eMedicine Specialties > Pulmonology > Occupational Lung Diseases

Silo Filler's Disease

Nader Kamangar, MD, FACP, FCCP, FAASM,, Associate Professor of Clinical Medicine, Director of Hospitalist/Intensivist Program, Division of Pulmonary, Critical Care and Sleep Medicine, David Geffen School of Medicine at University of California Los Angeles; Associate Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA/West Los Angeles Veterans Affairs Medical Center
Lex Chen, MD, Resident Physician, Department of Internal Medicine, University of California Los Angeles, Olive View Medical Center

Updated: Sep 17, 2009

Introduction

Background

Silo filler's disease (SFD) is an occupational disease that results from pulmonary exposure to oxides of nitrogen. Silo filler's disease is a preventable occupational hazard that can be eliminated by proper work practices.

Nitrogen dioxide is a reddish brown gas that emits an odor similar to that of household bleach. It forms rapidly in farm silos that are filled with fresh organic material (eg, corn, grains). Hours after the organic material is stored, toxic and lethal levels of nitrogen dioxide, which is heavier than air, develop on top of the silage.

The clinical presentation of silo filler’s disease depends on the duration of exposure and the concentration of this gas. Without proper precautions, farm workers entering a silo or remaining near the open hatches during the first 10 days after filling may experience various degrees of exposure. Most symptomatic exposures are mild and self-limiting; however, some events may cause sudden death from asphyxiation, pulmonary edema, or, weeks later, bronchiolitis obliterans. Low concentrations of nitrogen dioxide may cause cough, dyspnea, fatigue, upper airway irritation, and ocular irritation. With an increase in concentration and duration, the individual may experience cyanosis, vomiting, vertigo, and a loss of consciousness. More severe exposure can result in acute respiratory distress syndrome (ARDS), laryngeal spasm, bronchiolar spasm, reflex respiratory arrest, or asphyxia.

The first recorded incidence of a death from silo filler’s disease was in 1914 when 3 men fell into a silo and were asphyxiated by an unknown gas (ie, unknown at that time). The term silo filler's disease was coined in 1956.

Nitrogen dioxide, the main toxin found to cause silo filler’s disease, has been implicated in more instances of sudden infant death syndrome (SIDS), increased symptoms among asthmatic individuals, and higher rates of emergency department visits.

In a study with 169 cases of SIDS against age-matched controls, a higher nitrogen dioxide level increased the likelihood of SIDS. The level of nitrogen dioxide levels has seasonal trends. During the months with elevated nitrogen dioxide levels, the incidence of SIDS appears to increase. Even after adjusting for seasonal trends, nitrogen dioxide on the last day of infant exposure before death significantly increased the likelihood of SIDS.¹

Nitrogen dioxide increases the likelihood of pediatric asthma symptoms. In houses with the presence of a gas stove, which increases the levels of nitrogen dioxide, the incidence of respiratory symptoms among asthmatic persons is higher. The mean nitrogen dioxide level was 8.6 ppb (standard deviation [SD], 9.1 ppb) in homes with electric stoves and was 25.9 ppb (SD, 18.1 ppb) in homes with gas stoves. These levels are well below the Environmental Protection Agency’s outdoor standard of 53 ppb. In a study of 728 children with active asthma, children in households with gas stoves had an increased likelihood of wheezing, shortness of breath, and chest tightness.²

In a study of 400,000 emergency department visits to 14 hospitals in Canada during the 1990s and early 2000s, environmental pollutants, calculated by the 24-hour average concentrations of carbon monoxide and nitrogen dioxide levels, displayed a connection with an increase in visits for myocardial infarction/angina per 0.7 ppm of carbon monoxide and 18.4 ppb of nitrogen dioxide. Additionally, an increase in visits for heart failure was also noted in these patients. These associations tended to be greater during the warmer months.³

Pathophysiology

In the lung, nitrogen dioxide hydrolyzes to nitrous and nitric acid, causing profound chemical pneumonitis and pulmonary edema. Nitrogen dioxide hydrolyzes slower than some water-soluble gases, resulting in deep lung injury in the bronchioles and alveoli. Type I pneumocytes and ciliated airway cells are primarily affected, but damage also occurs from free radical generation, which results in protein oxidation, lipid peroxidation, and cell membrane damage. Nitrogen oxides can alter immune function and macrophage activity, leading to an impaired resistance to infection. Additionally, high levels of carbon dioxide in the silo may stimulate a deeper inspiration of the gases, causing a higher delivered dose.

