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Background: House dust mite allergen levels in humid coastal regions of Australia are high, particularly in beds. Because high allergen levels in beds are associated with more severe asthma, reduction of levels may be important for asthma control., Objective: We tested the effectiveness of an acaricidal treatment of bedding in combination with occlusive mattress and pillow encasings in reducing allergen levels in children's beds in a community setting., Methods: A total of 14 beds of children were selected for the active intervention. In each home the bed of a sibling of nearest age was selected as the control. Dust was vacuumed from beds by using a standard protocol, and Der p 1 levels were measured by using ELISA. Adjacent settling dust was collected by using opened Petri dishes. The intervention consisted of encasing mattresses and pillows in occlusive covers and washing all bedding with Acaril, an acaricidal additive. The acaricidal wash was repeated twice in 7 households at 2-month intervals. Control beds were not treated., Results: The mean Der p 1 concentration at baseline was 27.9 microg/g in the active beds and 18.1 microg/g in the control beds. At 4 days after intervention, Der p 1 decreased to 3.2 microg/g and 15.7 microg/g in active and control beds, respectively. The average difference (active minus control) over the first 8-week cycle was 78.5% (P <.0001), and the difference over 3 washing cycles was 125.1% (P <.05). The mean rate of settling Der p 1 adjacent to the actively treated beds decreased from 24.4 ng.m(-2).d(-1) at baseline to 10.0 ng.m(-2).d(-1) after intervention (P <.01)., Conclusion: A substantial reduction in Der p 1 levels in beds and in airborne dust in a humid region with naturally high house dust mite allergen levels can be achieved and sustained in a community setting with use of occlusive covers and a rigorous washing routine.

Background: Measurement of personal exposure to Der p 1 aeroallergen has previously been limited by the low quantity of material collected by sampling systems and the assay sensitivity. This has meant that exposure could only be detected if long sampling periods were used or reservoir dust was artificially disturbed. We have developed a sampling method to sample true personal exposure and combined it with a novel method which is sensitive enough to measure allergen exposure over shorter time frames., Objective: To describe normal domestic exposure to dust mite allergen during a range of activities in houses in Sydney, Australia., Methods: Inhaled particles containing mite allergen Der p 1 were collected using a nasal air sampler which impacts particles (> approximately 5 microm) onto a protein-binding membrane coated with a thin, porous, adhesive film. The allergen is bound to the membrane in the immediate vicinity of the particle and detected by immunostaining with monoclonal antibodies specific for Der p 1. In addition, samples were collected using a standard Institute of Occupational Medicine (IOM) personal air sampler and the amount of eluted Der p 1 was assayed by ELISA., Results: The median number (range) of inhaled particles containing Der p 1 collected in each 10-min sampling period was: dust raising 5 (2-10); lying in bed, 0 (0-2); sitting on the bed, 1 (0-2); walking around the bedroom, 0 (0-2). This represented 0-5.1% of all particles captured. The Der p 1 concentration of floor and bed dust was 19.4 and 55.1 microg/g, respectively. The standard IOM personal sampler and ELISA were unable to detect Der p 1 for any of the activities performed., Conclusions: We were able to count individual allergen-carrying particles inhaled over short time periods, during different domestic exposure situations. This will offer new insight into several aspects of personal allergen exposure.

House dust mite (HDM) allergens are important factors in the increasing prevalence of asthma. The lung epithelium forms a barrier that allergens must cross before they can cause sensitization. However, the mechanisms involved are unknown. Here we show that the cysteine proteinase allergen Der p 1 from fecal pellets of the HDM Dermatophagoides pteronyssinus causes disruption of intercellular tight junctions (TJs), which are the principal components of the epithelial paracellular permeability barrier. In confluent airway epithelial cells, Der p 1 led to cleavage of the TJ adhesion protein occludin. Cleavage was attenuated by antipain, but not by inhibitors of serine, aspartic, or matrix metalloproteinases. Putative Der p 1 cleavage sites were found in peptides from an extracellular domain of occludin and in the TJ adhesion protein claudin-1. TJ breakdown nonspecifically increased epithelial permeability, allowing Der p 1 to cross the epithelial barrier. Thus, transepithelial movement of Der p 1 to dendritic antigen-presenting cells via the paracellular pathway may be promoted by the allergen's own proteolytic activity. These results suggest that opening of TJs by environmental proteinases may be the initial step in the development of asthma to a variety of allergens.

Background: Infancy may be a critical time for exposure to house dust mite allergens, when exposure to high levels can increase the risk of allergic sensitization and the development of asthma in later life., Objective: To measure house dust mite allergen (Der p 1) concentration in the infants' environment and examine lifestyle factors which may influence mite allergen exposure., Methods: Infants aged between 4 and 12 months (n = 134) from the western region of Sydney, Australia. participated. Reservoir dust samples were collected from four sites within each home: infant's bed, second bed (adult or second child's bed), lounge floor and sheepskins (where available). Settling aeroallergen was collected for 10-14 d in Petri dishes in the infant's room. Der p 1 was measured by ELISA. A questionnaire on types of bedding, sleeping and playing patterns of the infant was completed by the parents at the time of dust collection., Results: All infants were exposed to at least one site with Der p 1 concentrations greater than 10 microg/g fine dust. The mean settling aeroallergen level in the infants' room was 24 ng De p l/m2 day and this was weakly related to bed allergen levels (r=0.21, P<0.05). Mattress type had a weak effect on Der p 1 levels as measured in the whole bed (P = 0.07), while bed cover and bed type had no effect (P>0.6). The mean product of time spent at a site and its allergen concentration was highest for beds in 69% of infants., Conclusion: The high level of allergen exposure in the environment of this group of infants places them at an increased risk of early sensitization and development of asthma. Any strategy to reduce asthma prevalence should address these high and avoidable levels.

