Cigarette smoke is a complex aerosol produced by the combustion of dried tobacco leaves, generating thousands of chemical substances that pose severe health risks to both smokers and non-smokers [1]. Among its most harmful constituents are , a highly addictive stimulant affecting the , , which impairs oxygen delivery by binding to , and , a carcinogenic mixture that accumulates in the lungs and contributes to respiratory diseases like [2]. The smoke contains over 7,000 chemicals, including known carcinogens such as , , and , which damage DNA and increase the risk of cancers, particularly [3]. Exposure occurs not only through active smoking but also via , which significantly raises the risk of cardiovascular diseases and respiratory conditions in non-smokers [4]. The addictive nature of nicotine, mediated through , reinforces dependency by stimulating the release of in the brain's reward system [5]. Public health organizations such as the and the recognize tobacco use as the leading preventable cause of death globally, responsible for over 90% of lung cancer cases and a major contributor to and [6]. Comprehensive strategies involving legislation, taxation, and cessation support through and are essential to reduce tobacco-related morbidity and mortality [7].

Chemical Composition of Cigarette Smoke

Cigarette smoke is a highly complex aerosol generated by the combustion of dried tobacco leaves, producing thousands of chemical substances with significant health implications. This intricate mixture arises not only from the burning of tobacco but also from the combustion of paper and various additives used in cigarette manufacturing [1]. The chemical profile of cigarette smoke is divided into two main phases: a gaseous phase, which constitutes approximately 87% of the smoke, and a particulate phase, known as total particulate matter (TPM), which includes and other condensed substances [9]. This section details the major chemical constituents, their formation during combustion, and the analytical methods used to study them.

Major Chemical Components and Their Health Impacts

The smoke from a single cigarette contains over 7,000 identified chemicals, of which at least 70 are classified as carcinogenic to humans by the International Agency for Research on Cancer (IARC) [10]. These substances are responsible for the wide array of diseases associated with smoking, including , , and .

  • : This primary alkaloid in tobacco is the key agent responsible for . It is a potent stimulant that rapidly crosses the blood-brain barrier, binding to in the and triggering the release of in the brain's reward system, which reinforces dependency [5].
  • : A colorless, odorless gas produced by the incomplete combustion of organic material, CO binds to with an affinity 200-250 times greater than oxygen, forming carboxyhemoglobin. This drastically reduces the oxygen-carrying capacity of the blood, leading to tissue hypoxia and contributing to cardiovascular strain and damage [12].
  • : This term refers to the sticky, brown residue of the particulate phase of smoke. It is a complex mixture of chemicals, including numerous carcinogens, that deposits in the lungs. Tar is a major contributor to lung damage, causing chronic bronchitis, emphysema, and acting as a primary carcinogen in the development of lung cancer [13].
  • : A volatile organic compound and a known human carcinogen (IARC Group 1), formaldehyde is a potent irritant to the respiratory tract. It is formed during the pyrolysis of sugars and other organic compounds in tobacco and is linked to cancers of the nose and throat [3].
  • : An aromatic hydrocarbon and a well-established carcinogen, benzene is formed during the incomplete combustion of tobacco. Chronic exposure is strongly associated with an increased risk of leukemia, particularly acute myeloid leukemia [15].
  • : This toxic compound damages the cilia lining the bronchial tubes, impairing the lungs' natural defense mechanism for clearing mucus and pathogens. This leads to chronic respiratory infections and contributes to the development of obstructive lung diseases [2].
  • : These are a class of organic compounds formed during the incomplete combustion of organic matter. A prominent example is benzo[a]pyrene, a potent mutagen that forms DNA adducts, leading to genetic mutations and cancer initiation, particularly in the lungs [17].
  • : These are among the most potent carcinogens in tobacco smoke, formed by the nitrosation of nicotine and other tobacco alkaloids during curing and combustion. Key TSNAs like NNK (4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone) and NNN (N'-nitrosonornicotine) are directly linked to cancers of the lung, oral cavity, esophagus, and pancreas [18].
  • Heavy metals: Cigarette smoke contains toxic heavy metals such as , , , and chromium, which are absorbed by tobacco plants from the soil. These metals accumulate in the body over time, contributing to kidney damage, cardiovascular disease, and neurotoxicity [19].

Formation of Chemicals During Combustion

The chemical composition of cigarette smoke is a direct result of the complex thermochemical processes that occur during combustion. The burning of a cigarette is a dynamic process that involves two primary phases: the high-temperature combustion (flame) at the tip, which can reach up to 880°C, and the lower-temperature pyrolysis and distillation of tobacco further down the cigarette [9].

  • During the mainstream combustion (when a smoker takes a puff), the high temperature leads to the production of gases like carbon monoxide, carbon dioxide, and volatile organic compounds (VOCs).
  • The sidestream smoke, which is emitted from the smoldering end of the cigarette between puffs, is produced at lower temperatures (around 400°C) and in an oxygen-poor environment. This incomplete combustion results in higher concentrations of many toxic and carcinogenic compounds, such as PAHs, carbon monoxide, and ammonia, compared to mainstream smoke [21]. This is a critical factor in the high toxicity of secondhand smoke.

Analytical Methods for Studying Cigarette Smoke

The analysis of cigarette smoke is a significant challenge due to its extreme chemical complexity and the instability of many of its components. Advanced analytical techniques are required to identify and quantify the thousands of substances present.

  • Gas Chromatography-Mass Spectrometry (GC-MS): This is the most widely used technique for analyzing volatile and semi-volatile organic compounds in smoke, such as benzene, toluene, and PAHs. It combines the separation power of gas chromatography with the identification capabilities of mass spectrometry [22].
  • Liquid Chromatography-Mass Spectrometry (LC-MS): This method is essential for analyzing non-volatile or thermally labile compounds, such as TSNAs and certain nicotine metabolites, which cannot be easily vaporized for GC-MS analysis [23].
  • Standardized Smoking Machines: To ensure reproducibility, laboratories use machines that "smoke" cigarettes according to standardized protocols (e.g., ISO 3308). These machines control the puff volume, duration, and frequency, allowing for the collection of mainstream smoke for analysis [24].
  • Biomarker Analysis: Complementary to smoke analysis, the measurement of biomarkers in biological samples (e.g., cotinine in urine or blood) provides a direct measure of an individual's exposure to tobacco smoke and its metabolites [25].

These sophisticated methodologies are crucial for toxicological risk assessment, regulatory compliance, and the development of public health policies aimed at reducing the harm caused by tobacco use.

Health Effects of Active and Passive Smoking

Cigarette smoke poses severe health risks to both individuals who actively smoke and those exposed to secondhand smoke, affecting multiple organ systems and significantly increasing the risk of chronic diseases and premature death. The complex mixture of over 7,000 chemicals in tobacco smoke includes known carcinogens, toxins, and addictive substances that damage the body through various biological mechanisms. These effects are not limited to the lungs but extend to the , , and other vital organs, making tobacco use one of the leading preventable causes of disease and mortality worldwide [6].

