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Skin Sensitization - Contact Dermatitis and Contact Urticaria

General Principles Of Contact Dermatitis


Why are we interested in the skin’s reaction to foreign chemicals? Perhaps because many of us have had blisters from poison ivy, rashes from nickel in metal items like earrings or necklaces, or eczematous reactions to other everyday objects. A friend comes to visit one evening with a red rash around her eyes; she has been diving in the Caribbean and reacted to the foreign-purchased black rubber goggles. A child comes to his mother crying that his feet are sore; they have reacted to the rubber in his sneakers. And a dental student has a serious life-threatening allergic reaction when donning latex gloves. These represent some common types of allergic contact hypersensitivity reactions.

This course is a survey of the mechanisms, detection, and causes of contact dermatitis. Understanding any individual case may require extensive literature search, physical examination and patch testing of the patient, and study of the product ingredients. There are many individual variations in sensitivity, due to genetic differences.

What is Allergic Hypersensitivity?

Allergic contact dermatitis (ACD) is synonymous with “eczema”, a term derived from the Greek word meaning “boiling out”. It is characterized by redness, oozing, crusting, weeping, and chronic scaling. Contact dermatitis occurs when the skin or mucous membrane meets foreign chemicals. Contact dermatitis may be allergic (due to different mechanisms) or irritant; it is important to distinguish between the two to know what to avoid.

Allergic skin sensitization is due to special mechanisms of the immune system and is found in genetically susceptible persons. An allergic skin reaction requires re-exposure or continuous exposure to the allergen, the substance causing the allergy. The first exposure “sensitizes” the person and the later exposure “elicits” the reaction. The hypersensitivity to an allergen can be immediate (Type I) – a sometimes-hazardous response that occurs within minutes to an hour of contact with the allergen – or delayed (Type IV), appearing at 24-72 hrs.

Immediate (Type I) Reactions versus Allergic Contact Dermatitis (Type IV)

Allergic Contact Dermatitis (ACD) usually is due to delayed hypersensitivity, which has a mechanism something like a tuberculin skin test. Most contact allergens are small, simple, lipophilic chemicals like nickel; these haptens must combine with a skin protein before becoming allergenic. The allergenic chemical (called an antigen) penetrates the skin, reaching the living cells below. Antigen-presenting cells such as Langerhans Cells present the chemical to special sets of genetically pre-programmed T-lymphocyte cells that recognize the chemical. The complex goes into draining lymph nodes and circulates in the body. More T-cells become sensitized. Thus, the contact dermatitis can spread from the primary contact site to distant parts of the body not in direct contact with the allergen. ACD susceptibility varies with the allergen, e.g., almost everyone can become sensitive to poison ivy, but most contact allergens affect fewer than 1% of the population.

The immediate (Type I) allergic reaction occurs through a different mechanism from delayed hypersensitivity. In this reaction a certain serum antibody, immunoglobulin E, is produced by the B lymphocytes, and pharmacological mediators like histamine are released from special cells known as mast cells.

Skin contact with antigens like latex protein or potatoes can cause the immediate skin condition called contact urticaria – characterized by hives, itching, tingling, burning, and an immediate “wheal and flare” skin reaction (having a raised area and redness). Sometimes tiny vesicles appear, and sometimes it is followed by eczema. The reaction may disseminate to become a generalized urticaria. Common allergens causing urticaria by contact are found in medicines, foods such as flour, cosmetics, and industrial chemicals. Exposure to allergens systemically (by eating certain foods or injection) may also cause urticaria. Raw fruits and vegetables may elicit reactions in the mouth, lips, and tongue, and throat hoarseness or irritation may occur.

Urticaria may be mediated immunologically, nonimmunologically, or through unknown mechanisms. Nonimmunological contact reactions occur without previous sensitization. Among the causes of nonimmunological reactions are cinnamic aldehyde (found in spices, flavors, and perfumes), benzoic acid and other preservatives. Acetylsalicylic acid or NSAIDS inhibits the reaction. Diagnosis is usually based on an open epicutaneous test. If negative, a prick test (antigen applied by puncture through the palm side of the forearm skin) or scratch test (antigen applied through a scratch in the skin) may be used. This identification is important for avoidance, since treatment is only palliative.

In the contact urticaria syndrome, immunologically-mediated systemic effects can appear in other organs, especially in atopic individuals (with a history of allergy). An additional immediate response is the severe body reaction known as anaphylaxis (a shock or drop in blood pressure). Anaphylaxis may occur in conjunction with urticaria, as with the serious allergic reactions to latex products. Other important immediate reactions may include rhinitis, bronchitis, and asthma. Certain people (atopics) have a family history of immediate allergy and are more prone to get Type I reactions; they constitute about 25% of the population.

The table below summarizes the classic types of hypersensitivity reactions that are involved in allergy. One chemical may elicit both immediate and delayed types of reactions.

Table I: Types of Hypersensitivity Rections

Although allergic contact dermatitis is generally due to direct contact, the allergen can be transmitted through the air, as with dust, pollen, pesticides, or aerosols. Contact dermatitis can spread systemically from the primary contact site to distant parts of the body not in direct contact with the allergen.

