Tobacco smoke contains numerous chemicals that exert inflammatory effects on the human body. Recent studies suggest that cigarette smoking may trigger the development of psoriasis through oxidative, inflammatory and genetic mechanisms. Smoking initiates formation of free radicals that stimulate cell signalling pathways active in psoriasis. Smoking damages the skin by increasing formation of reactive oxygen species (ROS) and decreasing the gene expression of antioxidants. Nicotine also stimulates innate immune cells integral to the pathogenesis of psoriasis. This perpetuates a cycle of chronic inflammation. Smoking also enhances expression of genes known to increase the risk of psoriasis.1,2,5

Research has found that increased smoking intensity corresponds to a higher risk of developing severe psoriasis whilst  longer cumulative duration of smoking (pack-years) increases the likelihood of developing psoriasis. The study also demonstrated a graded increase in psoriasis risk with increasing exposure to passive smoke.                              

In one study, researchers investigated the associations between smoking status, quantity,duration, and cessation and exposure to environmental tobacco smoke and the risk of incident psoriasis in a total population of 185,836 participants from the Nurses’ Health Study (NHS), the Nurses’ Health Study II (NHS II), and Health Professionals’ Follow-up Study (HPFS). They reported that in the NHS, 20% of the cases of incident psoriasis might have been prevented by the elimination of smoking. Similarly, the population-attributable risk was 15% in the NHS II and 19% in the HPFS. For all participants, 17.5% of the incidents of psoriasis were attributable to having ever smoked. Evidence from past association studies seemed to indicate a stronger association between smoking and psoriasis in women than in men.3

Research has also shown that the risk increases with the number of cigarettes smoked daily. Studies have shown that smoking more than 10 cigarettes per day by men who are psoriasis patients may be associated with a more severe expression of disease in their extremities. In addition, smoking among both men and women who are psoriasis patients has been shown to reduce improvement rates and hence difficulty in achieving remission during treatment.4 In a multicentre case-control study of 404 psoriasis patients and 616 controls, the risk for psoriasis was higher in smokers compared with non-smokers, and the association with smoking was stronger and more consistent among women than men. A particularly strong association was also found between smoking more than 15 cigarettes per day and Palmoplantar Pustular Psoriasis (PPP). Several observational and case-control studies have demonstrated up to 94% prevalence of tobacco use in patients with PPP.6 


As tobacco smoking also interferes with the bodies immunity by allowing colonization by perio -dontopathic bacteria and by acting as a local irritant, researchers have hypothesized that smoking may act as a trigger or permissive factor of periodontal disease in patients suffering from psoriasis. In order to test this hypothesis, the prevalence and severity of periodontal disease, Researchers assessed a group of smoking and non-smoking psoriasis patients and a group of smoking and non-smoking psoriasis-free controls. In this study it was statistically shown that psoriasis patients who smoke are at an approximately sixfold higher risk of developing severe periodontal disease, as compared to psoriasis patients who do not smoke.7

Another interesting observation was the frequent coexistence of a smoking habit and alcohol consumption in patients with psoriasis. In the literature, alcohol consumption has been described as a factor responsible for triggering psoriasis, but it is said that smoking increases the risk of the onset of the disease. Previous studies have indicated that smokers who drink are twice as likely to develop the disease as non-smokers and non-drinkers.8,9

It is well recognized that stress and anxiety acts in both the initiation and exacerbation of psoriasis. Psychosocial stressors include acute negative life events or chronic strains and have been implicated as risk factors for tobacco use. Psychological stress may influence smoking behaviour (e.g., initiation, maintenance, and relapse) through a number of mechanisms. Specifically, smoking may function as a coping behaviour, whereby nicotine is used to self-medicate in response to stress; it is also possible that exposure to stress may result in diminished self-regulation to control the urge to smoke. Previous observational studies illustrate that acute stressful events and greater exposure to chronic stressors (e.g., related to work, finances, or relationships) are associated with higher smoking prevalence compared to persons who did not experience these stressors.10

So in summary, studies suggest that cigarette smoking may trigger the development of psoriasis through oxidative, inflammatory and genetic mechanisms. Furthermore, smoking is associated with the clinical severity of psoriasis. Smoking also contributes to higher morbidity and mortality from smoking related disorders in these patients. It is, therefore, advisable, if possible to quit smoking, or at the very least, keep your smoking to a minimum, preferably under 10 cigarettes a day. Try to adopt other mechanisms to cope with your stress and anxiety and it is suggested that you read our other blogs on “Simple Physical and Mental Relaxation Techniques”.  Using these techniques you may be able to reduce your stress and anxiety levels and this may allow you to cut down on the number of cigarettes you smoke.