Immediate and Short-Term Effects of Active Smoking

The physiological effects of cigarette smoke begin within seconds of inhalation. , the primary addictive agent in tobacco, is rapidly absorbed into the bloodstream and reaches the brain in approximately 10 seconds, where it stimulates the release of in the brain's reward system, producing temporary feelings of pleasure and alertness [27]. This immediate neurochemical response reinforces the habit and contributes to dependency.

Concurrently, other components of smoke induce acute physiological changes:

  • Increased heart rate and elevated blood pressure due to nicotine's stimulation of the sympathetic nervous system [28]
  • Reduced oxygen delivery to tissues caused by , which binds to with an affinity 200–250 times greater than oxygen, forming carboxyhemoglobin and impairing oxygen transport [27]

Additional short-term effects include irritation of the respiratory tract, coughing, increased mucus production, and bronchoconstriction. Despite these adverse effects, the body begins to recover quickly after cessation: within 20 minutes, heart rate and blood pressure return to normal; within 48 hours, taste and smell start to improve, and the body begins eliminating toxins [30]. However, cessation can trigger withdrawal symptoms such as irritability, anxiety, difficulty concentrating, and increased appetite, which are transient and diminish over time [27].

Long-Term Health Consequences of Active Smoking

Chronic exposure to cigarette smoke leads to cumulative damage across multiple organ systems, resulting in some of the most serious and life-threatening diseases known to medicine.

Respiratory System Damage

The respiratory system bears a significant burden of tobacco-related disease. Smoking is the leading cause of chronic respiratory conditions, including:

  • Chronic bronchitis, characterized by persistent cough and excessive mucus production
  • **Chronic obstructive pulmonary disease (COPD)]], a progressive condition involving airflow obstruction and declining lung function [32]

The risk of developing lung cancer is dramatically elevated among smokers. It is estimated that smoking is responsible for approximately 90% of lung cancer cases in men and 70% in women [33]. This risk is driven by carcinogens such as , , and , which cause DNA adducts and mutations in critical genes like TP53 and KRAS [17].

Cardiovascular Disease

Smoking profoundly damages the cardiovascular system, increasing the risk of:

  • Atherosclerosis, due to endothelial dysfunction and plaque formation in arteries
  • **Myocardial infarction (heart attack)]]
  • **Stroke]]
  • **Peripheral artery disease]] [35]

Mechanisms include chronic inflammation, oxidative stress, reduced nitric oxide availability, and increased thrombosis. Smokers have up to 3–5 times higher risk of cardiovascular disease compared to non-smokers [36]. However, quitting smoking leads to rapid improvements: after one year, the risk of cardiovascular disease is halved; after five to ten years, it approaches that of a never-smoker [37].

Other Cancers and Systemic Effects

Beyond lung cancer, smoking increases the risk of malignancies in multiple organs, including:

  • Mouth, pharynx, and larynx
  • Esophagus
  • Bladder
  • Pancreas
  • Kidney [38]

The systemic toxicity of smoke also affects fertility, pregnancy outcomes (increasing risks of preterm birth and low birth weight), and accelerates skin aging. Furthermore, smoking is associated with type 2 diabetes, osteoarticular diseases, and immune system impairment [39].

Health Risks of Passive Smoking

Passive smoking, or secondhand smoke exposure, occurs when non-smokers inhale smoke exhaled by smokers or emitted from the burning end of a cigarette. This involuntary exposure is a major public health concern, as it contains the same toxic and carcinogenic substances found in mainstream smoke, including , , and [40].

Cardiovascular and Respiratory Effects

Even brief exposure to secondhand smoke can cause immediate harm:

  • A 25–30% increased risk of cardiovascular diseases, including heart attack and stroke, due to endothelial dysfunction, increased blood pressure, and thrombosis [40]
  • A 20–30% increased risk of lung cancer in non-smokers [40]
  • Exacerbation of asthma and increased incidence of respiratory infections, bronchitis, and pneumonia

The composition of sidestream smoke—emitted between puffs—is often more toxic than mainstream smoke because it is generated at lower temperatures and without filtration, resulting in higher concentrations of carcinogens and finer particulate matter (PM2.5) that penetrate deeper into the lungs [21].

Risks to Children and Vulnerable Populations

Children are particularly vulnerable to the effects of secondhand smoke. In Italy, approximately one in five children is exposed to secondhand smoke, primarily in the home environment [44]. This exposure increases the risk of:

  • Otitis media (middle ear infections)
  • Bronchitis and pneumonia
  • Impaired lung development
  • Sudden infant death syndrome (SIDS) [45]

Pregnant women exposed to secondhand smoke face higher risks of preterm delivery, intrauterine growth restriction, and placental complications, as toxins like carbon monoxide and nicotine cross the placenta and impair fetal oxygenation [46].

Sidestream vs. Mainstream Smoke: Toxicological Differences

The health risks of passive smoking are amplified by the chemical and physical differences between mainstream and sidestream smoke:

  • Sidestream smoke is produced at lower temperatures (~400 °C) and under oxygen-poor conditions, leading to incomplete combustion and higher concentrations of many toxins, including nicotine, formaldehyde, and carbon monoxide [47]
  • It contains smaller particulate matter, allowing deeper lung penetration and greater systemic absorption
  • It persists longer in indoor environments, contributing significantly to indoor air pollution [21]

Sidestream smoke constitutes about 85% of secondhand smoke, making it the primary contributor to passive exposure and associated health risks [49].

No Safe Level of Exposure

Critically, there is no safe level of exposure to cigarette smoke, whether active or passive. The World Health Organization (WHO) and the Istituto Superiore di Sanità (ISS) emphasize that even low levels of exposure increase the risk of cancer, cardiovascular disease, and respiratory illness [50]. This principle underpins public health recommendations that only completely smoke-free environments can fully protect non-smokers.

Benefits of Smoking Cessation

Quitting smoking yields substantial and measurable health benefits:

  • Within 20 minutes, heart rate and blood pressure normalize
  • Within one year, cardiovascular risk is halved
  • After ten years, the risk of lung cancer is significantly reduced and approaches that of a never-smoker [51]

Access to evidence-based interventions such as , counseling, and support from can significantly increase the likelihood of successful quitting [52]. The integration of pharmacological and behavioral approaches, including , is recommended by international guidelines as the most effective strategy for overcoming both physical and psychological dependence [53].

