Abstract Background Asthma emerging in late adulthood is uncommon and often misattributed to cardiac or infectious causes. In elderly nonsmokers, decades of passive smoke exposure can induce silent airway remodeling—epithelial injury, mucus hypersecretion, and smooth-muscle hyperreactivity—without symptoms for years. Exposure to new irritants such as menthol may then precipitate acute bronchospasm indistinguishable from asthma. Though perceived as soothing, menthol can paradoxically cause bronchoconstriction through TRPM8-mediated cold receptor activation and vagal reflexes. This case underscores how brief menthol exposure can trigger obstructive symptoms in a lifetime nonsmoker with smoke-primed airways, highlighting a preventable and underrecognized pathway for late-onset asthma-like disease. Case Presentation An 84-year-old woman with diabetes, hypertension, hyperlipidemia, and remote intermittent asthma presented with one week of progressive dyspnea and dry cough after daily use of an over-the-counter menthol nebulizer for congestion. She denied fever, chills, or chest pain. A lifelong nonsmoker, she had decades of heavy indoor secondhand smoke exposure from her spouse. On arrival, she was tachypneic (RR 26/min), tachycardic (HR 102 bpm), and hypoxic (SpO2 92% on room air). ABG showed pH 7.50, pCO2 26 mmHg, pO2 65 mmHg, and HCO3− 19.9 mmol/L, consistent with acute respiratory alkalosis and mild hypoxemia from hyperventilation. Exam revealed diffuse expiratory wheezes and prolonged expiration. Chest X-ray showed hyperinflated lungs with flattened diaphragms. Non-contrast CT demonstrated bilateral lower-lobe atelectasis with mild traction bronchiectasis. Echocardiogram showed grade I diastolic dysfunction with preserved systolic and valvular function. She was admitted to the ICU but improved rapidly with bronchodilators, corticosteroids, and oxygen, and was discharged on ICS/LABA therapy with pulmonary follow-up. Discussion This case demonstrates how passive smoke–induced airway remodeling can remain subclinical until reactivated by a chemical irritant. Menthol exposure triggered acute bronchospasm through neurogenic and inflammatory pathways in an already sensitized airway. The concordant findings—wheezing, hyperinflation, and respiratory alkalosis—confirmed obstructive physiology rather than infection or cardiac dysfunction. The presentation exemplifies an irritant-mediated, late-onset asthma phenotype, distinct from both chronic asthma and COPD, highlighting how even brief exposure to “benign” inhalants can reveal hidden airway hyperreactivity in older adults. Conclusion This case underscores a clinically and preventably significant phenomenon that brief menthol inhalation can unveil airway hyperreactivity shaped by years of secondhand smoke exposure. It expands awareness of irritant-mediated airway disease in nonsmokers and highlights the need for targeted history-taking and public education on menthol inhalant risks to reduce misdiagnosis and prevent avoidable respiratory exacerbations. This abstract is funded by: None
Jagra et al. (Fri,) studied this question.