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1.  Respiratory disease and cardiovascular morbidity 
Background: Work related dust exposure is a risk factor for acute and chronic respiratory irritation and inflammation. Exposure to dust and cigarette smoke predisposes to exogenous viral and bacterial infections of the respiratory tract. Respiratory infection can also act as a risk factor in the development of atherosclerotic and coronary artery disease.
Aims: To investigate the association of dust exposure and respiratory diseases with ischaemic heart disease (IHD) and other cardiovascular diseases (CVDs).
Methods: The study comprised 6022 dust exposed (granite, foundry, cotton mill, iron foundry, metal product, and electrical) workers hired in 1940–76 and followed until the end of 1992. National mortality and morbidity registers and questionnaires were used. The statistical methods were person-year analysis and Cox regression.
Results: Co-morbidity from cardiovascular and respiratory diseases ranged from 17% to 35%. In at least 60% of the co-morbidity cases a respiratory disease preceded a cardiovascular disease. Chronic bronchitis, pneumonia, and upper respiratory track infections predicted IHD in granite workers (rate ratio (RR) = 1.9; 95% CI 1.38 to 2.72), foundry workers (2.1; 1.48 to 2.93), and iron foundry workers (1.7; 1.16 to 2.35). Dust exposure was not a significant predictor of IHD or other CVD in any group. Dust exposure was related to respiratory morbidity. Thus, some respiratory diseases appeared to act as intermediate variables in the association of dust exposure with IHD.
Conclusion: Dust exposure had only a small direct effect on IHD and other CVD. IHD morbidity was associated with preceding respiratory morbidity. A chronic infectious respiratory tract disease appeared to play an independent role in the development of IHD.
doi:10.1136/oem.2004.017111
PMCID: PMC1741093  PMID: 16109822
2.  Cause-Specific Mortality Due to Malignant and Non-Malignant Disease in Korean Foundry Workers 
PLoS ONE  2014;9(2):e88264.
Background
Foundry work is associated with serious occupational hazards. Although several studies have investigated the health risks associated with foundry work, the results of these studies have been inconsistent with the exception of an increased lung cancer risk. The current study evaluated the mortality of Korean foundry workers due to malignant and non-malignant diseases.
Methods
This study is part of an ongoing investigation of Korean foundry workers. To date, we have observed more than 150,000 person-years in male foundry production workers. In the current study, we stratified mortality ratios by the following job categories: melting-pouring, molding-coremaking, fettling, and uncategorized production work. We calculated standard mortality ratios (SMR) of foundry workers compare to general Korean men and relative risk (RR) of mortality of foundry production workers reference to non-production worker, respectively.
Results
Korean foundry production workers had a significantly higher risk of mortality due to malignant disease, including stomach (RR: 3.96; 95% CI: 1.41–11.06) and lung cancer (RR: 2.08; 95% CI: 1.01–4.30), compared with non-production workers. High mortality ratios were also observed for non-malignant diseases, including diseases of the circulatory (RR: 1.92; 95% CI: 1.18–3.14), respiratory (RR: 1.71; 95% CI: 1.52–21.42 for uncategorized production worker), and digestive (RR: 2.27; 95% CI: 1.22–4.24) systems, as well as for injuries (RR: 2.36; 95% CI: 1.52–3.66) including suicide (RR: 3.64; 95% CI: 1.32–10.01).
Conclusion
This study suggests that foundry production work significantly increases the risk of mortality due to some kinds of malignant and non-malignant diseases compared with non-production work.
doi:10.1371/journal.pone.0088264
PMCID: PMC3914960  PMID: 24505454
3.  Interaction of smoking, uptake of polycyclic aromatic hydrocarbons, and cytochrome P450IA2 activity among foundry workers. 
An increased lung cancer risk has been described among foundry workers. Polycyclic aromatic hydrocarbons (PAHs) and silica are possible aetiological factors. This study describes a urinary PAH metabolite, 1-hydroxypyrene (hpU), as well as the degree of cytochrome P450IA2 activity/induction as reflected by the urinary caffeine ratio (IA2) in 45 foundry workers and 52 controls; IA2 was defined as the ratio of paraxanthine 7-demethylation products to a paraxanthine 8-hydroxylation product (1,7-dimethyluric acid). Mean exposure concentrations for foundry workers were defined by breathing zone hygienic samples (respirable dust 1.2 to 3.52 mg/m3 (93 samples)) and as total PAH (0.46 micrograms/m3) and pyrene concentrations (0.28 micrograms/m3) (six samples). Non-smoking controls and foundry workers had similar IA2 ratios (5.63, 95% confidence interval (95% CI) 4.56-6.70 and 4.40, 95% CI 3.56-5.24). The same was true for smoking controls and foundry workers (9.10, 95% CI 8.00-10.20 and 8.69, 95% CI 7.37-10.01). Both smoking groups had raised IA2 ratios compared with non-smokers (p less than 0.01). Non-smoking controls and foundry workers had similar hpU concentrations (0.16, 95% CI 0.10-0.22 and 0.11, 95% CI 0.09-0.13 mumol/mol creatinine). Smoking foundry workers had raised hpU concentrations (0.42, 95% CI 0.25-0.59) compared with smoking controls (0.26, 95% CI 0.18-0.34) (p less than 0.01). A small subgroup of smoking foundry workers with the highest exposures to both silica and PAH also had the highest hpU concentrations (0.70, 95% CI - 0.07-1.47 mumol/mol creatinine) (p less than 0.04). Increased hpU concentrations in smoking foundry workers suggest a more than additive effect from smoking and foundry exposures resulting in increased PAH uptake. Increased P450IA2 enzyme activity was only found in smokers and no additional effect of foundry exposures was seen. These data suggest that smoking as well as work related PAH exposure may be casually related to increased risk of lung cancer in foundry workers.
