Hart en vaten

Hart/vaten (Cardiovasculair)

Notitie, niet compleet!


Exposure to Traffic and the Onset of Myocardial Infarction.
Air pollution and cardiovascular injury epidemiology, toxicology, and mechanisms
Effects of inhalable particulate matter on blood coagulation.
Combustion- and friction-derived magnetic air pollution nanoparticles in human hearts
Ultrafine particulate matter exposure augments ischemia-reperfusion injury in mice
Inhalation of ultrafine particles alters blood leukocyte expression of adhesion molecules in humans
Cardiac and vascular changes in mice after exposure to ultrafine particulate matter


Exposure to Traffic and the Onset of Myocardial Infarction.
(Peters et al. 2004) NEJM, nog toe te voegen aan dropbox artikel van Jan Willem van de Wetering, niet in dropbox. Gaat over fijnstof niet over ultrafijnstof. Editorial beschikbaar. Wibren heeft een samenvatting gemaakt,hier niet bijgevoegd.
Background: An association between exposure to vehicular traffic in urban areas and the exacerbation of cardiovascular disease has been suggested in previous studies. This study was designed to assess whether exposure to traffic can trigger myocardial infarction.
Methods: We conducted a case-crossover study in which cases of myocardial infarction were identified with the use of data from the Cooperative Health Research in the Region of Augsburg Myocardial Infarction Registry in Augsburg, in southern Germany, for the period from February 1999 to July 2001. There were 691 subjects for whom the date and time of the myocardial infarction were known who had survived for at least 24 hours after the event, completed the registry’s standardized interview, and provided information on factors that may have triggered the myocardial infarction. Data on subjects’ activities during the four days preceding the onset of symptoms were collected with the use of patient diaries.
Results: An association was found between exposure to traffic and the onset of a myocardial infarction within one hour afterward (odds ratio, 2.92; 95 percent confidence interval, 2.22 to 3.83; P<0.001). The time the subjects spent in cars, on public transportation, or on motorcycles or bicycles was consistently linked with an increase in the risk of myocardial infarction. Adjusting for the level of exercise on a bicycle or for getting up in the morning changed the estimated effect of exposure to traffic only slightly (odds ratio for myocardial infarction, 2.73; 95 percent confidence interval, 2.06 to 3.61; P<0.001). The subject’s use of a car was the most common source of exposure to traffic; nevertheless, there was also an association between time spent on public transportation and the onset of a myocardial infarction one hour later.
Conclusions: Transient exposure to traffic may increase the risk of myocardial infarction in susceptible persons.
Long-Term Exposure to Air Pollution and Incidence of Cardiovascular Events in Women.
(Miller et al. 2007) In drobox artikel van Jan Willem, gaat over PM 2,5 of minder. Editorial beschikbaar.
Background Fine particulate air pollution has been linked to cardiovascular disease, but previous studies have assessed only mortality and differences in exposure between cities. We examined the association of long-term exposure to particulate matter of less than 2.5 μm in aerodynamic diameter (PM2.5) with cardiovascular events. Methods We studied 65,893 postmenopausal women without previous cardiovascular disease in 36 U.S. metropolitan areas from 1994 to 1998, with a median follow-up of 6 years. We assessed the women’s exposure to air pollutants using the monitor located nearest to each woman’s residence. Hazard ratios were estimated for the first cardiovascular event, adjusting for age, race or ethnic group, smoking status, educational level, household income, body-mass index, and presence or absence of diabetes, hypertension, or hypercholesterolemia. Results A total of 1816 women had one or more fatal or nonfatal cardiovascular events, as confirmed by a review of medical records, including death from coronary heart disease or cerebrovascular disease, coronary revascularization, myocardial infarction, and stroke. In 2000, levels of PM2.5 exposure varied from 3.4 to 28.3 μg per cubic meter (mean, 13.5). Each increase of 10 μg per cubic meter was associated with a 24% increase in the risk of a cardiovascular event (hazard ratio, 1.24; 95% confidence interval [CI], 1.09 to 1.41) and a 76% increase in the risk of death from cardiovascular disease (hazard ratio, 1.76; 95% CI, 1.25 to 2.47). For cardiovascular events, the between-city effect appeared to be smaller than the within-city effect. The risk of cerebrovascular events was also associated with increased levels of PM2.5 (hazard ratio, 1.35; 95% CI, 1.08 to 1.68). Conclusions Long-term exposure to fine particulate air pollution is associated with the incidence of cardiovascular disease and death among postmenopausal women. Exposure differences within cities are associated with the risk of cardiovascular disease.

Air pollution and cardiovascular injury epidemiology, toxicology, and mechanisms
(Simkhovich, Kleinman, and Kloner 2008) review in dropbox (
#UFP # cardiovascular
Recent epidemiologic studies show that increased levels of air pollutants are positively associated with cardiovascular morbidity and mortality. Inhalation of air pollutants affects heart rate, heart rate variability, blood pressure, vascular tone, blood coagulability, and the progression of atherosclerosis. Several categories within the general population (i.e., people with pre-existing cardiovascular disease and diabetic and elderly individuals) are considered to be more susceptible to air pollution-mediated cardiovascular effects. Major mechanisms of inhalation-mediated cardiovascular toxicity include activation of pro-inflammatory pathways and generation of reactive oxygen species. Although most studies focus on the influence of systemic effects, recent studies indicate that ultrafine particles may be translocated into the circulation and directly transported to the vasculature and heart where they can induce cardiac arrhythmias and decrease cardiac contractility and coronary flow.

