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Recurrent tuberculosis (TB) is due to exogenous re-infection with a new Mycobacterium tuberculosis strain or relapse with the initial strain. Genotyping can distinguish between genotypically identical (relapse) and dissimilar (re-infection) strains. In high TB incidence areas, recurrences are likely due to re-infection (assuming treatment guideline adherence and subsequent low relapse rates). However, in low-incidence areas, recurrences are likely due to relapse, provided infection control is adequate.1 Recurrent TB has been associated with treatment failure,2 drug resistance,3–5 and more complicated and expensive treatment regimens. Effectiveness of TB control programs is assessed in part by TB recurrence rates; however, programmatic data from the United States are limited.6–8 TB relapse rates vary from 2% to 6%,9–11 but are higher without appropriate treatment dosing,12 rifamycin-based therapy,13–15 or directly observed therapy (DOT).16 In TB Trials Consortium (TBTC) Study 22, non-Hispanic white race, low body weight, bilateral pulmonary or cavitary disease and positive sputum cultures after 2 months of treatment were all independent predictors of relapse.7,17 Chronic lung disease (CLD), including chronic obstructive pulmonary disease (COPD),18–20 asthma,21 and interstitial lung disease (particularly silicosis),22 are risk factors for developing TB, but have not been evaluated as risk factors for recurrence. In high TB incidence countries, human immunodeficiency virus (HIV) infection is a risk factor for TB re-infection.23–25 This association has not been shown in low-incidence areas, possibly due to lower likelihood of repeat exposure.26 Previous studies report conflicting results regarding HIV infection as a risk factor for TB relapse.8,26 TB relapse rates are used to determine optimal treatment duration, with desired rates of

Introduction. Silicosis, the most prevalent of the pneumoconioses, is caused by inhalation of crystalline silica particles. Silica-exposed workers are at increased risk for tuberculosis and other mycobacterium-related diseases. The risk of a patient with silicosis developing tuberculosis is higher (2.8 to 39 fold higher, depending on the severity of silicosis) than that found in healthy controls. Outline of Cases. The first patient was a 52-year-old male who was admitted in 2002 for the second time with dyspnoea, wheezing and fatigue over the last 11 years. He had worked in an iron smelting factory and was exposed to silica dust for 20 years. First hospitalization chest radiography showed bilateral pleural adhesions, diffuse lung fibrosis with signs of a specific lung process. Second hospitalization chest radiography showed bilateral massive irregular, non-homogenous calcified changes in the upper and middle parts of lungs. The patient died due to respiratory failure and chronic pulmonary heart in 2007. The main causes of his death were silicotuberculosis and chronic obstructive pulmonary disease. The second patient was a 50-year-old male who was admitted in 2005 for the second time with chest tightness, dyspnoea, wheezing and fatigue over the last 10 years. He had worked in an iron smelting factory and was exposed to silica dust for 30 years. First hospitalization chest radiography showed diffuse lung fibrosis and small nodular opacities. The patient was diagnosed with silicosis, small opacities sized level p/q, and profusion level 2/3. Second hospitalization chest radiography and CT showed diffuse lung fibrosis and small nodular opacities predominantly in the upper lobes. The patient was recognized as having an occupational disease, and received early retirement due to disability. Conclusion. In low-income countries, new cases of silicosis and associated lung cancer, chronic obstructive pulmonary disease and tuberculosis are likely to be seen for decades because necessary reduction of silica use will take time to be achieved.

Experimental silicosis and silicotuberculosis induced by intravenous injection of silicon dioxide particles are characterized by extensive degenerative and necrotic processes in the liver parenchyma. After 6 months, fibrosis of portal tracts in silicotuberculosis and silicosis was 2.8- and 1.4-fold more pronounced that in BCG granulomatosis and silicosis, respectively. Depression of cellular and intracellular regeneration processes in the liver parenchyma was also observed.

The stimulating effect of silicon dioxide on fibroblast proliferation in granulomas of male CBA mice surpasses that of BCG vaccine mycobacteria. The number of fibroblasts in granulomas after combined treatment with BCG and SiO 2 increased by more than 3 times compared to individual treatment with BCG and by 2 times compared to treatment with SiO 2 alone. In silicosis and silicotuberculosis, collagen and argyrophilic fibers in granulomas during the period from 4 to 6 months after administration of granulomogenic factors occupied more than 90% granuloma volume, which 3-fold surpassed the corresponding parameter in mice infected with BCG vaccine alone. In silicosis, pronounced fibrosis was determined by relatively high proliferative and synthetic activities of fibroblasts, while in silicotuberculosis it was achieved due to significantly higher proliferative activity against the background of lower synthetic activity.

