Health Effects Of Smoking Amr Badreldin Hamdy MD, FCCP
Smoking is a learned habit . The habit is culturally established in the developed world and has been for long enough to allow assessment of its effects on mortality and morbidity.
It has become almost common place to refer to the smoking problem in developing countries as tomorrow’s epidemic.
Tobacco use continues to be the leading cause of avoidable illness and death in economically advantaged countries , and is rapidly approaching that status worldwide.
Most smokers live in developing countries . Of the 1.1 billion smokers in the world in the early 1990’s, 800 million (75-75%) live in the developing world.
Between 1950 and 2000, tobacco caused over 60 million deaths in the developed countries ( 52 million men, and 10 million women ). Tobacco-caused deaths world-wide are expected to increase from about 5 mil/y today to about 10 mil/y by the 2030’s. Most of these deaths will occur in developing countries .
Smoking will kill about 500 million people alive in the world today.
One person dies every 5 minutes from smoking related diseases .
It is estimated that for each cigarette smoked, an average of 5.5 min of life is lost.
The 20-year-one-pack/day smoker has in-haled smoke over one million times; this repetitive act creates many strong cues for smoking throughout daily life.
A two-pack-a-day smoker spends 3 to 4 hours/day smoking, taking about 400 puffs and inhaling up to 1000mg of tar.
Failing immediate action , smoking disease will appear in developing countries before communicable diseases and malnutrition have been controlled , and the gap between the rich and poor countries will thus be further expanded.
Health care costs are about 40% higher for people who smoke.
The costs of smoking are far higher than the income from cigarette sales. Smoking causes millions of pounds each year in health-related costs, including the cost of lost productivity due to smoking. Death related productivity losses due to smoking among workers is high .
Treatment of tobacco dependence is cost-effective.
Healthy, young adult smokers have greater rates of hospitalization and lost work days than nonsmokers .
Tobacco use causes the majority of pulmonary disease , is the leading modifiable risk of cardiovascular disease , and causes more than 30% cancer deaths.
Current smokers have more acute and chronic illness as well as more restricted activity days, more bed disability days, and more school and work absenteeism than former smokers or those who never smoked.
Cigarette smokers have greater morbidity than nonsmokers.
Half of all regular cigarette smokers will eventually be killed by their habit.
On average, smokers die 7 years earlier than people who never smoked.
A heavy smoker at age 25 years can expect a life expectancy at least 25% shorter than a nonsmoker.
People who die from tobacco use do not die only in old age. About half of all smokers who are killed by tobacco die in middle age . On average, these smokers who die in middle age lose about 20-25 years of life expectancy .
Death rates of smokers are 2-3 times higher than for nonsmokers at all ages.
Cigarette smoking is the overwhelming reason men have a shorter life expectancy than women.
There is a clear dose-response relation-ship between smoking and life span , that, when compared with the median life span of men who never smoked, suggests a loss of one year for ex-smokers , three
years for light smokers , five years for moderate smokers , and eight years for heavy smokers.
Teenagers , in particular, may be overly complacent about smoking because they believe- incorrectly -that they can smoke for a few years and then quit without suffering and long-term effects.
The younger a person is when he or she begins to smoke, the more likely he or she is to develop nicotine addiction and even become heavily addicted and the more difficult it will be for them to quit .
Most people who become daily smokers (one or more cig/d during the previous 30 days) do so by the age of 18.
Smoking is most likely to become a habit during the teen years. When young people become cigarette smokers they are more likely to become addicted.
Tobacco serves as an entry drug and generally precedes use of other substances.
Smokers are much more likely to have used other substances, including alcohol, marijuana, and cocaine.
There is no safe cigarette , whether it is called ‘light’, ‘ultra-light’, or any other name.
Little difference in mortality has been found for lifelong filter versus non-filter smokers and for persistent smokers who switch from non-filter to filter cigarettes.
Tobacco is the most widely grown non-food crop in countries. Therefore, less land is available for food crop. Between 10 to 20 million people could be fed if food crop was grown in its place.
One whole tree is needed to cure the tobacco for 30 cigarettes. Each cigarette manufacturing machine uses 4 miles of paper/hour.
Cigarette production has increased in the USA, but domestic consumption has declined. Meanwhile exports overseas have markedly increased.
Why Do People Smoke?
Tobacco smoking is a learned habit . The habit is culturally established in the developed world and has been for long enough to allow assessment of its effects on mortality and morbidity.
Social and familial factors seem to be particularly important in smoking initiation.
Starting to smoke is clearly a cultural phenomenon which is opposed rather than reinforced by immediate pharmacological effects of tobacco.
Starting smoking may be due to peer group pressure , feeling left out while friends smoke and trying to fit in with the crowd.
It may be due to stress at home , work , school or in general by getting fed up with things.
It may be trying to attract attention , act cool or become popular .
It may calm down nerves!
