7-2013 English Edition International Journal for Applied Science • Personal Care • Detergents • Specialties J. Vollhardt, A. Janssen, Ch. Saecker Modern Sunscreens that Protect from more than just Sunburn COSMETICS SUN CARE J. Vollhardt, A. Janssen, Ch. Saecker* Modern Sunscreens that Protect from more than just Sunburn ■ Sunburn and what happens at duced damage level and undergo the ing level of pain on the affected spot. The lower UV dosages? programmed cellular death, a distinct corresponding energy dosage necessary to buildup of inflammatory cytokines oc- induce this skin answer is called one min- If our skin receives UV light with the first curs. The thus initiated inflammation imal erythemal dosage (1 MED). Dosages ray damaging effects will happen to vari- process causes blood vessels to widen, below this value usually do not induce ous cellular and extracellular constituents. and this turns the skin red. A sunburn be- any visible skin redness, with the excep- For keratinocytes, after »enough« cells comes manifest macroscopically not on- tion they are received subsequently for have been »disabled« by a certain UV-in- ly in skin reddening but also in a grow- a longer period of days. If a single UV Introduction fter 3 decades of intense episodes. But to draw the whole and therefore represents a strong public campaigns sun pro- picture: more than half of the UV driver to apply sun protection Atection is in the mind of al- dosage is not linked to vacation products. Most people consider most every consumer in particular times but rather to day by day ac- the avoidance of sunburn as a suc- if it concerns holiday or sport ac- tivities such as gardening, grill cess signal for their personal pro- tivities. Does this mean that in- parties or lunch breaks. People tection strategy and feel on the dustry stakeholders and con- have significantly lower aware- save side if they succeeded in do- sumers can lean back? Surely not. ness for sun protection in those ing so. But is this really true? Are There is still a lot more work and situations which might result in dosages below the erythemal education on safe sun exposure to occasional localized sunburn, e.g. dose level (1 MED) well compen- do, in particular because only one the facial area. In holiday sated in our body? This article country so far, Australia (1), has episodes most consumers have looks at such dosages in a few di- achieved a beginning decline of learnt how to avoid sunburn of mensions, e.g. DNA damage as the melanoma incidence. Holidays larger skin areas; however, quite mutagenic marker, oxidative and sport themes are often com- frequently they still have localized stress as anti-aging initiator and municated together with sun pro- weak sunburns on super-exposed immunosuppression as a cancer tection messages – with a com- skin parts or areas which had enhancement marker. It also gives pelling reason: a significant por- been treated only sparsely with recommendations based on the tion of the annual UV exposure sunscreen. Sunburn does cause findings to protect people of UV dose is collected in these pain and significant discomfort radiation beyond sunburn. 24 SOFW-Journal | 139 | 7-2013 COSMETICS SUN CARE dosage does not cause sunburn it is called suberythemal. UVB : UVA The energy or duration of UV radiation Natural day light, Europe noon, noon time, June 1 : 25 necessary to induce sunburn is not con- Natural day light, tropics noon 1 : 18 stant and can vary a lot from person to person mainly depending on skin type. Solar Simulated Radiation Sunburn is also wavelength dependent (SSR, artificial light for SPF measurements) 1 : 10 as UVB is more damaging than UVA. Be- Table 1 Light sources: Proportional energy ratios between UVB and UVA light ing in a holiday location in the tropics makes our skin burn faster, not only be- cause of a general higher radiation in- tensity but also because at that latitude due to absorption and some back scat- represent one major route to carcino- sunlight contains more UVB than e.g. in tering. The absorbed energy allows the genesis. The complex repair process, par- Europe (Table 1). But it is important to base pairs of the DNA to undergo a va- ticularly for the CPDs, takes place with- keep in mind that sunburn is not 100% riety of reactions which lead to alter- in hours and days and is therefore gen- UVB based. There is also an energy level ations in the structure of DNA. The ge- erally much slower than the time to pro- or time point at which pure UVA radia- netic code at that structurally altered lo- duce the damage under solar radiation. tion would cause erythema as well if UVB cation is not correctly readable anymore