Text prepared by Tee L. Guidotti and Niels Koehncke

University of Alberta

Edmonton, Alberta, Canada

25 November 1998




2 Silicosis remains the most prevalent occupational lung disease worldwide, especially in the developing world. However, the problem has not been completely solved in the fully industrialized world, either.


The problem


Exposure to crystalline silica as particles in the workplace remains an important public health concern worldwide (1,2). The biggest problem is in the developing world, especiall where rapid economic growth is occurring (3). Silica exposure itself, apart from or related to silicosis, can cause a variety of other health problems (3).

3 Any occupation, which disturbs, cuts, crushes or otherwise processes silica-containing rock can be considered to carry a potential risk for inhalation of silica particles (4). Mining, drilling, sandblasting, stone carving, knife grinding, glass manufacture, quarries and foundry work are all examples of occupations associated with risk of silica dust exposure. The probability of contracting a pneumoconiosis from this exposure depends on a complex interaction of many factors, both environmental and intrinsic to the individual (5). Different rates and volumes of respiration, personal characteristics, genetic susceptibility, and compromised host defenses on an acquired basis may all play a role in determining why some people in the workplace may develop silicosis and others may not. However, the most important factor by far, and the only factor amenable to control, is dust exposure.

4 The leading silica-related diseases of concern are silicosis, accelerated silicosis, acute silicosis (silica-induced alveolar proteinosis), silicotuberculosis, silica-associated lung cancer, systemic sclerosis and other silica-related immunopathies, silica related nephropathy, and chronic airflow obstruction usually comparable to that seen with smoking (1,2,6,7,8,9).

5 The primary determinants of silica toxicity are concentration and duration of dust exposure, particle size distribution, the crystalline isomorph (alpha-quartz, tridymite, cristobalite, in increasing order of potency), and the presence of a freshly fractured surface. Particles of about 5 : m or less in aerodynamic diameter penetrate to the small airways and alveoli and are then available for phagocytosis by macrophages, resulting in induction of an acute alveolitis and subsequent fibrosis. If the particle is fresh (fractured within 6 hours or less) or has adsorbed materials on the surface, toxicity may be greatly increased. Amorphous silica such as glass and fibrous glass is not so fibrogenic, but some forms of amorphous silica, such as diatomaceous earth and the biogenic silica formed in rice stalks and released by burning, contain enough crystalline silica to be occupational hazards.




6 Once inhalation of silica particles has occurred, the small particles penetrate to the lower respiratory tract. Here they can initially cause acute toxicity to macrophages and damage to other cells, such as Type 1 epithelium cells, in the lung. It is thought that the surface characteristics of the silica particle are responsible for the extreme toxicity of the dust. The fact that freshly crushed or fractured silica particles are much more potent in inducing inflammation and killing cells than silica particles that have aged in air for a time is further evidence that surface characteristics are important.

The silica particles are quickly ingested by macrophages into phagosomes, which then interact with lysosomes releasing proteolytic enzymes cytokines (mostly IL-1, IGF-1, PDGF, TNF-" ) and oxygen radicals (10,11,12,13,14). This massive release of lysosomal contents eventually may result in death of the cell and considerable inflammation in the form of lymphocyte and granulocyte recruitment and T-helper cell proliferation. Some macrophages maintain viability but become activated to produce these inflammatory mediators, initiating the disease process (15,16). Eventually, local fibrosis occurs with elaboration of collagen and fibronectin. Furthermore, this local reaction can secondarily cause altered antigenicity of self-proteins as well as immunoglobulin accumulation (B-cell activation).

7 While these early stages of inflammation may result in acute silicosis, characteristically they tend to produce an alveolitis which is the first stage of chronic silicosis. Brochoalveolar lavage at this stage demonstrates the presence of granulocytes, immunoglobulins, and type 2 pneumocytes. As collagen fibers are continually laid down in concentric fashion they eventually form the characteristic lesion of silicosis, the well-circumscribed silicotic nodule in the later stages (17). By this stage a chronic inflammatory response has set in and opacities become visible on the chest film. The silicotic nodule is a compact spherical structure which aggregates until it becomes radiologically visible and which projects on the chest film as a rounded opacity (characteristically visible in the upper lung fields). The later stages of silicosis then may involve infection with Mycobacterium tuberculosis, atypical mycobacteria, fungi, and Acinetobacter spp, greatly complicating the diagnosis and management and accelerating the fibrotic process. Carcinogenicity, nephritis, and systemic sclerosis may also emerge as features of silicosis in some cases, to be discussed later in this article.

