Excess lung function decline in gold miners following pulmonary tuberculosis.

BACKGROUND: Few if any studies of the association between pulmonary tuberculosis (TB) and lung function loss have had access to premorbid lung function values. METHODS: Using a retrospective cohort design, the study recruited employed South African gold miners who had undergone a pulmonary function test (PFT) between January 1995 and August 1996. The 'exposed' group comprised 185 miners treated for pulmonary TB after the initial PFT and the 'unexposed' group comprised 185 age-matched miners without TB. All participants had a follow-up PFT between April and June 2000. The outcome of interest was decline in lung function during the follow-up period as measured by forced vital capacity (FVC) and forced expiratory volume in 1 s(FEV(1)). RESULTS: After controlling for age, height, baseline lung function, silicosis, years of employment, smoking and other respiratory diagnoses, pulmonary TB during the follow-up period was associated with a mean excess loss of 40.3 ml/year in FEV(1) (95% CI 25.4 to 55.1) and 42.7 ml/year in FVC (95% CI 27.0 to 58.5). Lung function loss was greater among those with more severe or later clinical presentation of TB. Breathlessness was twice as common among TB cases (OR 2.20, 95% CI 1.18 to 4.11). CONCLUSION: There is a need for greater clinical recognition of the long-term respiratory consequences of treated pulmonary TB. Early detection of TB would help to reduce these sequelae and remains a priority, particularly in a workforce already subject to silica dust disease. However, strategies such as dust control, worker education about TB and dust and TB preventive therapy are also needed to avert the disease itself.

Workplace spirometry monitoring for respiratory disease prevention: a methods review.

This report reviews methods applicable in workplace spirometry monitoring for the identification of individuals with excessive lung function decline. Specific issues addressed include 1) maintaining longitudinal spirometry data precision at an acceptable level so that declines due to adverse physiological processes in the lung can be readily detected in an individual; 2) applying interpretative strategies that have a high likelihood of identifying workers at risk of developing lung function impairment; and 3) enhancing effectiveness of spirometry monitoring for intervention and disease prevention. Applications in ongoing computerized spirometry monitoring programs are described that demonstrate approaches to improving spirometry data precision and quality, and facilitating informed decision-making on disease prevention.

The precision of longitudinal lung function measurements: monitoring and interpretation.

BACKGROUND: The efficacy of decision making based on longitudinal spirometric measurements depends critically on the precision of the available data, which is determined by the magnitude of the within-person variation. AIMS: Firstly, to describe and investigate two statistical methods-a pairwise estimate of within-person standard deviation s(p) and the reliability coefficient G-for use in the monitoring of precision of longitudinal measurements of forced expiratory volume in one second (FEV1). Secondly, to investigate the effect of longitudinal data precision on the detectable excess rate of decline in FEV1. METHODS: The authors "monitored" retrospectively on a yearly basis the magnitude of the within-person variation s(p) and the coefficient G in 11 workplace based spirometric monitoring programmes conducted from 1987 to 2001 on 12 729 workers in various industrial plants. RESULTS: The plant-specific mean values s(p) (range 122-166 ml) and G (range 0.88-0.95), averaged over all years of follow up, correlated well with the plant-specific within-person standard deviation s(r) (range 130-177 ml) estimated from all longitudinal data. The correlations were 0.90 for s(p) and 0.68 for G. The average precision of the longitudinal FEV1 measurements affected the duration of follow up needed to identify a "true" excess rate of decline in FEV1 in an individual. CONCLUSIONS: The results show that monitoring of longitudinal spirometry data precision (1) allows that data precision can be improved or maintained at levels that allow individuals with a rapid decline to be identified at an earlier age; and (2) attaches a measure of precision to the data on which decision making is based.

Risk of silicosis in cohorts of Chinese tin and tungsten miners and pottery workers (II): Workplace-specific silica particle surface composition.

