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PubMed1987

Asbestos and cancer: a cohort followed up to death.

The mortality experience of 1074 white men who retired from a United States asbestos company during the period 1941-67 and who were exposed to asbestos working as production and maintenance employees for the company is reported to the end of 1980 when 88% of this cohort was known to be dead. As noted in earlier reports the mortality for respiratory and gastrointestinal cancer was raised. A more detailed examination of causes of death shows that the excess in gastrointestinal cancer was largely due to a statistically significant excess in stomach cancer. A statistically significant excess was also noted for kidney cancer, cancer of the eye, and non-malignant respiratory disease. Eight deaths from malignant mesothelioma were observed, two of which were peritoneal. Asbestos exposures for these mesothelioma cases were low relative to other members of the cohort. Continuing follow up of this cohort shows a dose response relation for respiratory cancer that has become increasingly linear. Standardised mortality ratios peaked 10 to 15 years after retirement and were relatively constant at around 250 in each five year interval starting in 1950. This excess might have been detected as early as 1960 but certainly by 1965. The mortality experience of this cohort reflects the ultimate effects of asbestos since nearly all of the cohort has now died.

Aged↗

PubMed1987

Relation between lung function, exercise capacity, and exposure to asbestos cement.

A group of 137 male workers with known exposure (mean 20 fibre years per millilitre) to asbestos cement who had symptoms or signs of pulmonary disease was studied together with a reference group of 49 healthy industrial workers with no exposure to asbestos. Lung function measurements were made at rest and during exercise. Evidence of lung fibrosis was found as well as of obstructive airways disease in the exposed group compared with the reference group. Asbestos cement exposure was related to variables reflecting lung fibrosis but not to variables reflecting airflow obstruction. Smoking was related to variables reflecting obstructive lung disease. Exercise capacity was reduced in the exposed workers and was related to smoking and to lung function variables, reflecting obstructive airways disease. There was no significant correlation between exercise capacity and exposure to asbestos cement.

Asbestos↗

PubMed1989

Progression of irregular opacities in asbestos miners.

All white and mixed race men who were employed in South African asbestos mines and mills between 30 November 1970 and 30 November 1975 were studied. The men who had two radiographs available, the first taken some time between the above two dates and the latest available radiograph which had to be at least two years after the first one numbered 1454: 793 continued exposure after the first radiograph and 661 did not. The films were read by a panel of three readers. Data available included age, years of exposure to asbestos and other mining, intensity of exposure to asbestos and other dust, and smoking habit. Progression was expressed as the difference between the average readings of radiograph 2--radiograph 1 in minor categories per year of irregular opacities. Changes in pleural abnormality were also measured. No differences of progression in the profusion or change in size of the irregular opacities were found between the two groups or in the number of zones affected. "New attacks" appeared equally frequently between the two groups. No difference in the change in extent of any type of pleural change was seen. It appears that once a dose of asbestos sufficient to initiate the disease has been retained it is inexorably progressive.

Asbestos↗

PubMed1991

Frequency of sister chromatid exchange and chromosomal aberrations in asbestos cement workers.

Exposure to asbestos minerals has been associated with a wide variety of adverse health effects including lung cancer, pleural mesothelioma, and cancer of other organs. It was shown previously that asbestos samples collected from a local asbestos factory enhanced sister chromatid exchanges (SCEs) and chromosomal aberrations in vitro using human lymphocytes. In the present study, 22 workers from the same factory and 12 controls were further investigated. Controls were matched for age, sex, and socioeconomic state. The peripheral blood lymphocytes were cultured and harvested at 48 hours for studies of chromosomal aberrations and at 72 hours for SCE frequency determinations. Asbestos workers had a raised mean SCE rate and increased numbers of chromosomal aberrations compared with a control population. Most of the chromosomal aberrations were chromatid gap and break types.

Adult↗

PubMed1991

Respiratory findings among ironworkers: results from a clinical survey in the New York metropolitan area and identification of health hazards from asbestos in place at work.

Diseases associated with asbestos are prevalent in the construction trades primarily as the result of the previously widespread use of insulation materials containing asbestos in the building industry. Workers in metal related trades, who are employed at construction sites, but who do not routinely use such materials in their work, may also be at risk for asbestos hazards. To assess such risk, a clinical survey was conducted on 869 ironworkers from the New York metropolitan area. A high prevalence of abnormalities on chest radiographs was found. Three hundred and twenty nine (38%) of the examined workers had pleural abnormalities on their chest radiographs consistent with asbestos induced effects. The prevalence of radiographic abnormalities indicating interstitial lung disease was low (7%) as was the prevalence of restrictive pulmonary function impairment (7%). Association was found between forced vital capacity (FVC) and pleural abnormalities on chest radiographs. Although ex-smokers appeared to have the highest prevalence of abnormalities, regression analyses showed that duration of employment in the ironworkers' trade was the most important factor associated with them.