Silicon dioxide in combination with Mycobacterium tuberculosis in BCG vaccine is characterized by a significantly higher granuloma-inducing activity than BCG or silicon dioxide alone. Cell "dissociation" from granulomas is not characteristic of granulomas induced by silicon dioxide or its combination with BCG (in contrast to BCG-induced granulomas). A steady increase in the counts and size, particularly on days 120-180, mainly at the expense of fibroblast accumulation and subtotal fibrosis, are intrinsic to these granulomas. Monocyte retention in the bone marrow is characteristic starting from day 56 until day 180 after injection of both granulomatous factors alone or in combination, particularly so in BCG granulomatosis.

Silicosis is a progressive interstitial lung disease, characterized by shortness of breath, cough, fever and bluish skin; it can present in three different forms: acute, accelerated and chronic. (1) It is caused by the lung tissue reaction to the inhalation of silica and occurs most commonly as an occupational disease of people working in the quarrying, manufacturing and building construction industries. Exposure to large amounts of free silica can go unnoticed because silica is odourless, non-irritant and does not cause any immediate health effects. As silicosis is incurable, clinical management includes removing the worker from the industry and giving symptomatic treatment. Public health goals are to detect early cases through monitoring of currently and formerly exposed workers, to establish surveillance programmes, to slow progression and to reduce disability. (2) In 1995, the World Health Organization and the International Labour Organization began a public awareness and prevention campaign to eliminate silicosis from the world by 2030. (3) Several countries--Brazil, Chile, China, Indonesia, Malaysia, Mexico, Poland, South Africa, Thailand, Turkey, Ukraine, the Bolivarian Republic of Venezuela and Viet Nam--have established national programmes for the elimination of silicosis. (3) However, in many low- to middle-income countries, including India, silicosis continues to be an occupational health hazard. India has a large mining industry, concentrated in the states of Chhattisgarh, Jharkhand, Orissa and West Bengal. In 1999, the Indian Council of Medical Research reported that around 3.0 million workers are at high risk of exposure to silica; of these, 1.7 million work in mining or quarrying activities, 0.6 million in the manufacture of non-metallic products (such as refractory products, structural clay, glass and mica) and 0.7 million in the metals industry. (4) There are also around 5.3 million construction workers at risk of silica exposure. (4) Due to variations in silica concentrations and duration of exposure in the work environment the reported prevalence of silicosis in India ranges widely--from 3.5% among 1977 workers in an ordnance factory to 54.6% in 593 workers in the slate-pencil industry. (5,6) The main challenge of eliminating silicosis in India is in the informal, unregulated sectors of industry which do not fall under the control of statutory tools such as the Factory Act of India (1948). (7) This Act mandates a well ventilated working environment, provisions for protection from dust, reduction of overcrowding and provision of basic occupational health care. Silicosis-affected workers in the informal sector are not entitled to statutory protection, which would remove them from the hazardous environment, or to compensation, which would enable them to leave work. Continued exposure makes it difficult for physicians to manage the disease. Furthermore, most primary-care physicians in India are not trained to manage occupational health diseases. Among the clinical complications of silicosis is tuberculosis (called silicotuberculosis), a disease which is still a major public health concern in low- and middle-income countries. (8) Chronic exposure to silica increases workers' risk of tuberculosis infection and aggravates pre-existing pulmonary tuberculosis. (9-11) Differential diagnosis is a challenge. Although treatable, tuberculosis in silicosis patients may go undiagnosed because cough, wheeze, expectoration, dyspnoea and vague chest pains are symptoms common to both diseases. Interpretation of the chest X-ray film of patients with silicosis is difficult due to the superimposition of silicotic nodules and tuberculous infiltrations. Mycobacterium tuberculosis bacilli may not be recovered from the sputum of silicotuberculosis patients because silicotic fibrosis prevents the discharge of tubercle bacilli into the sputum. (8) Acid-fast bacilli, if cultured, are mainly non-tuberculous mycobacteria. …

Through the concept of "thought collectives" in particular, Ludwik Fleck was a pioneer in demonstrating how much scientific knowledge is inherently made up of social and historical material. In this article, I propose to follow a Fleckian path by comparing the proceedings of the 1930 International Labour Office Conference on silicosis in Johannesburg on the one hand, and on the other the content of the debates that took place in France in the 2000s to revise the "tables" of occupational diseases which define the compensation rules for salaried workers in the French general (as well as the farm) health insurance scheme. The text offers an analysis of the striking similarities between these two distant sources, pointing out particularly the repetitiveness of ignorance and knowledge, and the nature of what can be admitted as a body of "evidence" in medico-legal issues such as the definition and compensation of occupational diseases.

