Mites, pets, cockroaches and fungi are the main sources of indoor aeroallergens. More occasionally, rare allergens such as those from plants can induce sensitization and symptoms.

House dust mites are arthropods belonging to the subphylum Chelicerata, class Arachnida, order Acari and suborder Astigmata. Other mites found in the Astigmata suborder include storage mites and scabies mites. Thirteen species of mites have been found in house dust, three of which are very common in homes around the world and are the major source of domestic allergens.

Mite bodies and mite faeces are the source of mite allergens. The allergens associated with mite faeces are enzymes that originate from the mite’s digestive tract. Other mite allergens may originate from saliva, supra-coxal gland secretions (involved in water uptake) and enzymes associated with the moulting process.

The most common mite species are Dermatophagoides farinae, Dermatophagoides pteronyssinus and Euroglyphus maynei, which are all found in temperate climates. In tropical and subtropical climates the storage mite, Blomia tropicalis, is also often found in house dust along with the other dust mites.

In the USA and continental Europe, most homes are co-inhabited with D. farinae and D. pteronyssinus, but one species usually predominates. In Europe and in most other countries, D. pteronyssinus species is found more frequently than D. farinae; an exception is the inland part of Finland, where D. farinae predominates. In some parts of Europe, such as Reykjavik (Iceland), Uppsala (Sweden) and Albacete (Spain), very few domestic samples contain detectable levels of group 1 mite allergens.

Mite allergens that are most often measured in the domestic environment are the major group 1 allergens: Der p 1, Dermatophagoides pteronyssinus 1 and Der f 1, Dermatophagoides farinae 1. Mattresses and mattress bases are the principal reservoir of mite allergens, but allergens are also found in dust from carpets, chairs, sofas and clothing. They may also be detected on soft toys and in dust from day-care centers and in various other public places such as cinemas, trains and buses.

Prospective studies have demonstrated that early domestic exposure to mite allergens is a risk factor for the development of specific sensitization, and that such sensitization is a risk factor for decreased lung function at school age. In mite-free environments, mite-allergic asthmatics have lower levels of specific IgE to mite, reduced specific and nonspecific bronchial hyper responsiveness and a decrease in air trapping and airway inflammation.

Patients with mite sensitization are rarely aware of a relationship between exposure and symptoms. Nevertheless, some of them describe rhinitis and/or asthma in contact with dust or in certain houses. The average time from exposure to the onset of symptoms is 30 min.

Cat allergens

Fel d 1 (Felis domesticus1). More than 80% of patients who are allergic to cats display IgE reactivity to Fel d 1 which is produced by the sebaceous, salivary and anal glands of domestic cats. Different species can produce different levels of allergen; moreover, the production of Fel d 1 depends on the hormonal status of the cat; male cats -especially those non-neutered – produce more allergen than females.

Fel d 2. Cat albumin (Fel d 2) is a minor allergen, sensitizing only about 15% of cat allergic patients. It is found in serum as well in epithelial extracts. Specific sensitization to cat albumin appears to be more common in patients with atopic dermatitis than in those with rhinitis.

Fel d 3. Fel d 3 is a cystein protease inhibitor (cystatin) and another major allergen, sensitizing between 60 and 90% of cat allergic people.

Fel d 4, a lipocalin, is also a major cat allergen with as many as 63% of cat allergic individuals having Fel d 4-specific IgE.

Cat immunoglobulins. These allergens are present in both the serum and epithelial extracts from cats and are occasional causes of specific sensitization.

Dog allergens

Can f 1 and Can f 2. Like most – but not all – mammalian allergens, these are lipocalin proteins. About 80% of patients with an allergy to dogs display IgE reactivity to Can f 1 and Can f 2. Can f 1 is produced by tongue epithelial tissue whereas Can f 2 is predominantly produced by parotid glands and only to a lesser extent by the tongue. Neither allergen is produced by the skin but both may be present on hair and dander. No significant amounts of these allergens have been found in dog urine or faeces. As with cats, there may be some inter-breed differences; Can f 1, for example, seems to be produced less by Labradors than other dog breeds.

Dog albumin (Can f 3) and immunoglobulin. Dog albumin and immunoglobulins are present in dog serum and in epithelial extracts but are minor allergens only, sensitizing just 5-30% of patients with dog allergies.

