Asbestos Workers Research Articles

RE: Study of smoking behavior in asbestos workers by Osinubi et al. Am J Ind Med 41:62–69, 2002. Reply to Lange and Thomulka's Letter to the Editor “Smoking prevalence of asbestos workers: A comment”

RE: Study of smoking behavior in asbestos workers by Osinubi et al. Am J Ind Med 41:62–69, 2002. Reply to Lange and Thomulka's Letter to the Editor “Smoking prevalence of asbestos workers: A comment”

Issues of causality in the history of occupational epidemiology.

Occupational epidemiology has its roots in classical medicine. However, it became a quantitative discipline only in the 20th century, through the pioneering work of individuals such as Case, Lloyd, and Selikoff and organizations such as the Division of Occupational Health of the U.S. Public Health Service. Studies of chemical dye workers, bituminous coal miners, smelting workers, and uranium miners have been especially important sources of innovations in methodology and in development of logical reasoning leading to acceptance of causal relationships of occupational exposures that lead to respiratory diseases and cancer. The cooperation of labor unions, such as those of steel and asbestos workers, has often been a crucial factor in providing essential data.

Respiratory impairment due to asbestos exposure in brake-lining workers

There is extensive evidence that exposure to asbestos causes pulmonary parenchymal fibrosis, pleural disease, and malignant neoplasm in asbestos-exposed workers. However, few data concerning brake-lining workers are available in the literature. In this study, we aimed to assess the long-term effects of chrysotile asbestos exposure on lung function and the risk of asbestos-related diseases in brake-lining workers. Seventy-four asbestos-exposed workers who processed brake-lining products and 12 unexposed office workers were offered pulmonary function tests (spirometry and transfer factor) in 1992 and 1999. In 1999, the mean duration of asbestos exposure was 10.00±4.07 and 11.02±4.81 years (7–31 years) in nonsmoking and smoking asbestos workers, respectively. Transfer factor ( T L, CO) and transfer coefficient ( K CO) decline were significant in the 7-year follow-up in both smoking and nonsmoking asbestos workers. However, lung function indices of the control group, whom were all current smokers; were also found to be decreased, including FEF 75, T L, CO and K CO. We found minimal reticular changes in 10 asbestos workers who were all current smokers, they underwent high-resolution computed tomography scans of the chest and we found that they had peribronchial thickening resulting from smoking. As a conclusion, even in the absence of radiographic asbestosis, T L, CO and K CO may decrease after a mean 10-year duration of exposure to asbestos in brake-lining workers and this is more noticeable with cigarette burden.

Incidence of cancer among the participants of the Finnish Asbestos Screening Campaign.

Cancer risk has been estimated for asbestos production workers or other heavily exposed asbestos workers in numerous studies. The bulk of the asbestos epidemic results come, however, from past intermittent exposures during asbestos product use. This study concentrated on estimating the risk of cancer in such a population. Altogether 23285 men and 930 women invited to a nationwide screening campaign for benign asbestos-related diseases in 1990-1992 were followed for cancer through the Finnish Cancer Register up to 1998. Standardized incidence ratios (SIR) were calculated in comparison with the total Finnish population. Altogether 1392 cases of cancer were found among the men. The risk was slightly, but significantly elevated for lung cancer [SIR 1.14, 95% confidence interval (95% CI) 1.01-1.26), mesothelioma (SIR 2.77, 95% CI 1.66-4.31), and prostate cancer (SIR 1.21, 95% CI 1.09-1.34). The risk of lung cancer was slightly higher among the invited nonparticipants (SIR 1.48, 95% CI 1.20-1.79) than among the participants (SIR 1.02, 95% CI 0.88-1.17). About 98% of the lung cancers occurred in current or ex-smokers. In a population of long-term construction workers, the risk of lung cancer and mesothelioma was increased, but considerably lower than among insulators, asbestos sprayers, or patients with asbestosis. As it was not possible to follow most of the invited nonparticipants in the original screening study, selection bias by smoking or other life-style factors possibly correlated to the individual's decision to participate in the health screening cannot be excluded.

