SummaryBackground International guidelines recommend allergen avoidance for asthma management, but do not include making assessments of allergen exposure. Mite allergen exposure cannot be assumed, especially in geographical regions where climatic conditions vary.Objective To develop a rapid test that would enable consumers to detect mite allergen in the home.Methods A lateral flow test using gold labelled antibody for mite group 2 allergen was developed as part of a detection kit incorporating the MITEST dust sampling device. Dust samples were assayed by ELISA for group 1 and group 2 allergens and by using the rapid test. The tests were compared as indices of mite allergen exposure.Results There was a good correlation between group 1 and group 2 levels by ELISA (n = 349, r = 0.60, P < 0.001). In a multi‐centre study of 65 homes (263 dust samples) in five countries, there was a strong correlation between ELISA and the rapid test. Most samples with high scores in the test (43/48, 90%) contained > 1 µg/m2 group 2 allergen, whereas most low samples contained < 1 µg/m2 (50/64, 78%). Differences between mean group 2 levels of samples that scored low (0.28 µg/m2), medium (1.68 µg/m2) or high (3.18 µg/m2) on the test were highly significant (P 0.007 to < 0.001).Conclusions A simple rapid test has been developed that detects mite allergen in the home within 10 min. The mite screening test should educate consumers about allergen exposure and encourage compliance with allergen‐avoidance procedures. This technology has applications for the detection of other common environmental allergens.

Clinical & Experimental AllergyVolume 22, Issue s2 p. 1-28 Free Access The control of allergens of dust mites and domestic pets: a position paper M. J. COLLOFF, Corresponding Author M. J. COLLOFF Department of Zoology, University of Glasgow, Glasgow G12 8QQ, U.K.Dr M. J. Colloff, Department of Zoology, University of Glasgow, Glasgow G12 8QQ, U.K.Search for more papers by this authorJ. AYRES, J. AYRES Regional Department of Respiratory Medicine, East Birmingham Hospital, Bordesley Green East, Birmingham B9 5ST, U.K.Search for more papers by this authorF. CARSWELL, F. CARSWELL Respiratory Research Group, Department of Child Health, Royal Hospital for Sick Children, Bristol BS2 8BJ, U.K.Search for more papers by this authorP. H. HOWARTH, P. H. HOWARTH Medicine I, Level D, Centre Block, Southampton General Hospital, Southampton SO9 4XY, U.K.Search for more papers by this authorT. G. MERRETT, T. G. MERRETT Allergy Analysis Centre, 31 Station Lane, Witney, Oxfordshire OX8 6AN, U.K.Search for more papers by this authorE. B. MITCHELL, E. B. MITCHELL The Blackrock Clinic, Blackrock, Co. Dublin, Republic of IrelandSearch for more papers by this authorM. J. WALSHAW, M. J. WALSHAW Cardiothoracic Centre, Broadgreen Hospital, Liverpool L14 3LB, U.K.Search for more papers by this authorJ. O. WARNER, J. O. WARNER Department of Child Health, Southampton General Hospital, Southampton S09 4XY, U.K.Search for more papers by this authorJILL A. WARNER, JILL A. WARNER Department of Child Health, Southampton General Hospital, Southampton S09 4XY, U.K.Search for more papers by this authorA. A. WOODCOCK, A. A. WOODCOCK Regional Department of Respiratory Physiology, Wythenshawe Hospital, Manchester M23 9LT, U.K.Search for more papers by this author M. J. COLLOFF, Corresponding Author M. J. COLLOFF Department of Zoology, University of Glasgow, Glasgow G12 8QQ, U.K.Dr M. J. Colloff, Department of Zoology, University of Glasgow, Glasgow G12 8QQ, U.K.Search for more papers by this authorJ. AYRES, J. AYRES Regional Department of Respiratory Medicine, East Birmingham Hospital, Bordesley Green East, Birmingham B9 5ST, U.K.Search for more papers by this authorF. CARSWELL, F. CARSWELL Respiratory Research Group, Department of Child Health, Royal Hospital for Sick Children, Bristol BS2 8BJ, U.K.Search for more papers by this authorP. H. HOWARTH, P. H. HOWARTH Medicine I, Level D, Centre Block, Southampton General Hospital, Southampton SO9 4XY, U.K.Search for more papers by this authorT. G. MERRETT, T. G. MERRETT Allergy Analysis Centre, 31 Station Lane, Witney, Oxfordshire OX8 6AN, U.K.Search for more papers by this authorE. B. MITCHELL, E. B. MITCHELL The Blackrock Clinic, Blackrock, Co. Dublin, Republic of IrelandSearch for more papers by this authorM. J. WALSHAW, M. J. WALSHAW Cardiothoracic Centre, Broadgreen Hospital, Liverpool L14 3LB, U.K.Search for more papers by this authorJ. O. WARNER, J. O. WARNER Department of Child Health, Southampton General Hospital, Southampton S09 4XY, U.K.Search for more papers by this authorJILL A. WARNER, JILL A. WARNER Department of Child Health, Southampton General Hospital, Southampton S09 4XY, U.K.Search for more papers by this authorA. A. WOODCOCK, A. A. WOODCOCK Regional Department of Respiratory Physiology, Wythenshawe Hospital, Manchester M23 9LT, U.K.Search for more papers by this author First published: September 1992 https://doi.org/10.1111/j.1365-2222.1992.tb01763.xCitations: 170AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat References 1 Marsh DG, Zwollo P, Huang SK, Ansari AA. Molecular genetics of human responsiveness to allergens. In: D Chadwick, D Evered, J Whelan, eds. IgE, Mast Cells and the Allergic Response. Ciba Foundation Symposium No 147. 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SummaryNatamycin, a fungicide marketed as Tymasil, is claimed to reduce house dust mite numbers and would therefore be expected to improve asthma in children with mite sensitivity. We have tested this assertion by a double‐blind, placebo‐controlled trial. There was no significant effect on levels of Der p I in mattress dust between active and placebo groups at the end of the spraying period. Histamine inhalation challenge PC20, clinic visit symptom scores and lung function tests reflecting either large or small airways obstruction were also unchanged. Therefore this product is not a therapeutic option for mite‐allergic patients using the manufacturer's recommended dose and method of administration. Other factors influencing the Der p I levels were also investigated. Of these, only month of measurement and bedroom wall humidity showed any association.

