J. Cosmet. Sci., 65, 315–345 (September/October 2014) 315 Need of UV protection and evaluation of effi cacy of sunscreens ANOOPINDER KAUR, PURVA THATAI, and BHARTI SAPRA, Pharmaceutics Division, Department of Pharmaceutical Sciences & Drug Research, Punjabi University, Patiala, 147002, Punjab, India Accepted for publication August 10, 2014. Synopsis Sun exposure has been coupled with numerous types of acute and chronic reactions in skin, for example, sun burns, photoimmune suppression, photoaging, and skin cancer. In scrutiny of growing understanding of the potentially unfavorable long-term side effects of solar irradiation, there is a universal call for harmless and effective photoprotectants. Photoprotective agents are used for protection against ultraviolet (UV) radiations. In support of best photoprotective measures, now sunscreens are in great demand. Safeguard from UVB is quantifi ed as a minimal erythema dose–based sun protection factor (SPF). UVA protection testing methods include evaluation of persistent pigment darkening (PPD) and critical wavelength. The rationale of this re- view is to present the contemporary information on the cutaneous pathophysiology of photooxidative stress, to study different UV fi lters with their UV spectrum and various commercially available sunscreens, with special emphasis on their active ingredients and SPFs. The characterization of different parameters to evaluate the effi cacy of sunscreens, for example, SPF, immune suppression factor, photostability, and water resistance, have been described on the basis of fi ndings from different researchers. INTRODUCTION Sunlight is composed of a continuous spectrum of electromagnetic radiation, that is, ultra- violet (UV) (45%), visible (5%), and infrared (50%). Furthermore, UV radiations (UVR) from the sun are classifi ed as UVA1 (340–400 nm), UVA2 (320–340 nm), UVB (290– 320 nm), and UVC (270–290 nm). UVB radiations are responsible for UV-induced skin damage. UVB suppresses immune reaction, induces tolerance toward antigens, and causes DNA damage that may further contribute to cancer. UV exposure of the skin results in the generation of reactive oxygen species (ROS), which are rapidly removed by nonenzymic (e.g., ascorbic acid, tocopherol, ubiquinol, and glutathione) and enzymic antioxidants (AO) (e.g., catalase, superoxide dismutase, glutathione peroxidase, and glutathione reduc- tase). Excessive ROS can overcome antioxidant defense and cause oxidative stress. UV exposure causes pigment darkening that can be immediate (occurs within seconds, disappears in 2 h after exposure), persistent where pigmentation is for 2–24 h (1), and Address all correspondence to Bharti Sapra at bhartijatin2000@yahoo.co.in

JOURNAL OF COSMETIC SCIENCE 316 delayed, that is, pigmentation is at peak at 72 h due to increase of tyrosinase activity and formation of new melanin (2). Exposure of skin to UVA (95% of solar radiation) leads to oxidative stress because of the increase in infl ammation due to infi ltration of infl ammatory blood leucocytes (macro- phages and neutrophils) increased production of prostaglandins (PGs) as a consequence of increased lipid peroxidation (LPx) release of tumor necrosis factor-alpha, nuclear factor-κB (NF-κB), infl ammatory cytokines (interleukins IL-1α, IL-1β, IL-6) and pro- duction of ROS (3). Responses of human skin toward UVB radiation can be acute or chronic. Acute responses include erythema, edema, pigment darkening followed by synthesis of vitamin D, de- layed tanning, and thickening of the dermis and epidermis, whereas chronic effects in- clude photoaging, immunosuppression and photocarcinogenesis (4). DNA damage by ROS leads to oxidation of 8-hydroxyguanine and pyrimidine bases that are responsible for mutagenesis and carcinogenesis (5,6). UVA penetrates deep into the epidermis and dermis. UVA and UVB are also known as tanning ray and burning ray, respectively. Long-term skin exposure to UVA can lead to skin aging (7), wrinkling, skin sagging (8), UV-induced immunosuppression (9), and burns (10). UVB absorbed by two adjacent cytosine residues in DNA causes the formation of cyclobutane pyrimidine dimers (CPD) and UVA induces the mutations at high frequency (11). UVC gets fi ltered by the ozone layer, as a result does not reach the earth (4). Figure 1 explains the spectrum of UV radia- tions as well as their hazardous effects on different layers of skin. Sunscreens are considered a useful approach for the photoprotection of skin. Sunscreen products that can absorb, refl ect or scatter UV photons are considered to be effective. Hence, they attenuate the amount and nature of UV radiations reaching viable cells in the skin. No sunscreen prevents photodamage, as it has been revealed that suberythemal Figure 1. Effects of UV radiation after penetration through different layers of skin.