Contact dermatitis: irritant vs allergic — the AU general practice approach

What contact dermatitis actually is

Contact dermatitis is inflammation of the skin caused by direct contact with a substance, rather than from within the body. It is one of the most common skin conditions seen in Australian general practice and the leading cause of occupational skin disease.

The condition divides into two mechanistically distinct forms. Irritant contact dermatitis (ICD) accounts for roughly 80% of cases. It is not an allergy — it results from direct physical or chemical damage to the skin barrier through repeated or sustained exposure to irritants: water, soaps, detergents, solvents, friction, acids, or alkalis. Any person exposed sufficiently will develop ICD; it is threshold-dependent, not immune-dependent.

Allergic contact dermatitis (ACD) accounts for the remaining ~20%. It is a type IV (delayed) hypersensitivity reaction: the immune system has become specifically sensitised to one substance (typically during 10–14 days of first sustained exposure), and on later re-exposure, a delayed inflammatory response develops 24–72 hours after contact. Common Australian allergens include nickel (the most prevalent — found in jewellery, watch clasps, buckles, and fasteners), fragrance mix, methylisothiazolinone (MI/MCI) preservative, paraphenylenediamine (PPD, black hair dye), rubber accelerators (thiurams, carbamates), neomycin, and lanolin. The Australasian Society for Contact Dermatitis Research (ASCDR) maintains the Australian Baseline Allergen Series used for patch testing.

A third variant — photocontact dermatitis — occurs when a substance on the skin reacts with UV radiation: either phototoxic (no immune memory needed, citrus and fig juice are typical causes) or photoallergic (immune-mediated, rare).

A. Core clinical — the AU general-practice framework

History

eTG and ASCIA stress that the history is the key to diagnosis. Core questions:

• Distribution — does the pattern match a likely contactant? Earlobe or umbilicus rash: nickel (earrings, belt buckle). Eyelid rash: cosmetics, nail polish (finger-to-eye transfer), preservatives. Hand dermatitis: occupational. Foot rash: shoe leather or rubber. Scalp and forehead: hair dye. Linear streaks on exposed skin: plant sap (phytophotodermatitis from citrus, fig, or grevillea).
• Timing — immediate onset (minutes–hours) suggests irritant exposure; 24–72 hour delay suggests ACD. Acute vs chronic pattern.
• Occupational history — specific duties, products handled, wet-work hours, soap and sanitiser frequency, glove type and compliance.
• Personal care products — recent introductions of new cosmetics, fragrances, sunscreens, or topical medicines.
• Jewellery and piercings — metal type, new pieces.
• Plants — gardening, native Australian plants, limes or fig leaves combined with sun exposure.
• Atopic history — atopic dermatitis predisposes to irritant contact dermatitis; the two commonly coexist.

Examination

Distribution is often diagnostic. Examine for:

• Morphology: acute phase — erythema, vesicles, oozing, oedema; subacute — crusting, scaling, excoriation; chronic — lichenification, fissuring, hyperpigmentation.
• Geometric or linear patterns (plant contact, clothing friction) vs diffuse involvement (systemic contact dermatitis).
• Secondary infection signs: warmth, honey-coloured crusting, spreading erythema.

Investigations

Most cases are diagnosed clinically. Selective investigations:

• Skin swab — where secondary bacterial infection is suspected.
• Skin scraping and fungal culture — where tinea manus or tinea pedis is in the differential (annular, scaling, asymmetric pattern).
• Patch testing — gold standard for ACD; performed by a dermatologist with ASCDR training. The Australian Baseline Series covers the most common local allergens. Readings at 48 and 96 hours. Stop potent topical corticosteroids one week before patch testing. Referral is appropriate for: refractory, recurring, or occupational contact dermatitis with unclear cause; suspected ACD where avoidance of the allergen will meaningfully change management.
• Skin biopsy — when the diagnosis is in doubt and cutaneous T-cell lymphoma, drug eruption, or autoimmune dermatosis needs exclusion.

Differential diagnoses

Atopic dermatitis (flexural, pruritic, atopic family history), psoriasis (well-demarcated, silvery scale), tinea (asymmetric, annular, positive scraping), nummular eczema, scabies (nocturnal itch, family members affected), seborrhoeic dermatitis (greasy scale, sebaceous areas), Stevens–Johnson syndrome / toxic epidermal necrolysis (mucosal involvement, systemic features — emergency), and drug eruption (medication timeline).

B. Evidence — what determines management in irritant versus allergic contact dermatitis

Trigger removal is the most important intervention

eTG, ASCIA, and ASCDR all emphasise this: removing or reducing the trigger contact is the foundation of management. Without it, topical treatments provide temporary relief but do not resolve the problem. For ACD, identifying the specific allergen through patch testing and then providing a written allergen-avoidance list (including product alternatives) is the most durable intervention.

