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The effect of PM2.5-related hazards on biomarkers of bronchial epithelial cells (A549) inflammation in Karaj and Fardis cities

Authors:
Tahereh Rahmatinia at TMU
Tahereh Rahmatinia
  • TMU
Majid Kermani at Iran University of Medical Sciences
Majid Kermani
Mahdi Farzadkia at Iran University of Medical Sciences
Mahdi Farzadkia
Ahmad Jonidi jafari at Iran University of Medical Sciences
Ahmad Jonidi jafari
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Abstract and Figures

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. Cells were separately exposed to three concentrations of PM2.5 (25, 50, and 100 μg/mL) and three times (12 h, 1 and 2 days). We evaluated cell viability by MTT assay [3- (4, 5-dimethylthiazol-2-yl) -2, 5-diphenyltetrazolium bromide] and liberation of pro-inflammatory cytokines (interleukin-6 and interleukin-8) by the ELISA method. The toxicological results of this study showed that increasing the concentration of PM2.5 particulates and contact time with it reduces cell viability and increases inflammatory responses. Seasonal cytotoxicity of PM2.5 particles in high-traffic areas at summer season compared to winter season was lower. The lowest percent of viability at 2 days of exposure and 100 μg/mL exposure in the winter sample was observed. Also, PM2.5 particles were influential in the amount of interleukins 8 and 6. The average release level of IL-6 and IL-8 in the cold season (winter) and the enormous exposure time and concentrations (2 days–100 μg/mL) was much higher than in the hot season (summer). These values were twice as high for winter PM2.5 samples as for summer samples. The compounds in PM2.5 at different seasons can cause some biological effects. The samples’ chemical characteristics in two seasons displayed that the PMs were diverse in chemical properties. In general, heavy metals and polycyclic aromatic hydrocarbons were more in the winter samples. However, the samples of wPM2.5 had a lower mass quota of metals such as aluminum, iron, copper, zinc, and magnesium. Concentrations of chromium, cadmium, arsenic, mercury, nickel, and lead were more significant in the sample of wPM2.5.
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RESEARCH ARTICLE
The effect of PM
2.5
-related hazards on biomarkers of bronchial
epithelial cells (A549) inflammation in Karaj and Fardis cities
Tahereh Rahmatinia
1,2
&Majid Kermani
1,2
&Mahdi Farzadkia
1,2
&Ahmad Jonidi Jafari
1,2
&Ali-Akbar Delbandi
3,4
&
Nesa Rashidi
3,4
&Farzad Fanaei
1,2
Received: 15 June 2021 / Accepted: 26 July 2021
#The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2021
Abstract
Fine particles (especially PM
2.5
particles) in ambient air can cause irreversible effects on human health. In the present study,
seasonal variations in toxicity PM
2.5
(cell viability and release of pro-inflammatory cytokines) were exposed human lung cells
(A549) to concentrations of PM
2.5
samples in summer (sPM
2.5
)andwinter(wPM
2.5
) seasons. Cells were separately exposed to
three concentrations of PM
2.5
(25, 50, and 100 μg/mL) and three times (12 h, 1 and 2 days). We evaluated cell viability by MTT
assay [3- (4, 5-dimethylthiazol-2-yl) -2, 5-diphenyltetrazolium bromide] and liberation of pro-inflammatory cytokines (interleu-
kin-6 and interleukin-8) by the ELISA method. The toxicological results of this study showed that increasing the concentration of
PM
2.5
particulates and contact time with it reduces cell viability and increases inflammatory responses. Seasonal cytotoxicity of
PM
2.5
particles in high-traffic areas at summer season compared to winter season was lower. The lowest percent of viability at 2
days of exposure and 100 μg/mL exposure in the winter sample was observed. Also, PM
2.5
particles were influential in the
amount of interleukins 8 and 6. The average release level of IL-6 and IL-8 in the cold season (winter) and the enormous exposure
time and concentrations (2 days–100 μg/mL) was much higher than in the hot season (summer). These values were twice as high
for winter PM
2.5
samples as forsummer samples. The compounds in PM
2.5
at different seasons can cause some biological effects.
