Hormones And Smelling Smoke


Link found between hormones and smelling smoke

It is important to understand the composition of cigarettes in order to understand how it can affect our health. Cigarettes contain up to thousands of different toxic components, such as polycyclic aromatic (benzene-like in structure) hydrocarbons that involve nicotine and cotinine. Some metals such as nitrosamines and arsenate are included as well, in addition to toxic cyanide, acrolein, cresols and acetaldehyde.1

Nicotine, as one of the distilled products of tobacco with its well-distinguished smell, can interfere with the hydroxylation process that is required for the synthesis of oestrogen, which is an essential hormone for reproductive fertility and feminine sexuality. . It is worth noting that such effects could reach a gene-level influence on the hydroxylation enzymes of activation of oestrogen, which are known as cytochrome enzymes.2

Moreover, smoking can lead to menopause-like symptoms such as  low bone mass density. This is not a direct relationship, but a consequence of decreased levels of oestrogen, which is essential for the preservation of bone mass density. This could  result in osteoporosis and  multiple pathological fractures  

Furthermore; several studies found smoking to be linked to low spermatic function with a subsequent lower fertility capability. In addition, erectile dysfunction was also associated with smoking. These are believed to cause oxidative stress that injures the lining of the penile vascularity. Smoking decreases the level of efficacy of testosterone by increasing the level of testosterone-binding proteins in the body, with a faster rate of deactivation of testosterone in the liver.4

Smoking was linked to thyroid gland disorders at different stages. This can also impact passive smokers, who are exposed to smoke rather than doing it. Evidence has found greater amounts of thyroid binding protein and thiocyanate in infants with smoking fathers than in those with non-smoking fathers. Thiocyanate is believed to be the cause of increased thyroid size, higher levels of thyroid hormones and lower levels of thyroid stimulating hormones due to the possibility of increased sympathetic activity in the body.5

The cyanide component of cigarettes is believed to be a factor in diffuse thyroid gland enlargement pathologies in females. This is more evident in diseases such as Grave's disease than in Hashimoto's disease. Smoking can increase eye protrusion in Grave's disease as accumulation of autoantibodies in the controlling muscles of the eye globe cause them to thicken. Nicotine can also  reduce  the efficacy of the treatment of thyroid disorders - a higher possibility of their recurrence was found.6,7

Smoking can affect the central axis of hormone secretion, affecting the pituitary gland hormone production. Nausea and vomiting were believed to due to smoking affecting the emetic centres with a subsequent rise in the anterior pituitary hormones such as growth hormone (GH), adrenocorticotropic hormone (ACTH), and antidiuretic hormone (ADH). Moreover, smoking can induce an increase in GH secretion in pregnancy due to the raised need of the foetus of a smoking mother for oxygenated blood. In addition, increased ADH secretion can mediate the sympathetic effect of nicotine on blood pressure.8 

Smoking shows multiple stimulatory effects on the adrenal gland. It was found to cause an increase in cortisol, even with a short period of nicotine exposure. This may result from the rise in ACTH or ADH. In addition, smoking increases the level of aldosterone, renin, and angiotensin hormones due to a possible sympathetic overstimulation.9

Concerning the adrenal medulla, smoking has a direct enhancing effect on adrenaline and noradrenaline, causing raised blood pressure. Smoking can increase the adrenal sex hormones due to its interference with the hydroxylation processes of androgens.10

Smoking is also linked to type 2 diabetes mellitus as it is  associated with increased  insulin secretion which can lead to  glucose intolerance. This owes to the decrease in the peripheral uptake and use of glucose, especially under the effect of glucose-increasing hormones such as GH and ACTH whose levels increase with smoking.11

Exposure to the smell of nicotine has been associated with a decrease in the ability to   distinguish smell.12 Although this can significantly affect the function of our olfactory system, several studies still consider this impact less than that of anosmia. In other words, it does not lead to  complete loss of smell.13

It is worth noting that tobacco smoking may induce stress which can be in the form of inflammation of the olfactory mucosa. This may be accompanied by the release of the previously anti-stress hormones, such as growth hormone, ACTH, cortisol and even thyroid hormones. Thus, this effect may exceed its locality by being more systemic, while affecting hormones that are carried in the blood. This would exacerbate the negative effect of smoking on smell by affecting the central affection of olfaction, rather than the peripheral affection.14


Although smoking has shown  recreational  and possible mood-stabilising benefits, its negative effects still require more studies. 


