Association of Fine Particulate Matter and Risk of Stroke in Patients With Atrial Fibrillation

Rhinehart, Zachary; Kinnee, Ellen; Essien, Utibe R.; Saul, Melissa; Guhl, Emily; Clougherty, Jane E.; Magnani, Jared W.

doi:10.1001/jamanetworkopen.2020.11760

Cited by 33 publications

(23 citation statements)

References 57 publications

(98 reference statements)

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“… PM 2.5 Seoul, Korea 2007 364 patients Increased risk of rupture-prone coronary plaque Yang et al (2019) 7. PM 2.5 Allegheny County, Pennsylvania 2007 - 2015 31,414 individuals with atrial Fibrillation (AF) Associated with high risk of ischemic stroke Rhinehart et al (2020) 8. PM 2.5 Shanghai, China 2014 - 2016 1,016,579 participants outpatients Increased risk of cardiac arrhythmias Yang et al (2020) 9.…”

Section: Impact Of Pm On the Cardiovascular Systemmentioning

confidence: 99%

Role of atmospheric particulate matter exposure in COVID-19 and other health risks in human: A review

Zhu

Maharajan

Liu

et al. 2021

Environmental Research

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Section: Impact Of Pm On the Cardiovascular Systemmentioning

confidence: 99%

Role of atmospheric particulate matter exposure in COVID-19 and other health risks in human: A review

Zhu

Maharajan

Liu

et al. 2021

Environmental Research

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“…Some epidemiologic studies have demonstrated that both short‐term and long‐term PM2.5 exposures are associated with a higher risk of ischemic stroke, especially with stroke characterized by large artery atherosclerosis (LAA) and small vessel occlusion 5‐7 . A recent large cohort study provided further evidence that PM2.5 exposure may be associated with ischemic stroke in individuals with prevalent atrial fibrillation 8 . In addition, high exposure to particulate matter (PM) before stroke may be independently associated with 3‐month mortality and cerebral edema after intravenous thrombolysis 9 .…”

Section: Introductionmentioning

confidence: 99%

Fine particulate matter exposure aggravates ischemic injury via NLRP3 inflammasome activation and pyroptosis

et al. 2022

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Aims Accumulating evidence has suggested that airborne fine particulate matter (PM2.5) exposure is associated with an increased risk of ischemic stroke. However, the underlying mechanisms have not been fully elucidated. In this study, we aim to investigate the role and mechanisms of NLRP3 inflammasome and pyroptosis in ischemic stroke after PM2.5 exposure. Methods The BV‐2 and HMC‐3 microglial cell lines were established and subjected to oxygen–glucose deprivation and reoxygenation (OGD/R) with or without PM2.5 exposure. We used the CCK‐8 assay to explore the effects of PM2.5 on cell viability of BV‐2 and HMC‐3 cells. Then, the effects of PM2.5 exposure on NLRP3 inflammasome and pyroptosis following OGD/R were detected by western blotting, ELISA, and the confocal immunofluorescence staining. Afterwards, NLRP3 was knocked down to further validate the effects of PM2.5 on cell viability, NLRP3 inflammasome activation, and pyroptosis after OGD/R in HMC‐3 cells. Finally, the intracellular reactive oxygen species (ROS) was measured and the ROS inhibitor N‐acetyl‐L‐cysteine (NAC) was used to investigate whether ROS was required for PM2.5‐induced NLRP3 inflammasome activation and pyroptosis under ischemic conditions. Results We found that PM2.5 exposure decreased the viability of BV‐2 and HMC‐3 cells in a dose‐ and time‐dependent manner under ischemic conditions. Furthermore, PM2.5 exposure aggravated NLRP3 inflammasome activation and pyroptosis after OGD/R, as indicated by an increased expression of NLRP3, ASC, pro‐caspase‐1, Caspase‐1, GSDMD, and GSDMD‐N; increased production of IL‐1β and IL‐18; and enhanced Caspase‐1 activity and SYTOX green uptake. However, shRNA NLRP3 treatment attenuated the effects of PM2.5 on cell viability, NLRP3 inflammasome activation, and pyroptosis. Moreover, we observed that PM2.5 exposure increased the production of intracellular ROS following OGD/R, while inhibiting ROS production with NAC partially attenuated PM2.5‐induced NLRP3 inflammasome activation and pyroptosis under ischemic conditions. Conclusion These results suggested that PM2.5 exposure triggered the activation of NLRP3 inflammasome and pyroptosis under ischemic conditions, which may be mediated by increased ROS production after ischemic stroke. These findings may provide a more enhanced understanding of the interplay between PM2.5 and neuroinflammation and cell death, and reveal a novel mechanism of PM2.5‐mediated toxic effects after ischemic stroke.

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“…According to Bourdrel et al, a 10 µg/m 3 increment in the PM 2.5 concentration had an influence on admissions for stroke up to two days after the exposure [32]. Besides the direct influence on ruptures of plaques in arteries, cerebral infarction pathomechanisms may also include the induction of atrial fibrillation, the consequent formation of thrombi, and their release to the bloodstream reaching the brain vessels [33,34].…”

Section: Discussionmentioning

confidence: 99%

Short-Term Effects of “Polish Smog” on Cardiovascular Mortality in the Green Lungs of Poland: A Case-Crossover Study with 4,500,000 Person-Years (PL-PARTICLES Study)

et al. 2021

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Previous studies conducted in highly polluted areas have reported associations between air pollution and daily mortality. The Green Lungs of Poland are characterized by unique natural features and a moderate pollution level. We aimed to assess the short-term impact of air pollution on cardiovascular (CVD)-, acute coronary syndrome (ACS)-, and cerebrovascular-related (CbVD) mortality. An analysis with 4,500,000 person-years and a time-stratified case-crossover design was performed. The interquartile range increase in the PM2.5 (OR 1.036, 95% CI 1.016–1.056, p < 0.001) and PM10 concentration (OR 1.034, 95% CI 1.015–1.053, p < 0.001) was associated with increased CVD mortality on lag 0, and this effect persisted on the following days. The effects of PMs were expressed more in association with ACS-related mortality (PM2.5-OR = 1.045, 95% CI 1.012–1.080, p = 0.01; PM10-OR = 1.044, 95% CI 1.010–1.078, p = 0.01) and CbVD mortality (PM10-OR = 1.099, 95% CI 1.019–1.343, p = 0.02). We also noted a higher CVD mortality OR in the cold season for PM10 in cities with area-source domination: Białystok (p = 0.001) and Suwałki (p = 0.047). The short-term impact of PMs on cardiovascular mortality is also observed in moderately polluted areas. This adverse health effect was more apparent in CbVD- and ACS-related mortality, and in the cold season. Further research focusing on the adverse health effects of “Polish smog” is sorely needed.

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Association of Fine Particulate Matter and Risk of Stroke in Patients With Atrial Fibrillation

Cited by 33 publications

References 57 publications

Role of atmospheric particulate matter exposure in COVID-19 and other health risks in human: A review

Role of atmospheric particulate matter exposure in COVID-19 and other health risks in human: A review

Fine particulate matter exposure aggravates ischemic injury via NLRP3 inflammasome activation and pyroptosis

Short-Term Effects of “Polish Smog” on Cardiovascular Mortality in the Green Lungs of Poland: A Case-Crossover Study with 4,500,000 Person-Years (PL-PARTICLES Study)

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