Cross reacting allergens between cat and dog

Patients very often display positive skin prick test responses to both cat and dog extracts and the question arises whether this reflects co-sensitization or cross sensitization. Since both cat and dog allergens (Can f 1 and 2 and Fel d 4) are lipocalins, some degree of cross-reactivity is plausible. The presence of a Fel d 1-like allergen in a dog extract has been demonstrated and may represent a target for the cross-reactive IgE antibodies present in the sera of 25% of cat- and dog-allergic patients; the clinical relevance of this allergen is unknown. Furthermore, albumin is an allergen present in both cat and dog secretions, although its clinical relevance too is still under discussion.

Cat allergens

In many parts of the world, exposure to Fel d 1 is ubiquitous; the allergen has been found and measured in the dust of mattresses, carpets, sofas, classrooms, clinical waiting rooms (including those of allergists), the upholstery of buses, trains and cars, and shopping areas. Moreover, 40% of airborne Fel d 1 is associated with particles less than 5μm and can be measured in undisturbed air. In school classrooms where there are pupils who are cat owners, the levels of airborne Fel d 1 may be higher than in houses without a pet cat.

In a US national survey, 13% of homes had at least one pet cat (but not a dog); 9% of homes contained measurable levels of Fel d 1 with a geometric mean concentration of 4.73 μg/g of dust. Feld 1 concentrations were significantly higher in homes in the more western regions, and in households with higher incomes and with white residents of above-average educations. Fel d 1 levels measured in house dust appear to be sufficiently stable so that single measurements can be used with confidence in longitudinal epidemiologic studies.

Dog allergens

Can f 1 can be found not only in the dust from sofas, carpets and mattresses of homes housing dogs, but also in houses without a dog. As with cat allergens, it may be detected in the dust from classrooms, and in the upholstered seats of private cars, where levels are higher in cars whose owners keep dogs at home.

Twenty-one per cent of US dwellings house at least one dog, but Can f 1 has been detected in up to 100% of US homes.

For mite, cat and dog allergens the gold standard of exposure measurement in dust or air is by the use of ELISA-based methods using monoclonal antibodies directed against the major allergens. For mite allergens, semi-quatitative home tests such as the Acarex test® and Rapid test® have been developed and show a good correlation with the ELISA methods.

Cat sensitization rates in population based studies have varied from 36% in 17-year-old Finnish teenagers to 3% in German children aged 9-11. For dog, in the same age groups, the prevalence of sensitization varied from 19% in Finland to 2.6% in Munich. In patients attending allergy clinics, the sensitization rate for cat allergen, assessed by skin prick test, varied between 23 and 30% in Northern Europe, between 10 and 28% in central Europe and between 13 and 43%, in southern Europe.

Children who attended classes where more than 18% of pupils were cat owners reported significantly decreased PEF, more days with asthma symptoms, and increased use of medication after school started. Immediate bronchial responses to cat allergen appeared to be localized in large airways.

The data on the effect on early pet ownership and indoor allergen exposure on the development of asthma in young children are conflicting. While several studies have shown that pet ownership during infancy decreased the risk of wheeze in later childhood, others have not found any association. However, most of the data show a trend of reduced risk for allergic disease in children exposed to animals early in life.

Measuring allergens in settled house dust and in domestic air suggests that, in some circumstances, levels of mouse allergens in indoor environments may be similar to those found in animal research facilities; in the USA, mouse allergens were detectable in 80% of dust samples collected in schools and in 100% of bedrooms in inner city homes; indeed, in a recent multicenter study performed in 75 different locations throughout the USA, 82% of randomly selected dwellings had measurable mouse allergen in house dust. Mouse allergen levels have consistently been found to be higher in kitchen dust than in bed dust. In contrast, concentrations of Mus m 1 and Rat n 1 (the major mouse and rat allergens, respectively) in Strasbourg (France) and in the UK seem to be far lower. The clinical significance of domestic rodent allergens (except in the case of pet animals) is unclear.

Rabbits, guinea pigs and hamsters are also often kept as pets and each is a source of several important allergens present mainly in fur, but also in dander, urine and saliva. In an Italian multicenter study, 2.4% of children were sensitized to rabbit allergens, only half of whom had daily or episodic contact with these animals. Only 10% of the sensitized subjects – exclusively pet rabbit owners with asthma – were mono-sensitized.

Rodents (especially rats and mice) are well-known as inducers of occupational respiratory symptoms in laboratory workers. In the domestic environment in the US, Mus m 1 and Rat n 1 were found in respectively 95 and 33% of the houses of inner-city children with asthma.

