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Year : 2009  |  Volume : 53  |  Issue : 5  |  Page : 618-627 Table of Contents     

Tobacco Interventions and Anaesthesia - A Review

Professor, Dept of Anaesthesiology, Lady Hardinge Medical College, Smt. Sucheta Kriplani & Kalawati Saran Childrens Hospital, New Delhi, 110001, India

Date of Web Publication3-Mar-2010

Correspondence Address:
Usha Saha
B5/108, Safdarjung Enclave, New Delhi 110029
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Source of Support: None, Conflict of Interest: None

PMID: 20640112

Rights and PermissionsRights and Permissions

Tobacco use is the leading preventable agent of death in the world. It is manufactured on a large scale in India and has a huge international market also. Death toll from tobacco use is on the rise. Use of tobacco is also increasing esp. in developing countries, in teenagers& in women, despite government, WHO and intervention by other statutory bodies. Prolonged use of tobacco or its products, as smoke or chew, endows significant risk of developing various diseases. With advances in surgical and anaethesia techniques& prolonged life expectancy, anaesthetist will be faced with management of these patients. Tobacco consumption affects every major organ system of the body; esp. lung, heart and blood vessels. Perioperative smoking cessation can significantly reduce the risk of postoperative complica­tions& duration of hospital stay. Anaesthetist can play an important role in motivating these patients to quit smoking preoperatively by providing brief counselling and nicotine replacement therapy in reluctant quitters. More of concern is the effect of passive smoking (second& third hand smoke) on non smokers.
This is a review of tobacco& its products, their health consequences, diseases caused, anaesthetic consider­ations& their role in helping these patients quit smoking Preventing nicotine addiction and improving smoking cessa­tion strategies should be the priority and despite these being only partially successful, strong measures at all levels should he continued& enforced.

Keywords: Tobacco, Smoking, Passive smoking, Second hand smoke, Health effects, Diseases, Lung cancer, Carcinogenesis, COPD, Anaesthetic considerations, Preoperative advice, Interventions

How to cite this article:
Saha U. Tobacco Interventions and Anaesthesia - A Review. Indian J Anaesth 2009;53:618-27

How to cite this URL:
Saha U. Tobacco Interventions and Anaesthesia - A Review. Indian J Anaesth [serial online] 2009 [cited 2021 Mar 6];53:618-27. Available from: https://www.ijaweb.org/text.asp?2009/53/5/618/60340

   Introduction Top

Tobacco use is the leading preventable agent of death in the world. It is responsible for more than five million deaths each year& the death toll from tobacco is expected to climb to > eight million people per year within next 25 years. It is estimated that eventually 50% of all smokers will be killed by direct or indirect effects of tobacco. As in 2002, some 1.22 billion people smoked. It was predicted that by 2010, 1.45 billion people will smoke and 1.5 to 1.9 billion by 2025 [1] .

The most popular type of substance that is smoked is tobacco. There are many different tobacco cultivars, which are made into a wide variety of mixtures and brands.

   History and Consumption Top

The history of smoking dates to 5000 BC. Early smoking evolved in association with religious ceremonies forpurpose of spiritual enlightenment. The practice quickly spread from Europe& America to rest of the world [2],[3] .

Perception surrounding smoking varied from being holy and sinful, sophisticated and vulgar, a panacea and a deadly health hazard [4] .Only recently smoking has come to be viewed in a complete negative light. Studies have proven that smoking is among the leading causes of many diseases such as lung cancer, heart attacks, etc [5] .

Smoking is the commonest method of consum­ing tobacco, and tobacco is the most common sub­stance smoked, less common drugs being cannabis and opium.

Smoking (dhumrapana "drinking smoke"
coined in 1700s) is a practice where tobacco is burned and smoke tasted, inhaled or actually drunk.

Tobacco `Brown gold', is an agro based prod­uct processed from fresh leaves of plants in genus "Nic­otiana'. Of the several species; Nicotianatabacutn. is commonly grown, but Nicotiana rustics also con­tains high concentrations of nicotine. The leaves are harvested, cured (slow oxidation and degradation of carotenoids in tobacco leaf) [6] , is treated, mixed with additives and then pyrolyzed. Tobacco is combined with upto 599 additivesto enhance the addictive po­tency, improve the effect& make it more palatable. The resultingvapors are inhaled and active substances absorbed through lung

Tobacco has Nicotine (2-5%,+/- 0.23%), Sug­ars (mainly reduced) (8-25%, +/- 1.8%) and Mois­ture (10-14% +/- 0.3%).