For ICD, the same principle applies: reducing wet-work hours, using soap substitutes (QV wash, Cetaphil, Aveeno), wearing cotton-liner gloves inside PVC for prolonged wet contact, and applying a protective emollient before and after work exposures.

Topical corticosteroids — site-matched potency

Per eTG and AMH, potency should match the body site and severity:

Site	Appropriate potency	Examples
Face, eyelids, skin folds	Mild	Hydrocortisone 1%
Body, limbs (short course)	Moderate to potent	Methylprednisolone aceponate 0.1% (Advantan), betamethasone valerate 0.02–0.1%
Palms, soles (short course)	Potent to very potent	Mometasone 0.1%, clobetasol 0.05%

Using potent corticosteroids on the face risks skin atrophy, telangiectasia, and perioral dermatitis. For chronic facial or skin-fold dermatitis, topical calcineurin inhibitors — pimecrolimus 1% or tacrolimus 0.1% — are effective steroid-sparing alternatives per AMH and ASCIA.

Emollients — the underused foundation

Liberal, regular use of fragrance-free, preservative-free emollients is central to barrier repair in both ICD and ACD. eTG recommends emollients multiple times daily as the backbone of chronic contact dermatitis management, supplementing rather than replacing trigger avoidance.

Systemic corticosteroids for severe acute ACD

For widespread or severe acute ACD — from contact with plants, industrial allergens, or hair dye — a short course of oral prednisolone (0.5–1 mg/kg/day, tapered over 2–3 weeks) provides symptomatic relief and reduces risk of rebound. Per eTG, abrupt cessation risks rebound flare; the taper is important.

C. Treatment hierarchy

Step 1 — Identify and reduce or remove the trigger

Diary of exposures, review of personal care products, occupational assessment. Patch testing referral for ACD where the cause is unclear or management will change based on the result.

Step 2 — Emollient and soap-free wash

Multiple daily applications of a fragrance-free, paraben-free emollient to clean, slightly damp skin. Replace soap with soap-free wash alternatives. This applies to all types and severities.

Step 3 — Site-matched topical corticosteroid

Short-to-medium course appropriate to the affected site and severity. Continuous long-term use of potent agents on the face or skin folds is not appropriate.

Step 4 — Barrier protection for ongoing exposure

Cotton-liner gloves under nitrile or PVC for wet work; latex avoidance if latex allergy suspected or confirmed. Pre-work moisturiser (not between glove layers). Regular hand-care routine per the Cleanse–Care–Protect framework endorsed by occupational dermatology.

Step 5 — Treat secondary infection if present

Oral cephalexin or flucloxacillin for clinically infected contact dermatitis. Topical mupirocin for limited impetiginisation, per eTG.

Step 6 — Specialist pathways for refractory or severe disease

Chronic, refractory, or severe hand or body dermatitis unresponsive to steps 1–5 warrants dermatology referral for: patch testing, phototherapy (NB-UVB or hand-bath PUVA), or systemic agents (methotrexate, ciclosporin, azathioprine, alitretinoin for chronic hand eczema). Dupilumab remains off-label for ACD in Australia as of mid-2026 — not PBS-funded for this indication.

D. Australian operations

MBS items

Standard consultations (MBS 23, 36, 44) cover the assessment. Skin swab (MBS 69300) for secondary infection. Skin biopsy (specialist MBS 30071 range) when diagnosis is uncertain. GPCCMP (MBS 965/967) is appropriate for chronic, occupational, or comorbid contact dermatitis where a management plan and allied health referrals (occupational therapist, psychologist) are clinically indicated.

PBS prescribing

Topical corticosteroids (hydrocortisone, betamethasone, mometasone, methylprednisolone aceponate, clobetasol) are on the general PBS schedule. Topical calcineurin inhibitors (pimecrolimus, tacrolimus) require Authority — PBS listing is for atopic dermatitis; use in contact dermatitis is off-label. Oral prednisolone, cephalexin, and flucloxacillin are on the general schedule. Methotrexate, ciclosporin, and azathioprine require Authority for specific dermatological indications; use in ACD is off-label, specialist-initiated.

Alitretinoin (Toctino) has limited TGA and PBS availability for severe chronic hand eczema in adults — specialist-initiated, requires pregnancy exclusion (Category X).

