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. cause. These cases are seen particularly in heavy Dessication by climatic, environmental or chemical industry, for instance 35% of "P.D.42" in the steel agencies at work causes dryness and fissuring industry is so accountable (Vickers, 1958). (chapping) and increased liability to mechanical An occupational traumatic dermatitis should stress and encourages chemical penetration. commence at the site of injury before complete October 1966 HODGSON: Industrial Dermatitis 645 Postgrad Med J: first published as 10.1136/pgmj.42.492.643 on 1 October 1966. Downloaded from

healing has occurred. The skin, in the vicinity of more prominent through contraction of erector pili recently healed abrasion, is however temporarily muscles. more susceptible (non-specific hypersensitivity) to other accepted irritants during the convalescent Environmental factors and sweat disturbances phase until hardening occurs. Keratin dehydration with chapping occurs from Continuous friction may increase the risk of variations in barometric pressure and the dew penetration by smoothing and thinning the horny point or from desiccation agents. layer as in pottery workers, paper mills and metal Outdoor workers in agriculture and fishing, those polishing, as can also constant handling of rough working in cold as ice cream or refrigeration men, or materials as rusty metal concrete or bricks. those in contact with solvents or alkali are particular- Keratin chains are stressed or the actual archi- ly liable to eczematogenic desiccation. tectural cementing loosened as when friction Asteatotic winter chapping may often precede blisters form from distortion of cells and acan- occupational eczema, and inadequate washing tholysis (Naylor, 1955). facilities or "paid ablution time" and wet towels or Combinations of friction and lacerative injury hand-cleansing solvents can contribute to this with infection however are most often eczemato- tendency. genic. For instance, clothing or footwear dirtied Constant climatic exposure in outdoor workers, with abrasive materials (coal miners or builders), clayey soil drying on the skin of agricultural workers, gloves stiffened by tar, or when synthetic glues heat in furnace workers and those in metal pro- cause the fingers to adhere together. Abrasive hard duction, smelting foundries and glass work also metal dusts as tantalum or zinc, metallic engineering dries the skin as can such hygroscopic chemicals as swarf in wipe rags adherent through oil, angular salt (fishermen) sugar (confectionery), and lime or particles of sugar or crumbs in confectionery works, cement dusts in the building trade. or harsh chrysotile asbestos fibres used for insulation On the other hand a constant exposure to waterProtected by copyright. (amphilole fibres for textiles are soft and flexible) and wet materials, electrolytes and emulsions may are other examples. Glass fibre causes pruritic, soften the keratin and, by maceration, increase erythematous or follicular traumatic dermatitis and penetration of larger chemical molecules; thus the risk may extend through contaminated clothing develop the initial patchy eczemas, with later to those at home. allergic sensitisations, of housewives, cleaners, Hardening of synthetic glues on the skin causes textile scourers (aggravated by alkaline keratin stripping of keratin with irritant effect and pre- degradation), catering and confectionery workers, disposes to entrance of some sensitisers as formalde- tanneries, paper pulp workers, and those in medical hyde (woodworkers) and epoxy resins. and allied trades. Persistent friction however also often causes a The added degree of keratin damage related to callus with localised thickening and hardening of minor irritants at home in all these cases always the horny layer; this gives considerable added presents considerable diagnostic difficulties. mechanical protection to injury at work. If there is a disturbance of normal cell shedding with hardening Disturbances of sweating. Sweat pore obstruction http://pmj.bmj.com/ and compression of the keratin lamellae (Rubin, may occur from hydration oedema as in maceration 1949) calluses occur to cause occupational stigmata; from sweating or wet work, or by poral hyperkera- they may also indicate diagnostically areas of skin tosis from micro-frictional trauma. Thus develop most exposed to irritation at work. sweat obstruction syndromes of the body (miliaria) Friction dermatitis will present with an initial or hands (dysidrotic pompholyx