BACKGROUND: It is hypothesized that surface occlusion by alumino-silicate affects the toxic activity of silica particles in respirable dust. In conjunction with an epidemiological investigation of silicosis disease risk in Chinese tin and tungsten mine and pottery workplaces, we analyzed respirable silica dusts using a multiple-voltage scanning electron microscopy-energy dispersive X-ray spectroscopy (MVSEM-EDS). METHODS: Forty-seven samples of respirable sized dust were collected on filters from 13 worksites and were analyzed by MVSEM-EDS using high (20 keV) and low (5 keV) electron beam accelerating voltages. Changes in the silicon-to-aluminum X-ray line intensity ratio between the two voltages are compared particle-by-particle with the 90th percentile value of the same measurements for a ground glass homogeneous control sample. This provides an index that distinguishes a silica particle that is homogeneously aluminum-contaminated from a clay-coated silica particle. RESULTS: The average sample percentages of respirable-sized silica particles alumino-silicate occlusion were: 45% for potteries, 18% for tin mines, and 13% for tungsten mines. The difference between the pottery and the metal mine worksites accounted for one third of an overall chi-square statistic for differences in change in measured silicon fraction between the samples. CONCLUSION: The companion epidemiological study found lower silicosis risk per unit cumulative respirable silica dust exposure for pottery workers compared to metal miners. Using these surface analysis results resolves differences in risk when exposure is normalized to cumulative respirable surface-available silica dust.

Chronic obstructive pulmonary disease due to occupational exposure to silica dust: a review of epidemiological and pathological evidence.

Occupational exposure is an important risk factor for chronic obstructive pulmonary disease (COPD), and silica dust is one of the most important occupational respiratory toxins. Epidemiological and pathological studies suggest that silica dust exposure can lead to COPD, even in the absence of radiological signs of silicosis, and that the association between cumulative silica dust exposure and airflow obstruction is independent of silicosis. Recent clinicopathological and experimental studies have contributed further towards explaining the potential mechanism through which silica can cause pathological changes that may lead to the development of COPD. In this paper we review the epidemiological and pathological evidence relevant to the development of COPD in silica dust exposed workers within the context of recent findings. The evidence surveyed suggests that chronic levels of silica dust that do not cause disabling silicosis may cause the development of chronic bronchitis, emphysema, and/or small airways disease that can lead to airflow obstruction, even in the absence of radiological silicosis.

Pooled exposure-response analyses and risk assessment for lung cancer in 10 cohorts of silica-exposed workers: an IARC multicentre study.

OBJECTIVES: Silica is one of the most common occupational exposures worldwide. In 1997 the International Agency for Research on Cancer (IARC) classified inhaled crystalline silica as a human carcinogen (group 1), but acknowledged limitations in the epidemiologic data, including inconsistencies across studies and the lack of extensive exposure-response data. We have conducted a pooled exposure-response analysis of 10 silica-exposed cohorts to investigate lung cancer. METHODS: The pooled cohort included 65,980 workers (44,160 miners, 21,820 nominees), and 1,072 lung cancer deaths (663 miners, 409 nonminers). Follow-up has been extended for five of these cohorts beyond published data. Quantitative exposure estimates by job and calendar time were adopted, modified, or developed to permit common analyses by respirable silica (mg/m3) across cohorts. RESULTS: The log of cumulative exposure, with a 15-year lag, was a strong predictor of lung cancer (p = 0.0001), with consistency across studies (test for heterogeneity, p = 0.34). Results for the log of cumulative exposure were consistent between underground mines and other facilities. Categorical analyses by quintile of cumulative exposure resulted in a monotonic trend with odds ratios of 1.0. 1.0, 1.3, 1.5, 1.6. Analyses using a spline curve also showed a monotonic increase in risk with increasing exposure. The estimated excess lifetime risk (through age 75) of lung cancer for a worker exposed from age 20 to 65 at 0.1 mg/m3 respirable crystalline silica (the permissible level in many countries) was 1.1-1.7%, above background risks of 3-6%. CONCLUSIONS: Our results support the decision by the IARC to classify inhaled silica in occupational settings as a carcinogen, and suggest that the current exposure limits in many countries may be inadequate. These data represent the first quantitative exposure-response analysis and risk assessment for silica using data from multiple studies.

Occupational respiratory diseases in South Africa--results from SORDSA, 1997-1999.

