen, thus probably reflecting more occupational exposure. Most patients with mesothelioma do have a history of exposure to asbestos, although it may have been brief and remote in time. The variability in percentages ofcases with identifiable asbestos exposure may be related to several factors: incompletehistory taking, unknown or hidden occupational exposures, or environmental exposure.

The beating room and the trimming machines were in a single building, but the grinder created somuch dust that Whipple was forced to close the door when the machine was operating. There were no warning labels on the asbestos bags, no ventilation fans, and no warning signs in the mill. The union complainedto the management about the dust, but Ruberoid always said it wash armless: ‘Nobody was scared of asbestos then’, Whipple later recalled:‘They didn’t understand it. Hugh Jackson spent his career working for Johns-Manville mostly inplant safety.

From 1952 to 1960 he was manager of the Industrial Health section and he reported directly to Dr Kenneth Smith, the corporation’s medical director. Jackson often visited the Waukegan factory in Illinois, where within a single complex Johns-Manville manufactured thermalinsulation, textiles, paper, mill board, and sheet materials. It also made pipe coverings, shingles, and flat boards. During the manufacture of shingles, asbestos, cement, and silica were combined into slurry, then pressed, dried, and cut into sections. According to Jackson, many of the jobs at Waukegan were dusty. The asbestos would arrive in 100 lb burlap bags, which along with the silica would be dumped by hand into the machines. There was no proper ventilation and the men would breathe in fiber. That pattern was repeated at numerous factories throughout the US. Asbestos dust scattered well beyond the factory gates. The streets around T&N’s Roberts’ plant in Leeds were awash with fibre and in the words of one resident: ‘It was as though we were practically eating dust. I rememberdust and fiber all around the streets near the factory. You could see thedust in the air. I have seen it blow around like a snowstorm.  In addition, workers brought dust home on their clothes.

A physician who worked for an American manufacturer described that problem in the following way: ‘Once asbestos gets into the home, carried home by the workmen, it is there virtually permanently—it gets into the rugs, into the carpets, it gets suspended by movement and actually you are getting 24 hour/day exposure. Most American, British, and French workers who came into contact with asbestos did not work in the primary industry, but were employedat oil refineries, shipyards, on building sites or in auto-repair shops. Inaddition to their exposure to a known hazard they shared a lack of knowledge about the dangers they faced.

The actor Steve McQueen, who died from mesothelioma at the age of 50, and who is said to have worked in shipyards and for a time in a brake-repair shop, is typical of the casualties. The US market for drum brake linings was dominated by Raybestos-Manhattan Inc. Its brake and clutch pads were marketed under the brand names Raybestos and Grey-Rock and sold to automotive warehouses, distributors and jobbers, car dealers, and repair shops. Raybestos also sold direct to ‘do-it-yourself’ car owners. Most drum linings were by weight between a third and three-quarters pure asbestos. Disc pads also contained chrysotile. According to the Asbestos Information Association, by 1972 worldwide over 300 million motor vehicles used asbestos-based brake linings. In that year in the US alone, more than 50,000 tonnes of asbestos was used in their manufacture.

As one manager of an auto-repair shopcommented in 1975: ‘Almost everything that moves uses some form ofasbestos friction material. All repair shops followed much the same procedures. After removing the wheel and brake drum, the brakes were usually cleaned out by compressed air or brushed by hand. Often the new linings were drilled, ground, and the SEC wanted to avoid the spectacle of a pandemic of ARDs in such asmall community. Today the town of Yallourn no longer exists.

Railroad machinists

Railroad machinists were exposed to significant amounts of mostly chrysotile asbestos, especially during the application and removal of asbestos insulation on the boilers of steam locomotives. The last steam engine repairs took place in the late 1950s. In 1988 Mancuso published a study investigating the risk of mesothelioma among railroad machinists. His cohort was railroad machinists employed by a company before 1935, and stillalive in 1945. He analysed the data for 181 people hired from 1920 to 1929. By 1986, 156 were identified as dead. There were 41 cancer deaths, 14 with mesothelioma.

