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1.  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
2.  Cause-Specific Mortality Due to Malignant and Non-Malignant Disease in Korean Foundry Workers 
PLoS ONE  2014;9(2):e88264.
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.
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.
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).
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.
PMCID: PMC3914960  PMID: 24505454
3.  The Causes of Death in Iron and Steel Workers (Non-foundry) 
Few studies have been made of the pathology associated with the iron and steel trades other than foundries. We review here the clinical, occupational, and pathological (post-mortem) findings in 10 grinders and 16 other non-foundry workers in iron and steel. Grinding is evidently a less dangerous trade than it was 100 or even 50 years ago, but silicosis and/or mixed dust fibrosis is still found amongst them. The risk of the onset of pneumoconiosis in other workers in these trades is small, but not absent.
PMCID: PMC1038014  PMID: 13774071
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
PMCID: PMC1740042  PMID: 11555687
5.  Mortality of copper cadmium alloy workers with special reference to lung cancer and non-malignant diseases of the respiratory system, 1946-92. 
OBJECTIVES--To identify and quantify any relations between occupational exposure to cadmium oxide fume and mortalities from lung cancer and from chronic non-malignant diseases of the respiratory system. METHODS--The mortality experience of 347 copper cadmium alloy workers, 624 workers employed in the vicinity of copper cadmium alloy work (vicinity workers), and 521 iron and brass foundry workers (all men) was investigated for the period 1946-92. All subjects were first employed in these types of work in the period 1922-78 and for a minimum period of one year at one of two participating factories. Two analytical approaches were used, indirect standardisation and Poisson regression. RESULTS--Compared with the general population of England and Wales, mortality from lung cancer among copper cadmium alloy workers was close to expectation (observed deaths 18, expected deaths 17.8, standardised mortality ratio (SMR) 101, 95% confidence interval (95% CI) 60 to 159). A significant excess was shown for lung cancer among vicinity workers but not among iron and brass foundry workers (vicinity workers: observed 55, expected 34.3, SMR 160, 95% CI 121 to 209, P < 0.01; iron and brass foundry workers: observed 19, expected 17.8, SMR 107, 95% CI 64 to 167). Increased SMRs for non-malignant diseases of the respiratory system were shown for each of the three groups (alloy workers: observed 54, expected 23.5, SMR 230, 95% CI 172 to 300, P < 0.001; vicinity workers: observed 71, expected 43.0, SMR 165, 95% CI 129 to 208, P < 0.001; iron and brass foundry workers: observed 34, expected 17.1, SMR 199, 95% CI 137 to 278, P < 0.01). Work histories of the copper cadmium alloy workers were combined with independent assessments of cadmium exposures over time to develop individual estimates of cumulative exposure to cadmium; this being a time dependent variable. Poisson regression was used to investigate risks of lung cancer and risks of chronic non-malignant diseases of the respiratory system in relation to three levels of cumulative cadmium exposure (< 1600, 1600-4799, > or = 4800 micrograms.m-3.y). After adjustment for age, year of starting alloy work, factory, and time from starting alloy work, there was a significant positive trend (P < 0.01) between cumulative exposure to cadmium and risks of mortality from chronic non-malignant diseases of the respiratory system. Relative to a risk of unity for the lowest exposure category, risks were 4.54 (95% CI 1.96 to 10.51) for the middle exposure category and 4.74 (95% CI 1.81 to 12.43) for the highest exposure category. There was a non-significant negative trend between cumulative cadmium exposure and risks of mortality from lung cancer. Relative to a risk of unity for the lowest exposure category, risks were 0.85 (95% CI 0.27 to 2.68) for the middle exposure category and 0.81 (95% CI 0.18 to 3.73) for the highest exposure category. Similar findings were obtained when adjustment was made for age only. CONCLUSIONS--The findings are consistent with the hypothesis that exposure to cadmium oxide fume increases risks of mortality from chronic non-malignant diseases of the respiratory system. The findings do not support the hypothesis that exposure to cadmium oxide fume increases risks of mortality for lung cancer.
