সদস্য:Gitartha.bordoloi/ধপাতৰ স্বাস্থ্যত প্ৰভাৱ
ধঁপাতৰ স্বাস্থ্যত প্ৰভাৱ বুলিলে ধঁপাত সেৱনে পৰা মানুহৰ স্বাস্থ্যত পেলোৱা প্ৰভাৱৰ পৰিঘটনা, প্ৰক্ৰিয়া আৰু কাৰকসমূহ বুজোৱা হয়। এপিডেমীঅ'ল'জিকেল গৱেষণাসমূহত মূলতঃ চিগাৰেটৰ ধঁপাত সেৱনক সামৰি লোৱা হৈছে, সেৱনৰ আন আন বিকল্পতকৈ ইয়াৰ বিষয়ে অধিক অধ্যয়ন কৰা হৈছে।
বিশ্বজুৰি ধঁপাত সেৱন হৈছে প্ৰতিৰোধ কৰিব পৰা মৃত্যুৰ প্ৰধানতম কাৰণ। ধঁপাতৰ ব্যৱহাৰে সাধাৰণতে হাওঁফাওঁ আৰু হৃদপিণ্ডৰ ৰোগ কৰে। হাৰ্ট এটেক, ষ্ট্ৰোক, ক্ৰ'নিক অব্ষ্ট্ৰাক্টিভ পালম'নেৰী ডিজিজ, ক্ৰনিক ব্ৰ'ঙ্কাইটিছ, কৰ্কট ৰোগ বিশেষকৈ হাওঁফাওঁৰ কৰ্কট, শ্বাসনলীৰ কৰ্কট, অগ্নাশয়ৰ কৰ্কট আদিৰ অন্যতম কাৰক হৈছে ধঁপাত। ই ৰক্তনলীকাৰ ৰোগ আৰু উচ্চ ৰক্তচাপৰো কাৰণ। এই প্ৰভাৱসমূহ ব্যক্তিজনে সেৱন কৰা চিগাৰেটৰ সংখ্যা আৰু সময়ৰ ওপৰত নিৰ্ভৰ কৰে। কম বয়সতে চিগাৰেট হুঁপা আৰম্ভ কৰা অধিক টাৰযুক্ত চিগাৰেট হুঁপিলে এই ৰোগবোৰৰ আশঙ্কা বাঢ়ে। ইয়াৰ লগতে পৰিৱেশিক চিগাৰেটৰ ধোঁৱা বা পৰোক্ষ চিগাৰেট সেৱনেও সকলো বয়সৰ লোকৰ স্বাস্থ্যৰ ক্ষতি কৰে। অনুন্নত দেশসমূহত বিক্ৰী হোৱা চিগাৰেটত টাৰৰ মাত্ৰা বেছি থাকে আৰু লগতে চেকনীৰ সুবিধাও নাথাকে, গতিকে এইসমূহ ঠাইত ধঁপাতৰ পৰা ক্ষতিও অধিক হয়। বিশ্ব স্বাস্থ্য সংস্থাৰ (WHO) হিছাপৰ মতে ২০০৪ চনত ধঁপাতৰ ফলত ৫.৪ নিযুত লোকৰ মৃত্যু হৈছে আৰু বিংশ শতিকাজুৰি এই সংখ্যা প্ৰায় ১০০ নিযুত। আমেৰিকা যুক্তৰাষ্টৰ ৰোগ নিয়ন্ত্ৰণ আৰু প্ৰতিৰোধ কেন্দ্ৰৰ মতে ধঁপাতৰ ব্যৱহাৰ "উন্নত দেশসমূহত মানুহৰ স্বাস্থ্যৰ ক্ষতি কৰিব পৰা প্ৰধান প্ৰতিৰোধযোগ্য কাৰক আৰু বিশ্বজুৰি কমবয়সীয়া মৃত্যুৰ গুৰুত্বপূৰ্ণ কাৰণ।"
চিগাৰেটৰ ধোঁৱাত কেইবাবিধো কাৰ্চিন'জেনিক পাইৰ'লাইটিক দ্ৰব্য থাকে যি ডিএনএ'ৰ লগত যুক্ত হৈ বহু জেনেটিক মিউটেছন কৰে। চিগাৰেটৰ ধোঁৱাত ১৯ বিধ ৰাসায়নিক কাৰ্চিন'জেন চিনাক্ত কৰা হৈছে। ধঁপাতত থকা নিক'টিন এবিধ মানসিক আসক্তিজনক যৌগ। গৰ্ভধাৰণত চিগাৰেট সেৱনে গৰ্ভপাত কৰিব পাৰে। লগতে কেঁচুৱাৰ দেহত ক্ষতি কৰি প্ৰাক্বয়স্ক জন্ম, জন্মৰ কম ওজন কৰাৰ লগতে চাডেন ইন্ফেণ্ট ডে'থ চিন্দ্ৰ'ম (SIDS)ৰ আশঙ্কা ১.৪ৰ পৰা ৩ গুণ পৰ্যন্ত বঢ়ায়। এন্দুৰৰ ওপৰত কৰা পৰীক্ষাৰ পৰা জানিব পৰা গৈছে যে গৰ্ভত চিগাৰেটৰ ধোঁৱাৰ প্ৰভাৱে শিশুৰ মগজুৱে হাইপ'ক্সিয়া চিনাক্ত কৰাত বাধা দিয়ে যাৰ ফলত দুৰ্ঘটনাবশতঃ এছ্ফাইক্সিয়া বা শ্বাসৰুদ্ধতা হ'ব পাৰে। পুৰুষৰ যৌন অসমৰ্থতাৰ হাৰ চিগাৰেট নোখোৱা লোকতকৈ চিগাৰেট খোৱাসকলৰ মাজত ৮৫% বেছি আৰু ধঁপাত লিঙ্গ শিথিলতাৰ এক অন্যতম কৰক।
স্বাস্থ্যত প্ৰভাৱ[সম্পাদনা কৰক]
এজন মানুহৰ ধঁপাতজনিত ৰোগ হোৱাৰ আশঙ্কা ধূমপান কৰা সময় আৰু তাৰ পৰিমাণৰ ওপৰত নিৰ্ভৰ কৰে। তেওঁ ধূমপান বাদ দিলে সেই আশঙ্কা লাহে লাহে কমি আহে আৰু শৰীৰৰ ক্ষতি নিজে নিজে মেৰামতি হ'বলৈ ধৰে। ধূমপান ত্যাগ কৰাৰ এবছৰৰ পিছত হৃদৰোগ হোৱাৰ আশঙ্কা ধূমপায়ী এজনতকৈ আধা হৈ পৰে। সকলো ধূমপায়ীৰে স্বাস্থ্যত প্ৰভাৱ একে নহয়। "পাতলীয়া চিগাৰেট" ("light" cigarettes)ৰ সেৱনেও ৰোগ প্ৰতিৰোধ কৰিব নোৱাৰে।
ধঁপাতৰ ব্যৱহাৰে মূলতঃ হৃদয় আৰু শ্বাস তন্ত্ৰৰ ৰোগৰ সৃষ্টি কৰে। হাৰ্ট এটেক, COPD, এম্ফাইচেমা, আৰু কৰ্কট ৰোগ, বিশেষকৈ হাওঁফাওঁৰ কৰ্কট, শ্বাসনলী তথা মুখৰ কৰ্কট, আৰু অগ্নাশয়ৰ কৰ্কটৰ মূল কাৰক হৈছে ধূমপান। নিয়মিত ধূমপান কৰাসকলৰ গড় আয়ুস ধূমপান নকৰাসকলতকৈ ১০ ৰ পৰা ১৭.৯ বছৰ কম হ'ব পাৰে। পুৰুষ ধূমপায়ীসকলৰ আধাসংখ্যক ধূমপানজনিত ৰোগৰ মৃত্যুমুকহ্ত পৰে। হাওঁফাওঁৰ কৰ্কট ৰোগৰ লগৰ ধূমপান জড়িত হোৱাৰ প্ৰমাণ সকলোতকৈ বেছি। পুৰুষ ধূমপাযীসকলৰ জীৱনকালত হাওঁফাওঁৰ কৰ্কট হোৱাৰ আশঙ্কা ১৭.২% আৰু মহিলাৰ ক্ষেত্ৰত ই ১১.৬% । ধূমপান নকৰাসকলৰ ক্ষেত্ৰত এই আশঙ্কা অতি কম; পুৰুষৰ ১.৩% আৰু মহিলাৰ ১.৪%। ধঁপাত সেৱন জাৰী ৰখা মানুহৰ ৰোগ হোৱাৰ আশঙ্কা ছয়জনৰ ভিতৰত এজনলৈ বাঢ়ে। প্ৰথম বিশ্বযুদ্ধৰ পূৰ্বে হাওঁফাওঁৰ কৰ্কট অতি কমকৈ হৈছিল আৰু বেছিভাগ চিকিৎসকেই এনে ৰোগী পৰীক্ষা কৰিবলৈ নাপাইছিল। বিশ্বযুদ্ধৰ পিছত ধূমপান বাঢ়ি অহাৰ লগে লগে হাওঁফাওঁৰ কৰ্কট অত্যধিক হাৰত বাঢ়িবলৈ ধৰিলে।
