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Occupational Lung Diseases

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Title: Occupational Lung Diseases


1
Occupational Lung Diseases
  • Internal Medicine Curriculum Presbyterian
    Hospital of Dallas
  • October 2003

2
A Brief History of Occupational Medicine
  • Ancient Times
  • The Middle Ages
  • Ramazzini (1633-1714)
  • The Industrial Revolution
  • The Modern Era

3
Ancient Times
  • Major economic activities included agriculture,
    mining for metals, and quarrying.
  • Pliny the Elder (AD 23-79) recorded the danger to
    miners from inhalation of fumes and vapors
  • Because mining was so dangerous, it was
    considered suitable only for slaves and as
    punishment for criminals.

4
The Middle Ages
  • The Erz Mountains in Bohemia was an important
    area for the mining and refining of useful and
    precious metals. A physician named Agricola
    became the town physician of Joachimsthal.
  • He recognized that mining activities could lead
    to conditions that caused chronic shortness of
    breath.
  • Agricola was probably observing silicosis and
    tuberculosis

5
Ramazzini
  • He published De Morbis Artificum Diatriba in 1700
    (Treatise on the Diseases of Workers). He
    describes
  • Dyspnea and metal poisoning in miners
  • Bronchitis from irritant fumes
  • Lung fibrosis in potters
  • Asthma from exposure to corn flour
  • Silicosis in stonemasons

6
Ramazzini
  • When a doctor visits a working class home he
    should be content to sit on a three-legged
    stool, if there isnt a guilded chair, and he
    should take time for his examination and to the
    questions recommended by Hippocrates, he should
    add one more what is your occupation?

7
Ramazzini
  • Medicine, like jurisprudence, should make a
    contribution to the well-being of workers, and
    see to it that, so far as possible, they should
    exercise their callings without harm. So I for my
    part have done what I could and have not thought
    it unbecoming to make my way into the lowliest
    workshops and study the mysteries of the mechanic
    arts.

8
The Industrial Revolution
  • Production of steel on an industrial scale.
  • Increased coal mining to make coke
  • Fabrics are made in factories from cotton and
    wool thanks to new machinery.
  • Charles Turner Thackrah, a town doctor, reported
    his observations on lung disease in miners and
    metal grinders and described a new method of
    measuring lung volume.

9
The Industrial Revolution Continued
  • Britain institutes Workmens Compensation Acts.
  • As of 1897, injured workers had rights to
    compensation from compensation from contributions
    paid by employers.
  • Silicosis (1919) and Asbestosis (1931) were later
    recognized and covered.

10
The Modern Era
  • E.R.A. Merewether (1892-1970) established the
    danger of asbestos and promoted the first
    legislation to control it.
  • Late 19th century, occupational lung cancers are
    described in miners.
  • Allergic alveolitis is described in 1932
  • Berylliosis is described in Germany in 1933
  • 1970, Congress passes OSHA legislation.

11
Principles of Occupational Lung Disease
  • Industrial processes change and become
    increasingly complex.
  • We should anticipate the appearance of a wider
    range of potentially toxic substances in the air.
  • It is unlikely that the lung will develop many
    new ways to react to inhaled substances.
  • Well see old lung diseases with new causes

12
Induction Periods
  • Short
  • Asthma
  • Infections
  • Allergic alveolitis
  • Toxic poisonings
  • Long
  • Pneumoconioses
  • Neoplasms

13
The Occupational History
  • All jobs held in their lifetime and the duration.
  • Do symptoms improve with weekends and vacations?
  • The longer they have had symptoms from
    occupational asthma, the less clear the
    connection between symptoms and work
  • What they did, not their title
  • brusher drills into hard rock
  • caulker uses electric arc equipment to gouge
    and fuse metal plates

14
The Occupational History
  • Toxic exposures can produce airway symptoms or an
    alveolitis.
  • If everyone in the workplace is affected in a
    dose-dependent manner, the etiology is likely to
    be toxic rather than immunologic.
  • Toxic reactions can occur on the first exposure.
    Immunologically-mediated diseases require
    re-exposure

15
Toxic Gases and Fumes
  • Asphyxiating gases displace oxygen in the
    alveolus, on the hemoglobin molecule, or prevent
    oxygen utilization by the cytochrome
  • Irritants are noticed quickly by the patients and
    create symptoms proximally to distally. (chlorine
    and ammonia)
  • Toxins that attack the alveolar membrane
    (phosgene and nitrogen dioxide)

16
Occupational Asthma
  • Symptoms usually begin several weeks after
    exposure begins.
  • Early in the syndrome, the patient may just
    notice a dry cough.
  • Patient may not be continuously exposed to
    provoking antigen.
  • A portable peak-flow meter and a diary is very
    helpful in determining if a work-place antigen is
    responsible

17
Industrial Bronchitis
  • Identical symptoms to chronic bronchitis seen
    with cigarette smoking
  • Coal workers
  • Grain Workers
  • Most non-smokers do not have a decrement in FEV
    1.0

18
Hypersensitivity Pneumonitis
  • An inflammatory, immunologically mediated
    response at the alveolar and bronchiolar level to
    organic particles or gases.
  • Acute, persistent, and subacute-recurrent forms
    of the disease.