OBJECTIVES: To describe the nature and extent of work-related respiratory diseases reported to the national Surveillance of Work-related and Occupational Respiratory Diseases in South Africa (SORDSA) reporting scheme. The causative agents and industrial categories in which they occurred are also characterised. DESIGN: Voluntary monthly reporting of newly diagnosed cases by pulmonologists, occupational medicine practitioners and occupational health nurses. SETTING: Medical and occupational health referral centres in the nine provinces of South Africa. SUBJECTS: Cases were workers from non-mining industries or ex-miners, suffering from a newly diagnosed occupational respiratory disease, reported to SORDSA between October 1996 and December 1999. OUTCOME MEASURES: Frequencies of reported occupational respiratory disease by year, reporting source, province and sex. Frequencies of short- and long-latency diseases by industry and causative agent. RESULTS: There was incomplete reporting coverage of the nine provinces in the first 3 years. Reporting was most comprehensive from Gauteng, KwaZulu-Natal and the Western Cape. Diseases with long latency periods made up 76.2% of the cases. Pneumoconiosis, even in non-mining industries, was the most frequently reported disease, followed by inhalation accidents. Occupational asthma was the fourth most reported disease. Apart from the prominence of pneumoconiosis, the results obtained by SORDSA are similar to those from a British occupational lung disease surveillance scheme. This study showed that newly diagnosed cases of occupational lung disease occurred in many industries and were caused by a variety of agents. CONCLUSION: SORDSA has contributed insight into the nature, extent and distribution of occupational respiratory diseases in South Africa. It has also highlighted important causes of occupational respiratory diseases in South Africa, as well as hazardous industries. The data indicate that South Africa has a widespread occupational lung disease problem, and provide a platform for targeted prevention strategies.

Occurrence and causes of occupational asthma in South Africa--results from SORDSA's Occupational Asthma Registry, 1997-1999.

OBJECTIVE: To present results for the first 3 years of the occupational asthma registry of the Surveillance of Work-related and Occupational Respiratory Diseases in South Africa (SORDSA) programme, ending December 1999. DESIGN: Surveillance was accomplished by collecting voluntary reports of occupational asthma cases from pulmonologists, occupational medicine practitioners and occupational health nurses. SETTING: Medical and occupational health referral centres in the nine provinces of South Africa. SUBJECTS: Patients diagnosed with new-onset occupational asthma with latency or irritant-induced asthma, reported to SORDSA during 1997-1999. OUTCOME MEASURES: Frequencies of cases, causative agents, industries causing exposure and diagnostic methods. Average annual incidence rates by province and by occupation. RESULTS: During this period 324 cases of occupational asthma were reported. The average annual incidence rate of occupational asthma was estimated in the three best-reporting provinces, namely Gauteng, KwaZulu-Natal and the Western Cape, as 17.5 per million employed people annually. This rate was highest in the Western Cape (25.1 per million). Semi-skilled operators had the highest incidence rate of 68.7 per million annually in the three provinces. Isocyanates and latex were the most common agents. Low molecular weight causative agents predominated (68.8%) over high molecular weight agents. Health care was the most frequently reported workplace for occupational asthma (OA) development. Serial peak flow testing was the method most often used for diagnosis. One-fifth of the cases were still occupationally exposed to the causative agent at time of diagnosis. CONCLUSION: Despite underreporting, SORDSA's estimate of the occupational asthma incidence rate was similar to that of the UK. SORDSA has also demonstrated that surveillance programmes in a developing country can provide useful information on which to base prevention activities.

Occupational asthma as identified by the Surveillance of Work-related and Occupational Respiratory Diseases programme in South Africa.

BACKGROUND: The nationwide Surveillance of Work-related and Occupational Respiratory Diseases in South Africa, SORDSA, was established in 1996 to provide systematic information on occupational respiratory diseases. OBJECTIVE: SORDSA's objectives are to monitor the nature, extent and distribution of occupational respiratory diseases, and to increase awareness of their diagnosis and prevention. This paper describes the programme and results obtained for occupational asthma in the first 2 years, ending in October 1998. METHODS: SORDSA identifies newly diagnosed cases of occupational respiratory disease through voluntary reporting by pulmonologists, occupational medicine doctors and occupational health nurses. Initially, recruitment of the above health care providers was done through the membership infrastructure of their respective professional societies. Booklets with prescribed monthly reporting forms were distributed annually to all reporting members and a core of reporting providers was established through a proactive method of data collection. Information dissemination and reporting feedback takes place through quarterly newsletters and issue-specific brochures on certain hazardous agents. RESULTS: Over the initial 2-year period, 3285 cases of occupational respiratory disease were reported to SORDSA by 203 doctors and 97 occupational health nurses. After pneumoconiosis and associated respiratory conditions, occupational asthma was the second most commonly reported disease with 225 cases (6.9%). The average annual incidence for occupational asthma in South Africa was 13.1 per million employed people, with the highest incidence reported from the Western Cape province (37.6 per million). Latex was the most frequently reported agent for occupational asthma, followed by isocyanates and platinum salts. Low molecular weight agents accounted for 59.6% of the cases of occupational asthma. CONCLUSION: The results from this initial phase show that despite some limitations, SORDSA has the potential to obtain useful data on the industries, agents and occupations causing occupational asthma in South Africa.

