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Tobacco smoking: Health impact, prevalence, correlates and interventions

Robert west.

a Department of Behavioural Science and Health , University College London , London, UK

Background and objectives : Despite reductions in prevalence in recent years, tobacco smoking remains one of the main preventable causes of ill-health and premature death worldwide. This paper reviews the extent and nature of harms caused by smoking, the benefits of stopping, patterns of smoking, psychological, pharmacological and social factors that contribute to uptake and maintenance of smoking, the effectiveness of population and individual level interventions aimed at combatting tobacco smoking, and the effectiveness of methods used to reduce the harm caused by continued use of tobacco or nicotine in some form.

Results and conclusions : Smoking behaviour is maintained primarily by the positive and negative reinforcing properties of nicotine delivered rapidly in a way that is affordable and palatable, with the negative health consequences mostly being sufficiently uncertain and distant in time not to create sufficient immediate concern to deter the behaviour. Raising immediate concerns about smoking by tax increases, social marketing and brief advice from health professionals can increase the rate at which smokers try to stop. Providing behavioural and pharmacological support can improve the rate at which those quit attempts succeed. Implementing national programmes containing these components are effective in reducing tobacco smoking prevalence and reducing smoking-related death and disease.

Introduction

The continued popularity of tobacco smoking appears to defy rational explanation. Smokers mostly acknowledge the harm they are doing to themselves and many report that they do not enjoy it – yet they continue to smoke (Fidler & West, 2011 ; Ussher, Brown, Rajamanoharan, & West, 2014 ). The reason is that nicotine from cigarettes generates strong urges to smoke that undermine and overwhelm concerns about the negative consequences of smoking, and the resolve not to smoke in those trying to stop (West & Shiffman, 2016 ). Progress is being made in many countries in reducing smoking prevalence but it remains one of the main causes of ill health and premature death worldwide (Gowing et al., 2015 ).

This paper provides a broad overview of smoking in terms of: the health effects, benefits of stopping, prevalence and patterns of use, psychological, pharmacological and social factors leading to uptake and maintenance of the behaviour, effectiveness of population level and individual level interventions to combat it, and methods used to reduce the harm despite continued use of tobacco or nicotine.

Definitions of smoking and smoking cessation

Tobacco smoking consists of drawing into the mouth, and usually the lungs, smoke from burning tobacco (West & Shiffman, 2016 ). The type of product smoked is most commonly cigarettes, but can also include cigarillos, cigars, pipes or water pipes. ‘Smokeless’ tobacco is also popular in some parts of the world. This typically involves using tobacco preparations for chewing, sniffing into the nose or placing as a wad in the mouth between the cheeks and gums (Critchley & Unal, 2003 ). Smokeless tobacco use has features that are similar to smoking and can carry significant health risks (Critchley & Unal, 2003 ); however, this article focuses on smoked tobacco only as this has been the subject of by far the largest volume of research and is the most harmful form of tobacco use.

Stopping smoking usually involves an intention not to smoke any more cigarettes from a given point in time (a ‘quit attempt’), followed by self-conscious resistance of urges to smoke resulting in a period of abstinence. If someone making a quit attempt smokes one or more cigarettes on an occasion but then resumes abstinence, this is usually termed a ‘lapse’. If this person resumes smoking on a regular basis s/he is said to have ‘relapsed’. ‘Short-term abstinence’ is commonly defined in terms of achieving up to 4 weeks of abstinence. ‘Long-term abstinence’ often refers to abstinence for at least 6 months but more typically involves abstinence for at least 12 months. There is no agreed criterion for deciding when someone has ‘stopped smoking’ so it is essential when using the term to be clear about how long the abstinence period has been.

Health impact of smoking and the benefits of stopping

Tobacco smoking increases the risk of contracting a wide range of diseases, many of which are fatal. Stopping smoking at any age is beneficial compared with continuing to smoke. For some diseases, the risk can be reversed while for others the risk is approximately frozen at the point when smoking stopped.

Health impact of smoking

Table ​ Table1 1 lists the main causes of death from smoking. Tobacco smoking is estimated to lead to the premature death of approximately 6 million people worldwide and 96,000 in the UK each year (Action on Smoking and Health, 2016b ; World Health Organization, 2013 ). A ‘premature death from smoking’ is defined as a death from a smoking-related disease in an individual who would otherwise have died later from another cause. On average, these premature deaths involve 10 years of life years lost (US Department of Health and Human Services, 2004 ). Many of these deaths occur in people who have stopped smoking but whose health has already been harmed by smoking. It also happens to be the case that smokers who do not stop smoking lose an average of 10 years of life expectancy compared with never-smokers and they start to suffer diseases of old age around 10 years earlier than non-smokers (Jha & Peto, 2014 ).

Most smoking-related deaths arise from cancers (mainly lung cancer), respiratory disease (mainly chronic obstructive pulmonary disease – COPD), and cardiovascular disease (mainly coronary heart disease) (Action on Smoking and Health, 2016b ). Smoking is an important risk factor for stroke, blindness, deafness, back pain, osteoporosis, and peripheral vascular disease (leading to amputation) (US Department of Health and Human Services, 2004 ). After the age of 40, smokers on average have higher levels of pain and disability than non-smokers (US Department of Health and Human Services, 2004 ).

Smoking in both women and men reduces fertility (Action on Smoking and Health, 2013 ). Smoking in pregnancy causes underdevelopment of the foetus and increases the risk of miscarriage, neonatal death, respiratory disease in the offspring, and is probably a cause of mental health problems in the offspring (Action on Smoking and Health, 2013 ).

People used to think that smoking was protective against Alzheimer’s disease but we now know that the opposite is the case: it is a major risk factor for both Alzheimer’s and vascular dementia (Ferri et al., 2011 ; US Department of Health and Human Services, 2004 ).

There is a positive association between average daily cigarette consumption and risk of smoking-related disease, but in the case of cardiovascular disease the association is non-linear, so that low levels of cigarette consumption carry a higher risk than would be expected from a simple linear relationship (US Department of Health and Human Services, 2004 ).

Tobacco smoke contains biologically significant concentrations of known carcinogens as well as many other toxic chemicals. Some of these, including a number of tobacco-specific nitrosamines (particularly NNK and NNN) are constituents of tobacco, largely as a result of the way it is processed, while others such as benzopyrine result from combustion of tobacco (Action on Smoking and Health, 2014b ). These chemicals form part of the particulate matter in smoke. Tobacco smoke also contains the gas, carbon monoxide (CO). CO is a potent toxin, displacing oxygen from haemoglobin molecules. However, acutely the amount of CO in tobacco smoke is too small to lead to hypoxia and the body produces increased numbers of red blood cells to compensate.

The nicotine in tobacco smoke may cause a small part of the increase in cardiovascular disease but none or almost none of the increase in risk of respiratory disease or cancer (Benowitz, 1997 , 1998 ). It is the other components of cigarette smoke that do almost all the damage. It has been proposed on the basis of studies with other species that nicotine damages the adolescent brain but there is no evidence for clinically significant deficits in cognition or emotion in adults who smoked during adolescence and then stopped (US Department of Health and Human Services, 2004 ).

Exposure to second-hand smoke carries a significant risk for both children and adults. Thus, non-smokers who are exposed to a smoky environment have an increased risk of cancer, heart disease and respiratory disease (Action on Smoking and Health, 2014a ).

Benefits of stopping smoking

Table ​ Table1 1 lists the main benefits of stopping smoking. Smokers who stop before their mid-30s have approximately the same life expectancy as never smokers (Doll, Peto, Boreham, & Sutherland, 2004 ; Pirie, Peto, Reeves, Green, & Beral, 2013 ). After the age of 35 years or so, stopping smoking recovers 2–3 months of healthy life expectancy for every year of smoking avoided, or 4–6 h for every day (Jha & Peto, 2014 ).

Stopping smoking has different effects on different smoking-related diseases. Excess risk of heart attack caused by smoking reduces by 50% within 12 months of stopping smoking. Stopping smoking returns the rate of decline in lung function to the normal age-related decline, but does not reverse this; it reduces the frequency of ‘exacerbations’ (acute attacks of breathing difficulty resulting in death or hospitalisation) in COPD patients (US Surgeon General, 1990 ). Stopping smoking ‘freezes’ the risk of smoking-related cancers at the level experienced when stopping occurs but does not decrease it in absolute terms (US Surgeon General, 1990 ).

Smokers who stop show reduced levels of stress and mood disorder than those who continue (Royal College of Physicians and Royal College of Psychiatrists, 2013 ). They also report higher levels of happiness and life satisfaction than those who continue (Shahab & West, 2009 , 2012 ). This suggests that smoking may harm mental health, though other explanations cannot be ruled out on the current evidence.

Prevalence and patterns of smoking

Smoking prevalence.

There are estimated to be approximately 1 billion tobacco smokers worldwide (Eriksen, Mackay, & Ross, 2013 ), amounting to approximately 30% of men and 7% of women (Gowing et al., 2015 ).

Cigarette smoking prevalence in Great Britain was estimated to be 16.9% in 2015, the most recent year for which figures are available at the time of writing: slightly lower in women than men (Office of National Satistics, 2016 ). Smoking in Great Britain has declined by 0.7 percentage points per year since 2001 (from 26.9% of adults in 2001). In Australia, daily cigarette smoking has declined by 0.6 percentage points per year over a similar time period (from 22.4% of adults aged 18 + years in 2001 to 14.5% in 2015) (Australian Bureau of Statistics, 2015 ). However, international comparisons are confused by different countries using a different definition of what counts as being a smoker, and different methods for assessing prevalence. Australia only counts daily smokers in their headline figures. The situation in the US is even more misleading. The headline prevalence figure for the US is below 16%, but this does not include occasional smokers and people who smoke cigarillos which are essentially cigarettes in all but name and which have become increasingly popular in recent years. So the figure for prevalence that is most comparable to the figure for Great Britain is 20% (Jamal, 2016 ).

With the above caveats in mind, the figures in Table ​ Table2 2 for smoking prevalence in world regions in men and women provide very broad estimates (Gowing et al., 2015 ). Most noteworthy is that smoking prevalence in men is more than four times that in women globally but that the difference is much less in most parts of Europe, and that Eastern Europe as a whole has the highest smoking prevalence of any region in the world.

Note: Current smoking of any tobacco product, adults aged 15 years and older, age-standardised rate, by gender. ‘Tobacco smoking’ includes cigarettes, cigars, pipes or any other smoked tobacco products. ‘Current smoking’ includes both daily and non-daily or occasional smoking. From Gowing et al. ( 2015 ).

Smoking patterns

The most common age of first trying a cigarette in countries that have been studied is 10–15 years (Action on Smoking and Health, 2015b ; Talip, Murang, Kifli, & Naing, 2016 ); take up of regular smoking usually continues up to early 20s (Dierker et al., 2008 ).

Average daily cigarette consumption among smokers in the US and UK has declined steadily since the 1970s. In the UK, it is currently 11 cigarettes per day, and non-daily smoking is very rare (Action on Smoking and Health, 2016c ; Jarvis, Giovino, O’Connor, Kozlowski, & Bernert, 2014 ). Smokers take in an average of 1–1.5 mg of nicotine per cigarette (US Department of Health Human Services, 2014 ). The US figures on patterns of smoking are distorted by not counting ‘cigarillos’ and other smoked tobacco products which are used very much like cigarettes, whose prevalence has increased in recent years (Jamal et al., 2015 ). The reduction in daily cigarette consumption has not been accompanied by a reduction in daily nicotine intake (Jarvis et al., 2014 ). This could be due to the use of other smoked tobacco products (in the case of the US) or smokers smoking their cigarettes more intensively (taking more, deeper or longer puffs).

Smokers in England spend an average of £23 per week on cigarettes and this figure is slowly rising (West & Brown, 2015 ). In the UK, hand-rolled cigarettes have become increasingly popular with 34% of smokers currently reporting use of these products (Action on Smoking and Health, 2016c ). Men and people in more deprived socio-economic groups are more likely to smoke hand-rolled cigarettes (Action on Smoking and Health, 2016c ).

In most countries, there are strong negative associations between smoking prevalence and educational level, affluence and mental health; and positive associations with alcohol use disorder and substance use disorder (Action on Smoking and Health, 2016a , 2016c ; Royal College of Physicians and Royal College of Psychiatrists, 2013 ; Talati, Keyes, & Hasin, 2016 ). In the UK, average daily cigarette consumption is higher for men than women, and higher in smokers in more deprived socio-economic groups and those with mental health problems (Action on Smoking and Health, 2016c ).

Psychological, pharmacological and social factors involved in smoking and smoking cessation

The natural history of smoking can be modelled as states and factors that influence the transition between these. Figure ​ Figure1 1 shows transitions that have been researched – the variables identified in the diagram are listed descriptively without attempting to explain how they may be connected.

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Factors associated with transitions in the natural history of smoking (parentheses indicate negative associations).

Smoking initiation

Important factors predicting initiation in western societies are: having friends who smoke, having parents who smoke, low social grade, tendency to mental health problems and impulsivity (Action on Smoking and Health, 2015b ). Transition to daily smoking follows a highly variable pattern sometimes being very rapid and sometimes taking several years (Schepis & Rao, 2005 ). Important factors predicting transition to regular smoking are: having friends who smoke, weak academic orientation, low parental support, pro-smoking attitudes, drinking alcohol and low socio-economic status (Action on Smoking and Health, 2015b ).

Smoking initiation has a ‘heritability’ (the proportion of variance in a characteristic that is attributable to genetic rather than environmental variance) of approximately 30–50% in western societies (Vink, Willemsen, & Boomsma, 2005 ). This means that differences in genetic make-up account for almost half of the difference in likelihood of starting smoking between individuals. This does not mean that environmental factors do not also play a crucial role as is evident from the very large decline in smoking initiation since the 1970s in many western countries.

The heritability of cigarette addiction (as distinct from smoking) is approximately 70–80% in western societies (Vink et al., 2005 ). Cigarette addiction here refers to the extent to which someone experiences a strong need to smoke. It is usually indexed by a combination of number of cigarettes per day and time from waking to smoking the first cigarette of the day (Kozlowski, Porter, Orleans, Pope, & Heatherton, 1994 ). It can also be indexed by the self-reported strength of urges to smoke (Fidler, Shahab, & West, 2011 ). Heritability of cigarette addiction, as indexed by failure of attempts to stop, is higher than the heritability for smoking and for initiation of smoking. This suggests that differences in genetic inheritance play a larger role in being able to stop smoking than in starting to smoke.

Cigarette addiction

Cigarette addiction stems from the fact that smoking provides highly controllable doses of the drug, nicotine, rapidly to the brain in a form that is accessible, affordable and palatable (West, 2009 ; West & Shiffman, 2016 ). Nicotine provided more slowly, for example by the nicotine transdermal patch, is much less addictive. It is possible that one or more mono-amine oxidase inhibitors in cigarette smoke add to, or synergise, the addictive properties of nicotine (Hogg, 2016 ).

The psychopharmacology of cigarette addiction is complex and far from fully understood. The following paragraphs summarise the current narrative.

Nicotine resembles the naturally occurring neurotransmitter, acetylcholine, sufficiently to attach itself to a subset of neuronal receptors for this neurotransmitter in the brain. These are called ‘nicotinic acetylcholine receptors’. When it does this with receptors in the ventral tegmental area in the midbrain, it causes an increased rate of firing of the nerves projecting forward from that area to another part of the brain called the nucleus accumbens. This causes release of another neurotransmitter called dopamine in the nucleus accumbens.

Dopamine release and uptake by neurones in the nucleus accumbens is believed to be central to all addictive behaviours. It acts as a neural ‘teaching signal’ which causes the brain to form an association between the current situation as perceived and the impulse to engage in whatever action immediately preceded this release. In the case of smoking, this creates an urge to smoke in situations in which smoking frequently occurs. These are often referred to as ‘cue-driven smoking urges’ or ‘situational cravings’ (West, 2009 ; West & Shiffman, 2016 ). This explains why even non-daily smokers often find it difficult to stop smoking altogether.

Repeated ingestion of nicotine from cigarettes causes changes to the functioning of the ventral tegmental area and nucleus accumbens such that when brain concentrations of nicotine are lower than usual, there is an abnormally low level of neural activity in these regions. This leads to feelings of need for behaviours that have in the past restored normal functioning, typically smoking. This feeling of need can be thought of as a kind of ‘nicotine hunger’, also called ‘background craving’ (West, 2009 ; West & Shiffman, 2016 ). This is probably why time between waking and first cigarette of the day is a useful predictor of difficulty stopping smoking (Vangeli, Stapleton, Smit, Borland, & West, 2011 ). So ‘cue-driven smoking urges’ and ‘nicotine hunger’ are important factors contributing to smoking behaviour and thought to be the primary mechanisms underpinning cigarette addiction (West, 2009 ; West & Shiffman, 2016 ).

When smokers abstain from cigarettes, within a few hours many of them start to experience nicotine withdrawal symptoms. Withdrawal symptoms from a drug are temporary symptoms that arise when the drug dose is reduced or use is terminated. They arise from neural adaptation to the presence of the drug in the central nervous system. For smoking, the most common early onset symptoms are: irritability, restlessness and difficult concentrating. Depression and anxiety have also been observed in some smokers. These symptoms typically last 1 to 4 weeks (West, 2009 ; West & Shiffman, 2016 ).

After a day or two of stopping smoking, many smokers experience other symptoms: increased appetite, constipation, mouth ulcers, cough, and weight gain. Increased appetite tends to last for at least 3 months; weight gain (averaging around 6 kg) tends to be permanent; other symptoms tend to last a few weeks. The increased appetite, weight gain and constipation arise from termination of nicotine intake but the others are probably related to other effects of stopping smoking (West, 2009 ; West & Shiffman, 2016 ).

Any of the above effects of abstinence may in individual cases promote resumption of smoking following a quit attempt but statistically the association is inconsistent and weak; the main factors driving relapse appear to be cue-driven smoking urges and nicotine hunger (Fidler & West, 2011 ; West, 2009 ; West & Shiffman, 2016 ).

Many smokers report that smoking helps them cope with stress and increases their ability to concentrate. However, this appears to be because when they go for a period without smoking they experience nicotine withdrawal symptoms that are relieved by smoking. Long-term smokers who stop report lower levels of stress than when they were smoking and no reduction in ability to concentrate (West, 2009 ; West & Shiffman, 2016 ).

It is commonly thought that smokers with mental health problems are using cigarettes to ‘self-medicate’ or treat their psychological symptoms. However, the evidence indicates that neither nicotine nor smoking improves psychological symptoms, and people with serious mental health disorders who stop smoking do not experience a worsening of mental health. In fact some studies have found an improvement (Royal College of Physicians and Royal College of Psychiatrists, 2013 ).

Smoking cessation

For most smokers, cessation requires a determined attempt to stop and then sufficient resolve in the following weeks and months to overcome what are often powerful urges to smoke. Factors that predict quit attempts differ from those that predict the success of those attempts (Vangeli et al., 2011 ). Approximately 5% of unaided quit attempts succeed for at least 6 months (Hughes, Keely, & Naud, 2004 ). Relapse after this point is estimated to be around 50% over subsequent years (Stapleton & West, 2012 ).

The most common self-reported reasons for smoking are stress relief and enjoyment, with around half of smokers reporting these smoking motives. Weight control, aiding concentration and socialising are also quite commonly cited (Fidler & West, 2009 ). Smoking for supposed stress relief, improved concentration, weight control or other functions has not been found to be related to attempts to stop or success of attempts to stop (Fidler & West, 2009 ). Smokers who report enjoying smoking are less likely to try to stop but not less likely to succeed if they do try (Fidler & West, 2011 ). In addition, having a positive smoker identity (liking being a smoker) predicts not trying to quit, over and above enjoyment of smoking (Fidler & West, 2009 ).

No clear association has been found between the number of times smokers have tried to stop in the past and their chances of success the next time they try (Vangeli et al., 2011 ). However, having tried to stop in the past few months is predictive of failure of the next quit attempt (Zhou et al., 2009 ). Belief in the harm caused by smoking is predictive of smokers making quit attempts but not the success of those attempts (Vangeli et al., 2011 ).

Some clinical studies have found that women were less likely to succeed in quit attempts than men but large population studies have found no difference in success rates between the genders (Vangeli et al., 2011 ) so it may be the case that women who seek help with stopping have greater difficulty than men who seek help with stopping.

Number of cigarettes smoked per day, time between waking and the first cigarette of the day and rated strength of urges to smoke prior to a quit attempt have been found to predict success of quit attempts (Vangeli et al., 2011 ).

Quit attempts that involve gradual reduction are less likely to succeed than those that involve quitting abruptly, even after controlling statistically for measures of cigarette addiction, confidence in quitting, other methods used to quit (e.g. nicotine replacement therapy) and sociodemographic factors (Lindson-Hawley et al., 2016 ).

Interventions to combat smoking

There is extensive evidence on interventions that can reduce smoking prevalence, either by reducing initiation or promoting cessation. Table ​ Table3 3 lists those that have the strongest evidence.

Population-level interventions

Increasing the financial cost of smoking through tax increases and control of illicit supply on average reduces overall consumption with a typical price elasticity globally of 0.4 (meaning that for every 10% increase in the real cost there is a 4% decrease in the number of cigarettes purchased). Most of the effect is in getting smokers to reduce their daily cigarette consumption so the effect on smoking prevalence has been found to be an average of a 1–2 percentage point prevalence reduction for every 10% increase in the real cost (Levy, Huang, Havumaki, & Meza, 2016 ). It has been claimed that increasing taxes on tobacco increases the amount of smuggling of cheap tobacco, but the evidence does not support this (Action on Smoking and Health, 2015a ; Joossens & Raw, 2003 ).