PMCID: PMC1012094  PMID: 1554617
4.  Dust exposure and impairment of lung function at a small iron foundry in a rapidly developing country 
OBJECTIVES—A cross sectional prospective study was carried out among iron foundry workers (exposed) and soft drink bottling and supply company workers (unexposed) to assess their occupational exposure to ambient respiratory dust in their work environment and its effect on their lung function profile.
PARTICIPANTS—Lung function was measured in 81 exposed and 113 unexposed workers. Personal respirable dust concentrations were measured for all the exposed and the unexposed workers. Information on respiratory signs and symptoms was also collected from the participants.
RESULTS—Among the exposed workers, midexpiratory flow (FEF25-75), forced expiratory volume in 1 second (FEV1), peak expiratory flow (PEF), FEV1/FVC, and FEV1/VC ratios were significantly lower whereas the vital capacity (VC) and forced vital capacity (FVC) were non-significantly higher. Job at the iron foundry was a significant predictor of lung function. Exposure to high concentration of respirable dust at the iron foundry was also a significant predictor. Workers working in high exposure areas (general works, furnace, continuous casting areas, and fabrication workshop) had lower lung function values than workers in medium and low exposure areas. Smoking did not enhance the effects of exposure to dust on lung function.
CONCLUSIONS—Exposure to respirable dust was higher among the iron foundry workers; and among these, general, furnace, rolling mill, and fabrication workers had higher exposures to dust than did workers in continuous casting, the mechanical workshop, and the bottling plant. Job type and exposure to dust were significant predictors of lung function. Implementation of industrial hygiene and proper and efficient use of personal protection equipment while at work could help to protect the respiratory health of industrial workers.


Keywords: lung function; dust exposure; foundry; smoking; personal protection
doi:10.1136/oem.58.10.656
PMCID: PMC1740042  PMID: 11555687
5.  Exposure of iron foundry workers to polycyclic aromatic hydrocarbons: benzo(a)pyrene-albumin adducts and 1-hydroxypyrene as biomarkers for exposure. 
Exposure to polycyclic aromatic hydrocarbons (PAHs) in foundry workers has been evaluated by determination of benzo(a)pyrene-serum albumin adducts and urinary 1-hydroxypyrene. Benzo(a)pyrene binding to albumin and 1-hydroxypyrene were quantitatively measured by enzyme linked immunosorbent assay (ELISA) and reverse phase high performance liquid chromatography (HPLC), respectively. 70 male foundry workers and 68 matched controls were investigated. High and low exposure groups were defined from breathing zone hygienic samples, consisting of 16 PAH compounds in particulate and gaseous phase. Mean total PAH was 10.40 micrograms/m3 in the breathing zone, and mean dust adsorbed PAH was 0.15 microgram/m. All carcinogenic PAH was adsorbed to dust. Median benzo(a)pyrene-albumin adduct concentrations (10-90% percentiles) were similar in foundry workers (smokers 0.55 (0.27-1.00) and non-smokers 0.58 (0.17-1.15)) pmol/mg albumin and age matched controls (smokers 0.57 (0.16-1.45) and non-smokers 0.70 (0.19-1.55) pmol/mg albumin). Median 1-hydroxypyrene concentrations were significantly higher (P < 0.0001) in smoking and non-smoking foundry workers (0.022 (0.006-0.075) and 0.027 (0.006-0.164)) mumol/mol creatinine than in smoking and non-smoking controls (0 (0-0.022) and 0 (0-0.010) mumol/mol creatinine). Dose-response relations between total PAH, pyrene, carcinogenic PAHs, and 1-hydroxypyrene for smokers, and polycyclic aromatic hydrocarbons adsorbed to dust for non-smokers are suggested. Exposure to PAHs adsorbed to dust showed an additive effect. There was no correlation between the concentrations of 1-hydroxypyrene and benzo(a)pyrene-albumin adducts. The change in 1-hydroxypyrene over a weekend was also studied. Friday morning median 1-hydroxypyrene concentrations were significantly higher in both smokers and non-smokers (0.021 (0-0.075) and 0.027 (0.06-0.164)) mumol/mol creatinine than Monday morning median concentrations (0.007 (0-0.021) and 0.008 (0-0.021) mumol/mol creatinine). Smoking did not affect the concentrations of 1-hydroxypyrene or benzo(a)pyrene-albumin adducts. These data suggest that 1-hydroxypyrene is a sensitive biomarker for low dose PAH exposure. Exposure to PAHs may be aetiologically related to increased risk of lung cancer in foundry workers.
PMCID: PMC1128029  PMID: 7951774
6.  Respiratory cancer and air pollution from iron foundries in a Scottish town: an epidemiological and environmental study. 
A geographical association between respiratory cancer and air pollution from steel foundries has been shown previously in Scotland and elsewhere. In the present study the iron-founding town of Kirkintilloch was found to have standardised mortality ratios (SMRs) for respiratory cancer in 1959-63, 1964-8, and 1969-73 that were unexceptional in comparison with Scotland. Nevertheless, when SMRs were calculated for respiratory cancer for the period 1966-76 in five zones of the town arranged, a priori, according to probable exposure to fumes from two iron foundries, and in the individual enumeration districts of the 1971 census, higher SMRs were found in the residential areas most exposed to pollution from the foundries. The gradient of the zones' SMRs--high close to the foundries to low at some distance from them--persisted despite standardisation of the SMRs for social class. A survey of the concentrations of several metals in soil cores sampled at 51 sites throughout the town showed a pattern of pollution that probably illustrated the effects of prevailing winds and topography on the pollution plumes from the foundries. The value of sampling soil cores in investigations where historical sources of metallic air pollution are of epidemiological interest was emphasised by the detection of high concentrations of Ni in an area where a nickel refinery had been located many decades previously.
PMCID: PMC1007923  PMID: 3689714
7.  Long-Term Exposure to Silica Dust and Risk of Total and Cause-Specific Mortality in Chinese Workers: A Cohort Study 
PLoS Medicine  2012;9(4):e1001206.
A retro-prospective cohort study by Weihong Chen and colleagues provides new estimates for the risk of total and cause-specific mortality due to long-term silica dust exposure among Chinese workers.
