Cigarette Smoke Health Implications

Introduction

Cigarettes?are, most likely, the most significant source of poisonous chemical compounds that cause human disease.?According to WHO data, cigarettes are the cause of at least four million deaths each year, this figure could double by 2020.?In the year 2000, it was calculated that about 5.7 billion cigarettes were consumed annually in the world, in America 845,337 million cigarettes, and in Colombia 17,171 million cigarettes;?consumption in Colombia is much lower than that observed in 1970 (2,1004 million cigarettes) but higher than in 1990 (13,647 million cigarettes) and 1997 (14,193 million cigarettes).?There are approximately one billion tobacco smokers in the world;?in turn, a high number of these smokers are addicted to nicotine.?The total number of cigarettes reported sold by the major manufacturers,?202.9 billion units?in 2019, decreased by 14.0 billion units (6.5 percent) from 2018

The cigarette is sold as a symbol of success and victory, attracting new generations to its consumption.?The aggressive advertising of tobacco companies added to the few efforts in public health makes it difficult to prevent smokers' illnesses.?

In recent years, cigarettes free of nitrosamines (a carcinogen found in cigarette smoke) have been promoted in Australia, Canada, and the United States.?It is striking that these cigarettes are advertised as "healthy" for consumers;?Although it is an effort, removing a carcinogen does not make a cigarette non-carcinogenic, nor does it help reduce mortality from cardiovascular disease associated with cigarette smoking.

Additionally, some studies show that smokers underestimate the risk of developing cancer or other medical complications.?Hanningfield and his colleagues found that only 8.7 percent of their study subjects believed they were at high risk of developing some type of cancer.

The cigarette is nothing more than a roll of tobacco wrapped in a strip of material that does not contain tobacco (unlike the cigar that is wrapped in tobacco).

Tobacco contains about 4000 particles, after its combustion 6000 are detected of which 65 are possible carcinogens and 11 are already proven carcinogens.

Cigarette smoke has two phases (particulate and gaseous) and two streams (main and secondary).?The main current is the one that passes through the cigarette and reaches the smoker's lungs;?the secondary current is the smoke current generated from the incandescent end of the cigarette.

A smoker is a person who uses a cigarette periodically or sporadically;?There is still no consensus on the definition of severe, moderate and light smoker, however many research studies mention as severe those who smoke more than 20 cigarettes a day, from 10 to 20 moderate and less than 10 light.?The passive smoker is the person who inhales cigarette smoke without smoking.

The costs of cigarette smoking on the quality of life of those who are exposed to it are incalculable.?Smoking has been associated with multiple types of cancer (lung, pancreas, larynx, pharynx, paranasal sinuses, stomach, esophagus, kidney), chronic lung disease, cardiovascular disease, and mental disorders.?Next we will return to the effects of cigarettes on active and passive smokers.

Effects in active smokers

The active smoker is exposed, not only to the toxic agents of the smoke streams, but also ingests some of them dissolved in saliva and mucus.?The pH of the smoke, additionally, favors the exchange of nicotine between the smoke and the smoker's tissues.?In this section we will discuss the main diseases suffered by active smokers: cancer, chronic obstructive pulmonary disease and cardiovascular disease.

Cancer

Since the 1950s (1950) the relationship between tobacco smoking and lung cancer has been known.?By 1986 it was known that tobacco smokers could suffer not only lung cancer but also a broad spectrum: pelvis, digestive tract (mouth, larynx, pharynx and esophagus) and pancreas.?Today, recent epidemiological evidence confirms the research of the past and illustrates new horizons in cancer epidemiology.

Carcinogens in cigarette smoke

Cigarette smoke contains significant amounts of known carcinogens, possible carcinogens, and probable human carcinogens.?In the long list of carcinogenic agents present in cigarette smoke, they must be named in the group of: polycyclic aromatic hydrocarbons, N-nitrosamines, aromatic amines, and metals.

