Mortality from lung cancer and population risk attributable to asbestos in an asbestos cement manufacturing town in Italy

OBJECTIVE: To estimate mortality from lung cancer and the risk attributable to asbestos separately for asbestos cement workers and for the general (non-occupationally exposed) population in the town of Casale Monferrato, where the largest Italian asbestos cement factory had been in operation in 1907-86. According to cancer registry data, in the same town the incidence of malignant mesothelioma in the general population is about 10 times higher than in comparable Italian provinces. METHOD: Decedents from lung cancer in 1989-95 were nominally identified in the list of decedents kept at the Local Health Authority of Casale Monferrato. Workers in the asbestos cement factory have been identified with a search in the nominal list of workers and the same was done for the wives of asbestos cement workers. These lists have already been used in cohort studies. Sensitivity and specificity of the linkage procedure with occupational activity in asbestos cement production have been evaluated in a previous study. Population at risk was estimated on the basis of official figures and on the results of the cohort study of asbestos cement workers. RESULTS: 227 deaths from lung cancer were included (184 men and 43 women). Among the asbestos cement workers mortalities were 234.0 x 100,000 person-years among men and 35.5 among women. Corresponding figures in the general (non- occupationally exposed) population in Casale Monferrato were 80.6 and 18.7. The rates in the general population were not higher than in the rest of the region. Attributable risk (AR) among the asbestos cement workers (and wives) is 67.5% (95% confidence interval (95% CI) 56.8 to 78.2) for men and 51.3% (95% CI 14.9 to 87.8) among women. Population AR to occupational or paraoccupational exposure in the asbestos cement production is 18.3% (95% CI 11.1 to 25.6) among men and 10.1% (95% CI 0 to 24.6) among women. CONCLUSION: This work did not show an increase in mortality from lung cancer for the population not exposed occupationally, but a large excess was found among men and women occupationally exposed in asbestos cement production. The total burden of lung cancer due to occupational exposure to asbestos may be underestimated, as only occupational exposure in asbestos cement production was taken into consideration. Nevertheless even a single factory can be responsible for a considerable proportion of deaths from lung cancer in a population.

 

     

Asbestos content of lung tissue in asbestos associated diseases: a study of 110 cases

Diseases associated with asbestos exposure include asbestosis, malignant mesothelioma, carcinoma of the lung, and parietal pleural plaques. In this study the asbestos content of lung tissue was examined in groups of cases representing each of these diseases and in several cases with non-occupational idiopathic pulmonary fibrosis. Asbestos bodies (AB), which are the hallmark of asbestos exposure, were present in the lungs of virtually everyone in the general population and present at increased levels in individuals with asbestos associated diseases. The highest numbers of AB occurred in individuals with asbestosis, all of whom had levels greater than or equal to 2000 ABs/g wet lung tissue. Every case with a content of 100,000 ABs/g or higher had asbestosis. Intermediate levels occurred in individuals with malignant mesothelioma and the lowest levels in patients with parietal pleural plaques. There was no overlap between the asbestos content of lung tissue from patients with asbestosis and those with idiopathic pulmonary fibrosis. Lung cancer was present in half the patients with asbestosis, and the distribution of histological patterns did not differ from that in patients with lung cancer without asbestosis. The asbestos body content in patients with lung cancer was highly variable. Control cases had values within our previously established normal range (0-20 ABs/g). There was a significant correlation (p less than 0.001) between AB counted by light microscope and AB and uncoated fibres counted by scanning electron microscopy. The previous observation that the vast majority of asbestos bodies isolated from human tissues have an amphibole core was confirmed.     

Asbestos content of lung tissue in asbestos associated diseases: a study of 110 cases.

Diseases associated with asbestos exposure include asbestosis, malignant mesothelioma, carcinoma of the lung, and parietal pleural plaques. In this study the asbestos content of lung tissue was examined in groups of cases representing each of these diseases and in several cases with non-occupational idiopathic pulmonary fibrosis. Asbestos bodies (AB), which are the hallmark of asbestos exposure, were present in the lungs of virtually everyone in the general population and present at increased levels in individuals with asbestos associated diseases. The highest numbers of AB occurred in individuals with asbestosis, all of whom had levels greater than or equal to 2000 ABs/g wet lung tissue. Every case with a content of 100,000 ABs/g or higher had asbestosis. Intermediate levels occurred in individuals with malignant mesothelioma and the lowest levels in patients with parietal pleural plaques. There was no overlap between the asbestos content of lung tissue from patients with asbestosis and those with idiopathic pulmonary fibrosis. Lung cancer was present in half the patients with asbestosis, and the distribution of histological patterns did not differ from that in patients with lung cancer without asbestosis. The asbestos body content in patients with lung cancer was highly variable. Control cases had values within our previously established normal range (0-20 ABs/g). There was a significant correlation (p less than 0.001) between AB counted by light microscope and AB and uncoated fibres counted by scanning electron microscopy. The previous observation that the vast majority of asbestos bodies isolated from human tissues have an amphibole core was confirmed.     