Lung function prediction equations derived from healthy South African gold miners.

OBJECTIVES: To estimate lung function prediction equations and to identify appropriate normal reference values for the population of about 250 000 of South African gold miners. METHODS: Data from a lung function screening programme conducted at a large South African gold mine from 1994 to 1998 were used to estimate the lung function prediction equations. The most reliable period of lung function testing was identified in a previous study of a temporal pattern in reliability, and lung function tests from this period were used. Miners with a history of pulmonary tuberculosis or with radiological abnormalities were excluded from the study. The prediction equations were estimated cross sectionally on 15 772 black and 2752 white miners, and published reference equations that fitted most closely the observed data were identified. RESULTS: The estimated prediction equations for forced vital capacity (FVC) are as follows: for black men, FVC (l)=- 2.901-0.025xage+4.655xheight; and for white men, FVC(l)=-4.407-0.036xage+ 5.940xheight. For forced expiratory volume in one second (FEV(1)) these equations are: for black men, FEV(1)(l)=-1.654- 0.30xage+3.665xheight; and for white men, FEV(1)(l)= -2.341- 0.038xage+4.314xheight. Units are years for age and metres for height. Knudson's and the European Community of Coal and Steel (ECCS) reference values provided the closest fit to the data on lung function of white miners, but the lower limits of normal from the ECCS equations were the closest to the observed one sided lower 95% confidence intervals (95% CIs). For black miners, reference equations that fitted best were derived by Louw et al on asymptomatic black South African men unexposed to occupational dust. There were significant differences between the two groups of miners in the estimated height adjusted mean lung function values for a 40 year old 1.7 m tall man (220 ml (5.2%) for FVC and 110 ml (3.2%) for FEV(1)); white men had higher FVC and FEV(1), but lower FEV(1)/FVC ratio. The ECCS reference values scaled by a conversion factor of 0. 93 for the FVC and 0.95 for the FEV(1) provided close fits to the data for black miners, but the rate of decline with age was higher than that in the observed data. None of the linear equations provided a good fit for the 20-29 and more than 55 years old age categories. CONCLUSION: The ECCS and Knudson equations provided the best fit to the data for white miners, whereas the equations by Louw et al estimated on asymptomatic black South African bank workers provided the best fit to the data for black miners. The ECCS reference values scaled by a factor of 0.93 for FVC and by 0.95 for FEV(1) provided close fits, but the rate of decline with age was higher than that in the data for black miners.

Correlation between autopsy findings for chronic obstructive airways disease and in-life disability in South African gold miners.

OBJECTIVES: In South Africa chronic obstructive airway disease (COAD), which could be due to working in a dusty atmosphere in scheduled mines or works, is a compensatable disease. Miners are compensated for in-life respiratory disability and for findings at autopsy of COAD, which includes emphysema, bronchitis assessed by mucus gland hyperplasia in the main bronchus, and bronchiolitis assessed by goblet cell metaplasia. The question arises as to whether the autopsy findings correlate with in-life impairment. The objectives of the study were: (1) to determine whether autopsy COAD outcomes relate to lung function and to respiratory symptoms and signs; and (2) to quantify the individual contributions of emphysema, bronchiolitis and bronchitis to lung function impairment. METHODS: On 724 gold miners, pathological findings of COAD--emphysema, bronchitis and bronchiolitis-- were related to lung function measurements and respiratory symptoms and signs observed within 5 years prior to death. RESULTS: Emphysema diagnosed at autopsy was the main determinant of airflow impairment. The emphysema score categories 0-5, 5-35, 35-65 and > 65 were associated with decreased forced expiratory volume in 1 s, expressed as percentage predicted (FEV1%) as follows: 78.8%, 66.2%, 52.0% and 46.0%, respectively. The score was also associated with increasing frequency of dyspnoea. After adjustment for emphysema, the bronchitis and bronchiolitis were not related to significant lung function loss, and in subjects without emphysema, the presence of moderate or marked bronchitis was associated with a mild impairment only. Bronchitis at autopsy was associated with increased frequency of rhonchi, sputum and cough, whereas bronchiolitis was associated with increased sputum only. Silicosis found at autopsy was associated with some obstructive and restrictive lung function impairment. Tobacco smoking was associated with all the COAD outcomes.