The word `Nicotine' is derived from Frenchman Jean Nicot who introduced tobacco to France in 1560 It is consumed in two forms, as -

1. Smoke

2. Smoke less


Tobacco for smoking is available as Beedi [7] (higher levels of CO, nicotine, andtar), Cigar, Cigarettes, Electronic cigarette (provides nicotine vapor from nico­tine solution), Hookah [8] (operates by waterfiltration and indirect heat), Kreteks (cigarettes introduced in Java) and Pipe. Vaporizer is usedto sublimate the active in­gredient in partial vacuum, rather than burning, with less production of irritating, toxic, carcinogenic by-products. Each cigarette can cause much damage [Table 1]

Non smoking exposures

Even non smokers are not exempt from the ad­verse health effects of smoking. Because of its negative implications; this form of consumption has played a key role in regulation oftobacco products. Smokeless to­bacco also contains nicotine. Passive smoking is in­voluntary consumption of tobacco smoke& falls into 3 categories [9]

1. Second-hand smoke (SHS)

2. Environmental tobacco smoke (ETS)

3. Third-hand smoke - smoke that remains after burn­ing end has been extinguished

4. Snuff- fine-ground smokeless tobacco product, in­troduced into nostrils

5. Chewing tobacco- put inside the mouth

Health effects­

It is highly addictive. Within 30 rains, nicotine equiva­lent to 4 cigarettes is ingested, and easy to become dependent upon

Contains >25 carcinogens, with 50% higher risk of Oropharyngeal cancer

Leukoplakia-from continued imtation of gums, tongue and oral mucosa

Increased risk of CVS diseases

Permanent discolouiation of teeth, halitosis and gum disease

Physiology Acetylcholine and Nicotine are chemically similar. Nicotine triggers cholinergic recep­tors, releasing adrenaline& nor adrenaline from adrenals, besides dopamine and endorphins. This gives apleasurable sensation, referred to as a"high"ranging between mild stimulus caused by nicotine to intense eu­phoria caused by heroin, cocaine and amphetamines Common result of smoking is the characteristic facial change known as smoker's face.

When tobacco is smoked, most ofthe nicotine is pyrolyzed, but remaining is sufficientto cause somatic and psychological dependency. Harmane (MAO in­hibitor) formed from acetaldehyde in tobacco smoke, has a role in nicotine addiction Not all drugs can be smoked, e.g. sulphate derivative is most commonly in­haled through nose, while purer free base forms require skill in administering. Also, not all smoke will be inhaled.

Cigarettes contain more than 4000 chemical. At least 400 are toxic. On inhaling, a cigarette burns at 700°C at the tip and 60°C in the core. This bums tobacco by incomplete combustion, to various toxic substances. As a cigarette bums, the residues get concentrated towards the butt. The products most damaging are

1. tar- a carcinogen.

2. nicotine- addictive and increases blood cholesterol, and

3. carbon monoxide (CO)- reduces O Z delivery to tissues

Consequences of smoking [10]

Causes cancers in most organs ofthe body, includ­ing kidney, cervix, and bone marrow, not previously linked to smoking.

Components ofthe gas and particulate phases cause COPD. The damage caused is influenced by the number of cigarettes smoked, filtered or not and method oftobacco preparation

Also causes cataracts and osteoporosis and in­creased risk for fractures.

Poor general health. Adverse effects begin before birth and continue across the life span

Reduced life expectancy by seven to eight years. The number of people <70 yrs age, who die from smoking -related diseases exceeds the total deaths caused by breast cancer, AIDS, traffic accidents and drug addiction.

Tobacco & cancer

In 18 th century, London physician Percival Pott made the first link between cancer and environmental agents when he noted a high incidence of scrotal can­cer among chimney sweeps and hypothesized the cause being exposure to coals and tars [9] .

Lung cancer is a leading cause of cancer death. Worldwide > one million people die each year. Ciga­rette smoking is the major cause of lung cancer. The risk diminishes after smoking cessation for > 5 years, but relative risk is still more than ofnon-smokers. The carcinogenic mechanism of tobacco smoking is a com­plex process. The tar fraction of cigarette smoke in­cludes both initiator and promoters of carcinogenesis, making it especially dangerous.