মৃত্যুৰ হাৰ[সম্পাদনা কৰক]
পুৰুষ আৰু মহিলা ধূমপায়ীয়ে ক্ৰমে গড়ে ১৩.২ আৰু ১৪.৫ বছৰ জীৱনৰ পৰা হেৰুৱায়।
৩৪,৪৮৬ জন ব্ৰিটিছ পুৰুষৰ ওপৰত কৰা এটা ৫০ বছৰীয়া সমীক্ষা অনুসৰি অন্ততঃ আজীৱন ধূমপায়ীসকলৰ আধাসংখ্যক ব্যক্তি সোনকালে মৃত্যুমুখত পৰে।
কৰ্কট ৰোগ[সম্পাদনা কৰক]
ধপাত ব্যৱহাৰৰ প্ৰাথমিক প্ৰভাৱ হৈছে বিভিন্ন প্ৰকাৰৰ কৰ্কট ৰোগ, বিশেষকৈ হাওঁফাওঁৰ কৰ্কট ৰোগ, বৃক্কৰ কৰ্কট ৰোগ, শ্বাসনলীৰ কৰ্কট ৰোগ, মূৰ আৰু ডিঙিৰ কৰ্কট ৰোগ, মূত্ৰাশয়ৰ কৰ্কট ৰোগ, খাদ্যনলীৰ কৰ্কট ৰোগ, অগ্ন্যাশয়ৰ কৰ্কট ৰোগ আৰু পাকস্থলীৰ কৰ্কট ৰোগ।
মায়েলইড লিউকেমিয়া, স্কোৱামাছ চে'ল কাৰ্চিন'মা, যকৃতৰ কৰ্কট ৰোগ, ক'ল'ৰেক্টেল কেন্সাৰ, গলব্লাডাৰ কেন্সাৰ, এড্ৰিনেল গ্ৰন্থিৰ কৰ্কট ৰোগ, ক্ষুদ্ৰান্ত্ৰৰ কৰ্কট ৰোগ আৰু শিশুকালৰ বিভিন্ন কৰ্কট ৰোগ হোৱাৰ প্ৰমাণো ধপাত সেৱনৰ ফলত পোৱা গৈছে। শেহতীয়া অধ্যয়নে পৰোক্ষ সেৱনকে ধৰি ধপাতৰ সেৱন আৰু মহিলাৰ চাৰ্ভিক্সৰ কৰ্কট ৰোগৰ সম্পৰ্ক থকাটো প্ৰমাণ কৰিছে।
আন কাৰক অবিহনে পুৰুষ ধূমপায়ীৰ বাবে হাওঁফাওঁৰ কৰ্কট ৰোগত ভুগি ৮৫ বছৰ বয়সৰ আগতে মৃত্যু হোৱাৰ আশঙ্কা ২২% আৰু মহিলাৰ বাবে ১১.৯%। আজীৱন ধূমপান নকৰাসকলৰ ক্ষেত্ৰত এই সংখ্যা ইউৰোপীয় পুৰুষৰ বাবে ১.১% আৰু মহিলাৰ বাবে ০.৮%।
ধূমপান কৰোঁতে ধোঁৱাত থকা যৌগসমূহে (যেনে- কাৰ্বন ম'ন'ক্সাইড, আৰু চায়ানাইড) হাওঁফাওঁৰ ক্ষতি কৰে আৰু loss of elasticity in the alveoli। ই emphysema আৰু COPD-ৰ কাৰণ বুলি বিশ্বাস কৰা হয়। কাৰ্চিন'জেন এক্ৰ'লিন আৰু ইয়াৰ উদ্ভুত যৌগই COPDত দেখা পোৱা প্ৰদাহৰ সৃষ্টি কৰে।
পৰোক্ষ ধূমপান হৈছে চিগাৰেট, পাইপ বা চিগাৰৰ পৰা ওলোৱা ধোঁৱা আৰু ধূমপায়ীৰ হাওঁফাওঁৰ পৰা নিৰ্গত ধোঁৱাৰ মিশ্ৰণ। ইয়াক নজনাকৈ সেৱন কৰা হয় আৰু ই চিগাৰেট জ্বলি শেষ হোৱাৰ বহু ঘণ্টাৰ পিছতো বতাহত থাকে। পৰোক্ষ ধূমপানে কৰ্কট ৰোগ, শ্বাসনলীৰ সংক্ৰমণ আৰু এজ্মাৰ সৃষ্টি কৰে। ঘৰ বা কৰ্মস্থলীত পৰোক্ষ ধূমপান কৰিবলগীয়া হোৱা লোকৰ হৃদৰোগৰ আশংকা ২৫-৩০% বাঢ়ে আৰু হাওঁফাওঁৰ কৰ্কটৰ আশংকা ২০-৩০% বাঢ়ে। পৰোক্ষ ধূমপানৰ পৰা প্ৰতি বছৰে প্ৰায় ৩৮,০০০ মানুহৰ মৃত্যু ঘটে বুলি অনুমান কৰা হয় আৰু ইয়াৰ ৩,৪০০ জন হাওঁফাওঁৰ কৰ্কট হোৱা ধূমপান নকৰা ব্যক্তি।
ধূমপানৰ ফলত হোৱা ক্ৰ'নিক অবষ্ট্ৰাক্টিভ পালমে'নেৰী ডিজিজ (COPD) এবিধ স্থায়ী, আৰোগ্যহীন ৰোগ য'ত হাওঁফাওঁৰ ক্ষমতা কমি যায়। ইয়াৰ ফলত উশাহ চুটি হৈ পৰে, উশাহ লওঁতে শব্দ হয়, খেকাৰৰ সৈতে কাঁহ হয় আৰু হাওঁফাওঁৰ ক্ষতি হৈ এম্ফাইচেমা বা ক্ৰ'নিক ব্ৰঙ্কাইটিছ ৰোগৰ সৃষ্টি হয়।
Inhalation of tobacco smoke causes several immediate responses within the heart and blood vessels. Within one minute the heart rate begins to rise, increasing by as much as 30 percent during the first 10 minutes of smoking. Carbon monoxide in tobacco smoke exerts its negative effects by reducing the blood’s ability to carry oxygen. Both of these conditions can become permanent with prolonged use of cigarettes.
