POSTGRAD. MED. J. (1966), 42, 643.

INDUSTRIAL DERMATITISGEOFFREY 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 theMinistry of National Insurance as P.D. 42 "a non-infective dermatitis of external origin, includingchrome ulceration of the skin but excluding der-matitis due to ionization particles of electromagneticradiations other than radiant heat." This hasreplaced "24b," dermatitis produced by dust,liquid or vapour.

It could also be described as the eczematousreaction of the skin to a hurtful agent or environ-mental factor which irritates it or to which it issensitive (allergic).

Accurate information is not easy to obtain but inthe years 1953 - 1956 in Great Britain industrialdermatitis accounted for 0.3% of 1.3% total lostworking days for all skin diseases in a workingpoulation of 20,500,000 (Thompson, 1958); Bourne(1960) gives similar figures, 0.32% of 1.6% skindiseases.

Eczematous reactions accepted under P.D. 42 are,however, not solely the contact result (dermatitis) ofan external irritant. Many are really eczemadetermined, often initially by external irritants, butpredisposed thereto by a constitution inferiority ofthe skin and inherited or acquired immuno-chemical relationships. These will both influencethe onset and the course of eczema, on a personalbasis.Behind these considerations lie most of the

difficulties relative to diagnosis of occupationaldermatitis.

Basically the development of industrial dermatitisrepresents a struggle between an external aggressor(mechanical, chemical or biological) at work, andthe defending epidermal defence with its varyinganatomical, architectural, molecular or physio-logical integrity.Rapid overwhelming of the defence leads to

acute contact dermatitis whilst more insidiousundermining predisposes to eczema.

Patterns of Dermatitis (P.D. 42).Eczematous reactions which may be accepted

under P.D. 42 or considered for aggravation bywork may be designated-(a) Contact dermatitis (contact pattern).(b) Exogenous "industrial" eczema (eczematousdermatitis), (patchy eczema pattern).

(c) Constitutional eczema (temporarily aggravatedby occupation) (constitutional patterns).

Fungal infections of the feet, epidermophytosis,in colliers may be accepted as an "industrialaccident" if there is evidence of pithead bathsbeing used.

In true contact dermatitis all exposed areas areaffected usually within hours or 2- 3 days ofcontact and recovery should occur in weeks to afew months when such contact ceases.

Patchy "industrial" eczema (eczematous derma-titis) usually presents in a patchy or discoid patternon the work-exposed skin but usually only aftermonths or years of exposure, its course beingchronic for months, years or sometimes permanently.Much patchy eczema is also initiated, however, byother exogenous factors (home or hobbies) actingalone or in concert with those at work.

Allergic sensitisation can occur in both patterns(contact and patchy eczema) but is preceded firstby some irritant or traumatic damage to the epider-mal protective structures allowing percutaneouspenetration of allergens.The constitutional patterns of eczema which may

be temporarily aggravated by work or environmentinclude dysidrotic (pompholyx), atopic (eczema-asthma-hayfever syndrome), seborrhoeic eczemasand neurodermatitis. Such skins are themselvesconstitutionally unstable and often susceptible toexogenic injury.Although theoretically a true contact dermatitis

and also an "industrial" eczema should recover,soon or eventually, when away from contact, manycases of accepted "P.D.42" become chronic; contactdermatitis developing later into a patchy eczema,and patchy eczema becoming chronic or progressinginto constitutional patterns. Factors which determinethis include constitutional predisposition itself,continued exposure to irritants or sensitisers atwork or in the home, secondary pyogenic infection,adverse effects of topical or systemic treatment, andpersisting functional disturbances such as vascularinstability and permeability, sweating and keratin-isation as sequels of the dermatitis even when theconvalescent skin appears clinically well. Emotionalfactors including neuroses (neurodermatitis), com-pensation, litigation, resettlement problems or frankmalingering (dermatitis artifacta) will also contribute.

POSTGRADUATE MEDICAL JOURNAL

Epidermal DefencePercutaneous chemical penetration, with irritant

action on deeper viable epidermal cells, or allergic-induced sensitisation through the dermal reticulo-endothelial system, is normally prevented by theintact keratinised stratum corneum. An ionic layer(water barrier) of cells, described by Szakall, (1955)below the stratum being electrically charged,repels anions and reattracts cations, and is alsorepellent to water and water soluble electrolytes.Fat-soluble chemicals may pass this barrier once itis damaged or may pass through the appendagealsebaceous glands. Entrance through sweat ducts isminimal although silver can enter thus to causeargyria (Buckley, 1963).

Later penetration through- viable malpigian andbasal cells is trans or intercellular in method.

In addition, there exists other "built-in" defencesas the neutralising buffer capacity of amphoterichorny keratin, and the "acid mantle" of shedstratum corneum horn cells, acidic sweat and fattyacids. Sebum also lessens water evaporation pro-tecting keratin.As the stratified horn layer constitutes the main

defence, this in turn relates to an intact grossarchitecture (cell-to-cell adhesion and dermosomebonding including that of other epidermal andepidemo-dermal junction levels) but also at a cellularlevel based upon the molecular structure of keratin.

