Bronchoconstriction provoked by exercise in a high-particulate-matter environment is attenuated by montelukast.
Airborne ultrafine and fine particulate matter (PM1 from fossil-fueled internal combustion engines may cause abnormal airway narrowing. Because of high PM1 exposure from ice resurfacing machines, the ice-rink athlete is especially vulnerable to PM1 toxicity. The purpose of this study was to evaluate protection by a single dose of montelukast in college ice hockey players following PM1 exposure exercise. Nine male ice hockey players (age 19.3+/-1.22 yr) performed 4 randomized, double-blinded, high-intensity, 6-min cycle ergometer trials in low [PM1] (2260+/-500 particles/cm3) and high [PM1] (348,600+/-121,600 particles/cm3) after placebo or montelukast. Pre- and postspirometry showed similar peak FEV1 (forced expiratory volume in 1 s) falls between placebo and montelukast after low [PM1] trials (14.5+/-18.06 vs. 9.5+/-11.75% of baseline, respectively). Peak FEV1 falls after high [PM1] trials were greater for placebo than for montelukast (17.3+/-9.79% vs. 1.7+/-5.77% of baseline; p<.0001). High [PM1] FEV1 fall after exercise following montelukast ingestion was less than after exercise following placebo ingestion under high and low [PM1] conditions and after exercise following montelukast ingestion under low [PM1] conditions at 5, 10, and 15 min postchallenge (p<.004, .0006, .009, respectively). Montelukast provided greater protection against bronchoconstriction after exercise during high [PM1] than low [PM1] exposure (approximately 90% vs. approximately 35%), suggesting that bronchoconstriction from PM1 exposure is predominately leukotriene mediated. The precise mechanism of airborne PM1-induced leukotriene-mediated airway narrowing remains unclear.