eczema.) redness, scaling, pigmentation or bullous formation Miliaria may precede eczema in body crevices or at the site affected. Later a patchy dry or moist on areas exposed to the friction of clothing. This on September 30, 2021 by guest. eczema may develop which on the forearms, thighs occurs in furnace men and soldiers in tropical and legs may simulate a constitutional discord or climates where heat exhaustion and thermogenic nummular eczema. Such industrial eczemas may anhidrosis may also develop with disturbed temper- affect the stokers, boilermen, dustmen, metal ature regulation. Miliarial eczemas also occur in workers, labourers, colliers and others in hot or colliers (papular eczemas of groins, axillae, cap band, dusty work. Secondary lichenification may occur belt and lamp battery areas), glass workers (sweat from continued friction or from habit scratching rags on neck), steel and other metal smelting, and in (neurodermatitis) but however can give some those working in overwarm or humid atmospheres protection and thus in time lessen incapacity. required by a particular chemical process or where Inferior skins intolerant of friction include those ventilation is inadequate, and when impervious prone to winter chapping, dry or atopic skins with protective clothing must be continuously worn, spicules of projecting keratin, hirsute persons and Obesity and alcoholism will contribute in many those with pilomotor instability, the hairs becoming instances. 646 POSTGRADUATE MEDICAL JOURNAL October 1966Postgrad Med J: first published as 10.1136/pgmj.42.492.643 on 1 October 1966. Downloaded from

Excessive sweating can localise frictional or chromic acid and chromates and cyanides (electro- contact dermatitis from noxious dusts in body plating), mercuric nitrate and metallic sodium, creases, increase skin staining from dyes and woods, ammonium nitrate and mercury fulminate or cause metal rusting ("rusters"), and by keratin (explosives), zinc chloride "Bakers fluid" (engineer- softening increase sensitisation. ing fluxes), unslaked lime (building trade). Ulceration Constitutional eczema (dysidrosis) may be initiat- of the nasal septum may be similarly caused. ed or aggravated in those with hyperidrosis where Among other common vesicants are acrylonitrile the handling of toxic chemicals requires long (vinyl cyanide) for acrylonitrile polymers and wearing of impervious plastic (P.V.C.) or rubber synthetic rubber, alkyl mustard compounds (syn- gloves and footgear. Some convalescent from thetic resins or flavours), chloroacrylates (acrylic dermatitis may also find protective gloves difficult resins), dinitrophenols (chemical industry), iodo- to wear. acetic acid (reagent for biochemical tests) and the Sweat obstruction caused by imperfect kera- alkyl organic tin (plasticisers for vinyl resins) and tinisation and poral closure in convalescent derma- organic mercury compounds (disinfectant agents titis or eczema subjects is a common cause of and agricultural seed dressings). relapse on their return to work. Vesicants very often induce sensitisation. Moderate irritants. These may cause contact Chemical irritants and sensitisers dermatitis on unprotected skin or after unusual Chemical irritants are graded as strong to moder- exposure. They include miscellaneous polyamines ate or weak in strength and action on the skin. as ethylene amines which are often alkaline (used Strong to moderate chemicals will normally cause in chemical synthesis or as hardeners for synthetic lesions varying from contact chemical burns with resin adhesives), hydrazines (engineering fluxes), erythema, vesication, bullae or ulcers to a classical fluoacetic acid and acetates (agricultural herbage contact dermatitis developing within hours or a few control), methyl salicylate (oil of wintergreen) andProtected by copyright. days of the exposure. methylene chloride (paint remover). Weak chemicals usually predispose to patchy Weak irritants. Transient erythema, or even eczema by slow disturbance of stratum corneum contact dermatitis patterns may be produced by this repair or its molecular protein structure. group in constitutionally inferior skins but most Secondary allergic sensitisation may complicate often the adverse effects are dehydration with harsh either. dry scaling and fissuring or persisting erythemas Most industrial dermatitis is initiated by chemical as in "housewives hands," grading over into patchy irritants or trauma (80%), allergic sensitisation only eczema with probable added allergic sensitisation. being responsible for some 