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Query: UMLS:C0037116 (silicosis)
 1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An IARC Working Group recently classified crystalline silica (quartz) into IARC's Group 1, i.e. a carcinogen. This classification is based on evidence of carcinogenicity in experimental animals and in humans. However, the evaluation stated that in making the overall evaluation, the Working Group noted that carcinogenicity to humans was not detected in all industrial circumstances studied and that carcinogenicity may be dependent on inherent characteristics of the crystalline silica or on external factors affecting its biological activity. The present review seeks to put the apparently conflicting findings of cancer incidence in quartz-exposed industries into a unifying thesis, based on mechanistic studies. These mechanistic studies have enabled the events leading from deposition of quartz to silicosis and cancer to be partially elucidated and have demonstrated that the biological effects of quartz can be understood in terms of surface reactivity. We particularly emphasise the ability of quartz to generate free radicals and cause oxidative stress and the fact that this could be modified by a range of substances that affect the quartz surface; some of these modifying substances could originate from other minerals. We therefore propose that the hazard posed by quartz is not a constant entity, but one that may vary dramatically depending on the origin of the silica sample or its contact with other chemicals/minerals within its complex constitution. The mechanistic data described here could assist in the interpretation of epidemiological studies and pose further hypotheses that could be tested in order to help resolve the quartz carcinogenesis anomaly. The data suggest that quartz cannot be death with as a single hazard entity, as is the case with most other chemicals.
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PMID:The quartz hazard: a variable entity. 972 16

Elevated disease rates have been documented among construction workers for cancer, pneumonoconiosis, asbestosis, and silicosis. However, methodologies for exposure assessment in construction are not well described in the U.S. literature. Working through a cooperative agreement with the National Institute for Occupational Safety and Health (NIOSH), the Center to Protect Workers' Rights--a research arm of the Building and Construction Trades Department, AFL-CIO--has developed and used a "Task-Based Exposure Assessment Model (T-BEAM)" for construction. The characteristic elements of T-BEAM are: (1) an emphasis on the identification, implementation, and evaluation of engineering and work practice controls; and (2) use of experienced, specially trained construction workers (construction safety and health specialists) in the exposure assessment process. A task-based approach was used because tasks, or specialized skills, form the single greatest thread of continuity in the dynamic environment of construction. Workers in the construction industry come from several crafts and are typically employed by a large number of contractors throughout their career. Project types (e.g., residential or industrial rehabilitation) are also highly variable and present unique health risks. Finally, because construction involves building, renovating, or dismantling physical surroundings, the work site is constantly changing. Between 1995 and 1996, T-BEAM was applied to the collection of approximately 200 personal exposure measurements associated with "hot work tasks"--welding and thermal cutting. Data were collected with the assistance of specially trained, journeyman ironworkers, pipe fitters, and boilermakers on nine construction sites located throughout the United States. Portable local exhaust ventilation was provided to participating contractors with the intent of measuring its impact on exposure. Results indicate that data collected in a standardized, systematic fashion from multiple work sites can be used to characterize exposures among sampled trades. Comparison of results to American Conference of Governmental Industrial Hygienists (ACGIH) threshold limit values (TLVs) demonstrate a significant health hazard among sampled trades posed by welding and thermal cutting fume, manganese, nickel, and chromium VI. Direct estimates of the probability of exceeding the ACGIH TLV for respirable particulate suggests that boilermakers (100%) and ironworkers (71%) are at greatest risk. Other task variables evaluated with respect to exposure include task, whether work was performed indoors or outdoors, intermittency of work, and use of ventilation. Use of local or mechanical ventilation reduced mean exposures to fumes significantly.
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PMID:The use of a task-based exposure assessment model (T-BEAM) for assessment of metal fume exposures during welding and thermal cutting. 1066 Sep 86