Chronic pulmonary function impairment caused by initial and recurrent pulmonary tuberculosis following treatment.

BACKGROUND: A study was undertaken to establish the chronic effect of initial and recurrent treated pulmonary tuberculosis on impairment of lung function. METHODS: A total of 27 660 black South African gold miners who had reliable pulmonary function tests from January 1995 to August 1996 were retrospectively followed for the incidence of pulmonary tuberculosis to 1970. The lung function measurements in 1995-6 were related to the number of previous episodes of tuberculosis and to the time that had lapsed from the diagnosis of the last episode of tuberculosis to the lung function test. Miners without tuberculosis or pneumoconiosis served as a comparison group. RESULTS: There were 2137 miners who had one episode of tuberculosis, 366 who had two, and 96 who had three or more episodes. The average time between the diagnosis of the last episode of tuberculosis and the lung function test was 4.6 years (range one month to 31 years). The loss of lung function was highest within six months of the diagnosis of tuberculosis and stabilised after 12 months when the loss was considered to be chronic. The estimated average chronic deficit in forced expiratory volume in one second (FEV(1)) after one, two, and three or more episodes of tuberculosis was 153 ml, 326 ml, and 410 ml, respectively. The corresponding deficits for forced vital capacity (FVC) were 96 ml, 286 ml, and 345 ml. The loss of function due to tuberculosis was not biased by the presence of HIV as HIV positive and HIV negative subjects had similar losses. The percentage of subjects with chronic airflow impairment (FEV(1) <80% predicted) was 18.4% in those with one episode, 27.1% in those with two, and 35.2% in those with three or more episodes of tuberculosis. CONCLUSIONS: Tuberculosis can cause chronic impairment of lung function which increases incrementally with the number of episodes of tuberculosis. Clearly, prevention of tuberculosis and its effect on lung function is important and can be achieved by early detection and by reduction of the risk of tuberculosis through intervention on risk factors such as HIV, silica dust exposure, silicosis, and socioeconomic factors.

Assessment of reliability of lung function screening programs or longitudinal studies.

The aim was to determine reliability of lung function measurements performed according to recommendations of the American Thoracic Society (ATS) at a screening program in a large South African gold mine and to determine the usefulness of the reliability coefficient G for monitoring the reliability of lung function measurements in a mass screening program. The reliability coefficient G estimates the amount of random error of measurement, relative to the total variation in a measurement. The coefficient G was calculated as a correlation coefficient between two consecutive lung function tests performed within 6 mo, over a period of 43 mo on 3,378 miners. There was significant temporal variability in the reliability. For FEV(1), the coefficient G showed increased variability over the first 5 mo and stabilized at a value of 0.93 for the next 23 mo, after which it systematically declined over the next 15 mo. We estimated that in a large screening program, an optimal sample size of around 900 miners, examined randomly throughout the year, on a yearly basis, would provide a sufficient sample to examine monthly or quarterly fluctuation in the reliability. The value of the reliability coefficient G did not change when the time between two consecutive tests increased up to 15 mo. In conclusion, monitoring of lung function reliability in a screening program by the reliability coefficient G should improve data quality, and provide a measure on which the confidence in a decision-making process could be based when examining temporal changes in lung function for individual subjects.

Risk of pulmonary tuberculosis relative to silicosis and exposure to silica dust in South African gold miners.