The samples’chemical characteristics in two seasons displayed that the PMs were diverse in chemical properties. In general,
heavy metals and polycyclic aromatic hydrocarbons were more in the winter samples. However, the samples of wPM
2.5
had a
lower mass quota of metals such as aluminum, iron, copper, zinc, and magnesium. Concentrations of chromium, cadmium,
arsenic, mercury, nickel, and lead were more significant in the sample of wPM
2.5
.
Keywords Pro-inflammatory cytokine .Lung epithelial cells (A549) .In vitro
Introduction
Inflammation of the airways is one of the short-term effects on
humans’lungs due to airborne PM (Schwartz et al. 2020).
Inflammation, when it happens with severity or for a long time
at the airway’s bottom, causes breathing system illnesses like
chronic obstructive pulmonary disease (COPD) and asthma
(Eapen et al. 2017; Fu et al. 2020). This process kills pro-
inflammatory intermediate using macrophages of alveolar
(AMs) and epithelial lung cells (ECs). Cytokines are signaling
proteins involved in regulating physiological factors that will
function as a pro-inflammatory or anti-inflammatory media-
tor. Chemokines are secreted only by cell damage or by mul-
tiple stimuli to absorb and activate immune cells (Ramgolam
et al. 2008). Two known pro-inflammatory cytokines are in-
terleukins 6 (IL-6) and 8 (IL-8). These proteins have special
functions. Since the first defense response is IL-8, it is released
Responsible Editor: Lotfi Aleya
*Majid Kermani
kermani.m@iums.ac.ir; majidkermani@yahoo.com
*Farzad Fanaei
farzadfanaei37@gmail.com
1
Research Center for Environmental Health Technology, Iran
University of Medical Sciences, Tehran, Iran
2
Department of Environmental Health Engineering, School of Public
Health, Iran University of Medical Sciences, Tehran, Iran
3
Immunology Research Center, Institute of Immunology and
Infectious Diseases, Iran University of Medical Sciences,
Tehran, Iran
4
Department of Immunology, School of Medicine, Iran University of
Medical Sciences, Tehran, Iran
https://doi.org/10.1007/s11356-021-15723-3
/ Published online: 7 August 2021
Environmental Science and Pollution Research (2022) 29:2172–2182
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
... 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. ...
Copper in airborne fine particulate matter (PM2.5) from urban sites causes the upregulation of pro-inflammatory cytokine IL-8 in human lung epithelial A549 cells
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  • May 2023
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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.
View
... 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 Cytotoxic Effects of Fine Particulate Matter (PM2.5) from Different Sources at the Air–Liquid Interface Exposure on A549 Cells
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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.
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... 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 disruptor concentrations in urine samples from Mexican Indigenous women
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  • May 2022
  • ENVIRON SCI POLLUT R
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.
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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. ...
Toxicological responses of A549 and HCE-T cells exposed to fine particulate matter at the air–liquid interface
Article
Full-text available
  • Mar 2024
  • ENVIRON SCI POLLUT R
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.
View
... 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 . ...
Investigating PM2.5 toxicity in highly polluted urban and industrial areas in the Middle East: human health risk assessment and spatial distribution
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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.
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... 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). ...