8 Eventually, increased parenchymal fibrosis and inflammation result in effacement of pulmonary vasculature, increased pulmonary arterial pressure, fixed pulmonary hypertension, right heart strain and cor pulmonale. These are very late outcomes of severe restrictive nodular silicosis. They are currently rare in the developed world but remain depressingly common in the developing world.


Silicosis and the Fibrotic Response


9 Silicosis can be characterized by radiological stages. There is a standard radiological system, the ILO Classification of the Pneumoconioses, that classifies these changes on a semi-quantitative basis.



Simple Silicosis


10 Simple silicosis is characterized by isolated rounded opacities, usually first visible in the upper lung fields. This may be associated with hypertrophy of the hilar lymph nodes. At times, the lymph node hypertrophy can be extreme. Rare cases may resemble sarcoidosis and may not show parenchymal opacities on the chest film at all. In these cases, the diagnosis must be made by biopsy. More often, the chest film is characterized by an appearance resembling miliary tuberculosis or sarcoidosis (with which it is frequently confused), gradually increasing in density and dispersion among the lung fields. As well, there is often a thin dense ring of calcification around the lymph nodes – the so-called “egg shell calcification” characteristic of silicosis and only rarely seen in other conditions such as sarcoidosis. Progression of the disease is associated with increases in the size and number of opacities.


Chronic Nodular Silicosis


11 In complicated silicosis, which is often called “conglomerative” or “chronic nodular silicosis”, the silicotic nodules coalesce into a fibrotic mass and a confluence of opacities on the chest film (“progressive massive fibrosis”). This leads to contraction of the upper lobes, traction emphysema and bullae. This often has the appearance of an “angel wing pattern” on the chest film, due to the dense bilateral crescentic shape that has reminded radiographers of an angel of death because it is a poor prognostic sign. Clinically, this massive fibrotic reaction in the lungs leads to dyspnea and progressive restrictive disease. Often, however, there may also be a concealed obstructive component reflecting some underlying emphysema or COPD. Unlike asbestosis, there are few physical signs that accompany even advanced silicosis; rales and clubbing are generally absent.

Chronic nodular silicosis, as mentioned above, is the advancement of the restrictive disease due to the progression of fibrotic nodules and associated clinically with progressive dyspnea. Ultimately, respiratory failure results because of the ventilatory defect. Right heart failure (cor pulmonale) may result if extensive emphysema and bullous disease is present. Eventually, the outcome of advanced conglomerative silicosis is respiratory failure and cardiopulmonary arrest if the disease continues to progress. Complications of chronic nodular silicosis may include superinfection with tuberculosis (silicotuberculosis) or atypical mycobacterial, other opportunistic infections (see below), pneumothorax (secondary to extensive fibrosis and bullae), systemic sclerosis in most of its forms (scleroderma and kidney disease) and rheumatoid nodules (as in Caplan’s syndrome).


Accelerated Silicosis


12 Accelerated silicosis is a very rare, diffuse, rapidly progressive form of nodular silicosis that arises from intense short term exposure to silica particles. Progressive massive fibrosis is seen more frequently in this condition and develops at a much faster rate. The disease is usually fatal within several years (18).


Acute Silicosis


13 In acute silicosis, the alveolitis that occurs early in the disease due to silica exposure predominates in the clinical picture and patients rarely survive to progress to more chronic forms. 14 Acute silicosis, or silica-induced alveolar proteinosis, is associated with massive outpouring of proteinaceous debris and fluid into alveolar spaces, presumably as a consequence of acute inflammation and diffuse alveolar injury. It occurs with short term exposures to very high concentrations of silica dust (4). The chest film appears much like a slowly evolving pulmonary edema or adult respiratory distress syndrome but without any other obvious precipitating cause. Acute silicosis may respond to lavage and administration of high dose steroids, but the prognosis is generally fatal. Respiratory failure eventually becomes untreatable due to continued accumulation of debris and lipoproteinaceous material in the airspaces (9). Occasionally acute silicosis is complicated by opportunistic infection by nocardia, fungi, and mycobacteria. Acute silicosis has sometimes caused multiple deaths among workers who have been heavily exposed at the same site. In view of the extremely poor prognosis and tendency for this form of silicosis to be seen in young workers, one must consider transplantation, whole lung lavage and other heroic measures if they are available.


