Document DGZ5zLzzd75mwynk41gobVdVn
review
Annals of Oncology 18: 985-990, 2007 doi:10.1093/annonc/mdl345
Published online 9 October 2006
Epidemiology of peritoneal mesothelioma: a review
P. Boffetta*
International Agency for Research on Cancer, Lyon, France
Received 4 April 2006; revised 2 August 2006; accepted 18 August 2006
The epidemiology of peritoneal mesothelioma is complicated by possible geographic and temporal variations in diagnostic practices. The incidence rates in industrialized countries range between 0.5 and three cases per million in men and between 0.2 and two cases per million in women. Exposure to asbestos is the main known cause of peritoneal mesothelioma. Results on peritoneal mesothelioma have been reported for 34 cohorts exposed to asbestos, among which a strong correlation was present between the percentages of deaths from pleural and peritoneal mesothelioma (correlation coefficient 0.8, P < 0.0001). Studies of workers exposed only or predominantly to chrysotile asbestos resulted in a lower proportion of total deaths from peritoneal mesothelioma than studies of workers exposed to amphibole or mixed type of asbestos. Cases of peritoneal mesothelioma have also been reported following exposure to erionite and Thorotrast, providing further evidence of common etiological factors with the pleural form of the disease. The role of other suspected risk factors, such as simian virus 40 infection and genetic predisposition, is unclear at present. Control of asbestos exposure remains the main approach to prevent peritoneal mesothelioma. Key words: asbestos, epidemiology, peritoneal mesothelioma, thorotrast
ffi
>
CD
introduction
The peritoneum is the second most frequent site of origin of mesothelioma, after the pleura. In developed countries, malignant mesothelioma (International Classification of Diseases for Oncology-Morphology codes 9050-9055) is the most frequent malignant neoplasm of the peritoneum [1]. Symptoms of peritoneal mesothelioma are unspecific, the most frequent being increased abdominal girth, pain and weight loss [2]; usually diagnosis occurs late. Treatment includes the combination of debulking surgery and i.p. chemotherapy. Survival remains poor; in the USA Surveillance, Epidemiology and End Results (SEER) cancer registry data median survival is 10 months and relative 5-year survival is 16% [3], however, in selected clinical series a longer survival (median >50 months) has been reported [2]. Although asbestos has been known for several decades to cause peritoneal mesothelioma, in addition to the pleural form of the disease [4], no detailed review of the epidemiological features of this disease has been published recently.
descriptive epidemiology
The descriptive epidemiology of peritoneal mesothelioma is complicated by temporal and geographic variability in diagnostic criteria. In addition, low sensitivity and low specificity of the diagnosis are important concerns, since
Correspondence to: Dr P. Boffetta, International Agency for Research on Cancer, 150 Cours Albert Thomas, 69008 Lyon, France. Tel +33-4-72738554; Fax: +33-4-72738320; E-mail: boffetta@iarc.fr
mesothelioma of the peritoneum can be misdiagnosed as a neoplasm originating from other abdominal organs, notably adenocarcinoma from the ovary, and vice versa [5, 6]. Furthermore, sensitivity and specificity of the diagnosis may vary by place and time, thus complicating geographic and temporal analyses of the occurrence of the disease. Furthermore, given the strong association between asbestos and mesothelioma, knowledge of previous exposure might influence diagnostic accuracy; if this is the case, a diagnosis of peritoneal mesothelioma would be more frequently made for a patient with recognized past asbestos exposure than for a patient with a similar clinical presentation but without history of asbestos exposure.
The consequences of these potential biases are difficult to assess. Although it is likely that occurrence of peritoneal mesothelioma is underestimated in most populations, overestimation might occur in circumstances of recognized asbestos exposure. In general, caution should be used in the interpretation of the available data on the incidence and mortality from this disease.
Recent international data on the incidence of peritoneal mesothelioma are available from Eurocim, a collaboration of European population-based cancer registries [7], and from the SEER program of the United States [3]. Only sparse data are available from the other countries. Figure 1 reports the most recent data from selected nationwide European cancer registries and the SEER registries; at this level of aggregation, agestandardized incidence rates among men range from 0.5 to about three cases per million population. However, higher rates
2006 European Society for Medical Oncology
Annals of Oncology
are reported in smaller areas with widespread past use of asbestos, such as the harbor city of Genoa, Italy (agestandardized rate in men in 1995, 5.5 per million). In most populations, rates among women are in the range 0.2-2 per million and are lower than in men; although in some countries, such as Sweden, rates are comparable in the two sexes. A correlation in incidence rates exists between the two sexes (correlation coefficient of 1991-1995 rates on the basis of 41 European and nine USA populations covered by cancer registry, 0.41; P = 0.003).