The mainstream smoke from the mouthpiece of a cigarette is an aerosol (10 [10] particles/mL). About 95% of smoke (vapor phase) is made of N 2 , NO, 0 2 & CO 2 .

The particulate phase contains at least 3500 com­pounds, mostcarcinogens and free radicals. The major free radical species is quinone-hydroquinone complex "held in a tar matrix". Free radical complex causes re­dox cycling, generating superoxides from 0 2 with for­mation of H Z O 2 , OH ions& DNA nicking. Nitric oxide acts synergistically with "tar"to cause DNA breakage.

Gas phase causes lipid peroxidation of blood plasma& formation of carbonyls (prevented by ascor­bic acid). Ascorbic acid levels are lower in smokers. Daily consumption of > 200 mg of Vit C / day is re­quired for serum ascorbate levels to be similarto those in nonsmokers.

There are about 55 carcinogens in cigarette smoke. [Table 2]. Some of them are:­

1. Benzo[á]pyrene (BaP) (PAH)- is a potent lung carcinogen

2. The tobacco-specific N-nitrosamine (NNK).

3. 1,3-Butadiene and Ethyl carbamate

4. Nickel, cluromium, cadmium, and arsenic

5. Polonium-210

6. Hydrazine

7. Toxins -Acrolein, Nitrogen oxides and Ac­etaldehyde

8. Weakly acidic compounds (Tumor Promot­ers) -Catechols. Pyrogallol, Decane, undecane, Pyrene, benzo [e]pyrene, and Fluoranthene

Sidestreamn smoke, released from the tip of a cigarette plus that which diffuses through cigarette pa pet; constitutes the maj orportion of ETS. Ratio of car­cinogens in sidestream to mainstream smoke is >1, but dilution with air ensures that passive uptake will be far less than in a smoker.

Measures of cigarette smoke uptake - Vari­ous biochemical markers to measure cigarette smoke uptake used, are:­

1. Exhaled CO, Carboxyhemoglobin and Tluocyanate

2. Urinary mutagenic metabolites-
NNK me­tabolites NNAL and NNAL-Glue. NNAL is a potent pulmonary carcinogen, while NNAL-Glue is not. Ra­tio of the two is used to assess susceptibility to lung cancer. This ratio is very low in black than in white smokers, suggesting poor detoxificationas a factor con­tributing to higher incidence of lung cancer in blacks

3. Cotinine, a nicotine metabolite, is the most specific andwidely used

Health hazards [Figure 1]

Smoking impairs physical fitness, general well being and endurance. Tobacco use affects every sys­tem of the body. Nicotine in cigarette smoke can dis­turb the functioning of the inner ear, sense of balance& dizziness. Most commonly affected organs are heart and lungs. Smoking is a maj or risk factor for heart at­tacks, strokes, COPD, cancel; fertility and pregnancy related problems, birth defects, blindness etc.

Cardiovascular Effects

Tobacco in any form trebles the risk of cardiac disease. About 30% of all deaths from heart disease are due to smoking. Cardiovascular effects ofsmoking occur within minutes with rise in HR upto 30 % in first 10 rains. This is short lived, but since most smoke ciga­rettes several times a day, these occur often, leadingto long-term problems. [11],[12]


Atherosclerosis is a normal aging process but smoking accelerates it. Depending on which blood ves­sels are involved, symptomatology varies.

.Coronary vessels: leading to IHD or MI. Smokers develop coronarythrombosis 10 years earlierthannon­smokers,& 9 out of 10 patients who undergo CABC; are smokers.

Cerebral vessels: leading to collapse, sub arach­noid hemorrhage (S AH), stroke, paralysis, coma & death.

Renal arteries- leading to renal hypertension or re­nal failure

Peripheral arteries- leading to peripheral vascular disease (Burgers disease, Raynaud's phenomenon), and gangrene.

Cardiomyopathy-CO in smoke damages the heart muscle& increases myocardium's susceptibility to vi­ral infections, cardiomyopathy and CCF.