Associations of personal exposure to domestic heating and cooking fuel emissions and epidemiological effects on rural residents in the Fenwei Plain, China
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  • SCI TOTAL ENVIRON
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Characterisation of PM2.5 – bound PAHs in outdoor air of Karaj megacity: the effect of meteorological factors
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Full-text available
  • Jul 2020
Aim: This study was conducted to evaluate the effects of ambient concentrations of PM2.5 and PM10 on the health‑related aspects including the total mortality, respiratory and cardiovascular diseases, and hospital admissions due to respiratory and cardiovascular diseases in Karaj, Alborz Province, Iran, during 2012–2016 using the AirQ2.2.3 software. The effects of meteorological parameters on the PM2.5 and PM10 levels were also investigated. Materials and Methods: Meteorological parameters, population, and the pollutant data were obtained from the Department of Environmental Protection, Karaj (Alborz, Iran). Statistical analysis was performed using the SPSS 24 software to study the relationship between the PM2.5 and PM10 concentrations and the meteorological parameters. Results: Our results showed a direct relationship between the PM10 concentration and the temperature (r = 0.34, P < 0.018) and relative humidity (r = 0.37, P < 0.5). However, there was a negative relationship between the PM10 concentration with wind speed (r < −0.328, P < 0.014) and precipitation (r < −0.179, P < 0.327). Similarly, there was a direct relationship between the PM2.5 concentration and the temperature (r = 0.41, P < 0.014) and relative humidity (r = 0.37, P < 0.05). On the other hand, a negative relationship was observed between the PM2.5 concentration with wind speed (r < −0.138, P < 0.010) and precipitation (r < −0.12, P < 0.201). The total number of death, death due to cardiovascular and respiratory diseases, and hospital admissions due to cardiovascular and respiratory diseases were equal to 1619, 1096, 306, and 4822, respectively. Conclusions: The results of this study showed that the concentrations of PM2.5 and PM10 should be reduced through applying the management strategies to improve the health of the residents in Karaj city.
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Concentrations and mortality due to short- and long-term exposure to PM2.5 in a megacity of Iran (2014–2019)
Article
Full-text available
  • Oct 2020
  • ENVIRON SCI POLLUT R
The present study aimed to survey the spatial and temporal trends of ambient concentration of PM2.5 and to estimate mortality attributed to short- and long-term exposure to PM2.5 in Isfahan from March 2014 to March 2019 using the AirQ+ software. The hourly concentrations of PM2.5 were obtained from the Isfahan Department of Environment and Isfahan Air Quality Monitoring Center. Then, the 24-h mean concentration of PM2.5 for each station was calculated using the Excel software. According to the results, the annual mean concentration of PM2.5 in 2014–2019 was 29.9–50.9 μg/m3, approximately 3–5 times higher than the WHO guideline (10 μg/m3). The data showed that people of Isfahan in almost 58% to 96% of the days of a year were exposed to PM2.5 higher than the WHO daily guideline. The concentrations of PM2.5 in cold months such as October, November, December and January were higher than those in the other months. The zoning of the annual concentrations of PM2.5 in urban areas showed that the highest PM2.5 concentrations were related to the northern, northwestern, southern and central areas of the city. On average, from 2014 to 2019, the number of deaths due to natural mortality, lung cancer (LC), chronic obstructive pulmonary disease (COPD), ischemic heart disease (IHD) and stroke associated with ambient PM2.5 were 948, 16, 18, 281 and 60, respectively. The present study estimated that on average, 14.29% of the total mortality, 17.2% of lung cancer (LC), 15.54% of chronic obstructive pulmonary disease (COPD), 17.12% of ischemic heart disease (IHD) and 14.94% of stroke mortalities were related to long-term exposure to ambient PM2.5. So provincial managers and politicians must adopt appropriate strategies to control air pollution and reduce the attributable health effects and economic losses.
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Analysis of PM10, Pb, Cd, and Ni atmospheric concentrations during domestic heating season in Sarajevo, Bosnia and Herzegovina, from 2010 to 2019
Article
Full-text available
  • Aug 2020
This paper examines atmospheric concentrations of particulate matter with an aerodynamic diameter smaller than 10 μm (PM10) and related particle-phase toxic heavy metals Cd, Ni, and Pb during domestic heating seasons from 2010 to 2019 in Sarajevo, Bosnia and Herzegovina. In total, 242 daily PM10 samples were collected using medium and high volume air samplers. The mean daily PM10 mass concentration for all measurements is 75.16 μg/m3 (with the range of 28.77–149.00 μg/m3). Variation of ambient PM10 was observed throughout the study in different years. Hourly values for PM10 measurements during two heating seasons are also presented. Metal concentrations in PM10 were analyzed by electrothermal atomic absorption spectrometry (ETAAS). Quantities of atmospheric mass concentrations of studied trace metals were observed in the following order: Pb > Ni > Cd. The mean concentrations of metals varied with Pb showing the highest concentration (ranging from 1.38 to 234.00 ng/m3), Ni ranging from 0.87 to 42.43 ng/m3, and Cd showing the lowest concentration ranging from 0.26 to 10.09 ng/m3. The concentration of Pb and Cd in PM10 was strongly correlated, suggesting a common source or dependence of these metals in PM10 in Sarajevo. Bioaccessibility of metals in the synthetic gastric juice was also estimated. The quantities of average bioaccessible metal fractions in PM10 samples showed the following trend: Cd > Pb > Ni. The health risk assessment shows that the population of Sarajevo is at increased lifetime risk of experiencing cancer because of exposure to these Cd concentrations in PM10. In addition, parallel PM10 sampling on two samplers showed that obtained results are highly comparable.
