Introduction: The use of biomass for cooking is a very common practice in Africa and Benin, and is associated with exposure to organic pollutants. The aim of this study was to assess carbon monoxide exposure and respi...Introduction: The use of biomass for cooking is a very common practice in Africa and Benin, and is associated with exposure to organic pollutants. The aim of this study was to assess carbon monoxide exposure and respiratory disorders in women at artisanal fish-smoking sites. Methods: This was a cross-sectional study of women fish smokers at two artisanal fish-smoking sites in Benin. Recruitment was exhaustive. An interview using a respiratory questionnaire inspired by the Union questionnaire, spirometry and carbon monoxide (CO) measurement were carried out. Descriptive analysis and comparison of means using Student’s t-test with a threshold of p = 0.05 were performed. Results: The median age of the 81 people surveyed was 40, with an interquartile range (IQT) of [25 to 75]. The median duration of daily exposure to smoke was 6 h IQT [4, 7]. Of those surveyed, 64 (79.01%) were illiterate and 39 (48.24%) had been working for 20 years. CO levels at the start of activity varied from 89 to 145 ppm in one case and from 40 to 89 ppm in the other. Respiratory symptoms were present in 19 (23.46%);18 (22.22%) had mild airway impairment on spirometry. There was a statistically significant decrease between the mean values of peak expiratory flow (PEF), mean expiratory volume in seconds (FEV1) and forced vital capacity (FVC) before and after exposure to smoke. Conclusion: CO levels are high on fish smoking sites and respiratory problems are common. Improved working conditions are important for these women.展开更多
An arumal model to study smoke inhalation injuries was established in the sheep.22adult mate sheep were forced to inhale saw-dust smoke of pine wood for 6 minutes through anendotracheal tube.Pulmonury compliance,arter...An arumal model to study smoke inhalation injuries was established in the sheep.22adult mate sheep were forced to inhale saw-dust smoke of pine wood for 6 minutes through anendotracheal tube.Pulmonury compliance,arterial blood gases,carboxyhemoglobin,andoxyhemoglobin were monitored and the morpholgical chanhes of the tracheobronchial tree andpulmonary parenchyma were studied with optical and eletron microscopy.Severe carbon monoxide poisorung with fatal blooa level of carboxyhemoglobin（higher than50％） was found at the end of smoie inhalation.Acute respiratory distress,progressivehypoxerrua decreased pulmonary compliance and increased P（A-α）O<sub>2</sub> and Q<sub>s</sub>/Q<sub>T</sub> oecurred af-ter the injury.Tracheobronchial blockage due to pseudomembranous cast,pulmonary edema,atelectasis,and necrosis of pulmonary epithelium were demonstrated on histological sections.The mechaniisms of carbon monoxide poisoning ane acute respiratory failure was discussed.展开更多
The primary objective of this article is to analyze the role of tobacco smoke compounds able to damage the cardiovascular system and, in particular, to interfere with blood pressure. They are products of tobacco plant...The primary objective of this article is to analyze the role of tobacco smoke compounds able to damage the cardiovascular system and, in particular, to interfere with blood pressure. They are products of tobacco plant leaves, like nicotine, thiocyanate and aromatic amines, and a chemical derived from cigarette combustion, carbon monoxide. Of the other thousands of chemicals, there is no clear evidence of cardiovascular damage. Nicotine and its major metabolite, cotinine, usually increase blood pressure by a direct action and an action stimulating neuro-humoral metabolites of the body as well as sympathetic stimulation. An indirect mechanism of damage exerted by elevated carboxyhemoglobin concentrations is mediated by carbon monoxide, which, mainly induces arterial wall damage and, consequently, late rising in blood pressure by a toxic direct action on endothelial and blood cells. Thiocyanate, in turn, reinforces the hypoxic effects determined by carbon monoxide. Aromatic amines, depending on their chemical structure, may exert toxic effects on the cardiovascular system although they have little effect on blood pressure. A rise in blood pressure determined by smoking compounds is a consequence of both their direct toxicity and the characteristics of their chemical chains that are strongly reactive with a large numberof molecules for their spatial shape. In addition, a rise in blood pressure has been documented in individuals smoking a cigarette, acutely and chronically, with irreversible artery wall alterations several years after beginning smoking. Since cigarette smoking has a worldwide diffusion, the evidence of this topic meets the interest of both the scientific community and those individuals aiming to control smoking.展开更多
