Background: It is important to assess risk factors for the development of allergic diseases, primarily because these diseases are so common and affect one third of all children in the western world, sometimes with serious manifestations, and also because these diseases have continued to increase over the last few decades.
Aims: To study the difference between the cumulative incidence of allergic diseases in 7-ycarold children in 1974 and 1994. To ascertain whether a/ urban as opposed to rural living, b/ maternal allergy, cl season of birth, and particularly, dl pertussis vaccination influence the development of allergic diseases.
Material & methods: Two cross-sectional and two prospective studies were evaluated in regard to allergic diseases and their relation to various risk factors. Diagnoses of allergic diseases were obtained from questionnaires and intensive prospective clinical evaluations. Skin prick tests and analyses of IgE to common allergens and pertussis toxin were performed.
Results: Allergic diseases increased from 15.1% to 26.1% with a relative risk of 1.7 (95% C.!. 1.4-2.1). The increase was attributed to the children having a heredity of allergic disease. Today, it is more common to have a family member with an allergic disease than not to have allergy in the immediate family. Bronchial asthma and allergic rhinoconjunctivitis in 7-year-old girls increased more than fourfold between 1974 and 1994 but the increase in 7-year-old boys was only 50%.
Urban as opposed to rural living during the first two years of life was a moderate risk factor for allergic disease up to 13-14 years of age. The risk was particularly high for bronchial asthma with a relative risk of 2.1 (95% C.!. 1.2-3.7) associated with urban living during the first year of life and 2.1 (1.2-3.6) with urban living the second year. The increase in risk remained after adjustment for family history of allergy, gender, environmental tobacco smoking, smoking during pregnancy, pets indoors, damp indoors and living area. Smoking during pregnancy was an independent risk factor for asthma in the child. The two crosssectional studies both showed significant increase (I 0%) in children if the mother had an allergic disease. Allergic diseases were associated with birth during the winter and negatively associated with birth during spring time. The acellular pertussis vaccines did not influence the development of allergy significantly more than the whole cell pertussis vaccines, or placebo (with diphtheria and tetanus only).
Discussion/Conclusions: The increased risk of allergic disease over the last few decades cannot be explained by genetic factors. The most plausible explanation is that there is some factor or factors that influence children with a genetic pre-disposition to allergy. Differences in microbial exposure and infections are conceivable reasons for the increase and may contribute to the difference seen between urban and rural areas. Other possible causes may be exposure to different adjuvants, e.g. nitrogen dioxide and diesel exhausts.
The increase in family size in families with an allergic mother, would be a survival advantage of being atopic. This could explain a long-term accumulation but not the dramatic increase during the second half of the 20th century.
The seasonal effect is moderate. One plausible explanation of the effect in relation to pollen allergy may be that the levels of maternal IgG to inhalants are dependent on the pollen season. However, the seasonal effects of IgE to egg in infancy may be attributable to the indoor environment.
In spite of the fact that acellular vaccines induced more IgE to pertussis toxin and that the Th2-type cytokines increased more than Thl-type cytokines after acellular pertussis vaccines, these vaccines did not significantly increase the risk of allergic disease in the children. Acellular vaccines are therefore recommended owing to their documented safety as well as effectiveness. All in all, several risk factors for allergic diseases have been found but none of them is strong enough to explain the increase over the last few decades.
Linköping: Linköpings universitet , 1998. , 78 p.
1998-08-25, Berzeliussalen, Universitetssjukhuset, Linköping, 09:00 (Swedish)
Papers, included in the Ph.D. thesis, are not registered and included in the posts from 1999 and backwards.