In view of the extended debate and differing opinions on whether crystalline silica is a human carcinogen, we have reviewed a selection of epidemiological reports, to identify the areas of uncertainty and disagreement. We have chosen to examine the papers which in a recent review were considered to provide the least confounded examinations of an association between silica exposure and cancer risk. We also refer to a study of the mortality of coalminers very recently reported by ourselves and colleagues. We find that parts of the evidence are coherent but there are contradictions. On examination this resolves mostly into differences between types of studies. The three types of epidemiological study included are: (i) exposure-response studies, the most powerful for the confirmation of a relationship between a specific exposure and a health effect; (ii) descriptive studies in which incidence of disease in an exposed population is compared with that in a reference population; and (iii) studies of incidence of disease in subjects on silicosis case-registers. Descriptive studies frequently though not invariably suggest an excess lung cancer risk in silica-exposed workers compared with the general population, but exposure-response studies consistently fail to confirm that the cause is exposure to quartz. A single exposure-response study of cristobalite suggests a positive relation. Both sets of evidence have weaknesses. There are uncertainties on whether the excess risks in the descriptive studies are related to silica exposure or to lifestyle, including smoking habits. There are doubts on whether the exposure estimates in some of the exposure-response studies were sufficiently reliable to detect a small risk or weak association, though they are unlikely to have missed a strong effect. Studies of subjects on silicosis case registers consistently show an excess of lung cancer, but it is not clear to what extent these increased risks represent a direct effect of silica exposure, a secondary effect of the silicosis, preferential inclusion of subjects suffering from the effects of smoking, or bias in diagnostic accuracy. This not unnaturally leads to differences in opinion, exacerbated by variations in the strength of proof required by different experts. The main scientific uncertainties in the evidence are: 1. Whether, in the descriptive studies, the excess lung cancer rates in silica-exposed workers are explicable in terms of smoking habits, socio-economic class differences and inappropriate comparison populations. Better smoking information and more carefully chosen comparison populations are needed; 2. Whether the exposure-response studies could have missed a real relationship between silica exposure and lung cancer, if one exists. Many of the exposure-response studies were conducted with great care, but weaknesses, in the available data on which the exposure estimations were based, could have caused a real relationship of lung cancer and silica exposure to be missed. These studies were sufficiently powerful to demonstrate relationships of silica exposure with silicosis and silico-tuberculosis, so it is unlikely that they would have missed any but a small risk, or weak relationship, for lung cancer. Our own recent study of coalminers used uniquely detailed and reliable exposure data, and failed to demonstrate convincingly an increased risk. This negative finding, though, applies only to a dust in which the proportion of quartz in the dust is usually less than 10%. Exposure-response studies are needed, with high quality exposure estimates, in populations exposed to respirable dust of which crystalline silica comprises more than 10%; 3. Whether the excess cancer risks in subjects on silicosis registers are the result of selection and diagnostic bias. Given these difficulties, case-register studies may not be capable of giving a reliable answer to the central question, though they have been useful in pointing to the possibility of a can
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PMID:Epidemiological evidence on the carcinogenicity of silica: factors in scientific judgement. 1102 42

In November 1997, a 61-year-old man was admitted to our hospital complaining of dyspnea. He had worked as a miner for 10 years and had received medical treatment based on a diagnosis of idiopathic interstitial pneumonia at our hospital since 1984. In conjunction with the progression of interstitial pneumonia, the patient's serum CA 19-9 had gradually increased since 1992, reaching 9,920 U/ml in 1997. Though cancer of the pancreas or other organs was suspected, an extensive examination revealed no malignancy. In April 1998, the patient died of bacterial pneumonia. Lung autopsy specimens disclosed severe interstitial fibrosis with prominent silicotic nodules. Based on these findings, silicosis was diagnosed. In immunohistochemical staining for CA 19-9, the lumina of severely fibrotic lesions covered with epithelial cells stained positively with anti-CA 19-9 antibody. These findings suggested that serum CA 19-9 may have been produced in the epithelial cells. We speculated that increased serum CA 19-9 levels in patients with interstitial pneumonia may occasionally be more indicative of the magnitude of destruction of lung architecture than the degree of disease activity.
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PMID:[Silicosis characterized by increasing serum CA 19-9 in parallel with progression of lung fibrosis]. 1077 74