Integrity of Keratin in Stratum CorneumThe fibrous protein keratin filling the firmly

packed denucleated cells of the stratum corneumhas been progressively synthesised by addition ofamino-acid polymerisation to polypeptide chains inthe viable basal cells and intermediate keratinocytes.A final cross linkage of adjacent polypeptide grids

by strong disulphide (S = S) bonds of cystine, orweaker salt (acid or basic) and electrically chargedhydrogen atoms of amino acids converts the gridsinto the rigid horny keratin and hardens dermosomecell adhesion. The keratin molecules themselvesadd mechanical strength being twisted in helicalform like ropes.

Water content

The 10 - 20% of water in the stratum corneum,replaced by diffusion from below, both plumps theindividual keratin molecules and acts as a lubricantbetween the polymer chains, similar to batchingemulsions used in spinning textiles, ropes or glassfibre. This reduces fibre to fibre friction, impartingsuppleness and abrasion proofing.

Dessication by climatic, environmental or chemicalagencies at work causes dryness and fissuring(chapping) and increased liability to mechanicalstress and encourages chemical penetration.

Under conditions of work therefore the stratumcorneum and deeper layers may be damagedprimarily by physical wounding or mechanicalstress with individual cell separation or proteindamage, by reduction of water content below 10%and at a cellular and molecular level, by chemicaldamage to protoplasm, to keratin and its crosslinks.

Occupational insult may also chemically damageenzymes responsible for cellular metabolism andprotein synthesis; bullous eruptions may thusdevelop. For instance, sulphydryl (-SH) containingenzymes are susceptible to chemicals as methylbromide, organic mercurials (seed dressings),arsenicals (Lewisite) or nitrogen mustards producingcontact vesicant dermatitis whilst other vesicantsact by blocking conversion and interfering withcellular respiratory metabolism relative to adenosinetriphosphate (ATP) (Burbach, 1964).During day-to-day exposures constant repair of

minor injuries or chemical damage occurs in thestratum corneum unless the result be at onceoverwhelming. While contact dermatitis is mainlydetermined by the concentration or allergenicity ofthe chemical or the degree of exposure, "eczematousdermatitis" occurs mostly in those with abnormallykeratinised or non-intact skins in which normalreparation less easily occurs.Among these constitutional inferior skins feature

dyskeratoses, icthyosis, xerosis, atopic persons, theseborrhoeic state and those with poor water-holding capacity (subject to winter chapping) orbuffering capacity. Thinning of the stratum corneum,inherited or acquired by primary collagen degener-ation in senile or aging skins also operates. Over useof topical steroids in treatment may itself lead tocollagenous degeneration with thinning and trans-parency and lessened resistance.

Aggressive Industrial AgentsInjurious agents at work (or in the home) may be

physical, environmental, chemical or biological.Chemicals are conveniently classified as irritants

or sensitisers, their potential for causing contactdermatitis or eczema is determined by chemicalreactivity, concentration, degree and conditions ofexposure, and by the constitutional resistance of theexposed skin.

Physical agentsPuncture wounds and lacerations with secondary

infection may lead to local traumatic dermatitis orinitiate eczema. Topical treatment is also a commoncause. These cases are seen particularly in heavyindustry, for instance 35% of "P.D.42" in the steelindustry is so accountable (Vickers, 1958).An occupational traumatic dermatitis should

commence at the site of injury before complete

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healing has occurred. The skin, in the vicinity ofrecently healed abrasion, is however temporarilymore susceptible (non-specific hypersensitivity) toother accepted irritants during the convalescentphase until hardening occurs.

Continuous friction may increase the risk ofpenetration by smoothing and thinning the hornylayer as in pottery workers, paper mills and metalpolishing, as can also constant handling of roughmaterials as rusty metal concrete or bricks.

Keratin chains are stressed or the actual archi-tectural cementing loosened as when frictionblisters form from distortion of cells and acan-tholysis (Naylor, 1955).

Combinations of friction and lacerative injurywith infection however are most often eczemato-genic. For instance, clothing or footwear dirtiedwith abrasive materials (coal miners or builders),gloves stiffened by tar, or when synthetic gluescause the fingers to adhere together. Abrasive hardmetal dusts as tantalum or zinc, metallic engineeringswarf in wipe rags adherent through oil, angularparticles of sugar or crumbs in confectionery works,or harsh chrysotile asbestos fibres used for insulation(amphilole fibres for textiles are soft and flexible)are other examples. Glass fibre causes pruritic,erythematous or follicular traumatic dermatitis andthe risk may extend through contaminated clothingto those at home.

Hardening of synthetic glues on the skin causesstripping of keratin with irritant effect and pre-disposes to entrance of some sensitisers as formalde-hyde (woodworkers) and epoxy resins.

Persistent friction however also often causes acallus with localised thickening and hardening ofthe horny layer; this gives considerable addedmechanical protection to injury at work. If there isa disturbance of normal cell shedding with hardeningand compression of the keratin lamellae (Rubin,1949) calluses occur to cause occupational stigmata;they may also indicate diagnostically areas of skinmost exposed to irritation at work.

Friction dermatitis will present with an initialredness, scaling, pigmentation or bullous formationat the site affected. Later a patchy dry or moisteczema may develop which on the forearms, thighsand legs may simulate a constitutional discord ornummular eczema. Such industrial eczemas mayaffect the stokers, boilermen, dustmen, metalworkers, labourers, colliers and others in hot ordusty work. Secondary lichenification may occurfrom continued friction or from habit scratching(neurodermatitis) but however can give someprotection and thus in time lessen incapacity.