Figure 2 shows the temporal trend in peritoneal mesothelioma incidence among men in selected countries [3, 7]. Rates between 1971 and 1995 remained stable in Sweden and United States (SEER), while they have increased in countries such as Denmark and Scotland. The analysis of age-specific rates provides a deeper insight in the pattern of disease incidence, but it is feasible only in populations with a large enough number of cases to provide meaningful results. Figure 3 shows such rates in England during 1971-1995 (men only); a birth cohort effect is indicated, with the highest rates experienced by men born between 1920 and 1930. A decline in the last time periods is apparent among young men, indicating that the overall incidence might decline in the future. Age- and time-specific trends in women cannot be adequately studied because of random variability.
In an analysis of 50 European and USA populations [3, 7], the incidence rates of peritoneal mesothelioma in men were one order of magnitude lower than those of pleural mesothelioma. Rates of peritoneal mesothelioma among men showed only
a modest correlation with that of the pleural form of the disease (Figure 4). A comparable analysis among women resulted in an even weaker correlation (correlation coefficient 0.14, P value 0.32). The modest correlation between peritoneal and pleural mesothelioma rates can be explained by differences in risk factors (e.g. circumstances of exposure to asbestos), but can also derive from bias in diagnostic and registration procedures.
exposure to asbestos
Data on the occurrence of peritoneal mesothelioma have been reported for 34 cohort studies of workers exposed to asbestos and asbestosis patients. The characteristics and key results of these cohorts are summarized in Table 1. A formal analysis of observed versus expected deaths (or cases) was presented in only few studies, because of difficulties in obtaining reliable reference rates. In order to provide some comparison between the cohorts, we used the proportion of peritoneal mesothelioma deaths over the total number of death as a measure of risk. This approach ignores differences in the age structure of the different study populations as well as temporal changes in the underlying rates. However, it is a relatively good indicator of the effect of an important determinant of the disease.
No peritoneal mesothelioma deaths were reported in 14 of the 34 studies; only two of these studies, however, comprised >1000 deaths, thus providing a reasonable power to detect a risk [13, 33]. The proportion over total deaths ranged in most of the remaining studies between 1/1000 and 1/100 (Table 1), with the
Downloaded from annonc.oxfordjoumals.org by guest on May 4, 2011
Figure 1. Incidence of peritoneal mesothelioma in selected countries
(1991-1995).
Figure 3. Age- and calendar time-specific incidence rates of peritoneal
mesothelioma in England (men).
- - - Denmark - - England 0 Scotland --U--Sweden -A- US SEER
* 1973-1975 for US SEER
Figure 2. Temporal trend in the incidence of peritoneal mesothelioma
in selected countries (men).
pleural mesothelioma
Figure 4. Correlation of peritoneal and pleural mesothelioma incidence
rates among men, 1991-1995 (41 European and nine surveillance, epidemiology and end results populations).