Asbestos bodies in the sputum of asbestos workers: correlation with occupational exposure.

A cross-sectional medical survey including collection of three consecutive sputum samples was carried out among 270 retired workers of a textile and friction materials factory, in order to investigate the relationship between asbestos body identification and asbestos exposure. The individual cumulative asbestos exposure, determined by means of a plant-specific job-exposure matrix based on asbestos air measurements in the workshops, proved to be heavy with a mean cumulative exposure of 217 fibres x mL(-1) x yr. Macrophages and asbestos bodies were identified in sputum samples by light microscopy. The lung origin of the sputum, suggested by the presence of macrophages and/or asbestos bodies, was confirmed in 82.6% of subjects, and 53% of these samples were positive for asbestos bodies. The prevalence of asbestos bodies was not related to sex, smoking status or latency. Conversely, multivariate analysis showed a positive relationship with cumulative exposure, duration and intensity of exposure to asbestos, as well as age and time since retirement. These findings suggest that sputum analysis for asbestos bodies may remain a relevant and noninvasive marker of heavy occupational exposure to asbestos, even years after retirement. Owing to the new perspectives in lung cancer screening, it might contribute to the identification of high-risk subjects.

Pi*S and Pi*Z alpha 1 antitrypsin polymorphism and the risk for asbestosis in occupational exposure to asbestos

Alpha 1 antitrypsin is a highly polymorphic anti-elastase enzyme, especially active in the protection of alveoli and liver. Here we studied the distribution of two deficient alleles Pi*Z and Pi* S, in 194 asbestos workers, of whom 100 were asbestosis cases, and 94 were controls without disease (exposed controls, EC). A second group of controls without asbestos exposure (non-exposed controls, NEC; n=122) was also included. Multivariate analysis adjusted by age and smoking habit showed ninefold risk for asbestosis in Pi*Z heterozygous individuals and 5.9-fold risk for Pi*S homozygous although differences were only significant in the first case (cases vs. EC: OR 8.9; p=0.04). Considering both genotypes (Pi*Z heterozygous, Pi*S homozygous) we obtained an OR of 8 ( p=0.01). Our results suggest that the alpha 1 antitrypsin polymorphisms, especially Pi*Z, could help to predict asbestosis risk and confirm the high prevalence of the Pi*S allele in Spain.

High prevalence of reversible airway obstruction in asbestos-exposed workers.

In this retrospective study of 97 male workers exposed to asbestos for 2-50 yr, data were collected on chest x-ray findings and lung function, including lung volumes, forced expiratory flow rates (i.e., forced expiratory volume in 1 sec [FEV1.0], forced expiratory flow measured between 25% and 75% of forced vital capacity [FEF(25-75%)]), airway resistance (R(aw)), carbon monoxide (CO)-diffusing capacity, and the existence of airway obstruction reversible by a beta-adrenergic agonist (RAO). The authors performed multiple-regression analyses to correlate the variations in lung function data with age, smoking habits, duration of asbestos exposure, and time since last exposure. Occupational activities of subjects that might induce specific lung abnormalities were also considered. No significant decrease was seen in lung volumes or CO-diffusing capacity; however, a decrease in FEV1.0 and an increase in R(aw) were measured in 65% of the subjects, and an isolated decrease in FEF(25-75%) occurred in only 18%. There was no difference in lung-function data between subjects who had chest x-ray signs of abnormalities (n = 59) and those who did not (n = 38). A significant relationship was found between the decrease in FEV1.0 and age; however, no correlation was noted between altered lung function and cigarette smoking, duration of asbestos exposure, or time since last exposure. RAO prevalence was higher (34%) than previously reported (9%) in subjects with chronic obstructive pulmonary disease (COPD) who were not exposed to asbestos or outdoor pollution. The RAO prevalence in asbestos-exposed workers was nearly the same as that measured in COPD subjects who lived downtown and who were exposed to outdoor pollution (36%). The high RAO prevalence in asbestos-exposed workers was found in 43% of subjects who were exposed only to asbestos, and in 33% of subjects who were also exposed to air pollution due to their occupational activities. It is hoped that the observations in this study will encourage practitioners to check for RAO in asbestos workers who use inhaled bronchodilators.