Guinea pigs, to which the prevalence of symptoms is about 30% in occupational settings, are often kept as pets and can induce indoor asthma. Similarly, a report of 30 cases suggests that hamster ownership is associated with mild to severe asthma, sometimes requiring hospital admission and becoming evident about 15 months after the onset of hamster exposure. In a large population-based survey in Japan, pet hamster ownership appeared independently to increase the risk of respiratory symptoms.

Severe asthma symptoms have been described in a patient washing a pet male ferret; specific IgE antibodies were detected against urinary proteins. Allergy to mink, a mammal from the same family as the ferret, has been described in occupational settings; keeping mink as pets is not unusual in certain countries. Household contact with chinchillas may lead to sensitization; allergic rhinitis and/or asthma in children and adults have been confirmed by nasal provocation testing.

Cockroaches are common allergens in many countries especially in the warm parts of North America and Asia, but are infrequent causes of allergic diseases in Europe. Of the 69 species recorded from North America, 24 species are invasive. The most common pest species are: the German cockroach (Blattela germanica), the American cockroach (Periplaneta Americana), the oriental cockroach (Blatta orientalis), the brow-banded cockroach (Supella longipalpa) and the smoky-brow cockroach (Periplaneta fuliginosa).

Several major cockroach allergens have been identified. In one study, twice as many cockroach allergic asthmatics had IgE antibodies against Bla g 2, compared with those against Bla g 1. An estimated 60-70% of cockroach-sensitive individuals have IgE antibodies to the allergens Bla g 4 and Bla g 5.

In some countries, cockroaches are one of the most common insects encountered by homeowners, especially those living in low-income housing. Even low numbers of cockroaches can produce significant amounts of allergen, and after extermination and/or reduction of cockroach numbers, and even with aggressive cleaning, allergens can be measured in dust for longer than 6 months. The most aggressive pest management strategies seem significantly to reduce allergen levels but often not below the ‘disease threshold’ of 8 U/g of house dust.

In some countries, exposure to cockroach allergens has an important role in asthma morbidity among inner city children. In inner cities in the USA, for example, more asthmatic children with cockroaches reported in their home were sensitized to cockroach allergens than those without exposure to cockroaches. In the same country, a study of urban, suburban and rural atopic patients found a higher prevalence of cockroach sensitivity among patients with a primary diagnosis of asthma (50%), than among those with a primary diagnosis of allergic rhinitis (30%). Exposure to cockroach allergens in early life has been associated with recurrent asthmatic wheezing in children with a family history of atopy. Exposure and sensitization to cockroach allergens increased rates of hospitalization, school absences and days with wheezing among asthmatic children.

In European and other countries, sensitization to cockroaches appears to be less common; as is any associated morbidity. In France, for example, the prevalence among children of specific IgE antibodies to cockroach allergens seems to be below 5%. Importantly, evidence of specific sensitization can be influenced by co-sensitization with other house dust allergens such as mites, which have cross reacting allergens (glutathion transferase and tropomyosin) with cockroaches.

Cockroaches present an additional, potential health problem; in a study of 80 cockroaches, around 70% were contaminated with Salmonella species, many of them resistant to antibacterial drugs.

Exposure of atopic children and adults to molds appears to be a risk factor for asthma. However, the fact that many studies have not been able to confirm an association points to the extreme difficulty of correctly assessing exposure to molds and, a fortiori, their allergens. Furthermore, although atopic individuals are at greater risk for asthma, the onset of cough and wheezing in atopic children and adults when exposed to molds might be not only the consequence of an allergic reaction but also an inflammatory response to the inhalation of mycotoxins and volatile organic substances liberated by molds.

Fungal growth indoors is influenced by various environmental factors, the most important of which is the availability of water. Water leaks, defective drainage, inadequate ventilation and moisture condensation resulting from faulty thermal insulation and heating, cooling and ventilation systems have been major contributors to moisture-related fungal problems in buildings. Prolonged high relative humidity has been shown to increase both dust and airborne fungal populations in indoor environments.

The indoor environment may also become a secondary source of exposure if fungal spores colonize interior or building materials. Although indoor fungal levels tend to reflect the levels found outdoors, housing characteristics and occupants’ behavior can affect exposure levels considerably.

Alternaria

Alternaria spores are common aeroallergens in many regions of the world, especially in warm inland climates and in arid regions. Alternaria exposure is often assessed by outdoor spore counts, because the most intense exposure is likely to occur outdoors. Nonetheless, fungal spores can enter a home from outside via ventilation or infiltration, or they can be carried in by occupants in their hair, skin, clothing or on their shoes as well as on their pets’ fur; the presence of a dog increases fungal populations in floor dust.

