Long-term residential exposure to urban air pollution, and repeated measures of systemic blood markers of inflammation and coagulation

Viehmann, Anja; Hertel, Sabine; Fuks, Kateryna; Eisele, Lewin; Moebus, Susanne; Möhlenkamp, Stefan; Nonnemacher, Michael; Jakobs, Hermann; Erbel, Raimund; Jöckel, Karl‐Heinz; Hoffmann, Barbara

doi:10.1136/oemed-2014-102800

Cited by 126 publications

(98 citation statements)

References 31 publications

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“…Convincing evidence from studies in vivo and in vitro suggested that PM 2.5 can induce cardiac toxicity (Cao et al, 2016;Li et al, 2015). A cohort study indicated that long-term PM 2.5 exposure associates with the increase of markers of inflammation (hs-CRP) in blood (Viehmann et al, 2015). In the present study, we found that PM 2.5 exposure caused cardiac fibrosis and cardiomyocyte hypertrophy.…”

Section: Discussionsupporting

confidence: 59%

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

Wu¹,

Zhang²

2018

J. Toxicol. Sci.

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-Epidemiological studies have confirmed that ambient fine particulate matter (PM 2.5 ) exposure is associated with cardiovascular disease (CVD). However, the underlying mechanisms in PM 2.5 exposure-induced heart injury are largely unknown. It has been acknowledged that NADPH oxidase (Nox) 4 plays a critical role in CVD development. To investigate the acute effects of PM 2.5 on the mouse heart and the role of Nox4 in PM 2.5 exposure-induced cardiac injury, C57BL/6J mice were instilled with saline or 1.5, 3.0, 6.0 mg/kg BW PM 2.5 suspension for two weeks (five days per week). The levels of malondialdehyde (MDA), super oxide dismutase (SOD), inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β in heart supernatants were determined using related kits. The expression of Nox4, p67 phox , p47 phox and p22 phox in heart tissue was evaluated by immunofluorescence staining or Western blotting, respectively. Protein levels of p53, Bax, Bcl-2 and Caspase-3 in the heart were examined using immunohistochemical staining and Western blotting. TUNEL assay was used to measure myocardial apoptosis. PM 2.5 exposure leads to obvious cardiac injury. PM 2.5 exposure increases MDA level and iNOS activity, and decreases activity of SOD in heart supernatants of mice. High levels of TNF-α and IL-1β in heart supernatants of mice with PM 2.5 instillation were determined. Nox4 and Noxassociated subunits such as p67 phox , p47 phox and p22 phox expression levels were increased in heart tissue of mice after PM 2.5 exposure. Additionally, PM 2.5 exposure causes myocardial apoptosis in the mouse heart. This study suggested that Nox4 is involved in PM 2.5 exposure-induced cardiac injury in mice.

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Section: Discussionsupporting

confidence: 59%

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

Wu¹,

Zhang²

2018

J. Toxicol. Sci.

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“…Elevated plasma concentrations of traditional inflammatory biomarkers such as interleukin-1 [40], interleukin-6 [40,41], granulocyte-macrophage colony-stimulating factor [40], tumor necrosis factor-alpha [41], fibrinogen [42], white blood cell and platelet count [42,43], C-reactive protein [42,43], and pentraxin-related protein 3 [44] after high-level exposure to PM 2.5 have been confirmed via a series of deep research studies in the past decade [43]. Pentraxin-related protein 3, in particular, was put forward as a new vascular inflammatory biomarker for the prognostic prediction of cardiovascular disease, especially in patients with ACS [45].…”

Section: Potential Cellular and Molecular Biology Mechanismsmentioning

confidence: 99%

“…Particulates in the blood can activate the platelet and blood coagulation systems, increasing the risk for coronary thrombosis. Increased circulative platelet counts [42,43] and increased concentrations of coagulation factors (e.g., fibrinogen [42]) have been observed in study populations, which appears as an inverse effect of a PM 2.5 -related inflammatory reaction. Additionally, the intrinsic blood coagulation pathway could be activated by endothelial injury or particles that directly enter the bloodstream, followed by platelet activation, blood coagulation, and thrombogenesis [104].…”

Section: Potential Physiopathologic Mechanisms Mediating Pm25-indmentioning

confidence: 99%

Potential Harmful Effects of PM2.5 on Occurrence and Progression of Acute Coronary Syndrome: Epidemiology, Mechanisms, and Prevention Measures

