Exposure to fine particulate matter promotes platelet activation and thrombosis via obesity-related inflammation

Dayu Hu; Xu Jia; Liyan Cui; Junxiu Liu; Jiahui Chen; Yazheng Wang; Wei Niu; Junhui Xu; Mark R. Miller; Miranda Loh; Furong Deng; Xinbiao Guo

doi:10.1016/j.jhazmat.2021.125341

Exposure to fine particulate matter promotes platelet activation and thrombosis via obesity-related inflammation

Dayu Hu, Xu Jia, Liyan Cui, Junxiu Liu, Jiahui Chen, Yazheng Wang, Wei Niu, Junhui Xu, Mark R. Miller, Miranda Loh, Furong Deng, Xinbiao Guo

Community, Environment and Policy

Research output: Contribution to journal › Article › peer-review

40 Scopus citations

Abstract

Short-term exposure to fine particulate matter (PM_2.5) increases thrombotic risk particularly in obese individuals, but the underlying mechanisms remain unclear. This study aims to compare the effects of PM_2.5 on inflammation and platelet activation in obese versus normal-weight adults, and investigate potential causal pathways. We conducted a panel study measuring blood markers in 44 obese and 53 normal-weight adults on 3 separate occasions in 2017–2018. Associations between PM_2.5/black carbon (BC) and biomarkers were estimated using mixed-effect models. An interaction analysis compared PM_2.5/BC-related effects between subgroups. Biomarker combinations and mediation analysis were performed to elucidate the biological pathways. There was a significant “low-high-low” trend of PM_2.5 levels across the 3 study periods. Increases in pro-inflammatory cytokines and changes of platelet activation and aggregation markers were associated with PM_2.5/BC in obese subgroup only. Among obese subjects, the combination of pro-inflammatory cytokines and that of platelet markers increased 26.8% (95% CI: 16.0%, 37.9%) and 14.7% (95% CI: 1.9%, 27.0%) per IQR increase in PM_2.5 over 5-day and 7-day averages. Inflammation mediated 24.5% of the pathways through which PM_2.5 promoted platelet activation. This study suggested obese people are susceptible to pro-thrombotic impacts of PM_2.5 exposures. PM_2.5 may aggravate thrombosis through obesity-related inflammation.

Original language	English (US)
Article number	125341
Journal	Journal of Hazardous Materials
Volume	413
DOIs	https://doi.org/10.1016/j.jhazmat.2021.125341
State	Published - Jul 5 2021

Keywords

Black carbon
Obesity
PM
Platelet
Prothrombotic state

ASJC Scopus subject areas

Environmental Engineering
Environmental Chemistry
Waste Management and Disposal
Pollution
Health, Toxicology and Mutagenesis

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10.1016/j.jhazmat.2021.125341

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title = "Exposure to fine particulate matter promotes platelet activation and thrombosis via obesity-related inflammation",

abstract = "Short-term exposure to fine particulate matter (PM2.5) increases thrombotic risk particularly in obese individuals, but the underlying mechanisms remain unclear. This study aims to compare the effects of PM2.5 on inflammation and platelet activation in obese versus normal-weight adults, and investigate potential causal pathways. We conducted a panel study measuring blood markers in 44 obese and 53 normal-weight adults on 3 separate occasions in 2017–2018. Associations between PM2.5/black carbon (BC) and biomarkers were estimated using mixed-effect models. An interaction analysis compared PM2.5/BC-related effects between subgroups. Biomarker combinations and mediation analysis were performed to elucidate the biological pathways. There was a significant “low-high-low” trend of PM2.5 levels across the 3 study periods. Increases in pro-inflammatory cytokines and changes of platelet activation and aggregation markers were associated with PM2.5/BC in obese subgroup only. Among obese subjects, the combination of pro-inflammatory cytokines and that of platelet markers increased 26.8% (95% CI: 16.0%, 37.9%) and 14.7% (95% CI: 1.9%, 27.0%) per IQR increase in PM2.5 over 5-day and 7-day averages. Inflammation mediated 24.5% of the pathways through which PM2.5 promoted platelet activation. This study suggested obese people are susceptible to pro-thrombotic impacts of PM2.5 exposures. PM2.5 may aggravate thrombosis through obesity-related inflammation.",

keywords = "Black carbon, Obesity, PM, Platelet, Prothrombotic state",

author = "Dayu Hu and Xu Jia and Liyan Cui and Junxiu Liu and Jiahui Chen and Yazheng Wang and Wei Niu and Junhui Xu and Miller, {Mark R.} and Miranda Loh and Furong Deng and Xinbiao Guo",

note = "Publisher Copyright: {\textcopyright} 2021 Elsevier B.V.",

year = "2021",

month = jul,

day = "5",

doi = "10.1016/j.jhazmat.2021.125341",

language = "English (US)",

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journal = "Journal of Hazardous Materials",

