PM2.5-induced inflammation and lipidome alteration associated with the development of atherosclerosis based on a targeted lipidomic analysis

Chen

Journal of Hazardous Materials

et al. 2021

Health effects induced by heavy metal components of particulate matter need further research. A total of 32 healthy volunteers were recruited to walk for 4 h in two different exposure scenarios in Wuhan from May 1 to Jun 30, 2019. Metabolomics technology was used to identify serum cardiovascular-related metabolites disturbance, and the health risk assessment model was employed to assess the non-carcinogenic and carcinogenic risks associated with airborne heavy metals. The results showed that the average mass concentrations of Co, Ni, Cd, Cu, Ag and Ba in PM 10 from May 1 to Jun 30, 2019 were 0.22, 0.49, 11.53, 2.23, 34.47 and 4.19 ng/m 3 , respectively, and were 0.86, 128.47, 291.85, 291.94, 98.55 and 422.62 ng/m 3 in PM 2.5 , respectively. Healthy young adults briefly exposed to heavy metals were associated with serum cardiovascular-related metabolites disturbance, including increased SM(d18:1/17:0) and Sphingomyelin, and decreased GlcCer(d16:1/18:0) and Galabiosylceramide, simultaneously accompanied by activation of the sphingolipid metabolism pathway. Non-carcinogenic and carcinogenic risks of airborne heavy metals via the inhalation route were observed, Ni and Cd most influenced to potential health risks. Findings indicated exposure to increment of heavy metals may increase health risks by causing cardiovascular-related metabolites disturbance via activating the sphingolipid metabolism pathway.

Section: Resultssupporting

confidence: 82%

Serum cardiovascular-related metabolites disturbance exposed to different heavy metal exposure scenarios

Chen

Journal of Hazardous Materials

et al. 2021

“…In a study of PM 2.5 -induced cytotoxicity to human lung cells, nineteen lipids were found to be increased and three decreased as a result of PM exposure, suggesting lipotoxicity. In a recent epidemiological study by Zhang et al ( 196 ), PM 2.5 exposure was found to cause inflammation and alterations in lipids associated with atherosclerosis. The findings of this study suggest that inflammation promoted plaque accumulation that was initiated through lipid dysregulation.…”

Section: Developments In the Fieldmentioning

confidence: 97%

Use of an Exposome Approach to Understand the Effects of Exposures From the Natural, Built, and Social Environments on Cardio-Vascular Disease Onset, Progression, and Outcomes

Juárez

Hood

Song

et al. 2020

Front. Public Health

Obesity, diabetes, and hypertension have increased by epidemic proportions in recent years among African Americans in comparison to Whites resulting in significant adverse cardiovascular disease (CVD) disparities. Today, African Americans are 30% more likely to die of heart disease than Whites and twice as likely to have a stroke. The causes of these disparities are not yet well-understood. Improved methods for identifying underlying risk factors is a critical first step toward reducing Black:White CVD disparities. This article will focus on environmental exposures in the external environment and how they can lead to changes at the cellular, molecular, and organ level to increase the personal risk for CVD and lead to population level CVD racial disparities. The external environment is defined in three broad domains: natural (air, water, land), built (places you live, work, and play) and social (social, demographic, economic, and political). We will describe how environmental exposures in the natural, built, and social environments "get under the skin" to affect gene expression though epigenetic, pan-omics, and related mechanisms that lead to increased risk for adverse CVD health outcomes and population level disparities. We also will examine the important role of metabolomics, proteomics, transcriptomics, genomics, and epigenomics in understanding how exposures in the natural, built, and social environments lead to CVD disparities with implications for clinical, public health, and policy interventions. In this review, we apply an exposome approach to Black:White CVD racial disparities. The exposome is a measure of all the exposures of an individual across the life course and the relationship of those exposures to health effects. The exposome represents the totality of exogenous (external) and endogenous (internal) exposures from conception onwards, simultaneously distinguishing, characterizing, and quantifying etiologic, mediating, moderating, and co-occurring risk and protective factors and their relationship to disease. Specifically, it assesses the biological mechanisms and underlying pathways through which chemical and non-chemical environmental Juarez et al. The Exposome and Cardiovascular Disease exposures are associated with CVD onset, progression and outcomes. The exposome is a promising approach for understanding the complex relationships among environment, behavior, biology, genetics, and disease phenotypes that underlie population level, Black: White CVD disparities.

“…Both macrophagederived foam cells and necrotic cells release various inflammatory factors (such as TNF, IL-1, and IL-6), thereby expanding the inflammatory response cascade and inducing persistent inflammation in local blood vessels [166]. Moreover, evidence from animal experiments has shown that inflammation is significantly unregulated in ApoE -/mice after exposure to PM 2.5 (10 mg/kg bw) for two months and that inflammation increases even if PM 2.5 exposure is stopped [6]. The above evidence focuses on the effects of PM 2.5 on inflammation and atherosclerosis.…”

Section: Ambient Pm 25 Induces An Inflammatory Responsementioning

confidence: 99%

“…Moreover, in ApoE -/mice exposed to a mixture of gasoline and diesel engine exhaust (MVE), the expression of LOX-1 was increased in cerebral microvascular endothelial cells, and at least in part, MVE altered the structure and integrity of the brain microvasculature via LOX-1 signaling [176]. Many studies have demonstrated that PM 2.5 contributes to lipid dysregulation in the sera of ApoE -/mice and promotes macrophage engulfment of ox-LDL through surface scavenger receptors to induce foam cell formation [6,12,177]. However, studies on the effect of PM 2.5 on lipid uptake and transport in endothelial cells are lacking, although limited evidence has shown that traffic-derived pollutants increase LOX-1 signaling in endothelial cells.…”

Section: Ambient Pm 25 Promotes Lipid Depositionmentioning

confidence: 99%

“…Thus, the global burden of cardiovascular disease caused by PM 2.5 may be much greater than that previously reported by WHO. Evidence has indicated that PM 2.5 induces lipid metabolism dysregulation and increases hypertension and the prevalence of cardiac arrhythmias, thus accelerating the progression of atherosclerosis, and increasing the risk of cardiovascular disease-and stroke-related mortality [6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The critical role of endothelial function in fine particulate matter-induced atherosclerosis

et al. 2020

Self Cite

Ambient and indoor air pollution contributes annually to approximately seven million premature deaths. Air pollution is a complex mixture of gaseous and particulate materials. In particular, fine particulate matter (PM2.5) plays a major mortality risk factor particularly on cardiovascular diseases through mechanisms of atherosclerosis, thrombosis and inflammation. A review on the PM2.5-induced atherosclerosis is needed to better understand the involved mechanisms. In this review, we summarized epidemiology and animal studies of PM2.5-induced atherosclerosis. Vascular endothelial injury is a critical early predictor of atherosclerosis. The evidence of mechanisms of PM2.5-induced atherosclerosis supports effects on vascular function. Thus, we summarized the main mechanisms of PM2.5-triggered vascular endothelial injury, which mainly involved three aspects, including vascular endothelial permeability, vasomotor function and vascular reparative capacity. Then we reviewed the relationship between PM2.5-induced endothelial injury and atherosclerosis. PM2.5-induced endothelial injury associated with inflammation, pro-coagulation and lipid deposition. Although the evidence of PM2.5-induced atherosclerosis is undergoing continual refinement, the mechanisms of PM2.5-triggered atherosclerosis are still limited, especially indoor PM2.5. Subsequent efforts of researchers are needed to improve the understanding of PM2.5 and atherosclerosis. Preventing or avoiding PM2.5-induced endothelial damage may greatly reduce the occurrence and development of atherosclerosis.