Smoking also increases the chance of heart disease, stroke, atherosclerosis, and peripheral vascular disease. Several ingredients of tobacco lead to the narrowing of blood vessels, increasing the likelihood of a blockage, and thus a heart attack or stroke. According to a study by an international team of researchers, people under 40 are five times more likely to have a heart attack if they smoke.
Recent research by American biologists has shown that cigarette smoke also influences the process of cell division in the cardiac muscle and changes the heart's shape.
The usage of tobacco has also been linked to Buerger's disease (thromboangiitis obliterans) the acute inflammation and thrombosis (clotting) of arteries and veins of the hands and feet.[উদ্ধৃতিৰ প্ৰয়োজন]
The current US Surgeon General’s Report concludes that there is no risk-free level of exposure to second-hand smoke. Even short exposures to second-hand smoke can cause blood platelets to become stickier, damage the lining of blood vessels, decrease coronary flow velocity reserves, and reduce heart rate variability, potentially increasing the risk of heart attack. New research indicates that private research conducted by cigarette company Philip Morris in the 1980s showed that second-hand smoke was toxic, yet the company suppressed the finding during the next two decades.
Although cigarette smoking causes a greater increase of the risk of cancer than cigar smoking, cigar smokers still have an increased risk for many health problems, including cancer, when compared to non-smokers. As for second-hand smoke, the NIH study points to the large amount of smoke generated by one cigar, saying "cigars can contribute substantial amounts of tobacco smoke to the indoor environment; and, when large numbers of cigar smokers congregate together in a cigar smoking event, the amount of ETS [i.e. second-hand smoke] produced is sufficient to be a health concern for those regularly required to work in those environments."
Smoking tends to increase blood cholesterol levels. Furthermore, the ratio of high-density lipoprotein (the "good" cholesterol) to low-density lipoprotein (the "bad" cholesterol) tends to be lower in smokers compared to non-smokers. Smoking also raises the levels of fibrinogen and increases platelet production (both involved in blood clotting) which makes the blood viscous. Carbon monoxide binds to haemoglobin (the oxygen-carrying component in red blood cells), resulting in a much stabler complex than haemoglobin bound with oxygen or carbon dioxide—the result is permanent loss of blood cell functionality. Blood cells are naturally recycled after a certain period of time, allowing for the creation of new, functional erythrocytes. However, if carbon monoxide exposure reaches a certain point before they can be recycled, hypoxia (and later death) occurs. All these factors make smokers more at risk of developing various forms of arteriosclerosis. As the arteriosclerosis progresses, blood flows less easily through rigid and narrowed blood vessels, making the blood more likely to form a thrombosis (clot). Sudden blockage of a blood vessel may lead to an infarction (stroke). However, it is also worth noting that the effects of smoking on the heart may be more subtle. These conditions may develop gradually given the smoking-healing cycle (the human body heals itself between periods of smoking), and therefore a smoker may develop less significant disorders such as worsening or maintenance of unpleasant dermatological conditions, e.g. eczema, due to reduced blood supply. Smoking also increases blood pressure and weakens blood vessels.
In addition to increasing the risk of kidney cancer, smoking can also contribute to additional renal damage. Smokers are at a significantly increased risk for chronic kidney disease than non-smokers. A history of smoking encourages the progression of diabetic nephropathy.
A study of an outbreak of A(H1N1) influenza in an Israeli military unit of 336 healthy young men to determine the relation of cigarette smoking to the incidence of clinically apparent influenza, revealed that, of 168 smokers, 68.5 percent had influenza, as compared with 47.2 percent of nonsmokers. Influenza was also more severe in the smokers; 50.6 percent of the smokers lost work days or required bed rest, or both, as compared with 30.1 percent of the nonsmokers.
According to a study of 1,900 male cadets after the 1968 Hong Kong A2 influenza epidemic at a South Carolina military academy, compared with nonsmokers heavy smokers (more than 20 cigarettes per day), had 21% more illnesses and 20% more bed rest, light smokers (less than 20 cigarettes per day) had 10% more illnesses and 7% more bed rest.
The effect of cigarette smoking upon epidemic influenza was studied prospectively among 1,811 male college students. Clinical influenza incidence among those who daily smoked 21 or more cigarettes was 21% higher than that of non-smokers. Influenza incidence among smokers of 1 to 20 cigarettes daily was intermediate between non-smokers and heavy cigarette smokers.
Surveillance of a 1979 influenza out-break at a military base for women in Israel revealed that, Influenza symptoms developed in 60.0% of the current smokers vs. 41.6% of the nonsmokers.
Smoking seems to cause a higher relative influenza-risk in older populations than in younger populations. In a prospective study of community-dwelling people 60–90 years of age, during 1993, of unimmunized people 23% of smokers had clinical influenza as compared with 6% of non-smokers.
Smoking may substantially contribute to the growth of influenza epidemics affecting the entire population.However the proportion of influenza cases in the general non-smoking population attributable to smokers has not yet been calculated.