Social marketing campaigns (e.g. TV advertising) can prevent smoking uptake, increase the rate at which smokers try to quit and improve the chances of success. This can lead to a reduction in smoking prevalence. Their effectiveness varies considerably with intensity, type of campaign and context (Bala, Strzeszynski, Topor-Madry, & Cahill, 2013 ; Hoffman & Tan, 2015 ).

Legislating to ban smoking in all indoor public areas may have a one-off effect on reducing smoking prevalence but findings are inconsistent across different countries (Bala et al., 2013 ). For example, in countries such as France it was not possible to detect an effect while in England, there did appear to be a decline in prevalence following the ban.

Although it is hard to show conclusively, circumstantial evidence suggests that banning tobacco advertising and putting large graphic health warnings on cigarette packets may have reduced smoking prevalence in some countries (Hoffman & Tan, 2015 ; Noar et al., 2016 ).

Individual-level interventions to promote smoking cessation

Brief advice.

Brief advice to stop smoking from a physician and offer of support to all smokers, regardless of motivation to quit, has been found in randomised trials to increase rate of quitting by an average of 2 percentage points of all those receiving it, whether or not they were initially interested in quitting (Stead et al., 2013 ). The offer of support appears to be more effective in getting smokers to try to quit than just advising smokers to stop (Aveyard, Begh, Parsons, & West, 2012 ).

Pharmacotherapy

Using a form of nicotine replacement therapy (NRT: transdermal patch, chewing gum, nasal spray, mouth spray, lozenge, inhalator, dissolvable strip) for at least 6 weeks from the start of a quit attempt increases the chances of long-term success of that quit attempt by about 3–7 percentage points if the user is under the care of a health professional or provided as part of a structured support programme (Stead et al., 2012 ). Some studies have found that NRT when bought from a shop and used without any additional structured support does not improve the chances of success at stopping (Kotz, Brown, & West, 2014a , 2014b ). A small proportion of people who use NRT to stop smoking continue to use it for months or even years after stopping smoking, but NRT appears to carry minimal risk to long-term users (Royal College of Physicians, 2016 ; Stead et al., 2012 ).

Data are sparse but at present, using an electronic cigarette in a quit attempt appears to increase the chances of success at stopping on average by an amount broadly similar to that from NRT; the variety of products available and the greater similarity to smoking appear to make them more attractive to many smokers as a means of stopping than NRT (McNeill et al., 2015 ; Royal College of Physicians, 2016 ). Electronic cigarettes deliver nicotine to users by heating a liquid containing nicotine, propylene glycol or glycerol and usually flavourings to create a vapour that is inhaled. They appear to carry minimal acute risk to users. If they are used long-term, their risk is almost certainly much less than that of smoking (based on concentrations of chemicals in the vapour) (McNeill et al., 2015 ; Royal College of Physicians, 2016 ).

‘Dual-form NRT’ (combining a transdermal NRT patch and one of the other forms) increases the chances of success at stopping more than ‘single-form NRT’ (just using one of the products) (Stead et al., 2012 ). Starting to use a nicotine transdermal patch several weeks before the target quit date may improve the chances of success at quitting compared with starting on the quit date (Stead et al., 2012 ).

Taking the prescription anti-depressant, bupropion (brand name Zyban), improves the chances of success of quit attempts by a similar amount to single-form NRT (Hughes, Stead, Hartmann-Boyce, Cahill, & Lancaster, 2014 ). Bupropion often leads to sleep disturbance and carries a very small risk of seizure. Bupropion probably works by reducing urges to smoke rather than any effect on depressed mood, but how it does this is not known. It is contra-indicated in pregnant smokers and people with an elevated seizure risk or history of eating disorder (Hughes et al, 2014 ). Taking the tricyclic anti-depressant, nortriptyline also improves the chances of success of quit attempts, probably by about the same amount as bupropion and NRT (Hughes et al., 2014 ). Its mechanism of action is not known. Nortriptyline often leads to dry mouth and sleep disorder and can be fatal in overdose (Hughes et al., 2014 ).

Taking the nicotinic-acetylcholine receptor partial agonist, varenicline (brand name Chantix in the US and Champix elsewhere), improves the chances of success by about 50% more than bupropion or single-form NRT (Cahill, Lindson-Hawley, Thomas, Fanshawe, & Lancaster, 2016 ). This is true for smokers with or without a psychiatric disorder (Anthenelli et al., 2016 ). Varenicline appears to work both by reducing urges to smoke and the rewarding effect of nicotine should a lapse occur (West, Baker, Cappelleri, & Bushmakin, 2008 ). Varenicline often leads to sleep disturbance and nausea. Serious neuropsychiatric and cardiovascular adverse reactions have been reported, but in comparative studies these have not been found to be more common than placebo or NRT (Anthenelli et al., 2016 ; Cahill et al., 2016 ; Sterling, Windle, Filion, Touma, & Eisenberg, 2016 ).

Taking the nicotinic-acetylcholine receptor partial agonist, cytisine, appears to improve the chances of success at least as much as single-form NRT and probably more (Cahill et al., 2016 ). Cytisine often causes nausea. No serious adverse reactions have been reported to date (Cahill et al., 2016 ). Where it is licensed for sale, cytisine is less than 1/10th the cost of other smoking cessation medications (Cahill et al., 2016 ).

Behavioural support

There is good evidence that behavioural interventions of many kinds, delivered though several modalities can help smokers to stop. Thus, behavioural support (encouragement, advice and discussion) from a trained stop-smoking specialist, provided at least weekly until at least 4 weeks following the target quit date can increase the chances of long-term success of a quit attempt by about 3–7 percentage points, whether it is given by phone or face-to-face (Lancaster & Stead, 2005 ). Group behavioural support (specialist-led groups of smokers stopping together and engaging in a structured discussion about their experiences), involving at least weekly sessions lasting until at least 4 weeks after the target quit date can increase the chances of success of a quit attempt by a similar amount or possibly more than individual support (Stead & Lancaster, 2005 ). Scheduled, multi-session telephone support can improve rates of success at stopping smoking by a broadly similar amount (Stead, Hartmann-Boyce, Perera, & Lancaster, 2013 ) but some large studies have failed to detect an effect so contextual factors and/or the precise type of support could be crucial to success. The effects of behavioural support and medication/NRT on success at stopping smoking appear to combine roughly additively (Stead, Koilpillai, & Lancaster, 2015 ). Smoking cessation support appears to be effective in primary care, secondary care and worksite settings (Cahill & Lancaster, 2014 ; West et al., 2015 ). Financial incentives, in the form of vouchers, have been found to increase smoking cessation rates for as long as they are in place (Cahill, Hartmann-Boyce, & Perera, 2015 ; Higgins & Solomon, 2016 ). Printed self-help materials can improve the chances of success at stopping long term by around 1–2 percentage points (Hartmann-Boyce, Lancaster, & Stead, 2014 ).

There is still relatively limited evidence on the effectiveness of digital support interventions for smoking cessation. Thus, while there is evidence that tailored, interactive websites can improve the chances of success at stopping smoking compared with no support, brief written materials or static information websites, many of those tested have not been found to be effective and it is not clear what differentiates those that are effective from those that are not (Graham et al., 2016 ). Text messaging programmes have been found to increase the chances of success of quit attempts by about 2–7 percentage points (Whittaker, McRobbie, Bullen, Rodgers, & Gu, 2016 ). There is currently insufficient evidence to know whether smartphone applications can improve success rates of quit attempts, although preliminary data suggest that they might (Whittaker et al., 2016 ). Evidence on alternative and complementary therapies is not sufficient to make confident statements about their effectiveness as aids to smoking cessation (Barnes et al., 2010 ; White, Rampes, Liu, Stead, & Campbell, 2014 ).

Overall, the highest smoking cessation rates appear to be achieved using specialist face-to-face behavioural support together with either varenicline or dual form NRT. With this support, continuous abstinence rates up to 52 weeks, verified by expired-air carbon monoxide tests, of more than 40% have been achieved (Kralikova et al., 2013 ). More commonly, 52-week continuous abstinence rates with this treatment are between 15 and 25% (West et al., 2015 ).

Smoking cessation support for pregnant smokers

In pregnant smokers, there is some evidence that NRT can help promote smoking cessation but evidence for an effect sustained to end of pregnancy is not conclusive (Sterling et al., 2016 ). There is also evidence that written self-help materials and face-to-face behavioural support can aid smoking cessation (Jones, Lewis, Parrott, Wormall, & Coleman, 2016 ), and financial incentives have also been found to improve quitting rates among pregnant smokers (Tappin et al., 2015 ). Almost half of women who stop smoking during pregnancy as a result of a clinical intervention relapse to smoking within 6 months of the birth (Jones et al., 2016 ).

Effectiveness of programmes to reduce smoking uptake

School-based programmes that involve both social competence training and peer-led social influence have been found to reduce smoking uptake (Georgie, Sean, Deborah, Matthew, & Rona, 2016 ) but educational programmes have not (Thomas, McLellan, & Perera, 2013 ). Mass media campaigns and increasing the financial cost of smoking reduce smoking uptake (Brinn, Carson, Esterman, Chang, & Smith, 2012 ; van Hasselt et al., 2015 ).

Reducing the harm from tobacco and nicotine use

Smokers who report that they are reducing their cigarette consumption smoke only 1–2 fewer cigarettes per day on average than when they say they are not (Beard et al., 2013 ). Clinical trials have found that use of NRT while smoking can substantially reduce cigarette consumption compared with placebo (Royal College of Physicians, 2016 ) but national surveys show very little reduction in cigarette consumption when smokers take up use of NRT in real-world settings (Beard et al., 2013 ). The benefit from using NRT while continuing to smoke appears to be in promoting subsequent smoking cessation. Using NRT (or varenicline) to reduce cigarette smoking with no immediate plans to quit leads to increased rates of quitting subsequently (Wu, Sun, He, & Zeng, 2015 ).

‘Snus’, a form of tobacco that is placed between the gums and the cheek and which is prepared in a way that is very low in carcinogens, gives high doses of nicotine but without evidence of an increase in risk of major tobacco-related cancers and either no, or a small, increase in risk of heart disease. It does appear to increase risk of periodontal disease, however. Snus is very popular in Sweden. Sweden has very low rates of smoking and tobacco-related disease indicating that a form of nicotine intake other than smoking can become popular and suggesting that this can contribute to a substantial reduction in tobacco-related harm (Royal College of Physicians, 2016 ).

The introduction of complete bans on smoking in indoor public areas can also be considered as a harm reduction measure. In this case, the main issue is harm to non-tobacco users. The evidence shows that such bans have been rapidly followed in the UK and several other jurisdictions by a reduction in heart attacks in non-smokers (Action on Smoking and Health, 2014a ).

Conclusions

Tobacco smoking causes death and disability on a huge scale and only about half of smokers report enjoying it. Despite this, approximately 1 billion adults engage in this behaviour worldwide and only around 5% of unaided quit attempts succeed for 6 months or more. The main reason appears to be that cigarettes deliver nicotine rapidly to the brain in a form that is convenient, and palatable. Nicotine acts on the brain to create urges to smoke in situations where smoking would normally occur and when brain nicotine levels become depleted. Concern about the harm from, and financial cost of, smoking are mostly not sufficient to counter this.

Governments can reduce smoking prevalence by raising the cost of smoking through taxation, mounting sustained social marketing campaigns, ensuring that health professionals routinely advise smokers to stop and offer support for quitting, and make available pharmacological and behavioural support for stopping.

Statement of competing interests

RW has, within the past 3 years, undertaken research and consultancy for companies that develop and manufacture smoking cessation medications (Pfizer, GSK, and J&J). He is an unpaid advisor to the UK’s National Centre for Smoking cessation and Training. His salary is funded by Cancer Research UK.

Disclosure statement

No potential conflict of interest was reported by the author.

This work was supported by Cancer Research UK [grant number C1417/A22962].

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  • Research article
  • Open access
  • Published: 30 June 2021

The negative impact of chronic tobacco smoking on adult neuropsychological function: a cross-sectional study

  • Mohammed Sh. Nadar   ORCID: orcid.org/0000-0003-4281-5630 1 ,
  • Abdullah M. Hasan 2 &
  • Mohammed Alsaleh 2  

BMC Public Health volume  21 , Article number:  1278 ( 2021 ) Cite this article

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The evidence on the effects of chronic tobacco smoking on neuropsychological functions is conflicting. The literature remains limited by inconsistent accounting for potentially confounding biomedical and psychiatric conditions. This study aimed to assess the neuropsychological functions of adult chronic tobacco smokers in comparison to group-matched non-smokers.

The study included 73 smokers and 84 group-matched non-smokers. The data was collected during the year 2019. After an initial interview to collect demographics and smoking profile, the subjects undertook neuropsychological assessments that targeted a wide range of cognitive domains.

The performance of smokers was poorer on almost all neuropsychological domains, namely selective attention ( p  ≤ .001, p  = .044), alternating attention ( p  = .002) working memory ( p  ≤ .001), Short-term memory ( p  = .006 and .003), Long-term memory ( p  ≤ .001), processing accuracy ( p  ≤ .001), and executive function ( p  = .011 and .026). Smokers were intact on processing speed. Smoking accumulation and lower age onset of regular smoking were correlated with lower neuropsychological function.

Our findings add to the growing body of evidence suggesting that chronic tobacco smoking impacts cognition negatively.

Peer Review reports

In 2015, around a quarter (24.9%) of the global population were current users of some form of tobacco [ 1 ]. Smoking is one form of tobacco exposure that is prevalent across the world.

The harmful impact of chronic tobacco smoking on physical health is well documented and includes cardiovascular diseases, respiratory diseases, and various forms of cancer [ 2 ]. Additionally, chronic smoking is implicated in the pathogenesis of neuropsychological dysfunction and has been directly linked to increased risk of depression and cognitive impairment [ 1 , 3 , 4 ].

A large number of studies have examined the effects of smoking on neuropsychological function across multiple variables. Compared to non-smokers, chronic smoking was cumulatively reported to have detrimental effects on various neuropsychological domains, including general intellectual abilities, processing speed, attention, memory, cognitive flexibility and executive functions [ 2 , 3 , 5 ]. The effects of smoking on cognition are believed to vary based on the dose and onset of regular use. Although the majority of studies provide evidence on the effect of chronic tobacco smoking on neuropsychological impairments, conflicting evidence also exists. For example, a 10-year longitudinal study of 1436 older adults found that smokers were less likely to develop cognitive impairment than those who had never smoked [ 6 ]. Another study consisting of 2553 adults found smokers to have lower rates of cognitive impairment compared to non-smokers [ 7 ], and both studies concluded that smoking may be protective of cognitive function. Several other studies also support the notion that cigarette smoking seems not to affect cognition or to have a positive effect on some aspects of cognitive function of smokers [ 8 , 9 , 10 , 11 ].

Based on the current literature, it is difficult to draw solid conclusions on the impact of smoking on neuropsychological function [ 2 ]. The influence of tobacco smoking on specific domains of cognition is complex and much remains to be known about its impact on neuropsychology and cognition. The literature remains limited by inconsistent accounting for potentially confounding biomedical and psychiatric conditions. For example, many of the studies did not account for confounding variables such as psychiatric disorders and comorbid substance abuse (i.e., alcohol, cannabis, and other drugs). In other studies, the duration of tobacco use was not taken into account [ 12 ]. Other studies varied in terms of which subcategories of specific neuropsychological domains were tested. Some controversy also remains regarding smoking effect on specific cognitive functions, and individual differences in smoking cognitive effects. Consequently, it is essential to continue to investigate the association between chronic tobacco smoking and potential neuropsychological impairments while controlling for possible confounding variables. This cross-sectional study aimed to assess the neuropsychological functions of chronic tobacco smokers in comparison to group-matched non-smokers. It was hypothesized that chronic tobacco smokers would have significantly poorer global neuropsychological functions compared to non-smokers.

Participants and procedure

We recruited the participants via social medial and local adverts during the year 2019. The participants were interviewed regarding cigarette smoking and use of other tobacco products. We excluded participants who reported current use of other substances that are known to affect cognition (i.e., alcohol, cannabis, and psychotropic medications, except for caffeine) up to 3 months prior to study enrollment. Since psychiatric illness is strongly correlated to cognitive impairment, we excluded subjects with any known psychiatric problems or mental diseases. Participants with any medical condition or history of serious head injury that are known to influence cognition were also excluded. To be included in the smoking group, the participant must have been a smoker for at least 10 years and smoked a minimum of one pack per day. The smokers and non-smokers were matched as a group for age, sex, ethnicity, educational, and socioeconomic status. Past smokers and second-hand smokers were excluded from the non-smokers’ group.

The study was approved by the Institutional Review Board, and all participants signed a written consent form to participate in the study before data collection. An initial interview collected information related to socio-demographic, health, and smoking profiles. After the interview session, all participants completed a comprehensive battery of outcome measures assessing neuropsychological functions that target a wide range of cognitive domains. All the measures used in this study have well-established and comprehensive psychometric properties, and were used in other studies on neuropsychological function (a brief description of each measure is provided in Table  1 ). In addition to the neuropsychological measures, we used the Grooved Pegboard (Lafayette Instrument, Lafayette, IN) as a measure of fine motor dexterity, which requires visual-spatial and motor coordination. The test battery was administered by a trained researcher, and the entire battery required about 60–70 min to complete. The participants were allowed short breaks between tests, and smokers were free to smoke during the breaks if desired. The sequence of outcome measures was administered consistently across all participants.

After completion of all measures, the participants were presented with two questions which they were required to answer by “Yes” or “No”. 1) “Do you believe that smoking increases the risk of physical health problems, such as getting heart disease, lung disease, stroke and cancer?”, and 2) “Do you believe that smoking increases the risk of cognitive health problems, such as reduced memory, attention, and concentration?”.

Statistical analysis

All statistical analysis was performed with Statistical Package for the Social Sciences (SPSS – Windows version 25; SPSS Inc., Chicago, IL). Comparison between groups of participants in terms of demographic characteristics and quantitative outcome measures were performed using t-tests for normally distributed data. Where homogeneity of variance was violated in a given model (Levine’s test), we used the Mann-Whitney U test for skewed data. Two-tailed statistics were used, and statistical significance was set at P  < 0.05. Cohen’s D effect sizes were reported when significant effects of group on a cognitive variable were identified. Pearson correlations were used to assess the influences of the smoking variables of accumulation (number of years smoking), Cigarettes/day, and Pack-Years of smoking and decline in cognitive function.

The final sample included 73 smokers (M = 52.1 years, SD = 7.2) and 84 non-smokers (M = 51.7 years, SD = 8.1). Independent t-tests showed that both groups were comparable across participant socio-demographic and health characteristics. Table  2 shows the general characteristics of the study population.

Data for all neuropsychological tasks are summarized in Table  3 . In the Montreal Cognitive Assessment (MoCA), both groups performed above the cutoff score of 26/30, indicating global cognition scores within the “normal” range. Nonetheless, the smokers’ group scored significantly lower than the non-smokers’ group ( p  = .042) with a moderate effect size of .49.

The Word condition (W) and Color condition (C) component of the Stroop Color and Word Test revealed no significant differences between both groups, demonstrating comparable processing speed abilities. The Color-word condition (CW) yielded a significant difference between groups ( p  ≤ .001, d = .62) demonstrating better selective attention of non-smokers. The Comprehensive Trail making test (CTMT) Trial 1 subtest, which measures processing speed, revealed no significant differences between groups, but the Trial 5 subtest revealed a significant difference ( p  = .002, d = .47) representing healthier alternating attention function of non-smokers. For the Wisconsin Card Sorting Test-64 (WCST-64), a small but significant effect size was detected in favor of the non-smokers’ group, showing a slightly better executive function capacity for non-smokers as evident by fewer Perseveration errors ( p  < .011, d = .34) and Non-perseveration errors ( p  < .026, d = 0.23).

In the Contextual Memory Test, the non-smokers’ group performed significantly better with small effect size for short-term memory ( p  = .006, d = .38), and with moderate effect size for long-term memory ( p  ≤ .001, d = .66). The Digit Span Task revealed comparable short-term memory results to the Contextual Memory Test, where the non-smokers’ group performed better than the smoking group ( p  = .003, d = .40). For working memory, a significant and large effect size of .75 was detected in favor of the non-smokers’ group ( p  ≤ .001).

The total number of items processed in the d2 Test of Attention was similar in both groups, indicating parallel processing speed. However, when factoring in the errors in performance, the smoking group had significantly poorer processing accuracy than their non-smokers’ counterpart in both measures of error (OE-Omission errors: p  ≤ .001, d = .55, CE-Commission errors: p  ≤ .001, d = .54, and TE-Total errors: p  ≤ .001, d = .67). The overall TP-Total performance of the d2 Test of Attention was significant with a small effect size ( p  = .044, d = .19) reflecting superior selective attention ability of the non-smokers’ group. As per the psychomotor domain, the non-smokers’ group outperformed the smoking group in the Grooved Pegboard test of fine motor dexterity ( p  = .007, d = .37).

A set of Pearson correlations were conducted to explore the relationship between smoking variables with scores of the neuropsychological measures. Higher smoking accumulation (total lifetime years of smoking) was significantly correlated with the lower neuropsychological performance of selective attention of the Stroop Color and Word Test ( r  = − 0.58; p  = .009), alternating attention of the Comprehensive Trail making test (CTMT) ( r  = − 0.32; p  = .027), and working memory of the Digit Span task ( r  = − 0.57; p  ≤ .001). There was an association between lifetime years of smoking and poorer performance on the Grooved Pegboard psychomotor measure of fine motor dexterity ( r  = −.41; p  = .047). The age onset of regular smoking was also correlated with the lower performance in the same measures above; namely selective attention ( r  = − 0.41; p  = .037), alternating attention ( r  = − 0.29; p  = .048), working memory ( r  = − 0.62; p  ≤ .001), and also processing accuracy of the d2 Test of Attention ( r  = − 0.46; p  = .039). There were no other significant correlations between the number of cigarettes smoked per day or Pack-Years and neuropsychological performance.