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PM2.5 Exposure Induces Inflammatory Response in Macrophages via the TLR4/COX-2/NF-κB Pathway
Article
Full-text available
  • Oct 2020
  • INFLAMMATION
Fine particulate matter with an aerodynamic diameter less than 2.5 μm (PM2.5) is a serious air pollutant associated with health problems. Macrophages play an important role in the process of PM2.5-induced inflammation in respiratory diseases. However, the detailed mechanism remains unclear. We aimed to examine the mechanism of PM2.5-induced inflammation and find possible anti-inflammatory inhibitors. PM2.5 was collected in Hangzhou, China, and the composition of adsorbed materials on PM2.5 was characterized. RAW 254.7 cells were then treated with PM2.5. Phagocytosis was observed, and inflammatory response was triggered as demonstrated by the release of high levels of monocyte chemoattractant protein-1(MCP-1), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) and increased mRNA expression of inducible nitric oxide synthase (iNOS) and TNF-α. Treatment with classic inhibitors suppressed the released pro-inflammatory factors in a dose-dependent manner. Using Immunology Inflammation Compound Library, we screened 70 inhibitors and clustered them based on similarities in their inhibitory effects, which we detected using cytometric bead array (CBA) assay. Molecular analysis revealed that the expression of toll-like receptor 4 (TLR4), nuclear factor kappa-B (NF-κB), and cyclooxygenase-2 (COX-2) was increased in PM2.5-stimulated RAW 254.7 cells. Corresponding inhibitors were selected, and the CBA assay verified their anti-inflammatory effects. These inhibitors reduced the expression of pro-inflammatory factors, and this reduction was correlated with the downregulation of the TLR4/NF-κB/COX-2 signaling pathway. In conclusion, PM2.5 induces an inflammatory response in macrophages via activation of TLR4/NF-κB/COX-2 signaling, and the inhibitors of this pathway are potential therapeutic candidates to treat inflammatory disorders.
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Prenatal exposure to polycyclic aromatic hydrocarbons and effects on neonatal anthropometric indices and thyroid-stimulating hormone in a Middle Eastern population
Article
  • Jan 2022
Prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) evokes extensive concerns regarding public health. Monitoring the pregnant women's exposure can be considered a suitable alternative to assess the fetus's exposure. This study aimed to monitor pregnant women's exposure (n = 126) to PAHs using a biomonitoring approach to evaluate effects on anthropometric indices and neonatal thyroid-stimulating hormone (TSH) in Shiraz, Iran. PAHs priority compounds were measured by gas chromatography-mass spectrometry (GC-MS) after separating blood serum and liquid-liquid extraction (LLE) method. Information on anthropometric indices, neonatal TSH levels, and data from the respondents was obtained from medical records and questionnaires. The mean PAHs concentrations ranged from 0.29 to 327.91 ng/g lipid. There was no significant difference between the measured PAHs in maternal serum at the seventh month and pregnancy termination except for ACY (p-Value<0.05). Regression analysis results showed a significant correlation (p-value<0.05) between exposure to passive smoke and total PAHs concentrations. There was no significant relationship between exposure to PAHs and weight, height, head circumference, and Apgar score of newborns. The results showed TSH decreased by 0.99 units as ACE increased per unit (β =-0.001). This study is the first to evaluate relationships between prenatal exposure to PAHs and effects on newborn health indicators, including TSH levels in a Middle Eastern population. Future studies are suggested to perform detailed assessments of PAHs intake sources, especially in vulnerable populations such as pregnant women and children.
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