The relative risk was mesothelioma in every 13 machinists hired. Similarly,  in 1986 Schenker completed a case-control analysis of mesothelioma among United States railroad employees. The United States Railroad Retirement Board notified investigators of all deaths among male railroad workers occurring in 1981–82. They reported 15 059 deaths during the study year. Twenty cases of mesothelioma were identified. More cases occurred among the workers in asbestos exposed job categories. The latency period was 30 years or more.

Jewelery industry

In the jewelery industry, asbestos has been used to make soldering forms. There have been case reports of mesothelioma among jewelery workers. However, Dubrow and Gute reported no cases of mesothelioma among 3141 Rhode Island jewelery workers who died during the decade 1968–78. This may have been a premature conclusion, since asbestos was not used in this industry in any significant amount until the 1940s. A cluster of 5 silversmiths with mesothelioma has also been observed in a Native American pueblo of 2000, where asbestos had been routinely used in the production of silver jewelery. After years of dispute, many of the investigators have come to some agreement: that amphiboles and particularly crocidolite are probably more carcinogenic than serpentines, but at high enough exposure levels, all the fiber types can cause mesothelioma.

Thirty per cent of the water distribution pipe sold in the United States in 1974 was asbestos cement. A mortality study of the members of the union of plumbers and pipefitters in the United States found significant excesses in proportional mortality ratios for malignancies, including 7 deaths due to mesothelioma. Two studies of sheet-metal workers in New York City found significantly increased mortality, and mesothelioma was recorded on death certificates in 9 out of 716 total deaths (1.3 per cent).

Studies in construction workers are difficult since specific exposures often are not known, and workers change jobs frequently. Epidemiological studies, however, consistently show that construction workers are one of the groups most at risk for asbestos-related disease and mesothelioma.

In 1967 a surgeon in Somerset hospital reported 17 cases of mesothelioma (9 pleural and 8 peritoneal) over a three year period. He explained the high concentration by the close proximity of the asbestosmill, 3 km from the hospital. There was also a large asbestos dump adjacent to a residential area. Radiologists from the same hospital also reported 10 cases, all with some occupational asbestos exposure. Several years later, the surgeons had treated another 36 cases, and searching through the medical records of neighboring hospitals they found an additional 19 cases, making the total 72. All of the cases where a history was available had an identifiable asbestos exposure in the nearby asbestos mill, except for 2 women who had environmental exposure. Over the years from 1951 to 1972 the incidence increased yearly from 1 per year to 8–9 per year.The discrepancy between these two studies is easy to explain, and highlights one of the difficulties with epidemiological studies of rare diseases with long latency periods. Enterline’s inclusion criteria required that members of the cohort had retired at a certain time, and had lived at least until age 65. They missed all the cases of mesothelioma in people who had already died, or who had not retired.This plant was also known to be extremely dusty, supporting the theory that the degree of exposure is a determining factor in the incidence of mesothelioma. Employees were quoted in the hospital charts as complaining ‘It was like working in a snowstorm’, and ‘I worked in an asbestos fog 20 minutes daily for 22 years’. In 1984 McDonald and colleagues conducted a study of 3641 workers employed for one month or more in a friction products plant in Connecticut from 1938 to 1958.

Like the Manville plant, this factory also used almost exclusively chrysotile asbestos. By 1983, of 3513 employees traced, 1267 had died; death certificates were obtained for 1228. No cases of mesothelioma were identified. These results support the amphibole hypothesis. However, exposures to asbestos in this plantwere probably very low since there were no deaths attributed to asbestosis, which is a disease marker for high exposures.

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.