The 1930 International Labour Office Conference on silicosis in Johannesburg was a turning point in the history of silicosis and in the recognition of the associated pathologic patterns. Since 1930, pneumoconioses such as silicosis have become much rarer in developed countries and can now be diagnosed at an early stage based on clinical and radiologic criteria. However, in spite of these advances, pathologists must remember to look for silica in tissues, particularly when clinical and radiologic findings are more uncertain. Furthermore, nowadays pathologists essentially observe silicotic lesions as incidental findings adjacent to lung cancers. In addition to identifying the characteristic lesions, pathologists must also try to identify their causative agent, in the case of crystalline silica firstly by using polarized light examination, followed as appropriate by more sophisticated devices. Finally, pathologists and clinicians must always keep in mind the various implications of exposure to silica compounds in a wide range of diseases.

Scholarly understanding of the nature of the science around silicosis has been strongly influenced, in recent years, by the idea that the mine doctors were responsible for hiding an epidemic, on the mines and in the countryside. In this paper, I try to show that the opposite was in fact the case, and that the science and government institutions for the regulation of silicosis and tuberculosis in white and black male workers were distinctively elaborated, and very largely successful in tracking and controlling the disease. This singular visibility, funded by the mines, stands in marked contrast with disease in general in South Africa, and forms a major part of the explanation for the very strong association of silicosis with mine work.

Very rapidly progressive "acute silicosis" was observed prior to the 1930 International Labour Office Conference on silicosis, but its clinical significance and pathologic relationship to classic silica caused pneumoconiosis were not settled.Textual analysis of the 1930 Conference proceedings identified data relevant to rapidly progressive silicosis. Standard bibliographic searches identified relevant biomedical literature dating from before and after the Conference.The 1930 Johannesburg Conference contained descriptions of acute silicosis, especially in the abrasive powders industry, but acute silica-related lung disease did not conform to a three-stage disease model in which tuberculosis supra-infection caused advanced disease, a model accepted at the Conference. Over following decades, additional reports appeared of rapidly progressive silicosis, unrelated to tuberculosis. Pulmonary alveolar proteinosis was identified only in 1958.Adoption by the 1930 Johannesburg Conference of a classification scheme into which acute rapidly progressive disease unrelated to tuberculosis fitted poorly may have impeded the understanding of acute silicosis and its importance.

The long-term exposure to dust in the hard coal mining industry can lead to various pathological lung changes, especially to chronic bronchitis without and with obstructive ventilation disorder, lung emphysema, pneumoconiosis (coal miner's pneumoconiosis, in Germany categorized as silicosis) and silicotuberculosis. These health disorders show a close pathogenetic and pathophysiological association and should not necessarily be regarded as individual entities. Most exposed subjects demonstrate more or less all of these pathological disorders. On account of individual (genetic?) susceptibility, their degree differs greatly. Some individuals are largely resistent, other subjects show severe effects like emphysema, progressive massive pneumoconiosis, or the Caplan syndrome. Several studies showed that the pathologically verified degree of lung fibrosis is associated with lung crystalline SiO(2) content whereas the emphysema score is inversely correlated with the coal content. With regard to diagnostics and medical expert opinion, it is important that conventional radiology has a low sensitivity. Further, health impairments of miners engaged for longtime which are insurance relevant (MdE) exist in cases without (BK 4111 if beginning after 12/31/1992) or with coalworkers' pneumoconiosis even for categories < 2/3.

Objectives: In East Germany, uranium mining was performed on a large scale for approximately 45 years (1946–1990). In particular, the poor working conditions during the post-war years until 1955 led to a high level of occupational diseases. The present study gives an overview of the occurrence of occupational diseases during the mining period as well as after uranium mining was stopped in 1990. Methods: The number of occupational diseases which occurred during the mining period was calculated from the files of the former Wismut SDAG. Although exposure to uranium ceased after 1990, new cases of occupational diseases were recognized after that date. These were recorded by the German Federation Of Institutions For Statutory Accident Insurance And Prevention (HVBG). Results and Conclusions: Today, more than 35,000 cases of occupational diseases are known, and many more are expected. About two-thirds of them are lung diseases: 16,376 cases of silicosis/silicotuberculosis and 7,695 cases of bronchial carcinomas. The increase in the number of recognized occupational diseases is shown and discussed against the background of changes in criteria for recognition and in working conditions as well as the duration of the latency period.