The main carcinogens include polycyclic aromatic hydrocarbons (such as benzopyrene), nitrosamines (aromatic amines), aldehydes, and inorganic compounds such as nickel, lead, and polonium 10. Polycyclic aromatic hydrocarbons (HPA) are formed after incomplete combustion of matter organic.?

The best-known compound of this type is benzo (a) pyrene;?PAHs cause cancer of the lung, trachea, oral cavity, larynx, and digestive tract when administered to laboratory animals.?N-nitrosamines are present in cigarette smoke in a volatile form and related to nicotine and other tobacco alkaloids.?Many of the N-nitrosamines are specific carcinogens for organs such as the lung and esophagus.?Aromatic amines were the first known carcinogens for their presence in industrialized environments.?Formaldehyde and acetaldehyde are also carcinogens proven by laboratory experiments.?Volatile hydrocarbons such as benzene cause leukemia in humans;?nickel and cadmium (metals) are also proven human carcinogens.

These compounds cause cellular apoptosis and cellular DNA damage.?In principle, the repair mechanisms are able to recover damaged genetic information, however, chronic exposure to carcinogens causes mutations in genes that control cell division, proliferation, and growth.

Lung cancer

Smoking cigarettes is the biggest risk factor for developing lung cancer.?The toxic agents present in cigarette smoke (both in the gaseous and particulate phases) cause significant damage to the lung epithelium.

?Generally, the integrity of the epithelium is maintained by a regenerative process, however, with repeated damage, significant telomere shortening occurs (replicative senescence) that can lead to metaplastic changes in squamous cells.?

Cellular senescence is an irreversible growth state of the cell induced by telomere shortening or telomere-dependent signals due to DNA damage and oxidative stress (stress-induced senescence).

?Carcinogenic compounds present in tobacco smoke produce mutations in the p53 gene that is related to cell growth and proliferation.

?The polycyclic aromatic hydrocarbons present in cigarette smoke are converted by the cytochrome oxidase P4501A1 complex (CyP1A1 gene products) from pre-carcinogenic to carcinogenic substances.?Benzo (a) pyrene is converted to epoxide diol (carcinogenic metabolite) that binds to mutable nucleotide sequences of the tumor suppressor oncogenes K-ras and p53.

?The polycyclic aromatic hydrocarbons present in cigarette smoke are converted by the cytochrome oxidase P4501A1 complex (CyP1A1 gene products) from pre-carcinogenic to carcinogenic substances.?Benzo (a) pyrene is converted to epoxide diol (carcinogenic metabolite) that binds to mutable nucleotide sequences of the tumor suppressor oncogenes K-ras and p53.?

The polycyclic aromatic hydrocarbons present in cigarette smoke are converted by the cytochrome oxidase P4501A1 complex (CyP1A1 gene products) from pre-carcinogenic to carcinogenic substances.?Benzo (a) pyrene is converted to epoxide diol (carcinogenic metabolite) that binds to mutable nucleotide sequences of the tumor suppressor oncogenes K-ras and p53 .

Nicotine binds to specific receptors on the epithelial cells of the respiratory tract.?Its action is coupled to the signaling cascade that induces an anti-apoptosis state, creating a favorable scenario for carcinogenesis.?

Although under conditions of non-consumption of nicotine, the pathway directed to apoptosis would occur, when the accumulated genetic damage is great, the activation of the anti-apoptosis pathway prevents it.?Nicotine also promotes angiogenesis associated with tumor growth and cell migration.

An important number of epidemiological studies make it possible to establish the relationship between the different histological types of lung cancer and cigarette smoking.?Of these, the four histological types with the highest incidence are squamous cell carcinoma, small cell carcinoma, undifferentiated long cell carcinoma, and adenocarcinoma.?The increase in the number of lung cancer cases in recent years occurs along with the increase in smokers.?The risk of developing it increases proportionally with the number of cigarettes consumed per day and with a younger age of onset of cigarette smoking.

Other types of cancer associated with cigarette smoking

Since the middle of the last century, important work has focused on establishing which types of cancer are related to cigarettes.

