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.

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.

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.

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.

With no particular affinity to any particular ethnic group, seen in all age groups and equally amongst males and females, the precise prevalence is not known.

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.

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.

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.

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

Other rashes that occur in a widespread distribution can look like an id reaction. These include atopic dermatitis, contact dermatitis, dyshidrosis, photodermatitis, scabies and drug eruptions.

Although wetness alone has the effect of macerating the skin, softening the stratum corneum, and greatly increasing susceptibility to friction injury, urine has an additional impact on skin integrity because of its effect on skin pH. While studies show that ammonia alone is only a mild skin irritant, when urea breaks down in the presence of fecal urease it increases pH because ammonia is released, which in turn promotes the activity of fecal enzymes such as protease and lipase. These fecal enzymes increase the skin's hydration and permeability to bile salts which also act as skin irritants.

There is no detectable difference in rates of diaper rash in conventional disposable diaper wearers and reusable cloth diaper wearers. "Babies wearing superabsorbent disposable diapers with a central gelling material have fewer episodes of diaper dermatitis compared with their counterparts wearing cloth diapers. However, keep in mind that superabsorbent diapers contain dyes that were suspected to cause allergic contact dermatitis (ACD)." Whether wearing cloth or disposable diapers they should be changed frequently to prevent diaper rash, even if they don't feel wet. To reduce the incidence of diaper rash, disposable diapers have been engineered to pull moisture away from the baby's skin using synthetic non-biodegradable gel. Today, cloth diapers use newly available superabsorbent microfiber cloth placed in a pocket with a layer of light permeable material that contacts the skin. This design serves to pull moisture away from the skin in to the microfiber cloth. This technology is used in most major pocket cloth diapers brands today.

The interaction between fecal enzyme activity and IDD explains the observation that infant diet and diaper rash are linked because fecal enzymes are in turn affected by diet. Breast-fed babies, for example, have a lower incidence of diaper rash, possibly because their stools have higher pH and lower enzymatic activity. Diaper rash is also most likely to be diagnosed in infants 8–12 months old, perhaps in response to an increase in eating solid foods and dietary changes around that age that affect fecal composition. Any time an infant’s diet undergoes a significant change (i.e. from breast milk to formula or from milk to solids) there appears to be an increased likelihood of diaper rash.

The link between feces and IDD is also apparent in the observation that infants are more susceptible to developing diaper rash after treating with antibiotics, which affect the intestinal microflora. Also, there is an increased incidence of diaper rash in infants who have suffered from diarrhea in the previous 48 hours, which may be because fecal enzymes such as lipase and protease are more active in feces which have passed rapidly through the gastrointestinal tract.

Eyelid dermatitis is commonly related to atopic dermatitis or allergic contact dermatitis. Volatile substances, tosylamide, epoxy hardeners, insect sprays, and lemon peel oil may be implicated, with many cases of eyelid contact dermatitis being caused by substances transferred by the hands to the eyelids.

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.

Many contact sensitizers or irritants are known to cause contact dermatitis superimposed on nummular dermatitis. Studies have implicated nickel, cobalt, chromate, and fragrance as likely culprits. Xerosis, or dehydration of skin is also a likely cause. Infection with "Staphylococcus aureus" bacteria or "Candida" may also play a role.

The prevalence of nummular dermatitis in the United States is approximately 2 per 1,000. It is considered a disease of adulthood, for it is rare in children.

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.

Rosin, the material commonly used to wax string instruments is known to cause allergic contact dermatitis in musicians. Nickel, a metal found in musical instruments causes allergic contact dermatitis on the fingers and hands of string instrumentalists and in the lip and neck of wind instrumentalists. Wind instrumentalists with lip and neck infection should switch to gold or plastic mouthpieces if allergic dermatitis occurs. (R)-4-methoxydalbergione present in rosewood may cause allergic contact dermatitis in violinists. Cane reed (causing chelitis in saxophone players), propolis (a wax used to close structural gaps in musical instruments), paraphenylenediamine (used to polish musical instruments) and potassium dichromate (tanning agent to the skin of the harp) also cause allergic contact dermatitis in musicians.

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.

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.

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.

Frequent, chronic contact of instruments to skin may make it callous by the thickening of stratum corneum. Use of 'thumb position' in cellists may cause callosity of left thumb. Garrod's pads are seen on the dorsal left second and third fingers over the proximal interphalangeal joints in violinists. Drummer's digit is the callosity seen on the lateral phalynx of the left finger. Callosities need treatment only when they are excessive or symptomatic.

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.

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.