OBJECTIVES: To investigate the following questions. (1) Is silica dust on its own, without the presence of silicosis, associated with an increased risk of pulmonary tuberculosis (PTB) in workers exposed to silica dust? (2) In the absence of silicosis is the excess risk dose related? (3) What is the predominant chronological sequence between the development of PTB and the development of silicosis after the end of exposure to dust? METHODS: A cohort of 2255 white South African gold miners has been followed up from 1968 to 1971, when they were 45-55 years of age, to 31 December 1995 for the incidence of PTB. During the follow up 1592 (71%) men died. Of these, 1296 (81%) had a necropsy done at the National Centre for Occupational Health (NCOH) to determine the presence of silicosis and PTB. The incidence of PTB in the cohort was studied relative to cumulative exposure to dust and the onset of silicosis. For the miners with necropsy, the incidence for PTB was studied relative to the severity of silicosis found at necropsy. RESULTS: There were 115 subjects who developed PTB. The total person-years of follow up was 39,319. For the whole cohort, the factors associated with increased risk of PTB were cumulative exposure to dust (mg/m3.y) (the adjusted rate ratio (RR) 1.07; (95% confidence interval (95% CI) 1.04 to 1.10)), silicosis diagnosed radiologically (3.96 (2.59 to 6.06)), and tobacco pack-years (1.02 (1.01 to 1.03)). The RR (95% CI) for PTB increased with increasing quartiles of cumulative exposure to dust 1.0, 1.51 (0.78 to 2.91), 2.35 (1.28 to 4.32), and 3.22 (1.75 to 5.90). In miners who did not have radiologically diagnosed silicosis (n = 1934, PTB = 74), the adjusted RR (95% CI) for PTB and cumulative exposure to dust was 1.10 (1.06 to 1.13), and increased with quartiles of cumulative exposure to dust as 1.00, 1.46 (0.70 to 3.03), 2.67 (1.37 to 5.23), and 4.01 (2.04 to 7.88). For the subjects who had a necropsy (n = 1296, PTB = 70), the adjusted RR (95% CI) for PTB increased with the severity of silicosis found at necropsy; 1.0 for no silicosis, 1.88 (0.97 to 3.64) for negligible, 2.69 (1.35 to 5.37) for slight, and 2.30 (1.16 to 4.58) for moderate or marked silicosis. For subjects who had a necropsy and no silicosis (n = 577, PTB = 18), the adjusted RR (95% CI) increased slightly with quartiles of cumulative dust 1.0, 1.11 (0.31 to 4.00), 1.42 (0.43 to 4.72), and 1.38 (0.33 to 5.62). CONCLUSION: Exposure to silica dust is a risk factor for the development of PTB in the absence of silicosis, even after exposure to silica dust ends. The risk of PTB increases with the presence of silicosis, and in miners without radiological silicosis, with quartiles of exposure to dust. The severity of silicosis diagnosed at necropsy was associated with increasing risk of PTB and even < 5 nodules--that is, undetectable radiologically--was associated with an increased risk of PTB. The diagnosis of PTB was on average 7.6 years after the end of exposure to dust, at around 60 years of age. The onset of radiological silicosis preceded the diagnosis of PTB in 90.2% of the cases with PTB who had silicosis. The results have implications for medical surveillance of workers exposed to silica dust after the end of exposure.

Lung cancer in relation to exposure to silica dust, silicosis and uranium production in South African gold miners.

BACKGROUND: A nested case-control study for lung cancer was performed on a cohort of 2260 South African gold miners in whom an association between exposure to silica dust and risk of lung cancer was previously reported. The objective was to investigate an expanded set of risk factors and also cancer cell type. METHODS: The 78 cases of lung cancer found during the follow up period from 1970 to 1986 were matched with 386 controls. Risk of lung cancer was related to smoking, exposure to silica dust, incidence of silicosis, and uranium production and the uranium content of the mine ore. RESULTS: The risk of lung cancer was associated with tobacco smoking, cumulative dust exposure, duration of underground mining, and with silicosis. The best predictive model included pack years of cigarette consumption (adjusted relative risk (RR) = 1.0 for < 6.5 pack years, 3.5 (95% confidence interval (CI) 0.7 to 16.8) for 6.5-20 pack years, 5.7 (95% CI 1.3 to 25.8) for 21-30 pack years, and 13.2 (95% CI 3.1 to 56.2) for more than 30 pack years) and silicosis (RR = 2.45 (95% CI 1.2 to 5.2)). No association was found with uranium production. The lung tumour cell type distribution was 40.3% small cell carcinoma, 38.8% squamous cell, 16.4% adenocarcinoma, and 4.5% large cell carcinoma. Small and large cell cancer combined were associated with exposure to dust. CONCLUSIONS: The results cannot be interpreted definitively in terms of causal association. Possible interpretations are: (1) subjects with high dust exposure who develop silicosis are at increased risk of lung cancer; (2) high levels of exposure to silica dust on its own is important in the pathogenesis of lung cancer and silicosis is coincidental; and (3) high levels of silica dust exposure may be a surrogate for the exposure to radon daughters.