Parental and sibling example.
Parental acceptance of children’s smoking.
Nicotine dependence : genetic, and psychosocial factors are relevant in maintenance of smoking behavior.
The factors that influence smoking initiation differ from those that influence maintenance of smoking behavior.
Genetic factors do contribute to tobacco use; heritable estimates range from 30-68%.
The mechanism for genetic influence may be constitutional differences in sensitivity or reactivity to nicotine’s toxic effects. Smokers are constitutionally sensitive to nicotine, and smoking initiation by these individuals leads to a rapid decrease in sensitivity , which in turn leads to tolerance of nicotine’s side effects .
Nicotine is neither a carcinogenic nor a co-carcinogen.
The problem of nicotine is that it addicts the individual to the inhalation of tobacco smoke, which permanently alters the structure and function of the human body .
It is by far the most important pharmacologically active substance in every form of tobacco and its smoke.
It is distilled from burning tobacco and carried on tar particles. The mainstream smoke of a filter-tipped cigarette on the average contains 15% of nicotine in its tobacco, although it may vary depending on individual smoking characteristics. It is ten times more concentrated, puff-to-puff, in the systemic arterial circulation than it is in the mixed-venous circulation.
Nicotine has the reputation as ‘ one of the dirtiest drugs in pharmacology ” because it does not have clean, isolated effects, but rather effects that vary according to dose and individual.
It is absorbed readily from tobacco smoke in the lungs, and it does not matter whether the tobacco smoke is from cigarettes, cigars, or pipes .
It enters the body in the form of thousands of little droplets , each suspended in a solid particle of partially burned tobacco (tar). These nicotine droplets are so small that they can penetrate into the tiniest branches of the lungs , where they are picked up by blood that has been sent to the lungs to take up oxygen.
From the lungs, it moves quickly to the left side of the heart , where nicotine is pumped to every corner of the body .
When a person inhales cigarette smoke, the nicotine it carries reaches the brain via the bloodstream, in about 8 seconds , which is less time than it would take to get the person injected intravenously .
By the time 15 to 20 sec have elapsed, the nicotine has spread throughout the whole body , and has even made it to the body’s last output, the big toe .
The overall level of nicotine climbs gradually through the day and falls during sleep.
The level is high enough and its fall gradual enough, however, that for most smokers, nicotine is active 24 hours a day, and they are never off the drug .
The ultrahigh arterial nicotine levels that cigarettes deliver to the brain literally give the smoking person fingertip control over mood, alertness, and vigor.
Arousal, relaxation, improved concentration and attention, and reduced anger and tension from stressful situations are some of the subjective beneficial effects.
It affects how a person feels , thinks , and functions at a cellular level .
Tolerance to some of the effects of nicotine is well recognized, which may develop quite rapidly.
Unpleasant symptoms of dizziness, nausea, and vomiting in first time smokers do not develop with repeat smoking.
Catecholamines (epinephrine and nor-epinephrine) released from the activation of the sympathetic nerves and adrenal gland are the cause of several nicotine’s biologic responses. It also increases levels of beta-endorphin, acetylcholine, serotinin , glutamate , and vasopressin in the CNS .
These mediators enhance concentration, alertness, and memory, decrease tension and anxiety, and promote a feeling of well-being.
Nicotine has a variety of complex CNS actions through its binding to the brain receptors.
Nicotine can mimic the effects of acetyl - choline in an array of areas: where ACH will work as a neurotransmitter , nicotine will work in its place. Since ACH works throughout the body, this also means that nicotine works in the body, wherever there are nicotinic receptors.
Therefore, nicotine’s effect can be explained by how it can serve the function of ACH at many receptor sites .
In small doses, it stimulates both sympathetic and parasympathetic ganglia; in larger doses, it has an opposite effect.
Autonomic ganglia are better known targets for nicotine.
Nicotine receptors are particularly concentrated in several areas that are key to effective functioning , survival , and re - production , the mesolimbic dopaminergic pathway, or pleasure reward pathway, and the locus ceruleus , a non-adrenergic center in the brain, which plays a critical role in cognitive processes and memory.
The activation of nicotine receptors throughout the brain increases brain production of numerous neurotransmitters , which in turn, produce a wide range of effects.
Nicotine in tobacco smoke increases the number of nicotine receptor sites in the brain by two-to threefold.
Nicotine is one of the most CNS active drug: milligram for milligram , it is ten times more potent a euphoria than heroin, cocaine, or d-amphetamine.
Tar is the name given to the aggregate of particulate matter in the cigarette smoke minus nicotine and moisture . In contradistinction to gases in the cigarette smoke, tar and nicotine are partly trapped in the filter tip.
It is a thick , dark liquid that is formed when tobacco burns . This tar covers the linings of the lungs , where it can cause disease.
It contains numerous compounds , known or suspected to be carcinogenic , tumor promoters , or co-carcinogens . Among them, poly-nuclear aromatic hydrocarbons are best known carcinogens.