A liquid-phase, antigen-binding radioimmunoassay measuring subclass IgG4 antibody (ab) to allergens has been developed. This assay, which uses monoclonal anti-IgG4 to bind IgG4, allows direct comparison of class (IgG)- and subclass (IgG4)-specific ab levels. These assays used radiolabeled purified allergens, Der p I (Ag P1) from the dust mite Dermatophagoides pteronyssinus, Lol p I (Rye 1), from ryegrass pollen, hen's egg ovalbumin, and β-lactoglobulin from cow's milk. We have investigated IgG4 abs in several clinical situations. The results confirm that IgG ab responses to both inhalants and food proteins unequivocally include IgG4 ab. On average, the proportion of IgG4 ab to these antigens is far higher than the contribution of IgG4 to total IgG. In patients with adult atopic dermatitis, levels of both class and subclass ab were higher than in control subjects; however, the ratio of IgG4:IgG varied widely in patients and control subjects. During desensitization treatment of patients with perennial rhinitis, levels of IgG4 ab to Der p I increased sharply, but there were also increases in the total IgG ab responses so that the precentage contribution of IgG4 was only moderately increased (mean values: before, 29%; after, 36%). In a prospective study of children from atopic families, IgG4 abs to food proteins were detectable as early as 3 months. IgG abs to hen's egg ovalbumin and β-lactoglobulin from cow's milk increased to a maximum at 3 years and declined by 5 years. However, specific IgG4 as a percentage of specific IgG increased progressively from a mean value of ∼15% at 6 months to ∼50% at 5 years of age. Overall, the results do not support a role for IgG4 in immediate skin reactivity as the sole blocking ab or in the production of allergic symptoms. However, given the known properties of the IgG4 subclass, changes in IgG4 abs to food allergens could well alter the impact of these proteins on young children.

Environmental factors were examined as determinants of clinical disease in a five year prospective study of 73 children born to atopic parents. Clinical follow up for evidence of eczema and wheezing was combined with regular skin testing, immunoglobulin assay, and respiratory viral culture where appropriate. Thirty six children developed eczema, which was often associated with a positive result of a skin test to ingestants in the first year and inhalants by the fifth year. Thirty two children developed one or more episodes of wheeze. Fifteen children wheezed once only, and not all of these developed atopy. No pattern of respiratory infection in early life was characteristic of children with recurrent wheeze. There was a significant difference in parental smoking habits between children with and without episodes of wheeze at the fifth birthday. No protective effect of breast feeding could be shown. The development of allergic disease in susceptible children is influenced by many environmental factors. Advice to families about reduction of environmental allergens continues to pose problems, but parents should be advised to avoid smoking in the child's presence.