Lung asbestos burden in shipyard and construction workers with mesothelioma: comparison with burdens in subjects with asbestosis or lung cancer

Although mesothelioma is generally considered to be caused by asbestos, epidemiologic studies indicate that some cases have another cause. In order to determine whether pulmonary asbestos burden can be used to define asbestos-related mesotheliomas, asbestos burden was quantified in 27 shipyard or construction workers with diffuse malignant mesothelioma of the pleura or peritoneum and a history of asbestos exposure. Their burden was significantly greater than the burden found in 19 unexposed men (P less than 0.001). The burdens were also compared to those of previously reported subjects with asbestosis or lung cancer. The median concentration for total amphibole fibers (2.7 million/g dry lung) in subjects with mesothelioma did not differ significantly from our previously reported median values for 14 subjects with asbestosis (1.3 million/g dry lung) or for 60 asbestos workers with lung cancer (1.3 million/g dry lung). Fiber size distribution for amosite, the most prevalent fiber type, was similar in all three subject groups. Fifteen of 25 (60%) subjects with mesothelioma had mild asbestosis. Asbestos body (AB) concentrations were greater than or equal to 1900/g dry lung, and total amphibole fiber concentrations were greater than or equal to 390,000/g dry lung. Counts of ABs greater than or equal to 0.5/cm2 in histologic sections always signified both of these concentrations in extracts. Thus, histologic sections showing greater than or equal to 0.5 ABs/cm2 or extracts containing asbestos body or amphibole fiber concentrations of at least 1900 or 390,000/g dry lung, respectively, will confirm an asbestos-related mesothelioma.     

Asbestos bodies or fibers and the diagnosis of asbestosis

A committee of the College of American Pathologists has proposed that the diagnosis of asbestosis requires fibrosis in respiratory bronchiolar walls and the presence of asbestos bodies (ABs) in tissue sections. To determine whether histologic ABs reliably reflect asbestos fiber concentrations in asbestosis, we compared the concentration of ABs in histologic sections to concentrations of ABs and fibers in tissue extracts of 14 asbestos workers with nonspecific interstitial fibrosis. ABs in histologic sections and extracts correlated well, r = 0.95. Counted and classified by electron microscopy, electron diffraction, and X-ray spectroscopy, commercial amphibole fibers (r = 0.94) also correlated well with ABs, but noncommercial amphiboles (r = -0.02) or chrysotile (r = 0.29) did not. In five subjects with a high percentage of noncommerical amphibole fibers, fewer than 0.5 histologic ABs/cm2 were present despite a total amphibole concentration that was similar to that in subjects with more histologic ABs. We conclude that ABs will be scarce or absent in histologic sections from some subjects with asbestosis, and that for such subjects, extracts of asbestos fibers should yield over 500,000 total amphibole fibers/g dry lung to signify that interstitial fibrosis may be caused by asbestos.     

Modeling mesothelioma risk associated with environmental asbestos exposure

BACKGROUND: Environmental asbestos pollution can cause malignant mesothelioma, but few studies have involved dose-response analyses with detailed information on occupational, domestic, and environmental exposures. OBJECTIVES: In the present study, we examined the spatial variation of mesothelioma risk in an area with high levels of asbestos pollution from an industrial plant, adjusting for occupational and domestic exposures. METHODS: This population-based case-control study included 103 incident cases of mesothelioma and 272 controls in 1987-1993 in the area around Casale Monferrato, Italy, where an important asbestos cement plant had been active for decades. Information collected included lifelong occupational and residential histories. Mesothelioma risk was estimated through logistic regression and a mixed additive-multiplicative model in which an additive scale was assumed for the risk associated with both residential distance from the plant and occupational exposures. The adjusted excess risk gradient by residential distance was modeled as an exponential decay with a threshold. RESULTS: Residents at the location of the asbestos cement factory had a relative risk for mesothelioma of 10.5 [95% confidence interval (CI), 3.8-50.1), adjusted for occupational and domestic exposures. Risk decreased rapidly with increasing distance from the factory, but at 10-km the risk was still 60% of its value at the source. The relative risk for occupational exposure was 6.0 (95% CI, 2.9-13.0), but this increased to 27.5 (95% CI, 7.8-153.4) when adjusted for residential distance. CONCLUSIONS: This study provides strong evidence that asbestos pollution from an industrial source greatly increases mesothelioma risk. Furthermore, relative risks from occupational exposure were underestimated and were markedly increased when adjusted for residential distance.     

