Size-fractionated ambient particulate matter induce toxicity: Oxidative potential, cytotoxic effect and inflammatory potential

Roy, Ritwika; Jan, Rohi; Bhor, Renuka; Pai, Kalpana; Satsangi, P. Gursumeeran

doi:10.1016/j.atmosenv.2023.120032

Cited by 5 publications

(1 citation statement)

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“…Only a few studies in the IGP examined the variation and chemical foundation of PM 2.5 pollution and its associations with PM 2.5 toxicity in Delhi. These studies often neglect the monsoon time or treat the entire monsoon period as an integrated clean season because of the low daily PM 2.5 concentrations that often fall within the National Ambient Air Quality Standard (NAAQS) of 60 μg m –3 . , Noteworthy, even lower concentrations (5 μg m –3 ) can still impact lung homeostasis and lead to various adverse outcomes. − Given this research gap and the threat of PM 2.5 exposure, it is essential to investigate the PM 2.5 OP and cytotoxicity during the monsoon period to address potentially overlooked health effects from air pollution in the IGP.…”

Section: Introductionmentioning

confidence: 99%

Variation of PM_2.5 Redox Potential and Toxicity During Monsoon in Delhi, India

Li,

Hakkim,

Sinha

et al. 2024

ACS EST Air

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This study investigates daily variations in redox potential of water-and organic-soluble PM 2.5 during Delhi's monsoon season, offering insights into its chemical composition, cytotoxicity, and oxidative threat to various lung conditions. PM 2.5 samples, categorized by pollution levels, showed an average intrinsic oxidative potential (OP m DTT ) of 27.5 pmol min −1 μg −1 , OH • generation of 51.1 pmol μg −1 , and antioxidant capacity (AOC) in both gallic acid and trolox equivalency of 62.5 and 35.3 pmol μg −1 , respectively. Water-soluble redox-active compounds (RACs) contributed to approximately 67% of the PM 2.5 redox potential.The polar-phase distribution of RACs in PM 2.5 can be modified by atmospheric photochemistry and precipitation. Biomass burning emerged as a pivotal pollution source, with polluted PM 2.5 samples exhibiting higher cytotoxicity and oxidative stress in A549 cells. All PM 2.5 compounds impaired cellular respiration, reducing the oxygen consumption rates in A549 cells. Intrinsic OP m DTT and OH • generation of PM 2.5 were influenced by lung fluid variants, such as exogenous nicotine and endogenous inflammatory protein. This study provides a comprehensive perspective on PM 2.5 pollution and its toxicity in Delhi, India during distinct pollution periods and also points out the importance of considering population disparities and individual health status in assessing PM 2.5 health impacts.

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