Wake Pulm Occupational Respiratory Disease

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Chrysotile

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- serpentines type
- one of the four fibers of asbestos
- readily cleared from the lung
- mesothelioma risk by itself or with tremolite contramination

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Crocidolite

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- amphiboles type
- one of the four fibers of asbestos
- More durable & fibrogenic
- Greater mesthelioma risk
- Readily form asbestos bodies

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Ferruginous Body

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Coated asbestos body… if you do an iron stain…this shows up

However, a ferruginous body does not mean asbestos…could be talc or something else

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Asbestos is found ...

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in > 3,000 products

40% of the workforce from 1940-1980 was exposed to asbestos

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What is the key to dx of asbestosis?

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key to Dx is complete history and high index of suspicion

there is a minimum of a 10 year latency... so you have to research back ... the early jobs are the most important

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What are the asbestos induced lung diseases?

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Benign pleural effusions/plaque
Asbestosis
Lung cancer
Mesothelioma

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What is seen on CXR and CT with asbestos exposure?

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CXR:
- Pleural plaque creates a ghost white shadow
- Blunting costophrenic angle = pleural effusion
- Thickening of visceral plueral.. Can cause restriction
- Pleural plaques along parietal pleura which can calcify (generally along the 6th-9th ribs posteriorly and bilaterally)… do not effect lung function

CT: Calcified pleural plaque

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Pleural Effusion for Asbestos

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May develop >= 10yrs after first exposure

May be benign or malignant

May be bloody

Seen on CXR at the parietal pleura... solitary abnormality in 48% of workers with a 20 year latency

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Asbestosis

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ILD

Fine reticular nodular markings (looks like spider web on CXR)

Starts in the lung bases

Latency often >20yrs

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Mesothelioma

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Exposure Hx in 70-80%

30-40 yr latency

Risk NOT dose dependent

Think there is a gene- environmental dz
b/c seem to run in families

There is no cure

Occurs in throrax > abdomen >>testicles

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What are the three types of cells in Mesothelioma?

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Epithelial (most common and best survival, only one surgeons will operate on)

Sarcomatous

Desmoplastic (looks like hyaline scaring… hard to dx pathologically)

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Mesothelioma on CXR

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Lumpy, bumpy pleural abnormality

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Mesothelioma
Signs and Symptoms

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Bloody pleural effusion

Cytology rarely Dx (tissue biopsy usually required)

Symptoms
- Pleuritic CP 60%
- Dyspnea 35%
- Cough 15%
- Weight loss 5%

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Progression of Mesothelioma

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Tumors grows around and surrounds the lungs.

It can grow out through the chest wall, pain when it gets to intercostal nerves.

Death from cor pulmonale as it grows into the pericardium and squishes the heart.

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Risk of Lung Cancer with smoking and/or asbestos

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10X greater chance of lung CA with smoking

5X greater chance of lung CA with asbestos exposure

If smoking and asbestos exposure, then 50-100 fold increase in bronchogenic CA risk

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Bronchogenic Cancer
and Asbestos induced lung disease

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5 X more common than in non exposed

Synergy with cigarette smoking yields 100 X risk

Cell types equal to smoking induced

Loosely exposure amount related

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Material Exposures of Asbestos

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Textiles
Building materials
Plastics
Paper products
Insulation
Caulks, putties cements, bond
Refractories

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Industrial Exposures of Asbestos

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Pipefitting
Plumbing
Foundry
Construction
Printers
Carpenters
Railroad
Shipyards

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Occupational Asthma

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"Variable airways narrowing causally related to exposure in the working environment to airborne dusts, gases, vapors or fumes" 

It is specific to the work place

Occupational exposures cause significant worsening in up to 15% of asthmatics

Estimated 2-5% of asthma cases in U.S. are de novo occupational asthma

Failure to diagnose and manage promptly can lead to long-term, irreversible sequelae

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Occupational Asthma Prevalence

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Plastics industry - 5%

Animal breeders/handlers - 6%

Bakers (flour... isocyanate) - 10-30%

Cotton workers (cardroom) - 20-30%

Metal refinery (platinum)- 30-50%

Western red cedar - 5%

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Does History Suggest Non-Occupational Basis?

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No relation between work and symptoms

Preexisting asthma / respiratory problems

Upper respiratory infection at onset of symptoms

Non-occupational allergies

Smoking

Medications (beta blockers, NSAIDs)

Gastroesophageal reflux symptoms 

Review medical records

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Occupational Asthma from Sensitizers

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Latent period of immunologic sensitization (1 year for small particles, 5 years for large)

Low levels cause symptoms

Sensitivity increases with continued exposure

If IgE mediated, correlation with skin tests, in vivo tests

Usually only in minority of workers

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Did the exposure cause the asthma?

