ABSTRACT
La exposición a las emanaciones de incendios forestales es un importante problema de salud pública nacional e internacional. El cambio climático que conlleva sequía y aumento de la temperatura estival aumenta el riesgo y magnitud de los episodios de incendios forestales, generándose grandes incendios cuyas emanaciones pueden afectar a poblaciones distanciadas del epicentro. La asociación entre la exposición a las emanaciones de los incendios forestales, el aumento de las concentraciones de material particulado aéreo y la morbilidad respiratoria (exacerbación de asma y enfermedades respiratorias crónicas) ha sido evidenciada en diversos estudios. Sin embargo, es difícil realizar un metaanálisis de ellos, ya que la metodología empleada es muy disímil. Entre los principales mecanismos de morbilidad se encontrarían: la producción de citoquinas proinflamatorias, la activación endotelial y la disfunción del sistema nervioso autónomo. Ante la exposición al humo de incendios forestales, se produce daño tisular, aumento de los mecanismos protrombóticos, aumento de la presión arterial y cambios en el ritmo cardiaco, que explicaría los efectos cardiovasculares. Los sujetos con patología cardiovascular preexistente podrían tener mayor riesgo cardiovascular; sin embargo, existen factores confundentes en esta asociación. Por otra parte, el posible riesgo cancerígeno con la exposición a estas emanaciones requiere mayores estudios poblacionales.
Exposure to forest fire fumes is a major national and international public health issue. Climate change that leads to drought and increased summer temperature increases the risk and magnitude of wildfires episodes, generating mega-fires whose fumes not only affect the boundary population, but they may become transcontinental. Association between exposure to forest fire fumes, mainly increased concentrations of air born particulate matter and respiratory morbidity (exacerbation of asthma and chronic respiratory diseases) has been evidenced by diverse studies. However, it is difficult to carry out meta-analysis with them since the methodology used is dissimilar. Among the main causes of morbidity have been postulated the production of pro-inflammatory cytokines, endothelial activation and dysfunction of the autonomic nervous system. Occurrence of tissue damage, increased prothrombotic mechanisms, increased blood pressure and changes in heart rate, would explain the cardiovascular effects associated with exposure to smoke from these fires. However, epidemiological outcomes have not been entirely consistent, as the association between cardiovascular morbidity and exposure to wildfire fumes may be mixed with confounding factors. Despite this, patients with pre-existing cardiovascular pathology may be at increased risk. Finally, the potential risk of carcinogen with exposure to these fumes requires further population studies.
Subject(s)
Humans , Respiratory Tract Diseases/epidemiology , Wildfires , Air Pollution/adverse effects , Particulate Matter/adverse effects , Respiratory Tract Diseases/etiology , Asthma/etiology , Asthma/epidemiology , Cardiovascular Diseases/etiology , Cardiovascular Diseases/epidemiology , Public HealthABSTRACT
Los incendios forestales representan un problema creciente de la salud pública a nivel mundial, especialmente para la población más vulnerable (niños, ancianos, embarazadas y portadores de enfermedades cardiovasculares o respiratorias crónicas) expuesta al humo y a otros contaminantes aéreos. A diferencia de la contaminación atmosférica habitual de grandes urbes, aquella derivada de los incendios forestales tiene una composición diferente y su ocurrencia es esporádica y difícil de prever. La exposición a contaminantes atmosféricos derivados de incendios forestales se asocia a aumento de la morbilidad respiratoria y cardiovascular, mediada por una respuesta inflamatoria pulmonar y sistémica, estrés oxidativo y disfunción endotelial. En sujetos expuestos a humo de incendios forestales se ha observado un aumento en la producción de citoquinas pro-inflamatorias, activación endotelial y disfunción del sistema nervioso autónomo, que produce daño tisular, aumento de los mecanismos protrombóticos, aumento de la presión arterial y cambios en el ritmo cardiaco. Esta revisión analiza los mecanismos que han sido involucrados en generar efectos nocivos para la salud de seres humanos expuestos a material particulado y gases emanados de incendios forestales.
Wildfires represent a growing global public health issue, especially to the most vulnerable segment of the population (children, old people, pregnant women, patients with cardiovascular or respiratory diseases) exposed to smoke and other air borne contaminants generated from these events. In contrast to great cities ' usual atmospheric pollution, that derives from forest fires differ in composition and its occurrence is sporadic and usually unpredictable. Exposure to atmospheric pollutants derived from forest fires has been associated to increased respiratory and cardiovascular morbidity, mediated by an inflammatory systemic response, oxidative stress and endothelial dysfunction. In people exposed to forest fire smoke an increased production of pro-inflammatory cytokines, endothelial activation and autonomic nervous system dysfunction has been observed, that leads to tissue injury, increased prothrombotic response, increased blood pressure and changes in heart rhythm. This review analyzes the mechanisms that have been involved in generating harmful health effects in humans exposed to inhaled particulate matter and gases steaming from wildfires.
Subject(s)
Humans , Cardiovascular Diseases/chemically induced , Wildfires , Air Pollution/adverse effects , Lung Diseases/chemically induced , Cardiovascular Diseases/physiopathology , Cerebrovascular Disorders/chemically induced , Cytokines/metabolism , Reactive Oxygen Species/metabolism , Oxidative Stress , Inhalation Exposure , Air Pollutants/adverse effects , Particulate Matter/adverse effects , Lung Diseases/physiopathologyABSTRACT
Background: Although the hamster model of elastase induced emphysema is well characterized, the rat model has received less attention. Aim: To evaluate the effect of a single intratracheal elastase dose on lung pathological changes of Sprague-Dawley rats. Material and methods: Rats were injected with a single intratracheal elastase dose of 28 U/100 g body weight or saline and studied 7, 15, 30 and 365 days after injection. Results: Forty percent of rats died in the first 48 hours after injection, six were sacrificed at 7 days, 6 at 15 days, 7 at 30 days and 12 at 365 days. Progressive centroacinar emphysema was found from day 7 after elastase, with a persistent inflammatory reaction in the vicinity of emphysematous areas. Conclusions: Present findings differ from the panacinar emphysema described in the hamster using a similar elastase dose