Allergens in the Environment
An allergen is any substance that can trigger an allergic response - Type-I hypersensitivity reaction in atopic (genetically predisposed) individuals.
The Reaction[✎ edit | edit source]
Acute response - the antigen is presented by an Antigen-Presenting Cell to TH2 lymphocytes. These TH2 lymphoctes cells interact with B lymphocytes and secrete Interleukin-4 (IL-4). The TH2 interaction and IL-4 cause the B-lymphocytes to respond by producing IgE antibodies. Secreted IgE circulates in the blood and binds to IgE-specific receptors on the surface of mast cells and basophils and sensitises these cells to the allergen. On subsequent exposure, the allergen binds to the IgE on the surface of sensitised mast cells or basophils. The cells are activated and undergo degranulation - release of histamine and other inflammatory mediators (cytokines, interleukins, leukotrienes, and prostaglandins) into the extracellular space. The effects of this include:
- Mucous secretion
- Nerve stimulation
- Smooth muscle contraction
This manifests clinically as rhinorrhea, itchiness, dyspnea, and anaphylaxis. Depending on various factors, the effects can be systemic (anaphylaxis), or localized (asthma in the respiratory system and eczema in the dermis)
Late-phase response - 2 to 24hours after acute reaction. It's mediated by other cells (neutrophils, lymphocytes, eosinophils and macrophages) that migrate to the inflamed site.
Risk Factors[✎ edit | edit source]
Risk factors can be divided into host and environmental factors.
Host factors Heredity (most important) Allergies are strongly familial: 70% concordance in identical twins and 40% in non-identical twins. Children with allergic parents are more likely to have the allergies and with increased severity compared to children of non-allergic parents. Others include: Gender Race Age
- Exposure to infectious diseases during early childhood - The hygiene hypothesis was developed when it was observed that hay fever and eczema were less common in children from larger families - where there are apparently more infectious agents present - than in children from one-child families. It states that insufficient stimulation of the TH1 arm of the immune system leads to an overactive TH2 arm, which in turn leads to allergic disease. It is supported by epidemiological data that shows immunological and autoimmune diseases are less common in developing countries than in industrialised countries.
- Environmental pollution
- Allergen levels in the environment
- Dietary changes
Transmission of Allergens[✎ edit | edit source]
Allergens are substances normally present in the environment and direct contact with allergen can be through:
- Surface contact with the allergen
They can also be contacted through
- Bite of allergen carrier
Common Allergens[✎ edit | edit source]
Foods - Ingestion The 'officially' recognised list changes across countries due to different genetic profiles and eating habits, the United States Food and Drug Administration recognises eight foods as common allergens - peanuts, tree nuts, eggs, milk, shellfish, fish, wheat and their derivatives, and soy and their derivatives, as well as sulphites (at 10ppm and over, found in food flavouring and colouring). Canada recognises these eight as well as sesame seeds and mustard. The European Union recognises the ten in Canada as well as celery.
Animal products - Inhalation / surface contact
- Dust mite - among the most common cause of allergies and triggers of asthma worldwide. They excrete least 15 allergens in their faeces and these are divided into groups. Groups 1 and 2 are the culprits of allergies. Group 1 consists of catalytic proteins (e.g. proteases) and group 2 are mite proteins (not as common as Group 1).
- Fel d 1 (cats)
- Fur and Dander
- Cockroach calyx
Drugs - By inoculation
Fungal allergies - Inhalation
- Fungal allergies are considered to be a major source of airborne allergens and are associated with seasonal asthma. Basidiospores are the dominant airborne fungal allergens and this family Includes - mushrooms, rusts, smuts, brackets,and puffballs.
- Bee sting venom
- Wasp sting venom
- Mosquito stings
Plant pollen (hay fever) - Fall under seasonal allergies - Inhalation
- Grass e.g. ryegrass
- Weeds e.g. nettle
- Trees e.g. birch, willow
Testing[✎ edit | edit source]
2 tests are widely used to detect the presence of allergen-specific IgE antibodies. A skin prick test and/or an allergy blood test. Both methods are recommended and have similar diagnostic value in terms of sensitivity and specificity.
Skin-prick testing Tiny punctures are made into the patient's skin, commonly on the forearm and back. Small amounts of suspected allergens and/or their extracts (e.g. pollen, peanut extract) are introduced to marked sites. A small plastic or metal device is used to puncture or prick the skin. Sometimes, the allergens are injected into the skin. If the reaction is positive, inflammation will occur within 30 minutes. This can range from slight reddening to hives.
Allergy blood test This measures the concentration of specific IgE antibodies in the blood. It's suitable for all regardless of age, skin condition, medication, symptom, illness or pregnancy. Multiple allergens can be detected with a single blood sample and it's safe since the patient isn't exposed to the allergen.
Treatment[✎ edit | edit source]
Traditional treatment is to simply avoid the allergen or reduce exposure.
Pharmacological intervention includes administering drugs that block the action of chemical allergy mediators or prevent activation of cells and degranulation. These include antihistamines, glucocorticoids, epinephrine (adrenaline), theophylline and cromolyn sodium.
Anti-allergy immunotherapy is a desensitisation treatment where the patient's production of IgG against the allergen is gradually stimulated. He/She is progressively larger doses of the allergen and this can either reduce the severity or eliminate hypersensitivity altogether.
Links[✎ edit | edit source]
Related Articles[✎ edit | edit source]
Bibliography[✎ edit | edit source]
Kay AB (2000). "Overview of 'allergy and allergic diseases: with a view to the future'". Br. Med. Bull. 56 (4): 843–64. doi:10.1258/0007142001903481
Food Allergy in children and young people. Costing report. Implementing NICE guidance, 2011. http://guidance.nice.org.uk/CG116/CostingReport/pdf/English
Kerkhof M, Dubois AE, Postma DS, Schouten JP, de Monchy JG (2003). "Role and interpretation of total serum IgE measurements in the diagnosis of allergic airway disease in adults". Allergy 58
Sicherer SH, Leung DY (2007). "Advances in allergic skin disease, anaphylaxis, and hypersensitivity reactions to foods, drugs, and insects". J. Allergy Clin. Immunol. 119
GREGORY, PH.; HIRST, JM. (Sep 1952). "Possible role of basidiospores as air-borne allergens". Nature 170 (4323): 414–414
Goldsby, Richard A., et al.,Immunology. 5th ed. New York: W.H. Freeman