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Silicosis and Screening

1-Introduction :
Pneumoconioses :
Parenchymal lung diseases due to chronic inhalation of inorganic (mineral) dusts are called pneumoconioses. Certain inorganic dusts, such as those containing silica, coal, asbestos, or beryllium, are fibrogenic. Rarely, hard metals and aluminum dust are associated with diffuse pulmonary fibrosis; clinical, x-ray, and physiologic changes resemble those in other diseases caused by dust inhalation and characterized by diffuse pulmonary fibrosis.
Several inert dusts, including iron oxide, barium, and tin, are non fibrogenic and can produce conditions known as siderosis, baritosis, and stannosis, respectively. The abnormal x-rays in these conditions reflect the radio dense appearance of the deposited materials and do not indicate disease because there are no symptoms or functional impairment.
Silicosis :
Silicosis is a pneumoconiosis usually caused by inhaling crystalline free silica (silicon dioxide, quartz) dust and characterized by discrete nodular pulmonary fibrosis and, in more advanced stages, by conglomerate fibrosis and respiratory impairment. Silicosis, one of the oldest occupational diseases, still kills thousands of people every year, everywhere in the world. It is an incurable lung disease caused by inhalation of dust containing free crystalline silica. It is irreversible and, moreover, the disease progresses even when exposure stops.
Usually, exposure of 20 to 30 years is necessary before the disease becomes apparent, altough it develops in less than 10 years when the exposure to dust is extremely high.
2-Etiology :
Silica, the causative agent :
Free crystalline silica, SiO2, is one of the most common minerals in the earth's crust. It is found in sand, many rocks such as granite, sandstone, flint and slate, and in some coal and metallic ores. The three most common forms are quartz, tridymite and cristobalite.
Crystalline silica :
As a general rule, the smaller the diameter of particles, the more efficient is the pulmonary clearance by the bronchi and acini.
The bronchial and alveolar retention of particles is the result of two opposing factors, deposition and clearance. Retention of dust will be at its peak, depending on the nature of dust, for the particles whose diameter ranges from 0.5 to 3 microns.
Quartz particles in the occupational setting range widely in size, but those less than 1 micron are believed to be the most pathogenic.
Since large particles impact and sediment in the nares and the major airways, only relatively small particles enter the acini.
The size of silica particles retained in the human lung is remarkably constant, with median diameters ranging from 0.5 to 0.7 micron.
The crystalline silica, alpha quartz, is the major cause of silicosis worldwide.
Although the silica polymorphs, cristobalite and tridymite, prove more toxic for cells and are highly fibrogenic under experimental conditions, these two mineralogic variants are of more limited health variance.
Respirable silica dust may be invisible to the naked eye and is so light that it can remain airborne for a long time. It can thus travel long distances in the air and so affect populations not otherwise considered to be at risk.
Sources :
Silica dust is released during operations in which rocks, sand, concrete and some ores are crushed or broken.
Work in mines, quarries, foundries, and construction sites, in the manufacture of glass,ceramics, and abrasive powders, and in masonry workshops is particularly risky.
The production and use of refractory brick containing silica may pose significant health hazards particularly after they have been exposed to high temperatures as a significant proportion of the silica is transformed to cristobalite or tridymite.
Bricklayers and others who maintain and dismantle the refractory brick of ovens, furnaces and other similar devices are exposed to a serious silica hazard.
Extremely high exposures, eg, in industries such as tunneling, abrasive soap making, and sand blasting, are associated with much shorter latency and more rapid disease progression.
Any abrasive blasting, even if the abrasive does not contain silica, may pose a silicosis hazard when it is used to remove materials that contain silica, such as remains of sand moulds from metal castings.
Some operations, like dry sweeping, the clearing of sand or concrete, or the cleaning of masonry with pressurized air can generate large dust clouds. Thus even in open air these activities can be hazardous.
3-Miscellaneous Epidemiologic Data :
In certain places in the world, an age-old scenario is being repeated. In the 16th century Agricola wrote of mines in the Carpathian mountains in Europe: " women are found to have married seven husbands, all of whom this terrible consumption (silico-tuberculosis) has carried off to a premature death ".
Only a few years ago certain villages in Northern Thailand were called " villages of widows " because of the large number of pestle-and-mortar-making workers who died early from silicosis.
1-During the period 1991 to 1995, China recorded more than 500 000 cases of silicosis,with around 6 000 new cases and more than 24 000 deaths occurring each year mostly among older workers.
2-In the USA, it is estimated that more than one million workers are occupationally exposed to free crystalline silica dusts (more than 100 000 of these workers are sandblasters), of whom some 59 000 will eventually develop silicosis. It is reported that each year in the USA about 300 people die from it, but the true number is not known.
3-Abrasive blasting with silica sand, often used to prepare surfaces for painting, has been associated with exposures 200 times greater than the level recommended by theUS National Institute for Occupational Safety and Health. This agency recommended that silica sand be prohibited as an abrasive blasting agent.
4-In Quebec, Canada, in the years 1988-1994, 40 newly diagnosed workers were compensated (12 were less than 40 years old).
4-Pathology and Pathophysiology :
Alveolar macrophages engulf respirable particles of free silica and enter the lymphatics and interstitial tissue. The macrophages cause cytotoxic enzymes to be released, and fibrosis of the lung parenchyma occurs. When a macrophage dies, the silica particles are released and engulfed by other macrophages, and the process may be repeated.
The typical initial pathologic change is the formation of discrete hyalinized silicotic nodules throughout the lungs. The dying macrophages release silica in the interstitial tissue around the second division of the respiratory bronchiole, where it forms a nodule. Later, coalescence of fibrosis results in conglomerate masses, contraction of the upper lung zones, and emphysema with marked distortion of lung architecture. Ventilatory and gas exchange functions are affected adversely. A reduction of all lung volumes distinguishes the overall physiologic pattern of conglomerate silicosis from that of advanced pulmonary emphysema. Severe functional impairment occurs in the late stages of conglomerate silicosis, and respiratory insufficiency - its ultimate consequence may progress along with radiographic worsening for a limited time (ie, 2 to 5 yr) even after exposure ceases. When the exposure to dust is extremely high and acute silicoproteinosis develops, the alveolar spaces fill with a proteinaceous material similar to that found in alveolar proteinosis, and mononuclear cells infiltrate the septa.
