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The Hidden Health Costs of Tobacco Use: Risking More Than Just Your Lungs

Thursday 2 July, 2026      |     Read Time: 4 mins

‍Beth Wright

‍

"Smoking is bad" does not do justice to the sheer amount of damage caused to the body by tobacco smoke [1].

Yet the normalisation of smoking is seeping back into 2026 culture, appearing online, in tabloids, and even being repopularised on the red carpet. It is a familiar foe, but with vaping and e-cigarettes adding new dimensions to an old problem, it is becoming increasingly clear that the battle for lung health is far from over.

The scale of the tobacco problem

Tobacco cultivation dates back over 12,000 years [2] and its origin lies with the indigenous populations in the Americas, where it held significant ceremonial and medicinal value, evolving from the species Nicotiana tabacum.

It wasn’t until 1964 that the dangers of tobacco use were officially recognised and the first public health warning was issued.

Considering how long it has been around, and how much research has been garnered to prove its deadly effect, tobacco use was supposed to be in long-term decline. For a while at least, it was, but this downhill trajectory among young people has plateaued. The rise of vaping, which is also aggressively marketed and flavoured to appeal to teens, has stalled the progress made pre-2010. The candy-style packaging of nicotine pouches is similarly targeted. Black-market tobacco has also closed the affordability gap that once deterred price-sensitive younger smokers.

The United Nations (UN) puts the tobacco usage among youth into global perspectives (3);

  • 15 million adolescents (aged 13–15) worldwide use e-cigarettes.
  • Adolescents are nine times more likely to vape than adults.
  • 40 million adolescents (aged 13–15) worldwide use tobacco.
These aren't abstract statistics. They represent developing brains being primed for lifelong nicotine dependence at the very stage of life when the neurological consequences are most severe.

Not all smoke is equal, but none of it is safe

Most people think of tobacco harm as a first-person issue, without understanding the true risk of second or third-hand smoke exposure. There are three distinct exposure types, each with its own chemistry and risk profile:

First-hand smoke

Directly inhaled smoke from cigarettes, cigars, or pipes contains the highest concentration of carcinogens and toxins. More than 7000 chemicals have been identified in cigarette smoke, with over 250 of these confirmed harmful and 70 confirmed or likely carcinogenic [4,5]. To put this into perspective, vehicle exhaust fumes contain

Second-hand smoke

This includes both exhaled smoke and the emissions from burning tobacco ends. This type of smoke can also contain up to the 70 known carcinogens, along with the chemicals that remain unknown, with no existing safe level of exposure [5].

Third-hand smoke

This is less well-known and often lumped in with second-hand smoke, yet it is important to distinguish it in its own category. It includes the smoke residue that clings to surfaces, clothing, and furniture. It is chemically reactive and particularly dangerous to infants and young children who touch and mouth surfaces.

Detailing Tobacco damage

The lungs: what looking at the statistics reveals

Each year, tobacco kills over 8 million people globally, which is more than malaria, HIV/AIDS, and road injuries combined.

Lungs take on the brunt of visible damage caused by smoking, with diseases such as chronic bronchitis, emphysema and squamous cell carcinoma [6,7,8] being increasingly likely to develop.

"All forms of tobacco use are harmful, and there is no safe level of exposure to tobacco." - WHO

With 10 forms of lung cancer, it should come as no surprise that 7 of these are directly linked to smoking [1]. The numbers related to tobacco-related deaths are just as harrowing. For instance, in 2021 tobacco was implicated in over 64% of deaths due to cancer of the trachea, bronchus and lung and over 38% of deaths from Chronic Obstructive Pulmonary Disease (COPD).

It does not stop here. Of the 8 million tobacco-related deaths, around 1.2 million are non-smokers dying from second-hand smoke exposure, including infants.

The effects of smoking during pregnancy are well-documented, with chemicals known to cross and directly enter placenta from the mother’s bloodstream. This exposure has been linked to premature birth, low birth weight, and in some cases, it can tragically end in sudden infant death syndrome (SIDS).

It is increasingly well-established that the body’s many systems are intricately connected, so it makes sense that the damage caused by smoking is not found within the lungs alone - smoking (regardless of whether it is first, second or third hand) has whole body/systemic implications.