Cigarette smoking is an important risk factor for the development of pathological changes directed to cancer of the aero-digestive tract.?The increased risk of developing cancer of the paranasal sinuses, nasal cavity and nasopharynx has been demonstrated in many case-control studies, with an important relationship between quantity and duration of cigarette smoking;?Among these, the most common histological type is squamous cell carcinoma.

Available epidemiological evidence shows a markedly increased risk of stomach cancer in smokers compared to non-smokers.?The association of cigarette smoking with alcohol consumption could pose a greater risk.?In turn, chronic?Helicobacter pylori infection?can also increase the risk in smokers.?

It is estimated that 11 percent of gastric cancer cases in men and 4 percent in women in developed countries and 17 percent in men and 11 percent in women in developing countries are attributable to cigarette smoking.

There is also an increased risk of developing liver cancer in smokers compared to non-smokers.?This is partly explained by the relationship between cigarette and alcohol consumption.?

Alcohol consumption remains the biggest risk factor for developing liver cancer.?However, some studies show a higher risk in non-alcoholic smokers of developing liver cancer compared with individuals who do not consume alcohol or tobacco.

Additionally, cigarette smoking is the most important risk factor for developing pancreatic cancer.?Many of the pathogenic effects of cigarettes are due to nicotine.?Nitrosamines are also derived from the metabolism of nicotine in the pancreas.?There, other molecules are formed that have the power to modify covalent bonds in DNA and proteins.

?In vitro, markers of pancreatic damage have been found in animals exposed to cigarette smoke: cytoplasmic vacuolation, interstitial edema, and cell necrosis.?Nicotine affects the cholinergic receptors of the central nervous system (CNS).

Activation of the nicotinic receptor is directed at the entry of calcium into the acinar cell.?Increased intracellular calcium promotes cytotoxicity;?activates a signaling cascade mediated by inositol triphosphate (affects cellular secretion);?and modifies the normal genetic expression of cells with the overexpression of proto-oncogenes, increased expression of the mutant p21 Ras protein and the H-Ras gene in pancreatic cells.?Ras proteins (encoded by RAS genes) play an important role in the transduction signals of mitogenic growth factors aimed at regulating the cell cycle.

Renal pelvic cancer and renal parenchymal adenocarcinoma are also associated with cigarette smoking.?For people who smoke 20 or more cigarettes a day, the risk of developing these types of cancer is 1.5 to two times higher compared to non-smokers.

Many studies have linked cigarette smoking and cervical cancer.?The analysis of the causality of cigarettes in the genesis of this type of cancer is complicated by the presence of the human papillomavirus (HPV).?Some laboratories have designed testing methods to identify HPV-positive and HPV-negative women.?Thus, they have been able to establish that the relative risk of HPV-negative women who smoke compared to non-smokers is 2.17.

The risk of developing myeloid leukemia is higher in smokers compared to nonsmokers.?Benzene is a powerful leukemogenic agent;?the levels of this substance in smokers are considerably increased.?The risk of smokers is 1.6 with a proportional relationship between the number of cigarettes consumed per day and the risk, even a causal relationship has been reported.

Chronic obstructive pulmonary disease (COPD)

Cigarette smoking is the biggest risk factor for developing COPD.?COPD is defined as a set of disorders in the respiratory system characterized by decreased peak expiratory flow and slow emptying of the alveolar sacs due to a combination of respiratory tract diseases and emphysema.?

This definition, however, does not account for the so-called systemic effects of COPD that new research has brought to light.?Such effects that will be discussed in this section include a systemic inflammatory state, nutritional abnormalities and weight loss, cardiovascular effects, effects on the nervous system and osteo-skeletal effects, and skeletal muscle dysfunction.

Systemic inflammation

The excessive inflammatory response within the lungs to the toxic agents of cigarette smoke is the pathogenetic mechanism of COPD;?abnormalities include increased numbers of T lymphocytes (predominantly LTCD8 +), macrophages, and neutrophils, increased levels of pro-inflammatory cytokines, and evidence of oxidative stress.?Pro-inflammatory changes have also been observed in the systemic circulation in addition to lung tissue.

