It consists of nodular fibrosis of the lungs and difficulty breathing caused by prolonged inhalation of chemical compounds containing crystalline silica (Silicon (IV) oxide). It often causes death, caused by breathing dust containing very small particles of crystalline silica (Silicon(IV) oxide). Exposure to crystalline silica can occur during mining, metallurgy, chemical-related industries, paints, ceramics, marble, stained glass, and less frequently in the filter, insulator, polishing, piping, heat-insulating, construction, and masonry industries. Activities such as cutting, breaking, crushing, drilling, grinding or abrasive cleaning of these materials can produce fine silica dust. It can also be in soil, mortar, plaster, and shingles. Very small particles of silica dust can be in the air you breathe and get trapped in your lungs. The smallest particles and fibers are the most dangerous since they are the ones that can reach the alveoli. It is generally considered that this size below which the risk of suffering from silicosis occurs is for particles smaller than 5 microns. As dust builds up in your lungs, your lungs become damaged and it becomes more difficult to breathe as you age.

At the cellular level, exposure to silica dust "Silicon (IV) oxide") produces the breakdown of lysosomes, which contain numerous enzymes that degrade both internal (deteriorated organelles) and external (proteins captured from the outside by endocytosis, for example) components. These enzymes are deposited in the lungs, causing significant damage to them.

Crystalline silica—silicon dioxide "Silicon(IV) Oxide") (SiO)—is what causes silicosis; It is found in nature in the form of quartz, cristobalite or tridymite, with quartz being the most abundant (12% of the Earth's crust); hence exposure to silica is very frequent. Although there are unusual sources of exposure, given its ubiquity, the most important is inland mining, although in some countries exposure is taking center stage in industries related to ornamental stone (granite, slate "Slate (rock)");[5]​ you must also be alert to industries that generate or use ground silica (silica flour). .

Because chronic silicosis is slow to develop, signs and symptoms may not appear until years after exposure. Signs and symptoms include:

In advanced cases, the following may also occur:

There are three types of silicosis:

There are two clinical forms according to radiology: simple silicosis and complicated silicosis.

Simple silicosis is by far the most common clinical form. It shows round opacities (the most common) and/or irregular opacities on simple postero-anterior chest x-ray (Rx). It does not usually produce functional alterations with clinical significance nor does it reduce life expectancy, as long as it does not progress to complications.

Complicated silicosis is characterized by the existence of Progressive Massive Fibrosis masses, also called conglomerate masses, with a diameter greater than 1 cm. It is a serious disease, especially if the masses are large, and significantly reduces the life expectancy of patients. The evolution from the simple to the complicated form is due to factors that are often unknown. Among the known factors are: high exposure to silica, abundant nodular profusion, tuberculosis and collagen diseases.

Rarely, the disease may present as diffuse pulmonary fibrosis,[6]​ interstitial pneumonia[7]​ or as a lung mass without apparent background nodulation (silicoma").

Patients with silicosis are particularly susceptible to tuberculosis (TB)—known as silicotuberculosis. The increased risk of incidence is almost 3 times greater than that of the healthy population, without having a certain explanation. It is believed that macrophages filled with silica decrease their ability to kill mycobacteria. Even workers with prolonged silica exposure, but without silicosis, are at increased risk for tuberculosis.

Pulmonary complications of silicosis also include chronic bronchitis and airflow limitation (indistinguishable from that caused by smoking), non-tuberculosis Mycobacterium infection, fungal lung infection, compensatory emphysema, and pneumothorax. There is some data revealing an association between silicosis and other autoimmune diseases, such as nephritis, scleroderma, and systemic lupus erythematosus, especially in acute or accelerated silicosis.

The diagnosis is based on a significant work history and typical X-ray findings. The ILO (International Labor Organization) has developed regulations in order to classify, describe and codify radiographic alterations attributable to pneumoconiosis and facilitate their comparability in epidemiological studies, without legal pretensions or connotations, although it is also used in the clinic; The 2000 edition is based on the comparison of the patient's X-ray with model plates provided by the organization.[8]​.