Looking outside the lungs

Smoking has serious consequences for your heart.

In fact, it doubles your risk of having a stroke (stroke foundation).

Smoking increases blood pressure (BP), damaging blood vessels over time and increasing chances of blood clot formation. This is a result of the many chemicals in smoke rapidly entering your blood stream and causing inflammation of vessel linings, allowing plaque to build up and leading to atherosclerosis (hardening of the arteries).

Smoking makes your blood stickier.

The platelets that seal your wounds externally also help seal wounds internally - and overactivation inside your blood vessels due to the damage caused by ongoing high blood pressure (hypertension) can lead to blood clot formation, something that is observed in smoking.

There are other ways that nicotine raises BP.

In fact, BP can be elevated following brain receptor stimulation caused by nicotine binding. This binding causes the release of adrenaline and noradrenaline (vital brain signaling chemicals or neurotransmitters), causing an increase in heart contractions per minute, and constricting blood vessels, raising BP [5]. For people with hypertension who already have an abnormally high BP, smoking can result in the loss of efficacy of anti-hypertensive drugs known as ACE-inhibitors. So, as well as increased stroke risk, kidney damage becomes a growing concern [9-11].

Alongside loss of heart health, bone health is rapidly affected by smoking.

Tobacco inhalation disrupts the essential bone remodeling cycle maintaining bone density. Your bone undergoes a continual process of resorption of mature bone tissue and formation of new tissue to maintain bone strength, repair damage and regulate calcium levels (a key player in muscle function).  This loss of regulation results in lower bone mass, increasing risks of osteoporosis and fracture [11].

So, lungs, heart, kidney, bones - what about the brain?

Cigarette smoking also has profound impacts on our brain - particularly on our mood-stabilising ‘happy chemical’ serotonin.

Smoking and serotonin: the mood trap.

This is perhaps the least discussed mechanism, and one of the most insidious.

Here’s how.

Nicotine temporarily increases the release of serotonin. This is the neurotransmitter central to mood regulation, emotional stability, and sleep. It also suppresses the brain's own serotonin synthesis over time.

The result is a biochemical trap: the more you smoke, the more your baseline serotonin drops and the more relief each cigarette seems to provide. Smokers frequently describe cigarettes as "calming", but the calm is the temporary relief of a deficiency that smoking itself created. Nicotine dependence and depression are deeply entangled, with causality running in both directions.

Quitting without support can trigger significant mood disruption. This is precisely why cessation should be treated as a medical event, not a willpower contest.

Quitting works and the body knows it fast

The case for quitting is overwhelming, and the body begins to repair itself within minutes of the last cigarette. These gains are real, measurable, and cumulative:

20 minutes

  • Your heart rate (HR) and BP drop following the initial stimulatory effect on the body associated with nicotine binding to the shoes. Both BP and HR begin normalising almost immediately after the cigarette in healthy individuals without existing lung disease.

12 hours

  • After 12 hours, the carbon monoxide (CO) in the lungs should have been removed, allowing blood oxygen levels to return to normal.
  • CO is an odorless toxic gas that can be introduced into the lungs by the incomplete combustion of tobacco when smoking. The intriguing thing about CO? It binds more strongly to your blood cells than oxygen, meaning it displaces the oxygen that otherwise would be delivered to your tissues and vital oxygen.
  • This explains the breathlessness caused by smoking, which is not always due to air sac (alveoli) death.

2-12 weeks

  • For long-time smokers, lung function can increase by up to 30% following just 3 months of quitting.

1 year and beyond

  • Coronary heart disease risk is roughly half that of a current smoker, with the risk of stroke matching a non-smoker by 5-10 years.
The resilience of the human body is unbelievable, as long as we give it the chance.

What methods actually work for quitting?

The most effective quitting approaches combine nicotine replacement therapy (NRT), such as patches, gum, lozenges, prescription options such as Varenicline (Champix/Chantix) and Bupropion, with behavioral support.

Yet, as over 32% of smokers may rely on smoking to manage a mental health issue [13,14] it's crucial to address the underlying reasons for their smoking in the first place.