986 | Boffetta
Volume 18 | No. 6 | June 2007
Downloaded from annonc.oxfordjournals.org by guest on May 4, 2011
Annals of Oncology
Table 1. Characteristics and results on peritoneal mesothelioma of cohorts of workers exposed to asbestos and of asbestosis patients
n Exposure circumstance
Fiber type Country
Period employment Sex Size Evidence TD PlMD PeMD LC SMR Reference
1 Gas mask manufacture
Cr
2 Gas mask manufacture
Ch
3 Gas mask manufacture
Cr
4 Textile product manufacture P Ch
5 Cement workers
P Ch
6 Cement workers
Mixed
7 Friction product manufacture Ch
8 Insulation manufacture
Am
9 Railroad repair workers
Mixed
10 Textile product manufacture P Ch
11 Cement workers
P Ch
12 Shipyard workers
Mixed
13 Cement workers
Mixed
14 Mixed exposure
P Ch
15 Mixed exposure
Mixed
16 Various product manufacture Am
17 Cement workers
Ch
18 Cement workers
P Ch
19 Vermiculite miners
Tre-Act
20 Mixed exposure
Mixed
21 Crocidolite miners
Cr
22 Cement workers
P Ch
23 Insulation workers
Mixed
24 Shipyard workers
P Ch
25 Miners
Am, Cr
26 Railroad construction work Mixed
27 Textile product manufacture Ch
28 Miners
Antho
29 Cement workers
P Ch
30 Asbestosis patients
Mixed
31 Cement workers
Mixed
32 Various product manufacture Ch
33 Asbestosis patients
Mixed
34 Cement workers
P Ch
UK UK UK United States UK Canada United States UK Sweden UK Sweden United States France Poland Germany United States UK United States United States United States Australia Austria United States Sweden South Africa Italy United States Finland Italy Italy Israel China Poland Norway
1938-1945 1939 1939 1938-1958 1936-1977 1955-1959 1939-1958 1945-1978 1939-1980 1933-1974 1943-1976 1950-1969 1940-1977 1945-1985 1930-1974 1941-1945 1941-1983 1937-1970 1970-1981 1941-1967 1943-1966 1950-1981 1967 1977-1979 1945-1981 1970-1989 1940-1965 1953-1967 1950-1980 1979a 1953-1992 1972 1970-1997a 1942-1976
F 578 MR F 570 DC F 757 DC M 4137 DC M 1592 DC M 535 DC M 3641 DC M 4820 DC M 3442 DC M 3211 DC M 1216 DC M 5191 CR M 1506 DC M 2403 DC PM 3070 DC M 820 BE MF 2167 DC M 6931 BE M 569 DC M 1074 DC PM 6916 DC NA 2816 DC M 17800 BE M 3893 DC M 7317 BE M 1534 DC MF 3022 DC M 736 CR M 2605 DC F 631 DC M 3057 BE M 515 MR M 907 DC M 541 CR
166 177 219 1392 351 108 1267 333 925 1113 220 668 206 527 185 593 486 2143 161 617 843 540 4951 NA 1225 194 1259 NA 1147 277 NA 132 300 NA
13 1 3
10 2 11 0 4 5 10 0 8 3 1 6 8 1 9 2 6 33 7 173 11 22 3 2 3 53 14 20 1 3 18
4 0 2 4 0 8 0 1 0 1 0 0 1 0 0 9 0 1 0 2 1 3 285 0 6 2 0 1 23 12 1 1 0 0
1.94 1.25 2.10 NA 0.93 4.90 1.49 1.96 1.16 1.32 1.23 1.09 2.17 1.41 1.44 4.97 0.97 NA 2.23 2.71 2.64 1.70 3.75 0.85 1.72 1.45 1.97 2.88 2.48 4.83 1.35 NA 1.68 3.10
[8] [9] [9] [10] [11] [12] [13] [14] [15] [16] [17] [18] [19] [20] [21] [22] [23] [24] [25] [26] [27] [28] [29] [30] [31] [32] [33] [34] [35] [36] [37] [38] [39] [40]
"Period of diagnosis. Fiber type: Ch, pure chrysotile; P Ch, predominantly chrysotile; Cr, crocidolite (pure or predominant); Am, amosite (pure or predominant); Antho, anthophillite; Tre-Act, tremolite-actinophyllite. Sex: M, males; F, females; MF, males and females; PM, predominantly males. Evidence: DC, death certificate; CR, cancer registry; BE, best evidence (ad hoc investigation); MR, routine medical records. TD, total deaths; PlMD, pleural mesothelioma deaths; PeMD, peritoneal mesothelioma deaths; LC SMR, standardized mortality ratio of lung cancer; NA, not available.
exception of cohorts of cement workers from Canada [12], insulators from United States [29] and asbestosis patients from Italy [36] in which >4% of total deaths were from peritoneal mesothelioma. There was a strong correlation between the percentage of peritoneal mesothelioma deaths and both the percentage of pleural mesothelioma deaths (Figure 5) and the standardized mortality ratio of lung cancer (not shown in detail, correlation coefficient 0.85, P < 0.0001). The latter result replicates the finding of a previous analysis of a smaller number of cohort studies [41].
