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Industrial Dermatitis Geoffrey A Postgrad Med J: first published as 10.1136/pgmj.42.492.643 on 1 October 1966. Downloaded from POSTGRAD. MED. J. (1966), 42, 643. INDUSTRIAL DERMATITIS GEOFFREY A. HODGSON, M.B.E., M.D. Consultant Dermatologist, United Cardiff Hospitals. Lecturer in Dermatology, Welsh National School of Medicine. INDUSTRIAL dermatitis is officially described by the (c) Constitutional eczema (temporarily aggravated Ministry of National Insurance as P.D. 42 "a non- by occupation) (constitutional patterns). infective dermatitis of external origin, including Fungal infections of the feet, epidermophytosis, chrome ulceration of the skin but excluding der- in colliers may be accepted as an "industrial matitis due to ionization particles of electromagnetic accident" if there is evidence of pithead baths radiations other than radiant heat." This has being used. replaced "24b," dermatitis produced by dust, In true contact dermatitis all exposed areas are liquid or vapour. affected usually within hours or 2- 3 days of It could also be described as the eczematous contact and recovery should occur in weeks to a reaction of the skin to a hurtful agent or environ- few months when such contact ceases. mental factor which irritates it or to which it is Patchy "industrial" eczema (eczematous derma- sensitive (allergic). titis) usually presents in a patchy or discoid pattern Accurate information is not easy to obtain but in on the work-exposed skin but usually only after the years 1953 - 1956 in Great Britain industrial months or years of exposure, its course beingProtected by copyright. dermatitis accounted for 0.3% of 1.3% total lost chronic for months, years or sometimes permanently. working days for all skin diseases in a working Much patchy eczema is also initiated, however, by poulation of 20,500,000 (Thompson, 1958); Bourne other exogenous factors (home or hobbies) acting (1960) gives similar figures, 0.32% of 1.6% skin alone or in concert with those at work. diseases. Allergic sensitisation can occur in both patterns Eczematous reactions accepted under P.D. 42 are, (contact and patchy eczema) but is preceded first however, not solely the contact result (dermatitis) of by some irritant or traumatic damage to the epider- an external irritant. Many are really eczema mal protective structures allowing percutaneous determined, often initially by external irritants, but penetration of allergens. predisposed thereto by a constitution inferiority of The constitutional patterns of eczema which may the skin and inherited or acquired immuno- be temporarily aggravated by work or environment chemical relationships. These will both influence include dysidrotic (pompholyx), atopic (eczema- the and the course of on a onset eczema, personal asthma-hayfever syndrome), seborrhoeic eczemas http://pmj.bmj.com/ basis. and neurodermatitis. Such skins are themselves Behind these considerations lie most of the constitutionally unstable and often susceptible to difficulties relative to diagnosis of occupational exogenic injury. dermatitis. Although theoretically a true contact dermatitis Basically the development of industrial dermatitis and also an "industrial" eczema should recover, represents a struggle between an external aggressor soon or eventually, when away from contact, many (mechanical, chemical or biological) at work, and cases of accepted "P.D.42" become chronic; contact the defending epidermal defence with its varying dermatitis developing later into a patchy eczema, on September 30, 2021 by guest. anatomical, architectural, molecular or physio- and patchy eczema becoming chronic or progressing logical integrity. into constitutional patterns. Factors which determine Rapid overwhelming of the defence leads to this include constitutional predisposition itself, acute contact dermatitis whilst more insidious continued exposure to irritants or sensitisers at undermining predisposes to eczema. work or in the home, secondary pyogenic infection, adverse effects of topical or systemic treatment, and Patterns of Dermatitis (P.D. 42). persisting functional disturbances such as vascular Eczematous reactions which may be accepted instability and permeability, sweating and keratin- under P.D. 42 or considered for aggravation by isation as sequels of the dermatitis even when the work may be designated - convalescent skin appears clinically well. Emotional (a) Contact dermatitis (contact pattern). factors including neuroses (neurodermatitis), com- (b) Exogenous "industrial" eczema (eczematous pensation, litigation, resettlement problems or frank dermatitis), (patchy eczema pattern). malingering (dermatitis artifacta) will also contribute. Postgrad Med J: first published as 10.1136/pgmj.42.492.643 on 1 October 1966. Downloaded from 644 POSTGRADUATE