Inferior skins intolerant of friction include thoseprone to winter chapping, dry or atopic skins withspicules of projecting keratin, hirsute persons andthose with pilomotor instability, the hairs becoming

more prominent through contraction of erector pilimuscles.

Environmental factors and sweat disturbancesKeratin dehydration with chapping occurs from

variations in barometric pressure and the dewpoint or from desiccation agents.Outdoor workers in agriculture and fishing, those

working in cold as ice cream or refrigeration men, orthose in contact with solvents or alkali are particular-ly liable to eczematogenic desiccation.

Asteatotic winter chapping may often precedeoccupational eczema, and inadequate washingfacilities or "paid ablution time" and wet towels orhand-cleansing solvents can contribute to thistendency.

Constant climatic exposure in outdoor workers,clayey soil drying on the skin of agricultural workers,heat in furnace workers and those in metal pro-duction, smelting foundries and glass work alsodries the skin as can such hygroscopic chemicals assalt (fishermen) sugar (confectionery), and lime orcement dusts in the building trade.On the other hand a constant exposure to water

and wet materials, electrolytes and emulsions maysoften the keratin and, by maceration, increasepenetration of larger chemical molecules; thusdevelop the initial patchy eczemas, with laterallergic sensitisations, of housewives, cleaners,textile scourers (aggravated by alkaline keratindegradation), catering and confectionery workers,tanneries, paper pulp workers, and those in medicaland allied trades.The added degree of keratin damage related to

minor irritants at home in all these cases alwayspresents considerable diagnostic difficulties.

Disturbances of sweating. Sweat pore obstructionmay occur from hydration oedema as in macerationfrom sweating or wet work, or by poral hyperkera-tosis from micro-frictional trauma. Thus developsweat obstruction syndromes of the body (miliaria)or hands (dysidrotic pompholyx eczema.)

Miliaria may precede eczema in body crevices oron areas exposed to the friction of clothing. Thisoccurs in furnace men and soldiers in tropicalclimates where heat exhaustion and thermogenicanhidrosis may also develop with disturbed temper-ature regulation. Miliarial eczemas also occur incolliers (papular eczemas of groins, axillae, cap band,belt and lamp battery areas), glass workers (sweatrags on neck), steel and other metal smelting, and inthose working in overwarm or humid atmospheresrequired by a particular chemical process or whereventilation is inadequate, and when imperviousprotective clothing must be continuously worn,Obesity and alcoholism will contribute in manyinstances.

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Excessive sweating can localise frictional orcontact dermatitis from noxious dusts in bodycreases, increase skin staining from dyes and woods,or cause metal rusting ("rusters"), and by keratinsoftening increase sensitisation.

Constitutional eczema (dysidrosis) may be initiat-ed or aggravated in those with hyperidrosis wherethe handling of toxic chemicals requires longwearing of impervious plastic (P.V.C.) or rubbergloves and footgear. Some convalescent fromdermatitis may also find protective gloves difficultto wear.

Sweat obstruction caused by imperfect kera-tinisation and poral closure in convalescent derma-titis or eczema subjects is a common cause ofrelapse on their return to work.

Chemical irritants and sensitisersChemical irritants are graded as strong to moder-

ate or weak in strength and action on the skin.Strong to moderate chemicals will normally cause

lesions varying from contact chemical burns witherythema, vesication, bullae or ulcers to a classicalcontact dermatitis developing within hours or a fewdays of the exposure.Weak chemicals usually predispose to patchy

eczema by slow disturbance of stratum corneumrepair or its molecular protein structure.

Secondary allergic sensitisation may complicateeither.Most industrial dermatitis is initiated by chemical

irritants or trauma (80%), allergic sensitisation onlybeing responsible for some 20% of cases.

Strong irritants and vesicants. Injury from strongchemicals is only likely to occur as an accidentthrough ignorance, or if normal safety precautionsand protective clothing be neglected. Processmen,fitters or other maintenance workers can howeverhave such accidental exposure from pipe breaks.Burns or dermatitis might occur from contact on

unprotected skin with such materials as liquidoxygen or hydrogen peroxide, concentrated in-organic acids and alkalis, chromic acid andchromates (electroplating), hydrofluoric acid andfluorides (glass etching, synthetic resin polymeri-sation and uranium manufacture), silico-fluorides,organic acids as phenols or cresols (manufacture ofphenolic resins), selenious acid (electrical industry),acetic acid and anhydrides (cellulose acetatemanufacture and rocket propellant fuels), silanesand chloro silanes (silicone resin manufacture), thechlorinated benzenes (chemical intermediates) andcatechols of cashew nut resins, shoe adhesives,copy paper, shellac and vegetation.Some however through abraded skin cause

ulcerations and leave scars which may act as dis-tinctive marks of occupation. Among these are

chromic acid and chromates and cyanides (electro-plating), mercuric nitrate and metallic sodium,ammonium nitrate and mercury fulminate(explosives), zinc chloride "Bakers fluid" (engineer-ing fluxes), unslaked lime (building trade). Ulcerationof the nasal septum may be similarly caused.Among other common vesicants are acrylonitrile

(vinyl cyanide) for acrylonitrile polymers andsynthetic rubber, alkyl mustard compounds (syn-thetic resins or flavours), chloroacrylates (acrylicresins), dinitrophenols (chemical industry), iodo-acetic acid (reagent for biochemical tests) and thealkyl organic tin (plasticisers for vinyl resins) andorganic mercury compounds (disinfectant agentsand agricultural seed dressings).

