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Erythema vs. Sunburning

Donald L. Smith
12/01/2001
Posted : 12/01/2001

Erythema vs. Sunburning

by Donald L. Smith

Erythema is a non-specific term used to define the redness of the skin produced by a congestion of the capillaries that can result from a variety of causes. Erythema can be caused in the skin by, among other things, friction, irritation and exposure to ultraviolet, visible and infrared (heat-producing) radiation. Sunburning is defined as an injury to the skin with erythema, tenderness and sometimes painful blistering, following excessive overexposure to ultraviolet radiation.

From these definitions it can be seen that while erythema is not synonymous with sunburning, one of the characteristics of a true sunburn is erythema. Therefore, the term "UVR-Induced Erythema (Sunburn)," which is defined as the redness of the skin produced by a congestion of the capillaries resulting from overexposure to ultraviolet radiation, should be universally used in order to be precise.

Overexposure is defined as a dose of ultraviolet radiation (UVR) sufficient to cause a sunburn and the level or dose of UVR sufficient to cause sunburning (overexposure) universally has been deemed to be 1 MED or more. MED is defined as "minimal erythemal dose" and you can see that this term is also imprecise. It should be ME(sb)D or "Minimal Erythemal (sunburning) Dose in order to be specific and precise.

Fact 1

Understanding the difference between erythema and sunburning will allow you to better explain these somewhat contradictory terms to your clients. For instance, we all know that sunburning should be avoided at all costs but we sell products--namely tingling lotions--that, because they irritate the skin, cause erythema. You can use this information to help sell tingling lotions by explaining that the "redness" of the skin that characterizes the erythema produced by tingling lotions is caused by the increased microcirculation of the blood through the skin which, theoretically, brings melanin closer to the surface of the skin where it can more easily be oxidized.

Fact 2

It was reported (in 1988) that visible light (400-700 nm) can cause erythema, immediate pigment darkening (IPD) and persistent (delayed) pigment darkening. The question of importance was whether or not this was erythema (redness) or sunburning.

Since the erythema disappeared within 24 hours, it was transient in nature and, therefore, not a true sunburn. There are two ways that are used clinically to determine the difference between erythema and sunburning. The first is an invasive procedure whereby a skin biopsy is examined for the presence of sunburn cells. The second is to grade the skin 24 hours after exposure or overexposure to UVR according to the following scale.

GradeDescription

0. Absent. No redness and not tender to the touch.

1. Barely perceptible redness and not tender to the touch.

2. Light pink color and tender to the touch.

3. Dark pink color and painful to the touch.

4. Dark pink color, painful to the touch and blistering.

5. Dark pink color, painful, blistering and requiring medical care.

As you can see, the transient erythema caused by visible light would be classified after 24 hours as a Grade 0. The erythema accompanying a true sunburn would persist after 24 hours and would be classified from Grade 1 to Grade 5.

In addition to setting the record straight regarding whether or not the visible portion of the electromagnetic spectrum can cause a sunburn (it can't), this article shows that these wavelengths can, and do, play a role in the creation of a tan. Since sunbeds have very low levels of visible irradiance, this study helps to explain why there is a slight difference between the facultative pigmentation (a "tan") produced outdoors as compared to the facultative pigmentation produced indoors by sunlamps.

Fact 3

The most common form of transient erythema (redness) that will be observed by tanning salon owners is the "heat flux" that sometimes occurs after a tanning session. This form of "redness" signifies that the blood flow to the surface vessels of the skin has increased in order to aid in cooling the skin and thereby helping to regulate body temperature.

Fact 4

Anti-tanning forces now are advocating using the production of CPDs (cyclobutane pyrimidine dimers) as a surrogate monitor of UVR-induced damage. We can, therefore, look to the measurement of CPDs to replace the time consuming and invasive measurement of sunburn cells.

Why is this important? Because it was found in a study published in the British Journal of Dermatology that the UVB wavelengths (280-320 nm) are responsible for 75 percent of the CPDs produced. Therefore, look for the anti-tanning faction to use this information to try to coerce the Food and Drug Administration (FDA) to adopt the same parameters (the CIE Erythemal Action Spectrum) regarding irradiance that are used in Europe.

If adopted, U.S. tanning salons would be forced to use low percentage UVB lamps and return to the 30-minute sessions (or longer) that are common in Europe.

What isn't being said? The proponents of CPDs as a surrogate for skin damage neglect to tell you that the normal homeostasis process of the body causes the CPDs to quickly be repaired. Moreover, they don't tell you that tanned skin is much less likely to produce CPDs than is untanned skin when exposed to a given dose of UVR.

The Bottom Line

Explain to your clients that the erythema (redness) produced by tingling lotions, and the "heat flux" that sometimes occurs in a tanning bed is not a sunburn; rather, these transient conditions show that there has been increased blood flow to the skin.

You also should point out that UV-induced erythema (redness) must persist for at least 24 hours in order to be considered a sunburn.

The next time you read something about CPD production--or if a client asks you a question--keep in mind that the production and the repair of cyclobutane pyrimidine dimmers (and other photoproducts) is a natural, normal and ongoing process. Moreover, the increased tolerance to UVR provided by a photoprotective tan protects against the production of CPDs for subsequent exposures.


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