Background
Human exposure to silica dust is very common in both working and living environments. However, the potential long-term health effects have not been well established across different exposure situations.
Methods and Findings
We studied 74,040 workers who worked at 29 metal mines and pottery factories in China for 1 y or more between January 1, 1960, and December 31, 1974, with follow-up until December 31, 2003 (median follow-up of 33 y). We estimated the cumulative silica dust exposure (CDE) for each worker by linking work history to a job–exposure matrix. We calculated standardized mortality ratios for underlying causes of death based on Chinese national mortality rates. Hazard ratios (HRs) for selected causes of death associated with CDE were estimated using the Cox proportional hazards model. The population attributable risks were estimated based on the prevalence of workers with silica dust exposure and HRs. The number of deaths attributable to silica dust exposure among Chinese workers was then calculated using the population attributable risk and the national mortality rate. We observed 19,516 deaths during 2,306,428 person-years of follow-up. Mortality from all causes was higher among workers exposed to silica dust than among non-exposed workers (993 versus 551 per 100,000 person-years). We observed significant positive exposure–response relationships between CDE (measured in milligrams/cubic meter–years, i.e., the sum of silica dust concentrations multiplied by the years of silica exposure) and mortality from all causes (HR 1.026, 95% confidence interval 1.023–1.029), respiratory diseases (1.069, 1.064–1.074), respiratory tuberculosis (1.065, 1.059–1.071), and cardiovascular disease (1.031, 1.025–1.036). Significantly elevated standardized mortality ratios were observed for all causes (1.06, 95% confidence interval 1.01–1.11), ischemic heart disease (1.65, 1.35–1.99), and pneumoconiosis (11.01, 7.67–14.95) among workers exposed to respirable silica concentrations equal to or lower than 0.1 mg/m3. After adjustment for potential confounders, including smoking, silica dust exposure accounted for 15.2% of all deaths in this study. We estimated that 4.2% of deaths (231,104 cases) among Chinese workers were attributable to silica dust exposure. The limitations of this study included a lack of data on dietary patterns and leisure time physical activity, possible underestimation of silica dust exposure for individuals who worked at the mines/factories before 1950, and a small number of deaths (4.3%) where the cause of death was based on oral reports from relatives.
Conclusions
Long-term silica dust exposure was associated with substantially increased mortality among Chinese workers. The increased risk was observed not only for deaths due to respiratory diseases and lung cancer, but also for deaths due to cardiovascular disease.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
Walk along most sandy beaches and you will be walking on millions of grains of crystalline silica, one of the commonest minerals on earth and a major ingredient in glass and in ceramic glazes. Silica is also used in the manufacture of building materials, in foundry castings, and for sandblasting, and respirable (breathable) crystalline silica particles are produced during quarrying and mining. Unfortunately, silica dust is not innocuous. Several serious diseases are associated with exposure to this dust, including silicosis (a chronic lung disease characterized by scarring and destruction of lung tissue), lung cancer, and pulmonary tuberculosis (a serious lung infection). Moreover, exposure to silica dust increases the risk of death (mortality). Worryingly, recent reports indicate that in the US and Europe, about 1.7 and 3.0 million people, respectively, are occupationally exposed to silica dust, figures that are dwarfed by the more than 23 million workers who are exposed in China. Occupational silica exposure, therefore, represents an important global public health concern.
Why Was This Study Done?
Although the lung-related adverse health effects of exposure to silica dust have been extensively studied, silica-related health effects may not be limited to these diseases. For example, could silica dust particles increase the risk of cardiovascular disease (diseases that affect the heart and circulation)? Other environmental particulates, such as the products of internal combustion engines, are associated with an increased risk of cardiovascular disease, but no one knows if the same is true for silica dust particles. Moreover, although it is clear that high levels of exposure to silica dust are dangerous, little is known about the adverse health effects of lower exposure levels. In this cohort study, the researchers examined the effect of long-term exposure to silica dust on the risk of all cause and cause-specific mortality in a large group (cohort) of Chinese workers.
What Did the Researchers Do and Find?
The researchers estimated the cumulative silica dust exposure for 74,040 workers at 29 metal mines and pottery factories from 1960 to 2003 from individual work histories and more than four million measurements of workplace dust concentrations, and collected health and mortality data for all the workers. Death from all causes was higher among workers exposed to silica dust than among non-exposed workers (993 versus 551 deaths per 100,000 person-years), and there was a positive exposure–response relationship between silica dust exposure and death from all causes, respiratory diseases, respiratory tuberculosis, and cardiovascular disease. For example, the hazard ratio for all cause death was 1.026 for every increase in cumulative silica dust exposure of 1 mg/m3-year; a hazard ratio is the incidence of an event in an exposed group divided by its incidence in an unexposed group. Notably, there was significantly increased mortality from all causes, ischemic heart disease, and silicosis among workers exposed to respirable silica concentrations at or below 0.1 mg/m3, the workplace exposure limit for silica dust set by the US Occupational Safety and Health Administration. For example, the standardized mortality ratio (SMR) for silicosis among people exposed to low levels of silica dust was 11.01; an SMR is the ratio of observed deaths in a cohort to expected deaths calculated from recorded deaths in the general population. Finally, the researchers used their data to estimate that, in 2008, 4.2% of deaths among industrial workers in China (231,104 deaths) were attributable to silica dust exposure.
What Do These Findings Mean?
These findings indicate that long-term silica dust exposure is associated with substantially increased mortality among Chinese workers. They confirm that there is an exposure–response relationship between silica dust exposure and a heightened risk of death from respiratory diseases and lung cancer. That is, the risk of death from these diseases increases as exposure to silica dust increases. In addition, they show a significant relationship between silica dust exposure and death from cardiovascular diseases. Importantly, these findings suggest that even levels of silica dust that are considered safe increase the risk of death. The accuracy of these findings may be affected by the accuracy of the silica dust exposure estimates and/or by confounding (other factors shared by the people exposed to silica such as diet may have affected their risk of death). Nevertheless, these findings highlight the need to tighten regulations on workplace dust control in China and elsewhere.