OBJECTIVES—To evaluate the association between silica, silicosis and lung cancer, the mortality of 724 patients with silicosis, first diagnosed by standard chest x ray film between 1964 and 1970, has been analysed by a cohort study extended to 31 December 1997. METHODS—Smoking and detailed occupational histories were available for each member of the cohort as well as the estimated lifetime exposure to respirable silica dust and radon daughters. Two independent readers blindly classified standard radiographs according to the 12 point International Labour Organisation (ILO) scale. Lung function tests meeting the American Thoracic Society's criteria were available for 665 patients. Standardised mortality ratios (SMRs) for selected causes of death were based on the age specific Sardinian regional death rates. RESULTS—The mortality for all causes was significantly higher than expected (SMR 1.35, 95% confidence interval (95% CI) 1.24 to 1.46) mainly due to tuberculosis (SMR 22.0) and to non-malignant chronic respiratory diseases (NMCRD) (SMR 6.03). All cancer deaths were within the expected numbers (SMR 0.93; 95% CI 0.76 to 1.14). The SMR for lung cancer was 1.37 (95% CI 0.98 to 1.91, 34 observed), increasing to 1.65 (95% CI 0.98 to 2.77) allowing for 20 years of latency since the first diagnosis of silicosis. Although mortality from NMCRD was strongly associated to the severity of radiological silicosis and to the extent of the cumulative exposure to silica, SMR for lung cancer was weakly related to the ILO categories and to the cumulative exposure to silica dust only after 20 years of lag interval. A significant excess of deaths from lung cancer (SMR 2.35) was found among silicotic patients previously employed in underground metal mines characterised by a relatively high airborne concentration of radon daughters and among ever smokers who showed an airflow obstruction at the time of the first diagnosis of silicosis (SMR 3.29). Mortality for lung cancer related to exposure was evaluated with both the Cox's proportional hazards modelling within the entire cohort and a nested case-control study (34 cases of lung cancer and 136 matched controls). Both multivariate analyses did not show any significant association with cumulative exposure to silica or severity of silicosis, but confirmed the association between mortality for lung cancer and relatively high exposure to radon, smoking, and airflow obstruction as significant covariates. CONCLUSIONS—The findings indicate that the slightly increased mortality for lung cancer in this cohort of silicotic patients was significantly associated with other risk factors—such as cigarette smoking, airflow obstruction, and estimated exposure to radon daughters in underground mines—rather than to the severity of radiological silicosis or to the cumulative exposure to crystalline silica dust itself. Keywords: silicosis; crystalline silica; lung cancer mortality

Eighty-five female quartz mill stone-grinding workers belonging to the Naika, Rathwa and Damor tribes of Chhotaudepur village of the Godhra region of Gujarat, Western India were surveyed and examined to assess health effects related to free silica dust exposure. The mean age for the subjects was 28.2 +/- 9.2 years, while the mean duration of exposure was 2.04 +/- 1.7 years. Chest radiographs showed findings suggestive of silicosis in 14%, silico-tuberculosis in 11.6% and tuberculosis in 8.1% of the study subjects. Respiratory morbidity was significantly associated with duration of exposure (X2 = 9.9, df = 2, p

Aim : To determine the magnetic resonance imaging (MRI) signal characteristics of progressive massive fibrosis (PMF) in silicosis. Subjects and Methods : We evaluated prospectively the MR appearances in 17 patients with 34 PMF lesions on the basis of pre-contrast signal intensity (SI) and SI pattern and post-contrast enhancement pattern, using a 0.5-T unit. There were 13 PMF lesions in six patients who had silicosis and 21 PMF lesions in 11 patients who had silicotuberculosis. The SI pattern on T2-weighted image (WI) was classified into four types and the pattern of contrast enhancement on T1-WI was classified into three types. MR appearances of PMF lesions were correlated with the findings of computed tomography (CT). Results : The commonest signal intensity characteristic was isointensity (70%) on T1-WI and hypointensity (68%) on T2-WI when compared with skeletal muscle. For signal pattern on T2-WI, a type with only internal high SI areas (46% in silicosis group, 38% in silicotuberculosis group) was most frequent. All of these areas corresponded to the low density areas at CT, suggestive of necrosis. After intravenous contrast medium enhancement, rim enhancement (54% in silicosis group, 52% in silicotuberculosis group) was most frequent, followed by no enhancement. Conclusion : The most common MRI appearance of PMF was isointensity on T1-WI and hypointensity on T2-WI when compared with skeletal muscle, with internal high SI areas on T2-WI and either rim enhancement or no enhancement.

To investigate the situation and causes of misdiagnosis of pneumoconiosis or silicotuberculosis in China by pooled analysis, and to provide a reference for the clinical diagnosis of pneumoconiosis in China and reduce the misdiagnosis rate.A computer search was performed to collect the studies on the misdiagnosis of pneumoconiosis or silicotuberculosis published in China from 1985 to 2013. The obtained data were subjected to pooled analysis to investigate the causes of misdiagnosis and seek the measures for reducing misdiagnosis.Fifty-nine studies involving 1178 cases of misdiagnosed pneumoconiosis or silicotuberculosis were collected. There were 13 causes of misdiagnosis, and the most common one was the poor ability of identification due to inadequate experience in reading chest X-ray films (45.93%), followed by neglect of patient's occupational history (44.99%). Other causes of misdiagnosis included complex X-ray findings that are difficult to judge (29.03%), poor quality of chest radiographs (23.09%), and lack of regular health supervision (19.95%).Inadequate experience of physicians is the main cause of misdiagnosis of pneumoconiosis or silicotuberculosis. To reduce misdiagnosis of the disease, measures should be taken to enhance the training and evaluation of knowledge and skills of diagnosis and differential diagnosis of pneumoconiosis among physicians.