Asbestos↗

PubMed1993

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.

Asbestos, Serpentine↗

PubMed1993

A cohort study on mortality among wives of workers in the asbestos cement industry in Casale Monferrato, Italy.

The study investigates mortality from cancer and other diseases in a cohort of wives of asbestos cement workers in Casale Monferrato (northwest Italy). After the exclusion of women with an occupational record in the asbestos cement industry, the cohort comprised 1964 women. Their domestic exposure was estimated according to their husbands' periods of employment in the plant: 1740 had a period of domestic exposure whereas the remaining 224 married an asbestos cement worker only after he definitely stopped his activity in the asbestos cement plant; these have, therefore, been considered as unexposed. The cohort of wives was constructed entirely through official records in the town offices and is both exhaustive and unaffected by recall bias. At the end of follow up (1988) 1669 women were alive, 270 were dead and 25 (1.2%) were untraced. Main mortality analyses were only up to age 79 to reduce the misclassification of causes of death. Expected mortality was based on local rates. Mortality analyses were limited to the period 1965-88 due to the availability of local rates: in that period 210 deaths occurred among women with domestic exposure v 229.1 expected. There were four deaths from pleural tumours (one diagnosed as mesothelioma at necropsis) and six from lung cancer v. 0.5 and 4.0 expected respectively. Two further cases of mesothelioma were diagnosed by histological examination after the end of follow up. None of the three wives with histologically diagnosed mesothelioma had been engaged in industrial activities. Corresponding information for the other three cases could not be traced.

Adult↗

PubMed1994

Asbestos, cement, and cancer in the right part of the colon.

OBJECTIVE: The aim was to investigate associations between exposure to mineral fibres and dust, and cancer in subsites within the large bowel. DESIGN: Pooled retrospective cohort studies. SUBJECTS AND SETTINGS: Blue collar workers, employed for at least one year in different trades; asbestos cement or cement workers (n = 2507), other industrial workers (n = 3965), and fishermen (n = 8092). MAIN OUTCOME MEASURES: Standardised incidence ratios (SIRs, national reference rates) were calculated for cause specific cancer morbidity between 1958 and 1989. The observation period began 15 years after first employment. RESULTS: The asbestos cement and cement workers had a slightly increased risk of colorectal cancer (SIR 1.5; 95% confidence interval (95% CI) 1.1-2.0). This was due to an increase only in the right part of the colon (SIR 2.5; 95% CI 1.6-3.8). The ratio of right (7th revision of the International Classification of Diseases ICD-7) 1530-1531)/left (ICD-7 1532-1533) colon cancer among the asbestos cement and cement workers of 4.8 differed significantly from the ratio both among the other blue collar workers (0.4) and among the fishermen (1.5). As the sensitivity and accuracy was insufficient, mortality data did not show the excess of cancers in the right part of the colon. CONCLUSIONS: An increased incidence of cancer in the right part of the colon was evident in the asbestos cement and cement workers. The distribution of cancers within the colon was noticeably different from that in other blue collar workers, indicating that our findings cannot be explained by socioeconomic confounding factors. A detailed and appropriate disease classification, based on incidence data, is necessary in order not to obscure or underestimate effects of exposure in epidemiological studies on colorectal cancer.

Asbestos↗

PubMed1994

Incidence of cancer among anthophyllite asbestos miners in Finland.

A cohort of 736 male and 167 female workers of two anthophyllite mines in Finland was followed up through the Finnish Cancer Registry for cancer in 1953-91. Compared with the total cancer incidence of the east Finnish population, the men had a raised risk of total cancer (standardised incidence ratio (SIR) 1.7; 95% confidence interval (95% CI) 1.4-1.9), mainly attributable to an excess in lung cancer (SIR 2.8; 95% CI 2.2-3.6). The risk of lung cancer was somewhat higher among workers classified as heavily exposed (SIR 3.2; 95% CI 2.4-4.1) than among those moderately exposed (SIR 2.3; 95% CI 1.5-3.6) and the risk increased with increasing smoking and with increasing time of work with exposure. There were four cases of mesothelioma v 0.1 expected, all in men who smoked and had had a long and heavy asbestos exposure. Among women, a non-significant excess in total cancer (SIR 1.5; 95% CI 0.9-2.4) was found in the subgroup with heavy exposure to asbestos. Anthophyllite asbestos seems to have high potency in the carcinogenesis of lung cancer and low potency in carcinogenesis of mesothelioma in comparison with the other types of asbestos.