Small round opacities are classified according to their diameter as p (the smallest), q (those that exceed 1.5 mm) and r (those that exceed 3 mm and do not exceed 10 mm) and irregular ones as s, t, u depending on their width (equivalent to the diameter in the round ones). The quantity or profusion is categorized from 0 to 3.

A combined notation is established based on profusion with 12 categories from 0/- (completely clean lung) 3/+ (the maximum imaginable profusion); for example 1/2 q/t. The first figure and the first letter would be the most probable.

The ILO classifies PMF masses according to their largest diameter as A (they exceed 10 mm), B (individually or together they exceed 5 cm) and C (they exceed an area equivalent to that of the right upper lobe.

In case of diagnostic doubts, High Resolution Computed Tomography (HRCT) can be used, which has been shown to be more sensitive and specific for the diagnosis.[9]​ It subjects the patient to much more radiation than X-ray and should not be used as a first-level diagnostic test but rather to clarify doubts. HRCT allows us to verify how PMF masses frequently originate in the subpleural region of posterior apical areas, progressively moving away from the pleura—a sign of detachment.[3]​.

Invasive techniques (such as biopsy) should not be indicated for the diagnosis of silicosis unless another entity susceptible to treatment is suspected.[3]​.

Primary prevention aims to limit cumulative exposure to silica to prevent the incidence of the disease from exceeding reasonable and acceptable limits. The most widely accepted exposure limit is 0.1 mg/m³ of respirable crystalline silica (average over the workday), proposed by OSHA (Occupational Safety and Health Administration).[10]​.

The National Silicosis Institute of Spain has developed standards for technical[11] and medical prevention.[12] The environmental limit value for daily exposure to silica (VLA-ED) for workers in extractive industries is established at 0.1 mg/m³ (0.05 in the case of cristobalite or tridymite); the respirable fraction of dust will not exceed 3 mg/m³. Primary prevention from a medical point of view is based on pre-work examinations. in order to avoid the concurrence of risk factors or lung diseases that could increase the risk. It is necessary to carry out periodic examinations of workers to remove those affected from risk.[13]​ Having radiological follow-up facilitates the diagnosis and avoids certain invasive examinations in doubtful cases (hilar lymphadenopathy due to exposure to silica, incipient PMF, etc.).[3]​.

Measures to control dust are based on irrigation with water so that the particles settle, use of appropriate means that do not re-enter the atmosphere, and removing them from the environment with aspiration and ventilation. To the extent these procedures fail, personal protection measures must be used. Devices can be used to filter and prevent inhalation of these materials when doing work such as mining.

It is important to avoid tobacco in any case, but especially in workers exposed to silica and take appropriate measures to prevent tuberculosis.

There is no specific treatment for silicosis, but it is important to remove the source of silica exposure to prevent worsening of the disease. Complementary treatment includes cough suppressants (a drug used to treat dry irritative cough), bronchodilators, and oxygen, if necessary. Antibiotics are prescribed for respiratory infections as needed.

Treatment also includes limiting exposure to irritants, stopping smoking, and routine skin testing for tuberculosis.

The problem is worrying because, in addition to producing silicosis, silica seems to be involved in other diseases[14]​ and the economic and social impact is important. Serious cases of silicosis continue to be observed. There is sufficient evidence that silica is involved in lung cancer,[15]​ in chronic obstructive pulmonary disease (COPD)[16]​ and in pulmonary tuberculosis.[17]​ Silicosis is considered a public health problem.[18]​ There are reasons to suspect a relationship with some collagenoses and perhaps with sarcoidosis.[19]​ Silica attacks a vital organ, putting the patient's life at risk; It is expected that the exhibition will continue in the future due to the expansion of industries related to ornamental stone and the fact that new industrial uses of silica appear (abrasive material, silica flour, etc.). Recommended exposure limits are difficult to achieve and do not appear to be sufficiently protective.[20]​.