In true respiratory hypersensitivity, characteristic changes occur in lung function tests; this does not usually occur with lung irritation and ill-defined conditions, such as sick building syndrome and multiple chemical sensitivity.

Allergy versus Irritation

Contact dermatitis can be caused by allergy or irritation; sometimes the same compound may cause both. Harvell et al (1995) indicate that nonimmunological reactions occur in about 70% of occupational dermatitis patients and in about 10% of patients coming to a skin clinic.

Irritant reactions are now considered to be complex processes, with a clinical appearance depending on multiple external and internal factors. Irritation does not require prior exposure and may occur on acute exposure, immediately, or after a delay. Lammintausta and Maibach (1990) classify irritant reactions as follows:

The prognosis is good on the first three types but variable on the remainder. Acute irritant contact dermatitis often results from accidental exposure. Recovery may take about four weeks. Repeated Irritant reactions, common in persons exposed to water, may lead to contact dermatitis. Delayed onset acute irritant contact dermatitis is easily confused with allergic contact dermatitis; they can be distinguished by patch tests. The common cumulative irritant dermatitis lasts for long periods and may become chronic. The frequency of exposure is too high in relation to skin recovery time. Traumatic irritant dermatitis has a prolonged healing time and the skin may not completely heal. Pustular and acneiform irritant dermatitis usually develops from exposure to metals, oils and greases, tar, asphalt, and certain chemicals.

Identification of risk groups is important in occupations with exposure to irritants, since work-related contact dermatitis is common. Many authors feel that persons with severe atopic dermatitis or a family history of respiratory atopy are especially prone to irritant contact dermatitis. In general, persons with prior skin disease are considered to be especially susceptible. Reactions to individual irritants may vary according to genetic differences. In some cases, the skin may become hardened to exposures.

Skin irritation has many pathologic appearances, depending on the causes. Among the many external factors influencing irritant reactions are mechanical causes such as occlusion, friction, pressure (calluses and blisters, reactions of violin players to wood at the collar, football players to pads). Continuous exposure in wet work causes redness and chapping (shampooers, house cleaners, food preparers, nurses, surgeons). Other factors include: sweating, temperature, occlusion, airborne irritation, and multiple chemical exposures.

Chemicals usually require a high exposing dose to cause irritation, but physical properties, vehicle, and corrosiveness may be important. Information on material Safety Data Sheets and results of animal tests may be important in avoiding workplace irritants. Exposure to multiple chemicals may have an additive effect. Some common irritants are:



soaps, detergents, and fabric conditioners

bleaches and disinfectants




foods – raw meat and fish, citrus and tomatoes

Irritation reactions first occur in the region of the body with the greatest exposure (e.g., the hand and fingers, areas with clothing contact, areas exposed to airborne allergens). Increased reactivity may occur in small children and decreased reactivity with age. It is uncertain whether irritation reactions are affected by race or gender.

The management of irritation reactions is by identifying the etiological agent and preventing recurrences, by avoiding harsh soaps and too frequent washing, and by using protective garments, lubrication, and topical corticosteroids when recommended by the specialist.

In contrast, eczematous reactions may be more delayed after exposure, have more itching and vesicles, and be more affected by the region of the body (e.g., thin eyelids) and preexisting skin disease.

Photoreactivity: Allergic or Irritant

Photoallergic contact dematitis reactions require light and certain chemicals that absorb visible or ultraviolet radiation, producing an allergenic molecule in sensitized individuals. Photoallergic dermatitis resembles other allergic delayed eczematous reactions in appearance. Causes include sunscreen compounds such as para-aminobenzoic acid (PABA), antibacterial agents such as hexachlorophene, therapeutic agents such as chlorpromazine or diphenhydramine, and other types of compounds such as thiourea.

Phototoxic (Photoirritant) dermatitis is a chemically-induced nonimmunological skin irritation reaction requiring light at certain wave lengths. More frequent than photosensitive reactions, they occur on first exposure, and are dose dependent. Agents include coal tar derivatives used in skin disease; certain drugs such as sulfonamide, dyes, and psoralens; and citrus and other plants. To prevent photoreactive dermatitis, avoid the responsible chemicals.

Predictive and Threshold Studies Predictive animal studies:

When a new product is developed, standard tests may be used to assess the allergenicity and toxicity of new components. Often these tests are performed in guinea pigs, but other species may be used. Large companies manufacturing potentially allergenic products may use human volunteers for screening. Attempts to develop in vitro predictive tests for allergenicity and irritation have not been especially successful. Predictive tests are described by Marzulli and Maibach (1996.)

Threshold studies

Some experimental studies have been performed to attempt to quantify the allergenic threshold of reaction to a given chemical. Theoretically, knowledge of the threshold would permit products to use a small quantity of a chemical without sensitizing or eliciting reactions. (See Emmett et al, 1994, Flyvhom, 1997).

Identifying the Cause

Examination and history

Every new case may pose a mystery. The dermatologist must be a detective to identify the cause of the skin reaction so the patient can avoid future exposure. After a physical examination to see the area of complaint and the pattern of the dermatitis, the doctor must make any differential diagnoses. For example, the dermatologist must distinguish allergic contact dermatitis from atopic eczema (a skin condition usually associated with a family history of Type I allergy) and other skin conditions. The doctor must take a thorough history, as illustrated in the texts by Guin (1995), Rycroft, Menne, and Frosch (1995), or Cronin (1980). The patient’s occupational exposures may require examination of product information sheets.

