i
sible
Effe
cts of Tob
co
mokingModel6 described the following as common features of a smoker’s face: lines or wrinkles on the face, typically radiating at right angles from the upper and lower lips or corners of the eyes, deep lines on the cheeks, or numerous shallow lines on the cheeks and lower jaw; a subtle gauntness of the facial features with prominence of the underlying bony contours; an atrophic, slightly pigmented grey appearance of the skin; and a plethoric, slightly orange, purple, and red complexion. These findings were shown to be independent of age, social class, exposure to sunlight, and recent change in weight. An additional feature that is sometimes present is large open and closed comedones with furrows and nodules in the periorbital area characteristic of Favre-Racouchot syndrome (smoker’s comedones).7 The nails of smokers may show a yellow discoloration, and in heavy smokers who suddenly cease smoking (e.g., due to an abrupt illness), a sharp demarcation line develops between the yellow nail plate and the newly developed proximal pink nail (referred to as Harlequin nail or quitter’s nail).8 Yellow discoloration of the hair and beard can also be seen in smokers, particularly in gray-haired individuals (e.g., smoker’s moustache). Furthermore, smoking has been linked to premature graying and loss of hair, although the supporting evidence remains circumstantial. Non-malignant changes in the oral mucosa of smokers are common and include gingival pigmentation (smoker’s melanosis), leukoplakia of the tongue (smoker’s tongue), and a gray-white keratinized palate with multiple red umbilicated papules that represent inflamed salivary glands (smoker’s palate/nicotine stomatitis).9
Smoking has been implicated as a causal or influencing factor for certain dermatologic disorders (Table 1). The obvious detrimental effects from smoking preclude experimental prospective interventions on human subjects, and therefore, the main body of evidence for these associations is derived from case-control studies. However, because of inherent biases connected with this type of research, as well as with cohort and observational studies, the conclusions that can be drawn from their findings are limited.
There is fairly good evidence to support a causal link between tobacco smoking and systemic lupus erythematosus (SLE), as it has been demonstrated that anti-malarial therapeutic agents for lupus are less effective in smokers.10 A metaanalysis of seven case-control studies and two cohort studies found a 1.5 times increased risk of SLE in current smokers, when compared with non-smokers. The finding remained significant after adjustment for age, sex, race, alcohol consumption, and socioeconomic status.11 However, the result may have been affected by publication bias due to an absence of studies reporting negative findings. Furthermore, former smoking was not found to be a risk factor for SLE. Exposure to smoking in early childhood or in utero was not associated with onset of SLE in a prospective cohort study.12 Discoid lupus erythematosus (DLE) has also been linked to smoking in several case-control studies, which have shown consistently higher smoking rates in DLE patients.13
| Prevalence in Smokers | Skin Disease | Level of Evidence |
| Higher Prevalence | Basal cell carcinoma | Case-control |
| Cutaneous squamous cell carcinoma | Prospective cohort and case-control | |
| Genital warts and HPV infection | Prospective cohort and case series | |
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