Airborne Contact Dermatitis (Ragweed Dermatitis; Dermatitis due to other chemical products – acids, alkalis, dichromate, insecticide, plastic, rubber, nylon; Dermatitis due to food in contact with the skin, eg, flour; Dermatitis due to paint, other solvents)

Are You Confident of the Diagnosis?

Airborne contact dermatitis is defined based on four criteria. These include the presence of environmental dust, droplets, or other volatile chemicals, clinical symptoms, the patient’s course and history, and results of epicutaneous testing. Airborne chemicals that contact the skin can result in either allergic or irritant dermatitis.

  • What to be alert for in the history

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Most reports of airborne contact dermatitis are occupational in nature. These patients will often begin to develop symptoms weeks or months after a new occupation or new exposure. Symptoms may initially develop on the eyelids. When plants are the responsible allergen patients may notice seasonal exacerbations (starting in the summer and ending in late autumn). New exposures in the workplace can be correlated to onset of the dermatitis. Suspicion for contact dermatitis should be higher if there is a lack of response to topical therapy.

  • Characteristic findings on physical examination

On physical examination, airborne allergic contact dermatitis (ACD) involves the face, V of neck, and forearms (Figure 1). Typical areas of involvement are the eyelids and Wilkinson’s triangle (behind the ears). Prolonged exposure can result in a dry lichenified appearance.

Figure 1.

Dermatitis resulting from airborne contact to fragrance mist.

A common cause of airborne allergic contact dermatitis stems from exposure to plants. This is known as ragweed dermatitis, which is in the Compositae family. The monoterpene lactones and the sesquiterpene lactones are thought to be responsible for Compositae allergy. Parthenium dermatitis is the most common form of airborne dermatitis in India. The plant is feverfew and also in the Compositae family.

Other potential airborne allergens include natural resins, woods, plastics (synthetic resins), rubbers, glues, metals, industrial and pharmaceutical chemicals, insecticides, pesticides, animal feed additives, herbicides, fungicides and miscellaneous allergens. Among the most common non-plant derived causes of airborne allergic contact dermatitis are components of epoxy resin systems, methylchloroisothiazolinone/methylisothiazolinone which is a preservative. Common causes of irritant airborne dermatitis arise from exposure to dust that contains fiberglass, asbestos, stone particles, cement (also potential allergen), and sawdust.

Irritant airborne reactions are typically accentuated around the collar line, belt line, or sleeve line. A lichenified eruption can be seen on the penis from when dust falls inside the clothes.

  • Expected results of diagnostic studies

Histopathology would be expected to show spongiosis and acanthosis of the epidermis and is most useful for excluding other potential causes including lymphoma, psoriasis, and tinea. Allergic airborne reactions can be diagnosed by means of epicutaneous patch testing. An initial screening series such as the TRUE test can be performed by most dermatologists. Additional patch test series to consider might include the following: plant series, plastic and glues, medicaments, rubber chemicals, bakery chemicals and acrylates.

  • Diagnosis confirmation

Photoallergic contact dermatitis, photoirritant contact dermatitis, phototoxicity and photoallergy to systemic medications can closely resemble airborne contact dermatitis. These reactions tend to be exacerbated by sunlight and often spare photoprotected areas, including the postauricular, submental, skin beneath the lower lips, above the eyelid, and nasolabial folds. These are areas where airborne contact dermatitis is often accentuated.

Other diagnostic considerations include adult atopic dermatitis (look for other features including personal or family history of atopy), mycosis fungoides (leonine facies and requires histologic confirmation). In diagnosing airborne ACD it is important to perform a careful history and exclude any potential topical or systemic photosensitizers. There should be a low threshold for patch testing.

Who is at Risk for Developing this Disease?

Outdoor workers are at greatest risk for photoallergic contact dermatitis including farmers, gardeners, and outdoor construction workers. Other high-risk professions include florists, industrial workers, and pharmaceutical workers. Those at risk for irritant airborne contact dermatitis include construction workers and wood workers, as they are often exposed to fiberglass and other forms of particulate dust.

What is the Cause of the Disease?