The physical examination and history may identify cause in 10% of the cases. Some items in the history might be:

  • Time of skin outbreak after exposure. May indicate urticaria or irritant reaction.
  • Occupational, domestic, or avocational exposure to common allergens
  • Prior allergies or family history

The patients that the dermatologist cannot diagnose initially probably require patch tests.

Patch Testing and Adverse Reactions

Some agents have been used as a standard patch test series by the American Academy of Dermatology and by European and Japanese groups. These are under review by an international committee (LaChapelle et al, 1997) but have included:



Cinnamic aldehyde

Ethylene diamine dichloride


Neomycin sulfate


Rubber chemicals

Paraphenylene diamine (PPD)

Potassium dichromate

Nickel sulfate

Balsam of Peru

Imidazolidinyl urea (Germall 115)

Quaternium 15

p-tert Butylphenol formaldehyde resin

Mercapto mix, MBT,Thiurams, Carba mix, etc.

Ethylene diamine was once used in Mycolog cream, a popular product for dermatitis therapy. Balsam of Peru is a fragrance from a plant resin, which is used in ointment, perfume, flavor, and hemorrhoid preparations. Colophony (rosin), a product of pine trees, is used on violin bows and to make glossy paper, solder, and compounds from varnish to lipstick. PPD is found in dyes, certain rubber products, and furs. Imidazolidinyl urea and Quaternium 15 represent two preservatives that may release formaldehyde; p-tert-Butylphenol formaldehyde resin is a plastic used as an adhesive; it may cause shoe dermatitis.

Special patch test series are available for certain purposes; e.g., shoe sensitivity, reactions of hairdressers or bakers, facial dermatitis, sensitivity to pharmaceuticals or textiles. Patch test series are available in the United States, Europe, and other countries. Patch testing is described in detail by Bruze (1995) and in a 1993 series in the American Journal of Contact Dermatitis, among others. For information in the U.S. communicate with the North American Contact Dermatitis Society (NACDG) c/o American Academy of Dermatology.

How to perform a patch test:

Patch tests are performed on the upper back. Patches are applied for about 48 hours, using an occluded patch. They must be a sufficient distance apart to avoid the “angry back syndrome” or “excited skin syndrome”, one of the principal causes of false positive results. In this phenomenon, a strong reaction at one location may cause other sites to react. This is especially likely with marginal irritants such as formaldehyde. The test must be performed on nondiseased skin, using non-irritating concentrations of the allergen. Many different techniques are used, but they must be standardized in the dose, the vehicle in which they are dissolved, occlusion method, the time applied, and the time when read. The most used applicators in the U.S. have been the Finn Chamber and Al-test. The thin-layer rapid-use epicutaneous test (TRUE) is being used increasingly. The Van der Bend Chamber is often used in Europe.

The Finn Chamber uses less space than the classic Al-test; it is a filter paper disk on which the allergen is placed and has an aluminum backing. The area is labeled for later reading. The test methods differ in sensitivity and specificity. The limits of the methodology should be clearly understood to interpret results and understand differing results in the literature.

False negative tests may result from use of a nonstandard allergen or poor storage of the allergen, use of topical corticosteroids, poor occlusion, premature removal of the patch, or early readings. Reading the patch test should occur from 48 to 72 hours. The patch test result may be negative due to inability to simulate actual exposure conditions. The patch test results must be found relevant, i.e., the physician must correlate the patch test results with the case history, location of the dermatitis, and known exposures. In vitro tests to replace patch tests have not been found to be practical and are primarily used in research. In vitro tests are being developed to predict irritancy.

Adverse reactions to skin tests for allergy:

Aside from “active sensitization,” a patch test actually causing sensitization, adverse reactions from patch tests are rare. Contact urticaria has occasionally occurred, however, with anaphylaxis.

“Use” Tests and Patient-supplied Products:

Not every sensitivity is detected by standard patch tests or even specialized tests for certain occupations. Patient-supplied allergens may be used, as they may contain additional sensitizers, different combinations of diluents, and relevant contaminants. Tests may be performed by occluded patch, open patch, or usage. The identity of the compounds should be confirmed in the original container and a portion of the sample carefully saved. Special procedures are available for woods, plants, foods, clothing, shoes, gloves and many other products (See Dooms Goosens, 1995).

ACD Differences due to Gender, Age, or Body Location

Differences between sexes reflect exposure:

Gender may affect contact allergy because of exposure differences. Occurrence at various sites may reflect differences in attire between men and women. For example, males may exhibit reactions to keys or belts on the trunk; to boots on the leg, or to a helmet on the scalp. Females may have dermatitis at the sites of nail varnish, bras, jewelry, or stockings.

Specific sensitizers may cause allergic dermatitis in common locations:

The hand is a common site of allergic dermatitis due to domestic or occupational exposures, especially in hairdressers, house cleaners, dentists, florists; kitchen or grocery workers, gloves, nickel or cobalt products.

