BACKGROUND: Epidemiologic surveys have revealed accelerated increases in adenocarcinoma but less rapid increases in squamous cell carcinoma of the lung among cigarette smokers in recent decades. Changes in the makeup of cigarettes and corresponding changes in smoke composition along with nicotine-compensating smoking patterns, such as the frequency of puff drawing and depth of inhalation, are suggested to have contributed to the observed epidemiologic profiles of these major histologic types of lung cancers. METHODS: The various changes in cigarette makeup leading to declining smoke yields from sales-weighted averages of 38 mg "tar" and 2.7 mg nicotine to 12 mg "tar" and 0.9 mg nicotine per cigarette are described. RESULTS: Higher nitrate content of tobacco blends is shown to be one of the major influences on lower smoke yields of carcinogenic polynuclear aromatic hydrocarbons (PAH) while causing increased yields of carcinogenic, tobacco-specific N-nitrosamines (TSNA). In vivo and in vitro bioassays incriminate PAH as inducers of squamous cell carcinoma, while TSNA are known to elicit primarily adenocarcinoma of the lung. CONCLUSIONS: The product changes, the smokers' dependence on nicotine which governs their smoking patterns, and the modified smoke chemistry support the hypothesis that differences in PAH and TSNA exposure may be linked to the observed different incidences of squamous cell cancer and adenocarcinoma of the lung.
BACKGROUND: Epidemiologic surveys have revealed accelerated increases in adenocarcinoma but less rapid increases in squamous cell carcinoma of the lung among cigarette smokers in recent decades. Changes in the makeup of cigarettes and corresponding changes in smoke composition along with nicotine-compensating smoking patterns, such as the frequency of puff drawing and depth of inhalation, are suggested to have contributed to the observed epidemiologic profiles of these major histologic types of lung cancers. METHODS: The various changes in cigarette makeup leading to declining smoke yields from sales-weighted averages of 38 mg "tar" and 2.7 mg nicotine to 12 mg "tar" and 0.9 mg nicotine per cigarette are described. RESULTS: Higher nitrate content of tobacco blends is shown to be one of the major influences on lower smoke yields of carcinogenicpolynuclear aromatic hydrocarbons (PAH) while causing increased yields of carcinogenic, tobacco-specific N-nitrosamines (TSNA). In vivo and in vitro bioassays incriminate PAH as inducers of squamous cell carcinoma, while TSNA are known to elicit primarily adenocarcinoma of the lung. CONCLUSIONS: The product changes, the smokers' dependence on nicotine which governs their smoking patterns, and the modified smoke chemistry support the hypothesis that differences in PAH and TSNA exposure may be linked to the observed different incidences of squamous cell cancer and adenocarcinoma of the lung.
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Authors: Maria Teresa Landi; Nilanjan Chatterjee; Kai Yu; Lynn R Goldin; Alisa M Goldstein; Melissa Rotunno; Lisa Mirabello; Kevin Jacobs; William Wheeler; Meredith Yeager; Andrew W Bergen; Qizhai Li; Dario Consonni; Angela C Pesatori; Sholom Wacholder; Michael Thun; Ryan Diver; Martin Oken; Jarmo Virtamo; Demetrius Albanes; Zhaoming Wang; Laurie Burdette; Kimberly F Doheny; Elizabeth W Pugh; Cathy Laurie; Paul Brennan; Rayjean Hung; Valerie Gaborieau; James D McKay; Mark Lathrop; John McLaughlin; Ying Wang; Ming-Sound Tsao; Margaret R Spitz; Yufei Wang; Hans Krokan; Lars Vatten; Frank Skorpen; Egil Arnesen; Simone Benhamou; Christine Bouchard; Andres Metspalu; Andres Metsapalu; Tonu Vooder; Mari Nelis; Kristian Välk; John K Field; Chu Chen; Gary Goodman; Patrick Sulem; Gudmar Thorleifsson; Thorunn Rafnar; Timothy Eisen; Wiebke Sauter; Albert Rosenberger; Heike Bickeböller; Angela Risch; Jenny Chang-Claude; H Erich Wichmann; Kari Stefansson; Richard Houlston; Christopher I Amos; Joseph F Fraumeni; Sharon A Savage; Pier Alberto Bertazzi; Margaret A Tucker; Stephen Chanock; Neil E Caporaso Journal: Am J Hum Genet Date: 2009-10-15 Impact factor: 11.025