Characterization of composite electrode material

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The dermatitis caused by contact with irritants is a local cutaneous response by direct action; that is, it is not mediated through an immunological reaction.

The inflammatory cutaneous changes that occur from skin irritation result from a direct, local, toxic effect on cellular elements of the skin, leading to cell death, release of lysosomal enzymes and soluble inflammatory mediators, recruitment of inflammatory cells and further tissue destruction. Obviously, exposure to strong irritants will produce massive damage quickly. However, under the right circumstances, virtually any substance is potentially capable of causing irritant contact dermatitis, and clinical irritant dermatitis generally results from multiple, cumulative exposures to (often) more than one potential skin irritant, rather than just a single substance.

There is a spectrum of degree of severity, depending on the strength of the irritant, the circumstances of exposure and the skin site affected. Since irritation depends on the lower, living layers of the epidermis, those factors that enhance penetration will increase severity of response.

A number of points should be emphasised:

■ Contact irritant dermatitis can occur from contact with several mild irritants, in which the effect is cumulative.

■ Continual irritant contact dermatitis can produce either a condition where even very mild irritants can produce irritation, or ‘hardening’ where the skin eventually tolerates repeated exposures.

■ Constant exposure to irritants impairs the barrier function of the skin and allows further penetration of other irritants.

■ Irritant and allergic contact dermatitis frequently coexist in the same person.

One further form of irritant contact dermatitis is light-induced change to chemicals on the skin surface (phototoxicity). The mechanism is nonimmunological, and some irritants, such as polycyclic aromatic hydrocarbons and some dyes, may be made more irritating by virtue of the action of sunlight. Some protection to this effect occurs in pigmented skin.

Some of the precise mechanisms of irritant contact dermatitis remain undefined.

Substances that dissolve skin proteins, such as keratin, or oxidising agents or dehydrating agents may be irritants. Changes in the water content of the skin also appear to be important.

Follow-up studies of people with occupational contact dermatitis indicate that (Cooley and Nethercott 1994):

■ about 25% fully resolve (that is, they become symptom free)

■ about 50% improve but continue to have periodic bouts of symptoms

■ the remaining 25% develop chronic, persistent dermatitis which is as severe (or worse) as the initial dermatitis.

About 30–40% of people with occupational dermatitis change their jobs to get away from the precipitating exposure. Job change is most beneficial (but not strikingly so) for sufferers with allergic contact dermatitis (Vestey et al. 1986). Job change does not always clear up the dermatitis, with perhaps a quarter of those changing jobs experiencing complete resolution of symptoms.

Allergic contact dermatitis A variety of agents are potential contact allergens, such as:

■ metal salts (nickel, chromium, cobalt)

■ rubber additives (mercaptobenzothiazole and other benzothiazoles, thiuram, resorcinol)

■ ethylenediamine componds

■ hydroquinone and p-aminophenol photographic developers

■ epoxy compounds

■ acrylates

■ aliphatic and aromatic amines

■ formaldehyde

■ phenolic compounds

■ therapeutics (neomycin, benzocaine, streptomycin antibiotics)

■ biocides (formaldehyde-releasing compounds, halogenated germicides, quaternary ammonium compounds).

A variety of natural products also cause allergic contact dermatitis, including grains (barley, oat, rye, wheat), foods (carrot, chicory, coconut, coffee, endive, lettuce, potato, radish), spices (cardamon, tamarind, tumeric, vanilla), plants (rhus, poison ivy, poison oak, sumac), and fragrances (balsam of Peru, cinnamic acid derivatives, citronella derivatives).

Unless they are primary irritants, most agents that cause allergic contact dermatitis do not produce a skin reaction on the first contact (if they did, they would be irritants).

The mechanism of effect of allergic dermatitis is a cell-mediated (or type VI) immune response. There are two main phases—the sensitisation phase and the elicitation phase.