In 1967, Enterline and Kendrik conducted a study of the effect of asbestos exposureon factory workers. They recorded the causes of deaths among 21 755 white men aged 15 to 65 who worked in several different asbestos-products plants in the United States at sometime during the period 1948 to 1951, identified from social security tax returns filed with theUnited States Bureau of Internal Revenue for the first quarters of 1948, 1949, 1950 and1951. Deaths were identified from death claims filed with the social security administration through 1963, and death certificates were reviewed. A cohort of 6281 cotton textile workerswas used as a control group for the asbestos textile workers. Among 1853 death certificates examined, only one listed mesothelioma.

Although respiratory cancer rates were increased overall, mortality was actually lower than for the general population. At most the follow-upwas only 17 years, so the full effect of asbestos exposure had probably not yet been seen.

Asbestos has been used to insulate the steam pipes and boilers of ships since the turn of the century. The asbestos may be woven in a mattress of cloth and wrapped around piping,  applied as a cement-like material, or sprayed as fire proofing. Not only the insulators were exposed – bystander exposure in this situation was probably significant, since the work was done in the enclosed spaces of ship boiler rooms.

Shipyard worker populations fluctuate greatly. In 1918 there were 318 500 shipyard workers in the United States, compared to 75 000 during the 1920s and 1930s. With the approach of World War II, the shipyards underwent a tremendous expansion and shipbuilding became the largest manufacturing industry in the United States for a time. By the end of 1943, 1 722 500 people were employed in shipyards. In some yards between 10 and 20 per cent of these workers were women. Turnover was very high, so it has been estimated that about 4.5 million people were employed in shipyards during World WarII.

After the war the number of shipyard workers rapidly decreased. Since no dust counts were taken, no one really knows what levels of asbestos fiber existed. They were likely very high at times. In 1975 the use of asbestos in shipbuilding and ship repair was largely abandoned. However, ship repair remained a problem because asbestos previously used as insulation on steam pipes and boilers had tobe ripped out and replaced during renovation and repair work.

A health survey of 1074 insulation workers in United States shipyards was conducted at the end of World War II. No significant evidence of disease was found. However, this was a little early to come to any conclusion. The risk of asbestos-relateddisease among shipyard workers was first recognised in England when five cases of mesothelioma were identified among employees of the Royal Navy Dockyard inDevonport. Evidence of asbestos-associated disease has also been reported among workers employed in United States shipyards during and after World War II.

Several studies since have shown high rates of asbestos-associated disease among shipyard workers in Connecticut, San Francisco and Georgia. In the Pacific Northwest, Hinds looked at all death certificates with mesothelioma listed as the cause of death for the years 1968 through 1976 for the Puget Sound region of Washington State. He found 40 cases of mesothelioma, and compared them to matched controls identified from the death files. He found a clear association between mesothelioma and employment in the Puget Sound Naval Shipyard. Lung burden studies in the Pacific Coast shipyard workers revealed amosite fibers in all cases of mesothelioma. The cases of mesothelioma also seemed to be associated with the presence of low aspect ratio amosite fibers, indicating a possible role for fiber size.

Before 1988, the United States did not even have a specific code formesothelioma, so many cases were misclassified on death certificates as lung cancers orabdominal cancers. In the United States, the best estimates of mesothelioma incidenceare derived from the Surveillance, Epidemiology and End Results (SEER) Program ofthe National Cancer Institute.

The SEER database2 includes about 9.5 per cent of theUnited States population. It covers 10 regional areas, in five states (Connecticut, Iowa,New Mexico, Utah and Hawaii), and five major urban areas – San Francisco–Oakland,New Orleans, Seattle, Atlanta, and Detroit. Although the SEER regions are reasonablyrepresentative of the United States population in terms of demographic and epidemiologicalfactors, the programme may not accurately reflect the country as a whole. Itincludes some shipbuilding areas, but large urban areas where asbestos was used inmanufacturing and construction are underrepresented. The database is organised bycase; each case is identified by age, sex, race, date of diagnosis and cancer type.

