| Clinical phenotype and type | Typical timing, severity, and course | Observed evidence and frequency | Suggested HPO label (identifier not assigned) |
|---|---|---|---|
| Cough and chest tightness — symptoms | May occur during or shortly after exposure; can improve transiently before delayed recurrence. Severity varies with exposure concentration and duration. | Described in human high-level NO₂ exposure and silo-filler disease reports; population frequency not established. (pqac-00000001, pqac-00000013) | Cough; Chest tightness |
| Dyspnea — symptom | Acute after substantial exposure or delayed by hours; may recur weeks later with bronchiolitis. Ranges from mild breathlessness to severe respiratory distress. | Present in the fatal 1982 CDC case and repeatedly described in clinical reviews; population frequency not established. (pqac-00000002, pqac-00000013) | Dyspnea |
| Wheeze or bronchospasm — clinical sign | Usually acute; may accompany bronchiolar irritation, respiratory distress, or pulmonary edema. | Wheezes and crackles were documented in the 1982 fatal case; high-level NO₂ can cause acute bronchospasm. Frequency not established. (pqac-00000013, pqac-00000019) | Wheezing; Bronchospasm |
| Hypoxemia and cyanosis — clinical sign/laboratory abnormality | Acute and potentially severe; reflects impaired gas exchange from alveolar-capillary injury and edema. | The 1982 patient was cyanotic and had PaO₂ 45 mmHg while receiving 2 L/min nasal oxygen. Frequency not established. (pqac-00000013) | Hypoxemia; Cyanosis |
| Acute lung injury — clinical syndrome | Acute or delayed over hours; may progress to ARDS, respiratory failure, or death. | A secondary review reports acute lung injury in 11 of 17 silo-gas-exposed Mayo Clinic patients (≈65%). This is a selected clinical series—not a population phenotype frequency or prevalence estimate. (pqac-00000010, pqac-00000016) | Acute lung injury; Acute respiratory distress syndrome |
| Noncardiogenic pulmonary edema — manifestation/pathology | Common severe early pattern, often developing within hours; may cause shock and fatal respiratory failure. | The 1982 autopsy showed grossly edematous lungs, bilateral pleural effusions, and alveoli flooded with proteinaceous material while alveolar walls remained intact. Frequency not established. (pqac-00000013) | Pulmonary edema |
| Shock — clinical sign | Acute, life-threatening complication of massive exposure and capillary leak; may progress rapidly despite treatment. | The 1982 patient had blood pressure 84/60 mmHg, remained in shock, and died five hours after admission. Frequency not established. (pqac-00000013) | Shock |
| Delayed bronchiolitis obliterans/constrictive bronchiolitis — complication | Typically arises after an apparent recovery, often 1–4 weeks after high-level exposure; may become persistent or irreversible because of bronchiolar fibrosis and obliteration. | Silo-gas exposure is a recognized cause. Reported findings include progressive exertional dyspnea, obstructive pulmonary-function abnormalities, hyperinflation, air trapping, mosaic attenuation, and bronchiolar-lumen obliteration. Frequency not established. (pqac-00000003, pqac-00000021, pqac-00000026, pqac-00000031) | Bronchiolitis obliterans; Constrictive bronchiolitis; Air trapping |
| Airflow obstruction — functional abnormality | May occur acutely from bronchospasm or persist after delayed bronchiolar fibrosis; severity is variable. | Airway obstruction was reported in the selected Mayo series; irreversible obstruction with reduced FEV₁ and air trapping characterizes constrictive bronchiolitis. Frequency not established. (pqac-00000010, pqac-00000022) | Obstructive ventilatory defect; Reduced forced expiratory volume |


*Table: Evidence-grounded clinical phenotype summary for silo-filler disease, including timing, course, documented measurements, and cautious frequency interpretation. Suggested HPO labels are provided without unverified ontology identifiers.*