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TOBACCO AND THE LUNGS

Dr. R. Umarani MD Professor of Medicine ,RMMCH, A.U.

TOBACCO AND THE LUNGS

is the single most preventable risk to human health


is an important cause of premature death worldwide is the cause for raising incidence of lung cancers in the youth . scientifically proved relationship between lung disorders and smoking risk also to second hand or passive smoking

TO QUOTE A FEW
chronic obstructive pulmonary disease (COPD -this includes chronic bronchitis or blue bloaters and emphysema or pink puffers) bronchial asthma respiratory infections (the association with pulmonary tuberculosis is a well known fact) interstitial lung diseases-[a few of them] gastroesophageal reflux disorder(GERD) the dreaded lung cancer

Low birth weight babies, SIDS,Pneumonia, middle ear infections

POISONS IN TOBACCO SMOKING

Carbon Monoxide--Nitrites Ammonia--Nitrosamines---Hydrogen Cyanide--Sulfur Compounds--Vinyl Chloride HydrocarbonsVolatile AlcoholsUrethane-Formaldehyde-Hydrazine

WHY DO THESE OCCUR? Tobacco smoke This contains 4000and more chemicals Most of them are harmful to our lungs Mix together to form a sticky TAR Tar sticks to the cilia in our lungs and plays havoc Defensive mechanism by cilia is lost Tissue injury by inhaled particulars Immune mechanisms impairedlungs injured

PATHOGENESIS The lung injury by smoking leads to a sequence of events which are hypertrophy of goblet cells and mucous glands increased mucus secretion narrowing of the airways and fibrosis destruction of airways and fibrosis injury to lung parenchyma vascular changes &increase in inflammatory cells oxidative stress imbalance of proteinases and antiproteinases. advanced cases of lung injury remodeling of airways parenchymal destruction pulmonary vascular changes reduces lungs capacity for gas exchange to hypoxemia and hypercapnia.

COPD/COAD leading cause of death economic burden to the individual and the society 80% to 90% of COPD are due to smoking cause for 5.3% deaths in the globe in 1990 expected to cause 9.3% deaths in 2020. Indian studies also highlight a high prevalence rate ( A prevalence rate of 4.1% has been reported by Ray et al in Tamilnadu in 1995.) Does the high prevalence rate stop with only tobacco smoking? No. The relationship of COPD with tobacco smoking seems independent of the type of the product smoked i.e. cigarettes, beedis or chutta as proved by various studies. THE ESTIMATED GROSS BURDEN OF COPD IS APPROXIMATELY 12 MILLION PEOPLE IN INDIA .

52 million sufferers in the world progressive in nature includes chronic bronchitis and emphysema airflow limitation, inflammatory changes, irreversible changes symptoms for three months of a year for at least two consecutive years

When to suspect and diagnose COPD? The clinical features are as follows; ----- chronic cough . -----chronic sputum production. Sputum production and chronic cough is more in the early morning hours. Sputum is usually tenacious,sticky and occasionally streaked with blood. -----breathlessness. This develops in the course of the disease. -----acute exacerbations.

------Physical examination reveals signs of emphysema such as barrel shaped chest, use of accessory muscles, hyper-resonant note on percussion, decreased breath sounds ,and rhonchi on auscultation.

-----To confirm the diagnosis pulmonary function test using spirometry is done and FVC,FEV1 values are measured. The severity of the disease can be staged based on the findings.

What are its complications? Chronic cor pulmonaleheart failure Respiratory failure Recurrent respiratory infections Pneumothorax

TUBERCULOSIS AND SMOKING How grave is the disease?


-----Various studies in India especially in Tamilnadu To quote a few; -the risk of smokers dying from tuberculosis was four times more compared among non-smokers --prevalence of TB was three times higher in smokers than non-smokers --the prevalence ratio was positively related to daily smoking ,both to cigarettes and particularly to beedis. --the death of half TB cases could have been avoided if the patients had been non smokers. --the heavier the smoking ,the greater the prevalence of TB --smoking contributes to half the deaths in the males from TB in India and a quarter of deaths in middle age(25--69) How does this occur ? Smoking weakens the immune system increased suscepility to pulmonary tuberculosis damages the respiratory mucosa

SMOKING AND LUNG CANCERS


--- contributory factor for lung cancers. -- 87% of males and 85% of females with lung cancers had strong history of smoking. -- risk increased with both the duration and quantity of all smoking products.

Why do lung cancers occur in smokers? The definite carcinogenic substances in tobacco smoke implicated in lung cancer are; 4-Aminobiphenyl , Benzene , Cadmium Chromium , 2-Naphthylamine , Nickel Polonium-210 , Radon , Vinyl chloride Probably carcinogenic to humans: Acrylonitrile Possibly carcinogenic to humans: Acetaldehyde (the high solubility of polonium 210 the inhibition of the clearing action of the cilia in the respiratory tract by tobacco smoke, the stickiness of the particles of tar precipitated from the smoke, and deposits within the lung of insoluble lead 210 which then breaks down into polonium 210,) Even after having stopped smoking for a year, concentrations of lead 210 and polonium 210 in rib bones and alveolar lung tissue remain twice as high in ex-smokers as in those who had never smoked. These are the two main culprits in the causation of lung cancers.

