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Fine particles (especially PM2.5 particles) in ambient air can cause irreversible effects on human health. In the present study, seasonal variations in toxicity PM2.5 (cell viability and release of pro-inflammatory cytokines) were exposed human lung cells (A549) to concentrations of PM2.5 samples in summer (sPM2.5) and winter (wPM2.5) seasons. Cell...
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Laboratory and epidemiological researches have indicated that ambient air particulate matter have a plays critical role in causing diseases. The current research evaluated the chemical attributes of PM2.5 in the ambient air of the cities of Karaj and Fardis and determined its toxicological effects on human lung epithelial cells (A549). In the study...
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... However, epithelial cells were exposed to air for a long period of time, and using traditional immersion exposure to evaluate the cytotoxicity of PM 2.5 clearly does not meet the requirements. Current research has shown that in traditional immersion exposure, the duration of exposure significantly affects the cytotoxicity of particulate matter, leading to decreased cell activity and increased inflammatory response (Rahmatinia et al. 2022). However, at the ALI, the debate is not unanimous. ...
Fine particulate matter (PM2.5) can enter the human body in various ways and have adverse effects on human health. Human lungs and eyes are exposed to the air for a long time and are the first to be exposed to PM2.5. The “liquid immersion exposure method” has some limitations that prevent it from fully reflecting the toxic effects of particulate matter on the human body. In this study, the collected PM2.5 samples were chemically analyzed. An air–liquid interface (ALI) model with a high correlation to the in vivo environment was established based on human lung epithelial cells (A549) and immortalized human corneal epithelial cells (HCE-T). The VITROCELL Cloud 12 system was used to distribute PM2.5 on the cells evenly. After exposure for 6 h and 24 h, cell viability, apoptosis rate, reactive oxygen species (ROS) level, expression of inflammatory factors, and deoxyribonucleic acid (DNA) damage were measured. The results demonstrated significant dose- and time-dependent effects of PM2.5 on cell viability, cell apoptosis, ROS generation, and DNA damage at the ALI, while the inflammatory factors showed dose-dependent effects only. It should be noted that even short exposure to low doses of PM2.5 can cause cell DNA double-strand breaks and increased expression of γ-H2AX, indicating significant genotoxicity of PM2.5. Increased abundance of ROS in cells plays a crucial role in the cytotoxicity induced by PM2.5 exposure These findings emphasize the significant cellular damage and genotoxicity that may result from short-term exposure to low levels of PM2.5.
... Some related studies have found that different seasons and sources of particulate matter had varying degrees of influence on the secretion of inflammatory factors (IL-8 and IL-6). The metals, PAHs, endotoxin, and other components in particulate matter played an important role in the inflammatory response induced by PM 2.5 [34,35]. These results suggested that the source and spatiotemporal distribution of particulate matter could lead to different components of particulate matter, which in turn affected its biological toxicity. ...
... Some related studies have found that different seasons and sources of particulate matter had varying degrees of influence on the secretion of inflammatory factors (IL−8 and IL−6). The metals, PAHs, endotoxin, and other components in particulate matter played an important role in the inflammatory response induced by PM2.5 [34,35]. These results suggested that the source and spatiotemporal distribution of particulate matter could lead to different components of particulate matter, which in turn affected its biological toxicity. ...
The health of humans has been negatively impacted by PM2.5 exposure, but the chemical composition and toxicity of PM2.5 might vary depending on its source. To investigate the toxic effects of particulate matter from different sources on lung epithelial cells (A549), PM2.5 samples were collected from residential, industrial, and transportation areas in Nanjing, China. The chemical composition of PM2.5 was analyzed, and toxicological experiments were conducted. The A549 cells were exposed using an air–liquid interface (ALI) exposure system, and the cytotoxic indicators of the cells were detected. The research results indicated that acute exposure to different sources of particulate matter at the air–liquid interface caused damage to the cells, induced the production of ROS, caused apoptosis, inflammatory damage, and DNA damage, with a dose–effect relationship. The content of heavy metals and PAHs in PM2.5 from the traffic source was relatively high, and the toxic effect of the traffic–source samples on the cells was higher than that of the industrial– and residential–source samples. The cytotoxicity of particulate matter was mostly associated with water–soluble ions, carbon components, heavy metals, PAHs, and endotoxin, based on the analysis of the Pearson correlation. Oxidative stress played an important role in PM2.5–induced biological toxicity.
... Multiple prior studies have suggested that as the concentration of PM 2.5 rises and the duration of exposure increases, the rate of cell survival tends to decline[56][57][58][59] . Moreover, previously conducted studies around the world showed that ambient PM in summer, with the same concentration and usage, have a lower toxic effects on A549 compared to PM 2.5 in winter season20,29,31,60 . ...