Management of the serotonin disruption smokers experience, through counselling or antidepressant support, has also been shown to significantly improve quit rates in people with comorbid depression or anxiety.

No single method works for everyone, though the research consistently shows that doing nothing about the psychological dependence, while only managing the physical one, or vice versa, leads to higher relapse rates.

If you think the message of “No Smoking” is outdated, think again.

The tobacco pandemic continues and the statistics are unambiguous. Tobacco kills 8 million people a year, including over 1.2 million from second-hand smoke who never lit a cigarette [16].

‍

Disclaimer: The content provided on Diag-Nose.io is intended solely for informational and educational purposes. It does not constitute, and should not be relied upon as, medical advice, diagnosis, or treatment. Every effort is made to ensure the information provided is accurate and up-to-date. Users should consult a licensed physician or qualified healthcare provider before making any health-related decisions.

‍

‍

References

  1. Effects of smoking and tobacco | Australian Government Department of Health, Disability and Ageing
  2. Tushingham, S., Snyder, C. M., Brownstein, K. J., Damitio, W. J., & Gang, D. R. (2018). Biomolecular archaeology reveals ancient origins of indigenous tobacco smoking in North American Plateau. Proceedings of the National Academy of Sciences of the United States of America, 115(46), 11742–11747. https://doi.org/10.1073/pnas.1813796115
  3. United Nations (2025). WHO: Despite smoking decline, tobacco still hooks one in five adults worldwide | UN News.
  4. [Harms of Cigarette Smoking and Health Benefits of Quitting - NCI](https://www.cancer.gov/about-cancer/causes-prevention/risk/tobacco/cessation-fact-sheet#:~:text=Of the more than 7%2C000 chemicals in tobacco,tobacco smoke%2C at least 69 can cause cancer.)
  5. U.S. Dept of Health and Human Services. The Health Consequences of Smoking—50 Years of Progress: A Report of the Surgeon General. U.S. Dept of Health and Human Services; 2014.
  6. Bozinovski, S., Vlahos, R., Anthony, D., McQualter, J., Anderson, G., Irving, L., & Steinfort, D. (2016). COPD and squamous cell lung cancer: aberrant inflammation and immunity is the common link. British journal of pharmacology, 173(4), 635–648. https://doi.org/10.1111/bph.13198
  7. Casara, A., Turato, G., Marin-Oto, M., Semenzato, U., Biondini, D., Tinè, M., Bernardinello, N., Cocconcelli, E., Cubero, P., Balestro, E., Spagnolo, P., Marin, J. M., Cosio, M. G., Saetta, M., & Bazzan, E. (2022). Chronic Bronchitis Affects Outcomes in Smokers without Chronic Obstructive Pulmonary Disease (COPD). Journal of clinical medicine, 11(16), 4886. https://doi.org/10.3390/jcm11164886
  8. Mathew, A. R., Bhatt, S. P., Colangelo, L. A., Allen, N. B., Jacobs, D. R., Jr, Auer, R., Dransfield, M. T., Hitsman, B., Washko, G. R., & Kalhan, R. (2019). Life-Course Smoking Trajectories and Risk for Emphysema in Middle Age: The CARDIA Lung Study. American journal of respiratory and critical care medicine, 199(2), 237–240. https://doi.org/10.1164/rccm.201808-1568LE
  9. Al-Bashaireh, A. M., Haddad, L. G., Weaver, M., Chengguo, X., Kelly, D. L., & Yoon, S. (2018). The Effect of Tobacco Smoking on Bone Mass: An Overview of Pathophysiologic Mechanisms. Journal of osteoporosis, 2018, 1206235. https://doi.org/10.1155/2018/1206235
  10. Mahmud, A, Feely, J. Effect of Smoking on Arterial Stiffness and Pulse Pressure Amplification. Hypertension. 2002; 41(1):183-7. https://doi.org/10.1161/01.HYP.0000047464.66901.60
  11. Leone A. (2011). Does Smoking Act as a Friend or Enemy of Blood Pressure? Let Release Pandora's Box. Cardiology research and practice, 2011, 264894. https://doi.org/10.4061/2011/264894
  12. Gould, T. Epigenetic and long-term effects of nicotine on biology, behavior, and health. Pharmacological Research. 2023;192(106741):1043-6618.https://doi.org/10.1016/j.phrs.2023.106741.
  13. Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to smoking: 50 years' observations on male British doctors. BMJ. 2004; 328(7455):1519-1527.
  14. The Department of Health and Ageing, SANE. smoking-and-mental-illness-a-guide-for-health-professionals_0.pdf
  15. WHO. Tobacco: The Health Benefits of Smoking Cessation.Tobacco: Health benefits of smoking cessation
  16. WHO. Preventing non-communicable diseases. Tobacco kills 8 million people every year

