According to the GOLD 2006 definition, COPD is a preventable and treatable pathological situation characterized by the partially reversible airflow limitation determined by a variable proportion mixture of small airways disease (obliterative bronchiolitis) and parenchyma destruction (emphysema). A major impediment in the study of the COPD is represented by the fact the fundamental morphological changes that determine the major pulmonary dysfunction take place in the small, peripheral, airways, at the bronchiolo-alveolar attachments. That is why the experimental model of COPD developed progressively to the transgenic mouse. There are many experimental studies on the animal models that have obtained emphysema rapidly through intratraheal instillation of elastasis or bronchitis/bronchiolitis through intratraheal instillation of particles. It is accepted that the unnatural character of aggression, that does not permit the natural evolution of the inflammatory phenomenon, limits these models and tissue remodeling that take place in COPD patients. It is well known that cigarette smoking is a major cause of COPD. There have been reported some cases of COPD in never smoking patients exposed to air pollutants. We aimed to create an experimental model of COPD in rat through exposure to smoke resulted from solid combustibles burn for the same period and in the same conditions of cigarette smoke exposure and to compare the pulmonary morphological changes. Thirty Wistar rats were divided into three groups (n = 10): (1) the control group (C), (2) the cigarette smoke group (CS), and (3) the solid combustible smoke group (SCS). Apart from the control group, these were treated with solid combustibles smoke (SCS group) or cigarette smoke (CS group) for six months. Morphological and morphometry studies have been assessed. We have established a rat COPD model based on natural cigarette smoke exposure versus solid combustible burn resulted smoke, usable for a further approach in human non-smoker COPD investigation. Out procedures resulted in clear pulmonary morphological lesions that are characteristic for COPD. The achieved data support the idea that solid combustible burn resulted smoke determines emphysematous parenchyma lesions that are similar, but with an attenuated morphological appearance when comparing to the cigarette smoke exposure.