Additional Information
Please access these websites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001206.
The American Lung Association provides information on silicosis
The US Centers for Disease Control and Prevention provides information on silica in the workplace, including links to relevant US National Institute for Occupational Health and Safety publications, and information on silicosis and other pneumoconioses
The US Occupational Safety and Health Administration also has detailed information on occupational exposure to crystalline silica
What does silicosis mean to you is a video provided by the US Mine Safety and Health Administration that includes personal experiences of silicosis; Dont let silica dust you is a video produced by the Association of Occupational and Environmental Clinics that identifies ways to reduce silica dust exposure in the workplace
The MedlinePlus encyclopedia has a page on silicosis (in English and Spanish)
The International Labour Organization provides information on health surveillance for those exposed to respirable crystalline silica
The World Health Organization has published a report about the health effects of crystalline silica and quartz
doi:10.1371/journal.pmed.1001206
PMCID: PMC3328438  PMID: 22529751
8.  Blood anti-oxidant parameters at different stages of pneumoconiosis in coal workers. 
The pneumoconioses are associated with chronic inflammatory processes during which increased amounts of reactive oxygen species are formed in the lower respiratory tract. To characterize the effect(s) of these processes on the defense system against free radicals, we studied 91 individuals with long-term occupational exposure to coal mine dust. Thirty-one subjects were classified with radiological evidence to be pneumoconiotics, while 58 control miners had no pulmonary disorders. We measured antioxidant parameters in red blood cells, considering the latter to reflect the oxidative stress in the lung. Glutathione levels were significantly decreased (p = 0.04) in red blood cells of miners with coal workers' pneumoconiosis with radiograph classification 0/1 to 2/1, while in miners with classification 3/2 to 3/3, the plasma iron concentrations were significantly decreased (p = 0.04). Moreover, some factors of the anti-oxidant system (superoxide dismutase, catalase, glutathione peroxidase) were correlated in the diseased but not in the control miners. Taken together, all data support the role of the erythrocyte as a circulating anti-oxidant carrier and also that changes in red blood cell anti-oxidant factors reflect the oxidative stress imposed by the pneumoconiotic (inflammatory) processes in the lung.
PMCID: PMC1567629  PMID: 2351120
9.  Mortality among a cohort of United Kingdom steel foundry workers with special reference to cancers of the stomach and lung, 1946-90. 
OBJECTIVE--The aim was to describe cause specific mortality among steel foundry workers and to determine if any part of the experience may be due to occupation. DESIGN--Historical prospective cohort study. SETTING--Nine steel foundries in England and one in Scotland. SUBJECTS--10,438 male production employees first employed in the period 1946-65 and with a minimum period of employment of one year. MAIN OUTCOME MEASURES--Observed and expected numbers of deaths for the period 1946-90. RESULTS--Compared with the general population of England and Wales, standardised mortality ratios (SMRs) for all causes and all neoplasms were 115 (observed deaths (Obs) 3976) and 119 (Obs 1129) respectively. Statistically significant excesses were found for cancer of the stomach (Obs 124, expected deaths (Exp) 92.5, SMR 134, 95% confidence interval (95% CI) 111-160) and cancer of the lung (Obs 551, Exp 378.3, SMR 146, 95% CI 134-158). A raised SMR (153) was also found for non-malignant diseases of the respiratory system. Classifications of jobs attracting either higher dust or higher fume exposures did not usefully predict these increased SMRs. Poisson regression was used to investigate risks of mortality from all cancers, cancer of the stomach, cancer of the lung, and non-malignant diseases of the respiratory system associated with duration of employment in the foundry area, the fettling shop, the foundry area/fettling shop, and the industry in general. Monotonic dose-response relations were not found, although there were positive trends for lung cancer and employment in the foundry area/fettling shop (1.0, 1.21, 1.44, 1.26) and for diseases of the respiratory system and employment in the fettling shop (1.0, 1.37, 1.18, 1.35). CONCLUSIONS--Confident interpretation of the causes of the raised SMRs was not possible. There was limited evidence of an occupational role in the excesses of lung cancer and diseases of the respiratory system. Smoking history was shown, in an indirect way, to be an unlikely explanation.
PMCID: PMC1127976  PMID: 8199681
10.  Gaseous and adsorbed PAH in an iron foundry. 
The increased risk of lung cancer among foundry workers is assumed to be associated with the inhalation of gaseous and particle bound polycyclic aromatic hydrocarbons (PAH). These compounds are produced during pyrolysis of carbon containing loading material in the moulding sand. The concentrations of 20 PAH, some of which are carcinogenic, have been determined in the dusty casting area of an iron foundry by means of gas chromatography and mass spectrometry. The total dust was fractionated by means of a precision cascade impactor. It was possible to differentiate the PAH load in microgram/mg dust in seven particle size fractions ranging from 0.36- greater than or equal to 24.95 microns. Initially, there was an increase of the adsorbed PAH mass concentration with increasing particle diameter up to a maximum of 1.1 microgram/mg in the dust of the 1.57 micron fraction. Thereafter there was a continuous decrease of PAH mass concentration with increasing particle size. When the differing weights of the seven fractions are taken into account, however, the total PAH load of the individual fractions increases steadily with increasing particle size. The inhalable fine dust, 31.4% of the total dust, contains 49.9% of the total adsorbed PAH. The gas phase contained on average three times more carcinogenic PAH with four and five rings than was adsorbed on the dust. Thus the percentage of the gaseous substances amounts to 77% of the total PAH load at the place of work in an iron foundry.
PMCID: PMC1007764  PMID: 3801335
11.  In vitro characterization of DNA adducts formed by foundry air particulate matter. 
Environmental Health Perspectives  1996;104(Suppl 3):687-690.
