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 .
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.
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.
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.
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 .
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.
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 .
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 .
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.
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.
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.
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 .
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.
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.
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.
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.
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.
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.
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.
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 .
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.
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.
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.
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 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.
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 .
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 .
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.
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.
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 .
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.
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.
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.
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.
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.
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.
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.
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.
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.