Occult exposure to asbestos in steel workers revealed by bronchoalveolar lavage

To investigate the asbestos burden in a steelplant environment, we counted asbestos bodies (ABs) in the bronchoalveolar lavage fluid (BALF) of 65 steel workers who had retired during the previous 5 y. They had worked for at least 15 y in the same area of the plant (coke oven or blast furnace) as maintenance or production workers. On the basis of occupational anamnesis, 28 had occasional past professional exposure to asbestos; the remaining 37 workers denied any contact with asbestos. A total of 54 white-collar workers who had no occupational exposure to asbestos were included in the study as controls. An increased prevalence and concentration of ABs was found in the BALF of steel workers. Electron microscopy and EDAX analysis of AB from steel workers revealed that the core fibers were mainly amphiboles. More ABs were found in the BALF of maintenance workers than in production workers. However, the BALF from steel workers who denied any contact with asbestos revealed an increased AB burden v. controls. This demonstrates that steel workers may be subject to an occult exposure to amphiboles in the steelplant environment.     

Death certificates in epidemiological studies, including occupational hazards: inaccuracies in occupational categories.

We compared death certificates for asbestos-associated diseases (mesothelioma, lung cancer, asbestosis) in two asbestos workers' cohorts. One (insulation workers) had current or recent employment and a strong, continuing union support system which gave them much information about the effects of asbestos exposure. The second cohort, asbestos factory workers, had no such advantage. The factory had closed almost 30 years before, and its workers had dispersed into many areas of the state and nation. Accuracy of medical diagnosis was comparable in the two groups, but occupational listings were not. Three-quarters of the insulators' death certificates told of asbestos work, while virtually none of the factory workers' certificates provided such information, even for deaths of mesothelioma and asbestosis. The data indicate that disease categories, based on medical and pathological diagnoses, at least for asbestos-associated disease, tend to be accurate. Attempts to identify groups at risk by sorting occupational categories can give variable results, good for those with current exposures, much less satisfactory for those with long-past occupational exposures.     

Exposure-response analysis of risk of respiratory disease associated with occupational exposure to chrysotile asbestos.

OBJECTIVES: To evaluate alternative models and estimate risk of mortality from lung cancer and asbestosis after occupational exposure to chrysotile asbestos. METHODS: Data were used from a recent update of a cohort mortality study of workers in a South Carolina textile factory. Alternative exposure-response models were evaluated with Poisson regression. A model designed to evaluate evidence of a threshold response was also fitted. Lifetime risks of lung cancer and asbestosis were estimated with an actuarial approach that accounts for competing causes of death. RESULTS: A highly significant exposure-response relation was found for both lung cancer and asbestosis. The exposure-response relation for lung cancer seemed to be linear on a multiplicative scale, which is consistent with previous analyses of lung cancer and exposure to asbestos. In contrast, the exposure-response relation for asbestosis seemed to be nonlinear on a multiplicative scale in this analysis. There was no significant evidence for a threshold in models of either the lung cancer or asbestosis. The excess lifetime risk for white men exposed for 45 years at the recently revised OSHA standard of 0.1 fibre/ml was predicted to be about 5/1000 for lung cancer, and 2/1000 for asbestosis. CONCLUSIONS: This study confirms the findings from previous investigations of a strong exposure-response relation between exposure to chrysotile asbestos and mortality from lung cancer, and asbestosis. The risk estimates for lung cancer derived from this analysis are higher than those derived from other populations exposed to chrysotile asbestos. Possible reasons for this discrepancy are discussed.     

