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Refining Assessment of PAH Exposure and Potential Carcinogenic Risk Assessment from Biomass Burning Incorporating Internal Dosimetry Metrics

机译:结合内部剂量测定法的生物质燃烧对PAH暴露的改进评估和潜在致癌风险评估

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The current study deals with the assessment of the cancer risk attributable to exposure to PAHs associated to an increased use of biomass for space heating in Greece in the winter of 2012-2013. The study incorporated ambient air PM sampling in several sites in the city of Thessaloniki, as well as chemical analysis of PAHs and levoglucosan, used here as the most specific tracer of biomass combustion. Internal exposure to PAHs was estimated taking into account the deposition of the respective PM fractions across the human respiratory tract (HRT) and the respective PAHs concentration of the respective PM fractions. Deposition at different regions of the HRT was estimated using the Multiple-Path Particle Dosimetry (MPPD) model. Potential cancer risk due to exposure to the mixture of urban ambient air PAHs was calculated using the toxicity equivalence factor (TEF) approach using as basis the benzo(a)pyrene (B[a]P) cancer potency. The BaP-TEQ (Toxicity Equivalent Quotient) (carcinogenic equivalent expressed in ng/m3) was calculated by multiplying the concentrations of each compound in the PAH mixture with the respective TEF for cancer potency relative to BaP. Cancer risk was estimated by multiplying the TEQ of the respective fraction of particulate matter deposited daily across HRT by a slope-factor equal to 0.25 10-6 ng/kg_bw/day) function, initially derived by the B[a]P Inhalation Unit Risk (equal to 0.88 10-6 (ng/m3)-1). Significant variation in internal exposure to PAHs (and respectively to the estimated risk) was observed among different age groups, much larger than variation due to geospatial attributes. Bodyweight normalized uptake (and the attributed risk) for children is four times higher than for adults. Only limited difference was found between traffic and urban background sites in the winter; the latter indicates that biomass emitted PM are not significantly different in terms of carcinogenic potency compared to traffic ones.
机译:当前的研究涉及对因暴露于多环芳烃而引起的癌症风险的评估,这与希腊在2012-2013年冬季增加生物质用于空间供暖的使用有关。该研究在塞萨洛尼基市的多个地点进行了环境空气PM采样,并对多环芳烃和左旋葡聚糖的化学分析进行了分析,在这里将其用作生物质燃烧的最具体示踪剂。考虑到各个PM组分在人类呼吸道(HRT)上的沉积以及各个PM组分的各个PAHs浓度,估计了PAH的内部暴露量。使用多径颗粒剂量法(MPPD)模型估算了HRT不同区域的沉积。使用毒性当量因数(TEF)方法以苯并(a)((B [a] P)癌症效力为基础,计算了由于暴露于城市环境空气PAHs混合物而导致的潜在癌症风险。 BaP-TEQ(毒性当量商)(致癌当量,以ng / m3表示)是通过将PAH混合物中每种化合物的浓度乘以各自的TEF相对于BaP的癌症效力来计算的。通过每天通过HRT沉积的颗粒物各个部分的TEQ乘以等于0.25 10-6 ng / kg_bw / day的斜率因子来估算癌症风险,该斜率因子最初是由B [a] P吸入单位风险得出的(等于0.88 10-6(ng / m3)-1)。在不同年龄组之间观察到内部暴露于PAHs的显着差异(以及对估计风险的显着差异),远大于由于地理空间属性引起的差异。儿童的体重正常摄入量(及相关风险)是成人的四倍。在冬季,交通与城市背景地点之间的差异很小。后者表明,与交通运输相比,PM排放的生物量在致癌效力方面没有显着差异。

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