What are the consequences of smoking on the skin?

In a clinical study, Douglas MODEL found, by comparing the facial characteristics of smokers and non-smokers, that those who smoke exhibited a slightly pigmented and greyish appearance of the skin. Indeed, the facial skin of smokers tends to take on a dull and greyish hue, which gives the impression of advanced ageing.

It is important to note that carbon monoxide present in tobacco smoke is absorbed into the blood and binds to haemoglobin, which reduces the blood's oxygen-carrying capacity. Consequently, skin cells will be less oxygenated, and this can lead to a reduction in the production of new skin cells and an accumulation of dead cells on the skin's surface.

In a study, Jan N. BOUWES BAVINCK and his colleagues investigated the potential association between smoking and skin cancer. To do this, a case study was conducted in a hospital setting, involving 161 patients with squamous cell carcinoma, 301 with nodular basal cell carcinoma, 153 with superficial multifocal basal cell carcinoma, 125 with malignant melanoma, and 386 controls. Information on smoking history was collected during personal interviews. An association between smoking and squamous cell carcinoma of the skin was found (relative risk: 2.3), with a higher risk for current smokers (relative risk: 3.3) than for former smokers (relative risk: 1.9). There was a dose-response relationship with the number of cigarettes smoked.

The effects of tobacco on the development of skin cancers can be explained through various means. Firstly, tobacco smoke can act as a skin carcinogen, either directly on the skin or systemically in the bloodstream. It contains various compounds proven to be carcinogenic, such as nitrosamines, phenolic compounds, and aromatic amines. These substances can form DNA adducts and thus cause cancers. Furthermore, mutations in the p53 gene, a tumour suppressor, have been associated with tobacco smoke in relation to squamous cell carcinoma of the skin, particularly by certain carcinogens. This event could therefore be responsible for the development of skin cancers when one smokes.

In a study conducted by Karen H. CALHOUN, researchers sought to determine whether smokers have a higher risk of complications following the reconstruction of facial skin defects. 91 patients with reconstructed facial skin defects were examined. 38 (42%) were active smokers, 12 (13%) had not smoked for at least a year before the operation, and the rest were non-smokers. Complications occurred in 25% of patients (37% among smokers, 17% among ex-smokers and 17% among non-smokers). Full-thickness skin losses occurred in active smokers. Therefore, active smokers may have a higher risk of complications during reconstructive surgery.

The toxic components of cigarette smoke, particularly nicotine, carbon monoxide, and hydrogen cyanide, interfere with the processes involved in wound healing. The pathobiological effects of tobacco products on wound healing are similar to those that cause premature ageing of the skin. For instance, the reduction in collagen production and the alteration of extracellular matrix renewal with increased levels of MMP are both reported as contributing to aberrant wound healing. Furthermore, smoking can also delay wound healing due to a decrease in blood flow, associated with an increase in vasopressin secretion.

The precise mechanisms have not yet been elucidated.

Ehrin J. ARMSTRONG and his team aimed to assess the prevalence of smoking among patients suffering from psoriasis and the contribution of smoking to the incidence of this skin condition. The meta-analysis of prevalence studies involved a total of 146,934 psoriasis patients and 529,111 non-affected patients.

Analyses have revealed a significant association between psoriasis and current smoking. Indeed, individuals with a history of smoking were 139 times more likely to develop incident psoriasis, and current smokers were almost twice as likely to develop psoriasis than non-smokers. There also appears to be a link with the intensity of smoking: individuals who smoke between one to 14 cigarettes per day are 181 times more at risk of developing psoriasis than non-smokers.

Several mechanisms are likely at the root of the associations between smoking and psoriasis. Smoking induces oxidative stress and damage caused by free radicals on the dermal membrane. It should be noted that cigarette smoke contains approximately 1,017 free radicals per puff. This increased exposure to free radicals is likely to trigger a cascade of systemic consequences, including the development of psoriasis. In addition, nicotine, a major substance in tobacco, induces an increased secretion of IL-12, a pro-inflammatory cytokine, by dendritic cells. Numerous other inflammatory cells and cytokines, including tumour necrosis factor, IFN-γ and IL-2 are produced by pathways activated by nicotine. This situation therefore promotes skin inflammation and the onset of conditions such as psoriasis.

Mauro PICARDO and his colleagues sought to verify the presence of a correlation between the frequency of non-inflammatory acne and smoking through an analysis of possible differences in sebum composition in a group of smokers suffering from acne compared to healthy smokers and non-smokers.

Out of 277 female smokers, 155 were suffering from acne (56%), and out of 723 non-smokers, 70 were suffering from acne (9.7%). These results demonstrate a strong correlation between tobacco use and acne. Furthermore, the analysis revealed significant differences in the sebum composition between smokers and non-smokers. In smokers, the levels of vitamin E were halved compared to non-smokers. The decrease in levels of vitamin E was associated with an increase in the degree of oxidative lipid peroxidation, which was assessed taking into account the quantity of squalene, a lipid characteristic of human sebum, and its peroxide (P-Sq). Smokers showed a decrease in squalene, equivalent to 50% compared to non-smokers, and an increase in its peroxide.

Among the alterations caused to the skin by smoking, an important role could be played by changes in the composition of sebum. Smoking appears to cause an increase in oxidative stress and reduce the levels of α-tocopherol (vitamin E) in the plasma, which is the main antioxidant transported by sebum to the skin's surface to maintain low levels of sebaceous lipid peroxides. Among the peroxidised lipids, squalene is particularly important as its peroxides have a hyperproliferative effect on keratinocytes, which will clog the pores when in excess, and these effects are comedogenic. Thus, these peroxides produced by free radicals induced during oxidative stress can lead to the onset of acne.

The cited consequences are applicable to active smoking, but also to passive smoking, that is, not smoking oneself but being in contact with tobacco smoke, due to the deposition of toxic compounds on the skin.