Smoking skin lesions F17.1 + Hauterkrankung

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 04.08.2022

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Synonym(s)

Skin and smoking; Skin and tobacco; Skin changes due to smoking; Skin symptoms due to smoking; Smoker's skin; smoking, skin changes; Smoking Skin lesions; The skin and smoking; Tuxedo and the Skin

Definition
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Cutaneous changes induced by mostly long-term tobacco consumption. Smoking is now considered the most common avoidable cause of death. In Germany it causes about 140,000 deaths every year. The main causes are diseases of the cardiovascular system and oncological complications.

Classification
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Chronic noise has the following effects on the skin:

  • General effects:
    • Skin aging is accelerated
    • Wound healing is delayed
    • Induction of inflammatory responses/initiation or exacerbation of disease (Thomsen SF et al 2010):
      • Pustulosis palmaris et plantaris (smokers suffer more often from pustulosis palmoplantaris than non-smokers)
      • Psoriasis vulgaris (clear connection)
      • Dermatitis atopische (connection not clear)
      • Dyshidrotic dermatitis - heavy smokers/serum nicotine level >3 ng/ml - suffer from chronic (dyshidrotic)hand dermatitis 5x more often than non-smokers - Lai YC et al 2016).
      • Acne inversa/hidradenitissuppurativa (confirmed association; smoking is a contributory trigger. 89% of patients with acne inversa are smokers).
      • Acne vulgaris (correlation possible but not confirmed; in postpubertal acne in women, the proportion of smokers - compared to non-smokers - is significantly higher)
      • pyoderma gangraenosum
      • Type IV sensitizations (nicotine itself does not cause type IV sensitizations. More commonly, "tobacco allergies are found in tobacco retailers, couriers, and cigar makers-Bonamonte D et al. 2016).
      • Lupus erythematosus
  • Induction of chronic vascular disease:

Induction of malignant tumors of the skin and mucous membranes:

Occurrence/Epidemiology
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In Central Europe, about 40% of men and 30% of women smoke. The average cigarette consumption per day is 15 cigarettes. 75 to 80% of all smokers meet the criteria of nicotine dependence:

  • Compulsive smoking
  • Tolerance development
  • Physical withdrawal symptoms with abstinence
  • Continued tobacco consumption despite consequential damage
  • Changes in lifestyle to maintain tobacco consumption
  • Limited control over smoking behaviour

Etiopathogenesis
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The clinical effects of tobacco consumption on the skin have been known in part since the introduction of the tobacco plant in Europe in the 16th century. The alkaloid nicotine contained in the plant, named after its discoverer Jean de Nicot, is considered the main toxin of cigarette smoke. Each cigarette is inhaled with approximately 2 - 3 mg. If the amount inhaled is constant, the level of nicotine concentration in the blood varies from person to person. It depends on various factors such as the pH of the urine or the metabolism by microsomal liver enzymes.

About 5000 different substances can be detected in cigarette smoke extracts, 43 of which are classified as carcinogenic (criteria of IARC = International Agency for Research on Cancer). It is therefore difficult to attribute the effects of smoking on the skin and the whole organism to a single ingredient or to a single effect. They rather result from complex summation effects, partly in combination with environmental factors.

Manifestation
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Heavy smokers appear to be clearly pre-aged even at a relatively young age. The skin of the long-time smoker appears wrinkled, the complexion pale, the face grey and less well supplied with blood. The connection between extrinsic skin aging and high cigarette consumption (pack-years) is proven (Vierkötter A et al. 2010; Puri P et al. 2017).

Actinic elastosis: It is known that tobacco smoke is phototoxic due to various components (aromatic hydrocarbons). This also explains the frequent occurrence of actinic elastosis and the M. Favre-Racouchaud in intensive smokers. Responsible for this effect are the influences of tobacco inhalates, partly in combination with solar radiation on epithelium and skin connective tissue. Experimentally, an extract of cigarette smoke inhibited cell division and the growth of fibroblasts.

Circulatory disorders: Nicotine leads to vasoconstriction. Furthermore, the carbon monoxide contained in cigarette smoke impedes the transport of oxygen and thus the oxygenation of the tissue. At the same time, inflammatory cytokines such as interleukin-1, interleukin-6, interleukin-8 and TNF-alpha are released. Video-capillaroscopically, disturbances of the microcirculation caused by tobacco constituents are detectable which are apparently irreversible (Scardina GA et al. 2019).

Smoking causes a reduction in the hydration of the stratum corneum. In addition, the proliferation rate of the basal cells is reduced. Furthermore, nicotine influences keratinocyte proliferation, differentiation and apoptosis via the nicotinic and muscarinic acetylcholine receptors (ACh-R /nACh-R) (Ortiz A et al. 2012). Since nACh-R also occurs in sweat and sebaceous glands, a stimulating effect on sweat and sebum secretion is likely.

Smoking and allergies: Contact allergies(nickel allergies) are more common among smokers than among non-smokers.

