ArticlePloS one2013
The role of metal components in the cardiovascular effects of PM2.5.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Long-Term PMJournal of the American Heart Association · 2021Pooled it
- Exposure to PM2.5 via vascular endothelial growth factor relationship: Meta-analysis.PloS one · 2018Pooled it
- Fine Particulate Matter Concentrations in Urban Chinese Cities, 2005-2016: A Systematic Review.International journal of environmental research and public health · 2017Pooled it
- SRM 1650b Administration to Isolated Rat Heart Aggravates Ischemia-Reperfusion Injury via Mitochondrial Dysfunction and Downregulation of PI3K/Akt Signaling Pathways.Journal of biochemical and molecular toxicology · 2026Article
- Lung Deposition of Particulate Matter as a Source of Metal Exposure: A Threat to Humans and Animals.Toxics · 2025Review
- Cross-sectional associations between multiple plasma heavy metals and lung function among elderly Chinese.Scientific reports · 2025Article
- Fine particulate matter‑induced cardiac developmental toxicity (Review).Experimental and therapeutic medicine · 2025Review
- Exposure to air pollution and cardiovascular risk in young children - a pilot project.Pediatric research · 2024Article
- Sources and Specified Health Risks of 12 PMToxics · 2024Article
- Disease-associated metabolic pathways affected by heavy metals and metalloid.Toxicology reports · 2023Review
- The Impact of Fine Particulate Matter 2.5 on the Cardiovascular System: A Review of the Invisible Killer.Nanomaterials (Basel, Switzerland) · 2022Review
- Susceptibility of patients with chronic obstructive pulmonary disease to heart rate difference associated with the short-term exposure to metals in ambient fine particles: A panel study in Beijing, China.Science China. Life sciences · 2022Article
- Tempol Preserves Endothelial Progenitor Cells in Male Mice with Ambient Fine Particulate Matter Exposure.Biomedicines · 2022Article
- Air Pollution Exposure Induces Vascular Injury and Hampers Endothelial Repair by Altering Progenitor and Stem Cells Functionality.Frontiers in cell and developmental biology · 2022Review
- Circulating Endothelial Progenitor Cells Are Preserved in Female Mice Exposed to Ambient Fine Particulate Matter Independent of Estrogen.International journal of molecular sciences · 2021Article
- Endothelial progenitor cells as critical mediators of environmental air pollution-induced cardiovascular toxicity.American journal of physiology. Heart and circulatory physiology · 2021Review
- Health Risk Analysis of Elemental Components of an Industrially Emitted Respirable Particulate Matter in an Urban Area.International journal of environmental research and public health · 2021Article
- Effects of ambient particulate matter on vascular tissue: a review.Journal of toxicology and environmental health. Part B, Critical reviews · 2020Review
- PM2.5 exposure induces vascular dysfunction via NO generated by iNOS in lung of ApoE-/- mouse.International journal of biological sciences · 2020Article
- Toxic Effects of Particulate Matter Derived from Dust Samples Near the Dzhidinski Ore Processing Mill, Eastern Siberia, Russia.Cardiovascular toxicology · 2019Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Exposure to ambient fine particulate matter (PM2.5) increases risks for cardiovascular disorders (CVD). However, the mechanisms and components responsible for the effects are poorly understood. Based on our previous murine exposure studies, a translational pilot study was conducted in female residents of Jinchang and Zhangye, China, to test the hypothesis that specific chemical component of PM2.5 is responsible for PM2.5 associated CVD. Daily ambient and personal exposures to PM2.5 and 35 elements were measured in the two cities. A total of 60 healthy nonsmoking adult women residents were recruited for measurements of inflammation biomarkers. In addition, circulating endothelial progenitor cells (CEPCs) were also measured in 20 subjects. The ambient levels of PM2.5 were comparable between Jinchang and Zhangye (47.4 and 54.5 µg/m(3), respectively). However, the levels of nickel, copper, arsenic, and selenium in Jinchang were 82, 26, 12, and 6 fold higher than Zhangye, respectively. The levels of C-reactive protein (3.44 ± 3.46 vs. 1.55 ± 1.13), interleukin-6 (1.65 ± 1.17 vs. 1.09 ± 0.60), and vascular endothelial growth factor (117.6 ± 217.0 vs. 22.7 ± 21.3) were significantly higher in Jinchang. Furthermore, all phenotypes of CEPCs were significantly lower in subjects recruited from Jinchang than those from Zhangye. These results suggest that specific metals may be important components responsible for PM2.5-induced cardiovascular effects and that the reduced capacity of endothelial repair may play a critical role.
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Registered trials
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