Allergic diseases are strongly familial: identical twins are likely to have the same allergic diseases about 70% of the time; the same allergy occurs about 40% of the time in non-identical twins. Allergic parents are more likely to have allergic children, and those children's allergies are likely to be more severe than those in children of non-allergic parents. Some allergies, however, are not consistent along genealogies; parents who are allergic to peanuts may have children who are allergic to ragweed. It seems that the likelihood of developing allergies is inherited and related to an irregularity in the immune system, but the specific allergen is not.

The risk of allergic sensitization and the development of allergies varies with age, with young children most at risk. Several studies have shown that IgE levels are highest in childhood and fall rapidly between the ages of 10 and 30 years. The peak prevalence of hay fever is highest in children and young adults and the incidence of asthma is highest in children under 10.

Overall, boys have a higher risk of developing allergies than girls, although for some diseases, namely asthma in young adults, females are more likely to be affected. These differences between the sexes tend to decrease in adulthood.

Ethnicity may play a role in some allergies; however, racial factors have been difficult to separate from environmental influences and changes due to migration. It has been suggested that different genetic loci are responsible for asthma, to be specific, in people of European, Hispanic, Asian, and African origins.

Chronic stress can aggravate allergic conditions. This has been attributed to a T helper 2 (TH2)-predominant response driven by suppression of interleukin 12 by both the autonomic nervous system and the hypothalamic–pituitary–adrenal axis. Stress management in highly susceptible individuals may improve symptoms.

Venom from stinging or biting insects such as Hymenoptera (ants, bees, and wasps) or Triatominae (kissing bugs) may cause anaphylaxis in susceptible people. Previous systemic reactions, which are anything more than a local reaction around the site of the sting, are a risk factor for future anaphylaxis; however, half of fatalities have had no previous systemic reaction.

When infants consume peanut proteins while 4 to 11 months old, the risk of developing peanut allergy before the age of 5 years decreases by 11-25%, specifically in children with higher allergy risk via their parents with peanut allergy. From these results, the American Academy of Pediatrics rescinded their recommendation to delay exposure to peanuts in children, also stating there is no reason to avoid peanuts during pregnancy or breastfeeding.

There is conflicting evidence on whether maternal diet during pregnancy has any effect on development of allergies due to a lack of good studies. A 2010 systematic review of clinical research indicated that there is insufficient evidence for whether maternal peanut exposure, or early consumption of peanuts by children, affects sensitivity for peanut allergy.

Any medication may potentially trigger anaphylaxis. The most common are β-lactam antibiotics (such as penicillin) followed by aspirin and NSAIDs. Other antibiotics are implicated less frequently, and the reactions to NSAIDs are agent specific meaning that those who are allergic to one NSAID can typically tolerate a different one. Other relatively common causes include chemotherapy, vaccines, protamine and herbal preparations. Some medications (vancomycin, morphine, x-ray contrast among others) cause anaphylaxis by directly triggering mast cell degranulation.

The frequency of a reaction to an agent partly depends on the frequency of its use and partly on its intrinsic properties. Anaphylaxis to penicillin or cephalosporins occurs only after it binds to proteins inside the body with some agents binding more easily than others. Anaphylaxis to penicillin occurs once in every 2,000 to 10,000 courses of treatment, with death occurring in fewer than one in every 50,000 courses of treatment. Anaphylaxis to aspirin and NSAIDs occurs in about one in every 50,000 persons. If someone has a reaction to penicillins, his or her risk of a reaction to cephalosporins is greater but still less than one in 1,000. The old radiocontrast agents caused reactions in 1% of cases, while the newer lower osmolar agents cause reactions in 0.04% of cases.

