Exposure to mold during infancy increases the risk of asthma. Tendency to development of asthma is three times higher among children living in mold contaminated areas. More on this topic can be found in the August issue of Annals of Allergy, Asthma & Immunology, scientific journal of the American College of Allergy, Asthma and Immunology (ACAAI).
Atopic asthma is a chronic inflammatory disorder of the airways wherein on exposure to allergens, the body mounts an immune response. In the course of this response hyperreactivity of the airways can be observed, resulting in symptoms related to bronchial obturation, often reversible spontaneously or after treatment. The etiology of asthma is complex and multi-factorial. Environmental, immunological, infectious and genetic factors have been associated with its development. Most current data suggest that asthma drives development of a Th2 lymphocyte-predominant immune response, which is associated with atopy and IgE mediated inflammation via pathways involving the production of proinflammatory cytokines. Asthma is characterized not only with bronchial hyperreactivity, but also remodeling and eosinophilic inflammation of the airways. In addition, an increased secretion of the bronchial mucus is present and high levels of the IgE antibodies in the serum are observed.
The problem of asthma is one of the more frequently raised in large population studies. In the opinion of the ACAAI allergic diseases constitute the third (after infectious diseases and tumors, a group of illnesses with the highest rate of susceptibility and the associated maximum activity of the research, both basic science, clinical studies and epidemiology. In developed countries an increasing incidence of the allergic diseases can be found. Model of life prevalent there and, in particular hygiene, prevents contact with the commonly occurring pathogens. On the one hand, the lack of children exposure on infections caused by micro-organisms, effects with developing allergies at a higher age. Through this lack of a natural sequence of events after contact with the antigen, the production of antigen-specific Th1 lymphocytes is blocked. We also know, however, that the problem of allergies and related diseases is very complex. The more interesting are the reports suggesting that exposure to mold, increases the risk of asthma development among children.
In the latest publication from the Annals of Allergy, Asthma & Immunology, data of 176 children, coming from a larger population (700), involved in the Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS) were analyzed. This project was devoted to childhood allergies associated with air pollution. Little patients were observed for 7 years. Since asthma has also genetic background, children with positive family history of allergic diseases were singled out. The mold exposure level has been measured by a DNA-based test, on The U.S. Environmental Protection Agency (EPA) methods. Module test combined an analysis of the presence or absence of 36 different molds that affect the level of exposure in homes. This index was used to assess the impact of the presence of mold on the asthma development among participants of the study. It turned out that up to 18% of children enrolled in CCAAPS, showed symptoms of asthma at the age of 7. It is estimated that approximately 9% of children in the United States will have this disease. The percentage increases among children from poor families in urban areas. The most practical application from this study is the parents motivation, especially those burdened with positive history of allergic disorders to the upkeep of good housing conditions. The fight with fungus on the wall started.
1. Tiina Reponen, Stephen Vesper, Linda Levin, Elisabet Johansson, Patrick Ryan, Jeffery Burkle, Sergey A. Grinshpun, Shu Zheng, David I. Bernstein, James Lockey, Manuel Villareal, Gurjit K. Khurana Hershey, Grace LeMasters. High environmental relative moldiness index during infancy as a predictor of asthma at 7 years of age. Annals of Allergy, Asthma & Immunology, 2011; 107 (2): 120 DOI: 10.1016/j.anai.2011.04.018
2. ScienceDaily. Retrieved August 5, 2011, from http://www.sciencedaily.com /releases/2011/08/110804082002.htm