A higher proportion of studies of cohorts of workers exposed to chrysotile (either as unique or as predominant fiber type) reported no peritoneal mesothelioma deaths (nine of 15) as compared with studies of cohorts of workers to amphiboles or mixed fibers (four of 17; Table 2, column 3; chi-square test, P value 0.04). The proportion of mesothelioma deaths over total
8
6
0
E 4
2468
% pleural meso.
correlation coefficient 0.80, p<0.0001
Figure 5. Correlation of percentage of pleural and peritoneal
mesothelioma deaths in cohorts of asbestos-exposed workers.
deaths was higher in cohorts exposed to amphiboles or mixed fibers than in cohorts exposed to chrysotile (Table 2), but the difference was not statistically significant (P value after
Volume 18 | No. 6 | June 2007
doi:10.1093/annonc/mdl345 | 987
jDownloaded from annonc.oxford ournals.org by guest on May 4, 2011
Annals of Oncology
Table 2. Percentage of peritoneal mesothelioma deaths (PMDs) over total deaths (TDs), by type of asbestos fiber
Asbestos type
Overall Pure chrysotile Predominant chrysotile Amphiboles Mixed
Cohort number (see Table 1)
2, 7, 17, 22, 32 4, 5, 10, 11, 14, 18, 22, 24, 29, 34 1, 3, 8, 16, 21, 25 6, 9, 12, 13, 15, 20, 23, 26, 30, 31, 33
n cohorts with no PMD
13 of 32 4 of 5 5 of 10 0 of 6 4 of 11
PMD/TD (%)a Median
0.2 0.8 0.3 0.7 2.7
"Information on proportion of PMD available for 30 cohorts (see Table 1 for details), excluding cohorts with no PMD. Two cohorts (number 19 and 28) excluded from the analysis. NA, not applicable.
Range
0.05-7.4 NA 0.05-2.0 0.1-2.4 0.3-7.4
adjustment for geographic region, 0.09). It was not possible to assess the effect of different types of amphibole fibers. Similar conclusions were noticed in a previous analysis of a smaller number of cohorts [41]. No effect of geographic region on the proportion of mesothelioma deaths over total deaths was detected [P value, on the basis of four regions (United States, UK, Western Europe, other countries) and adjusted for asbestos type, 0.9]. Only four studies were available of women (Table 1), pre-empting detailed analyses. No difference was found in the proportion of peritoneal mesothelioma deaths over total deaths according to diagnostic accuracy (death certificate versus best evidence, results not shown in detail). An effect of period of employment was apparent, with the cohorts of workers first employed before 1950 having a lower proportion of peritoneal mesothelioma deaths over total deaths than cohorts of workers employed later (P value after adjustment for geographic region, 0.005). This finding might reflect improved diagnostic accuracy during recent decades.
The dose-response relationship between occupational asbestos exposure and peritoneal mesothelioma risk has been investigated on the basis of the studies providing information on quantitative asbestos exposure [41]. The risk of peritoneal mesothelioma for workers exposed to amphiboles was proportional to the square of cumulative exposure, while a similar estimate could not be obtained for chrysotile-exposed workers [41, 42].
The important role of occupational exposure to asbestos in causing peritoneal mesothelioma has been confirmed in two community-based studies. A study from 24 of the United States [43] included 657 death certificates with peritoneal cancer (not specified as to histological type) as underlying cause recorded during 1984-1992. The occupation listed on the death certificate of these decedents (typically, the last occupation) was more frequently a job-entailing exposure to asbestos than the occupation of controls (deaths from other causes, matched 10 : 1 to cases). In particular, the odds ratio (OR) of peritoneal cancer was 180 [95% confidence interval (CI) 23, 1375] for insulation workers and 7.6 (95% CI 2.3, 25) for manufacturers of nonmetallic mineral products, including asbestos. When the authors applied a matrix for asbestos exposure on the basis of the jobs listed on the death certificate, they found a strong relationship with probability and intensity of exposure.
In a case-control study from Los Angeles and New York, USA, 20 cases of (or deaths from) peritoneal mesothelioma among men were compared with death certificate controls [44].
Interviews were conducted with next of kin. Exposure to asbestos, either self-reported or derived from occupational history, was present for 17 of the cases (OR 3.1, 95% CI 0.8,15). The fraction of peritoneal mesothelioma attributable to asbestos exposure in this population was 58% (95% CI 20, 89).