Perhaps the most serious oral condition that can arise is that of oral cancer. However, smoking also increases the risk for various other oral diseases, some almost completely exclusive to tobacco users. The National Institutes of Health, through the National Cancer Institute, determined in 1998 that "cigar smoking causes a variety of cancers including cancers of the oral cavity (lip, tongue, mouth, throat), esophagus, larynx, and lung." Pipe smoking involves significant health risks, particularly oral cancer. Roughly half of periodontitis or inflammation around the teeth cases are attributed to current or former smoking. Smokeless tobacco causes gingival recession and white mucosal lesions. Up to 90% of periodontitis patients who are not helped by common modes of treatment are smokers. Smokers have significantly greater loss of bone height than nonsmokers, and the trend can be extended to pipe smokers to have more bone loss than nonsmokers. Smoking has been proven to be an important factor in the staining of teeth. Halitosis or bad breath is common among tobacco smokers. Tooth loss has been shown to be 2 to 3 times higher in smokers than in non-smokers. In addition, complications may further include leukoplakia, the adherent white plaques or patches on the mucous membranes of the oral cavity, including the tongue, and a loss of taste sensation or salivary changes.[উদ্ধৃতিৰ প্ৰয়োজন]
Tobacco is also linked to susceptibility to infectious diseases, particularly in the lungs. Smoking more than 20 cigarettes a day increases the risk of tuberculosis by two to four times, and being a current smoker has been linked to a fourfold increase in the risk of invasive pneumococcal disease. It is believed that smoking increases the risk of these and other pulmonary and respiratory tract infections both through structural damage and through effects on the immune system. The effects on the immune system include an increase in CD4+ cell production attributable to nicotine, which has tentatively been linked to increased HIV susceptibility. The usage of tobacco also increases rates of infection: common cold and bronchitis, chronic obstructive pulmonary disease, emphysema and chronic bronchitis in particular.[উদ্ধৃতিৰ প্ৰয়োজন]
Smoking reduces the risk of Kaposi's sarcoma in people without HIV infection. One study found this only with the male population and could not draw any conclusions for the female participants in the study.
যৌন অসমৰ্থতা[সম্পাদনা কৰক]
Incidence of impotence is approximately 85 percent higher in male smokers compared to non-smokers, and it is a key cause of erectile dysfunction (ED). Smoking causes impotence because it promotes arterial narrowing.
মহিলাৰ সন্তানহীনতা[সম্পাদনা কৰক]
Smoking is harmful to the ovaries, potentially causing female infertility, and the degree of damage is dependent upon the amount and length of time a woman smokes. Nicotine and other harmful chemicals in cigarettes interfere with the body’s ability to create estrogen, a hormone that regulates folliculogenesis and ovulation. Also, cigarette smoking interferes with folliculogenesis, embryo transport, endometrial receptivity, endometrial angiogenesis, uterine blood flow and the uterine myometrium. Some damage is irreversible, but stopping smoking can prevent further damage. Smokers are 60% more likely to be infertile than non-smokers. Smoking reduces the chances of IVF producing a live birth by 34% and increases the risk of an IVF pregnancy miscarrying by 30%.
"Smokers often report that cigarettes help relieve feelings of stress. However, the stress levels of adult smokers are slightly higher than those of nonsmokers, adolescent smokers report increasing levels of stress as they develop regular patterns of smoking, and smoking cessation leads to reduced stress. Far from acting as an aid for mood control, nicotine dependency seems to exacerbate stress. This is confirmed in the daily mood patterns described by smokers, with normal moods during smoking and worsening moods between cigarettes. Thus, the apparent relaxant effect of smoking only reflects the reversal of the tension and irritability that develop during nicotine depletion. Dependent smokers need nicotine to remain feeling normal." 
ক্ষিপ্ৰ প্ৰভাৱ[সম্পাদনা কৰক]
Users report feelings of relaxation, sharpness, calmness, and alertness. Those new to smoking may experience nausea, dizziness, and rapid heart beat. Generally, the unpleasant symptoms will eventually vanish over time, with repeated use, as the body builds a tolerance to the chemicals in the cigarettes, such as nicotine.
The deleterious mood effects of abstinence explain why smokers suffer more daily stress than non-smokers, and become less stressed when they quit smoking. Deprivation reversal also explains much of the arousal data, with deprived smokers being less vigilant and less alert than non-deprived smokers or non-smokers.
Recent studies have shown a positive relationship between psychological distress and salivary cotinine levels in smoking and non-smoking adults, indicating that both firsthand and secondhand smoke exposure may lead to higher levels of mental stress.
সামাজিক আৰু আচৰণগত[সম্পাদনা কৰক]
Cognitive function[সম্পাদনা কৰক]
The usage of tobacco can also create cognitive dysfunction. There seems to be an increased risk of Alzheimer's disease, although "case–control and cohort studies produce conflicting results as to the direction of the association between smoking and AD". Smoking has been found to contribute to dementia and cognitive decline, reduced memory and cognitive abilities in adolescents, and brain shrinkage (cerebral atrophy).
Most notably, some studies have found that patients with Alzheimer's disease are more likely not to have smoked than the general population, which has been interpreted to suggest that smoking offers some protection against Alzheimer's. However, the research in this area is limited and the results are conflicting; some studies show that smoking increases the risk of Alzheimer's disease [উদ্ধৃতিৰ প্ৰয়োজন]. A recent review of the available scientific literature concluded that the apparent decrease in Alzheimer risk may be simply because smokers tend to die before reaching the age at which Alzheimer normally occurs. "Differential mortality is always likely to be a problem where there is a need to investigate the effects of smoking in a disorder with very low incidence rates before age 75 years, which is the case of Alzheimer's disease," it stated, noting that smokers are only half as likely as non-smokers to survive to the age of 80.
Evidence suggests that non-smokers are up to twice as likely as smokers to develop Parkinson's disease or Alzheimer's disease. A plausible explanation for these cases may be the effect of nicotine, a cholinergic stimulant, increasing the levels of acetylcholine in the smoker's brain; Parkinson's disease occurs when the effect of dopamine is less than that of acetylcholine. In addition, nicotine stimulates the mesolimbic dopamine pathway (as do other drugs of abuse), causing an effective increase in dopamine levels. Opponents counter by noting that consumption of pure nicotine may be as beneficial as smoking without the risks associated with smoking, although this is unlikely due to the importance of the MAO-B inhibitor compounds of tobacco in preventing neurodegenerative diseases.[উদ্ধৃতিৰ প্ৰয়োজন]
In many respects, nicotine acts on the nervous system in a similar way to caffeine. Some writings have stated that smoking can also increase mental concentration; one study documents a significantly better performance on the normed Advanced Raven Progressive Matrices test after smoking.
