Compositions, sources and health risks of dioxins/furans, polycylic aromatic hydrocarbons and trace metals in ambient air of Kuala Lumpur

Abstract

Polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) are persistent organic pollutants that are prone to bind with fine particulate matter (PM2.5). PM2.5 might contain other toxic air pollutants, such as polycyclic aromatic hydrocarbons (PAHs) and trace metals (TMs), posing potential health risks by inhalation. This study aimed to quantify the levels of PCDDs/PCDFs in PM2.5, total suspended particles (TSP) and in the gaseous phase, as well as PAHs and TMs in PM2.5 in the urban air of Kuala Lumpur across different monsoon cycles. The potential sources contributing to atmospheric PCDDs/PCDFs and the health risks associated with inhalation exposure were also investigated. PM2.5 and TSP were collected using high-volume samplers from December 2021 to October 2022. Particulate samples were collected on quartz microfibre, whereas the gaseous phase was captured on polyurethane foam. The congener profiles of 17 PCDDs/PCDFs, 16 PAHs, and 11 TMs were determined. The possible sources were apportioned using positive matrix factorisation (PMF). Carcinogenic and non-carcinogenic health risk assessments for children and adults were estimated using the United States Environmental Protection Agency (USEPA) approach. The average PM2.5 and TSP concentrations were 18.4 ± 8.9 μg m-3 and 36.6 ± 11.6 μg m-3, respectively. Approximately 62% of daily PM2.5 samples exceeded the World Health Organization 2018 guideline. The Ʃ17PCDDs/PCDFs concentration in ambient air is 7748 ± 3323 fg m-3, whereas PM2.5, TSP, and gaseous phase concentrations are 6332 ± 3558 fg m-3, 4358 ± 2747 fg m-3 dan 3304 ± 1514 fg m-3, respectively. The hepta- and octa-group congeners dominated up to 80% of the Ʃ17PCDDs/PCDFs and are more likely to bind with the particle phase than the gaseous phase. The Ʃ17PCDDs/PCDFs displayed a significant seasonal trend and a significant difference between gaseous and particle concentrations (p <0.001). Active and passive samples showed comparable Ʃ17PCDD/PCDF profiles with estimated uptake rate for PCDDs/PCDFs using passive sampling is 1.65 m3 day-1. The PM2.5-bound Ʃ16PAH concentrations ranged from 3.18 to 9.74 ng m–3, with 4–6-ring PAHs contributing 95% of the total Ʃ16PAHs. The Ʃ11TM concentrations in PM2.5 ranged from 116.4 to 464.5 ng m-3, with Fe as the most abundant metal. The PMF model suggests that traffic-related emissions are the primary sources of PCDDs/PCDFs, PAHs and TMs in PM2.5 (32–38%). Exposure to the gaseous phase of Ʃ17PCDDs/PCDFs resulted in a greater inhalation lifetime cancer risk (5.3E-06 ± 2.8E-06) than exposure to the particulate phases of TSP and PM2.5. Non-carcinogenic effects are negligible in all cases. This study has successfully provided comprehensive information on the atmospheric PCDDs/PCDFs in different phases in Kuala Lumpur, where the toxic equivalent (TEQ) concentrations are dominant in the gaseous phase, while cancer risks from exposure to PM2.5-bound PCDDs/PCDFs, PAHs and TMs are tolerable in children and adults.