It consists of nodular fibrosis of the lungs and difficulty breathing caused by prolonged inhalation of chemical compounds containing crystalline silica (Silicon (IV) oxide). It often causes death, caused by breathing dust containing very small particles of crystalline silica (Silicon(IV) oxide). Exposure to crystalline silica can occur during mining, metallurgy, chemical-related industries, paints, ceramics, marble, stained glass, and less frequently in the filter, insulator, polishing, piping, heat-insulating, construction, and masonry industries. Activities such as cutting, breaking, crushing, drilling, grinding or abrasive cleaning of these materials can produce fine silica dust. It can also be in soil, mortar, plaster, and shingles. Very small particles of silica dust can be in the air you breathe and get trapped in your lungs. The smallest particles and fibers are the most dangerous since they are the ones that can reach the alveoli. It is generally considered that this size below which the risk of suffering from silicosis occurs is for particles smaller than 5 microns. As dust builds up in your lungs, your lungs become damaged and it becomes more difficult to breathe as you age.

At the cellular level, exposure to silica dust "Silicon (IV) oxide") produces the breakdown of lysosomes, which contain numerous enzymes that degrade both internal (deteriorated organelles) and external (proteins captured from the outside by endocytosis, for example) components. These enzymes are deposited in the lungs, causing significant damage to them.

Crystalline silica—silicon dioxide "Silicon(IV) Oxide") (SiO)—is what causes silicosis; It is found in nature in the form of quartz, cristobalite or tridymite, with quartz being the most abundant (12% of the Earth's crust); hence exposure to silica is very frequent. Although there are unusual sources of exposure, given its ubiquity, the most important is inland mining, although in some countries exposure is taking center stage in industries related to ornamental stone (granite, slate "Slate (rock)");[5]​ you must also be alert to industries that generate or use ground silica (silica flour). .

Because chronic silicosis is slow to develop, signs and symptoms may not appear until years after exposure. Signs and symptoms include:

In advanced cases, the following may also occur:

There are three types of silicosis:

There are two clinical forms according to radiology: simple silicosis and complicated silicosis.

Simple silicosis is by far the most common clinical form. It shows round opacities (the most common) and/or irregular opacities on simple postero-anterior chest x-ray (Rx). It does not usually produce functional alterations with clinical significance nor does it reduce life expectancy, as long as it does not progress to complications.

Complicated silicosis is characterized by the existence of Progressive Massive Fibrosis masses, also called conglomerate masses, with a diameter greater than 1 cm. It is a serious disease, especially if the masses are large, and significantly reduces the life expectancy of patients. The evolution from the simple to the complicated form is due to factors that are often unknown. Among the known factors are: high exposure to silica, abundant nodular profusion, tuberculosis and collagen diseases.

Rarely, the disease may present as diffuse pulmonary fibrosis,[6]​ interstitial pneumonia[7]​ or as a lung mass without apparent background nodulation (silicoma").

Patients with silicosis are particularly susceptible to tuberculosis (TB)—known as silicotuberculosis. The increased risk of incidence is almost 3 times greater than that of the healthy population, without having a certain explanation. It is believed that macrophages filled with silica decrease their ability to kill mycobacteria. Even workers with prolonged silica exposure, but without silicosis, are at increased risk for tuberculosis.

Pulmonary complications of silicosis also include chronic bronchitis and airflow limitation (indistinguishable from that caused by smoking), non-tuberculosis Mycobacterium infection, fungal lung infection, compensatory emphysema, and pneumothorax. There is some data revealing an association between silicosis and other autoimmune diseases, such as nephritis, scleroderma, and systemic lupus erythematosus, especially in acute or accelerated silicosis.

The diagnosis is based on a significant work history and typical X-ray findings. The ILO (International Labor Organization) has developed regulations in order to classify, describe and codify radiographic alterations attributable to pneumoconiosis and facilitate their comparability in epidemiological studies, without legal pretensions or connotations, although it is also used in the clinic; The 2000 edition is based on the comparison of the patient's X-ray with model plates provided by the organization.[8]​.

