Chemical Characteristics and Cytotoxicity to GC-2spd(ts) Cells of PM2.5 in Nanjing Jiangbei New Area from 2015 to 2019

Abstract

PM2.5 is an air pollutant with complex components. After entering the body through respiration, PM2.5 can not only cause respiratory diseases, but also break through the blood–testis barrier and influence the reproductive system. PM2.5 with different components may result in different toxic effects. In the first five years of Nanjing Jiangbei New Area, industrial transformation would change the concentration and chemical fraction of PM2.5 in the local environment to a certain extent. In this study, PM2.5 collected in Nanjing Jiangbei New Area every autumn and winter from 2015 to 2019 was analyzed. PM2.5 concentration generally decreased year by year. The large proportion of secondary inorganic ions indicated the presence of secondary pollution at the sampling site. PM2.5 was mainly emitted from fossil fuel combustion and vehicle exhaust. The cytotoxicity of PM2.5 samples was evaluated by PM2.5 exposure to mouse spermatocytes (GC-2spd(ts) cells). Cell viability was relatively low in 2016 and 2018, and relatively high in 2017 and 2019. Reactive oxygen species levels and DNA damage levels followed similar trends, with an overall annual decrease. The cytotoxicity of PM2.5 on GC-2spd(ts) cells was significantly correlated with water-soluble ions, water-soluble organic carbon, heavy metals and polycyclic aromatic hydrocarbons (p < 0.01). According to principal component analysis and multiple linear regression, fossil fuel combustion, secondary transformation of pollutants and construction dust were identified as the major contributors to cytotoxic effects, contributing more than 50%.

New health index derived from oxidative potential and cell toxicity of fine particulate matter to assess its potential health effect

“…The WSOC was moderately and strongly correlated with secondary inorganic ions at the Beijing (0.6 < r < 0.8) and Gwangju (0.6 < r < 0.9) sites, respectively. In other studies, secondary aerosols have been reported to contribute to an increase in OP [ 11 ] and biological responses (e.g., cell toxicity, ROS, and inflammation) [ 54 , 55 ]. Secondary inorganic ions can increase the solubility of metals in particles and change their pH (e.g., acidification) to indirectly affect OP [ 39 , 56 , 57 ].…”

The Cytotoxic Effects of Fine Particulate Matter (PM2.5) from Different Sources at the Air–Liquid Interface Exposure on A549 Cells

“…The NO 3 − /SO 4 2− ratio was often used to determine the main source of atmospheric particulate pollution. When the ratio was larger than 1, it meant that mobile sources, like car exhausts, dominated the emission source; when it was less than 1, it meant that stationary sources, such as coal combustion, dominated [ 4 , 30 ]. The NO 3 − /SO 4 2− ratios of the PM 2.5 samples from the residential, industrial, and traffic sources were 0.99, 1.35, and 1.30, respectively.…”

“…A common biomarker of DNA double–strand breaks (DSBs) is γ–H2AX, which is produced when H2AX is phosphorylated. The level of γ–H2AX might indicate the extent of DNA damage [ 4 , 36 ]. In this experiment, stained γ–H2AX showed green fluorescence under a fluorescence microscope ( Figure 5 a–c).…”

“…The International Agency for Research on Cancer (IARC) has classified fine particulate matter (<2.5 μm, PM 2.5 ) as a Class I carcinogen. PM 2.5 was a major air pollutant that was produced by traffic exhausts, industrial emissions, burning coal and fuel, and other human activities, as well as aerosol formation in natural processes [ 2 , 3 , 4 ]. PM 2.5 could be suspended in the air for a long time and carry various harmful substances (such as polycyclic aromatic hydrocarbons, heavy metals, etc.).…”

“…Previous studies have shown that the chemical components (water–soluble ions, carbonaceous components, heavy metals, and polycyclic aromatic hydrocarbons) in PM 2.5 were one of the key factors leading to its toxic effects on cells [ 12 , 13 , 14 ]. Water–soluble ions could lead to adverse effects such as cellular oxidative stress and inflammatory reactions [ 4 , 15 ]. Heavy metals, polycyclic aromatic hydrocarbons (PAHs), and their oxygen–containing derivatives could induce cytotoxicity, oxidative stress, inflammatory response, and DNA damage [ 15 , 16 , 17 , 18 , 19 ].…”