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OCCUPATIONAL LUNG DISEASE PowerPoint Presentation on CD

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eBay item number:
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Last updated on  Nov 09, 2013 06:18:40 PST  View all revisions

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 All derivative (i.e. change in media; by compilation) work from this underlying U.S. Government public domain/public release data is COPYRIGHT © GOVPUBS

$3.00 first class shipping in U.S. and rest of world.

Includes the Adobe Acrobat Reader for reading and printing publications.

Numerous illustrations and matrices.

Contains the following key public domain (not copyrighted) U.S. Government publication(s) on one CD-ROM in both Microsoft PowerPoint and Adobe Acrobat PDF file formats:

TITLE:  Occupational Lung Disease, 74 pages (slides)

SLIDE TOPICS, SUBTOPICS and CONTENTS:

Occupational Lung Disease
Patrick Allan, MD
Maj USAF MC
Staff, Pulm/Critical Care/Sleep Medicine

Occupational Lung Disease
What is that we as Air Force personnel are exposed to that has been associated with symptoms or evident damage to the lung?
Warfighter – pilots, security personnel, munitions
Weaponry – heat tolerant high strength materials
Fire retardants on APC’s and tanks
Deployed environment
Nonspecific – dust, fine sand, fumes
Hospital workers
Latex
Detergents

Case #1
37 y.o. AD Lt. Col presents with complaints of worsening dyspnea and dry cough for 9 months.  He has been provided fluticasone/salmeterol and albuterol inhalers along with several courses of different empiric antibiotics for what PCP’s have labeled as bronchitis and asthma, all without subjective benefit.
Pmedhx: nummular excema
Medications:  Advair, PRN albuterol
PSocHx: no recent travel outside of CONUS, no inhalants/fume exposures, nonsmoker
PFamhx: M-DM, F-COPD
Occupation:  High-velocity weapon propulsion systems






Munitions
Beryllium
Cobalt
Tungsten
Cadmium
Vanadium

Common features
Used in all aspects of:
Airplane manufacturing
Weaponry
Nuclear industry
Space industry


Berylliosis









Case #2
29 y.o. SrA just took up smoking during his tour at Balad AB, Iraq.  He works in CE and was recently taking down a plaster wall from an old Iraqi barracks when he became suddenly dyspneic with a dry cough. 
Radiographic evaluation at the EMEDS disclosed the following:


Patient became progressively hypoxic despite marked breathing efforts necessitating intubation with mechanical ventilation
CCATT airlift provided same-day transport to Landstuhl Germany
Bronchoscopy in the intensive care unit disclosed the following:

Diagnosis: Acute Eosinophilic Pneumonia
March 2003 through March 2004
There were 18 cases of AEP identified among 183 000 military personnel deployed in or near Iraq
incidence of 9.1 per 100 000 person-years (95% confidence interval, 4.3-13.3).
89% were men and the median age was 22 (range, 19-47) years.
All patients used tobacco, with 78% recently beginning to smoke.
All but 1 reported significant exposure to fine airborne sand or dust. (JAMA. 2004;292:2997-3005).

Two soldiers died; the remainder responded to corticosteroids and/or supportive care. Twelve individuals were reevaluated a median of 3 months after diagnosis.
At that point, 3 patients reported mild dyspnea and 1 reported wheezing
Case #3
22 y.o. housekeeper at WHMC complains of a 6 month h/o worsening cough and wheezing.  An ER staff member gave her an albuterol inhaler to help her out – she notes transient near-normalization of her breathing with albuterol use.  She denies a single incident exposure to accidental chemical/detergent spills.
PMHx/other meds-none, no prior asthma history
PSocHx-+1 ppd smoker, -PPD one year ago, constantly exposed to numerous cleaning agents
PFamHx:  NC
All: NKDA
Occupation-Associated Airway Diseases

Case #3 continued
CXR:  WNL, no acute cardiopulmonary process identified
CBC, TSH - WNL
Patient was returned to work by her PCM but told to do peak flow monitoring three to four times a day for four weeks with:
At least three measurements 2-3 hours apart at work
Continue to do 3-4 measurements a day at home on the weekends as well