Eye-vision disturbances, blindness, optic neuropa­thy& macular degeneration


Lung cancer was a rarity before the invention of cigarettes. Smokers are 5-10 times as likelyto develop lung cancer. Each yeas; > one million smokers die of lung cancer in USA, accounting for 25% of total smok­ing-related deathsi [13] . 1 in 10 moderate smokers and 1 in 5 heavy smokers (>15 cigarettes/day) will die of lung cancer: About 85% of smokers with lung cancer die within 5 yrs& > half die within one year.

Smoking also causes cancer on lip, tongue, or other locations in the mouth, often requiring surgery, Cancer of nose, (rare, less fatal), Pancreas (80% die within a year), Oesophagus (cause of 80 to 90 % of oesophageal cancers, always in combination with al­cohol use), Bladder;& Cervix (probably due increased susceptibilityto sexuallytransmitted virus [14] .

Respiratory system

Smoking impairs pulmonary functions by damag­ingthe cilia, alveoli, and bronchioles& increasing irri­tability of the bronchial tree [15] . Smoking is the most com­mon cause of COPD. It's estimated that 94% of 20-a-day smokers have some emphysema when exam­ined post mortem, while ? 90 % non-smokers have none. It starts between the ages of 35 and 45 when lung function starts to decline anyway. In smokers, the rate of decline trebles with onset of symptoms.

Management [16],[17]

Of foremost importance is Cessation of Smoking

Patient should avoid being around smokers and fume-laden polluted air

Use a face mask or nose filter

Those above 60 yrs age must receive Influenza& Pneumonia vaccination

Maintaining hydration& healthy diet

Deep breathing exercises (Belly breathing)

Physical activity (exercise, walking and yoga)

Controlled Oxygen therapy increases survival rates, alleviates symptoms, and improves quality of life in patients with severe COPD


beta z agonist and ipratropium (Combivent)


use is not advocated. Oral or inhaled are useful in acute exacerbation (shorten recovery time; improve FEV I& oxygenation, de­creased relapse and shorter length of hospital stay). Common corticosteroids are- Flovent, Solumedml and Prednisone

Other medications- NRT, antidepressants, Clonidine (in hypertensives, helps in withdrawal symptoms)

Management of complications of COPD e.g., heart failure, pulmonary hypertension

Long-term oxygen therapy ifhypoxemia, pulmo­nary hypertension, respiratory failure are present

Newer Developments -Antitrypsin replacement therapy -for inherited deficiency of a antitrypsin in


Pulmonary rehabilitation - for end stage COPD. There are three types of surgical options - Bullectomy Lung Volume Reduction Surgery (LVRS) and Lmig Transplantation.

Kidney -
Smoking causes and worsens renal dam­age in those with medical problems affecting kidneys, e.g. diabetes mellitus or hypertension. Urinary tract problems are more common among smokers, because tobacco components in urine irritate urinary tract, caus­ing frequent micturation& nocturnal dysuria.

Eye -Heavy smokers are more likely to get cata­ Ract [18] . Exhaled

Infections & immunity - Smoking interferes with cell mediated immunity and makes smokers prone to gum infections and periodontal diseases [19] .

Bone and muscle pain - Smokers are more likely to have back ache, bone and muscle pain& injuries, partly due to compromised peripheral circulation.

Smoking and Thyroid Disease -Cyanide, in tobacco smoke, interferes with thyroid hormone pro­duction. Smoking triples the risk for developing thy­roid disease and goitre. Women smokers with sub clini­cal hypothyroidism have a high risk for developing full­blown hypothyroidism.

Reproductive system

Women are more likely to have menstrual irregu­larities, infertility problems, cramps& hot flashes dur­ing menopause. Smoking lowers estrogen levels and attain early menopause with increased risk of os­teoporosis& fractures.

Problems during pregnancy [20]

Immediate problems -
Continuing to smoke during pregnancy carries risks forthe foetus due to lower immunity, CO in maternal blood& hypoxemia

Greater risk for ectopic, miscarriage, premature rup­ture of membranes, placenta previa, and abruptio

• Effect on foetus- increased risk for stillbirth, prema­turity, and low birth weight babies

Increased risk of babies born with cleft lip

Long-tern problems in children born to smoking mothers­

Increased risk of allergies

Childhood hypertension, obesity, diabetes mellitus

Poorer lungfunetions&chances ofdeveloping early asthma

Increased risk of mental retardation, learning and behaviour problems

Smoking & elderly-Elderly face increased risk of fractures, cataracts, and COPD. Certain age-related conditions occur at higher rates and earlier in smokers e.g. Cataracts, Age-related macular degeneration (AMD), Gum disease, tooth loss, Wrinkles, Baldness, premature greying, Hearing loss, urinary& faecal in­continence.