5-Symptoms and Signs :
The form and severity in which silicosis manifests itself depend on the type and extent of exposure to silica dusts.
Patients with simple nodular silicosis have no respiratory symptoms and usually no respiratory impairment. They may cough and raise sputum, but these symptoms are due to industrial bronchitis and occur as often in persons with normal x-rays. Although simple silicosis has little effect on pulmonary function, patients with category 2 or 3 disease occasionally have slightly reduced lung volumes, but the values are seldom outside the predicted range.
Conglomerate silicosis, in contrast, may lead to severe shortness of breath, cough,and sputum. The severity of the shortness of breath is related to the size of the conglomerate masses in the lungs. When the masses are extensive, the patient becomes severely disabled. As the masses encroach on and obliterate the vascular bed, pulmonary hypertension and right ventricular hypertrophy supervene. In an advanced state, there may be physical findings of consolidation and of pulmonary hypertension.
Nonhypoxemic cor pulmonale eventually causes death.
In conglomerate (complicated) silicosis, especially in the late stages, pulmonary function abnormalities are common. They include decreased lung volumes and diffusing capacity, and airway obstruction, frequently with pulmonary hypertension and, occasionally, mild hypoxemia. CO2 retention is unusual. In many patients with silicosis, the serum contains lung autoantibodies and antinuclear factor. Persons who are occupationally exposed to silica and who have a positive tuberculin test are at greater risk of developing TB. Generally, the more silica in the lungs, the greater the risk.
A frequent cause of death in people with silicosis is pulmonary tuberculosis (silico-tuberculosis).
Respiratory insufficiencies due to massive fibrosis and emphysema (respiratory tissue loss is not always present), as well as heart failure, are other causes of death.
6-Diagnosis :
Diagnosis is based on characteristic chest x-ray changes and a history of exposure to free silica. Simple silicosis is recognized by the presence of multiple, small, rounded or regular opacities on the chest x-ray and is classified as category 1, 2, or 3 according to their profusion. Conglomerate silicosis is recognized by the development of an opacity > 1 cm in diameter on a background of category 2 or 3 simple silicosis. Numerous other diseases may resemble simple silicosis, including miliary TB, welders' siderosis, hemosiderosis, sarcoidosis, and coal workers' pneumoconiosis.
However, the presence of eggshell calcifications in the hilar and mediastinal lymph nodes distinguishes silicosis from other occupational lung diseases.
Silicotuberculosis resembles conglomerate silicosis on x-rays. The distinction can be made by sputum culture.
7-Treatment :
No effective treatment is known other than lung transplantation. Persons with airway obstruction should be treated as for chronic airway obstruction. Those exposed to silica who have a positive tuberculin test but negative sputum TB cultures should be given isoniazid for at least 1 yr. Some authorities recommend lifelong treatment because the function of alveolar macrophages may be permanently compromised by silica. Lifelong isoniazid prophylaxis may be indicated for those who have been treated previously for active pulmonary TB. Patients with silicosis and active pulmonary TB require extension of standard multidrug therapy by at least 3 to 6 mo.
8-Screening for silicosis :
Introduction :
Diagnosis and health surveillance are essential components of any programme aiming at eliminating silicosis. Although medical and radiological examinations can only detect and not prevent silicosis, these are important complements to primary prevention.
However, surveillance should be considered as a complement to control strategies and never as a replacement for primary prevention.
According to Quebec's guidelines, chest X-ray is the only tool recommended to screen for silicosis. Pulmonary lesions can be found on chest X-rays before the presence of symptoms.
It is an effective screening test depending on the importance of exposure (amount and duration).
Naturally films must be read by a B-reader, a radiologist with a special training.
Pulmonary function testing is useless when workers do not experience pulmonary symptoms.
Physical examination is also useless at the screening level.
The use of a standardized pulmonary questionnaire may be useful only to screen for chronic bronchitis, mainly related to tobacco smoking.
Medical surveillance :
High risk workers :
As in sandblasting where the exposure to respirable crystalline silica may be in the vicinity of, and even more than 2½ times the exposure limit, chest X-ray should be done every year until important corrective measures are put in place to lower the exposure to safer levels after prompt and vigorous intervention by the team responsible for occupational health and safety.
These high-risk levels should not be tolerated for being very hazardous.
When adequate protective gears are supplied, chest X-ray could be done less frequently for obvious reasons, one good exemple would be every 3 years.
Cumulative dose :
If workers' level of exposure is in the vicinity of 0.1mg/m3, for 8 hours a day and 40 hours a week, a first chest X-ray is suggested after the first 10 years of exposure, then another one10 years later and finally, one every 5 years. This pattern of medical surveillance is determined using the "cumulative dose" concept which goes as follows :
level of exposure (mg/m3) x years of exposure = cumulative dose (mg/m3/year)
At the level of 1mg/m3/year, a first chest X-ray should be performed. And, at 2mg/m3/year, another chest X-ray should be prescribed.
When the score is higher than 2.0 mg/m3/year, a chest X-ray should be done everytime the cumulative dose increases by 0.5 mg/m3/year.
Therefore, a worker exposed to very low levels, like 0.025 mg/m3, shall not have a chest X-ray before 40 years of exposure.
Mine and quarry workers are covered by a special by-law :
They must have a pulmonary examination every 3 years including a physical examination and a chest X-ray. The first examination for employees who have never been exposed to silica or asbestos should take place within the first 6 years after being hired.
A pre-employment examination is mandatory and also include a questionnaire of pulmonary symptoms and a lung physiology evaluation.
These guidelines have been suggested since 1996.
9-Exposure limits :
Quebec's exposure limits :





