The risk factors

A genetic predisposition

In allergic individuals, there is a type of antibody called IgE, which recognizes the allergens to which the individual is sensitive. These antibodies then trigger inflammation upon contact.

The predisposition of certain individuals to develop an IgE response to environmental allergens is called atopy. It has been shown that there is a family predisposition also called an "atopic" tendency, which makes it possible to determine the risk of allergic manifestations in a child:

 

 If neither parent is allergic

12.5% to 15%

 If one of the parents is allergic

25% to 40%

 If both parents are allergic

50% to 65%

 If both parents plus another close family member are allergic

< ou = à 75%

 

 

The environment

Changes in the environment and lifestyles, increasing urbanisation, pollution, tobacco use or passive smoking (secondhand smoke) and the changes in our eating habits are all factors that promote the development of allergies.

Individuals are constantly confronted by new allergens. Atmospheric pollutants are not the cause of allergic manifestations but they appear as aggravating factors.

The hygiene hypothesis

The first explanation is tied to the hygiene hypothesis [1] developed by Strachan in 1989.

Several recent studies have demonstrated in reproducible fashion that there is a lower prevalence of allergic rhinitis and asthma in children who have several siblings (especially older siblings), in children who go to the nursery regularly and starting at an early age, or in children who were born on dairy farms.

Studies provide arguments that lend support to the possible protective function of early exposure to pets on the subsequent risk of allergy: seven times out of eight, exposure to a cat or dog is associated, at least in a subgroup, with a lower risk of at least one allergy indicator (asthma, wheezing, atopic dermatitis, atopic sensitisation).

In a single study, the allergic risk is significantly increased in cat owners, solely when the mother has a history of asthma. Nevertheless, it is not possible to confirm that such exposure protects individuals from allergic disease.

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[1] Liu et al. J allergy Clin Immunol. 2003 ; 111 :471-8