Silicosis is a fibrosing lung disease induced by silica particle inhalation. In addition to its effects on pulmonary physiology, the disease is also associated with clinically important immune dysfunction, detectable both systemically and in the lung. An important local pulmonary manifestation of silicosis-associated immune dysfunction is impaired host defense against mycobacteria. Normal host defense against mycobacteria is accomplished through cell-mediated responses by T cells and macrophages. The mechanism underlying impaired antimycobacterial defense and silicotuberculosis in silicotics is unknown. Despite impaired host defense against mycobacteria, silicosis appears to be associated with increased and dysregulated antibody production, as evidenced by the presence of hypergammaglobulinemia, circulating immune complexes, and autoantibodies in many patients with silicosis. The apparent paradox of excess antibody production, but impaired cell-mediated immunity, is not unique to silicosis. In a ...

Setting : A medical facility for approximately 90 000 gold miners employed on 24 South African gold mines. Objective : To evaluate the effectiveness of rifampicin, isoniazid and pyrazinamide given for 3 months for the prevention of tuberculosis in men with silicosis. Design : A randomised double-blind placebo controlled trial with active 4-year follow up of subjects by routine radiographic screening. Results : A total of 382 gold miners with silicosis were randomised to receive rifampicin 600 mg, isoniazid 400 mg and pyrazinamide 1.25 g daily as Rifater® or a placebo. These men have been followed for 4 years since the end of the treatment period. Eleven men who received the combination tablet and 15 men who received the placebo tablet have developed tuberculosis ( χ 2 dfl=0.66, P = 0.4). Conclusion : This multi-drug short course chemoprophylaxis regimen has failed to prevent tuberculosis in miners with silicosis. Even if a larger study had demonstrated a statistically significant effect of the regimen as compared with placebo, the rate of tuberculosis in the men who received the three-drug regimen was unacceptably high.

Setting: A medical facility for approximately 90 000 gold miners employed on 24 South African gold mines. Objective: To establish the long-term risk attributable to silicosis of relapse from pulmonary tuberculosis treated with short-course chemotherapy. Design: A consecutive sample of gold miners with pulmonary tuberculosis allocated to receive rifampicin, isoniazid, pyrazinamide and streptomycin given on weekdays for 5 months. Radiographs were assessed at the time of diagnosis for the presence of silicosis. All of the men were followed for at least 5 years after completing their treatment, or until they left mine service or suffered a relapse of tuberculosis. Results: The sample included 549 men of whom 167 had silicosis. The incidence density for relapse in silicosis was 1.55 (95% CI 0.97, 2.48) times that for the men without silicosis. There was no difference in the pattern of relapse over time between the two groups: the mean period to relapse in the men with silicosis was 2.6 years (SD 1.89 years) and for the men without silicosis was 3.1 years (SD 2.23 years) (P = 0.6). Conclusion: Silicosis causes a small increase in the risk of relapse of tuberculosis. Relapses in both groups were not confined to the first 2 years after completion of treatment.

We conducted a retrospective survey of nocardiosis in 9 city hospitals in northern Italy from 1982 to 1992. The medical records of 30 patients with documented nocardiosis were reviewed. Microbiological data included morphology, biochemical characteristics, serology and in vitro susceptibility testing. The 29 isolates (1 case was diagnosed on the basis of serological results) were Nocardia asteroides (n = 25) and Nocardia farcinica (n = 4). Predisposing factors included immunosuppression for organ transplant rejection prophylaxis, lung disease (silicotuberculosis and pulmonary fibrosis), solid tumours and hematological malignancies, and AIDS. Three patients had no identified risk factors. 20 cases of pulmonary nocardiosis were observed. Sites of infection in patients without previous pulmonary involvement were: brain abscesses, soft tissues, pericardium, blood, and cerebrospinal fluid. Most strains tested were susceptible to amikacin and imipenem. Resistance to several antimicrobial agents was found, parti...

