Silicosis

Co, Eunice Victoria M. Co, Gregory Allan C.

Sources and Exposure

Silica
common, naturallyoccurring crystal rock beds main part of sand forms dust during mining, quarrying, tunneling, and working with many metal ores mines, quarries, foundries, and construction sites, in the manufacture of glass, ceramics, and abrasive powders, and in masonry workshops

Occupations at Risk

Cases of Silicosis
mining establishment of Delamar, Nevada ruined by a drymining process that produced a silicosiscausing dust the town was nicknamed The Widowmaker

Cases of Silicosis
certain villages in Northern Thailand were called "villages of widows" large number of pestle-and-mortarmaking workers who died early from silicosis

Silicosis
potters disease, sand cutters disease or grinders rot. one of the oldest occupational diseases incurable lung disease disease progresses even when exposure stops caused by inhalation of dust crystalline silica dust (SiO2)
quartz cristobalite tridymite

Formation of Silicosis
Composition
Free silica Higher percentage increased risk

Concentration
5 million particles per cubic foot (mppcf)

Particle size
Respirable size reach alveoli: 1-3 microns or less

Time of exposure (duration)

6-7 years of contact

Susceptibility of individual
Previous/concurrent lung infection Age, smoking history

Phagocytosis Theory
macrophages ingest the dust particles tumor necrosis factors, interleukin-1, leukotriene B4 and other cytokines fibroblasts proliferate and produce collagen around the silica particle fibrosis and the formation of the nodular lesions

Mechanical Theory
Insoluble Sharp edged Tissue irritation

Chemical Theory
Silanol (SiOH) groups on surface of particles may react with cell membranes Negative surface charge on SiOgroups may underlie direct toxicity React with tissue and produce Salicylic acid

Colloidal Reaction Theory

Piezo Electric Theory Electric discharge emitted when pressure is applied to one end of crystal

Immunologic Theory
Silicotics High gamma globulin Hyaline matter of silicotic nodules
Beta and gamma globulin

Gross Pathology

Fibrotic chages Milliary nodulations

Normal lung Silicotic lung

X-ray
normal x-ray silicosis (upper lobes) silicosis -- diffuse

Histopathology

Fibrotic nodues Concentric onion-skin arrangement of collagen fibers Central hyalinization Cellular peripheral zone Acute: PAS(+) alveolar exudate (alveolar lipoproteinosis), cellular infiltrate of alveolar walls

 Occupational Safety and Health Administration is the main federal agency charged with the enforcement of safety and health legislation for the US Dept. of Labor The permissible exposure limits refer to a time-weighted average (TWA) which shall not be exceeded for an 8-hour workday within a 40-hour workweek. OSHA classifies silica glass dust as a "nuisance dust" with a TWA for total dust of 15 mg/m3 and respirable fraction of 5mg/m3 The OSHA TWA for 100% silica quartz is 0.3mg/m3 total dust and 0.1mg/m3 respirable fraction. Concentration of coal mines respirable dust (avg of 4.9 mg/m3)
National Safety Council, Fundamentals of Industrial Hygiene, Second Edition. Chapter 7 , Particulates, pp 171-200. Chicago, Ill, 1979. General Occupational Health Standards, Volume I, State of Washington, Department of Labor and Industries.

Clinical Presentation: Signs and Symptoms

Primary complaints: Chronic dry cough SOB w/ exercise Chest tightness Insomnia, pleural pain and hemoptysis Possible complications: risk for TB Progressive massive fibrosis

Types of Silicosis
Asymptomatic silicosis
Early cases of the disease do not present any symptoms

Chronic silicosis
after 1520 years of exposure to moderate to low levels of silica dust. Patients with this type of silicosis may not have obvious symptoms
SOB following physical exertion Severe dry cough fatigue loss of appetite chest pains fever

chest X-ray is necessary to determine if there is lung damage.

http://www.cdc.gov/niosh/silfact1.html

 Accelerated silicosis
Silicosis that develops 510 years after high exposure to silica dust. Symptoms include severe shortness of breath, weakness, and weight loss.

Acute silicosis
develops a few months to 2 years after exposure to very high concentrations of silica dust. severe disabling SOB, pleuritic pain, weakness, and weight loss, often leading to death.

http://www.cdc.gov/niosh/silfact1.html

Diagnosis and Tests

History Jobs, hobbies, other activities - Exposure to silica dust Physical Exam chest expansion breath sounds Request for: 1. Chest x-ray 2. Pulmonary Function Tests (PFT) 3. PPD
http://www.who.int/mediacentre/factsheets/fs238/en/

Chest X-Ray
Chest X-Ray Differential Diagnosis
Miliary TB Histoplasmosis Byssinosis Bagassosis

Ground glass appearance- frank mottling Bilateral changes

Chest X-Ray
Stages of disease by xray:
1st Stage discrete nodular circular shadows; 2 mm diameter (present as emphysema) 2nd Stage nodular shadows in the whole lung; some coalesce to form higher opacities 3rd Stage massive consolidation
http://emedicine.medscape.com/article/302027-overview

PFT / PPD
Pulmonary Function Test- Spirometry lung capacity Prolonged expiratory phase PPD Screening for TB

Prognosis
Incurable Develop TB Heart failure due to increased workload of the heart to the lungs Depend on the amount of damage to the lungs

Treatment
Silicosis is an irreversible condition with no cure. Treatment focus: Maintain patient comfort Slow the progression of silicosis

Treatment
1. 2. 3. 4. 5. 6. 7. Stop further exposure Stop smoking Antibiotics and anti-TB drugs infections Cough suppressants Chest physiotherapy Breathe easier Oxygen administration Bronchodilators

http://www.osha.gov/Publications/silicosis.pdf

Prevention
Identify source Use local exhaust ventilations Water spray is often used where dust emanates Control dust through dry air filtering Do not eat, drink or smoke near crystalline silica dust. Wash hands and face before eating, drinking or smoking away from exposure area. Use respiration equipment and protective clothing Undergo medical examination

http://www.osha.gov/Publications/silicosis.pdf

Extra slides

Pathology
Fibrotic nodules
are most common usually less than 1 cm. in diameter Spherical hard and gray to black.

On histologic examination:
Whorled appearance with concentrically arranged collagen On the periphery: aggregates of mononuclear cells:
Lymphocytes Fibroblasts

Pathology
Progressive massive fibrosis
Morphological
Central cavitation: related to amount of silica Disability due to amt of destruction of tissue

Radiological
Noduclar masses >2cm in diameter in a background of silmple silicosis Larger lesions: coalesce of smaller nodules
Nodules: 5-10 cm in diameter In the upper zones of the lungs= bilateral

Pathology
Alveolar proteinosis
Heavy exposure to finely particulate silica: sand blasting, boiler scaling Associated with diffuse fibrosis of the lung Silicotic nodules not found Dense eosinophilic material accumulate in alveolar spaces = produce an appearance that resembles alveolar lipoproteins Radiology:
Linear fibrosis and reduced lung volume