Preliminary Findings for Pleural Mesothelioma among Women in the Quebec Chrysotile Mining Regions

Introduction. We conducted a descriptive study to compare cases of pleural mesothelioma among female residents of Quebec’s asbestos mining regions to matched controls for residential, domestic and occupational asbestos exposures. Methods. We visited hospitals throughout the province of Quebec to identify women aged ≥50 yr whose hospital records mentioned any possible mesothelioma between 1970 and 1989. Hospital records and biological materials were reviewed by three expert pathologists to identify individuals who had lived in a mining region in Quebec at the time of diagnosis. For each case, 15 controls matched for year (±2) of birth and area of residence were selected from a previously interviewed sample of 817 female asbestos mining area residents alive in 1989. Relatives of the cases were similarly interviewed regarding lifetime occupational and residential histories and cohabitation with asbestos worker(s). Cumulative exposure from each source was estimated in fibers/ml-yr from indirect data. Results. We identified six ‘definite or probable’ and four ‘possible’ pleural mesothelioma cases. All resided in Thetford Mines (none in the town of Asbestos) and were born before 1935. Five cases (50%) worked in the asbestos industry (versus 2.7% of controls; relative risk = 53.8). Nine (90%) had lived with one or more asbestos workers (versus 65% of controls); six (60%) with two or more workers (versus 36% of controls). Mean cumulative exposure (residential, domestic, and occupational combined) was estimated as 226.1 fibers/ml-yr (range 84–525) for cases and 84.1 fibers/ml-yr (range 0–189) for controls, with a plausible 5-fold error on either side.

Study of smoking behavior in asbestos workers*

Asbestos exposure and concomitant cigarette smoking markedly increase the risk of lung cancer and contribute to the prevalence and severity of pulmonary interstitial fibrosis. A cross-sectional survey of 214 asbestos workers was initiated to determine the prevalence of smoking and their readiness to quit smoking using the stage of change theory. The study was comprised of 61 never smokers (28.5%), 118 ex-smokers (55.1%), and 35 current smokers (16.4%). Reasons for smoking cessation in ex-smokers included perception of ill-health (51%) and knowledge of smoking-asbestos hazards (3.4%). Stage of change of current smokers revealed: precontemplation (26.5%), contemplation (35%), preparation (29%), and action (8.8%). Current smokers had the highest prevalence of small airway obstruction on spirometry. A detailed smoking history during medical surveillance activities will enable the occupational physician to identify asbestos workers who have difficulty quitting and to develop a system in which such individuals can be referred to comprehensive smoking cessation programs.

Pulmonary function in long-term asbestos workers in China.

The relationship of pulmonary function to exposure to asbestos and radiographic abnormalities has been controversial, especially when smoking is present as a confounder. The aim of the study was to provide further understanding on the radiographic-physiologic associations in nonsmoking and smoking asbestos workers. Radiographic asbestosis, pleural lesion, and pulmonary function were studied in 269 Chinese asbestos workers, with average exposure years of 23 for male workers and 18 for female workers. Their functional data were compared with those of 274 controls without exposure to dust. Although most of the male workers were smokers, none of the female workers smoked. In comparison with controls, asbestos workers had significantly lower lung volume and diffusing capacity, irrespective of gender. Female workers and smoking male workers had lower measurements of forced expiratory volume in 1 second and instantaneous forced expiratory flow at 50% and 25% of forced vital capacity. After adjustment for relevant covariates, asbestos exposure, asbestosis, and pleural abnormalities were associated with decreased parameters of pulmonary function, including lung volume, diffusing capacity, and airway flow. These data indicate that asbestos-related functional defects manifested by lung restriction and mild airway obstruction correlate with exposure to asbestos and with parenchymal and pleural abnormalities, independent of smoking.