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TDI (diisocyanates) 5-10%, wood dusts 4%, pine resins (colophony) 4-21%, salts of nickel chromiun & platinum

RADS
- acute overwhelming exposure
- nonspecific bronchial hyperreactivity (methacholine positive)

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Reactive Airways Dysfunction Syndrome
(RADS)

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No previous history of asthma

Acute, high level exposure to toxic/irritant agent

Respiratory symptoms within 24 hours of exposure

Persistent respiratory symptoms, non-specific bronchial hyperreactivity

Pulmonary functions normal (with + methacholine challenge) or show reversible obstruction
- Obstruction less reversible than asthma

Eosinophilic infiltration not characteristic

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Etiologies of occupational asthma
Low Molecular Weight Chemicals

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Isocyanates (HDI, MDI, TDI, IPDI)

Woods (red cedar, exotic, sawmills)

Glues (methacrylates, cyanoacrylates)

Epoxies (anhydrides, amines...)

Colophony

Dyes

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Etiologies of occupational asthma
High Molecular Weight Chemicals

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Flour - cereals

Animals handlers

Latex

Psyllium (in metamucil)

Crab processing

Antibiotics, enzymes

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Postive

Interpretation of specific challenges

Occupational Asthma

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A positive challenge is usually defined by a sustained fall in FEV1 of ≥ 20%, as compared to the control mock day.
- This confirms the diagnosis of occupational asthma

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Negative

Interpretation of specific challenges

Occupational Asthma

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A negative challenge however does not exclude entirely the diagnosis of occupational asthma

- Wrong agent (or sensitizing process not active)

- Loss of sensitization

- Medication not allowed

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Occupational Asthma Management

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Reduce / avoid exposure in work place

Removal of worker in some cases, particularly if sensitizer present

Surveillance measures
- Periodic monitoring of work place exposures, spirometry, tests for immunologic sensitization

Medications

Address any non-occupational factors

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Occupational Asthma Prognosis

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Timely removal should result in improvement

Residual disease
- Reported from isocyanates, red cedar, snow crab, some irritants, other agents

- Worse prognosis if greater duration exposure; greater severity / frequency of symptoms, airway obstruction or hyper-reactivity, dual bronchial responses

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OCCUPATIONAL ASTHMA

Was this the heralding asthma event?

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Hx of allergic rhinnitis

family Hx of asthma

Hx of frequent URI

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OCCUPATIONAL ASTHMA

Can the patient return to work?

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Is there a physiologic link between the workplace and the functional abnormality

Is the patient optimally controled

Is the patient compliant with their meds

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Silicosis

Epidemiology

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1500 new cases of silicosis projected annually by statewide NJ surveillance 1979-1987.

Among new cases of pneumonitis diagnosed 1/33 - silicosis/asbestos

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Niosh Major Occupational Exposures Categories

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1. Metal mining

2. Coal mining

3. Nonmetallic minerals

4. Stone, clay and glass products

5. Foundries

6. Sandblasting (most common in /US)

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Classical Findings of Silicosis

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1. Shortness of breath on exertion (Spirometry= obstructive)

2. Cough/sputum production

3. Chest tightness

4. Wheezing

Often confounded by exposure to tobacco smoke, polycyclic hydrocarbons, and radiation

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Silicosis

CXR Abnormalities

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1. Rounded (p, q, r) opacities approximately 1 mm in diameter

2. Upper lung zones

3. May coalesce or Calcify (progressive, massive fibrosis)

4. May have associated lower lung bullae that cause pneumothorax (b/c scar tissue contracts)

5. Egg-shell calcification of mediastinal, hilar nodes

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Immunity and Silicosis

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1. High incidence of RF and ANA (scleroderma and rheumatoid arthritis)

2. High incidence of TB or m. Avium

3. Caplan’s Syndrome

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Silicosis and Onset

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Chronic – 10-30 years

Accelerated – 10 yrs

Acute ... silicoproteinosis – immediately

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Silicoproteinosis

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Prominent alveolar illing with eosinophilic proteinaceous material

Mild interstitial thickening is also present

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Most important considerations with Asbestosis

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All employment important

Second hand exposure

latency

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Most important considerations with occupational asthma

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Is asthma caused by or exacerbated by employment

Does the asthma preclude working in the environment

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Most important considerations with Silicosis

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Upper lobe

Alveolar proteinosis

Autoimmune overlap