Differences between inhaled and intravenous bronchial challenge to detect O(3)-induced hyperresponsiveness

Area of Science:

• Environmental Health
• Pulmonary Medicine
• Toxicology

Background:

• Ozone (O3) exposure is a known risk factor for respiratory diseases.
• Airway hyperresponsiveness (AHR) is a hallmark of asthma and other obstructive lung diseases.
• Assessing AHR typically involves dose-response curves using bronchoconstrictor agonists, but route comparability is unclear.

Purpose of the Study:

• To compare the effectiveness of inhaled versus intravenous administration of bronchoconstrictor agonists in detecting ozone-induced airway hyperresponsiveness.
• To investigate whether ozone exposure affects acetylcholinesterase activity, potentially explaining differences in agonist effectiveness.

Main Methods:

• Guinea pigs were exposed to ozone (3 ppm, 1 hour) or air.
• Airway responsiveness to inhaled or intravenous acetylcholine (ACh) and histamine was measured using two plethysmographic methods.
• Acetylcholinesterase activity was assessed in lung homogenates and blood samples.

Main Results:

• Ozone exposure induced significant airway hyperresponsiveness to intravenous agonists.
• No significant airway hyperresponsiveness was detected with inhaled agonists after acute ozone exposure.
• Inhaled agonist effectiveness was confirmed after antigen challenge or prolonged ozone exposure (3 hours).
• Ozone exposure did not alter acetylcholinesterase activity in lung or blood.

Conclusions:

• Intravenous administration of agonists is more sensitive than inhalation for detecting acute ozone-induced airway hyperresponsiveness.
• The route-dependent difference in detecting AHR is not explained by ozone-induced inhibition of acetylcholinesterase activity.
• Findings highlight the importance of agonist administration route in assessing ozone's respiratory effects.