  • Etiology

Airborne contact dermatitis occurs when a volatilized or aerosolized chemical contacts the skin and behaves as an allergen or irritant. Some individuals in the population are genetically susceptible to airborne ACD. All individuals in the population are subjected to irritation at varying thresholds.

  • Pathophysiology

Airborne ACD is a classic delayed type hypersensitivity or a type IV immunologic reaction. It is immune mediated rather than antibody mediated. The airborne allergen or hapten initially sensitizes the skin and creates memory lymphocytes. The small chemical molecules responsible for allergic contact dermatitis must bind to antigen presenting cells or Langerhans cells, which are situated within the suprabasilar layer of the epidermis. Langerhans cells interact with CD4+(helper) T cells leading to the inflammatory response.

Irritant contact dermatitis is a nonspecific response of the skin to direct chemical damage that releases mediators of inflammation predominately from epidermal cells.

Filaggrin barrier defects that predispose individuals to atopic dermatitis might also predispose them to allergic contact dermatitis by allowing greater penetration of chemical haptens. Initial sensitization requires 10 to 14 days.

Systemic Implications and Complications

Some of the airborne allergens through different immunologic pathways may be asociated with respiratory symptoms including bronchospasm. Additional history taking might focus on this symptomatology.

Treatment Options

Treatment options are summarized in Table I.

Table I.
Medical Treatment Physical Modalities
Topical corticosteroids Avoidance protocols
Topical calcineurin inhibitors Tacrolimus Pimecrolimus Narrowband (short wavelength) UVB
Psoralen photochemotherapy (PUVA)
Systemic corticosteroids
Mycophenolate mofetil (MMF)

Optimal Therapeutic Approach for this Disease

The treatment of airborne contact dermatitis lies chiefly in the avoidance of the offending agent. In certain circumstances (eg, outdoor plant allergens), avoidance protocols cannot be achieved, and therapy is rendered to reduce the inflammatory component and its consequent objective and subjective findings.

Discuss with the patient the importance of removing the provocative agent. In cases of airborne ACD stress only, minute amounts of allergen are required for a reaction to occur. This may require a careful and detailed history of all potential exposures both at home and in the workplace.

Occupational counseling may be required in cases of occupational exposure. This often requires complete removal from the workplace but at times may be ameliorated by improved ventilation and protective barrier clothing.

Effectiveness of topical steroids in the treatment of airborne allergic contact dermatitis has been well documented. A list of steroids by potency is outlined in Table II.

Table II.
Class Potency Corticosteroid
Class 1 Super potent Clobetasol propionate
Halobetasol proprionate
Class 2 Potent Betamethasone dipropionate
Diflorasone diacetate
Class 3 Upper mid-strength Mometasone furoate
Class 4 Mid-strength Fluocinolone acetonide
Class 5 Lower mid-strength Triamcinolone acetonide
Hydrocortisone butyrate
Class 6 Mild Alclometasone diproprionate
Class 7 Least potent Hydrocortisone

Topical calcineurin inhibitors, while approved for atopic dermatitis, can be used to treat airborne ACD. Topical 0.1% tacrolimus has the advantage of being a steroid-free agent. While the onset of action can be slow, it has demonstrated efficacy in reducing the inflammatory manifestations of nickel contact dermatitis. The disadvantage is the initial stinging and burning associated with the use of this agent. Topical pimecrolimus has the advantage of better tolerance but is less potent than topical tacrolimus. Consider combination therapy using topical calcineurin inhibitors on the weekdays and topical steroids in a pulsed fashion on the weekends.

Oral corticosteroids are a mainstay in the acute phase of the dermatitis. Similar to other causes of acute contact dermatitis patients typically require at least a 2-week course to prevent a rebound phenomenon. Most adults require an initial dosage of 40-60mg per day.

Antihistamines can be used for their antipruritic effect. Generally more soporific antihistamines are required, including hydroxyzine, diphenhydramine, and doxepin (tricyclic).