20% of cases. These weak eczematogenic irritants are found in a large variety of occupations. They all predispose to Strong irritants and vesicants. Injury from strong irritation of viable cells or to sensitisation by chemicals is only likely to occur as an accident desiccating, damaging the keratin architecture or through ignorance, or if normal safety precautions cellular protein, or by loosening molecular links and protective clothing be neglected. Processmen, and by increasing percutaneous penetration. For http://pmj.bmj.com/ fitters or other maintenance workers can however instance, alkalis damage protein by reducing the have such accidental exposure from pipe breaks. disulphide link (S =S) freeing sulphydryl groups Burns or dermatitis might occur from contact on (-SH), weak acids dissociate salt links and may unprotected skin with such materials as liquid dehydrate; oxidisers as perchlorates and perborates oxygen or hydrogen peroxide, concentrated in- affect hydrogen bonds and chlorine compounds as organic acids and alkalis, chromic acid and chlorinated lime (bleaching powder) or bisulphites, chromates (electroplating), hydrofluoric acid and as reducers, also affect the strong disulphide link. fluorides (glass etching, synthetic resin polymeri- The over use of these latter as stain removers may be on September 30, 2021 by guest. sation and uranium manufacture), silico-fluorides, eczematogenic. Textile, ink and dye workers are organic acids as phenols or cresols (manufacture of mainly at risk. phenolic resins), selenious acid (electrical industry), Solvent or alkaline agents which remove sebum acetic acid and anhydrides (cellulose acetate expose the keratin to dehydration and bacterial manufacture and rocket propellant fuels), silanes infections by removal of the "acid mantle." and chloro silanes (silicone resin manufacture), the Among other weak irritants which usually cause chlorinated benzenes (chemical intermediates) and patchy eczema are engineering cutting oils especially catechols of cashew nut resins, shoe adhesives, "suds" emulsion oils. There ase assessed as causa- copy paper, shellac and vegetation. tive of 15 - 20% of cases of industrial dermatitis. Some however through abraded skin cause Synthetic anionic detergents and alkaline "built" ulcerations and leave scars which may act as dis- washing agents are accepted as eczematogenic. tinctive marks of occupation. Among these are Although occasional acute irritant effects are seen Postgrad Med J: first published as 10.1136/pgmj.42.492.643 on 1 October 1966. Downloaded from October 1966 HODGSON: Industrial Dermatitis 647 from some concentrated anionic detergents as tion may occur although this is often postulated on moderate irritants, the bad reputation of detergents the grounds of multiple reactions which may be may be unjustified for as Suskind and Whitehouse irritant effects of patch testing. Group- or cross- (1963) have shown by immersion tests, that house- sensitisation is where substances of apparently wives eczema, allegedly due to detergents, can still dissimilar chemistry have a common immune support daily immersion in weak solutions without chemical group or molecular nucleus determining ill effect. group reactions. This was first described by Mayer Solvents vary in their action, most aggressive (1928) in respect of the "para group." Many other being petroleum hydrocarbons (petrol, naphtha, examples have been since described including:- white spirit, kerosene), coal tar hydrocarbons (benzene and toluene), chlorinated hydrocarbons List of Common Group Sensitisers (carbon tetrachloride for rubber, paint, dry cleaning Antibiotics (penicillin, tetracyclines, "mycins") and fire extinguishers), and trichlorethylene for Arsenicals (inorganic, organic) metal degreasing. True turpentine is both irritant Bisphenols (epoxy resins and phenols) and sensitising. Catechols (copying inks, shoes and resins, Ana- Ketones are usually eczematogenic after long cardinacae trees) exposure and may attack hydrogen bonds; methyl Chloro-cresols and xylenols (preservatives) ethyl ketone used in synthetic resin adhesives has Essential oils (essences, balsams) caused eczema when used to remove adherent Esters - Para-aminobenzoic acid esters ("Para- epoxy or polyester glues from the skin. Alcohols are bens") (ointment and cosmetic preservatives) less irritant causing usually a temporary whitening Paraphenylamine diamine. of the skin; the volatile esters and ethers provoking "Para" group - Aniline compounds (dye stuffs), mainly mucous membrane irritation.