MEDICAL JOURNAL October 1966 Epidermal Defence Under conditions of work therefore the stratum Percutaneous chemical penetration, with irritant corneum and deeper layers may be damaged action on deeper viable epidermal cells, or allergic- primarily by physical wounding or mechanical induced sensitisation through the dermal reticulo- stress with individual cell separation or protein endothelial system, is normally prevented by the damage, by reduction of water content below 10% intact keratinised stratum corneum. An ionic layer and at a cellular and molecular level, by chemical (water barrier) of cells, described by Szakall, (1955) damage to protoplasm, to keratin and its cross below the stratum being electrically charged, links. repels anions and reattracts cations, and is also Occupational insult may also chemically damage repellent to water and water soluble electrolytes. enzymes responsible for cellular metabolism and Fat-soluble chemicals may pass this barrier once it protein synthesis; bullous eruptions may thus is damaged or may pass through the appendageal develop. For instance, sulphydryl (-SH) containing sebaceous glands. Entrance through sweat ducts is enzymes are susceptible to chemicals as methyl minimal although silver can enter thus to cause bromide, organic mercurials (seed dressings), argyria (Buckley, 1963). arsenicals (Lewisite) or nitrogen mustards producing Later penetration through- viable malpigian and contact vesicant dermatitis whilst other vesicants basal cells is trans or intercellular in method. act by blocking conversion and interfering with In addition, there exists other "built-in" defences cellular respiratory metabolism relative to adenosine as the neutralising buffer capacity of amphoteric triphosphate (ATP) (Burbach, 1964). horny keratin, and the "acid mantle" of shed During day-to-day exposures constant repair of stratum corneum horn cells, acidic sweat and fatty minor injuries or chemical damage occurs in the acids. Sebum also lessens water evaporation pro- stratum corneum unless the result be at once overwhelming. While contact dermatitis is mainly tecting keratin. Protected by copyright. determined by the concentration or allergenicity of As the stratified horn layer constitutes the main the chemical or the degree of exposure, "eczematous defence, this in turn relates to an intact gross dermatitis" occurs mostly in those with abnormally architecture (cell-to-cell adhesion and dermosome keratinised or non-intact skins in which normal bonding including that of other epidermal and reparation less easily occurs. epidemo-dermal junction levels) but also at a cellular Among these constitutional inferior skins feature level based upon the molecular structure of keratin. dyskeratoses, icthyosis, xerosis, atopic persons, the seborrhoeic state and those with poor water- Integrity of Keratin in Stratum Corneum holding capacity (subject to winter chapping) or The fibrous protein keratin filling the firmly buffering capacity. Thinning ofthe stratum corneum, packed denucleated cells of the stratum corneum inherited or acquired by primary collagen degener- has been progressively synthesised by addition of ation in senile or aging skins also operates. Over use amino-acid polymerisation to polypeptide chains in of topical steroids in treatment may itself lead to the viable basal cells and intermediate keratinocytes. collagenous degeneration with thinning and trans- A final cross linkage of adjacent polypeptide grids parency and lessened resistance. http://pmj.bmj.com/ by strong disulphide (S = S) bonds of cystine, or weaker salt (acid or basic) and electrically charged Aggressive Industrial Agents hydrogen atoms of amino acids converts the grids Injurious agents at work (or in the home) may be into the rigid horny keratin and hardens dermosome physical, environmental, chemical or biological. cell adhesion. The keratin molecules themselves Chemicals are conveniently classified as irritants add mechanical strength being twisted in helical or sensitisers, their potential for causing contact form like ropes. dermatitis or eczema is determined by chemical on September 30, 2021 by guest. reactivity, concentration, degree and conditions of Water content exposure, and by the constitutional resistance of the The 10 - 20 % of water in the stratum corneum, exposed skin. replaced by diffusion from below, both plumps the individual keratin molecules and acts as a lubricant Physical agents between the polymer chains, similar to batching Puncture wounds and lacerations with secondary emulsions used in spinning textiles, ropes or glass infection may lead to local traumatic dermatitis or fibre. This reduces fibre to fibre friction, imparting initiate eczema. Topical treatment is also a common suppleness and abrasion proofing.
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