Vesicants very often induce sensitisation.Moderate irritants. These may cause contact

dermatitis on unprotected skin or after unusualexposure. They include miscellaneous polyaminesas ethylene amines which are often alkaline (usedin chemical synthesis or as hardeners for syntheticresin adhesives), hydrazines (engineering fluxes),fluoacetic acid and acetates (agricultural herbagecontrol), methyl salicylate (oil of wintergreen) andmethylene chloride (paint remover).

Weak irritants. Transient erythema, or evencontact dermatitis patterns may be produced by thisgroup in constitutionally inferior skins but mostoften the adverse effects are dehydration with harshdry scaling and fissuring or persisting erythemasas in "housewives hands," grading over into patchyeczema with probable added allergic sensitisation.

These weak eczematogenic irritants are found in alarge variety of occupations. They all predispose toirritation of viable cells or to sensitisation bydesiccating, damaging the keratin architecture orcellular protein, or by loosening molecular linksand by increasing percutaneous penetration. Forinstance, alkalis damage protein by reducing thedisulphide link (S =S) freeing sulphydryl groups(-SH), weak acids dissociate salt links and maydehydrate; oxidisers as perchlorates and perboratesaffect hydrogen bonds and chlorine compounds aschlorinated lime (bleaching powder) or bisulphites,as reducers, also affect the strong disulphide link.The over use of these latter as stain removers may beeczematogenic. Textile, ink and dye workers aremainly at risk.

Solvent or alkaline agents which remove sebumexpose the keratin to dehydration and bacterialinfections by removal of the "acid mantle."Among other weak irritants which usually cause

patchy eczema are engineering cutting oils especially"suds" emulsion oils. There ase assessed as causa-tive of 15 - 20% of cases of industrial dermatitis.Synthetic anionic detergents and alkaline "built"washing agents are accepted as eczematogenic.Although occasional acute irritant effects are seen

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from some concentrated anionic detergents asmoderate irritants, the bad reputation of detergentsmay be unjustified for as Suskind and Whitehouse(1963) have shown by immersion tests, that house-wives eczema, allegedly due to detergents, can stillsupport daily immersion in weak solutions withoutill effect.

Solvents vary in their action, most aggressivebeing petroleum hydrocarbons (petrol, naphtha,white spirit, kerosene), coal tar hydrocarbons(benzene and toluene), chlorinated hydrocarbons(carbon tetrachloride for rubber, paint, dry cleaningand fire extinguishers), and trichlorethylene formetal degreasing. True turpentine is both irritantand sensitising.

Ketones are usually eczematogenic after longexposure and may attack hydrogen bonds; methylethyl ketone used in synthetic resin adhesives hascaused eczema when used to remove adherentepoxy or polyester glues from the skin. Alcohols areless irritant causing usually a temporary whiteningof the skin; the volatile esters and ethers provokingmainly mucous membrane irritation.The use of petroleum solvents, white spirit or

"turps" substitute (decalin and tetralin) by paintersand printers for cleaning machinery or stained handsis often a cause of eczema.

Harsh abrasives or alkaline "built" soaps andover use of strong solvent-alkali containing handor waterless cleansers and over-washing of thehands by those with obsessional traits may besimilarly provocative.

Biological irritantsBanal infections with monilia are relatively

common in industry, particularly in the cateringtrade where maceration of the skin and sugarysolutions predispose to candida albicans growth.Dentists may develop similar infections of the fingersfrom patients' mouths; occasionally these maybecome eczematised.

Less obvious however are miscellaneous zoonoticmite infections which may cause urticarial, papulo-vesicular and sometimes frank dermatitis. Dockworkers (prunes, figs), millers and grocers (cerealmites), tobacco workers, poultry men includingrailway personnel (pigeons) are so prone.

The Allergic Sensitisation ProcessAllergic sensitisation is of the delayed eczematous

type induced by contact and percutaneous pene-tration. The minimal contact time for sensitisationis some 6 - 8 hours, and the incubation time beforeclinical evidence 6- 10 days or shorter. Contactwith the antigen should cause the delayed eczematousresponse in 12 - 48 hours or within a few days.Allergic sensitisation to industrial chemicals isusually specific to one agent but polyvalent sensitisa-

tion may occur although this is often postulated onthe grounds of multiple reactions which may beirritant effects of patch testing. Group- or cross-sensitisation is where substances of apparentlydissimilar chemistry have a common immunechemical group or molecular nucleus determininggroup reactions. This was first described by Mayer(1928) in respect of the "para group." Many otherexamples have been since described including:-

List of Common Group SensitisersAntibiotics (penicillin, tetracyclines, "mycins")Arsenicals (inorganic, organic)Bisphenols (epoxy resins and phenols)Catechols (copying inks, shoes and resins, Ana-

cardinacae trees)Chloro-cresols and xylenols (preservatives)Essential oils (essences, balsams)Esters- Para-aminobenzoic acid esters ("Para-bens") (ointment and cosmetic preservatives)Paraphenylamine diamine."Para" group- Aniline compounds (dye stuffs),amino-azo dyes, nitrophenols (picric and trini-trotoluene explosives), sulphamides, sapamine(brilliantines Paschoud 1963).