  1. Prevention (US) C for DC and, Promotion (US) NC for CDP and H, Health (US) O on S and. Chemistry and toxicology of cigarette smoke and biomarkers of exposure and harm [Internet]. Centers for Disease Control and Prevention (US); 2010 [cited 2022 Dec 28]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK53014/
  2. Marom-Haham L, Shulman A. Cigarette smoking and hormones. Current Opinion in Obstetrics & Gynecology [Internet]. 2016 Aug [cited 2023 Feb 5];28(4):230–5. Available from: https://journals.lww.com/00001703-201608000-00003
  3. Daniel M, Martin AD, Drinkwater DT. Cigarette smoking, steroid hormones, and bone mineral density in young women. Calcif Tissue Int. 1992 Apr;50(4):300–5.
  4. Jandíková H, Dušková M, Stárka L. The influence of smoking and cessation on the human reproductive hormonal balance. Physiol Res. 2017 Sep 26;66(Suppl 3):S323–31.
  5. Utiger RD. Effects of smoking on thyroid function. Eur J Endocrinol. 1998 Apr;138(4):368–9.
  6. Wiersinga WM, Bartalena L. Epidemiology and prevention of Graves’ ophthalmopathy. Thyroid. 2002 Oct;12(10):855–60.
  7. Vestergaard P. Smoking and thyroid disorders--a meta-analysis. Eur J Endocrinol. 2002 Feb;146(2):153–61.
  8. Kapoor D, Jones TH. Smoking and hormones in health and endocrine disorders. European Journal of Endocrinology [Internet]. 2005 Apr 1 [cited 2022 Dec 28];152(4):491–9. Available from: https://eje.bioscientifica.com/view/journals/eje/152/4/1520491.xml
  9. Frederick SL, Reus VI, Ginsberg D, Hall SM, Munoz RF, Ellman G. Cortisol and response to dexamethasone as predictors of withdrawal distress and abstinence success in smokers. Biol Psychiatry. 1998 Apr 1;43(7):525–30.
  10. García Calzado MC, García Rojas JF, Mangas Rojas A, Millán J. [Tobacco and arterial pressure (Ii.). The acute effects on the angiotensin-converting enzyme]. An Med Interna. 1990 Aug;7(8):392–5.
  11. Chiodera P, Volpi R, Capretti L, Speroni G, Necchi-Ghiri S, Caffarri G, et al. Abnormal effect of cigarette smoking on pituitary hormone secretions in insulin-dependent diabetes mellitus. Clin Endocrinol (Oxf). 1997 Mar;46(3):351–7.
  12. Katotomichelakis M, Balatsouras D, Tripsianis G, Davris S, Maroudias N, Danielides V, et al. The effect of smoking on the olfactory function. Rhinology. 2007 Dec;45(4):273–80.
  13. Gudziol H, Graul J, Bitter T, Guntinas-Lichius O. Riechsinn wird durch akutes Rauchen reversibel und durch chronisches Rauchen dauerhaft geschädigt. Laryngorhinootologie [Internet]. 2013 Oct [cited 2022 Dec 28];92(10):663–6. Available from: http://www.thieme-connect.de/DOI/DOI?10.1055/s-0033-1349082
  14. Çengel Kurnaz S, Tahir E, Kavaz E. Olfactory dysfunction in passive vs active smoking. Laryngoscope Investig Otolaryngol. 2021 Oct;6(5):932–9.
This content is purely informational and isn’t medical guidance. It shouldn’t replace professional medical counsel. Always consult your physician regarding treatment risks and benefits. See our editorial standards for more details.

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Mohamed Abulfadl

Master of Medical Biochemistry and Molecular Biology- Faculty of Medicine, Aswan University, Egypt

Mohamed is a medical doctor with neurology and nephrology research interest. He has an experience
of working for three years as a dual specialist of diagnostic Medicine (both diagnostic imaging and
Laboratory medicine).
Additionally, he has an interest in supporting university students, either as a teaching assistant, mentor
or even invigilator since 2016.
He is currently on a PHD study on translational neuroscience in Bristol medical school in UK.

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