Each year a one-pack-a-day smoker smears the equivalent to a cup of tar over his or her respiratory tract.
Tar and CO are not found in smokeless tobacco .
Tar produces chronic irritation of the respiratory system and is a major cause of lung cancer. In tobacco smoke it has a direct cancer-causing action.
The amount of tar delivered in mainstream smoke in each cigarette constitutes its content.
Nicotine is the principal cause of physiologic addiction to smoking and it meets the criteria of a highly addictive drug.
The powerful addicting properties of nicotine are the cause of failure to quit smoking by most cigarette smokers.
Mg for mg, the nicotine contained in all cigarette smoke is more potent than heroin.
The physical withdrawal of nicotine from the body takes approximately 2-3 weeks . After that time period, cravings are more psychological in origin.
Nicotine is highly addictive . It is both stimulant and a sedative to the CNS. The ingestion of nicotine results in an almost immediate kick because it causes a
discharge of epinephrine from the adrenal cortex. This stimulates the CNS , and other endocrine glands , which causes a sudden release of glucose . Stimulation is then followed by depression and fatigue , leading the abuser to seek more nicotine .
Stress and anxiety affect nicotine tolerance and dependence . The stress hormone corticosterone reduces the effect of nicotine; therefore, more nicotine must be consumed to achieve the same effect. This increases tolerance to nicotine and leads to increased dependence .
Like other psychoactive drugs, e.g. heroin , cocaine , or alcohol , nicotine serves as a reinforce for abuse liability in humans .
Most of the nicotine from cigarette smoke is adsorbed through the wide surface of the alveoli after its inhalation.
Nicotine in cigar and pipe smoke and smokeless tobacco is absorbed from the oral mucous membrane .
Within seconds after inhalation of cigarette smoke, a huge bolus of nicotine passes up the internal carotid arteries to the brain. There, the molecules bind to nicotine receptors.
The amount of nicotine that a smoker absorbs with each cigarette is determined not only by its nicotine content and the physical properties of its filter tip , but by the puff volume, depth of inhalation, rate of puffing, and duration of breath holding after each inhalation.
Smokeless tobacco does not contain tar and CO, but it does contain nicotine, which makes it just as addictive.
Carboxy-hemoglobin level in the blood-stream is a pretty good way to judge a person’s actual intake of cigarette smoke products.
With appropriate genetic substrate, a tobacco user can become nicotine addicted. About 90% of cigarette smokers are, in fact, physiologically nicotine addicted . They fall into a spectrum ranging from minimally nicotine addicted to severe nicotine addicted.
For these 90%, stopping is not a matter of choice, or free will. It is a medical and physiological problem that requires accurate diagnosis and appropriate medical treatment.
Thus, an individual, usually a child or early adolescent, must possess those genotypes that form the biological basis for nicotine addiction .
Then environmental and social factors must act on the child to induce genetic expression.
Without the proper genetic substrate, a smoker cannot become nicotine dependent.
About 10% of cigarette smokers lack the requisite genes and have no physiological nicotine dependence. These individuals do not experience any of the nicotine withdrawal symptoms.
They can smoke 1 or 2 cigarettes every now and then, or even 10 or 30 cigarettes in a social setting one evening and then nothing for days , weeks , or longer , and not even think about cigarettes.
These are truly ‘ social smokers ’ and do have complete, volitional control over when they will smoke. Scientifically , they are called chippers.
EFFECT ON THE RESPIRATORY SYSTEM
Cigarette smoking alters both the structure and function of central and peripheral airways, alveoli and capillaries, and the immune system of the lung.
Smoking during youth can impair lung growth and diminish the level of maximum lung function .
Girls are more susceptible than boys to smoking and adverse effects on the growth of the lung and lung function .
Smokers show evidence of impairment of pulmonary clearance, including cilia and alveolar macrophage functions.
Smoking is the chief factor for spontaneous pneumothorax in young tall thin people, increasing the risk more than 20-fold in men and nine fold in women.
Post-operative pulmonary complications are seen more frequently in cigarette smokers than in nonsmokers.
Respiratory infections are more prevalent and severe among cigarette smokers, than among nonsmokers.
Smoking during childhood not only increases the risk of developing COPD in adulthood, but also lowers the age of its onset.
Smoking is a cause of heightened airway responsiveness , which in turn may be a risk factor for the development of COPD . Only 10-15% of cigarette smokers develop COPD, but cigarette smoking accounts for about 80-90% of the risk of developing COPD.
Cigarette smokers have a higher COPD mortality than smokers , and have higher rates of other respiratory symptoms , bronchitis , and decline in FEV1.
These differences between smokers and nonsmokers increase with pack-years of smoking.
The delicate lining where air passes through the blood stream is 4 times as permeable ( leakier ) in smokers than non-smokers. When a smoker stops smoking for only one day, the lung’s leakiness diminishes considerably.
