Early-life cockroach allergen and polycyclic aromatic hydrocarbon exposures predict cockroach sensitization among inner-city children

Department of Environmental Health Sciences, Mailman School of Public Health, New York, NY. Electronic address: .
The Journal of allergy and clinical immunology (Impact Factor: 11.48). 01/2013; 131(3). DOI: 10.1016/j.jaci.2012.12.666
Source: PubMed


BACKGROUND: Sensitization to cockroach is one of the strongest identified risk factors for greater asthma morbidity in low-income urban communities; however, the timing of exposures relevant to the development of sensitization has not been elucidated fully. Furthermore, exposure to combustion byproducts, including polycyclic aromatic hydrocarbons (PAHs), can augment the development of allergic sensitization. OBJECTIVE: We sought to test the hypotheses that domestic cockroach allergen measured prenatally would predict cockroach sensitization in early childhood and that this association would be greater for children exposed to higher PAH concentrations. METHODS: Dominican and African American pregnant women living in New York City were enrolled. In the third trimester expectant mothers wore personal air samplers for measurement of 8 nonvolatile PAHs and the semivolatile PAH pyrene, and dust was collected from homes for allergen measurement. Glutathione-S-transferase μ 1 (GSTM1) gene polymorphisms were measured in children. Allergen-specific IgE levels were measured from the children at ages 2, 3, 5, and 7 years. RESULTS: Bla g 2 in prenatal kitchen dust predicted cockroach sensitization at the ages of 5 to 7 years (adjusted relative risk [RR], 1.15; P = .001; n = 349). The association was observed only among children with greater than (RR, 1.22; P = .001) but not less than (RR, 1.07; P = .24) the median sum of 8 nonvolatile PAH levels. The association was most pronounced among children with higher PAH levels and null for the GSTM1 gene (RR, 1.54; P = .001). CONCLUSIONS: Prenatal exposure to cockroach allergen was associated with a greater risk of allergic sensitization. This risk was increased by exposure to nonvolatile PAHs, with children null for the GSTM1 mutation particularly vulnerable.

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    • "Several studies showed that especially fetal and infantile exposure to tobacco smoke increased the risk of asthma symptoms and lower respiratory tract infection in early childhood.59,60 ETS exposure also increases the vulnerability of the lungs to other air pollutants such as PM.61 Additionally, a recent study showed that prenatal exposure to cockroach allergen increased the risk of allergic sensitization in children at the age of 5-7 years and that exposure to nonvolatile polyaromatic hydrocarbons (PAHs) augmented the risk.62 Moreover, VOCs are emitted from interior products such as synthetically coated furniture, carpets, and polyvinylchloride flooring, which means that newly built or renovated houses have higher levels of these compounds. "
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    • "Antioxidant redox systems and antioxidant enzymes neutralize ROS, but oxidative stress may induce posttranslational modifications in proteins modulating ROS activities. Emerging evidence suggests that environmental pollutants may promote allergic sensitisation: a recent pediatric study found that the risk of allergic sensitisation was increased by exposure to non-volatile polycyclic aromatic hydrocarbons (PAH) in children without the common GSTM1 gene polymorphism, who seemed to be more susceptible to sensitisation by combined cockroach allergen and PAH exposure [45]. "
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