Some examples:

- Allergic asthma

- Allergic conjunctivitis

- Allergic rhinitis ("hay fever")

- Anaphylaxis

- Angioedema

- Urticaria (hives)

- Eosinophilia

- Penicillin allergy

- Cephalosporin allergy

- Food allergy

- Sweet itch

A child's allergy is an immune system reaction. The child is reacting to a specific substance, or allergen. The immune system of a child responds to the invading allergen by releasing histamine and other chemicals that typically trigger symptoms in the nose, lungs, throat, sinuses, ears, eyes, skin, or stomach lining. In some children, allergies can also trigger symptoms of asthma—a disease that causes wheezing or difficulty breathing. If a child has allergies and asthma, controlling the allergies is important because the lack of treatment may make the allergies worse. Compounds such as phthalates are associated with asthma in children. Asthma in children is associated with exposure to indoor allergens. in early childhood may prevent the development of asthma, but exposure at an older age may provoke bronchoconstriction. Use of antibiotics in early life has been linked to the development of asthma. Exposure to indoor volatile organic compounds may be a trigger for asthma; formaldehyde exposure, for example, has a positive association.

Each home contains possible allergens that can develop into allergies after exposure to:

- Dust mites

- Dogs and cats

- Other furry pets

- Cockroaches

- Mice and rats)

- Plants

- Mold

Vitamin D deficiency at the time of birth and exposure to egg white, milk, peanut, walnut, soy, shrimp, cod fish, and wheat makes a child more susceptible to allergies. Soy-based infant formula is associated with allergies in infants.

The majority of children outgrow egg allergy. One review reported that 70% of children will outgrow this allergy by 16 years. In subsequently published longitudinal studies, one reported that for 140 infants who had challenge-confirmed egg allergy, 44% had resolved by two years. A second reported that for 203 infants with confirmed IgE-mediated egg allergy, 45% resolved by two years of age, 66% by four years, and 71% by six years. Children will be able to tolerate eggs as an ingredient in baked goods and well-cooked eggs sooner than under-cooked eggs. Resolution was more likely if baseline serum IgE was lower, and if the baseline symptoms did not include anaphylaxis.

Milk allergy typically presents in the first year of life. The majority of children outgrow milk allergy by the age of ten years. One large clinical trial reported resolutions of 19% by age 4 years, 42% by age 8 years, 64% by age 12 years, and 79% by 16 years. Children are be able to tolerate milk as an ingredient in baked goods relative to liquid milk. Resolution was more likely if baseline serum IgE was lower, or if IgE-mediated allergy was absent so that all that was present was cell-mediated, non-IgE allergy.

People with confirmed cow's milk allergy may also demonstrate an allergic response to beef, moreso to rare beef versus well-cooked beef. The offending protein appears to be bovine serum albumin. This is not the same beef allergy that is seen primarily in the southeastern United States, triggered by being bitten by a Lone Star tick.

Milk allergy has consequences. In a U.S. government diet and health surveys conducted in 2007-2010, 6,189 children ages 2-17 years were assessed. For those classified as cow's milk allergic at the time of the survey, mean weight, height and body-mass index were significantly lower than their non-allergic peers. This was not true for children with other food allergies. Diet assessment showed a significant 23% reduction of calcium intake and near-significant trends for lower vitamin D and total calorie intake.

Treatment usually involves adrenaline (epinephrine), antihistamines, and corticosteroids.

If the entire body is involved, then anaphylaxis can take place, which is an acute, systemic reaction that can prove fatal.

Allergies to a specific pollen are usually associated with OAS reactions to other certain foods. For instance, an allergy to ragweed is associated with OAS reactions to banana, watermelon, cantaloupe, honeydew, zucchini, and cucumber. This does not mean that all sufferers of an allergy to ragweed will experience adverse effects from all or even any of these foods. Reactions may be associated with one type of food, with new reactions to other foods developing later. However, reaction to one or more foods in any given category does not necessarily mean a person is allergic to all foods in that group.

One way to prevent allergic rhinitis is to wear a respirator or mask when near potential allergens.

Growing up on a farm and having multiple brothers and or sisters decreases the risk.

OAS produces symptoms when an affected person eats certain fruits, vegetables, and nuts. Some individuals may only show allergy to only one particular food, and others may show an allergic response to many foods.

