Hospital: Report by phone, fax, or mail
Lab: Report by phone, fax, or mail
Physician/Health care providers: Report by phone, fax, or mail
Medical Examiners: Report by phone, fax, or mail
Poison Control Centers: Report by phone, fax, or mail
Occupational Nurses: Report by phone, fax, or mail
Local Public Health Agency (LPHA): No follow-up required, unless outbreak occurrence
Report to the IDPH Division of Environmental Health:
Iowa Department of Public Health
Division of Environmental Health
Lucas State Office Building
321 E. 12th Street
Des Moines, Iowa 50319-0075
Phone (Mon-Fri 8 am - 4:30 pm): 800-972-2026
24-hour Disease Reporting Hotline: (For use outside of EH office hours) 800-362-2736
Silo filler's disease (SFD) is an occupational pulmonary disease resulting from exposure to oxides of nitrogen.
A. Clinical Description
Inhalation of oxides of nitrogen (NOx) can cause sudden death, pulmonary edema, and/or bronchiolitis obliterans. Significant exposure can also result in methemoglobinemia. Nitrogen dioxide binds to hemoglobin with 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.
Low concentrations of nitrogen dioxide cause cough, dyspnea, fatigue, and upper airway and ocular irritation. With an increase in concentration and duration, the exposed person additionally may experience cyanosis, vomiting, vertigo, and a loss of consciousness. More severe exposure can result in laryngeal spasm, bronchiolar spasm, reflex respiratory arrest, or asphyxia, leading to death. Most symptomatic exposures are mild and self-limiting; however, some cause sudden death from asphyxiation, pulmonary edema, or weeks later, bronchiolitis obliterans.
B. Sources of Exposure
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 (e.g., 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. When farm workers enter the silo or are near its open hatches during the first 10 days after filling (without proper precautions), they may experience various degrees of silo filler’s disease. The first recorded incidence of a death from SFD was in 1914. This occurred when three men fell into a silo and were asphyxiated by a gas that was unknown at that time. The term, "silo filler’s disease," was established in 1956.
C. Population at Risk
Although probably not common, the true scope of exposure to NOx is thought to be underestimated. An unpublished survey in the late 1960's revealed that 4.2 percent of Wisconsin farm operators had developed symptoms of NOx inhalation when working in or near freshly filled silos. Other statistics on the frequency of agricultural NOx exposure are not available, but a number of deaths have been documented through the years. The severity of the hazard rests partially in the high case fatality rate: 29 percent of cases cited in medical literature have been fatal.
D. Diagnosis, Treatment, and Prognosis
Patients in the acute stages of silo filler's disease will present with moderate to severe respiratory distress. Systemic hypotension and evidence of severe hemoconcentration may be present, as may methemoglobinemia and severe metabolic acidosis. Leukocytosis is typical. Pulmonary function tests show a reduced vital capacity, increased airways resistance, impaired gas transfer, and hypoxemia.
Because the initial illness may be mild, patients may present to a physician for the first time during a relapse, two to six weeks after exposure to NOx. At this time, cough, tachypnea, dyspnea, fever, tachycardia, cyanosis, or other symptoms of respiratory distress are due to bronchiolitis obliterans. Small, discrete nodules, with or without confluence, will be evident on the chest radiograph.
Silo filler's disease may be confused with a number of illnesses, including hypersensitivity pneumonitis or toxic organic dust syndrome, which result from exposure to moldy hay or grain. When working around a silo, exposure to mold typically occurs while uncapping the silo and removing moldy silage from the top silo layers well after the harvest season. Thus, the timing is different than it would be for silo filler's disease. The chest radiograph of bronchiolitis obliterans may resemble miliary tuberculosis among other diseases; an accurate occupational history and negative sputum smears for acid-fast bacillus will help avoid confusion. A detailed medical and occupational history is crucial to correct diagnosis. In addition to noting exposure to a recently filled silo, most commonly in late summer or early fall, a patient may recall seeing signs of NOx near the silo or experiencing the transient symptoms described previously. Since exposure to silo gas may have occurred from hours to weeks prior to onset of severe respiratory symptoms, the patient may not associate symptoms with exposure to silo gas. Prompt diagnosis and treatment of patients with acute symptoms are vital to prevent possible death and, in the case of initial illness, to lessen the probability of relapse.