Silicotuberculosis and Opportunistic Infections


15 Studies have demonstrated that patients with silicosis have a greatly increased risk of developing and dying from tuberculosis (6,19,21,22,23). Significantly higher mortality from tuberculosis associated with silicosis has been documented in the United States, even recently (20).  16 The diagnosis of silicotuberculosis is suggested when there is a change in the rate of progression of silicotic nodules on the chest film so that the disease appears to be developing much more rapidly, or when there is onset of systemic symptoms such as fever, weight loss or new cough (especially hemoptysis). The infection tends to favor upper lobes and may develop early when fibrosis is not far advanced. The recovery of acid-fast bacilli from sputum may be difficult because the mycobacteria burden is much less than in other forms of tuberculosis. Repeated sputum induction and even gastric washings may be required if the diagnosis is strongly suspected. While Mycobacterium tuberculosis is the most common organism, atypical mycobacteria are becoming increasingly common (Mycobacterium kansasii, Mycobacterium avium-intracellulare) (24). Silicotuberculosis usually represents reactivation of old disease, not primary infection.

Silicotuberculosis tends to be refractory to treatment due to poor penetration into the fibrotic mass by antibiotics. Often, patients require life-long suppression using triple therapy. With the introduction of rifampin, however, some short course regimes have been successful in treating silicosis-associated tuberculosis (25,26)

Other opportunistic infections are relatively uncommon. Presumably they result from a primary infection establishing a nidus in compromised lung tissue. Acinetobacter spp. resulting in cavitation and abscess formation has been described in several foundry workers. Deep fungal infections (aspergillosis, cryptococcosis, sporotrichosis, and nocardiosis) have also been described.



Systemic Sclerosis (Scleroderma)


17 Silica exposure is also associated with systemic sclerosis (scleroderma) and its many manifestations. This syndrome usually occurs in a worker with radiologically obvious silicosis.

18 The association of sclerodactyly or systemic sclerosis with “dusty trades” or silicosis has been described in the past (27,28). Systemic sclerosis is a generalized disorder of connective tissues and small blood vessels, thought to be the result of an autoimmune process. Scleroderma is the characteristic pattern of changes seen in the skin, particularly over the digits and face. Raynaud’s phenomenon is the demonstration of vasoconstriction and subsequent ischemia in the fingers induced by cold stress and is characteristic of patients with systemic sclerosis. CREST syndrome is derived from the acronym for “calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia”, all individual cardinal features of systemic sclerosis and constituting a syndrome when they occur together; when this occurs, there is a particular risk of renal involvement and progressive renal failure. “Erasmus syndrome”, a common term in the French literature, is systemic sclerosis in association with silica exposure.

19 The diagnosis of systemic sclerosis must meet the major criterion and two out of three minor criteria as established by the American Rheumatism Association. Major criterion (required): typical sclerodermatous skin changes (tightness, thickening and nonpitting induration, exclude local forms of scleroderma) involving areas proximal to the metacarpophalangeal or metatarsophalangeal joints, affecting other parts of extremities, face, neck, or trunk (thorax or abdomen); usually bilateral, symmetrical, and almost always including similar changes in the digits (fingers and toes, sclerodactyly).

Minor criteria (two out of three required): 1) Sclerodactyly (sclerodermatous skin changes as described above limited to the digits). 2) Digital pitting scars or loss of substance (tissue) from finger pad (depressed areas at tip of digits or loss of digital pad tissue as a result of digital ischemia rather than trauma or exogenous causes). 3) Bibasilar pulmonary fibrosis (bilateral reticular pattern of linear or lineoreticular densities which are most pronounced in basilar portions of the lungs on standard chest roentgenogram) which may assume the appearance of diffuse mottling or “honeycomb lung” and should not be attributed to primary lung disease.

