Cytotoxic Free Radicals on Air-Borne Soot Particles Generated by Burning Wood or Low-Maturity Coals

Abstract

The traditional cook stove is a major contributor to combustionderived soot particles, which contain various chemical species that may cause a significant impact to human health and ecosystems. However, properties and toxicity associated with environmentally persistent free radicals (EPFRs) in such emissions are not well known. This paper investigated the characteristics and cytotoxicity of soot-associated EPFRs discharged from Chinese household stoves. Our results showed that the concentrations of EPFRs were related to fuel types, and they were higher in wood-burning soot (8.9−10.5 × 10 16 spins/g) than in coal-burning soot (3.9−9.7 × 10 16 spins/g). Meanwhile, EPFR concentrations in soot decreased with an increase of coal maturity. The soot EPFRs, especially reactive fractions, readily induced the generation of reactive oxygen species (ROS). Potential health effects of soot EPFRs were also examined using normal human bronchial epithelial cell line 16HBE as a model. Soot particles were internalized by 16HBE cells inducing cytotoxicity. The main toxicity inducers were identified to be reactive EPFR species, which generated ROS inside human cells. Our findings provided valuable insights into potential contributions of soot EPFRs associated with different types of fuel to health problems. This information will support regulations to end or limit current stove usage in numerous households.

Elucidation of the Critical Role of Core Materials in PM2.5-Induced Cytotoxicity by Interrogating Silica- and Carbon-Based Model PM2.5 Particle Libraries

“…Cell suspensions containing 5000 cells in 100 μL were seeded in 96-well plates. After incubation for 24 h, cells were incubated with different concentrations of model PM 2.5 particles and PM 2.5 -JN (10,25,50,100,200,400, and 800 μg/ mL) for another 48 h. The CCK-8 kit (Dojindo, Japan) was used to detect the viability of 16HBE cells after various treatments according to the manufacturer's instructions.…”

“…Carbon black and silica constitute insoluble parts of PM 2.5 , depending on their environmental sources . Due to wind and anthropogenic activities, soil, construction, and urban fugitive dust are major sources of airborne silica particles, − while biomass burning, automobiles, and gas flaring release high contents of carbon black particles into the atmosphere. − Carbon black and silica have distinctly different physicochemical properties, e . g ., silica is more polar than carbon black.…”

Characteristics of Environmentally Persistent Free Radicals in PM2.5 and the Influence of Air Pollutants in Shihezi, Northwestern China

“…The secondary sources of EPFRs are derived from the intermediate products formed by the degradation of organic compounds under natural conditions, such as the degradation of aromatic hydrocarbons and their auto-oxidation processes [ 19 ]. Polycyclic aromatic hydrocarbons (PAHs), as precursors, can react heterogeneously with ozone to produce oxygenated functional groups [ 20 ], which can stabilize on transition metal surfaces to form EPFRs [ 21 ]. Researchers have found that the formation of EPFRs may involve many organic chemical degradation processes [ 19 , 20 , 21 , 22 ].…”

“…Polycyclic aromatic hydrocarbons (PAHs), as precursors, can react heterogeneously with ozone to produce oxygenated functional groups [ 20 ], which can stabilize on transition metal surfaces to form EPFRs [ 21 ]. Researchers have found that the formation of EPFRs may involve many organic chemical degradation processes [ 19 , 20 , 21 , 22 ]. Compared with EPFRs formed under extreme conditions, such as during combustion or under high temperature [ 22 ], the formation of EPFRs in natural ambient surroundings is common, but few studies have explored this environmental process.…”

Are the new atmospheric health risk substances EPFRs oxidatively toxic? : Results from a large urban road dust study in Northwest China

“…Meanwhile, in a laboratory simulation of EPFRs generation experiments, it was found that a single EPFR can catalyze the generation of 10 reactive oxygen species (ROS) 22,23,24 ; in studies of municipal solid waste incinerator fly ash, there was a significant correlation between EPFRs concentrations and hydroxyl and superoxide radical concentrations 25 ; EPFRs adsorbed on PM2.5 induced hydroxyl radical production in aqueous and hydrogen peroxide solutions, and the concentration of hydroxyl radical increased consistently with the time of induction 26 . The major toxicity inducer EPFRs were found to produce ROS in human cells when the potential health effects of EPFRs in coal soot were investigated using the healthy human bronchial epithelial cell line 16HBE as a model 27 .…”