Small round opacities are classified according to their diameter as p (the smallest), q (those that exceed 1.5 mm) and r (those that exceed 3 mm and do not exceed 10 mm) and irregular ones as s, t, u depending on their width (equivalent to the diameter in the round ones). The quantity or profusion is categorized from 0 to 3.

A combined notation is established based on profusion with 12 categories from 0/- (completely clean lung) 3/+ (the maximum imaginable profusion); for example 1/2 q/t. The first figure and the first letter would be the most probable.

The ILO classifies PMF masses according to their largest diameter as A (they exceed 10 mm), B (individually or together they exceed 5 cm) and C (they exceed an area equivalent to that of the right upper lobe.

In case of diagnostic doubts, High Resolution Computed Tomography (HRCT) can be used, which has been shown to be more sensitive and specific for the diagnosis.[9]​ It subjects the patient to much more radiation than X-ray and should not be used as a first-level diagnostic test but rather to clarify doubts. HRCT allows us to verify how PMF masses frequently originate in the subpleural region of posterior apical areas, progressively moving away from the pleura—a sign of detachment.[3]​.

Invasive techniques (such as biopsy) should not be indicated for the diagnosis of silicosis unless another entity susceptible to treatment is suspected.[3]​.

Primary prevention aims to limit cumulative exposure to silica to prevent the incidence of the disease from exceeding reasonable and acceptable limits. The most widely accepted exposure limit is 0.1 mg/m³ of respirable crystalline silica (average over the workday), proposed by OSHA (Occupational Safety and Health Administration).[10]​.

The National Silicosis Institute of Spain has developed standards for technical[11] and medical prevention.[12] The environmental limit value for daily exposure to silica (VLA-ED) for workers in extractive industries is established at 0.1 mg/m³ (0.05 in the case of cristobalite or tridymite); the respirable fraction of dust will not exceed 3 mg/m³. Primary prevention from a medical point of view is based on pre-work examinations. in order to avoid the concurrence of risk factors or lung diseases that could increase the risk. It is necessary to carry out periodic examinations of workers to remove those affected from risk.[13]​ Having radiological follow-up facilitates the diagnosis and avoids certain invasive examinations in doubtful cases (hilar lymphadenopathy due to exposure to silica, incipient PMF, etc.).[3]​.

Measures to control dust are based on irrigation with water so that the particles settle, use of appropriate means that do not re-enter the atmosphere, and removing them from the environment with aspiration and ventilation. To the extent these procedures fail, personal protection measures must be used. Devices can be used to filter and prevent inhalation of these materials when doing work such as mining.

It is important to avoid tobacco in any case, but especially in workers exposed to silica and take appropriate measures to prevent tuberculosis.

There is no specific treatment for silicosis, but it is important to remove the source of silica exposure to prevent worsening of the disease. Complementary treatment includes cough suppressants (a drug used to treat dry irritative cough), bronchodilators, and oxygen, if necessary. Antibiotics are prescribed for respiratory infections as needed.

Treatment also includes limiting exposure to irritants, stopping smoking, and routine skin testing for tuberculosis.

The problem is worrying because, in addition to producing silicosis, silica seems to be involved in other diseases[14]​ and the economic and social impact is important. Serious cases of silicosis continue to be observed. There is sufficient evidence that silica is involved in lung cancer,[15]​ in chronic obstructive pulmonary disease (COPD)[16]​ and in pulmonary tuberculosis.[17]​ Silicosis is considered a public health problem.[18]​ There are reasons to suspect a relationship with some collagenoses and perhaps with sarcoidosis.[19]​ Silica attacks a vital organ, putting the patient's life at risk; It is expected that the exhibition will continue in the future due to the expansion of industries related to ornamental stone and the fact that new industrial uses of silica appear (abrasive material, silica flour, etc.). Recommended exposure limits are difficult to achieve and do not appear to be sufficiently protective.[20]​.