Different molecular biological markers were filtered out (Table 2). This situation and thus could give rise to mutations. are known to track the buildup of this may evolve with sunscreens providing no Two neighboring thymines in the DNA damage and repair process, which hap- or little UVA protection. strand are prone to a particular muta- pens unnoticed by the consumer until When reporting on human trials involv- tion: they form in a photo-catalyzed re- the skin shows visible signs of redness ing UV radiation, the wavelength and in- action a dimer, called cyclobutane pyri- due to exposure to erythemal UV dosages dividual sensitivity dependency of the midine dimer (CPD) or more specific, (> 1 MED). Indicative damage markers MED is less suitable and may lead to con- thymine dimer (TT). Fortunately, our cells after UV radiation can be: relative num- fusion in data comparisons. Additional have evolved several DNA repair mecha- ber of SBCs and CPDs. Also monitoring parameters would have to be measured nisms such as the nucleotide excision re- of p53 by immunofluorescence can be and reported to make experiments com- pair (NER). While it is well known that helpful, as it indicates the cells’ begin of parable. The Standard Erythemal Dosage UVB is the major source of DNA damage, repair. In addition to molecular biologi- (SED) has therefore been introduced (2) only recently it has been shown that UVA cal methods requiring biopsies, measure- to avoid or define dependencies. For a could also induce direct DNA damage ment of the erythemal index represents reference example: 1 MED for a skin type particularly in deeper layers of the skin a sensitive technology to follow up the 2 person is about 2 SED. Table 2 (3-6) lists (7). UVA light interacts also with DNA in subsequent rise towards sunburn before average energy values to induce 1 MED in more indirect mechanism through for- it is really visible to the human eye. a skin type 2 person of some commonly mation of excited oxygen species which used light sources, note the much higher finally might lead to the formation of number for UVA to induce sunburn. CPDs, 8-oxoguanine and strand breaks. ■ Damages revealed before onset p53, a key protein, orchestrates the re- of sunburn after single and subse- pair process. It also initiates apoptosis, quent suberythemal UV Exposure ■ Molecular components related the programmed cell death to protect to sunburn and evolvement of against mutagenesis. Such affected cells UV damage until sunburn are called sunburn cells (SBCs). Damage Fig. 1 shows the slow evolvement of skin on p53 itself and persisting mutations of redness by a series of subsequent subery- It is widely accepted that sunburn is that protein are very critical as they can themal dosages (11 x 0.6 MED of SSR) linked with DNA damage in the cellular nucleus, followed by apoptosis of the keratinocytes and in consequence in- Type of Light Energy necessary to induce duction of an inflammation, which leads 1 MED in a skin type II finally to skin redness. However not all 2 connections in this cascade of events are Monochromatic UVB (300 nm) median 25 mJ/cm fully understood. The most prominent Monochromatic UVA (360 nm) median 32 J/cm2 primary target for UV interaction with Simulated Day Light (SDL) 15.2 J/cm2 skin is DNA. UVB light gets physically ab- Sun (295–400 nm) ~5–12 J/cm2 sorbed e.g. by the thymine chromophore. Solar Simulated Radiation (SSR) as used for SPF measurement ~2 J/cm2 The epidermis is densely packed with cells and therefore UVB does not pene- Table 2 Energy values of certain light sources to induce 1 MED in a skin type 2 person trate much deeper than the basal layer 26 SOFW-Journal | 139 | 7-2013 COSMETICS SUN CARE volunteers of skin type I and II were ex- of either SSR or SDL was enough to gen- uneven skin tone (13) delivers informa- posed to (8). At a value of about 80 skin erate p53 upregulated cells. SBCs were tion for a visional judgment on age. The redness gets visually perceivable. Over present at a significant level already at desire to look attractive is high, being the the whole period of 11 days there seems only 0.25 MED SSR, while SDL needed 0.5 main driver of the global demand for to be a gradually rising level of damage MED to generate a similar number. effective treatment concepts. A second indicated by progressing skin redness strategy, which actually should be the (blue line, Fig. 1). During the first 8 – 10 primary one to fight signs of aging is to days this damage goes on unnoticed, on- ■ UVA radiation is setting an aging protect skin against their origin before ly at the last day it seemed to have be- process into motion aging signs appear or get worse.