Cigarette smoking allows an imbalance between proteolysis and anti-proteolysis activity in the lung, possibly resulting in parenchyma destruction and airflow obstruction .
Smokers suffer from a decreased lung reserve . They are unable to run or even walk as far or as fast as their peers who have never smoked.
An estimated 10 to 15% of all smokers develop clinically significant airflow obstruction.
Approximately one third of cigarette smokers develop chronic cough and phlegm production , but only one seventh of smokers develop accelerated rates of loss of lung function .
Respiratory symptoms are greatly increased among cigarette smokers. A dose-response relationship exists for chronic cough and phlegm production
wheeze, and dyspnea.
Smoking-induced changes in airway epithelium including loss of cilia, mucous gland hypertrophy, an increase in the number of goblet cells , and increased permeability underlie the development of these respiratory symptoms .
Smoking leads to acceleration of the normal aging process of the lungs , with l oss of elastic recoil resulting in expansion of the distal airspaces . Physiologically , this results in hyper-expansion and decreased FEV1 .
Every smoker and nonsmoker alike experience a low decline in lung function starting at about 30.
Cigarette smoking and age are the only factors consistently associated with increase loss of FEV1 . Smokers with the lowest FEV1 also have the greatest fall per year.
About 20% of lifelong smokers develop airflow obstruction detectable by PFT s. Asymptomatic smokers have impaired ventilatory function when compared with nonsmokers of the same age.
Nonsmokers lose FEV1 at an accelerated range with age; the average loss is 30-70 mL/year . Some susceptible smokers (15%) loose function much more rapidly, approximately 150 mL/year .
Current smokers have a lower FEV1 and an accelerated decline in FEV1 compared to those who formerly or never smoked . Both of these associations show a dose-response relationship and are more dramatic in men than women.
There is increased mortality from COPD , pneumonia, and influenza among cigarette smokers compared with nonsmokers.
With sustained abstinence from smoking, the rate of decline in pulmonary function among smokers returns to normal; but lung reserve remains decreased relative to those who have never smoked.
Smoking cessation decreases accelerated decline by the first year to half that of smokers.
A relatively low FEV1, by middle age and a faster-than-expected annual fall in FEV1, are the two most useful findings in identifying smokers who are likely to develop severe pulmonary impairment.
Tobacco smoking is clearly the dominant causative factor in 80-85% of cases of bronchogenic carcinoma , and the risk is also dose-dependent.
All types of lung cancer are caused by tobacco use for both men and women.
A multi-step transformation from normal pseudostratified ciliated epithelium to squamous metaplasia , carcinoma in situ, and eventually invasive bronchogenic carcinoma has been reported by several prospective studies.
Lung cancer potential from smoking has been largely attributed to polycyclic aromatic hydrocarbons , and tobacco specific nitrosamines, with a small contribution to polonium-210 and volatile aldehydes.
Smoking transforms cells from normal to malignant.
The tar content of cigarettes is the major factor in carcinogenesis of smoking.
Brands of cigarettes that contain less tar and nicotine only marginally reduce the risk of lung cancer mortality.
Individuals who start smoking before the age of 15 y are 4 times more likely to develop lung cancer than those who begin after the age of 25 years .
The amount and duration of smoking determine the risk of lung cancer for smokers. Men or women who smoke more than 40 cig/day have twice the lung cancer risk of those who smoke less than 20 cig/day .
Lung cancer is more than 10 times higher in smokers than nonsmokers.
Its incidence increases by a power of 4-5 as the duration of smoking increases . There is a clear dose-response relationship between the number of cigs smoked per day and the increasing risk of death from lung cancer. Pipe and cigar smokers have an increased risk of lung cancer, but lower than that of cigarette smokers .
About 90-95% of male lung cancer deaths in developed countries, and 70-75% of female lung cancer deaths, are due to smoking.
In the last 30 years, there has been a 400% increase in women’s lung cancer deaths.
There is a risk reduction of lung cancer with smoking cessation. After 10 years , the risk is about 30-40% the risk of ongoing smoking.
The risk of lung cancer in ex-smokers always remains increased compared to that in nonsmokers.
Premature coronary heart disease is one of the most important medical consequences of smoking. Male and female smokers are at greater risk of myocardial infarction, recurrent heart attacks, and sudden death from coronary heart disease than nonsmokers.
Smokers have a two- to fourfold increased incidence of CHD and a two- to fourfold greater risk of sudden death than non-smokers. Mortality from CHD can be predicted by the number of cigarettes smoked/day, the depth of inhalation, the age of smoking onset , and the number of years smoked.
Cigarette smoking produces acute and chronic myocardial changes that directly contribute to the development of CHD and its associated complications.
Cigarette smokers have a significantly higher CO exposure than nonsmokers. CO binds Hb to form CO-Hb, with consequently reduced oxygen-carrying capacity.
