Columbia Center for Children's Environmental Health, Mailman School of Public Health, Columbia University, New York, NY 10032, USA.
J Allergy Clin Immunol. 2013 Mar;131(3):886-93. doi: 10.1016/j.jaci.2012.12.666. Epub 2013 Feb 4.
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.
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.
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.
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).
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.
蟑螂致敏是低收入城市社区哮喘发病率增加的最强危险因素之一;然而,与致敏发展相关的暴露时间尚未完全阐明。此外,接触燃烧产物,包括多环芳烃(PAHs),可以增强过敏致敏的发展。
我们试图检验以下假设:孕期测量的室内蟑螂过敏原可预测儿童早期的蟑螂致敏,并且这种关联在接触较高 PAH 浓度的儿童中更为明显。
在纽约市,招募了多米尼加和非裔美国孕妇。在妊娠晚期,孕妇佩戴个人空气采样器,以测量 8 种非挥发性 PAHs 和半挥发性 PAH 芘,从家中采集灰尘以进行过敏原测量。测量儿童谷胱甘肽 S-转移酶 μ1(GSTM1)基因多态性。在 2、3、5 和 7 岁时,测量儿童的过敏原特异性 IgE 水平。
产前厨房灰尘中的 Bla g 2 预测了 5 至 7 岁时的蟑螂致敏(调整后的相对风险 [RR],1.15;P =.001;n = 349)。该关联仅见于高于(RR,1.22;P =.001)而非低于(RR,1.07;P =.24)中位数 8 种非挥发性 PAH 水平总和的儿童中。该关联在 PAH 水平较高的儿童中最为明显,而 GSTM1 基因则不存在(RR,1.54;P =.001)。
孕期暴露于蟑螂过敏原与过敏致敏的风险增加相关。这种风险因接触非挥发性 PAHs 而增加,而 GSTM1 基因突变缺失的儿童尤其易受影响。