Skin and hair are subjected to various harmful environmental agents, including tobacco smoke. Comprising thousands of substances, tobacco smoke inflicts damage on the skin, with nicotine itself also being detrimental.
Beyond its established connections to cancer, and lung and heart diseases, smoking is implicated in early skin aging, impeded wound healing, and heightened infection risks, in addition to various skin conditions such as psoriasis, hidradenitis suppurativa, and cutaneous lupus erythematosus. It has been observed that smokers generally suffer more severely from most inflammatory skin diseases—including acne—than non-smokers, and these conditions are often more challenging to treat effectively in smokers.
Tobacco smoke induces oxidative stress, leading to inadequate oxygen supply to the skin, tissue ischemia, and occlusion of blood vessels. It diminishes innate and host immune responses and triggers the production of metallo-proteinase MMP-1, an enzyme that breaks down collagen.
Although nicotine replacement is less harmful to the skin than smoking, nicotine itself causes vasoconstriction, inhibits inflammation, delays wound healing, and contributes to skin aging.
The temporary adverse effects of tobacco smoking on the skin and mucosa include:
– Yellowing of fingers and fingernails temporarily
– Teeth discoloration
– Development of a black hairy tongue.
Over time, the appearance of a 40-year-old heavy smoker’s skin can resemble that of a 70-year-old non-smoker:
– Development of facial wrinkles and furrows, such as crow’s feet and vertical ear crease, and smoker’s lines around the lips
– Baggy eyelids and a slack jawline
– Uneven skin coloring, appearing greyish or yellow with visible blood vessels (telangiectasia)
– Dry and coarse skin texture.
The exact mechanisms through which smoking accelerates aging of facial skin are speculative but may include:
– Direct burning of the skin by cigarette heat
– Changes in skin’s elastic fibres (elastosis)
– Vasoconstriction, limiting blood supply and leading to alterations in skin elastic fibres and collagen loss
– Reduction of vitamin A levels and skin moisture.
Smoking hampers wound healing, affecting skin injuries and surgical wounds, elevating the risk of infection, failure of grafts or flaps, tissue death, and blood clot formation. The underlying mechanisms include vasoconstriction and reduced oxygen delivery, delayed keratinocyte migration, diminished collagen synthesis, and slowed new blood vessel growth within wounds.
Smoking aggravates the development and persistence of leg ulcers, especially arterial and diabetic foot ulcers, and calciphylaxis. It is linked to a higher likelihood or severity of:
– Bacterial wound infections, predominantly caused by Staphylococcus aureus and Streptococcus pyogenes
– Candida albicans infections, especially in the mouth
– Viral infections, notably human papillomavirus (HPV), including genital warts.
Cigarette smoking doubles the risk of squamous cell carcinoma of the skin compared to non-smokers and increases the risk of oral leukoplakia (precancer) and oral cancer; 75% of oral and lip cancer cases occur in smokers. Smoking does not seem to elevate the risk of basal cell carcinoma.
Quitting smoking reduces the metastasis risk from lip cancer by two to threefold.
Palmoplantar pustulosis, a chronic and disabling dermatosis characterized by pustules, erythema, and scaling on the palms and soles, predominantly affects middle-aged women, most of whom are smokers. The condition’s mechanism involves nicotine interacting with acetylcholine receptors in sweat glands and ducts, altering their structure and causing inflammation.
Cessation of smoking leads to gradual improvement, and many patients may eventually see their pustules clear.
Studies have shown that smokers typically exhibit more extensive and severe psoriasis than non-smokers. Patients with chronic plaque psoriasis tend to smoke more than those without the condition. Obesity or metabolic syndrome and quality of life issues complicate this research.
The mechanism is believed to involve smoking-induced inflammatory mediators and the promotion of keratinocyte proliferation, with nicotine binding to dendritic cells, T-cells, and keratinocytes.
Most patients with hidradenitis suppurativa (HS) are smokers, experiencing a greater disease burden than non-smokers. HS’s pathogenesis is linked to nicotine/acetylcholine-induced follicular occlusion, follicular rupture, and immune dysregulation, with smokers responding poorly to current treatments.
Some inflammatory diseases appear less common or severe in smokers than in non-smokers, including:
– Aphthous ulcers
– Rosacea
– Labial herpes simplex
– Pemphigus vulgaris
– Dermatitis herpetiformis
– Pyoderma gangrenosum.
However, smoking is not recommended as a treatment due to its adverse effects and addiction risk.
For those seeking to quit smoking, various support options are available, including telephone support, consultations with family doctors, nicotine replacement therapies, and prescription medications like varenicline (Champix™) or bupropion (Zyban™). Vaping or e-cigarettes are also options, though they come with their own health concerns. A multi-faceted approach is often most effective, with devices like carbon monoxide breath meters aiding in treatment guidance.
The cutaneous effects of smoking cessation can vary, with nicotine-containing patches, gum, lozenges, nasal spray, inhalers, and e-cigarettes potentially beneficial or detrimental to skin health. Cutaneous side effects from these treatments may impact patient adherence.