文摘Introduction: The use of biomass for cooking is a very common practice in Africa and Benin, and is associated with exposure to organic pollutants. The aim of this study was to assess carbon monoxide exposure and respiratory disorders in women at artisanal fish-smoking sites. Methods: This was a cross-sectional study of women fish smokers at two artisanal fish-smoking sites in Benin. Recruitment was exhaustive. An interview using a respiratory questionnaire inspired by the Union questionnaire, spirometry and carbon monoxide (CO) measurement were carried out. Descriptive analysis and comparison of means using Student’s t-test with a threshold of p = 0.05 were performed. Results: The median age of the 81 people surveyed was 40, with an interquartile range (IQT) of [25 to 75]. The median duration of daily exposure to smoke was 6 h IQT [4, 7]. Of those surveyed, 64 (79.01%) were illiterate and 39 (48.24%) had been working for 20 years. CO levels at the start of activity varied from 89 to 145 ppm in one case and from 40 to 89 ppm in the other. Respiratory symptoms were present in 19 (23.46%);18 (22.22%) had mild airway impairment on spirometry. There was a statistically significant decrease between the mean values of peak expiratory flow (PEF), mean expiratory volume in seconds (FEV1) and forced vital capacity (FVC) before and after exposure to smoke. Conclusion: CO levels are high on fish smoking sites and respiratory problems are common. Improved working conditions are important for these women.
文摘An arumal model to study smoke inhalation injuries was established in the sheep.22adult mate sheep were forced to inhale saw-dust smoke of pine wood for 6 minutes through anendotracheal tube.Pulmonury compliance,arterial blood gases,carboxyhemoglobin,andoxyhemoglobin were monitored and the morpholgical chanhes of the tracheobronchial tree andpulmonary parenchyma were studied with optical and eletron microscopy.Severe carbon monoxide poisorung with fatal blooa level of carboxyhemoglobin（higher than50％） was found at the end of smoie inhalation.Acute respiratory distress,progressivehypoxerrua decreased pulmonary compliance and increased P（A-α）O<sub>2</sub> and Q<sub>s</sub>/Q<sub>T</sub> oecurred af-ter the injury.Tracheobronchial blockage due to pseudomembranous cast,pulmonary edema,atelectasis,and necrosis of pulmonary epithelium were demonstrated on histological sections.The mechaniisms of carbon monoxide poisoning ane acute respiratory failure was discussed.
文摘The primary objective of this article is to analyze the role of tobacco smoke compounds able to damage the cardiovascular system and, in particular, to interfere with blood pressure. They are products of tobacco plant leaves, like nicotine, thiocyanate and aromatic amines, and a chemical derived from cigarette combustion, carbon monoxide. Of the other thousands of chemicals, there is no clear evidence of cardiovascular damage. Nicotine and its major metabolite, cotinine, usually increase blood pressure by a direct action and an action stimulating neuro-humoral metabolites of the body as well as sympathetic stimulation. An indirect mechanism of damage exerted by elevated carboxyhemoglobin concentrations is mediated by carbon monoxide, which, mainly induces arterial wall damage and, consequently, late rising in blood pressure by a toxic direct action on endothelial and blood cells. Thiocyanate, in turn, reinforces the hypoxic effects determined by carbon monoxide. Aromatic amines, depending on their chemical structure, may exert toxic effects on the cardiovascular system although they have little effect on blood pressure. A rise in blood pressure determined by smoking compounds is a consequence of both their direct toxicity and the characteristics of their chemical chains that are strongly reactive with a large numberof molecules for their spatial shape. In addition, a rise in blood pressure has been documented in individuals smoking a cigarette, acutely and chronically, with irreversible artery wall alterations several years after beginning smoking. Since cigarette smoking has a worldwide diffusion, the evidence of this topic meets the interest of both the scientific community and those individuals aiming to control smoking.