The Interaction of Asbestos and Smoking in Lung Cancer

Both cigarette smoke and inhaled asbestos fibres can cause lung cancer, but the assessment of how these agents act in combination is a matter of great difficulty. In non-smokers, the condition is so rare that, in any cohort of asbestos workers, the standardised mortality ratio (SMR, that is the ratio of the numbers of deaths observed and expected) is quite imprecise. The SMR for smokers, with which it has to be compared, is also subject to sampling error, making the interaction even more unstable. This accounts for much of the variation that has bedevilled evaluation. The debate has been concentrated on two hypotheses: additive (asbestos and cigarette smoke act independently) and multiplicative (asbestos produces an effect proportional to the effect of smoking). The very few data available until 1977 failed to fit the former and fitted the latter only poorly. They would have fitted better a hypothesis of greater synergism, but the only one proposed was too convoluted. So the multiplicative model appeared the only alternative, and was deemed 'accepted'. The ratio of lung cancer SMRs for non-smokers and smokers was generalised into the relative asbestos effect, RAE, with all the advantages of a parametric statistic (Berry et al., 1985, British Journal of Industrial Medicine 42, 12). On the multiplicative hypothesis, RAE=1, while RAE>1 indicates less synergism. The RAEs for the three most recent of the six results then available were >1; for one, P<0.005. From the six results combined, it was concluded that 'overall non-smokers have a relative risk of lung cancer due to asbestos that is 1.8 times that of smokers'. Some admitted uncertainty about the figure 1.8 was seized upon and even the thrust of the conclusion has been very largely disregarded. So too has the RAE and all its benefits. As a result, all later reviewers have been led into error, much of it serious: in particular, they have failed to appreciate how much of the variation arises from the inevitable imprecision of all RAEs. This failure led reviewers in 1994 to discard, quite without justification, those interactions which were less than multiplicative and came from cohort studies. Although case-referent studies seemed to support the multiplicative hypothesis, the information from them is essentially unreliable. Thus it cannot weaken the conclusions from the cohort studies, that the multiplicative hypothesis is untenable and that the relative risk of lung cancer from asbestos exposure is about twice as high in non-smokers as in smokers; the best estimate of RAE is 2.04, with 95% confidence interval 1.28-3.25. This finding is not only of high statistical significance but of great social and scientific importance.

Changes in low molecular weight DNA fragmentation in white blood cells of workers highly exposed to asbestos.

The aim of this study was to determine low molecular weight (LMW)-DNA fragmentation changes after white blood cell (WBC) incubation in lysis buffer followed by constant-field gel electrophoresis (CFGE). WBCs were isolated from blood samples of workers highly exposed to asbestos fibres at the workplace in Germany, and were compared with those from healthy adults. This study was conducted parallel to the study presented in our preceding paper (Marczynski et al. 2000b) in which we described significant increases in the levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG) adducts in the DNA of white blood cells from the same highly exposed workers relative to the levels found in the control group in all three study years (1994 to 1997). We found that 15-h incubation in lysis buffer of WBCs embedded in agarose-plugs from healthy control donors with 2% SDS, proteinase K and Na2-EDTA at 42 degrees C followed by 0.5 h at 4 degrees C produced a characteristic DNA fragmentation pattern below 23 kbp using CFGE. In the 1st year of the study (1994-1995) changes were found in LMW-DNA fragmentation in 54.8% of the asbestos workers studied, compared with the DNA fragmentation pattern of controls. Interestingly, in the 2nd year of the study (1995 1996) changes in DNA fragmentation were found in only 39.9% of exposed subjects. In the 3rd year of the study (1996-1997) the highest number of workers exposed to asbestos (67.3%) with changes in the LMW-DNA fragmentation pattern was found. The Chi-square test for each year of the study revealed significant changes (P < 0.001). These changes may be due to the presence of hydrogen peroxide (H2O2), as has been shown in vitro. It is likely that a Fenton reaction involving the heterolytic reduction of H2O2 by traces of reduced transition metals such as Fe2+ and Cu+ is involved in the fragmentation of DNA. No difference was found in the changes in DNA fragmentation between asbestos-exposed subjects with and without benign asbestos-associated diseases (asbestosis, asbestos-associated pleural plaques). Significant correlations were not found after analysis of the changes in DNA fragmentation in relation to different possible occupational and non-occupational confounding factors, such as the duration of asbestos exposure, the latency period, estimated cumulative fibrous dust dose ("fibre-years"), and non-occupational confounding factors, such as age, smoking status, acute febrile infections, the intake of medicines, aspirin, Ca2+, Mg2+ and/or hormones, the intake of vitamins, and cases of cancer. Our data confirm that oxidative stress occurs in the WBCs of workers highly exposed to asbestos fibres, thus supporting the hypothesis that asbestos fibres damage cells through an oxidative mechanism. Oxidative stress and oxidative DNA damage may be induced by long-term exposure to asbestos. The new insights into the oxidative effects of asbestos fibres are of great importance because they provide a way forward for new preventive strategies. Preventive and therapeutic approaches using antioxidants should be taken into consideration.