amino-azo dyes, nitrophenols (picric and trini- Protected by copyright. The use of petroleum solvents, white spirit or trotoluene explosives), sulphamides, sapamine "turps" substitute (decalin and tetralin) by painters (brilliantines Paschoud 1963). and printers for cleaning machinery or stained hands Hydrazines (engineering fluxes, rocket fuels, is often a cause of eczema. pharmaceuticals) Harsh abrasives or alkaline "built" soaps and Hydroxyquinolines (topical dermatological therapy) over use of strong solvent-alkali containing hand Phenothiazines (pharmaceutical) or waterless cleansers and over-washing of the Thioglycollic acid and salts (cold wave hairdressers) hands by those with obsessional traits may be Vegetation (tars, terpenes, essential oils). similarly provocative. Other examples are continually reported indicating Biological irritants that allergic sensitisation may begin at home or in Banal infections with monilia are relatively pursuits outside of work. latrogenic sensitisation common in industry, particularly in the catering established by drugs may for instance cause cross trade where maceration of the skin and sugary sensitisation reactions in industry. Apresoline http://pmj.bmj.com/ solutions predispose to candida albicans growth. (hydrazinophthazine), phenyl hydrazine and isoni- Dentists may develop similar infections of the fingers cotinic acid hydrazine (INAH) may pave the way for from patients' mouths; occasionally these may hydrazine salts used as metal soldering fluxes to become eczematised. cause sensitisation dermatitis (Frost and Hjorth Less obvious however are miscellaneous zoonotic 1959). mite infections which may cause urticarial, papulo- vesicular and sometimes frank dermatitis. Dock Industrial chemicals which induce photosensitive dermatitis include the germicides tetrachlorsalicyl workers (prunes, figs), millers and grocers (cereal on September 30, 2021 by guest. anilides (which provoked an epidemic of mites), tobacco workers, poultry men contact including dermatitis in a toilet railway personnel (pigeons) are so prone. soap), bithionol, and hexa- chlorophene used in cosmetics and soaps, or in The Allergic Sensitisation Process pharmaceutical products. Allergic sensitisation is of the delayed eczematous Other iatrogenic or pharmaceutical exposures type induced by contact and percutaneous pene- under poor factory hygiene conditions are the tration. The minimal contact time for sensitisation phenothiazines (antihistamines, tranquillisers), oral is some 6 - 8 hours, and the incubation time before antidiabetic drugs (Tolbutamide), diuretics (chloro- clinical evidence 6- 10 days or shorter. Contact thiazide) and griseofulvin. with the antigen should cause the delayed eczematous Irritant phototoxicity caused by altered light response in 12 - 48 hours or within a few days. absorption is caused also industrially by petroleum Allergic sensitisation to industrial chemicals is oils, creosote, tar and pitch, perfumes (oil of usually specific to one agent but polyvalent sensitisa- Bergamot) and furocoumarins from the Umbelli- 648 POSTGRADUATE MEDICAL JOURNAL October 1966 Postgrad Med J: first published as 10.1136/pgmj.42.492.643 on 1 October 1966. Downloaded from ferae plant family; photo-dermatitis in celery or piperidine, hexamethylene amine). Ethylene amines parsnip pickers occurs. which are often alkaline and irritant used as harden- ing agents with epoxy resin glues have been respon- Common trade allergic sensitisations sible for dermatitis. Sensitisers only account for some 20% of indus- Antibiotics and other topical agents. Sensitisation trial dermatitis, physical and irritant agents being may occur during manufacture in pharmaceutical much more important. workers but mainly contact dermatitis occurs from Space does not permit of a full list but some are topical treatments of minor injuries with sensitisers important in a wide range of occupations or handling as commercial neomycin (B.C. and neamine neo- consumer products. mycin A), penicillin and the tetracyclines (chlor- The sensitisation may however be also often tetracycline and oxytetracycline). Neomycin is acquired outside industry or on a group basis becoming more recognised as a source of contact causing difficulty in incriminating the work. Among sensitisation, and a cross sensitiser with framycetin, important common sensitisers may be listed:- soframycin, bacitracin, kanamycin and strepto- Arsenic. Both the inorganic and organic arsenic mycin. compounds are sensitising. Dermatitis has occurred Other topical agents occasionally causing in metal production from copper ore (including dermatitis when used in treatment of industrial those in villages around), glass manufacture, injuries or skin diseases are the hydroxy quinolines, sheep dips, hide preservation, vine growers, wood acriflavine, quaternary ammonium salts and lanoline preservation and pharmaceuticals, or as agricultural or other emulsifiers and germicides as "Parabens" insecticides. used in ointment bases. Necrotising ulcerations are Chromates. Hexavalent chromate is definitely reported from the quaternary ammonium de- antigenic and so is the trivalent form (Fregert and qualinium chloride. Rorsman 1964). Trivalent chromate may also be Dyestuffs. Dyes used are mainly synthetic andProtected by copyright. oxidised