Skin Reactions to Light

18
Skin Reactions to Light

Ultraviolet radiation (UVR) has a mixture of beneficial and harmful effects. Our species, Homo sapiens, arose in Africa probably around 200 000 years ago. In contrast to our primate cousins, we have lost our covering of fur. In combination with the high volumes of sweat we can produce, this enables us to lose heat effectively, and originally we found our ecological niche as a long distance hunter, able to track our prey until heat and exhaustion fatally weakened it. With this loss of fur, however, has come the need to cope with the effects of the sun directly striking our epidermis. In the last 80 000 years we have scattered from our ancestral African homeland to populate the globe. The range of environments in which we have settled, from the tropics to the polar regions, and Himalayan heights to below sea level, has further altered our exposure to sunlight and imposed powerful evolutionary pressures on our skin. The most obvious effect of this has been in the range of pigmentation we show. This has been caused by two opposing evolutionary pressures. On the one hand we need pale enough skin to synthesise vitamin D, and, on the other, our skin needs enough eumelanin to protect from carcinogenesis and neural tube defect-inducing folate destruction. Recent large-scale population movements have led to high rates of skin cancer in white Australians, and high rates of rickets in immigrants from the Indian subcontinent to Scotland.

The UVR spectrum is divided into three parts (Figure 18.1), each having different effects on the skin, although UVC does not penetrate the ozone layer of the atmosphere and is therefore currently irrelevant to skin disease. Virtually all of the UVB is absorbed in the epidermis, whereas some 30% of UVA reaches the dermis. The B wavelengths (UVB: 290–320 nm) cause sunburn and are effectively screened out by window glass. The A spectrum (UVA) is longwave ultraviolet light, from 320 nm to the most violet colour perceptible to the eye (about 400 nm). It ages and tans the skin. The differences between the wavelengths can be recorded conveniently in the form of action spectra, which show how effective each is at producing different biological effects, such as clearing psoriasis or causing erythema. UVR is non-ionizing, but changes the skin by reacting with endogenous light-absorbing chemicals (chromophores), which include DNA, RNA, urocanic acid and melanin.

images — **Figure 18.1** Skin disorders and the wavelengths that cause them.

The variation in consitutive skin pigmentation and response to UVR is conventionally divided into six types (Table 18.1). These skin types require different degrees of protection against the sun.

Table 18.1 Skin types classified by their reactions to ultraviolet radiation (UVR).

Type	Definition	Description
I	Always burns but never tans	Pale skin, red hair, freckles
II	Usually burns, sometimes tans	Fair skin
III	May burn, usually tans	Darker skin
IV	Rarely burns, always tans	Mediterranean
V	Moderate constitutional pigmentation	Latin American, Middle Eastern
VI	Marked constitutional pigmentation	Black

Beneficial effects of sunlight

A considerable body of epidemiological data suggest beneficial health effects of sunlight but the interpretation of these data can be contentious. Rickets is a disease of poor diet or inadequate sun exposure resulting in low vitamin D levels and correction of either of these factors is therapeutic. The case for the benefits of vitamin D in other conditions is less clear-cut. Observational studies show that subjects with high levels of circulating vitamin D are less likely to have cardiovascular disease, hypertension, type 2 diabetes or multiple sclerosis than those with low levels. Correlation should not be confused with causation, however, and the results of intervention studies in which vitamin D supplementation has been given have been disappointing. Ill health may lead to reduced sun exposure and thus low vitamin D levels (reverse causation), or vitamin D levels might be acting as a marker for sunlight exposure, which is beneficial via a different mechanism (confounding). A newly identified alternative mechanism is mediated by the vasodilator nitric oxide. The skin contains large stores of nitrate and nitrite, which are converted by sunlight to the nitric oxide from where it enters the circulation and lowers blood pressure. Other mechanisms may also exist.

Clinically, UVR is helpful in the treatment of diseases such as psoriasis and eczema, but at the same time use of tanning lamps, particularly by young people, increases the risk of developing melanoma and non-melanoma skin cancers. Excess UV exposure also leads to photoageing, and may cause or worsen several skin disorders (Figure 18.2).

Sunburn

Cause

UVB penetrates the epidermis and superficial dermis, stimulating the production and release of prostaglandins, leukotrienes, histamine, interleukin 1 (IL-1) and tumour necrosis factor α (TNF-α). These cause pain and stimulate the production of the inducible nitric oxide synthase (iNOS) enzyme. This generates very high local concentrations of nitric oxide which causes the characteristic dermal vasodilatation and redness.

Presentation and course

Skin exposed to too much UVB smarts and becomes red several hours later. Severe sunburn is painful and may blister. The redness is maximal after 1 day, contemporaneously with peak levels of the iNOS enzyme, and then settles over the next 2–3 days, leaving sheet-like desquamation (Figure 18.3), diffuse pigmentation (a ‘tan’) and, sometimes, discrete lentigines.

Differential diagnosis

Phototoxic reactions caused by drugs are like an exaggerated sunburn.

Investigations

None are required.

Treatment

The treatment is symptomatic. Baths may be cooling and oily shake lotions (e.g. oily calamine lotion) or creams are comforting. Potent topical corticosteroids (Formulary 1, p. 401) help if used early and briefly. Oral aspirin (a prostaglandin synthesis inhibitor) relieves the pain.