Effects of the ambient fine particulate matter (PM2.5) exposure on urinary metabolic profiles in rats using UPLC-Q-TOF-MS

2019 ◽  
Vol 30 (1) ◽  
pp. 90-94 ◽  
Author(s):  
Lin Zhang ◽  
Tengfei Xu ◽  
Zifeng Pi ◽  
Meizhu Zheng ◽  
Fengrui Song ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Fine Particulate Matter ◽  
Metabolic Profiles ◽  
Fine Particulate ◽  
Pm2.5 Exposure ◽  
Tof Ms

scholarly journals The Combined Effects of Fine Particulate Matter and Temperature on Preterm Birth in Seoul, 2010–2016

2021 ◽  
Vol 18 (4) ◽  
pp. 1463
Author(s):  
Youngrin Kwag ◽  
Min-ho Kim ◽  
Shinhee Ye ◽  
Jongmin Oh ◽  
Gyeyoon Yim ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Preterm Birth ◽  
Pregnant Women ◽  
Low Temperatures ◽  
Fine Particulate Matter ◽  
Temperature Data ◽  
Fine Particulate ◽  
The Mean ◽  
Pm2.5 Exposure ◽  
Pm2.5 Concentration

Background: Preterm birth contributes to the morbidity and mortality of newborns and infants. Recent studies have shown that maternal exposure to particulate matter and extreme temperatures results in immune dysfunction, which can induce preterm birth. This study aimed to evaluate the association between fine particulate matter (PM2.5) exposure, temperature, and preterm birth in Seoul, Republic of Korea. Methods: We used 2010–2016 birth data from Seoul, obtained from the Korea National Statistical Office Microdata. PM2.5 concentration data from Seoul were generated through the Community Multiscale Air Quality (CMAQ) model. Seoul temperature data were collected from the Korea Meteorological Administration (KMA). The exposure period of PM2.5 and temperature were divided into the first (TR1), second (TR2), and third (TR3) trimesters of pregnancy. The mean PM2.5 concentration was used in units of ×10 µg/m3 and the mean temperature was divided into four categories based on quartiles. Logistic regression analyses were performed to evaluate the association between PM2.5 exposure and preterm birth, as well as the combined effects of PM2.5 exposure and temperature on preterm birth. Result: In a model that includes three trimesters of PM2.5 and temperature data as exposures, which assumes an interaction between PM2.5 and temperature in each trimester, the risk of preterm birth was positively associated with TR1 PM2.5 exposure among pregnant women exposed to relatively low mean temperatures (<3.4 °C) during TR1 (OR 1.134, 95% CI 1.061–1.213, p < 0.001). Conclusions: When we assumed the interaction between PM2.5 exposure and temperature exposure, PM2.5 exposure during TR1 increased the risk of preterm birth among pregnant women exposed to low temperatures during TR1. Pregnant women should be aware of the risk associated with combined exposure to particulate matter and low temperatures during TR1 to prevent preterm birth.

scholarly journals In Utero Exposure to Fine Particulate Matter Causes Hypertension Due to Impaired Renal Dopamine D1 Receptor in Offspring

2018 ◽  
Vol 46 (1) ◽  
pp. 148-159 ◽  
Author(s):  
Zhengmeng Ye ◽  
Xi Lu ◽  
Yi Deng ◽  
Xinquan Wang ◽  
Shuo Zheng ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Particulate Matter ◽  
Sodium Excretion ◽  
Fine Particulate Matter ◽  
In Utero ◽  
D1 Receptor ◽  
In Utero Exposure ◽  
Fine Particulate ◽  
Pm2.5 Exposure ◽  
Renal Dopamine