The scalp is only rarely a site of dermatitis, but it may occur from hair dye, conditioner, caps, or hair clips. Shampoo is usually rinsed rapidly from the head.

The face is a common site of dermatitis; it may result from fragrances, preservatives, hair products, nail polish from the hand, or sunscreen. Near the eye it may be due to cosmetics, applicators, or eyelash curler rubber. On the ear or earlobe, dermatitis may be due to ear piercing or various metals in earrings (even 14 K gold or sterling silver). It also may be caused by putting metal objects in the ear canal.

The trunk may be exposed to allergens from nickel in clothing, zippers and jeans buttons; rubber in undergarments; fragrances in soap and skin care products; formaldehyde resin; and clothing dyes

The thighs, legs, and feet may acquire dermatitis from objects in pockets, stocking dyes, or rubber in shoe constituents. Sometimes contact dermatitis may occur as part of other symptoms or in unusual presentations.

Importance of age:

Is skin sensitivity affected by age? Opinions vary, but certain products are likely to be used by small children and others by the elderly, causing ACD. Allergic contact dermatitis in children is commonly produced by:

  • Poison ivy, oak, and sumac
  • MBT, a rubber chemical in shoes
  • Potassium dichromate in shoes
  • Nickel in ear piercing devices or earrings,identification bands, metal jeans buttons

In the elderly, various medications, salves, and black dyes may cause reactions.

Treatment of Contact Dermatitis

The main principles of treating ACD include avoidance of the causative agent and substitution of other products. For symptoms, treat itching with palliative topical agents. For signs, treat weeping eruptions with drying agents and dry eruptions with emollients. Sweating may be controlled medically or decreased by keeping environmental air at 50% humidity and temperature from 17-22o C (62.6 to 71.6o F).

Avoid all other potential allergens and irritants including lotions, lubricants, and medicated products. Remember the injunction, “Do no additional harm”. Products aggravating dermatitis may be shampoos, soaps, cosmetics, or abrasive cleansers in the house. In addition, the dermatitis may be made worse by rubbing hard with a washcloth, by solvents like nail polish remover, and by bleach, raw meat, and fresh tomatoes. Remove all materials potentially causing the reaction, and test individually by recommencing use slowly.

Treating Acute versus Chronic Illness

Poison ivy is an example of an acute allergic contact dermatitis. To control it, avoidance is the most important factor. Recognize the plant and wear protective clothing. Attempts to use oral desensitization have had only short-term success. Poison ivy has been treated with corticosteroids, cool wet compresses, and anti-itching medication such as calamine.

Chronic allergic contact dermatitis may be caused by almost anything, including compounds used for ACD treatment. The responsible agent should be identified and avoided. Treatment consists of short term corticosteroids. Dermatologists use special treatments, such as UV light, for stubborn cases.

Common Causes Of Allergic Contact Dermatitis

Nickel The prevalence of nickel sensitization in normal individuals is about 10% in this country. Ear piercing is an important risk factor for nickel sensitivity. Traditionally higher in females, its occurrence may change with men having pierced ears today and both sexes increasing the piercing of other body parts. Ear piercing may cause increased reaction to other metals, such as gold and mercury.

Examples of exposure to nickel include:

jewelry, clothing snaps and buttons, coins, keys, buckles, blue jeans buttons (some are nickel-free), scissors, window hardware, eyeglass frames, hooks and garter snaps, identification tages, knitting needles, watch straps, acupuncture needles, nonstainless steel, thimbles.

Nickel sensitization is aggravated in body locations when sweat leaches the nickel out of metal. Similarly, in dental amalgams and prostheses, saliva helps the nickel leach out. It is controversial whether nickel in foods or water can cause sensitization. Nickel may produce either allergic contact dermatitis or urticaria. With contact urticaria from nickel in necklaces not made of sterling silver or a high percent of gold, the neck begins to itch almost immediately and turns red. Nickel may also cause a runny nose and other Type I allergic symptoms. Jewelry can be tested chemically for nickel with a simple spot test kit, the dimethglyoxime test. Some companies make special jewelry for people sensitive to nickel or other metals. Burruss and Fowler (1995) list some of these and products helpful to metal-sensitive individuals.

Chromium Chromium and chromates are important sensitizers. The highest exposures are occupational – from cement, mortar and plaster; thus, chromium allergy has traditionally been more common in men, but this is changing. Most cases of eczema are on the hands and fingers. Some shoe dermatitis is derived from chrome tanned leather. Other common exposures include tanning leather, pigments, corrosion inhibitors, tattoos, photography, inks, and dyes. Additional metals causing contact allergy include: cobalt, gold, palladium, beryllium, platinum, and mercury. There are many occupational exposures. In dentistry, acrylates are responsible for most cases of dermatitis in dentists and patients, but metals causing reactions include nickel, mercury, aluminum, gold, nickel, platinum, palladium, and chromate.

To avoid contact with sensitizing metals:

  • Pierce ears with surgical steel posts
  • Coat jewelry and clothing buttons causing reactions with clear nonsensitizing polish.
  • Make keys of aluminum or other nonsensitizing metals.
  • Test objects with dimethglyoxime
  • If perspiring, change shoes and socks often
  • Wear cotton gloves under leather work gloves
  • Avoid direct contact with cement and construction materials by using face masks and protective clothing.