Hydrazines (engineering fluxes, rocket fuels,pharmaceuticals)

Hydroxyquinolines (topical dermatological therapy)Phenothiazines (pharmaceutical)Thioglycollic acid and salts (cold wave hairdressers)Vegetation (tars, terpenes, essential oils).

Other examples are continually reported indicatingthat allergic sensitisation may begin at home or inpursuits outside of work. latrogenic sensitisationestablished by drugs may for instance cause crosssensitisation reactions in industry. Apresoline(hydrazinophthazine), phenyl hydrazine and isoni-cotinic acid hydrazine (INAH) may pave the way forhydrazine salts used as metal soldering fluxes tocause sensitisation dermatitis (Frost and Hjorth1959).

Industrial chemicals which induce photosensitivedermatitis include the germicides tetrachlorsalicylanilides (which provoked an epidemic of contactdermatitis in a toilet soap), bithionol, and hexa-chlorophene used in cosmetics and soaps, or inpharmaceutical products.

Other iatrogenic or pharmaceutical exposuresunder poor factory hygiene conditions are thephenothiazines (antihistamines, tranquillisers), oralantidiabetic drugs (Tolbutamide), diuretics (chloro-thiazide) and griseofulvin.

Irritant phototoxicity caused by altered lightabsorption is caused also industrially by petroleumoils, creosote, tar and pitch, perfumes (oil ofBergamot) and furocoumarins from the Umbelli-

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ferae plant family; photo-dermatitis in celery orparsnip pickers occurs.

Common trade allergic sensitisationsSensitisers only account for some 20% of indus-

trial dermatitis, physical and irritant agents beingmuch more important.

Space does not permit of a full list but some areimportant in a wide range of occupations or handlingconsumer products.The sensitisation may however be also often

acquired outside industry or on a group basiscausing difficulty in incriminating the work. Amongimportant common sensitisers may be listed:-

Arsenic. Both the inorganic and organic arseniccompounds are sensitising. Dermatitis has occurredin metal production from copper ore (includingthose in villages around), glass manufacture,sheep dips, hide preservation, vine growers, woodpreservation and pharmaceuticals, or as agriculturalinsecticides.

Chromates. Hexavalent chromate is definitelyantigenic and so is the trivalent form (Fregert andRorsman 1964). Trivalent chromate may also beoxidised in tissues, as in tattoo marks, to hexavalentform. Industrial substances and occupations at riskare paint primers, chromated animal glue as inmatch heads, boot and shoe tanning, buildingindustry (cement), electroplating, metallurgy (alloys),ink and lithography and photoengraving printing,engineering oils (contaminated with chromate),refractory foundry cores, photography, wood andfuels (chromate preserved wood ash), anti-rustradiation coolants for railways engines and dyemordants for furs and textiles.The metallic chromium or chrome plating is not

antigenic.Cobalt and nickel. At least 86.5% (Marcussen,

1960) of nickel sensitisation occurs from non-industrial sources but 4% from industrial processesas electroplating, metal alloys and fat and margarinemanufacture. Cobalt is a sensitiser and, as theelement may be associated with nickel, it can bedifficult to produce a completely pure metal.Metallic alloys and pigments used in paints, enamelsand ceramics are the main exposures.

Formaldehyde. This is a commonly used preserva-tive in medical and allied trades, and for leather,textiles and for coagulation of rubber latex. Com-bined with phenols or cresols (phenolic) or urea andmelamine (aminoplast) it is condensed to makeformaldehyde resins. Plywood and the woodadhesives and anti-crease textile resins have beensources of formaldehyde sensitisation.

Amines. These have widespread use in industryand as aniline type intermediates in dye stuffmanufacture and as rubber accelerators (toluidine,

piperidine, hexamethylene amine). Ethylene amineswhich are often alkaline and irritant used as harden-ing agents with epoxy resin glues have been respon-sible for dermatitis.

Antibiotics and other topical agents. Sensitisationmay occur during manufacture in pharmaceuticalworkers but mainly contact dermatitis occurs fromtopical treatments of minor injuries with sensitisersas commercial neomycin (B.C. and neamine neo-mycin A), penicillin and the tetracyclines (chlor-tetracycline and oxytetracycline). Neomycin isbecoming more recognised as a source of contactsensitisation, and a cross sensitiser with framycetin,soframycin, bacitracin, kanamycin and strepto-mycin.

Other topical agents occasionally causingdermatitis when used in treatment of industrialinjuries or skin diseases are the hydroxy quinolines,acriflavine, quaternary ammonium salts and lanolineor other emulsifiers and germicides as "Parabens"used in ointment bases. Necrotising ulcerations arereported from the quaternary ammonium de-qualinium chloride.

Dyestuffs. Dyes used are mainly synthetic andderived from coal tar or petroleum chemicals.Soluble dyes are more likely to cause contactdermatitis than insoluble dyes and pigments. Mostrisk comes not from the fully developed dye, oftenfirmly anchored chemically or mechanically in thefabric or material, but from residual dye intermedi-ates left in the final product or improperly washedtextile. Azo dyes are used in colouring of petrol,textiles, food, paint and ink colours. Contactsensitisation has occurred from ball-point pen inksand hosiery dyes, reds and yellows. Amino azo dyesused as food colourings are not thought to induceprimary epidermal sensitisation by ingestion butthey may, on a cross sensitisation basis, sometimesevoke cross reactions in persons already sensitisedby the "para group" (Baer and Leider, 1949).

