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