eMedicine Specialties > Pulmonology > Occupational Lung Diseases

Silo Filler's Disease

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
Coauthor(s): Lex Chen, MD, Resident Physician, Department of Internal Medicine, University of California Los Angeles, Olive View Medical Center
Contributor Information and Disclosures

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.

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