Most smokers, when denied access to nicotine, exhibit symptoms such as irritability, jitteriness, dry mouth, and rapid heart beat. The onset of these symptoms is very fast, nicotine's half-life being only 2 hours.[উদ্ধৃতিৰ প্ৰয়োজন] Withdrawal symptoms can appear even if the smoker's consumption is very limited or irregular, appearing after only 4–5 cigarettes in most adolescents.[উদ্ধৃতিৰ প্ৰয়োজন] The psychological dependence may linger for months or even many years. Unlike some recreational drugs, nicotine does not measurably alter a smoker's motor skills, judgement, or language abilities while under the influence of the drug. Tobacco withdrawal has been shown to cause clinically significant distress.
Former and current smokers have a lower incidence of Parkinson's disease compared to people who have never smoked, although the authors stated that it was more likely that the movement disorders which are part of Parkinson's disease prevented people from being able to smoke than that smoking itself was protective. Another study considered a possible role of nicotine in reducing Parkinson's risk: nicotine stimulates the dopaminergic system of the brain, which is damaged in Parkinson's disease, while other compounds in tobacco smoke inhibit MAO-B, an enzyme which produces oxidative radicals by breaking down dopamine.
A very large percentage of schizophrenics smoke tobacco as a form of self medication. The high rate of tobacco use by the mentally ill is a major factor in their decreased life expectancy, which is about 25 years shorter than the general population. Following the observation that smoking improves condition of people with schizophrenia, in particular working memory deficit, nicotine patches had been proposed as a way to treat schizophrenia. Some studies suggest that a link exists between smoking and mental illness, citing the high incidence of smoking amongst those suffering from schizophrenia and the possibility that smoking may alleviate some of the symptoms of mental illness, but these have not been conclusive.
Recent studies have linked smoking to anxiety disorders, suggesting the correlation (and possibly mechanism) may be related to the broad class of anxiety disorders, and not limited to just depression. Current and ongoing research attempt to explore the addiction-anxiety relationship. Data from multiple studies suggest that anxiety disorders and depression play a role in cigarette smoking. A history of regular smoking was observed more frequently among individuals who had experienced a major depressive disorder at some time in their lives than among individuals who had never experienced major depression or among individuals with no psychiatric diagnosis. People with major depression are also much less likely to quit due to the increased risk of experiencing mild to severe states of depression, including a major depressive episode. Depressed smokers appear to experience more withdrawal symptoms on quitting, are less likely to be successful at quitting, and are more likely to relapse.
Environmental tobacco smoke exposure and maternal smoking during pregnancy have been shown to cause lower infant birth weights.
Studies have shown an association between prenatal exposure to environmental tobacco smoke and conduct disorder in children. As well, post-natal tobacco smoke exposure may cause similar behavioral problems in children. 
Women who smoke have about a 50% higher chance of giving birth to a child with behavioral disorders, such as ADD, but a recent study in a book called "ADD a different perspective" overturns this, saying that ADD is a genetic trait. Proof of this comes from a study showing that the people with Attention Deficit Disorder had higher levels of certain hormones as Thom Hartman explains the theory of Hunter vs. farmer theory 
আন আন প্ৰভাৱ[সম্পাদনা কৰক]
Studies suggest that smoking decreases appetite, but did not conclude that overweight people should smoke or that their health would improve by smoking. This is also a cause of heart diseases.  Smoking also decreases weight by overexpressing the gene AZGP1 which stimulates lipolysis.
Smoking causes about 10% of the global burden of fire deaths, and smokers are placed at an increased risk of injury-related deaths in general, partly due to also experiencing an increased risk of dying in a motor vehicle crash.
Smoking increases the risk of symptoms associated with Crohn's disease (a dose-dependent effect with use of greater than 15 cigarettes per day). There is some evidence for decreased rates of endometriosis in infertile smoking women, although other studies have found that smoking increases the risk in infertile women. There is little or no evidence of a protective effect in fertile women. Some preliminary data from 1996 suggested a reduced incidence of uterine fibroids, but overall the evidence is unconvincing.
Current research shows that tobacco smokers who are exposed to residential radon are twice as likely to develop lung cancer as non-smokers. As well, the risk of developing lung cancer from asbestos exposure is twice as likely for smokers than for non-smokers.
New research has found that women who smoke are at significantly increased risk of developing an abdominal aortic aneurysm, a condition in which a weak area of the abdominal aorta expands or bulges.
ৰোগ বিতৰণ[সম্পাদনা কৰক]
Tobacco may be consumed by either smoking or other smokeless methods such as chewing, the World Health Organization (WHO) only collect data on smoked tobacco. Smoking has therefore been studied more extensively than any other form of consumption.
In 2000, smoking was practiced by 1.22 billion people, predicted to rise to 1.45 billion people in 2010 and 1.5 to 1.9 billion by 2025. If prevalence had decreased by 2% a year since 2000 this figure would have been 1.3 billion in 2010 and 2025. Despite dropping by 0.4 percent from 2009 to 2010, the United States still reports an average of 17.9 percent usage.
As of 2002, about twenty percent of young teens (13–15) smoke worldwide, with 80,000 to 100,000 children taking up the addiction every day—roughly half of whom live in Asia. Half of those who begin smoking in adolescent years are projected to go on to smoke for 15 to 20 years.
The WHO states that "Much of the disease burden and premature mortality attributable to tobacco use disproportionately affect the poor". Of the 1.22 billion smokers, 1 billion of them live in developing or transitional nations. Rates of smoking have leveled off or declined in the developed world. In the developing world, however, tobacco consumption is rising by 3.4% per year as of 2002.
The WHO in 2004 projected 58.8 million deaths to occur globally, from which 5.4 million are tobacco-attributed, and 4.9 million as of 2007. As of 2002, 70% of the deaths are in developing countries.
The shift in prevalence of tobacco smoking to a younger demographic, mainly in the developing world, can be attributed to several factors. The tobacco industry spends up to $12.5 billion annually on advertising, which is increasingly geared towards adolescents in the developing world because they are a very vulnerable audience for the marketing campaigns. Adolescents have more difficulty understanding the long term health risks that are associated with smoking and are also more easily influenced by “images of romance, success, sophistication, popularity, and adventure which advertising suggests they could achieve through the consumption of cigarettes”. This shift in marketing towards adolescents and even children in the tobacco industry is debilitating to organizations’ and countries’ efforts to improve child health and mortality in the developing world. It reverses or halts the effects of the work that has been done to improve health care in these countries, and although smoking is deemed as a “voluntary” health risk, the marketing of tobacco towards very impressionable adolescents in the developing world makes it less of a voluntary action and more of an inevitable shift.