Significant exposure can also result in methemoglobinemia. Nitrogen dioxide binds to hemoglobin with a great affinity, forming nitrosyl hemoglobin, which is readily oxidized to methemoglobin. Methemoglobin results in a leftward shift of the oxygen disassociation curve, which impairs the oxygen delivery and compounds the already present hypoxia.

Frequency

United States

Silo filler's disease is prevalent during the harvest months of September and October. During other months, consider other etiologies first. An estimated annual incidence of 5 cases per 100,000 silo-associated farm workers per year was reported in New York.^4,5 Silo filler's disease is likely significantly underreported.

Mortality/Morbidity

Exposure is usually mild and self-limiting; however, some exposure results in pulmonary edema, bronchiolitis obliterans, or rapid asphyxiation. In one study, approximately one third of people with severe exposures died from pulmonary edema and bronchiolitis obliterans.

• Sudden death and asphyxiation: Death can result from bronchiolar spasm, laryngeal spasm, reflex respiratory arrest, or asphyxia. Nitrogen dioxide concentrations can be sufficiently high, causing displaced oxygen, complete asphyxiation, and death. High concentrations can render a person helpless within 2-3 minutes.
• Pulmonary edema: The chemical irritation of the alveoli and bronchioles results in rapid destruction of the epithelial cells generating fluid accumulation in the lung tissue by breakdown of the pulmonary capillary bed.
• Bronchiolitis obliterans: Failure to treat silo filler’s disease with corticosteroids can result in the development of fibrous granulation tissue within small airways and alveolar ducts, occurring weeks or months after the initial incident. This results in a permanent restrictive lung disease.

Race

No epidemiologic studies indicate a racial predilection for silo filler's disease.

Sex

Silo filler's disease is an agricultural occupational disease, and it historically has predominantly affected the male farm worker; however, sex is unlikely to play a role in the pathophysiologic response.

Age

Adults are at highest risk to develop silo filler's disease; however, nitrogen dioxide exposure can also affect children and livestock near a fresh silage pile.

Clinical

History

• Occupational medical history in silo filler's disease
  • Obtain a complete occupational medical history and be familiar with the pattern of disease caused by nitrogen dioxide.
  • If the patient presents immediately postexposure, the full injury may not be appreciated; effects may occur up to 24 hours after the event.
  • September and October (ie, harvest season) are the primary months that silo filler's disease occurs and should influence diagnostic decision-making.
• Acute symptoms of silo filler's disease
  • Common symptoms are coughing, light-headedness, dyspnea, tightness in the chest, choking, diaphoresis, and loss of consciousness.
  • Coughing is the most common symptom; however, it may not occur in all patients.
  • Wheezing, chest pain, weakness, throat and ocular irritation, and nausea are less common symptoms.
  • Nitrogen dioxide is not as soluble as other gases (eg, chlorine); consequently, mucous membrane irritation is not common.
• Persistent or delayed symptoms of silo filler's disease
  • These may appear days or even weeks later. 
  • Symptoms include dyspnea, coughing, chest pain, rapid breathing, tightness in the chest, headache, and fever.
  • Less frequent symptoms include insomnia, wheezing, chills, light-headedness, myalgias, nausea, hemoptysis, palpitations, and blue lips.
  • Some cases of silo filler’s disease resolve with no persistent or delayed symptoms.

Physical

The findings on physical examination in a patient with silo filler's disease may appear normal initially, but findings often include the following:

• Decreased breath sounds
• Rales
• Rhonchi
• Wheezing
• Conjunctival injection
• Cyanosis (caused by the presence of methemoglobin and impaired pulmonary gas exchange)
• Hemoptysis
• Unresponsiveness
• Systemic hypotension: Nitric oxide formation generates vasodilation and reduced systemic vascular resistance, resulting in hypotension.

