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Oral Session 9 – Mortality studies and lung disease

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O9.1 AUTOPSY BASED RESPIRATORY OUTCOMES AMONG SOUTH AFRICAN COALMINERS

R. N. Naidoo1, T. Robins2, J. Murray3.1University of Natal; Durban, South Africa; 2University of Michigan; Ann Arbor, MI, USA; 3National Institute for Occupational Health, Johannesburg, South Africa

Introduction: The objectives of the study were to describe the prevalence of autopsy diagnosed respiratory outcomes, particularly emphysema, among South African coalminers, and to determine whether dose–response relationships existed between these outcomes and measures of exposure (years worked in coalmining), using data from the Pathology Automation System (PATHAUT) database of South African miners, one of the largest autopsy databases in the world.

Methods: All autopsies (n = 7760) conducted on coalworkers and recorded on PATHAUT from 1975 to 1997 were evaluated for prevalence of emphysema, coal workers’ pneumoconiosis (CWP), silicosis and tuberculosis. Analyses were restricted to those with exclusive coalmining exposure and information on years of exposure (n = 3167). Logistic regression was conducted to determine relationships between exposure and outcomes, controlling for covariates such as race, smoking, and age.

Results: The average number of years of coalmining exposure was 11.0 years, and mean age of the workers was 41.1 years. There were 66.1% black miners and 33.6% white in the cases, and 31% of the cases had information on smoking. Among those with exclusive coal exposure, the prevalences of silicosis, tuberculosis (TB), CWP, and moderate to marked emphysema were 10.2%, 5.5%, 7.0% and 5.2% respectively. With the exception of TB, all respiratory outcomes were associated with years worked (p<0.0001). A significant relationship was found between smoking and all autopsy outcomes, except CWP. Black miners had a 6.59-fold and a 1.35-fold greater risk for TB and CWP respectively compared with white miners, while white miners had an increased risk of 1.28 times and 5.26 times for silicosis and emphysema respectively. Moderate to marked emphysema was strongly associated with years worked (odds ratio (OR) of 9.5 with 95% confidence interval 2.31 to 39.9) for highest tercile of years worked compared with lowest tercile. The OR for current smokers was lower: 3.60 (1.4 to 4.2).

Conclusions: There were significant dose related associations of key outcomes, including emphysema, with coal dust exposure; greater odds among workers with the higher categories of years worked. These findings strongly suggest that exposure to dust in coal miners is causally related to these outcomes of interest.

O9.2 MORTALITY OF FORMER MINERS AND MILLERS OF CROCIDOLITE AT WITTENOOM

A. W. Musk2, N. H. de Klerk2, A. Reid2, G. L. Ambrosini2, L. Fritschi2, N. J. Olsen3, E. Merler4, M. S. T. Hobbs2, G. Berry1.1School of Public Health, University of Sydney, NSW, Australia; 2School of Population Health, University of Western Australia, WA, Australia; 3Sir Charles Gairdner Hospital, Nedlands, WA, Australia; 4Occupational Health Unit, Department of Prevention, Local Health Unit, National Health System, Padua, Italy

Objective: To report the numbers and causes of death that have occurred in former Wittenoom crocidolite workers to the end of 2000, and to compare the numbers with expected numbers based on national death rates allowing for age, sex and time period.

Methods: A group of 6493 men and 415 women who had worked at the former Wittenoom crocidolite mine and mill at some time between 1943 and 1966 have been followed up to the end of 2000. The duration of employment was usually short, with 45% of men working at Wittenoom for <3 months and <3% remaining for 5 years or longer. Dust concentrations, particularly in the old mill, have been documented as high.

Results: Of the former workers, 2549 are known to have died by the end of 2000; 888 of the deaths were due to neoplasms, 743 to circulatory diseases, 267 to respiratory diseases, 117 to digestive diseases, and 256 to injuries and poisonings. Of the 888 neoplasms, 296 were due to cancer of the trachea, bronchus, and lungs, 199 to pleural mesothelioma, and 32 to peritoneal mesothelioma.

Conclusions: As a consequence of the exposure to crocidolite asbestos, the main excess mortality in this group of former workers is due to lung cancer and mesothelioma.

O9.3 LUNG CANCER MORTALITY AND IRON OXIDE EXPOSURES IN A FRENCH STEEL PRODUCING FACTORY

E. Bourgkard1, J. J. Moulin1, B. Courcot2, M. Diss3, G. Duval2, J. Ettlinger2, P. Goutet4, D. Hémon5, N. Marquis6, J. M. Mur7, C. Rigal2, M. P. Rohn-Janssens2.1INRS; 2SOLLAC Atlantique; 3ARCELOR; 4LICE; 5INSERM-U170-IFR69; 6LECES Environnement; 7INSERM U420, France

Introduction: A mortality study was carried out among workers employed in a French steel producing factory to assess the possible association between iron oxide exposures and lung cancer risk.

Methods: A historical cohort was set up of all workers ever employed for at least 1 year on the site between 1959 and 1997. The cohort was followed up from January 1968 to December 1998. Causes of death were ascertained from death certificates. Job histories and smoking habits were available for 99.7% and 72.3% respectively. Occupational exposures were assessed by a specific job exposure matrix (JEM) developed by a committee of experts and validated with atmospheric measurements. Standardised mortality ratios (SMRs) were computed using local death rates as external references. Poisson regressions were used to estimate the relative risks (RRs) due to occupational exposures (internal references), taking into account potential confounding factors.

