Download Asbestos Related Lung Disease

Occupational Lung Disease
Respiratory Block: 2016
Sunita Mulpuru MD FRCPC
&
Steven T. Bencze MD FRCPC
Respiratory Medicine
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Session Objectives
List
common occupational exposures
that lead to occupational asthma
Describe key
causes, symptoms and
types of occupational lung disease
Occupational Lung Disease Key Features
•
Respiratory illness caused by the work environment
•
May occur years after the exposure (decades)
•
Exposures can affect:
– Airways (bronchi/alveoli)
– Lung Interstitium (area around the airspaces)
– Pleura
Lung Structure
Bernardino Ramazzini (1633 - 1714):
De Morbis Artificum, 1713
Occupational Asthma: Definition
“Disease characterized by variable
airflow obstruction and/or airway
hyper-responsiveness due to causes
and conditions attributable to a
particular work environment and not to
stimuli encountered outside the
workplace”
• It is usually new-onset asthma, but can
occur in people with pre-existing
asthma
• Pathophysiology:
– Immunologically mediated (via IgE
antibodies to HMW of LMW agents)
– Induced by respiratory irritant at work
(less common)
Can Respir J Vol 5 No 4 1998
Occupational Asthma: Breakdown
Occupational Asthma: Mechanisms 1
• Sensitization to a High or Low molecular weight agent occurs, with a
latency period of weeks to years
– Re exposure can cause an asthmatic response
• Sensitization by an immunologic mechanism occurs for many agents
(latex proteins, flour, animal allergens)
Occupational Asthma: Mechanisms 2
• Alternatively, OA can be caused by high
level irritant exposure at work
– Starts within 24 hrs, no latency
period, no sensitization, re-exposure
will usually not trigger asthma
OA: HIGH MOLECULAR WEIGHT antigens
Sensitizers
Occupation
Animal, insect
Animal handlers, Health Care Workers
Food , animal protein, bacteria, fungi
Food processing
Latex
Health Care Workers
Flour
Bakers
Vegetable gums
Printers
OA: Low MOLECULAR WEIGHT Antigens
Sensitizers
Occupation
Isocyanates
Painters , autobody, glues
Wood dust
Carpenters, forestry
Dyes
Textile workers
Epoxy
Auto industry
Persulfate
Hairdresser
Fluxes
Electronics
Metal dust
Welders
Occupational Asthma: Clinical History
• Must have a high index of suspicion
• Occupational history
– exposure to a known asthma inducing agent (get the
material safety data sheets)
– Symptoms started after employment
– Improvement of symptoms during weekends and
holidays
– Worsening of symptoms on returning to work
• History alone is insufficient, so
objective testing is needed
Occupational Asthma: Objective Testing
•
Demonstrate the presence of asthma
objectively
–
Spirometry pre and post bronchodilator (Beta 2
agonist) with 24 hrs of work place exposure or
during symptoms
–
Methacholine challenge test (if spirometry
normal)
•
Use Objective tests to assess the relationship
with work
–
–
–
–
Immunological tests (identify specific IgE
antibodies to a work place allergen)
Serial PEF measurements both on and off work
On and off work methacholine challenge tests
Specific inhalation challenges or occupational
type of exposure tests - "gold standard"
OA Diagnosis: Monitoring of PEF - How to do it ?