19
Acute HP
  • Fever, muscular aches, and malaise 4-8 hours
    after exposure to the antigen.
  • May be associated with dry cough or chest
    tightness.
  • Shortness of breath is a feature of a severe
    attack.
  • Symptoms peak 8-12 hours after exposure and
    improve over the next 12-24 hours.

20
Persistent HP (acute)
  • An atypical pneumonia picture with bilateral
    infiltrates on CXR, hypoxemia, and rales.
  • May return to hospital within days after
    improving on antibiotics.

21
Recurrent HP
  • Malaise, dry cough, shortness of breath
  • Often mistakenly receive multiple courses of
    antibiotics or psychiatric referral.
  • Some may progress to pulmonary fibrosis.
  • In severe cases, CXR, pulmonary functions, and
    lung biopsy may be indistinguishable from
    end-stage idipathic pulmonary fibrosis

22
RADS the Reactive Airways Dysfunction Syndrome
  • The onset of an asthma like syndrome after a
    single severe exposure to a respiratory irritant.
  • Not immunologically mediated
  • Positive methacholine challenge test
  • Symptoms of asthma may persist for more than one
    year after the event.

23
Pneumoconiosis
  • The term is currently defined by the
    International Labour Organisation (ILO) as the
    accumulation of dust in the lungs and the tissue
    reactions to its presence tissue reaction may be
    non-collagenous (minimal stromal reaction) or
    collagenous (when scarring is permanent.

24
The Pneumoconioses
  • Asbestosis
  • Silicosis
  • Coal Workers pneumoconiosis
  • Berylliosis

25
ILO radiologic classification
  • Rounded opacities p (lt1.5mm), q, and r (gt3 mm)
  • Irregular opacities s, t, or u
  • Profusion 12 point scale (0/0 thru 3/3)
  • Grading of pleural thickening

26
Asbestos
  • A very fibrogenic dust, that causes pulmonary
    fibrosis
  • pleural plaques, benign pleural effusions
  • Mesothelioma, carcinoma of the lung

27
Pleural Reaction - Asbestos
28
Asbestosis
  • Diffuse fibrosis caused by a persistent alveolar
    inflammation
  • Irregular opacities predominately in the lung
    bases
  • Rales invariably present
  • Clubbing is common

29
Asbestos-related pleural plaques
30
Asbestos plaques
31
Gross appearance of Plaque
32
Silicosis
  • Simple Silicosis small nodules, predominately
    upper lobes patient often asymptomatic
  • Complicated Silicosis (Progressive Massive
    Fibrosis) coalescence into large nodules or
    masses with retraction of upper lobes
  • Tuberculosis is a common complication

33
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34
Coal Workers Pneumoconiosis (CWP)
  • Coal dust is inert and not particularly
    fibrogenic.
  • Can cause industrial bronchitis, emphysema, and
    progressive massive fibrosis.
  • Xray looks worse than patient
  • Many symptomatic coal miners have silicosis or
    tobacco induced COPD

35
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36
Simple CWP
  • An asymptomatic patient with normal pulmonary
    functions.
  • CXR shows small rounded opacities predominately
    in the upper lobes.

37
Complications of CWP
  • Tuberculosis
  • PMF
  • Caplans Syndrome a syndrome with rheumatoid
    arthritis features, PMF, and , usually (gt70), a
    ppositive rheumatoid factor.

38
Hard Metal Disease
  • Cobalt is the offending agent
  • Used in metal cutting or grinding tools and in
    jet engine turbine blades
  • Pulmonary fibrosis probably due to fibrogenic
    properties of metal
  • Asthma and hypersensitivity pneumonitis due to
    metals ability to provoke an immune response
    (?hapten)

39
Dung Lung
  • Dont ask

40
Sick Building Syndrome
  • Reports began to appear about the time that new,
    tighter, more energy efficient office buildings
    were built.
  • Hundreds of organic compounds have been
    identified in indoor air.
  • Formaldehyde is an ubiquitous indoor organic that
    is a mucosal irritant.

41
Multiple Chemical Sensitivity
  • Mucosal complaints
  • Asthma like symptoms
  • Neuro-cognitive complaints

42
Occupational Lung Cancers
  • Asbestos
  • Arsenic
  • Bischloromethyl ether
  • Coke oven fumes
  • Insoluble Hexavalent chromium cmpds
  • Soluble nickel
  • Mustard gas
  • Radon daughters

43
Mesothelioma
44
Mesothelioma
45
Small Cell Carcinoma of the Lung
  • Bischloromethyl ether (BCME) used as industrial
    intermediate for organic synthesis, organic
    solvents, bactericides, fungicides, and
    cross-linking agents.
  • Radon Daughters Radon-222 a decay product of
    U-238 is a gas and an alpha particle emitter as
    are its decay products polonium-218,-214, and
    -210. Present in some metal mines.

46
Legal Aspects of Industrial Disease
  • I was never ruined but twice, once when I lost a
    lawsuit and once when I won.
  • Voltaire
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