Neutrophils and lymphocytes from COPD patients show increased chemotaxis and extracellular proteolysis;?neutrophils also produce more ROS (reactive oxygen species).?The increase in the expression of CD 11b in the neutrophils of patients with COPD and the abnormalities in the transduction of this signal, the increase in the expression of cell adhesion proteins and the increase in vesicular transport suggest an exaggerated response of the neutrophils in COPD.

The CD4 + / CD8 + T lymphocyte (LT) ratio is characteristic of an inflammatory state in COPD;?there is a significant increase in the number of LT CD8 + and a decrease in the number of LT CD4 +.?They have even reported an increase in the number of circulating "activated" T lymphocytes in the blood of smokers.?

The levels of cytokines and acute phase proteins show high levels: tumor necrosis factor (TNF-a) and its receptor, interleukins (IL), reactive protein, binding protein lipopolysaccharide, (Granulocyte-macrophage colony stimulating factor), all of them are markers of inflammatory status and are also associated with cardiovascular disease.

Nutritional abnormality and weight loss

The nutritional abnormalities described in COPD patients include alterations in calorie metabolism, basal metabolic rate, and body composition.?Unexplained weight loss is observed in approximately 50 percent of patients.?

Increased metabolic rate does not keep pace with calorie intake;?This may be due to either the drugs indicated in COPD (?2 adrenergic agonists), the inflammatory response typical of COPD and the relationship between metabolic breakdown and increased levels of pro-inflammatory cytokines, and tissue hypoxia and its complications (congestive heart failure).

?There is also a direct relationship between the activity of cytochrome oxidase and the degree of hypoxia present in COPD.

Skeletal muscle dysfunction

Patients with advanced COPD have exercise intolerance and dyspnea.?Little by little, the patient with COPD assumes a sedentary lifestyle as a consequence of the decrease in their respiratory function, decreasing the resistance to fatigue of the skeletal muscle.

?Exercise in these patients increases the release of alanine and glutamine from skeletal muscle, this suggests the existence of abnormalities in metabolism within myocytes.?

The chronic hypoxia to which the muscle tissue is exposed in COPD causes alterations in the metabolism of proteins in the muscle tissue (myosin synthesis) and loss of muscle mass.?The systemic inflammation typical of COPD has important pathogenic effects on muscle.?Tumor necrosis factor (TNF) induces the expression of several genes related to a greater inflammatory response;?TNF also activates FN-k? (nuclear factor kB) and degrades myosin heavy chains.?

Some advanced cases of COPD show the presence of oxidative stress that causes muscle fatigue and proteolysis.?Nitric oxide, a free radical that is produced under normal conditions in muscle, can play an important role in tissue damage: cytokines increase the production of nitric oxide and the number of blood vessels is lower than normal, it can also cause failure of muscle contraction.?

Some advanced cases of COPD show the presence of oxidative stress that causes muscle fatigue and proteolysis.?Nitric oxide, a free radical that is produced under normal conditions in muscle, can play an important role in tissue damage: cytokines increase the production of nitric oxide and the number of blood vessels is lower than normal, it can also cause the failure of muscle contraction.

?Some advanced cases of COPD show the presence of oxidative stress that causes muscle fatigue and proteolysis.?Nitric oxide, a free radical that is produced under normal conditions in muscle, can play an important role in tissue damage: cytokines increase the production of nitric oxide and the number of blood vessels is lower than normal, it can also cause the failure of muscle contraction.

Other effects

Endothelial function is abnormal in the lungs, heart, and kidneys.?Coronary artery disease is not uncommon in COPD patients.

The bioenergetics metabolism of the brain is altered, it is believed that it may be due to adaptation to hypoxia, or to another systemic effect of COPD or to a mechanism that is not yet known.?

Many cases of depression have been reported in those who suffer from this disease, the triggering of this state is due in part to a psychological effect due to the weakening caused by the disease and the presence of the mediators of the inflammatory state (cytokines).?Serum leptin levels are also decreased compared to healthy people, which could mean the beginning of imbalances in the circadian rhythm.