•
At least 2 weeks at work and off work
–
At least 4 times daily, preferably every 2 hours
•
Medication allowed:
1. Keep it constant and at minimum dose
2. Short acting Beta-2 agonist as needed
3. Continue asthma controllers
4. Avoid, if possible, long-acting beta-2-agonist
•
False positive
– Subject not exposed during monitoring
– Poor compliance
False negative
– Change in medication (inhaled steroids)
– Malingering (falsification of results)
•
PEF Monitoring: Example
American Thoracic Society: Occupational Asthma
Occupational Asthma: Methacholine Challenge
Testing
• Have patient on / off work for 2
week periods
• Complete methacholine challenge
testing while working, then at the
end of a 2-4 week period off work
• If improvement in the PC20 level
(concentration of MCT at which FEV1 falls
improves while off work: highly
supportive of OA
20%)
– Looking for a 3-4 fold increase in the
concentration of methacholine that
produces a drop in FEV1
Reactive Airways Dysfunction: Diagnosis
• Generally not confirmed by objective
tests
– Depends on history
– Objective confirmation of asthma
– Onset within 24 hrs of large
exposure
– Symptom duration of at least 3
months
• Reactive Airways Dysfunction
Syndrome (RADS) among Rescue and
Recovery Workers in the World Trade
Center Health Registry (WTCHR)
– (Am J Respir Crit Care Med 179;2009:A5853)
RADS: Diagnostic Criteria
ACCP: Diagnosis and Management of Work-Related Asthma
RADS: Some Causative Agents
Sensitizers
Smoke
Chlorine
Sulphur dioxide
Cleaning agents
Isocyanates (paints)
Diesel exhaust
Other Occupational Lung Diseases
1) Hypersensitivity Pneumonitis
–
Hypersensitivity (allergic) reaction to
inhalation of antigenic organic
particles/fumes
2) Pneumoconioses
– Airway and Interstitial pulmonary
disease resultant from inhalation of
inorganic and organic dusts
Hypersensitivity Pneumonitis (HP)
• First recognized in 1713, in wheat
reapers
• 5 -15% prevalence in population
exposed to known inciting antigens
• Presents along a spectrum of acute,
subacute, and chronic
• May hear about HP as “Farmer’s
Lung” or “Bird Fancier’s Lung”
depending on the exposure that
caused it
– > 200 different organic antigens
associated with HP
• More common among non-smokers
Hypersensitivity Pneumonitis: Clinical Presentation and
Diagnosis
•
Acute form:
– occurs several hours after exposure
– subside within a few days
•
Subacute form:
– can occur with gradual onset of dyspnea over
weeks and months, chronic productive cough
•
Chronic form:
– Long standing exposure to the offending
antigen can lead to irreversible fibrotic
changes in the lung
•
Diagnosis:
– Compatible History of exposure to known
causative agent
– Classic Radiology patterns
– Resolution with removal of the offending
exposure
Hypersensitivity Pneumonitis: Known Inciting Antigens
Hypersensitivity Pneumonitis: Factors in Pathogenesis
Host
factors
Agents
Genetic
background
antigens
Smoking
history
Non-antigenic
elements
HP
Viral
infection(s)
Hypersensitivity Pneumonitis: Management
• Avoidance of the antigen is the key
– May continue farming without development of irreversible
fibrosis
• Precautions
– Dust masks with filters
– Appropriate ventilation
– Mechanisation feeding process
– Close monitoring
• Despite avoidance of antigen
– Chronic form may fail to improve (development of fibrosis)
• For severe cases
– Prednisone 40-60 mg/day x 7-14 days
– Tapering dose over 4-6 weeks
• Not recommended to continue steroid therapy past 6 months
Pneumoconioses: Inhalation of Inorganic/Organic
Dusts Compounds
•
Definition:
– Lung disease (non-neoplastic) resulting from inhalation of inorganic and organic dusts
– Examples: Silicosis, Asbestosis, Coal Worker’s Pneumoconiosis, Talc-related lung disease,
Bauxite Pneumoconiosis
•
Sources of exposures:
– Coal: Coal miners
– Silica: Sandblasters, Miners, Foundry workers, Potters, Dental Workers, Construction,
Glass workers, Stone cutters (sandstone, granite)
– Asbestos: Mining, Shipyard workers, Plumbers, Electricians, Construction
•
Factors that determine severity of lung reaction to these materials
– Intensity and duration of exposure
– Individual sysceptibility
– Nature and properties of the dust (size, toxicity, etc.)
Coal Workers Pneumoconiosis (Coal Workers Lung)
• Coal Worker’s Pneumoconiosis:
– Small particles are inhaled, causes an
inflammatory state, pulmonary architecture is
damaged
– Pulmonary nodules and progressive massive
fibrosis can result (usually stops when exposure stops)
– Years – Decades to develop
– Symptoms: Chronic cough, sputum production
(melanoptysis), dyspnea
– PFT: Progressive airflow limitation (obstruction)
• Exposure to coal dust can also result in chronic
bronchitis and chronic obstructive pulmonary
disease “industrial bronchitis”
Imaging Examples: Coal Worker’s
Pneumoconiosis
Progressive Massive Fibrosis
Silicosis
• Silicosis
– Silica is silicon dioxide (SiO2) which
comprises large part of granite, sandstone
and slate