In the dust of 831 houses in 75 locations throughout the USA, Alternaria antigen was detected in 95% of samples. Different factors may influence exposure to Alternaria; for example, antigen concentrations are significantly higher in homes that use dehumidifiers. The presence of a dehumidifier may be an indication of a persistent humidity or moisture problem, but dehumidifiers can also become reservoirs for fungi. Predictors of domestic Alternaria antigen concentrations vary by location because the activities of occupants and pets can affect each location in the home differently. Having carpeting in bedrooms predicts lower concentrations in beds, whereas kitchens with carpeting have significantly higher levels than kitchens without carpeting; frequent cooking may also result in higher temperature and humidity levels in kitchen. Furthermore, the presence of children predicts higher antigen levels in beds but not in floor or upholstery dusts. Less frequent cleaning contributes to higher Alternaria antigen levels in floor and upholstery dusts, especially in living rooms; correspondingly, levels in beds are lower if bedding is washed more frequently. Washing temperature (cold, warm, hot) does not seem to influence antigen levels.

Other molds

Aspergillus, Cladosporium and Penicillium levels in indoor environments are highest in the autumn, correlating with outdoor concentrations. Where indoor air levels are higher than those outside, this appears to be associated with home characteristics including damp (Cladosporium and Alternaria), the ownership of a pet cat (Aspergillus), cockroach infestation (Aspergillus) and a ‘musty’ smell (Penicillium).

The most frequent indoor molds are Aspergillus, Penicillium, Cladosporium and Alternaria. ELISA tests have been developed for measuring the major allergens of Alternaria (Alt a 1) and Aspergillus fumigatus (Asp f 1), but in most domestic environments, measurable levels are found in fewer than 10% of homes. It has been demonstrated that several common fungal species including Aspergillus and Alternaria release more allergen on germination than before germination and Asp f 1 can more often be measured in domestic air if its spores have germinated. However the clinical relevance of allergens associated with fungal germination remains to be resolved; ungerminated spores might be deposited in the favorable environment of warmth and moisture in the lung or nasal cavity, subsequently germinate and act as an additional source of allergen.

In a European survey from the GA²LEN network, between 2.6 and 4% of patients in Northern Europe who were skin prick tested for inhalant allergens were found to be sensitized to Alternaria. Corresponding figures for central and southern Europe respectively were 1.7-16.4% and 10-20.5%. In general European population samples the prevalence is probably lower (1.1-5.1%).

Among 4962 European subjects aged between 3 and 80 years and with rhinitis and asthma, 19% had a positive skin test at least to one mold; 15% of them were sensitized only to one or more molds (Alternaria 60%, Candida 33%, Trichophyton 4.6%) and not to other common aeroallergens. Among 4-year-old atopic children, the prevalence of a positive skin prick test to Alternaria alternata or Cladosporium herbarum was 6%.

Exposure to Alternaria alternata may be a risk factor for asthma. In some studies the prevalence of current symptomatic asthma increased with increasing domestic Alternaria concentrations. In 414 children from seven urban American communities, all of them sensitized to molds, a correlation with indoor concentrations of Alternaria and Cladosporium has been reported. In centers with a higher prevalence of asthma, the prevalence of reported indoor mold exposure was also high.

Asthma is the most common disease in children sensitized to molds. In a pediatric survey, at 4 years of age Alternaria and Cladosporium were the third most common causes of sensitization after house dust mite and grass pollen; and sensitization to molds correlated positively with a clinical diagnosis of asthma. An association between daily emergency department visits for asthma to the Children’s Hospital of Ontario, and daily concentrations of both pollen grains and fungal spores over a five-year period was found. The percentage increase associated with each group was 1.9% for deuteromycetes (Alternaria, Cladosporium, Penicillium, Aspergilus, Epicoccum). Mold exposure has also been associated with asthma symptoms and bronchial responsiveness, the effect being stronger in subjects sensitized to Cladosporium species. For children sensitized to Alternaria and heavily exposed to this mold there is a markedly increased risk of severe asthma.

In a multicenter European epidemiological survey, data from people aged 20-44 with asthma and skin prick tests suggested that the severity of asthma was associated with sensitization to airborne molds rather than to pollens and cats. The frequency of sensitization to molds (Alternaria alternata or Cladosporium herbarum, or both) increased significantly with increasing asthma severity. Multiple mold reactions were also much commoner in the group with multiple admissions and the number of asthma admissions was related to the number and size of positive mold skin allergy tests and less strongly correlated to the number and size of non-mold allergy tests.