PMCID: PMC1128381  PMID: 8563843
6.  Biological monitoring of foundry workers exposed to polycyclic aromatic hydrocarbons. 
This investigation describes benzo(a)pyrene (BP) serum protein adduct concentrations in 45 foundry workers and 45 matched non-occupationally exposed controls. High and low BP exposure groups were defined using breathing zone hygienic samples for both quartz and BP exposures. A newly developed enzyme linked immunosorbent assay detected benzo(a)pyrenediolepoxide-I binding to serum protein. Mean BP protein adduct concentrations (SD) for non-smoking (24.0 BP equivalents/100 micrograms protein (21.0] and smoking (28.0 (18.2] foundry workers were significantly higher than mean values for non-smoking (7.23 (8.72] and smoking (14.2 (24.4] controls. Foundry workers with high exposures to either quartz (28.4 (15.5] or BP (30.7 (19.3] had slightly raised mean adduct concentrations compared with foundry workers with low exposure for quartz (23.9 (23.1] or BP (24.5 (19.4). Highest mean adduct concentrations were found among a small group of workers with simultaneous high exposures to both quartz and BP (39.2 (6.5] suggesting an additive effect. These data support the ideas of a possible aetiological connection between an increased risk of lung cancer and BP exposure among foundry workers, and an additive effect between BP and quartz. Measurement of BP serum protein adduct concentrations appears to be a useful method by which groups exposed to BP may be biologically monitored.
PMCID: PMC1035205  PMID: 2383513
7.  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
8.  Mortality of workers in an automobile engine and parts manufacturing complex. 
A proportionate mortality ratio (PMR) study was conducted using data on workers from three local unions representing an integrated automobile factory composed of forge, foundry, and engine (machine and assembly) plants. Ninety four percent of the death certificates were obtained for all active and non-active workers who died during the period 1 January 1970 to 31 December 1979 and were vested in union and company benefit programmes. Observed numbers of deaths were compared with expected numbers based on two standards, the proportionate mortality among men in the United States 1970-9 and among men in Erie County 1975. There was close agreement between the number of observed and expected deaths by either standard of comparison among white auto workers in the forge and foundry plants. Valid analyses of cause specific mortality among non-whites could be conducted for the foundry plant only. Although there was raised PMR for deaths due to diseases of the circulatory system using the Erie County standard, none of the other cause specific PMRs was significant. Although based on small numbers, the risk of cancer of the lung was significantly high in non-whites under age 50 in the foundry (PMR = 2.6; p less than 0.05). The cause specific PMRs for whites in the engine plant were statistically significant for malignant neoplasms (1.2) and all external causes (0.62) based on the US white male standard. Analysis of cancer specific mortality among white men in the machining/assembly plant showed significant excesses for cancer of the digestive system (PMR=1.5), particularly of the liver (PMR=2.6) and pancreas (PMR=1.9); cancers of the respiratory system (PMR=1.4 using the Erie County standard); and cancer of the urinary bladder (PMR=2.3). Workers employed for more than 20 years showed statistically increased mortality ratios for cancers of the digestive system (1.9), particularly cancer of the pancreas (2.3) and cancer of the rectum (2.8). Individuals whose employment began during or before 1950 exhibited increased PMRs for cancers of the digestive organs (1.8), particularly of the pancreas (2.5) and of the bladder (3.4). Workers whose employment began after 1950, on the other hand, exhibited raised PMRs for cancers of the respiratory system (1.5) and of the kidney (3.2). Since the foundry and forge plants did not start production until 1955, mortality associated with those work settings may be greater in the future.