This relative lack of oxygen causes an increase in hematopoiesis and a relative polycythemia. Clinically, this results in increased resting cardiac output and myocardial work at all levels.
The hypercoaguable state from higher levels of fibrinogen and hematocrit among smokers is likely related more to combustion products and gases than to nicotine. Nicotine enhances platelet aggregation.
Several mechanisms contribute to ischemic heart disease among smokers, including atherosclerosis, thrombosis , coronary artery spasm, cardiac arrhythmias, unfavorable lipid profiles, reduced oxygen-carrying capacity of the blood, and increased myocardial work.
About one third of all heart attack deaths and 40% of stroke deaths are attributable to tobacco use.
Smoking can lower the threshold of dysrythmia , especially ventricular fibrillation , leading to sudden death .
Sudden death is 4 times more likely to occur in young male cig smokers than nonsmokers. Women who use both cigs and oral contraceptive pills increase their risk of developing CHD tenfold . The risk level in quitters does not return to that of nonsmokers until 15 years after quitting.
Smoking even only 1-5 cigs/day presents a significant risk for myocardial infarction .
Myocardial infarction is 5 times more common among smokers than among nonsmokers under age 50.
Acutely , smoking may cause myocardial ischemia through an increase in oxygen demand or by reducing blood supply. This latter change may result from smoking-related coronary artery spasm and/or platelet aggregation and adhesiveness.
Chronically , cigarette smoking can result in coronary atherosclerosis , possibly by causing repetitive endothelial injury ; increased platelet adherence with stimulation of smooth muscle proliferation ; and increased low density lipoprotein cholesterol and/ or reduced high-density lipoprotein cholesterol .
Smoking-induced peripheral vascular disease is the most common organic cause of impotence and causes premature skin wrinkles , especially in people with generous sun or other ultraviolet light exposure.
With the first cigarette of the day, heart rate will increase by 10 to 20 beats/min. Blood pressure will go up 5 to 10 points. Body temperature will drop in the fingertips as the blood vessels there are constricted. Smokeless tobacco also increases the blood pressure.
Smoking among hypertensive patients increases complication rates , including progression of atherosclerosis , renal disease , and malignant hypertension .
Heart rates in smokers are noted to be elevated even during sleep, when no cigarettes are smoked.
Smoking cessation reduces the risk of peripheral vascular disease and its sequels. Complications from peripheral vascular disease in individuals who quit smoking are reduced , and performance and overall survival are increased .
After one year of smoking cessation , the excess risk of CHD mortality is reduced by about one-half and continues to decline with time. But patients who continue to smoke after a myocardial infarction have a double risk of dying within 15 years of the attack.
CENTRAL NERVOUS SYSTEM
Smoking causes stroke in both men and women. Smokers have an increased relative risk, approximately two, for ischemic stroke. The incidence of silent strokes’- events that are harbingers of both severe strokes and dementia- is increased in anyone who has ever smoked. Smoking increases the risk for subarachnoid hemorrhage .
Stroke risk decreases to baseline by five years after smoking cessation, but an ex-smoker’s risk of cerebrovascular accident remains high for at least 20 years after cessation.
CNS sensitivity and responsiveness to nicotine is genetically determined.
Smoking has long been associated with an increased risk of a variety of cancers . The role of cigarette smoke and the pathophysiology of cancer is complex.
A younger age of smoking initiation is associated with an increased risk , whereas pack-years of cigarettes shows a significant dose-response.
Smokers are at increased risk for a second smoking-related cancer once they have a tobacco-associated malignancy.
Of some 4000 components of tobacco, more than 50 have been shown to be carcinogenic in vivo and in vitro.
There appears to be a dose-response relationship for smoking and cervical cancer , because smokers consistently show an increased risk of cervical neoplasia.
Most tobacco-related head and neck cancers are squamous cell carcinoma.
Oral cancer and pre-malignant changes of the oral mucosa are much more common among users of smokeless tobacco compared to non users.
The origin of oral cancer is multi-factorial, but it can be traced to past or present use of alcohol and tobacco products (cigarettes, cigars, pipe and spit tobacco); exposure to the sun (lip cancer); and exposure to carcinogens in the work place. In comparison to nonsmokers, smokers have a 2-18 fold increase in risk of developing oral cancer .
The role of tobacco in esophageal cancer is stronger for squamous cell than adeno-carcinoma and stronger in women than in men.
The risk of distal stomach cancer is associated with stomach ulcers and pack-years of smoking.
Smoking increases the risk of pancreatic cancer in both men and women. The pro-portion of deaths attributable to smoking is estimated at about 30%, and there does appear to be a dose response relationship. Patients with this form of cancer have one of the poorest 5-year survival rates for any form of cancer.