The prognosis for systemic sclerosis associated with silica exposure (Eramus syndrome) appears to be the same as for other forms of systemic sclerosis. One study demonstrated that “silica-associated systemic sclerosis is clinically, serologically and immunologically indistinguishable from idiopathic systemic sclerosis (29). The prognosis is therefore highly variable, ranging from mild disease and slow progression with minimal disability (usually because of painful Raynaud’s phenomenon) to rapid progression and death when there is extensive involvement of kidney, lung or heart.


Silica-Associated Lung Cancer

20 Lung cancer may appear against a background of preexisting silicosis. However, lung cancer may also occur in persons exposed to silica in the absence of silicosis. As always, the question is whether the cancer is related to the underlying fibrotic disease, in this case silicosis.

21 Available data support the conclusion that silicosis produces increased risk for lung cancer and that the association between silica exposure and lung cancer is causal. Furthermore, it appears that the direct and cumulative effect of silica exposure, rather than the development of silicosis, is responsible for the increased risk of lung cancer (31,32,33). The International Agency for Research on Cancer (IARC, 1987) has accepted silica as a Class 1 human carcinogen and a definite animal carcinogen. Animal studies have generally required long survival times to demonstrate this effect. To date, there has been no suggestion that silica-associated lung cancer is different in presentation, distribution of histological type, responsiveness to treatment, or prognosis from lung cancer in general. Some studies have shown an interactive risk with cigarette smoking, and identification of cancer by periodic screening by either chest film or sputum cytology has not been shown to increase survival or improve prognosis.



Other Associations


22 Other disorders associated with silica exposure have included chronic nephritis (34), silica nephropathy (glomerulonephritis associated with intense exposure) (35), and airways disease. Less common autoimmune conditions have also been associated with silica exposure (2).


Surveillance of Silica-Exposed Workers


23 A thorough occupational history will almost always identify workers at risk of silica dust exposure. Interim symptom histories are usually too insensitive and nonspecific to be of much value in following groups of silica-exposed workers. A chest x-ray is the essential surveillance modality; while not very sensitive it can be very specific in the presence of an occupational history limited to significant silica exposure. Radiographic appearance of early silicosis (discussed previously) is characteristic, and that of late stage silicosis is often pathognomonic. [Table 1 is provided at the end of this text to provide guidance to answer inquiries about recommended surveillance.]

Pulmonary function tests may show early small airways disease, presumably because of a bronchitic component associated with irritation from the dust. Later, restrictive changes predominate as fibrosis develops. The presence of extensive emphysema may result in mixed restrictive and obstructive components, with restrictive changes usually predominating. Diffusion capacity becomes abnormal as destruction of parenchyma affects the pulmonary vascular bed. Diffusion capacity is more useful in following patients with silicosis than as a screening tool, however.

Finally, CT scans, MRIs, and other specialized imaging techniques are almost never required to make the diagnosis of silicosis and have no place in a screening program. One important point to bear in mind is that with gradual declining incidence of the disease (and hence reduced prevalence), the screening programs become less effective and risks of misdiagnosis are increased. This is becoming a serious problem in developed countries where silicosis is increasingly rare and physicians tend to forget about it.

Silicosis is most likely to be mistaken form sarcoidosis, other pneumoconioses, or miliary tuberculosis. Even at a Canadian institution with a high level of awareness there has been one case of a 49-year old man who worked as a sandblaster in his native Chile prior to emigrating to Canada. When a diffuse fibrotic process was discovered on a screening chest film, it was initially suspected to be sarcoidosis because silicosis has been rare in the province of Alberta since the 1970’s. Once a biopsy was performed, the process was identified as silicotuberculosis. Ideally, such invasive procedures should not be necessary to make this diagnosis.


Management of Silicosis


24 As there is no specific treatment for silicosis, management generally involves delaying progression and providing supportive care. Removal from exposure is the obvious first step. While removal from exposure does not necessarily stop the gradual progression of simple silicosis, faster progression of the disease is less likely and less severe when it occurs if exposure to silica dust ceases (17). Oxygen supplementation (if necessary), smoking cessation, and surveillance for infection (with early treatment if detected) are also important components of management. Cor pulmonale can be alleviated by preload reduction (diuresis) but is not responsive to digoxin or direct measures to reverse pulmonary hypertension. Several therapeutic interventions have been attempted to halt or reverse the fibrotic process such as aluminum powder, d-penicillamine, polyvinyl pyridine-N-oxide (PPNO) and tetrandine. The Chinese herbal extract tetrandine is in early clinical trials to assess its ability to slow progression of silicosis. Unfortunately none have shown striking success, although Chinese studies suggest that in combination they may retard progression of the disease. PPNO has shown encouraging results in animal studies but has also been demonstrated to be carcinogenic in animal studies.  25 Future directions for management options may include cytokine inhibitors, modulators of collagen biosynthesis, and antioxidant treatment (acutely) (36).  26 Nothing on the horizon promises to cure silicosis. Once it begins, silicosis is incurable.