Carcinogenic and Toxic Mechanisms of Tobacco Smoke

Cigarette smoke exerts its detrimental health effects through a complex array of chemical constituents that act via multiple biological pathways, leading to the development of cancer, cardiovascular disease, and respiratory disorders. The combustion of tobacco generates over 7,000 chemicals, including more than 70 known human carcinogens and numerous toxicants that induce cellular damage through mechanisms such as DNA adduct formation, oxidative stress, chronic inflammation, and endothelial dysfunction [3]. These mechanisms operate synergistically, amplifying the overall toxic burden on the body.

Carcinogenic Mechanisms: DNA Damage and Mutagenesis

The carcinogenic potential of tobacco smoke is primarily driven by its ability to cause direct and indirect damage to cellular DNA, leading to mutations in critical oncogenes and tumor suppressor genes. This process is mediated by several classes of carcinogens present in the particulate and gaseous phases of smoke.

One of the most potent groups of carcinogens is the tobacco-specific nitrosamines (TSNAs), such as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and N'-nitrosonornicotine (NNN). These compounds are formed during the curing and combustion of tobacco and are metabolically activated in the body into reactive intermediates. These intermediates form covalent bonds with DNA, creating DNA adducts that disrupt normal replication and repair processes [18]. The resulting mutations in key genes like KRAS and TP53 are frequently observed in lung, oral, and pancreatic cancers, driving uncontrolled cellular proliferation and tumorigenesis [56]. Furthermore, TSNAs can bind to , promoting tumor cell survival and proliferation, thereby linking carcinogenesis with the addictive properties of tobacco [56].

Another major class of carcinogens is the polycyclic aromatic hydrocarbons (PAHs), such as benzo[a]pyrene. These compounds are products of incomplete combustion and, like TSNAs, are metabolized into highly reactive epoxides. These metabolites form bulky DNA adducts, which are particularly effective at inducing mutations in the TP53 gene, a hallmark of many smoking-related cancers, especially [17]. The presence of these adducts in the lung tissue of smokers provides direct evidence of the genotoxic impact of smoke exposure.

Additionally, benzene, a volatile organic compound in smoke, is a well-established hematotoxin and carcinogen. Chronic exposure damages the bone marrow and causes genetic alterations in hematopoietic stem cells, significantly increasing the risk of developing acute myeloid leukemia [15]. The combined action of these and other carcinogens, such as formaldehyde and arsenic, results in a cumulative mutagenic load that overwhelms the body's DNA repair mechanisms, initiating and promoting the development of various cancers, including those of the larynx, bladder, and esophagus [60].

Toxic Mechanisms in Cardiovascular Disease

The cardiovascular toxicity of cigarette smoke arises from a combination of factors that impair blood vessel function, promote atherosclerosis, and increase the risk of thrombotic events like myocardial infarction and stroke.

A primary mechanism involves hypoxia induced by carbon monoxide (CO). CO binds to hemoglobin with an affinity 200-250 times greater than that of oxygen, forming carboxyhemoglobin and drastically reducing the blood's oxygen-carrying capacity [12]. This chronic oxygen deprivation places significant stress on the myocardium, increasing cardiac workload and contributing to ischemic heart disease.

Simultaneously, nicotine plays a critical role by stimulating the sympathetic nervous system. It triggers the release of adrenaline and noradrenaline, leading to tachycardia, elevated blood pressure, and vasoconstriction [62]. This chronic activation of the cardiovascular system accelerates vascular damage. Moreover, nicotine promotes the proliferation of vascular smooth muscle cells and contributes to endothelial dysfunction by reducing the production of nitric oxide (NO), a key vasodilator [63]. This dysfunction is a critical early step in the development of atherosclerosis.

The smoke also directly damages the vascular endothelium, triggering a state of chronic inflammation. This inflammatory response leads to the recruitment of immune cells and the formation of atherosclerotic plaques. The risk of cardiovascular events is substantially elevated in smokers, who face a 2- to 4-fold higher risk of developing coronary heart disease, stroke, and peripheral arterial disease compared to non-smokers [64].

Toxic Mechanisms in Respiratory Disease

The respiratory system is directly exposed to the highest concentrations of smoke constituents, leading to a cascade of pathological changes that result in chronic obstructive pulmonary disease (COPD), including chronic bronchitis and emphysema.

The tar fraction of smoke, a complex mixture of organic compounds, deposits in the airways and alveoli. This deposition damages the ciliated epithelial cells of the bronchial lining, impairing the mucociliary clearance system. This failure allows mucus and pathogens to accumulate, leading to chronic bronchitis, characterized by a persistent cough and recurrent infections [65].

Key toxicants like formaldehyde and hydrogen cyanide further exacerbate respiratory damage. Formaldehyde is a potent irritant that causes chronic inflammation of the airways, while hydrogen cyanide inhibits cytochrome c oxidase, a crucial enzyme in cellular respiration, thereby damaging lung tissue at a metabolic level [66].

The hallmark of emphysema is the destruction of alveolar walls. This is driven by smoke-induced chronic inflammation, which recruits neutrophils and macrophages to the lungs. These inflammatory cells release proteolytic enzymes, such as elastase, which break down the elastic fibers of the alveoli. The resulting loss of alveolar structure severely impairs gas exchange, leading to progressive shortness of breath and respiratory failure [32]. This process is further accelerated by an imbalance between proteases and their inhibitors, a condition known as the protease-antiprotease imbalance.

Role of Sidestream Smoke and Passive Exposure

The toxicity of tobacco smoke is not limited to the mainstream smoke inhaled by the smoker. Sidestream smoke, which is generated from the smoldering end of a cigarette between puffs, is often more toxic than mainstream smoke. It is produced at lower temperatures and with less oxygen, resulting in higher concentrations of many carcinogens and toxicants, including carbon monoxide, nicotine, formaldehyde, and PAHs [21]. Sidestream smoke also contains smaller particulate matter (PM2.5), which can penetrate deeper into the lungs and the systemic circulation.

Secondhand smoke, which is composed of approximately 85% sidestream smoke and 15% exhaled mainstream smoke, exposes non-smokers to these hazardous compounds. This involuntary exposure significantly increases the risk of lung cancer and cardiovascular disease in non-smokers, highlighting that the carcinogenic and toxic mechanisms of tobacco smoke affect not only active users but also the broader population [50].

Nicotine Addiction and Neurobiological Effects

Nicotine, the primary psychoactive alkaloid in tobacco, is the principal agent responsible for the addictive properties of cigarette smoke. Its potent effects on the initiate a complex cascade of neurobiological changes that lead to both physical and psychological dependence, making smoking cessation one of the most challenging behavioral modifications to achieve. The addictive potential of nicotine is comparable to that of other controlled substances like heroin or cocaine, as it hijacks the brain's natural reward pathways to create a powerful cycle of reinforcement [70].