About WHO

Founded in 1948, the World Health Organization (WHO) is the United Nations agency responsible for international public health. Operating across 150 countries, WHO connects nations, partners, and people with a single mandate: to ensure that everyone, everywhere can attain the highest possible standard of health.

WHO leads global efforts to expand universal health coverage, directs and coordinates the international response to health emergencies, and advances evidence-based policies that promote health across the full course of life. Progress is measured against the Triple Billion targets - a commitment to extend universal health coverage, emergency protection, and improved wellbeing to one billion additional people in each category.

About Diag-Nose.io

Diag-Nose.io, founded in 2020, is a TechBio company focused on translating the complexities of the unified airway into precision diagnostic and drug discovery solutions.

Their precision medicine technology combines advanced proteomics, computational biology, and AI (machine learning) to create a scalable respiratory biology model. This innovation aims to help clinicians prescribe the right treatments faster and enable researchers to accelerate the development of new therapies.

The company’s flagship platform, RhinoMAP™, leverages proteomic data to predict respiratory disease activity, monitor therapy response and predict treatment efficacy in advance, with an initial focus on anti-Th2 biologics.

Learn more at Diag-Nose.io

About the author

Beth Wright

Junior Researcher

Beth Wright, a Junior Researcher at Diag-Nose, expertly aims to improve accessibility of medical information and research in the field of Respiratory Disease.

Beth holds a BBiomedSc. from Monash University.

Thursday 2 July, 2026      |     Read Time: 4 mins

‍Beth Wright

‍

"Smoking is bad" does not do justice to the sheer amount of damage caused to the body by tobacco smoke [1].

Yet the normalisation of smoking is seeping back into 2026 culture, appearing online, in tabloids, and even being repopularised on the red carpet. It is a familiar foe, but with vaping and e-cigarettes adding new dimensions to an old problem, it is becoming increasingly clear that the battle for lung health is far from over.

The scale of the tobacco problem

Tobacco cultivation dates back over 12,000 years [2] and its origin lies with the indigenous populations in the Americas, where it held significant ceremonial and medicinal value, evolving from the species Nicotiana tabacum.

It wasn’t until 1964 that the dangers of tobacco use were officially recognised and the first public health warning was issued.

Considering how long it has been around, and how much research has been garnered to prove its deadly effect, tobacco use was supposed to be in long-term decline. For a while at least, it was, but this downhill trajectory among young people has plateaued. The rise of vaping, which is also aggressively marketed and flavoured to appeal to teens, has stalled the progress made pre-2010. The candy-style packaging of nicotine pouches is similarly targeted. Black-market tobacco has also closed the affordability gap that once deterred price-sensitive younger smokers.

The United Nations (UN) puts the tobacco usage among youth into global perspectives (3);

  • 15 million adolescents (aged 13–15) worldwide use e-cigarettes.
  • Adolescents are nine times more likely to vape than adults.
  • 40 million adolescents (aged 13–15) worldwide use tobacco.
These aren't abstract statistics. They represent developing brains being primed for lifelong nicotine dependence at the very stage of life when the neurological consequences are most severe.

