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Sunscreen
– The ultraviolet (UV) wavelengths of light associated with cutaneous damage are UVB (290–320 nm) and UVA (320–400 nm) light.
– UVB absorption by DNA results in a p53 tumor suppressor gene mutation resulting in pyrimidine dimer formation, which is mutagenic and linked to cutaneous carcinogenesis.
– Acute UVB exposure results in a sunburn (Fig. 2.1).
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– Repeat acute UVB exposures over time have been associated with the formation of basal cell carcinoma and melanoma.
– Chronic UVB exposure has been linked to the development of actinic keratoses and squamous cell carcinoma.
– UVA is unaffected by window glass, altitude, time of day, or season and can produce a tan and dyspigmentation without preceding erythema.
– UVA light penetrates deeply into the dermis, producing many of the clinical findings associated with photo damage (Fig. 2.2).
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– UVA absorption by DNA results in formation of oxygen free radicals, thought to contribute to carcinogenesis. It causes immunosuppression through the depletion of Langerhans’ cells and reduced antigen presenting cell activity.
– UVA exposure has been linked to the development of melanoma in animal models.
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Chemical sunscreen (Table 2.1)—absorbs light in the UV wavelength of light (UVB 290–320 nm) and UVA 320–400 nm), transforming this light into harmless long wave radiation and re-emitting as heat energy.
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Physical screen (Table 2.2)—scatters or reflects UV radiation. Can also absorb UV light and release it as heat.
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Sun protective factor—optimally a sunscreen would provide protection against the full spectrum of UV radiation. The sun protective factor (SPF) is the only internationally standardized measure of a sunscreen’s ability to filter UV radiation. It is the ratio of the UV energy needed to produce a minimal erythema dose (MED) on sunscreen-protected skin to the UV energy required to produce an MED on ...