Cigarettes have been associated with an approximate 2-fold increase in risk of colon adenomas or polyps, which are in turn strongly related to colon cancer. It may lead to as long as 35 years for the colon cancer secondary to smoking to appear.
The risk of death for colon cancer and rectal cancer is 16-22% higher, respectively, in tobacco users compared with never users. The risk increase holds for cigarettes, pipe and cigar smoking and smokeless tobacco.
Smoking is a contributory factor to excess risk of cancer of the bladder and renal carcinoma . The risk is significantly related to duration of smoking, inversely related to the age initiation , and inversely related to time since smoking cessation.
ORGAN SECONDARY EFFECTS
Smoking decreases our senses , particularly the sense of smell and taste (that’s why a smoker cannot smell the stink he carries around with him).
Smoking stains the fingers and teeth, and leaves a stale smell on the hair , breath and clothes .
Smoking causes premature facial wrinkling through vasoconstriction of the capillaries of the face . This is visible in deep “ crow’s feet ” radiating from the corners of the eyes and pale, grayish, wrinkled skin on the cheeks.
Smoking more than triples the average person’s chance of premature facial wrinkling , and the severity of wrinkling increases with the number of pack years, doubling and in some cases quadrupling depending on the number of packs smoked per day, over a ling period of time.
As the small blood vessels constrict, the skin temperature may also decrease , causing the fingers, toes, and skin to feel cold.
Gum disease and tooth loss are common among smokers.
Cigarette smoke irritants can permanently damage the tissues of the larynx . The effect of this is a noticeable deepening and hoarseness in the voices of chronic smokers.
Vocal cord polyps (non-cancerous) are strongly related to tobacco exposure, and such polyps rarely disappear without surgery.
Smoking decreases esophageal sphincter pressure. This allows acid to reflux from the stomach into the esophagus. This can lead to esophagitis and to permanent esophageal stricture.
Cigarette smoking is associated with symptomatic gastro-esophageal reflux disease .
Peptic ulcer is significantly associated with the number of cigarettes smoked/day, but not significantly with either tar or nicotine yield.
Duodenal ulcers heal more slowly in smokers even when treated.
Smoking cessation is associated with fewer duodenal ulcers, compared with current smoking.
There is a 2- to 3-fold increased rate among both smokers and ex-smokers of developing macular degeneration , an irreversible form of blindness.
Smoking causes vision loss by restricting blood flow to the eye.
There is a 40% higher rate of cataracts among smokers.
Smoking is associated with osteoporosis in women, and with spinal disk disease in both sexes.
OCCUPATION AND SMOKING
Cigarette smoking can increase the risk of developing occupationa l lung disease and trigger exacerbations of existing work-related disease.
Workers who smoke and are exposed to coal, silica, grain, or cotton dust are more likely to develop chronic bronchitis than nonsmoking workers with similar exposure or non-exposed smokers. The risk appears to be additive .
Smokers exposed to asbestos, radon , arsenic, diesel exhaust, aromatic amines, and silica are more likely to develop cancer than nonsmoking workers.
Smoking increases the risk of developing IgE antibodies and asthma among selected workers exposed to potential workplace allergens, such as platinum and humidifier-associated antigens.
HORMONES AND SMOKING
Cigarette smokers have a higher incidence of hormone-related cancers such as breast, prostate , and cervical cancers .
Because of the anti-estrogenic effect of tobacco use, a variety of hormone-dependent disorders are related to tobacco.
Endometrial cancer, which depends on estrogens for its pathogenesis, is reduced among women who smoke.
A variety of benign disorders related to hormone levels are increased among smokers such as gall bladder disease and prostate hyperplasia.
Among both men and women, osteoporosis, lowered bone mineral density , and osteoporosis features are more frequent among smokers.
Women who smoke experience menopause at an earlier age.
PREGNANCY AND SMOKING
Maternal mortality rates are increased in smokers.
Smoking during pregnancy is the main preventable cause of perinatal morbidity and mortality.
Smoking may reduce tube motility , delay ovum entry into the uterus , and increase the risk of pelvic inflammatory disease ( ectopic pregnancy ).
Miscarriage is 2 to 3 times more common in smokers, as are still birth due to fetal O2 deprivation and placental abnormalities induced by the CO and nicotine in cigarette smoke.
Women who smoke at the time of conception or during pregnancy are more likely to have spontaneous abortions and pregnancy complications of placenta previa , placental abruption , and premature rupture of membranes than nonsmoking women.
Smoking-related fetal intra-uterine growth retardation is a major health concern because it is associated with increased per-inatal mortality from a variety of causes.
Women who smoke during pregnancy are 50% more likely to have a child with mental retardation of unknown cause than are nonsmoking women.
In utero exposure of the infant to active maternal smoking has been associated with deficits in lung function , an increased risk of wheezing respiratory illness in early infancy, impairment of somatic (height ) growth in childhood , and small deficits in intelligence and behavior as measured on standardized tests.