Asbestos, Amphibole↗

PubMed1997

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.

Adult↗

PubMed1999

Increased serum concentrations of growth factor receptors and Neu in workers previously exposed to asbestos.

OBJECTIVES: Epidermal growth factor receptor (EGFR) and oncogene Neu belong to a family of growth factor receptors which may play a part in carcinogenesis. Although increased serum concentrations of Neu and EGFR have been shown in several patients with asbestosis who later developed cancer, serum concentrations have not been studied in workers exposed in the past to asbestos but without asbestos related diseases. METHODS: Serum concentrations of secreted growth factor receptors were studied in 300 workers exposed in the past to asbestos and the results were compared with those of 70 controls. RESULTS: In the controls 4.3% (3/70) had EGFR values > 912 units/ml, compared with 39% (117/299) of the exposed group (p < 0.001). The difference in high values was even more pronounced for Neu with 4.3% of controls having Neu values > 2580 fmol/ml compared with 72% (216/299) of the exposed workers (p < 0.001). Pleural plaques predicted lower serum concentrations of EGFR but not lower Neu concentrations, and this finding remained significant after adjustment for age, exposure time, smoking, and time from initial exposure. CONCLUSIONS: Enhanced secretion of EGFR and Neu was found in a large cohort of retired asbestos workers with a wide range of exposure and latency periods. They did not have asbestosis or cancer and their EGFR values were higher in those without plaques. Further studies are needed to confirm our results, to determine the source of the secreted growth factor receptors, and to study their possible value as risk factors in the development of cancer.

Adult↗

PubMed2004

History of asbestos related disease.

The first medical article on the hazards of asbestos dust appeared in the British Medical Journal in 1924. Following inquiries by Edward Merewether and Charles Price, the British government introduced regulations to control dangerous dust emissions in UK asbestos factories. Until the 1960s these appeared to have addressed the problem effectively. Only then, with the discoveries that mesothelioma was an asbestos related disease and that workers other than those employed in the dustiest parts of asbestos factories were at risk, were the nature and scale of the hazard reassessed. In Britain, America, and elsewhere new and increasingly strict regulations were enacted.

Asbestos↗

PubMed2005

SV40-dependent AKT activity drives mesothelial cell transformation after asbestos exposure.

Human malignant mesothelioma is an aggressive cancer generally associated with exposure to asbestos, although SV40 virus has been involved as a possible cofactor by a number of studies. Asbestos fibers induce cytotoxicity in human mesothelial cells (HMC), although cell survival activated by key signaling pathways may promote transformation. We and others previously reported that SV40 large T antigen induces autocrine loops in HMC and malignant mesothelioma cells, leading to activation of growth factor receptors. Now we show that SV40 induces cell survival via Akt activation in malignant mesothelioma and HMC cells exposed to asbestos. Consequently, prolonged exposure to asbestos fibers progressively induces transformation of SV40-positive HMC. As a model of SV40/asbestos cocarcinogenesis, we propose that malignant mesothelioma originates from a subpopulation of transformed stem cells and that Akt signaling is a novel therapeutic target to overcome malignant mesothelioma resistance to conventional therapies.

Apoptosis↗

PubMed2000

Incidence of malignant pleural mesothelioma due to environmental asbestos fiber exposure in the southeast of Turkey.

BACKGROUND: Inhabitants of the southeast of Turkey (ST) have been exposed since childhood to inhalation of asbestos, from a material containing tremolite, used for whitewashing. This has resulted in an increased incidence of malignant pleural mesothelioma (MPM). OBJECTIVES: To review the epidemiological features of MPM cases in ST; to calculate and compare the incidence with the previously reported ones. SUBJECTS AND METHODS: The study included 176 MPM cases from different places in ST. The incidence of MPM was calculated for those places according to the distribution of the cases. RESULTS: In the previously identified regions of asbestos (region 1) where the population had been informed of the danger with the soil some decades ago, the MPM incidence was decreased, as compared to the previous reports. The annual incidence of MPM in these places was found to be 42.9 per million in this study while it had been reported to be 105.5 per million in the previous studies. In contrast, the incidence that was reported previously to be 2.75 per million in the regions where asbestos exposure had not been identified before (region 2) was found to be 8.6 per million in this study. In region 2 the incidence of MPM increased even in the second half of the last decade (5.9 versus 11.9 per million). CONCLUSIONS: Use of asbestos-containing soil continues in different places in ST. Even if the use of this soil is abandoned today, MPM will be an important health problem in this region till the third or fourth decades of this century. Informing the villagers of the danger and preventing the use of this soil may result in a considerable decrease in the incidence of MPM.

