Allergic disorders are the chronic diseases of greatest pediatric morbidity, affecting over 25 % of the pediatric population. Indeed, this situation has been referred to as an "allergic epidemic". In comparison with asthma, atopic dermatitis and allergic rhinitis have been less extensively investigated, although this does not mean that they should be regarded as minor disorders but rather as alterations that affect the quality of life of the patients and their families, which generate considerable direct and indirect costs. Despite an important research effort, the reason for this allergic epidemic is not well known. These are multifactor disorders without a single causal agent, in which the most important component is the genetic predisposition of the patient (atopy), modulated by environmental factors, exposure to allergens, infections and irritants, among others. A confounding element is the fact that the concept of allergic diseases encompasses phenotypes of rhinitis, atopic dermatitis or asthma in which no IgE-mediated atopic mechanism is demonstrated, and which can manifest in a way similar to true allergic phenotypes. Differentiation between the two is difficult to establish on the basis of self-administered questionnaires alone, in the absence of a precise etiological diagnosis. The present article reviews the numerous factors suggested to be responsible for the increase in allergic diseases recorded in the last few decades, and for the differences in prevalence observed among centres. For most of these factors the results published in the literature are contradictory, in some cases due to a lack of control of the associated interacting or confounding factors. Consensus exists for only some of these causal factors, such as the established parallelism between the increase in allergic diseases and the reduction in infectious processes on one hand, and the increase in particles generated by diesel fuel combustion on the other. In addition, the implicated factors could act differently (and in some cases even antagonically) upon atopy and on the different disease phenotypes, thereby complicating the study of these interactions even further.