Infants born to mothers who smoke during pregnancy are on average 200 gm lighter and 1 cm shorter than infants on nonsmoking mothers.
The lungs of children whose mother smoke grow at only 93% the rate of children whose mother do not.
Nicotine and other components of smoke are present in breast milk of nursing mothers who smoke ; infants who ingest such milk take smaller volumes , gain weight more slowly , have more vomiting , diarrhea , and restless behavior than infants of nonsmoking mothers.
ENVIRONMENTAL TOBACCO SMOKE
ETS is composed of side-stream and mainstream smoke.
Burning tobacco is the main source of indoor pollution in the developed world as it contains over 4000 dangerous chemicals.
Side-stream smoke , which is emitted from the burning end of a lit cigarette, contains the same compounds found in mainstream smoke, which is inhaled into the smoker’s lung and exhaled.
Many of the 4000 known compounds and more than 40 known carcinogens found in MS are present in greater concentrations in SS.
Increased levels of some of the known constituents of ETS have been measured in exposed nonsmokers and vary, in part, with room size, ventilation, number of smokers, and rate of smoking .
Respiratory symptom frequency is increased in exposed nonsmoking spouses.
Evidence appears to show that ETS does play a role in the development of lung cancer in nonsmokers. Its risk is about 20-30% higher than for never smokers not exposed to ETS .
There is an increased risk of 20-50% of CHD among nonsmokers living with smokers.
In a dose-dependent relationship , exposure to environmental tobacco smoke increases the average relative risk of coronary heart disease to 1.25 and of progression of atherosclerosis to 1.20 .
The risk of lower respiratory tract diseases (such as croup, bronchitis, pneumonia) is estimated to be about 50-60% higher in children exposed to ETS during the first 1-2 years of life, compared with unexposed children.
Chronic respiratory symptoms such as cough, phlegm, and wheeze are all more common in children whose parents smoke.
Involuntary smoking reduces the growth rate and of lung function in children.
There is increased bronchial responsiveness in children from homes of smokers.
In children, exposure to ETS is causally associated with increased prevalence of fluid in the middle ear , symptoms of upper respiratory tract irritation , and a small but significant reduction in lung function.
Second hand smoke is classified as a Group A carcinogen.
When smokers stop smoking cold turkey , most experience one or more nicotine withdrawal symptoms. These are not psychological, they are physical and physiological . Their origin begins directly in altered CNS neurons.
Nicotine withdrawal symptoms occur and are caused by nicotine’s sudden removal from the increased number of nicotine receptor sites present in the smoker’s brain.
Generally , nicotine withdrawal symptoms can be completely relieved within minutes after smoking only one cigarette.
All CNS induced symptoms caused by abrupt discontinuation of tobacco use are promptly reversed, in dose-dependent fashion, by resumption of tobacco use or administration of any nicotine pharmaceutical agent via any route, e.g. nasal spray, intravenous, or trans-dermal.
Nicotine withdrawal symptoms include :
2. Anxiety , nervousness ( drink a lot of water to flush the nicotine out of the system).
3. Lack of concentration ( rest, exercise).
4. Tiredness ( get an extra hour of sleep, brisk exercise).
5. Frustration, anger .
6. Depression and depressed mood.
8. Craving for cigarettes.
9. Nocturnal awakenings.
10 . Constipation ( include more whole-grain foods and fresh fruit and vegetables, exercise).
11. Sleeplessness ( exercise regularly).
12. Headache ( plenty of rest, exercise).
13. Sore throat ( drinking liquids may help).
14. Increased appetite and weight gain.
14. Decreased heart rate.
TIPS FOR CUTTING DOWN ON SMOKING GRADUALLY
1. Switch brands to one you find distasteful.
2. Smoke only half of each cigarette.
3. Smoke without inhaling.
4. Buy cigarettes by the pack , not the carton.
5. Try to eliminate the cigarettes.
6. Set a daily quota and reduce the number of cigarettes you smoke each day.
7. Increase your exercise .
8. Postpone your cigarette until you can go all day without one.
9. Smoke only in uncomfortable places.
10. Spend time where smoking is prohibited.
BENEFITS OF QUITTING
It is better never to start smoking cigarettes- and become addicted to nicotine-than it is to smoke with the thought of quitting later .
Smoking is not a bad habit that can be easily overcome with a modicum of determinate, better known as will power.
Interventions are needed which target smokers for whom addiction, need, and reinforcement play a key role in maintaining their dependency.
The health benefits of smoking cessation are immediate and substantial, extending to men and women of all ages, both sick and healthy.
Smoking cessation has major and immediate health benefits for men and women of all ages. Benefits apply to persons with and without smoking-related disease .
The only way to avoid the health hazards of smoking is to quit completely or to never start smoking.
It is important to note that the extent to which the risks of smoking decrease depends on how much the person smoked, the age the person started smoking, and the amount of inhalation.