Application of inhalant allergens in high concentration to the mildly abraded skin of sensitive patients with atopic dermatitis gave rise to eczematous skin responses at 48 h. These lesions, infiltrated by basophils, eosinophils and mononuclear cells, are examples of cutaneous basophil hypersensitivity. Repeated application of allergen induced an increase in skin mast cells by 6 days, the mast cell hyperplasia replacing the earlier basophil infiltration. No electron microscopic evidence of mast cell heterogeneity among the recruited cells was found.

Sixty patients with atopic dermatitis attending an allergy clinic were assessed for evidence of skin sensitivity and serum antibodies to egg and milk proteins. Prick skin test responses to egg were found in 23 patients and in 74% of these positive egg radioallergosorbent test (RAST) was demonstrable. Positive prick test for milk were present in 10 patients, but only 30% gave a positive milk RAST. Quantitative intradermal skin testing, RAST, and a double antibody antigen binding radioimmunoassay confirmed the presence of IgE antibody to egg proteins but indicated that the levels were very low when compared to those seen to the house dust mite antigen in sensitive patients. In contrast, IgG antibody to purified egg and milk proteins was present in large amount in most patients, the levels being significantly higher than in non-allergic controls.

Patients with atopic dermatitis have IgE antibodies to common environmental antigens, both foods and inhalants. Such antibodies are probably relevant and exposure to the corresponding antigens can give rise to eczema. Nevertheless, the mechanisms involved and the role of other etiologies, e.g. contact reactions, remain to be elucidated. Patients with atopic dermatitis should have comprehensive evaluations to determine the role of environmental antigens.

We have recently shown that peripheral blood mononuclear cells from patients sensitive to the house dust mite, D. pteronyssinus, will proliferate in vitro in response to the purified major allergen, antigen P1. Such cell populations, separated on Ficoll gradients, were shown to contain basophils, and had an average histamine content of 12 ng/10(6) cells. Incubation with antigen P1 resulted in the release of histamine, and histamine is known to activate T suppressor cells. In the present experiments we observed up to 80% inhibition of proliferation (mean 50-60%) with histamine added at 3.3 X 10(-7)-3.3 X 10(-5) M. Cultures of T cells supplemented with irradiated non-T cells, that had been depleted of cells bearing surface membrane IgG, IgM and IgE, contained on average 63% less histamine than unseparated cultures. However, no consistent difference in the proliferative response to antigen P1 was observed. Depletion of histamine by pre-incubation of the cells with antigen P1 at 10(-3)-10(-4) micrograms/ml followed by washing of the cells before culture also produced no significant change in the proliferative response. Passage of cell population over nylon wool resulted in depletion of basophils, as well as other cell types, and generally led to a decrease in proliferation. We conclude that release of mediators from basophils in cell cultures does not markedly affect the magnitude of the proliferative response to antigen P1. The varied responses seen with cells from different individuals are likely to reflect differences in the numbers of circulating allergen sensitized T cells.

Immunoglobulin E (IgE) has a central role in allergic reactions although it rarely exceeds 5 micrograms ml-1 even in the serum of severely allergic individuals. Both mast cells and basophils possess receptors which bind the Fc portion of IgE with high affinity; crosslinking of membrane-bound IgE by allergen results in degranulation of the cell and release of a variety of pharmacologically active mediator including histamine. Myeloma IgE has been successfully used to block the skin sensitizing activity of allergic sera; however, human myeloma IgE is clearly in limited supply. The emergence of techniques allowing the stable introduction of immunoglobulin gene DNA into myeloma cells has allowed us to construct a mouse cell line that secretes a chimaeric IgE, lambda 1 antibody whose heavy chain is composed of a human C epsilon constant region fused to a mouse variable (VH) region. This chimaeric IgE is specific for the hapten 4-hydroxy-3-nitro-phenacetyl (NP) and can, when crosslinked by antigen, trigger the degranulation of human basophils. When not crosslinked, however, the chimaeric IgE can prevent the passive sensitization of these cells by sera from allergic subjects.

SummaryHouse dust mite sensitivity is very common in patients with bronchial asthma, yet dust mite avoidance frequently receives little attention in clinical management. It is likely that any reduction in allergen levels associated with routine cleaning is insufficient to allow clinical improvement. In the present study the acaricide pirimiphos methyl is shown to reduce the levels of Dermatophagoides pteronyssinus, antigen P1 in homes. Following a single application the level of antigen P1 in dust from carpets was reduced by up to 73% and by more than 50% in soft furnishings. Serial sampling showed a reduction for 6 weeks under conditions where carpets and chairs treated with solvent showed a progressive rise in allergen level. Furthermore the survival of mites in cultures or infested carpet segments was markedly inhibited, with antigen PI accumulation reduced by >90%. These results suggest major reductions in house dust mite allergen levels in the home can be achieved.