This study is part of an ongoing investigation of biomarkers in iron foundry workers exposed to polycyclic aromatic compounds. Foundry workers with the highest exposures had elevated levels of DNA adducts in their white blood cells in previous studies. The purpose of this study was to characterize the nature of DNA reactive chemicals in foundry air samples through incubating the foundry filter extract with DNA and activation enzymes. Calf thymus DNA was incubated with foundry filter extract and activated by either rat liver activation mixture (S9 mix) or xanthine oxidase. A complex pattern of adducts was observed on thin-layer chromatography (TLC) by the 32P-postlabeling assay. Two selected polycyclic aromatic hydrocarbons (PAHs)--1-NP-and anti(+/-)benzo[a]pyrene-trans-7,8-dihydrodiol-9,10-epoxide [anti(+/-) BPDE]-DNA adducts--were used as marker compounds in characterizing the postlabeled DNA adducts by TLC combined with high-performance liquid chromatography (HPLC). After an initial separation of DNA adducts by TLC, individual spots were isolated and separated further on HPLC. HPLC analysis and spiking with anti(+/-)BPDE-DNA standard confirmed the co-migration of the anti(+/-)BPDE-DNA standard with one PAH adduct formed by the S9 mix-activated DCM extract in calf thymus DNA.
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PMCID: PMC1469650  PMID: 8781406
12.  Hut lung: a domestically acquired pneumoconiosis of mixed aetiology in rural women. 
Thorax  1991;46(5):334-340.
A form of pneumoconiosis in rural African women termed "Transkei silicosis" has been thought to be due to silica particles inhaled while they are hand grinding maize between rocks. Twenty five women were studied who were considered to have this condition according to the following criteria: rural domicile, radiographic and lung biopsy evidence of pneumoconiosis, no exposure to mining or industry and no evidence of active tuberculosis. They were assessed for radiological, pathological, physiological and bronchoalveolar lavage fluid features. Potential aetiological factors were assessed by determining levels of exposure to respirable quartz and non-quartz containing dusts and smoke in rural dwellings during maize grinding and cooking. Most of the women were symptomless. Radiological findings ranged from a miliary pattern to extensive fibrosis resembling progressive massive fibrosis. Histological features included simple "anthracosis" in 12, anthracosis with macules in six, and mixed dust fibrosis in seven. Cell numbers and their proportions in lavage fluid were normal. More than 60% of macrophages were heavily laden with inorganic inclusions. Respirable quartz concentrations and calculated cumulative time weighted exposures were below those recommended for industry during grinding with sandstone (100% quartz) and they were even lower during grinding with dolerite containing no quartz despite the presence of an appreciable amount of quartz in the ground maize. Total respirable dust and smoke concentrations were greater than the recommended safe levels. Three women had no exposure to maize grinding. It is concluded that the inhalation of non-quartz containing dust and smoke from biomass fuelled fires is more important in the aetiology of this condition than exposure to quartz dust. The term "hut lung" may be more appropriate.
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PMCID: PMC463130  PMID: 2068688
13.  Dust exposure, pneumoconiosis, and mortality of coalminers. 
General mortality in approximately 25 000 British coalminers over 22 year periods ending in 1980 was 13% lower on average than in English and Welsh men in the same regions of Britain. There were significant within region variations between collieries, and standardised mortality ratios increased during the later years of the follow up, approaching or slightly exceeding 100 in most of the 20 coalmines studied. Age specific comparisons of 22 year survival rates were made in subgroups. Relative risks of death from all non-violent causes for men with the earliest stage of progressive massive fibrosis (PMF category A), compared with risks in miners with no pneumoconiosis (category O), ranged from 1.2 in those aged 55-64 initially to 3.5 for those aged 25-34. Mortality in miners with higher categories of PMF (B or C) was even more severe. Survival rates in men with category 1 simple pneumoconiosis were about 2% to 3% lower than in miners with radiographs classified as category O, but there was no consistent evidence of an increase in mortality with increasing category of simple pneumoconiosis. Mortality from all non-violent causes increased systematically with increases in estimates of exposure to dust before the start of the follow up. That gradient was attributable primarily to deaths certified as due to pneumoconiosis and those recorded as due to bronchitis and emphysema (p less than 0.001). There was some evidence of a dust related increase in deaths from cancers of the digestive system (p approximately equal to 0.05), but none of an association between exposure to coalmine dust and lung cancer. Lung cancer mortality, assessed over 17 year periods, was about 5.5 times higher in smokers than in life long non-smokers. Smokers with no pneumoconiosis had slightly higher lung cancer death rates than smokers with pneumoconiosis. We conclude that miners exposed to excessive amounts of respirable coalmine dust are at increased risk of premature death, either from progressive massive fibrosis or from chronic bronchitis or emphysema.
PMCID: PMC1007567  PMID: 4063215
14.  Pneumoconiosis in Carbon Electrode Makers 
In the absence of adequate preventive measures the manufacture of carbon electrodes is attended by a considerable dust hazard. The present paper is based on a study of the clinical, radiological, and pathological changes resulting from inhalation of this dust, which is derived from crushed coke and anthracite.
An account is given of the findings in a clinical survey of 15 men who had been employed for at least 10 years in manufacturing carbon electrodes. Four of these men were suffering from complicated and five from simple pneumoconiosis.
In addition, the findings in three necropsied cases (two complicated and one simple) are recorded in detail. Bacteriological examination of the lungs and analysis of the lung dust was carried out in the two cases of complicated pneumoconiosis.
It is shown that carbon electrode makers may develop simple pneumoconiosis with focal emphysema and that this may complicated by the development of massive fibrotic lesions. Both the simple and the complicated pneumoconiosis are indistinguishable from the corresponding conditions in other coalworkers.
Quartz was almost entirely absent from the lung dust of the two necropsied cases with massive fibrosis and in one of these cases virulent tubercle bacilli were shown. The significance of these findings is discussed in relation to the aetiology of progressive massive fibrosis. While it is evident that they are incompatible with the “silica” theory they provide some limited support for the “tuberculosis” theory.
