The typical clinical manifestations of Chronic Obstructive Pulmonary Disease (COPD) are explained by the presence of an obstructive process involving the air flow, accompanied by an exaggerated inflammatory response against external agents [1]. The causal factors for COPD are not yet fully understood, but they are related with significant exposure to harmful particles and gasses [2]. The disease is associated to cigarette smoking, in particular, for long stretches of time [3]; but only 20% of smokers develop COPD [4]. There has also been an increase of cases of COPD observed in consumers of other inhaled products or substances [5] and even in non-smokers [6]. Globally, cannabis or marihuana is the most commonly used illegal substance, the prevalence of having used the drug on occasion during life may reach 10% in some populations [7]. Cannabis consumption seems to present some short term beneficial pulmonary effects such as immediate bronchodilation, secondary to reduced airway resistance, which can be compromised in the long term as the cannabis smoke inhaled can have the same harmful effects as those attributed to tobacco [8,9]. The purpose of this article is to preset a case of secondary COPD associated to regular cannabis consumption or dependency. 1.1. The case A 62-year-old male patient, living in an upper income area of the city, with over six months of clinical symptoms of grade 2 dyspnea (mMRC). Physical examination revealed blood pressure of 120/70 mm HG, a heart rate of 61 beats/minute, breathing rate of 20 breaths/minute, weight of 81 kg, height 184 cm and BMI of 23.92, with no other clinically relevant findings. Significant personal antecedents include an over 40-year history of cannabis consumption with occasional cocaine base use. The patient denied cigarette consumption and biomass exposition. The patient's clinical history also documented esophagus cancer of the adenocarcinoma type and benign prostatic hypertrophy. Both conditions were treated through surgery. Evaluation using the COPD Assessment Test, (CAT): 7 (cough: 2, phlegm: 2, chest tightness: 0, dyspnea: 3, domestic activity: 0, sleep: 0, energy: 0, fear: 0). A chest x-ray revealed hyperlucency in the upper lobes and ballooning in the left posterior arch of the tenth rib (Fig. 1). There was also evidence of thickening of bronchial walls (Fig. 2). Pre- and post-bronchodilator spirometry informed forced expiratory volume in the first second (VEF1)/forced vital capacity (CVF): 65%, VEF1: 89% of the predicted, CVF: 106% of the predicted, FEF 25–75%: 63 (Fig. 3), carbon monoxide diffusion capacity: reduced, moderate. High resolution chest CT shows radiolucides with focal and central air attenuation located in the upper lobes without an identifiable wall (centrilobullar emphysema). No bullous emphysema are observed (Fig. 4). Category A COPD diagnosis was confirmed (GOLD 2018) and pharmacological management with one 150 μg indacaterol capsule inhaled once daily was initiated with an important remission of symptoms, without clinically significant exacerbations through one year of follow-up. Open in a separate window Fig. 1 Posteroanterior radiography.