Effect of High Levels of Oxygen and Smoking on the Lungs in Human Volunteers

Stress such as high oxygen or inflammation can result in damage to proteins by processes such
as oxidation or alternative regulation of signaling pathways by post-translational
modification of proteins (e.g., phosphorylation). Delivery of oxygen in high concentrations
to the lungs can result in damage, which is mediated in large part by reactive oxygen
species. Inflammation can result in activation of intracellular signaling pathways. This
study will evaluate modification of proteins and nucleic acids in bronchoalveolar lavage
fluid, bronchial epithelial cells, and peripheral blood of individuals exposed to oxygen or
who are smokers. In doing so, it will determine the effects of hyperoxia or inflammation on
the lung.

- INCLUSION CRITERIA:

History - good overall health without history of recent (within 3 months) acute disease;

Physical examination within normal limits;

Laboratory evaluation; including complete blood count (CBC), serum electrolyte
determinations, clotting times, chest x-ray, pulmonary function testing, and an
electrocardiogram (EKG) - within normal limits;

Non-smokers defined as having never smoked or not smoked in the past 2 years;

Smokers defined as moderate (1 pack per day for 3+ years) or heavy (1-2 packs for 10+
years);

Subjects must be willing to make the time commitment necessary for the study.

EXCLUSION CRITERIA:

Any study subject who does not fulfill the criteria for eligibility.

Individuals with a history of allergy or adverse reactions to atropine or any local
anesthetic;

Individuals testing positive for the human immunodeficiency virus or hepatitis virus;

Individuals on chronic medications or currently receiving medications;

Pregnant or lactating individuals, since the effects of hyperoxia on the fetus are unclear.