Meng

Zhang

Yang

et al. 2016

IJERPH

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The harmful effects of particulate matter with an aerodynamic diameter of <2.5 µm (PM2.5) and its association with acute coronary syndrome (ACS) has gained increased attention in recent years. Significant associations between PM2.5 and ACS have been found in most studies, although sometimes only observed in specific subgroups. PM2.5-induced detrimental effects and ACS arise through multiple mechanisms, including endothelial injury, an enhanced inflammatory response, oxidative stress, autonomic dysfunction, and mitochondria damage as well as genotoxic effects. These effects can lead to a series of physiopathological changes including coronary artery atherosclerosis, hypertension, an imbalance between energy supply and demand to heart tissue, and a systemic hypercoagulable state. Effective strategies to prevent the harmful effects of PM2.5 include reducing pollution sources of PM2.5 and population exposure to PM2.5, and governments and organizations publicizing the harmful effects of PM2.5 and establishing air quality standards for PM2.5. PM2.5 exposure is a significant risk factor for ACS, and effective strategies with which to prevent both susceptible and healthy populations from an increased risk for ACS have important clinical significance in the prevention and treatment of ACS.

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“…UFP are of particular concern due to their small size, which allows them to penetrate deeper into the lungs, cross biological barriers, and be translocated to other organs where they can cause adverse health effects (Geiser et al, 2005; HEI Review Panel on Ultrafine Particulates, 2013; Oberdörster et al, 2005). Since the 2013 HEI report new studies have reported associations between traffic-generated UFP and markers of cardiovascular disease risk and mortality (Lane et al., 2016; Ostro et al, 2015; Viehmann et al, 2015). …”

Section: Introductionmentioning

confidence: 99%

Comparisons of traffic-related ultrafine particle number concentrations measured in two urban areas by central, residential, and mobile monitoring

Simon

Hudda

Naumova

et al. 2017

Atmospheric Environment

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Traffic-related ultrafine particles (UFP; <100 nanometers diameter) are ubiquitous in urban air. While studies have shown that UFP are toxic, epidemiological evidence of health effects, which is needed to inform risk assessment at the population scale, is limited due to challenges of accurately estimating UFP exposures. Epidemiologic studies often use empirical models to estimate UFP exposures; however, the monitoring strategies upon which the models are based have varied between studies. Our study compares particle number concentrations (PNC; a proxy for UFP) measured by three different monitoring approaches (central-site, short-term residential-site, and mobile on-road monitoring) in two study areas in metropolitan Boston (MA, USA). Our objectives were to quantify ambient PNC differences between the three monitoring platforms, compare the temporal patterns and the spatial heterogeneity of PNC between the monitoring platforms, and identify factors that affect correlations across the platforms. We collected >12,000 hours of measurements at the central sites, 1,000 hours of measurements at each of 20 residential sites in the two study areas, and >120 hours of mobile measurements over the course of ~1 year in each study area. Our results show differences between the monitoring strategies: mean one-minute PNC on-roads were higher (64,000 and 32,000 particles/cm3 in Boston and Chelsea, respectively) compared to central-site measurements (23,000 and 19,000 particles/cm3) and both were higher than at residences (14,000 and 15,000 particles/cm3). Temporal correlations and spatial heterogeneity also differed between the platforms. Temporal correlations were generally highest between central and residential sites, and lowest between central-site and on-road measurements. We observed the greatest spatial heterogeneity across monitoring platforms during the morning rush hours (06:00–09:00) and the lowest during the overnight hours (18:00–06:00). Longer averaging times (days and hours vs. minutes) increased temporal correlations (Pearson correlations were 0.69 and 0.60 vs. 0.39 in Boston; 0.71 and 0.61 vs. 0.45 in Chelsea) and reduced spatial heterogeneity (coefficients of divergence were 0.24 and 0.29 vs. 0.33 in Boston; 0.20 and 0.27 vs. 0.31 in Chelsea). Our results suggest that combining stationary and mobile monitoring may lead to improved characterization of UFP in urban areas and thereby lead to improved exposure assignment for epidemiology studies.

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Long-term residential exposure to urban air pollution, and repeated measures of systemic blood markers of inflammation and coagulation

Cited by 126 publications

References 31 publications

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

Potential Harmful Effects of PM2.5 on Occurrence and Progression of Acute Coronary Syndrome: Epidemiology, Mechanisms, and Prevention Measures

Comparisons of traffic-related ultrafine particle number concentrations measured in two urban areas by central, residential, and mobile monitoring

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