Exposure to environmental tobacco smoke (ETS) increases the risk of respiratory illness in children but data are inconclusive regarding the risk of IgE sensitisation.
To elucidate whether exposure to smoking prenatally and/or postnatally is related to IgE sensitisation in children at 4 years of age.
As part of a prospective birth cohort study (BAMSE), a total of 4089 families with children answered questionnaires when the child was 2 months, 1, 2 and 4 years old on environmental factors and symptoms of allergic disease. Blood collected at age 4 years from 2614 children was analysed for IgE antibodies to common inhalant and food allergens. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using logistic regression with adjustments for potential confounders.
There was no evident association between maternal smoking during pregnancy and risk of IgE sensitisation. In contrast, a dose-response effect was found for exposure to ETS from parental smoking during the first few months of life and IgE sensitisation. There was an increased risk of sensitisation to inhalant and/or food allergens (OR(adj) 1.28 (95% CI 1.01 to 1.62)) among children exposed to ETS at 2 months of age. The risk appeared particularly elevated for indoor inhalant allergens, such as cat (OR(adj) 1.96 (95% CI 1.28 to 2.99)) and for food allergens (OR(adj) 1.46 (95% CI 1.11 to 1.93)). The IgE sensitising effect of ETS seemed to be confined to infants of parents without allergic diseases and to ETS exposure during early infancy.
Our data indicate that exposure in early infancy to ETS increases the risk of IgE sensitisation to indoor inhalant and food allergens.
"Recently, some studies have reported a positive association between environmental tobacco smoke (ETS) exposure and atopic sensitization25,26,27,28). The German Multicentre Allergy Study found a significantly higher risk of sensitization to food allergens in infancy among children who had been exposed to prenatal or postnatal smoking26). "
[Show abstract][Hide abstract] ABSTRACT: Atopic sensitization is a complex phenomenon that changes dynamically with age throughout childhood; its prevalence increases with age in young children. Additionally, with increasing age, the prevalence of sensitization to inhalant allergens and the prevalence of polysensitization to allergens increase. It is also well established that the development of atopic sensitization is the result of a complex interplay of genetic and environmental factors. However, there is considerable heterogeneity in the literature in terms of the effect of different environmental exposures in young children on the subsequent risk of atopic sensitization and allergic diseases. Previous studies on the relationship, in early life, between pet ownership, sex, exposure to secondhand smoke, exposure to traffic-related air pollution components, and atopic sensitization have yielded different results. Recent studies have highlighted the importance of gene-environment interactions, especially during early childhood, on the risk of subsequent atopic sensitization and allergic diseases. Therefore, pediatricians should consider the genetic and environmental determinants of atopic sensitization in infants and young children when diagnosing and treating patients with allergic diseases. Determining ways in which early exposure to these risk factors in young children may be reduced could be beneficial in preventing the likelihood of developing atopic sensitization.
Korean Journal of Pediatrics 05/2014; 57(5):205-10. DOI:10.3345/kjp.2014.57.5.205
"Early prenatal and postnatal exposure to environmental tobacco smoke has been associated with decreased lung growth and childhood asthma.3 Early exposure to ETS during infancy may enhance potential for later sensitization to environmental allergens.4 "
[Show abstract][Hide abstract] ABSTRACT: The rising incidence of allergic disorders in developed countries is unexplained. Exposure to traffic related air pollutants may be an important cause of wheezing and asthma in childhood. Experimental evidence from human studies suggests that diesel exhaust particles, constituents of fine particulate matter less than 2.5 microns (PM(2.5)), may act to enhance IgE mediated aeroallergen sensitization and Th2 directed cytokine responses. To date, epidemiologic investigations indicate that children living in close proximity to heavily travelled roads are more likely to be atopic and wheeze. The Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS) birth cohort study was initiated to test the hypothesis that early high exposure to traffic related air pollutants is associated with early aeroallergen sensitization and allergic respiratory phenotypes. Using an exposure cohort design, more than 700 infants born to atopic parents were recruited at age 1 living either less than 400 meters (high traffic pollutant exposure) or greater than 1,500 meters (low exposure) from a major road. Children were medically evaluated and underwent skin prick testing with aeroallergen at screening, and re-evaluated sequentially at ages 1, 2, 3, 4, and 7. In this study, both proximity and land use regression (LUR) models of traffic air pollutant exposure have been assessed. Proximity to stop and go traffic with large concentrations of bus and truck traffic predicted persistent wheezing during infancy. The LUR model estimated elemental carbon attributable to traffic (ECAT) as a proxy for diesel exhaust particulate exposure. High ECAT was significantly associated with wheezing at age 1 as well as persistent wheezing at age 3. High mold exposure predicted a well defined asthma phenotype at age 7.
"After consulting and reviewing a lot literature offline and online and making sure that a dynamic human health risk assessment system is required, in the second steps, the HRAQ was made up of total 58 questions divided in four major sections of personal history, environmental status, occupational health status (clinical history and disease history), and socioeconomic status. "
[Show abstract][Hide abstract] ABSTRACT: An online human health risk assessment system (OHHRAS) has been designed and developed in the form of a prototype database-driven system and made available for the population of India through a website - www.healthriskindia.in. OHHRAS provide the three utilities, that is, health survey, health status, and bio-calculators. The first utility health survey is functional on the basis of database being developed dynamically and gives the desired output to the user on the basis of input criteria entered into the system; the second utility health status is providing the output on the basis of dynamic questionnaire and ticked (selected) answers and generates the health status reports based on multiple matches set as per advise of medical experts and the third utility bio-calculators are very useful for the scientists/researchers as online statistical analysis tool that gives more accuracy and save the time of user. The whole system and database-driven website has been designed and developed by using the software (mainly are PHP, My-SQL, Deamweaver, C++ etc.) and made available publically through a database-driven website (www.healthriskindia.in), which are very useful for researchers, academia, students, and general masses of all sectors.
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