This is a preliminary communication of the ECCO project that studies the interaction between lung cancer, COPD and SAHS. They are very common respiratory diseases, whose confluence is not rare and whose main trigger is tobacco. The main objective of this communication is to observe the effect of tobacco on tumor development and progression in lung cancer. Female mice of the susceptible strain A/JOlaHsd are initially administered with a NNK carcinogen and then chronically exposed to tobacco smoke. The evolution of the body weight gain of the mice is recorded. Before necropsies, pulmonary ventilation is studied by PET/CT using a radioactive gas (SF6); and the lung function of the mice is also analyzed. The lungs are then removed, from which a histological image and a gene expression study are obtained by qPCR of 84 genes related to oncogenesis, angiogenesis and hypoxia. In the context of lung cancer, tobacco produces a decrease in body weight gain; it produces a functional irregularity in the ventilation with hypoventilated areas; decreases the maximum inspiratory volume at 25mbar. There is an increase in the number of tumors and the total tumor area, as well as an increase in the area of pure papillary tumors. The gene expression of lung tissue is modified by tobacco, decreasing the expression levels of several genes related to tumor proliferation (Angptl6, Cdknia (p21), Cdkn2b (p15), lgf1, lgfbp4, NFkbia,...). We have found that tobacco alters tumor histology, both in extension and in the type of tumor induced by the carcinogen. Furthermore, it seems to decrease the expression of certain genes related to tumor proliferation. These conclusions are open until the results of the control group without lung cancer are available.