Background/Aims: Adverse environment in utero can modulate adult phenotypes including blood pressure. Fine particulate matter (PM2.5) exposure in utero causes hypertension in the offspring, but the exact mechanisms are not clear. Renal dopamine D1 receptor (D1R), regulated by G protein-coupled receptor kinase type 4 (GRK4), plays an important role in the regulation of renal sodium transport and blood pressure. In this present study, we determined if renal D1R dysfunction is involved in PM2.5–induced hypertension in the offspring. Methods: Pregnant Sprague–Dawley rats were given an oropharyngeal drip of PM2.5 (1.0 mg/kg) at gestation day 8, 10, and 12. The blood pressure, 24-hour sodium excretion, and urine volume were measured in the offspring. The expression levels of GRK4 and D1R were determined by immunoblotting. The phosphorylation of D1R was investigated using immunoprecipitation. Plasma malondialdehyde and superoxide dismutase levels were also measured in the offspring. Results: As compared with saline-treated dams, offspring of PM2.5-treated dams had increased blood pressure, impaired sodium excretion, and reduced D1R-mediated natriuresis and diuresis, accompanied by decreased renal D1R expression and GRK4 expression. The impaired renal D1R function and increased GRK4 expression could be caused by increased reactive oxidative stress (ROS) induced by PM2.5 exposure. Administration of tempol, a redox-cycling nitroxide, for 4 weeks in the offspring of PM2.5-treated dam normalized the decreased renal D1R expression and increased renal D1R phosphorylation and GRK4 expression. Furthermore, tempol normalized the increased renal expression of c-Myc, a transcription factor that regulates GRK4 expression. Conclusions: In utero exposure to PM2.5 increases ROS and GRK4 expression, impairs D1R-mediated sodium excretion, and increases blood pressure in the offspring. These studies suggest that normalization of D1R function may be a target for the prevention and treatment of the hypertension in offspring of mothers exposed to PM2.5 during pregnancy.

Ambient Fine Particulate Matter and Preterm Birth in California: Identification of Critical Exposure Windows

2019 ◽  
Vol 188 (9) ◽  
pp. 1608-1615 ◽  
Author(s):  
Paige Sheridan ◽  
Sindana Ilango ◽  
Tim A Bruckner ◽  
Qiong Wang ◽  
Rupa Basu ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Preterm Birth ◽  
Proportional Hazards ◽  
Fine Particulate Matter ◽  
Cox Proportional Hazards ◽  
Distributed Lag ◽  
Fine Particulate ◽  
Cox Proportional Hazards Models ◽  
Pm2.5 Exposure ◽  
Exposure Windows

Abstract Exposure to ambient fine particulate matter (particulate matter ≤2.5 μm in aerodynamic diameter (PM2.5)) during pregnancy is associated with preterm birth (PTB), a leading cause of infant morbidity and mortality. Results from studies attempting to identify etiologically relevant exposure periods of vulnerability have been inconsistent, possibly because of failure to consider the time-to-event nature of the outcome and lagged exposure effects of PM2.5. In this study, we aimed to identify critical exposure windows for weekly PM2.5 exposure and PTB in California using California birth cohort data from 2005–2010. Associations were assessed using distributed-lag Cox proportional hazards models. We assessed effect-measure modification by race/ethnicity by calculating the weekly relative excess risk due to interaction. For a 10-μg/m3 increase in PM2.5 exposure over the entire period of gestation, PTB risk increased by 11% (hazard ratio = 1.11, 95% confidence interval: 1.09, 1.14). Gestational weeks 17–24 and 36 were associated with increased vulnerability to PM2.5 exposure. We find that non-Hispanic black mothers may be more susceptible to effects of PM2.5 exposure than non-Hispanic white mothers, particularly at the end of pregnancy. These findings extend our knowledge about the existence of specific exposure periods during pregnancy that have the greatest impact on preterm birth.

scholarly journals A city-level analysis of air pollution, climate and COVID-19 early spread during the Spanish lockdown

2020 ◽  
Author(s):  
Alvaro Briz-Redon ◽  
Carolina Belenguer-Sapina ◽  
Angel Serrano-Aroca
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Environmental Conditions ◽  
Fine Particulate Matter ◽  
Epidemic Curve ◽  
Fine Particulate ◽  
The World ◽  
Pm2.5 Exposure ◽  
Level Analysis ◽  
Good Agreement

The COVID-19 outbreak has escalated into the worse pandemic of the present century. The fast spread of the new SARS-CoV-2 coronavirus has caused devastating health and economic crises all over the world, with Spain being one of the worst affected countries in terms of confirmed COVID-19 cases and deaths per inhabitant. In this situation, the Spanish Government declared the lockdown of the country. The variations of air pollution in terms of fine particulate matter (PM2.5) levels in seven cities of Spain are analyzed here considering the effect of meteorology during the national lockdown. The possible associations of PM2.5 pollution and climate with COVID-19 accumulated cases were also analyzed. While the epidemic curve was flattened, the results of the analysis show that the 4-week Spanish lockdown significantly reduced the PM2.5 levels in only one of the cities despite the drastically reduced human activity in good agreement with our previous study of changes in air quality in terms of CO, SO2, PM10, O3 and NO2 levels. Furthermore, no associations between either PM2.5 exposure or environmental conditions and COVID-19 transmission were found during the early spread of the pandemic.

