Molecular distribution, sources and potential health risks of fine particulate-bound polycyclic aromatic hydrocarbons during high pollution episodes in a subtropical urban city

• Published in: Chemosphere (Oxford) Vol. 340; p. 139943
• Main Authors: Singh, Abhishek, Banerjee, Tirthankar, Latif, Mohd T., Ramanathan, Sharanya, Suradi, Hamidah, Othman, Murnira, Murari, Vishnu
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 01-11-2023
• Subjects: Aerosol exposure; Carcinogenicity; PAHs; Receptor model; Respiratory deposition; Receptor model; PAHs; Aerosol exposure; Respiratory deposition; Carcinogenicity
• ISSN: 0045-6535; 1879-1298
• DOI: 10.1016/j.chemosphere.2023.139943

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 monitoring days accounting ≥100 μgm−3 of PM2.5 concentration, frequently from November to January (99% of monitoring 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.
Sources, exposure and health risks of airborne PAHs. [Display omitted]
•Ambient PM2.5 concentration was roughly 20 times higher than WHO standard.•Both low and high molecular weight PAHs were prominent with minor seasonal variation.•Biomass burning, fuel combustion including coal combustion are major PAHs emitter.•Respiratory deposition at the upper airway is most prominent PAHs exposure pathway.•Incremental risk of developing cancer by PAH exposure was high in children than adult.