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