Smoking and its effects on the skin

Introduction

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.

How does smoking damage the skin?

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.

Smoking and ageing skin

Tobacco smoking has unpleasant temporary cutaneous and mucosal effects:

Temporary yellowing of fingers and fingernails
Discoloured teeth
Black hairy tongue.

Longer term, the gaunt skin of a 40-year-old heavy smoker resembles that of non-smoking 70-year-old:

Facial wrinkles and furrows (eg, crows’ feet at lateral canthus, vertical ear crease, smoker’s lines around lips)
Baggy eyelids and slack jawline
Uneven skin colouring: greyish, yellow with prominent blood vessels (telangiectasia)
Dry, coarse skin.

How does smoking cause ageing of the skin?

It is not certain exactly how smoking causes early ageing of the facial skin. Theories include:

Heat from the cigarette directly burning the skin
Changes in the elastic fibres of the skin (elastosis )
Narrowing of blood vessels (vasoconstriction), which reduces blood supply to the skin and can cause changes in skin elastic fibres and loss of collagen
Reducing vitamin A levels and moisture of the skin.

Smoking and wound healing

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:

Vascoconstriction and lack of oxygen reaching skin cells
Delayed migration of keratinocytes
Decreased collagen synthesis
Delayed growth of new blood vessels within the wound.

Smoking contributes to the development and persistence of leg ulcers, particularly arterial ulcers, diabetic foot ulcers and calciphylaxis.

Slow healing wounds in smokers

Smoking and infections

Smoking is associated with a greater likelihood or severity of:

Bacterial wound infections, most often caused by Staphylococccus aureus and Streptococcus pyogenes
Candida albicans infection, particularly in the mouth
Viral infections, especially human papillomavirus (HPV), including genital warts.

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 and skin 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.

Smoking and skin cancer

Smoking and palmoplantar pustulosis

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.

Smoking and pustulosis

Smoking and psoriasis

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.

Smoking and psoriasis

Smoking and hidradenitis suppurativa

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.

Smoking and vascular disease

Nicotine causes vasoconstriction and hypercoagulability, increasing the chance of blood clots occluding blood vessels.

Smoking can aggravate or initiate:

Chilblains
Frostbite
Primary or secondary vasospastic disease (Raynaud phenomenon)
Ulceration, in patients with systemic sclerosis
Thromboangiitis obliterans (Buerger disease), in which blood clots occur in small blood vessels
Cholesterol emboli associated with atherosclerosis
Thrombosis caused by thrombophilia, antiphospholipid syndrome or drugs — including oral contraceptives.

Visual Effects of smoking

Smoking and cutaneous lupus erythematosus

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.

Discoid lupus erythematosus: severe in smokers

Smoking and oral diseases

Conditions affecting the mouth tend to be more common in smokers. These include:

Oral candidiasis (thrush)
Oral lichen planus and erosive lichen planus
Hairy tongue (lingua villosa). In this condition the surface of the tongue has elongated hair-like processes and is yellow, brown, green or black due to bacterial overgrowth. The condition is due to soft diet, poor oral hygiene, lack of saliva and smoking.
Nicotine stomatitis
Hairy leukoplakia associated with HIV infection
Gingival enlargement and gingivitis
Actinic cheilitis ie, dry peeling lips due to sun damage.

Effect of smoking on medicines

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.