Mechanism of Action in the Brain

When inhaled, nicotine is rapidly absorbed through the lungs and reaches the brain within 10 to 20 seconds, crossing the blood-brain barrier due to its high lipophilicity [27]. Its primary mechanism of action involves binding to and activating specific receptors in the brain known as (nAChRs), which are ligand-gated ion channels composed of various subunits, most notably α4β2 and α7 [72]. The activation of these receptors triggers a depolarization of neurons, leading to the release of a wide array of neurotransmitters.

The most critical neurochemical event in nicotine addiction is the surge of in the brain's reward circuitry, particularly in the , a key component of the mesolimbic pathway [73]. This dopamine release produces immediate sensations of pleasure, gratification, and euphoria, which strongly reinforce the act of smoking. Beyond dopamine, nicotine also stimulates the release of other neurotransmitters that contribute to its diverse effects: and increase alertness and heart rate, can elevate mood, enhances attention and cognitive function, and help reduce stress and pain, providing a powerful, albeit temporary, sense of emotional relief [74].

Neuroadaptations and Tolerance

Chronic exposure to nicotine induces significant neuroplastic changes in the brain. A hallmark of this adaptation is the up-regulation of nAChRs, where the brain increases the number of these receptors in response to the persistent presence of nicotine [75]. This neuroadaptation leads to tolerance, meaning that over time, the smoker requires higher or more frequent doses of nicotine to achieve the same pleasurable effects. This process alters the functionality of neural networks involved in learning, memory, and impulse control, embedding the smoking behavior deeply into the smoker's daily routines and cognitive processes [76]. Furthermore, research has identified additional molecular mechanisms, such as the activation of intracellular signaling pathways like MAPK/ERK and epigenetic modifications, which help to stabilize the addicted state [77].

The Withdrawal Syndrome and Negative Reinforcement

When nicotine intake ceases, the brain's adapted state is disrupted, leading to a well-defined syndrome of withdrawal. The absence of nicotine results in a temporary dysfunction of the reward system and a state of dopaminergic hypofunction, manifesting as a cluster of distressing physical and psychological symptoms. These include intense cravings, anxiety, irritability, depressed mood, difficulty concentrating, insomnia, and a significant increase in appetite [78]. The rapid onset of these symptoms—often within hours of the last cigarette—creates a powerful negative reinforcement cycle. The smoker is driven to resume nicotine use not to achieve pleasure, but to obtain rapid relief from the discomfort of withdrawal. This mechanism of avoiding negative states is a primary driver for the chronic maintenance of the addiction [79].

Comparison with Other Psychoactive Substances

Nicotine is considered one of the most addictive substances known, with an addiction potential that surpasses that of alcohol, cocaine, and even heroin according to some comparative assessments [80]. Its unique power lies in its method of delivery and pharmacokinetics. The rapid delivery of nicotine to the brain via smoking creates an almost instantaneous "hit," while its short half-life of about two hours means its effects wear off quickly. This combination necessitates frequent, repeated use throughout the day, which powerfully reinforces the addiction through classical and operant conditioning [81]. Unlike heroin, which primarily acts on the opioid system, nicotine exploits the brain's natural cholinergic system, subtly but persistently altering its normal function to create a state of dependence.

Impact on Cardiovascular and Respiratory Systems

Cigarette smoke exerts profound and damaging effects on both the and the , leading to a range of chronic diseases that are among the leading causes of preventable death worldwide. The complex mixture of toxic and carcinogenic chemicals in tobacco smoke, including , , , and various aldehydes, acts synergistically to impair organ function, promote inflammation, and accelerate disease progression.

Cardiovascular Damage Mechanisms

The cardiovascular system is particularly vulnerable to the toxic components of cigarette smoke. Key mechanisms of damage include:

  • Carbon monoxide (CO): This gas binds to with an affinity 200–250 times greater than that of oxygen, forming carboxyhemoglobin and significantly reducing the blood's oxygen-carrying capacity [82]. This leads to tissue hypoxia, especially affecting oxygen-sensitive organs such as the heart and brain, and increases the workload on the [83].

  • Nicotine: While not directly carcinogenic, nicotine is a potent cardiovascular toxin. It stimulates the release of adrenaline and noradrenaline, resulting in increased , elevated , and vasoconstriction [62]. These effects increase cardiac workload and oxygen demand, predisposing smokers to ischemic events such as [85]. Nicotine also contributes to endothelial dysfunction by reducing the availability of , a key vasodilator, thereby promoting atherosclerosis [63].

  • Atherosclerosis and thrombosis: Tobacco smoke induces chronic inflammation and oxidative stress, damaging the vascular endothelium and accelerating the formation of atherosclerotic plaques [87]. Smokers have a 2 to 4 times higher risk of developing , , and compared to non-smokers [36]. The risk of acute cardiovascular events, such as heart attack, increases by 25–30% even with brief exposure to secondhand smoke [40].

  • Radical species and oxidative stress: Cigarette smoke contains over 10^15 free radicals per puff, which oxidize low-density lipoprotein (LDL) cholesterol. Oxidized LDL is readily taken up by macrophages, forming foam cells and initiating plaque development in arterial walls [90].

Respiratory System Impairment

The respiratory system bears the brunt of direct exposure to inhaled smoke, resulting in both acute irritation and chronic structural damage.

  • Tar deposition and ciliary damage: Tar, the particulate fraction of smoke, accumulates in the airways and alveoli, damaging the ciliated epithelium. This impairs the mucociliary clearance mechanism, leading to mucus buildup, chronic cough, and increased susceptibility to respiratory infections [65].

  • Chronic obstructive pulmonary disease (COPD): Smoking is the primary cause of , accounting for over 80% of cases. COPD encompasses chronic bronchitis and emphysema, characterized by persistent airflow limitation. The inflammatory response triggered by smoke recruits neutrophils and macrophages, which release proteolytic enzymes like elastase, leading to alveolar wall destruction and loss of lung elasticity [32].

  • Acrolein and aldehyde toxicity: Acrolein, a highly reactive aldehyde formed during tobacco pyrolysis, is a major contributor to respiratory damage. It irritates the airways, induces bronchoconstriction, and promotes mucus hypersecretion, exacerbating conditions like and [70]. It also contributes to systemic inflammation and endothelial dysfunction.

  • Lung cancer and mutagenesis: While not exclusive to the respiratory system, the carcinogenic impact on the lungs is profound. Carcinogens such as and form DNA adducts, causing mutations in critical genes like TP53 and KRAS, which drive the development of [17].

Impact of Secondhand Smoke

Secondhand smoke, composed primarily of sidestream smoke (85%) and exhaled mainstream smoke, poses significant risks to non-smokers. Sidestream smoke is generated at lower temperatures and undergoes incomplete combustion, resulting in higher concentrations of many toxins, including CO, nicotine, formaldehyde, and PAHs [21]. Non-smokers exposed to secondhand smoke face a 25–30% increased risk of developing cardiovascular disease and a 20–30% higher risk of lung cancer [40]. Children are especially vulnerable, with exposure linked to increased rates of bronchitis, pneumonia, asthma, and sudden infant death syndrome (SIDS) [45].

