Kulkarni Neeta, Pierse Nevil, Rushton Lesley, Grigg Jonathan
Division of Child Health, Department of Infection, Immunity, and Inflammation, University of Leicester, Leicester, United Kingdom.
N Engl J Med. 2006 Jul 6;355(1):21-30. doi: 10.1056/NEJMoa052972.
Epidemiologic studies indirectly suggest that the inhalation of carbonaceous particulate matter impairs lung function in children. Using the carbon content of airway macrophages as a marker of individual exposure to particulate matter derived from fossil fuel, we sought direct evidence of this association.
Airway macrophages were obtained from healthy children through sputum induction, and the area of airway macrophages occupied by carbon was measured. Lung function was measured with the use of spirometry. We modeled the exposure to primary particulate matter (PM) that is less than 10 mum in aerodynamic diameter (PM10) at or near each child's home address. Linear regression was used to evaluate associations between carbon content of alveolar macrophages and variables that may affect individual exposure. To determine whether lung function that is reduced for other reasons is associated with an increase in the carbon content of airway macrophages, we also studied children with severe asthma.
We were able to assess the carbon content of airway macrophages in 64 of 114 healthy children (56 percent). Each increase in primary PM10 of 1.0 microg per cubic meter was associated with an increase of 0.10 microm2 (95 percent confidence interval, 0.01 to 0.18) in the carbon content of airway macrophages, and each increase of 1.0 microm2 in carbon content was associated with a reduction of 17 percent (95 percent confidence interval, 5.6 to 28.4 percent) in forced expiratory volume in one second, of 12.9 percent (95 percent confidence interval, 0.9 to 24.8 percent) in forced vital capacity, and of 34.7 percent (95 percent confidence interval, 11.3 to 58.1 percent) in the forced expiratory flow between 25 and 75 percent of the forced vital capacity. The carbon content of airway macrophages was lower in children with asthma than in healthy children.
There is a dose-dependent inverse association between the carbon content of airway macrophages and lung function in children. We found no evidence that reduced lung function itself causes an increase in carbon content.
流行病学研究间接表明，吸入含碳颗粒物会损害儿童的肺功能。我们以气道巨噬细胞中的碳含量作为个体接触化石燃料衍生颗粒物的标志物，试图寻找这种关联的直接证据。
通过诱导痰液从健康儿童获取气道巨噬细胞，并测量气道巨噬细胞中被碳占据的面积。使用肺活量测定法测量肺功能。我们对每个儿童家庭住址处或附近空气动力学直径小于10微米的一次颗粒物（PM10）暴露情况进行建模。采用线性回归评估肺泡巨噬细胞碳含量与可能影响个体暴露的变量之间的关联。为了确定因其他原因导致的肺功能降低是否与气道巨噬细胞碳含量增加有关，我们还研究了重度哮喘患儿。
我们能够评估114名健康儿童中64名（56%）的气道巨噬细胞碳含量。每立方米一次PM10增加1.0微克，气道巨噬细胞碳含量增加0.10平方微米（95%置信区间为0.01至0.18），碳含量每增加1.0平方微米，一秒用力呼气量降低17%（95%置信区间为5.6至28.4%），用力肺活量降低12.9%（95%置信区间为0.9至24.8%），用力肺活量25%至75%之间的用力呼气流量降低34.7%（95%置信区间为11.3至58.1%）。哮喘患儿气道巨噬细胞的碳含量低于健康儿童。
儿童气道巨噬细胞的碳含量与肺功能之间存在剂量依赖性负相关。我们没有发现肺功能降低本身会导致碳含量增加的证据。
