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ASBESTOS

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Title: ASBESTOS


1
ASBESTOS
  • Francine Lortie-Monette, MD, MSc, CSPQ, MBA
  • Department of Epidemiology and Biostatistics
  • University of Western Ontario
  • 2003

2
Asbestosis
  • Asbestosis is a model for other dust diseases as
    well as other forms of pulmonary fibrosis
  • Some dust diseases take years for clinical
    symptoms to develop

3
Dust Diseases
  • Following removal from exposure, coal
    pneumoconioses may stop progressing but
  • Silicosis and asbestosis often do progress

4
Asbestosis
  • Model for
  • Restrictive ventilatory impairment (vs
    obstructive)
  • Interstitial lung disease

5
Why Study Asbestosis?
  • Exposure has continued in European construction
    industry till the mid-1970s
  • What about developing countries?

6
Why Study Asbestosis?
  • The resulting epidemic of mesothelioma in
    building workers born after 1940 did not become
    apparent until the 1990s owing to the long
    latency of the disease
  • Incidence rates are still rising

7
ASBESTOS
  • A broad term for a group of naturally occurring
    fibrous mineral silicates of magnesium and iron.
  • Asbestos-containing rock is mined, crushed and
    milled to obtain fibrous material, processed
    further into finer fibers.

8
ASBESTOS
  • Asbestos fibers are categorized into 2 groups
  • Amphiboles
  • Serpentines

9
ASBESTOS Amphiboles (straight fibers)
  • Those used commercially include
  • Amosite (brown)
  • Anthophylite
  • Crocidolite (blue)
  • Others (e.g. tremolite and actinolite) are
    frequent contaminants of other silicates,
    including some vermiculites and talcs.

10
ASBESTOS Serpentines
  • Used commercially
  • Chrysotile (3MgO-2SiO2-2H2O)
  • (the most common)

11
The Characteristics of ASBESTOS
  • Natural resistance to heat and acid
  • Tensile strength
  • Remarkable thermal, electrical and sound
    insulating properties
  • Have resulted in thousands of commercial
    applications, including floor tiles, boiler and
    pipe insulation, roofing materials, brake
    linings, and cement pipes.

12
Routes of Exposure
  • Some ingestion (e.g. contaminated water)
  • Mostly inhalation
  • Aerosols generated by mining, milling,
    product-manufacture, end use of product, and
    disturbance of asbestos-containing materials
    (e.g. renovations)

13
Pathogenesis
  • Fibers provoke the accumulation of macrophages in
    alveolar ducts and peribronchial regions, which
    become thickened.
  • This fibrotic process progresses, leading to a
    stiffened, smaller lung with diminished capacity
    for gas exchange.
  • Progression can occur after exposure has ceased,
    due to the retention of fibers in the lung and
    persistent inflammatory response.

14
Effects
  • Pulmonary Fibrosis
  • Pleural Thickening
  • Pleural Effusion
  • Cancer

15
Pulmonary Fibrosis
  • Results in restrictive lung disease that
    generally becomes manifest clinically 15-20 years
    after the onset of exposure.

16
Pulmonary Fibrosis (Contd)
  • Most Prominent Symptom
  • Insidious onset of dyspnea on exertion
  • Signs
  • End-inspiratory basilar rales which persist after
    cough
  • Decreased forced vital capacity (FVC), total lung
    capacity (TLC) and diffusing capacity (DLCO)
  • Eventually, extensive fibrosis obstructs the
    blood flow throughout the pulmonary bed, causing
    pulmonary hypertension and compensatory right
    ventricular hypertrophy.

17
Benign Pleural Effusion
  • May occur within the first 10 years of exposure,
    and may be the first manifestation of illness.
  • Diagnosis by exclusion, i.e. negative cultures
    of pleural fluid and pathological examination
    showing no malignant cells.
  • Patients may be asymptomatic spontaneous
    resorption may occur within several weeks.

18
Pleural Thickening (localized or diffuse)
  • The most common consequence of occupational
    exposure to asbestos.
  • Latency 20, and up to 40 years.
  • Associated with reduced FVC

19
Lung Cancer
  • Latency of ? 20 years.
  • Same cell types and histological features as
    other primary lung cancers.

20
Malignant Mesothelioma of the pleura and
peritoneum
  • Considered a signal neoplasm because of its
    rarity in the absence of exposure to asbestos.
  • Latency ? 20 years
  • Presenting symptoms often are chest pain and
    dyspnea, due to pleural effusions.
  • At high concentrations cancer of the
    gastrointestinal tract, kidney, pancreas and
    larynx (also post ingestion).

21
Asbestos
  • Summary of a typical case
  • Severe restrictive pulmonary impairment with
    progressive dyspnea on exertion
  • No response to steroids
  • Deteriorates without ongoing exposure hypoxemia
    develops
  • Severe exercise limitation, with arterial
    desaturation
  • Ultimately terminal respiratory failure

22
Silicosis
  • Silica hard crystalling mineral, silicon dioxide
    (SiO2), known as quartz
  • Commonly found in most igneous rocks and most
    types of sand

23
Silicosis
  • Persons at risk
  • Hard rock miners (gold, iron, uranium)
  • Smelter workers
  • Sand-blasters

24
Silicosis
  • Most silicosis results from chronic exposure over
    years
  • Acute silicosis can occur from high exposure
    (sand-blasters), and can cause death from massive
    pulmonary fibrosis.

25
Silicosis recommended reading
  • Finkelstein MM Silica, silicosis, and lung
    cancers a risk assessment.
  • Am J Ind Med 2000 38 8-18
  • Copies will be available at LRC on February 10,
    2003
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