Within the workplace, individuals may be exposed to significant amounts of nickel, airborne from the combustion of fossil fuels, or from contact with tools that are nickel-plated. Historically, workplaces where prolonged contact with soluble nickel has been high, have shown high risks for allergic contact nickel dermatitis. For example, nickel dermatitis was common in the past among nickel platers. Due to improved industrial and personal hygiene practices, however, over the past several decades, reports of nickel sensitivity in workplaces, such as the electroplating industry, have been sparse. In the workplace, exposure reduction includes personal protection equipment and other risk management measures.

Nickel allergy results in a skin response (rash) after the skin comes in direct and sustained contact with any item which releases a large amount of free nickel from its surface. The skin reaction can occur at the site of contact, or sometimes spread beyond to the rest of the body. Cutaneous exposure can cause localized erythematous, pruritic, vesicular, and scaly patches. Ingestion of nickel may cause a systemic reaction, that will affect a larger skin surface. Examples of systemic reactions can include hand dermatitis, baboon syndrome, or generalized eczematous reactions.

According to the hygiene hypothesis, when children are brought up exposed to allergens in the environment at a young age, their immune system is more likely to tolerate them, while children brought up in a modern "sanitary" environment are less likely to be exposed to those allergens at a young age, and, when they are finally exposed, develop allergies. There is some support for this hypothesis with respect to AD. Those exposed to dogs while growing up have a lower risk of atopic dermatitis. There is also support from epidemiological studies for a protective role for helminths against AD. Likewise children with poor hygiene are at a lower risk for developing AD, as are children who drink unpasteurised milk.

In a small percentage of cases, atopic dermatitis is caused by sensitization to foods. Also, exposure to allergens, either from food or the environment, can exacerbate existing atopic dermatitis. Exposure to dust mites, for example, is believed to contribute to one's risk of developing AD. A diet high in fruits seems to have a protective effect against AD, whereas the opposite seems true for fast foods. Atopic dermatitis sometimes appears to be associated with celiac disease and non-celiac gluten sensitivity, and the improvement with a gluten-free diet indicates that gluten is a causative agent in these cases.

Urushiol-induced contact dermatitis is caused by contact with a plant or any other object containing urushiol oil. The oil adheres to almost anything with which it comes in contact, such as towels, blankets, clothing, and landscaping tools. Clothing or other materials that touch the plant and then, before being washed, touch the skin are common causes of exposure.

For people who have never been exposed or are not yet allergic to urushiol, it may take 10 to 21 days for a reaction to occur the first time. Once allergic to urushiol, however, most people break out 48 to 72 hours after contact with the oil. Typically, individuals have been exposed at least once, if not several times, before they develop a rash. The rash typically persists one to two weeks, but in some cases may last up to five weeks.

Urushiol is primarily found in the spaces between cells beneath the outer skin of the plant, so the effects are less severe if the plant tissue remains undamaged on contact. Once the oil and resin are thoroughly washed from the skin, the rash is not contagious. Urushiol does not always spread once it has bonded with the skin, and cannot be transferred once the urushiol has been washed away.

Although simple skin exposure is most common, ingestion of urushiol can lead to serious, systemic reactions. Burning plant material is commonly said to create urushiol-laden smoke that causes a systemic reaction, as well as a rash in the throat and eyes. Firefighters often get rashes and eye inflammation from smoke-related contact. A high-temperature bonfire may incinerate urushiol before it can cause harm, while a smoldering fire may vaporize the volatile oil and spread it as white smoke. However, some sources dispute the danger of burning urushiol-containing plant material.

Common allergens implicated include the following:

- Nickel (nickel sulfate hexahydrate) – has been recognized as a significant cause of allergy. This metal is frequently encountered in stainless steel cookware, jewelry and clasps or buttons on clothing. Current estimates gauge are that roughly 2.5 million US adults and 250,000 children suffer from nickel allergy, which costs an estimated $5.7 billion per year for treatment of symptoms. A significant portion of nickel allergy is preventable.

- Gold (gold sodium thiosulfate) – precious metal often found in jewelry and dental materials

- Balsam of Peru (Myroxylon pereirae) – used in food and drink for flavoring, in perfumes and toiletries for fragrance, and in medicine and pharmaceutical items for healing properties; derived from tree resin. It may also be a component of artificial vanilla and/or cinnamon flavorings.

- Chromium – used in the tanning of leather. Also a component of uncured cement/mortar, facial cosmetics and some bar soaps.

- Urushiol – oily coating from plants of Toxicodendron genus – poison ivy, poison oak, and poison sumac. Also found in mango plants and cashews.