Exposure to molds can cause human disease through several well-defined mechanisms including the generation of a harmful immune response, direct infection by the organism and toxic irritant effects from mold byproducts. In addition, many new mold-related illnesses have in recent years been hypothesized; many of these remain largely or completely unproven. Concerns about mold exposure and its effects are so common that all healthcare providers, particularly allergists and immunologists, are frequently faced with issues regarding both real and asserted mold-related illnesses.

Homes occasionally contain a large number of storage mites, such as Lepidoglyphus destructor, Tyrophagus putrescentiae and longior, Aleuroglyphus ovatus and Gohieria fusca. Sensitization rates to storage mites are highest in city dwellers; approximately 10% of the general population in Ohio (urban, suburban and rural) are sensitized to L. destructor and/or T. putrescentiae.

House dust contains significant levels of silver fish (Lepisma saccharina) antigen, the clinical significance of which is unclear.

Insects of the Coleopters order cause occupational sensitization in mill workers. In the indoor environment, cough and rhino-conjunctivitis during housekeeping were related to larvae of dermestidae (Attagenus pelio), a diagnosis of specific allergy being confirmed by epicutaneous tests, and specific IgE determination to larval proteins. A case of asthma has been reported, induced by dermestidae larvae present in wooden floors in a dwelling with stuffed animals on the wall. Environmental control measures such as scraping and disinfesting the wooden floor and covering it with a varnish, as well as removal of the stuffed animals, were sufficient to control the patient’s symptoms. Another example is allergic asthma to Psocus spp. (Pscoptera). These insects have been shown to proliferate in hemp fibers, which are sometimes used for house insulation.

Other inhalant insect allergens have been described as outdoor agents responsible for epidemic asthma, possibly induced by crickets, locusts and moths (caddis fly). Some allergies to moths are related to hobbies: for instance, anglers may be in contact with different kinds of moths and their larvae. Other food products such as crustaceans or different worms and larvae can also lead to sensitization in fish hobbyists. In Japan, a higher frequency of IgE antibody responses to insects (moth, butterfly, caddis fly and chironomids) was found in patients with bronchial asthma; and air sampling revealed the presence of insect-related particles less than 10 μm in diameter.

Scaly animals such as lizards were assumed not to be allergenic. However, allergy to iguana has been reported and confirmed by skin tests and in vitro studies to iguana scales.

Respiratory sensitization to avian allergens has also been described. The responsible allergens, especially Gal d 5, an alphalivetin, are implicated in bird egg syndrome.

Green algae (chlorella) grow under similar conditions to molds and can be found as indoor allergens. Sensitization to chlorella has been described in children (6% of outpatients in a study from Germany) and is mainly found among mold-sensitized patients. The clinical relevance, however, has not been clearly demonstrated.

Among ornamental plants, Ficus spp., especially Ficus benjamina, was found to sensitize 6% of 395 outpatients in Sweden; among them 3% were symptomatic with perennial asthma, rhinitis or conjunctivitis. Specific Ficus allergens have been detected in house dust samples including those that are also present in natural rubber latex derived from a species of the same family (Hevea brasiliensis). Other latex plants, such as Euphorbia pulcherina and Araujia sericifera can induce immediate allergies in atopic patients. Other clinical cases of allergy to ornamental plants have been described, including allergy to the coffee plant, to papyrus (Cyperus alternifolius) and to Tradescantia albifloxia. Cut and dried flowers are potential allergenic sources but in the domestic setting seem to be less frequently a problem than they are for gardeners and florists.

Allergens introduced by stinging insects can induce allergic manifestations in the indoor environment. An example is given by fleas and especially cat fleas as well as by ground bugs. The European pigeon ‘soft tick’ (Argas reflexus) lives inside houses and is increasingly widespread due to growing pigeon colonies in urban areas. Bites by ticks usually occur at night and severe allergic reactions have been reported.

Exposure to airborne food allergens by handling and cooking can be induced by odors, fumes, vapors or sprays, which have a potential role in provoking clinical manifestations such as asthma, rhinitis and conjunctivitis in sensitized patients. Reactions induced by peeling vegetables such as raw potatoes, carrots and fresh asparagus are well-known, but the elicitation of asthma by the steam of cooking vegetables such as chick peas and lentils is also possible. The inhalation of steam when boiling fish or shrimps or other crustacean can also be an inadvertent exposure to allergens in the kitchen. Exposure to airborne allergens, even in low amounts, can induce moderate to severe symptoms in highly sensitized patients. Patients with peanut allergy may develop respiratory symptoms in closed environment such as an airplane cabin where peanut packages are opened.

