Volume XIX - Nr.2 - November 2004
Skin and Sun Radiations
Excessive skin exposure to sun radiations may acutely cause inflammation, while chronically leading to skin ageing and cancer.
UV.B negative effects are the following: sunburn; DNA damages; early skin ageing, skin cancer; immuno-suppression; photodynamic reactions; photodermatitis; eye inflammations. UV.A negative effects are the following: collagen damage; loss of skin elasticity; immuno-depression; photodynamic reactions; photodermatitis; eye inflammation.
Individuals who, as children or adolescents, have once or several times suffered from sunburns with blisters have double probability to develop malignant melanoma. Among these individuals, the risk for those with a light skin is three times higher [R.S. Stern, M.C. Weinstein, S.G. Baker: Risk reduction for non melanoma skin cancer with childhood sunscreen use. Arch. Dermatol. 122:537-545 (1986)].
The regular use of sunscreens reduces the incidence of non melanoma skin cancer by only 70%, with a 78% value when sunscreens are regularly used since childhood.
The results thought to be obtained from oral administration of b-carotene do not exactly meet the expectations. As a matter of fact, a-carotene and not b-carotene, has a ten times higher antiproliferative effect (H. Nishino, J. Takayasu, A. Iwashima, M. Murakoshi, J. Imanishi, 1988).
Moreover, of the three different carotenes which in nature are always mixed together, namely a, b and ?-carotene, a-carotene is the only optically active one with different cyclic ends: one is an a-ionone, the other a b-ionone.
Therefore, in order to obtain the same effect as a, b-carotene should be taken in great quantities, which would even stain the skin. Moreover, empirical oral administration of natural substances, namely those containing the three carotenes, is only potentially effective. Therefore b-carotene is no guarantee today.
From a biologic point of view, the most active part of the solar electromagnetic spectrum lies between 280 and 700 nm. UV.C radiations, namely those with wave length below 290 nm, are filtered through the stratosphere.
These radiations are more exactly filtered by the ozone layer. Therefore, should the excessive use of chlorofluorocarbonates lead to the loss of this protective layer, UV.C radiations will have to be taken into account.
UV.C radiations are used for their germicidal action.
Quite often, observations based on few experimental data were for a long time considered to be sufficient to correctly define the course of a phenomenon. This was also the case of UV.B and UV.C radiations induced erythemas which, on the basis of studies conducted many years ago, were thought to have a different course.
Namely the UV.C induced erythema was thought to have its onset, reaching its maximum intensity and disappearing more rapidly than when induced by UV.B. This assumption is based on data reports resulting from limited studies which do not specify whether the compared UV.B and UV.C erythemas had the same intensity.
Since a different course of these two types of erythema is likely to involve also a different pathogenetic mechanism, with a particular role played by prostaglandins as inflammation mediators, Farr and coworkers correctly decided to review the problem under experimental conditions permitting a more exact lesion degree quantification (1988). They conducted their research on 8 adult volunteers (4 males and 4 females) by using their central back skin. T
he radiation equipment employed was supplying 30 W/m2 between 200 and 290 nm (namely within the UV.C spectrum, with 96% emission at 254 nm wavelength) and 80 W/m2 between 290 and 320 nm (namely within the UV.B spectrum). At both sides of the median dorsal line, 6 areas were identified with a 20 mm diameter each, 5 of which underwent increasing UV.B radiation doses for factors 1, 3 or increasing UV.C radiations for factor 2, with an initial minimum amount of 0.6-1.2 kJ/m2 UV.B and 0.08-0.25 kJ/m2 UV.C radiation dose respectively.
The erythema degree was assessed after 4-8-12-24-36 and 48 hours after radiation exposure with a suitable reflectance instrument to evaluate the quantity of red and green light reflected by the skin. This method is employed to obtain an “erythema index” which is proportional to skin blood content. The sixth radiation-free area was used as control.
Radiation induced vasodilation increase was calculated by subtracting from the values obtained at several time intervals the erythema index value recorded at zero time. A 0.05 increase corresponds to a minimum erythema producing dose, namely a uniform clear-cut edge rash in the radiation exposed area, whereas a 0.3 increase corresponds to marked erythema. Finally, to better identify the erythema course in each subject, data obtained under different radiation dosages at each observation time have been added together thus obtaining a dose independent index.
The results have shown that at both wave lengths, namely with both UV.B and UV.C, the erythema appears 4 hours after radiation exposure with its peak between 8 and 24 hours. Moreover, although peak time varies considerably from person to person, in each of them the peak for both radiation types seemed to coincide.
Obviously enough, UV.B and UV.C radiation induced inflammation duration depended on radiation dose and, when the erythema index increase at 12 hours was lower than 0.1, the erythema subsided within 48 hours. Finally, by comparing the course of UV.B and UV.C induced erythemas, significant differences were observed only in three out of eight subjects examined. Major differences were observed between individual subjects regarding erythema course, especially with reference to the time interval from exposure to inflammation peak.
Yet, in most of them, UV.B and UV.C radiations were observed to lead to an alteration sequence which was substantially similar with respect to time-dependence. This would suggest that in both radiation types the same action mechanism is at the origin of inflammation.
Furthermore, the results obtained would indicate that previous reports about a more rapid onset and shorter course of UV.C radiation induced erythemas should be considered as questionable and even likely to be wrong, since they were based on the comparison of radiation doses causing different intensity and duration reactions.