The reported cases of osteoporosis link a significant number of people with COPD.?Osteoporosis occurs as a result of the other systemic effects of COPD (inflammatory state, skeletal muscle dysfunction, hypoxia, sedentary lifestyle).

Cardiovascular disease

Cardiovascular disease?is one of the leading causes of death in the world.?Cigarette smoke has greatly increased its prevalence in the population around the world.?Oxidative stress is the mechanism through which vascular endothelial injury and atherogenesis occur.?At present, it is assumed that atherosclerosis is an inflammatory disease where oxidation of LDL (low-density lipoproteins), hypertension, and hypertriglyceridemia occur.

Cigarette smoke generates considerable amounts of ROS within the human body, which play an important role in atherogenesis by promoting the oxidation of lipoproteins circulating in the bloodstream.?

ROS also favor the adherence of phagocytes to the vascular endothelium.?ROS suppresses nitric oxide activity in vascular endothelium, oxidize LDL, is atherogenic, and activates DNA-binding factors, such as activator protein 1 and Nuclear Factor k, which promote the expression of genes that encode proinflammatory proteins.

Markers of inflammation (blood levels of C-reactive protein, fibrinogen, lymphocytes, and leukocytes), as well as the number of platelets, are found in high concentrations in smokers compared to non-smokers or people who have quit smoking, in turn. once are at risk of thrombosis.

Effects on passive smokers

People who, without smoking, are exposed to secondhand smoke, are at risk of acquiring cigarette-related diseases;?in children and newborns it has been associated with low birth weight, sudden death syndrome, middle ear infection, asthma, bronchitis, and pneumonia;?in adults cardiovascular disease, lung cancer and cancer of the nasal cavity;?Additionally, the relationship between passive smoking and the risk of miscarriage, development and learning problems in children, meningococcal infections, leukemia in children, exacerbation of asthma in adults, exacerbation of cystic fibrosis, decreased lung function, and cancer is studied. of cervix.

Newborns, children, and pregnant women as passive smokers

Exposure to cigarette smoke of pregnant women and children has negative consequences for their health.

Cigarette smoking is associated in pregnant women with a significant number of obstetric complications: spontaneous abortion, ectopic pregnancies, premature birth, placental abruption, and premature rupture of membranes.?Likewise, exposure to environments saturated with cigarette smoke pollutants can cause premature birth.

Experiments carried out on animals have shown that exposure to cigarette smoke during pregnancy slows the movements of the fetus, these, in turn, are important for the development of the lungs.?

In humans, it has been observed that the movements of the fetuses of women who are exposed to cigarette smoke are less than those of women who are not exposed.?The lungs of children whose mothers had this exposure are hypoplastic and will affect their function in adulthood since the "programming" of lung function occurs during the embryonic period.

Exposure of the fetus to cigarette toxins increases the risk of low birth weight, however, genetic variations have been reported in this regard.?Low birth weight increases the future incidence of coronary heart disease, hypertension, type II diabetes mellitus, insulin resistance, dyslipidemia, and premature death.?In developing countries, these associations are closer.?The risk of neonatal sepsis, neonatal neunomy, and other infections is also increased.

Exposure to cigarette smoke during childhood is the greatest risk factor for infant premature death syndrome.?Although the sleeping position and economic status are important risk factors, the fact that the breast smokes doubles the risk of the syndrome.?

Possible explanations are abnormalities in brain development with a tendency to apnea and abnormal respiratory control mechanisms (reduced ventilation in response to hypoxia);?Another possible explanation is the development of respiratory diseases as a consequence of exposure to cigarette smoke.?

In the first years of life, second-hand smoke is associated with a high incidence of respiratory infections,?they also include an increased risk of developing tuberculosis and meningococcal infection (this is due to the decrease in the humoral immune response and a greater adherence of the bacteria to the lung tissue).?The risk for middle ear infections is also higher for children whose parents smoke.

Prenatal exposure to cigarette smoke increases the risk of developing asthma in the first years of life;?Although the risk is also high for those who begin to be passive smokers after birth, this is more related to cases of bronchitis.?