Occupational contact dermatitis and workers’ compensation

Safe Work Australia data confirm skin disease is among the most prevalent categories of compensable occupational injury. When the cause is occupational:

• Document: occupation, specific products handled, wet-work hours, duration of exposure, timeline, examination findings, and photographs
• Refer for patch testing with the Australian Baseline Series ± occupational-specific panels
• Write a workplace modification certificate (reduced wet work, alternative glove or cleaning product, rest breaks)
• Assist with a workers’ compensation claim under the relevant state or territory legislation
• Consider referral to occupational rehabilitation if career change may be necessary for severe cases

ASCIA and ASCDR patient resources

ASCIA provides patient education resources on allergen avoidance by category. ASCDR lists practitioners with contact dermatitis patch-testing expertise in Australia.

E. Special populations

Occupational groups at highest risk

Healthcare workers, hairdressers, food handlers, cleaners, and construction workers have the highest burden of occupational contact dermatitis in Australia. Early recognition and occupational review prevent progression to chronic, treatment-refractory disease. Hairdressers in particular face high rates of nickel, PPD (hair dye), and ammonium persulfate sensitisation; career-affecting ACD is a recognised occupational injury.

Nickel sensitisation in young people

Nickel is the most prevalent sensitiser in Australia, affecting approximately 5–10% of adults, with higher rates in women due to jewellery and piercing exposure. Sensitisation commonly begins in adolescence with ear or body piercings. Counselling about nickel-free jewellery (surgical steel, titanium, gold ≥18 carat) at the time of sensitisation reduces ongoing elicitation. Children with recurring earlobe rashes from earrings are likely sensitised; switching to nickel-free pieces is the management.

Atopic dermatitis as a predisposing factor

Atopic dermatitis impairs the skin barrier (reduced filaggrin), significantly predisposing to ICD. In patients with concurrent atopic and contact dermatitis — a common combination in hand dermatitis — both conditions need to be addressed. Patch testing helps distinguish which component is allergic. Management addresses both the atopic baseline (see the separate article on atopic dermatitis) and the contact triggers.

Pregnancy

Topical corticosteroids are generally safe in pregnancy for limited area and duration; potent formulations over large body surface areas in the first trimester are approached with caution. Calcineurin inhibitors have limited pregnancy safety data; large-area use is avoided. Patch testing in pregnancy is generally deferred — the stress of provocating a reaction and the limitations of subsequently managing a new allergen identification are reasons for delay, per eTG.

Photocontact dermatitis and Australian outdoor exposures

Australia’s high UV intensity amplifies the risk of phytophotodermatitis. Common sources: citrus fruit handling (particularly lime and lemon juice) followed by sun exposure, fig leaf contact, and some grevillea species. The rash appears where plant juice was on the skin during sun exposure — often drip or streak patterns on hands and forearms — delayed 24–72 hours. Strict sun protection and topical corticosteroids manage the acute phase; hyperpigmentation may persist for months.

When to escalate

Urgent or emergency referral:

• Fever, mucosal involvement, blistering, or widespread skin loss — Stevens–Johnson syndrome / toxic epidermal necrolysis; call emergency services or attend ED immediately
• Erythroderma (>90% body surface area involvement) — systemic instability risk; admit
• Severe systemic reaction — urticaria plus angio-oedema, bronchospasm (rare from contact alone, more typical of protein contact urticaria from latex or food)

Same-week dermatology referral:

• Severe acute ACD not responding within a few days to topical treatment
• Suspected severe drug-induced dermatitis (DRESS, SJS/TEN differential)
• Occupational dermatitis with significant functional impact

Routine outpatient dermatology referral:

• Refractory, recurring, or occupational ACD requiring patch testing
• Chronic hand or body dermatitis unresponsive to 4–8 weeks of adequate topical management
• Eyelid or facial dermatitis where allergen identification is important before further treatment

What this article is and is not

This article draws on current Australian dermatology guidelines — Therapeutic Guidelines (eTG), ASCIA, ASCDR, Australasian College of Dermatologists, AMH, and Safe Work Australia. It is general health information, not personal medical advice, and does not create a doctor–patient relationship. Treatment decisions — including choice of corticosteroid formulation, need for patch testing, and systemic agents — are made with your GP and treating dermatologist based on individual clinical circumstances.

Australian consumer resources: HealthDirect — Contact dermatitis, Better Health Channel — Contact dermatitis, ASCIA, ASCDR.

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Sources cited

1. Therapeutic Guidelines — Contact dermatitis
2. ASCIA — Contact dermatitis
3. Australasian Society for Contact Dermatitis Research (ASCDR)
4. Australasian College of Dermatologists
5. AMH — Topical corticosteroids
6. Safe Work Australia — Skin diseases
7. HealthDirect — Contact dermatitis
8. Better Health Channel — Contact dermatitis