Prenatal and perinatal risk factors of food allergy in Taiwanese young children.

Background: In recent decades, the prevalence of food allergy (FA) in children has increased in Western countries; however, there have been only limited studies on FA, especially among young children, in Asian countries, including Taiwan. In this study, we identified prenatal and perinatal risk factors associated with FA in young children in Taiwan. Methods: For this prospective birth cohort study, we adopted the Southern Taiwan Allergy Research Alliance (STARA)-FA questionnaire to collect data related to prenatal and perinatal risk factors and self-reported allergic symptoms in children aged 1-3 years in the well-baby clinics of 4 medical centers located in 3 cities, Chia-Yi, Tainan, and Kaohsiung, Taiwan. The STARA-FA questionnaire consisted of 99 questions to investigate the association of prenatal and perinatal risk factors with FA. Results: We recruited 903 young children aged 1-3 years in Taiwan. Among those, 95 (14.7%) children had allergic reactions to foods. The most common food allergens were eggs (26/95, 27.3%), milk (22/95, 23.2%), fruits (13/95, 13.7%), and seafood (12/95, 12.6%). We also found that there were 134 (14.8%) children with eczema, 86 (9.5%) with wheezing, and 240 (26.6%) with rhinitis. Children with a personal history of eczema (adjusted odds ratio [AOR], 2.48; 95% confidence interval [CI], 1.38-4.45) and a family allergy history (AOR, 2.06; 95% CI, 1.18-3.57) had a significantly increased risk of FA. Maternal peanut consumption during pregnancy was associated with a decreased risk of FA in children (AOR, 0.57; 95% CI, 0.33-0.98). Conclusions: In this study, the prevalence of FA in a cohort of Taiwanese young children was 14.7%. Risk factors associated with FA were a personal eczema history and a family allergy history, which might serve as predictive or prevention factors for the development of FA in young children in Taiwan.

Epigenetic regulation in allergic diseases and related studies

Asthma, a chronic inflammatory disorder of the airway, has features of both heritability as well as environmental influences which can be introduced in utero exposures and modified through aging, and the features may attribute to epigenetic regulation. Epigenetic regulation explains the association between early prenatal maternal smoking and later asthma-related outcomes. Epigenetic marks (DNA methylation, modifications of histone tails or noncoding RNAs) work with other components of the cellular regulatory machinery to control the levels of expressed genes, and several allergy- and asthma-related genes have been found to be susceptible to epigenetic regulation, including genes important to T-effector pathways (IFN-γ, interleukin [IL] 4, IL-13, IL-17) and T-regulatory pathways (FoxP3). Therefore, the mechanism by which epigenetic regulation contributes to allergic diseases is a critical issue. In the past most published experimental work, with few exceptions, has only comprised small observational studies and models in cell systems and animals. However, very recently exciting and elegant experimental studies and novel translational research works were published with new and advanced technologies investigating epigenetic mark on a genomic scale and comprehensive approaches to data analysis. Interestingly, a potential link between exposure to environmental pollutants and the occurrence of allergic diseases is revealed recently, particular in developed and industrialized countries, and endocrine disrupting chemicals (EDCs) as environmental hormone may play a key role. This review addresses the important question of how EDCs (nonylphenol, 4 octylphenol, and phthalates) influences on asthma-related gene expression via epigenetic regulation in immune cells, and how anti-asthmatic agents prohibit expression of inflammatory genes via epigenetic modification. The discovery and validation of epigenetic biomarkers linking exposure to allergic diseases might lead to better epigenotyping of risk, prognosis, treatment prediction, and development of novel therapies.

The Effects of Environmental Toxins on Allergic Inflammation

The prevalence of asthma and allergic disease has increased worldwide over the last few decades. Many common environmental factors are associated with this increase. Several theories have been proposed to account for this trend, especially those concerning the impact of environmental toxicants. The development of the immune system, particularly in the prenatal period, has far-reaching consequences for health during early childhood, and throughout adult life. One underlying mechanism for the increased levels of allergic responses, secondary to exposure, appears to be an imbalance in the T-helper function caused by exposure to the toxicants. Exposure to environmental endocrine-disrupting chemicals can result in dramatic changes in cytokine production, the activity of the immune system, the overall Th1 and Th2 balance, and in mediators of type 1 hypersensitivity mediators, such as IgE. Passive exposure to tobacco smoke is a common risk factor for wheezing and asthma in children. People living in urban areas and close to roads with a high volume of traffic, and high levels of diesel exhaust fumes, have the highest exposure to environmental compounds, and these people are strongly linked with type 1 hypersensitivity disorders and enhanced Th2 responses. These data are consistent with epidemiological research that has consistently detected increased incidences of allergies and asthma in people living in these locations. During recent decades more than 100,000 new chemicals have been used in common consumer products and are released into the everyday environment. Therefore, in this review, we discuss the environmental effects on allergies of indoor and outside exposure.