Smoking and autoimmune diseases: There is a slightly increased incidence (factor 2.0) of systemic lupus erythematosus, which is more severe in smokers than in non-smokers. It has also been known for a long time that the effect of chloroquine is lower in smokers than in non-smokers. This must be taken into account in the treatment of autoimmune diseases.

Nicotine and components of cigarette smoke can induce the following effects:

  • Increase in the concentration of carbon monoxide as well as a reduced oxygen binding and consequently a reduced oxygen supply in the blood
  • Stimulation of the sympathetic nervous system and increased catecholamine release leads to vascular constriction
  • Reactive oxygen species and free radicals lead to oxidative stress
  • Inhibition of fibroblasts and myoblasts lead to delayed tissue formation
  • Polycyclic aromatic hydrocarbons, nitrosamines, heterocyclic aromatic amines, -cadmium, benzene and formaldehyde in tobacco inhalates have oncogenic and sometimes photosensitizing effects.
  • Induction of MMPs and inhibition of TIPMs leads to degradation of elastic fibres and collagen
  • Wound healing disorders: The disturbed collagen production and reduction of tissue perfusion lead to poorer wound healing (Balaji SM 2008; Frick WG et al. 1994). Smokers developed wound healing disorders postoperatively in 48.2% of cases, non-smokers only in 21.0% of cases. When smoking was stopped 6 weeks prior to surgery, this was still 30.8% of patients (Goertz O et al. 2012). It is recommended to stop smoking 6-8 weeks before a planned operation. A higher complication rate is also to be expected in smokers with flap plasty (flap necrosis, dehiscence).

Note(s)
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Data from the USA show that 440,000 Americans die annually from cigarette-related diseases.

Smokers die on average 13 or 14 years earlier than non-smokers. The treatment of these diseases costs 75 billion dollars per year in the USA.

Smoking cigarettes can promote the development of carcinomas of the throat, kidney, pancreas, esophagus, bladder, stomach, as well as lead to aneurysms of the abdominal aorta, granulocytic leukemia, heart disease, vascular disease (atherosclerosis), cataracts, or restrictions in lung function.

The influence of "second-hand smoke" on smokers and non-smokers should not be underestimated.

E-cigarettes: Electronic cigarettes (E-Cigs) account for a considerable and increasing share of the consumption of tobacco products. They are now a problem for oral health. E-cigs with flavourings have been shown to cause increased oxidative/carbonyl stress and inflammatory cytokine release in human periodontal ligament fibroblasts and epigingival epithelium.

Literature
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  1. Balaji SM (2008) Tobacco smoking and surgical healing of oral tissues: a review.Indian J Dent Res 19:344-348.
  2. Bonamonte D et al (2016) Tobacco-induced contact dermatitis. Eur J Dermatol 26(:223-231.
  3. Chaumont M et al (2018) Differential Effects of E-Cigarette on Microvascular Endothelial Function, Arterial Stiffness and Oxidative Stress: A Randomized Crossover Trial. Sci Rep 8:10378.
  4. Frick WG et al (1994) Smoking and wound healing: a review. Tex Dent J 111:21-23.
  5. Goertz O et al (2012) Wound healing disorders in smokers, nonsmokers, and after smoking cessation. Surgeon J 83:652-656.
  6. Krug M et al (2004) Tobacco dependence and the consequences on the skin. Dermatologist 55: 301-316
  7. Lai YC et al (2016) Smoking and hand dermatitis in the United States adult population. Ann Dermatol 28:164-171.
  8. Ortiz A et al (2012) Smoking and the skin. Int J Dermatol 51:250-262.
  9. Panconesi E (1954) Occupational dermatoses caused by tobacco. In tema di dermatosi professionali da tabacco. Rass Dermatol Sifilogr 7:85-100.
  10. Placzek M et al (2004) Tabacco smoke is phototoxic. Br J Dermatol 150: 991-993.
  11. Puri P et al (2017) Effects of air pollution on the skin: A review. Indian J Dermatol Venereol Leprol 83:415-423.
  12. Scardina GA et al (2019) Permanence of modifications in oral microcirculation in ex-smokers. Med Sci Monit 25:866-871.
  13. Strzelak A et al. (2018) Tobacco Smoke Induces and Alters Immune Responses in the Lung Triggering Inflammation, Allergy, Asthma and Other Lung Diseases: A Mechanistic Review. Int J Environ Res Public Health 15:1033.
  14. Sundar IK et al. (2016) E-cigarettes and flavorings induce inflammatory and pro-senescence responses in oral epithelial cells and periodontal fibroblasts. Oncotarget 7:77196-77204.
  15. Thomsen SF et al (2010) Smoking and skin disease. Skin Therapy Lett 15:4-7.
  16. Vierkötter A et al (2010) J. Airborne particle exposure and extrinsic skin aging. J Invest Dermatol 130:2719-2726.
  17. Wollina U (2017) Smoking and the skin. Skinmed 15:197-202.

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Please ask your physician for a reliable diagnosis. This website is only meant as a reference.

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Last updated on: 04.08.2022