Causes

• Silos filled with freshly cut corn, oats, grass, alfalfa, or other plant material generates oxides of nitrogen within hours. Maximum concentrations of nitrogen dioxide are reached within 1-2 days, and then the levels begin to fall after 10-14 days. In well-sealed silos, nitrogen dioxide can be present for weeks. Silage that is heavily fertilized, has experienced drought, or is derived from immature plants results in much higher concentrations of nitrogen oxides within the silo.
• During storage, nitrogen dioxide, which is 1.5 times heavier than air, can remain in deep depressions of the silage material. Exposure can develop while attempting to level the silage without proper ventilation or breathing apparatus. One documented case occurred in an individual who traversed the ladder at the opening of a silo. The heavier-than-air nitrogen dioxide flowed down the side of the silo, exposing the worker to toxic levels of gas.

Differential Diagnoses

Other Problems to Be Considered

Acute lung injury
Pneumonitis, other chemical
Pneumoconiosis 
Conjunctivitis 
Smoke inhalation 
Toxicity, carbon monoxide
Toxicity, chlorine gas
Toxicity, hydrogen sulfide
Toxicity, carbamate
Toxicity, phosgene
Toxicity, ozone
Toxic organic dust syndrome

Workup

Laboratory Studies

• Silo filler's disease (SFD) cannot be diagnosed using any laboratory studies; however, the following studies can be helpful in excluding other causes of the symptoms.
• Arterial blood gas level
  • Measuring arterial blood gas (ABG) levels establishes the presence and severity of gas exchange impairment. Initial blood gas levels are extremely important in the decision to intubate.
  • Some available literature supports obtaining serial ABG levels during follow-up visits to ascertain whether bronchiolitis obliterans is developing.
• Lactate level: Metabolic acidosis can occur by dissolution of nitrous oxide in body fluids, resulting in tissue hypoxemia and subsequent lactic acid formation.
• Methemoglobin level
  • Perform a methemoglobin (MHb) test to evaluate cyanosis that does not respond to oxygen administration. MHb is an inactive oxidized form of hemoglobin that does not contribute to oxygen transport. Cyanosis results from an MHb test result that is greater than 10-15%.
  • Methylene blue administration can affect this test result.
• Complete blood cell count: Leukocytosis is often present in silo filler’s disease.

Imaging Studies

• Chest radiography
  • Findings may be normal.
  • During acute injury, the chest radiograph shows ill-defined, alveolar opacities, which are characteristic of pulmonary edema or ARDS.
  • Subacute injury reveals small opacities or confluent woolly opacities. The small opacities can be mistaken for miliary tuberculosis.

Other Tests

• Pulmonary function testing
  • As soon as the patient is able to undergo tests, conduct a pulmonary function test (PFT) to chart the progress and document the severity of disease.
  • A baseline PFT is helpful as the patient recovers.
  • Conduct PFTs at regular intervals toward the end of the inpatient stay and during follow-up visits.
• Electrocardiography
  • Symptoms of silo filler’s disease can mimic cardiovascular events; ECG may help rule out such occurrences.
  • Serial ECGs are helpful for baseline and initial encounters; however, only abnormal findings are helpful.
• Pulse oximetry monitoring: Pulse oximetry monitoring may be misleading in the presence of methemoglobinemia.
• Pulmonary artery catheter: In patients who are critically ill, monitoring of mixed venous oxygenation and pulmonary vascular resistance may assist in the management of oxygenation requirements, fluids, ARDS, and physiologic variables.

Procedures

• Intubation and mechanical ventilation may be necessary if gas exchange is severely impaired.

Histologic Findings

In patients who quickly die, hemorrhagic edema and patches of pneumonia are revealed in their airways. Small palpable nodules and hemorrhagic areas appear in those patients who survive for several weeks.

Microscopic evaluation of tissues from patients with acute silo filler’s disease shows edema and extensive damage of the respiratory epithelium, which may be completely shed in the small bronchi and bronchioles. In patients who survive for longer periods, generalized infiltration of the alveolar walls with lymphocytes (ie, numerous macrophages in alveolar spaces) occurs. Bronchiolitis obliterans occurs in various stages of organization and is responsible for the palpable nodules.

Treatment

Medical Care

• Prehospital care in silo filler's disease (SFD): Safely remove the patient from exposure without endangering rescuers.
• Medical care for silo filler's disease is as follows:
  • Hospitalize the patient for 12-24 hours for observation or longer if gas exchange is compromised.
  • Administer oxygen to the patient for hypoxemia.
  • Use mechanical ventilatory support for hypoxemic or hypercapnic respiratory failure. Treat secondary infection, if present.
  • Administer volume expanders cautiously.
  • The patient may require invasive monitoring because excessive administration of volume expanders can cause hydrostatic pulmonary edema. Nitrogen dioxide forms nitric oxide, causing vasodilation and an apparent volume depletion.⁶
  • Monitor continuous pulse oximetry.