When asking the participants about the effects of smoking on health, 100% of non-smokers and 92% of smokers believe that smoking has negative effects on physical health, while 37% of non-smokers and 19% of smokers believed that smoking has negative effects on cognitive health.

The current study aimed to assess and compare the neuropsychological functions of chronic tobacco smokers in comparison to non-smokers. As hypothesized, the results indicated that chronic tobacco smokers had significantly poorer neuropsychological functions compared to their group-matched non-smokers. The poorer performance was apparent in almost all cognitive domains, namely attention, memory, processing accuracy, and executive function, but not processing speed.

With respect to global neuropsychological function, the performance of smokers in the Montreal Cognitive Assessment (MoCA) was not impaired since they scored within the “normal” range. Nonetheless, their performance was significantly weaker compared to their matched non-smokers. Despite the “normal” results of the MoCA, the more dedicated measures in this study clearly revealed a sub-optimal neuropsychological performance of our smokers’ group.

The effects of smoking on memory performance is inconsistent in the literature, with studies reporting significant differences between smokers and non-smokers in some memory measures [ 4 , 21 , 22 , 23 , 24 , 25 ] while others reporting insignificant differences [ 10 , 21 , 22 , 26 , 27 , 28 ]. Our results showed the neuropsychological domain of memory to be affected in our smoking sample and with group differences of moderate to strong effect sizes, as our non-smokers’ group outperformed the smokers in all components of memory measures. The non-smokers’ group had better short-term and long-term memory as indicated by their superior capacity to recall information in the Contextual Memory Test, which involves visual presentation of pictures, as well as the Digit Span Task, which involves auditory and verbal presentation of numbers. Working memory was particularly compromised in our chronic tobacco smokers, as evident by the largest effect size (d = .75) amongst the neuropsychological measures employed in this study. Similar results for working memory impairments were found in middle-aged adults [ 22 , 29 ], young adults [ 30 , 31 , 32 , 33 ] and even adolescent smokers [ 34 ]. Based on the compromised overall memory performance of smokers, it is plausible to state that chronic tobacco smoking may predispose the development of dementia.

While the effects of tobacco smoking on memory have been widely studied, their effects on attention have been less investigated. Attention is central for learning and memory since encoding information requires attention in the first place. The smokers in our study were less able to block irrelevant information and focus their selective attention on the task at hand. This was strongly demonstrated in the Stroop Color and Word Test and less significantly demonstrated in the d2 Test of Attention. Alternating attention was also affected in our smokers’ CTMT test, indicating more difficulty to disengage and reengage the focus of attention in response to environmental stimuli, in comparison to the non-smokers’ group. Our findings on the domain of attention are consistent with the literature where attention was found to be affected in smokers [ 28 , 31 ], but contrasted several other studies where attention was not affected [ 10 , 26 , 33 , 34 ]. Given the intertwined relationship between attention and memory, it is reasonable to suggest that smoking may diminish memory as a result of decreasing attentional capacities, reflected in reduced ability to resist distraction and blocking irrelevant stimuli.

Executive function involves the simultaneous use of a set of cognitive abilities to allow the individual to perform higher-level complex tasks. The findings in our study detected a significant executive function difference in favor of the non-smokers’ group, who performed better in both subtests of the WCST-64. These results are consistent with previous literature findings of executive function limitation among smokers [ 9 , 10 , 22 , 23 , 25 , 26 , 31 , 35 ], indicating that chronic tobacco smokers have inferior mental flexibility and abstract thinking compared to non-smokers.

Interestingly, processing speed was not significantly affected in the smoking group across all the four subtests we used in this study, albeit two of the subtests were statistically borderline ( p  = .052, .055). These findings agree with few studies [ 10 , 26 , 31 , 33 ], but contrast with most other studies that assessed processing speed for their smoking participants [ 4 , 21 , 22 , 36 , 37 , 38 ]. Despite this finding, the processing accuracy of our smokers’ sample was significantly lower than non-smokers ( p  ≤ .001). That is, the smokers’ processing speed matched that of non-smokers, but with a significantly higher number of errors. The substandard performance of smokers on measures of processing accuracy, as evident by a significantly higher number of cognitive errors, should be added to a growing list of neuropsychological sequelae associated with persistent smoking.

Within the smoker group, smoking onset was correlated with lower performance on working memory, selective attention, alternating attention, and the number of errors made. This means that individuals who start smoking at a younger age are at a greater risk of developing neuropsychological dysfunction. The impairments appear to manifest very early in smokers, as demonstrated in the inferior working memory of adolescents with a mean of only 4 years of smoking [ 34 ]. Additional support on the effects of smoking on the young brain was objectively shown in functional magnetic resonance imaging where young adult smokers had reduced prefrontal cortex activation during attentional tasks when compared with non-smokers [ 39 ]. This pronounced negative effects of smoking on the young brain might be explained by the fact that the prefrontal cortex has not completed its maturation, as the prefrontal cortex is one of the last brain areas to mature and is still developing during adolescence and early adulthood [ 40 ]. This stage of ongoing development makes the brain more susceptible to the influence of tobacco smoking and other psychoactive substances [ 40 ].

Correspondingly, smoking accumulation in this study similarly affected neuropsychological function, meaning the longer an individual smoked during their lifetime, the more prone they become to cognitive dysfunction. These results are consistent with other studies that reported total lifetime years of smoking to be correlated with inferior neuropsychological efficiency [ 22 ] and executive function [ 27 ]. Interestingly, the number of cigarettes per day or pack-years were not associated with neuropsychological performance in this study, contrasting the main findings of a recent review conducted by Conti et al. (2019), in which several studies included in their review reported a negative link between the number of pack-years and neuropsychological function [ 2 ]. This discrepancy in results may be confounded by the considerable variations in the number of pack-years reported across studies (ranging from 4.26 to 73.73) [ 2 ].

The magnitude of differences between smokers and non-smokers in this study extend beyond neuropsychological function to include the psychomotor domain as well. Our non-smokers’ group outperformed the smoking group in the Grooved Pegboard test of fine motor dexterity, albeit with a relatively small effect size of .37. Durazzo et al. [ 22 ] also reported significantly poorer fine motor dexterity performance in their smoking sample, but with much larger effect sizes (i.e., .72). The psychomotor function was also negatively correlated with smoking accumulation, where longer lifetime smoking was associated with reduced fine motor dexterity.

The question arises related to the reasons for heterogeneity in study outcomes between studies of comparable designs. For example, processing speed was reported in some studies to be reduced among smokers [ 4 , 21 , 22 , 36 , 37 , 38 ] but not in other studies [ 10 , 26 , 31 , 33 ]. The same point can be raised for memory and attention. Several reasons could explain such variations in the performance; 1) The outcome measures used to assess the target variable (i.e., processing speed) are different across studies, which may vary in their sensitivity and other psychometric properties. 2) Some studies did not report which version of the tests they used (e.g., original version, modified version, pen and paper, or electronic version). Depending on the assessment used, it could involve a visual task, an auditory task, or even a motor task. An assessment that involves the use of pen and paper will recruit a variety of motor and cognitive pathways in the brain to facilitate writing or tracing, while an electronic version of the same assessment will involve different brain pathways. Such variations in assessment components could yield different results. These factors make it less accurate to perform cross-study comparisons or to compare the study scores with normative data. A possible solution to help makes the results more comparable across studies, and thus more clinically meaningful, is to use complete reporting of the specific testing procedures (e.g., test version, subtests used, and scoring methods) and to use consistent and systematic data collection and analysis procedures.

The participants awareness about the negative effects of smoking on physical health were very high. However, their awareness about the negative effects of smoking on neuropsychological health was low, particularly among smokes (37% of non-smokers and 19% of smokers). This very low awareness of the negative consequences of smoking on neuropsychological function among smokers and non-smokers is a major public health issue that should be properly addressed.

Since tobacco smoking remains highly prevalent across the globe and is known to be influenced by public perception of risk and associations with negative outcomes [ 31 ], it is imperative to invest further in policy initiatives to control smoking. The emphasis of public health campaigns primarily focuses on physical health, and less commonly address neuropsychological health. Increasing public awareness should go beyond the already established physical health consequences to include the negative impact of smoking on neuropsychological function. We hope that raising awareness about the wider effects of tobacco smoking on cognition could help encourage people to stop smoking.

Limitations and future research

There are several limitations and areas for improvement in future research. Although we attempted group matching for demographics and health variables, the self-reported health & medical profile can be problematic due to matters of inaccuracy of some participants. Future research should adopt standardized screening measures to provide accurate objective measures. The scope of neuropsychological impairment associated with chronic cigarette smoking has yet to be fully delineated. Large-scale prospective studies with more consistent, highly sensitive, and robust cognitive outcome measures are required to determine the true links between smoking and neuropsychological dysfunction.

Chronic tobacco smoking seems to be a prospective risk factor for neuropsychological impairment, as expressed in our data by reduced attention, memory, executive function, and processing accuracy of smokers compared to their group-matched non-smokers. The cognitive performance of participants decreased as the number of years smoking increased. Similarly, the younger the age when regular smoking started, the lower was the cognitive performance. The consequences of smoking go beyond neuropsychological performance to encompass fine motor dexterity tasks as well.

Availability of data and materials

The datasets used during the current study are available from the corresponding author on reasonable request.

Abbreviations

Montreal Cognitive Assessment

Comprehensive Trail making test

Wisconsin Card Sorting Test-64

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MN designed the study, coordinated the implementation of the study and data collection, and drafted the manuscript. AH and MA managed the literature review and references cited. AH and MA reviewed and revised the manuscript. All authors have read and approved the final manuscript.

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Nadar, M.S., Hasan, A.M. & Alsaleh, M. The negative impact of chronic tobacco smoking on adult neuropsychological function: a cross-sectional study. BMC Public Health 21 , 1278 (2021). https://doi.org/10.1186/s12889-021-11287-6

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harmful effects of smoking research paper

February 14, 2024

Smoking May Compromise Immune Health, Even Years After Quitting

A new study found persistent effects of smoking on the adaptive immune system, but how this translates to health risks remains unclear

By Alejandra Manjarrez

Close-up of person in red shirt smoking a cigarette

incamerastock/Alamy Stock Photo

Numerous factors shape how a person’s immune system reacts to infections and other challenges. Age, sex and genetics are fundamental contributors—as the COVID pandemic highlighted. Now a new study shows that smoking has an equally important impact on certain immune responses, with some of its effects possibly lasting well beyond when a person quits.

To explore which environmental factors had the biggest role, researchers measured the production of cytokines—key messenger molecules that mediate inflammation—in the blood of 1,000 healthy people after exposing the samples to either bacteria, fungi, antibodies or other agents known to elicit an immune response. Smoking was found to greatly alter both the innate response—the body’s general and immediate first line of defense—and the slower, more threat-specific adaptive response. The data suggest that the cytokine secretion in the innate immune response rapidly returns to the level of nonsmokers after a person quits smoking but that the effects on the adaptive response appear to endure for years or decades through a process called epigenetic memory. The results were published today in Nature .

“It was a very large study, so that gives you confidence [in] the results,” says Yasmin Thanavala , an immunologist at Roswell Park Comprehensive Cancer Center who did not participate in the research. Moreover, “[the authors] looked across a broad range of [immune] stimuli, and that’s an interesting aspect,” she adds.

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The new findings add to the vast body of evidence on the damaging health effects of cigarette smoking. Smoking increases the risk for cardiovascular disease and lung cancer . It is responsible for about 90 percent of all lung cancer deaths and 80 percent of all deaths from chronic obstructive pulmonary disease. Smoking also harms many other organs and increases the risk of dying from nonlung cancers. Quitting smoking, on the other hand, reverses the risk for most of these diseases. But the magnitude and persistence of smoking’s effects on the immune system are less understood.

Between 2011 and 2012 a team led by researchers at the Pasteur Institute in France recruited people to donate blood and other types of samples for the Milieu Intérieur project , a population-based study designed to explore the factors that influence the variability in human immune responses, which has already resulted in the publication of several papers. The cohort comprised men and women of European descent between the ages of 20 and 69.

While the blood samples were still fresh, the team exposed each one to 11 different immune challenges or no agent (as a control) during a 22-hour period. The stimuli included Escherichia coli and influenza, which trigger the immune system’s innate response, as well as agents such as the Staphylococcus aureus enterotoxin B superantigen (SEB) that directly activate cells in the adaptive immune system called T cells. “That’s really the strength of this [analysis] because not so many studies ... look at this diversity of immune responses from the same individual,” says Darragh Duffy , an immunologist at the Pasteur Institute and senior author of the paper.

Using statistical analyses, the team assessed how sociodemographic, environmental, clinical and nutritional factors reported by each person influenced the secretion of 13 cytokines in response to the various stimuli. They found, for instance, that variations in body mass index and a latent infection with cytomegalovirus—a type of herpes virus that many people are exposed to during their lifetime—altered cytokine production in response to certain stimuli. But of all the variables the researchers studied, smoking showed the most associations with immune changes.

When exposed to E. coli , concentrations of CXCL5, a cytokine that recruits and activates white blood cells, were significantly higher in the blood of individuals who currently smoked compared with those who didn’t. In those who had quit smoking, however, CXCL5 secretion resembled that of nonsmokers. The toxin SEB, on the other hand, increased the production of the proinflammatory cytokine IL-2 and the anti-inflammatory cytokine IL-13 in the blood of people who smoked, but unlike the response to E. coli stimulation, this pattern persisted in people who had stopped smoking years or decades ago.

In the new study, “adaptive immune response changes are more long-lasting and innate immune changes are more transient, and that also makes sense,” Thanavala says. She and her colleagues have previously reported that mice exposed to cigarette smoke have a defective adaptive immune response even weeks after their last smoke exposure. The responses may improve over time, she adds, “but they never go back to a nonsmoking condition, so the effects are very long-lasting, even in our mouse system.” Findings in mice can’t always be extrapolated to humans, however.

Duffy and his colleagues found that smoking’s persistent effects on cytokine production were linked to long-lived B cell and T cell populations and changes in DNA methylation, which involves the addition of chemical markers that can modify gene activity. The researchers observed a reduction in the presence of these markers—known as DNA hypomethylation—at five genes whose low methylation levels were previously associated with smoking. The more cigarettes a person smoked and the more years they smoked, the lower these DNA methylation levels were—suggesting a dose-response effect.

The researchers aren’t sure which ingredients in tobacco are responsible for the effects, but there was nothing to suggest that it was nicotine, Duffy says. “Given those five methylation genes that are quite diverse and implicated in processing toxins, I suspect it’s not nicotine-related,” he adds. It is also unclear whether electronic cigarettes induce similar effects to those described in the new study. “They’re definitely less toxic than regular cigarettes” but still not without risk, Duffy cautions.

Toxicologist Irfan Rahman of the University of Rochester Medical Center, who was not involved in the new study, says the findings could have implications for vaccine effectiveness in smokers and former smokers. Because immune cells in these populations are so greatly affected, they might not be able to trigger a good antibody response, he says. Thanavala, who has observed that smoke exposure compromises vaccine response in mice, notes that generally, the same vaccine is given to all individuals, regardless of their smoking habits. “Maybe this will help us to understand that in people who have smoked for a long time, you need to make a different approach because their adaptive immune response is going to be poor.”

Thanavala cautions, however, that the cytokine profiles in smokers or former smokers do not translate directly to a worse adaptive immune response to real-world infections or toxin exposures. “But it’s the first step to understanding that smoking is controlling certain factors of immune function,” she says. Duffy acknowledges that his team’s approach is only a model of how an individual might respond and adds that the research “can’t say anything about [a specific] outcome to any kind of disease.” He and his colleagues are now addressing that question in a new 10-year follow-up study that includes a subset of the original cohort and will assess who remains healthy and who doesn’t.

Experts also point out the similar genetic background of the study cohort as a limitation. “Will this result hold true [in] a diverse population?” Thanavala asks. Duffy says he hopes that other researchers can replicate these findings in other populations. He adds that he and his colleagues are also testing these associations in cohort studies in Africa and Hong Kong.

Just last week another population-based study that involved more than two million people in South Korea aged 30 and older concluded that cancer risk started going down 10 years after people quit smoking. “Their message was [that] it’s always a good time to stop smoking” because you’ll start seeing benefits over time, Duffy says, adding that his team’s findings on the innate immune response are in line with that. “The best time to quit smoking is as soon as possible.”

Harmful health effects of cigarette smoking

  • Published: November 2003
  • Volume 253 , pages 159–165, ( 2003 )

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  • Salil K. Das 1  

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This is a comprehensive review on the harmful health effects of cigarette smoking. Tobacco smoking is a reprehensible habit that has spread all over the world as an epidemic. It reduces the life expectancy among smokers. It increases overall medical costs and contributes to the loss of productivity during the life span. Smoking has been shown to be linked with various neurological, cardiovascular, and pulmonary diseases. Cigarette smoke not only affects the smokers but also contributes to the health problems of the non-smokers. Exposure to environmental tobacco smoke contributes to health problems in children and is a significant risk factor for asthma. Cigarette smoke contains several carcinogens that alter biochemical defense systems leading to lung cancer.

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Das, S.K. Harmful health effects of cigarette smoking. Mol Cell Biochem 253 , 159–165 (2003). https://doi.org/10.1023/A:1026024829294

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Harmful health effects of cigarette smoking

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  • 1 Department of Biochemistry, Meharry Medical College, Nashville, TN 37208, USA. [email protected]
  • PMID: 14619966
  • DOI: 10.1023/a:1026024829294

This is a comprehensive review on the harmful health effects of cigarette smoking. Tobacco smoking is a reprehensible habit that has spread all over the world as an epidemic. It reduces the life expectancy among smokers. It increases overall medical costs and contributes to the loss of productivity during the life span. Smoking has been shown to be linked with various neurological, cardiovascular, and pulmonary diseases. Cigarette smoke not only affects the smokers but also contributes to the health problems of the non-smokers. Exposure to environmental tobacco smoke contributes to health problems in children and is a significant risk factor for asthma. Cigarette smoke contains several carcinogens that alter biochemical defense systems leading to lung cancer.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.
  • Asthma / etiology*
  • Cardiovascular Diseases / etiology*
  • Lung Neoplasms / etiology*
  • Nervous System Diseases / etiology*
  • Smoking / adverse effects*
  • Tobacco Smoke Pollution / adverse effects
  • Tobacco Smoke Pollution

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  • 2S06 GM08037/GM/NIGMS NIH HHS/United States
  • Open access
  • Published: 30 July 2021

Impact of tobacco and/or nicotine products on health and functioning: a scoping review and findings from the preparatory phase of the development of a new self-report measure

  • Esther F. Afolalu   ORCID: orcid.org/0000-0001-8866-4765 1 ,
  • Erica Spies 1 ,
  • Agnes Bacso 1 ,
  • Emilie Clerc 1 ,
  • Linda Abetz-Webb 2 ,
  • Sophie Gallot 1 &
  • Christelle Chrea 1  

Harm Reduction Journal volume  18 , Article number:  79 ( 2021 ) Cite this article

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Measuring self-reported experience of health and functioning is important for understanding the changes in the health status of individuals switching from cigarettes to less harmful tobacco and/or nicotine products (TNP) or reduced-risk products (RRP) and for supporting tobacco harm reduction strategies.

This paper presents insights from three research activities from the preparatory phase of the development of a new self-report health and functioning measure. A scoping literature review was conducted to identify the positive and negative impact of TNP use on health and functioning. Focus groups ( n  = 29) on risk perception and individual interviews ( n  = 40) on perceived dependence in people who use TNPs were reanalyzed in the context of health and functioning, and expert opinion was gathered from five key opinion leaders and five technical consultants.

Triangulating the findings of the review of 97 articles, qualitative input from people who use TNPs, and expert feedback helped generate a preliminary conceptual framework including health and functioning and conceptually-related domains impacted by TNP use. Domains related to the future health and functioning measurement model include physical health signs and symptoms, general physical appearance, functioning (physical, sexual, cognitive, emotional, and social), and general health perceptions.

Conclusions

This preliminary conceptual framework can inform future research on development and validation of new measures for assessment of overall health and functioning impact of TNPs from the consumers’ perspective.

As a leading cause of preventable morbidity and mortality worldwide, smoking remains a major public health problem. Compared with those who do not smoke, people who smoke are significantly more likely to develop heart diseases, lung cancer, chronic obstructive pulmonary disease (COPD), and other diseases [ 1 , 2 ]. It is well established that the best way to avoid the health risks associated with smoking is for people to never start and for those who smoke to quit [ 1 , 3 ]. Tobacco harm reduction is one way to alleviate the health risk for individuals who choose not to quit smoking [ 4 ], by providing less harmful tobacco and/or nicotine products (TNP), such as reduced-risk products (RRP) (used here to refer to products that present, are likely to present, or have the potential to present, less risk of harm to people who smoke and switch to these products versus continued smoking) or modified risk tobacco products (MRTP).

Several smokeless tobacco products and a heated tobacco product were recently authorized for marketing with modified risk claims through the United States (US) Food and Drug Administration (FDA) MRTP pathway [ 5 ]. The guidance on MRTP applications [ 6 ] specifies that health outcomes should be assessed during premarket evaluation and postmarket surveillance of modified risk TNPs such as these. These health outcomes comprise not only objective clinical and biological measures but also self-reported outcomes [ 6 , 7 ]. Studies and reports have recently started providing evidence on the health impact of new TNPs [ 8 ]. For instance, recent papers have investigated the effects of e-cigarettes and heated tobacco products on cardiopulmonary outcomes [ 9 , 10 , 11 , 12 , 13 , 14 ]. However, the papers have mainly focused on clinical measurements, such as spirometry and other lung function tests; consumer perception is rarely explored or the focus of the research. Measuring self-reported experience is important for understanding the changes in the health status of individuals switching from cigarettes to RRPs and is a key component of tobacco harm reduction strategies [ 7 ]. Self-reported ratings of RRP effectiveness or adverse events might differ from clinical measures and provide another perspective as useful as the clinicians. In addition, consumer perception of positive changes in health status, functioning and other behavioral outcomes will also subsequently influence use behaviors and switching to RRPs rather than continuing smoking.