In a prospective study of 92 children with at least one atopic parent, the development of the specific antibody responses to food and inhalant allergens during the first 5 years of life were assessed. By the radioallergosorbent test egg specific IgE antibody occurred in about 30% of the children with the mean peak concentration at 12 months. By the second year the prevalence of this antibody had increased whereas the mean concentration had decreased. Milk specific IgE antibody could not be shown in any subject, including four whose skin tests yielded positive results. Food specific IgG antibody was noted by antigen binding radioimmunoassays at 3 months in most children. These responses had peaked and began to fall by the fifth year. In contrast few children had detectable IgE or IgG antibody to inhalant allergens before the first 2 years of life. Both the concentration and prevalence of specific antibody, however, increased from the second to the fifth year and was greater in children whose skin tests yielded positive results. Breast feeding was associated with an increase in the prevalence of positive results from skin tests but was not associated with detectable IgE antibody to both food proteins, a lower concentration of IgG antibody to cows' milk, and was not associated with protection against the development of disease. A high level of exposure to dust mite was associated with an increased prevalence of positive results from skin tests to dust mite and appreciably higher antibody concentration. This study indicates differences in the humoral responses to food and inhalant allergens. Environmental factors appear to influence the development of these responses.

Peripheral blood mononuclear cells (PBMC) from the majority of the allergic patients that we tested who were skin test-sensitive to the house dust mite Dermatophagoides pteronyssinus (D. pt.) (46/67) showed significant proliferation in response to the purified major allergen Antigen P1; PBMC from 14/15 nonsensitive controls showed no significant response. Optimal responses were seen with 10 micrograms Antigen P1/ml, but 21 of 43 patients tested showed significant proliferation at 0.01 microgram Antigen P1/ml. The results of three types of experiments showed that the responding cells were T cells, predominantly of the helper phenotype. First, purified T cells in the presence of irradiated or mitomycin C-treated antigen-presenting cells showed good proliferation to Antigen P1. Secondly, flow cytometry analysis showed a progressive increase in the percentage of viable cells bearing the Leu-3a marker--up to 88% by day 7--and demonstrated that the larger, blast-transformed cells bore this marker. Finally, interleukin 2 production was demonstrated in antigen-stimulated cultures at days 3 to 5, i.e., about 2 days before the peak of proliferation. When patients were grouped according to their disease symptoms, no clear differences were seen between the T cell responses of patients with asthma, eczema, or rhinitis, or with asthma and eczema, although patients with rhinitis alone tended to show weaker responses. Overall, there was a significant correlation between serum IgE antibody to Antigen P1 and T cell proliferation (rs = 0.579, p less than 0.001); however, excluding individuals with no IgE antibody, the quantitative correlation was poor (rs = 0.26, p less than 0.1). These results indicate that most patients showing immediate hypersensitivity to D. pt. have circulating T cells sensitized to Antigen P1. These sensitized T cells probably act as helper cells for antibody production, but may also play a role in the pathogenesis of allergic lesions and in the delayed or chronic symptoms of these allergic diseases.

Inhalant allergens applied to the skin of sensitive atopic dermatitis patients by means of a modified patch test technique, induce acute eczematous lesions. These lesions contain basophils, eosinophils, mononuclear cells, and neutrophils and represent an example of human cutaneous basophil hypersensitivity. The role of IgE antibody in this eczematous reaction was studied by systemic and local passive transfer experiments. Plasma with high IgE antibody when infused into patients with hypogammaglobulinemia as part of their replacement treatment resulted, post infusion, in cutaneous mast cell and blood basophil sensitization as measured by quantitative skin testing and leukocyte histamine release. Subsequent patch tests on these patients using the house dust mite antigen, antigen P1, produced macroscopic erythematous responses containing mononuclear cells, and eosinophils but not basophils. Local transfer of atopic dermatitis serum with high IgE antibody produced weak macroscopic responses and in these lesions mononuclear cells and both basophils and eosinophils were present. The serum activity which allowed transfer of basophil and eosinophil recruitment was heat labile. Specifically purified antibody to the mite antigen P1 (containing IgE and IgG antibody), when transferred, allowed eosinophil but not basophil recruitment to patch test sites. These results suggest that while the allergen-induced patch test response may involve IgE antibodies, as well as the cells normally involved in delayed responses, another serum activity is also involved.