Many government regulations have been passed to protect citizens from harm caused by public environmental tobacco smoke. The "Pro-Children Act of 2001" prohibits smoking within any facility that provides health care, day care, library services, or elementary and secondary education to children. On May 23, 2011, New York City enforced a smoking ban for all parks, beaches, and pedestrian malls in an attempt to eliminate threats posed to civilians by environmental tobacco smoke.
In the 1930s German scientists showed that cigarette smoking caused lung cancer. In 1938 a study by a Johns Hopkins University scientist suggested a strongly negative correlation between smoking and lifespan. In 1950 five studies were published in which "smoking was powerfully implicated in the causation of lung cancer". These included the now classic paper "Smoking and Carcinoma of the Lung" which appeared in the British Medical Journal. This paper reported that "heavy smokers were fifty times as likely as non-smokers to contract lung cancer".
In 1953, scientists at the Sloan-Kettering Institute in New York City demonstrated that cigarette tar painted on the skin of mice caused fatal cancers. This work attracted much media attention; the New York Times and Life both covered the issue. The Reader's Digest published an article entitled "Cancer by the Carton".
A team of British scientists headed by Richard Doll carried out a longitudinal study of 34,439 medical specialists from 1951 to 2001, generally called the "British Doctors Study." The study demonstrated that about half of the persistent cigarette smokers born in 1900–1909 were eventually killed by their addiction (calculated from the logarithms of the probabilities of surviving from 35–70, 70–80, and 80–90) and about two thirds of the persistent cigarette smokers born in the 1920s would eventually be killed by their addiction. After a ban on smoking in all enclosed public places was introduced in Scotland in March 2006, there was a 17 percent reduction in hospital admissions for acute coronary syndrome. 67% of the decrease occurred in non-smokers.
The health effects of tobacco have been significant for the development of the science of epidemiology. As the mechanism of carcinogenicity is radiomimetic or radiological, the effects are stochastic. Definite statements can be made only on the relative increased or decreased probabilities of contracting a given disease; Philosophically and theoretically speaking, it is impossible to definitively prove a direct causative link between exposure to a radiomimetic poison such as tobacco smoke and the cancer that follows. Tobacco companies have capitalized on this philosophical objection and exploited the doubts of clinicians, who consider only individual cases, on the causal link in the stochastic expression of the toxicity as actual disease.
There have been multiple court cases on the issue that tobacco companies have researched the health effects of tobacco, but suppressed the findings or formatted them to imply lessened or no hazard.
A study published in the journal Pediatrics refers to the danger posed by what the authors call "third-hand smoke" — toxic substances that remain in areas where smoking has recently occurred. The study was reviewed in an story broadcast by the Voice of America.
অনিয়মিত ধূমপান[সম্পাদনা কৰক]
The term "smoker" is used to mean a person who habitually smokes tobacco on a daily basis. This category has been the focus of the vast majority of tobacco studies. However, the health effects of less-than-daily smoking are far less well understood. Studies have often taken the data of "occasional smokers" (those who have never smoked daily) and grouped them with those who have never smoked.
A recent European study on occasional smoking published findings that the risk of the major smoking-related cancers for occasional smokers was 1.24 times that of those who have never smoked at all but the result was not statistically significant. (For a confidence interval of 95%, this data showed an incidence rate ratio of 0.80 to 1.94.) This compares to studies showing that habitual heavy smokers have greater than 50 times the incidence of smoking-related cancers.
ৰাসায়নিক কাৰ্চিন'জেন[সম্পাদনা কৰক]
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Smoke, or any partially burnt organic matter, contains carcinogens (cancer-causing agents). The potential effects of smoking, such as lung cancer, can take up to 20 years to manifest themselves. Historically, women began smoking en masse later than men, so an increased death rate caused by smoking amongst women did not appear until later. The male lung cancer death rate decreased in 1975 — roughly 20 years after the initial decline in cigarette consumption in men. A fall in consumption in women also began in 1975 but by 1991 had not manifested in a decrease in lung cancer related mortalities amongst women.
Smoke contains several carcinogenic pyrolytic products that bind to DNA and cause genetic mutations. Particularly potent carcinogens are polynuclear aromatic hydrocarbons (PAH), which are toxicated to mutagenic epoxides. The first PAH to be identified as a carcinogen in tobacco smoke was benzopyrene, which has been shown to toxicate into an epoxide that irreversibly attaches to a cell's nuclear DNA, which may either kill the cell or cause a genetic mutation. If the mutation inhibits programmed cell death, the cell can survive to become a cancer cell. Similarly, acrolein, which is abundant in tobacco smoke, also irreversibly binds to DNA, causes mutations and thus also cancer. However, it needs no activation to become carcinogenic.
There are over 19 known carcinogens in cigarette smoke. The following are some of the most potent carcinogens:
- Polynuclear aromatic hydrocarbons are tar components produced by pyrolysis in smoldering organic matter and emitted into smoke. Many of them are highly carcinogenic and mutagenic, because they are toxicated to mutagenic epoxides, which are electrophilic alkylating agents. The first PAH to be identified as a carcinogen in tobacco smoke was benzopyrene, which been shown to toxicate into a diol epoxide and then permanently attach to nuclear DNA, which may either kill the cell or cause a genetic mutation. The DNA contains the information on how the cell function; in practice, it contains the recipes for protein synthesis. If the mutation inhibits programmed cell death, the cell can survive to become a cancer cell, a cell that does not function like a normal cell. The carcinogenity is radiomimetic, i.e. similar to that produced by ionizing nuclear radiation. Tobacco manufacturers have experimented with combustionless vaporizer technology to allow cigarettes to be consumed without the formation of carcinogenic benzopyrenes. Although such products have become increasingly popular, they still represent a very small fraction of the market, and no conclusive evidence has shown to prove or disprove the positive health claims.[উদ্ধৃতিৰ প্ৰয়োজন]
- Acrolein is a pyrolysis product that is abundant in cigarette smoke. It gives smoke an acrid smell and an irritating, lachromatory effect and is a major contributor to its carcinogenity. Like PAH metabolites, acrolein is also an electrophilic alkylating agent and permanently binds to the DNA base guanine, by a conjugate addition followed by cyclization into a hemiaminal. The acrolein-guanine adduct induces mutations during DNA copying and thus causes cancers in a manner similar to PAHs. However, acrolein is 1000 times more abundant than PAHs in cigarette smoke, and is able to react as is, without metabolic activation. Acrolein has been shown to be a mutagen and carcinogen in human cells. The carcinogenity of acrolein has been difficult to study by animal experimentation, because it has such a toxicity that it tends to kill the animals before they develop cancer. Generally, compounds able to react by conjugate addition as electrophiles (so-called Michael acceptors after Michael reaction) are toxic and carcinogenic, because they can permanently alkylate DNA, similarly to mustard gas or aflatoxin. Acrolein is only one of them present in cigarette smoke; for example, crotonaldehyde has been found in cigarette smoke. Michael acceptors also contribute to the chronic inflammation present in tobacco disease.