– Silicosis is lung disease caused by
inhalation of fine silica dust (acute or
chronic) and subsequent inflammatory
reaction (continues even without exposure)
– Acute Silicosis: alveolar filling with
inflammatory infiltrates (rare)
– Chronic Silicosis: nodules, and progressive
massive fibrosis (coalescing of the
nodules), 20-30 years after exposure
– Symptoms: Cough, dyspnea
• Patients are susceptible to
Mycobacterial infections (like
M.Tuberculosis)
Imaging Examples: Silicosis
Silicosis (Nodular Disease)
Silicosis (progressive, massive
fibrosis)
Asbestos Related Lung Disease
Asbestos Related Lung Disease
• Naturally occurring fibre used widely in the
construction and insulation industries (high
tensile strength)
• Two Types of Asbestos Fibres
– Serpentine Fibres (Chrysotile, 90% of
commercial use, less toxic)
– Amphibole Fibres (crocidolite, amosite,
tremolite )
• Cause clinical respiratory disease by direct toxic
effects on pulmonary cells, and subsequent
release of cytokines, reactive oxygen species
Asbestos Related Lung Disease: Occupation & Clinical
Manifestations
• Some Occupations Associated with
Exposure:
– Plumbers, Pipefitters, Electricians, Insulation
Workers, Carpenters, Boilermakers, Welders, Work
with Brakes (linings), Shipyard workers, Textile
workers (making fireproof clothing and blankets)
– Other forms of exposure: living near asbestos mines,
residential remodelling
• Clinical Manifestations:
– Pleural effusion (benign)
– Pleural plaques
– Diffuse pleural thickening, rounded
atelectasis
– Asbestosis (interstitial lung fibrosis)
– Malignant mesothelioma (cancer of
the pleura)
– Bronchogenic carcinoma
Asbestos Related Lung Disease: Effusion
• Benign Asbestos-Related Pleural Effusion
(BAPE)
– Usually seen within 15 years of
exposure (much before appearance of
interstitial lung disease)
– Usually unilateral
– Often “exudative” in nature
– May recur, persist, or leave pleural
thickening
Asbestos Related Lung Disease: Pleural Plaques
•
Pleural Plaques - Benign
– Calcifications usually involving the parietal pleura, usually asymptomatic
– Occur in approximately 50% of asbestos-exposed individuals (significant exposure)
– Most common manifestation of previous asbestos exposure
– 20-40 year latency (at time of detection)
Asbestos Related Lung Disease: Asbestosis (ILD)
Asbestosis: Fibrotic lung disease secondary to asbestos exposure:
- Usually 20-30 yr latency period, inversely proportional to exposure
intensity
- CT example of lung fibrosis caused by Asbestos Exposure: “Honeycomb Cysts”
Asbestos Related Lung Disease: Malignant Mesothelioma
• Mesothelioma is a cancer of the mesothelial
surfaces of the pleura or periotoneum
• 10% lifetime risk of developing
mesothelioma in asbestos workers (high
estimate)
• Dose-response relationship between
exposure and mesothelioma
• Latency period of 30-40 years
• Not known to be independently associated
with smoking
– Asbestos exposure and smoking act synergistically
to increase the risk of lung cancer to 60x’s that of a
non-smoker, non-asbestos exposed person
Asbestos Related Lung Disease: Malignant Mesothelioma
Clinical Presentation:
• More common in men, presenting age 5070
• Most common to present with pleural
effusion
• Symptoms: breathlessness, pleuritic chest
pain, constitutional symptoms (with
disease progression)
• X ray may show pleural effusion, or pleural
thickening, CT can show diffuse
circumfrential nodular pleural thickening
1.
Diagnosis:
• Pleural biopsy
• CT Guided
• Thoracoscopy
1. Drug Discovery Today:Disease Mechanisms Vol 4, No.2, 2007
Pneumoconioses: Summary
American Thoracic Society, Occupational Lung Diseases
Occupational Lung Disease Key Features
•
Obtain an Occupational history (this is key)
• Type of work, setting, duration, exposures
• Seek objective evidence of cause and effect
relationship
•
Reduction of exposure is the key to prevention
•
Advise Patients about Workplace Safety and
Insurance Board (WSIB) and compensation
(if warranted)
Occupational Lung Disease: Summary
• Many lung disorders can be caused or exacerbated by
occupational or non-occupational factors and
exposures
• Some occupational exposures can cause several
different lung disorders
• Multiple different exposures (including cigarette
smoke) may be important for development of clinical
disease
• Exposure dose matters
• Individual differences in susceptibility are important
• Some disorders take a long time to develop
• Occupational & exposure history is crucial!!
Occupational Lung Disease Summary
Occupational
Asthma
Hypersensitivity
Pneumonitis
Pneumoconioses
Mechanism
Immune or
Irritant
Immune /
Allergic
Immune / Chronic
Inflammation
Onset
Weeks-Months
Immediate (RADS)
Months-Years
Long Latency
Diagnosis
- Methacholine
Testing
- Compatible
History
- Compatible History
- Radiographic
Findings
- Improves with
removal of antigen
- Compatible history
(workplace)
- Radiographic
Findings
(Asbestos/Coal/
Silica)
Any Questions?