Effects of inhalable particulate matter on blood coagulation.
(Bonzini et al. 2010) associatie tussen PM1 en PM 10 en bloedstollingsfactoren. Het betreft metingen.
Summary. Background: Particulate matter (PM) exposure has been linked to increased risk of cardiovascular disease, possibly resulting from hypercoagulability and thrombosis. Lung and systemic inflammation resulting from PM inhalation may activate blood coagulation, but mechanisms for PM-related hypercoagulability are still largely unknown. Objectives: To identify coagulation mechanisms activated by PM in a population with well-characterized exposure. Methods: We measured prothrombin time (PT), activated partial thromboplastin time, endogenous thrombin potentials (ETPs) with/ without exogenous triggers and with/without soluble thrombomodulin, tissue-type plasminogen activator (t-PA) antigen, Ddimer and C-reactive protein (CRP) in 37 workers in a steel production plant with well-characterized exposure to PM with aerodynamic diameter of < 1 lm (PM1) and coarse PM (PM10 – PM1). Blood samples were collected from each subject on the first (baseline) and last (postexposure) day of a 4-day work week. We analyzed differences between baseline and postexposure levels using a paired Students t-test. We fitted multivariate mixed-regression models to estimate the associations of interquartile range PM1 and coarse PM exposure with parameter levels. Results: None of the parameters showed any significant changes from baseline in postexposure samples. However, exposure levels were associated with shorter PT (b[PM1] = )0.33 s, P = 0.08; b[PMcoarse] = ) 0.33 s, P = 0.01), and higher ETP without exogenous triggers and with thrombomodulin (b[PM1] = + 99 nM min, P = 0.02; b[PMcoarse] = + 66 nM min, P = 0.05), t-PA (b[PM1] =+ 0.72 ng mL)1 , P = 0.01; b[PMcoarse] = + 0.88 ng mL)1 , P = 0.04), and CRP (b[PM1] = + 0.59 mg L)1 , P = 0.03; b[PMcoarse] = + 0.48 mg L)1 , P = 0.01). Conclusions: PM exposure did not show any short-term effect within the week of the study. The association of PM exposure with PT, ETP and CRP provides some evidence of long-term effects on inflammation and coagulation.

Combustion- and friction-derived magnetic air pollution nanoparticles in human hearts
(Calderón-Garcidueñas et al. 2019) in dropbox ( is mooi paper, maar de controle groepen zijn raar)
#Heart #Human physiology #UFP #pathology #mechanism
Air pollution is a risk factor for cardiovascular and Alzheimer’s disease (AD). Iron-rich, strongly magnetic, combustion- and friction-derived nanoparticles (CFDNPs) are abundant in particulate air pollution. Metropolitan Mexico City (MMC) young residents have abundant brain CFDNPs associated with AD pathology. We aimed to identify if magnetic CFDNPs are present in urbanites’ hearts and associated with cell damage. We used magnetic analysis and transmission electron microscopy (TEM) to identify heart CFDNPs and measured oxidative stress (cellular prion protein, PrP(C)), and endoplasmic reticulum (ER) stress (glucose regulated protein, GRP78) in 72 subjects age 23.8 ± 9.4y: 63 MMC residents, with Alzheimer Continuum vs 9 controls. Magnetite/maghemite nanoparticles displaying the typical rounded crystal morphologies and fused surface textures of CFDNPs were more abundant in MMC residents’ hearts. NPs, ∼2-10 × more abundant in exposed vs controls, were present inside mitochondria in ventricular cardiomyocytes, in ER, at mitochondria-ER contact sites (MERCs), intercalated disks, endothelial and mast cells. Erythrocytes were identified transferring ‘hitchhiking’ NPs to activated endothelium. Magnetic CFDNP concentrations and particle numbers ranged from 0.2 to 1.7 μg/g and ∼2 to 22 × 10(9)/g, respectively. Co-occurring with cardiomyocyte NPs were abnormal mitochondria and MERCs, dilated ER, and lipofuscin. MMC residents had strong left ventricular PrP(C) and bi-ventricular GRP78 up-regulation. The health impact of up to ∼22 billion magnetic NPs/g of ventricular tissue are likely reflecting the combination of surface charge, ferrimagnetism, and redox activity, and includes their potential for disruption of the heart’s electrical impulse pathways, hyperthermia and alignment and/or rotation in response to magnetic fields. Exposure to solid NPs appears to be directly associated with early and significant cardiac damage. Identification of strongly magnetic CFDNPs in the hearts of children and young adults provides an important novel layer of information for understanding CVD pathogenesis emphasizing the urgent need for prioritization of particulate air pollution control.

