Tobacco smoke has been considered the main cause of lung cancer;however, epidemiological studies have identified several etiologic factors that could be involved in lung cancer onset in never smokers.In developing countries the exposure to biomass smoke (wood, dung and charcoal) has been associated with lung cancer pathogenesis.Our research group has been studying lung cancer associated with wood smoke exposure.We found that the incidence of this pathology was higher in women than in men, adenocarcinoma was the predominant reported histologic subtype and these patients had a better response to cis-platin first line chemotherapy (OR=4.9, 95% CI =1.25-20.15, p =0.019).Wood smoke exposure patients compared to tobacco smokers, had an increase in p53 and in phospho-p53 (serine392) levels (p < 0.0025) that indicates that both groups are probably exposed to the same carcinogens.Matrix metalloproteinases (MMPs) gelatinase activity that is associated with cancer progression, was lower in wood smoke than in smoker patients (p =0.017).This data had a correlation with the response to treatment (OR 6.11, 95% CI =1.28-31.6, p =0.018).The increase in the gelatinase activity in both groups when compared to control subjects is mainly due to an increase in MMP-2 activity, however MMP-2 and MMP-9 enzymatic activity was significantly increased in smoker patients (p =0.0006 and p =0.0033, respectively).MMP-9 and MT1-MMP plasma levels were increased in tobacco smoker subjects.There were no significant differences in MMP-2, TIMP-1 and TIMP-2 plasma concentration among both groups.In conclusion there are clinical and molecular differences among wood smoke and tobacco induced lung cancer that must be taken into consideration for the election of the most effective treatment.