Two studies provided evidence of an increased risk of peritoneal mesothelioma following nonoccupational exposure to asbestos. In a study from England, two cases of peritoneal mesothelioma were reported in women with household exposure [45]. No cases were reported among individuals with neighborhood exposure, while for seven cases, including three in men, there was no evidence of occupational or environmental exposure to asbestos. In a study from United States, eight cases of peritoneal mesothelioma were reported among women without occupational exposure; household exposure was reported for seven of them and residential exposure for three, including the case without household exposure [46]. In the case-control study from Los Angeles and New York mentioned above, no cases of peritoneal mesothelioma had residential exposure to asbestos [44].
exposure to other mineral fibers
Erionite is a silicate fiber belonging to the family of zeolites [47]. An increased risk of pleural mesothelioma and lung cancer has been reported among residents in a contaminated area from Cappadocia, Turkey, in which no sources of asbestos exposure were identified [48-50]. In particular, in a survey of 141 deaths in four villages, during 1979-1983, 29 deaths from pleural mesothelioma (20.5%) and four deaths from peritoneal mesothelioma (3.5%) were identified [50]. In a study of 162 Cappadocian migrants to Sweden, one case of peritoneal mesothelioma was identified [51].
There is no evidence of an increased risk of peritoneal mesothelioma among workers exposed to man-made vitreous fibers [52], although the available studies do not have a sufficient statistical power to detect a small increase in risk.
ionizing radiation
Three cohorts of patients receiving Thorotrast for radiological examinations reported results on peritoneal mesothelioma risk (Table 3). Although a formal estimate of the risk is complicated by uncertainties in the calculation of expected deaths, these
988 | Boffetta
Volume 18 | No. 6 | June 2007
Downloaded from annonc.oxfordjournals.org by guest on May 4, 2011
Annals of Oncology
Table 3. Peritoneal mesothelioma in patients exposed to Thorotrast
Country, circumstance of exposure Denmark, cerebral arteriography
Germany, limb or cerebral arteriography
Japan, arteriography
Follow-up period; method 1935-1992; CR
NR; AS 1945-1992; AS
n patients 999
2326 370
n perit. meso 6
4 1
n pl. meso 2
5 0
Comments Pathological verification. p53 mutation
in peritoneal meso: 0 of 6
Three additional retroperitoneal neoplasms
Reference [53]
[54] [55]
perit., peritoneal; meso, mesothelioma; pl., pleural; CR, cancer registry; AS, active surveillance; NR, not reported.
patients experienced a cumulative incidence of peritoneal mesothelioma between 0.2% and 0.6%, higher than that of many cohorts of asbestos-exposed workers listed in Table 1. The incidence of peritoneal mesothelioma among Thorotrast patients was comparable with, or even greater than, that of pleural mesothelioma. The deposition of a-particles in abdominal organs adjacent to the peritoneum, such as the liver, spleen and lymph nodes is a plausible explanation of these findings. The time of appearance of peritoneal mesotheliomas in the Danish cohort of Thorotrast patients was longer than that of other cancers whose risk was also increased, such as liver and lung cancer [53]. An additional three cohorts of Thorotrast patients have been studied [56-58], but results for peritoneal mesothelioma have not been reported. The evidence on the risk of peritoneal mesothelioma following exposure to other sources of ionizing radiation is limited to a few case reports, e.g. of cancer patients who underwent radiotherapy [59].
other risk factors
A large number of studies detected sequences of the papovavirus, simian virus 40 (SV40) in samples of pleural mesothelioma [60]; however, the causal nature of this association has been questioned [61], and laboratory contamination may explain some of the findings [62]. In one of these studies, 11 German cases of peritoneal mesothelioma were also included, seven of which were positive for SV40 Tag sequences [63].
A possible role of chronic pancreatitis in peritoneal mesothelioma has been indicated, but not formally evaluated [64]. Genetic factors have been indicated to play a role in pleural mesothelioma [65]. Very limited information is available on the peritoneal form of the disease. In the case-control study from Los Angeles and New York mentioned above, the mother of an asbestos-exposed case of peritoneal mesothelioma was reported to have suffered from the same neoplasm [66]. No studies are available on other potential risk factors (e.g. nutrition).
conclusions
The rarity of the peritoneal mesothelioma and its diagnostic uncertainties limit our understanding of its epidemiological features. Asbestos is the main known cause of the disease, but other risk factors are likely to be involved in its etiology and pathogenesis. Although the evidence is not conclusive, this review of cohort and case-control studies indicates that the association between asbestos exposure and peritoneal
mesothelioma is less strong than in the case of pleural mesothelioma. This might explain the relatively low correlation between the incidence of the two diseases. The other known risk factors explain only a very small proportion of cases of peritoneal mesothelioma. Despite these limitations, control of exposure to asbestos, in particular at the workplace, remains the main approach for the prevention of peritoneal mesothelioma.
references
1. Mack TM. Sarcomas and other malignancies of soft tissue, retroperitoneum, peritoneum, pleura, heart, mediastinum, and spleen. Cancer 1995; 75: 211-244.