Screening of autopsy populations for previous occupational exposure to asbestos

A screening procedure to select, in autopsy populations, subjects having a major likelihood of previous occupational exposure to asbestos is described. To test our necropsy population we searched for pleural plaques (PPs); the optical count of both lung asbestos bodies (ABs) and uncoated mineral fibers (UMFs) at least 10 microns in length was recorded. In the adult autopsy population studied in the Turin area, the predictive value given by a positive test for large-size PPs (mostly bilateral) was about 55%. This level of probability did not rise in relation to the AB counts, whereas an increase to over 75% was observed if more than 10,000 UMFs/g dry lung were present. In subjects without PPs or with small-size plaque lesions (mostly unilateral), predictive values of positive tests were 20 to 30% when ABs and UMFs were found to be below 100 and 10,000/g, respectively, and increased to approximately 40% if the AB count exceeded 500/g and to almost 70% for an UMF count above 100,000/g. In subjects without PPs or with small-size plaque lesions, the probability of being nonexposed was greater than 90% if neither ABs nor UMFs were found. This autopsy screening may be a reliable tool in selecting cases most probably related to occupational exposure.     

Correlation between fibre content of the lung and disease in east London asbestos factory workers

The lungs from 36 past workers at an east London asbestos factory who had died from asbestos related disease were compared with lung tissue from 56 matched control patients being operated on in east London for carcinoma of the lung, correlating the severity of asbestosis and the presence of pulmonary carcinoma or mesothelioma of the pleura or peritoneum with an asbestos exposure index and type and amount of mineral fibre in the lungs. Asbestosis was associated with far heavier fibre burdens than mesothelioma. There was also a striking difference in the degree of asbestosis between the subjects with mesothelioma and those with carcinoma of the lung, the asbestosis being more severe in the latter. A further finding was that crocidolite and amosite were strongly associated with asbestosis, carcinoma of the lung complicating asbestosis, and mesothelioma, whereas no such correlation was evident with chrysotile or mullite. It is suggested that more emphasis should be placed on the biological differences between amphibole and serpentine asbestos fibre.     

Relationship between pleural plaques prevalence and extension and biomarkers of cumulative asbestos dose. A necropsy study

Background:The relationship between pleural plaques and cumulative asbestos exposure is controversial.Objectives:To evaluate the relationship between lung asbestos bodies (AB) and fibres (AF) and plaques presence and extension.Methods:In a necropsy series of shipyard workers with asbestos-related diseases, we measured counts (per g of dry lung tissue) of AB (thousands) and AF>1 μm (millions). Pleural plaques were classified into three extension grades. We fitted univariate and multivariable linear (dependent variables: AB and AF, log₁₀ transformed) and multinomial (dependent variable: plaques grade) regression models.Results:We analysed 124 subjects, 13 without plaques 20 with grade 1, 69 with grade 2, and 22 with grade 3 plaques. Geometric means (GM) of AB were 10.6, 23.3, 126, and 140 in the four groups respectively (P=0.0001). GMs for AF (mostly amphiboles) were 1.2, 1.4, 7.3, and 12.9 (P=0.0001). AB and AF were strongly correlated (r=0.81). The likelihood of no plaques and grade 1 plaques decreased with increasing AB and AF doses, with a corresponding increase of grade 2 and 3 plaques. Plaque presence and extension was also associated with histologically verified asbestosis (P<0.001).Conclusions:Our study showed a strong positive relationship between pleural plaque presence and extension and both lung asbestos burden and asbestosis.Key words: Pleural plaques, lung asbestos fibre burden     

Pleural malignant mesothelioma and non-occupational exposure to asbestos in Casale Monferrato, Italy.

OBJECTIVES--To assess and quantify the occurrence of pleural malignant mesotheliomas in people who neither experienced occupational exposure to asbestos nor were married to (or known to live with) workers exposed to asbestos in the workplace. The study was conducted in the area of the local health authority of Casale Monferrato, in north western Italy, where a large factory that produced asbestos cement was active up to 1985. No other major activities related to asbestos have ever been present in the area. METHODS--A retrospective survey covering the period 1980 to 1991 identified 126 incident pleural malignant mesotheliomas histologically diagnosed among residents in the local health authority (population at the 1981 census 98,000). Submission of 83 of 95 cases diagnosed during 1980-9 for revision by a panel of five expert pathologists led to the exclusion of 21. The 31 cases diagnosed in 1990-1 were not submitted for revision. For 64 of the 105 retained cases, information derived from different sources (rosters of the employees in the asbestos cement factory dated back to 1907, list of their spouses, clinical records) did not suggest occupational or paraoccupational exposure to asbestos. RESULTS--Incidence excludes cases for which there was some suggestion of occupational or paraoccupational exposure to asbestos. Incidence of histologically confirmed malignant mesothelioma among residents in the local health authority (annual x 100,000; age adjusted) was 4.2 in men and 2.3 in women (based on 26 and 18 cases respectively). In both sexes, rates in 1985-9 were higher than in the previous quinquennium. Corresponding estimates for 1990-1 (based on unrevised diagnoses) suggest similar rates in men and women. CONCLUSION--Rate ratios which are four to six times those measured by conventional Italian cancer registries can hardly be totally explained by bias produced by lack of recognition of occupational or paraoccupational exposure. The problem of proving this type of negative data is common to other circumstances of alleged cancer clusters of environmental (non occupational) origin.     