NLRP3 Inflammasome: A Potential Therapeutic Target in Fine Particulate Matter-Induced Neuroinflammation in Alzheimer’s Disease

2021 ◽  
Author(s):  
Jian-Quan Shi ◽  
Bian-Rong Wang ◽  
Teng Jiang ◽  
Li Gao ◽  
Ying-Dong Zhang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Particulate Matter ◽  
Nlrp3 Inflammasome ◽  
Molecular Mechanisms ◽  
Fine Particulate Matter ◽  
Transport Pathway ◽  
Critical Gap ◽  
Fine Particulate ◽  
Pm2.5 Exposure

As one of the most harmful air pollutants, fine particulate matter (PM2.5) has been implicated as a risk factor for multiple diseases, which has generated widespread public concern. Accordingly, a growing literature links PM2.5 exposure with Alzheimer’s disease (AD). A critical gap in our understanding of the adverse effects of PM2.5 on AD is the mechanism triggered by PM2.5 that contributes to disease progression. Recent evidence has demonstrated that PM2.5 can activate NLRP3 inflammasome-mediated neuroinflammation. In this review, we highlight the novel evidence between PM2.5 exposure and AD incidence, which is collected and summarized from neuropathological, epidemiological, and neuroimaging studies to in-depth deciphering molecular mechanisms. First, neuropathological, epidemiological, and neuroimaging studies will be summarized. Then, the transport pathway for central nervous system delivery of PM2.5 will be presented. Finally, the role of NLRP3 inflammasome-mediated neuroinflammation in PM2.5 induced-effects on AD will be recapitulated.

scholarly journals Astaxanthin Suppresses PM2.5-Induced Neuroinflammation by Regulating Akt Phosphorylation in BV-2 Microglial Cells

2020 ◽  
Vol 21 (19) ◽  
pp. 7227 ◽  
Author(s):  
Ryeong-Eun Kim ◽  
Chan Young Shin ◽  
Seol-Heui Han ◽  
Kyoung Ja Kwon
Keyword(s):  
Nitric Oxide ◽  
Air Pollution ◽  
Particulate Matter ◽  
Fine Particulate Matter ◽  
Microglial Cells ◽  
Akt Phosphorylation ◽  
Fine Particulate ◽  
Pm2.5 Exposure ◽  
Anti Inflammatory ◽  
The Brain

Air pollution has become one of the most serious issues for human health and has been shown to be particularly concerning for neural and cognitive health. Recent studies suggest that fine particulate matter of less than 2.5 (PM2.5), common in air pollution, can reach the brain, potentially resulting in the development and acceleration of various neurological disorders including Alzheimer’s disease, Parkinson’s disease, and other forms of dementia, but the underlying pathological mechanisms are not clear. Astaxanthin is a red-colored phytonutrient carotenoid that has been known for anti-inflammatory and neuroprotective effects. In this study, we demonstrated that exposure to PM2.5 increases the neuroinflammation, the expression of proinflammatory M1, and disease-associated microglia (DAM) signature markers in microglial cells, and that treatment with astaxanthin can prevent the neurotoxic effects of this exposure through anti-inflammatory properties. Diesel particulate matter (Sigma-Aldrich) was used as a fine particulate matter 2.5 in the present study. Cultured rat glial cells and BV-2 microglial cells were treated with various concentrations of PM2.5, and then the expression of various inflammatory mediators and signaling pathways were measured using qRT-PCR and Western blot. Astaxanthin was then added and assayed as above to evaluate its effects on microglial changes, inflammation, and toxicity induced by PM2.5. PM2.5 increased the production of nitric oxide and reactive oxygen species and upregulated the transcription of various proinflammatory markers including Interleukin-1β (IL-1β), Interleukin-6 (IL-6), Tumor necrosis factor α (TNFα), inducible nitric oxide synthase (iNOS), triggering receptor expressed on myeloid cells 2 (TREM2), Toll-like receptor 2/4 (TLR2/4), and cyclooxygenase-2 (COX-2) in BV-2 microglial cells. However, the mRNA expression of IL-10 and arginase-1 decreased following PM2.5 treatment. PM2.5 treatment increased c-Jun N-terminal kinases (JNK) phosphorylation and decreased Akt phosphorylation. Astaxanthin attenuated these PM2.5-induced responses, reducing transcription of the proinflammatory markers iNOS and heme oxygenase-1 (HO-1), which prevented neuronal cell death. Our results indicate that PM2.5 exposure reformulates microglia via proinflammatory M1 and DAM phenotype, leading to neurotoxicity, and the fact that astaxanthin treatment can prevent neurotoxicity by inhibiting transition to the proinflammatory M1 and DAM phenotypes. These results demonstrate that PM2.5 exposure can induce brain damage through the change of proinflammatory M1 and DAM signatures in the microglial cells, as well as the fact that astaxanthin can have a potential beneficial effect on PM2.5 exposure of the brain.

