Silo filler’s disease is associated with inhalation of biologic dusts and results from inhalation of nitrogen dioxide (NO2) gas from fresh silage.
The clinical manifestations are variable depending on level of exposure.
If NO2 gas penetrates throughout the lung, it can result in a severe form of acute respiratory distress syndrome: pulmonary edema, hyalinized alveolar membranes, congestion and other respiratory illnesses.
NO2 is derived from the nitrates in corn or hay that are converted to nitrites and oxygen by anaerobic fermentation, which eventually yield NO2.
NO2 fumes ranges from yellow to reddish brown, and its odor is similar to that of household bleach.
NO2 gas begins to form within a few hours after the silo has been filled, reaches a peak 1 to 5 days later, and may produce toxic levels for 2 to 6 weeks.
Farmers are exposed when they enter the silo on the day of filling or within 1 to 2 days thereafter.
Levels of 200 to 2,000 parts per million (ppm) are common.
Levels of 50 to 100 ppm are capable of producing pulmonary disease.
Four phases: asymptomatic, pulmonary edema, progressive pulmonary insufficiency, and chronic pulmonary insufficiency.
The disease does not necessarily progress in such phases.
The clinical and pathologic classification: collapse and sudden death, acute alveolar injury and pulmonary edema, early and reversible bronchiolitis obliterans, and late scarring and irreversible bronchiolitis obliterans.
Collapse and sudden death in silos are a serious problem since they were first built.
Sudden death can occur immediately after filling of the silo.
Sudden death can also occur when levels of NO2 are high but also potentially almost anytime silage is in the silo when levels of oxygen are low.: oxygen levels as low as 3.48% have been found in silos.
NO2 may cause bronchospasm and nitrites may cause cardiac dysfunction.
Death is likely due to asphyxiation from low inspired oxygen.
Low oxygen levels can cause death from falls as well.
Acute alveolar injury and pulmonary edema result from exposure to NO2.
There may be a latency period of several hours after exposure with symptoms of fever, cough, myalgias, and progressive dyspnea.
Patients present in acute respiratory distress, often with cyanosis and coarse crackles.
Chest X-rays may indicate pulmonary edema or patchy infiltrates.
Autopsy findings: lungs full of frothy white fluid, consolidation, alveolar edema and exudation of neutrophils into alveolar spaces; alveolar walls with lymphocytic infiltrates, and necrotizing bronchiolitis.
Early administration of oxygen and high-dose corticosteroid therapy, with recent studies indicate a good prognosis.
Bronchiolitis obliterans is also associated with exposure to NO2.
Bronchiolitis obliterans is often, reversible in silo-filler’s disease.
With bronchiolitis obliterans NO2
exposure occurs as previously described but at less concentrated levels or for a briefer duration.
Patients often recover completely from the acute respiratory inflammatory, but symptoms but return 2 to 4 weeks later with fever, chills, and cough.
Bronchiolitis obliterans characterized by partial or complete obstruction of bronchioles with granulation tissue and organized fibrin plug.
The lesions are reversible with immediate corticosteroid and oxygen therapy.
With bronchiolitis obliterans relapses may occur, and corticosteroid therapy may be necessary for several weeks or even 6 to 12 months.
With bronchiolitis obliterans the diffusing capacity is abnormal, and chest X-rays show nodular opacities and sometimes patchy infiltrates, or organizing pneumonia.
The differential diagnosis: allergic alveolitis and grain-dust asthma, cigarette-related emphysema and chronic bronchitis with associated airflow obstruction.
Prevention : no one enters the silo for any purpose from the time of filling until 7 to 10 days thereafter, provide good ventilation, provide barriers to prevent children or animals from straying into any space adjoining the silo, and always activate the blower fan before entering the silo.
With early recognition the NO2-related acute alveolar injury with pulmonary edema and the bronchiolitis obliterans lesion are treatable and do not result in irreversible scarring and disabling airflow obstruction.