Background: Since 1953, the sales-weighted average "tar" and nicotine yields of commercial cigarettes in developed countries have significantly declined. However, the risk for chronic obstructive pulmonary disease (COPD) and for cancer of the lung has not decreased; adenocarcinoma incidence even continues to rise faster than the rate of squamous cell carcinoma of the lung. Undiminished risk of cigarette smokers for COPD and lung cancer is largely due to more intense smoking and deeper inhalation of the smoke of "low-yield" cigarettes and to significant changes in the smoke yields of certain lung carcinogens.
Methods: Puff frequency, puff duration, and puff volume of cigarette smokers were determined by a microcomputer-assisted flow transducer. These parameters were then programmed into a smoking machine to generate mainstream smoke for quantifying nicotine and lung carcinogens.
Results: Simulating the human smoking characteristics increases the yields of "tar" and nicotine per cigarette two- to threefold above Federal Trade Commission-reported levels. Smoke yields of lung carcinogens like benzo[alpha]pyrene and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone parallel those of nicotine and "tar."
Conclusions: The way people smoke and the total number of cigarettes consumed daily determine the uptake, i.e., the administered dose of nicotine, other toxic, and genotoxic smoke constituents. It is important to communicate this to consumers rather than letting the smokers believe that they are truly smoking a cigarette of lower smoke yields when they choose "light" or "ultralight" products.