Also read our blog “Psoriasis and Alcohol Intake”, “Stress, Anxiety, Depression and Psoriasis”, “Stressed about Psoriasis – Identify Your Stressors and Yours Stress Responses”, “Simple Physical Relaxation Techniques for Psoriasis Patients” and  “Simple Mental/Mind Relaxation Techniques Part 1 and Part 2”


  • Armstrong AW, Armstrong EJ, Fuller EN, et al. Smoking and pathogenesis of psoriasis. Br J Dermatol 2011; 165: 1162-8.
  • Al-Rubaii A, Al-Ward N, Al-Waiz M. The age of onset of psoriasis and its relationship to smoking habits and stressful life events. Saudi Med J2003; 24:108.
  • Wenqing Li et al.; Smoking and Risk of Incident Psoriasis Among Women and Men in the United States: A Combined Analysis; American Journal of Epidemiology Advance Access published January 12, 2012;
  • Behnam SM,Behnam SE, Koo JY.; Smoking and psoriasis.; Skinmed. 2005 May-Jun;4(3):174-6.
  • Armstrong AW, ; Psoriasis and smoking: a systematic review and meta-analysis; British Journal of DermatologyVolume 170, Issue 2, Article first published online: 18 FEB 2014
  • Freiman A. et al.; Cutaneous Effects of Smoking; Journal of Cutaneous Medicine and Surgery Volume 8 Number 6 December 2004
  • Antal M. et al.; Smoking as a Permissive Factor of Periodontal Disease in Psoriasis; PLOS ONE |; March 2014 | Volume 9 | Issue 3 | e92333
  • Agnieszka B. Owczarczyk-Saczonek , Roman Nowicki; The association between smoking and the prevalence of metabolic syndrome and its components in patients with psoriasis aged 30 to 49 years; Postep Derm Alergol 2015; XXXII (5): 331–336 DOI: 10.5114/pdia.2015.54743
  • Naldi L, Peli L, Parazzini F. Association of early-stage psoriasis with smoking and male alcohol consumption: evidence from an Italian case-control study. Arch Dermatol1999; 135:1479–84.
  • Slopen N. et al.; Psychosocial stress and cigarette smoking persistence, cessation, and relapse over 9–10 years: a prospective study of middle-aged adults in the United States; Cancer Causes Control DOI 10.1007/s10552-013-0262-5



Human beings are continuously exposed to environmental pollutants. Because of its critical location, the skin is a major interface between the body and the environment and provides a biological barrier against an array of chemical and physical environmental pollutants. The skin can be defined as our first defense against the environment because of its constant exposure to oxidants, including ultraviolet (UV) radiation and other environmental pollutants such as diesel fuel exhaust, cigarette smoke (CS), halogenated hydrocarbons, heavy metals, and ozone (O3). The exposure to environmental pro-oxidant agents leads to the formation of reactive oxygen species (ROS) and the generation of bioactive molecules that can damage skin cells.1

 The skin is a potential target for oxidative injury, as it is continuously exposed to UV radiation and other environmental stresses generating reactive oxygen species (ROS). ROS mediated oxidative damage involves a vast number of biological molecules since it causes lipid peroxidation, DNA modification, and secretion of inflammatory cytokines.2 ROS induced oxidation of polyunsaturated fatty acids results in the metabolization of the lipid peroxidation into malondialdehyde (MDA). Lipids are structural components of cell membranes, critical in the formation of the permeability barrier of cells, whilst MDA is used as a biomarker of lipid peroxidation.2,3


Alterations that disturb the skin barrier function in either stratum corneum lipid metabolism or protein components of the corneocytes are involved in the development of various mild or severe skin diseases, including erythema, oedema, hyperplasia, “sunburn cell” formation, skin aging, contact dermatitis, atopic dermatitis, psoriasis, and skin cancers.1

The mechanism by which environmental insults exert a detrimental effect the skin barrier function is through the generation of oxidative stress, which overwhelms the skin’s defenses by quickly depleting the enzymatic (glutathione peroxidase, glutathione reductase, superoxide dismutase, catalase) and nonenzymatic (vitamin E, vitamin C, and glutathione) antioxidant capacity, thus leading to deleterious effects.1 The enzymes, including glutathione peroxidase, superoxide dismutase (SOD) and catalase (CAT) decrease the concentration of the most harmful oxidants, hence an inadequate antioxidant protection or excess ROS production generates oxidative stress and contributes to the development of cutaneous diseases and disorders.

