A 38-year-old woman from Mumbai presents with acute onset of severe dyspnea, chest tightness, and wheezing that began 2 hours after exposure to heavy smog during a traffic jam. She has a history of mild asthma (well-controlled on salbutamol PRN). On examination, peak expiratory flow (PEF) is 220 L/min (baseline 380 L/min), and diffuse bilateral wheezing is heard. Ambient air quality index is 380 (severe) with elevated ozone (O₃) levels of 180 µg/m³ and NO₂ levels of 95 µg/m³. Which air pollutant is most likely responsible for her acute asthma exacerbation?

Explanation

## Diagnosis: Acute Asthma Exacerbation Triggered by Ozone Exposure ### Clinical Presentation This patient presents with acute-onset asthma exacerbation (PEF drop from 380 to 220 L/min, wheezing, dyspnea) within 2 hours of exposure to severe smog with elevated ozone levels. This rapid onset is characteristic of ozone-induced airway hyperresponsiveness. ### Ozone (O₃) Mechanism in Acute Asthma **Key Point:** Ozone is a secondary oxidant pollutant formed from NOₓ and volatile organic compounds (VOCs) in sunlight. It causes acute, reversible airway inflammation and hyperresponsiveness, particularly in susceptible individuals (asthmatics, children, outdoor workers). ### Pathophysiology of Ozone-Induced Asthma Exacerbation | Feature | Ozone Effect | |---------|-------------| | **Onset** | Acute (minutes to 2 hours) | | **Mechanism** | Direct oxidative injury to airway epithelium → inflammatory cascade | | **Target cells** | Airway epithelial cells, mast cells, eosinophils | | **Airway response** | Hyperresponsiveness, increased mucus production, bronchoconstriction | | **Reversibility** | Largely reversible with bronchodilators and removal from exposure | | **Duration** | Hours to days | | **Susceptibility** | Asthmatics > healthy individuals | **High-Yield:** Ozone is the most potent air pollutant for triggering acute asthma exacerbations. Even brief exposures (< 2 hours) at concentrations > 100 µg/m³ can precipitate symptoms in susceptible asthmatics. ### Why Ozone, Not Other Pollutants? **Clinical Pearl:** The 2-hour latency and acute bronchospasm in a known asthmatic during high ozone exposure is pathognomonic for ozone-induced exacerbation. Ozone levels of 180 µg/m³ are well above the WHO guideline (100 µg/m³ for 8-hour exposure) and sufficient to cause acute symptoms. ### Mechanism of Ozone-Induced Airway Hyperresponsiveness 1. Ozone penetrates to the tracheobronchial region (larger particles than PM₂.₅) 2. Oxidative stress → epithelial cell damage and apoptosis 3. Release of inflammatory mediators (IL-8, TNF-α, reactive oxygen species) 4. Mast cell degranulation → histamine and tryptase release 5. Increased airway smooth muscle tone and mucus secretion 6. Transient increase in airway responsiveness to methacholine and allergens ### Differential Consideration: Why Not PM₂.₅? While PM₂.₅ is elevated in smog, it typically causes **chronic** airway disease (as in the previous case), not acute exacerbations in the 2-hour timeframe. PM₂.₅ effects develop over months to years of exposure. [cite:Park 26e Ch 9; Harrison 21e Ch 244]