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- Material and methods
Background: The aim of this study was to compare the prevalence of atopic sensitization and possible risk factors for allergies in two ethnically similar but geographically widely separated urban populations.
Methods: Data from two centers of the European Community Respiratory Health Survey, Reykjavík, Iceland, and Uppsala, Sweden, were utilized. This included a structured interview, skin prick tests, and blood samples for total and specific IgE for common aeroallergens. Additional measurements of specific IgE antibodies to common food antigens were performed. Furthermore, data on social environment, lifestyle, air pollution, and meteorologic variables were compared.
Results: Skin prick tests were done on 540 individuals in Reykjavík and 527 in Uppsala. The overall prevalence of at least one positive prick test was 20.5% in Reykjavík and 34.2% in Uppsala (P<0.001). Total and specific IgE were measured in serum from 521 subjects in Reykjavík and 472 in Uppsala. The geometric mean value for total IgE was significantly lower in Reykjavík (13.4 kU/l) than in Uppsala (24.7 kU/l) (P<0.001). Similarly, the overall prevalence of at least one specific IgE to airborne allergens was 23.6% in Reykjavík and 32.3% in Uppsala (P<0.01). Specific IgE to a food panel (fx5) was measured in 502 subjects in Reykjavík, and 434 in Uppsala. In Reykjavík, 20 individuals (4.0%) were positive to one or more of the allergens in the food panel compared to 27 (6.0%) in Uppsala. When the single allergens present in the food panel were measured, altogether 16 positive reactions were found in Reykjavík compared to 47 in Uppsala (P<0.05).
Conclusions: The prevalence of sensitization to both airborne and food allergens was lower in Reykjavík than in Uppsala. The difference may be due to environmental and/or dietary differences or to some yet undefined factor.
Atopy is partly due to genetic susceptibility ( 1), but recent surveys from several developed countries have revealed an increasing prevalence of this condition, indicating an important role of environmental factors ( 2–5). Simultaneously, atopic diseases have been increasing in prevalence ( 6–10).
Several possible explanations of these findings have been advanced ( 11–13). The causative role of air pollution and cigarette smoking, once held to be at least partly responsible for the increasing prevalence of allergy, has not been borne out by the data from eastern and western Europe ( 14). Similarly, allergic diseases are increasing in the UK despite a steady decrease in air pollution since the 1950s ( 15). Other differences that seem pertinent to this comparison include differences in living standards between East and West, which will affect factors such as dietary habits and the indoor environment.
The purpose of this study, which is partly based on the protocol used in the European Community Respiratory Health Survey (ECRHS), was to compare the prevalence of atopic sensitization in two ethnically similar urban populations, living under different climatic, environmental, and dietary conditions.
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- Material and methods
The first part of the ECRHS suggested that there was considerable variation in the prevalence of allergic diseases within Europe ( 30). In this first part, Iceland had prevalence values that were among the lowest in Europe, while Sweden had midrange values. As these populations are genetically closely related, we felt that these differences deserved a closer look.
In this study, the prevalence rates of atopic sensitization were compared between Reykjavík and Uppsala. We found a significant difference between these two populations in allergic sensitization, estimated with skin tests and measurements of specific IgE to airborne allergens as well as some food allergens. Not only were different types of atopic sensitization more common in Uppsala than Reykjavík, but multisensitization was also more common in Uppsala. The difference in prevalence of sensitization is in accordance with the self-reported difference in respiratory symptoms and use of asthma medication between the two study groups ( 23). The causes are, however, obscure.
Ethnically, the study populations are similar; therefore, ethnic causes are rather unlikely. The climatologic differences explain the difference in prevalence of birch and wheat sensitization, as birch trees and wheat fields are common in Sweden, but not in Iceland. However, climatologic differences are not likely to explain the overall differences in specific and total IgE sensitization. The role of air pollution as an adjuvant factor to atopic sensitization is controversial, and air pollution in the two study areas was comparable and low.
Evidence has been put forward that the dose of allergens in house dust to which children are exposed is important in determining whether they become sensitized ( 31, 32). In our study, there is no information about house-dust-mite allergen load in the environment of the participants, but the prevalence of childhood exposure to cats and dogs was higher in Uppsala. Surprisingly, atopic sensitization was more common among those not exposed to these animals in childhood, and exposure to cat or dog in childhood was an independent negative risk factor for atopy in both Reykjavík and Uppsala. This finding should, however, favor lower prevalence rates in Uppsala and does not explain the reverse situation which was observed.
The effect of smoking on atopic sensitization is controversial. Active smokers have previously been found to have higher total IgE, but not a higher rate of allergic skin test reactivity ( 33). Higher cord-blood IgE has been found in the children of mothers who smoke ( 34), and some investigators have found a correlation between exposure in infancy to maternal smoking and specific IgE ( 35). In our study, both current and previous smoking was more common in Reykjavík, but this factor does not explain the lower prevalence of atopy seen there. The reported parental smoking habits did not differ significantly between the centers.
Small sibship size has been reported to be a risk factor for atopic sensitization ( 36, 37). The number of brothers and sisters in Reykjavík is 50% higher than in Uppsala, a finding that might explain some of the lower prevalence found in Reykjavík. However, in the multivariate analysis, this finding did not stand out as an independent risk factor.
The only clue provided by the multivariate analysis to the differences in prevalence rates between centers was that respiratory infections in early life seemed to be a protective factor in Reykjavík, but not in Uppsala. However, the number of reports of such infections did not differ between the centers, and their number was not associated with the number of siblings.
There are some possible risk factors for atopy that differ between these countries but were not assessed by this study. Firstly, socioeconomic factors have been discussed as a cause of increasing atopic sensitization. In the study areas, both social and economic standards were relatively high and comparable. There was some difference in household habits, and more detached or semidetached dwellings and fitted carpets are found in Reykjavík. All houses in the Reykjavík area use geothermal heating, which in Iceland is inexpensive and allows ventilation via open windows. Secondly, vaccination early in childhood might play a role, and an inverse association between tuberculin responses and atopy has been reported ( 38). In both study areas, the vaccination practice was the same with one exception; in Uppsala, the population of this age is BCG vaccinated, but this is only rarely done in Reykjavík.
Thirdly, consumption of oily fish might possibly protect against asthma in childhood ( 39). Black & Sharpe have discussed the possible protective effect of the consumption of oily fish against atopic diseases ( 40). There is no individual information available about fish consumption in our study groups, but fish consumption in Iceland was almost triple that of Sweden at the time of the study, and daily consumption of cod liver oil is still very common in Iceland.
When we compared corresponding age groups in both centers, the difference in prevalence of atopy was greater in the older age groups. Interestingly, there was no significant difference in reported parental allergies between Reykjavík and Uppsala. Hence, it is possible that the population of Iceland, receiving the full impact of modern lifestyle later than their counterparts in Sweden, have yet to experience the vast increase in allergic diseases seen in other western countries. This and the influence of difference in fish consumption between Iceland and Sweden on the prevalence of allergic diseases in these countries are now only speculation, but these issues may be clarified by the ongoing follow-up of the ECRHS.
Our cross-sectional study provides objective evidence of a lower prevalence of sensitization to both airborne and food allergens in Reykjavík than in Uppsala. These differences could partly be explained by lower allergic exposure, higher number of siblings, and more fish consumption in Reykjavik than in Uppsala. In addition, there may be some yet undefined factor, protective in Iceland or causative in Sweden.