Photosensitivity and Diving

by Bruce Miller, MD
Dr. Miller, a Dermatologist, is a Consultant for Diving Medicine Online. This is a lecture presented to Medical Seminars, 2000

A brief review of the physics and photobiology of ultraviolet radiation (UVR):

Transformation of H to He in sun’s interior liberates vast amounts of energy which reaches the earth’s surface in the form of electromagnetic radiation (EMR) : x-rays, cosmic rays, electric waves, radio waves, infrared, visible light, and ultraviolet radiation (UVR).
EMR travels in the form of waves containing packets of energy called photons. In the case of x-rays and cosmic rays, the wavelengths are very short, measuring only a few nanometers(nm):1 nanometer = 1 billionth of a meter. On the other hand radio waves are very long, measuring several kilometers (km):
1 km=1000 meters. The amount of energy contained in EMR is inversely proportional to its wavelength. The ozonosphere blocks all EMR shorter than 297 nm (thank goodness!).

UVA vs. UVB-what’s the difference and why it’s important:

UVR includes wavelengths of EMR between 297-400 nm. Convention divides this spectrum into UVB = 297-320 and UVA = 320-400. UVA may be further divided into UVA II = 320-340 and UVA I = 340-400. UVB is also known as the “sunburn spectrum” and is the prime factor in photo aging and photocarcinogenesis. UVA also contributes to photo trauma but is the spectrum primarily responsible
for photosensitivity reactions because of its deeper penetration into the skin.
UVB only penetrates into the epidermis and the papillary (uppermost) dermis and is blocked by window glass. UVA penetrates into the reticular (deep) dermis and passes through window glass unchanged. Unlike UVB these rays don’t vary in intensity with the time of day or the season. Compared to UVB, 100 times as many reach the surface of the earth.

Ozone depletion due to fluorocarbons found in aerosols, auto air conditioners, refrigerators, etc., pose a significant threat to us all in the form of an increased incidence of melanomas and other skin cancers, depressed immunity, accelerated aging, etc., due to high energy particles and increased UVR reaching the earth’s surface.

Under photosensitivity diseases, we will cover phototoxic and photoallergic systemic photoeruptions (mainly drugs), phototoxic and photoallergic contact dermatoses (mainly plants and perfumes), nature’s phototoxic diseases (the porphyrias), and a common photo eruption of unknown etiology, polymorphous
light eruption (PMLE).

Photoxic vs. Photoallergic:

Fundamental to both is the absorption of photons of light by a chromophore. However, once this event occurs, the mechanisms leading to cellular damage diverge.

In phototoxic reactions the photosensitivity is mediated by non-immunologic mechanisms. Absorption of photons of a specific wavelength (UVA in nearly all cases) by the photosensitizing chromophore results in electrons changing their orbits and creating unstable singlet or triplet states, which release
energy when the molecule returns to a stable ground state. This energy causes cellular damage and the release of products of inflammation, as well as free radicals, causing cellular damage and resultant erythema, edema, and occasionally vesiculation, i.e., an exaggerated sunburn reaction, which is restricted to sun-exposed areas. This reaction can occur upon first exposure to the drug.These chromophores are typically polycyclic ring structures withalternating single and double bonds, and fluorination at critical sites onthe molecule. The fluoroquinolones are typical examples, as are the porphyrins. Apart from sunburn, phototoxic drug eruptions are the commonest photosensitivity reactions.

In photoallergic reactions, following absorption of the specific photons, a new compound is formed, which acts as a haptene. This molecule then combines with a protein to form a complete antigen, which possesses immunologic properties. The mechanism of the host response is then similar to other forms
of delayed hypersensitivity and is mediated by T-lymphocytes. Morphologically, this response presents as an eczematous eruption, and while it may start in sun exposed areas, it may spread to non-sun exposed parts of the body. These reactions are relatively unusual and require at least one prior exposure to the drug
Diseases such as discoid and systemic lupus, PMLE, solar urticaria, and dermatomyositis may also fall into this category, although their morphologies vary widely.