The interaction of asbestos and smoking in lung cancer

Both cigarette smoke and inhaled asbestos fibres can cause lung cancer, but the assessment of how these agents act in combination is a matter of great difficulty. In non-smokers, the condition is so rare that, in any cohort of asbestos workers, the standardised mortality ratio (SMR, that is the ratio of the numbers of deaths observed and expected) is quite imprecise. The SMR for smokers, with which it has to be compared, is also subject to sampling error, making the interaction even more unstable. This accounts for much of the variation that has bedevilled evaluation.The debate has been concentrated on two hypotheses: additive (asbestos and cigarette smoke act independently) and multiplicative (asbestos produces an effect proportional to the effect of smoking). The very few data available until 1977 failed to fit the former and fitted the latter only poorly. They would have fitted better a hypothesis of greater synergism, but the only one proposed was too convoluted. So the multiplicative model appeared the only alternative, and was deemed ‘accepted’.The ratio of lung cancer SMRs for non-smokers and smokers was generalised into the relative asbestos effect, RAE, with all the advantages of a parametric statistic (Berry et al., 1985, British Journal of Industrial Medicine42, 12). On the multiplicative hypothesis, RAE=1, while RAE>1 indicates less synergism. The RAEs for the three most recent of the six results then available were >1; for one, P<0.005. From the six results combined, it was concluded that ‘overall non-smokers have a relative risk of lung cancer due to asbestos that is 1.8 times that of smokers’. Some admitted uncertainty about the figure 1.8 was seized upon and even the thrust of the conclusion has been very largely disregarded. So too has the RAE and all its benefits. As a result, all later reviewers have been led into error, much of it serious: in particular, they have failed to appreciate how much of the variation arises from the inevitable imprecision of all RAEs. This failure led reviewers in 1994 to discard, quite without justification, those interactions which were less than multiplicative and came from cohort studies. Although case-referent studies seemed to support the multiplicative hypothesis, the information from them is essentially unreliable. Thus it cannot weaken the conclusions from the cohort studies, that the multiplicative hypothesis is untenable and that the relative risk of lung cancer from asbestos exposure is about twice as high in non-smokers as in smokers; the best estimate of RAE is 2.04, with 95% confidence interval 1.28–3.25. This finding is not only of high statistical significance but of great social and scientific importance.

Epidemiology of occupational asbestos-related diseases in China.

In 1950s and 60s, asbestosis had been a major health hazard for asbestos exposed workers. In the late 1970s, lung cancers with or without asbestosis were found among asbestos workers. All cohort studies on asbestos workers and on chrysotile miners in China showed excess deaths from lung cancer. In a large scale of cohort study on asbestos workers, a synergistic effect was found between cigarette smoking and asbestos exposure in the production of lung cancer. There have been not so many cases of malignant mesotheliomas reported, so far. In the cohort of chrysotile miners, 4 cases of pleural mesothelioma were observed. In the large scale of cohort study on asbestos workers in 9 factories using only chrysotile only one case of pleural mesothelioma was detected for 10 years' observation. In another 2 cohort studies, 2 cases of peritoneal mesotheliomas were found, one in Shanghai asbestos factory where a small amount of crocidolite had been used in 1960s, and one in Anqing asbestos factory that was located near tremolite mine. Further study is needed especially for the relationship between exposure to Chinese chrysotile and malignant mesotheliomas.