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PMCID: PMC1037965  PMID: 13843110
15.  Carbon Pneumoconiosis 
The occurrence of carbon pneumoconiosis in rubber-factory workers is unusual: the case reported here was discovered in a routine post-mortem examination. The report includes the clinical, radiological, morbid anatomical, and histological findings on a man who had worked in the carbon black store of a rubber works for a continuous period of 21 years, followed by 11 years in the calender department of the same factory. At the age of 65 years the man was retired on the grounds of age and indifferent health: he collapsed and died soon afterwards.
The medical history of severe cough with expectoration suggested that he may have had pulmonary tuberculosis in earlier life and some supporting evidence of this infection was found in that his wife contracted this disease after marriage and subsequently died from tuberculosis.
The appearances of massive fibrosis in the upper lobes of the lungs suggested that the combined action of carbon black and tuberculosis had produced an “infective” type of pneumoconiosis: in the lower lobes there was far less fibrosis and the appearances were those of simple pneumoconiosis. In addition to the fibrosis the lungs showed nodules of black dust with severe perifocal emphysema. Electron microscopy of the lung dust showed two distinct components and they were similar to samples of channel and thermal blacks which were the main types of carbon used in the factory.
This case is an example of pneumoconiosis due to virtually non-siliceous carbon and illustrates that prolonged exposure to heavy dust concentration produces such lesions as described in this paper.
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PMCID: PMC1038100  PMID: 13770721
16.  Silicosis and coal workers' pneumoconiosis. 
Environmental Health Perspectives  2000;108(Suppl 4):675-684.
Exposure to coal mine dust and/or crystalline silica results in pneumoconiosis with initiation and progression of pulmonary fibrosis. This review presents characteristics of simple and complicated coal workers' pneumoconiosis (CWP) as well as pathologic indices of acute and chronic silicosis by summarizing results of in vitro, animal, and human investigations. These results support four basic mechanisms in the etiology of CWP and silicosis: a) direct cytotoxicity of coal dust or silica, resulting in lung cell damage, release of lipases and proteases, and eventual lung scarring; b) activation of oxidant production by pulmonary phagocytes, which overwhelms the antioxidant defenses and leads to lipid peroxidation, protein nitrosation, cell injury, and lung scarring; c) activation of mediator release from alveolar macrophages and epithelial cells, which leads to recruitment of polymorphonuclear leukocytes and macrophages, resulting in the production of proinflammatory cytokines and reactive species and in further lung injury and scarring; d) secretion of growth factors from alveolar macrophages and epithelial cells, stimulating fibroblast proliferation and eventual scarring. Results of in vitro and animal studies provide a basis for proposing these mechanisms for the initiation and progression of pneumoconiosis. Data obtained from exposed workers lend support to these mechanisms.
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PMCID: PMC1637684  PMID: 10931786
17.  Cancer mortality in a cohort of United Kingdom steel foundry workers: 1946-85. 
The mortality experienced by a cohort of 10,491 United Kingdom steel foundry workers during the period 1946-85 has been investigated. These workers were all male operatives first employed in any one of the 10 participating foundries in 1946-65; all had worked in the industry for a minimum period of one year. Compared with the general population of England and Wales, statistically significant excesses relating to cancer mortality were found for cancer of the stomach (E = 77.4, O = 106, SMR = 137) and cancer of the lung (E = 229.2, O = 441, SMR = 147). A statistically significant deficit was found for cancer of the brain (E = 19.4, O = 10, SMR = 51). Involvement of occupational exposures was assessed by the method of regression models and life tables (RMLT). This method was used to compare the duration of employment in the industry, in "dust exposed" jobs, in "fume exposed" jobs, in foundry area jobs, in fettling shop jobs, and in foundry area or fettling shop jobs, of those dying from cancers of the stomach and lung with those of all matching survivors. The RMLT analyses provided evidence of an occupational involvement in the risk of death from lung cancer from work in the foundry area or fettling shop, and weaker evidence of an occupational involvement in the risk of death from stomach cancer from work in the foundry area.
PMCID: PMC1009731  PMID: 2923828
18.  Pneumoconiosis in China-Clay Workers 
A 70 mm. radiographic survey in 914 workmen exposed to china-clay dust was made in 1959 in an industrial plant in which kaolin deposits are processed for the earthenware industry in Ayyat, United Arab Republic. All were ex-agricultural workers and thus not exposed to any industrial dust hazards.
The purpose of the survey was to study the prevalence of pneumoconiosis and active tuberculosis. Fifty subjects were considered to require further investigation and large films were therefore taken which showed the following results: five cases of pneumoconiosis; one case of pneumoconiosis and tuberculosis; and 13 cases of active tuberculosis. Of the five pneumoconiosis cases, two were classified as progressive massive fibrosis (P.M.F.), two as category 3 and one as category 1 simple pneumoconiosis. All had been heavily exposed for 15 years or more.
Case records of the pneumoconiosis group are given with follow-up observations for two and a half years. There were no important clinical or radiographic changes except that one of the two patients with P.M.F. died of cor pulmonale. Correlation of the clinical features and radiographic abnormalities was poor. The low prevalence of pneumoconiosis, in spite of the heavy and prolonged exposure, is emphasized. A sample of the airborne dust contained about 2% of SiO2.
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PMCID: PMC1039204  PMID: 14046160
19.  Two Cases of Lung Cancer in Foundry Workers 
Background
Iron and steel foundry workers are exposed to various toxic and carcinogenic substances including crystalline silica, polycyclic aromatic hydrocarbons, and arsenic. Studies have been conducted on lung cancer in iron and steel founding workers and the concentration of crystalline silica in foundries; however, the concentration of crystalline silica and cases of lung cancer in a single foundry has never been reported in Korea. Therefore, the authors report two cases of lung cancer and concentration of crystalline silica by the X-ray diffraction method.