- Nitrosamines are a group of carcinogenic compounds found in cigarette smoke but not in uncured tobacco leaves. Nitrosamines form on flue-cured tobacco leaves during the curing process through a chemical reaction between nicotine and other compounds contained in the uncured leaf and various oxides of nitrogen found in all combustion gases. Switching to Indirect fire curing has been shown to reduce nitrosamine levels to less than 0.1 parts per million.
Sidestream tobacco smoke, or exhaled mainstream smoke, is particularly harmful. Because exhaled smoke exists at lower temperatures than inhaled smoke, chemical compounds undergo changes which can cause them to become more dangerous. As well, smoke undergoes changes as it ages, which causes the transformation of the compound NO into the more toxic NO2. Further, volatilization causes smoke particles to become smaller, and thus more easily embedded deep into the lung of anyone who later breathes the air.
Radioactive carcinogens[সম্পাদনা কৰক]
In addition to chemical, nonradioactive carcinogens, tobacco and tobacco smoke contain small amounts of lead-210 (210Pb) and polonium-210 (210Po) both of which are radioactive carcinogens. The presence of polonium-210 in mainstream cigarette smoke has been experimentally measured at levels of 0.0263–0.036 pCi (0.97–1.33 mBq),[উদ্ধৃতিৰ প্ৰয়োজন] which is equivalent to about 0.1 pCi per milligram of smoke (4 mBq/mg); or about 0.81 pCi of lead 210 per gram of dry condensed smoke (30 Bq/kg).
Research by NCAR radiochemist Ed Martell determined that radioactive compounds in cigarette smoke are deposited in "hot spots" where bronchial tubes branch. Since tar from cigarette smoke is resistant to dissolving in lung fluid, the radioactive compounds have a great deal of time to undergo radioactive decay before being cleared by natural processes. Indoors, these radioactive compounds linger in secondhand smoke, and therefore greater exposure occurs when these radioactive compounds are inhaled during normal breathing, which is deeper and longer than when inhaling cigarettes. Damage to the protective epithelial tissue from smoking only increases the prolonged retention of insoluble polonium 210 compounds produced from burning tobacco. Martell estimated that a carcinogenic radiation dose of 80–100 rads is delivered to the lung tissue of most smokers who die of lung cancer.
Smoking an average of 1.5 packs per day gives a radiation dose of 60-160 mSv/year, compared with living near a nuclear power station (0.0001 mSv/year) or the 3.0 mSv/year average dose for Americans. Some of the mineral apatite in Florida used to produce phosphate for U.S.A. tobacco crops contains uranium, radium, lead 210 and polonium 210 and radon. The radioactive smoke from tobacco fertilized this way is deposited in lungs and releases radiation even if a smoker quits the habit. The combination of carcinogenic tar and radiation in a sensitive organ such as lungs increases the risk of cancer. If the smoker also breathes in the asbestos fibers which commonly occur in urban and industrial environments, the risk of cancer is greatly increased.
Nicotine that is contained in cigarettes and other smoked tobacco products is a stimulant and is one of the main factors leading to continued tobacco smoking. Although the amount of nicotine inhaled with tobacco smoke is quite small (most of the substance is destroyed by the heat) it is still sufficient to cause physical and/or psychological dependence. The amount of nicotine absorbed by the body from smoking depends on many factors, including the type of tobacco, whether the smoke is inhaled, and whether a filter is used. Despite the design of various cigarettes advertised and even tested on machines to deliver less of the toxic tar, studies show that when smoked by humans instead of machines, they deliver the same net amount of smoke. Ingesting a compound by smoking is one of the most rapid and efficient methods of introducing it into the bloodstream, second only to injection, which allows for the rapid feedback which supports the smokers' ability to titrate their dosage. On average it takes about ten seconds for the substance to reach the brain. As a result of the efficiency of this delivery system, many smokers feel as though they are unable to cease. Of those who attempt cessation and last three months without succumbing to nicotine, most are able to remain smoke free for the rest of their lives. There exists a possibility of depression in some who attempt cessation, as with other psychoactive substances. Depression is also common in teenage smokers; teens who smoke are four times as likely to develop depressive symptoms as their nonsmoking peers.
Although nicotine does play a role in acute episodes of some diseases (including stroke, impotence, and heart disease) by its stimulation of adrenaline release, which raises blood pressure, heart rate, and free fatty acids, the most serious longer term effects are more the result of the products of the smouldering combustion process. This has enabled development of various nicotine delivery systems, such as the nicotine patch or nicotine gum, that can satisfy the addictive craving by delivering nicotine without the harmful combustion by-products. This can help the heavily dependent smoker to quit gradually, while discontinuing further damage to health.
Nicotine is a highly addictive psychoactive chemical. When tobacco is smoked, most of the nicotine is pyrolyzed; a dose sufficient to cause mild somatic dependency and mild to strong psychological dependency remains. There is also a formation of harmane (a MAO inhibitor) from the acetaldehyde in cigarette smoke, which seems to play an important role in nicotine addiction probably by facilitating dopamine release in the nucleus accumbens in response to nicotine stimuli. According to studies by Henningfield and Benowitz, nicotine is more addictive than cannabis, caffeine, ethanol, cocaine, and heroin when considering both somatic and psychological dependence. However, due to the stronger withdrawal effects of ethanol, cocaine and heroin, nicotine may have a lower potential for somatic dependence than these substances. About half of Canadians who currently smoke have tried to quit. McGill University health professor Jennifer O'Loughlin stated that nicotine addiction can occur as soon as five months after the start of smoking.
Recent evidence has shown that smoking tobacco increases the release of dopamine in the brain, specifically in the mesolimbic pathway, the same neuro-reward circuit activated by drugs of abuse such as heroin and cocaine. This suggests nicotine use has a pleasurable effect that triggers positive reinforcement. One study found that smokers exhibit better reaction-time and memory performance compared to non-smokers, which is consistent with increased activation of dopamine receptors. Neurologically, rodent studies have found that nicotine self-administration causes lowering of reward thresholds—a finding opposite that of most other drugs of abuse (e.g. cocaine and heroin). This increase in reward circuit sensitivity persisted months after the self-administration ended, suggesting that nicotine's alteration of brain reward function is either long lasting or permanent.[উদ্ধৃতিৰ প্ৰয়োজন] Furthermore, it has been found that nicotine can activate long term potentiation in vivo and in vitro.[উদ্ধৃতিৰ প্ৰয়োজন] These studies suggest nicotine’s "trace memory" may contribute to difficulties in nicotine abstinence.[মৌলিক গৱেষণা ?]
The carcinogenity of tobacco smoke is not explained by nicotine per se, which is not carcinogenic or mutagenic. However, it inhibits apoptosis, therefore accelerating existing cancers. Also, NNK, a nicotine derivative converted from nicotine, can be carcinogenic.