Increased body mass index is related to apparent circumscribed pleural thickening on plain chest radiographs.

Diffuse pleural thickening and pleural plaques are the commonest radiological manifestations of asbestos exposure. Differentiation between subpleural fat and non-calcified pleural plaques is important clinically and medico-legally. This study aims to determine if apparent circumscribed pleural thickening on chest radiographs is related with obesity. Surveillance chest x-rays of 693 former asbestos workers were read with the ILO classification. Subjects with costophrenic angle obliteration (n = 57) were analyzed separately. The remaining subjects were subdivided according to their body mass index (BMI): Group 1 < 26 kg/m(2); Group 2 26-30 kg/m(2); Group 3 > 30 kg/m(2). Baseline characteristics, asbestos exposure, and profusion scores were evenly distributed. BMI of > 30 kg/m(2) was associated with a higher prevalence of pleural thickening on CXR (Gp1 = 8.5%; Gp2 = 9.3%; Gp3 = 18.3%). This relationship was strongest in the subgroups with 25-50% of the lateral chest wall involved and pleural thickness of < 10 mm. Obesity (BMI > 30 kg/m(2)) is related to apparent circumscribed pleural thickening on CXR, especially thin (< 1 cm) shadows covering 25-50% of the lateral chest wall.

Application of statistical models for secondary data usage of the US Navy's Occupational Exposure Database (NOED).

Many organizations around the world have collected data related to individual worker exposures that are used to determine compliance with workplace standards. These data are often warehoused and thereafter rarely used as an information resource. Using appropriate groupings and analysis of OSHA data, Gómez showed that such stored data can provide additional insight on factors affecting occupational exposures. Using data from the Occupational Exposure Database of the United States Navy, the usefulness of statistical models for defining probabilities of exposure above permissible limits for observed work conditions is examined. Analyses have highlighted worker Similar Exposure Groups (SEGs) with potential for overexposure to asbestos and lead. In terms of grouping data, Rappaport et al. defined the Within-Between Lognormal Model, a scale-independent measure for quantifying between-worker variability within a selected worker group: (B)R.95 = exp[3.92s(sB)], representing the ratio of arithmetic mean exposures received by workers in the 97.5th and 2.5th percentiles. To help search for groups, the Proportional Odds Model, a generalization of the logistic model to ordinal data, can predict probabilities for group exposure above the Occupational Exposure Limit (OEL), or the Action Level (AL), which is one-half of the OEL. Worker SEGs have been identified for asbestos workers removing friable asbestos ((B)R.95 = 11.0) and nonfriable asbestos ((B)R.95 = 6.5); metal cleaning workers sandingspecialized equipment ((B)R.95 = 11.3), and workers at target shooting ranges cleaning up lead debris ((B)R.95 = 10). Estimated probabilities for the categories <AL, AL-OEL, and >OEL support current understanding of work processes examined. Differences in probability noted between tasks and levels of ventilation validate this method for evaluating other available workplace exposure determinants, and for predicting probability of membership in categories that may help further define worker exposure groups, and determinants of excessive exposures. Thus, analyses of retrospective exposure data can help identify work site and work practice factors for efficient targeting of remediation resources.

Mortality from all cancers of asbestos factory workers in east London 1933–80

OBJECTIVETo give the observed and expected deaths due to cancer at all separate sites in asbestos workers in east London, and to analyse these for overall effect and exposure-response trend.METHODSThe...