Not all smoke is equal, but none of it is safe

Most people think of tobacco harm as a first-person issue, without understanding the true risk of second or third-hand smoke exposure. There are three distinct exposure types, each with its own chemistry and risk profile:

First-hand smoke

Directly inhaled smoke from cigarettes, cigars, or pipes contains the highest concentration of carcinogens and toxins. More than 7000 chemicals have been identified in cigarette smoke, with over 250 of these confirmed harmful and 70 confirmed or likely carcinogenic [4,5]. To put this into perspective, vehicle exhaust fumes contain

Second-hand smoke

This includes both exhaled smoke and the emissions from burning tobacco ends. This type of smoke can also contain up to the 70 known carcinogens, along with the chemicals that remain unknown, with no existing safe level of exposure [5].

Third-hand smoke

This is less well-known and often lumped in with second-hand smoke, yet it is important to distinguish it in its own category. It includes the smoke residue that clings to surfaces, clothing, and furniture. It is chemically reactive and particularly dangerous to infants and young children who touch and mouth surfaces.

Detailing Tobacco damage

The lungs: what looking at the statistics reveals

Each year, tobacco kills over 8 million people globally, which is more than malaria, HIV/AIDS, and road injuries combined.

Lungs take on the brunt of visible damage caused by smoking, with diseases such as chronic bronchitis, emphysema and squamous cell carcinoma [6,7,8] being increasingly likely to develop.

"All forms of tobacco use are harmful, and there is no safe level of exposure to tobacco." - WHO

With 10 forms of lung cancer, it should come as no surprise that 7 of these are directly linked to smoking [1]. The numbers related to tobacco-related deaths are just as harrowing. For instance, in 2021 tobacco was implicated in over 64% of deaths due to cancer of the trachea, bronchus and lung and over 38% of deaths from Chronic Obstructive Pulmonary Disease (COPD).

It does not stop here. Of the 8 million tobacco-related deaths, around 1.2 million are non-smokers dying from second-hand smoke exposure, including infants.

The effects of smoking during pregnancy are well-documented, with chemicals known to cross and directly enter placenta from the mother’s bloodstream. This exposure has been linked to premature birth, low birth weight, and in some cases, it can tragically end in sudden infant death syndrome (SIDS).

It is increasingly well-established that the body’s many systems are intricately connected, so it makes sense that the damage caused by smoking is not found within the lungs alone - smoking (regardless of whether it is first, second or third hand) has whole body/systemic implications.

Looking outside the lungs

Smoking has serious consequences for your heart.

In fact, it doubles your risk of having a stroke (stroke foundation).

Smoking increases blood pressure (BP), damaging blood vessels over time and increasing chances of blood clot formation. This is a result of the many chemicals in smoke rapidly entering your blood stream and causing inflammation of vessel linings, allowing plaque to build up and leading to atherosclerosis (hardening of the arteries).

Smoking makes your blood stickier.

The platelets that seal your wounds externally also help seal wounds internally - and overactivation inside your blood vessels due to the damage caused by ongoing high blood pressure (hypertension) can lead to blood clot formation, something that is observed in smoking.

There are other ways that nicotine raises BP.

In fact, BP can be elevated following brain receptor stimulation caused by nicotine binding. This binding causes the release of adrenaline and noradrenaline (vital brain signaling chemicals or neurotransmitters), causing an increase in heart contractions per minute, and constricting blood vessels, raising BP [5]. For people with hypertension who already have an abnormally high BP, smoking can result in the loss of efficacy of anti-hypertensive drugs known as ACE-inhibitors. So, as well as increased stroke risk, kidney damage becomes a growing concern [9-11].

Alongside loss of heart health, bone health is rapidly affected by smoking.

Tobacco inhalation disrupts the essential bone remodeling cycle maintaining bone density. Your bone undergoes a continual process of resorption of mature bone tissue and formation of new tissue to maintain bone strength, repair damage and regulate calcium levels (a key player in muscle function).  This loss of regulation results in lower bone mass, increasing risks of osteoporosis and fracture [11].

So, lungs, heart, kidney, bones - what about the brain?

Cigarette smoking also has profound impacts on our brain - particularly on our mood-stabilising ‘happy chemical’ serotonin.

Smoking and serotonin: the mood trap.

This is perhaps the least discussed mechanism, and one of the most insidious.

Here’s how.

Nicotine temporarily increases the release of serotonin. This is the neurotransmitter central to mood regulation, emotional stability, and sleep. It also suppresses the brain's own serotonin synthesis over time.