Emphysema and airway obstruction in non-smoking South African gold miners with long exposure to silica dust.

OBJECTIVE: Occupational exposure to silica dust is associated with significant impairment of lung function. The present study investigates which pathological changes in the lung are associated with impairment of lung function in silica dust exposed workers who were life-long non-smokers. METHODS: 242 South African white gold miners who were lifelong non-smokers and who had a necropsy at death were studied. The pathological features identified at necropsy were the degree and type of emphysema, the presence of airway disease, and the degree of silicosis in the lung parenchyma and pleura. These features were related to lung function tests done a few years before death, to type of impairment (obstructive or restrictive), and to cumulative silica dust exposure. RESULTS: The degree of emphysema found at necropsy was not associated with a statistically significant impairment of lung function or with dust exposure. The degree of silicosis in the lung parenchyma and the large airways disease (based on mucus gland hyperplasia) were associated with a statistically significant impairment of lung function. The large airway disease was, however, not positively associated with dust exposure or silicosis. In miners with a moderate or a higher degree of limitation of airflow the main findings were silicosis, heart disease, and obesity. The presence of small airways disease could not be established from the necropsy material. CONCLUSION: The results indicate that the level of exposure to silica dust to which these miners were exposed, without a confounding effect of tobacco smoking, is not associated with a degree of emphysema that would cause a statistically significant impairment of lung function. Silicosis of the lung parenchyma was associated with loss of lung function. Other factors that may play a part in impairment of lung function in these miners are obesity and heart disease.

Correlation between radiological and pathological diagnosis of silicosis: an autopsy population based study.

The radiological findings for the profusion of rounded opacities were compared to pathological findings for parenchymal silicosis in 557 gold miners who had, on average, 2.7 years between the radiological and pathological examination. Three readers read the radiographs, and ILO category 1/1 or more was defined as a positive diagnosis of silicosis. The sensitivity values were 0.393, 0.371, and 0.236, and the specificity values were 0.987, 0.965, and 0.978, for the three readers, respectively. The sensitivity of the readers improved with increasing degree of autopsy silicosis, but a large proportion of those with a moderate and marked degree of silicosis were not diagnosed radiologically. The diagnostic sensitivity of the radiological test could be improved by using category 0/1 as a cutoff point for workers exposed to a high average concentration of respirable silica dust. The diagnostic specificity of radiology could be improved by using category 1/0 or 1/1 as a cutoff point for a positive diagnosis for workers exposed to a low average concentration of respirable silica dust.

Risk of silicosis in a cohort of white South African gold miners.

The risk of silicosis was investigated in a cohort of 2,235 white South African gold miners who had, on average, 24 years of net service from 1940 to the early 1970s and who were followed up to 1991 for radiological signs of onset of silicosis (ILO category 1/1 or more). There were 313 (14%) miners who developed signs of silicosis at an average age of 55.9 years. The latency period was largely independent of the cumulative dust exposure. In 57% of the silicosis, the radiological signs developed, on average, 7.4 years after mining exposure ceased. The risk of silicosis increased exponentially with the cumulative dust dose, the accelerated increase being after 7 mg/m3-years. At the highest exposure level of 15 mg/m3-years, which represents approximately 37 years of gold mining at an average respirable dust concentration of 0.4 mg/m3, the cumulative risk for silicosis reached 77%. In conclusion, the risk of silicosis was strongly dose dependent; however, the latency period was largely independent of the dose.