Impairment Evaluation in Silicosis


27 Documentation of exposure opportunity is the first step in impairment evaluation. This involves a detailed occupational history and, if possible, exposure assessment of the workplace. The presence of a possibly silica-associated condition must then be established by a compatible history and physical examination, along with appropriate laboratory and imaging techniques (always including a chest x-ray). Establishment of probable causation is concluded by demonstrating that the clinical presentation is consistent in a workplace setting involving exposure to airborne silica; a biopsy is not necessary. Finally, an impairment assessment is made.

In North America, the most common impairment rating system is the American Medical Association’s Guides to the Evaluation of Permanent Impairment.

The AMA Guides are a useful way to classify impairment. The lowest pulmonary function measurement defines the class. Assessing a percentage of impairment within the class is a judgement, taking into account nonoccupational conditions that are present in the same worker, factors affecting these tests other than respiratory disease (such as obesity), and the worker’s ability to function. The impairment rating (class or specific percentage) is used by many insurance companies and workers’ compensation systems to calculate disability. Disability is an estimate of how badly reduced is the worker’s ability to work at their occupation and to earn a living, given the degree of functional impairment. It is the basis for pension, benefits to make up for lost wages and other forms of compensation in these systems. [Table 2 is provided at the end the text because it is too complicated for a slide. It can be used to answer questions.]




28 There are a few simple take-home messages from this presentation:

Support the elimination of silicosis by educating workers and employers and by advocating measures to control exposure to silica dust.



29 This program was developed for you by the International Commission on Occupational Health, the international, interdisciplinary organization of occupational health professionals.

Table 1

Surveillance of Silica-Exposed Workers




The baseline medical surveillance examination for silica-exposed workers should include the following (9):


    1. History
    2. Physical examination
    3. Pulmonary function testing
    4. Chest film
    5. Urinalysis


Annual examinations should be done thereafter, including the following (9):


1) Repeat questionnaire (utility of this debatable, however)

2) Spirometry

3) Chest filme (see below)

4) further testing as indicated (e.g. urinalysis


Chest X-ray Schedule for Silica-Exposed Workers (9)


Exposure Duration Age X-ray Schedule


< 10 yrs all ages every 5 years

> 10 yrs < 35 every 5 years

> 10 yrs 35-44 every 2 years

> 10 yrs > 45 every year




Table 2

Classes of Respiratory Impairment from the AMA Guides to the Evaluation of Permanent Impairment


Pulmonary Function Measurement* Class 1:

0%, no impairment of the whole person

Class 2:

10-25%, mild impairment of the whole person

Class 3:

26-50%, moderate impairment of the whole person

Class 4:

51-100%, severe impairment of the whole person















VO2 Max**


FVC$ 80% of predicted;



FEV1/FVC $ 70%





DCO $ 70% of predicted.



>25 mL/(kg min);




7.1 METS


FVC between

60% and 79%

of predicted;


FEV1 between

60% and 79% of predicted;


DCO between 60% and 69% of predicted.



20 and 25 mL/kg min);


5.7-7.1 METS


FVC between

51% and 59% of predicted;


FEV1 between 41% and 59% predicted;



DCO between 41% and 59% of predicted.


Between 15 and 20 mL/(kg min);


4.3-5.7 METS




FVC # 50% of predicted;



FEV1 # 40% of predicted;




DCO # 40% of predicted.



<15 mL/(kg min);



< L/min; or <4.3 METS


* FVC = forced vital capacity, FEV1 = forced expiratory volume in the first second,

DCO = diffusing capacity of carbon monoxide. The DCO is primarily of value for persons with restrictive lung disease.

In classes 2 and 3, if the FVC, FEV1 and FEV1/FVC ratio are normal and the DCO is between 41% and 79%, then an exercise test is required.