How does the patient present?

--- fever, cough ,expectoration, blood stained sputum(hemoptysis)loss of weight and appetite, difficulty in swallowing, hoarseness of voice, dilated veins(SVC obstruction). ---Clinical examination reveals signs of a mass lesion with or without collapse .pleural effusion, rib erosion,etc. ---The diagnosis can be confirmed by radio imaging and histological finding. -------Surgery,radiotherapy and chemotherapy are the modalities of treatment.

CONCLUSION To conclude, by following the 5A strategy, ASK(about tobacco smoking) ASSESS(about the status and severity of use) ADVISE(TO STOP) ASSIST(in smoking cessation) ARRANGE(follow-up programme) we can achieve a tobacco free world like our tobacco free university. The final wordSMOKING CESSATION IS THE MOST EFFECTIVE AND IMPORTANT STEP IN TREATMENT AND PREVENTION OF THE ABOVE MENTIONED PROBLEMS.

FREQUENTLY ASKED QUESTIONS 1]Does it produce only lung cancers? The WHO estimates 90% of oral and nasopharyngeal cancers could be attributed to the use of tobacco. The habit of chewing betel liquid with tobacco in addition to particularly beedi smoking were main reasons of causing oral cancers.

2]Is there any difference between bidi and cigarette smoking? A recent study by CHABBRA et al have found a high prevalence rate of chest symptoms in bidi smoking than cigarettes.The toxicity of compounds like ammonia,tar nicotine,radioactive uranium were found to be higher in bidis than cigars.

3] I have been smoking two packets of cigarette a day for 20 years. What is my risk of developing Lung cancer ? This can be calculated by using a] Pack years- Duration of smoking in years x number of packets of cigarettes smoke per day. The risk of development of lung cancer increases if pack years exceeds forty. b] Smoking index: Is the number of cigarettes or beedis smoked per day x the of smoking duration. Smoking index greater than 300 is a risk factor for lung cancer.

4] What are the dangers of passive cigarette smoking? A non smoker living with the smoker is exposed to approximately 1 % of the level of tobacco smoke to which the smoker of 20 cigarettes a dayis exposed. It causes 5 % of all cancer deaths. Children of smoking parents have increased prevalence of respiratory tract infections and decreased levels of pulmonary functions. 5] Can this risk be measured? Yes. The levels of Plasma Cotinine, a metabolite of nicotine can be measured.

REFERENCES American Thoracic Society. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1995; 152(5 Pt 2):S77-S121. British Thoracic Society. Guidelines for the management of chronic obstructive pulmonary disease. Thorax 1997;52(SuppI 5): S1-S28. Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management and prevention of chronic obstructive lung disease. NHLBI/WHO workshop report. Bethesda, National Heart, Lung and Blood Institute. 2001; NIH Publication No. 2701:1-100. Siafakas NM, Vermeire P, Pride NB, Paoletti P, Gibson J, Howard P, et al. Optimal assessment and management of chronic obstructive pulmonary disease (COPD). The European Respiratory Society Task Force. Eur Respir J 1995;8:1398-1420. Jindal SK, Aggarwal AN, Gupta D. Areview of population studies from India to estimate national burden of chronic obstructive pulmonary disease and its association with smoking. Indian J Chest Dis Allied Sci 2001 ;43:139-47.

Wig KL, GuleriaJS, Bhasin RC, Holmes E Or),VasudevaYL,Singh H. Certain clinical and epidemiological patterns of chronic obstructive lung disease as seen in Northern India. Indian J Chest Dis 1964;6:183-94. Sikand BK, Pamra SP, Mathur GP. Chronic bronchitis in Delhi as revealed by mass survey. Indian J Tuberc 1966;13:94-101. Viswanathan R. Epidemiology of chronic bronchitis: Morbidity survey in Patna urban area. Indian J Med Res 1966;54:105-11. Bhattacharya SN, Bhatnagar JK, Kumar S, Jain PC. Chronicbronchitis in rural population. Indian J Chest Dis 1975;17:l-7. Radha TG, Gupta GK, Singh A, Mathur N. Chronic bronchitis in an urban locality of New Delhi: An epidemiological survey. Indian J Med Res 1977;66:273-95. Chabbra SK,Rajpal S,Gupta R.Patterns of smoking in Delhi and comparison of chronic Respiratory Morbidity among bidi and cigarette Smokers.Indian J Chest Diseases and Sci 2001 43;19--26

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