Individuals with an allergy to tree pollen may develop OAS to a variety of foods. While the tree pollen allergy has been worked out, the grass pollen is not well understood. Furthermore, some individuals have severe reactions to certain fruits and vegetables that do not fall into any particular allergy category. In recent years, it has also become apparent that when tropical foods initiate OAS, allergy to latex may be the underlying cause.

Because the allergenic proteins associated with OAS are usually destroyed by cooking, most reactions are caused by eating raw foods. The main exceptions to this are celery and nuts, which may cause reactions even after being cooked.

The most common food allergens account for about 90% of all allergic reactions; in adults they include shellfish, peanuts, tree nuts, fish, and egg. In children, they include milk, eggs, peanuts, and tree nuts. Six to 8% of children under the age of three have food allergies and nearly 4% of adults have food allergies.

For reasons not entirely understood, the diagnosis of food allergies has apparently become more common in Western nations recently. In the United States, food allergy affects as many as 5% of infants less than three years of age and 3% to 4% of adults. A similar prevalence is found in Canada.

About 75% of children who have allergies to milk protein are able to tolerate baked-in milk products, i.e., muffins, cookies, cake, and hydrolyzed formulas.

About 50% of children with allergies to milk, egg, soy, peanuts, tree nuts, and wheat will outgrow their allergy by the age of 6. Those who are still allergic by the age of 12 or so have less than an 8% chance of outgrowing the allergy.

Peanut and tree nut allergies are less likely to be outgrown, although evidence now shows that about 20% of those with peanut allergies and 9% of those with tree nut allergies will outgrow them.

In Japan, allergy to buckwheat flour, used for soba noodles, is more common than peanuts, tree nuts or foods made from soy beans.

Corn allergy may also be prevalent in many populations, although it may be difficult to recognize in areas such as the United States and Canada where corn derivatives are common in the food supply.

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 rhinitis is the type of allergy that affects the greatest number of people. In Western countries, between 10 and 30 percent of people are affected in a given year. It is most common between the ages of twenty and forty.

Food allergies develop more easily in people with the atopic syndrome, a very common combination of diseases: allergic rhinitis and conjunctivitis, eczema, and asthma. The syndrome has a strong inherited component; a family history of allergic diseases can be indicative of the atopic syndrome.

The cause of allergic conjunctivitis is an allergic reaction of the body's immune system to an allergen. Allergic conjunctivitis is common in people who have other signs of allergic disease such as hay fever, asthma and eczema.

Among the most common allergens that cause conjunctivitis are:

- Pollen from trees, grass and ragweed

- Animal skin and secretions such as saliva

- Perfumes

- Cosmetics

- Skin medicines

- Air pollution

- Smoke

- Dust mites

- Balsam of Peru (used in food and drink for flavoring, in perfumes and toiletries for fragrance, and in medicine and pharmaceutical items for healing properties)

- Eye drops

Most cases of seasonal conjunctivitis are due to pollen and occur in the hay fever season, grass pollens in early summer and various other pollens and moulds may cause symptoms later in the summer.

Many environmental factors have been associated with asthma's development and exacerbation including allergens, air pollution, and other environmental chemicals. Smoking during pregnancy and after delivery is associated with a greater risk of asthma-like symptoms. Low air quality from factors such as traffic pollution or high ozone levels has been associated with both asthma development and increased asthma severity. Over half of cases in children in the United States occur in areas with air quality below EPA standards. Low air quality is more common in low-income and minority communities.

Exposure to indoor volatile organic compounds may be a trigger for asthma; formaldehyde exposure, for example, has a positive association. Also, phthalates in certain types of PVC are associated with asthma in children and adults. While exposure to pesticides is linked to the development of asthma it is unclear if this is a cause and effect relationship.

There is an association between acetaminophen (paracetamol) use and asthma. The majority of the evidence does not, however, support a causal role. A 2014 review found that the association disappeared when respiratory infections were taken into account. Use by a mother during pregnancy is also associated with an increased risk as is psychological stress during pregnancy.