The datafor mesothelioma are published only intermittently. However, this database providesthe most comprehensive national incidence data available for this disease.In 1997 Price3 analysed the SEER data for mesothelioma. He divided the data intofive-year age groups in each diagnosis year. He found a consistently higher rate of mesotheliomain men than in women. The rate for women remained relatively constant overthe years. On the other hand, the rate for men increased until 1992, when it peaked at 1.9 per 100 000 people. Since then the incidence rate in men has been slowly decreasing(Fig. 1.1).2 This trend is presumably due to occupational asbestos exposure, which washighest during the years 1930–60.

The highest lifetime risk was for the 1925–30 birthcohort – a group that would have been at work in shipyards, manufacturing and constructionduring the years 1930–60. In recent years in the United States, the incidence has beenapproximately 2000–3000 cases per year, or 11.4 cases per million men and 2.8 cases permillion women.4 The mortality rate in people with prolonged heavy exposure to asbestosvaries from 2 to 10 per cent in different studies, and the latency period between initialexposure and manifestation of disease is usually 20–50 years.

From 1987 to 1996 an averageof 520 people died per year in the United States of malignant mesothelioma.Data from the United States Department of Health and Human Services5 show thatstates with the highest incidence of mesothelioma are all coastal or Great Lakes States.Florida has displaced New York as the State with the highest number of deaths per yearfrom mesothelioma.

In 1996, 78 people died of mesothelioma in Florida. The states withthe highest age-adjusted mortality rates were Washington and Oregon, probably due tothe presence of shipyards. The most frequently recorded occupation on death certificatesof people with mesothelioma in the United States was homemaker (10.6 per cent of alldeaths), followed by managers and administrators, plumbers, pipefitters and steamfitters,production supervisors, labourers, electricians, farmers, carpenters and machinists. Themost common industry was construction, followed by ship building and railroads. Otherareas with significant mesothelioma incidence were schools and government.

Most of the mines were open pit mines, where 13-metre (40-foot) holeswere drilled in asbestos-containing ore deposits, and were then blasted with explosives.Workers loaded the loose ore onto trucks and then transported it to a crushingmachine. Moisture was removed by heating the crushed ore in huge dryers. Duringmilling the ore went through stages of screening and vacuum separation in whichloose asbestos fibre was lifted from the rock.

Conveyor belts, chutes, and vacuumexhaustpipes transported the ore and fibre through the mills. Most employees workedin the mills, cleaning up spilled asbestos fibre, feeding asbestos into storage bins, andmaintaining equipment. Before 1970, only total dust counts were made – asbestosfibre concentrations were not measured separately. Virtually all jobs in this industrywere very dusty. In the 1970s asbestos fibre concentrations were measured, and it wasfound that average asbestos-fibre concentrations were significant, especially in thedrying and crushing operation, and greatly exceeded the asbestos standard of 5 fibresper cubic centimetre (5 f/cm3) of air then in effect in the United States.

Several groups have studied the miners and millers in the Thetford and Asbestosmines over the years. Initially it was thought that this group might reflect exposureonly to chrysotile asbestos, and therefore could answer the question of whetherchrysotile was carcinogenic by itself. McDonald and colleagues began a comprehensivestudy of respiratory morbidity and mortality in a cohort of almost 12 000 workers, born between 1891 and 1920, who had worked in the Quebec asbestos industry, includingthe mines and mills near Asbestos and Thetford. After exclusion of men lost tofollow-up, the cohort consisted of 9780 men: 4175 from the main complex of minesand mills of Thetford mines, 4031 in the mine and mill of Asbestos, 708 in the asbestosproducts factory of Asbestos, and the others from smaller mines in the Thetford region.Initially they found very few deaths due to mesothelioma. Among 2413 maledeaths in the cohort as of the end of 1966, there were only three deaths due to mesothelioma.31 The overall death rate was much lower than that found in other groups.