- Sap from certain species of mangrove and agave

- Thiomersal – mercury compound used in local antiseptics and in vaccines

- Neomycin – topical antibiotic common in first aid creams and ointments, cosmetics, deodorant, soap, and pet food. Found by itself, or in Neosporin or Triple Antibiotic

- Fragrance mix – group of the eight most common fragrance allergens found in foods, cosmetic products, insecticides, antiseptics, soaps, perfumes, and dental products

- Formaldehyde – preservative with multiple uses, "e.g.", in paper products, paints, medications, household cleaners, cosmetic products, and fabric finishes. Often released into products by the use of formaldehyde releasers such as imidazolidinyl urea, diazolidinyl urea, Quaternium-15, DMDM Hydantoin, and 2-bromo-2-nitropropane-1,3-diol.

- Cobalt chloride – metal found in medical products; hair dye; antiperspirant; metal-plated objects such as snaps, buttons or tools; and in cobalt blue pigment

- Bacitracin – topical antibiotic found by itself, or as Polysporin or Triple Antibiotic

- Quaternium-15 – preservative in cosmetic products (self-tanners, shampoo, nail polish, sunscreen) and in industrial products (polishes, paints and waxes).

- Colophony (Rosin) – rosin, sap or sawdust typically from spruce or fir trees

- Topical steroid – "see" steroid allergy

- Photographic developers, especially those containing metol

- Topical anesthetics – such as pramoxine or diphenhydramine, after prolonged use

- Isothiazolinones – preservatives used in many personal care, household, and commercial products.

- Mercaptobenzothiazole – in rubber products, notably shoes, gloves, and car tires.

- Soluble salts of platinum – "see" platinosis

Chemical irritant contact dermatitis is either acute or chronic, which is usually associated with strong and weak irritants respectively. The following definition is provided by Mathias and Maibach (1978): The mechanism of action varies. Detergents, surfactants, extremes of pH, and organic solvents all directly affecting the barrier properties of the epidermis. These effects include removing fat emulsion, defatting of dermal lipids, inflicting cellular damage on the epithelium, and increasing the transepidermal water loss by damaging the horny layer water-binding mechanisms and damaging the DNA, which causes the layer to thin. Concentrated irritants have an acute effect, but this is not as common as the accumulative, chronic effect of irritants whose deleterious effects build up with subsequent doses (ESCD 2006).

Chemical irritants are often strong alkalis as found in drain cleaners and soap with lye residues. Many other chemical compounds can also cause contact dermatitiis.

Irritant contact dermatitis (ICD) can be divided into forms caused by chemical irritants, and those caused by physical irritants. Common chemical irritants implicated include: solvents (alcohol, xylene, turpentine, esters, acetone, ketones, and others); metalworking fluids (neat oils, water-based metalworking fluids with surfactants); latex; kerosene; ethylene oxide; surfactants in topical medications and cosmetics (sodium lauryl sulfate); and alkalis (drain cleaners, strong soap with lye residues).

Physical irritant contact dermatitis may most commonly be caused by low humidity from air conditioning. Also, many plants directly irritate the skin.

Urushiol-induced contact dermatitis (also called Toxicodendron dermatitis and Rhus dermatitis) is the medical name given to allergic rashes produced by the oil urushiol, which is contained in various plants, most notably those of the "Toxicodendron" genus: the Chinese lacquer tree, poison ivy, poison oak, and poison sumac. The name is derived from the Japanese word for the sap of the Chinese lacquer tree, "urushi". Other plants in the sumac family (including mango, pistachio, the Burmese lacquer tree, the India marking nut tree, and the shell of the cashew) also contain urushiol, as do unrelated plants such as "Ginkgo biloba."

As is the case with all contact dermatitis, urushiol-induced rashes are a Type IV hypersensitivity reaction, also known as delayed-type hypersensitivity. Symptoms include itching, inflammation, oozing, and, in severe cases, a burning sensation.

The American Academy of Dermatology estimates that there are up to 50 million cases of urushiol-induced dermatitis annually in the United States alone, accounting for 10% of all lost-time injuries in the United States Forest Service. Poison oak is a significant problem in the rural Western and Southern United States, while poison ivy is most rampant in the Eastern United States. Dermatitis from poison sumac is less common.

Common causes of allergic contact dermatitis include: nickel allergy, 14K or 18K gold, Balsam of Peru ("Myroxylon pereirae"), and chromium. In the Americas they include the oily coating from plants of the "Toxicodendron" genus: poison ivy, poison oak, and poison sumac. Millions of cases occur each year in North America alone. The alkyl resorcinols in "Grevillea banksii" and "Grevillea" 'Robyn Gordon' are responsible for contact dermatitis. Bilobol, another alkyl resorcinol found in "Ginkgo biloba" fruits, is also a strong skin irritant.

