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Is Primary Prevention of Allergy-Mediated Asthma a Viable Idea?  Jim
Stout, MD, MPH IN THIS issue of the ARCHIVES, Dr Tsitoura and her colleagues 1 report on a remarkable international dataset of infants and young children at high risk for becoming allergic to, but not yet sensitized to, house dust mites. In a primary prevention trial, these children were randomized either to an intervention group that received a simple house dust mite–reduction strategy (mattress encasement and detailed preventive environmental recommendations, such as hot-washing of sheets and bedding) or to a control group, whose parents received information about general indoor environmental issues. After 1 year, children in the intervention group were less than half as likely as controls to have developed allergy to house dust mites (3.0% vs 6.5%). Furthermore, the frequency of asthma symptoms and asthma diagnoses was greater among the children who became sensitized to house dust mites during the study year. How potentially significant are these findings in the context of allergies and asthma? To consider this question, it is helpful to review selected issues focusing on the public health problem of asthma, which, unlike allergic rhinitis, frequently results in exacerbations that require hospitalization and other types of rescue care.The health burden of asthma is enormous and has steadily increased during the last 3 decades in the United States, although since 1995 has shown signs of stabilizing.2 Studies from England, Sweden, and Australia show a doubling of prevalence of allergic rhinitis during this time.3 These increases in respiratory allergies and asthma have been observed primarily in westernized societies. The pharmaceutical industry has developed agents for controlling asthma and allergy symptoms and exacerbations (without serious adverse effects!), and clinicians receive a plethora of reminders to use them. Health care professionals have responded with clinical management guidelines for allergic rhinitis and asthma that are based on a growing body of evidence.3, 4 A chronic care model now exists for responding to the specific needs of patients with chronic illness such as asthma, and methods for disseminating this model in the primary care setting have been developed and deployed (for more information, see reference 5, http://www.healthdisparities.net, http://www.nichq.org, and http://www.ihi.org). Underlying all of this effort and activity, however, remains a
fundamental question Based on the results of one longitudinal birth cohort of more than 1000
subjects, it seems that what we diagnose as asthma in childhood can be
organized into 3 distinct phenotypes, which vary in their long-term health
consequences and are the presumed result of different pathophysiologic
processes. Although they can cause significant illness, the first 2 types Allergy-mediated asthma, the third phenotype, usually persists into later life.7 This more permanent asthma presupposes that the susceptible child first becomes allergic, which occurs in 2 primary ways: by generating antigen-specific immunoglobulin E, and by generating Th2 (type 2 T helper) cells from undifferentiated T helper cells. Our current understanding is that, once changed, these Th2 cells produce mostly allergy-mediating cytokines (their Th1 differentiated counterparts produce mostly infection response-mediating cytokines).8 The dose, duration, and timing of the allergic exposures resulting in these changes are all fertile areas of inquiry. Most (80%) cases of allergy-mediated asthma first manifest before age 6 years and more than half before age 3 years. The sooner in life a child develops allergy-mediated asthma, the more severe it tends to be, a clinical finding that supports the probable cumulative effect of the inflammatory component of asthma.6 As Martinez6 points out in this article, "if the adverse effects of persistent (allergy-mediated) asthma are to be prevented, diagnosis and intervention would seem to be necessary before the age of 5 or 6 years." Allergy to house dust mites is the best known predictor of allergy-mediated asthma.13 Although this report focused on house dust mites only, there are additional clinically important allergens found in bedding.10 In a recent sample of inner-city children with allergy-mediated asthma from 7 US cities, 79% were sensitized to 2 or more and 51% to 3 or more indoor airborne allergens.11 In the United States, the most important of these other bed-borne allergens seems to be from cockroaches.10 Thus, bed encasements and sheet washing can facilitate avoidance of other important allergens besides dust mites, which was likely an unmeasured benefit of the intervention in this trial. Indoor sensitivity results from inhaling small quantities of an allergen repeatedly over a period of months or years.9 The house dust mite is arguably the best understood of these allergens, and based on literature from several different countries, there is now an established threshold of antigen-load exposure beyond which the development of allergy or asthma becomes much more likely.12 Epidemiologic data on antigen burden in low-income vs high-income housing are mostly unavailable. However, it is reasonable to suspect that the antigen load in low-income housing stock is greater than that in larger and newer housing, which is also likely to be better equipped for cleaning. The asthma morbidity patterns from small area analyses certainly support this idea.13, 14 Is it possible that our urban cores have become antigen harborages in which these offending pest- and pet-derived proteins have accumulated over the last few decades and that inner city occupants, and especially children, have played the role of canaries in these man-made mines? Could a simple environmental intervention in early childhood similar to the one described by Tsitoura and colleagues not just delay the onset of allergy-mediated asthma but fundamentally alter its expression, for example, by allowing more appropriate (ie, less allergic) differentiation of the T helper cell lines?8 The potential impact of this provocative finding deserves further attention and understanding. We should look forward to other reports from these data and from other projects focusing on primary prevention of allergy-mediated asthma.
REFERENCES
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© 2002 American Medical Association. All rights reserved. |
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Where is
all the asthma and allergy coming from? The atopic response is a combination
of genetic predisposition and environmental exposure; since we are basically
the same genetic species as our parents and grandparents, we must,
therefore, look for environmental changes over this period as an explanation
for these increases in prevalence. For asthma, the most likely environmental
culprits are irritants (primarily environmental tobacco smoke although
outdoor diesel exhaust may also play a role in some communities),
respiratory infectious agents (primarily viruses), and indoor airborne
allergens (primarily house dust mites, cockroaches, molds, and pet dander).|
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