Author: Dr Susan Simpkin, Medical Registrar, Waikato Hospital, Hamilton, New Zealand, 2010. Updated by Hon Assoc Prof Amanda Oakley, Dermatolgist, Waikato Hospital, Hamilton, New Zealand, November 2016.
Skin and hair are exposed to various environmental noxious agents, including tobacco smoke. Tobacco smoke consists of thousands of substances that damage the skin, and nicotine itself is harmful.
Beyond its known links to cancer, lung and heart disease, smoking is associated with premature skin ageing, delayed wound healing, and increased infections, as well as a number of skin disorders, particularly psoriasis, hidradenitis suppurativa and cutaneous lupus erythematosus. There is a general observation that smokers tend to be more severely affected than non-smokers by the majority of inflammatory skin diseases — even acne —and various conditions are often more difficult to treat effectively in smokers.
Tobacco smoke causes oxidative stress so that insufficient oxygen is supplied to the skin resulting in tissue ischaemia and blood vessel occlusion. It reduces innate and host immune responses, and induces metallo-proteinase MMP-1, an enzyme that specifically degrades collagen.
Nicotine replacement is safer for the skin than smoking, although nicotine itself induces vasoconstriction, inhibits inflammation, delays wound healing and accelerates skin ageing.
Tobacco smoking has unpleasant temporary cutaneous and mucosal effects:
Longer term, the gaunt skin of a 40-year-old heavy smoker resembles that of non-smoking 70-year-old:
It is not certain exactly how smoking causes early ageing of the facial skin. Theories include:
Smoking delays wound healing, including skin injuries and surgical wounds. It increases the risk of wound infection, graft or flap failure, death of tissue and blood clot formation. The reasons for this are unclear but involve:
Smoking is associated with a greater likelihood or severity of:
If you have genital warts and you smoke, you have a greater chance of developing wart-virus associated cancers, including cervical cancer, vulval intraepitheial cancer, vulval cancer or penile intraepithelial cancer.
Smoking cigarettes doubles the risk of developing a type of skin cancer called squamous cell carcinoma, compared to non-smokers. There is also an increased risk of oral leukoplakia (precancer) and oral cancer; 75% of cases of oral cancer and lip cancer occur in smokers. Smoking does not appear to increase the risk of basal cell carcinoma.
Smoking cessation reduces the risk of metastasis (spread) from lip cancer by 2–3-fold.
Palmoplantar pustulosis is treatment-resistant, chronic, and disabling dermatosis characterised by pustules, erythema and scaling on the soles and palms. It mainly affects middle-aged women, >90% of whom smoke. The mechanism relates to nicotine binding with acetylcholine receptors in the sweat gland and duct, to change their structure and induce inflammation.
Cessation of smoking gradually results in improvement and the pustules may eventually clear up in many patients.
Several studies have confirmed that smokers tend to have more extensive and severe psoriasis than those that do not. Patients with chronic plaque psoriasis smoke more than patients without psoriasis. The research is confounded by those with obesity or metabolic syndrome and quality of life issues.
The mechanism appears to be that smoking induces inflammatory mediators and promotes keratinocyte proliferation. Nicotine itself binds to dendritic cells, T-cells and keratinocytes.
The majority of patients with hidradenitis suppurativa (HS) are smokers, and smokers have a greater burden of disease than non-smokers. There is genetic predisposition to HS, and it is particularly prevalent in obese women. The pathogenesis involves nicotine/acetylcholine-induced follicular occlusion, follicular rupture, and immune dysregulation. Smokers respond poorly to current treatment options.
Nicotine causes vasoconstriction and hypercoagulability, increasing the chance of blood clots occluding blood vessels.
Smoking can aggravate or initiate:
There is more than ten-fold risk of chronic cutaneous lupus erythematosus (especially discoid lupus erythematosus) in smokers compared to non-smokers. Smoking increases autoimmune activity by activating the lymphocytes. There is also suspicion that treatment of chronic cutaneous LE is less effective in smokers.
Treatment of cutaneous lupus erythematosus with hydroxychloroquine and other medications is less effective in smokers.
Conditions affecting the mouth tend to be more common in smokers. These include:
Polycyclic aromatic hydrocarbons from smoking induces CYP1A2 enzymes in the liver. These enzymes destroy toxins. The result is that smokers need higher doses of many medicines compared to non-smokers to achieve the same result. These include insulin, pain relievers, antipsychotics, anticoagulants, caffeine and alcohol.
Alcohol intake and caffeine intake are on average double in smokers. This tolerance of alcohol and caffeine is quickly lost when a smoker stops smoking. Previously tolerated amounts of alcohol and caffeine can thus result in unexpected toxicity.
Alcohol ingestion can also lead to smoking more.
Some inflammatory diseases are less common or less severe in smokers than non-smokers. These include:
However, smoking is not recommended as treatment due to its adverse effects and risk of addiction.
If you want to stop smoking or are thinking about quitting, there are people and services who can help.
A combination of approaches is often best. A meter to measure carbon monoxide in breath can be used to guide treatment.
Nicotine-containing patches, gum, lozenges, nasal spray, inhalers and e-cigarettes may or may not be beneficial to the skin in patients attempting to stop smoking.
Cutaneous side effects may result in poor patient adherence to treatment.
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