2. Mohamed F, Sugarbaker PH. Peritoneal mesothelioma. Curr Treat Options Oncol 2002; 3: 375-386.
3. Surveillance, Epidemiology, and End Results (SEER) Program. SEER*Stat Database: Incidence--SEER 9 Regs Public-Use, Nov 2003 Sub (1973-2001), National Cancer Institute, DCCPS, Surveillance Research Program, Cancer Statistics Branch, released April 2004, based on the November 2003 submission; http://www.seer.cancer.gov (28 September 2006, date last accessed).
4. Wagner JC, Gilson JC, Berry G et al. Epidemiology of asbestos cancers. Br Med Bull 1971; 27: 71-76.
5. Krasuski P, Poniecka A, Gal E. The diagnostic challenge of peritoneal mesothelioma. Arch Gynecol Obstet 2002; 266: 130-132.
6. Nielsen AM, Olsen JH, Madsen PM et al. Peritoneal mesotheliomas in Danish women: review of histopathologic slides and history of abdominal surgery. Acta Obstet Gynecol Scand 1994; 73: 581-585.
7. European Network of Cancer Registries. Eurocim Version 4.0. European Incidence Database V2.3, CI5 Dictionary (2001). Lyon, France: IARC 2001.
8. Jones JS, Smith PG, Pooley FD et al. The consequences of exposure to asbestos dust in a wartime gas-mask factory. IARC Sci Publ 1980; 30: 637-653.
9. Acheson ED, Gardner MJ, Pippard EC et al. Mortality of two groups of women who manufactured gas masks from chrysotile and crocidolite asbestos: a 40-year follow-up. Br J Ind Med 1982; 39: 344-348.
10. McDonald AD, McDonald JC, Pooley FD. Mineral fibre content of lung in mesothelial tumours in North America. Ann Occup Hyg 1982; 26: 417-422.
11. Thomas HF, Benjamin IT, Elwood PC et al. Further follow-up study of workers from an asbestos cement factory. Br J Ind Med 1982; 39: 273-276.
12. Finkelstein MM. Mortality among employees of an Ontario asbestos-cement factory. Am Rev Respir Dis 1984; 129: 754-761.
13. McDonald AD, Fry JS, Woolley AJ et al. Dust exposure and mortality in an American chrysotile asbestos friction products plant. Br J Ind Med 1984; 41: 151-157.
14. Acheson ED, Gardner MJ, Winter PD et al. Cancer in a factory using amosite asbestos. Int J Epidemiol 1984; 13: 3-10.
15. Ohlson CG, Klaesson B, Hogstedt C. Mortality among asbestos-exposed workers in a railroad workshop. Scand J Work Environ Health 1984; 10: 283-291.
16. Peto J, Doll R, Hermon C et al. Relationship of mortality to measures of environmental asbestos pollution in an asbestos textile factory. Ann Occup Hyg 1985; 29: 305-355.
Volume 18 | No. 6 | June 2007
doi:10.1093/annonc/mdl345 | 989
Downloaded from annonc.oxfordjournals.org by guest on May 4, 2011
Annals of Oncology
17. Ohlson CG, Hogstedt C. Lung cancer among asbestos cement workers. A Swedish cohort study and a review. Br J Ind Med 1985; 42: 397-402.
18. Kolonel LN, Yoshizawa CN, Hirohata T et al. Cancer occurrence in shipyard workers exposed to asbestos in Hawaii. Cancer Res 1985; 45: 3924-3928.
19. Alies-Patin AM, Valleron AJ. Mortality of workers in a French asbestos cement factory 1940-82. Br J Ind Med 1985; 42: 219-225.
20. Szeszenia-Dabrowska N, Wilczynska U, Szymczak W. Risk of cancer in women occupationally exposed to asbestos dust. Med Pr 1986; 37: 243-249.
21. Woitowitz HJ, Lange HJ, Beierl L et al. Mortality rates in the Federal Republic of Germany following previous occupational exposure to asbestos dust. Int Arch Occup Environ Health 1986; 57: 161-171.
