Abstract：
:The prevalence of asthma is increasing worldwide. The increase has been found for both sexes, for all races and age groups. The factors responsible are unclear. The short period of increase makes it unlikely that a genetic change is responsible but rather suggests that either air pollutants or a behavioral change may be involved. Behavioral changes may include decreased exercise and outdoor activity due to, for example increased usage of television and computers. What is the role of allergy in the development of asthma? In allergic sensitization, allergens initiate the inflammation and IgE antibodies are typically present. Once asthma has developed, factors such as irritants, infections and exercise may result in acute symptomatology. Infancy is a high risk period for allergic sensitization since natural defense mechanisms are not fully developed. Epidemiologic evidence suggests that microbial stimuli during early childhood can influence induction of atopic diseases. In animal studies, pre-infection with respiratory virus has resulted in enhanced response to allergens. Another factor implicated in the surge of allergic disease is airborne particulates. Evidence has been obtained for an association of environmental tobacco smoke (ETS) with development of allergic sensitization. ETS enhances IgE production as does diesel and aluminum silicate, the latter a component of fly ash. What are the mechanisms responsible for the environmental influences on development of allergy? Th2 cytokine responses, with suppression of Th1 cytokines, are prominent in children. Th1 maturation appears to be promoted by microbial exposure. Increased understanding of the complex interactions of environmental factors with the developing immune system is essential to reverse the current upward trend in allergic respiratory disease.
journal_name
Toxicologyjournal_title
Toxicologyauthors
Karol MHdoi
10.1016/s0300-483x(02)00298-6keywords:
subject
Has Abstractpub_date
2002-12-27 00:00:00pages
305-10eissn
0300-483Xissn
1879-3185pii
S0300483X02002986journal_volume
181-182pub_type
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