It is worth noting that nicotine, although frequently implicated in producing tobacco addiction, is not significantly addictive when administered alone. The addictive potential manifests itself after co-administration of an MAOI, which specifically causes sensitization of the locomotor response in rats, a measure of addictive potential.
ধঁপাত সেৱনৰ আন পথ[সম্পাদনা কৰক]
ধঁপাত চোবোৱা[সম্পাদনা কৰক]
Chewing tobacco has been known to cause cancer, particularly of the mouth and throat. According to the International Agency for Research on Cancer, "Some health scientists have suggested that smokeless tobacco should be used in smoking cessation programmes and have made implicit or explicit claims that its use would partly reduce the exposure of smokers to carcinogens and the risk for cancer. These claims, however, are not supported by the available evidence." Oral and spit tobacco increase the risk for leukoplakia a precursor to oral cancer.
Like other forms of tobacco use, cigar smoking poses a significant health risk depending on dosage: risks are greater for those who inhale more when they smoke, smoke more cigars, or smoke them longer. The risk of dying from any cause is significantly greater for cigar smokers, with the risk particularly higher for smokers less than 65 years old, and with risk for moderate and deep inhalers reaching levels similar to cigarette smokers. Little cigars are commonly inhaled and likely pose the same health risks as cigarettes. The increased risk for those smoking 1–2 cigars per day is too small to be statistically significant, and the health risks of the 3/4 of cigar smokers who smoke less than daily are not known and are hard to measure; although it has been claimed that people who smoke few cigars have no increased risk, a more accurate statement is that their risks are proportionate to their exposure. Health risks are similar to cigarette smoking in nicotine addiction, periodontal health, tooth loss, and many types of cancer, including cancers of the mouth, throat, and esophagus. Cigar smoking also can cause cancers of the lung and larynx, where the increased risk is less than that of cigarettes. Many of these cancers have extremely low cure rates. Cigar smoking also increases the risk of lung and heart diseases such as chronic obstructive pulmonary disease.
A common belief among users is that the smoke is significantly less dangerous than that from cigarettes. The water moisture induced by the hookah makes the smoke less irritating and may give a false sense of security and reduce concerns about true health effects. Doctors at institutions including the Mayo Clinic have stated that use of hookah can be as detrimental to a person's health as smoking cigarettes, and a study by the World Health Organization also confirmed these findings.
Each hookah session typically lasts more than 40 minutes, and consists of 50 to 200 inhalations that each range from 0.15 to 0.50 liters of smoke. In an hour-long smoking session of hookah, users consume about 100 to 200 times the smoke of a single cigarette; in a 45-minute smoking session a typical smoker would inhale 1.7 times the nicotine  of a single cigarette. A study in the Journal of Periodontology found that water pipe smokers were five times more likely than non-smokers to show signs of gum disease [উদ্ধৃতিৰ প্ৰয়োজন]. According to USA Today, people who smoked water pipes had five times the risk of lung cancer of non-smokers.
A study on hookah smoking and cancer in Pakistan was published in 2008. Its objective was "to find serum CEA levels in ever/exclusive hookah smokers, i.e. those who smoked only hookah (no cigarettes, bidis, etc.), prepared between 1 and 4 times a day with a quantity of up to 120 g of a tobacco-molasses mixture each (i.e. the tobacco weight equivalent of up to 60 cigarettes of 1 g each) and consumed in 1 to 8 sessions". Carcinoembryonic antigen (CEA) is a marker found in several forms of cancer. Levels in exclusive hookah smokers were lower compared to cigarette smokers although the difference was not statistically significant between a hookah smoker and a non-smoker. Also the study concluded that heavy hookah smoking (2–4 daily preparations; 3–8 sessions a day ; >2 hrs to ≤ 6 hours) substantially raises CEA levels. A recent study published in the Asia Pacific Journal of Cancer Prevention (Koul PA et al. Hookah Smoking and Lung Cancer in the Kashmir Valley of the Indian SubcontinentAsian Pacific J Cancer Prev, 12, 519-524; doi.) documented that hookah smokers were nearly 6-times at risk for development of lung cancer as compared to healthy non-smokers in Kashmir (India). Hookah in Kashmir has some peculiar features in having a direct contact of the live embers with the burning tobacco thus resulting in high temperatures that augments the production of carcinogenic products from tobacco burning. Additionally water in the hookah base is not changed after every session that renders the water contaminated to a greater degree and thus a possible source of dissolved carcinogens.
Users of snuff are believed to face less risk of some cancers than smokers, but are still at greater risk than people who do not use any tobacco products. They also have an equal risk of other health problems directly linked to nicotine such as increased rate of atherosclerosis.
Concern about the health effects of tobacco has a long history. As early as 1604 James I wrote A Counterblaste to Tobacco, in which he said that tobacco users were "harming your selves both in persons and goods" and the Word of Wisdom of The Church of Jesus Christ of Latter-day Saints, written in 1833, prohibits the ingestion of tobacco thus: "...tobacco is not for the body, neither for the belly, and is not good for man, but is an herb for bruises and all sick cattle, to be used with judgment and skill." (Doctrine and Covenants 89:8).
The late-19th century invention of automated cigarette-making machinery in the American South made possible mass production of cigarettes at low cost, and cigarettes became elegant and fashionable among society men as the Victorian era gave way to the Edwardian. In 1912, American Dr. Isaac Adler was the first to strongly suggest that lung cancer is related to smoking. In 1929, Fritz Lickint of Dresden, Germany, published a formal statistical evidence of a lung cancer-tobacco link, based on a study showing that lung cancer sufferers were likely to be smokers. Lickint also argued that tobacco use was the best way to explain the fact that lung cancer struck men four or five times more often than women (since women smoked much less).
Prior to World War I, lung cancer was considered to be a rare disease, which most physicians would never see during their career. With the postwar rise in popularity of cigarette smoking, however, came an epidemic of lung cancer.
In 1950, Richard Doll published research in the British Medical Journal showing a close link between smoking and lung cancer. Four years later, in 1954, the British Doctors Study, a study of some 40,000 doctors over 20 years, confirmed the suggestion, based on which the government issued advice that smoking and lung cancer rates were related. The British Doctors Study lasted until 2001, with results published every ten years and final results published in 2004 by Doll and Richard Peto. Much early research was also done by Alton Ochsner. Reader's Digest magazine for many years published frequent anti-smoking articles. In 1964, the United States Surgeon General's Report on Smoking and Health, led millions of American smokers to quit, the banning of certain advertising, and the requirement of warning labels on tobacco products.
The Canadian province of British Columbia has the Tobacco Damages and Health Care Costs Recovery Act.
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বহিঃ সংযোগ[সম্পাদনা কৰক]
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