Self-perceived health status is a complex concept to define and measure, particularly within the context of TNP use [ 15 ]. While generic health status measures, such as the Medical Outcomes Study 36-item Short-Form Health Survey (SF-36), have been used to evaluate the health status of people who smoke [ 16 , 17 ], comparisons have mainly been made between those who currently smoke, those who used to smoke, and those who never smoked [ 18 , 19 ]. Results from these studies strongly suggest that, in healthy populations, existing generic measures are not sensitive enough to detect change over time when stopping or switching from cigarettes to other TNPs, owing to high ceiling effects [ 20 ]. While a few smoking-specific quality of life measures have been developed, these measures have not been widely implemented or standardized [ 15 , 17 , 21 , 22 ], and the application of these smoking-specific measures to different TNP use across the risk continuum is scarce [ 20 ].

As part of the A ssessment of B ehavioral OU tcomes related to T obacco and Nicotine Products (ABOUT™) Toolbox initiative [ 23 ], the present project aims at developing a new self-report measure (ABOUT™— Health and Functioning ) to address the current gap and assess the impact of TNPs on health and functioning (including health status, functional status and other health-related quality of life constructs). This paper presents insights from three research activities [ 24 , 25 ] from the preparatory phase of development of the measure—that is, a scoping literature review, reanalysis of consumer focus groups/interviews, and expert opinion. These three activities serve as background research to support the development of a preliminary conceptual framework of health and functioning associated with the use of TNPs.

Scoping literature review

The purpose of the review was to address two main questions among individuals who use TNPs:

What are the positive and negative health and functioning impacts of TNP use?

What concepts are evaluated by measures used to assess the positive and negative impacts of TNP use?

Given the nature and breadth of the research questions and the number of potentially relevant publications, a scoping literature review was used as it provides a means of identifying the literature and mapping the concepts and evidence on a topic by using an informative and iterative research process [ 26 ]. The scoping review involved a PubMed search (August 2018) and application of Sciome’s rapid Evidence Mapping (rEM) [ 27 ], followed by additional manual screening and review. rEM is a proprietary methodology developed by Sciome ( https://www.sciome.com/ ) to rapidly summarize and produce a quantitative representation of the available body of scientific evidence in a particular area. The study by Lam et al. demonstrated a proof-of-concept application of the rEM methodology [ 27 ]. The PubMed search terms targeted qualitative and quantitative research among people who use TNPs (Table 1 ). This was supplemented by a second, parallel step of manually identifying relevant literature through other known sources. Table 2 describes the general inclusion and exclusion criteria that were applied to the scoping literature review.

After the initial rEM exercise, two reviewers (EC, SG) further manually screened the titles and abstracts of the articles identified through the automated rEM exercise against the inclusion and exclusion criteria. Finally, the selected publications underwent a full screening by two reviewers (VL and DF) for determining their relevance to the research questions for data extraction and one of the co-authors (LA-W) cross-checked the screening and resolved differences in opinion among the reviewers.

The World Health Organization (WHO) International Classification of Functioning, Disability and Health (ICF) [ 28 ] framework and the revised Wilson and Cleary [ 29 , 30 ] model were used as a guide to broadly inform categories for data extraction from the literature on TNP use and health and functioning. These established models enable the conceptualization and description of health status and functioning (the combination of which is often referred to as health-related quality of life) [ 31 , 32 ], and related outcomes and determinants. To complement and refine this and to ensure relevance to those who use TNPs, the data extracted from the literature was also grouped and labeled based on the contents of the literature reviewed.

The elements extracted from the selected papers were as follows:

Author, citation details, and publication type

Objectives and/or research questions

Sample type, size, and principle demographics

Type(s) of TNP and definitions of levels of consumption

Methodology, questionnaires, and statistical methods used

Main results

Results grouped in broad categories: Health Signs and Symptoms; General Health Perceptions; Quality of Life, Health-Related Quality of Life, and Functional Status; Individual Characteristics; Environmental and Social Characteristics; Biomarkers and Biological Endpoints.

Reanalysis of focus groups/in-depth interviews

The objective of the secondary analyses of existing qualitative data in people who use TNPs was to inform the drafting of the initial conceptual framework, as well as interview guides for planned concept elicitation qualitative studies to identify concepts and develop items to detect what is relevant to measure in this context. Two sets of qualitative data containing information related to health and functioning were reanalyzed and participants had consented for their data to be used in future studies. The first was from 29 focus groups (total number of participants n  = 229) that were originally designed to discuss perceived risk, appeal, and intent to use TNPs [ 33 , 34 ]. The focus groups—stratified by smoking status—were conducted in the United States (US; n  = 12), Japan ( n  = 4), Italy ( n  = 4), and the United Kingdom (UK; n  = 9) between December 2012 and August 2013. The second dataset included 40 in-depth interviews conducted in North Carolina, USA, with people who use TNPs, to discuss issues centered on perceived dependence on TNPs [ 35 ]. While 21 interviewees were people who were poly-TNPs users, 19 were people who were exclusive users of one of the following types of TNPs: cigarettes ( n  = 5), smokeless tobacco ( n  = 5), e-cigarettes ( n  = 5), or another type of TNP (pipes, waterpipes, or nicotine replacement therapy [NRT] products; n  = 4). These interviews were conducted in August 2017. The demographics of both data sets are presented in Table 3 . For reanalyzing the data, an initial codebook guided by the literature review data extraction categories was developed; however, new codes were created to complement these categories based on the thematic content analysis of the transcripts. The qualitative analysis software Quirkos [ 36 ] was used for the reanalysis.

Expert panel review

An expert panel consisting of five key opinion leaders (KOL) and five technical consultants was convened in August 28, 2018, in Neuchâtel, Switzerland. The KOLs were subject matter experts in the fields of nicotine and smoking cessation ( n  = 1), Patients Reported Outcomes (PRO) evaluation and scale development ( n  = 3), and health economics ( n  = 1). The consultants were experts on nicotine dependence ( n  = 1), psychometric validation ( n  = 2), market research ( n  = 1), and PRO development and validation ( n  = 1). The meeting followed an agenda and semi-structured discussion guide to facilitate conversations. First, the panel was presented with the principles underlying the tobacco harm reduction assessment strategy [ 4 ]. This session was followed by an open elicitation phase, during which two experienced moderators asked the panel to identify and discuss concepts related to health and functioning in people who use TNPs that different stakeholders might find important. Then, the panel was asked to review and respond to the concepts identified in the literature review and in the qualitative research reanalysis. These findings were discussed in depth to arrive at a consolidated preliminary conceptual framework. Each concept was presented, and the experts were asked to rank and agree on concepts to be included and how the concepts should be grouped by domains in the framework. In generating the framework, the project team and expert panel considered the themes and concepts identified under each of the categories from the scoping literature review, specific concepts from the secondary analyses of the qualitative data, and the expert panel meeting. The authors then synthesized and re-organized concepts emerging from the different preparatory phase activities under main health and functioning and conceptually-related domains. The participants also provided their input on the best strategies for planned qualitative studies to inform and support the development and validity of the proposed health and functioning measure.

The literature search identified 4761 articles. Figure  1 (flow diagram) depicts the results of the search and screening process. Titles and abstracts were screened by the rEM exercise until the machine learning algorithms predicted 97.7% relevant references; thus, 707 abstracts were not screened. After applying the inclusion/exclusion criteria to the remaining 4,054 abstracts, 281 were identified as part of the rEM exercise. After additional manual screening and review of the abstracts and articles against the inclusion/exclusion criteria, 90 full-text articles were included for data extraction [ 20 , 37 – 125 ]. Seven additional full-text articles were also included on the basis of a manual search [ 126 , 127 , 128 , 129 , 130 , 131 , 132 ]. Findings are summarized in Table 4 and a detailed description and data extracted from all the articles from the literature review is presented in Additional File 1 .

figure 1

Flow diagram Sciome’s rapid Evidence Mapping (rEM) and manual screening processes of the scoping literature review

Fifty-six publications (56/97; 58%) presented data related to health signs and symptoms . These are grouped under five core areas: mental health and cognitive functioning (28/97; 29%); pain and physical trauma (6/97; 6%); respiratory, cardiovascular and inflammatory conditions (5/97; 5%); “other” health conditions , which included insomnia, liver disease, eye health, and hearing loss (5/97; 5%); and oral health (4/97; 4%). There were also eight publications related to the effects of smoking cessation on health signs and symptoms, mostly benefits of cessation but also including perceived dependence, addiction, and withdrawal symptoms (8/97; 8%). Overall, the burden and impact of cigarette smoking on both physical and mental health symptoms was negative and generally worse among people who smoke relative to those who do not smoke. On the other hand, quitting smoking was accompanied by improvements in general physical health and psychological wellbeing. However, in spite of the positive impact of quitting smoking, loss of moments of pleasure, struggle to manage stress, the social aspects of smoking, and withdrawal symptoms were seen as barriers to quitting.

The general health perceptions of various adults who use TNPs were reported in 18 of the 97 articles (18%), with 9 of them detailing the general health perceptions related to cigarettes and 9 being related to e-cigarettes and other TNPs. Perceptions were determined by questionnaires and focus groups for evaluating the health impacts, fear of diseases, harm to others and self, social impacts (both positive [e.g., inclusion and looking “cool”] and negative [e.g., stigma and exclusion]), and other reasons for taking up or considering/attempting smoking cessation.

Quality of life, health-related quality of life, and functional status was studied in 9 of the 97 included articles (9%). These studies mostly demonstrated with generic and specific QoL, HRQoL, or functional status questionnaires that cigarette smoking was associated with a worse quality of life and that smoking cessation often resulted in an improved quality of life. However, in some cases, the use of TNPs also reportedly enabled individuals to manage their levels of anxiety and improve some aspects of social engagement and functional status.

Individual, environmental and social characteristics were found to influence the decision to smoke and/or consider or attempt to quit smoking or switching to other TNPs, as reported in 8 (8%) and 11 (11%) of 97 publications, respectively. Some key characteristics and determinants of smoking behavior included low socioeconomic status, male sex, living alone, family, and close social environment, societal stigma, and local regulations.

Finally, 12 of the 97 publications (12%) were related to studies on biomarkers and biological endpoints in people who use TNPs and showed that smoking cigarettes negatively influenced cardiovascular, respiratory, oral, renal, stress, metabolic, and inflammatory-related biomarkers and physiological assessments.

The themes from this reanalysis are summarized below and organized on the basis of the narrative of the participants of their experiences.

Perceived negative impact of smoking

Other than health, the biggest and most salient reported negative impact of smoking was the perceived lack of control related to addiction and emotional health and wellbeing. Participants reported feeling that cigarette smoking was running their lives or “holding them hostage.” They reported that this perceived lack of a sense of control or willpower often led to feelings of weakness or a feeling that they were a “slave” to cigarettes. Many respondents reported smoking even when they did not necessarily want to and experiencing feelings of obsession and craving.

Perceived lack of control and addiction were also related to the activities of the participants throughout the day. People who smoke often reported altering their activities to smoke because of patterns of behavior or routine and the experienced need for a smoke. They reported that the “need for a smoke” sensation would cause them to leave work or social events early, not attend events if smoking was not allowed, interrupt what they were doing to smoke, and get up in the middle of the night.

Fear of withdrawal symptoms, with a strong emphasis on mental/emotional health, was also prominent among reported negative impacts of smoking. This fear was often reported as limiting the willingness of individuals to try to quit smoking or facilitating a return to prior smoking behavior. Individuals reported fearing the following symptoms they associated with withdrawal: mood swings and irritability, violent or aggressive behavior, inability to concentrate, anxiety, anger, and weight gain.

Perceived benefits of smoking

Several perceived benefits were identified that keep individuals smoking or using cigarettes. These included perceptions of enhanced cognitive functioning, relaxation, a way to take a break, use as a coping strategy, a social function, a weight management tool, the perception that it feels good, and being part of one’s identity. It is also important to note that the perceived benefits of smoking often outweighed the risks and the feeling of lack of control in the participant discussions. Even people who used to smoke noted they missed the relaxation and breaks they associated with smoking.

Recognition of symptoms/diseases related to smoking

Table 5 summarizes the negative symptoms and diseases related to smoking recognized by participants in both the focus groups and interviews. These were mostly related to six main body systems (cardiovascular, digestive, oral, neurological, reproductive, and respiratory).

Impacts on physical functioning

The participants noted how smoking impacts their physical functioning. In particular, they noted how their exercise capacity during running, playing sports, walking upstairs, and general physical activity was diminished. They also reported reduced stamina and endurance, decreased physical strength, and feeling tired more easily.

Effects on emotional health

The participants also described how smoking impacts their emotional health and wellbeing. People who smoke reported feelings of shame, guilt, weakness, and a lack of control or powerlessness. They also reported feelings of depression and anxiety associated with worry about health risks. Furthermore, the participants indicated that they experienced a fear of going to places where they could not smoke, being a bad role model for their children, and (in case of people who used to smoke) going back to smoking.

Positive and negative social impacts

Smoking was perceived to have both negative and positive impacts on the social lives of participants. Smoking impacted life negatively when it was not allowed in certain environments, such as in homes, at work, and in cars and airplanes. Stigma was also associated with smoking in an environment where peers and family members do not smoke, but it was also seen as a source of group identity within social networks that had a higher prevalence of smoking behaviors. Participants reported that smoking had some positive impacts on their social interaction, because it facilitated work breaks and increased communication with peers.

Reasons people decided to try to quit

Throughout the focus groups and interviews, individuals identified several reasons why they tried to quit smoking. These included: health, diagnosis of cancer (self, family, or friend), gum disease, pregnancy, hospital stay, worry that it will “kill me,” dislike of taste or odor, social reasons, change in surroundings (fewer smoking spaces), and price.

Reasons people do not like alternatives to cigarettes

The participants’ reasons for not liking alternatives to cigarettes (i.e., less harmful TNPs/RRPs) included perceptions that the alternatives did not work (i.e., the participants still had cravings and experienced withdrawal symptoms), made them feel or get ill (nausea and vomiting), were not “the same” as cigarettes in terms of the ritual, taste, or “feeling,” or were inconvenient/too big to carry.

The conclusions of the expert panel widely supported the findings of the literature review and the input from the reanalyzed focus groups and interviews. Some of the experts working in field of tobacco and nicotine provided additional insights based on their extensive experience with people who use TNPs; they highlighted the importance of the enjoyment of smoking for people who find it difficult to quit, the positive immediate benefits of quitting, and the smoking-related biomarkers that might be on a causal pathway between switching and changes in health and functioning status.

The following main areas were discussed and agreed during the meeting: (1) utility of use, referring to the perceived satisfaction and enjoyment of smoking (e.g., craving relief, weight control, and social affiliation); (2) signs and symptoms of withdrawal (e.g., anxiety, depression, and anger) and the positive immediate physical health effects of quitting smoking (e.g., better general and oral hygiene, less coughing, and improved exercise capacity); (3) functioning, including cognitive, physical, sexual, social, emotional, and role functioning; (4) worry associated with smoking and smoking-related diseases; (5) general health perceptions and quality of life; (6) association with smoking-related biomarkers that could be on the causal pathway between switching and changes in health and functioning; and (7) TNP use patterns and maintenance of switching to RRPs.

Generation of the preliminary conceptual framework

Triangulation of the findings from the literature review, qualitative input from people who use TNPs, and expert panel feedback helped generate a preliminary descriptive conceptual framework that includes the health and functioning and conceptually-related domains impacted by TNP use (Fig.  2 ).

figure 2

Health and functioning conceptual framework related to tobacco and/or nicotine product use from the preparatory phase research findings

Four domains related to the future health and functioning measurement model for TNP use are indicated in grey rectangular boxes and include (moving down from proximal to distal parameters) physical health symptoms (e.g., oral and respiratory symptoms), general physical condition (e.g., appearance and hygiene), functioning (physical, sexual, cognitive, emotional, and social functioning), and general health perceptions, which will be the most distal measure of health and functioning. The preparatory phase research also identified six conceptually-related domains (in dashed rectangular boxes), which are not direct indicators of health status but might influence the impact of TNP use on health and functioning. These include attitudinal variables (worry about the health risks of using TNPs and perceived dependence/fear of withdrawal symptoms associated with quitting smoking), and utilitarian ones (perceived appeal, satisfaction, and benefits of TNP use). In addition, personal factors (e.g., sociodemographic) and environmental factors (e.g., peer/family influence, policies and regulations and sociocultural context) are also reflected in the conceptual framework as indirect indicators of health and functioning.

The framework further indicates that specific behavioral indicators (i.e., TNP use patterns over time) might influence any impact of TNP use on health and functioning. Whilst other causal and reciprocal relationships and hierarchies might exist within the domains, these are not explicitly characterized in this initial draft of the framework and will have to be tested with further empirical data. Finally, identified biomarkers of potential harm (in italics and dashed box) are also integrated in this conceptual framework as part of the conceptually-related domains, because they are on a causal pathway between TNP use and changes in health and functioning [ 133 , 134 ]. Biomarkers are not part of the measurement model that will be considered for a new self-report measure; however, because they are the most proximal parameters to health and functioning, they will be assessed independently as appropriate endpoints by objective clinical or biological analyses.

Triangulation of published literature, reanalysis of qualitative data, and expert opinion helped develop the presented preliminary conceptual framework as the foundation for a new measure to assess the impact of TNPs on self-reported health and functioning. This is essential for identifying relevant concepts and understanding what is important to measure in people who use TNPs. The findings reveal the importance of not only the perceived impacts of TNP use on physical health and physical functioning, but also on aspects of mental health and social interactions and functioning, and general perceptions of health and health-related quality of life.

For the literature review, the WHO ICF [ 28 ] and Wilson and Cleary model [ 29 , 30 ] served as useful guides to develop categories for data abstraction. The scoping literature review yielded 97 articles on TNP use and the relationship to health, perceptions of health, social and individual functioning, and quality of life. Overall, most studies had focused on the known negative effects of cigarette smoking (e.g., mental, respiratory, and oral health) and the rationale and motivation to quit smoking. The WHO ICF and Wilson and Clearly models were not always sufficient for identifying the breadth of relevant concepts, especially from the perspective of TNP use. Development of new codes for the reanalysis of existing qualitative data allowed for the development, extension, and exploration of the topic and provided valuable insights reported in the qualitative data reanalysis, such as the perceived benefits/satisfaction from cigarette smoking, and the rationale for quitting smoking or switching to an RRP. The findings show how this manner of secondary analysis can be valuable in health-related fields where the topic is broad and an existing body of knowledge can contribute by offering a different perspective [ 135 ].

The presentation of the preliminary conceptual framework from this preparatory phase is specific to TNP use and marks a slight departure from the established norms and characterization of the variables typically observed in existing generic health and functioning and health-related quality of life models, such as the WHO ICF and Wilson and Clearly models. Notably, specific hypothesized relationships and the hierarchy between domains are not explicitly characterized in the current draft of the framework. The framework provided an exploratory representation of the current findings to reflect a measurement instrument in people who use TNPs that would ideally be able to assess and demonstrate improvements in self-reported health and functioning status, stability of perceived positive aspects of using TNPs, and no worsening in key areas of physical and emotional health and functioning upon switching to RRPs. Nevertheless, the framework could still undergo further refinement to support the development and validation of a new measure and to further characterize and test the relationships and hierarchies between domains.

This work is not without limitations. For the scoping literature review, among the reviewed articles, not many reported on the use of e-cigarettes and other alternative tobacco or nicotine-delivery devices, because most studies had focused exclusively on cigarettes. It is possible that concepts associated with health and functioning that are relevant to other TNPs were not identified. This is most likely the consequence of the large number of publications related to cigarette use. Some concepts might also have been missed, given the large evidence base on health and functioning-related themes and concepts. However, this was also not a systematic literature search; a scoping review is generally broader than a systematic review in terms of the former having a less-defined research question, broader inclusion and exclusion criteria, and no systematic appraisal of study quality [ 26 ]. Nevertheless, the present scoping review methodology provides a lens on the overall evidence base, and regular updates on the search—specifically related to RRPs and novel TNPs and their health and functioning impacts—could be considered for fully understanding the evolving state of the art in this context. The reanalysis of existing qualitative data also has limitations related to data fit and completeness of preexisting data [ 136 ]. The insights collected from these reanalyzed studies were originally for a different purpose several years prior to the present research, and this might not completely and accurately reflect the objectives of the new project.

Considering the findings of the current research, the development of a health and functioning measure can continue to follow the FDA’s Guidance on PRO measures. As specified within the guideline, gaining input directly from the intended use populations through concept elicitation is a critical activity for ensuring content validity during the development of any new self-reported measure [ 137 ]. Continuous engagement with an expert panel can also support the refinement of the conceptual framework as well as the development of the draft and final measure.

The goal of this research was to identify from varied research activities key concepts and aspects of health and functioning and related changes associated with the use of TNPs. The resulting preliminary conceptual framework provides the basis for informing future research to further understand health and functioning concepts important to measure in individual who switch to RRPs and to develop a new self-report measure to assess this from the consumers’ perspective.

Availability of data and materials

All data generated or analyzed during this study are included in this published article and its supplementary information files.