Correlation between fibre content of the lung and disease in east London asbestos factory workers.

The lungs from 36 past workers at an east London asbestos factory who had died from asbestos related disease were compared with lung tissue from 56 matched control patients being operated on in east London for carcinoma of the lung, correlating the severity of asbestosis and the presence of pulmonary carcinoma or mesothelioma of the pleura or peritoneum with an asbestos exposure index and type and amount of mineral fibre in the lungs. Asbestosis was associated with far heavier fibre burdens than mesothelioma. There was also a striking difference in the degree of asbestosis between the subjects with mesothelioma and those with carcinoma of the lung, the asbestosis being more severe in the latter. A further finding was that crocidolite and amosite were strongly associated with asbestosis, carcinoma of the lung complicating asbestosis, and mesothelioma, whereas no such correlation was evident with chrysotile or mullite. It is suggested that more emphasis should be placed on the biological differences between amphibole and serpentine asbestos fibre.     

Lung cancer in a female non-smoker with occupational exposure to asbestos: a case report

BACKGROUND: Until recently, asbestos was widely used in a variety of industrial processes. Workers exposed to asbestos may develop lung and pleural diseases such as asbestosis, lung cancer, benign pleural effusion, pleural plaques and mesothelioma. OBJECTIVE: To describe a clinical case of lung cancer in a female non-smoker with occupational exposure to asbestos. METHODS: The clinical and occupational history was based on the information kindly provided by the Occupational Unit of the National Health Service and on the case history of a hospital admittance in 2001, when the patient underwent surgery for lung cancer. RESULTS: The patient worked for 6 years in an asbestos manufacturing industry where she was exposed to high concentrations of asbestos, and then worked for 14 years in a sugar refinery only during the summer. She had benign pleural effusion, pleural plaques, asbestosis and lung cancer. CONCLUSIONS: We concluded that a six-year exposure to high doses of asbestos may induce lung cancer and asbestosis in a female non-smoker.     

Increased risk of malignant mesothelioma of the pleura after residential or domestic exposure to asbestos: a case-control study in Casale Monferrato, Italy.

The association of malignant mesothelioma (MM) and nonoccupational asbestos exposure is currently debated. Our study investigates environmental and domestic asbestos exposure in the city where the largest Italian asbestos cement (AC) factory was located. This population-based case-control study included pleural MM (histologically diagnosed) incidents in the area in 1987-1993, matched by age and sex to two controls (four if younger than 60). Diagnoses were confirmed by a panel of five pathologists. We interviewed 102 cases and 273 controls in 1993-1995, out of 116 and 330 eligible subjects. Information was checked and completed on the basis of factory and Town Office files. We adjusted analyses for occupational exposure in the AC industry. In the town there were no other relevant industrial sources of asbestos exposure. Twenty-three cases and 20 controls lived with an AC worker [odds ratio (OR) = 4.5; 95% confidence interval (CI), 1.8-11.1)]. The risk was higher for the offspring of AC workers (OR = 7.4; 95% CI, 1.9-28.1). Subjects attending grammar school in Casale also showed an increased risk (OR = 3.3; 95% CI, 1.4-7.7). Living in Casale was associated with a very high risk (after selecting out AC workers: OR = 20.6; 95% CI, 6.2-68.6), with spatial trend with increasing distance from the AC factory. The present work confirms the association of environmental asbestos exposure and pleural MM, controlling for other sources of asbestos exposure, and suggests that environmental exposure caused a greater risk than domestic exposure.     

Study of occupational lung cancer in asbestos factories in China.