Results: The cohort comprised 16 742 males and 959 females (400 218 person years). Among males, the observed mortality was lower than expected for all causes (2338 deaths, SMR 0.81, 95% confidence interval (CI) 0.78 to 0.85) and for lung cancer (233 deaths, SMR 0.89, 95% CI 0.78 to 1.01). No lung cancer excess was observed for exposure to iron oxides (RR 0.80, 95% CI 0.55 to 1.17) and no dose–response relationship with intensity and duration of exposure was observed. A non-significant excess was observed for asbestos (RR 1.22, 95% CI 0.91 to 1.64) and silica (RR 1.29, 95% CI 0.78 to 2.14) compared with the non-exposed groups, and no dose–response relationship was observed with intensity and duration of exposure. A significant bladder cancer excess was observed among workers exposed to oil mists (RR 2.44, 95% CI 1.06 to 5.60) compared with those non-exposed. This risk was found to increase significantly with intensity and duration of exposure. Adjustments for smoking habits did not change any results.

Conclusion: This study did not detect any relationship between exposure to iron oxides and lung cancer mortality.

O9.4 MORTALITY AMONG INDUSTRIAL SILICA SAND WORKERS

T. P. Brown, L. Rushton.MRC Institute for Environment and Health, Leicester, UK

Introduction: Occupational exposure to respirable crystalline silica dust (RCSD) has been shown to cause silicosis, pulmonary tuberculosis, chronic bronchitis, and chronic obstructive pulmonary disease, and, more recently, autoimmune diseases and renal disease. This paper describes the mortality patterns among a cohort of British industrial silica sand workers.

Methods: The cohort consists of 2704 workers, employed for more than a year at one of seven quarries after 1951. RCSD samples collected after 1978 were used to develop a job exposure matrix (JEM). No dust measurements were available before 1978, so exposure for each job and quarry group was estimated using linear regression. Cause of death information was obtained from the National Health Service Central Register. Standardised mortality ratios (SMR) were calculated using the national rates as comparison.

Results: There was a total of 764 deaths, and mortality from all causes was significantly reduced. Mortality from cardiovascular and respiratory diseases overall was also less than expected. There was a slight deficit in cancer mortality. Bladder cancer mortality was increased and mortality from lung cancer was as expected for men, but raised for women (four cases only). Mortality did not show any pattern with quarry group or job category, with the exception of bladder and lung cancers that were significantly raised at one quarry. Lung cancer mortality was significantly increased overall in those workers employed for <5 years and for those starting work between 1950 and 1959 at one quarry. It also showed a negative trend with cumulative RCSD exposure, even after lagging the data.

Conclusions: Mortality was generally lower than expected. This study has not demonstrated any consistent relationship between RCSD exposure and the development of cancer, especially lung cancer. However, only one case of silicosis was identified, highlighting a limitation of the use of death certificates.

O9.5 URBAN ENVIRONMENT AND CANCER: A MORTALITY STUDY AMONG BUS DRIVERS AND TRAFFIC POLICE OFFICERS

A. C. Pesatori1, D. Consonni1, P. A. Bertazzi1, A. Colombi1, M. Bonzini1, F. Merlo2.1Department of Occupational Health, Istituti Clinici di Perfezionamento and University of Milan, Milan, Italy; 2National Cancer Research Institute, Genoa, Italy

Introduction: A multicentre European study identified occupational groups exposed to low or very low benzene levels. The research had two components: cross sectional biomarkers and historical cohort mortality study. We report the main findings of the mortality study among bus drivers and traffic police officers in Genoa and Milan, Italy.

Methods: We identified three cohorts of male workers employed in the period 1949–79, comprising 7105 bus drivers and 1563 traffic police officers in Genoa, and 3390 traffic police officers in Milan. The follow up covered the period 1960-1998. Expected deaths and standardised mortality ratios (SMR) were computed using national (before 1970) and regional (1970 onwards) mortality rates.

Results: The tracing was over 99% complete. Among bus drivers there were 2296 deaths (SMR 0.92); elevated risks for several causes were found, notably lung cancer (309 deaths, SMR 1.18, 95% confidence interval (CI) 1.06 to 1.32), and Hodgkin’s disease (13 deaths, SMR 2.07, 95% CI 1.20 to 3.56); mortality from respiratory, cardiovascular, and digestive diseases was markedly reduced. Lung cancer risk increased with duration of employment (SMR in the category 30+ years 1.27, 95% CI 1.06 to 1.52) and with time since first employment (test for trend p = 0.04; SMR in the category 30+ years 1.26, 95% CI 1.11 to 1.44). Among traffic police officers in Genoa we observed 592 deaths (SMR 0.92); elevated risks were found for liver cancer (15 deaths, SMR 1.66, 95% CI 1.00 to 2.76), while lung cancer mortality was close to the expected (60 deaths, SMR 0.96). There were 1325 deaths among traffic police officers in Milan (SMR 0.92); we observed slightly elevated risks for Hodgkin’s disease (five deaths, SMR 1.56, 95% CI 0.65 to 3.74), and leukaemia (14 deaths, SMR 1.23, 95% CI 0.73 to 2.08).

Conclusions: Workers exposed to urban traffic showed a suggestive increase of some lymphatic and haematopoietic cancers. Lung cancer risk among bus drivers was elevated and positively associated with length of employment and latency. Airborne pollutants are a plausible explanation for these findings.

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