Common causes of irritant contact dermatitis include solvents, metalworking fluids, latex, kerosene, ethylene oxide, paper, especially papers coated with chemicals and printing inks, certain foods and drink, food flavorings and spices, perfume, surfactants in topical medications and cosmetics, alkalis, low humidity from air conditioning, and many plants. Other common causes of irritant contact dermatitis are harsh, alkaline soaps, detergents, and cleaning products.

There are three types of contact dermatitis: irritant contact dermatitis; allergic contact dermatitis; and photocontact dermatitis. Photocontact dermatitis is divided into two categories: phototoxic and photoallergic.

Irritant contact dermatitis is a form of contact dermatitis that can be divided into forms caused by chemical irritants and those caused by physical irritants.

The hygiene hypothesis postulates that the cause of asthma, eczema, and other allergic diseases is an unusually clean environment. It is supported by epidemiologic studies for asthma. The hypothesis states that exposure to bacteria and other immune system modulators is important during development, and missing out on this exposure increases risk for asthma and allergy.

While it has been suggested that eczema may sometimes be an allergic reaction to the excrement from house dust mites, with up to 5% of people showing antibodies to the mites, the overall role this plays awaits further corroboration.

There is no good evidence that a mother's diet during pregnancy, the formula used, or breastfeeding changes the risk. There is tentative evidence that probiotics in infancy may reduce rates but it is insufficient to recommend its use.

People with eczema should not get the smallpox vaccination due to risk of developing eczema vaccinatum, a potentially severe and sometimes fatal complication.

Garlic allergy or allergic contact dermatitis to garlic is a common inflammatory skin condition caused by contact with garlic oil or dust. It mostly affects people who cut and handle fresh garlic, such as chefs, and presents on the tips of the thumb, index and middle fingers of the non-dominant hand (which typically hold garlic bulbs during the cutting). The affected fingertips show an asymmetrical pattern of fissure as well as thickening and shedding of the outer skin layers, which may progress to second- or third-degree burn of injured skin.

Garlic dermatitis is similar to the tulip dermatitis and is induced by a combined mechanical and chemical action. Whereas the former mechanism acts via skin rubbing which progresses into damage, the major cause of the latter is the chemical diallyl disulfide (DADS), together with related compounds allyl propyl disulfide and allicin. These chemicals occur in oils of plants of the genus "Allium", including garlic, onion and leek.

Garlic allergy has been known since at least 1950. It is not limited to hand contact, but can also be induced, with different symptoms, by inhaling garlic dust or ingesting raw garlic, though the latter cases are relatively rare. DADS penetrates through most types of commercial gloves, and thus wearing gloves while handling garlic has proven inefficient against the allergy. Treatment includes avoiding any contact with garlic oil or vapours, as well as medication, such as administering acitretin (25 mg/day, orally) or applying psoralen and ultraviolet light to the affected skin area over a period of 12 weeks (PUVA therapy).

Allergic contact dermatitis (ACD) is a form of contact dermatitis that is the manifestation of an allergic response caused by contact with a substance; the other type being irritant contact dermatitis (ICD).

Although less common than ICD, ACD is accepted to be the most prevalent form of immunotoxicity found in humans. By its allergic nature, this form of contact dermatitis is a hypersensitive reaction that is atypical within the population. The mechanisms by which these reactions occur are complex, with many levels of fine control. Their immunology centres on the interaction of immunoregulatory cytokines and discrete subpopulations of T lymphocytes.

Natural rubber latex can also cause irritant contact dermatitis, a less severe form of reaction that does not involve the immune system. Contact dermatitis causes dry, itchy, irritated areas on the skin, most often on the hands. Latex-glove induced dermatitis increases the chance of hospital-acquired infections, including blood-borne infections, being transmitted.

Occupational skin diseases are ranked among the top five occupational diseases in many countries.

Contact Dermatitis due to irritation is inflammation of the skin which results from a contact with an irritant. It has been observed that this type of dermatitis does not require prior sensitization of the immune system. There have been studies to support that past or present atopic dermatitis is a risk factor for this type of dermatitis. Common irritants include detergents, acids, alkalies, oils, organic solvents and reducing agents.

The acute form of this dermatitis develops on exposure of the skin to a strong irritant or caustic chemical. This exposure can occur as a result of accident at a workplace . The irritant reaction starts to increase in its intensity within minutes to hours of exposure to the irritant and reaches its peak quickly. After the reaction has reached its peak level, it starts to heal. This process is known as decrescendo phenomenon. The most frequent potent irritants leading to this type of dermatitis are acids and alkaline solutions. The symptoms include redness and swelling of the skin along with the formation of blisters.