PMCID: PMC1007428  PMID: 3970876
9.  Respiratory health of workers exposed to metal dusts and foundry fumes in a copper refinery. 
OBJECTIVES--To assess airflow limitation in workers exposed long term to metal dust, the prevalence of pleural plaques in those workers exposed in the past to asbestos, the influence of pleural plaques on lung function, and the possible association with airway disease caused by asbestos. METHODS--A cross sectional and longitudinal (seven year) survey of 494 long term (mean (SEM) 21(1) years) workers in a copper refinery was carried out from medical questionnaires, chest radiographs, and forced spirometry. RESULTS--The prevalence of lifetime non-smokers was 19%, current smokers 39%, and ex-smokers 42%. The prevalence of chronic obstructive pulmonary diseases (COPD) (forced expiratory volume in one second (FEV1) < 80% predicted) was 5%, small airway dysfunction (SAD) (maximal mid-expiratory flow (MMEF) < 60% predicted) was 7%, and this did not differ from the control population. The COPD and SAD were associated with cumulative smoking index but not with the cumulative work years at the plant or with any type of work at the plant. The mean (SEM) reduction of FEV1 was 20(7) ml in non-smokers, 26(4) ml in smokers, and 26(5) ml in ex-smokers (P > 0.05). In the smokers and ex-smokers with COPD, the loss of FEV1 was 53(10) (P < 0.02). The prevalence of pleural plaques was 11% (P < 0.0001); pleural plaques were found in older workers with known exposure to asbestos. The pleural plaques were circumscribed and associated with a non-significant 196 ml reduction in forced vital capacity (FVC) and non-significant reduction of FVC over time. The pleural plaques were not associated with COPD or SAD. The cumulative smoking index obtained by a technician did not differ from that by a chest physician. CONCLUSIONS--Despite exposures to asbestos that produced pleural plaques and exposures to metal dusts and foundry fumes the long term workers of this plant did not have excessive prevalence of COPD or SAD. The data suggest that low level long term exposure to metal dusts, gases, and foundry fumes do not necessarily cause respiratory dysfunction, circumscribed pleural plaques with low grades of width and extent do not reduce FVC significantly, and exposure to asbestos dust that produced pleural plaques does not necessarily produce airway dysfunction.
PMCID: PMC1128188  PMID: 7735395
10.  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.
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.
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
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
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
PMCID: PMC3328438  PMID: 22529751
11.  Rheumatism in Foundry Workers 
In order to investigate loss of work from rheumatic diseases in the metal trades, employees in 10 foundries were questioned.
Of 325 foundry workers aged 35 to 74 years, who had worked for at least 10 years on the foundry floor, 299 were examined clinically and radiologically for evidence of rheumatic disease. Radiographs of the hands, knees, and dorsal and lumbar spine were taken as a routine, and the pelvis was included in those aged 45 and over. A comparison was made with a control series of radiographs, from men, matched for age, in a random population sample examined earlier in the town of Leigh.
Rheumatic complaints in general were less frequent in the foundry workers than in the random sample, and the foundry workers less often gave a history of prolonged incapacity (three months or more) due to this cause.
Radiological evidence of disc degeneration in the lumbar spine, however, was more frequent in the foundry workers than in the controls and was of greater severity. Further, the foundry workers more commonly had symptoms and signs of lumbar disc prolapse. On the other hand, the controls had more osteo-arthrosis of the hips and knees and lost more work from pain at these sites. This was associated with a difference of body habitus, obesity being less frequent in the foundry workers.
Foundry workers directly exposed to hot conditions did not have less back or leg pain than those not so exposed despite a greater prevalence of disc degeneration.
Measurements of air temperature, humidity, and radiant heat were made in a foundry while pouring was in progress. The air temperature rose from 18°C. to 26°C. and the humidity ranged from 70% to 54%. The mean intensity of radiation incident on the clothed surface of a foundry worker was 0·12 watt/cm.2. This was compared with conditions during therapeutic exposure to radiant heat. The radiant heat under conditions of `heat therapy' varied between 0·16 and 0·37 watt/cm.2. The possible influence of radiant heat on the prevalence of rheumatic complaints is discussed.
PMCID: PMC1008347  PMID: 5295324
12.  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.
PMCID: PMC1469650  PMID: 8781406
13.  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
14.  Respiratory abnormalities among workers in an iron and steel foundry. 
A study of the health of 78 workers in an iron and steel foundry in Vancouver, British Columbia, was carried out and the results compared with those found in 372 railway repair yard workers who were not significantly exposed to air contaminants at work. The foundry workers were exposed to PepSet, which consists of diphenyl methane diisocyanate (MDI) and phenol formaldehyde and their decomposition products as well as to silica containing particulates. A questionnaire was administered by trained interviewers, and chest radiography, allergy skin tests, pulmonary function tests, and methacholine inhalation tests were carried out as well as measurement levels of dust and MDI. Compared with the controls, the foundry workers had more respiratory symptoms and a significantly lower mean FEV1 and FEF25-75% after adjustments had been made for differences in age, height, and smoking habit. Three workers (4.8%) had radiographic evidence of pneumoconiosis and 12 (18.2%) had asthma defined as presence of bronchial hyperreactivity, cough, and additional respiratory symptoms such as wheeze, chest tightness, or breathlessness. Sensitisation to MDI is probably the cause of asthma in these workers.