Abbreviations

Assessment of Behavioral OUtcomes related to Tobacco and Nicotine Products Toolbox

Chronic obstructive pulmonary disease

Food and Drug Administration

Health-related quality of life

International Classification of Functioning, Disability and Health

  • Modified risk tobacco products

Nicotine replacement therapy

Patient-Reported Outcomes

Quality of life

Reduced-risk products

Rapid Evidence Mapping

  • Tobacco and/or nicotine products

United Kingdom

United States

36-Item Short-Form Health Survey

World Health Organization

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Acknowledgements

We thank the team at Sciome LLC for their assistance and contribution to the literature review. We thank Vivienne Law and David Floyd for their contributions to the literature review, reanalysis of qualitative data, and assistance with review of the draft manuscript. We thank Catherine Acquadro for her review of the draft manuscript. We also thank John Ware, Jed Rose, Ashley Slagle, Donald Patrick, Karl Fagerström, Stefan Cano, and Thomas Salzberger for their input and review.

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EA, ES and CC performed conceptualization. EA, ES and LA-W performed methodology. EA, ES, SG, EC and LA-W were involved in the investigation. EA and ES were involved in writing—original draft. EA, EC, LA-W and CC were involved in writing—review & editing. EA performed visualization. ES and CC performed supervision. AB, EC and SG were involved in data curation. AB and EC were involved in project administration. LA-W performed formal analysis. CC was involved in funding acquisition. All authors read and approved the final manuscript.

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Esther F. Afolalu, Emilie Clerc, and Christelle Chrea are employees of Philip Morris International. Agnes Bacso, Erica Spies, and Sophie Gallot completed the work during prior employment with Philip Morris International. Linda Abetz-Webb is a consultant for Philip Morris International.

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Summary tables of results of scoping literature review

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Afolalu, E.F., Spies, E., Bacso, A. et al. Impact of tobacco and/or nicotine products on health and functioning: a scoping review and findings from the preparatory phase of the development of a new self-report measure. Harm Reduct J 18 , 79 (2021). https://doi.org/10.1186/s12954-021-00526-z

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  • Health and functioning
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Harm Reduction Journal

ISSN: 1477-7517

harmful effects of smoking research paper

Health Effects of Cigarette Smoking

Smoking and death, smoking and increased health risks, smoking and cardiovascular disease, smoking and respiratory disease, smoking and cancer, smoking and other health risks, quitting and reduced risks.

Cigarette smoking harms nearly every organ of the body, causes many diseases, and reduces the health of smokers in general. 1,2

Quitting smoking lowers your risk for smoking-related diseases and can add years to your life. 1,2

Cigarette smoking is the leading cause of preventable death in the United States. 1

  • Cigarette smoking causes more than 480,000 deaths each year in the United States. This is nearly one in five deaths. 1,2,3
  • Human immunodeficiency virus (HIV)
  • Illegal drug use
  • Alcohol use
  • Motor vehicle injuries
  • Firearm-related incidents
  • More than 10 times as many U.S. citizens have died prematurely from cigarette smoking than have died in all the wars fought by the United States. 1
  • Smoking causes about 90% (or 9 out of 10) of all lung cancer deaths. 1,2  More women die from lung cancer each year than from breast cancer. 5
  • Smoking causes about 80% (or 8 out of 10) of all deaths from chronic obstructive pulmonary disease (COPD). 1
  • Cigarette smoking increases risk for death from all causes in men and women. 1
  • The risk of dying from cigarette smoking has increased over the last 50 years in the U.S. 1

Smokers are more likely than nonsmokers to develop heart disease, stroke, and lung cancer. 1

  • For coronary heart disease by 2 to 4 times 1,6
  • For stroke by 2 to 4 times 1
  • Of men developing lung cancer by 25 times 1
  • Of women developing lung cancer by 25.7 times 1
  • Smoking causes diminished overall health, increased absenteeism from work, and increased health care utilization and cost. 1

Smokers are at greater risk for diseases that affect the heart and blood vessels (cardiovascular disease). 1,2

  • Smoking causes stroke and coronary heart disease, which are among the leading causes of death in the United States. 1,3
  • Even people who smoke fewer than five cigarettes a day can have early signs of cardiovascular disease. 1
  • Smoking damages blood vessels and can make them thicken and grow narrower. This makes your heart beat faster and your blood pressure go up. Clots can also form. 1,2
  • A clot blocks the blood flow to part of your brain;
  • A blood vessel in or around your brain bursts. 1,2
  • Blockages caused by smoking can also reduce blood flow to your legs and skin. 1,2

Smoking can cause lung disease by damaging your airways and the small air sacs (alveoli) found in your lungs. 1,2

  • Lung diseases caused by smoking include COPD, which includes emphysema and chronic bronchitis. 1,2
  • Cigarette smoking causes most cases of lung cancer. 1,2
  • If you have asthma, tobacco smoke can trigger an attack or make an attack worse. 1,2
  • Smokers are 12 to 13 times more likely to die from COPD than nonsmokers. 1

Smoking can cause cancer almost anywhere in your body: 1,2

  • Blood (acute myeloid leukemia)
  • Colon and rectum (colorectal)
  • Kidney and ureter
  • Oropharynx (includes parts of the throat, tongue, soft palate, and the tonsils)
  • Trachea, bronchus, and lung

Smoking also increases the risk of dying from cancer and other diseases in cancer patients and survivors. 1

If nobody smoked, one of every three cancer deaths in the United States would not happen. 1,2

Smoking harms nearly every organ of the body and affects a person’s overall health. 1,2

  • Preterm (early) delivery
  • Stillbirth (death of the baby before birth)
  • Low birth weight
  • Sudden infant death syndrome (known as SIDS or crib death)
  • Ectopic pregnancy
  • Orofacial clefts in infants
  • Smoking can also affect men’s sperm, which can reduce fertility and also increase risks for birth defects and miscarriage. 2
  • Women past childbearing years who smoke have weaker bones than women who never smoked. They are also at greater risk for broken bones.
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  • Smoking is a cause of type 2 diabetes mellitus and can make it harder to control. The risk of developing diabetes is 30–40% higher for active smokers than nonsmokers. 1,2
  • Smoking causes general adverse effects on the body, including inflammation and decreased immune function. 1
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  • Quitting smoking is one of the most important actions people can take to improve their health. This is true regardless of their age or how long they have been smoking. Visit the Benefits of Quitting  page for more information about how quitting smoking can improve your health.
  • U.S. Department of Health and Human Services. The Health Consequences of Smoking—50 Years of Progress: A Report of the Surgeon General . Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014 [accessed 2017 Apr 20].
  • U.S. Department of Health and Human Services. How Tobacco Smoke Causes Disease: What It Means to You . Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010 [accessed 2017 Apr 20].
  • Centers for Disease Control and Prevention. QuickStats: Number of Deaths from 10 Leading Causes—National Vital Statistics System, United States, 2010 . Morbidity and Mortality Weekly Report 2013:62(08);155. [accessed 2017 Apr 20].
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  • U.S. Department of Health and Human Services. Reducing the Health Consequences of Smoking: 25 Years of Progress. A Report of the Surgeon General . Rockville (MD): U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 1989 [accessed 2017 Apr 20].

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  • Published: 18 May 2021

An updated overview of e-cigarette impact on human health

  • Patrice Marques   ORCID: orcid.org/0000-0003-0465-1727 1 , 2 ,
  • Laura Piqueras   ORCID: orcid.org/0000-0001-8010-5168 1 , 2 , 3 &
  • Maria-Jesus Sanz   ORCID: orcid.org/0000-0002-8885-294X 1 , 2 , 3  

Respiratory Research volume  22 , Article number:  151 ( 2021 ) Cite this article

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The electronic cigarette ( e-cigarette ), for many considered as a safe alternative to conventional cigarettes, has revolutionised the tobacco industry in the last decades. In e-cigarettes , tobacco combustion is replaced by e-liquid heating, leading some manufacturers to propose that e-cigarettes have less harmful respiratory effects than tobacco consumption. Other innovative features such as the adjustment of nicotine content and the choice of pleasant flavours have won over many users. Nevertheless, the safety of e-cigarette consumption and its potential as a smoking cessation method remain controversial due to limited evidence. Moreover, it has been reported that the heating process itself can lead to the formation of new decomposition compounds of questionable toxicity. Numerous in vivo and in vitro studies have been performed to better understand the impact of these new inhalable compounds on human health. Results of toxicological analyses suggest that e-cigarettes can be safer than conventional cigarettes, although harmful effects from short-term e-cigarette use have been described. Worryingly, the potential long-term effects of e-cigarette consumption have been scarcely investigated. In this review, we take stock of the main findings in this field and their consequences for human health including coronavirus disease 2019 (COVID-19).

Electronic nicotine dispensing systems (ENDS), commonly known as electronic cigarettes or e-cigarettes , have been popularly considered a less harmful alternative to conventional cigarette smoking since they first appeared on the market more than a decade ago. E-cigarettes are electronic devices, essentially consisting of a cartridge, filled with an e-liquid, a heating element/atomiser necessary to heat the e-liquid to create a vapour that can be inhaled through a mouthpiece, and a rechargeable battery (Fig.  1 ) [ 1 , 2 ]. Both the electronic devices and the different e-liquids are easily available in shops or online stores.

figure 1

Effect of the heating process on aerosol composition. Main harmful effects documented. Several compounds detected in e-cigarette aerosols are not present in e-liquid s and the device material also seems to contribute to the presence of metal and silicate particles in the aerosols. The heating conditions especially on humectants, flavourings and the low-quality material used have been identified as the generator of the new compounds in aerosols. Some compounds generated from humectants (propylene glycol and glycerol) and flavourings, have been associated with clear airways impact, inflammation, impairment of cardiovascular function and toxicity. In addition, some of them are carcinogens or potential carcinogens

The e-liquid typically contains humectants and flavourings, with or without nicotine; once vapourised by the atomiser, the aerosol (vapour) provides a sensation similar to tobacco smoking, but purportedly without harmful effects [ 3 ]. However, it has been reported that the heating process can lead to the generation of new decomposition compounds that may be hazardous [ 4 , 5 ]. The levels of nicotine, which is the key addictive component of tobacco, can also vary between the commercially available e-liquids, and even nicotine-free options are available. For this particular reason, e-cigarettes are often viewed as a smoking cessation tool, given that those with nicotine can prevent smoking craving, yet this idea has not been fully demonstrated [ 2 , 6 , 7 ].

Because e-cigarettes are combustion-free, and because most of the damaging and well-known effects of tobacco are derived from this reaction, there is a common and widely spread assumption that e-cigarette consumption or “vaping” is safer than conventional cigarette smoking. However, are they risk-free? Is there sufficient toxicological data on all the components employed in e-liquids ? Do we really know the composition of the inhaled vapour during the heating process and its impact on health? Can e-cigarettes be used to curb tobacco use? Do their consumption impact on coronavirus disease 2019 (COVID-19)? In the present review, we have attempted to clarify these questions based on the existing scientific literature, and we have compiled new insights related with the toxicity derived from the use of these devices.

Effect of e-cigarette vapour versus conventional cigarette exposure: in vivo and in vitro effects

Numerous studies have been performed to evaluate the safety/toxicity of e-cigarette use both in vivo and in in vitro cell culture.

One of the first studies in humans involved the analysis of 9 volunteers that consumed e-cigarettes , with or without nicotine, in a ventilated room for 2 h [ 8 ]. Pollutants in indoor air, exhaled nitric oxide (NO) and urinary metabolite profiles were analysed. The results of this acute experiment revealed that e-cigarettes are not emission-free, and ultrafine particles formed from propylene glycol (PG) could be detected in the lungs. The study also suggested that the presence of nicotine in e-cigarettes increased the levels of NO exhaled from consumers and provoked marked airway inflammation; however, no differences were found in the levels of exhaled carbon monoxide (CO), an oxidative stress marker, before and after e-cigarette consumption [ 8 ]. A more recent human study detected significantly higher levels of metabolites of hazardous compounds including benzene, ethylene oxide, acrylonitrile, acrolein and acrylamide in the urine of adolescent dual users ( e-cigarettes and conventional tobacco consumers) than in adolescent e-cigarette -only users (Table 1 ) [ 9 ]. Moreover, the urine levels of metabolites of acrylonitrile, acrolein, propylene oxide, acrylamide and crotonaldehyde, all of which are detrimental for human health, were significantly higher in e-cigarette -only users than in non-smoker controls, reaching up to twice the registered values of those from non-smoker subjects (Table 1 ) [ 9 ]. In line with these observations, dysregulation of lung homeostasis has been documented in non-smokers subjected to acute inhalation of e-cigarette aerosols [ 10 ].

Little is known about the effect of vaping on the immune system. Interestingly, both traditional and e-cigarette consumption by non-smokers was found to provoke short-term effects on platelet function, increasing platelet activation (levels of soluble CD40 ligand and the adhesion molecule P-selectin) and platelet aggregation, although to a lesser extent with e-cigarettes [ 11 ]. As found with platelets, the exposure of neutrophils to e-cigarette aerosol resulted in increased CD11b and CD66b expression being both markers of neutrophil activation [ 12 ]. Additionally, increased oxidative stress, vascular endothelial damage, impaired endothelial function, and changes in vascular tone have all been reported in different human studies on vaping [ 13 , 14 , 15 , 16 , 17 ]. In this context, it is widely accepted that platelet and leukocyte activation as well as endothelial dysfunction are associated with atherogenesis and cardiovascular morbidity [ 18 , 19 ]. In line with these observations the potential association of daily e-cigarettes consumption and the increased risk of myocardial infarction remains controversial but benefits may occur when switching from tobacco to chronic e-cigarette use in blood pressure regulation, endothelial function and vascular stiffness (reviewed in [ 20 ]). Nevertheless, whether or not e-cigarette vaping has cardiovascular consequences requires further investigation.

More recently, in August 2019, the US Centers for Disease Control and Prevention (CDC) declared an outbreak of the e-cigarette or vaping product use-associated lung injury (EVALI) which caused several deaths in young population (reviewed in [ 20 ]). Indeed, computed tomography (CT scan) revealed local inflammation that impaired gas exchange caused by aerosolised oils from e-cigarettes [ 21 ]. However, most of the reported cases of lung injury were associated with use of e-cigarettes for tetrahydrocannabinol (THC) consumption as well as vitamin E additives [ 20 ] and not necessarily attributable to other e-cigarette components.

On the other hand, in a comparative study of mice subjected to either lab air, e-cigarette aerosol or cigarette smoke (CS) for 3 days (6 h-exposure per day), those exposed to e-cigarette aerosols showed significant increases in interleukin (IL)-6 but normal lung parenchyma with no evidence of apoptotic activity or elevations in IL-1β or tumour necrosis factor-α (TNFα) [ 22 ]. By contrast, animals exposed to CS showed lung inflammatory cell infiltration and elevations in inflammatory marker expression such as IL-6, IL-1β and TNFα [ 22 ]. Beyond airway disease, exposure to aerosols from e-liquids with or without nicotine has also been also associated with neurotoxicity in an early-life murine model [ 23 ].

Results from in vitro studies are in general agreement with the limited number of in vivo studies. For example, in an analysis using primary human umbilical vein endothelial cells (HUVEC) exposed to 11 commercially-available vapours, 5 were found to be acutely cytotoxic, and only 3 of those contained nicotine [ 24 ]. In addition, 5 of the 11 vapours tested (including 4 that were cytotoxic) reduced HUVEC proliferation and one of them increased the production of intracellular reactive oxygen species (ROS) [ 24 ]. Three of the most cytotoxic vapours—with effects similar to those of conventional high-nicotine CS extracts—also caused comparable morphological changes [ 24 ]. Endothelial cell migration is an important mechanism of vascular repair than can be disrupted in smokers due to endothelial dysfunction [ 25 , 26 ]. In a comparative study of CS and e-cigarette aerosols, Taylor et al . found that exposure of HUVEC to e-cigarette aqueous extracts for 20 h did not affect migration in a scratch wound assay [ 27 ], whereas equivalent cells exposed to CS extract showed a significant inhibition in migration that was concentration dependent [ 27 ].

In cultured human airway epithelial cells, both e-cigarette aerosol and CS extract induced IL-8/CXCL8 (neutrophil chemoattractant) release [ 28 ]. In contrast, while CS extract reduced epithelial barrier integrity (determined by the translocation of dextran from the apical to the basolateral side of the cell layer), e-cigarette aerosol did not, suggesting that only CS extract negatively affected host defence [ 28 ]. Moreover, Higham et al . also found that e-cigarette aerosol caused IL-8/CXCL8 and matrix metallopeptidase 9 (MMP-9) release together with enhanced activity of elastase from neutrophils [ 12 ] which might facilitate neutrophil migration to the site of inflammation [ 12 ].

In a comparative study, repeated exposure of human gingival fibroblasts to CS condensate or to nicotine-rich or nicotine-free e-vapour condensates led to alterations in morphology, suppression of proliferation and induction of apoptosis, with changes in all three parameters greater in cells exposed to CS condensate [ 29 ]. Likewise, both e-cigarette aerosol and CS extract increased cell death in adenocarcinomic human alveolar basal epithelial cells (A549 cells), and again the effect was more damaging with CS extract than with e-cigarette aerosol (detrimental effects found at 2 mg/mL of CS extract vs. 64 mg/mL of e-cigarette extract) [ 22 ], which is in agreement with another study examining battery output voltage and cytotoxicity [ 30 ].

All this evidence would suggest that e-cigarettes are potentially less harmful than conventional cigarettes (Fig.  2 ) [ 11 , 14 , 22 , 24 , 27 , 28 , 29 ]. Importantly, however, most of these studies have investigated only short-term effects [ 10 , 14 , 15 , 22 , 27 , 28 , 29 , 31 , 32 ], and the long-term effects of e-cigarette consumption on human health are still unclear and require further study.

figure 2

Comparison of the degree of harmful effects documented from e-cigarette and conventional cigarette consumption. Human studies, in vivo mice exposure and in vitro studies. All of these effects from e-cigarettes were documented to be lower than those exerted by conventional cigarettes, which may suggest that e-cigarette consumption could be a safer option than conventional tobacco smoking but not a clear safe choice

Consequences of nicotine content

Beyond flavour, one of the major issues in the e-liquid market is the range of nicotine content available. Depending on the manufacturer, the concentration of this alkaloid can be presented as low , medium or high , or expressed as mg/mL or as a percentage (% v/v). The concentrations range from 0 (0%, nicotine-free option) to 20 mg/mL (2.0%)—the maximum nicotine threshold according to directive 2014/40/EU of the European Parliament and the European Union Council [ 33 , 34 ]. Despite this normative, however, some commercial e-liquids have nicotine concentrations close to 54 mg/mL [ 35 ], much higher than the limits established by the European Union.

The mislabelling of nicotine content in e-liquids has been previously addressed [ 8 , 34 ]. For instance, gas chromatography with a flame ionisation detector (GC-FID) revealed inconsistencies in the nicotine content with respect to the manufacturer´s declaration (average of 22 ± 0.8 mg/mL vs. 18 mg/mL) [ 8 ], which equates to a content ~ 22% higher than that indicated in the product label. Of note, several studies have detected nicotine in those e-liquids labelled as nicotine-free [ 5 , 35 , 36 ]. One study detected the presence of nicotine (0.11–6.90 mg/mL) in 5 of 23 nicotine-free labelled e-liquids by nuclear magnetic resonance spectroscopy [ 35 ], and another study found nicotine (average 8.9 mg/mL) in 13.6% (17/125) of the nicotine-free e-liquids as analysed by high performance liquid chromatography (HPLC) [ 36 ]. Among the 17 samples tested in this latter study 14 were identified to be counterfeit or suspected counterfeit. A third study detected nicotine in 7 of 10 nicotine-free refills, although the concentrations were lower than those identified in the previous analyses (0.1–15 µg/mL) [ 5 ]. Not only is there evidence of mislabelling of nicotine content among refills labelled as nicotine-free, but there also seems to be a history of poor labelling accuracy in nicotine-containing e-liquids [ 37 , 38 ].

A comparison of the serum levels of nicotine from e-cigarette or conventional cigarette consumption has been recently reported [ 39 ]. Participants took one vape from an e-cigarette , with at least 12 mg/mL of nicotine, or inhaled a conventional cigarette, every 20 s for 10 min. Blood samples were collected 1, 2, 4, 6, 8, 10, 12 and 15 min after the first puff, and nicotine serum levels were measured by liquid chromatography-mass spectrometry (LC–MS). The results revealed higher serum levels of nicotine in the conventional CS group than in the e-cigarette group (25.9 ± 16.7 ng/mL vs. 11.5 ± 9.8 ng/mL). However, e-cigarettes containing 20 mg/mL of nicotine are more equivalent to normal cigarettes, based on the delivery of approximately 1 mg of nicotine every 5 min [ 40 ].

In this line, a study compared the acute impact of CS vs. e-cigarette vaping with equivalent nicotine content in healthy smokers and non-smokers. Both increased markers of oxidative stress and decreased NO bioavailability, flow-mediated dilation, and vitamin E levels showing no significant differences between tobacco and e-cigarette exposure (reviewed in [ 20 ]). Inasmuch, short-term e-cigarette use in healthy smokers resulted in marked impairment of endothelial function and an increase in arterial stiffness (reviewed in [ 20 ]). Similar effects on endothelial dysfunction and arterial stiffness were found in animals when they were exposed to e-cigarette vapor either for several days or chronically (reviewed in [ 20 ]). In contrast, other studies found acute microvascular endothelial dysfunction, increased oxidative stress and arterial stiffness in smokers after exposure to e-cigarettes with nicotine, but not after e-cigarettes without nicotine (reviewed in [ 20 ]). In women smokers, a study found a significant difference in stiffness after smoking just one tobacco cigarette, but not after use of e-cigarettes (reviewed in [ 20 ]).