Consultations

• Consult a pulmonary medicine or critical care specialist if the patient requires endotracheal intubation or hemodynamic monitoring.
• Consult a medical toxicologist or poison control center to provide additional information and patient care guidelines.

Activity

Advise the patient to avoid exercise for 1-2 days after exposure.

Medication

Methylene blue is indicated for significant methemoglobinemia. Other possible treatments may include antibiotics if infection becomes evident, and vasopressor drugs are required to correct the normovolemic shock. Corticosteroids may be important in the prevention of bronchiolitis obliterans.

Antidotes

Methylene blue (ie, tetramethyl thionine chloride) is the recommended antidote for methemoglobinemia. It is reduced to leukomethylene blue, which is then available to reduce methemoglobin to hemoglobin.

Methylene blue (Urolene Blue)

Used if methemoglobin exceeds 30%. Administer IV.

Dosing

Adult

1-2 mg/kg IV over 5 min at 1% solution; repeat dosing in 1 h if continued symptomatology or significant methemoglobinemia is present; not to exceed 7 mg/kg

Pediatric

Administer as in adults; 0.3-1.0 mg/kg IV over 5 min for neonates

Interactions

None reported

Contraindications

Documented hypersensitivity; intraspinal administration; severe renal insufficiency; treatment of methemoglobinemia in cyanide poisoning

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

High doses (5-10 mg/kg) or rapid IV administration may induce acute hemolytic anemia or cause further methemoglobin production; patients with a glucose-6-phosphate deficiency may not benefit from this treatment; toxic effects include dyspnea, precordial pain, restlessness, apprehension, a sense of oppression, and tremors

Corticosteroids

These agents do not benefit the patient during the acute phase, but they are effective in treating bronchiolitis obliterans. Because not all patients with acute lung injury develop bronchiolitis, judge the risk factors and choose between prescribing the patient corticosteroids as prevention and monitoring the patient for clinical or radiographic evidence of bronchiolitis obliterans.

Methylprednisolone (Adlone, Solu-Medrol, Depo-Medrol)

Reduces inflammatory response of bronchiolitis obliterans and can be tapered over 8 wk, adjusting the dose based on clinical symptoms, radiographs, and spirometry.

Dosing

Adult

125 mg IV q6h initially; follow with 40 mg/d PO, tapering to 20 mg/d over the first mo, then gradually wean off over the next mo

Pediatric

Not to exceed 30 mg/kg IV

Interactions

Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use

Inhalational agents

One case report described a patient with ARDS secondary to silo filler’s disease who required nitric oxide (NO) therapy because of worsening oxygenation. Great care should be instituted with nitric oxide therapy because of the possibility of worsening pulmonary damage and methemoglobinemia, which are already present in silo filler’s disease.

Nitric oxide (INOmax)

Produced endogenously from action of enzyme NO synthetase on arginine; relaxes vascular smooth muscle by binding to heme moiety of cytosolic guanylate cyclase, activating guanylate cyclase and increasing intracellular levels of cGMP, which then leads to vasodilation; when inhaled, NO decreases pulmonary vascular resistance and improves lung blood flow.

Dosing

Adult

20 ppm via respirator initially; not to exceed 80 ppm; effect of pulmonary vasodilatation may still be observed at 5 ppm; deliver by system that measures concentrations of NO in breathing gas with constant concentration throughout respiratory cycle; deliver by system that does not cause generation of excessive inhaled nitrogen dioxide

Pediatric

20 ppm via respirator initially; not to exceed 80 ppm; most children respond at 20 ppm and can be weaned to lower doses; effect of pulmonary vasodilatation may still be observed at 5 ppm; deliver by system that measures concentrations of NO in breathing gas with constant concentration throughout respiratory cycle; deliver by system that does not cause generation of excessive inhaled nitrogen dioxide

Interactions

Concomitant administration with NO donor compounds (eg, nitroprusside, nitroglycerin) may have additive effects and may increase risk of methemoglobinemia

