Risk factors for<unk>  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<unk> c 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,<unk> n levels, and dietary changes. Dust mites Dust mite<unk> , also known as house dust<unk> , is a sensitization and<unk> c reaction to the droppings of house dust mites. The<unk>  is common and can trigger<unk> c reactions such as asthma, eczema or itching. It is the manifestation of a parasitosis. The mite's gut contains potent digestive enzymes (notably peptidase 1) that persist in their feces and are major inducers of<unk> c reactions such as wheezing. The mite's exoskeleton can also contribute to<unk> c reactions. Unlike scabies mites or skin follicle mites, house dust mites do not burrow under the skin and are not parasitic. Foods A wide variety of foods can cause<unk> c reactions, but 90% of<unk> c responses to foods are caused by cow's milk, soy, eggs, wheat, peanuts, tree nuts, fish, and shellfish. Other food<unk> es, affecting less than 1 person per 10,000 population, may be considered "rare". The use of hydrolysed milk baby formula versus standard milk baby formula does not appear to change the risk. The most common food<unk>  in the US population is a sensitivity to crustacea. Although peanut<unk> es are notorious for their severity, peanut<unk> es are not the most common food<unk>  in adults or children. Severe or life-threatening reactions may be triggered by other<unk> ns, and are more common when combined with asthma. Rates of<unk> es differ between adults and children. Peanut<unk> es can sometimes be outgrown by children. Egg<unk> es affect one to two percent of children but are outgrown by about two-thirds of children by the age of 5. The sensitivity is usually to proteins in the white, rather than the yolk. Milk-protein<unk> es are most common in children. Approximately 60% of milk-protein reactions are immunoglobulin E-mediated, with the remaining usually attributable to inflammation of the colon. Some people are unable to tolerate milk from goats or sheep as well as from cows, and many are also unable to tolerate dairy products such as cheese. Roughly 10% of children with a milk<unk>  will have a reaction to beef. Beef contains small amounts of proteins that are present in greater abundance in cow's milk. Lactose intolerance, a common reaction to milk, is not a form of<unk>  at all, but rather due to the absence of an enzyme in the digestive tract. Those with tree nut<unk> es may be<unk> c to one or to many tree nuts, including pecans, pistachios, pine nuts, and walnuts. Also seeds, including sesame seeds and poppy seeds, contain oils in which protein is present, which may elicit an<unk> c reaction.<unk> ns can be transferred from one food to another through genetic engineering; however genetic modification can also remove<unk> ns. Little research has been done on the natural variation of<unk> n concentrations in unmodified crops. Latex Latex can trigger an IgE-mediated cutaneous, respiratory, and systemic reaction. The prevalence of latex<unk>  in the general population is believed to be less than one percent. In a hospital study, 1 in 800 surgical patients (0.125 percent) reported latex sensitivity, although the sensitivity among healthcare workers is higher, between seven and ten percent. Researchers attribute this higher level to the exposure of healthcare workers to areas with significant airborne latex<unk> ns, such as operating rooms, intensive-care units, and dental suites. These latex-rich environments may sensitize healthcare workers who regularly inhale<unk> nic proteins. The most prevalent response to latex is an<unk> c contact dermatitis, a delayed hypersensitive reaction appearing as dry, crusted lesions. This reaction usually lasts 48–96 hours. Sweating or rubbing the area under the glove aggravates the lesions, possibly leading to ulcerations. Anaphylactic reactions occur most often in sensitive patients who have been exposed to a surgeon's latex gloves during abdominal surgery, but other mucosal exposures, such as dental procedures, can also produce systemic reactions. Latex and banana sensitivity may cross-react. Furthermore, those with latex<unk>  may also have sensitivities to avocado, kiwifruit, and chestnut. These people often have perioral itching and local urticaria. Only occasionally have these food-induced<unk> es induced systemic responses. Researchers suspect that the cross-reactivity of latex with banana, avocado, kiwifruit, and chestnut occurs because latex proteins are structurally homologous with some other plant proteins. Medications About 10% of people report that they are<unk> c to penicillin; however, 90% turn out not to be. Serious<unk> es only occur in about 0.03%. Insect stings Typically, insects which generate<unk> c responses are either stinging insects (wasps, bees, hornets and ants) or biting insects (mosquitoes, ticks). Stinging insects inject venom into their victims, whilst biting insects normally introduce anti-coagulants. Toxins interacting with proteins Another non-food protein reaction, urushiol-induced contact dermatitis, originates after contact with poison ivy, eastern poison oak, western poison oak, or poison sumac. Urushiol, which is not itself a protein, acts as a hapten and chemically reacts with, binds to, and changes the shape of integral membrane proteins on exposed skin cells. The immune system does not recognize the affected cells as normal parts of the body, causing a T-cellmediated immune response. Of these poisonous plants, sumac is the most virulent. The resulting dermatological response to the reaction between urushiol and membrane proteins includes redness, swelling, papules, vesicles, blisters, and streaking. Estimates vary on the percentage of the population that will have an immune system response. Approximately 25 percent of the population will have a strong<unk> c response to urushiol. In general, approximately 80 percent to 90 percent of adults will develop a rash if they are exposed to of purified urushiol, but some people are so sensitive that it takes only a molecular trace on the skin to initiate an<unk> c reaction. Genetics<unk> c diseases are strongly familial: identical twins are likely to have the same<unk> c diseases about 70% of the time; the same<unk>  occurs about 40% of the time in non-identical twins.<unk> c parents are more likely to have<unk> c children, and those children's<unk> es are likely to be more severe than those in children of non-allergic parents. Some<unk> es, however, are not consistent along genealogies; parents who are<unk> c to peanuts may have children who are<unk> c to ragweed. It seems that the likelihood of developing<unk> es is inherited and related to an irregularity in the immune system, but the specific<unk> n is not. The risk of<unk> c sensitization and the development of<unk> es 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. Ethnicity may play a role in some<unk> es; 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. Hygiene hypothesis<unk> c diseases are caused by inappropriate immunological responses to harmless antigens driven by a TH2-mediated immune response. Many bacteria and viruses elicit a TH1-mediated immune response, which down-regulates TH2 responses. The first proposed mechanism of action of the hygiene hypothesis was that insufficient stimulation of the TH1 arm of the immune system leads to an overactive TH2 arm, which in turn leads to<unk> c disease. In other words, individuals living in too sterile an environment are not exposed to enough pathogens to keep the immune system busy. Since our bodies evolved to deal with a certain level of such pathogens, when they are not exposed to this level, the immune system will attack harmless antigens and thus normally benign microbial objects—like pollen—will trigger an immune response. The hygiene hypothesis was developed to explain the observation that hay fever and eczema, both<unk> c diseases, were less common in children from larger families, which were, it is presumed, exposed to more infectious agents through their siblings, than in children from families with only one child. The hygiene hypothesis has been extensively investigated by immunologists and epidemiologists and has become an important theoretical framework for the study of<unk> c disorders. It is used to explain the increase in<unk> c diseases that have been seen since industrialization, and the higher incidence of<unk> c diseases in more developed countries. The hygiene hypothesis has now expanded to include exposure to symbiotic bacteria and parasites as important modulators of immune system development, along with infectious agents. Epidemiological data support the hygiene hypothesis. Studies have shown that various immunological and autoimmune diseases are much less common in the developing world than the industrialized world and that immigrants to the industrialized
Allergy
Foodborne illness
Hypersensitivity
Food intolerance
Alloimmunity
Bronchiolitis
Pseudoallergy
Scombroid food poisoning