![]() There is no safe level of exposure to cigarette smoke. Even a brief exposure to SHS can cause platelet aggregation and other hemodynamic changes favoring AMI onset and this effects seem to disappear a short time after SHS exposure cessation. Moreover SHS is responsible for accelerating atherosclerosis by lipid profile alteration, endothelial dysfunction and damage, hemodynamic stress, oxidant injury, neutrophil activation, enhanced thrombosis, increased fibrinogen and blood viscosity (3). Second hand smoking may induce AMI through such mechanisms as the prothrombotic state, increased myocardial workload, reduced oxygen-carrying capacity of blood caused by carbon monoxide, coronary vasoconstriction, and cathecholamine release. Several studies, have shown the reduction of AMI incidence after implementation of smoking bans in public places in a variety of countries ( 5, 6, 7, 8, 9). Toxins produced by SHS directly affect the cardiovascular system through well known multiple mechanisms, such as an increase in platelet activation, endothelial dysfunction, oxidative stress and inflammation, among others ( 2, 3, 4). Passive smoke is one of the most preventable causes of coronary artery disease (CAD), and of acute myocardial infarction (AMI) ( 1) next to obesity and a sedentary lifestyle. This review summarises the effects of passive smoke and takes a look at smoking ban laws - with a particular view to acute myocardial infarction. It provides a framework for tobacco measures to be implemented. The 2005 WHO Framework convention, the first international treaty under the auspices of the World Health Organization has been ratified by 168 parties - the US is one of the 9 countries such as Cuba and Switzerland that have signed yet have not ratified the treaty). In Europe, the European Union started issuing laws regarding promotion and advertising of tobacco in 2001. In 1964, the United States Surgeon General's Report on smoking and Health was published this led millions of American smokers to quit, the banning of certain advertising, and the requirement of warning labels on tobacco products.Ī section of the 1972 Surgeon General's report was devoted to second-hand smoke for the fist time and was the object of f ull report in 19 thereafter. ![]() ![]() The results of that epidemiological study showed - with a degree of certainty close to that of a randomised controlled study -, that both lung cancer and myocardial infarction occurred more often in smokers than in non-smokers. Richard Dole continued his inquiry with the British Doctors Study, where 2/3rd of all British male physicians (40,000) volunteered to answer questionnaires regarding their health and smoking habits. World of goo second hand smoke free#Indeed, alongside the publications of two American researchers and a German one, British psychologist and epidemiologist Richard Dole, (together with statistician Austin Bradford Hill), presented the results of a case-control study showing that among lung cancer cases, there were more smokers than among those free of lung cancer. This smoke is a mixture of gases and particles containing thousands of chemicals of which hundred cause disease.Īctive smoking was first shown as being statistically linked to lung cancer a century and a year ago, but it wasn't until after 1950 that smoking as causally linked to respiratory and cardiovascular disease was established. ![]() The burning cigarette produces side-stream smoke and makes up 85% of passive smoke while what the smoker exhales, mainstream smoke, contributes to second-hand smoke by only 15%. Also called passive smoke, second-hand smoke is what a smoker produces for those around him/her to inhale themselves: what emanates from the burning tip of the cigarette or cigar or pipe being smoked added to the smokers' actual breathing out of the inhaled substance. A person smoking causes bystanders to inhale second-hand smoke (SHS). ![]()
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