The result is a biochemical trap: the more you smoke, the more your baseline serotonin drops and the more relief each cigarette seems to provide. Smokers frequently describe cigarettes as "calming", but the calm is the temporary relief of a deficiency that smoking itself created. Nicotine dependence and depression are deeply entangled, with causality running in both directions.

Quitting without support can trigger significant mood disruption. This is precisely why cessation should be treated as a medical event, not a willpower contest.

Quitting works and the body knows it fast

The case for quitting is overwhelming, and the body begins to repair itself within minutes of the last cigarette. These gains are real, measurable, and cumulative:

20 minutes

  • Your heart rate (HR) and BP drop following the initial stimulatory effect on the body associated with nicotine binding to the shoes. Both BP and HR begin normalising almost immediately after the cigarette in healthy individuals without existing lung disease.

12 hours

  • After 12 hours, the carbon monoxide (CO) in the lungs should have been removed, allowing blood oxygen levels to return to normal.
  • CO is an odorless toxic gas that can be introduced into the lungs by the incomplete combustion of tobacco when smoking. The intriguing thing about CO? It binds more strongly to your blood cells than oxygen, meaning it displaces the oxygen that otherwise would be delivered to your tissues and vital oxygen.
  • This explains the breathlessness caused by smoking, which is not always due to air sac (alveoli) death.

2-12 weeks

  • For long-time smokers, lung function can increase by up to 30% following just 3 months of quitting.

1 year and beyond

  • Coronary heart disease risk is roughly half that of a current smoker, with the risk of stroke matching a non-smoker by 5-10 years.
The resilience of the human body is unbelievable, as long as we give it the chance.

What methods actually work for quitting?

The most effective quitting approaches combine nicotine replacement therapy (NRT), such as patches, gum, lozenges, prescription options such as Varenicline (Champix/Chantix) and Bupropion, with behavioral support.

Yet, as over 32% of smokers may rely on smoking to manage a mental health issue [13,14] it's crucial to address the underlying reasons for their smoking in the first place.

Management of the serotonin disruption smokers experience, through counselling or antidepressant support, has also been shown to significantly improve quit rates in people with comorbid depression or anxiety.

No single method works for everyone, though the research consistently shows that doing nothing about the psychological dependence, while only managing the physical one, or vice versa, leads to higher relapse rates.

If you think the message of “No Smoking” is outdated, think again.

The tobacco pandemic continues and the statistics are unambiguous. Tobacco kills 8 million people a year, including over 1.2 million from second-hand smoke who never lit a cigarette [16].

‍

Disclaimer: The content provided on Diag-Nose.io is intended solely for informational and educational purposes. It does not constitute, and should not be relied upon as, medical advice, diagnosis, or treatment. Every effort is made to ensure the information provided is accurate and up-to-date. Users should consult a licensed physician or qualified healthcare provider before making any health-related decisions.

