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.

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.

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.

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.

Allergic contact dermatitis (ACD) is accepted to be the most prevalent form of immunotoxicity found in humans, and is a common occupational and environmental health problem. By its allergic nature, this form of contact dermatitis is a hypersensitive reaction that is atypical within the population. The mechanisms by which this reaction occurs are complex, with many levels of fine control. Their immunology centres on the interaction of immunoregulatory cytokines and discrete subpopulations of T lymphocytes.

Allergens include nickel, gold, Balsam of Peru ("Myroxylon pereirae"), chromium, and the oily coating from plants of the "Toxicodendron" genus, such as poison ivy, poison oak, and poison sumac.

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

In adults, the prevalence of IgE sensitization to allergens from house dust mite and cat, but not grass, seem to decrease over time as people age. However, the biological reasons for these changes are not fully understood.

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.

Three main factors play an essential role in the development of chronic hand eczema: excessive contact with water and irritants (cumulative-toxic stress), contact with allergens, and atopic diathesis, which has a genetic component. Individual hand eczema types are identified and named according to the main catalysts involved, i.e. cumulative-toxic, contact-allergenic, or atopic hand eczema. Activities that are stressful for the skin or involve repeated, excessive contact with water or skin-irritating substances at work or home can cause damage to the skin's protective abilities and increase the chances of inflammation. This also applies to prolonged wearing of protective rubber gloves and similar materials, since sweating occurs within these gloves. Disturbance of the skin's protective barrier also facilitates penetration by allergenic substances and promotes the development of contact dermatitis. Contact allergies play a very important role in the development of hand eczema. If the hand is subjected to repeated contact with a substance that leads to an allergy, the skin reacts with signs of inflammation. Numerous people affected by hand eczema also experience skin inflammation on their feet. Often, a contact allergy to an ingredient in shoe leather treatment may be the catalyst. Contact allergies in certain types of employment are especially problematic, particularly if the work involves the handling of allergenic materials, e.g. masonry work or hairdressing.

People allergic to Balsam of Peru may experience a flare-up of hand eczema if they use or consume products that use it as an ingredient.

Severe and chronic eczema qualifies as one of the most frequent occupational illnesses. Patients should therefore be referred to an occupational-dermatological specialist as soon as possible. Patients with a history of neurodermitis, hay fever, or allergic asthma often develop hand eczema. These sicknesses reflect the individual's particular susceptibility or genetic predisposition to react over-sensitively to various environmental influences. This is described as atopy or atopy diathesis. Atopic diathesis is frequently accompanied by genetically conditioned problems with the skin's protective barriers, which causes a weakening of the skin's resistance against irritating substances and moisture, as well as easier penetration by allergens, which may lead to the development of contact allergies.

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.

Prevention includes avoiding exposure to the sun and wearing sun block on the affected area.

- Cover up: wear long sleeves, slacks, and a wide-brimmed hat whenever harsh exposure is probable

- Avoid chemicals that may trigger a reaction

- Wear sunscreen at least factor 30 with a high UVA protection level

- Wear gloves and/or remain indoors after handling fruits or plants which increase sensitivity to light

Hand eczema is a common condition: study data indicates a one-year prevalence of up to 10% in the general population. It is estimated that only 50–70% of people affected consult a doctor. The frequency of severe, chronic and recurrent forms of hand eczema is estimated at 5–7%. Approximately 2–4% of hand eczema patients also report that external (topical) therapy is insufficient.

Several factors adversely affect the long-term prognosis, including the development of the condition prior to the 20th birthday, the severity of initial manifestations, and eczema during childhood. Women, especially those under 30, are more frequently affected than men.

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.

A rarely cited double-blind study in 1982 reported that a course of oral urushiol usually hyposensitized subjects.

Atopic reactions are caused by localized hypersensitivity reaction to an allergen. Atopy appears to show a strong hereditary component. One study concludes that the risk of developing atopic dermatitis (3%) or atopy in general (7%) "increases by a factor of two with each first-degree family member already suffering from atopy". As well, maternal stress and perinatal programming is increasingly understood as a root cause of atopy, finding that "...trauma may be a particularly robust potentiator of the cascade of biological events that increase vulnerability to atopy and may help explain the increased risk found in low-income urban populations.”

Environmental factors are also thought to play a role in the development of atopy, and the 'hygiene hypothesis' is one of the models that may explain the steep rise in the incidence of atopic diseases, though this hypothesis is incomplete and in some cases, contradictory to findings. This hypothesis proposes that excess 'cleanliness' in an infant's or child's environment can lead to a decline in the number of infectious stimuli that are necessary for the proper development of the immune system. The decrease in exposure to infectious stimuli may result in an imbalance between the infectious-response ("protective") elements and the allergic-response ("false alarm") elements within the immune system.

Some studies also suggest that the maternal diet during pregnancy may be a causal factor in atopic diseases (including asthma) in offspring, suggesting that consumption of antioxidants, certain lipids, and/or a Mediterranean diet may help to prevent atopic diseases.

The multicenter PARSIFAL study in 2006, involving 6630 children age 5 to 13 in 5 European countries, suggested that reduced use of antibiotics and antipyretics is associated with a reduced risk of allergic disease in children.

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.

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.

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.

Physical irritant contact dermatitis is a less-researched form of ICD due to its various mechanisms of action and a lack of a test for its diagnosis.

A complete patient history combined with negative allergic patch testing is usually necessary to reach a correct diagnosis. The simplest form of PICD results from prolonged rubbing, although the diversity of implicated irritants is far wider. Examples include paper friction, fiberglass, and scratchy clothing.

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.

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.

The exact causes of dyshidrosis are unknown. In 2013, a randomized, double-blind, placebo-controlled cross-over study by the University Medical Center Groningen reported that dyshydrosis outbreaks on the hands increased significantly among those allergic to house dust mites, following inhalation of house dust mite allergen.

Food allergens may be involved in certain cases. Cases studies have implicated a wide range of foods including tuna, tomato, pineapple, chocolate, coffee, and spices among others. A number of studies have implicated balsam of Peru.

Id reaction and irritant contact dermatitis are possible causes.