Case presentation
A 55-year-old blasting and grinding worker who worked in a foundry for 33 years was diagnosed with lung cancer. Another 64-year-old forklift driver who worked in foundries for 39 years was also diagnosed with lung cancer. Shot blast operatives were exposed to the highest level of respirable quartz (0.412 mg/m3), and a forklift driver was exposed to 0.223 mg/m3.
Conclusions
The lung cancer of the two workers is very likely due to occupationally related exposure given their occupational history, the level of exposure to crystalline silica, and epidemiologic evidence. Further studies on the concentration of crystalline silica in foundries and techniques to reduce the crystalline silica concentration are required.
doi:10.1186/2052-4374-25-16
PMCID: PMC3923328  PMID: 24472520
Crystalline silica; Iron and steel founding; Lung cancer; Occupational exposure
20.  Polymorphisms in chemokine and chemokine receptor genes and the development of coal workers' pneumoconiosis 
Cytokine  2006;33(3):171-178.
Chemokines and their receptors are key regulators of inflammation and may participate in the lung fibrotic process. Associations of polymorphisms in CCL5 (G-403A) and its receptor CCR5 (Δ32), CCL2 (A-2578G) and CCR2 (V64I), and CX3CR1 V249I and T280M with Coal Worker’s Pneumoconiosis (CWP) were investigated in 209 miners examined in 1990, 1994 and 1999. Coal dust exposure was assessed by job history and ambient measures. The main health outcome was lung computed tomography (CT) score in 1990. Internal coherence was assessed by studying CT score in 1994, 4-year change in CT score, and CWP prevalence in 1999. CCR5 Δ32 carriers had significantly higher CT score in 1990 and 1994 (2.15 vs. 1.28, p=0.01; 3.04 vs. 1.80, p=0.04). The CX3CR1 1249 allele was significantly associated with lower 1990 CT score and lower progression in 4-year change in CT score in CCR5 Δ32 carriers only (p for interaction=0.03 and 0.02). CX3CR1 V249I was associated with lower 1999 CWP prevalence (16.7%, 13.2%, 0.0% for VV, VI and II); the effect was most evident in miners with high dust exposure (31.6%, 21.7%, 0.0%). Our findings indicate that chemokine receptors CCR5 and CX3CR1 may be involved in the development of pneumoconiosis.
doi:10.1016/j.cyto.2006.01.001
PMCID: PMC1913495  PMID: 16524739
Adult; Chemokine CCL2; genetics; Chemokines; genetics; Chemokines, CC; genetics; Coal Mining; Gene Frequency; Genotype; Humans; Membrane Proteins; genetics; Middle Aged; Phenotype; Pneumoconiosis; diagnosis; epidemiology; genetics; Polymorphism, Genetic; Polymorphism, Single Nucleotide; Prevalence; Receptors, CCR5; genetics; Receptors, Chemokine; genetics; chemokines; interaction; occupational exposure; pneumoconiosis; polymorphism
21.  Population Studies of Chronic Respiratory Disease: A Comparison of Miners, Foundryworkers, and Others in Staveley, Derbyshire 
Mortality and morbidity statistics suggest that miners and foundryworkers are more prone to bronchitis than other industrial workers but it is not yet certain that this excess is due to occupational factors. The present investigation was designed to compare the prevalence of bronchitis and respiratory disability in a representative sample of miners, foundryworkers, and other industrial groups living in Staveley, Derbyshire, a town of some 18,000 inhabitants, and to study some of the possible aetiological factors. A random sample of 776 men, stratified by age into two groups, 25 to 34 and 55 to 64 years, and by occupation into four groups, non-dusty, miners and ex-miners, foundry and ex-foundryworkers, and other dusty jobs, was used. Respiratory symptoms were recorded on a standardized questionnaire and the ventilatory capacity was assessed by means of the forced expiratory volume (F.E.V.0·75) and recorded as the indirect maximum breathing capacity (M.B.C.).
Miners and ex-miners recorded a higher prevalence of respiratory symptoms and a lower mean M.B.C. than men who had worked only in dust-free occupations. In the older age group the differences were not large and were not statistically significant but in the younger men the difference in the mean M.B.C. was significant. Foundry and ex-foundryworkers with a pure industrial history recorded a similar prevalence of symptoms to the men who had never worked in dusty occupations and their mean M.B.C. was only slightly and insignificantly lower. A higher prevalence of symptoms and a lower mean M.B.C. was, however, recorded by the foundrymen who had also been exposed to other dusts or fumes and the occupational histories suggested that such exposure was more likely than foundry work to account for the findings.
The number of years spent on the coal-getting shift was used to assess the importance of exposure to coal dust. In the elderly miners without pneumoconiosis there was a significant increase in the prevalence of breathlessness, accompanied by a reciprocal fall in the mean M.B.C. with increasing years spent on the coal-getting shift; but in no other group was a consistent trend found.
In both age groups the prevalence of respiratory symptoms was lower and the mean M.B.C. higher in non-smokers than in smokers and ex-smokers. Heavy smokers (those smoking 15g. and over/day) recorded a higher prevalence of symptoms and a lower mean M.B.C. than light smokers, and the values for ex-smokers approximated to those of the non-smokers.
The wives of the elderly men in the sample were studied to try to determine how far the apparently high rates of bronchitis shown by national mortality statistics are attributable to social factors. The findings suggested that the wives of the men who worked in dusty jobs had a somewhat higher prevalence of cough and/or sputum and of chest illness during the past three years than the wives of those who had worked only in dust-free occupations.
PMCID: PMC1037963  PMID: 14401755
22.  Pneumoconiosis in Makers of Artificial Grinding Wheels, Including a Case of Caplan's Syndrome* 
Mass miniature radiography surveys in a factory producing artificial grinding wheels detected cases of pneumoconiosis, mostly of the silicotic type. All cases were traced to the department where the so-called “bond” is prepared and mixed with the abrasive grains of carborundum and artificial corundum. This ceramic-vitrified bond, similar in composition to English general earthenware, contained until recently a significant proportion of free silica.