in tissues, as in tattoo marks, to hexavalent derived from coal tar or petroleum chemicals. form. Industrial substances and occupations at risk Soluble dyes are more likely to cause contact are paint primers, chromated animal glue as in dermatitis than insoluble dyes and pigments. Most match heads, boot and shoe tanning, building risk comes not from the fully developed dye, often industry (cement), electroplating, metallurgy (alloys), firmly anchored chemically or mechanically in the ink and lithography and photoengraving printing, fabric or material, but from residual dye intermedi- engineering oils (contaminated with chromate), ates left in the final product or improperly washed refractory foundry cores, photography, wood and textile. Azo dyes are used in colouring of petrol, fuels (chromate preserved wood ash), anti-rust textiles, food, paint and ink colours. Contact radiation coolants for railways engines and dye sensitisation has occurred from ball-point pen inks mordants for furs and textiles. and hosiery dyes, reds and yellows. Amino azo dyes The metallic chromium or chrome plating is not used as food colourings are not thought to induce

antigenic. primary epidermal sensitisation by ingestion but http://pmj.bmj.com/ Cobalt and nickel. At least 86.5% (Marcussen, they may, on a cross sensitisation basis, sometimes 1960) of nickel sensitisation occurs from non- evoke cross reactions in persons already sensitised industrial sources but 4% from industrial processes by the "para group" (Baer and Leider, 1949). as electroplating, metal alloys and fat and margarine Other azo dyes liable to sensitise and photo- manufacture. Cobalt is a sensitiser and, as the sensitise are flavine (azo-acridine), eosin used in element may be associated with nickel, it can be lipsticks (azo-xanthene) and optical blanchophores difficult to produce a completely pure metal. (azo-stilbene) used in textiles and detergents. Metallic alloys and pigments used in paints, enamels Azo pigments may occasionally leach out of on September 30, 2021 by guest. and ceramics are the main exposures. synthetic resins and solvents during use. Formaldehyde. This is a commonly used preserva- Other sensitisers include the triphenyl methanes tive in medical and allied trades, and for leather, (auramine, brilliant green, crystal and methyl textiles and for coagulation of rubber latex. Com- violet), vat indigoid, alizarin and amine dyes bined with phenols or cresols (phenolic) or urea and as paraphenylene diamine used for hair or textile melamine (aminoplast) it is condensed to make dyes which has an azo cross sensitisation. Para- formaldehyde resins. Plywood and the wood phenylene diamine may cause a contact dermatitis adhesives and anti-crease textile resins have been or possibly, via toxic enzymal damage also a sources of formaldehyde sensitisation. lichenoid dermatosis quite indistinguishable clinic- Amines. These have widespread use in industry ally from lichen planus. This has occurred in and as aniline type intermediates in dye stuff photographic workers using substituted parapheny- manufacture and as rubber accelerators (toluidine, lene diamine colour developers. Postgrad Med J: first published as 10.1136/pgmj.42.492.643 on 1 October 1966. Downloaded from October 1966 HODGSON: Industrial Dermatitis 649

Essential oils of vegetation cross linkage for final use or consumer products. Trees and timber. The essential oils and oleo- Miscellaneous catalysts, solvents, plasticisers, fillers, resins and other secondary products formed during pigments and special additives also being included the photosynthetic metabolism of trees and plants in the formulation. Plasticisers are often pro- may act as irritants or sensitisers to those handling ductive of contact dermatitis in the consumer them. article. Chemically these secondary products include As the manufacture is mainly enclosed, contact organic acids, phenols, resorcinols, catechols, dermatitis at that stage is uncommon but initiators quinones, tars, terpenes, alkaloids etc.; cross such as organic peroxides or metallic halides may sensitisations may occur. Foreign woods are more cause accidental skin burns. Anti-oxidant amines likely to cause contact dermatitis in wood workers or phenols, used to stop the polymer at the required than native. This occurs from naphthoquinones length, may be irritant or sensitising as can hydro- (lepachols) in teak, Greenheart, Peroba do Campos quinone used later to stabilise the polymer. Raw and Jacaranda, and catechols in the Anacardinaceae material condensates or intermediates are only trees as Poison Ivy and Sumac, Japanese lacquer, potential hazards till fully polymerised and in the Indian ink trees and Cashew nut used for synthetic case of the former when cured to harden as with resins. adhesives. The principle is accepted that a fully The Conifer family (Pinaceae) of all the native polymerised or hardened polymer is inert. woods are most likely to cause alpha-pinene Personnel exposed to more risk are those pro- sensitisation in furniture factories or house building. cessing the partly polymerised resin as in adhesives, Sensitivity to alga-fungal tree lichens of trees and laminates or mouldings to a final product, or woods may cause contact dermatitis; usnic acid is occasionally when handling the consumer article.

