A review of effects of particulate matter-associated nickel and vanadium species on cardiovascular and respiratory systems

Zhang, Zhihong; Chau, Patsy Yuen-Kwan; Lai, Hak Kan; Wong, Chit Ming

doi:10.1080/09603120802460392

Cited by 56 publications

(26 citation statements)

References 51 publications

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“…Also, nickel (Ni) and vanadium (V) are higher in the PM sample than some of the other metals probably due to the large amount of fossil fuel combustion in the area. Ni and V are common components in many particulate matter samples and studies investigating the effects of PM containing Ni and V have observed CVD endpoints (Afridi et al 2011; Zhang et al 2009). (Lippmann et al 2006) exposed ApoE −/− mice to PM containing high concentrations of Ni.…”

Section: Discussionmentioning

confidence: 99%

Particulate Matter From Saudi Arabia Induces Genes Involved in Inflammation, Metabolic Syndrome and Atherosclerosis

Brocato

Sun

Shamy

et al. 2014

Journal of Toxicology and Environmental Health, Part A

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Airborne particulate matter (PM) exposure is a major environmental health concern and is linked to metabolic disorders, such as cardiovascular diseases (CVD) and diabetes, which are on the rise in the Kingdom of Saudi Arabia. This study investigated changes in mouse lung gene expression produced by administration of PM10 collected from Jeddah, Saudi Arabia. FVB/N mice were exposed to 100 µg PM10 or water by aspiration and euthanized 24 hr later. The bronchoalveolar lavage fluid (BALF) was collected and analyzed for neutrophil concentration and TNF-α and IL-6 levels. RNA was extracted from the lungs and whole transcript was analyzed using Affymetrix Mouse Gene 1.0 ST Array. Mice exposed to PM10 displayed an increase in neutrophil concentration and elevated TNF-α and IL-6 levels. Gene expression analysis revealed that mice exposed to PM10 displayed 202 genes that were significantly up-regulated and 40 genes that were significantly down-regulated. PM10 induced genes involved in inflammation, cholesterol and lipid metabolism, as well as atherosclerosis. This is the first study to demonstrate that Saudi Arabia PM10 increases in vivo expression of genes located in pathways associated with diseases involving metabolic syndrome and atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

Particulate Matter From Saudi Arabia Induces Genes Involved in Inflammation, Metabolic Syndrome and Atherosclerosis

Brocato

Sun

Shamy

et al. 2014

Journal of Toxicology and Environmental Health, Part A

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“…And in the absence of metals sources, the residual oil combustion source category induces the cellular effect due to presence of Ni. Zhang et al (2009) considered all findings on Ni and V of exposure, epidemiological, and toxicological studies, and concluded that Ni and V are positively correlated with human cardiovascular and respiratory diseases. The recent review by Lippmann and Chen (2009) implicated residual oil fly ash as the most toxic source-related mixture, and Ni and V, as particularly influential components in terms of acute cardiac function changes and excess short-term mortality.…”

Section: Discussionmentioning

confidence: 99%

Oxidant generation capacity of source-apportioned PM2.5

Maciejczyk

Zhong

Lippmann

et al. 2010

Inhalation Toxicology

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While many studies found associations between ambient particulate matter (PM) and morbidity or mortality outcomes, it is unclear whether these associations are dependent on the composition of PM, which varies with the source of that PM. We addressed this knowledge gap by conducting a time-series PM-health effects assessment that specifically investigated the role of source-apportioned fine PM (PM2.5) on the oxidant generation capacity that might be responsible for respiratory and cardiovascular health outcomes. Daily PM2.5 composition speciation and blakc carbon (BC) measurements, conducted in rural New York for 303 days between March 2003 and January 2005, were analyzed by a factor analysis source apportionment model, and five source categories (transported aerosol/secondary sulfate, resuspended soil, metals, residual oil combustion, industrial/incineration) were identified. After the exposure of human epithelial cells (BEAS-2B) to our PM2.5 samples, cellular NFkB activation showed a relatively significant association with the Ni concentration averaging 38 ng/m3, and weaker but still significant correlations with Ba (13 ng/m3), Mn (9 ng/m3), and Fe (500 ng/m3). The single-source category regression analysis of NF-κB signal showed a significant association only with the metals source Thus, three metals, which together constitute only 60 ng/m3 to the PM2.5 mass (107 ug/m3), appear to be more influential on lung cell responses than BC (6 ug/m3) and sulfate ions (36 ug/m3) that are present at much higher mass concentrations.

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“…The roles of finer particles in determining cardiovascular effects have been pointed out by several epidemiological studies (Brook et al, 2010). PM components, as well as metals with strong pro-inflammatory actions, have been also shown to play key roles in determining PM-related cardiovascular effects (Zhang et al, 2009). PM-induced systemic inflammation has been suggested as a primary mediator of PM effects (Seaton et al, 1995; Ghio et al, 2003; Baccarelli et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Extracellular histones mediate the effects of metal-rich air particles on blood coagulation

Cantone

Angelici

Bollati

et al. 2014

Environmental Research

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Background Epidemiological studies have shown associations of particulate matter (PM) exposure with hypercoagulability and thrombosis. Extracellular circulating histones have recently been identified as novel mediators of inflammatory and procoagulant responses. The potential roles of extracellular histones in PM-related hypercoagulability have yet not been investigated. Objectives In 63 steel workers, we evaluated the effects of exposure to PM and PM metal components on two extracellular histone modifications (H3K4me3 and H3K9ac); and the association of H3K4me3 and H3K9ac with coagulation markers. Methods Extracellular H3K4me3 and H3K9ac were determined in plasma through enzyme-linked immunosorbent assays. Coagulation markers included endogenous thrombin potentials (ETPs), tissue-type plasminogen activator antigen (t-PA) and d-dimer. Exposure to PM with aerodynamic diameters <1 µm (PM1) or <10 µm (PM10) and PM10 metal components were estimated for each participant. Results The coagulation marker ETP, measured in the presence of soluble thrombomodulin (ETP TM+), showed significant positive associations with PM1 (β=107.84, p=0.03), PM10 (β=83.06, p=0.02), and zinc (β=75.14, p=0.03); and a marginal association with iron (β=122.58, p=0.07). Additional PM effects were observed on t-PA, D-dimer, and ETP TM+. PM1 exposure was associated with increased plasma H3K4me3 and H3K9ac (β=0.20, p=0.02; β=0.16, p=0.05, respectively). H3K4me3, but not H3K9ac, was associated with zinc (β=0.13, p=0.03) and iron (β=0.32, p=0.01) contained in PM. ETP TM+ was increased in association with higher plasma H3K4me3 (β=0.50, p=0.05) and H3K9ac (β=0.54, p=0.05). Conclusions This observational study suggests potential roles of extracellular histones in PM-induced hypercoagulability. Experimental studies are warranted to further characterize these findings.

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A review of effects of particulate matter-associated nickel and vanadium species on cardiovascular and respiratory systems

Cited by 56 publications

References 51 publications

Particulate Matter From Saudi Arabia Induces Genes Involved in Inflammation, Metabolic Syndrome and Atherosclerosis

Particulate Matter From Saudi Arabia Induces Genes Involved in Inflammation, Metabolic Syndrome and Atherosclerosis

Oxidant generation capacity of source-apportioned PM2.5

Extracellular histones mediate the effects of metal-rich air particles on blood coagulation

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