Contraindications

Right to left shunting of blood; methemoglobin reductase deficiency

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Abrupt discontinuation of NO may lead to worsening oxygenation and increasing PAP; toxic effects include methemoglobinemia and pulmonary inflammation resulting from reactive nitrogen intermediates; caution in thrombocytopenia, anemia, leukopenia, or bleeding disorders; monitor for PaO₂, methemoglobin, and NO₂; abrupt withdrawal causes rebound pulmonary hypertension

Follow-up

Further Inpatient Care

• Admit silo filler's disease (SFD) patients for at least 24 hours if they have signs of dyspnea, altered mental status, hypoxemia, or a widened alveolar-arterial oxygen gradient.
• If no initial symptoms are present, observe the patient for at least 12 hours for hypoxemia.
• Pulmonary edema can take up to 48 hours to develop. Educate the silo filler's disease patient on the possible symptoms and instruct the patient to return if the symptoms develop.
• Clinical improvement and resolution of hypoxemia and methemoglobinemia are helpful endpoints for discharge.

Further Outpatient Care

• Conduct a follow-up examination at 1 week, 1 month, and 3 months after exposure, with serial pulmonary function testing and radiographs.

Inpatient & Outpatient Medications

• When the silo filler's disease patient is discharged, prescribe corticosteroid taper for at least 8 weeks. A longer duration (ie, 6-12 mo) may be indicated if symptoms of bronchiolitis obliterans persist or recur after initial steroid taper.
• Inhaled sympathomimetics (eg, albuterol), anticholinergics (eg, ipratropium bromide), and steroids (eg, fluticasone propionate) may also be indicated if the patient has additional symptoms of reactive airway disease. A typical asthma disease management plan can be used for these patients.

Transfer

• Transferring the silo filler's disease patient to a tertiary care center for further diagnostic evaluation and ventilatory support may be necessary.

Deterrence/Prevention

• Educate farm workers at risk for exposure and development of silo filler's disease.

Complications

• Secondary infection: Infection (eg, pneumonia) is possible because of the mucosal injury caused by pulmonary edema and the inhibition of immune function by nitrogen dioxide.
• Bronchiolitis obliterans: Fibrous granulation tissue develops within small airways and alveolar ducts, occurring weeks or months after the initial incident.

Prognosis

• Pulmonary function may not improve (without permanent disability) for weeks or months; however, mild dysfunction likely due to bronchiolitis obliterans may occur. This manifests as mild hyperinflation; abnormal V_max50, V_max75, or FEF_25-75; increased respiratory resistance; and airway obstruction.
• The lungs clear quickly with steroid treatment, and the chest radiograph may reveal no evidence of residual lung damage.
• Treat deconditioning by referring the patient to a pulmonary rehabilitation program.

Patient Education

• Offer the following preventive advice to the patient:
  • Stay out of the silos during the 2-week danger period after the initial filling.
  • Close all doors before putting in the silage.
  • Go up the outside ladder to the level of silage.
  • If the silo is not completely full, remove the doors that lead down to the silage.
  • Enter the silo only with a complete oxygen support system (ie, air supply, self-contained breathing apparatus).
  • Ventilate the silo by opening the cover flaps and running the silo blower for 24-48 hours before entering.
  • Never enter the silo alone or without a lifeline for rescue during the danger period.
  • If entering a silo during filling is necessary, enter immediately after the last load.

Miscellaneous

Medicolegal Pitfalls

• Failure to inform the patient about delayed symptoms, including life-threatening pulmonary edema and dyspnea due to bronchiolitis obliterans
• Failure to consider the asymptomatic period and the delayed onset of symptoms associated with nitrogen dioxide toxicity
• Discharging the patient too soon from the emergency department
• Failure to consider nitrogen dioxide toxicity in patients who present with dyspnea and who have occupations allowing exposure
• Failure to recognize early signs of significant respiratory distress and to document either a PO₂, an Aa gradient, or oxygen saturation via pulse oximetry
• Failure to monitor the patient in a setting where respiratory support is immediately available
• Failure to monitor the patient for bronchiolitis obliterans or to prescribe the patient steroids when signs manifest

References

1. Klonoff-Cohen H, Lam PK, Lewis A. Outdoor carbon monoxide, nitrogen dioxide, and sudden infant death syndrome. Arch Dis Child. Jul 2005;90(7):750-3. [Medline].

