Lung cancer risk from PAHs emitted from biomass combustion.
Lung cancer risk from PAHs emitted from biomass combustion.
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DOI：
10.1016/j.envres.2014.12.009
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发表时间：
2015-02
影响因子：
8.3
通讯作者：
D. Sarigiannis;S. Karakitsios;D. Zikopoulos;S. Nikolaki;M. Kermenidou
中科院分区：
文献类型：
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作者：
D. Sarigiannis;S. Karakitsios;D. Zikopoulos;S. Nikolaki;M. Kermenidou
这项研究涉及评估的癌症风险归因于多环芳烃暴露，归因于在2012-2013年冬季在希腊增加使用生物质空间加热。三个部分的颗粒物（PM 1，PM2.5和PM10）进行了测量，在两个采样点（城市/住宅和交通影响），然后通过化学分析19多环芳烃和左旋葡聚糖（用作生物标志物示踪剂）。PAH诱导的肺癌风险是通过一种综合方法来估计的，该方法结合了人体呼吸道沉积建模，以估计每个靶组织的毒性当量浓度（TEQ）。这使我们能够进一步区分年龄组的内部暴露和风险。结果表明，所有PM分数较高，在希腊在寒冷的月份，主要是由于生物质用于空间加热。PAH和左旋葡聚糖水平高度相关，表明生物质燃烧排放的颗粒物比其他来源排放的PM更具毒性。对于靠近城市背景监测点的居民，估计的肺癌风险不可忽略。由于较高的体重标准化剂量和人体呼吸道（HRT）生理学，估计婴儿和儿童的风险较高。青少年的HRT结构和生理学有利于每单位质量更小、毒性更大的颗粒的沉积。在所有情况下，估计风险（城市背景站点为5.7E-07和1.4E-06，交通站点为1.4E-07至5.0E-07）低于传统方法估计的值（2.8E−06和9.7E−07分别适用于城市背景和交通站点），基于吸入单位风险;后者假设吸附在颗粒物上的所有多环芳烃都被人类吸收。采用本文提出的方法，两个采样点的估计风险相差5-7倍（取决于年龄组）。如果我们仅仅依靠传统的风险评估方法，这些差异是无法确定的。因此，生物质燃烧排放的PM中多环芳烃的实际癌症风险将被大大低估。
This study deals with the assessment of the cancer risk attributable to PAH exposure, attributable to the increased use of biomass for space heating in Greece in the winter of 2012–2013. Three fractions of particulates (PM1, PM2.5 and PM10) were measured in two sampling sites (urban/residential and traffic-influenced) followed by chemical analysis of 19 PAHs and levoglucosan (used as a biomarker tracer). PAH-induced lung cancer risk was estimated by a comprehensive methodology that incorporated human respiratory tract deposition modelling in order to estimate the toxic equivalent concentration (TEQ) at each target tissue. This allowed us to further differentiate internal exposure and risk by age groups. Results showed that all PM fractions are higher in Greece during the cold months of the year, mainly due to biomass use for space heating. PAH and levoglucosan levels were highly correlated, indicating that particles emitted from biomass combustion are more toxic than PM emitted from other sources. The estimated lung cancer risk was non-negligible for residents close to the urban background monitoring site. Higher risk was estimated for infants and children, due to the higher bodyweight normalized dose and the human respiratory tract (HRT) physiology. HRT structure and physiology in youngsters favor deposition of particles that are smaller and more toxic per unit mass. In all cases, the estimated risk (5.7E−07 and 1.4E−06 for the urban background site and 1.4E−07 to 5.0E−07 for the traffic site) was lower to the one estimated by the conventional methodology (2.8E−06 and 9.7E−07 for the urban background and the traffic site respectively) that is based on Inhalation Unit Risk; the latter assumes that all PAHs adsorbed on particles are taken up by humans. With the methodology proposed herein, the estimated risk presents a 5–7 times difference between the two sampling sites (depending on the age group). These differences could not have been identified had we relied only on conventional risk assessment method. Consequently, the actual cancer risk attributable to PAHs on PM emitted from biomass burning would have been significantly underestimated.