Spatially resolved distribution, sources and health risks of heavy metals in size-fractionated road dust from 57 sites across megacity Kolkata, India.

This work reports the first assessment of contamination levels, source contributions and health risks associated with heavy metals (HMs) in road dust from Kolkata, the second-most polluted metropolis in India. To this end, samples collected from 57 locations across 6 land-use categories: residential, roadside, traffic, railway, port and industrial areas in the city during 2018 were analyzed for 11 major and trace metals (Ca, Mg, Fe, Al, Mn, Ni, V, Cu, Zn, Cr, Pb) in three size fractions: <75 μm, 75-125 μm and 125-300 μm. Overall, Mn, Zn, Cr, Pb, V, Cu and Ni were enriched in the smallest fraction by factors of 1.2-2.7. Based on metal distribution across land-use categories, crustal dust (Fe, Al, V), construction activities (Ca, Mg), metallurgical processes (Pb), and non-exhaust abrasive emissions from brake, tire and paint wear (Cu, Zn, Cr) were found to be significant. HMs such as Cu, Zn, Cr and Pb were considerably enriched over background levels as suggested by three contamination indices: Enrichment Factor (EF; overall range: 2.4-12.0), Index of Geo-accumulation (I; overall range: 1.1-3.4), and Pollution Index (PI; overall range: 3.1-15.6). Geospatial mapping identified HM contamination hotspots (integrated PI >4) in west-central and northern parts (the older sections) of the city represented by industrial, port, and traffic-congested residential areas. Using positive matrix factorization (PMF), the following sources were apportioned for the three size fractions: crustal dust (48-66%), construction activities (18-20%), vehicular abrasion (7-21%), industrial emissions (5-8%), a Cr-dominated mixed source (6%) and an unassigned source (7%). Finally, health risk assessment in the form of cumulative hazard index (HI) and incremental lifetime cancer risk (ILCR) found that children (mean HI: 1.29 and ILCR: 2E-04) are comparatively more vulnerable than adults (mean HI: 0.22 and ILCR: 8E-05) to HM exposure, with the ingestion exposure pathway dominating over dermal contact and inhalation.