Broad spectrum protection from visible light

The Earth’s atmosphere absorbs most of the high energy X-ray and gamma radiation, while ultraviolet radiation (UVR, 100–400 nm), visible light (VL, 400-760 nm), and infrared (IR, 760 nm- 0.1 mm) manage to penetrate Earth’s atmosphere and reach Earth’s surface. In the UVR range, UVB (290-315 nm) and UVA (315-400 nm), are able to reach the earth’s surface, while UVC (100-290 nm) is mostly absorbed by the ozone layer. Human skin acts as a barrier between the body and the environment against various physical, chemical and biological attacks. Thus one of the main functions of skin is to protect against various ill effects including that of solar radiation. Due to increased incidences of skin cancer, the last few decades have seen an increased effort by researchers to understand the interaction of sunlight with skin. Skin’s response to sunlight is determined by the skin type. The Fitzpatrick classification4 of skin types is based on the response of skin to sun exposure and the constitutive skin colour. Skin types I and II burn more easily. Individuals with these skin types do not tan and have an increased incidence of skin cancer compared to those with skin types III to VI. Skin type III burns minimally and tans moderately and gradually. Skin type IV has light brown skin, burns minimally and tans well; Type V with dark brown colour rarely burns and tans deeply; Type VI has dark brown/black skin, never burns, but tans deeply.

Effect of UV radiation

UVR on Earth’s surface includes both UVB and UVA radiation and constitutes about 3%-4% of total sunlight received. In skin types I-II, exposure to UVB radiation leads to erythema and sunburns. The redness induced due to exposure to UVB is called erythema. Large doses of UVB exposure lead to sunburn. Exposure to large doses of UVA also leads to erythema, however to a lesser extent. The erythema caused by UVB is attributed to capillary dilatation since it can penetrate only up to the upper dermis while the erythema caused by UVA is attributed to the dilatation of vessels of the subpapillary plexus. Until few decades ago, UVB was considered to be responsible for sunburn and solar induced carcinogenessis. However recent studies have indicated that UVA can be attributed with about 10%-20% of the carcinogenicity of sunlight. Further evidence generated in the last decade on the effect of UVA on skin has led to the European Commission’s recommendations to provide extended protection against UVA in addition to the protection provided against UVB, highlighting the damage potential of UVA. According to the recent US FDA regulations, a ‘broad spectrum sunscreen’ should have a critical wavelength greater or equal to 370 nm highlighting the importance of UVA protection. In addition to erythema, skin pigmentation or tanning is also induced by UVR and occurs in three different phases – immediate pigment darkening (IPD), persistent pigment darkening (PPD) and delayed tanning (DT). IPD is the transient skin pigmentation induced due to small doses of UVA (1–5 J/cm2) exposure, and fades within 20 minutes to 2 hours. IPD is attributed to the photo oxidation and redistribution of pre-existing melanin and its precursors. When skin is exposed to high doses of UVA (>10 J/cm2), the induced pigmentation persists for more than 24 hours and is termed as PPD. PPD also results from oxidation and redistribution of pre-existing melanin. In contrast to IPD and PPD, DT occurring many days after exposure, is attributed to the synthesis of new melanin. Both UVB and UVA are capable of inducing DT. However UVB is found to be more efficient than UVA in inducing erythema and DT. While erythema, IPD and DT are noticeable effects of short-term UVR exposure of skin, repeated UV exposure also leads to immunosuppression and photo carcinogenesis which results in skin cancer. It has been found that the more energetic UVB induces genotoxic effects in skin by damaging various molecules including DNAs and proteins. Incorrect repair of this DNA damage can lead to mutations and carcinogenesis.5 Repeated exposure to UVR can also result in chronic effects such as photoageing which in turn leads to development of deep wrinkles and spots on the sun exposed skin. Both UVA and UVB can induce this premature skin ageing either directly or indirectly. UVR activates critical genes which may have a prime role in skin inflammatory responses. Activation of such genes can lead to increases in inflammation through the release of signalling molecules such as cytokines (eg. IL-1, IL-6, VEGF and TNF-).6 These ultimately lead to increased oxidative damage through production of reactive oxygen species (ROS). Additionally, the ROS generated by UVR also activates cell surface receptors and cytokines leading to heightened inflammatory reactions.7 The molecules can affect the appearance of the skin via the modulation of extracellular skin matrix. Prolonged high levels of these cytokines can lead to irreversible tissue damage and development of photoaged skin. UVR is capable of inducing vascular change which may contribute to the telangiectases (dilated blood vessels) and neoplasm (abnormal tissue mass) seen in sun-exposed areas. UVR can also induce alterations in skin structural components like collagen, elastin and glycosamino glycans. This can occur by the damage to the existing extracellular matrix and reduced synthesis of new collagen by decrease in pro-collagen synthesis. The physical manifestations of these underlying molecular changes would be perceived and seen by an individual as age spots, lentigens, increased wrinkles and leathery skin giving an overall aged appearance. In order to identify the underlying changes in skin that happen with UVR exposure, Unilever has conducted genomics and proteomics studies with skin Type III, IV and V. In this study, skin samples from different individuals of different skin colour (obtained as a discard from surgical interventions) were exposed to UVR. Genomic material was extracted after 24 hours from the tissues and analysed using one of the latest tools of molecular biology, viz., Differential display. This methodology helps to determine the levels of different genes expressed in a tissue and can be used to differentiate gene expression levels in response to a stimulus. As shown in Figure 2, several genes relevant to skin health were found to be modulated by UV exposure. These modulations were found to vary with skin colour.