0.05 mg/m3



0.10 mg/m3

Pr, C2, EM


0.05 mg/m3



0.10 mg/m3


Pr = Respirable dust.(Poussière respirable)
C2 = Suspected carcinogen to humans
EM = Substance that should be kept at the lowest practicable level
10-Prophylaxis :
Action should be taken before exposure happens.Silicosis is prevented by avoiding inhalation of dust containing free crystalline silica. Alice Hamilton (1869-1970), pioneer occupational physician and hygienist who conducted major studies on silicosis in the USA said: " obviously the way to attack silicosis is to prevent the formation and escape of dust".
1-At the turn of the 20th century in Vermont, USA, introduction of pneumatic tools to the granite cutting industry was followed by a dramatic rise in death rate from silicosis.(Pneumatic tools generated much larger quantities of free crystalline silica-containing dust.) In the late 1930s, dust control measures were introduced and the number of new cases of disease gradually decreased, until there were virtually none by 1967.
2-In Switzerland, stricter controls in the 1970s and 1980s led to approximately six-fold reduction in the number of silicosis cases per year (many residual from previous exposure).
Because dust suppression cannot reduce the risk in sandblasting, external-air-supplied hoods should be used. Such protection may not be available to personnel performing other jobs in the area (eg, painting, welding). Thus substituting other abrasive materials for sand is desirable.
So, good housekeeping of your studio is very important; to do so you may, among other things, use wet processes, or even a vacuum system whose air is exhausted outside of the workshop.
Avoidance of processes generating unnecessary dust is also important. To this, we may add work in closed systems and improvement of the general ventilation.
The wearing of an approved dust mask for this kind of hazard is also recommended when the level of exposure seems problematic.
References :
1-Important aerosols in occupational settings, André Dufresne Ph.D.(McGill University), Montreal,Canada.
2-Toxicologie Industrielle et Intoxications Professionnelles, Robert R. Lauwerys, 1999.
3-Les Maladies Respiratoires d'Origine Professionnelle, Marinet Y., Anthoine D., Petiet G.,1999
4-Silicosis, the WHO, fact sheet # 238, May 2000.
5-The Merck Manual of Diagnosis and Therapy, on-line publication.

By Edouard Bastarache

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