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T1 - Exposure to fine particulate matter promotes platelet activation and thrombosis via obesity-related inflammation

AU - Hu, Dayu

AU - Jia, Xu

AU - Cui, Liyan

AU - Liu, Junxiu

AU - Chen, Jiahui

AU - Wang, Yazheng

AU - Niu, Wei

AU - Xu, Junhui

AU - Miller, Mark R.

AU - Loh, Miranda

AU - Deng, Furong

AU - Guo, Xinbiao

PY - 2021/7/5

Y1 - 2021/7/5

N2 - Short-term exposure to fine particulate matter (PM2.5) increases thrombotic risk particularly in obese individuals, but the underlying mechanisms remain unclear. This study aims to compare the effects of PM2.5 on inflammation and platelet activation in obese versus normal-weight adults, and investigate potential causal pathways. We conducted a panel study measuring blood markers in 44 obese and 53 normal-weight adults on 3 separate occasions in 2017–2018. Associations between PM2.5/black carbon (BC) and biomarkers were estimated using mixed-effect models. An interaction analysis compared PM2.5/BC-related effects between subgroups. Biomarker combinations and mediation analysis were performed to elucidate the biological pathways. There was a significant “low-high-low” trend of PM2.5 levels across the 3 study periods. Increases in pro-inflammatory cytokines and changes of platelet activation and aggregation markers were associated with PM2.5/BC in obese subgroup only. Among obese subjects, the combination of pro-inflammatory cytokines and that of platelet markers increased 26.8% (95% CI: 16.0%, 37.9%) and 14.7% (95% CI: 1.9%, 27.0%) per IQR increase in PM2.5 over 5-day and 7-day averages. Inflammation mediated 24.5% of the pathways through which PM2.5 promoted platelet activation. This study suggested obese people are susceptible to pro-thrombotic impacts of PM2.5 exposures. PM2.5 may aggravate thrombosis through obesity-related inflammation.

AB - Short-term exposure to fine particulate matter (PM2.5) increases thrombotic risk particularly in obese individuals, but the underlying mechanisms remain unclear. This study aims to compare the effects of PM2.5 on inflammation and platelet activation in obese versus normal-weight adults, and investigate potential causal pathways. We conducted a panel study measuring blood markers in 44 obese and 53 normal-weight adults on 3 separate occasions in 2017–2018. Associations between PM2.5/black carbon (BC) and biomarkers were estimated using mixed-effect models. An interaction analysis compared PM2.5/BC-related effects between subgroups. Biomarker combinations and mediation analysis were performed to elucidate the biological pathways. There was a significant “low-high-low” trend of PM2.5 levels across the 3 study periods. Increases in pro-inflammatory cytokines and changes of platelet activation and aggregation markers were associated with PM2.5/BC in obese subgroup only. Among obese subjects, the combination of pro-inflammatory cytokines and that of platelet markers increased 26.8% (95% CI: 16.0%, 37.9%) and 14.7% (95% CI: 1.9%, 27.0%) per IQR increase in PM2.5 over 5-day and 7-day averages. Inflammation mediated 24.5% of the pathways through which PM2.5 promoted platelet activation. This study suggested obese people are susceptible to pro-thrombotic impacts of PM2.5 exposures. PM2.5 may aggravate thrombosis through obesity-related inflammation.

KW - Black carbon

KW - Obesity

KW - PM

KW - Platelet

KW - Prothrombotic state

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VL - 413

JO - Journal of Hazardous Materials

JF - Journal of Hazardous Materials

M1 - 125341

ER -

Exposure to fine particulate matter promotes platelet activation and thrombosis via obesity-related inflammation

Abstract

Keywords

ASJC Scopus subject areas

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