Legal Requirements for Medical Surveillance of Asbestos Workers in Malaysia, the USA and Under International Law

Worldwide, regulatory actions have consistently required for occupational exposure to asbestos. Regulatory agencies use medical surveillance as a method of verifying the effectiveness of engineering controls to prevent work-related disease. In many countries it is also used to detect longitudinal changes in the prevalence and incidence of occupational disease in light of stated regulatory goals. It is therefore an important component of regulatory programs designed to avert and curtail asbestos-related occupational disease. In 1986, the International Labor Organization (ILO) drafted C. 162, Concerning Safety in the Use of Asbestos; Malaysia promulgated Asbestos Process Regulations (1986) under the Factories and Machinery Act; and the USA revised its Safety and Health Act, Occupational Exposure to Asbestos, Tremolite, Anthophyllite and Actinolite, (1986). One can infer from these and other developments around the world that there is a strong international regulatory trend towards increased protection against occupational exposure to asbestos. This article examines in detail the regulatory requirements for of asbestos workers (excluding worker's compensation) under laws in Malaysia and the USA, using the ILO Convention 162 as an analytical framework. For the purposes of this paper, medical surveillance of asbestos workers refers to monitoring of workers' health, as contemplated by C. 162, Part IV, Article 21 Surveillance of the Working Environment and Workers' Health. C.162 Article 21 provides that shall be comprised of five components: (1) examinations; (2) monitoring at no cost to workers; (3) information and individual advice to workers regarding results of examinations; (4) alternative sources of income for those workers for whom asbestos exposure is medically inadvisable; (5) a notification system for asbestos-related disease. C.162 allows for expansive protections of exposed workers, through its requirements. Even though many important components of the program are not expressly stated, the key elements of a good program are included within its purview. C.162 therefore is a good blueprint for evaluating programs.

Sputum cytopathology and other clinical findings as early risk factors for lung cancer in amosite asbestos workers

Sputum cytopathology and other clinical findings as early risk factors for lung cancer in amosite asbestos workers

Association between 8-hydroxy-2′-deoxyguanosine levels in DNA of workers highly exposed to asbestos and their clinical data, occupational and non-occupational confounding factors, and cancer

In the preceding paper [B. Marczynski, P. Rozynek, T. Kraus, St. Schlösser, H.J. Raithel, X. Baur, Levels of 8-hydroxy-2′-deoxyguanosine in DNA of white blood cells from workers highly exposed to asbestos in Germany, Mutat. Res. (2000) submitted] we described significant increases ( p<0.001) in the levels of 8-hydroxy-2′-deoxyguanosine (8-OHdG) adducts in the DNA of white blood cells (WBC) of workers highly exposed to asbestos fibers at the workplace relative to those found in the control group in all three study years (period between 1994 and 1997). The results show that the oxidative DNA damage in exposed individuals is between 1.7 times and twice that found in control samples for all 3 years of the study ( p<0.001). The aim of this study was to examine the association between the 8-OHdG levels in WBC DNA of workers highly exposed to asbestos fibers at the workplace and clinical data, occupational and non-occupational confounding factors, and cancer. There is no obvious correlation between the steady-state levels of 8-OHdG in the circulating WBC DNA of asbestos workers and possible confounding factors, such as the presence of benign asbestos-associated diseases, the duration of asbestos exposure, the latency period, the fixed cumulative fibrous dust dose (“fiber years”), age, smoking status, acute febrile infections, medicines, aspirin, calcium (Ca 2+), magnesium (Mg 2+), and the hormone and vitamin intake. This indicates that previous inhalation of asbestos fibers is the major factor responsible for the difference observed in oxidative DNA damage between asbestos workers and controls. For patients suffering from respiratory cancer, cancer of the gastrointestinal tract, mouth/pharynx/larynx, and urogenital tract the mean DNA-adduct level was significantly higher ( p<0.01) than that found in controls, but not significantly higher ( p>0.05) than that for asbestos-exposed patients without tumours. The formation of 8-OHdG adduct levels in WBC DNA of patients with hematopoietic cancer, chondrosarcomas and multiform glioblastomas was not significantly higher than that found in the control group ( p>0.05). Our results support the hypothesis that oxidative DNA damage in man caused by asbestos fibers plays a role in the formation of malignant tumours.