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

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

2 Dust Diseases Following removal from exposure, coal pneumoconioses may stop progressing but Silicosis and asbestosis often do progress Asbestosis Model for: Restrictive ventilatory impairment (vs obstructive) Interstitial lung disease 2

3 Why Study Asbestosis? Exposure has continued in European construction industry till the mid- 1970s What about developing countries? 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 3

4 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. ASBESTOS Asbestos fibers are categorized into 2 groups: Amphiboles Serpentines 4

5 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. ASBESTOS: Serpentines Used commercially: Chrysotile (3MgO-2SiO 2-2H 2 O) (the most common) 5

6 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. 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) 6

7 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. Effects Pulmonary Fibrosis Pleural Thickening Pleural Effusion Cancer 7

8 Pulmonary Fibrosis Results in restrictive lung disease that generally becomes manifest clinically years after the onset of exposure. Pulmonary Fibrosis (Cont d) 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 (D L CO) Eventually, extensive fibrosis obstructs the blood flow throughout the pulmonary bed, causing pulmonary hypertension and compensatory right ventricular hypertrophy. 8

9 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. 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 9

10 Lung Cancer Latency of 20 years. Same cell types and histological features as other primary lung cancers. 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). 10

11 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 Silicosis Silica: hard crystalling mineral, silicon dioxide (SiO 2 ), known as quartz Commonly found in most igneous rocks and most types of sand 11

12 Silicosis Persons at risk: Hard rock miners (gold, iron, uranium) Smelter workers Sand-blasters 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. 12

13 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,

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