Non smoking dangers of tobacco -Fire deaths- Smoking causes 6% of all fires, but it is the leading cause of deaths in fire accidents. Smoking-re­lated fires are deadlier because they occur in homes, at night, when everyone is asleep. [21],[22]

Smoking and Surgical Recovery - Smoking increases the risk of perioperative cardiac& respira­tory problems, delayed wound healing and prolonged hospital stay.

Quitting [10]

The benefits of quitting begin within 20 minutes of the last cigarette.

At 8 hrs-BP& PR decreases, CO level in blood drops, O Z levels& body temperature increase to normal.

At 24 hours-Chance of heart attack decreases

By 3 Months-PFT improve,& worst of nicotine withdrawal symptoms subside.

By 9 Months- clinical improvement in respiratory symptoms occurs.

By Year- there is 50% reduction in risk of CAD

By 5 years- CVA& CAD risk is reduced to same as non smokers

By 10 years-50% decrease in risk of lung& other cancers

By 15 years- risk of CAD& death becomes similar to non smokers

Anaesthetic interventions [23]

Up to now, primary care physicians have been the focus of health care system efforts to address smok­ing. Cigarette smoking exacts an enormous toll in hu­man suffering and economic costs. The risk of prema­ture death and disability is dramatically reduced when smokers quit, even if they have already developed smoking related disease or have smoked for decades. Specialists like anaesthesiologists were ignored. ATask Force oftheASAappointed in 2006, adapted the evi­dence-based US clinical practice guidelines for physi­cians into a strategy relevant and efficient for anaesthesiologists [24] .

Why should anaesthesiologists bother to address tobacco use?

1. First reason - Doing something about a patient's smoking can improve short term clinical outcomes. Smoking is an important risk factor for perioperative cardiac, respiratory, and wound healing complications. Also, those who quit 3 weeks preoperatively have re­duced risk ofperioperative complications and shorter hospital stay. Even shorter period of abstinence has some benefits. [25],[26]

2. Second reason-Anaesthesiologists encounter smokers at a unique moment. Patients facing surgery feel vulnerable and are eager to complyto reduce one's risk of surgical complications. Surgery under anaes­thesia is a powerful motivation to change behavior. Preop counseling and use of quitting aids increases the proportion of quitters [25] .

3. Third reason - Smoking interventions in the hospital increase the odds that a smoker will quit long­term after discharge as long as there is continued sup­port [27]

The AS A's Smoking Cessation Initiative Task Force has designed a simple three-step system (Ask-Advise-Refer orAAR) that tailors evidence­based smoking cessation strategies for anaesthesiology practice. It is designed to be quick and efficient to implement 2S. Here, the physician­

A-Asks a patient about smoking status

A- Advises smokers to quit, and

R- Refers smokers to free national telephone quithne

Anaesthetic management

As far as possible patient's condition should be optimized preoperatively and all procedures undertaken as elective, except for emergency or life saving proce­dures.

Choice of anaesthesiatechnique is dictated bythe surgical procedure to be undertaken. Neuraxial or re­gional anaesthesia should be preferred wherever pos­sible, keeping in mindthe increased risk of complica­tions following GA in smokers because of adverse res­piratory (hyperirritable respuatorytree)& cardiovas­cular effects. Approach to management remains the same as for non smokers.

Irrespective of the anaesthesia technique to be used, athorough detailed preoperative evaluation should be done with medical and drug history, history of aller­gies, details of tobacco use (amount, duration) and past experiences with anaesthesia Alcohol increases the risk of anaesthesia in smokers,& this history should be es­tablished. History regarding each maj or organ system must be established (cardiac, CNS, respiratory, renal, hepatic and GIT).

Athorough general physical& systemic exami­nation must be carried out to confirm the findings in history; or establish a new one.

Besides routine investigations, complete blood counts (TLC, DLC), LFT, KFT, X ray chest, pulmo­nary function tests, blood gas analysis, electrolytes, ECG, echocardiography and blood sugar (for diabetic control) must be done. Thyroid functions need to be done if suggested bythe history, besides investigations pertaining to the surgical procedure.