It is well known that nicotine is extremely addictive and has a multitude of harmful effects. Nicotine has significant biologic activity and adversely affects several physiological systems including the cardiovascular, respiratory, immunological and reproductive systems, and can also compromise lung and kidney function [ 41 ]. Recently, a sub-chronic whole-body exposure of e-liquid (2 h/day, 5 days/week, 30 days) containing PG alone or PG with nicotine (25 mg/mL) to wild type (WT) animals or knockout (KO) mice in α7 nicotinic acetylcholine receptor (nAChRα7-KO) revealed a partly nAChRα7-dependent lung inflammation [ 42 ]. While sub-chronic exposure to PG/nicotine promote nAChRα7-dependent increased levels of different cytokines and chemokines in the bronchoalveolar lavage fluid (BALF) such as IL-1α, IL-2, IL-9, interferon γ (IFNγ), granulocyte-macrophage colony-stimulating factor (GM-CSF), monocyte chemoattractant protein-1 (MCP-1/CCL2) and regulated on activation, normal T cell expressed and secreted (RANTES/CCL5), the enhanced levels of IL-1β, IL-5 and TNFα were nAChRα7 independent. In general, most of the cytokines detected in BALF were significantly increased in WT mice exposed to PG with nicotine compared to PG alone or air control [ 42 ]. Some of these effects were found to be through nicotine activation of NF-κB signalling albeit in females but not in males. In addition, PG with nicotine caused increased macrophage and CD4 + /CD8 + T-lymphocytes cell counts in BALF compared to air control, but these effects were ameliorated when animals were sub-chronically exposed to PG alone [ 42 ].

Of note, another study indicated that although RANTES/CCL5 and CCR1 mRNA were upregulated in flavour/nicotine-containing e-cigarette users, vaping flavour and nicotine-less e-cigarettes did not significantly dysregulate cytokine and inflammasome activation [ 43 ].

In addition to its toxicological effects on foetus development, nicotine can disrupt brain development in adolescents and young adults [ 44 , 45 , 46 ]. Several studies have also suggested that nicotine is potentially carcinogenic (reviewed in [ 41 ]), but more work is needed to prove its carcinogenicity independently of the combustion products of tobacco [ 47 ]. In this latter regard, no differences were encountered in the frequency of tumour appearance in rats subjected to long-term (2 years) inhalation of nicotine when compared with control rats [ 48 ]. Despite the lack of carcinogenicity evidence, it has been reported that nicotine promotes tumour cell survival by decreasing apoptosis and increasing proliferation [ 49 ], indicating that it may work as a “tumour enhancer”. In a very recent study, chronic administration of nicotine to mice (1 mg/kg every 3 days for a 60-day period) enhanced brain metastasis by skewing the polarity of M2 microglia, which increases metastatic tumour growth [ 50 ]. Assuming that a conventional cigarette contains 0.172–1.702 mg of nicotine [ 51 ], the daily nicotine dose administered to these animals corresponds to 40–400 cigarettes for a 70 kg-adult, which is a dose of an extremely heavy smoker. We would argue that further studies with chronic administration of low doses of nicotine are required to clearly evaluate its impact on carcinogenicity.

In the aforementioned study exposing human gingival fibroblasts to CS condensate or to nicotine-rich or nicotine-free e-vapour condensates [ 29 ], the detrimental effects were greater in cells exposed to nicotine-rich condensate than to nicotine-free condensate, suggesting that the possible injurious effects of nicotine should be considered when purchasing e-refills . It is also noteworthy that among the 3 most cytotoxic vapours for HUVEC evaluated in the Putzhammer et al . study, 2 were nicotine-free, which suggests that nicotine is not the only hazardous component in e-cigarettes [ 24 ] .

The lethal dose of nicotine for an adult is estimated at 30–60 mg [ 52 ]. Given that nicotine easily diffuses from the dermis to the bloodstream, acute nicotine exposure by e-liquid spilling (5 mL of a 20 mg/mL nicotine-containing refill is equivalent to 100 mg of nicotine) can easily be toxic or even deadly [ 8 ]. Thus, devices with rechargeable refills are another issue of concern with e-cigarettes , especially when e-liquids are not sold in child-safe containers, increasing the risk of spilling, swallowing or breathing.

These data overall indicate that the harmful effects of nicotine should not be underestimated. Despite the established regulations, some inaccuracies in nicotine content labelling remain in different brands of e-liquids . Consequently, stricter regulation and a higher quality control in the e-liquid industry are required.

Effect of humectants and their heating-related products

In this particular aspect, again the composition of the e-liquid varies significantly among different commercial brands [ 4 , 35 ]. The most common and major components of e-liquids are PG or 1,2-propanediol, and glycerol or glycerine (propane-1,2,3-triol). Both types of compounds are used as humectants to prevent the e-liquid from drying out [ 2 , 53 ] and are classified by the Food and Drug Administration (FDA) as “Generally Recognised as Safe” [ 54 ]. In fact, they are widely used as alimentary and pharmaceutical products [ 2 ]. In an analysis of 54 commercially available e-liquids , PG and glycerol were detected in almost all samples at concentrations ranging from 0.4% to 98% (average 57%) and from 0.3% to 95% (average 37%), respectively [ 35 ].

With regards to toxicity, little is known about the effects of humectants when they are heated and chronically inhaled. Studies have indicated that PG can induce respiratory irritation and increase the probability of asthma development [ 55 , 56 ], and both PG and glycerol from e-cigarettes might reach concentrations sufficiently high to potentially cause irritation of the airways [ 57 ]. Indeed, the latter study established that one e-cigarette puff results in a PG exposure of 430–603 mg/m 3 , which is higher than the levels reported to cause airway irritation (average 309 mg/m 3 ) based on a human study [ 55 ]. The same study established that one e-cigarette puff results in a glycerol exposure of 348–495 mg/m 3 [ 57 ], which is close to the levels reported to cause airway irritation in rats (662 mg/m 3 ) [ 58 ].

Airway epithelial injury induced by acute vaping of PG and glycerol aerosols (50:50 vol/vol), with or without nicotine, has been reported in two randomised clinical trials in young tobacco smokers [ 32 ]. In vitro, aerosols from glycerol only-containing refills showed cytotoxicity in A549 and human embryonic stem cells, even at a low battery output voltage [ 59 ]. PG was also found to affect early neurodevelopment in a zebrafish model [ 60 ]. Another important issue is that, under heating conditions PG can produce acetaldehyde or formaldehyde (119.2 or 143.7 ng/puff at 20 W, respectively, on average), while glycerol can also generate acrolein (53.0, 1000.0 or 5.9 ng/puff at 20 W, respectively, on average), all carbonyls with a well-documented toxicity [ 61 ]. Although, assuming 15 puffs per e-cigarette unit, carbonyls produced by PG or glycerol heating would be below the maximum levels found in a conventional cigarette combustion (Table 2 ) [ 51 , 62 ]. Nevertheless, further studies are required to properly test the deleterious effects of all these compounds at physiological doses resembling those to which individuals are chronically exposed.

Although PG and glycerol are the major components of e-liquids other components have been detected. When the aerosols of 4 commercially available e-liquids chosen from a top 10 list of “ Best E-Cigarettes of 2014” , were analysed by gas chromatography-mass spectrometry (GC–MS) after heating, numerous compounds were detected, with nearly half of them not previously identified [ 4 ], thus suggesting that the heating process per se generates new compounds of unknown consequence. Of note, the analysis identified formaldehyde, acetaldehyde and acrolein [ 4 ], 3 carbonyl compounds with known high toxicity [ 63 , 64 , 65 , 66 , 67 ]. While no information was given regarding formaldehyde and acetaldehyde concentrations, the authors calculated that one puff could result in an acrolein exposure of 0.003–0.015 μg/mL [ 4 ]. Assuming 40 mL per puff and 15 puffs per e-cigarette unit (according to several manufacturers) [ 4 ], each e-cigarette unit would generate approximately 1.8–9 μg of acrolein, which is less than the levels of acrolein emitted by a conventional tobacco cigarette (18.3–98.2 μg) [ 51 ]. However, given that e-cigarette units of vaping are not well established, users may puff intermittently throughout the whole day. Thus, assuming 400 to 500 puffs per cartridge, users could be exposed to up to 300 μg of acrolein.

In a similar study, acrolein was found in 11 of 12 aerosols tested, with a similar content range (approximately 0.07–4.19 μg per e-cigarette unit) [ 68 ]. In the same study, both formaldehyde and acetaldehyde were detected in all of the aerosols tested, with contents of 0.2–5.61 μg and 0.11–1.36 μg, respectively, per e-cigarette unit [ 68 ]. It is important to point out that the levels of these toxic products in e-cigarette aerosols are significantly lower than those found in CS: 9 times lower for formaldehyde, 450 times lower for acetaldehyde and 15 times lower for acrolein (Table 2 ) [ 62 , 68 ].

Other compounds that have been detected in aerosols include acetamide, a potential human carcinogen [ 5 ], and some aldehydes [ 69 ], although their levels were minimal. Interestingly, the existence of harmful concentrations of diethylene glycol, a known cytotoxic agent, in e-liquid aerosols is contentious with some studies detecting its presence [ 4 , 68 , 70 , 71 , 72 ], and others finding low subtoxic concentrations [ 73 , 74 ]. Similar observations were reported for the content ethylene glycol. In this regard, either it was detected at concentrations that did not exceed the authorised limit [ 73 ], or it was absent from the aerosols produced [ 4 , 71 , 72 ]. Only one study revealed its presence at high concentration in a very low number of samples [ 5 ]. Nevertheless, its presence above 1 mg/g is not allowed by the FDA [ 73 ]. Figure  1 lists the main compounds detected in aerosols derived from humectant heating and their potential damaging effects. It would seem that future studies should analyse the possible toxic effects of humectants and related products at concentrations similar to those that e-cigarette vapers are exposed to reach conclusive results.

Impact of flavouring compounds

The range of e-liquid flavours available to consumers is extensive and is used to attract both current smokers and new e-cigarette users, which is a growing public health concern [ 6 ]. In fact, over 5 million middle- and high-school students were current users of e-cigarettes in 2019 [ 75 ], and appealing flavours have been identified as the primary reason for e-cigarette consumption in 81% of young users [ 76 ]. Since 2016, the FDA regulates the flavours used in the e-cigarette market and has recently published an enforcement policy on unauthorised flavours, including fruit and mint flavours, which are more appealing to young users [ 77 ]. However, the long-term effects of all flavour chemicals used by this industry (which are more than 15,000) remain unknown and they are not usually included in the product label [ 78 ]. Furthermore, there is no safety guarantee since they may harbour potential toxic or irritating properties [ 5 ].

With regards to the multitude of available flavours, some have demonstrated cytotoxicity [ 59 , 79 ]. Bahl et al. evaluated the toxicity of 36 different e-liquids and 29 different flavours on human embryonic stem cells, mouse neural stem cells and human pulmonary fibroblasts using a metabolic activity assay. In general, those e-liquids that were bubblegum-, butterscotch- and caramel-flavoured did not show any overt cytotoxicity even at the highest dose tested. By contrast, those e-liquids with Freedom Smoke Menthol Arctic and Global Smoke Caramel flavours had marked cytotoxic effects on pulmonary fibroblasts and those with Cinnamon Ceylon flavour were the most cytotoxic in all cell lines [ 79 ]. A further study from the same group [ 80 ] revealed that high cytotoxicity is a recurrent feature of cinnamon-flavoured e-liquids. In this line, results from GC–MS and HPLC analyses indicated that cinnamaldehyde (CAD) and 2-methoxycinnamaldehyde, but not dipropylene glycol or vanillin, were mainly responsible for the high cytotoxicity of cinnamon-flavoured e-liquids [ 80 ]. Other flavouring-related compounds that are associated with respiratory complications [ 81 , 82 , 83 ], such as diacetyl, 2,3-pentanedione or acetoin, were found in 47 out of 51 aerosols of flavoured e-liquids tested [ 84 ] . Allen et al . calculated an average of 239 μg of diacetyl per cartridge [ 84 ]. Assuming again 400 puffs per cartridge and 40 mL per puff, is it is possible to estimate an average of 0.015 ppm of diacetyl per puff, which could compromise normal lung function in the long-term [ 85 ].

The cytotoxic and pro-inflammatory effects of different e-cigarette flavouring chemicals were also tested on two human monocytic cell lines—mono mac 6 (MM6) and U937 [ 86 ]. Among the flavouring chemicals tested, CAD was found to be the most toxic and O-vanillin and pentanedione also showed significant cytotoxicity; by contrast, acetoin, diacetyl, maltol, and coumarin did not show any toxicity at the concentrations assayed (10–1000 µM). Of interest, a higher toxicity was evident when combinations of different flavours or mixed equal proportions of e-liquids from 10 differently flavoured e-liquids were tested, suggesting that vaping a single flavour is less toxic than inhaling mixed flavours [ 86 ]. Also, all the tested flavours produced significant levels of ROS in a cell-free ROS production assay. Finally, diacetyl, pentanedione, O-vanillin, maltol, coumarin, and CAD induced significant IL-8 secretion from MM6 and U937 monocytes [ 86 ]. It should be borne in mind, however, that the concentrations assayed were in the supra-physiological range and it is likely that, once inhaled, these concentrations are not reached in the airway space. Indeed, one of the limitations of the study was that human cells are not exposed to e-liquids per se, but rather to the aerosols where the concentrations are lower [ 86 ]. In this line, the maximum concentration tested (1000 µM) would correspond to approximately 80 to 150 ppm, which is far higher than the levels found in aerosols of some of these compounds [ 84 ]. Moreover, on a day-to-day basis, lungs of e-cigarette users are not constantly exposed to these chemicals for 24 h at these concentrations. Similar limitations were found when five of seven flavourings were found to cause cytotoxicity in human bronchial epithelial cells [ 87 ].

Recently, a commonly commercialized crème brûlée -flavoured aerosol was found to contain high concentrations of benzoic acid (86.9 μg/puff), a well-established respiratory irritant [ 88 ]. When human lung epithelial cells (BEAS-2B and H292) were exposed to this aerosol for 1 h, a marked cytotoxicity was observed in BEAS-2B but not in H292 cells, 24 h later. However, increased ROS production was registered in H292 cells [ 88 ].

Therefore, to fully understand the effects of these compounds, it is relevant the cell cultures selected for performing these assays, as well as the use of in vivo models that mimic the real-life situation of chronic e-cigarette vapers to clarify their impact on human health.

The e-cigarette device

While the bulk of studies related to the impact of e-cigarette use on human health has focused on the e-liquid components and the resulting aerosols produced after heating, a few studies have addressed the material of the electronic device and its potential consequences—specifically, the potential presence of metals such as copper, nickel or silver particles in e-liquids and aerosols originating from the filaments and wires and the atomiser [ 89 , 90 , 91 ].

Other important components in the aerosols include silicate particles from the fiberglass wicks or silicone [ 89 , 90 , 91 ]. Many of these products are known to cause abnormalities in respiratory function and respiratory diseases [ 89 , 90 , 91 ], but more in-depth studies are required. Interestingly, the battery output voltage also seems to have an impact on the cytotoxicity of the aerosol vapours, with e-liquids from a higher battery output voltage showing more toxicity to A549 cells [ 30 ].

A recent study compared the acute effects of e-cigarette vapor (with PG/vegetable glycerine plus tobacco flavouring but without nicotine) generated from stainless‐steel atomizer (SS) heating element or from a nickel‐chromium alloy (NC) [ 92 ]. Some rats received a single e-cigarette exposure for 2 h from a NC heating element (60 or 70 W); other rats received a similar exposure of e-cigarette vapor using a SS heating element for the same period of time (60 or 70 W) and, a final group of animals were exposed for 2 h to air. Neither the air‐exposed rats nor those exposed to e-cigarette vapor using SS heating elements developed respiratory distress. In contrast, 80% of the rats exposed to e-cigarette vapor using NC heating units developed clinical acute respiratory distress when a 70‐W power setting was employed. Thus, suggesting that operating units at higher than recommended settings can cause adverse effects. Nevertheless, there is no doubt that the deleterious effects of battery output voltage are not comparable to those exerted by CS extracts [ 30 ] (Figs.  1 and 2 ).

E-cigarettes as a smoking cessation tool

CS contains a large number of substances—about 7000 different constituents in total, with sizes ranging from atoms to particulate matter, and with many hundreds likely responsible for the harmful effects of this habit [ 93 ]. Given that tobacco is being substituted in great part by e-cigarettes with different chemical compositions, manufacturers claim that e -cigarette will not cause lung diseases such as lung cancer, chronic obstructive pulmonary disease, or cardiovascular disorders often associated with conventional cigarette consumption [ 3 , 94 ]. However, the World Health Organisation suggests that e-cigarettes cannot be considered as a viable method to quit smoking, due to a lack of evidence [ 7 , 95 ]. Indeed, the results of studies addressing the use of e-cigarettes as a smoking cessation tool remain controversial [ 96 , 97 , 98 , 99 , 100 ]. Moreover, both FDA and CDC are actively investigating the incidence of severe respiratory symptoms associated with the use of vaping products [ 77 ]. Because many e-liquids contain nicotine, which is well known for its powerful addictive properties [ 41 ], e-cigarette users can easily switch to conventional cigarette smoking, avoiding smoking cessation. Nevertheless, the possibility of vaping nicotine-free e-cigarettes has led to the branding of these devices as smoking cessation tools [ 2 , 6 , 7 ].

In a recently published randomised trial of 886 subjects who were willing to quit smoking [ 100 ], the abstinence rate was found to be twice as high in the e-cigarette group than in the nicotine-replacement group (18.0% vs. 9.9%) after 1 year. Of note, the abstinence rate found in the nicotine-replacement group was lower than what is usually expected with this therapy. Nevertheless, the incidence of throat and mouth irritation was higher in the e-cigarette group than in the nicotine-replacement group (65.3% vs. 51.2%, respectively). Also, the participant adherence to the treatment after 1-year abstinence was significantly higher in the e-cigarette group (80%) than in nicotine-replacement products group (9%) [ 100 ].

On the other hand, it is estimated that COPD could become the third leading cause of death in 2030 [ 101 ]. Given that COPD is generally associated with smoking habits (approximately 15 to 20% of smokers develop COPD) [ 101 ], smoking cessation is imperative among COPD smokers. Published data revealed a clear reduction of conventional cigarette consumption in COPD smokers that switched to e-cigarettes [ 101 ]. Indeed, a significant reduction in exacerbations was observed and, consequently, the ability to perform physical activities was improved when data was compared with those non-vapers COPD smokers. Nevertheless, a longer follow-up of these COPD patients is required to find out whether they have quitted conventional smoking or even vaping, since the final goal under these circumstances is to quit both habits.

Based on the current literature, it seems that several factors have led to the success of e-cigarette use as a smoking cessation tool. First, some e-cigarette flavours positively affect smoking cessation outcomes among smokers [ 102 ]. Second, e-cigarettes have been described to improve smoking cessation rate only among highly-dependent smokers and not among conventional smokers, suggesting that the individual degree of nicotine dependence plays an important role in this process [ 97 ]. Third, the general belief of their relative harmfulness to consumers' health compared with conventional combustible tobacco [ 103 ]. And finally, the exposure to point-of-sale marketing of e-cigarette has also been identified to affect the smoking cessation success [ 96 ].

Implication of e-cigarette consumption in COVID-19 time

Different reports have pointed out that smokers and vapers are more vulnerable to SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) infections or more prone to adverse outcomes if they suffer COVID-19 [ 104 ]. However, while a systematic review indicated that cigarette smoking is probably associated with enhanced damage from COVID-19, a meta-analysis did not, yet the latter had several limitations due to the small sample sizes [ 105 ].

Interestingly, most of these reports linking COVID-19 harmful effects with smoking or vaping, are based on their capability of increasing the expression of angiotensin-converting enzyme 2 (ACE2) in the lung. It is well known that ACE2 is the gate for SARS-CoV-2 entrance to the airways [ 106 ] and it is mainly expressed in type 2 alveolar epithelial cells and alveolar macrophages [ 107 ]. To date, most of the studies in this field indicate that current smokers have higher expression of ACE2 in the airways (reviewed by [ 108 ]) than healthy non-smokers [ 109 , 110 ]. However, while a recent report indicated that e-cigarette vaping also caused nicotine-dependent ACE2 up-regulation [ 42 ], others have revealed that neither acute inhalation of e-cigarette vapour nor e-cigarette users had increased lung ACE2 expression regardless nicotine presence in the e-liquid [ 43 , 110 ].

In regard to these contentions, current knowledge suggests that increased ACE2 expression is not necessarily linked to enhanced susceptibility to SARS-CoV-2 infection and adverse outcome. Indeed, elderly population express lower levels of ACE2 than young people and SARS-CoV-2/ACE2 interaction further decreases ACE2 expression. In fact, most of the deaths provoked by COVID-19 took place in people over 60 years old of age [ 111 ]. Therefore, it is plausible that the increased susceptibility to disease progression and the subsequent fatal outcome in this population is related to poor angiotensin 1-7 (Ang-1-7) generation, the main peptide generated by ACE2, and probably to their inaccessibility to its anti-inflammatory effects. Furthermore, it seems that all the efforts towards increasing ACE2 expression may result in a better resolution of the pneumonic process associated to this pandemic disease.

Nevertheless, additional complications associated to COVID-19 are increased thrombotic events and cytokine storm. In the lungs, e-cigarette consumption has been correlated to toxicity, oxidative stress, and inflammatory response [ 32 , 112 ]. More recently, a study revealed that while the use of nicotine/flavour-containing e-cigarettes led to significant cytokine dysregulation and potential inflammasome activation, none of these effects were detected in non-flavoured and non-nicotine-containing e-cigarettes [ 43 ]. Therefore, taken together these observations, e-cigarette use may still be a potent risk factor for severe COVID-19 development depending on the flavour and nicotine content.

In summary, it seems that either smoking or nicotine vaping may adversely impact on COVID-19 outcome. However, additional follow up studies are required in COVID-19 pandemic to clarify the effect of e-cigarette use on lung and cardiovascular complications derived from SARS-CoV-2 infection.