** VO2 Max, or measured exercise capacity, is useful in assessing whether a person’s complaint of dyspnea (see Table 1) is a result of respiratory or other conditions. A person’s cardiac and conditioning status must be considered in performing the test and in interpreting the results.




NOTES: Two important caveats apply to silicosis:


  1. “In evaluating the cause of abnormality in any of the listed measures, the physician should consider the possible contribition of extrapulmonary factors to respiratory system impairment. For example, obesity may decrease the forced vital capacity, and anemia may decrease the DLCO. However, only pulmonary dysfunction should be considered in evaluating impairment according to Table 8... Impairment of other organ systems may be evaluated according to the criteria given in other Guides chapters and then combined with the respiratory system impairment...”

    [Note: In the AMA Guides, individual impairments may be added sequentially or “combined” by a formula that reflects relative contribution to impairment of the total person.]




  3. “It is important to recognize that such conditions as asthma, hypersensitivity pneumonitis, and pneumoconiosis may require that the individual refrain from working in a specific occupational setting where he or she is exposed to the offending agent. This does not necessarily indicate that the individual has permanent pulmonary impairment in occupational settings other than those causing the abnormality.”






Disk #33: Silica Document





  1. Banks D, Balaan M, Wang M. Silicosis in the 1990s, revisited. Chest 1997; 11(4): 837-838.

  3. Steeland K, Goldsmith D. Silica exposure and autoimmune diseases. Am J Ind Med 1995; 28:603-608.

  5. International Agency for Research on Cancer. Silica, some silicates, coal dust and para-aramid fibrils. Vol. 8 of: IARC Monographs on the Evaluation of Carcinogenic Risks of Humans. Lyon, IARC, 1997.

  7. Beckett W et al. Adverse Effects of crystalline silica exposure. Am J Respir Crit Care Med 1997; 155:761-765

  9. Polzik E.V. et al. The principles of predicting the individual risk of silicosis and silicotuberculosis. Med Lav 1990; 81(2):87-95.

  11. Cowie R. The epidemiology of tuberculosis in gold miners with silicosis. Am J Respir Crit Care Med 1994; 150:1460-1462.

  13. Weill H, McDonald JC. Exposure to crystalline silica and risk of lung cancer: the epidemiological evidence. Thorax 1996; 51:97-102.

  15. Roseman K et al. Silicosis in the 1990s. Chest 1997; 111:779-786.

  17. Donaldson K, Borm PJA. The quartz hazard: A variable entity. Ann Occ Hyg 1998; 42(5):287-294.

  19. Davis GS. Pathogenesis of silicosis: current concepts and hypothesis. Lung 1986; 164:139-154.

  21. Lugano EM, Dauber JH, Daniele RP. Acute experimental silicosis. Am J Pathol 1982; 109:27-36.

  23. Adamson I, Bowden DH. Role of polymorphonuclear leukocytes in silica-induced pulmonary fibrosis. Am J Pathol 1984; 117:37-43.

  25. Dubois CM et al. Asbestos fibers and silica particles stimulate rat alveolar macrophages to release tumor necrosis factor. Am Rev Repir Dis 1969; 139:1257-1264.

  27. Gupta GS, Kaw JL. Formation of lipid peroxides in the subcellular fractions of silicotic lung in rats. Eur J Respir Dis 1993; 49:163-166.

  29. Davis GS. The pathogenesis of silicosis. Chest 1986; 89:166S-169S.

  31. Bowden DH, Adamson IYR. The role of cell injury and the continuing inflammatory response in the generation of silicotic pulmonary fibrosis. J Pathol 1984; 144:149-161.

  33. Zenz, C. Occupational Medicine, 3rd ed. Mosby-Year Book, Inc. 1994.

  35. LaDou J. Occupational & Environmental Medicine, 2nd ed. Appleton & Lange, 1997.

  37. Sherson D, Lander F. Morbidity of pulmonary tuberculosis among silicotic and nonsilicotic foundry workers in Denmark. J Occup Med 1990; 2:110-113.

  39. Althouse R et al. Tuberculosis comortality with silicosis: United States, 1979-1991. Appl Occup Environ Hyg 1995; 10:1037-1041.
  40. Sherwin RP et al. Silicate pneumoconiosis of farm workers. Lab Invest 1979; 40:576-582.

