occupational lung disease

Question 1

1. Know the major determinants of site and severity of lung disease

Answer 1

1. Dose= duration x concentration. 2. Solubility= More water-soluble agents deposit in the upper airway (i.e. chlorine - nasopharyngeal mucosa); less water-soluble agents affect the distal airways/bronchioles (i.e. nitrogen oxides). 3. Particle size= Particles > 10 microns are filtered in the upper airway, particles <2.5 microns may affect the small airways and alveoli.

Question 2

2. Know the questions used in evaluation of occupational lung disease

Answer 2

History: Where do you work? What is your job title? What are your job duties? What are you exposed to?

Question 3

Physical exam findings in evaluation of occupational lung disease

Answer 3

usually non specific

Question 4

Diagnostic tests used in evaluation of occupational lung disease

Answer 4

Pulmonary function testing (PFTs), cardio-pulmonary exercise tolerance test, bronchial challenge testing, chest imaging (chest x-ray, high resolution chest CT), blood tests (eg, BeLPT or tests for antigen-specific antibodies), occasionally lung biopsy

Question 5

3. Know the 2 major categories of occupational/environmental lung diseases

Answer 5

Airway diseases and interstitial lung diseases

Question 6

4. Know the types of airways diseases and examples

Answer 6

occupational asthma, reactive airways dysfunction syndrome (RADS) aka irritant asthma, chronic obstructive pulmonary disease (COPD) from coal mine dust, constrictive/obliterative bronchiolitis

Question 7

5. Know the types of interstitial lung diseases and examples

Answer 7

Pneumoconioses: asbestos-related lung diseases (asbestosis), silicosis, coal worker’s pneumoconiosis. Others: hypersensitivity pneumonitis, chronic beryllium disease

Question 8

•HMW compounds: animal proteins, baking flours and enzymes that trigger a specific IgE immunologic reaction.LMW compounds: isocyanates (spray paint/auto-body

Answer 8

PFTs show obstruction (low FEV1) and/or air trapping (increased RV) and/or decreased DLCO. Imaging : may be normal or show airway wall thickening, air trapping, emphysema

Question 9

Interstitial disease PFTs and imaging

Answer 9

•Pulmonary function testing: shows restriction (low TLC/FVC), decreased DLCO. Imaging: inflammation (centrilobular nodules, groundglass opacities) or fibrosis (rounded or linear opacities)

Question 10

Occupational asthma causes and mechanisms

Answer 10

•HMW compounds: animal proteins, baking flours and enzymes that trigger a specific IgE immunologic reaction. LMW compounds: isocyanates (spray paint/auto-bodyrepair), plicatic acid (western red cedar), epoxy resins, platinum compounds that may combine with endogenous proteins to create new antigenic determinants

Question 11

Occupational asthma presentation

Answer 11

Months to years after initial exposure. May have a temporal pattern such as getting better on weekends. Variable airflow obstruction, airway hyperresponsiveness, and airway inflammation

Question 12

Reactive airway dysfunction syndrome presentation

Answer 12

•NO LATENCY, symptom onset within 24-48 hours of exposure. Airway epithelial injury leads to persistent hyperresponsiveness and airflow obstruction

Question 13

Reactive airway dysfunction syndrome causes and mechanism

Answer 13

Causes: exposure to noxious irritant gas/vapor/dusts (i.e. World Trade Center workers exposed to high pH alkaline dust), chlorine exposure. Mechanism: denudation of the mucosa with fibrinohemorrhagic exudates in the submucosa, followed by proliferation of basal cells and supepithelial edema; may expose airway c-fibers, triggering cough and bronchospasm
Causes: exposure to noxious irritant gas/vapor/dusts (i.e. World Trade Center workers exposed to high pH alkaline dust), chlorine exposure. Mechanism: denudation of the mucosa with fibrinohemorrhagic exudates in the submucosa, followed by proliferation of basal cells and supepithelial edema; may expose airway c-fibers, triggering cough and bronchospasm