Formaldehyde Formaldehyde is a ubiquitous chemical, a colorless gas with a characteristic odor. It is present in emissions and in air and water. Exposures include permanent press clothing, plastics, and paper products, which release formaldehyde gas from resins, and cosmetics and other products using small amounts of formaldehyde or preservatives that break down to formaldehyde* There are many occupational exposures. Formalin (formaldehyde dissolved in water) is found in biology labs and mortuaries. The solid paraformaldehyde is used as pesticide, moth repellent, and fumigant. Formaldehyde releasers are found in preservatives that are used in cosmetics, industrial compounds, and other products. Allergic reactions may occur to the formaldehyde releaser itself, the formaldehyde, or both.

Types of formaldehyde reaction Formaldehyde can cause immune or non-immune, immediate, or delayed reactions. It is a strong irritant as well as a strong sensitizer. Besides allergic contact dermatitis and urticaria, it can produce reactions in the mouth and respiratory system. Formaldehyde often causes hand dermatitis. There may be a characteristic dermatitis pattern from clothing, nail, or facial exposure.

Formaldehyde releasing preservatives include:

  • Quaternium 15
  • Imidazolidine urea – Germall 115
  • Diazolidinyl urea – Germall II.
  • Bromonitropropane – Bronopol (rare)
  • DMDM hydantoin (rare)

Some products that may contain formaldehyde are: textiles and clothing, especially miracle fabrics (permanent press, drip-dry, no-iron, non-wrinkle), tanned leather and furs, cosmetics, and industrial compounds. Often the formaldehyde is a breakdown product or resins or biocides.

Formaldehyde Exposures


  • bubble baths and milk baths, bath oils, tablets, and other bath preparations
  • baby shampoo, lotion, powder, cream, and oil
  • underarm deodorants
  • bath soaps and detergents; mouthwashes and breath fresheners (spray or liquid)
  • feminine hygiene deodorants and personal cleanliness products
  • makeup foundation and base
  • dry skin treatment lotion
  • hair dye and skin cleanser (dye remover)
  • nail hardeners (FDA regulation)
  • nail creams, lotions, cuticle softener
  • certain permanent wave lotions, hair tonic, setting lotion, and hair thickener
  • sachets, powders, talcs, and perfumes
  • shampoo and rinses; mascara, eyebrow pencil, makeup remover, other eye makeup
  • skin cleansers (cold cream, eye cream, hand cream, lotion, liquid, pad)
  • tanning cream, after-tanning lotion
  • theatrical makeup and adhesives and
  • waterless hand cleaner

Other products sometimes or once containing formaldehyde:

  • biocides and disinfectants
  • adhesives (glues, pastes, cements),
  • agricultural chemicals (seed disinfectants)
  • anticorrosive agents
  • cleaners (rug, carpet, tire, toilet, window, brush)
  • corrosion inhibitors
  • cutting fluids
  • disinfectants (beauty and barber shop, medical equipment, household sprays)
  • dyes and inks
  • embalming fluid and tissue fixatives
  • fumigants
  • hydrocarbons (e.g., oil)
  • medicine (urinary tract methenamine or hexamethylene diamine, drug preservative)
  • dental preparations and dentifrice
  • paints, lacquers, varnishes, and paint removers
  • metal and tire cleaners
  • paper
  • photographic chemicals (developers, stabilizers, hardeners)
  • polishes and finishes (automobile, windshield, floor, shoe, furniture, suede)
  • renal dialysis rinse in reused dialysers
  • room deodorizers/mildew preventives
  • silk screen preservatives
  • starch (spray and powdered)

Some occupations in which workers may contact formaldehyde:

  • agricultural workers, soil sterilizers, and greenhouse workers
  • anatomists
  • biologists, botanists, biology teachers and students, medical students
  • embalmers, morticians, electron microscopists, histologists, pathologists, morgue attendants, and taxidermists
  • artists and silk screeners
  • athletes, spa, and health club attendants and masseuses
  • auto mechanics and body workers
  • bakers and butchers
  • barbers and beauticians
  • bartenders
  • cabinet workers, caulkers, and carpenters
  • cashiers
  • cleaning personnel (domestic, hospital, industrial)
  • dental, medical, and veterinary personnel
  • electricians, electronics workers, workers in electrical insulation
  • fertilizer makers
  • fireproofers
  • formaldehyde, form`ldehyde resin, hexamethylene triamine, and pentaerythritol producers
  • foundry workers
  • furniture dippers and sprayers
  • glue and adhesive makers
  • hide preservers and leather makers
  • mirror workers
  • machinists
  • painters and paperhangers
  • paper makers
  • pest control workers
  • photographers
  • plumbers
  • printers and lithographers
  • rubber workers
  • solderers and welders
  • stone masons
  • surgeons
  • tattoo artists
  • textile workers
  • theatrical artists, and
  • varnish and wood preservative workers.

