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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
- 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
- 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
- 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
- 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
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 :
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
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.
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.
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
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'
- However, the
presence of eggshell calcifications in the hilar and mediastinal
lymph nodes distinguishes silicosis from other occupational lung
- Silicotuberculosis resembles conglomerate
silicosis on x-rays. The distinction can be made by sputum
- 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 :
- 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.
surveillance should be considered as a complement to control
strategies and never as a replacement for primary
- 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
function testing is useless when workers do not experience
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.
- High risk
- 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
- 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
- level of
exposure (mg/m3) x years of exposure = cumulative dose
- 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 :
exposure limits :
- Pr = Respirable
- C2 = Suspected
carcinogen to humans
- EM = Substance
that should be kept at the lowest practicable level
- 10-Prophylaxis :
- Action should
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
- The wearing of an
approved dust mask for this kind of hazard is also recommended
when the level of exposure seems problematic.
aerosols in occupational settings, André Dufresne
Ph.D.(McGill University), Montreal,Canada.
Industrielle et Intoxications Professionnelles, Robert R.
- 3-Les Maladies
Respiratoires d'Origine Professionnelle, Marinet Y., Anthoine D.,
the WHO, fact sheet # 238, May 2000.
- 5-The Merck
Manual of Diagnosis and Therapy, on-line publication.
Out Bound Links
In Bound Links
Edouard Bastarache M.D.
Occupational & Environmental Medicine
Author of "Substitutions for Raw Ceramic Materials"
Tracy, QuÃ©bec, CANADA