PMCID: PMC1007429  PMID: 2982392
15.  Chronic exposure to zinc of furnace operators in a brass foundry 
Hamdi, A. E. (1969).Brit. J. industr. Med.,26, 126-134. Chronic exposure to zinc of furnace operators in a brass foundry. Twelve furnace operators with chronic exposure to zinc oxide fumes in a brass foundry and 10 normal non-exposed control subjects were studied. Simultaneous determinations of zinc concentrations in the plasma, blood corpuscles, whole blood, and urine were made for each worker and control subject, and in the basal fasting gastric juice and in the gastric secretion half an hour and one hour after gastric stimulation by alcohol in eight workers and seven control subjects.
The workers showed a statistically significant increase of zinc concentration in the blood corpuscles, whole blood, and basal fasting gastric juice compared with the control subjects. Urinary zinc excretion was slightly increased in the exposed workers. The increase in the plasma zinc in the workers was not statistically significant.
Stomach aspiration after alcohol showed a depression of the mean zinc concentration in the gastric secretion after half an hour with a subsequent increase to approximately the fasting level after one hour in both the normal subjects and the workers. Mean zinc concentrations in the gastric juice half an hour and one hour after stomach stimulation were higher in the workers, but the increase was not statistically significant.
It is suggested that the zinc absorbed by these workers is rapidly eliminated from the plasma to be excreted through the gastro-intestinal and urinary tracts; excess zinc is stored in the blood corpuscles. The increased zinc concentration in the gastric secretion of these workers might account, in part, for the high incidence of gastric complaints among them.
PMCID: PMC1008906  PMID: 5780104
16.  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
17.  Two Cases of Lung Cancer in Foundry Workers 
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.
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.
PMCID: PMC3923328  PMID: 24472520
Crystalline silica; Iron and steel founding; Lung cancer; Occupational exposure
18.  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
19.  Cancer Morbidity of Foundry Workers in Korea 
Journal of Korean Medical Science  2010;25(12):1733-1741.
Foundry workers are potentially exposed to a number of carcinogens. This study was conducted to describe the cancer incidence associated with employment in small-sized Korean iron foundries and to compare those findings to the Korean population. Cancer morbidity in 208 Korean foundries was analyzed using the Standardized Incidence Ratio (SIR) and Standardized Rate Ratio (SRR). Overall cancer morbidity in foundry workers (SIR=1.11, 95% confidence interval [CI]=1.01-1.21) was significantly higher than that of Korean general population. Lung cancer (SIR=1.45, 95%CI=1.11-1.87) and lymphohematopoietcic cancer (SIR=1.58, 95%CI=1.00-2.37) in production workers were significantly high compared to Korean general population. Stomach cancer in fettling (SRR=2.10, 95%CI=1.10-4.01) and lung cancer in molding (SRR=3.06, 95%CI=1.22-7.64) and in fettling (SRR=2.63, 95%CI=1.01-6.84) were there significant elevations compared to office workers. In this study, statistically significant excess lung cancer was observed in production workers comparing to Korean general population and office workers. Also, cancer morbidity of overall cancer, lung cancer and stomach cancer was significantly increased with duration of employment at ten and more years comparing to Korean general population. These findings suggest in causal association between exposure to carcinogens during foundry work and cancer morbidity.