Benefits of Smoking Cessation

The damage caused by smoking is not entirely irreversible. Cessation leads to rapid and progressive improvements in both systems:

  • Within 20 minutes, heart rate and blood pressure begin to normalize [98].
  • After one year, the risk of cardiovascular disease is halved compared to that of a continuing smoker.
  • After 10 years, the risk of lung cancer decreases significantly, approaching that of a never-smoker [51].

Public health interventions, including access to , , and pharmacological treatments like varenicline, are essential to support individuals in quitting and reducing the overall burden of tobacco-related disease [52].

Public Health Burden and Epidemiology in Italy

Cigarette smoking remains a critical public health challenge in Italy, representing one of the leading preventable causes of death and disease. Despite a gradual decline in traditional cigarette use among adults over the past two decades, tobacco consumption continues to impose a substantial burden on the population, particularly through its strong association with major chronic diseases such as , , and . The epidemiological landscape is further complicated by emerging trends, including the rising use of alternative nicotine products and persistent disparities across age, gender, and geographic regions.

Prevalence and Demographic Trends

According to the most recent data from the in 2024, approximately one in four adults in Italy is a smoker, corresponding to a prevalence rate of about 24% among individuals aged 18 to 69 years [101]. This rate shows a stabilization after years of decline, indicating that tobacco use remains deeply entrenched in certain segments of the population.

A particularly concerning trend is observed among youth. While traditional cigarette smoking is decreasing among adolescents, there is a significant increase in the use of alternative nicotine delivery systems. Approximately 30.2% of young people between the ages of 14 and 17 use at least one nicotine-containing product, including conventional cigarettes, , or [101]. The phenomenon of policonsumo (poly-use), defined as the concurrent use of multiple tobacco and nicotine products, has doubled in recent years, posing new challenges for prevention and cessation efforts [103].

Gender differences in smoking prevalence persist, with higher rates among men (31.1%) compared to women (22.3%) [104]. However, the gap is narrowing, and there are signs of stabilization or even slight increases in smoking rates among younger women, which may reflect shifting social norms and targeted marketing strategies by the tobacco industry [105].

Geographic and Socioeconomic Disparities

Significant regional disparities exist in tobacco use across Italy. Southern regions, such as Sicily, Calabria, and Campania, report higher smoking rates compared to northern regions like Lombardy, Trentino-Alto Adige, and Friuli-Venezia Giulia [106]. These differences are influenced by a combination of socioeconomic factors, cultural attitudes toward smoking, and variations in the availability and utilization of smoking cessation services.

Smoking prevalence is also closely linked to socioeconomic status. Individuals with lower levels of education and income are more likely to smoke, highlighting the role of social determinants in shaping health behaviors [107]. This socioeconomic gradient contributes to health inequities, as disadvantaged populations bear a disproportionate burden of tobacco-related diseases.

Disease Burden and Mortality

The public health impact of smoking in Italy is profound. Tobacco use is responsible for over 93,000 deaths annually, accounting for approximately 15% of all deaths in the country [108]. Some estimates place the number at more than 80,000 deaths per year specifically due to lung cancer alone [109]. Additionally, smoking is linked to about 24.5% of all cancer deaths in Italy [110].

The diseases with the highest relative risk associated with smoking include:

  • Lung cancer: Smoking is responsible for about 90% of cases, with smokers facing a 15 to 30 times higher risk compared to non-smokers [111].
  • Chronic obstructive pulmonary disease (COPD): The primary cause of COPD, smoking increases the risk by 5 to 20 times [32].
  • Cardiovascular diseases: Smokers have a 60-70% higher risk of myocardial infarction and a 50% increased risk of stroke [36].

Impact of Secondhand Smoke

Exposure to contributes significantly to the overall disease burden, particularly in domestic and occupational settings. The fumes exhaled by smokers and those released from the burning end of a cigarette contain high concentrations of toxic and carcinogenic substances. In Italy, it is estimated that secondhand smoke causes thousands of premature deaths each year among non-smokers, primarily due to cardiovascular diseases and lung cancer [114]. Children exposed to secondhand smoke at home are at increased risk of respiratory infections, asthma, and impaired lung development [45].

Effectiveness of Tobacco Control Policies

The implementation of comprehensive tobacco control policies has yielded measurable public health benefits. The introduction of Law 3/2003, commonly known as the "Sirchia Law," which banned smoking in enclosed public places and workplaces, marked a turning point in Italy's approach to tobacco control. Epidemiological studies have demonstrated a significant reduction in secondhand smoke exposure following the law's enactment, evidenced by decreased levels of particulate matter (PM2.5) in public venues and lower urinary cotinine levels in non-smokers [116].

Furthermore, the legislation has been associated with a notable decline in hospital admissions for acute coronary events. A national study reported an 11% reduction in myocardial infarction hospitalizations in the years following the ban, with the most significant benefits observed among non-smokers [117]. These findings underscore the effectiveness of smoke-free policies in protecting public health and reducing the burden of tobacco-related diseases.

More recently, cities like Milan have extended smoking bans to outdoor public areas, including parks and pedestrian zones, reflecting an ongoing commitment to creating healthier environments [118]. These evolving regulations, supported by robust epidemiological evidence, are essential for sustaining progress and addressing new challenges posed by the changing tobacco landscape.

Prevention and Cessation Strategies

Tobacco use remains the leading preventable cause of death and disease globally, prompting national and international health authorities to implement comprehensive strategies aimed at reducing tobacco consumption and supporting cessation. These strategies integrate legislative, fiscal, educational, and clinical approaches to protect non-smokers, prevent youth initiation, and assist current smokers in quitting. In Italy, the and the have established evidence-based guidelines that emphasize three core objectives: protecting non-smokers from secondhand smoke, reducing the prevalence of new smokers, and promoting effective cessation programs [7].

National and European Policy Frameworks

In Italy, tobacco control is anchored in the Legge 3/2003, commonly known as the "Sirchia Law," which prohibits smoking in all enclosed public places, including bars, restaurants, workplaces, hospitals, and public transportation [120]. This landmark legislation was further strengthened by the Decreto-legge 15 settembre 2023, n. 123, later converted into Legge 13 novembre 2023, n. 159, which enhanced preventive measures and expanded smoke-free environments [121]. These policies are aligned with the recommendations of the and the European Union’s Framework Convention on Tobacco Control (FCTC), which advocate for 100% smoke-free environments as the only effective way to protect public health [50].