The uses of silica and the potential health hazards for workers or others exposed to dust particles date back thousands of years and are documented. Hippocrates and Pliny both mentioned silica's ability to cause disease and Pliny even described miners who used forms of respiratory protection. The first study of silicosis, in the time of the industrial revolution, was that of Johnstone in 1796 who noted the high mortality of needlepointers at Redditch, England. By 1918, English workers received compensation for disability as a result of silicosis. Silicosis is a pneumoconiosis, but the terms must not be used synonymously. Silicosis, of all the pneumoconioses, has probably claimed the largest number of victims, either alone or in combination with tuberculosis, a condition frequently associated with silicosis. Betts gave the first description of acute silicosis in the United States. In 1932, the American Public Health Association (APHA) developed the definition for the fibrotic lung disease silicosis as A disease due to breathing air containing silica (SiO2), characterized anatomically by generalized fibrotic changes and the development of miliary nodulations in both lungs, and clinically by shortness of breath, decreased chest expansion, lessened capacity for work, absence of fever, increased susceptibility to tuberculosis (some or all of which symptoms may be present) and by characteristic X-ray findings.”. In 1917, Dr. Alice Hamilton described the life of stonecutters in the Barre, Vermont area of the United States. Later the United States Public Health Service studied these workers and issued a report giving preventive measures to combat silicotuberculosis and silicosis resulting from the inhalation of silica-containing dusts for Barre workers and also for other exposed workers. Silica is a natural mineral composed of silicon dioxide, which occurs in either the crystalline or amorphous form. Silica makes up 21% of the earth's crust and is the most common of all chemical compounds. Pure silicon dioxide crystals are found naturally in three polymorphic forms: quartz, the most common; tridymite; and cristobalite. Each of the three is important to human health and make up the crystalline form of silica. Both tridymite and cristobalite appear more fibrogenic than quartz. Silicon dioxide is an acidic oxide, which is practically insoluble in water, but can be attacked by hydrogen fluoride. The amorphous form of silicon dioxide, also called vitreous silica, does not pose a significant threat to human health because it has not been associated with pneumoconiosis. In the few reports that have claimed an association between amorphous silica and disease, the truly amorphous nature of the material has been in doubt. Therefore, for the purposes of this discussion, the review and comments relate to quartz (the most common silicate), which is sometimes called free silica. Human exposures to silica were encountered from the first time man dug into the ground because silica deposits are found in every land mass and stratum from every era and period of geological time. The use of silica in the production of glass probably dates back thousands of years. It is difficult to get accurate figures on the use and production of silica because it is such a universal material and has a multitude of uses. The uses of silica are quite varied and so is the production of silica. Processing operations depend upon the nature of the deposit as well as the desired end product and include crushing, secondary milling to refine particle size, and other methods to further refine the particles. World production was estimated by Davis and Tepordei at 182 million tons in 1983, Asia was the largest producer, followed by Europe, South America, North America, and Africa. This production pattern has been relatively stable for the last 10–15 years. Case reports and surveys by the U.S. Bureau of Mines and the Public Health Service documented the occurrence of pulmonary disease in various worker groups exposed to silica. Public attention was galvanized by the Gauley Bridge (WV) outbreak of acute silicosis among tunnelers of nearby pure quartz. This incident provided an impetus for industrial health reform in the United States and led in 1937 to dust control standards and to the Walsh–Healy legislation. Silicosis rates among granite workers in Vermont decreased dramatically during subsequent decades. From that time to the present, standards have been under continued reevaluation, and decremental changes in permissible exposures to “free” silica dust have reduced but have not eliminated silicosis as a health hazard. Keywords: Silica; Silicon; Nonmining sector; Female workers; Male workers; Exposure assessment; Toxic effects; Cancer; Lung tumor; Amorphous silica; Quartz; Standards; Mica; Pumice; Mining; Portland cement; Standards; non-U.S.

A prospective study of 53,753 coal miners was undertaken at the Instituto Nacional de Silicosis (INS) in Asturias, Spain, during the period 1971 to 1985. This included a complete medical history, physical examination, pulmonary function tests, and intensive search for pulmonary tuberculosis. A total of 1,136 new cases of active pulmonary tuberculosis were found, all of which were confirmed by bacteriology. The average incidence was 150 +/- 31 cases per 100,000 miners year-1. Annual analysis revealed that this figure remained fairly stable during the period of study. Only a reduction of the prevalence in the subgroup of miners with massive pulmonary fibrosis was seen in later years. The risk of tuberculosis among miners was three times greater than that for the general population of the same area. Our inability to reduce the incidence of pulmonary tuberculosis in a large group of coal miners, in spite of the fact that the treatments given were effective and that in the last eight years chemoprophylaxis was given to close contacts, should be emphasized.