PMCID: PMC2995226  PMID: 21165287
Foundry; Stomach Neoplasms; Lung Neoplasms; Lymphohematopietic Cancer
20.  Respiratory disease in foundry workers. 
A survey was carried out in a steel foundry in Brisbane to evaluate the nature and frequency of respiratory symptoms and to assess ventilatory function. The foundry used many moulding processes including the Furane, Isocure, Shell, carbon dioxide, and oil sand systems. Nasal symptoms and wheeze were often reported, particularly by workers in the general foundry and core shop, and on a semiautomated line. By contrast, workers in the aftercast section not exposed to fumes or vapours from the various moulding processes reported these symptoms less often. Of 46 workers exposed to moulding fumes and vapours, 11 had developed a wheeze while working at the foundry. Wheeze and other respiratory tract symptoms were often attributed by the workers to exposure to substances at work, particularly from the Shell process which uses phenol formaldehyde resin and hexamethylenetetramine. Symptoms were reported also, but less often, on exposure to materials used in the Furane process (urea formaldehyde and furfuryl alcohol) and the Isocure process (methylene diphenyl diisocyanate, phenol formaldehyde, and dimethylethylamine). Ventilatory function studied over Monday and Friday showed a small and inconsistent changes. The six subjects working on the semiautomated line showed a small decrease in FEV1 (+/- SEM) (208 +/- 70 ml) only on Monday; this differed significantly from that in 17 aftercast workers (9 +/- 50 ml, p less than 0.05). Ventilatory function recorded before work on Monday morning showed no evidence of chronic airway obstruction in any group. Most environmental measurements were below the threshold limit values (TLV) except in the general foundry, where furfuryl alcohol was detected at concentrations of up to 50 ppm and formaldehyde at 4 ppm. The onset of symptoms in relation to exposure to various fumes and vapours suggests that both irritant and hypersensitivity mechanisms are present. As environmental modifications had occurred recently the apparent hypersensitivity may relate to past exposure levels above the TLV.
PMCID: PMC1007430  PMID: 3970867
21.  Hexachlorobenzene and octachlorostyrene in plasma of aluminium foundry workers using hexachloroethane for degassing. 
OBJECTIVES: To study the load of selected organochlorine compounds in the blood of aluminium foundry workers who use hexachloroethane as a degassing agent for aluminium and to measure some possible effects on internal organs. METHODS: Plasma from nine male aluminium foundry workers with past experience of use of hexachloroethane and 18 controls (two controls per exposed case) matched for residence, sex, age, and socioeconomic status was analysed for hexachlorobenzene (HCB), (P-HCB), and octachlorostyrene (P-OCS) with low resolution gas chromatography-mass spectrometry. Serum samples from the same subjects were analysed for standard kidney, pancreas, and liver function variables. Analysis of variance (ANOVA) with the triplets retained, a non-parametric test, and linear regression were used for the analysis. RESULTS: A fourfold increase of mean P-HCB was found among the exposed subjects compared with the controls (313.1 v 66.9 ng/g lipid; P < 0.01; (ANOVA model)). For P-OCS this difference was even larger (54.6 v 0.7 ng/g lipid; P < 0.01). Results were still significant (P < 0.05) with non-parametric testing. Within the exposed group there was a good correlation between the ln P-HCB (r = 0.80) and ln P-OCS (r = 0.91), respectively, with the cumulative number of years of exposure to hexachloroethane. No significant difference in kidney, pancreas, or liver function was found between the two groups. CONCLUSIONS: Aluminium degassing with hexachloroethane may increase the body burden of selected organochlorine compounds as reflected by HCB and OCS measurements. With the inherent limitations of this investigation no signs of subclinical organ toxicity were found.
PMCID: PMC1128987  PMID: 9326166
22.  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.