At the European level, the EU has adopted a multi-pronged approach to tobacco control. The Tobacco Products Directive (2014/40/EU), set for an update in 2026, mandates large, graphic health warnings on cigarette packaging, bans flavored tobacco products that appeal to youth (such as slim and aromatic cigarettes), and regulates the marketing of tobacco and nicotine products [123]. Additionally, the Directive 2003/33/EC prohibits cross-border advertising and sponsorship of tobacco products, including in sports and cultural events [124]. In 2024, the European Parliament proposed extending smoke-free zones to outdoor public areas frequented by children, such as playgrounds, school grounds, and public transport stops, with the long-term goal of achieving a "tobacco-free generation" by 2040 [125].

Fiscal and Economic Interventions

Taxation is a powerful tool in tobacco control. The Italian government has supported initiatives to increase the price of cigarettes by up to 5 euros per pack, aiming to reduce consumption, particularly among youth, and allocate the additional revenue to the [126]. This approach is supported by the EU, which in 2025 proposed a 139% increase in tobacco excise duties across member states to discourage smoking and combat illicit trade [127]. Higher prices have been shown to be especially effective in preventing smoking initiation among adolescents and encouraging cessation among low-income populations.

Clinical Support and Smoking Cessation Programs

The Italian healthcare system provides robust support for smokers seeking to quit through a network of Centri Antifumo (CAF), distributed across the country. These centers offer personalized cessation programs that combine pharmacological treatments, psychological counseling, and behavioral support [52]. The Numero Verde Antifumo (800 554 088), managed by the ISS, provides free, confidential advice and guidance to individuals attempting to quit, serving as a critical first point of contact [129].

Pharmacological interventions available through the CAF include (such as patches, gums, and inhalers), , and . In recent years, the has approved the reimbursement of innovative medications, including those based on , which are dispensed exclusively through antismoking centers to ensure proper medical supervision [130]. The integration of these treatments with behavioral support has been shown to significantly increase the success rates of quitting.

Psychological and Behavioral Interventions

Psychological factors play a crucial role in both the initiation and maintenance of smoking. Many individuals use smoking as a coping mechanism for stress, anxiety, or emotional regulation, creating a powerful psychological dependency [131]. The terapia cognitivo-comportamentale (TCC) is a cornerstone of effective cessation support, helping individuals identify triggers, modify dysfunctional beliefs (such as "smoking helps me relax"), and develop healthier coping strategies [132]. TCC addresses both positive reinforcement (the pleasure derived from nicotine) and negative reinforcement (the relief from withdrawal symptoms), breaking the cycle of addiction [133].

Digital tools, such as mobile apps and text messaging services, are increasingly used to provide ongoing support, motivational reminders, and craving management techniques, particularly among younger populations [134]. These tools enhance accessibility and adherence to cessation programs.

Monitoring and Evaluation

The effectiveness of tobacco control policies in Italy is continuously monitored through the PASSI (Progressi delle Aziende Sanitarie per la Salute in Italia) surveillance system, coordinated by the ISS. PASSI collects epidemiological data on smoking prevalence, secondhand smoke exposure, and cessation attempts, providing essential feedback for policy evaluation and refinement [135]. According to 2024 data, approximately one in four adults in Italy smokes, while 30% of youth use at least one nicotine-containing product, highlighting the ongoing challenge of youth tobacco use and the need for targeted interventions [101].

In conclusion, the prevention and cessation of tobacco use in Italy and across Europe relies on a synergistic approach that combines strict legislation, economic disincentives, accessible clinical support, and evidence-based psychological interventions. The continuous evolution of tobacco products, particularly the rise of and , necessitates adaptive policies and ongoing public health vigilance to protect population health and achieve long-term tobacco control goals.

Regulatory Policies and Smoke-Free Environments

The regulation of cigarette smoke and the establishment of smoke-free environments are critical components of public health strategies aimed at reducing the burden of disease associated with both active and passive smoking. Scientific evidence confirms that no level of exposure to tobacco smoke is safe, prompting governments and international organizations to implement comprehensive legislative frameworks to protect populations, especially vulnerable groups such as children and pregnant women [137]. These policies are grounded in robust epidemiological data demonstrating the severe health risks of secondhand smoke, including a 25–30% increased risk of cardiovascular diseases and a 20–30% higher risk of lung cancer among non-smokers [40]. The absence of a safe threshold for exposure has led to the adoption of strict, evidence-based regulations designed to eliminate tobacco smoke from public and private spaces alike.

National Legislation in Italy

Italy has been a pioneer in tobacco control legislation within Europe, particularly with the introduction of Law 3/2003, commonly known as the "Sirchia Law," which came into effect in 2005. This landmark legislation banned smoking in all enclosed public places, including bars, restaurants, workplaces, hospitals, and public transportation, with the primary goal of protecting non-smokers from the dangers of secondhand smoke [120]. The law was a direct response to the classification of secondhand smoke as a Group 1 carcinogen by the International Agency for Research on Cancer (IARC), signifying that it is definitively carcinogenic to humans [40].

The impact of this legislation has been significant. Studies conducted by the showed a marked reduction in particulate matter (PM2.5) levels in public venues and a measurable decline in hospital admissions for acute coronary events, particularly among non-smokers [116]. Furthermore, the law contributed to a shift in social norms, making smoking less socially acceptable and encouraging more smokers to attempt cessation. The legislation has been reinforced by subsequent decrees, such as the Decree-Law of September 15, 2023, converted into Law 159 of November 13, 2023, which further strengthened preventive measures and addressed emerging challenges posed by new tobacco products [121].

European Union Framework and Recommendations

At the European level, tobacco control is guided by the recommendations of the and the , which are aligned with the World Health Organization's (WHO) Framework Convention on Tobacco Control (FCTC). The EU has established a comprehensive regulatory framework through directives such as Directive 2014/40/EU, which governs the manufacture, presentation, and sale of tobacco and related products. This directive mandates large, graphic health warnings on packaging, bans the use of characterizing flavors (such as menthol) that appeal to youth, and prohibits misleading terms like "light" or "mild" [123].

A key EU recommendation, issued on November 30, 2009, calls on member states to ensure 100% smoke-free environments in all indoor public places, workplaces, and public transport to protect public health [144]. In 2024, the European Parliament advanced new proposals to extend smoke-free policies to outdoor areas frequently used by children and families, such as playgrounds, public transport stops, and restaurant terraces, reflecting a growing consensus on the need for comprehensive protection [125]. The ultimate goal is to create a "tobacco-free generation" by 2040, a vision that requires sustained political commitment and cross-border cooperation.

