Our study detected a prevalence of post-adolescent acne of 18.5% (), slightly higher than that reported by other authors (12–14%),2,3
and particularly frequent among smokers ( and ). Post adolescent acne is commonly described as a mild to moderate acne, mainly inflammatory and localized on the chin, on the lower jaw and the neck.2,3
However, we found that APAA was clearly the most frequent form (74.6%), and that it was particularly frequent among smokers (p = 0.0003). Among smokers, APAA seems to represent a peculiar form, which in the most serious cases could be considered a true “smoker’s acne,” analogous to the “smoker’s face” described by other authors.5
In fact, in our study 81.8% of subjects with severe APAA were smokers. The only two non-smokers with serious APAA were patients who lived in environmental predisposing conditions: a 32-year-old woman strongly exposed to passive smoking (both parents were heavy smokers) (), and a 36-year-old cook. Among smokers, CPAA was scarcely represented (), while it prevailed among the non-smokers (61.6%), and was always mild-moderate in severity ().
Data on the correlation between acne and smoking are still controversial. The absence of published data comparable to our data could probably be explained by a different approach to the problem. In fact published statistics were mainly carried out on adolescent acne or on a non-homogenous population. A study by Schäfer et al. on a general population showed a higher prevalence of acne among smokers compared to non-smokers and a linear correlation between the severity of acne and the number of cigarettes smoked.9
These results seem to be confirmed by a more recent study by Chuh et al.10
In the meanwhile, Mills et al. reported an inverse correlation between the incidence of acne and smoking,11
but authors considered a highly selected population, consisting of hospitalized male patients affected by serious inflammatory acne. A recent study by Klaz et al.12
reported an inverse correlation between the severity of acne and the number of cigarettes smoked. Also in this case, data are not comparable to ours because the cohort consisted exclusively of young male adults.
In a study by Cunliffe et al. on post-adolescent acne, among possible pathogenetic factors (hormonal alteration, stress, cosmetic use, occupational), smoking has inexplicably not been taken into consideration.3
Williams and Layton claimed that data on the correlation between acne and smoking could be confounded by the fact that they do not clearly indicate a temporal correlation between smoking and acne.2
Indeed, in our sample, only approximately 1/3 of the APAA group referred the appearance of acne 1–2 years after starting smoking, moreover this finding was not considered completely reliable due to the difficulty encountered in the collection of history data. Despite this, the strong correlation found made the temporal correlation between smoking habits and acne of secondary importance. Moreover, among patient who had experienced adolescent acne, smokers were more frequently affected by active acne (). This finding suggest that smoking could be a major contributing factor for post-adolescent acne in predisposed patients.
Several factors (hormonal alterations, stress, environmental pollution, light exposure), other than smoking, can contribute to the pathogenesis of APAA.13
In our study, 33 non-smokers were affected by APAA (2 with a severe form). In 16 of these patients predisposing factors were identified (). In particular, light exposure is a predisposing condition to the onset of retentional lesions, as described in Favre-Rochochout syndrome.14
In our geographical area light exposure is widespread and this could have influenced our statistics, even if, according to our biopsies, the presence of severe acne in young women in the absence of elastosis, suggested that the influence of light exposure on APAA was only marginal. Experimental evidence supports the hypothesis of a pathogenetic role of smoking on APAA. Keratinocytes have nicotine acetylcholine receptors that increase their adhesion, differentiation, apoptosis and inhibit migration.7,15
At higher concentrations of 100 µg/ml, nicotine induces cutaneous hyperkeratinisation. 16
Nicotine and other components of cigarette smoke induce microcirculation alterations with consequent vasoconstriction and hypoxyemia17,18
and exhibit an inhibitory effect on the chemotaxis of neutrophils and lymphocytes.19
Among alterations caused on the skin by smoking an important role could be played by alterations in sebum composition; in fact smoking seems to cause an increase in oxidative stress and reduces the levels of α-tocopherol in plasma.20
Our data show that the oxidative damage of smoke is also affecting sebum production: sebum of smokers presented significant lower concentrations of α-tocopherol, which is the principal antioxidant transported by sebum on the skin surface,21
probably in order to maintain low levels of peroxidated products of sebaceous lipids.3,21,22
These products seem to be involved in the pathogenesis of acne; previous studies demonstrated that patients affected by acne had a higher grade of lipid peroxidation.24
Among peroxidated lipids, squalene is particularly important because it is a characteristic lipid of human sebum and because its peroxides have a hyperproliferative effect on keratinocytes and are, therefore, comedogenic.25,26
Our data show that along with a decrease in α-tocopherol there is also an increase in squalene peroxide in the sebum of smokers. Thus, cigarette smoke produces an alteration in sebum composition, through the production of reactive oxygen species (ROS), which is similar to that found in acne. Although we detected no difference between the sebum of healthy smokers and smokers with acne, it could be hypothesized that smoking is associated with a higher susceptibility to acne and in particular to APAA. Taking into consideration the role of lipid peroxidation in acne, and the incidence of acne subjects in our sample, there could be a possible association between smoking habits and this particular type of acne. The ability of cigarette smoke to induce peroxidation on sebaceous lipids and the relative deficiency of antioxidants could be considered as an element capable of contributing to the onset and/or exacerbation of this pathology in subjects already predisposed to this disease, such as individulas that present an excess of sebum production considered one of the principal factors involved in the pathogenesis of acne.
The lack of significant statistical difference between smokers with and without acne regarding the cumulative smoking dose (considering that the calculation does not take numerous variables into account such as type of cigarettes smoked, manner of smoking, passive smoking, possible suspension periods, inaccurate number of cigarettes referred, possible variations in the number of cigarette smoked) could suggest that the clinical expression of acne in these patients could be related to genetic predisposition. Several studies demonstrated that smoking is an independent risk factor for the early onset of facial wrinkles27
and that there is an association between premature facial wrinkling and pulmonary function impairment. Kadunce et al. have suggested a common pathogenesis for the early development of facial wrinkles and chronic-obstructive pulmonary disease (COPD).28
In agreement with this hypothesis, Lange et al. found a significant association of both conditions in smokers.29
A recent work by Patel et al. demonstrated a correlation between cutaneous aging in smokers and COPD.30
Future studies would verify, if the presence of APAA could be a marker for predisposition to systemic damage by smoke as for early cutaneous aging.
The percentage of adult women affected by acne is increasing.31
External factors such as cosmetics and active occupation do not seem to play a significant pathogenetic role.32
However, stress-induced alterations of the curaneous androgen metabolism remain a hypothesis which has still to be verified.33,34
Our data confirm that APAA affects a high percentage of adult women. Among these patients the number of smokers is so high, which might partially explain the noticeable increase in this pathology.
Recognizing this form is fundamental for proper information on the effects of tobacco on the skin and can contribute to the anti-smoking information programs, especially among adolescents where aesthetic motivation plays an important role.
In some patients the severity of acne, the clinical variation, the strong correlation with smoking and the biochemical data could lead to consider APAA as a new entity among smoking-related cutaneous diseases (“smoker’s acne face”).