occupational health - silicosis

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    Silicosis

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

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    Sources and Exposure

    Silica common, naturally-

    occurring crystal

    rock beds

    main part of sand

    forms dust during mining,quarrying, tunneling, andworking with many metalores

    mines, quarries,foundries, and

    construction sites, in themanufacture of glass,ceramics, and abrasivepowders, and in masonryworkshops

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    Occupations at Risk

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    Cases of Silicosis

    mining establishment

    of Delamar, Nevada

    ruined by a dry-

    mining process thatproduced a silicosis-

    causing dust

    the town was

    nicknamed The

    Widowmaker

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    Cases of Silicosis

    certain villages in

    Northern Thailand

    were called "villages

    of widows" large number of

    pestle-and-mortar-

    making workers who

    died early fromsilicosis

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    Silicosis

    potters disease, sand cuttersdisease or grinders rot.

    one of the oldest occupationaldiseases

    incurable lung disease

    disease progresses even whenexposure stops

    caused by inhalation of dustcrystalline

    silica dust (SiO2)

    quartz cristobalite

    tridymite

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    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

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    Phagocytosis Theory

    macrophages ingestthe dust particles

    tumor necrosisfactors, interleukin-1,

    leukotriene B4 andother cytokines

    fibroblasts proliferateand produce collagen

    around the silicaparticle

    fibrosis and theformation of thenodular lesions

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    Mechanical Theory

    Insoluble

    Sharp edged

    Tissue irritation

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    Chemical Theory

    Silanol (SiOH)groups on surface ofparticles may reactwith cell membranes

    Negative surfacecharge on SiO-groups may underliedirect toxicity

    React with tissue andproduce Salicylic acid

    http://upload.wikimedia.org/wikipedia/commons/4/4b/Silica.svg
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    Colloidal Reaction Theory

    Piezo Electric Theory

    Electric discharge emitted when pressure is

    applied to one end of crystal

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    Immunologic Theory

    Silicotics

    High gamma globulin

    Hyaline matter of

    silicotic nodules Beta and gamma

    globulin

    http://www.osha.gov/SLTC/etools/silica/silicosis/silicosis.html
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    Gross Pathology

    Fibrotic chages

    Milliary nodulations

    Silicotic lung

    Normal lung

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    X-ray

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

    http://images.google.com/imgres?imgurl=http://a248.e.akamai.net/7/248/430/20040913134745/www.merck.com/mrkshared/mmanual/plates/p75_3.jpg&imgrefurl=http://www.merck.com/mrkshared/mmanual/plates/75pla3.jsp&h=437&w=500&sz=63&tbnid=xj5yAJK0ZvIJ:&tbnh=110&tbnw=127&hl=en&start=13&prev=/images%3Fq%3Dsilicosis%26svnum%3D10%26hl%3Den%26lr%3D%26sa%3DNhttp://images.google.com/imgres?imgurl=http://www4.umdnj.edu/cswaweb/rad_teach/images/silic_10.jpg&imgrefurl=http://www4.umdnj.edu/cswaweb/rad_teach/silicosis.html&h=699&w=600&sz=347&tbnid=hddVe1MpbdoJ:&tbnh=138&tbnw=118&hl=en&start=18&prev=/images%3Fq%3Dsilicosis%26svnum%3D10%26hl%3Den%26lr%3D%26sa%3DNhttp://images.google.com/imgres?imgurl=http://a248.e.akamai.net/7/248/430/20040913134745/www.merck.com/mrkshared/mmanual/plates/p75_3.jpg&imgrefurl=http://www.merck.com/mrkshared/mmanual/plates/75pla3.jsp&h=437&w=500&sz=63&tbnid=xj5yAJK0ZvIJ:&tbnh=110&tbnw=127&hl=en&start=13&prev=/images%3Fq%3Dsilicosis%26svnum%3D10%26hl%3Den%26lr%3D%26sa%3DNhttp://images.google.com/imgres?imgurl=http://a248.e.akamai.net/7/248/430/20040913134745/www.merck.com/mrkshared/mmanual/plates/p75_3.jpg&imgrefurl=http://www.merck.com/mrkshared/mmanual/plates/75pla3.jsp&h=437&w=500&sz=63&tbnid=xj5yAJK0ZvIJ:&tbnh=110&tbnw=127&hl=en&start=13&prev=/images%3Fq%3Dsilicosis%26svnum%3D10%26hl%3Den%26lr%3D%26sa%3DN
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    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

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    Occupational Safety and Health Adm inistrat ionis the mainfederal agency charged with the enforcement of safety andhealth legislation for the US Dept. of Labor

    The permissible exposure limits refer to a time-weightedaverage (TWA) which shall not be exceeded for an 8-hourworkday within a 40-hour workweek.

    OSHA class i f ies s i l ica glass dus t as a " nuisance dus t"w ith a TWA fo r total dust o f 15 mg/m3 and respirablefract ion o f 5mg/m3

    The OSHA TWA for 100% sil ica quartz is 0.3mg /m3 total

    dust and 0.1mg /m3 resp irable fract ion.

    Concentration of coal mines respirable dust (avg of 4.9mg/m3)

    General Occupational Health Standards, Volume I, State of Washington, Department of Labor and Industries.National Safety Council, Fundamentals of Industrial Hygiene, Second Edition. Chapter 7 , Particulates, pp 171-200. Chicago, Ill, 1979.

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    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

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    Types of Silicosis

    Asymp tomat ic s i l icos is Early cases of the disease do not present any symptoms

    Chronic si l ico sis

    after 1520 years of exposure to moderate to low levels of silicadust.

    Patients with this type of silicosis may not have obvioussymptoms

    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

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    Accelerated si l icosis

    Silicosis that develops 510 years afterhigh exposure

    to silica dust. Symptoms include severe shortness of

    breath, weakness, and weight loss.

    Acute s i l icos is

    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

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    Diagnosis and TestsHistory

    Jobs, hobbies, other activities - Exposure to silicadust

    Physical Exam

    chest expansion breath sounds

    Request for:

    1. Chest x-ray2. Pulmonary Function Tests (PFT)

    3. PPD

    http://www.who.int/mediacentre/factsheets/fs238/en/

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    Chest X-Ray

    Chest X-Ray Differential Diagnosis

    Miliary TB

    Histoplasmosis

    Byssinosis

    Bagassosis

    Ground glass appearance- frank mottling Bilateral changes

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    Chest X-Ray

    Stages of disease by x-

    ray:

    1st Stage discrete

    nodular circular shadows; 2mm 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

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    PFT / PPD

    Pulmonary Function Test- Spirometry

    lung capacity

    Prolonged expiratory phase

    PPD

    Screening for TB

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    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

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    Treatment

    Silicosis is an irreversible condition with no

    cure.

    Treatment focus:

    Maintain patient comfort

    Slow the progression of silicosis

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    Treatment

    1. Stop further exposure

    2. Stop smoking

    3. Antibiotics and anti-TB drugs infections4. Cough suppressants

    5. Chest physiotherapy

    6. Oxygen administration7. Bronchodilators

    Breathe easier

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

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    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 smokingaway from exposure area.

    Use respiration equipment and protective clothing

    Undergo medical examination

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

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    Extra slides

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    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

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    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

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    Pathology

    Alveolar proteinosisHeavy 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 lipoproteinsRadiology:

    Linear fibrosis and reduced lung volume