22. Seidman H, Selikoff IJ, Gelb SK. Mortality experience of amosite asbestos factory workers: dose-response relationships 5 to 40 years after onset of short-term work exposure. Am J Ind Med 1986; 10: 479-514.
23. Gardner MJ, Winter PD, Pannett B et al. Follow up study of workers manufacturing chrysotile asbestos cement products. Br J Ind Med 1986; 43: 726-732.
24. Hughes JM, Weill H, Hammad YY. Mortality of workers employed in two asbestos cement manufacturing plants. Br J Ind Med 1987; 44: 161-174.
25. Amandus HE, Wheeler R. The morbidity and mortality of vermiculite miners and millers exposed to tremolite-actinolite: part II. Mortality. Am J Ind Med 1987; 11: 15-26.
26. Enterline PE, Hartley J, Henderson V. Asbestos and cancer: a cohort followed up to death. Br J Ind Med 1987; 44: 396-401.
27. Armstrong BK, de Klerk NH, Musk AW et al. Mortality in miners and millers of crocidolite in Western Australia. Br J Ind Med 1988; 45: 5-13.
28. Neuberger M, Kundi M. Individual asbestos exposure: smoking and mortality--a cohort study in the asbestos cement industry. Br J Ind Med 1990; 47: 615-620.
29. Selikoff IJ, Seidman H. Asbestos-associated deaths among insulation workers in the United States and Canada, 1967-1987. Ann N Y Acad Sci 1991; 643:1-14.
30. Sanden A, Jarvholm B, Larsson S et al. The risk of lung cancer and mesothelioma after cessation of asbestos exposure: a prospective cohort study of shipyard workers. Eur Respir J 1992; 5: 281-285.
31. Sluis-Cremer GK, Liddell FD, Logan WP et al. The mortality of amphibole miners in South Africa, 1946-80. Br J Ind Med 1992; 49: 566-575.
32. Menegozzo M, Belli S, Bruno C et al. Mortality due to causes correlatable to asbestos in a cohort of workers in railway car construction. Med Lav 1993; 84: 193-200.
33. Dement JM, Brown DP, Okun A. Follow-up study of chrysotile asbestos textile workers: cohort mortality and case-control analyses. Am J Ind Med 1994; 26: 431-447.
34. Meurman LO, Pukkala E, Hakama M. Incidence of cancer among anthophyllite asbestos miners in Finland. Occup Environ Med 1994; 51: 421-425.
35. Magnani C, Terracini B, Ivaldi C et al. Tumor mortality and from other causes in asbestos cement workers at the Casale Montferrato plant. Med Lav 1996; 87: 133-146.
36. Germani D, Belli S, Bruno G et al. Cohort mortality study of women compensated for asbestosis in Italy. Am J Ind Med 1999; 36: 129-134.
37. Tulchinsky TH, Ginsberg GM, Iscovich J et al. Cancer in ex-asbestos cement workers in Israel, 1953-1992. Am J Ind Med 1999; 35: 1-8.
38. Yano E, Wang ZM, Wang XR et al. Cancer mortality among workers exposed to amphibole-free chrysotile asbestos. Am J Epidemiol 2001; 154: 538-543.
39. Szeszenia-Dabrowska N, Urszula W, Szymczak W et al. Mortality study of workers compensated for asbestosis in Poland, 1970-1997. Int J Occup Med Environ Health 2002; 15: 267-278.
40. Ulvestad B, Kjaerheim K, Martinsen JI et al. Cancer incidence among workers in the asbestos-cement producing industry in Norway. Scand J Work Environ Health 2002; 28: 411-417.
41. Hodgson JT, Darnton A. The quantitative risks of mesothelioma and lung cancer in relation to asbestos exposure. Ann Occup Hyg 2000; 44: 565-601.
42. Coggon D, Inskip H, Winter P et al. Differences in occupational mortality from pleural cancer, peritoneal cancer, and asbestosis. Occup Environ Med 1995; 52: 775-777.
43. Cocco P, Dosemeci M. Peritoneal cancer and occupational exposure to asbestos: results from the application of a job-exposure matrix. Am J Ind Med 1999; 35: 9-14.
44. Spirtas R, Heineman EF, Bernstein L et al. Malignant mesothelioma: attributable risk of asbestos exposure. Occup Environ Med 1994; 51: 804-811.