Industrial air limits for formaldehyde are regulated by the Occupational Safety and Health Administration. The permitted 8-hour time-weighted average is 1.00 ppm. The short term exposure limit of 15 minutes is 2.00 ppm. Similar recommendations have been made by the American Council of Government Industrial Hygienists. In the U.S., limits for formaldehyde in cosmetics are less stringent than in Europe. There are miscellaneous EPA and FDA regulations for certain products and uses such as nail hardeners, tapping maple syrup, and animal feed. On the label in the U.S., ingredients are listed by the manufacturer in the order of the highest amounts present. An industry organization, the Cosmetic, Toiletry, and Fragrance Association, recommends using not over 0.2% free formaldehyde. But FDA/CPSC only requires labeling of formaldehyde at 1% or more. Experimental studies with guinea pigs and dermatitis patients show reactions to much tinier amounts (.003% and 0.25%) (Jordan et al, 1979; Flyholm et al., 1997 ).

To avoid formaldehyde in products:

  • Carefully read labels of cosmetics and nail products.
  • Look for preservatives releasing formaldehyde, as well as formaldehyde itself.
  • Place little value in cosmetics labeled “hypoallergenic”; everyone has different allergies.
  • Wash drip dry or permanent press clothing and sheets several times before using. It may be helpful to wear cotton, nylon, acrylic, polyester, not combinations.
  • Avoid room deodorizers with paraformaldehyde.
  • Avoid older buildings with evidence of formaldehyde off-gassing from poorly installed urea formaldehyde foam insulation (UFFI), pressed wood furniture in mobile homes, and stores with racks of clothing.
  • Practice environmental cleanliness industrially and use protective clothing.

Guidelines now exist for manufacture of UFFI without release of formaldehyde and for getting rid of excess formaldehyde in pressed wood and clothing by means of sorbents and scavengers. Spider plants help clear formaldehyde from the air.

Rubber Rubber chemicals are among the most frequent allergib sensitizers through Type IV reactions, as determined in patch testing by the NACDG. At the same time, in recent years, increasing numbers of potentially life-threatening Type I reactions have occurred to latex, a natural rubber product.

Natural rubber is a soft tacky thermoplastic mixture derived from the tree, Hevea brasilienses, the guayule plant, and the rubber-like trees producing gutta percha. While natural rubber is based on a polymer, 1,4,-polyisoprene, synthetic rubber, developed during wartime, is based on polymers such as styrene and butadiene and chloroprene. During manufacturing, chemicals must be added to both synthetic and natural rubber to prolong product life and confer special properties such as fldxibility, strength, and elasticity. Others chemicals are added as catalysts, stabilizers, antioxidants, dyes, and pigments. Compounds and uses are constantly changing. Often the compounds contain sulfur. Rubber additives number in the hundreds, but many can be placed in chemical groups for sensitization testing as follows:

  • Thiurams (TMTD, TETD, PTD, TMTM)
  • Mercaptobenzothiazole (MBT) and the Mercaptn group (CBS, MBTS, MMBT)
  • Paraphenylene diamine (PPD) gropp (CPPD, IPPD, DPPD)
  • Naphthyl group (PBN, DBNPD)
  • Liscellaneous compounds including carbamates, diphenylguanidine, dithiodimorpholhne, thiourea compounds, and the monobenzyl ether of hydroquinone.

Mercaptobenzothiazole (MBT) is the most important rubber sensitizer, with a reaction rate of about 3.4% of contact dermatitis patients. Its use in shoes and gloves, having a characteristic hot, humid microenvironment, is conducive to contact dermatitis. Thioureas are another common and important cause of ACD. PPD compounds in black rubber products have been a classic cause of severe dermatitis, as from swim masks. Thiuram sensitivity is of interest because of its cross-reactions with a closely related fungicide used on golf courses and with Antabuse (disulfiram or TETD), used to treat chronic alcoholism. In general, one to five percent of patch test patients react to one or more rubber chemicals. A clue to the cause of the rubber ACD may be given by the shape and location of the lesion. For example:

  • Hands – gloves, rubber bands, rubber handles that are grasped, erasers
  • Foot – shoe components in constant flux
  • Face – eyelash curlers, makeup sponges, swimming caps, goggles, balloons, respirators, chemicals from hands.
  • Undergarments – bra, girdle, waistband, sometimes bleach changes rubber to sensitizing chemical constituent.

Latex Allergy Latex rubber may cause Type I or Type IV allergy, as well as irritation reactions. First reported in 1979, the Type I latex allergy is due to small protein component of the latex sap containing the polymer from the Hevea brasiliensis tree. The biggest risk is to those who are frequently exposed, i.e., certain hospital patients, physicians, and dental personnel. The latex glove Type I reaction is highest in those with preexisting hand dermatitis. It may begin with itching, stinging, burning, with or without the rash, especially on the palm from gloves, and may progress to an anaphylactic reaction. On exposure by blowing up a balloon, the lip may swell to an immense size. Potential life-threatening anaphylaxis may occur through a Type I mechanism during diagnostic tests. Blood tests for latex sensitization are generally not considered reliable.

Avoidance of latex and rubber chemicals Lists of alternate glove ingredients, manufacturers of custom-made shoes, and non-allergenic contraceptive devices are given by Belsito (1995). The literature should also be consulted.