‍

‍

References

  1. Effects of smoking and tobacco | Australian Government Department of Health, Disability and Ageing
  2. Tushingham, S., Snyder, C. M., Brownstein, K. J., Damitio, W. J., & Gang, D. R. (2018). Biomolecular archaeology reveals ancient origins of indigenous tobacco smoking in North American Plateau. Proceedings of the National Academy of Sciences of the United States of America, 115(46), 11742–11747. https://doi.org/10.1073/pnas.1813796115
  3. United Nations (2025). WHO: Despite smoking decline, tobacco still hooks one in five adults worldwide | UN News.
  4. [Harms of Cigarette Smoking and Health Benefits of Quitting - NCI](https://www.cancer.gov/about-cancer/causes-prevention/risk/tobacco/cessation-fact-sheet#:~:text=Of the more than 7%2C000 chemicals in tobacco,tobacco smoke%2C at least 69 can cause cancer.)
  5. U.S. Dept of Health and Human Services. The Health Consequences of Smoking—50 Years of Progress: A Report of the Surgeon General. U.S. Dept of Health and Human Services; 2014.
  6. Bozinovski, S., Vlahos, R., Anthony, D., McQualter, J., Anderson, G., Irving, L., & Steinfort, D. (2016). COPD and squamous cell lung cancer: aberrant inflammation and immunity is the common link. British journal of pharmacology, 173(4), 635–648. https://doi.org/10.1111/bph.13198
  7. Casara, A., Turato, G., Marin-Oto, M., Semenzato, U., Biondini, D., Tinè, M., Bernardinello, N., Cocconcelli, E., Cubero, P., Balestro, E., Spagnolo, P., Marin, J. M., Cosio, M. G., Saetta, M., & Bazzan, E. (2022). Chronic Bronchitis Affects Outcomes in Smokers without Chronic Obstructive Pulmonary Disease (COPD). Journal of clinical medicine, 11(16), 4886. https://doi.org/10.3390/jcm11164886
  8. Mathew, A. R., Bhatt, S. P., Colangelo, L. A., Allen, N. B., Jacobs, D. R., Jr, Auer, R., Dransfield, M. T., Hitsman, B., Washko, G. R., & Kalhan, R. (2019). Life-Course Smoking Trajectories and Risk for Emphysema in Middle Age: The CARDIA Lung Study. American journal of respiratory and critical care medicine, 199(2), 237–240. https://doi.org/10.1164/rccm.201808-1568LE
  9. Al-Bashaireh, A. M., Haddad, L. G., Weaver, M., Chengguo, X., Kelly, D. L., & Yoon, S. (2018). The Effect of Tobacco Smoking on Bone Mass: An Overview of Pathophysiologic Mechanisms. Journal of osteoporosis, 2018, 1206235. https://doi.org/10.1155/2018/1206235
  10. Mahmud, A, Feely, J. Effect of Smoking on Arterial Stiffness and Pulse Pressure Amplification. Hypertension. 2002; 41(1):183-7. https://doi.org/10.1161/01.HYP.0000047464.66901.60
  11. Leone A. (2011). Does Smoking Act as a Friend or Enemy of Blood Pressure? Let Release Pandora's Box. Cardiology research and practice, 2011, 264894. https://doi.org/10.4061/2011/264894
  12. Gould, T. Epigenetic and long-term effects of nicotine on biology, behavior, and health. Pharmacological Research. 2023;192(106741):1043-6618.https://doi.org/10.1016/j.phrs.2023.106741.
  13. Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to smoking: 50 years' observations on male British doctors. BMJ. 2004; 328(7455):1519-1527.
  14. The Department of Health and Ageing, SANE. smoking-and-mental-illness-a-guide-for-health-professionals_0.pdf
  15. WHO. Tobacco: The Health Benefits of Smoking Cessation.Tobacco: Health benefits of smoking cessation
  16. WHO. Preventing non-communicable diseases. Tobacco kills 8 million people every year

About WHO

Founded in 1948, the World Health Organization (WHO) is the United Nations agency responsible for international public health. Operating across 150 countries, WHO connects nations, partners, and people with a single mandate: to ensure that everyone, everywhere can attain the highest possible standard of health.

WHO leads global efforts to expand universal health coverage, directs and coordinates the international response to health emergencies, and advances evidence-based policies that promote health across the full course of life. Progress is measured against the Triple Billion targets - a commitment to extend universal health coverage, emergency protection, and improved wellbeing to one billion additional people in each category.

About Diag-Nose.io

Diag-Nose.io, founded in 2020, is a TechBio company focused on translating the complexities of the unified airway into precision diagnostic and drug discovery solutions.

Their precision medicine technology combines advanced proteomics, computational biology, and AI (machine learning) to create a scalable respiratory biology model. This innovation aims to help clinicians prescribe the right treatments faster and enable researchers to accelerate the development of new therapies.

The company’s flagship platform, RhinoMAP™, leverages proteomic data to predict respiratory disease activity, monitor therapy response and predict treatment efficacy in advance, with an initial focus on anti-Th2 biologics.

Learn more at Diag-Nose.io

About the author

Beth Wright

Junior Researcher

Beth Wright, a Junior Researcher at Diag-Nose, expertly aims to improve accessibility of medical information and research in the field of Respiratory Disease.

Beth holds a BBiomedSc. from Monash University.