PMCID: PMC1741093  PMID: 16109822
23.  Non-malignant chest x ray changes in patients with mesothelioma in a large cohort of asbestos insulation workers. 
To assess the prevalence of non-malignant chest x ray abnormalities in cases of mesothelioma 184 cases of mesothelioma (72 pleural and 112 peritoneal) which had occurred in a cohort of asbestos insulation workers followed up since 1967 were studied. Chest x ray films of satisfactory quality, on which the presence or absence of non-malignant radiological changes indicating interstitial pulmonary fibrosis or pleural fibrosis or both, could be assessed with a high degree of certainty were available. In some cases (20% for pleural mesothelioma, 11.6% for peritoneal mesothelioma) non-malignant radiological changes were not radiologically detectable. Parenchymal interstitial fibrosis (small irregular opacities) only was found in a proportion of cases (25.4% of pleural mesotheliomas, 12.5% of peritoneal mesotheliomas). Pleural fibrosis only was detected in 17% of cases of pleural mesothelioma and 27% of cases of peritoneal mesothelioma. Most patients had both parenchymal and pleural fibrosis. Although these results tend to indicate that in peritoneal mesothelioma the proportion of pleural fibrosis is significantly higher, these findings might have been due to the fact that in most cases of pleural mesothelioma non-malignant changes were interpreted in one hemithorax only. In 46 cases (21 pleural, 25 peritoneal) in which sufficient lung tissue was available histopathology of lung parenchyma indicated the presence of interstitial fibrosis; in 20 (43.5%) of these the chest x ray film had been read as negative. Thus the absence of radiologically detectable small opacities on the chest x ray film does not exclude the existence of interstitial pulmonary fibrosis in cases of mesothelioma among insulation workers. With lower levels of exposure (such as in family contacts of asbestos workers) it is conceivable that mesothelioma might occur in the absence of interstitial pulmonary fibrosis.
PMCID: PMC1007841  PMID: 3606969
24.  Humoral immunosuppression in men exposed to polycyclic aromatic hydrocarbons and related carcinogens in polluted environments. 
Environmental Health Perspectives  1994;102(3):302-304.
We evaluated humoral immunity by measuring IgG, IgA, IgM, and IgE concentrations in 274 male workers in an iron foundry in Cracow, Poland. There were two groups: 199 coke oven workers and 76 cold-rolling mill workers. The groups were similar with respect to age, length of work (average 15 years), and smoking habits. Exposure to polycyclic aromatic hydrocarbons (PAHs), assessed by personal and area monitoring, ranged from 0.2 to 50 micrograms/m3 benzo[a]pyrene in coke plant workers and was of 3-5 magnitudes higher than in the cold-rolling mill employees. Comparison of the two groups revealed a marked depression of mean serum IgG and IgA in coke oven workers (p < 0.001, Student's unpaired t-test). In the same subjects, serum IgM had a tendency to decrease, whereas serum IgE showed a trend toward higher values. Thus, workers exposed chronically to complex mixtures of air pollutants, composed primarily of PAHs, develop immunosuppression. It remains to be established whether the immunosuppression described here is related to the frequent development of lung cancer reported in coke plant employees. Workers exposed chronically to PAHs should have serum immunoglobulins monitored regularly.
PMCID: PMC1567104  PMID: 8033871
25.  Historical cohort study of a New Zealand foundry and heavy engineering plant 
OBJECTIVES: To investigate the mortality of workers who had been exposed to asbestos, machining fluids and foundry work in a foundry and heavy engineering plant in the railway rolling stock manufacturing industry in New Zealand. METHODS: Historical cohort study design. RESULTS: For the total workforce of 3522 men employed between 1945 and 1991, follow up was 90% of person-years to 31 December 1991. Significantly increased standardised mortality ratios (SMRs) were found for all causes of death combined (SMR 1.07; 95% confidence interval (95% CI) 1.01 to 1.14), all malignancies (SMR 1.15; 95% CI 1.01 to 1.31), circulatory (SMR 1.16; 95% CI 1.07 to 1.27) and musculoskeletal diseases (SMR 3.06; 95% CI 1.39 to 5.84), all digestive cancers (SMR 1.29; 95% CI 1.04 to 1.59), all respiratory cancers (SMR 1.34; 95% CI 1.08 to 1.65), cancer of the oesophagus (SMR 1.97; 95% CI 1.01 to 3.45), and mesothelioma of the pleura (SMR 6.58; 95% CI 1.24 to 19.49). Three deaths from pleural mesothelioma were recorded, with latency times of 51, 53, and 57 years. There were no dose-response relations between exposure to asbestos, machining fluids or foundry work, or by duration of employment in the plant, and any cause of death. CONCLUSIONS: This study found small increases in risk for several causes of death among foundry and heavy engineering workers; however, these increases were small and the possible effects of smoking and other lifestyle factors could not be excluded. There was evidence of asbestos related disease in those involved in engineering work in the past.
PMCID: PMC1757697  PMID: 10448319

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