the sensitiser (Mitchell, 1965); clothes may be affected Possibility of contact with reactive chemicals Protected by copyright. by dried dusts. Preservation of timber with creosote, under such conditions include persistence of arsenical chromate or chlorinated organic chemicals, unreacted monomers, intermediates or catalysts, often in solvents, can also be sources of dermatitis. leaching of plasticisers to which may be added Plants. Horticultural workers, florists and house 25 - 50% of the whole especially from addition workers are prone to irritant acidic juices from a polymers, machining of cured plastics and thermal large variety of vegetation or to traumatic injuries decomposition. Resins being completely poly- from stiff hairs, spines or bristles. merised in synthetic fibres (with the exception of Only a few families however cause dermatitis. some nylon), emulsion and solvent paints, and such They include daffodils and narcissi (Amaryllidaceae), addition polymers as polyethylene, polypropylene daisies, chrysanthemums (Compositae), lilies, tulips are without hazard. and hyacinths (Liliaceae), Primula obconica (Primu- Synthetic resins have widespread industrial and laceae) and buttercups and anemones (Ranuncul- consumer use. aceae). Some reported examples of contact dermatitis and

Among classic examples of contact dermatitis are the responsible agents are: http://pmj.bmj.com/ "tulip finger" in florists especially from Rose Cope- Addition polymers land and Preludin tulips (Rook, 1961), and hyacinth Celluloses - dermatitis from plasticisers in scabies with papulo-vesicular or follicular eruptions. spectacle frames. Onions and garlic bulbs may irritate handlers. Vinyls - dermatitis from plasticisers in poly- vinylchloride watch straps, rainwear, Catering trade floor tiles, babies' drawers, artificial Essential oils as a source of sensitisation include leather moulded domestic articles. limonene ofcitrus fruits (lemons, grapefruit, oranges, Triphenyl (TPP) and tricresyl phos- on September 30, 2021 by guest. tangerines), cinnamon and vanilla (cross sensitisers phate (TCP) have both caused re- with Balsam of Peru (Hjorth, 1961), and synthetic actions in the vinyls and cellulose essences as bitter almond (eugenol), almond oil articles. (benzaldehyde oil). Many vegetables also carry an Acrylics -dermatitis from moulding powders irritant risk but an unusual adverse effect arises from used for dentures, car accessories and proleolytic enzymes in pineapples (bromelin) or consumer goods. The offending pancreatic juices. Constant exposure to fruit or agents here are partially polymerised vegetable juices and wet conditions being also poly methyl methacrylate catalysts as eczematogenic. amines, mercaptans, hydrazines in the moulding powder and hydroquinone, Synthetic resins and rubber chemicals phenols and pyrogallol inhibitors, The technology here is based upon addition or cobalt accelerators and peroxide cata- condensation polymer formation of resins with later lysts of the hardening liquid. Postgrad Med J: first published as 10.1136/pgmj.42.492.643 on 1 October 1966. Downloaded from 650 POSTGRADUATE MEDICAL JOURNAL October 1966

Condensation polymers. The hazards here relate in isobutylene polymers), stabilisers (phenyl-alpha- mainly to the incompletely polymerised resin and to naphthylamine and epichlorhydrin in chlorobuta- catalyst hardening agents until the final product is diene "Neoprene" polymers) or plasticisers. set. Their final use is mainly for cast resins, ad- Only rarely is the synthetic rubber itself a contact hesives and laminating agents and in paints. risk as chloroprene, butadiene or polysulphide Polyamides. Although pure nylon polymers are rubbers. considered inert contact reactions have rarely been Most contact dermatitis occurs from consumer described to Nylon 6 episilon Caprolactam polymers products relative to additives as accelerators, and (Morris, 1960). Other textile fibres and other nylons, antioxidants which, being uncombined, leach from celluloses, polyvinylidene chloride (Saran), iso- the final article. cyanates (Perlon), acrylonitrile (Orlon), linear The large range of additives used makes exact polyester (terylene) and regenerated protein are not designation difficult but commonly at fault are productive of dermatitis although various texiile accelerators as tetramethyl thiuram monosulphide coning oils, sizes and finishes may be. (also used as insecticides (TMT)), mercapto benzo- Formaldehyde resins. Mainly used are phenol thiazole (MBT), dipenta methylene thiuram mono- formaldehyde (phenolic) and urea or melamine sulphide (PTD), paraphenylene diamine (PPD) condensates (aminoplast). (Wilson, 