Other azo dyes liable to sensitise and photo-sensitise are flavine (azo-acridine), eosin used inlipsticks (azo-xanthene) and optical blanchophores(azo-stilbene) used in textiles and detergents.Azo pigments may occasionally leach out of

synthetic resins and solvents during use.Other sensitisers include the triphenyl methanes

(auramine, brilliant green, crystal and methylviolet), vat indigoid, alizarin and amine dyesas paraphenylene diamine used for hair or textiledyes which has an azo cross sensitisation. Para-phenylene diamine may cause a contact dermatitisor possibly, via toxic enzymal damage also alichenoid dermatosis quite indistinguishable clinic-ally from lichen planus. This has occurred inphotographic workers using substituted parapheny-lene diamine colour developers.

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Essential oils of vegetationTrees and timber. The essential oils and oleo-

resins and other secondary products formed duringthe photosynthetic metabolism of trees and plantsmay act as irritants or sensitisers to those handlingthem.

Chemically these secondary products includeorganic acids, phenols, resorcinols, catechols,quinones, tars, terpenes, alkaloids etc.; crosssensitisations may occur. Foreign woods are morelikely to cause contact dermatitis in wood workersthan native. This occurs from naphthoquinones(lepachols) in teak, Greenheart, Peroba do Camposand Jacaranda, and catechols in the Anacardinaceaetrees as Poison Ivy and Sumac, Japanese lacquer,Indian ink trees and Cashew nut used for syntheticresins.The Conifer family (Pinaceae) of all the native

woods are most likely to cause alpha-pinenesensitisation in furniture factories or house building.Sensitivity to alga-fungal tree lichens of trees andwoods may cause contact dermatitis; usnic acid isthe sensitiser (Mitchell, 1965); clothes may be affectedby dried dusts. Preservation of timber with creosote,arsenical chromate or chlorinated organic chemicals,often in solvents, can also be sources of dermatitis.

Plants. Horticultural workers, florists and houseworkers are prone to irritant acidic juices from alarge variety of vegetation or to traumatic injuriesfrom stiff hairs, spines or bristles.

Only a few families however cause dermatitis.They include daffodils and narcissi (Amaryllidaceae),daisies, chrysanthemums (Compositae), lilies, tulipsand hyacinths (Liliaceae), Primula obconica (Primu-laceae) and buttercups and anemones (Ranuncul-aceae).Among classic examples of contact dermatitis are

"tulip finger" in florists especially from Rose Cope-land and Preludin tulips (Rook, 1961), and hyacinthscabies with papulo-vesicular or follicular eruptions.Onions and garlic bulbs may irritate handlers.

Catering tradeEssential oils as a source of sensitisation include

limonene of citrus fruits (lemons, grapefruit, oranges,tangerines), cinnamon and vanilla (cross sensitiserswith Balsam of Peru (Hjorth, 1961), and syntheticessences as bitter almond (eugenol), almond oil(benzaldehyde oil). Many vegetables also carry anirritant risk but an unusual adverse effect arises fromproleolytic enzymes in pineapples (bromelin) orpancreatic juices. Constant exposure to fruit orvegetable juices and wet conditions being alsoeczematogenic.

Synthetic resins and rubber chemicalsThe technology here is based upon addition or

condensation polymer formation of resins with later

cross linkage for final use or consumer products.Miscellaneous catalysts, solvents, plasticisers, fillers,pigments and special additives also being includedin the formulation. Plasticisers are often pro-ductive of contact dermatitis in the consumerarticle.As the manufacture is mainly enclosed, contact

dermatitis at that stage is uncommon but initiatorssuch as organic peroxides or metallic halides maycause accidental skin burns. Anti-oxidant aminesor phenols, used to stop the polymer at the requiredlength, may be irritant or sensitising as can hydro-quinone used later to stabilise the polymer. Rawmaterial condensates or intermediates are onlypotential hazards till fully polymerised and in thecase of the former when cured to harden as withadhesives. The principle is accepted that a fullypolymerised or hardened polymer is inert.

Personnel exposed to more risk are those pro-cessing the partly polymerised resin as in adhesives,laminates or mouldings to a final product, oroccasionally when handling the consumer article.

Possibility of contact with reactive chemicalsunder such conditions include persistence ofunreacted monomers, intermediates or catalysts,leaching of plasticisers to which may be added25 - 50% of the whole especially from additionpolymers, machining of cured plastics and thermaldecomposition. Resins being completely poly-merised in synthetic fibres (with the exception ofsome nylon), emulsion and solvent paints, and suchaddition polymers as polyethylene, polypropyleneare without hazard.

Synthetic resins have widespread industrial andconsumer use.Some reported examples of contact dermatitis and

the responsible agents are:Addition polymersCelluloses - dermatitis from plasticisers in

spectacle frames.Vinyls - dermatitis from plasticisers in poly-

vinylchloride watch straps, rainwear,floor tiles, babies' drawers, artificialleather moulded domestic articles.Triphenyl (TPP) and tricresyl phos-phate (TCP) have both caused re-actions in the vinyls and cellulosearticles.

