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 From these results, the American Academy of Pediatrics rescinded their recommendation to delay exposure to peanuts in children, also stating there is no reason to avoid peanuts during pregnancy or breastfeeding.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.

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.

Risk factors for allergy can be placed in two general categories, namely host and environmental factors. Host factors include heredity, sex, race, and age, with heredity being by far the most significant. However, there have been recent increases in the incidence of allergic disorders that cannot be explained by genetic factors alone. Four major environmental candidates are alterations in exposure to infectious diseases during early childhood, environmental pollution, allergen levels, and dietary changes.

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.

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.

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.

Estimates of latex sensitivity in the general population range from 0.8% to 8.2%.

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.

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.

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.

In countries in North America and western Europe, where use of cow's milk based infant formula is common, chicken egg allergy is the second most common food allergy in infants and young children after cow's milk. However, in Japan, egg allergy is first and cow's milk second, followed by wheat and then the other common allergenic foods. A review from South Africa reported egg and peanut as the two most common allergenic foods.

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. Egg 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. One review estimates that in North American and western European populations the prevalence of egg allergy in children under the age of five years is 1.8-2.0%. A second described the range in young children as 0.5-2.5%. Although the majority of children develop tolerance as they age into school age years, for roughly one-third the allergy persists into adulthood. Strong predictors for adult-persistent allergy are anaphylactic symptoms as a child, high egg-specific serum IgE, robust response to the skin prick test and absence of tolerance to egg-containing baked foods. Self-reported allergy prevalence is always higher than food-challenge confirmed allergy.

For all age groups, a review of fifty studies conducted in Europe estimated 2.5% for self-reported egg allergy and 0.2% for confirmed. National survey data in the United States collected in 2005 and 2006 showed that from age six and older, the prevalence of serum IgE confirmed egg allergy was under 0.2%.

Adult-onset of egg allergy is rare, but there is confirmation of cases. Some were described as having started in late teenage years; another group were workers in the baking industry who were exposed to powdered egg dust.

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%.

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.

Contact sensitivity, atopic dermatitis, eczema, and urticaria appear to be related phenomena, the cause of which is generally believed to be the hydrophobic prolamin components of certain Triticeae, Aveneae cultivars. In wheat one of these proteins is ω-gliadin (Gli-B1 gene product). A study of mothers and infants on an allergen-free diet demonstrated that these conditions can be avoided if wheat sensitive cohort in the population avoid wheat in the first year of life. As with exercise induced anaphylaxis aspirin (also: tartrazine, sodium benzoate, sodium glutamate (MSG), sodium metabisulfite, tyramine) may be sensitizing factors for reactivity. Studies of the wheat-dependent exercise induced anaphylaxis demonstrate that atopy and EIA can be triggered from the ingestion of that aspirin and probably NSAIDs allow the entry of wheat proteins into the blood, where IgE reacts within allergens in the dermal tissues. Some individuals may be so sensitive that low dose aspirin therapy can increase risk for both atopy and WDEIA.

Wheat allergies were also common with contact dermatitis. A primary cause was the donning agent used for latex gloves prior to the 1990s, however most gloves now use protein free starch as donning agents.

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.

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.

Risk factors for drug allergies can be attributed to the drug itself or the characteristics of the patient. Drug-specific risk factors include the dose, route of administration, duration of treatment, repetitive exposure to the drug, and concurrent illnesses. Host risk factors include age, sex, atopy, specific genetic polymorphisms, and inherent predisposition to react to multiple unrelated drugs (multiple drug allergy syndrome).

A drug allergy is more likely to develop with large doses and extended exposure.

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.

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.

Alpha-gal allergies develop after a person has been bitten by the lone star tick in the United States, the European castor bean tick, and the paralysis tick in Australia. Alpha-gal is not naturally present in apes and humans, but is in all other mammals. If a tick feeds on another mammal, the alpha-gal will remain in its alimentary tract. The tick will then inject the alpha-gal into a person's skin, which in turn will cause the immune system to release a flood of IgE antibodies to fight off the foreign carbohydrate. Researchers still do not know which specific component of tick saliva causes the reaction.

A 2012 preliminary study found unexpectedly high rates of alpha-gal allergies in the Western and North Central parts of the United States, which suggests that the allergy may be spread by unknown tick species. Examples of alpha-gal allergies were even present in Hawaii, where none of the ticks identified with the allergies live. Human factors were suggested but no specific examples were provided.

Alpha-gal is present in the anti-cancer drug cetuximab, as well as the IV fluid replacements Gelofusine and Haemaccel. Blood thinners derived from porcine intestine and replacement heart valves derived from porcine tissue may also contain alpha-gal.

There has been at least one instance of a man with an alpha-gal allergy going into anaphylaxis after receiving a heart valve transplant. Some researchers have suggested that the alpha-gal which is prevalent in pig's tissue and used for xenografts may contribute to organ rejection.

For those allergic to fruits, cooking may help reduce or eliminate the reaction to some fruits.

People with this allergy might not necessarily be allergic to citrus fruits.

There are many different types of fruits that people have been shown to react allergically such as mangoes and bananas. Some foods are clearly more allergenic than others. In adults, peanuts, tree nuts, finned fish, crustaceans, fruit, and vegetables account for 85% of the food-allergic reactions(O'Neil, Zanovec and Nickla).

People suffering from allergies may suffer from a hypersensitivity to the allergic food, which is what causes the allergic reaction. Most fruit allergies are oral syndrome allergies because they are consumed but may also be an external allergy if the fruit touches the skin.