Childhood exposure to fine particulate matter and black carbon and the development of new wheeze between ages 5 and 7 in an urban prospective cohort.

Childhood exposure to fine particulate matter and black carbon and the development of new wheeze between ages 5 and 7 in an urban prospective cohort.
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DOI:
10.1016/j.envint.2012.03.012
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发表时间:
2012-09-15
影响因子:
11.8
通讯作者:
Miller, Rachel L.
Miller, Rachel L.
中科院分区:
环境科学与生态学1区
文献类型:
--
作者:
Jung, Kyung Hwa;Hsu, Shao-I;Yan, Beizhan;Moors, Kathleen;Chillrud, Steven N.;Ross, James;Wang, Shuang;Perzanowski, Matthew S.;Kinney, Patrick L.;Whyatt, Robin M.;Perera, Frederica P.;Miller, Rachel L.

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虽然暴露于城市细颗粒物(PM2.5)和烟黑碳(soot-BC)与哮喘加重有关,但关于这些污染物是否与市中心年幼儿童哮喘或过敏的新发展有关的证据有限。我们假设,儿童时期暴露于PM2.5和烟尘- bc成分可能与内城出生队列中新的喘息和血清学发展的报告有关。作为纽约市哥伦比亚儿童环境健康中心(CCCEH)出生队列研究的一部分,在2005年10月至2011年5月期间,对408名5-6岁儿童进行了为期两周的PM2.5、煤烟- bc(基于多波长积分球法)和修正吸收系数(Abs*;基于烟染反射计)的综合住宅监测。6个月后重复住宅监测(n=262),以捕捉季节变化。在长达3年的随访期间,通过国际儿童哮喘和过敏研究(ISAAC)问卷调查确定了新的喘息症状,并与报告从未喘息、喘息缓解或持续喘息的参照组进行了比较。测定5岁和7岁儿童血清中抗蜚蠊、小鼠、猫和尘螨的特异性免疫球蛋白(Ig) E和总IgE水平。第一次访问时测量的PM2.5、烟尘- bc和Abs*与第二次访问时测量的PM2.5、烟尘- bc和Abs*具有中等相关性(Pearson r = 0.44)。使用逻辑回归模型,PM2.5与新呼吸之间呈正相关,校正优势比[95%置信区间]为每四分位数范围(IQR) 1.51[1.05-2.16]。新发病与烟灰- bc和(OR 1.40[0.96-2.05])、Abs* (OR 1.57[0.91-2.68])呈正相关,但不显著;当限制那些间隔6个月重复家庭室内测量的参与者时,发现空气污染物测量与新喘息之间存在显著的正相关。没有发现污染物和IgE水平之间的联系。我们的研究结果表明,儿童暴露于室内空气污染,其中大部分很容易从室外渗透,可能导致5至7岁儿童出现喘息症状。
While exposures to urban fine particulate matter (PM2.5) and soot-black carbon (soot-BC) have been associated with asthma exacerbations, there is limited evidence on whether these pollutants are associated with the new development of asthma or allergy among young inner city children. We hypothesized that childhood exposure to PM2.5 and the soot-BC component would be associated with the report of new wheeze and development of seroatopy in an inner city birth cohort. As part of the research being conducted by the Columbia Center of Children’s Environmental Health (CCCEH) birth cohort study in New York City, two-week integrated residential monitoring of PM2.5, soot-BC (based on a multi-wavelength integrating sphere method), and modified absorption coefficient (Abs*; based on the smoke stain reflectometer) was conducted between October 2005 and May 2011 for 408 children at age 5–6 years old. Residential monitoring was repeated 6 months later (n=262) to capture seasonal variability. New wheeze was identified through the International Study of Asthma and Allergies in Childhood (ISAAC) questionnaires during up to 3 years of follow-up and compared to a reference group that reported never wheeze, remitted wheeze, or persistent wheeze. Specific immunoglobulin (Ig) E against cockroach, mouse, cat, and dust mite and total IgE levels were measured in sera at ages 5 and 7 years. PM2.5, soot-BC, and Abs* measured at the first visit were correlated moderately with those at the second visit (Pearson r > 0.44). Using logistic regression models, a positive association between PM2.5 and new wheeze was found with adjusted odds ratio [95% confidence intervals] of 1.51 [1.05–2.16] per interquartile range (IQR). Positive but nonsignificant association was found between the development of new wheeze and soot-BC and (OR 1.40 [0.96–2.05]), and Abs* (OR 1.57 [0.91–2.68]); Significantly positive associations were found between air pollutant measurements and new wheeze when restricting to those participants with repeat home indoor measurements 6 months apart. Associations between pollutants and IgE levels were not detected. Our findings suggest that childhood exposure to indoor air pollution, much of which penetrated readily from outdoor sources, may contribute to the development of wheeze symptoms among children age 5 to 7 years.
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