title: Pulmonary arterial hypertension and cor pulmonale associated with chronic domestic woodsmoke inhalation.
abstract: We describe the clinical, radiologic, functional, and pulmonary hemodynamic characteristics of a group of 30 nonsmoking patients with a lung disease that may be related to intense, long-standing indoor wood-smoke exposure. The endoscopic and some of the pathologic findings are also presented. Intense and prolonged wood-smoke inhalation may produce a chronic pulmonary disease that is similar in many aspects to other forms of inorganic dust-exposure interstitial lung disease. It affects mostly country women in their 60s, and severe dyspnea and cough are the outstanding complaints. The chest roentgenograms show a diffuse, bilateral, reticulonodular pattern, combined with normalized or hyperinflated lungs, as well as indirect signs of pulmonary arterial hypertension (PAH). On the pulmonary function test the patients show a mixed restrictive-obstructive pattern with severe hypoxemia and variable degrees of hypercapnia. Endoscopic findings are those of acute and chronic bronchitis and intense anthracotic staining of the airways appears to be quite characteristic. Fibrous and inflammatory focal thickening of the alveolar septa as well as diffuse parenchymal anthracotic deposits are the most prominent pathologic findings, although inflammatory changes of the bronchial epithelium are also present. The patients had severe PAH in which, as in other chronic lung diseases, chronic alveolar hypoxia may play the main pathogenetic role. However, PAH in wood-smoke inhalation-associated lung disease (WSIALD) appears to be more severe than in other forms of interstitial lung disease and tobacco-related COPD. The patients we studied are a selected group and they may represent one end of the spectrum of the WSIALD.
authors.affiliation: Cardiopulmonary Department, Instituto Nacional de Cardiologìa, Ignacio Chavez, Mexico City, Mexico.
authors.forename: J
authors.initials: J
authors.lastname: Sandoval
authors.forename: J
authors.initials: J
authors.lastname: Salas
authors.forename: M L
authors.initials: ML
authors.lastname: Martinez-Guerra
authors.forename: A
authors.initials: A
authors.lastname: Gómez
authors.forename: C
authors.initials: C
authors.lastname: Martinez
authors.forename: A
authors.initials: A
authors.lastname: Portales
authors.forename: A
authors.initials: A
authors.lastname: Palomar
authors.forename: M
authors.initials: M
authors.lastname: Villegas
authors.forename: R
authors.initials: R
authors.lastname: Barrios
mesh_terms: D001794:Blood Pressure / Q000502:physiology; D001991:Bronchitis / Q000473:pathology; D003371:Cough / Q000209:etiology; D004417:Dyspnea / Q000209:etiology; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D008875:Middle Aged; D010100:Oxygen / Q000097:blood; D011651:Pulmonary Artery / Q000503:physiopathology; D011659:Pulmonary Gas Exchange / Q000502:physiology; D011660:Pulmonary Heart Disease / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D012115:Residual Volume / Q000502:physiology; D015656:Respiratory Mechanics / Q000502:physiology; D012906:Smoke / Q000009:adverse effects*; D015208:Smoke Inhalation Injury / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D014109:Total Lung Capacity / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology; D014797:Vital Capacity / Q000502:physiology; D014934:Wood
chemical_list: D012906:Smoke; D010100:Oxygen