45. Newhouse ML, Thompson H. Mesothelioma of pleura and peritoneum following exposure to asbestos in the London area. 1965. Br J Ind Med 1993; 50: 769-778.
46. Vianna NJ, Polan AK. Non-occupational exposure to asbestos and malignant mesothelioma in females. Lancet 1978; i: 1061-1063.
47. International Agency for Research on Cancer. Silica and Some Silicates. IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Volume 42. Lyon, France: IARC 1997; 225.
48. Baris YI, Saracci R, Simonato L et al. Malignant mesothelioma and radiological chest abnormalities in two villages in Central Turkey. An epidemiological and environmental investigation. Lancet 1981; i: 984-987.
49. Saracci R, Simonato L, Baris Y et al. The age-mortality curve of endemic pleural mesothelioma in Karain, Central Turkey. Br J Cancer 1982; 45: 147-149.
50. Baris YI, Simonato L, Artvinli M et al. Epidemiological and environmental evidence of the health effects of exposure to erionite fibres: a four-year study in the Cappadocian region of Turkey. Int J Cancer 1987; 39: 10-17.
51. Metintas M, Hillerdal G, Metintas S. Malignant mesothelioma due to environmental exposure to erionite: follow-up of a Turkish emigrant cohort. Eur Respir J 1999; 13: 523-526.
52. International Agency for Research on Cancer. Man-Made Vitreous Fibres. IARC Monographs on the Evaluation of The Carcinogenic Risks to Humans. Volume 81. Lyon, France: IARC 2002.
53. Andersson M, Wallin H, Jonsson M et al. Lung carcinoma and malignant mesothelioma in patients exposed to Thorotrast: incidence, histology and p53 status. Int J Cancer 1995; 63: 330-336.
54. Van Kaick G, Dalheimer A, Hornik S et al. The German thorotrast study: recent results and assessment of risks. Radiat Res 1999; 152 (Suppl): S64-S71.
55. Ishikawa Y, Mori T, Machinami R. Lack of apparent excess of malignant mesothelioma but increased overall malignancies of peritoneal cavity in Japanese autopsies with Thorotrast injection into blood vessels. J Cancer Res Clin Oncol 1995; 121: 567-570.
56. Nyberg U, Nilsson B, Travis LB et al. Cancer incidence among Swedish patients exposed to radioactive thorotrast: a forty-year follow-up survey. Radiat Res 2002; 157: 419-425.
57. Dos Santos Silva I, Malveiro F, Jones ME et al. Mortality after radiological investigation with radioactive Thorotrast: a follow-up study of up to fifty years in Portugal. Radiat Res 2003; 159: 521-534.
58. Travis LB, Hauptmann M, Gaul LK et al. Site-specific cancer incidence and mortality after cerebral angiography with radioactive thortrast. Radiat Res 2003; 160: 691-706.
59. Gilks B, Hegedus C, Freeman H et al. Malignant peritoneal mesothelioma after remote abdominal radiation. Cancer 1988; 61: 2019-2021.
60. Gazdar AF, Butel JS, Carbone M. SV40 and human tumours: myth, association or causality? Nat Rev Cancer 2002; 2: 957-964.
61. Klein G, Powers A, Croce C. Association of SV40 with human tumors. Oncogene 2002; 21: 1141-1149.
62. Lopez-Rios F, Illei BP, Rusch V et al. Evidence against a role for SV40 infection in human mesotheliomas and high risk of false-positive PCR results owing to presence of SV40 sequences in common laboratory plasmids. Lancet 2004; 364: 1157-1166.
63. Shivapurkar N, Wiethege T, Wistuba II et al. Presence of simian virus 40 sequences in malignant pleural, peritoneal and noninvasive mesotheliomas. Int J Cancer 2000; 85: 743-745.
64. Peterson JT Jr, Greenberg SD, Buffler PA. Non-asbestos-related malignant mesothelioma. A review. Cancer 1984; 54: 951-960.
65. Carbone M, Kratzke RA, Testa JR. The pathogenesis of mesothelioma. Semin Oncol 2002; 29: 2-17.
66. Heineman EF, Bernstein L, Stark AD et al. Mesothelioma, asbestos, and reported history of cancer in first-degree relatives. Cancer 1996; 77: 549-554.
990 | Boffetta
Volume 18 | No. 6 | June 2007