2. Belanger K, Gent JF, Triche EW, Bracken MB, Leaderer BP. Association of indoor nitrogen dioxide exposure with respiratory symptoms in children with asthma. Am J Respir Crit Care Med. Feb 1 2006;173(3):297-303. [Medline].

3. Stieb DM, Szyszkowicz M, Rowe BH, Leech JA. Air pollution and emergency department visits for cardiac and respiratory conditions: a multi-city time-series analysis. Environ Health. Jun 10 2009;8:25. [Medline].

4. MMWR. Silo-Filler's disease in rural New York. MMWR Morb Mortal Wkly Rep. Jul 23 1982;31(28):389-91. [Medline].

5. Zwemer FL Jr, Pratt DS, May JJ. Silo filler's disease in New York State. Am Rev Respir Dis. Sep 1992;146(3):650-3. [Medline].

6. Ichinose F, Roberts JD Jr, Zapol WM. Inhaled nitric oxide: a selective pulmonary vasodilator: current uses and therapeutic potential. Circulation. Jun 29 2004;109(25):3106-11. [Medline].

7. do Pico GA. Lung (agricultural/rural). Otolaryngol Head Neck Surg. Feb 1996;114(2):212-6. [Medline].

8. Douglas WW, Hepper NG, Colby TV. Silo-filler's disease. Mayo Clin Proc. Mar 1989;64(3):291-304. [Medline].

9. Goldstein E, Peek NF, Parks NJ, Hines HH, Steffey EP, Tarkington B. Fate and distribution of inhaled nitrogen dioxide in rhesus monkeys. Am Rev Respir Dis. Mar 1977;115(3):403-12. [Medline].

10. Gurney JW, Unger JM, Dorby CA, Mitby JK, Von Essen SG. Agricultural disorders of the lung. Radiographics. Jul 1991;11(4):625-34. [Medline].

11. Leavey JF, Dubin RL, Singh N, Kaminsky DA. Silo-Filler's disease, the acute respiratory distress syndrome, and oxides of nitrogen. Ann Intern Med. Sep 7 2004;141(5):410-1. [Medline].

12. Maurer WJ. Silo-filler's disease. A historical perspective and report of a case. Wis Med J. Aug 1985;84(8):13-6. [Medline].

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Keywords

silo filler’s disease, silo filler disease, silo unloader disease, nitrogen dioxide poisoning, SFD, silo-filler's disease, proliferative pulmonary disease, pulmonary edema, bronchiolitis obliterans, asphyxiation, methemoglobinemia, chemical pneumonitis, acute respiratory distress syndrome, ARDS, acute lung injury, nitrogen oxides, bronchioles lung injury, alveoli lung injury, arterial blood gas, ABG, methemoglobin, MHb, methemoglobinemia

Contributor Information and Disclosures

Author

Nader Kamangar, MD, FACP, FCCP, FAASM,, Associate Professor of Clinical Medicine, Director of Hospitalist/Intensivist Program, Division of Pulmonary, Critical Care and Sleep Medicine, David Geffen School of Medicine at University of California Los Angeles; Associate Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA/West Los Angeles Veterans Affairs Medical Center
Nader Kamangar, MD, FACP, FCCP, FAASM, is a member of the following medical societies: American Academy of Sleep Medicine, American Association of Bronchology, American College of Chest Physicians, American College of Physicians, American Lung Association, American Medical Association, American Thoracic Society, California Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Lex Chen, MD, Resident Physician, Department of Internal Medicine, University of California Los Angeles, Olive View Medical Center
Lex Chen, MD is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.

Medical Editor

Gregory Tino, MD, Director of Pulmonary Outpatient Practices, Associate Professor, Department of Medicine, Division of Pulmonary, Allergy, and Critical Care, University of Pennsylvania Medical Center and Hospital
Gregory Tino, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gregg T Anders, DO, Medical Director, Great Plains Regional Medical Command , Brook Army Medical Center; Clinical Associate Professor, Department of Internal Medicine, Division of Pulmonary Disease, University of Texas Health Science Center at San Antonio
Gregg T Anders, DO is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, Rebecca Bascom, MD, MPH, and Mark D Rasmussen, MD, to the development and writing of this article.

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