Phototherapy has been reserved generally for patients with refractory ACD that is unresponsive to topical or oral corticosteroids or for patients who cannot avoid all provoking factors in their daily environment. Narrowband UVB is more convenient for the patient and associated with fewer side effects than psoralen plus ultraviolet A (PUVA) . PUVA can be considered in more refractory cases.

Systemic immunomodulators can be considered when avoidance is not obtainable. Generally this pertains to cases of airborne ACD from naturally occurring outdoor ubiquitous plants. Most of the evidence stems from case reports and small case series and is more anecdotal in nature.

MMF is appealing due to somewhat lower toxicities. Similar to treatment of adult atopic dermatitis, typical adults can be started on a dosage of 1 gram twice a day with adjustments made according to response. In persistent and severe instances cyclosporine may have more reliability. Patients from India with parthenium dermatitis have been adequately managed with azathioprine and methotrexate.

Patient Management

Explain the pathogenesis to the patient. Other than outdoor ubiquitous plants, emphasize that the best prognosis lies with complete avoidance.

In cases of Compositae induced airborne ACD, handle patients as you would any chronic disease. Therapy needs to be balanced against any potential risk. If exacerbations are seasonal, therapy can be episodic. It may be possible to take a break from therapy during the winter months in cooler climates.

Unusual Clinical Scenarios to Consider in Patient Management

Airborne contact dermatitis can be more difficult to diagnose when superimposed on other dermatoses. There was a case of a farmer with multiple allergens responsible for his airborne ACD. He presented with features of rosacea due to years of treatment with topical steroids. Because of this he had difficulty qualifying for worker’s compensation.

It is important to correctly link responsible occupational airborne allergens to the dermatitis. Failure to do so may disqualify a worker from deserved compensation claims.

What is the Evidence?

Santos, R, Goossens, A. “An update on airborne contact dermatitis: 2001–2006”. Contact Dermatitis. vol. 57. 2007. pp. 353-60. (A comprehensive review of the common allergens responsible for airborne dermatitis.)

Paulsen, E, Christensen, LP, Andersen, KE. “Compositae dermatitis from airborne parthenolide”. Br J Dermatol. vol. 156. 2007. pp. 510-15. (A study of 12 patients with feverfew dermatitis from Europe. Through use of chromatography, the responsible allergen was shown to be parthenolide, which is a sesquiterpene lactone.)

Kanerva, L, Jolanki, R, Estlander, T. “Airborne occupational allergic contact dermatitis from triglycidyl-p-aminophenol and tetraglycidyl-4,4’-methylene dianiline in preimpregnated epoxy products in the aircraft industry”. Dermatology. vol. 201. 2000. pp. 29-33. (This a well-documented case report demonstrating airborne allergy to epoxy in an aircraft assembler. Epoxy is a more commonly reported cause of occupational airborne ACD.)

Cohen, DE, Heidary, N. “Treatment of irritant and allergic contact dermatitis”. Dermatol Ther. vol. 17. 2004. pp. 334-40. (This review summarizes both standard and more innovative treatment options for allergic contact dermatitis.)

Ponyai, G, Hidvegi, B, Nemeth, I, Temesvari, E, Karpati, S. “Contact and aeroallergens in adult atopic dermatitis”. J Eur Acad Dermatol Venerol. vol. 22. 2008. pp. 1346-55. (This study of 34 patients found that aeroallergens played a significant role in exacerbating adult atopic dermatitis.)

Spiewak, R, Dutkiewicz, J. “A farmer’s occupational airborne dermatitis masqueraded by coexisting rosacea: delayed diagnosis and legal acknowledgement”. Ann Agric Environ Med. vol. 11. 2004. pp. 329-33.

Dekoven, JG, Yu, AM. “Occupational airborne contact dermatitis from proton pump inhibitors”. Dermatitis. vol. 26. 2015. pp. 287-90.

Breuer, K, Uter, W, Geier, J. “Epidemiological data on airborne contact dermatitis-results of the IVDK”. Contact Dermatitis. vol. 73. 2015. pp. 239-47. (A rare case of airborne occupational dermatitis in a farmer that presented as rosacea due to treatment. The diagnostic confusion interfered with the ability to qualify for worker’s compensation.)