Occupational Lung Disease Flashcards
Major airway diseases related to occupational exposure
- occupational asthma
- reactive airways dysfxn syndrome (RADS)
- COPD
- constrictive/obliterative bronchiolitis
Major interstitial lung diseases related to occupational exposure
- asbestos-related lung diseases (asbestosis),
- silicosis
- coal worker’s pneumoconiosis
- hypersensitivity pneumonitis
- chronic beryllium disease
Major Hx questions to determine presence of occupational lung disease
- Where do you work?
- What is your job title?
- What are your job duties?
- What are you exposed to?
- Review exposure assessment: MSDS, OSHA reports, exposure sampling
Major determinants of site/severity of lung disease
- dose: duration*concentration
- solubility
- particle size
Impact of solubility on site/severity of lung disease
- more water-soluble agents ==> upper airway (i.e. nasopharyngeal mucosa, eg, chlorine)
- less water-soluble agents ==> distal airways/bronchioles (eg, nitrogen oxides).
Impact of particle size on site/severity of lung disease
- particles > 10 microns = upper airway
- particles <10 microns are “respirable” = more deeply into the lung
- particles <2.5 microns = small airways and alveoli
Occupational asthma (OA) general characteristics
- airway dz w/variable otuflow obstruction + airway hyperresponse + airway inflammation due to occupational exposure
- caused by agents w/immunologic/sensitizing properties
- OA and asbestos-related lung disease = most common occupational lung diseases
- OA accounts for up to 15% of adult asthma.
OA: causes/mechanisms
i. High-molecular weight compounds – eg, animal proteins, baking flours and enzymes that trigger a specific IgE immunologic reaction
ii. Low-molecular weight compounds – eg, isocyanates, plicatic acid (found in western red cedar), epoxy resins, platinum compounds <== combine w/self proteins to create new “foreign” antigens
OA: Dx & Tx
- asthma w/latency = onset long after exposure
- usually improves w/time away from work
- confirm asthma w/PFTs and imaging
- Tx: remove causal exposure + normal asthma tx
RADS general characteristics
Airway epithelial injury from exposure to inhalants with irritant properties, leading to persistent bronchial hyperresponsiveness and airflow obstruction
RADS: causes & mechanism
i. Causes: exposure to noxious irritant gas/vapor/dusts (eg, World Trade Center workers exposed to high pH alkaline dust)
ii. Mechanism: denudation of the mucosa with fibrinohemorrhagic exudates in the submucosa, followed by proliferation of basal cells and subepithelial edema. May expose airway c-fibers, triggering cough and bronchospasm.
RADS: Dx & Tx
- No latency = sx w/in 24-48 hrs of expsure
- Dx w/Hx, PFTs, imaging
- Tx w/asthma Rx
COPD (occupational): Causes & Mechanism
i. 15% of COPD due to occupational causes including biomass combustion, respirable silica and coal mine dusts (mining), organic dusts
ii. Mechanism: probably similar to tobacco-smoke induced COPD – oxidant injury, imbalance of proteases and anti-proteases
COPD: Dx & Tx
- Sx: cough, sputum, wheezing, chest tightness, dyspnea
- Dx w/PFTs, imaging, hx
- Tx: remove from exposure, COPD rx
Constrictive/Obliterative Bronchiolitis: definition
Pathologic injury of small airways (eg, less than 2 mm in diameter), with extrinsic or intrinsic bronchiolar narrowing
Constrictive/Obliterative Bronchiolitis: causes & mechanism
i. Causes: Exposure to some noxious gases (eg, oxides of nitrogen and sulfur), dusts (combustion products), and chemicals (eg, diacetyl flavoring in buttered popcorn)
ii. Mechanism: a. Injury to the bronchiolar epithelium ==> granulation tissue ==> narrowing or obliteration of the airway.
b. Submucosal or peribronchiolar fibrosis ==> extrinsic narrowing or obliteration of the bronchiolar lumen.
Constrictive/Obliterative Bronchiolitis: Dx & Tx
- sx: subtle onset, cough, dyspnea, chest tight
- dx: hx, PFTs, CT shows air trapping
- tx: remove from exposure (poor prognosis)
Asbestos-related Lung diseases: causes & mechanism
- asbestos = metallic fiber ==> shape/size (aspect ratio) confer disease risk
- main exposures: construction demolition/remodels, commercial brake mechanics
- Direct toxic effects of fibers on pulmonary parenchymal cells
- Free radicals react with and damage a variety of cellular macromolecules and may disrupt DNA, increasing risk for malignancy.
Types of non-malignant asbestos-related lung disease
- benign asbestos pleural effusion
- pleural thickening/calcification/plaque
- rounded atelectasis
- asbestosis
Types of malignant asbestos-related lung disease
- lung cancer <== syngery with smoking (asbestos + smoking = 50x increased risk)
- mesothelioma (pleural, peritoneal)
- no increased risk w/ smoking
- sentinel cancer for asbestos exposure
Asbestos-related lung diseases: Dx & Tx
- Hx (early occupations), PFTs (restricted), imaging (plaques, scarring)
- Tx: benign=supportive, malignant=oncology; remove from exposure
Silicosis: causes & mechanism
- Workers who blast, cut, grind with/on respirable silica containing materials
- Hard rock miners, foundry workers, sandblasters, stone-washed jeans manufacturers
- O2 radicals injure target pulmonary cells such as alveolar macrophages ==> inflammatory cytokines ==> resulting in inflammation and fibrosis
Silicosis: Types
- simple silicosis
- complicated silicosis (progressive massive fibrosis)
- acute silicoproteinsosis
- accelerated silicosis
- other conditions can result (infections, cancer, etc.)
Silicosis: Dx & Tx
- Dx: exposure history, PFTs (restriced or mixed)
- imaging: upper lobe, nodular, silicoprotein=~PNA-looking
- biopsy
- Tx: removal from exposure
Workers pneumoconiosis (Black lung): causes, mechanism, dx, tx
- Cause: inhalation of coal mine dust , underground > surface
- Mechanism: similar to silica toxicity
- Diagnosis: exposure hx, PFTs (normal or abormal), imaging (upper lobe small rounded nodular opacities)
- Pathologic feature = “dust macule”
- Treatment: remove exposure, pulmonary supportive care
Chronic Beryllium disease (CBD): cause & mechanism
- Beryllium (Be) = metal in aerospace/bomb manufacture ==> beryllium sensitization
- Mechanism: Immune response to beryllium ==> granulomatous lung inflammation.
- some genetic susceptibility possible
- dose-response relationship
Chronic Beryllium disease (CBD): Dx & Tx
- Dx: hx of exposure, latency, dyspnea, cough
- blood levels of BeLPT
- lung biopsy
- Tx: remove from exposure, inhaled steriods
Hypersensitivity Pneumonitis: causes & mechanism
i. Causes :
1. Some animal proteins (mainly birds) – parrots, cockatiels, cockatoos, finches (Bird fancier’s lung)
2. Microbial aerosols: 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
3. A few low molecular weight chemicals: isocyanates
ii. Mechanism
1. T-cell-mediated immune response, with antigen-specific antibodies
Hypersenstivity Pneumonitis: Dx & Tx
- Acute: flu-like, respiratory illness, 6-12 hrs after high-dose exposure
- Subacute/Chornic: respiratory + systemic symptoms
- Dx: exposure hx, PFTs (restricted usuallly), CT w/ upper lobe centrilobular nodes, ground glass, air trapping