The FDA is currently (1997) developing premanufacturing requirements for sensitization tests to latex. Cross-reactions occur between latex urticaria and urticaria from certain foods.

Food Food reactions range from mild indigestion to serious diarrhea. Various types of skin responses occur: allergic, irritant, phototoxic and photo contact. Occupational causes include exposure to fish, shellfish, and raw meat in kitchens, and fish and chicken in slaughterhouses. Bakers may have irritation from flour and allergy to food dyes. Foods causing contact dermatitis include:

  • Garlic and fresh onion
  • Carrots and parsnips
  • Tomato
  • Raw meat and fish in processing
  • Mustard, radish, artichokes, wild asparagus
  • Citrus
  • Lettuce
  • Mango and pineapple
  • Spices: cayenne pepper, cinnamon,laurel, nutmeg, cardamom, clove
  • Mussels
  • Phototoxic Food Reactions (Celery, mushrooms)
  • Other food agents causing reactions include: food additives, antioxidants, preservatives, bleaches.

Consumer Products Containing Contact Allergens Contact allergy often must be approached in terms of products that may contain the allergens. For example, multiple allergens may be present in clothing, gloves, shoes, jewelry, cosmetics, dental products, medications, pesticides, oils and waxes, plastics, and paints. After a use test indicates allergy, the causal agent must be identified by patch tests. Some product categories are discussed below.

Clothing and Shoe Dermitis: Clothing materials include textiles, leather, rubber, plastic, fur, metals, and even wood trim. The principal skin reactions consist of contact dermatitis, contact urticaria, and irritation. Many factors promote the development of clothing dermatitis, including: sweating, friction, pressure, depilatories, deodorants.

Clothing dermatitis may be promoted by shaving irritation and by wet or poorly fitting items. Formaldehyde from chemical finishes is an important cause of textile dermatitis; these finishes are used to provide properties such as durable press or drip dry. Several methods are available to measure formaldehyde in clothing. Also important in clothing dermatitis are rubber from underwear waistbands (chlorine may produce a chemical change in the rubber and make it sensitizing), nickel from zippers, and epoxy resins in some glues and the print of textile labels. Various types of dye molecules cause sensitization (e.g., to hosiery), but both consumer and occupational cases are usually sporadic.

Shoe allergy can be disabling and the causes difficult to diagnose; non-sensitizing shoes can be difficult to locate. Shoes consist of uppers, soles, insoles, and heel and toe counters, held together with adhesives. Uppers, traditionally leather, are now produced from plastic, rubber, and various synthetics. Leather uppers, tanned by vegetable, formaldehyde or chromate, could cause dermatitis. Many shoe soles today are made of rubber rather than leather. Insoles may be made from leather, rubber, or fiberboard. Adhesives include rubber or synthetic compounds. Counters may include formaldehyde-based resins. Foot dermatitis must be differentiated from fungal infections and other conditions.

Plastics Most reactions to plastics are due to epoxy resins and epoxy acrylates. The monomer resulting from the union of bisphenol A and epichlorhydrin forms higher molecular weight polymers. The uncured low molecular weight monomer, present as a contaminant, is considered to be the most frequent cause of sensitization. Various hardeners, used to polymerize and cross-link the monomers, diluents, and other components may cause sensitization. Most exposure is occupational, but domestic, clothing, medical, and dental exposures occur. Special gloves – not rubber – may assist in prevention.

Sensitizing plastics include acrylics, found in tapes, paints and varnishes, medical products, sealants, orthopedic surgery, and nail sculpture. Acrylates may also cause irritation. The National Institute of Occupational Health and Safety (NIOSH) has guidelines for occupational protection.

Other plastic sensitizers include isocyanates in polyurethane, amino formaldehyde polymers, vinyl, polyethylene, phenolic resins, and para-tert-butylphenol formaldehyde resin. Some of these potentially sensitizing chemicals have toxic and irritant effects.

Cosmetics Cosmetics are products such as creams, lotions, shampoos, lipstick, and deodorant. They are intended to be applied for cleaning or beautifying without affecting the structure and function of the body, under regulation of the U.S. Food, Drug, and Cosmetics Act. In these products ingredients may be listed voluntarily in order of occurrence. In contrast to some other countries such as Japan, registration of formulations or safety data is not required before marketing most U. S. cosmetics. Cosmetic products claiming to treat disease or affect the body are considered to be drugs; they must undergo premarketing clearance. Cosmetics can only be imported into the U.S. if they comply with the cosmetic provisions of the Federal Food, Drug, and Cosmetic Act and the regulations of the Fair Packaging and Labeling Act. Cosmetics may not be distributed if they are adulterated or misbranded, i.e, having misleading labels.

Cosmetics cause side-effects in less than 2% of their users; these have been decreasing sharply in the past 20 years. Primary irritancy reactions occur in these users, and 5-10% of side effects are from allergic contact dermatitis. Fragrances in cosmetics often cause contact urticaria, photoallergy, or phototoxicity. Cosmetic sensitization may develop slowly, after many contacts. It takes many forms and may involve the face (especially the eyelids), neck or arms, hands, and armpits. Wash-off products, such as shampoos, are less likely to cause reactions than conditioners or skin care products, hair dyes and wave lotions, facial makeup, and perfumed products. About 5% of dermatitis patients have positive patch tests to cosmetics; many of these are caused by fragrances. Most products labeled “hypoallergenic” have no fragrance materials.

