

Not all types of pollen are allergenic. Those responsible for respiratory allergies mainly belong the Poaceae family (fodder and cereal grasses: Dactylis (Cocksfoot or orchard grass), Timothy grass, Compositae family (e.g. ragweed, and ragwort), herbaceous plants (Pellitory-of-the-Wall (Parietaria officinalis) and for trees, from the Betulaceae family (e.g. Birch), Fagaceae family, Oleaceae family (ash, olive, oak, plane, etc.), and Cupressaceae family (cypress, juniper, thuja, white cedar and cedar).
House dust mites are the leading cause of respiratory allergies in both children and adults. The most allergenic species which are also commonly found in Europe- are house dust mites Dermatophagoides pteronyssinus and Dermatophagoides farinae.
House dust mites feed on dead skin and proliferate under well-determined conditions of relative humidity and temperature: 80% relative humidity and temperatures above productid 20°C.
House dust mites are perennial allergens. Mattresses and pillows provide the perfect ecological niche for reproduction but the highest densities of allergens are found in carpets and rugs, and stuffed toys.
House dust mite allergens are carried in their excrement and dead bodies.
The risk of sensitisation to dust mites depends on the density of mites in the home is high.
On the contrary, the prevalence of both sensitisation to house dust mites and asthma is relatively low in children who are brought up at high altitude where conditions are not conducive to mites growth.[1]
Example : House dust mites
Storage mites
Rural and agricultural areas have long been considered to have a monopoly on storage mites, which cause occupational allergies in farmers. However, recent studies have shown that urban populations, in particular those living in humid habitats, could become sensitised to storage mites.[2] Storage mites have even been found in bedding as is the case with house dust mites. High relative humidity promotes the growth of molds, which themselves comprise a nutritional environment for storage mites.
Therefore, it seems important to bear in mind a possible sensitisation to storage mites in the allergy diagnosis.
Over the last twenty years, increasing number of pets has resulted in a significant increase in the prevalence of hypersensitivity to related allergens[3].
Dogs and above all cats are the main animals responsible for allergic disease.
Horses also represent a potent allergen. Small rodents (hamsters, rabbits, mice, etc.), which are common inhabitants of children's bedrooms or classrooms, are often the cause of allergic symptoms.
Cat-derived allergens are mainly found on its skin, in the saliva and urine, and on the fur. They can also reach a relatively high density in the air in the form of particles of 2.5 µm in size.[4] Such particles may remain suspended in the air for several months even after the removal of the animal. Recently, it has been shown that even subjects who do not have a cat at home can develop hypersensitivity, and that the indirect exposure of an asthmatic child to cat allergens at school can worsens the disease. [5]
The inhalation of insect debris can induce respiratory allergies. Cockroaches are very allergenic. This allergy is particularly widespread in collective housing.[6] It may be the cause of severe asthma.
Bees, wasps or hornets are all hymenoptera. Their venom can cause immediate or delayed allergic reactions.
Hymenoptera venom: Examples:
Molds are ubiquitous organisms, due to their function as a degradation agent of food or industrial products. Molds can cause respiratory allergies. The small size of their spores (3 to 10 µm) encourages their penetration in the respiratory tract. During massive spore formation in the environment, molds can cause real epidemics of allergic asthma.
Molds result in both seasonal and perennial allergies, including rhinitis, conjunctivitis, and asthma. Most often held responsible, since they are the best-known: Alternaria, interior molds and exterior (in arid and desert areas) molds.[7] Penicillium and Cladosporium are predominant inside living quarters. Aspergillus is a mold that can induce both type I allergic reactions and type III reactions (Bronchopulmonary aspergillosis).
An extract from rubber trees (Hevea brasiliensis), natural latex is industrially treated and forms part of the composition of medical and surgical gloves, syringe joints, infusion tubing, cleaning gloves, balloons, pacifiers, soles, shoes, condoms, etc.
Since the middle of the 1980's, the expansion of the use of gloves by care providers and laboratory staff (due to the risk of infection with the HIV, HBV and HCV viruses) has led to a considerable rise in the number of latex allergies. In Europe, the data on prevalence vary between 0.04% and 1% of the general population. However, prevalence is much higher in certain at-risk groups such as healthcare staff, professions exposed to latex, patients having had multiple operations (e.g. children with spina bifida).[8]
Latex allergy is most frequently manifested by urticaria, but also by rhinitis, conjunctivitis and asthma (following the inhalation of latex particles transported by corn starch grains, present in the surgical or medical gloves). On occasion, severe systemic reactions or even anaphylactic shock may occur after contact with latex or during the ingestion of foods containing allergens that are cross-reactive with those of latex (kiwi, avocado, chestnut and banana).
Interior and urban pollution exacerbate rhinitis and asthma.
Urban pollution is linked to automobiles, and the main atmospheric pollutants are ozone, nitrogen dioxide (NO2) and sulfur dioxide (SO2).[9]
No less important if not predominant, pollution inside homes includes, in addition to allergens, polluting gases and aerosols, formaldehyde and tobacco smoke.
[1] Charpin D. et al. Rev Prat (paris) 1996 ; 46 : 942-8
[2] Olsson S. et al. Clin Exp Allergy. 2000 ; 30(7) : 912-9
[3] De Blay F. et al. Rev Mal Respi 2000; 017: 167-177
[4] De Blay F. et al. Rev Fr Allergol, 1998; 38: 839-841
[5] Almqvist C. et al. Am J Respir Crit Care Med 2001; 163: 695-8.
[6] De Blay F. et al. J Allergy Clin Immunol 1997; 99: 107-12.
[7] Halonen M. et al. Am J Crit Care med 1997; 155: 359-63.
[8] Cullinan P. et al. Clin Exp Allergy 2003; 33: 1484-1499.
[9] ARIA. J Allergy Clin Immunol. 2001; 108 (5 Suppl): S147-334.