List of drugs that may cause photosensitivity reactions

Phototoxic reactions:
tetracycline photox. eruption, photo -onycholysis, vesicles
PUVA photo-onycholysis

Photoallergic reactions:
Lomotil (erythema multiforme)
Tetracycline (lichenoid)

Porphyria Cutanea Tarda (PCT) and Erythropoetic Protoporphyria (EPP):

These photoxic diseases are caused by an increased concentration of porphyrins in the blood. Porphyrins are pyrimidines arranged in a ring-shaped structure with alternating double bonds and are derived from the metabolic breakdown of old RBC’s. Due to enzymatic defects,which are probably hereditary in both types, porphyrins build up in the bloodstream and act as chromophores, absorbing UVA and causing cellular damage by energy transfer. Which type of porphyria develops depends on the specific defect. PCT causes elevated porphyrin levels in the serum. EPP causes elevated levels within the

Photocontact dermatoses:

Usually caused by plants containing furocoumarins (psoralens) and called “phytophotodermatoses”. Also seen with perfumes and colognes containing oil of bergamot -”berlock dermatitis”. Shalimar perfume was a prime example. These phototoxic reactions are typically blistering and leave a brownish hyperpigmentation in their wake
Plants which can cause this are parsnips, fennel, dill, parsley, masterwort, celery, coriander, common rue, gas plant, bergamot, lime and other citrus, buttercup, mustard, blindweed, agrimony, yarrow, meadow grass, S. John’s wort, buckwheat, and ragweed. They all contain furocoumarins. We’ve
frequently seen this in celery pickers here in Oregon.

These reactions are now rare since halogenated salicylanilides were removed as antibacterial agents from soaps, and people learned to stop handling phenothiazine drugs.


Review of the ideal characteristics of a sunscreen reveals that while there are many excellent products on the market, they are primarily effective against UVB. Protection against UVA from 350-400nm has yet to be achieved, despite claims to the contrary.
“The physical agents we tested provided only weak UVA protection in both the shorter (320-340) and the longer (340-400) UVA ranges. Dibenzoylmethane derivatives (eg., parsol 1789) are much more efficient in the shorter but not in the longer UVA ranges. The best UVA protection over the entire UVA range is, without doubt, provided by the combination of real UVA filters (eg., benzophenones, parsol 1789, eusolex 6300 and 8020, lawsone with dihydroxy acetone, diphenylacrylate, methyl anthranilate, and octocrylene) and physical agents (eg., titanium dioxide, red petrolatum, talc, kaolin, and zinc oxide). The protection afforded by this combination also appears to be cumulative.”

Roelandts R. Which components in broad-spectrum sunscreens are most necessary for adequate UVA protection? J Am Acad Dermatol 1991;25:999-1004.

In a broad-spectrum sunscreen, the UVA filters are combined in varying combinations with UVB absorbing chemicals: PABA and its esters, methoxycinnamates, homosalate, salicylate, sulfonic acid, digalloyl trioleate, diphenyl acrylate, and lawson with dihydroxyacetone.

Sun Protection Factor (SPF). If your burn time (MED=minimal erythema dose, defined as the minimum amount of energy required to produce a uniform, clearly demarcated erythema response at 24 hours) without a sunscreen is 10 minutes, then a SPF of 15 will extend your MED to 150 minutes. This does NOT mean you can stay out in the sun all day. A SPF of 15 should be the absolute minimum level of protection, and we recommend higher numbers. The SPF only measures protection against UVB. There is no analogous number available for UVA protection. However, you should always use a “broad-spectrum” , UVA-UVB sunscreen that is labeled as WATERPROOF, not water resistant.

There are two new UVA filters : Parsol 1789, aka “Avobenzone”, a dibenzoylmethane derivative, and octocrylene.

We are currently doing a study for Galderma/L’Oreal in PMLE using a combination sunscreen with two UVB and two UVA filters. Mexoryl is the investigational UVA filter.
Photoprotective clothing is the only sure way to block the longer wavelengths.
For a catalog, write to:

Sun Precautions
2815 Wetmore Ave.
Everett, WA 98210


1. Gonzalez E, Gonzalez S. Drug photosensitivity, idiopathic photodermatoses,
and sunscreens.. J Am Acad Dermatol 1996;35:871-885.

2. Gould J, Mercurio M, Elmets C. Cutaneous photosensitivity diseases induced
by exogenous agents. J Am Acad Dermatol 1995;33:551-571.

3. Miller, B Sunning-and still having fun. Alert Diver 1996;Nov-Dec:37-39.


Ernest S. Campbell, M.D., FACS

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