Patients peak flow show a daytime periodicity – i.e. they get worse when she is at work
PCM orders pulmonary function testing which shows the following:






Reactive Airway Dysfunction Syndrome
a.k.a. irritant-induced asthma
RADS occurs after a single exposure to high level – symptoms must occur within 24 hours of the accidental exposure
Symptoms should persist for at least 12 weeks

Of note patient’s PEF do not worsen upon returning to work unless the irritant can also act as a long-term sensitizer




Occupational Asthma




Factoids
Dose-response relationship for several agents
Cedar, colophony, flour, platinum salts, acid anhydrides, laboratory animal proteins
Concentration required for sensitization is typically 1-2 fold greater than the minimum  concentration to elicit symptoms in those that are sensitized
i.e. PEL for sensitization is higher than for eliminating asthmatic symptoms
Atopy and cigarette smoking are risk factors only for HMW
Latency between sensitization and OA can be several years
Often preceded by rhinoconjunctivitis (11%) (HMW not LMW)
70% of sensitized patients will develop long-term asthma
Sensitization is not OA (60% of + skin tests occur in asymptomatic individuals)

Treatment for airways disease


Who is likely not to improve/remit?
Those with clinically severe bronchospasm at presentation
Those with methacholine responsiveness to low dose challenges
Frequent oral corticosteroids courses to regain control
Case #4
66 y.o. military retiree volunteers moving patients at WHMC when he was exposed to a spill site of cleaning supplies containing bleach.  Feels fine initially but after returning home from work develops a worsening cough. 
PMHx-HTN, HLP
Meds:  Amlodipine, Zocor
PSocHx-never smoker, negative PPD 2 months ago
PFamHx: noncontributory

The cough persists for 6 weeks before he finally decides to see his PCM.
CXR:  WNL, no acute cardiopulmonary process identified
PFT: Normal, no evidence of reversibility

PCM refers pt to pulmonologist (fellow):
methacholine test performed:  normal

Senior staff is concerned given the patient’s incident exposure for potential RADS or a rarer form of chemical bronchitis.
Repeat methacholine test: negative
Sputum sample shows the following:

Pulmonologist then recommends bronchoscopy which reveals the following on endobronchial biopsy:

Diagnosis:  Eosinophilic bronchitis
Patient is started on inhaled fluticasone/salmeterol
Symptoms resolve within 3 days of therapy.
With discontinuation of inhaler his symptoms promptly resume
Case #5
44 y.o. scene commander for the SAFD responds to a chlorine gas spill subsequent to a train collision in SW Texas.  Was wearing his “bunker gear” – consisting of respirator, full mask and standard fire-retardant firefighter uniform.
He did fine at the scene but subsequently noted eye and throat irritation upon returning home followed by a progressive cough.

His PCM, concerned for long-lasting chemical effects refers the patient to pulmonary
CXR: WNL, no acute cardiopulmonary process identified
PFT’s: no obstruction
Methacholine testing was negative
Sputum sampling did not disclose eosinophils on cytology



OA Prevention and Therapy
Prevention and Therapy overlap at two points
Evaluate the workspace – obtain all material safety data sheets for all solid, liquid, vapor, or fume substances found in the person’s workspace.
Removing the offending agent from the workspace
Ensures NIOSH/OSHA limits are enforced
Explores alternative non-irritating/sensitizing agents
Reducing exposure to the offending agent
Patient works in another physically separate work space
Employs NIOSH/OSHA approved filters
Prevention
Prevention



Summary
Occupational Lung Disease
Covers a spectrum from lung tissue to airways disorders
Can only be diagnosed through an appreciation of the symptoms and potential toxic substances present in your patient’s work environment.
Requires objective evidence of disease
Leads to persistent and in many cases recalcitrant disabling lung processes
Treatment is often supportive with appropriate interventions tailored to:
Substance avoidance/minimization
Indicated medical therapy
Appropriate disability support – often has the greatest benefit to the disabled patient and their family
Limits
Lecture did not discuss coal workers, silica, kaolinite, asbestos-related lung disease
Why?  I have separate lectures for each as each requires dedicated discussion.


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