There are a number of steps in sensitisation:

■ absorption of the allergic agent or antigen (or hapten)

■ binding of the antigen to a carrier protein, which forms the complete antigen

■ binding of the complete antigen to the cell surface of macrophages or Langerhans cells within the epidermis

■ these cells alter the configuration of the antigen where it then interacts with T lymphocytes

■ antigen-bearing lymphocytes then undergo clonal proliferation in the regional lymph node, where two populations of sensitised lymphocytes arise

■ effector lymphocytes which are distributed to the skin surface through the blood stream

■ memory cells will form new populations of sensitised lymphocytes on repeat contact with the antigen.

Sensitisation usually takes 10–21 days. Following sensitisation, the immune system is in a state of readiness (elicitation phase) should further contact with the allergic agent occur.

When this happens, effector T lymphocytes are activated (from formation of the complete antigen). Activated lymphocytes then interact with other skin cells and processes to synthesise a range of substances called cytokines, which mediate the inflammatory response. The elicitation phase can fade with time, as antigen memory is lost, although it can persist for life in many individuals.

Strong allergens have molecular weights of less than about 500 and are quite reactive with proteins. The number of potent allergens is quite small, although several thousand substances have been reported to have caused sensitisation in one or a few individuals.

Other important points to note about allergic contact dermatitis should be noted:

■ Differentiation of mild irritants from skin allergens can be quite difficult.

■ Allergic contact dermatitis may not develop for months or years after first exposure to an agent.

■ Many sensitisers are also irritants (for example, chromates, nickel salts, formaldehyde, wood turpentine).

■ Elicitation reactions can be produced or maintained by minute amounts of exposure, often in concentrations insufficient to irritate the nonallergic skin.

■ Cross-sensitivity may occur where a worker exposed to one allergen will also react to one or more closely related allergens, even without being exposed to the second allergen before.

■ Diagnostic patch testing is the most accurate means of distinguishing between allergic contact from irritant contact dermatitis.

As with phototoxicity and irritant contact dermatitis, photoallergic reactions (an interaction of a chemical and sunlight) are also possible. Photoallergens include phenothiazides and some coumarin derivatives. Photoallergic reactions are quite rare in the occupational environment, but are very serious if they occur.

The factors that should be taken into account in the development of skin irritation are summarised in Table 5.5.

Thermal burns

Skin tissue is not thick and can be susceptible to extremes of temperature. Burns cause problems because the body can loose fluids, thereby leading to dehydration and electrolyte imbalance, and increasing susceptibility to infection.

Thermal burns are classified thus:

■ first degree burns: damage to epidermis only

■ second degree burns: damage to epidermis and upper dermis (blisters may be seen)

■ third degree burns: full thickness burns, usually leading to scarring.

Critical, that is life-threatening, burns are those where there are:

Table 5.5 Factors in the development of skin

Frequency and number of exposures Possibility of occlusion to the skin Exposure

■ second degree burns to over 25% of the skin

■ third degree burns to over 10% of the skin surface

■ third degree burns to face, hands, feet and joints.

Scalds are a subclass of burns caused by hot liquids or hot, moist vapours like steam.

Pigmentary disorders

Vitiligo is a condition characterised by the destruction of melanocytes. The destruction can be over small or large areas of skin, resulting in patches of depigmentation, often with a hyperpigmented border, and often enlarging slowly. While vitiligo is considered an autoimmune disease, some occupational exposures may produce similar depigmentation. For example, skin absorption of materials that resemble some of the precursors to melanin synthesis (such as phenolic or catecholic derivatives which resemble tyrosine) may inhibit synthesis at low doses, and cause melanocyte death at high exposures. These materials are antioxidants or germicidal disinfectants, which may be found in a range of products, including rubber products, photographic developers, lubricating oils, plastics, adhesives and disinfectant or cleaning solutions.

Compounds known to cause hypopigmentation include:

■ antiseptics such as o-benzylchlorophenol and pyrocatechol

■ organic compounds such as o-phenylphenol and p-butylphenol

■ photographic chemicals such as hydroquinone and its monoethyl and monobenzyl ethers

■ disinfectants such as p-cresol

■ astringents such as p-tertiary butylcatechol.