This large cohort of chrysotile miners and millers in Quebec has been followed eversince, with updated results published periodically, and a review of the data relating tomesothelioma published in 1997. By 1993, almost 80 per cent of the cohort had died, andthe youngest survivors were in their mid-70s. From the total of more than 8000 deaths, were probably due to mesothelioma – all except one probably pleural mesothelioma. Thirty three were miners and millers, and 5 were factory workers. Eight had a history of only minimal known exposure to the asbestos industry, although on further analysis 2 of these were employed in gas mask manufacture, which involved exposure to crocidolite.

When the results were analysed further, the investigators found 25 mesotheliomas in Thetford Minesand only 8 in Asbestos. This corresponded to a rate 33.7 versus 13.2 per 100 000 subject years.At the factory in Asbestos where the 708 employees were potentially exposed to crocidoliteand/or amosite, there were 5 deaths due to mesothelioma out of a total of 553 deaths – a rateof 46.2 per 100 000 subject years. The cases at Thetford were more common in miners thanmillers, whereas those at Asbestos were all in millers. Within the Thetford Mines there weregeographical differences in the rates of mesothelioma, with a substantially increased riskassociated with years of employment in a localised group of 5 mines. The authors felt thatthis indicated that the explanation might be mineralogical.

Multiple lung tissue analyses were done in some of the cases, 39–42 and revealed that even though these men were exposed overwhelmingly to chrysotile, tremolite fibres predominatedin the lungs of the miners and millers, especially those from the region ofThetford mines with the highest incidence of mesothelioma. In the two factory workersand three of the five miners and millers from Asbestos, there were substantial concentrationsof crocidolite. The authors concluded that perhaps the chrysotile was not carcinogenicat all, and the cases of mesothelioma were entirely due to the presence of amphiboles– tremolite in the mines and crocidolite in the factory. Churg and colleagues also found high concentrations of chrysotile fibres in the lungs of people with mesothelioma.

However, other studies contradicted the findings of McDonald and colleagues. Begin and colleagues reviewed the 120 cases of mesothelioma that came before the Worker’s Compensation Board of Quebec from 1967 to 1990. This was a different databasethan that used by McDonald and colleagues. The 49 cases from the chrysotile miningand milling area were compared with 50 cases in manufacturing and construction, and 21 cases from industries where asbestos was not a major work material – often an ‘incidental’material. The first group had a significantly older mean age with longer exposuretime.

In the mining towns of Thetford and Asbestos, the incidence of mesotheliomawas proportional to the workforce (20 in Asbestos and 29 in Thetford), suggesting thatthe greater tremolite contamination in Thetford was not a significant factor in causingmesothelioma. Begin reported an incidence of 2.5 cases per year from 1980 to 1990 or62.5 cases per million per year, and 150–250 cases per million per year among the minersand millers. These numbers were significantly more than those reported by McDonaldin his earlier cohort. The number of cases overall increased significantly in the 1960s to1990s, a time during which most of the McDonald cohort was deceased, suggesting thatMcDonald’s cohort definition may have missed the peak incidence of mesothelioma inQuebec.

The longer exposure duration in the cases with mesothelioma is consistentwith Churg’s finding of increased chrysotile fibres in the lungs of mesothelioma cases.Nicholson, Selikoff and others  also undertook a study of mortality in Canadianminers and millers, in an attempt to determine the carcinogenicity of chrysotile. Theytried to define a cohort that would be comparable to previously published cohorts offactory workers and insulation workers. They identified 544 employees who had spent asleast 20 years working in the mines and mills in the Thetford area, and found only onecase of mesothelioma.

The lower rate of mesothelioma found in this study could be dueto a variety of factors. Fibre type may play a role, with amphiboles likely somewhat morecarcinogenic. However, the difference may also be due to the size or concentration of thefibres inhaled, or it might have just been too early to see the cases of mesothelioma.Two small cohorts of vermiculite miners in the United States have also beenstudied, 44 one of which had also experienced substantial exposure to fibrous tremolite.These studies revealed 4 cases among 165 deaths (406 subjects). Notably, thesestudies were earlier – only 12–21 per cent of the subjects had died.