Question 14

Occupational COPD presentation

Answer 14

•cough, sputum, wheezing, chest tightness and dyspnea

Question 15

Occupational COPD causes and mechanism

Answer 15

•Causes: exposure to biomass combustion, respirable silica and coal mine dusts (mining), vanadium, organic dusts. Mechanism: oxidant injury, imbalance of proteases and anti-proteases

Question 16

Constrictive/Obliterative Bronchiolitis presentation

Answer 16

•subtle onset with cough, dyspnea, chest tightness. Pathologic injury of small airways causes extrinsic or intrinsic bronchiolar narrowing

Question 17

Constrictive/Obliterative Bronchiolitis causes

Answer 17

•exposure to noxious gases such as oxides of nitrogen and sulfur, dusts (combustion products), and chemicals (i.e. diacetyl flavoring in buttered popcorn – think flavor workers lung disease)

Question 18

Constrictive/Obliterative Bronchiolitis mechanism

Answer 18

Injury to bronchiolar epithelium results in excessive proliferation of granulation tissue, leading to narrowing or obliteration of the airway; submucosal or peribronchiolar fibrosis may lead to extrinsic narrowing or obliteration of bronchiolar lumen

Question 19

Asbestos lung disease cause and mechanism

Answer 19

•Cause: asbestos fibers – group of naturally-occurring hydrated magnesium silicates that when crushed, break into fibers (friable) Mechanism: direct toxic effects of fibers on pulmonary parenchymal cells, with release of various mediators by inflammatory cells

Question 20

Asbestos related lung diseases

Answer 20

Malignant: lung cancer and mesothelioma. Non malignant: benign asbestos pleural effusion, pleural thickening/calcifications/plaques, rounded atelectasis, and asbestosis (fibrosis usually affecting lower lung zones)

Question 21

Silicosis presentation

Answer 21

usually long latency, includes SOB and cough. Causes interstitial lung disease which can progress to fibrotic lung disease

Question 22

Silicosis causes and mechanism

Answer 22

•Causes: crystalline silica, exposed workers such as gold miners, foundry workers, sandblasters (stone-washed jean manufacturers. Mechanism: : generation of oxygen radicals that injure target pulmonary cells such as alveolar macrophages, leads to generation of inflammatory cytokines

Question 23

Coal Workers Pneumoconiosis presentation

Answer 23

usually cough, shortness of breath; pulmonary function testing may be normal, chest imaging typically demonstrates upper lobe small rounded nodular opacities; pathology may be notable for “dust macules”.

Question 24

Coal Workers Pneumoconiosis causes and mechanism

Answer 24

Causes: inhalation of coal mine dust. Mechanism: generation of oxygen radicals that injure target pulmonary cells such as alveolar macrophages, leads to generation of inflammatory cytokines

Question 25

Chronic Beryllium Disease presentation

Answer 25

Subtle cough, dyspnea, chest tightness. Indistinguishable from sarcoidosis excepft for exposures

Question 26

Chronic Beryllium Disease causes and mechanism

Answer 26

Causes: beryllium (lightweight, strong metal used in aerospace engineering, nuclear bomb manufacturing, nuclear reactors, etc.). Mechanism: immune response to beryllium, often leading to granulomatous lung inflammation; some workers have a genetic susceptibility to beryllium’s effects, but there is also a dose-response relationship

Question 27

Hypersensitivity Pneumonitis presentation

Answer 27

acute symptoms – flu-like illness with respiratory symptoms; subacute/chronic HP – insidious onset. Immune response to animal proteins

Question 28

Hypersensitivity Pneumonitis cause and mechanism

Answer 28

Causes: some animal proteins (mainly birds), fungi, bacteria inhaled from contaminated hay (farmer’s lung), hot tubs & indoor pools (due to non-tuberculous mycobacteria and gram-negative organisms), humidifiers, machining/metal-working fluids. Mechanism: T cell response