Exposure to particulate matter (PM) can be considered as a factor affecting human health. The aim of this study was to investigate the concentration of PM2.5 and heavy metals and their influence on survival of A549 human lung cells in exposure to PM2.5 breathing air of Ahvaz city. In order to assess the levels of PM2.5 and heavy metals, air samples were collected from 14 sampling stations positioned across Ahvaz city during both winter and summer seasons. The concentration of heavy metals was determined using ICP OES. Next, the MTT assay [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] was employed to ascertain the survival rate of A549 cells. The findings from this research demonstrated that average PM2.5 of the study period was (149.5 μg/m³). Also, the average concentration of PM2.5 in the urban area in winter and summer was (153.3- and 106.9 μg/m³) and in the industrial area this parameter was (191.6 and 158.3 μg/m³). The average concentration of metals (ng/m³) of urban areas against industrial, Al (493 vs. 485), Fe (536 vs. 612), Cu (198 vs. 212), Ni (128 vs. 129), Cr (48.5 vs. 54), Cd (118 vs. 124), Mn (120 vs. 119), As (51 vs. 67), Hg (37 vs. 50), Zn (302 vs. 332) and Pb (266 vs. 351) were obtained. The results of the MTT assay showed that the highest percentage of cell survival according to the exposure concentration was 25 > 50 > 100 > 200. Also, the lowest percentage of survival (58.8%) was observed in the winter season and in industrial areas with a concentration of 200 μg/ml. The carcinogenic risk assessment of heavy metals indicated that except for Cr, whose carcinogenicity was 1.32E−03, other metals were in the safe range (10–4–10–6) for human health. The high concentration of PM2.5 and heavy metals can increase respiratory and cardiovascular diseases and reduce the public health level of Ahvaz citizens.
... Environ Geochem Health from Karaj, Iran (Rahmatinia et al., 2022). Therefore, PM 2.5 can produce inflammatory cytokines from both macrophages and epithelial cells and induce inflammation. ...
... Our results revealed that PM 2.5 from the Kawasaki site induced the gene expression of IL-8 but not that of genes that encode other cytokines, such as pro-IL-1β and IL-6, in lung epithelial A549 cells (Fig. S2). The difference in the concentration of the metals and/or organic carbon in PM 2.5 from Karaj and Kawasaki affected the inflammatory responses differently, even in the same types of cells (Rahmatinia et al., 2022). Similarly, as shown in "PM2.5 from Kawasaki and Fukue sites affected lung epithelial A549 cells differently" section, PM 2.5 from Kawasaki (industrial area) and Fukue (domestic area) showed distinctly different metal compositions and inflammatory responses in lung epithelial cells (Fig. 3). ...
... Mbelambela et al. conducted an epidemiological study showing a correlation between PM 2.5 and chronic obstructive pulmonary disease (COPD) (Mbelambela et al., 2020). Furthermore, it is reported that exposure to PM 10 induced lung inflammation in a mouse model (Rahmatinia et al., 2022). Thus, IL-8 production following exposure to PM 2.5 can be considered a potential risk factor for pulmonary diseases. ...
Fine atmospheric particles, such as PM2.5, are strongly related to the onset and exacerbation of inflammatory responses leading to the development of respiratory and cardiovascular diseases. PM2.5 is a complex mixture of tiny particles with different properties (i.e., size, morphology, and chemical components). Moreover, the mechanism by which PM2.5 induces inflammatory responses has not been fully elucidated. Therefore, it is necessary to determine the composition of PM2.5 to identify the main factors causing PM2.5-associated inflammation and diseases. In the present study, we investigated PM2.5 from two sites (Fukue, a remote monitoring site, and Kawasaki, an urban monitoring site) with greatly different environments and PM2.5 compositions. The results of ICP-MS and EDX-SEM indicated that PM2.5 from Kawasaki contained more metals and significantly induced the expression of the pro-inflammatory cytokine gene IL-8 compared to the PM2.5 from Fukue. We also verified the increased secretion of IL-8 protein from exposure to PM2.5 from Kawasaki. We further investigated their effects on inflammatory response and cytotoxicity using metal nanoparticles (Cu, Zn, and Ni) and ions and found that the Cu nanoparticles caused a dose-dependent increase in IL-8 expression together with significant cell death. We also found that Cu nanoparticles enhanced the secretion of IL-8 protein. These results suggest that Cu in PM2.5 is involved in lung inflammation.
... Many studies have shown that PM 2.5 has a distinct effect on the levels of IL-8. For example, the mean levels of IL-6 and IL-8 in human lung cells (A549) in the cold season (winter) are twice that in the hot season (summer), following that the PM 2.5 concentration in winter (56.4 μg m −3 ) is also double of that in summer (26.9 μg m −3 ) (Rahmatinia et al., 2022). A study conducted in Milan, Italy found that PM 2.5 led to the accumulation of IL-8 in intracellular vesicles (Longhin et al., 2018). ...