Adult↗

PubMed1980

Maximal expiratory flow volume curves in workers exposed to asbestos.

We have studied 40 workers with varying industrial exposure to asbestos, using routine spirometry and maximal expiratory flow volume curves (MEFVC). Abnormalities of MEFVC were common and seen in those with normal spirometry and total lung capacity. The high incidence of abnormal MEFVC suggests that air flow dysfunction in small airways may follow prolonged asbestos exposure. Our findings support, therefore, the idea that asbestos exposure may cause an obstruction to airflow arising particularly in small airways, and that one of the common functional abnormalities attributable to asbestos exposure is airways obstruction.

Adult↗

PubMed1980

Asbestos-related disease from household exposure.

The importance of nonoccupational asbestos exposure has been emphasized recently. To illustrate this problem, we report 4 persons with asbestos-related disease from household exposure. There were 2 wives of asbestos workers, who cleaned their husbands' work clothes. One developed a mesothelioma and the other plaques, calcification, benign asbestos pleural effusion and subpleural parenchymal fibrosis. 2 men were exposed as children while playing in a cellar room which was also used for their father's muffler repair business. At ages 27 and 33, they had pleural and diaphragmatic calcifications.

Adult↗

PubMed1994

Longitudinal changes in lung function among asbestos-exposed workers.

To prospectively identify the determinants of persistent or accelerated loss of lung function among workers occupationally exposed to asbestos and assess the relative contribution of cigarette smoking, asbestos-induced pleural fibrosis, and specific findings from bronchoalveolar lavage and high resolution CT scans, we examined the determinants of lung function changes in 117 subjects occupationally exposed to asbestos for at least 1 yr in a high exposure setting. A minimum of 20 yr was required between the first exposure to asbestos and entry into the study. Baseline studies included an independent assessment of dyspnea, lung volumes, diffusing capacity of carbon monoxide (DLCO), a chest radiograph, a high resolution CT (HRCT) scan, and bronchoalveolar lavage (BAL). Subjects were observed for an average of 2 yr (range, 0.5 to 4.0 yr), and lung function was measured on at least two separate occasions (mean, 4.1 separate tests). During the period of observation, there was an average 1.5% decrease in the TLC and a 2.5% decrease in the DLCO. In this longitudinal data set, after controlling for age, height, pack-years of cigarette smoking, and follow-up time, persistently lower measures of TLC were independently related to moderate to severe dyspnea (p = 0.005), diffuse pleural thickening (p = 0.007), and higher concentrations of fibronectin in BAL fluid (p = 0.01). Interstitial lung disease either on the chest radiograph or HRCT scan was not independently associated with persistently lower measures of TLC during the period of observation. However, none of the clinical variables we examined were associated with an accelerated decline in TLC.(ABSTRACT TRUNCATED AT 250 WORDS)

Asbestos↗

PubMed1989

Asbestos fibers and silica particles stimulate rat alveolar macrophages to release tumor necrosis factor. Autoregulatory role of leukotriene B4.

Alveolar macrophages (AM) can play a crucial role in the pathogenesis of pulmonary disease via their ability to produce potent inflammatory and fibrogenic mediators. We found that rat AM cultured with 1 to 100 micrograms/ml of silica particles or asbestos fibers produced tumor necrosis factor (TNF) and leukotriene B4 (LTB4) in a concentration-dependent fashion, whereas latex beads, an inert phagocytic stimulus, failed to induce significant augmentation of either TNF or LTB4. In a time course study, AM stimulated for 2 h with silica or asbestos produced an increased amount of LTB4, which preceded the rise in TNF activity detected 7 and 24 h after culture initiation. The induction appears to involve the synthesis of new protein since actinomycin D and cycloheximide abrogate the majority of the stimulatory effect. We next examined the role of LTB4 in mineral-dust-induced TNF production. The lipoxygenase inhibitors nordihydroguaiaretic acid (NDGA) and AA861 used at 1 to 50 micrograms/ml reduced in a concentration-dependent fashion asbestos- or silica-stimulated TNF release. On the other hand, "reconstitutive" experiments in which we added exogenous LTB4 (10(-14) to 10(-8) M) to AM treated with lipoxygenase inhibitors showed partial restoration of TNF production induced by chrysotile or silica, with peak effect at 10(-10)M LTB4. The present study demonstrated that AM incubated in the presence of chrysotile A or silica can produce both LTB4 and TNF and that endogenous lipoxygenase metabolites as well as exogenous LTB4 can act to amplify TNF production. These observations suggest a common mechanism by which asbestos and silica may modulate the production of inflammatory and fibrogenic cytokines.

Animals↗