  42. Watkins-Pitchford W. The silicosis of the South African gold mines and the changes produced in it by legislative and administrative effort. J Ind Hyg 1927; 9:109-139.

  44. Gordon D. Dust and history. Med J Austral 1954; 2:161-166.

  46. Bailey WC et al. Silicomycobacterial disease in sandblasters. Am Rev Respir Dis 1974; 110:115-125.

  48. Lin TP et al. Short-course chemotherapy for pulmonary tuberculosis in pneumonconiotic patients. Am Rev Respir Dis 1987; 136:808-810.

  50. Cowie RL. Silicotuberculosis: long term outcome after short course chemotherapy. Tuber Lung Dis 1995; 76:39-42.

  52. Erasmus LD. Scleroderma in gold-miners on the Witwatersrand with particular reference to pulmonary manifestations. S Afr J Lab Clin Med 1957; 3:209-231.

  54. Rodnan GP et al. The association of progressive systemic sclerosis (scleroderma) with coal miners’ pneumonconiosis and other forms of silicosis. Ann Intern Med. 1967; 66:323-334.

  56. Rustin MHA et al. Silica-associated systemic sclerosis is clinically, serologically and immunologically indistinguishable from idiopathic systemic sclerosis. Br J Dermatol. 1990; 123:725-734.

  58. Smith et al. Meta-analysis of studies of lung cancer among silicotics. Epidemiol 1995; 617-624.

  60. Checkoway H et al. Dose-response associations of silica with nonmalignant respiratory disease and lung cancer mortality in the diatomaceous earth industry. Am J Epidemiol 1997; 145:680-8.

  62. Hua F et al. Lung cancer among tin miners in southeast China: Silica exposure, silicosis, and cigarette smoking. Am J Ind Med 1994; 26:373-381.

  64. Guidotti T. Silica exposure and risk of lung cancer: Pathophysiological hypothesis in research amenable to testing by epidemiological methods. Appl Occup Environ Hyg 1995; 10(12):1075-1080.

  66. Collis EL, Yule GU. The mortality experience of an occupational group exposed to silica dust, compared with that of the general population and an occupational group exposed to dust not containing silica. J Ind Hyg 1933; 15:395-417.

  68. Banks DE et al. Silicon nephropathy mimicking Fabry’s disease. Am J Nephrol 1983; 3:279-284.

  70. Goldstein RH, Fine A. Potential theraputic initiatives for fibrogenic lung diseases. Chest 1995; 108:848-55.






N indicates a slide change to slide number N.


This test can be read but it is more effective if you use your own words (but be careful of the terminology).


Comments that are for you only and are not intended to be read are enclosed in brackets.


Tables 1 and 2 can be copied and used as handouts if there is a need, but they will only be useful to physicians and nurses who expect routinely to perform surveillance and impairment assessment on silica-exposed workers. Health professionals who do not follow silica-exposed workers and who are more likely to see a case once silicosis has already begun will have little need for these tables.


Please do not stop on slide #28. Many people have worked hard on this project and the groups that support it deserve recognition. Please show slide #29.













  1. Title Slide
  2. Introduction
  3. Silica Exposure
  4. Silica-Related Disease
  5. Determinants of Silica Toxicity
  6. Pathophysiology of Silicosis
  7. Outcomes of the Process
  8. Complications of the Process
  9. Radiologic Presentations of Silicosis
  10. Simple Silicosis (Chest film)
  11. Chronic Nodular Silicosis (Chest film)
  12. Accelerated Silicosis (Chest film)
  13. Acute Silicosis (Chest film)
  14. Acute Silicosis
  15. Silicotuberculosis (Chest film)
  16. Silicotuberculosis
  17. Systemic Sclerosis (Chest film)
  18. Systemic Sclerosis
  19. Diagnostic Criteria for Systemic Sclerosis
  20. Silica-Associated Lung Cancer (Chest film)
  21. Silica-Associated Lung Cancer
  22. Other Silica-Associated Diseases
  23. Surveillance of Silica-Exposed Workers
  24. Conventional Management of Silicosis
  25. Future Directions in Management of Silicosis
  26. Silicosis is Incurable
  27. Impairment Evaluation in Silicosis
  28. Messages to Take Home
  29. Credits

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