Solid fuel combustion for domestic heating in northern China in the wintertime is of great environmental and health concern. This study assesses personal exposure to particulate matter with different aerodynamic diameters and multiple gaseous pollutants from 123 rural residents in Yuncheng, the Fenwei Plain. The subjects are divided into groups based on the unique energy source applied, including biomass, coal, and electricity/no heating activities. The health effects of the exposures are expressed with four urinary biomarkers. The personal exposure levels to three different aerodynamic particle sizes (i.e., PM10, PM2.5, and PM1) of the electricity/no heating group are 5.1 %–12 % lower than those of the coal group. In addition, the exposure levels are 25 %–40 % lower for carbon monoxide (CO) and 10.8 %–20.3 % lower for ozone (O3) in the electricity/no heating group than the other two fuel groups. C-reactive protein (CRP) in the urine of the participants in biomass and coal groups is significantly higher than that in the electricity/no heating group, consistent with the observations on other biomarkers. Increases in 8-hydroxy-2 deoxyguanosine (8-OHdG), interleukin-8 (IL-8), and vascular endothelial growth factor (VEGF) are observed for the exposures to higher concentrations of air pollutants. For instance, PMs and nitrogen dioxide (NO2) show significant impacts on positive correlations with 8-OHdG and IL-8, while O3 positively correlates with CRP. PM1 exhibits higher effects on the biomarkers than the gaseous pollutants, especially on VEGF and IL-8. The study indicates that excessive use of traditional domestic solid fuels could pose severe health effects on rural residents. The promotion of using clean energy is urgently needed in the rural areas of northern China.
... PAHs are part of a complex mixture of particulate matter (PM) in the environment (Rahmatinia et al. 2021b). PM is divided into three types: coarse, fine, and ultrafine particle fractions based on their size (Bourdrel et al. 2017); fine particles (0.1-2.5 µm) (PM 2.5 ) are related to the development of adverse effects due to PM 2.5 has significant capability to penetrate into human airways (Rahmatinia et al. 2021a) effect of PM2.5. Additionally, several studies have reported that PM 2.5 are the principal PM related to increased risk of kidney cancer, lung cancer, heart, and respiratory disease (Bourdrel et al. 2017;Kim et al. 2018;Rahmatinia et al. 2021a). ...
... PM is divided into three types: coarse, fine, and ultrafine particle fractions based on their size (Bourdrel et al. 2017); fine particles (0.1-2.5 µm) (PM 2.5 ) are related to the development of adverse effects due to PM 2.5 has significant capability to penetrate into human airways (Rahmatinia et al. 2021a) effect of PM2.5. Additionally, several studies have reported that PM 2.5 are the principal PM related to increased risk of kidney cancer, lung cancer, heart, and respiratory disease (Bourdrel et al. 2017;Kim et al. 2018;Rahmatinia et al. 2021a). ...
Environmental endocrine disruptors are a risk factor for produce adverse cardiovascular, reproductive, developmental, metabolic, and neurological effects. Most of these endocrine disruptors are plastics components such as phthalates and bisphenol A, or polycyclic aromatic hydrocarbons generated through indoor air pollution. Among populations vulnerable to pollution, indigenous people are of particular concern due to their limited access to health care, direct dependency on natural resources, traditions, and low levels of support. The aim of this study was to evaluate the exposure to phthalate metabolites, 1-hydroxypyrene (1OH-P), and bisphenol A (BPA) through biomonitoring data from an indigenous population of the Huasteca Potosina in Mexico. The urinary concentrations of 4 phthalate metabolites and BPA were analyzed by ultra-performance liquid chromatography coupled to tandem mass spectrometry, and 1OH-P exposure was evaluated by high-performance liquid chromatography coupled to a fluorescence detector. A total of 45 women were included, with a high percentage of overweight (59%). The use of plastics containers and burning garbage were the main pollution sources (98-100%). Mono-2-ethyl phthalate, mono-n-butyl phthalate and 1OH-P concentrations were identified in 100% of the study population, with a median (25 th – 75 th percentile) of 17478 (11362- 37355), 113.8 (61.7-203.5) and 1.2 (0.9-1.7) μg/g creatinine, respectively. Urinary mono-2-ethyl phthalate concentrations tend to be higher than those measured from other studies, which reflects an impressive exposure to di(2-ethylhexyl) phthalate. Considering the magnitude of the indigenous population exposed to pollutants and the possible effects, it is important to design strategies that mitigate exposure and evaluate the effectiveness through biological monitoring and effects.
