WOOLCOCK AJ. Changing prevalence of asthma in Australian children

Department of Medicine, University of Sydney, NSW, Australia.
BMJ Clinical Research (Impact Factor: 14.09). 07/1994; 308(6944):1591-6. DOI: 10.1136/bmj.308.6944.1591
Source: PubMed


To investigate whether prevalence of asthma in children increased in 10 years.
Serial cross sectional studies of two populations of children by means of standard protocol.
Two towns in New South Wales: Belmont (coastal and humid) and Wagga Wagga (inland and dry).
Children aged 8-10 years: 718 in Belmont and 769 in Wagga Wagga in 1982; 873 in Belmont and 795 in Wagga Wagga in 1992.
History of respiratory illness recorded by parents in self administered questionnaire; airway hyperresponsiveness by histamine inhalation test; atopy by skin prick tests; counts of house dust mites in domestic dust.
Prevalence of wheeze in previous 12 months increased in Belmont, from 10.4% (75/718) in 1982 to 27.6% (240/873) in 1992 (P < 0.001), and in Wagga Wagga, from 15.5% (119/769) to 23.1% (183/795) (P < 0.001). The prevalence of airway hyperresponsiveness increased twofold in Belmont to 19.8% (173/873) (P < 0.001) and 1.4-fold in Wagga Wagga to 18.1% (P < 0.05). The prevalence of airway hyperresponsiveness increased mainly in atopic children only, but the prevalence of atopy was unchanged (about 28.5% in Belmont and about 32.5% in Wagga Wagga). Numbers of house dust mites increased 5.5-fold in Belmont and 4.5-fold in Wagga Wagga.
We suggest that exposure to higher allergen levels has increased airway abnormalities in atopic children or that mechanisms that protected airways of earlier generations of children have been altered by new environmental factors.

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    • "A potential limitation of this study is the use of questionnaire data to define two of the three phenotypes evaluated here (i.e., asthma and croup). Questionnaire reports of physician reported asthma have been used by others and have been found to be reliable [38, 39]. However, associations identified still require careful consideration of the lack of a gold standard for asthma at this time. "
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    ABSTRACT: Background: The CD14 gene has an important role in the detection of inflammatory provoking pathogens and in the ensuing signaling of the innate immune response. We assessed the role of CD14 C-159T, G-1359T in the expression of asthma, croup, and allergy in Canadian school children of ages 6 to 14 years. Methods: Children attending schools in a rural community participated in a cross-sectional survey of respiratory health. Following consent, we conducted clinical assessments to collect buccal swabs for genotyping and perform skin prick testing (SPT) to determine atopic status. Genotyping and SPT results were available for 533 and 499 children, respectively. Separate multivariable analyses that included both polymorphisms were conducted for each phenotype. Results: The prevalence of asthma, allergy, and croup was 18.6%, 22.4%, and 6.6%, respectively. Children with the T/T variant of CD14 G-1359T were more likely to have physician diagnosed asthma (26.8%). Children with C/C variant of CD14 C-159T had a significantly lower prevalence of croup (2.6%). Haplotype analyses of the two CD14 polymorphisms showed that individuals with the T|T haplotype combination were significantly more likely to have asthma (P = 0.014). Conclusions: In this study, CD14 variants are important for the expression of croup and asthma but not atopy.
    Disease markers 11/2013; 35(6):765-771. DOI:10.1155/2013/434920 · 1.56 Impact Factor
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    • "Longitudinal studies have also reported a close association between changes in BHR and atopic status. In the aforementioned Australian study, the prevalence of atopy and BHR for 8- to 10-year-old children was assessed in 1982 and 1992; the prevalence of atopy did not change after 10 years, whereas the prevalence of BHR increased 1.5- to 2.2-fold, and was more prominent among the atopic group.6 Therefore, Australian study is a good example that presented atopy as an important risk factor for both current and future BHR. "
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    ABSTRACT: Both atopy and bronchial hyperresponsiveness (BHR) are characteristic features of asthma. They are also found among non-asthmatic subjects, including allergic rhinitis patients and the general population. Atopy and BHR in asthma are closely related. Atopy induces airway inflammation as an IgE response to a specific allergen, which causes or amplifies BHR. Moreover, significant evidence of the close relationship between atopy and BHR has been found in non-asthmatic subjects. In this article, we discuss the relationship between atopy and BHR in the general population, asthmatic subjects, and those with allergic rhinitis. This should widen our understanding of the pathophysiology of atopy and BHR.
    Allergy, asthma & immunology research 07/2013; 5(4):181-8. DOI:10.4168/aair.2013.5.4.181 · 2.43 Impact Factor
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    • "The prevalence of atopic disease has increased tremendously in the second half of the twentieth century (Peat et al., 1994). Although the cause of this increase is not known though, a genetic cause is unlikely due to the time span in which the increase took place. "
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    ABSTRACT: Over the last years insight in the complex interactions between innate and adaptive immunity in the regulation of an inflammatory response has increased enormously. This has revived the interest in stress proteins; proteins that are expressed during cell stress. As these proteins can attract and trigger an immunological response they can act as important mediators in this interaction. In this respect, of special interest are proteins that may act as modulators of both innate and adaptive immunity. Heat shock proteins (HSPs) are stress proteins that have these, and more, characteristics. More than two decades of studies on HSPs has revealed that they are part of intrinsic, "natural" mechanisms that steer inflammation. This has provoked comprehensive explorations of the role of HSPs in various human inflammatory diseases. Most studies have focused on classical autoimmune diseases. This has led to the development of clinical studies with HSPs that have shown promise in Phase II/III clinical trials. Remarkably, only very little is yet known of the role of HSPs in atopic diseases. In allergic disease a number of studies have investigated the possibility that allergen-specific regulatory T cell (Treg) function is defective in individuals with allergic diseases. This raises the question whether methods can be identified to improve the Treg repertoire. Studies from other inflammatory diseases have suggested HSPs may have such a beneficial effect on the T cell repertoire. Based on the immune mechanisms of atopic diseases, in this review we will argue that, as in other human inflammatory conditions, understanding immunity to HSPs is likely also relevant for atopic diseases. Specifically, we will discuss why certain HSPs such as HSP60 connect the immune response to environmental antigens with regulation of the inflammatory response. Thus they provide a molecular link that may eventually even help to better understand the immune pathological basis of the hygiene hypothesis.
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