Most of our understanding of dermal effects or of systemic toxicity that affects the skin comes from knowledge of the circumstances for adults.

A useful online reference for dermatological conditions is The Electronic Textbook of Dermatology by The Internet Dermatology Society, Inc. 2000.

Exposure to substances such as mercury, silver, gold, arsenic, coal tar pitch, creosote and some aromatic chlorinated hydrocarbons is known to result in increased pigmentation.

Environmental agents associated with the appearance of scleroderma-like lesions include vinyl chloride, silica, dioxin, epoxy resins, rapeseed oil, solvents and L-tryptophan.

Clinical Signs

Clinical signs of environmentally induced dermal effects will vary depending on the environmental agent involved. The most common such skin disorders, or those most readily recognized as being related to environmental exposure, include:

• rash
• dermatitis
• pigmentary changes
• photosensitivity reactions
• urticaria
• scleroderma-like conditions
• chloracne lesions
• malignancy

In most cases, the nature of the relationship between environmental exposure and dermal effects is not always clearly understood.24 There is also little written on dermatological effects specifically in children from exposure to environmental agents. Most of our understanding of dermal effects or of systemic toxicity that affects the skin comes from knowledge of the circumstances for adults. This may not provide an entirely accurate portrayal of the nature of environmentally induced dermal disorders in children; however, it is some basis for understanding. We concentrate here on describing those skin conditions that are most relevant in a clinical practice or that pose an important public health concern.

Dermatitis

The most common cutaneous reaction to environmental chemicals is dermatitis, specifically, contact dermatitis or CD. CD is defined clinically as skin inflammation with intercellular edema arising from direct contact between a chemical agent and skin.25 It can be acute or chronic and it can result either from a direct irritation response (ICD) (the majority of CD cases) or from a delayed cell-mediated immune or allergic reaction (ACD). Solvents, acids, alkalis, metal salts and oxidants are all chemical agents associated with irritant CD. Nickel, chromium and formaldehyde are common chemicals associated with allergic CD.

The nature and severity of symptoms of CD vary depending upon the mode of induction. ICD is more typically restricted to the region exposed to the irritant agent and can present as burning, mild erythema through to necrosis and ulceration that appears in a period of minutes to hours. ACD is characterized by appearing days or weeks after exposure and may start with itching that progresses to erythema or vesicles. Prior sensitization to an allergen that causes ACD will reduce the reaction time between subsequent exposure and expression.26

Photosensitivity Reactions

Photosensitivity reactions produce dermatitis-like lesions on the sun-exposed regions of the body, including face, back of the neck, upper chest, arms, dorsal surfaces of hands and feet and the anterior aspect of the lower legs. The photosensitivity contact dermatitis occurs when a chemical substance is “activated” or transformed on the surface of the skin by the action of ultraviolet radiation (UV-A wavelengths). There are two types of photosensitivity reactions: photoallergic responses are immune-mediated and are analagous to ACD and require previous sensitization to the photoactive substance; phototoxic responses are analogous to ICD and are not immune-mediated.

A number of different substances and products can cause photosensitivity reactions. Products applied to the skin including fragrance-containing lotions, some suntanning products and some germicidal soaps and detergents can cause photosensitivity reactions. Citrus fruits (especially limes) and celery are also sources of the naturally occurring phototoxic agent psoralens.27,28

Pigmentary Changes

Discolouration, hypopigmentation and hyperpigmentation of skin can occur secondary to systemic absorption of certain chemicals and usually occurs after an inflammatory effect from such exposures.29 Pigment alteration can occur as a result of damage to melanocytes, alteration in synthesis of melanin or by other specific mechanisms that cause pigment build-up or loss.

Hyperpigmentation is most commonly a result of a non-specific skin lesion such as the post-inflammatory reaction in CD that secondarily leads to excess manufacture of melanin or deposition of hemosiderin.30 Exposure to substances such as mercury, silver, gold, arsenic, coal tar pitch, creosote and some aromatic chlorinated hydrocarbons or PCBs is known to result in increased pigmentation. In some cases, hyperpigmentation occurs as a result of exposure to a photosensitizing substance and subsequent exposure to UVR. Hyperpigmentation responses can persist for long periods and are more common in individuals with dark complexions.