Conclusions

The harmful effects of CS and their deleterious consequences are both well recognised and widely investigated. However, and based on the studies carried out so far, it seems that e-cigarette consumption is less toxic than tobacco smoking. This does not necessarily mean, however, that e-cigarettes are free from hazardous effects. Indeed, studies investigating their long-term effects on human health are urgently required. In this regard, the main additional studies needed in this field are summarized in Table 3 .

The composition of e-liquids requires stricter regulation, as they can be easily bought online and many incidences of mislabelling have been detected, which can seriously affect consumers’ health. Beyond their unknown long-term effects on human health, the extended list of appealing flavours available seems to attract new “never-smokers”, which is especially worrying among young users. Additionally, there is still a lack of evidence of e-cigarette consumption as a smoking cessation method. Indeed, e-cigarettes containing nicotine may relieve the craving for smoking, but not the conventional cigarette smoking habit.

Interestingly, there is a strong difference of opinion on e-cigarettes between countries. Whereas countries such as Brazil, Uruguay and India have banned the sale of e-cigarettes , others such as the United Kingdom support this device to quit smoking. The increasing number of adolescent users and reported deaths in the United States prompted the government to ban the sale of flavoured e-cigarettes in 2020. The difference in opinion worldwide may be due to different restrictions imposed. For example, while no more than 20 ng/mL of nicotine is allowed in the EU, e-liquids with 59 mg/dL are currently available in the United States. Nevertheless, despite the national restrictions, users can easily access foreign or even counterfeit products online.

In regard to COVID-19 pandemic, the actual literature suggests that nicotine vaping may display adverse outcomes. Therefore, follow up studies are necessary to clarify the impact of e-cigarette consumption on human health in SARS-CoV-2 infection.

In conclusion, e-cigarettes could be a good alternative to conventional tobacco cigarettes, with less side effects; however, a stricter sale control, a proper regulation of the industry including flavour restriction, as well as further toxicological studies, including their chronic effects, are warranted.

Availability of data and materials

Not applicable.

Abbreviations

Angiotensin-converting enzyme 2

Angiotensin 1-7

Bronchoalveolar lavage fluid

Cinnamaldehyde

US Centers for Disease Control and Prevention

Carbon monoxide

Chronic obstructive pulmonary disease

Coronavirus disease 2019

Cigarette smoke

Electronic nicotine dispensing systems

e-cigarette or vaping product use-associated lung injury

Food and Drug Administration

Gas chromatography with a flame ionisation detector

Gas chromatography-mass spectrometry

Granulocyte–macrophage colony-stimulating factor

High performance liquid chromatography

Human umbilical vein endothelial cells

Interleukin

Interferon γ

Liquid chromatography-mass spectrometry

Monocyte chemoattractant protein-1

Matrix metallopeptidase 9

α7 Nicotinic acetylcholine receptor

Nickel‐chromium alloy

Nitric oxide

Propylene glycol

Regulated on activation, normal T cell expressed and secreted

Reactive oxygen species

Severe acute respiratory syndrome coronavirus 2

Stainless‐steel atomizer

Tetrahydrocannabinol

Tumour necrosis factor-α

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The authors gratefully acknowledge Dr. Cruz González, Pulmonologist at University Clinic Hospital of Valencia (Valencia, Spain) for her thoughtful suggestions and support.

This work was supported by the Spanish Ministry of Science and Innovation [Grant Number SAF2017-89714-R]; Carlos III Health Institute [Grant Numbers PIE15/00013, PI18/00209]; Generalitat Valenciana [Grant Number PROMETEO/2019/032, Gent T CDEI-04/20-A and AICO/2019/250], and the European Regional Development Fund.

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Smoking has long-term effects on the immune system

Like other factors such as age, sex and genetics, smoking has a major impact on immune responses. This is the finding recently made by a team of scientists at the Institut Pasteur using the Milieu Intérieur cohort of 1,000 healthy volunteers, established to understand variability in immune responses. In addition to its short-term impact on immunity, smoking also has long-term consequences. For many years after they have quit the habit, smokers are left with effects on some of their bodies' defense mechanisms acquired while smoking. These findings, which for the first time reveal a long-term memory of the effects of smoking on immunity, will be published in the journal Nature on February 14, 2024.

Individuals' immune systems vary significantly in terms of how effectively they respond to microbial attacks. But how can this variability be explained? What factors cause these differences? "To answer this key question, we set up the Milieu Intérieur cohort comprising 1,000 healthy individuals aged 20 to 70 in 2011," comments Darragh Duffy, Head of the Translational Immunology Unit at the Institut Pasteur and last author of the study. While certain factors such as age, sex and genetics are known to have a significant impact on the immune system, the aim of this new study was to identify which other factors had the most influence."

The scientists exposed blood samples taken from individuals in the Milieu Intérieur cohort to a wide variety of microbes (viruses, bacteria, etc.) and observed their immune response by measuring levels of secreted cytokines (1) . Using the large quantities of data gathered for individuals in the cohort, the team then determined which of the 136 investigated variables (body mass index, smoking, number of hours' sleep, exercise, childhood illnesses, vaccinations, living environment, etc.) had the most influence on the immune responses studied. Three variables stood out: smoking, latent cytomegalovirus infection (2) and body mass index. "The influence of these three factors on certain immune responses could be equal to that of age, sex or genetics," points out Darragh Duffy.

As regards smoking, an analysis of the data showed that the inflammatory response, which is immediately triggered by infection with a pathogen, was heightened in smokers, and moreover, the activity of certain cells involved in immune memory was impaired. In other words, this study shows that smoking disrupts not only innate immune mechanisms, but also some adaptive immune mechanisms. "A comparison of immune responses in smokers and ex-smokers revealed that the inflammatory response returned to normal levels quickly after smoking cessation, while the impact on adaptive immunity persisted for 10 to 15 years," observes Darragh Duffy. "This is the first time it has been possible to demonstrate the long-term influence of smoking on immune responses."

Basically, the immune system appears to have something resembling a long-term memory of the effects of smoking. But how? "When we realized that the profiles of smokers and ex-smokers were similar, we immediately suspected that epigenetic processes were at play (3) ," says Violaine Saint-André, a bioinformatician in the Institut Pasteur's Translational Immunology Unit and first author of the study. "We demonstrated that the long-term effects of smoking on immune responses were linked to differences in DNA methylation (4) -- with the potential to modify the expression of genes involved in immune cell metabolism -- between smokers, ex-smokers and non-smokers." It therefore appears that smoking can induce persistent changes to the immune system through epigenetic mechanisms.

"This is a major discovery elucidating the impact of smoking on healthy individuals' immunity and also, by comparison, on the immunity of individuals suffering from various diseases," concludes Violaine Saint-André.

(1) proteins secreted by a large number of immune cells to communicate among themselves and participate in immune defense.

(2) a virus in the herpes family that is often asymptomatic though dangerous to fetuses.

(3) changes in DNA that affect how genes are expressed, i.e. how they are used by cells.

(4) methylation is a type of chemical modification. Methyl groups position themselves on DNA, changing the way in which the genome is read in the cell.

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  • Violaine Saint-André, Bruno Charbit, Anne Biton, Vincent Rouilly, Céline Possémé, Anthony Bertrand, Maxime Rotival, Jacob Bergstedt, Etienne Patin, Matthew L. Albert, Lluis Quintana-Murci, Darragh Duffy, Laurent Abel, Andres Alcover, Hugues Aschard, Philippe Bousso, Nollaig Bourke, Petter Brodin, Pierre Bruhns, Nadine Cerf-Bensussan, Ana Cumano, Christophe D’Enfert, Caroline Demangel, Ludovic Deriano, Marie-Agnès Dillies, James Di Santo, Gérard Eberl, Jost Enninga, Jacques Fellay, Ivo Gomperts-Boneca, Milena Hasan, Gunilla Karlsson Hedestam, Serge Hercberg, Molly A. Ingersoll, Olivier Lantz, Rose Anne Kenny, Mickaël Ménager, Frédérique Michel, Hugo Mouquet, Cliona O’Farrelly, Antonio Rausell, Frédéric Rieux-Laucat, Lars Rogge, Magnus Fontes, Anavaj Sakuntabhai, Olivier Schwartz, Benno Schwikowski, Spencer Shorte, Frédéric Tangy, Antoine Toubert, Mathilde Touvier, Marie-Noëlle Ungeheuer, Christophe Zimmer. Smoking changes adaptive immunity with persistent effects . Nature , 2024; DOI: 10.1038/s41586-023-06968-8

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Research Article

The Health Effects of Passive Smoking: An Overview of Systematic Reviews Based on Observational Epidemiological Evidence

Affiliation School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

* E-mail: [email protected]

  • Shiyi Cao, 
  • Chen Yang, 
  • Yong Gan, 

PLOS

  • Published: October 6, 2015
  • https://doi.org/10.1371/journal.pone.0139907
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Fig 1

We aim to systematically summarize the available epidemiological evidence to identify the impact of environmental tobacco smoke on health.

A systematic literature search of PubMed, Embase, Web of Science, and Scopus for meta-analyses was conducted through January 2015. We included systematic reviews that investigated the association between passive smoking and certain diseases. Quantitative outcomes of association between passive smoking and the risk of certain diseases were summarized.

Sixteen meta-analyses covering 130 cohort studies, 159 case-control studies, and 161 cross-sectional studies and involving 25 diseases or health problems were reviewed. Passive smoking appears not to be significantly associated with eight diseases or health problems, but significantly elevates the risk for eleven specific diseases or health problems, including invasive meningococcal disease in children (OR 2.18; 95% CI 1.63–2.92), cervical cancer (OR 1.73; 95% CI 1.35–2.21), Neisseria meningitidis carriage (OR 1.68; 95% CI 1.19–2.36), Streptococcus pneumoniae carriage (OR 1.66; 95% CI 1.33–2.07), lower respiratory infections in infancy (OR 1.42; 95% CI 1.33–1.51), food allergy (OR 1.43; 95% CI 1.12–1.83), and so on.

Conclusions

Our overview of systematic reviews of observational epidemiological evidence suggests that passive smoking is significantly associated with an increasing risk of many diseases or health problems, especially diseases in children and cancers.

Citation: Cao S, Yang C, Gan Y, Lu Z (2015) The Health Effects of Passive Smoking: An Overview of Systematic Reviews Based on Observational Epidemiological Evidence. PLoS ONE 10(10): e0139907. https://doi.org/10.1371/journal.pone.0139907

Editor: Yan Li, Shanghai Institute of Hypertension, CHINA

Received: April 23, 2015; Accepted: September 19, 2015; Published: October 6, 2015

Copyright: © 2015 Cao et al. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Data Availability: All relevant data are within the paper and its Supporting Information files.

Funding: The authors have no support or funding to report.

Competing interests: The authors have declared that no competing interests exist.

Introduction

Smoking is a major public health problem worldwide. There have been thousands of studies investigating the impact of active smoking on health, and the overall toxic effects of active smoking are generally recognized [ 1 ]. In comparison, the effects of passive smoking on health are not fully understood. Existing studies suggest that passive smoking and active smoking might equally increase the risk of certain diseases, such as female breast cancer [ 2 ], allergic rhinitis, allergic dermatitis, and food allergy [ 3 ]. As early as 1928, Schonherr suspected that inhalation of husbands’ smoke could cause lung cancer among non-smoking wives [ 4 ]. Since then a substantial body of research about environmental tobacco smoke and health has appeared [ 5 ]. But the impact of passive smoking on health remains largely inconclusive and has not been systematically summarized.

Due to the relative small health risks associated with exposure to passive smoking, investigation of this issue requires large study sizes. Difficulties in measuring passive smoking and controlling various confounding factors further add to the uncertainty in any investigation of the effects of passive smoking. Consequently, a meta-analysis, pooling together individual original studies quantitatively, has played an important part in establishing the evidence about the health effects of passive smoking [ 5 ]. Since Zmirou evaluated the respiratory risk of passive smoking by a meta-analysis in the early 1990s, many meta-analyses of observational epidemiological studies have been published to identify the impact of passive smoking on health.

Recognizing that the evidence is accumulating constantly worldwide, we conducted an overview of systematic reviews that have summarized the evidence from observational epidemiological studies on the health effects of passive smoking.

No protocol exists for this overview of systematic reviews.

Data for this research was acquired from previously published papers. Written consent and ethical approval were not required.

Literature search strategy

We attempted to conduct this overview of systematic reviews in accordance with the rationale and guideline recommended by Cochrane handbook 5.1.0 [ 6 ] ( S1 Checklist ). A systematic literature search of PubMed, Embase, Web of Science, and Scopus was conducted in January 2015 using the following search terms with no restrictions: passive smoking, secondhand smoking, environmental tobacco smoke, involuntary smoking, and tobacco smoke pollution. The reference lists of the retrieved articles were also reviewed. We did not contact authors of the primary studies for additional information.

Selection of relevant systematic reviews

Systematic reviews meeting the following criteria were regarded as eligible: (1) the design was meta-analysis, (2) passive smoking was an exposure variable and the outcome was the incidence of certain diseases or health problems, (3) the included original studies were cross-sectional, case-control, or/and cohort study design, (4) the literature search was international or worldwide, and (5) the pooled relative risk (RR) or odds ratio (OR) and the corresponding 95% confidence interval (CI) of specific diseases relating to exposure to passive smoking were reported or could be calculated from the data provided. Systematic reviews in which all included original studies were conducted in one country or region were excluded. We also excluded the meta-analyses that investigated the association between maternal smoking in pregnancy and the health risk of offspring. All potential meta-analyses were independently screened by two authors (SC and CY), who reviewed the titles or/abstracts first and then conducted a full-text assessment. Disagreements between the two reviewers were resolved through discussion with the third investigator (ZL).

Data extraction

The following information was extracted from the studies by two investigators (SC and CY): first author, publication year, country, number and design of the included original studies, and main quantitative estimates of the association of interest.

Quality appraisal

We appraised all the included meta-analyses using the Assessment of Multiple Systematic Reviews (AMSTAR) standard, an 11-item assessment tool designed to appraise the methodological quality of systematic reviews [ 7 ]. The maximum score is 11, and 0–4, 5–8, and 9–11 respectively indicates low, moderate, and high quality [ 8 ]. Disagreements on assessment scores were resolved by discussion among the authors.

Synthesis of the evidence

There may be more than one meta-analysis published regarding the association between passive smoking and risk of a specific disease. We only included the latest meta-analysis and excluded all the previous ones. For each included meta-analysis, we summarized the number and design of the included original studies, the main quantitative estimates of association of interest, heterogeneity between original studies, and so on. In any included meta-analyses, when estimates of association between passive smoking and certain diseases were reported separately for subgroups, we combined the results of the subgroups and calculated common estimates using a fixed-effects model if appropriate.

Literature search

Fig 1 shows the process of study identification and inclusion. Initially, we retrieved 2,079 articles from Pubmed, Emabse, Web of Science, and Scopus. After 1,105 duplicates were excluded, 974 articles were screened through titles and abstracts, of which 858 were excluded mainly because they were original studies or irrelevant reviews. After full-text review of the remaining 116 articles, 100 were further excluded because they did not report the outcomes of interest or their findings were already updated by newer systematic reviews. Finally, 16 meta-analyses were included [ 3 , 9 – 23 ].

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https://doi.org/10.1371/journal.pone.0139907.g001

Characteristics and quality of the included systematic reviews

The main characteristics of the sixteen meta-analyses were summarized in Table 1 . These meta-analyses covered a total of 130 cohort studies, 159 case-control studies, and 161 cross-sectional studies. They were published between 1998 and 2014. The quality scores of these meta-analyses appraised using AMSTAR ranged from 3 to 10. The numbers of meta-analyses with high quality, middle quality, and low quality were 5, 9, and 2 respectively (see Table 2 ).

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https://doi.org/10.1371/journal.pone.0139907.t001

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https://doi.org/10.1371/journal.pone.0139907.t002

The Main Health Consequences of Passive Smoking

Fig 2 shows the integrated results on the impact of passive smoking on specific diseases. The included 16 meta-analyses covered 25 diseases or health problems. There was statistically significant positive relationship between exposure environmental tobacco smoke and the risk of eleven diseases, especially invasive meningococcal disease in children (OR 2.18; 95% CI 1.63–2.92) and other three diseases or health problems with a 1.5 to 2.0-fold increase in the risk: cervical cancer (OR 1.73; 95% CI 1.35–2.21), Neisseria meningitidis carriage (OR 1.68; 95% CI 1.19–2.36), and Streptococcus pneumoniae carriage (OR 1.66; 95% CI 1.33–2.07). The increase in the risk of other seven diseases associated with exposure to passive smoking was statistically significant but small in impact size (OR was less than 1.5): lower respiratory infections in infancy (OR 1.42; 95% CI 1.33–1.51), food allergy (OR 1.43; 95% CI 1.12–1.83), childhood asthma (OR 1.32; 95% CI 1.23–1.42), lung cancer (OR 1.27; 95% CI 1.17–1.37), stroke (OR 1.25; 95% CI 1.12–1.38), allergic rhinitis (OR 1.09; 95% CI 1.04–1.14), and allergic dermatitis (OR 1.07; 95% CI 1.03–1.12). Of these 25 diseases or health problems, eight diseases were not found to be significantly associated with passive smoking. They were invasive Haemophilus influenzae type B (Hib) disease, invasive pneumococcal disease, Crohn's disease, pancreatic cancer, ulcerative colitis, breast cancer, bladder cancer, and pharyngeal carriage for Hib. In addition, the effects of passive smoking on increased risk of coronary heart disease, tuberculosis, diabetes, and middle ear disease in children (recurrent otitis media, middle ear effusion, and glue ear) were not conclusive, because the number of included studies was small or the quality of the corresponding meta-analysis was low.

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https://doi.org/10.1371/journal.pone.0139907.g002

Passive smoking and cancer risk

We investigated the association of passive smoking with the risk of lung cancer, cervical cancer, pancreatic cancer, breast cancer, and bladder cancer. Based on 55 observational studies (7 cohort studies, 25 population-based case-control studies and 23 non-population-based case-control studies), passive smoking were found to be associated with the increased risk of lung cancer (OR 1.27; 95% CI 1.17 to 1.37). The ORs for lung cancer in North America, Asia, and Europe were similar [ 19 ]. 11 case-control studies, involving 3,230 cases and 2,982 controls, suggested a positive relationship between passive smoking and cervical cancer (OR 1.73; 95% CI 1.35–2.21) [ 15 ]. Pancreatic cancer [ 21 ], breast cancer [ 13 ], and bladder cancer were not found to be associated with passive smoking.

Passive smoking and allergic diseases

A meta-analysis of observational studies published in PLOS Medicine systematically reviewed the effects of exposure to environmental smoke on allergic diseases [ 3 ]. The pooled ORs of 63 studies for allergic rhinitis, 58 studies for allergic dermatitis, and 6 studies for food allergies were 1.07 (95% CI 1.03–1.12), 1.09 (95% CI 1.04–1.14), and 1.43 (95% CI 1.12–1.83) respectively. Another meta-analysis investigated the association between passive smoking and the risk of physician-diagnosed childhood asthma [ 9 ], and suggested that there was consistent evidence of a modest positive association between them (OR 1.32; 95% CI: 1.23–1.42).

Passive smoking and pediatric invasive bacterial disease and bacterial carriage

Passive smoking was also thought to be associated with pediatric invasive bacterial disease and bacterial carriage. A meta-analysis involving 30 case-control studies for invasive bacterial disease and 12 cross-sectional studies for bacterial carriage indicated that the risk of invasive meningococcal disease, pharyngeal carriage for Neisseria, meningitidies and Streptococcus pneumoniae were significantly associated with passive smoking, and the ORs were 2.18, 95% CI 1.63 to 2.92), 1.68 (95% CI, 1.19–2.36), and 1.66 (95% CI 1.33–2.07), respectively. The risk of invasive pneumococcal disease, invasive Hib disease, and pharyngeal carriage for Hib were not found to be related to exposure to environmental smoke.

The health effects of environmental tobacco smoke are attracting more and more attention worldwide. Increasing numbers of original studies and meta-analyses are being published focusing on this important issue. In the present overview of systematic reviews based on sixteen systematic reviews involving 450 original observational studies, we found that passive smoking could significantly increase the risk of eleven diseases, especially invasive meningococcal disease in children, cervical cancer, Neisseria meningitidis carriage, and Streptococcus. pneumoniae carriage, but not associated with other eight diseases. Cancers were one of the most common investigated health outcomes associated with passive smoking. We found that exposure to environmental tobacco smoke could increase the risk of lung cancer and cervical cancer, but was not the risk of pancreatic cancer, breast cancer, or bladder cancer. It appears that passive smoking could increase the risk of some diseases among children, especially bacterial infections (e.g., lower respiratory infections in infancy, middle ear disease in children, invasive meningococcal disease in children, allergic diseases in children, and childhood asthma).

Previously, there were some reviews focusing on the health effects of exposure to environmental tobacco smoke. But they were qualitative or only involved children or limited to several diseases [ 24 – 26 ]. We used a systematic overview to summarize the quantitative estimates of the associations between passive smoking and various diseases based on all latest available meta-analyses. It should be noted that, in the present overview, we excluded meta-analyses evaluating the effects of smoking during pregnancy on fetus or offspring health, because the effects was obviously different from the health effects of active smoking or conventional passive smoking in the general population.

The quality of included original studies influences the reliability of the results and conclusions of the corresponding meta-analysis; similarly, the validity of the results of an overview of systematic reviews depends on the quality of the included systematic reviews. We used AMSTAR protocol, an internationally recognized assessment tool, to appraise the methodological quality of all included meta-analyses, and found that there were two meta-analyses with low quality. Accordingly, the conclusions drawn based on these two meta-analyses involving middle ear disease in children and coronary heart disease need to be interpreted with caution.