1960); and the anti-oxidant monobenzyl Sensitising agents are formaldehyde, intermedi- ether of hydroquinone which has also caused ates, phenylol methanes or methylol ureas and contact leucodermia. Plasticisers and dyes are much hardening agents as hexamethylene tetramine. less common causes. Dermatitis has occurred from those resins used for Protective industrial gloves, clothing, boots and moulding powders, copying papers (para-tertiary shoes, personal clothing, elasticised textiles and foam rubber may affect the wearer. butyl catechol), shoe adhesives (para-tertiary butyl Protected by copyright. phenol) and anti-crease amino-plast "non-crush" Other hazards from rubber are the eczematogenic textile resins. effect of alkaline rubber latices, and solvent rubber adhesives or those requiring a vulcanisation system Epoxy resins. These have caused contact derma- as used in the boot and titis not only from the epoxy resin itself but also from shoe industry. the polyamines used as cross linkage catalysts. Diagnosis and Management Until adequate protective measures were employed, Where the dermatitis is contact in pattern, the incidence was considerable. diagnosis is made on the clinical appearance and Exposure occurs in encapsulating "potting" industrial exposure to a known irritant or sensitiser. electrical insulation, non-drip and resistant surface In the case of patchy eczema the diagnosis is often coatings and industrial paints, and as adhesives for a matter of the physician's opinion and assessment metals, glass, ceramics and plastics. of the importance of the operative occupational and Epichlorhydrin and Bisphenol A (isopropylidene non-occupational agent in relationship to the diphenol) the raw materials are both aggressive and

constitutional http://pmj.bmj.com/ actively sensitising. Glass fibre laminates by diathesis of the patient. skin In both patterns allergic sensitisation may be traumatising the encourage penetration of assessed by patch testing. These are single specified sensitisers. tests or batch tests. For instance, in hand eczemas Polyesters. The linear textile fibres are without such batteries may include common sensitisers or hazard but occasional contact dermatitis may occur nickel, chromate, formaldehyde, balsam of peru, from solvent based lacquers or when used as rubber, antihistamines, antibiotics, ointment bases, adhesives on glass fibre laminates. The cure agents, etc., other group sensitisers or the main hazards of or solvents, as also lacquers, are mainly at fault; the the suspect occupation such as rubber compounding on September 30, 2021 by guest. resins themselves having only a low sensitisation chemicals. index. Difficulties in interpretation include false irritant Rubber. Artificial rubber may be made from iso- positive reactions and multiple false positives in prene (natural rubber)-like polymers as butadiene "status eczematicus" from testing during active or chloroprene or from high elastomers of such dermatitis; false negative reactions also occur synthetic resins as vinyl, and silicones polymerised through non-penetration. Eosin, for example, in to a rubbery state. As with natural rubbers the risks lipsticks may react on the thin lip-skin but not on of contact dermatitis reside mainly in the compound- the thick skin of the back. Stripping with adhesive ing materials necessary to achieve vulcanisation cure scotch tape has been used to overcome this difficulty. for consumer products. Delayed positive reactions, 72 hours or in 6 - 7 days Occasional dermatitis may occur during manu- after the test, usually indicate true allergic sensitisa- facture of the polymers from catalysts as mercaptans, tion. Delayed positives after 7 - 10 days indicate boron trifluoride and aluminium chloride (initiators sensitisation by the patch test itself. A latent Postgrad Med J: first published as 10.1136/pgmj.42.492.643 on 1 October 1966. Downloaded from October 1966 HODGSON: Industrial Dermatitis 651 sensitivity can be awakened by the patch test itself, Conditioning creams with lanoline, soft paraffin which would wrongly suggest responsibility for the or oil/water emulsions are helpful in maintaining dermatitis. Eric Skog (1965) has shewn a significant the keratin integrity to water content and water/oil increasing number of positive test reactions to para- emulsion creams such as Ung.Aquosum may phenylene diamine, sensitisation being induced by benefit the person whose hands tend to chap in the the test, more so by the higher concentrations. Thus winter or those with patchy eczema in atopic or pre-employment patch tests are not advised. ichthyotic skins. Sensitisations may also have been initiated by