Former smokers live longer than continuing smokers!
People who stop smoking at younger ages experience the greatest health benefits from quitting. Those who quit by age 35 avoid 90% of the risk due to tobacco use. Even smoker who quit after age 50 substantially reduce their risk of dying early. It is never too late to quit smoking on assumption that the damage is already done.
People who quit smoking before age 50 have one-half risk of dying over the next 15 years compared to people who continue to smoke.
A smoker who gives up the habit at the age of 65 reduces his or her risk of dying from a tobacco-related disease by half.
Within 20 minutes of smoking the last cigarette, the body begins to restore itself.
The heart rate drops 20 minutes after stopping.
Twelve hours after quitting the CO level in the blood drops to normal.
Two weeks to three months after quitting , the circulation improves and the lung function increases.
Quitting improves pulmonary function by about 5% within a few months of cessation
One to nine months after quitting , cough and shortness of breath decrease; cilia regain normal function in the lungs, increasing the ability to handle mucus, clean the lungs, and reduce the risk of infection.
One year after quitting , the excess risk of coronary heart disease is half that of a smoker’s.
Five years after quitting , the stroke risk is reduced to that of a nonsmoker.
Ten years after quitting, the lung cancer death rate is about half that of a continuing smoker’s.
The risk of cancer of the mouth, throat, esophagus, bladder, cervix, and pancreas decrease .
Fifteen years after quitting , the risk of coronary heart disease is that of a nonsmoker’s.
In most cases, if a person quits smoking by age 40 , there will be no significant difference in lung function compared with those who never smoked.
Susceptible smokers who stop smoking at age of 50 do not regain lost function or regain only a little, but they subsequently lose function at the same rate as people who never smoked.
Cessation of cigarette smoking is the only intervention that slows the rate of decline in lung function in COPD, with an average loss of 14.4 mL/year in sustained quitters, versus 60.2 mL/year in continuing smokers.
Smoking cessation is the only way to slow the decline in lung function in emphysema.
Women who stop smoking before pregnancy or during the first 3 to 4 months of pregnancy reduce their risk of having a low birth weight baby to that of women who never smoked.
Smoking cessation decreases the risk of myocardial infarction by 50% within two years. After 5-15 years, the risk of stroke decreases to that of those who never smoked.
After 10 years, lung cancer risk is 30-50% that of continuing smokers.
Smoking cessation also reduces the risk of other tobacco-related malignancies, including cancers of the larynx, esophagus pancreas and urinary bladder.
It also decreases morbidity and mortality from peripheral vascular disease, gastric and duodenal ulcers, pneumonia, stroke, and COPD.
Smoking cessation after the establishment of psychological and physical dependency becomes a most difficult complex task.
Tobacco dependence is a chronic condition that often requires repeated intervention.
People do not quit smoking, INDIVIDUALS do! Just like only you can quit smoking. No one can quit smoking for YOU . Only YOU can quit smoking for yourself.
Withdrawal symptoms are accounted for by the withdrawal of nicotine, as they also occur with the cessation of smokeless tobacco and nicotine gum, and are relieved by the administration of nicotine.
Tobacco dependence treatments are clinically effective and cost-effective relative to other medical and disease prevention interventions.
Numerous effective pharmacological therapies for smoking cessation exist. They should be used with all patients attempting to stop smoking ( except in the presence of contra-indications).
First-line pharmacological therapies are bupropion SR and nicotine replacement therapy products ( patch, gum, nasal spray, inhaler).
Second-line pharmacological therapies are nortriptyline and clonidine.
Success rate of buprion is between 22-40%.
Events in the developing countries strongly support the view that the introduction of advertising increases smoking.
Mass media education campaigns are a valuable way of reaching population subgroups of all educational levels.
The withdrawal of all advertising rate measures , is associated with lower smoking rates, both among young people and in older subjects.
Two advertising approaches are particularly effective in preventing teens from smoking, truth and scare tactics.
Public health goals are :
1. To increase smoking cessation.
2. Decrease initiation.
3. Lower exposure to ETS.
4. Eliminate disparities in prevalence and health effects among population groups.
A public information campaign can:
1. Raise public awareness about smoking and health.
2 . Persuade smokers to give up smoking and provide advice and materials on how this might be done.
3. Influence nonsmokers to remain so (especially the young).
4. Create awareness that smoking is neither normal nor majority behavior.
5. Establish the rights of the nonsmoker.
6. Provide information on potentially less hazardous forms of smoking.
7. Introduce notions of legislation and health policy.
8. Criticize tobacco industry activities.
Policy initiatives work, only if properly funded and implemented :
1. Services to treat tobacco dependence.
2. High intensity mass media campaigns.
3. Bans on tobacco advertising.
4. Passage of local ordinances to promote smoke-free indoor environment.
6. School-based prevention and treatment programs.
7. Decreased access to tobacco products by youth act in concert.