Asthma is associated with exposure to indoor allergens. Common indoor allergens include dust mites, cockroaches, animal dander (fragments of fur or feathers), and mold. Efforts to decrease dust mites have been found to be ineffective on symptoms in sensitized subjects. Certain viral respiratory infections, such as respiratory syncytial virus and rhinovirus, may increase the risk of developing asthma when acquired as young children. Certain other infections, however, may decrease the risk.

Incidence and prevalence are terms commonly used in describing disease epidemiology. Incidence is newly diagnosed cases, which can be expressed as new cases per year per million people. Prevalence is the number of cases alive, expressible as existing cases per million people during a period of time. Milk allergies are usually observed in infants and young children, and often disappear with age (see Prognosis), so prevalence of egg allergy may be expressed as a percentage of children under a set age. Milk allergy affects between 2% and 3% of infants in developed countries. This estimate is for antibody-based allergy; prevalence of allergy based on cellular immunity is unknown.

For all age groups, a review of fifty studies conducted in Europe estimated 6.0% for self-reported milk allergy and 0.6% for confirmed. National survey data in the United States collected 2005-2006 showed that from age six and older, the prevalence of serum IgE confirmed milk allergy was under 0.4%.

PKC results from a delayed hypersensitivity/inflammatory reaction to antigens expressed by various pathogens. Common agents include Staph. aureus, Mycobacterium tuberculosis, Chlamydia and Candida.

The disorder is thought to be caused by an anomaly in the arachidonic acid metabolizing cascade which leads to increased production of pro-inflammatory cysteinyl leukotrienes, a series of chemicals involved in the body's inflammatory response. When medications like NSAIDs or aspirin block the COX-1 enzyme, production of thromboxane and some anti-inflammatory prostaglandins is decreased, and in patients with aspirin-induced asthma this results in the overproduction of pro-inflammatory leukotrienes to causes severe exacerbations of asthma and allergy-like symptoms. The underlying cause of the disorder is not fully understood, but there have been several important findings:

- Abnormally low levels of prostaglandin E (PGE), which is protective for the lungs, has been found in patients with aspirin-induced asthma and may worsen their lung inflammation.

- In addition to the overproduction of cystinyl leukotrienes, overproduction of 15-lipoxygenase-derived arachidonic acid metabolites viz., 15-hydroxyicosatetraenoic acid and eoxins by the eosinophils isolated from the blood of individuals with AERD; certain of these products may help promote the inflammatory response.

- Overexpression of both the cysteinyl leukotriene receptor 1 and the leukotriene C synthase enzyme has been shown in respiratory tissue from patients with aspirin-induced asthma, which likely relates to the increased response to leukotrienes and increased production of leukotrienes seen in the disorder.

- The attachment of platelets to certain leukocytes in the blood of patients with aspirin-sensitive asthma has also been shown to contribute to the overproduction of leukotrienes.

- There may be a relationship between aspirin-induced asthma and "TBX21", "PTGER2", and "LTC4S".

- Eosinophils isolated from the blood of aspirin-induced asthma subjects (as well as severe asthmatic patients) greatly overproduce 15-hydroxyicosatetraenoic acid and eoxin C4 when challenged with arachidonic acid or calcium ionophore A23187, compared to the eosinophils taken from normal or mildly asthmatic subjects; aspirin treatment of eosinophils from aspirin intolerant subjects causes the cells to mount a further increase in eoxin production. These results suggest that 15-lipoxygenase and certain of its metabolites, perhaps eoxin C4, as contributing to aspirin-induced asthma in a fashion similar to 5-lipoxygenase and its leukotriene metabolites.

There is a strong genetic predisposition toward atopic allergies, especially on the maternal side. Because of the strong familial evidence, investigators have tried to map susceptibility genes for atopy. Genes for atopy (C11orf30, STAT6, SLC25A46, HLA-DQB1, IL1RL1/IL18R1, TLR1/TLR6/TLR10, LPP, MYC/PVT1, IL2/ADAD1, HLA-B/MICA) tend to be involved in allergic responses or other components of the immune system. C11orf30 seems to be the most relevant for atopy as it may increase susceptibility to poly-sensitization.