Background: In coastal Australia, mean house-dust-mite allergen concentration is 20-40 times higher in homes than in public buildings. Allergen concentrations in university colleges, which share some characteristics of both homes and public buildings, are not known. The study aimed to compare bed mite-allergen concentration in colleges with local homes., Methods: Mattress dust was collected from three colleges (n = 60 in each) and local homes (n = 68) during summer. Der p 1 was measured by ELISA. Information was collected on the floor plan of the colleges, cleaning practices, age of building, and orientation of room., Results: Most college mattresses (94%) had Der p 1 concentrations less than the mean of homes in the same climate. The geometric means of Der p 1 in the mattresses of the colleges were as follows: A, 8.9 micrograms Der p 1/g fine dust (95% CI 6.9, 11.5); B, 1.9 (1.5, 2.3); and C, 1.5 (1.2, 2.0), compared to homes, 22.5 (17.6, 28.7). The percentages of college mattresses with less than 2 micrograms/g were 7%, 48%, and 58%, respectively, compared to 4% for homes. Higher Der p 1 concentrations were weakly associated with age of building in college A, and orientation in college B. Der p 1 concentrations were independent of floor level and age of mattress., Conclusions: These findings indicate that low allergen concentrations are achievable without extreme hygiene and cleaning measures in a climate which supports mite proliferation in homes.

House dust mite (HDM) allergen exposure and its relation to HDM allergy and asthma was assessed in a case-control study conducted over three seasons in 74 Sydney schoolchildren, 33 of whom were allergic to HDM and 12 of whom had current asthma. In each season histamine inhalation tests and skin prick tests were performed, symptom questionnaires were administered, and dust samples were collected. The mean concentrations of HDM allergen (in micrograms of Der p 1 per gram of fine dust) were: bed, 38.9 (95% confidence interval [CI], 31.8 to 47.5); bedroom floor, 22.4 (95% CI, 18.3 to 27.5); and lounge room floor, 13.7 (95% CI, 10.7 to 17.6). The mean of the highest allergen concentration in each house was 51.0 (95% CI, 43.2 to 60.1). All but two subjects had at least one site in all seasons with an HDM allergen concentration greater than 10 micrograms/gm, the proposed threshold for asthma symptoms. Subjects with allergy to HDM, symptoms of asthma, or airway hyperresponsiveness did not have higher HDM allergen concentrations in their house. In this study we were unable to test hypotheses concerning proposed thresholds for risk of sensitization and for risk of asthma symptoms because virtually all subjects were exposed to HDM allergen levels above the proposed thresholds.

To measure the association between changes in house dust mite (HDM) allergen Der p I exposure and changes in the severity of asthma, we re-analysed data from a clinical trial in which 34 HDM-allergic subjects with asthma (18 women, mean age 35 years) were followed for between 3 and 12 months. The concentration of Der p I in fine dust from the bed, the bedroom floor and the living room floor was measured at 3-monthly intervals along with assessment of subjects' spirometric function and airway hyperresponsiveness (AHR, measured by histamine inhalation test). Daily symptom scores, morning peak expiratory flow rate and peak flow variability were measured throughout the study period. The mean Der p I concentration in the bed at baseline was 25.4 micrograms/g (95% CI: 15.8-40.6). During the course of the study large within-subject fluctuations were observed in allergen concentrations and in the measurements of the severity of asthma. Changes in allergen concentration in the bed were significantly correlated with changes in AHR (P = 0.003) and symptom score (P = 0.04). Changes in allergen concentration in the living room floor were correlated with changes in symptom scores (P = 0.01). Although these correlations were significant the magnitude of the effect was relatively modest. We conclude that a large reduction in HDM allergen concentration, particularly in the bed, results in a modest reduction in AHR and improvement in symptoms in HDM-allergic subjects with asthma.

To test the effectiveness of a house dust mite (HDM) allergen avoidance strategy we conducted a randomized controlled trial in 35 atopic subjects with asthma, aged 13 to 60 living in Sydney - a high HDM allergen environment. After a 3 month run-in period, subjects were randomized to active allergen avoidance treatment (n = 17) or placebo (n = 18) groups and followed for 6 months. The active treatment involved placing impermeable covers over the mattress, pillows and duvet and spraying the remaining bedding, as well as the carpets and furniture, with a tannic acid/acaricidal spray. Subjects kept a daily record of symptoms and peak expiratory flow rates and had 3 monthly assessments of lung function and airway hyperresponsiveness (AHR). Dust samples were collected from the bed, the bedroom floor and the living room floor at 3 monthly intervals and 2 weeks after the treatment. Mean HDM allergen levels at baseline at these sites were, in the active group, 15.5, 9.6 and 10.2 micrograms Der p I/g of fine dust, and, in the placebo group 25.7, 11.8 and 6.3 micrograms/g. Two weeks after the allergen avoidance treatment the HDM allergen level in the beds was reduced to 29% of baseline (95% CI 16-50%, P = 0.038 compared with placebo), but was not significantly different at 3 or 6 months. There was also no significant effect of the allergen avoidance treatment on symptom scores, peak flow variability, lung function or AHR P > 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)