non- industrial contacts. Where contact dermatitis has occurred the work- man should be left on his own or alternative work if REFERENCES possible unless the dermatitis is severe. In sensi- tisation he should come off contact unless it is BAER, R. L., and LEIDER, M. (1949): Effects of Feeding Certified Food Azodyes in Paraphenylenedi-amine- known the de-sensitisation hardening will occur. hypersensitive Subjects, J. invest. Derm., 13, 223. Accommodation hardening to irritants as oils, BETTLEY, F. Ray (1965): Diagnosis of Industrial paraffin, soaps and detergents can and does occur Dermatitis, Brit. med. J., ii, 1340. with continued contact. BOURNE, L. B. (1960): Industrial Health and Welfare, Med. Press, 244, 186. Most recover from contact dermatitis after months BUCKLEY, W. R. (1963): Localized Argyria, Arch. Derm., but some remain sensitive and have further attacks 88, 531. on re-exposure. Where a patchy eczema or a consti- BURBACH, J. P. E. (1964): In: Progress in the Biological Sciences in Relation to Dermatology -2. Edited by tutional eczema pattern has emerged effort should A. Rook and R. H. Champion. pp. 443-450. London: be made to get the man back to his own job (if not Cambridge Univ. Press. sensitised) or alternative work as soon as possible; FREGERT, S., and RORSMAN, H. (1964): Allergy to Protected by copyright. Hellier's (1958) figures indicate 770% of those with Trivalent Chromium, Arch. Derm., 90, 4. industrial eczema had recurrences whether or not FROST, J., and HJORTH, N. (1959): Contact Dermatitis from Hydrazine Hydrochloride in Soldering Flux. their jobs were changed. Cross Sensitization to Apresoline and Isoniazid. Psychoneurotic factors soon begin adversely to Acta derm-venereol. (Stockh.), 39, 82. affect complete recovery where there is a prolonged HELLIER, F. F. (1958): The Prognosis in Industrial Dermatitis, Brit. med. J., i, 196. absence from work. HJORTH, N. (1961): Eczematous Allergy to Balsams, An increment on the normal sickness benefit in Acta derm-venereol. (Stockh.), 41, Suppl. 46. the form of industrial benefit may itself increase the MARCUSSEN, P. V. (1960): Ecological Considerations on Nickel Dermatitis, Brit. J. industr. Med., 17, 65. chances of eczema being diagnosed as occupational MAYER, R. L. (1928): Die Uberempfindlichkeit gegen (Bettley, 1965), and could also militate against an Korper von Chinonstruktur, Arch. Derm. Syph. early return to work. (Berl.), 156, 331. MITCHELL, J. C. (1965): Allergy to Lichens, Arch. Derm., 92, 142. Prevention and Protection MORRIs, G. E. (1960): Nylon Dermatitis, New Erngl. J. http://pmj.bmj.com/ Med., 263, 30. Prevention of industrial dermatitis is mainly NAYLOR, P. F. D. (1955): Experimental Friction Blisters, referable to safety precautions, machine design and Brit. J. Derm., 67, 327. protective equipment to reduce skin contact, with PASCHOUD, J. M. (1963): Quelques Cas d'Eczema de proper factory floor and personal cleanliness and Contact avec Sensibilisation de Groupe, Dermatologica. (Basel), 127, 349. adequate washing facilities. ROOK, A. (1961): Plant Dermatitis. The Significance of Industrial eczema is commonly initiated by the Variety-Specific Sensitization, Brit. J. Derm., 73, 283. ill use of abrasives, high alkali soap or detergent RUBIN, L. (1949): Hyperkeratosis in Response to Mechanical Irritation, J. invest. Derm., 13, 313. on September 30, 2021 by guest. cleaners, or solvents as white spirit, paint thinners, SKOG, E. (1965): Sensitization to p-Phenylenediamine, paraffin, petrol or trichlorethylene used on the site. Arch. Derm., 92, 276. SUSKIND, R. R., and WHITEHOUSE, H. S. (1963): The Occasional cases of contact dermatitis are related Housewife and Her Exposure to Washing Products, to sensitivity to rubber or plastic gloves and to Arch. Derm., 88, 130. barrier creams. Barrier creams are sub judice as to SZAKALL, A. (1955): Uber die Eigenschaften, Herkunft their effectiveness. They certainly aid in cleansing und Physiologischen Funktionen der die H-Ionen- konzentration Bestimmenden Wirkstoffe in der the skin after work. They are not entirely useless Verhornten Epidermis, Arch. klin. exp. Derm., 201, but must be limited in protective faculty under 331. conditions of use which tend to remove them or THOMSON, S. (1958): Some Aspects of Industrial Derma- interrupt the continuous film needed for protection. titis, Brit. med. J., i, 1135. VICKERS, H. R. (1958): Dermatitis in the Steel Industry in They do not stop the penetration of sensitisers and Sheffield, Brit. med. J., i, 199. are not effective in continuous exposure to oils, WILSON, H. T. H. (1960): Rubber-Glove Dermatitis, Brit. cement or wet working conditions. med. J., ii, 21.