Occupational or environmental exposure to plant dusts has been shown to increase the risk of obstructive lung diseases, primarily by non-immunological activity.¹ However, the causative agents and the underlying mechanisms have not been established. We have recently suggested that the polyphenolic fraction of hydrolysable tannins in plant derived dusts, with tannic acid (TA) as the main constituent, may contribute to airway constriction.² Here we present experimental evidence that TA causes acute airway obstruction by non-competitive inhibition of the constitutive endothelial isoform of nitric oxide synthase (eNOS) in the tracheobronchial epithelium, which is reported to provoke airway hyperresponsiveness and bronchoconstriction.³

Organ bath experiments were performed using the trachea and main bronchi of non-sensitised guinea pigs. The tracheobronchial tree was dissected out of CO₂ sacrificed guinea pigs of either sex weighing 300–450 g and cut into rings of 3–4 cartilage segments wide. Isometric contractions were recorded as described previously.⁴ Briefly, individual rings were mounted in organ baths containing 10 ml carbogen aerated Tyrode solution (pH 7.4, 37°C), kept at a preload of 25 mN, left to equilibrate for 60 minutes, and precontracted by addition of 25 μmol/l prostaglandin F_2α to 30–40% of their individual isometric maximum (100%).

NO release was determined in real time by an amperometric microsensor as described elsewhere.⁴ Briefly, …