Preoperative advice -

Fasting overnight or for at least 6 hours Preop

Smoking cessation-advise fiber rich, lots of fruits, vegetables, plenty of water, milk, calcium& Vit D supplements, strengthening exercises, nicotine re­placement therapy (NRT), Alternative therapies such as acupuncture and hypnosis

Care for smoking related medical diseases

Care for incidental medical problems

Preop and post treatment PFT


Great care needs to be exercised to prevent­

Respiratory complications such as lanyngo or broneho spasm (hyperirritability)

Hemodynamic disturbances

Careful dosing of drugs esp. relaxants

Care with narcotics, esp. morphine. Short acting drugs (fentanyl, remifentanil, sufentanyl) and NSAIDS should be preferred.

Maintaining adequate hydration& output

Care with ventilation- IPPV with smalltidal volume & higher rate.

Avoid PEEP, high Fi0 2 , hyperventilation (CO, wash­out)

With neuraxial block- avoid over transfusion& pre­cipitation of CCF

Intra op monitoring -non invasive monitoring is sufficient for most operations for HR, BP, temperature & respiration, Fi0 2 , EtCO 2 , Sp0 2 , intake output, ar­terial blood gas analysis, CVP

Indications for invasive monitoring­

  • ASA 3 or 4 patients
  • Extensive general surgical operation
  • Cardiac surgery
  • Neuro surgical procedures
  • Organ transplants
  • Hepatic resections, etc

Post op instructions -

  • Monitoring to be continued for at least 6-8 hours
  • Controlled 0 2 therapy
  • No driving or use of machinery for at least 24 hours after GA
  • No Alcohol or unprescribed drugs

Post operative side effects - Smokers have more complications following anaesthesia. Some of these are:­

  • Delayed recovery
  • Respiratory infections
  • Prolonged hospital stay
  • Excessive drowsiness, dizziness and headache (from CO 2 washout, hypertension)
  • Nausea and vomiting
  • Shivering -should be avoided (increases 0 2 con­sumption)

Most side effects wear off within 24 hours. Risk of complications depends on patient's age, sex, weight, current medical condition and use of alcohol or drugs

Changes in cigarettes to reduce yields of tar and nicotine have no benefits. Hence, measures to prevent smoking initiation need to be strong and enforced, es­pecially among young adults.

Although current rates of intervention provided by anaesthesiologists and surgeons are low, there is considerable interest amongthese physicians in learn­ing more about interventions. Given the relatively high prevalence of smoking in Japan and the potential for surgery to serve as a `teachable moment' to promote abstinence from smoking, leadership by these special­ists in the area of tobacco control could have amajor impact on public health in Japan [29],[30]

There is insufficient evidence about long-term benefit to give firm support the use of interventions in­tended to help smokers reduce tobacco use. Some people who do not wish to quit can be helped to cut down the number of cigarettes smoked and reduce their CO levels by using NRT Preventingnicotineaddiction and improving smoking cessation strategies should be the priority, but despite these being only partially suc­cessful, strong measures at all levels should be contin­ued& enforced.

   References Top

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2.Lock S, Reynolds LA and Tansey EM. Ashes to Ashes: The History of Smoking and Health 1998; 2nd ed. Rodopi.  Back to cited text no. 2      
3.Gilman SL; XunZhou. Smoke: AGlobal History of Smok­ing, 2004; Reaktion Books.  Back to cited text no. 3      
4.Burns E. The Smoke of the Gods: A Social History of Tobacco. 2007; Philadelphia: Temple University Press.  Back to cited text no. 4      
5.World Health Organization Report on the Global To­bacco Epidemic, 2008: the MPOWER package. World Health Organization, Geneva, 2008, p. 8.  Back to cited text no. 5      
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18.Christen WG, Manson JE, Seddon lM, G1ynnRJ, Buring JE, Rosner B, Hennekens CH. Aprospective study of cigarette smoking and risk of cataract in men. Journal of the American Medical Association 1992; 268:989­993.  Back to cited text no. 18      
19.Kerdvongbundit t; Wikesjo UM. Prevalence and sever­ity of periodontal disease at mandibular molar teeth in smokers with regular oral hygiene habits. J of Periodon­tology 2002; 73:735-740.  Back to cited text no. 19      
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  [Figure 1]

  [Table 1], [Table 2]


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