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



In this blog we will concentrate on the role of physical contact with chemicals and the effect on psoriasis. For Oral Drug Induced Psoriasis please refer to out blog “PSORIASIS – the Relationship with Drugs”


Various studies have suggested that hypersensitivity to contact  allergens, namely chemicals, in psoriasis is an important and often underestimated, provocative/exacerbating factor in the manifestation and the course of psoriasis.

Dollarphotoclub_80345209 Chemicals

Recently research has focused on allergic contact dermatitis in psoriasis and results have supported the role of contact allergy in provoking psoriatic lesions on palms and soles. Studies of incidence of contact allergy in patients with palmar and plantar psoriasis report the following results:-

  • Positive patch-tests were found in 39.5% of the psoriatic cases with palmo-plantar involvement therefore indicating a significantly greater hypersensitivity to contact allergen in the group of patients with palmo-plantar psoriatic lesions. Some of the allergens that elicited as positive response were – nickel sulphate, epoxy resin, cobalt chloride, phenylenediamine, paraben mix, detergents, potassium dichromate, nickel sulphate, soap for hands, thiuram mix, neomycin sulfat and nickel.1                                                                                                                                                                                                                                                                              
  • In another study in patients with various presentations of psoriasis vulgaris, the researchers concluded that the result of 68% of patients with a positive patch-test, points to delayed type hypersensitivity to contact allergens as a possibly relevant factor in the presentation or course of psoriasis. The most common allergens were tars, nickel sulphate, perfume and balsam of Peru.2.3                                                                                                                                                                                      
  • In another study, the researchers found 19 patients (25%) with different forms of psoriasis (inverse psoriasis, palmoplantar psoriasis, chronic plaque psoriasis, guttate psoriasis and pustular psoriasis) who had positive patch tests. The most common positive patch-tests were to nickel, fragrance mix, coal tar, colophony and neomycin.4                                                                                                                                                                                                                                                                                 
  • Another study reported allergic disease in 21% of patients tested, but a positive RAST test was obtained in 44%. In chronic plaque-type psoriasis a positive RAST test was significantly more common (58%) than in active psoriasis (22%). Grass pollen and house dust mite were the most prevalent sensitizing allergens, with frequencies of 64% and 53%, respectively in the sensitized subjects. Sensitization increased with age and polysensitization was common. Contact dermatitis was verified with patch tests in 12 men and 20 women, of whom 10 had chronic plaque-type psoriasis and 22 active psoriasis. Tar, nickel sulphate, corticosteroid mixture and thiomersal were the most common allergens. No irritant reactions were seen at the concentrations used.5                             

In some of the studies it was found that when the patients with positive patch-tests avoided the topical products containing the incriminated allergens, they showed improvement in their psoriasis. This strongly suggests that hypersensitivity to contact allergens in psoriasis is a relevant provocative/perpetuating factor in manifestations and the course of psoriasis.1

Other research has suggested that there is a possible interaction between the clinical evolution of psoriasis and the production of the cytokines that intervene in immunoreactions involved in cell-mediated responses and in atopy. The Th1 lymphocytes involved in cell-mediated responses seem to act during the active phase of psoriasis, whereas the Th2 lymphocytes active in atopy are active during the non-active plaque-type phase and, for this reason, are more associated with IgE-mediated allergies. In clinical practice, patients with chronic psoriasis are more likely to develop IgE-mediated diseases, whereas in the active phase they will be more affected by contact dermatitis: the greater application of topical treatments during this phase increases the risk of contact dermatitis.5

Researchers concluded that:-

  • Allergic contact dermatitis has a great role in the provoking and maintenance of the psoriasis lesions.
  • Patch-tests should be included as a routine diagnostic procedure in psoriasis, especially in palmo-plantar psoriasis, in long standing psoriasis and in psoriasis resistant to therapy.
  • Avoidance/elimination of selective previously identified materials/antigens with positive patch-test responses may alleviate and make the treatment of chronic, recalcitrant psoriasis more effective.1

The theory proposed for the most likely cause is thought to be due to skin injury caused by exposure to the chemical/material/antigen and the subsequent initiation of the Koebner effect.

See our blog “Koebner Phenomenon”, blog “Psoriasis and Chemical Exposure to Pollution”, “Psoriasis and Smoking” and “Psoriasis and Alcohol Intake”


  1. Heule F. et al.; Delayed-type hypersensitivity to contact allergens in psoriasis; Contact Dermatitis; Volume 38,Issue 2, pages 78–82, February 1998
  2. Heule F, Tahapary GJM, Belloc R, Van Joost Th. Delayed-type hypersensitivity to contact allergens in psoriasis: A clinical evaluation. Contact Dermatitis 1998; 38: 78 -82
  3. Binden A. D., Muston H., Beck M. H. (1994): Intolerance and contact allergy to tar and dithranol in psoriasis. Contact Dermatitis. 31: 185–186.
  4. Fleming C. J., Burden A. D. (1997): Contact allergy in psoriasis. Contact Dermatitis. 36: 274–276.
  5. Pigatto P.D.; Atopy and Contact Sensitization in Psoriasis; Acta Derm Venereol 2000; Suppl 211: 19-20
  6. Thappa DM. The isomorphic phenomenon of Koebner. Indian J Dermatol Venereol Leprol 2004;70:187-9