A retrospective cohort study (1972-81) of occupational cancers in asbestos (chrysotile) factories has been previously published. In this paper the results of continued tracing and interviewing of members of this cohort from 1982 to 1986 is reported. The cohort included 5893 persons (45,974 person-years for men and 39,445 person-years for women). Malignant tumours played a large part in causes of death (36.9%). There were 183 cancers and 67 lung cancers among 496 deaths. The mortality due to lung cancer had a tendency to increase. By comparison with a control group, the RR of lung cancer was 5.32 (p < 0.01), and the SRR of lung cancer was 4.2 (p < 0.01), significantly higher than those of a control group. Among 148 cases of death from asbestosis there were 33 cases complicated with lung cancer (22.3%). The dose-response relations between exposure to asbestos and incidence of asbestosis and lung cancer were also studied in one asbestos factory. There was a positive correlation. A synergistic effect was found between cigarette smoking and lung cancer. Preventive and control measures and exposure limits for asbestos dust in the air of workplaces were recommended.     

The effect of asbestosis on lung cancer risk beyond the dose related effect of asbestos alone

Aims: To determine if the presence of asbestosis is a prerequisite for lung cancer in subjects with known exposure to blue asbestos (crocidolite). Methods: Former workers and residents of Wittenoom with known amounts of asbestos exposure (duration, intensity, and time since first exposure), current chest x ray and smoking information, participating in a cancer prevention programme (n = 1988) were studied. The first plain chest radiograph taken at the time of recruitment into the cancer prevention programme was examined for radiographic evidence of asbestosis according to the UICC (ILO) classification. Cox proportional hazards modelling was used to relate asbestosis, asbestos exposure, and lung cancer. Results: Between 1990 and 2002 there were 58 cases of lung cancer. Thirty six per cent of cases had radiographic evidence of asbestosis compared to 12% of study participants. Smoking status was the strongest predictor of lung cancer, with current smokers (OR = 26.5, 95% CI 3.5 to 198) having the greatest risk. Radiographic asbestosis (OR = 1.94, 95% CI 1.09 to 3.46) and asbestos exposure (OR = 1.21 per f/ml-year, 95% CI 1.02 to 1.42) were significantly associated with an increased risk of lung cancer. There was an increased risk of lung cancer with increasing exposure in those without asbestosis. Conclusion: In this cohort of former workers and residents of Wittenoom, asbestosis is not a mandatory precursor for asbestos related lung cancer. These findings support the hypothesis that it is the asbestos fibres per se that cause lung cancer, which can develop with or without the presence of asbestosis.     

Retention of Asbestos Bodies in the Lungs of Welders

Examination of asbestos bodies (AB) retained in the lungs is a useful way of assessing past occupational exposure to this material. AB retention has been extensively studied in workers directly exposed to asbestos, but less so in those end users, such as welders, who use asbestos-containing products. We therefore retrospectively studied AB retention in 211 welders, for whom biological testing procedures had been requested by a chest physician, between 1988 and 1991. Optical microscopy of AB was performed on samples of sputum (40 subjects), bronchoalveolar lavage fluid (BAL) (147 subjects), and lung tissue obtained after thoracotomy (38 subjects). Information on previous jobs and exposure was obtained using a questionnaire (the mean duration of welding activities was 16.6 years). Eighty-two subjects (38.9%) had elevated lung retention of AB in all the samples studied. Significant AB retention occurred in only 30% of sputum samples, but in 40.1% of BAL samples and 39.5% of lung tissue samples. The duration of welding activities correlated with the density of AB in BAL or lung tissue (r = 0.31, p < 0.01 and r = 0.49, p < 0.05, respectively). On the basis of the questionnaire, only two of the welders with significant AB retention had other occupational exposure to asbestos. Our findings suggest that welding activities may increase lung retention of AB, and consequently might produce higher risks of fibrotic and/or malignant pulmonary diseases. These potential risks need to be brought to the attention of doctors; a longitudinal follow-up may also be warranted in such populations, even after individuals have ceased their welding jobs.     

Pleural mesothelioma: forecasts of the death toll in the area of Casale Monferrato,Italy

In the city of Casale Monferrato, the largest Italian factory that produced asbestos‐cement goods was active from 1907 to 1985. Consequently, asbestos fibers scattered in the surrounding area and caused an enormous number of cases of pleural mesothelioma. Owing to the very long latency of this disease, many subjects have not exhibited its symptoms yet. The aim of this paper is to model and predict the future evolution of the number of deaths due to this disease among residents in the area around that city. The model used here is based on a cellular automata that is assumed to pass through three steps: exposure, contamination, and diagnosis. In this way, forecasts of the future evolution take into account the environmental conditions that changed over the last century because of different levels of plant activity. The model is fitted to annual diagnosis data from 1954 to 2008. Results show that deaths will not end until 2031 and that in the next two decades, at least 505 more subjects will be diagnosed with this disease. Copyright © 2012 John Wiley & Sons, Ltd.