本研究调查了印度瓦拉纳西市细颗粒物中16种优先多环芳烃（PAHs）的丰度，以确定其来源和潜在的致癌健康风险。该城市是南亚典型的城市居民点，颗粒物暴露水平远高于标准，有关污染诱发的死亡和疾病的报道不计其数。从2019年10月到2020年5月，对细颗粒物（PM2.5）进行了监测，其中有32％的天数PM2.5浓度达到或超过100μg/m3，其中大多数发生在11月至1月之间（99％的天数）。16种优先PAHs的浓度在24.1至44.6 ng/m3之间变化（平均：33.1±3.2 ng/m3），季节变化不大。低分子量PAHs（LMW，占56％）和高分子量PAHs（HMW，占44％）都很丰富，其中芴（3.9±0.4ng/m3）和荧蒽（3.5±0.3ng/m3）是最主要的PAHs。苯并[a]芘（B(a)P）的浓度（0.5±0.1ng/m3）低于国家标准，其贡献了总PAHs含量的13％。PAH同系物的诊断比值表明热源是主要来源，包括生物质燃烧和柴油和汽油驱动车辆的排放。使用受体模型进行源解析显示，PAHs的主要来源为生物质燃烧和燃料燃烧（贡献了源份的54％），其次是燃煤进行住宅供暖和烹饪（贡献了源份的44％）。苯并[a]芘当量的潜在毒性范围从0.003到1.365，累积毒性为2.13ng/m3。在PAHs物种中，二苯并[h]蒽的毒性贡献最大，其次是苯并[a]芘，二者共占PAHs诱导的致癌性的86％。终身暴露（ILCR）下患癌风险在儿童中更高（3.3×10-4），其中56％由低分子量PAHs通过摄入和皮肤接触引起。相比之下，成年人更易吸入空气中的PAHs，累积ILCR为2.2×10-4。然而，由于未计入金属丰度，对PM2.5暴露的ILCR可能被低估，因此需要针对特定来源的控制措施。版权所有©2023 Elsevier Ltd.

Abundance of fine particulate-bound 16 priority polycyclic aromatic hydrocarbons (PAHs) was investigated to ascertain its sources and potential carcinogenic health risks in Varanasi, India. The city represents a typical urban settlement of South Asia having particulate exposure manyfold higher than standard with reports of pollution induced mortalities and morbidities. Fine particulates (PM2.5) were monitored from October 2019 to May 2020, with 32% of days accounting ≥100 μgm-3 of PM2.5 concentration, frequently from November to January (99% of days). The concentration of 16 priority PAHs varied from 24.1 to 44.6 ngm-3 (mean: 33.1 ± 3.2 ngm-3) without much seasonal deviations. Both low (LMW, 56%) and high molecular weight (HMW, 44%) PAHs were abundant, with Fluoranthene (3.9 ± 0.4ngm-3) and Fluorene (3.5 ± 0.3ngm-3) emerged as most dominating PAHs. Concentration of Benzo(a)pyrene (B(a)P, 0.5 ± 0.1ngm-3) was lower than the national standard as it contributed 13% of total PAHs mass. Diagnostic ratios of PAH isomers indicate predominance of pyrogenic sources including emissions from biomass burning, and both from diesel and petrol-driven vehicles. Source apportionment using receptor model revealed similar observation of major PAHs contribution from biomass burning and fuel combustion (54% of source contribution) followed by coal combustion for residential heating and cooking purposes (44%). Potential toxicity of B[a]P equivalence ranged from 0.003 to 1.365 with cumulative toxicity of 2.13ngm-3. Among the PAH species, dibenzo[h]anthracene contributed maximum toxicity followed by B[a]P, together accounting 86% of PAH induced carcinogenicity. Incremental risk of developing cancer through lifetime exposure (ILCR) of PAHs was higher in children (3.3 × 10-4) with 56% contribution from LMW PAHs, primarily through ingestion and dermal contact. Adults in contrast, were more exposed to inhale airborne PAHs with cumulative ILCR of 2.2 × 10-4. However, ILCR to PM2.5 exposure is probably underestimated considering unaccounted metal abundance thus, require source-specific control measures.Copyright © 2023. Published by Elsevier Ltd.