Decreased pigmentation is common after exposure to industrial chemicals such as alkylphenols, but can also result from physical damage to the skin due to chemical or thermal burns or local trauma.31 The hypopigmentation response requires one to six months to manifest and may persist for months to years after exposure.

Urticaria

Urticaria or hives can be mediated by immunologic, non-immunologic or uncertain mechanisms and can be generalized or localized. Contact urticaria is the localized form that appears immediately after direct dermal absorption of a substance. Symptoms are generally short-lived and consist of itching, burning or tingling sensation.

Allergic contact urticaria produces a range of symptoms depending upon the degree of reaction and individual sensitivity to a given allergen. Skin symptoms consist of rash, erythema and edema. It can involve remote areas of skin and in the anaphylactic reaction can produce generalized effects that involve the respiratory, gastrointestinal and orolaryngeal systems.

Allergic contact urticaria is elicited in previously sensitized individuals by a wide variety of biological allergens (including animal, plant, food and textile allergens), certain medications, common chemicals, cosmetic products and physical agents (e.g., heat, cold, water and light). Latex rubber, eggs, silk and animal fur are associated with the most severe allergic responses.

Nonallergic contact urticaria is the more common type of contact urticaria and represents a localized response from a substance that directly affects skin vasculature or is mediated by the release of inflammatory mediators such as bradykinin. The nonallergic urticaria is elicited by exposure to acids, alcohols and a number of miscellaneous substances.

The contact urticaria of uncertain mechanism can have features of both allergic and nonallergic responses. Exposure to formaldehye, ammonium persulfate (used in peroxide hair bleaches), sunlight or aqueous substances (water, saline and perspiration) produces urticaria of uncertain mechanism.32

Scleroderma-Like Conditions

Sclerodermatous conditions are characterized by a thickening and “bound down” appearance of the skin as well as mottling of pigmentation. Environmental agents associated with the appearance of scleroderma-like lesions include vinyl chloride, silica, dioxin, epoxy resins, rapeseed oil, solvents and L-tryptophan.33 In 1989, ingestion of contaminated L-tryptophan supplements caused an epidemic of Eosinophilia-Mylagia Syndrome (EMS) in the United States. L-tryptophan was touted as a treatment for “hyperactivity” and therefore there were substantial numbers of children affected. EMS affects multiple systems including blood, immune and pulmonary and is associated with scerodermiform skin changes.

Chloracne 

Chloracne is a rare, but particularly severe, recalcitrant type of acne that is the hallmark of extreme exposure (usually occupational) to industrial substances such as dioxin or other chlorinated or brominated aromatic compounds (e.g., PCBs, PBBs). The acne cysts appear within months of exposure and can last about two years after exposure has ceased.

They occur primarily in the cheeks (below and lateral to the eyes) and behind the ears, saving the central regions of the face, but they can involve other regions of the head and body with increasing severity of exposure. Chloracne lesions are particularly painful, can be permanently disfiguring and are resistant to treatment. Removal from exposure is the most important intervention and the condition does resolve eventually.

Follow-up studies of populations exposed to accidental release of large volumes of such chemicals have demonstrated the variety of skin lesions associated with acute, high dose exposures. These accidental exposures also provide the few data available on the effects of such exposures in children. In Japan and Taiwan, there were widespread accidental exposures to PCBs through contaminated cooking oil in 1968 and 1979, respectively.

Chloracne and other dermal effects including hyperpigmentation and keratoses stem from direct ingestion of PCBs and PCDFs in individuals of any age. It appears that they result solely from such high-dose exposures and are not linked with exposure to the lower background levels we all experience.34 Those children who were prenatally exposed to high doses demonstrated abnormal development of hair and nails and excess pigmentation among other severe health and developmental effects.

In Seveso, Italy, a large number of people were exposed to 2,3,7,8-tetrachlorodibenzo-para-dioxin (TCDD), the most toxic of the dioxins, due to an industrial accident in 1976. The exposure to TCDD was via dermal absorption and children likely received a higher absorbed dose for a given exposure compared to adults.35 These children developed chloracne that was most severe on areas of the body unprotected by clothing.36,37

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