Any symptomatic patient who has been exposed to NOx should be monitored closely by a physician for 48 hours because of the possibility of sudden pulmonary edema. Typically, these patients are hospitalized. In certain cases, patients could remain at home, but should be warned to report immediately to the physician upon development of respiratory distress. Persons developing pulmonary edema or respiratory embarrassment must be placed on steroids for a minimum of eight weeks, to decrease the probability of bronchiolitis obliterans. Persons presenting for the first time with bronchiolitis obliterans also should receive steroid treatment. Patients may require intensive supportive therapy, including oxygen, bronchodilators, or assisted ventilation. Antibiotics may be required for secondary respiratory infection.
Reactions to NOx depend on the concentration of gas inhaled and the length of exposure. Relatively mild exposure to NOx produces ocular irritation and a transient upper respiratory tract syndrome manifest as cough, possibly with dyspnea, fatigue, nausea, cyanosis, vomiting, vertigo, or somnolence. Symptoms may be severe enough to induce workers to leave the silo. However, when reactions to NOx are minimal, workers may stay in the silo and increase the probability of a more severe reaction. Although symptoms may persist one to two weeks, chest films, pulmonary function tests, and blood gases are normal, and recovery is complete.
Very high concentrations of NOx induce immediate distress, resulting in collapse and death within minutes. The mechanism of this reaction is not completely understood: death may be due to airway spasm or laryngospasm, reflex respiratory arrest, or simple asphyxiation due to low ambient oxygen concentrations. People who collapse in silos and are rescued immediately, may survive only to experience the respiratory responses described below.
At somewhat lower concentrations, NOx induces pulmonary edema (normally within 30 hours following exposure), bronchiolitis obliterans (within days to weeks), or both. These reactions are commonly called "silo filler's disease." At the time of exposure, patients may have had no or minimal symptoms, or they may have experienced those symptoms associated with mild exposures listed previously. However, a slowly evolving and progressive inflammation of the lungs results in massive pulmonary edema most commonly from 6 to 12 hours later. Death from asphyxiation may occur within hours, but the majority of patients recover completely with appropriate therapy within days or weeks.
In a small percentage of cases, recovery from this first phase of illness may appear to be complete, including clearing of chest films, only to be followed by a relapse characterized by bronchiolitis obliterans, typically two to four weeks following exposure. This fibrocellular obliteration of the bronchioles also may be the initial clinical manifestation. Relapse may lead to death or to slow recovery over a period of weeks to months. Most patients who survive the pulmonary edema, bronchiolitis obliterans, or both do not develop significant respiratory impairment, although subclinical small airways obstruction may persist. Bronchiolitis obliterans responds to steroids. However, occasionally a patient may experience persistent pulmonary dysfunction of variable severity.
E. Prevention of Exposure
Silo filler's disease is a preventable occupational hazard that can be eliminated by proper work practices. Farmers need to thoroughly understand the hazards associated with newly filled silos. Once filled, no one should enter the silo for at least two weeks. If entrance is imperative during the filling process, the blower should be run for 30 minutes prior to entering the silo and kept running while anyone is inside. All silo doors should be kept closed during and after filling to prevent NOx from flowing down the chute. The door between the silo room and barn should be kept closed. Children and animals should be kept away from the silo and adjacent feed room during filling and for two weeks afterward. A few days before the silo is entered for the first time, the filler opening should be pulled open from the ground (not from the chute) with a rope. The blower should be operated for at least one-half hour prior to entrance, and other means of ventilation should be maximized. Detector tubes (also called colorimetric tubes) that measure the concentration of NO2 are reasonably priced and reliable if properly used.