Crystalline silica was recently classified as a human carcinogen by the International Agency for Research on Cancer (IARC). However, the direct genotoxic effect of silica in humans remains unclear. We examined the p53 and K-ras gene mutations in lung cancer in workers with silicosis (LCWS). DNA was extracted from paraffin-embedded tissues and examined by PCR-RFLP, PCR-SSCP, and DNA sequencing. The mutation frequencies of p53 gene were high, but the mutation distributions in exons and among the histological types of LCWS differed from those of common (i.e., not silicosis-related) lung cancer. Furthermore, no mutations in codon 12 of K-ras gene (predominant in common lung cancer) were found in LCWS. These findings in the mutational spectrum support a carcinogenic effect of silica dust at the DNA molecular level.
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PMID:A distinct mutational spectrum of p53 and K-ras genes in lung cancer of workers with silicosis. 1090 1

The International Agency for Research on Cancer (IARC) determined that crystalline silica inhaled from occupational sources should be classified as carcinogenic to humans and upgraded it from group 2A to group 1. It has also been found that silicosis may be associated with cancer of various organs and with autoimmune diseases. We studied both the cytogenetic effects and the influence on cell-mediated immunity of mineral dust inhalation in patients with pneumoconiosis, including silicosis. The frequency of sister chromatid exchanges and micronucleus in the pneumoconiosis group were significantly higher than in the controls, suggesting a cytogenetic influence of the occupationally inhaled dust. Alterations in the immunoregulatory T cells were observed in the pneumoconiosis groups, suggesting that inhaled mineral dust may cause immunotoxic effects. Based on these findings, we can consider that cytogenetic damages and immunoregulatory abnormalities in pneumoconiosis patients may play a role in the pathogenesis of various cancers and autoimmune diseases associated with pneumoconiosis.
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PMID:Cytogenetic damage and cell-mediated immunity in pneumoconiosis. 1090 16

The 'Sendzimir' Steel Mill, Cracow, Poland, gives employment to approximately 17,000 workers. During the years 1994-98, 1396 compensation claims for diseases related to occupational hazards were registered. After a scrupulous investigation, 851 cases were certified as occupation-related diseases. Of this number, 481 cases (56.5%) were diagnosed as pulmonary diseases, including silicosis (n = 225, 46.7%); chronic bronchitis (n = 138, 28.7%); lung carcinoma (n = 59, 12.3%); epithelial cancer (n = 42); adenocarcinoma (n = 12); microcellular carcinoma (n = 5); asthma, 12 atopic and 24 non-atopic (n = 36, 7.5%); and asbestosis (n = 23, 4.8%). Chronic bronchitis was diagnosed in patients exposed to industrial dusts, containing SiO2, NOx, and SO2. Asthma occurred most frequently among those exposed mainly to Cr+6, Co and Ni containing dusts, and lung carcinoma in those exposed to policyclic aromatic hydrocarbons, including benz(a)pyren, asbestos, chromium, vapours of oils and lubricants. In 1994-96, chronic bronchitis and silicosis, and in 1997-98, lung carcinoma and asthma were most frequently diagnosed in the workers under study. It is likely that the diminishing frequency of chronic bronchitis and silicosis was the consequence of technological progress, and greater concern for hygiene standards. Increasing incidence of lung cancer reflects long latency characteristic of this illness.
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PMID:Occurrence of pulmonary diseases in steel mill workers. 1096 40

39 years old man with granulomatous lesions in both lungs caused by occupational contact with glass fibers was described. He has been working as an bricklayer-plasterer for 18 years and was in contact with lime, cement, plaster, asbestos, dust of coal and wood and with glass fibers. For the last two years before admission in 1993 he has had frequent bronchial infections. On admission he was in good general condition, his spirometric examination and blood gases were within normal limits. On chest x-ray disseminated lesions were found. Those lesions were of the round shapes on chest CT. Many sputum cultures for tubercle bacilli were negative. ANA and ANCA were not found in the serum. ACE was within normal limits. No precipitins to environmental antigens were found. Cancer metastases were suspected and lung biopsy during videothoracoscopy was done. Many foreign body type granulomas were found throughout the specimen. The character of the lesions was not typical for tuberculosis, sarcoidosis, extrinsic allergic alveolitis, silicosis or asbestosis. There are some reports concerning the possibility of development of such lesions after the exposition to glass fibers. We suspect that case is an example of such pathology. His occupational exposition was stopped in 1993 and he was observed without treatment. During the 5 years of observation (up till 1998) he was in good health with stable chest x-ray picture and results of respiratory system function.
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PMID:[Granulomatous lung lesions after occupational exposure to glass fibers]. 1100 67