Acrylics -dermatitis from moulding powdersused for dentures, car accessories andconsumer goods. The offendingagents here are partially polymerisedpoly methyl methacrylate catalysts asamines, mercaptans, hydrazines in themoulding powder and hydroquinone,phenols and pyrogallol inhibitors,cobalt accelerators and peroxide cata-lysts of the hardening liquid.

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Condensation polymers. The hazards here relatemainly to the incompletely polymerised resin and tocatalyst hardening agents until the final product isset. Their final use is mainly for cast resins, ad-hesives and laminating agents and in paints.

Polyamides. Although pure nylon polymers areconsidered inert contact reactions have rarely beendescribed to Nylon 6 episilon Caprolactam polymers(Morris, 1960). Other textile fibres and other nylons,celluloses, polyvinylidene chloride (Saran), iso-cyanates (Perlon), acrylonitrile (Orlon), linearpolyester (terylene) and regenerated protein are notproductive of dermatitis although various texiileconing oils, sizes and finishes may be.

Formaldehyde resins. Mainly used are phenolformaldehyde (phenolic) and urea or melaminecondensates (aminoplast).

Sensitising agents are formaldehyde, intermedi-ates, phenylol methanes or methylol ureas andhardening agents as hexamethylene tetramine.Dermatitis has occurred from those resins used formoulding powders, copying papers (para-tertiarybutyl catechol), shoe adhesives (para-tertiary butylphenol) and anti-crease amino-plast "non-crush"textile resins.Epoxy resins. These have caused contact derma-

titis not only from the epoxy resin itself but also fromthe polyamines used as cross linkage catalysts.Until adequate protective measures were employed,the incidence was considerable.Exposure occurs in encapsulating "potting"

electrical insulation, non-drip and resistant surfacecoatings and industrial paints, and as adhesives formetals, glass, ceramics and plastics.

Epichlorhydrin and Bisphenol A (isopropylidenediphenol) the raw materials are both aggressive andactively sensitising. Glass fibre laminates bytraumatising the skin encourage penetration ofsensitisers.

Polyesters. The linear textile fibres are withouthazard but occasional contact dermatitis may occurfrom solvent based lacquers or when used asadhesives on glass fibre laminates. The cure agents,or solvents, as also lacquers, are mainly at fault; theresins themselves having only a low sensitisationindex.

Rubber. Artificial rubber may be made from iso-prene (natural rubber)-like polymers as butadieneor chloroprene or from high elastomers of suchsynthetic resins as vinyl, and silicones polymerisedto a rubbery state. As with natural rubbers the risksof contact dermatitis reside mainly in the compound-ing materials necessary to achieve vulcanisation curefor consumer products.

Occasional dermatitis may occur during manu-facture of the polymers from catalysts as mercaptans,boron trifluoride and aluminium chloride (initiators

in isobutylene polymers), stabilisers (phenyl-alpha-naphthylamine and epichlorhydrin in chlorobuta-diene "Neoprene" polymers) or plasticisers.Only rarely is the synthetic rubber itself a contact

risk as chloroprene, butadiene or polysulphiderubbers.Most contact dermatitis occurs from consumer

products relative to additives as accelerators, andantioxidants which, being uncombined, leach fromthe final article.The large range of additives used makes exact

designation difficult but commonly at fault areaccelerators as tetramethyl thiuram monosulphide(also used as insecticides (TMT)), mercapto benzo-thiazole (MBT), dipenta methylene thiuram mono-sulphide (PTD), paraphenylene diamine (PPD)(Wilson, 1960); and the anti-oxidant monobenzylether of hydroquinone which has also causedcontact leucodermia. Plasticisers and dyes are muchless common causes.

Protective industrial gloves, clothing, boots andshoes, personal clothing, elasticised textiles and foamrubber may affect the wearer.

Other hazards from rubber are the eczematogeniceffect of alkaline rubber latices, and solvent rubberadhesives or those requiring a vulcanisation systemas used in the boot and shoe industry.

Diagnosis and ManagementWhere the dermatitis is contact in pattern,

diagnosis is made on the clinical appearance andindustrial exposure to a known irritant or sensitiser.In the case of patchy eczema the diagnosis is oftena matter of the physician's opinion and assessmentof the importance of the operative occupational andnon-occupational agent in relationship to theconstitutional diathesis of the patient.

In both patterns allergic sensitisation may beassessed by patch testing. These are single specifiedtests or batch tests. For instance, in hand eczemassuch batteries may include common sensitisers ornickel, chromate, formaldehyde, balsam of peru,rubber, antihistamines, antibiotics, ointment bases,etc., other group sensitisers or the main hazards ofthe suspect occupation such as rubber compoundingchemicals.

Difficulties in interpretation include false irritantpositive reactions and multiple false positives in"status eczematicus" from testing during activedermatitis; false negative reactions also occurthrough non-penetration. Eosin, for example, inlipsticks may react on the thin lip-skin but not onthe thick skin of the back. Stripping with adhesivescotch tape has been used to overcome this difficulty.Delayed positive reactions, 72 hours or in 6 - 7 daysafter the test, usually indicate true allergic sensitisa-tion. Delayed positives after 7 - 10 days indicatesensitisation by the patch test itself. A latent

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sensitivity can be awakened by the patch test itself,which would wrongly suggest responsibility for thedermatitis. Eric Skog (1965) has shewn a significantincreasing number of positive test reactions to para-phenylene diamine, sensitisation being induced bythe test, more so by the higher concentrations. Thuspre-employment patch tests are not advised.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 ifpossible unless the dermatitis is severe. In sensi-tisation he should come off contact unless it isknown the de-sensitisation hardening will occur.Accommodation hardening to irritants as oils,paraffin, soaps and detergents can and does occurwith continued contact.Most recover from contact dermatitis after months

but some remain sensitive and have further attackson re-exposure. Where a patchy eczema or a consti-tutional eczema pattern has emerged effort shouldbe made to get the man back to his own job (if notsensitised) or alternative work as soon as possible;Hellier's (1958) figures indicate 770% of those withindustrial eczema had recurrences whether or nottheir jobs were changed.