Expansion to Outdoor and Public Spaces

Recognizing that secondhand smoke exposure is not limited to indoor environments, there has been a growing trend to extend smoke-free regulations to outdoor public spaces. In Italy, cities like Milan have taken the lead. In 2025, the Milan City Council approved a new regulation that extends the smoking ban to all outdoor public areas, including parks, gardens, and pedestrian zones, to further reduce public exposure and promote healthier urban living [118]. This move is supported by evidence that sidestream smoke, which makes up the majority of secondhand smoke, contains higher concentrations of some toxins than mainstream smoke and can linger in the air, posing a risk even in open areas [21].

The expansion of smoke-free zones to outdoor settings is also driven by concerns over thirdhand smoke—the residual contamination of surfaces and dust with toxic chemicals from tobacco smoke—which can be particularly harmful to children who crawl and play on contaminated floors [40]. These policies are part of a broader strategy to denormalize smoking and reduce the visibility of tobacco use, thereby decreasing its appeal, especially to young people.

Economic and Fiscal Measures

Regulatory policies are complemented by economic instruments designed to reduce tobacco consumption. A cornerstone of this approach is the imposition of high excise taxes on tobacco products. The EU's Directive 2011/64/EU sets minimum levels of excise duty on manufactured tobacco, and in 2025, the European Commission proposed a significant increase—up to 139%—to further discourage consumption and combat illicit trade [127]. In Italy, a public campaign has advocated for increasing the price of cigarettes by 5 euros, with the additional revenue directed toward the National Health Service (SSN) [126].

These fiscal measures are highly effective, particularly in reducing smoking initiation among youth and low-income populations, who are more price-sensitive. The combination of high prices, comprehensive smoke-free laws, and public awareness campaigns creates a powerful deterrent against tobacco use and supports those who wish to quit.

Monitoring, Enforcement, and Public Support

The success of regulatory policies depends on effective monitoring and enforcement. In Italy, the PASSI (Progressi delle Aziende Sanitarie per la Salute in Italia) surveillance system, coordinated by the , tracks smoking prevalence and exposure to secondhand smoke, providing essential data to evaluate the impact of policies and guide future interventions [135]. Public support for smoke-free laws is generally high, especially once the benefits are realized, such as improved air quality and health.

National support systems, such as the anti-smoking centers (Centri Antifumo) and the free helpline 800 554 088, play a crucial role in helping individuals quit by providing access to , counseling, and behavioral support [52]. The integration of these services with regulatory policies ensures a holistic approach to tobacco control, addressing both the environmental and individual dimensions of the smoking epidemic. This multi-faceted strategy, combining legislation, taxation, education, and cessation support, represents the most effective way to reduce the immense public health burden of tobacco use.

Emerging Trends: E-Cigarettes and Heated Tobacco Products

The landscape of tobacco consumption is undergoing a significant transformation with the rise of alternative nicotine delivery systems, particularly e-cigarettes and heated tobacco products (HTPs). These devices have gained substantial popularity, especially among younger demographics, as they are often marketed as less harmful alternatives to traditional combustible cigarettes. However, their long-term health effects, role in smoking cessation, and impact on public health remain subjects of intense scientific and regulatory scrutiny.

E-Cigarettes: Mechanism and Chemical Composition

E-cigarettes, also known as vapes or electronic nicotine delivery systems (ENDS), operate by heating a liquid—commonly referred to as e-liquid or vape juice—to produce an aerosol that users inhale. Unlike traditional cigarettes, e-cigarettes do not involve the combustion of tobacco, which significantly alters their chemical output [153]. The e-liquid typically contains a base of propylene glycol and vegetable glycerin, water, flavorings, and, in many cases, nicotine [154].

While the absence of combustion reduces the formation of many toxicants found in cigarette smoke, e-cigarette aerosols are not harmless. They can contain potentially harmful substances such as formaldehyde, acetaldehyde, and acrolein, particularly when devices are used at high temperatures or with malfunctioning components [153]. Some flavoring agents may also degrade into toxic compounds when heated, posing additional risks to respiratory health [156]. Notably, e-cigarette aerosols contain levels of carcinogens that are estimated to be 10 to 25 times lower than those in conventional cigarette smoke, suggesting a reduced but not eliminated toxicological risk [157].

Heated Tobacco Products: A Middle Ground?

Heated tobacco products, such as IQOS, represent another category of alternative nicotine delivery systems. These devices heat processed tobacco leaves to a controlled temperature—typically around 350 °C—without burning them, thereby releasing nicotine and other volatile compounds in an aerosol form [158]. By avoiding combustion, HTPs significantly reduce the production of harmful chemicals compared to traditional cigarettes, with studies indicating up to a 95% reduction in the concentration of certain toxicants [159].

However, HTPs are not risk-free. Independent research has detected the presence of tobacco-specific nitrosamines (TSNAs), aromatic hydrocarbons, and even radionuclides like polonium-210 in the aerosol produced by these devices, albeit at lower levels than in cigarette smoke [160]. The nicotine delivered by HTPs maintains a high potential for addiction, and the long-term effects on the respiratory system and cardiovascular health are still not fully understood [161]. Furthermore, the perception of reduced harm may lead to dual use with combustible cigarettes, undermining their potential as a harm reduction tool.

Health Implications and Regulatory Perspectives

From a toxicological standpoint, both e-cigarettes and HTPs present a lower risk profile than traditional cigarettes due to the absence or reduction of combustion-related toxins [153]. However, this reduction does not equate to safety. The inhalation of any foreign chemical substance poses inherent risks, and cases of severe lung injury, such as EVALI (E-cigarette or Vaping product use-Associated Lung Injury) in the United States, have highlighted the potential dangers, particularly with unregulated or contaminated products [163].

Regulatory bodies such as the and the in Italy emphasize that neither e-cigarettes nor HTPs are recommended as first-line tools for smoking cessation [164]. While they may offer a harm reduction strategy for adult smokers unable or unwilling to quit nicotine entirely, their use among non-smokers, especially adolescents, is a major public health concern. The appealing flavors, sleek designs, and aggressive marketing of these products have contributed to a significant increase in youth nicotine use, raising fears of a new generation becoming addicted to nicotine [165].

Trends Among Youth and the Challenge of Policonsumo

Recent data from Italy highlight a worrying trend: while traditional cigarette use among adolescents is declining, the use of e-cigarettes and HTPs is on the rise. In 2024, approximately 30% of young people between the ages of 14 and 17 reported using at least one nicotine-containing product, and the phenomenon of policonsumo—the concurrent use of multiple tobacco and nicotine products—has doubled in recent years [101]. This pattern of use complicates cessation efforts and may perpetuate nicotine dependence.

Metanalyses have shown that non-smoking youth who use e-cigarettes are at a significantly higher risk of transitioning to combustible cigarette use, with relative risks ranging from 2.2 to 3.5 [167]. This gateway effect, combined with the neurobiological vulnerability of the adolescent brain to nicotine addiction, underscores the need for stringent regulations on marketing, flavor bans, and age restrictions to protect young people [168].

