TRANSDERMAL NICOTINE SUPPRESSES CUTANEOUS INFLAMMATION

Background: Cigarette smoking significantly alters the inflammatory re sponse in the skin following application of irritants and rubefacients . The mechanism of this effect is unknown. There are thousands of comp onents in cigarette smoke that may be pharmacologically important, but there is evidence to suggest that nice tine may play an important rol e in the observed effect on the inflammatory process. Design: This was an interventional study to assess cutaneous responsiveness to differe nt stimuli after transdermal nicotine administration in volunteer subj ects. Cutaneous testing was performed at baseline and at weeks 2 and 4 (the end) of the study. Setting: The Department of Dermatology, Unive rsity Hospital of Wales, Cardiff.Participants: Ten lifelong nonsmokers were recruited for the study. Intervention: Nicotine patches were app lied daily for 1 month. Main Outcome Measures: The following tests wer e performed: application of 2 times the minimal irritancy dose of sodi um lauryl sulfate, irradiation with 2 times the minimal erythema dose of UV-B, measurement of cutaneous vasodilation following application o f ethyl and hexyl nicotinate, and reactive hyperemia following arteria l occlusion. Results: There was a significant reduction in the cutaneo us inflammatory response to sodium lauryl sulfate (P<.001) and irradia tion with UV-B (P<.003) and a reduction in reactive hyperemia (P<.03) after 2 weeks of treatment, which returned values to normal at 4 weeks . There was no change in blood flow following application of topical n icotinates. Conclusions: Nicotine administration via a transdermal del ivery system suppresses the cutaneous inflammatory response to sodium lauryl sulfate and W-B, as well as triggers a transient suppression of reactive hyperemia following arterial occlusion. The apparent anti-in flammatory effects of smoking cigarettes can therefore only partially be explained as a long-term effect of nicotine.