The chronic form occurs as a result of repeated exposure of the skin to weak irritants over long periods of time.

Clinical manifestations of the contact dermatitis are also modified by external factors such as environmental factors (mechanical pressure, temperature, and humidity) and predisposing characteristics of the individual (age, sex, ethnic origin, preexisting skin disease, atopic skin diathesis, and anatomic region exposed.

Another occupational skin disease is glove-related hand urticaria, believed to be caused by repeated wearing and removal of the gloves. It has been reported as an occupational problem among the health care workers. The reaction is caused by the latex or the nitrile present in the gloves.

Natural rubber latex is known to cause Type I and Type IV allergic reactions, as well as irritant contact dermatitis.

Defatting can be prevented by wearing appropriate protective clothing such as gloves, lab coats and aprons when working regularly with defatting agents. Prolonged skin contact or chronic defatting of the skin increases the possibility for developing irritant contact dermatitis and has the potential to worsen pre-existing skin conditions. Patients with chronic dermatitis are advised to use non-irritating soaps and dishwashing liquids sparingly and to choose those with a neutral pH and minimal defatting capability.

Cosmetics play an important role as causal factors for perioral dermatitis. Regular generous applications of moisturising creams cause persistent hydration of the horny layer causing impairment and occlusion of the barrier function, irritation of the hair follicle and proliferation of skin flora. Combining this with night cream and foundation significantly increases risk of perioral dermatitis by 13-fold.

Prevention measures include avoidance of the irritant through its removal from the workplace or through technical shielding by the use of potent irritants in closed systems or automation, irritant replacement or removal and personal protection of the workers.

The aim of treatment is to relieve the allergy-induced itch and to remove the fleas from the pet and its home environment. In some cases, secondary bacterial or yeast infections will also need treatment before the itching subsides. Environmental flea control includes using flea foggers or bombs, vacuuming, and treating pet bedding by washing on a hot cycle (over 60 degrees Celsius) in the washing machine. The current on-pet treatment recommended by veterinary dermatologists is spinosad (Comfortis) monthly and nitenpyram (Capstar or generics) every 48 hours until improvement.

Many pets with FAD may also have other allergies, such as allergies to food, contact allergies, and atopic dermatitis.

The cause of perioral dermatitis is unclear. The use of topical steroids and cosmetics have the most important role. Although light exposure has been discounted as a causal factor, some reports of perioral dermatitis have been made by some patients receiving Psoralen and ultraviolet A therapy.

The diagnosis of flea allergy dermatitis is complicated by the grooming habits of pets. Cats in particular are very efficient at grooming out fleas, often removing any evidence of infestation. Fleas begin biting within 5 minutes of finding a host, and there are no flea treatments that kill fleas before biting occurs.

Atopy is a hereditary and chronic (lifelong) allergic skin disease. Signs usually begin between 6 months and 3 years of age, with some breeds of dog, such as the Golden Retriever showing signs at an earlier age. Dogs with atopic dermatitis are itchy, especially around the eyes, muzzle, ears and feet. In severe cases the irritation is generalised. If the allergens are seasonal, the signs of irritation are similarly seasonal. Many dogs with house dust mite allergy have perennial disease. Some of the allergens associated with atopy in dogs include pollens of trees, grasses and weeds, as well as molds and House dust mite. Ear and skin infections with the bacteria "Staphylococcus pseudintermedius" and the yeast "Malassezia pachydermatis" are common secondary to atopic dermatitis.

Food allergy can be associated with identical signs and some authorities consider food allergy to be a type of atopic dermatitis.

Diagnosis of atopic dermatitis is by elimination of other causes of irritation including fleas, scabies and other parasites such as Cheyletiella and lice. Food allergy can be identified through the use of elimination diet trials in which a novel or hydrolysed protein diet is used for a minimum of 6 weeks and allergies to aeroallergens can be identified using intradermal allergy testing and/or blood testing (allergen-specific IgE ELISA).

Treatment includes avoidance of the offending allergens if possible, but for most dogs this is not practical or effective. Other treatments modulate the adverse immune response to allergens and include antihistamines, steroids, ciclosporin and immunotherapy (a process in which allergens are injected to try to induce tolerance). In many cases shampoos, medicated wipes and ear cleaners are needed to try to prevent the return of infections.

New research into T-cell receptor peptides and their effects on dogs with severe, advanced atopic dermatitis are being investigated.