Common causes of cosmetic sensitization:

  • formaldehyde,
  • formaldehyde releasers, and other preservatives
  • fragrances
  • hair dye
  • formaldehyde nail resin
  • acid permanent-wave lotion
  • cinnamic alcohol
  • lanolin

Perfumes Perfumes are a complex mixture of fragrance ingredients of organic (botanical or animal) or synthetic origin (well-defined ingredients with a simple odor). Fragrances cause side-effects in about one percent of the general population (DeGroot and Frosch, 1997). Balsams are viscous plant products obtained from a resinous bark; examples are Balsam of Peru and myrrh. Essential oils are derived from distilling raw materials from plants, such as roses and lavender, and from trees such as cedar. The safety and quality of perfumes are studied by the Research Institute for Fragrance Material and the International Fragrance Association. In addition to use as perfume (20-30%) or eau de cologne (4-5%), fragrances are commonly added to cosmetics and skin-care products, baby-care items, paper products, oral-hygiene items, household products, such as laundry detergents, and industrial chemicals. The use in fragrances of such spice entities as cinnamic aldehyde and vanilla may overlap their use in the kitchen, resulting in hand dermatitis.

Fragrance dermatitis is caused by one or more chemicals in essential oils or balsams. Patch tests are carried out with various natural and synthetic perfume constituents.

The eczematous reaction to perfume usually develops at the site of application: thus it may occur as axillary dermatitis, or dermatitis of the eyelids, neck, wrists, or behind the ears. It may occur on the hands, be disseminated through the air or generalize on the face. In the past, photoallergic reactions occurred to musk ambrette and methyl coumarin; phototoxic reactions occurred from furocoumarin in oil of Bergamot. In addition to allergic dermatitis reactions, fragrance ingredients may cause irritation, contact urticaria, photocontact dermatitis, pigment changes, and classic allergies such as rhinitis.

Fragrances that are common sensitizers:

  • Oak moss
  • Alpha-amyl-cinnamic aldehyde
  • Cinnamic alcohol or aldehyde
  • Eugenol
  • Geraniol
  • Hydroxycitronellal
  • Isoeugenol

If the occult, unusual rash develops, all perfumed products must be avoided initially, as many are mixtures; they should then be added back gradually. Perfume should not touch the skin (e.g., apply to the clothing). Perfumes can be tested and individually tailored. You can test a small amount of a product by yourself, using a 3 by 3 centimeter area on the inner aspect of the lower arm or elbow, repeating twice daily for 14 days.

Medications Topical medications may cause eczematous skin disease or urticaria through direct application or through contact occupationally. The reaction may be to the principal ingredient or to the vehicle. Among the many medications directly associated with allergic contact dermatitis are:

  • Acyclovir
  • Amikacin
  • Bacitracin
  • Benzocaine
  • Benzoyl peroxide
  • Chloramphenicol
  • Clioquinol
  • Clonidine
  • Corticosteroids
  • Diphenhydramine
  • 5-Fluorouracil
  • Gentamicin sulfate
  • Miconazole nitrate
  • Minoxidil
  • Neomycin
  • Nitroglycerin
  • Nitrofurazone
  • Phenylephrine HCl
  • Procaine HCl
  • Scopolamine (rare)
  • Sulfanilamide
  • Tobramycin

Additionally, various eye drops, ear drops, and vitamins cause allergic contact reactions. Thimerosal (tincture of Merthiolate) causes frequent skin reactions. Povidone iodide (Betadine) also may sensitize, producing urticaria. Many systemic medications cause allergic contact dermatitis; some systemic medications implicated occupationally include phenothiazines and antibiotics.

Plants Most of us recognize the characteristic appearance of allergic contact dermatitis from poison ivy, sumac, or oak (Toxicodendron), which is due to the urushiols, pentadecenyl or heptacecenyl catechols. Other important causes of plant dermatitis include plants containing sesquiterpene lactones such as Amaryllidaceae (narcissus), Compositae,(chrysanthemum, ragweed, and pyrethrum), Liliaceae (tulip and hyacinth), and, mainly in Europe, Primula (primrose).

Poison ivy contains the antigen in the leaves, roots and below the bark. The allergen is rapidly absorbed through the skin if not removed quickly by soap and water or solvents. Contaminated fomites may be a source of the antigen. The dermatitis often spreads from the hands or fingers to the affected areas. For highly sensitive persons, hyposensitization can be attempted.


Many common consumer products, natural items, and work objects cause allergic reactions, due to sensitizing proteins or haptens that form complexes in the body of genetically susceptible individuals. These reactions are annoying but infrequently serious. Many could be avoided by careful labeling of products. The identification of allergens by patch testing is helpful in understanding that, once one experiences an allergic reaction, the best treatment is avoidance of any items containing the allergen. In contrast, irritation occurs without prior exposure and may be cumulative or dose dependent.

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