The evidence level of meta-analyses partly depends on the number and the design type of included original studies. Although there was no consensus about the minimum number of original studies included in meta-analysis, but more caution is needed when an association is assessed based on a small number of original studies. In our overview, we found a significant positive association between passive smoking and tuberculosis (OR 4.01; 95% CI 2.54–6.34), but it was only based on 4 case-control studies. More studies should be conducted to further assess the relationship between them. Similarly, the effect of passive smoking on diabetes was based on 6 cohort studies (OR 1.21; 95% CI 1.07–1.38), and more original studies are also needed.

There were several strengths in our research. Firstly, we followed the primary rationale and method of Cochrane overviews of reviews [ 6 ] to summarize the health consequences of certain exposure. Overview of systematic reviews is primarily intended to summarize multiple reviews addressing the effects of two or more potential interventions for a single condition or health problem. Up to now, most of overviews have been conducted to evaluate the effects of several interventions [ 27 , 28 ], and very few overviews have addressed the effects of a single exposure factor on multiple diseases or health problems based on observational studies. Our present overview expands the application of overviews of systematic reviews. Additionally, our study provides robust and comprehensive scientific information for smoking ban in public places and for educational pamphlets about passive smoking.

Some limitations in our overview should be noted. Firstly, we only included systematic reviews but not original studies. The associations of passive smoking with some diseases might have been investigated by original studies but not synthesized by meta-analyses and, therefore, were not summarized in this overview. Secondly, the mechanism on the health effects of passive smoking was not be examined since our study only intended to summarize relevant observational epidemiological evidence.

In summary, our overview of systematic reviews of up-to-date epidemiological evidence suggests that passive smoking is significantly associated with an increasing risk of many diseases and health problems, especially diseases in children and cancers. This study provides comprehensive population-based evidence about toxic effect of exposure to environmental tobacco smoke and should benefit developing health promotion strategies of smoking control. Stricter regulations against cigarette smoking should be formulated and implemented, because smoking harms not only own health but also the health of neighboring people.

Supporting Information

S1 prisma checklist..

https://doi.org/10.1371/journal.pone.0139907.s001

Acknowledgments

Access to data.

All the data in this review are from publicly published papers, and we take responsibility for the integrity of the data and the accuracy of the data analysis.

Author Contributions

Conceived and designed the experiments: ZL. Performed the experiments: SC CY. Analyzed the data: SC YG. Contributed reagents/materials/analysis tools: CY. Wrote the paper: SC.

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  • 14 February 2024

Smoking’s lasting effect on the immune system

  • Yang Luo   ORCID: http://orcid.org/0000-0001-7385-6166 0 &
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Yang Luo is at the Kennedy Institute of Rheumatology, University of Oxford, Oxford OX3 7FY, UK.

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Simon Stent is a research scientist based in Oxford, UK.

When our bodies encounter pathogens such as bacteria and viruses, immune cells release molecules called cytokines to coordinate the body’s defence mechanisms. These cytokines send signals to other immune cells to mount an appropriate response against the invading pathogens. The secretion of cytokines can vary among individuals and is influenced by both environmental and inherited factors. Writing in Nature , Saint-André et al . 1 report their examination of data from the Milieu Intérieur project 2 , a research initiative designed to study the variability in the immune system among 1,000 healthy individuals.

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Nature 626 , 724-725 (2024)

doi: https://doi.org/10.1038/d41586-024-00232-3

Saint-André, V. et al. Nature 626 , 827–835 (2024).

Article   Google Scholar  

Thomas, S. et al. Clin. Immunol. 157 , 277–293 (2015).

Article   PubMed   Google Scholar  

Burgos, M. et al. Ther. Adv. Med. Oncol . 14 , 17588359211072621 (2022).

Prüss-Ustün, A. et al. BMJ 364 , l265 (2019).

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Smoking is the factor that most alters our defenses, even years after quitting

An experiment with 1,000 people from the same city that began over a decade ago reveals the unknown persistent effects of tobacco on our immune responses.

Fumar

The Covid pandemic was a master class in understanding that each person has characteristic defenses against diseases. Some people who got infected with the coronavirus did not even realize it, while others died in a matter of days. A little over a decade ago, the Spanish biologist Lluís Quintana-Murci and his American colleague Matthew Albert began a bold experiment to understand the determining factors of this variability. They recruited 1,000 healthy people between 20 and 70 years of age in the French city of Rennes, choosing 100 volunteers of each sex for each decade. They all provided blood and stool samples and filled out a 44-page questionnaire about their lifestyle. Skin biopsies were even taken to grow their cells in the laboratory. The latest results were presented on Wednesday, and they show that smoking is the factor that most alters defenses, even years after having stopped smoking.

There are more than 100 reasons to reject tobacco, according to a count kept by the World Health Organization: the greater risk of suffering from cancer or a heart attack, bad body odor, the expense, facial wrinkles, yellowish teeth, damage to people exposed to second-hand smoke. Reasons 79, 80, 81 and 82 detail that the toxic substances in tobacco weaken the immune system and increase the risk of infections, tumors, autoimmune diseases and AIDS. The new study, published today in the journal Nature , warns that the white blood cells of ex-smokers remain altered for years. It is the environmental factor that has the most influence of the 136 variables that were analyzed, followed by body mass index and latent infections by cytomegalovirus, a pathogen known to leave consequences in one in five affected babies.

The authors of the study, from the Pasteur Institute in Paris, focused on the production of cytokines, proteins that are released in cells when they detect a pathogen and help coordinate the immune response. The researchers, led by biologist Violaine Saint-André and immunologist Darragh Duffy, observed that smoking affects the non-specific innate defenses with which we are born, causing greater inflammatory responses. This harmful effect disappears when you quit smoking. However, scientists detected that the cells responsible for specific immunity — those acquired during life — remain altered for years after quitting. Smoking is the only factor with effects that are comparable to immutable variables such as age, sex and genetics.

The Spanish biologist Lluís Quintana-Murci (first row, center) with his team at the Pasteur Institute.

The researchers assert that their results “have potential clinical implications for the risk of developing infections, cancers or autoimmune diseases,” but they are cautious. They have not yet studied the relationship between this alteration of white blood cells and tumors. “However, it is well known from much other previous work that smoking increases the risk of multiple types of cancer, but the longer it has been since you stopped smoking, the lower the risk,” explains Duffy. The immunologist cites a recent study with almost three million participants in South Korea where researchers observed a 50% reduction in the risk of cancer after 15 years of quitting smoking.

The 1,000 volunteers in Rennes have Western European ancestors, to facilitate analysis in a genetically homogeneous population, but the authors are already working on similar experiments in other locations, such as Senegal and Hong Kong.

The president of the Spanish Society of Immunology, Marcos López Hoyos, applauded the new work, in which he has not participated. “In many patients with chronic smoking and COPD [chronic obstructive pulmonary disease] we have always seen a clinical finding: we found hypogammaglobulinemia [low levels of antibodies], which is a cause of secondary immunodeficiency,” he points out. “In COPD with smoking there are more infections and there is more cancer. The alteration of the cytokines that they have observed clearly indicates that it can favor an alteration in the regulation of the immune response and generate these diseases, although they do not prove it,” says López Hoyos, who is the scientific director of the Marqués de Valdecilla Research Institute in Santander. “It’s a beautiful experiment.”

The new results are “very interesting, but not surprising,” according to oncologist Alberto Ocaña, who urges caution. “The study only shows that tobacco alters the immune system, not that these alterations are the cause of cancer . Cancer is a genetic disease that also requires other added alterations, such as a dysfunctional immune system,” explains Ocaña, coordinator of the Experimental Cancer Therapies Unit at the San Carlos Clinical Hospital in Madrid.

The Pasteur Institute team has grown cells from volunteers, put them in contact with different substances in the laboratory and analyzed how they behave. Immunologist África González, from the University of Vigo, is surprised by the duration of the effects of smoking. “It is striking that this signature is persistently maintained in the immune system, as if to say: “You have smoked.” And those cells, when they have been exposed to tobacco, are going to behave differently against a pathogen,” she reflects. “They cannot say categorically that this alteration increases your risk of cancer, but tobacco itself not only alters the immune response, but also contains many substances that are carcinogenic in themselves.”

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This article has been reviewed according to Science X's editorial process and policies . Editors have highlighted the following attributes while ensuring the content's credibility:

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Research shows lasting effects of smoking after quitting

smoke

Researchers are still discovering how smoking continues to harm people's health even years after they quit, with a new study on Wednesday revealing tobacco's lasting effect on the immune system.

Despite the tobacco industry long fighting to conceal the dangers of smoking, tobacco is now known to kill more than eight million people globally a year, according to the World Health Organization.

But the myriad of ways the habit damages bodies are still coming to light.

The new study, published in the journal Nature , found that smoking alters the immune system , which protect bodies from infection, for far longer than previously thought.

It particularly highlighted changes to what is called adaptive immunity, which is built up over time as the body's specialized cells remember how to fight back against foreign pathogens they have encountered before.

The findings were based on analyzing blood and other samples taken from 1,000 healthy people in France starting from more than a decade ago.

Smoking was found to have more influence on adaptive immunity than other factors such as amount of sleep or physical activity , the researchers said.

The study also confirmed previous research which has shown smoking's effect on "innate immunity," which is the body's first line of defense against invading pathogens.

While innate immunity rebounded immediately after people stopping smoking, adaptive immunity remained effected for years, even decades after quitting, the study said.

The sample size was too small to give a precise timeline for how long these changes last.

The researchers emphasized that the effect does wear off—so the sooner people quit the better.

Of course, it is still better "for long term immunity to never start smoking," lead study author Violaine Saint-Andre of France's Pasteur Institute told a press conference.

The researchers could not say for sure what consequences these changes may have on health. But they hypothesized that it could affect people's risk of infections, cancer or autoimmune diseases.

The sooner the better

Another study, published last week in the journal NEJM Evidence , aimed to determine how much quitting smoking was linked to a lower risk of disease and dying early.

It covered 1.5 million people across the United States, Canada, Norway and the UK, some of them active smokers, some who never started—and everyone in between.

When people quit smoking, it took 10 years for their average life expectancy to return to the same level as non-smokers, according to the study.

Again, the researchers emphasized the importance of quitting as soon as possible—some benefits were evident as early as three years after kicking the habit.

The effect was noticeable no matter what age people quit, however the benefits were more pronounced for those under 40.

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Smoking and Its Negative Effects on Human Beings Research Paper

Smoking is one of the most common negative habits that people indulge in. Many health experts have warned that smoking is unhealthy and dangerous to the human health. This essay will discuss the negative effects of smoking on human beings.

Smoking cigarette is addictive that is why many smokers have difficulties in giving up the habit. Cigarettes are produced of tobacco with a large percent of other additives, which account for the largest number of preventable deaths in the world. People who smoke commonly face different health problems, which are caused by tobacco consumption. Therefore, smoking has negative health consequences for smokers and people who live with them and become passive smokers as a result.

The WHO and other health organisations have sensitised people on the dangers of smoking. There are many health conditions which smokers are likely to suffer from (Pampel 61). Their bodies absorb harmful toxins which cigarettes contain which are dangerous to their health.

Smoking is a major health risk which results in heart attacks, strokes, bronchitis, and other respiratory diseases. The accumulation of tobacco and other toxins in the respiratory tract of a smoker makes a person suffer from respiratory health conditions.

Smokers, therefore, are likely to incur huge medical bills when they seek for treatment for these diseases. Many governments spend a lot of money on treating smoking related diseases, which increases the cost of healthcare. Pampel argues that smokers can succumb to such illnesses unless they stop smoking (64).

Tobacco consumption causes dental problems which are difficult to reverse. Smokers are likely to have bad breath, stained teeth and smelly gums. Toxic elements, which cigarettes contain, for instance, tar, have dangerous impacts on human health. These substances cause smokers to have poor dents and even lose their teeth (Peate 362).

Smokers are likely to suffer emotionally and psychologically because poor health and unattractive appearance, caused, for example, by stained or broken teeth, make a person lose his/her own self-esteem. Smokers are likely to be shunned by people close to them because of fetid breath, bad body odour and poor outward appearance. Therefore, people need to be made aware of dental and other health problems they are likely to experience as a result of smoking.

Tobacco consumption causes a lot of deaths in developing countries. These countries have weak laws which do not effectively regulate cigarette selling and consumption. Advertisement implicit messages encourage the young to become smokers. Tobacco advertising in many developed countries has been prohibited. However, some third world countries still allow tobacco advertising, which encourages more people to acquire this bad habit.

The images of sophistication, bravery and glamour which are carried by tobacco adverts easily persuade the young to become smokers. Peate reveals that tobacco companies target adolescents and women to increase their sales (363). These people are easily influenced by what they see in the media. People who begin smoking at early age are likely to be addicted for a longer period than those who develop the habit at mature age (Cox).

Smokers are exposed to various carcinogens in cigarettes. These carcinogens cause cancer and negatively affect human health. Lung, throat, brain, bladder, cervical cancer as well as other forms are caused by smoking. The symptoms are often detected at the time when the smoker’s health condition is already chronic.

Cancer is one of the leading causes of death world wide. A significant number of cancer patients have a history of smoking and tobacco consumption (Peate 365). If people get exposed to exhaled smoke, they are likely to be affected by it. They breathe in toxic components of the exhaled smoke that deposit in their lungs and other respiratory organs. These people can suffer from respiratory illnesses as well.

Women, who smoke during pregnancy, are likely to expose their unborn babies to toxic substances contained in cigarettes. The tar that is present in cigarettes is likely to be embedded in the DNA of a mother, who may pass it on to the child in her womb. These toxic components inhibit the normal growth of a baby in the fetus, which results in death and still births. Cox reveals that if the pregnancy proceeds to full term, the delivered child can have severe brain disorders.

Such children are very slow at learning because their cognitive functions are impaired. Female smokers are likely to become infertile or their reproductive abilities are limited. Nicotine restricts the ability of the female reproductive system to generate estrogen. Many physiological and reproductive functions in women depend on estrogen.

Nicotine is a substance found in cigarettes which is very addictive. People who try to give up smoking experience severe withdrawal symptoms, which restrict their ability to function effectively. They are likely to experience several episodes of depression.

This is because their bodies are used to the intake of nicotine and have difficulties in performing its functions without it (Cox). Nicotine stimulates the human mind just like any other drug, which increases the risk of high blood pressure in a smoker. From the above mentioned, it is easy to conclude that smoking has negative effects on people’s health.

Works Cited

Cox, Jack. “The Lesser Known Harmful Effects of Smoking.” The Register , 21 Nov. 2012. Orange Country Register News . Web. < https://www.ocregister.com/2012/11/21/the-lesser-known-harmful-effects-of-smoking/ >.

Pampel, Fred C. Tobacco Industry and Smoking . New York: Infobase Publishing, 2009. Print.

Peate, Ian. “The Effects of Smoking on the Reproductive Health of Men”. British Journal of Nursing 14.7 (2005): 362–366. Print.

  • Chicago (A-D)
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IvyPanda. (2020, July 8). Smoking and Its Negative Effects on Human Beings. https://ivypanda.com/essays/smoking-effects/

"Smoking and Its Negative Effects on Human Beings." IvyPanda , 8 July 2020, ivypanda.com/essays/smoking-effects/.

IvyPanda . (2020) 'Smoking and Its Negative Effects on Human Beings'. 8 July.

IvyPanda . 2020. "Smoking and Its Negative Effects on Human Beings." July 8, 2020. https://ivypanda.com/essays/smoking-effects/.

1. IvyPanda . "Smoking and Its Negative Effects on Human Beings." July 8, 2020. https://ivypanda.com/essays/smoking-effects/.

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IvyPanda . "Smoking and Its Negative Effects on Human Beings." July 8, 2020. https://ivypanda.com/essays/smoking-effects/.

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AFP

Research shows lasting effects of smoking after quitting

R esearchers are still discovering how smoking continues to harm people's health even years after they quit, with a new study on Wednesday revealing tobacco's lasting effect on the immune system.

Despite the tobacco industry long fighting to conceal the dangers of smoking, tobacco is now known to kill more than eight million people globally a year, according to the World Health Organization.

But the myriad of ways the habit damages bodies are still coming to light. 

The new study, published in the journal Nature, found that smoking alters the immune system, which protect bodies from infection, for far longer than previously thought.

It particularly highlighted changes to what is called adaptive immunity, which is built up over time as the body's specialised cells remember how to fight back against foreign pathogens they have encountered before.

The findings were based on analysing blood and other samples taken from 1,000 healthy people in France starting from more than a decade ago.

Smoking was found to have more influence on adaptive immunity than other factors such as amount of sleep or physical activity, the researchers said.

The study also confirmed previous research which has shown smoking's effect on "innate immunity," which is the body's first line of defence against invading pathogens.

While innate immunity rebounded immediately after people stopping smoking, adaptive immunity remained effected for years, even decades after quitting, the study said.

The sample size was too small to give a  precise timeline for how long these changes last.

The researchers emphasised that the effect does wear off -- so the sooner people quit the better.

Of course, it is still better "for long term immunity to never start smoking," lead study author Violaine Saint-Andre of France's Pasteur Institute told a press conference.

The researchers could not say for sure what consequences these changes may have on health. But they hypothesised that it could affect people's risk of infections, cancer or autoimmune diseases.

- The sooner the better -

Another study, published last week in the journal NEJM Evidence, aimed to determine how much quitting smoking was linked to a lower risk of disease and dying early.

It covered 1.5 million people across the United States, Canada, Norway and the UK, some of them active smokers, some who never started -- and everyone in between.

When people quit smoking, it took 10 years for their average life expectancy to return to the same level as non-smokers, according to the study.

Again, the researchers emphasised the importance of quitting as soon as possible -- some benefits were evident as early as three years after kicking the habit.

The effect was noticeable no matter what age people quit, however the benefits were more pronounced for those under 40.

A new study has shown how smoking alters the body's immune system for years after people quit

IMAGES

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  5. 20 Devastating😳😳 Health Problems Caused by Smoking 🚭 #shorts #short video viral #shorts #smoking

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    This paper reviews the extent and nature of harms caused by smoking, the benefits of stopping, patterns of smoking, psychologi-cal, pharmacological and social factors that contribute to uptake and mainte-nance of smoking, the effectiveness of population and individual level interventions aimed at combatting tobacco smoking, and the effectiveness...

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    Smoking increases the risk for cardiovascular disease and lung cancer. It is responsible for about 90 percent of all lung cancer deaths and 80 percent of all deaths from chronic obstructive ...

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    Tobacco causes human deaths, more than by all deaths from HIV, illegal drug use, alcohol use, and motor vehicle injuries, suicides, and murders combined [ ]. Smokers die 14 years earlier than nonsmokers [ ]. Tobacco smoking is a leading cause of human cancer and deaths which are higher in developing countries than in developed countries.

  10. Harmful health effects of cigarette smoking

    2 Altmetric Explore all metrics Abstract This is a comprehensive review on the harmful health effects of cigarette smoking. Tobacco smoking is a reprehensible habit that has spread all over the world as an epidemic. It reduces the life expectancy among smokers.

  11. Harmful health effects of cigarette smoking

    This is a comprehensive review on the harmful health effects of cigarette smoking. Tobacco smoking is a reprehensible habit that has spread all over the world as an epidemic. It reduces the life expectancy among smokers. It increases overall medical costs and contributes to the loss of productivity ….

  12. (PDF) Cigarettes and Its Effects on Health

    Various studies have found that smoking is a risk factor for NCD. Conclusion: Cessation of smoking can save sufferers and also save people around smokers. When a smoker starts quitting...

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    Measuring self-reported experience of health and functioning is important for understanding the changes in the health status of individuals switching from cigarettes to less harmful tobacco and/or nicotine products (TNP) or reduced-risk products (RRP) and for supporting tobacco harm reduction strategies. This paper presents insights from three research activities from the preparatory phase of ...

  14. Health Effects of Cigarette Smoking

    References Cigarette smoking harms nearly every organ of the body, causes many diseases, and reduces the health of smokers in general. 1,2 Quitting smoking lowers your risk for smoking-related diseases and can add years to your life. 1,2 Smoking and Death Cigarette smoking is the leading cause of preventable death in the United States.1

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    Read the paper: Smoking changes adaptive immunity with persistent effects ... Although the authors' findings demonstrate the short-term and long-term effects of smoking on cytokine responses in ...

  21. Scientists discover smoking has a harmful impact on the ...

    Cigarette smoking has a long-term impact on the immune system, according to a new study. Scientists from the French Institut Pasteur have found that years after smokers quit, the effects tobacco ...

  22. Smoking's effects on the immune system can last years, study finds

    CNN —. Smoking tobacco is so harmful to the body that it changes a person's immune system, leaving them vulnerable to more disease and infection even years after they've quit, a new study ...

  23. Smoking is the factor that most alters our defenses, even years after

    This harmful effect disappears when you quit smoking. However, scientists detected that the cells responsible for specific immunity — those acquired during life — remain altered for years after quitting. Smoking is the only factor with effects that are comparable to immutable variables such as age, sex and genetics.

  24. Research shows lasting effects of smoking after quitting

    Credit: CC0 Public Domain. Researchers are still discovering how smoking continues to harm people's health even years after they quit, with a new study on Wednesday revealing tobacco's lasting ...

  25. Smoking and Its Negative Effects on Human Beings Research Paper

    Smoking and Its Negative Effects on Human Beings Research Paper Exclusively available on IvyPanda Smoking is one of the most common negative habits that people indulge in. Many health experts have warned that smoking is unhealthy and dangerous to the human health. This essay will discuss the negative effects of smoking on human beings.

  26. Research shows lasting effects of smoking after quitting

    Research shows lasting effects of smoking after quitting. Researchers are still discovering how smoking continues to harm people's health even years after they quit, with a new study on Wednesday ...