Transdermal nicotine suppresses cutaneous inflammation.
BACKGROUND
Cigarette smoking significantly alters the inflammatory response in the skin following application of irritants and rubefacients. The mechanism of this effect is unknown. There are thousands of components in cigarette smoke that may be pharmacologically important, but there is evidence to suggest that nicotine may play an important role in the observed effect on the inflammatory process.


METHODS
This was an interventional study to assess cutaneous responsiveness to different stimuli after transdermal nicotine administration in volunteer subjects. Cutaneous testing was performed at baseline and at weeks 2 and 4 (the end) of the study.


METHODS
The department of Dermatology, University Hospital of Wales, Cardiff.


METHODS
Ten lifelong nonsmokers were recruited for the study.


METHODS
Nicotine patches were applied daily for 1 month.


METHODS
The following tests were performed: application of 2 times the minimal irritancy dose of sodium lauryl sulfate, irradiation with 2 times the minimal erythema dose of UV-B, measurement of cutaneous vasodilation following application of ethyl and hexyl nicotinate, and reactive hyperemia following arterial occlusion.


RESULTS
There was a significant reduction in the cutaneous inflammatory response to sodium lauryl sulfate (P < .001) and irradiation 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 nicotinates.


CONCLUSIONS
Nicotine administration via a transdermal delivery system suppresses the cutaneous inflammatory response to sodium lauryl sulfate and UV-B, as well as triggers a transient suppression of reactive hyperemia following arterial occlusion. The apparent anti-inflammatory effects of smoking cigarettes can therefore only partially be explained as a long-term effect of nicotine.
Mills
C M
CM
Department of Dermatology, University Hospital of Wales, Cardiff.
Hill
S A
SA
Marks
R
R
D000279:Administration, Cutaneous; D000328:Adult; D001157:Arterial Occlusive Diseases / Q000503:physiopathology; D001916:Brachial Artery / Q000503:physiopathology; D000697:Central Nervous System Stimulants / Q000008:administration & dosage / Q000494:pharmacology*; D003872:Dermatitis / Q000209:etiology / Q000503:physiopathology*; D003877:Dermatitis, Contact / Q000209:etiology / Q000503:physiopathology; D017453:Dermatitis, Irritant / Q000209:etiology / Q000503:physiopathology; D004890:Erythema / Q000209:etiology / Q000503:physiopathology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006940:Hyperemia / Q000209:etiology / Q000503:physiopathology; D007509:Irritants / Q000009:adverse effects; D008297:Male; D009538:Nicotine / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology; D009539:Nicotinic Acids / Q000009:adverse effects; D011109:Polymethacrylic Acids / Q000008:administration & dosage / Q000494:pharmacology*; D011145:Polyvinyls / Q000008:administration & dosage / Q000494:pharmacology*; D011829:Radiation Dosage; D012039:Regional Blood Flow; D012867:Skin / Q000098:blood supply / Q000187:drug effects* / Q000528:radiation effects; D012907:Smoking / Q000503:physiopathology; D012967:Sodium Dodecyl Sulfate / Q000009:adverse effects; D013501:Surface-Active Agents / Q000009:adverse effects; D061485:Tobacco Use Cessation Devices; D014466:Ultraviolet Rays / Q000009:adverse effects; D014664:Vasodilation / Q000187:drug effects
D000697:Central Nervous System Stimulants; D007509:Irritants; D009539:Nicotinic Acids; D011109:Polymethacrylic Acids; D011145:Polyvinyls; D013501:Surface-Active Agents; D012967:Sodium Dodecyl Sulfate; D009538:Nicotine; C049457:hexyl nicotinate; C037328:ethylnicotinate