The miniature film survey was followed up by an investigation on full-sized films, in which 92% of all workers in the bond department participated. The radiographs were subjected to dual independent viewing and it was found that 66% of the men who had worked in the bond department for more than 10 years showed radiological evidence of pneumoconiosis with a high proportion of progressive massive fibrosis (P.M.F.)
Recently the amount of free silica in the ceramic bond has been reduced by the introduction of “frits” in place of powdered flint and part of the factory has been rebuilt and new methods of dust suppression and dust extraction have been introduced. One of the cases presented with the rheumatoid-pneumoconiotic syndrome, first described by Caplan.
It is suggested that some of the cases of pneumoconiosis, attributed to carborundum, may be due to the binding materials of artificial grinding wheels.
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PMCID: PMC1038033  PMID: 14434374
23.  Respiratory symptoms, lung function, and pneumoconiosis among self employed dental technicians. 
From the registry of self employed workers living in Paris, a group of 105 dental technicians was studied to evaluate occupational exposure, to determine respiratory manifestations, and to investigate immune disturbances. Seventy one dental technicians (age range 43-68: group D), 34 dental technicians younger than 43 or older than 68 (group d), and 68 control workers (age range 43-66: group C) were investigated. The demographic characteristics and the smoking habits of the groups D and C did not differ significantly. The dental technicians often worked alone (43.7%) or in small laboratories without adequate dust control. The mean duration of their exposure was long (group D 34.0 (SD 8.4) years). The prevalence of respiratory symptoms did not differ between groups D and C except for the occurrence of increased cough and phlegm lasting for three weeks or more over the past three years (group D 16.9%, group C 2.9%, p < 0.007). The effect of cigarette smoking on respiratory symptoms and lung function was obvious. All mean values of lung function for dental technicians and controls were within normal limits. Significant decreases in all mean lung function values were found among smokers by comparison with non-smokers, however, and a positive interaction with occupational exposure was established. The x ray films of dental technicians (n = 102, groups D and d) were read independently by four readers and recorded according to the International Labour Office classification of pneumoconioses. The prevalence of small opacities greater than 1/0 was 11.8% with a significant increase with duration of exposure. The prevalence among dental technicians with 30 years or exposure or more was significantly higher (22.2%) than those with less than 30 years (3.5, p < 0.004). The prevalence of autoantibodies (rheumatoid factors, antinuclear antibodies, and antihistone antibodies) was not significantly different in the groups D and C. When positive, autoantibodies only occurred at low concentrations. This finding contrasts with previous reports on the occurrence of autoantibodies and even of connective tissue diseases in dental technicians. In conclusion, the study confirms an increased risk of pneumoconiosis among dental technicians. Moreover, there may be other lung disorders such as impairment of lung function especially in association with cigarette smoking.
PMCID: PMC1012163  PMID: 8507597
24.  A Survey of the Methods Developed in the National Coal Board's Pneumoconiosis Field Research for Correlating Environmental Exposure with Medical Condition 
The correlation of the medical and environmental data (i.e. the derivation of the dosage-response relationship) in a study such as the National Coal Board's Pneumoconiosis Field Research (P.F.R.) is subject to many complicating factors compared with the more conventional types of biological assay. Several methods have been developed within the Research to overcome these difficulties, and the new procedures are described. Each is concerned with the estimation of the direct relation between the radiological abnormality associated with simple pneumoconiosis and some single measure of the past hazard, but the basic techniques are sufficiently general to be applicable in other fields of study.
The first development involves the definition of an underlying continuous scale of radiological abnormality. This prepares the way for the derivation of the “quantitative” relation between exposure and response, to replace the “semi-quantal” relation which is inherent in the use of a small number of discrete categories of radiological abnormality. The effect of errors of observation of dosage and response on the corresponding quantitative and quantal relationships is then determined.
The second development concerns the use of a “multi-dimensional” representation of past hazard. Most of the men under observation had worked in a number of different mining occupations before their first chest radiograph was taken, but this exposure cannot be assessed in terms of dust concentrations, for which reliable data are not available. Nevertheless, it is shown that past hazard can usefully be represented by three “dimensions” corresponding to the periods spent in three main types of environment—(a) the coal-face (coal-getting shift), (b) the coal-face (preparation shift) and (c) elsewhere underground. Each man's past exposure up to the time of his first chest radiograph can be expressed in terms of these three dimensions and the effect of each environment separately can be determined.
The third development extends the multi-dimensional approach to cover not only the working history before the first medical examination, but also the recorded exposure (in terms of measured dust concentrations), to which each man has been subject between the first and subsequent “follow-up” surveys. This measured exposure is regarded as one dimension of the man's total exposure up to the time of his second (or later) examination, and it is possible in this way to determine the direct relation between radiological abnormality and measured exposure, even when this component represents only part of the total hazard to which the man has been subject.
The application of the methods is illustrated by the analysis of some of the data which have been obtained in the Pneumoconiosis Field Research.
PMCID: PMC1038147  PMID: 13698432
25.  Reactive oxygen species: their relation to pneumoconiosis and carcinogenesis. 
Environmental Health Perspectives  1998;106(Suppl 5):1151-1155.
Occupational exposures to mineral particles cause pneumoconiosis and other diseases, including cancer. Recent studies have suggested that reactive oxygen species (ROS) may play a key role in the mechanisms of disease initiation and progression following exposure to these particles. ROS-induced primary stimuli result in the increased secretion of proinflammatory cytokines and other mediators, promoting events that appear to be important in the progression of cell injury and pulmonary disease. We have provided evidence supporting the hypothesis that inhalation of insoluble particles such as asbestos, agricultural dusts, coal, crystalline silica, and inorganic dust can be involved in facilitating multiple pathways for persistent generation of ROS, which may lead to a continuum of inflammation leading to progression of disease. This article briefly summarizes some of the recent findings from our laboratories with emphasis on the molecular events by which ROS are involved in promoting pneumoconiosis and carcinogenesis.
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PMCID: PMC1533374  PMID: 9788890

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