Pathogenic mechanisms in chronic obstructive pulmonary disease due to biomass smoke exposure

Arch Bronconeumol. 2015 Jun;51(6):285-92. doi: 10.1016/j.arbres.2014.10.005. Epub 2015 Jan 20.
[Article in English, Spanish]

Abstract

Chronic obstructive pulmonary disease (COPD) mortality and morbidity have increased significantly worldwide in recent decades. Although cigarette smoke is still considered the main risk factor for the development of the disease, estimates suggest that between 25% and 33% of COPD patients are non-smokers. Among the factors that may increase the risk of developing COPD, biomass smoke has been proposed as one of the most important, affecting especially women and children in developing countries. Despite the epidemiological evidence linking exposure to biomass smoke with adverse health effects, the specific cellular and molecular mechanisms by which this pollutant can be harmful for the respiratory and cardiovascular systems remain unclear. In this article we review the main pathogenic mechanisms proposed to date that make biomass smoke one of the major risk factors for COPD.

Keywords: Biomass smoke; Chronic obstructive pulmonary disease; Enfermedad pulmonar obstructiva crónica; Genotoxicidad; Genotoxicity; Humo de biomasa; Inflamación; Inflammation; Pathogenesis; Patogenia.

Publication types

  • Review

MeSH terms

  • Adult
  • Air Pollutants / adverse effects
  • Air Pollution, Indoor / adverse effects
  • Animals
  • Biomass*
  • Child
  • Cooking
  • Cytokines / metabolism
  • Environmental Exposure
  • Female
  • Gases / adverse effects
  • Heating
  • Humans
  • Inflammasomes / drug effects
  • Inflammation / etiology
  • Inflammation Mediators / metabolism
  • Male
  • Mice
  • Oxidative Stress
  • Particulate Matter / adverse effects
  • Pregnancy
  • Prenatal Exposure Delayed Effects
  • Pulmonary Disease, Chronic Obstructive / etiology*
  • Rural Population
  • Smoke / adverse effects*
  • Smoke Inhalation Injury / complications*
  • Transient Receptor Potential Channels / drug effects

Substances

  • Air Pollutants
  • Cytokines
  • Gases
  • Inflammasomes
  • Inflammation Mediators
  • Particulate Matter
  • Smoke
  • Transient Receptor Potential Channels