Increased capacity for chemotaxis (the directional movement of cells in response to chemical stimuli), adhesion (the interaction of a cell with a neighbouring cell or with the underlying extracellular matrix, via specialized multi-protein adhesive structures) and increased ROS production in neutrophils, keratinocytes and fibroblasts of the skin matrix, have been reported in patients with psoriasis. Research results have shown that increased oxidative stress in these patients, as demonstrated by the high plasma malondialdehyde (MDA) levels and compromised levels of the antioxidant defense enzymes, have been observed even at the time of diagnosis itself. Other reports have suggested that, fibroblasts in the lesion-free skin of psoriasis patients have shown signs of increased oxidative damage even before the formation of the characteristic psoriatic plaque/lesions which may indicate the involvement of abnormal immune reactions leading to the onset of the disease.2

Sun UV rays, Ozone (O3 – the primary constituent of smog), cigarette smoke (CS) exposure, and pollutants, in addition to the natural process of aging, contribute to the generation of free radicals and reactive oxygen species (ROS) that interact with lipid-rich plasma membrane and initiate the so-called lipid peroxidation reaction cascade. The progressive depletion of antioxidant content in the stratum corneum leads to the cascade of effects which result in an active cellular response in the deepest layers of the skin. ROS is known to stimulate the release of pro-inflammatory mediators from a variety of skin cells. Skin inflammation, in turn, leads to skin infiltration by activated neutrophils and other phagocytic cells that generate further free radicals (both reactive oxygen and nitrogen species), thus establishing a vicious circle.1

 There is no doubt that the skin is continuously and simultaneously exposed to several oxidative stressors, and these can have additive, if not synergistic, effects. Whilst UV ray therapy has been proven to be an effective treatment for psoriasis and there is certainly anecdotal information that indicates sun exposure also improves psoriatic lesions, there has been little or no research on the effects of combined UV and O3 on the inducement and or exacerbation of psoriasis.  While environmental UV radiation penetrates into the epidermis (UV-B) or into the dermis (UV-A) and is known to induce the release of tissue-degrading enzymes, O3 oxidizes biological systems only at the surface. Therefore, because O3 and UV cooperatively damage subcutaneous (SC) components they exert an additive effect in cutaneous tissues. Research results have suggested that UV irradiation has been shown to compromise the skin barrier and simultaneous exposure to O3 may enhance this phenomenon by perturbing SC lipid constituents that are known to be critical determinants of the barrier function. It has been proposed that the by-products of O3-induced lipid oxidation penetrate the outer skin barrier and cause effects on constituents of the deeper epidermis that can lead to activation of transcription factors, such as Nuclear factor kappa B (NF-?B), which regulates a variety of proinflammatory cytokines. NF-?B is a protein transcription factor that orchestrates inflammation and other complex biological processes. It is a key regulatory element in a variety of immune and inflammatory pathways, in cellular proliferation and differentiation and in apoptosis. Therefore NF-?B is a crucial mediator involved in the pathogenesis of psoriasis.1,3,4,6

It has been theorized that responses to air pollutants may be age related, and several recent studies have shown that skin responses to pollutants are modulated by age. The free radical theory of aging is supported by finding that oxidative damage to biomolecules accumulates and increases with age. In aging skin, the process oxidative damage involves not only proteins, lipids and DNA but also is linked with alteration of the collagenous extracellular matrix in the dermis. The extensive research in the aging process of human skin found that levels of MMP-1 increased with age and contributed to fragmentation and disorganization of collagen fibers in the dermis. Researchers have also found that both a contact of fibroblasts with collagen fibers and collagen cross-links of collagen fibers are strongly reduced in aged skin (80% and 75%, respectively). Despite a large body of knowledge a detailed molecular mechanism of the skin aging is not fully recognized.1,5

Further research is required to determine exactly how air pollutants can induce and/or exacerbate psoriasis and other skin conditions. However one theory proposed for the most likely cause is thought to be due to skin injury caused by exposure to the chemical pollutant and the subsequent initiation of the Koebner effect.

See our blog “Koebner Phenomenon”, “Psoriasis and Chemical Exposure” and “Psoriasis and Smoking”


  • Valacchi et al.; Cancer Cutaneous responses to environmental stressors ; Annals Of The New York Academy Of Sciences;  Issue: Nutrition and Physical Activity in Aging, Obesity, and Cancer; Ann. N.Y. Acad. Sci. ISSN 0077-8923;
  • Ayala A. et al.; Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal; Oxidative Medicine and Cellular Longevity Volume 2014, Article ID 360438, 31 pages; file:///C:/Documents%20and%20Settings/marg/My%20Documents/Downloads/360438.pdf
  • Kadam P. et al.; Role of Oxidative Stress in Various Stages of Psoriasis; Ind J Clin Biochem (Oct-Dec 2010) 25(4):388–392; file:///C:/Documents%20and%20Settings/marg/My%20Documents/Downloads/12291_2010_Article_43.pdf
  • Goldminz AM. Et al.; NF-?B: an essential transcription factor in psoriasis.; J Dermatol Sci.2013 Feb;69(2):89-94. doi: 10.1016/j.jdermsci.2012.11.002. Epub 2012 Nov 14.
  • Kruk J., Duchnik E.; Oxidative Stress and Skin Diseases: Possible Role of Physical Activity; Asian Pacific Journal of Cancer Prevention, Vol 15, 2014
  • Burke KE,Wei H.; Synergistic damage by UVA radiation and pollutants.; Toxicol Ind Health May/June 2009 25: (4-5): 219-224