In 1997, the International Agency for Research on Cancer determined that crystalline silica was a human carcinogen but noted inconsistencies in the epidemiology. There are few exposure-response analyses. The authors examined lung cancer mortality among 4,626 industrial sand workers, estimating exposure via a job-exposure matrix based on 4,269 industrial hygiene samples collected in 1974--1995. The average length of employment was 9 years, and estimated average exposure was 0.05 mg/m(3) (the National Institute of Occupational Safety and Health Recommended Exposure Limit). Results confirmed excess mortality from silicosis/pneumoconioses (standardized mortality ratio = 18.2, 95% confidence interval: 10.6, 29.1; 17 deaths). The lung cancer standardized mortality ratio was 1.60 (95% confidence interval: 1.31, 1.93; 109 deaths). Limited data suggested that smoking might account for 10--20% of the lung cancer excess. Exposure-response analyses by quartile of cumulative exposure (15-year lag) yielded standardized rate ratios of 1.00, 0.78, 1.51, and 1.57 (p for trend = 0.07). Nested case-control analyses after exclusion of short-term workers, who had high overall morality, yielded odds ratios by quartile of cumulative exposure (15-year lag) of 1.00, 1.35, 1.63, and 2.00 (p for trend = 0.08) and odds ratios by quartile of average exposure of 1.00, 0.92, 1.44, and 2.26 (p = 0.005). These data lend support to the labeling by the International Agency for Research on Cancer of silica as a human carcinogen. There are approximately 2 million US workers exposed to silica; 100,000 are exposed to more than 0.1 mg/m(3).
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PMID:Lung cancer among industrial sand workers exposed to crystalline silica. 1159 92

In 1997, the International Agency for Research on Cancer (IARC) upgraded its evaluation of crystalline silica to a Group 1 human carcinogen. Criticism against such decision is based on the lack of consistency in experimental results across animal species, violation of an important principle for causality, such as the replication of findings under different circumstances of exposure, and the lack of a clear dose-response curve. The most recent epidemiological literature on the silica-silicosis-lung cancer link replicates the inconsistent findings that have been characterising 50 years of scientific debate in the occupational arena. Exposure circumstances capable of modifying the silica-lung cancer association include chronic bronchitis, composition of the dust mixing, particularly concerning co-occurrence of other known or probable lung carcinogens, total respirable dust, concentration of silica in respirable dust, type of crystalline silica and particle surface characteristics. The hypothesis of a silicosis-mediated pathway points toward an unspecific mechanism shared with other fibrotic conditions, for which silica might be just one of the triggers. In envisaging a multivariate multistep model of lung cancer among silica-exposed workers, silica might be considered as a "passive components of the sufficient cause", i.e., one of the associated risk factors, concurrent or subsequent to the "active component(s) of the sufficient cause" (including, for instance, smoking, asbestos, radon-daughters, arsenic, hexavalent chromium, nickel, polycyclic aromatic hydrocarbons (PAH), and diesel exhausts among the external risk factors; and DNA repair enzymes polymorphism and spontaneous inactivation of tumour suppressor genes among the internal risk factors), which adds up in modulating the tumoral development in not easily predictable directions. If silica acts as a human lung carcinogen depending on certain occupational exposure circumstances, perhaps those circumstances and not silica itself should be classified for their human carcinogenicity potential.
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PMID:Multifactorial aetiology of lung cancer among silica-exposed workers. 1160 27


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