Conclusion: Balancing Harm Reduction and Public Health Protection

E-cigarettes and heated tobacco products represent a complex and evolving challenge for public health policy. While they may offer a less harmful alternative for adult smokers, their widespread appeal to youth and the lack of long-term safety data necessitate a cautious approach. The and other health authorities advocate for comprehensive regulation that promotes harm reduction for current smokers while preventing initiation among non-smokers [134]. Rigorous monitoring, independent research, and evidence-based policies are essential to ensure that these emerging trends do not undermine decades of progress in tobacco control.

Psychological and Social Factors in Tobacco Use

Tobacco use is driven not only by the pharmacological effects of but also by a complex interplay of psychological, emotional, and social factors that influence both the initiation and maintenance of smoking behavior. In Italy, as in many other countries, these factors are deeply embedded in individual identity, social interactions, and cultural norms, particularly during adolescence—a critical period for the development of lifelong habits.

Psychological and Emotional Drivers of Smoking Initiation

The decision to start smoking is often rooted in psychological and emotional needs rather than a simple desire for nicotine. Adolescence, a stage marked by identity formation and emotional volatility, is the most common period for smoking initiation [131]. Key psychological motivators include the search for identity and self-affirmation, where smoking is perceived as a symbol of maturity, independence, or rebellion against authority [131]. This desire to assert autonomy can override awareness of health risks, especially when smoking is framed as an act of personal freedom.

Another major factor is the use of smoking as a coping mechanism for negative emotions. Many young people turn to cigarettes to manage anxiety, stress, insecurity, or emotional discomfort [172]. However, this strategy is counterproductive: long-term studies show that smoking can actually exacerbate symptoms of anxiety and depression, creating a vicious cycle of emotional dependence [173]. The temporary relief provided by nicotine reinforces the behavior, making it difficult to discontinue.

Curiosity and normalization also play significant roles. Exposure to smoking in family members, peers, or media can normalize the behavior, making it appear common or even attractive [165]. In Italy, despite public health efforts, smoking is still perceived by some youth as a socially acceptable or trendy behavior, especially with the aggressive marketing of products like that are often presented as modern, safe, or stylish alternatives [165].

Social Influences and Peer Pressure

Social dynamics, particularly peer pressure and the desire for belonging, are among the most powerful predictors of smoking initiation. The fear of social exclusion—often linked to the psychological phenomenon known as FOMO (Fear of Missing Out)—can drive adolescents to smoke to gain acceptance within a group [176]. Smoking becomes a shared ritual, reinforcing social bonds and group identity [131]. This effect is amplified in environments where smoking is prevalent among peers, creating a self-reinforcing social norm.

In adulthood, social smoking often persists in specific contexts such as after meals, during work breaks, or in social gatherings, where the act of smoking is intertwined with relaxation and conversation [178]. These behavioral routines become deeply ingrained, making cessation difficult even when health concerns are acknowledged.

Psychological Mechanisms of Behavioral Reinforcement

The maintenance of smoking behavior is sustained by powerful psychological reinforcement mechanisms. The positive reinforcement provided by nicotine—its rapid stimulation of the brain's reward system and the release of —creates a strong association between smoking and feelings of pleasure, alertness, and improved concentration [179]. This immediate gratification reinforces the habit, making it resistant to change.

Equally important is negative reinforcement, where smoking alleviates the unpleasant symptoms of nicotine withdrawal, such as irritability, anxiety, difficulty concentrating, and cravings [133]. The relief from these symptoms reinforces the behavior, creating a cycle in which smoking is used to maintain emotional equilibrium [181].

Over time, classical conditioning strengthens the habit. Neutral stimuli—such as drinking coffee, finishing a meal, or feeling stressed—become conditioned triggers that automatically elicit the urge to smoke [182]. These cues can provoke intense cravings even in the absence of physical dependence, making them a major obstacle to quitting [183].

Cognitive Distortions and Barriers to Quitting

Many smokers struggle with cognitive distortions that hinder cessation efforts. A common belief is that smoking helps with relaxation or stress management, when in reality, the perceived relief is due to the temporary resolution of withdrawal symptoms rather than a true anxiolytic effect [184]. This self-deception perpetuates the illusion that smoking is beneficial, reducing motivation to quit.

Additionally, cognitive dissonance arises when smokers are aware of the health risks but continue to smoke. To reduce this internal conflict, individuals may rationalize their behavior with thoughts like "I don't smoke that much" or "I'll quit soon," which serve to minimize guilt and delay action [185].

Fear of failure and low self-efficacy are also significant barriers. Many smokers have attempted to quit multiple times and fear another relapse, leading to discouragement and resignation [186]. This lack of confidence in one’s ability to quit can prevent individuals from even attempting cessation.

Cultural and Contextual Factors in Italy

In the Italian context, smoking is often embedded in social rituals and daily routines, such as smoking after meals or during social gatherings, which reinforces its role as a cultural practice [187]. While smoking rates among adults have declined, there is a growing concern about the rise in use of nicotine-containing products among youth, including e-cigarettes and heated tobacco products [101].

This shift is driven by marketing strategies that target young people with appealing flavors and digital lifestyles, transforming nicotine use into a form of social status or digital identity [165]. As a result, the psychological profile of young users is evolving, with increasing rates of poly-use—the simultaneous use of multiple nicotine products—posing new challenges for prevention and intervention [103].

Interventions Targeting Psychological and Social Factors

Effective smoking cessation programs must address these psychological and social dimensions. Cognitive-behavioral therapy (CBT) is a cornerstone of behavioral intervention, helping individuals identify triggers, modify dysfunctional beliefs (e.g., "smoking helps me relax"), and develop healthier coping strategies [132]. CBT also teaches techniques for managing cravings, such as "urge surfing" and mindfulness, and focuses on relapse prevention through personalized action plans [192].

Pharmacological support, such as , , or , is most effective when combined with psychological interventions, as it addresses the physical dependence while therapy targets the behavioral and emotional components [192]. In Italy, the integration of these approaches is supported by the national network of smoking cessation centers (Centri Antifumo), which offer multidisciplinary care, and the national quitline (800 554 088), providing free, evidence-based counseling [52].

Environmental interventions, such as smoke-free policies in public places and workplaces, also play a crucial role by reducing exposure to triggers and normalizing non-smoking behavior [195]. Digital tools, including mobile apps and text messaging programs, offer continuous support and have been shown to improve adherence to cessation efforts, particularly among younger populations [134].

In conclusion, the psychological and social dimensions of tobacco use are central to understanding why people start smoking and why they find it so difficult to quit. Addressing these factors through integrated, personalized, and culturally sensitive interventions is essential for achieving sustainable smoking cessation and reducing the overall burden of tobacco-related disease.

References