Silicoproteinosis is a rare disease, which can cause the rapid onset of respiratory failure following massive exposure to silica dust.A 25-year-old patient presented with altered state and dyspnea. The diagnosis of military pulmonary tuberculosis was first considered and antituberculous treatment was started. The diagnosis was reconsidered due to a lack of improvement and the discovery of an 18-month history of exposure to silica. The patient had stopped work 6 months prior to hospitalization. High-resolution CT showed air space condensation associated to centrilobular nodules throughout the lungs and multiple mediastinal lymph nodes, suggesting sarcoidosis. Bronchoalveolar lavage (BAL) suggested the diagnosis of lipoproteinosis. Because of discordance between the bacteriological, radiological and the BAL results, a surgical lung biopsy was performed which led to the diagnoses of a secondary lipoproteinosis. The diagnosis of silicoproteinosis was then considered. Over a one-year follow up, the patient's respiratory failure has progressed markedly despite treatment with corticosteroids.Silicoproteinosis is a distinct pathological entity, the diagnosis of which depends on clinical and radiological features as well as BAL findings, which may avoid the need for more invasive investigations.

We studied the effect of preliminary loading of peritoneal macrophages with silicium dioxide on in vitro viability, phagocytosis of BCG strain mycobacteria, and the capability to destroy the phagocytosed mycobacterium tuberculosis. It was shown that preliminary loading of macrophages with silicium dioxide did not reduce their viability and stimulated phagocytosis of BCG strain mycobacteria, but reduced their antibacterial activity.

For better or for worse, the date 31 May will remain embedded in the annals of South African history. On this date in 1902 the second Anglo-Boer War officially ended, and in 1910 the four British colonies of the Cape of Good Hope, Natal, Transvaal and the Orange Free State united to form a single country under British dominion. Bar this event, these colonies would have traversed separate historical trajectories eventually leading to four independent sovereign states. Ironically, the name South Africa (and the ZA international country code) harks back to Paul Kruger's Zuid-Afrikaanse Republiek, itself an amalgamation of several tiny Afrikaner republics in the territory that came to be known as the Transvaal. Finally, on 31 May 1961, South Africa was declared a republic, with Hendrik Verwoerd exulting 'God regeer!' (God reigns!).

Background South Africa has the third highest annual number of new tuberculosis (TB) cases globally. The resurgence of TB which has particularly affected gold miners in South Africa, is attributed to occupational risk factors for TB including silica dust exposure and high HIV prevalence. Isoniazid preventive therapy (IPT) is recommended for individuals at high risk to prevent both HIV-related TB and silicotuberculosis, but global uptake has been poor. We describe the design of a cluster randomised study, “Thibela TB”, which compares routine IPT targeted to those identified as at higher risk of TB (due to HIV infection or silicosis) against a “community-wide” approach in which IPT is offered to all employees. The trial is registered with the Current Controlled Trials: Registration number ISRCTN63327174. Methods We describe the rationale for the intervention of community-wide IPT, drawing on studies conducted in 1950–1960s in the pre-HIV era. The design of the study, including the definition of the cluster, is presented and advantages and limitations of such a design are discussed. Conclusion If successful in reducing TB incidence and prevalence, this trial has potential to make a major contribution to TB control policy in high HIV settings, providing evidence concerning efficacy, and additionally safety and population-level effects on drug susceptibility patterns. Such rigorous evaluation is essential to provide policy makers with an evidence base to guide community-level TB prevention strategies.

Silicosis is the most common occupational lung disease worldwide. It leads to respiratory impairment and may have associated infections that decrease pulmonary function. We describe the case of a 55-year-old man with chronic silicosis who presented with hemoptysis and a cavitated conglomerate mass. The final diagnosis was silicotuberculosis.

The authors revealed features of clinical course and outcomes in patients with silicosis and silicotuberculosis, who worked on iron industry enterprise. The article covers comparative analysis of survival rate and mortality among silicosis patients over 14 years of observation.

Erasmus' syndrome involves the association of systemic scleroderma (SS) and exposure to silica. Silicosis may precede the SS but the latter may be the presentation, in which case a history of exposure to silica should be sought as part of the diagnosis.A 46-year-old man with history of pulmonary tuberculosis presented with dyspnoea and dysphagea. Clinical examination revealed thickening of the facial skin with a pointed nose, erythema and telangiectasia, Raynaud's syndrome and sclerodactyly. A thoracic CT scan revealed bilateral, fibrotic, pseudo-tumoural masses. Antinuclear antibodies, anti-topoisomerase 1 and antihistone were positive.The clinical presentation of Erasmus' syndrome associating systemic scleroderma and pulmonary pseudo-tumours may pose a problem of differential diagnosis from lung cancer. This condition requires regular clinical and radiological monitoring, particularly as both scleroderma and silicosis increase the risk of lung cancer.