Immunoglobulin E (IgE) levels are higher in children of smoking mothers, so it is possible that these children develop allergies more easily.

Children exposed to cigarette smoke more easily develop attention deficit syndrome and may show antisocial behavior patterns.?In animals, nicotine has been observed to affect cell proliferation and differentiation and produce abnormal patterns in synapse formation, possibly these abnormalities also occur in humans.

The incidence of cancer cases in children exposed to cigarette smoke is unclear.?Although an increased risk for certain brain tumors and leukemia has been reported, this could be the effect of other distracting factors.

Effects in adults

The scenarios of exposure to the toxins of cigarettes for an adult are numerous: from the same workplace to the meeting places.?This makes intervention difficult and it is necessary to direct efforts towards the education of potential passive smokers so that they stay away from the places where people smoke.

The available medical literature (recent and old) corroborates the assumptions about the risk of developing lung cancer for passive smokers, presenting a direct relationship level of exposure-higher risk.

The relationship is causal, that is, secondhand smoke causes lung cancer.?The risk of developing airway cancer is also higher in passive smokers compared to nonsmokers without exposure to cigarette smoke.

In the last 20 years, the results of at least 14 studies have been presented that support the relationship between being a passive smoker and increased cardiovascular risk, the risk of dying from coronary heart disease is 20 percent.?It has recently been shown that both active and passive smokers are at risk of developing atherosclerosis.

Implications for public health

The negative effects on the health of all people periodically exposed to environments with cigarette toxins have already been demonstrated, the immense need to limit the public places where it can be smoked comes to light.?

Smoke-free places should be guaranteed for non-smokers in all public places (restaurants, parks, offices, etc.).?It is also important to mention the need to educate parents who smoke, so that they do so away from their children and thus avoids the complications that this exposure will bring to their health.

Although progress has already begun in Colombia in this regard, there is still a long way to go: it is not difficult to meet a smoker anywhere, nor to see parents teaching their children cigarettes, nor to see doctors smoking in front of their patients and students.

Nicotine dependence

Nicotine is perhaps the chemical compound present in the most famous cigarette.?Nicotine is a very addictive agent - Nicotine is actually a socially accepted drug.?The risk of developing an addiction to this substance is the combination of pharmacological, genetic, psychological, and socioeconomic factors;?the behavior of these addicts is similar to that of addicts to other drugs.

The criteria used to define and diagnose nicotine dependence can be grouped into two: a group that takes into account the signs and symptoms of tolerance and withdrawal;?the other group includes behaviors related to the continuation of nicotine consumption.

Tolerance is defined as the need to use more and more nicotine to achieve the desired physiological or psychological effect.?When the use of the substance is stopped abruptly, related symptoms appear.?So-called "substance-seeking behavior" may also appear in consumers.?Dependence on the substance becomes evident after compulsive use of it.

Genetics

Genes that influence nicotine metabolism and subsequent nicotine tolerance play an important role in determining individual dependence.?People who possess more efficient alleles of genes (that is, who do not feel the acute adverse effects of smoking such as nausea and headaches) are at a higher risk of developing nicotine dependence.?The CYP2A6 and CYP2D6 genes encode proteins that participate in nicotine metabolism;?some individuals show less active alleles of these genes, they have been shown to smoke less than people with more active genes.

Certain polymorphic alleles of genes for the dopamine D2 receptor are also implicated in the development of dependence.?Nicotine acts on the dopaminergic reticular system in the brain, where it activates receptors for nicotine which in turn stimulates the release of dopamine throughout this system.?

?Another study in lung cancer patients found that the B 1 B 2 genotype was more common in smokers than non-smokers.?Smokers with the common A 1 or B 1 alleles tend to start smoking younger and have rarely tried to quit compared to subjects with the more common?alleles.

Another functional polymorphism is found in the region of the gene for the serotonin transporter, which consists of two versions of the promoter: one long and one short.?

The short variant results in less transcription of the transporter;?individuals homozygous for this polymorphism have lower levels of serotonin reabsorption.?

