OR WAIT 15 SECS
For most of the outcomes assessed, the UV-induced changes were numerically less in the skin pretreated with the sunscreen.
The study evaluated the performance of the patented, commercially available sunscreen system to inhibit UV-induced epidermal and dermal injury by assessing an array of molecular and cellular markers. The tested product has an SPF value of 30, contains avobenzone, oxybenzone, homosalate, octisalate, octocrylene and the photostabilizer diethylhexyl 2,6-naphthalate, and provides high absorbance of UVB (290 nm to 320 nm) and UVA (320 to 400 nm) wavelengths.
After undergoing minimum erythema dose (MED) testing, one site on the lower back of each subject was treated with 2 mg/cm2 of the broad-spectrum sunscreen prior to UV irradiation with 30 MED. There were two control sites consisting of untreated skin that was either exposed to UV 1 MED or left not irradiated.
Findings from biopsies taken 24 hours after UV exposure demonstrated no differences in erythema between the three sites, as assessed by microvessel dilation. Compared with the untreated control site, skin exposed to 1 MED irradiation exhibited significant increases in levels of MMP-9, sunburn cells, mast cells, thymine dimers and microvessel density, demonstrating the damaging effects of the UV treatment. Other markers assessed included Langerhans cells and MMP-1, but they were not significantly altered by the minimal UV exposure.
Comparisons between the two irradiated sites showed that the sunscreen pretreatment significantly mitigated induction of MMP-9 expression, a marker of collagen degradation. Otherwise, there were no significant differences in the levels of any of the other histological markers between the 1 MED site and the skin that was sunscreen protected and exposed to the intense UV insult. In fact, for most of the outcomes assessed, the UV-induced changes were numerically less in the skin pretreated with the sunscreen.
"There has been a long-standing need for photostable sunscreen products effective for protecting against the harmful effects of UVA.
"Using a comprehensive set of histological markers, the present study substantiated the SPF rating of this novel sunscreen system and its efficacy for preventing UVA-induced immune-suppression and photodamage. Although this was a single use study, the activity demonstrated by the sunscreen formulation suggests that, with appropriate use, it should be helpful for reducing photoaging and the development of skin cancer," Dr. Draelos says.
Similar methodology has been used in a follow-up study to test the performance of the SPF 55 formulation of the broad-spectrum absorbent sunscreen in protecting against a 55 MED UVA insult. The results were positive and were presented at the annual meeting of the American Academy of Dermatology this month.
Previously, Dr. Draelos participated as an investigator in a multicenter study that demonstrated the efficacy of the SPF 55 product for protecting against outbreaks of polymorphous light eruption (PMLE). That trial enrolled 46 adult men and women with clinically-confirmed PMLE at three centers, which provided geographic diversity. The participants were instructed to apply the sunscreen daily to one side only (right vs. left was randomly selected) and to seek up to four hours of continuous sun exposure over a two to three day period.
Reactions to sun exposure were graded by the dermatologist and the patients using independent grading scales. A positive PMLE reaction was defined as an increase (worsening) of one or more grades in any of five investigator-evaluated and four patient-assessed PMLE attributes.
The results showed the sunscreen was uniformly effective in preventing positive PMLE reactions, and for all of the parameters evaluated, there was only a minimal increase in mean grading scale scores on sunscreen-treated skin. In contrast, with the exception of patient-rated stinging/burning, the untreated skin exhibited worsening of approximately one grade or higher in all rated signs and symptoms of PMLE.