NLRP3 Inflammasome: A Potential Therapeutic Target in Fine Particulate Matter-Induced Neuroinflammation in Alzheimer’s Disease

2020 ◽  
Vol 77 (3) ◽  
pp. 923-934
Author(s):  
Jian-Quan Shi ◽  
Bian-Rong Wang ◽  
Teng Jiang ◽  
Li Gao ◽  
Ying-Dong Zhang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Particulate Matter ◽  
Nlrp3 Inflammasome ◽  
Molecular Mechanisms ◽  
Fine Particulate Matter ◽  
Transport Pathway ◽  
Critical Gap ◽  
Fine Particulate ◽  
Pm2.5 Exposure

As one of the most harmful air pollutants, fine particulate matter (PM2.5) has been implicated as a risk factor for multiple diseases, which has generated widespread public concern. Accordingly, a growing literature links PM2.5 exposure with Alzheimer’s disease (AD). A critical gap in our understanding of the adverse effects of PM2.5 on AD is the mechanism triggered by PM2.5 that contributes to disease progression. Recent evidence has demonstrated that PM2.5 can activate NLRP3 inflammasome-mediated neuroinflammation. In this review, we highlight the novel evidence between PM2.5 exposure and AD incidence, which is collected and summarized from neuropathological, epidemiological, and neuroimaging studies to in-depth deciphering molecular mechanisms. First, neuropathological, epidemiological, and neuroimaging studies will be summarized. Then, the transport pathway for central nervous system delivery of PM2.5 will be presented. Finally, the role of NLRP3 inflammasome-mediated neuroinflammation in PM2.5 induced-effects on AD will be recapitulated.

scholarly journals Association of Fine Particulate Matter Exposure with Acute Noncardiovascular Critical Illnesses and In-hospital Outcomes in Patients Receiving Intensive Cardiac Care

2020 ◽  
Author(s):  
Fei Chen ◽  
Qi Liu ◽  
Baotao Huang ◽  
Fangyang Huang ◽  
Yiming Li ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Particulate Matter ◽  
Respiratory Failure ◽  
Fine Particulate Matter ◽  
Kidney Injury ◽  
Cardiac Care ◽  
Short Term ◽  
Fine Particulate ◽  
Exposure Levels ◽  
Pm2.5 Exposure

Abstract Background The effect of short-term exposure to fine particulate matter (PM2.5) on the incidence of acute noncardiovascular critical illnesses (ANCIs) and clinical outcomes is unknown in patients with acute cardiovascular diseases. Methods We conducted a retrospective study in 2,337 admissions to an intensive cardiac care unit (ICCU) from June 2016 to May 2017. We used the 2-day average PM2.5 concentration before ICCU admission to estimate the individual exposure level, and patients were divided into 3 groups according to the concentration tertiles. Major ANCI was defined as the composite of acute respiratory failure, acute kidney injury, gastrointestinal hemorrhage, or sepsis. The primary endpoint was all-cause death or discharge against medical advice in extremely critical condition. Results During the 12-month study period, the annual median concentration of PM2.5 in Chengdu, China was 48 µg/m3 (IQR, 33-77 µg/m3). More than 20 percent of admissions were complicated by major ANCI, and the primary endpoints occurred in 7.6% of patients during their hospitalization. The association of short-term PM2.5 exposure levels with the incidence of acute respiratory failure (adjusted OR [odds ratio] =1.31, 95%CI [confidence interval]1.12-1.54) and acute kidney injury (adjusted OR=1.20, 95%CI 1.02-1.41) showed a significant trend. Additionally, there were numerically more cases of sepsis (adjusted OR=1.21, 95%CI 0.92-1.60) and gastrointestinal hemorrhage (adjusted OR=1.29, 95%CI 0.94-1.77) in patients with higher exposure levels. After further multivariable adjustment, short-term PM2.5 exposure levels were still significantly associated with incident major ANCI (adjusted OR=1.32, 95%CI 1.12-1.56), as well as a higher incidence of the primary endpoint (adjusted OR=1.52, 95%CI 1.09-2.12). Conclusion Short-term PM2.5 exposure before ICCU admission was associated with an increased risk of incident major ANCI and worse in-hospital outcomes in patients receiving intensive cardiac care.

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