The lower reabsorption of serotonin is related to aggressive and impulsive behavior, in turn, people with this type of neurotic behavior have an anxious, depressive, impulsive personality and with a greater risk of becoming dependent on nicotine.?Certain polymorphisms of the gene are responsible for smoking behavior and nicotine dependence.

Neuropharmacology and neuroendocrinology

Nicotine is a psychomotor stimulant.?The normal plasma levels of nicotine present in the smoker are between 10 and 60 ng / mL, a small limit that can easily trigger compensatory effects.?The nicotine within the central nervous system reinforces (increases) the function of neuro-regulatory mechanisms mediated by dopamine, norepinephrine,

?-endorphin;?facilitates action mediated by acetylcholine and norepinephrine and improves memory formation mediated by acetylcholine, norepinephrine and arginine vasopressin.?Reduces anxiety and tension (by increasing - ? - endorphins), depresses blood pressure and respiratory function by action on catecholamine;?it can also mediate anti-nociception and act on the reticular system (directly through dopaminergic pathways).?

Nicotine has very important effects on stress hormones: it increases the release of CRF (corticotrophin-releasing factor) and ACTH (adrenocorticotropic hormone), it also increases the release of corticosteroids.?Regulatory effects from nicotine exposure occur almost immediately;

Management of the nicotine-dependent patient

At present, there are several methods indicated for the management of patient who depends on nicotine.?Withdrawal syndrome characterized by depressed mood, insomnia, irritability, anxiety, difficulty concentrating, restlessness, decreased heart rate, and weight gain occurs when smoking is suddenly discontinued.

The aids available for the intervention are: talks with the doctor, individual counseling, group counseling, telephone counseling, self-help, nicotine replacement therapy (patches, gum, inhalers, nasal spray), antidepressants, anxiolytics, acupuncture, and exercise, among others.

Prevention of diseases associated with cigarette smoking

The harmful effects of cigarette smoking on health have been illustrated.?Undoubtedly, cigarettes are a great public health problem.?Laws should prevent smoking in public places or where the health of those who do not smoke is affected at all costs.?

Likewise, they should prevent the sale of any form of tobacco to minors.?The medical literature reports on the powerful effect that cigarette advertisements have on the decision to start smoking and on the decision to continue smoking.?

Although proposals to reduce consumption should be born from the highest spheres of power, doctors and other health professionals and students of health sciences can and should play an important role in raising awareness among the population,

Lack of incentives can be the cause of doctors avoiding meddling in smoking prevention programs.?

However, the doctor can easily start awareness: through posters on the walls of their offices, handing out small flyers with information on the harmful effects, making a small talk about diseases related to cigarettes, making analogies about occupations. of the patient and the toxins of cigarette smoke (for example that the smoke contains formaldehyde and that this substance is used in the preservation of corpses or cyanide that was used in the execution chambers during the Second World War).?Delivering an individualized message has better effects on the patient;?likewise, take care not to hurt susceptibilities in smokers.

Intervention in adolescents is of vital importance and requires special attention.?In this group are potential smokers and therefore, the focal points of intervention of tobacco companies.

Conclusion

Cigarettes contain substances that are harmful to health, including many known carcinogens.?These poisons cause cancer of the lung, of the aero-digestive tract, of the esophagus, of the stomach, of the paranasal sinuses, of the cervix, adenocarcinoma of the renal parenchyma, carcinoma of the renal pelvis, leukemia, pancreatic cancer, and liver cancer.?Cigarette smoke can also trigger the destruction of lung tissue resulting in the appearance of chronic obstructive pulmonary disease that decreases the quality of life of those who acquire it.?Cardiovascular events and the higher incidence of respiratory infections are also a consequence of cigarette smoking.

Unfortunately, these effects are not limited to smokers but affect those who are periodically exposed to smoke (passive smokers), they show high risks of acquiring "smoking diseases".

Against this background, all those who work in the health area must play an active role in the prevention of cigarette consumption, making use of political pressure, but also building from their trades.