ACETAMINOPHEN AND ASTHMA

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. 1. Prolonged use of acetaminophen in therapeutic doses provokes oxidative stress in human airways. 2. Prolonged use of therapeutic doses of acetaminophen results in increased concentrations of bronchoconstricting prostanoids in human airways. Specific aims 1. To test the hypothesis that chronic use of acetaminophen in therapeutic doses provokes oxidative stress in the airways in normal and asthmatic human subjects. 2. To test the hypothesis that chronic use of therapeutic doses of acetaminophen causes inhibition of prostacyclin and increases thromboxane A2 levels in the airways in normal and asthmatic subjects.