Silicotuberculosis is an independent disease that arising in patients with silicosis from exacerbation of old tuberculous foci in the lung, less frequently in the lymph nodes and other organs. In silicotiberculosis, there are common secondary tuberculosis forms that are located mainly in the lung, which are rarely accompanied by a rapid progression. Characteristic morphological signs of early, nodal and nodular silicosis are observed. Silicotuberculosis is an independent disease that arises in patients from an exacerbation of old tuberculous foci in the lung, less frequently in the lymph nodes and other organs. In silicotuberculosis, there are usually secondary tuberculosis forms that are located mainly in the lung, which are rarely accompanied by a rapid progression. The characteristic morphological signs of early, nodal, and nodular silicosis are observed. Thoracic and abdominal lymph nodes, lymphatic and blood vessels, the bronchi and pulmonary surfactant system were explored. In silicosis, tuberculosis, and silicotuberculosis, silicon levels and spodograms of some visceral organs were studied and trace elements were determined in the lung.

A 68-year-old man who had worked as a stone mason for more than 50 years with a heavy smoking history consulted our clinic with symptoms of cough, low grade fever, weightloss, malaise and a single expectoration of hemo-sputum. He had been diagnosed as silicosis by the mass survey 5 years ago based on nodular shadows with egg-shell calcification in hilar lymphnodes on his chest radiography, and has received chest radiographic examination once a year. As the author was not so familiar with the radiographic features of silicotuberculosis, it was difficult to interprete ill-defined contour of silicotic nodules accompanied by patchy opacities formation in right midlung field and silicotic conglomeration accompanied by an ischemic cavity in the left basal segments. A definitive diagnosis could not be established until 10 months later when a second attack of exacerbation of silicotuberculosis occurred showing multiple thin walled fresh tuberculous cavities on the chest radiography with positive smear and culture. Among multiple tuberculous cavities, there was a cirrhotic-walled cavity caused by endogenous reactivation of a quiescent tuberculous lesion on the right apex. This lesion was considered to be the source of dissemination of this case. Finally, it took about two and a half years before establishing the diagnosis in this case because of a series of doctors delays. He was treated successfully with antituberculous drugs for one and a half years including one year rifampicin medication. The clinico-pathological findings of silicotic conglomeration in the left basal segments were discussed based on the findings of transbronchial biopsy from occluded B10 and chest radiographic findings, and it was revealed that silicotic conglomeration might consist of inflammatory granulation combined with granulomatous tubercle, but not a fibrous lesion.

The study has defined criteria for the concomitant development of tuberculosis as secondary to silicosis. Factorial and discriminant analyses identified the most significant factors of immune homeostasis in silicotuberculosis. The major signs of possible development of tuberculosis in the presence of silicosis are the elevated levels of total IgE and IgG, fibronectin; the cells expressing CD4+ and CD20+ markers; and the decreased concentration of the mucinic antigen 3EG5. The findings were used to construct models of immunity in tuberculosis, silicosis, and silicotuberculosis. The use of a complex of immunological studies promoted the better early diagnosis of silicotuberculosis.

To study the gene mutation and streptomycin, isoniazid or rifampicin resistance of Mycobacterium isolated from silico-tuberculosis patient's sputum so as to find a more effective therapy for this disease.Mycobacteria tuberculosis were separated from 96 coal worker with silico-tuberculosis firstly. Then rpsL, KatG and rpoB fragments of genome were copied with PCR and compared their SSCP profiles with standard strains.67 strains of streptomycin, isoniazid or rifampicin resistant Mycobacteria tuberculosis were found in routine drug resistance test, with the percentages of 80.5% (54/67), 58.2% (39/67) respectively. PCR-SSCP showed that out of 67 drug-resistant strains, 66(98.5%) of rpsL, 47(70.1%) of rpoB and 42(62.7%) of KatG appeared abnormal.Most of the resistant strains appeared gene mutation. The mution rates were higher than the results from routine drug resistance test.

The present cross sectional study was carried out among 134 ex-workers from quartz stone crushing units. Using the interview technique as a tool for data collection, demographic and occupational details of the subjects were recorded on the predesigned proforma. Standard diagnostic criteria were used for diagnosing silicosis and silico-tuberculosis. The pulmonary functions of the subjects were measured with Spirovit SP-10. The mean age of the males was found to be 33.18 +/- 10.39 yr and that of the females was 30.10 +/- 9.3 yr and for the whole group was 31.77 +/- 9.99 yr. Mean duration of exposure was 2.74 +/- 1.65 yr. The study variables included age, sex, duration of exposure, smoking and respiratory morbidity. Forced Vital Capacity (FVC) which suggests lung parenchymal disorders was found to be significantly reduced with female sex, presence of smoking, increasing duration of exposure and presence of pneumoconiosis, whereas the lung function parameters indicating the status of airways were found to be significantly reduced with all the factors. Therefore, it was concluded that quartz stone workers exposed to approximately 100% free silica had deteriorated lung function which can be attributed mainly to respiratory disorders along with other epidemiological factors such as age, sex, duration of exposure and smoking.