In assessing new or less well-known allergic etiologies, it is essential to document clinical cases by immunological tests. This requires expert laboratory support. The publication of well documented clinical cases increases the number of accessible and useful references in the literature, and will assist in the provision of evidence-based advice on the avoidance of relevant etiological factors that may lead to complete and definitive recovery.

There is no clear evidence that the primary prevention of allergic sensitization and/or disease by environmental allergen reduction in the home is effective. In contrast, there is valuable evidence relating to ‘tertiary preventive’ methods (the prevention of symptoms in allergic patients) for several allergens.

Mite allergens

Several studies have demonstrated a clinical benefit in mite-sensitive asthmatic children when global allergen avoidance has been performed; for example, symptoms in such children improve when they stay at altitudes of 1800 m or more. In contrast, three meta-analyses have underlined the absence of any consistent efficacy of methods of dust mite allergen exposure reduction and consequent clinical improvement. Major weaknesses in the published literature, however, make a definitive conclusion difficult.

Cat allergens

Two clinical studies, each using a vacuum cleaner with HEPA filter and an air cleaner in patients allergic to cat but who kept a cat at home, had contradictory findings. The first showed a benefit in terms of bronchial hyper responsiveness; the second showed no benefit.

Cockroach allergens

It is essential to identify the pest species; the use of commercial traps is further important in determining the extent and severity of the problem. Control strategies should include elimination of potential pest reservoirs and conduits and, when necessary, the application of insecticidal sprays, with minimal exposure to people and pets; a community action plan may be necessary. Post-treatment evaluations are essential.

Global allergen avoidance

Home visits by an Indoor Environment Medical counselor who has the time to measure, counsel and control compliance appears necessary. This new job has been validated by a multicenter study in France and two other larger studies in the USA.

A randomized, controlled study included 937 children aged from 5 to 11 years with moderate to severe allergic asthma. After one year of global allergen avoidance using an indoor technician and different allergen reduction methods a significant decrease in allergen exposures was observed. This was associated with a 19% reduction in symptoms, a 13% reduction in emergency visits and a 20% reduction in school absenteeism. There was a correlation between clinical improvement and reductions in allergen exposures. The authors claimed that all the reduction methods were costeffective. Under such conditions, global avoidance must be regarded as part of the treatment of severely allergic asthma in children who are exposed to domestic allergens.

Further reading

Celedon, J., Milton, D., Ramsey, C. et al. (2007) Exposure to dust mite allergen and endotoxin in early life and asthma and atopy in childhood. J. Allergy Clin. Immunol. 120: 144-149.

Chew, G., Rogers, C., Burge, H. et al. (2003) Dustborne and airborne fungal propagules represent different spectrum of fungi with differing relations to home characteristics. Allergy 58: 13-20.

De Blay, F., Fourgaut, G., Hodelin, G. et al. (2003) Medical indoor environment counselor (MIEC) role in the compliance with advice on mite allergen avoidance and on mite allergen exposure. Allergy 58: 27-33.

Gotzsche, P., Johansen, H. (2008) House dust mite control measures for asthma. Cochrane Database Syst. Rev. 2: CD001187. Review.

Mahillon, V., Saussez, S., Michel, O. (2006) High incidence of sensitization to ornamental plants in allergic rhinitis. Allergy 61: 1138-1140.

Morgan, W., Crain, E., Gruchalla, R. et al. (2004) Results of a home-based environmental intervention among urban children with asthma. New Engl. J. Med. 351: 1068-1080.

Platt-Mills, T., Vaughan, J., Squillace, S. et al. (2001) Sensitization, asthma and modified Th2 response in children exposed to cat allergen: a population-based cross-sectional study. Lancet 357: 752-756.

Rust, M.K., (2008) Cockroaches. In Public Health Significance of Urban Pests, Bonnefoy, X., Kampen, H., Sweeney K. (eds). WHO: Copenhagen; 53-84.

Zock, J., Jarvis, D., Luczynskz, C. et al. (2002) Housing characteristics, reported mold exposure and asthma in the European Community Respiratory Health Survey. J. Allergy Clin. Immunol. 110: 285-292.