Psychoneurotic factors soon begin adversely toaffect complete recovery where there is a prolongedabsence from work.An increment on the normal sickness benefit in

the form of industrial benefit may itself increase thechances of eczema being diagnosed as occupational(Bettley, 1965), and could also militate against anearly return to work.

Prevention and ProtectionPrevention of industrial dermatitis is mainly

referable to safety precautions, machine design andprotective equipment to reduce skin contact, withproper factory floor and personal cleanliness andadequate washing facilities.

Industrial eczema is commonly initiated by theill use of abrasives, high alkali soap or detergentcleaners, or solvents as white spirit, paint thinners,paraffin, petrol or trichlorethylene used on the site.

Occasional cases of contact dermatitis are relatedto sensitivity to rubber or plastic gloves and tobarrier creams. Barrier creams are sub judice as totheir effectiveness. They certainly aid in cleansingthe skin after work. They are not entirely uselessbut must be limited in protective faculty underconditions of use which tend to remove them orinterrupt the continuous film needed for protection.They do not stop the penetration of sensitisers andare not effective in continuous exposure to oils,cement or wet working conditions.

Conditioning creams with lanoline, soft paraffinor oil/water emulsions are helpful in maintainingthe keratin integrity to water content and water/oilemulsion creams such as Ung.Aquosum maybenefit the person whose hands tend to chap in thewinter or those with patchy eczema in atopic orichthyotic skins.

REFERENCES

BAER, R. L., and LEIDER, M. (1949): Effects of FeedingCertified Food Azodyes in Paraphenylenedi-amine-hypersensitive Subjects, J. invest. Derm., 13, 223.

BETTLEY, F. Ray (1965): Diagnosis of IndustrialDermatitis, Brit. med. J., ii, 1340.

BOURNE, L. B. (1960): Industrial Health and Welfare,Med. Press, 244, 186.

BUCKLEY, W. R. (1963): Localized Argyria, Arch. Derm.,88, 531.

BURBACH, J. P. E. (1964): In: Progress in the BiologicalSciences in Relation to Dermatology -2. Edited byA. Rook and R. H. Champion. pp. 443-450. London:Cambridge Univ. Press.

FREGERT, S., and RORSMAN, H. (1964): Allergy toTrivalent Chromium, Arch. Derm., 90, 4.

FROST, J., and HJORTH, N. (1959): Contact Dermatitisfrom Hydrazine Hydrochloride in Soldering Flux.Cross Sensitization to Apresoline and Isoniazid.Acta derm-venereol. (Stockh.), 39, 82.

HELLIER, F. F. (1958): The Prognosis in IndustrialDermatitis, Brit. med. J., i, 196.

HJORTH, N. (1961): Eczematous Allergy to Balsams,Acta derm-venereol. (Stockh.), 41, Suppl. 46.

MARCUSSEN, P. V. (1960): Ecological Considerations onNickel Dermatitis, Brit. J. industr. Med., 17, 65.

MAYER, R. L. (1928): Die Uberempfindlichkeit gegenKorper von Chinonstruktur, Arch. Derm. Syph.(Berl.), 156, 331.

MITCHELL, J. C. (1965): Allergy to Lichens, Arch. Derm.,92, 142.

MORRIs, G. E. (1960): Nylon Dermatitis, New Erngl. J.Med., 263, 30.

NAYLOR, P. F. D. (1955): Experimental Friction Blisters,Brit. J. Derm., 67, 327.

PASCHOUD, J. M. (1963): Quelques Cas d'Eczema deContact avec Sensibilisation de Groupe, Dermatologica.(Basel), 127, 349.

ROOK, A. (1961): Plant Dermatitis. The Significance ofVariety-Specific Sensitization, Brit. J. Derm., 73, 283.

RUBIN, L. (1949): Hyperkeratosis in Response toMechanical Irritation, J. invest. Derm., 13, 313.

SKOG, E. (1965): Sensitization to p-Phenylenediamine,Arch. Derm., 92, 276.

SUSKIND, R. R., and WHITEHOUSE, H. S. (1963): TheHousewife and Her Exposure to Washing Products,Arch. Derm., 88, 130.

SZAKALL, A. (1955): Uber die Eigenschaften, Herkunftund Physiologischen Funktionen der die H-Ionen-konzentration Bestimmenden Wirkstoffe in derVerhornten Epidermis, Arch. klin. exp. Derm., 201,331.

THOMSON, S. (1958): Some Aspects of Industrial Derma-titis, Brit. med. J., i, 1135.

VICKERS, H. R. (1958): Dermatitis in the Steel Industry inSheffield, Brit. med. J., i, 199.

WILSON, H. T. H. (1960): Rubber-Glove Dermatitis, Brit.med. J., ii, 21.