Ultrafine particulate matter exposure augments ischemia-reperfusion injury in mice
(Cozzi et al. 2006) in dropbox
#Early study #UFP #Cardio #Mechanism #animal model
Epidemiological studies have linked ambient particulate matter (PM) levels to an increased incidence of adverse cardiovascular events. Yet little is definitively known about the mechanisms accounting for the cardiovascular events associated with PM exposure. The goal of this study was to determine the effects of ultrafine (<0.1 microm) PM exposure on ischemia-reperfusion (I/R) injury. ICR mice were exposed to 100 microg of PM or vehicle by intratracheal instillation. Twenty-four hours later, mice were anesthetized with pentobarbital sodium (60 mg/kg), the left anterior descending coronary artery was ligated for 20 min, flow was restored for 2 h, and the resulting myocardial infarct (MI) size was evaluated. PM exposure doubled the relative size of the MI compared with the vehicle control. No difference was observed in the percentage of the left ventricle at risk for ischemia. PM exposure increased the level of oxidative stress in the myocardium after I/R. The density of neutrophils in the reperfused myocardium was increased by PM exposure, but differences in the number of blood leukocytes, expression of adhesion molecules on circulating neutrophils, and activation state of circulating neutrophils 24 h after PM exposure could not be correlated to the increased I/R injury observed. Additionally, aortas isolated from PM-exposed animals and studied in vitro exhibited a reduced endothelium-dependent relaxation response to acetylcholine. These results indicate that exposure to ultrafine PM increases oxidative stress in the myocardium, alters vascular reactivity, and augments injury after I/R in a murine model.

Inhalation of ultrafine particles alters blood leukocyte expression of adhesion molecules in humans
(Frampton et al. 2006) in dropbox
#Early study #human # UFP # Cardio vascular
Ultrafine particles (UFPs; aerodynamic diameter < 100 nm) may contribute to the respiratory and cardiovascular morbidity and mortality associated with particulate air pollution. We tested the hypothesis that inhalation of carbon UFPs has vascular effects in healthy and asthmatic subjects, detectable as alterations in blood leukocyte expression of adhesion molecules. Healthy subjects inhaled filtered air and freshly generated elemental carbon particles (count median diameter approximately 25nm, geometric standard deviation approximately 1.6), for 2 hr, in three separate protocols: 10 microg/m3 at rest, 10 and 25 microg/m3 with exercise, and 50 microg/m3 with exercise. In a fourth protocol, subjects with asthma inhaled air and 10 microg/m3 UFPs with exercise. Peripheral venous blood was obtained before and at intervals after exposure, and leukocyte expression of surface markers was quantitated using multiparameter flow cytometry. In healthy subjects, particle exposure with exercise reduced expression of adhesion molecules CD54 and CD18 on monocytes and CD18 and CD49d on granulocytes. There were also concentration-related reductions in blood monocytes, basophils, and eosinophils and increased lymphocyte expression of the activation marker CD25. In subjects with asthma, exposure with exercise to 10 microg/m3 UFPs reduced expression of CD11b on monocytes and eosinophils and CD54 on granulocytes. Particle exposure also reduced the percentage of CD4+ T cells, basophils, and eosinophils. Inhalation of elemental carbon UFPs alters peripheral blood leukocyte distribution and expression of adhesion molecules, in a pattern consistent with increased retention of leukocytes in the pulmonary vascular bed.

Cardiac and vascular changes in mice after exposure to ultrafine particulate matter
(Cascio et al. 2007)
#UFP #cardiovascular #animal model #mechanism
Increased ambient air particulate matter (PM) concentrations are associated with risk for myocardial infarction, stroke, and arrhythmia, and ultrafine PM (UFPM) might be particularly toxic to the cardiovascular system. Recent epidemiological studies are beginning to offer mechanistic insights, yet the rodent model remains a valuable tool to explore potential mechanisms. This article reviews a series of studies from our laboratory demonstrating the promise of mouse models to link health effects to biological mechanisms. Specifically, data from 6- to 10-wk-old male ICR mice exposed to intratracheal instillation of 100 microg of UFPM collected from the Chapel Hill, NC airshed are described. Studies of ischemia/reperfusion, vascular function, and hemostasis are described. In summary, UFPM exposure doubles the size of myocardial infarction attendant to an episode of ischemia and reperfusion while increasing postischemic oxidant stress. UFPM alters endothelial-dependent and -independent regulation of systemic vascular tone; increases platelet number, plasma fibrinogen, and soluble P-selectin levels; and reduces bleeding time, implying enhanced thrombogenic potential. Taking these findings together, this model of acute UFPM exposure in the mouse indicates that UFPM induces a prothrombotic state and decreases vasomotor responsiveness, thereby offering insight into how UFPM could contribute to vascular events associated with thrombosis and ischemia and increasing the extent of infarction.
Ultrafine particles from diesel engines induce vascular oxidative stress via JNK activation
(Li et al. 2009) In dropbox note: particles in this publication are not defined but in https://www.sciencedirect.com/science/article/abs/pii/S0021850201002105. E.g. <150nm
#UFP # mechanism #oxidative stress
Exposure to particulate air pollution is linked to increased incidences of cardiovascular diseases. Ambient ultrafine particles (UFP) from diesel vehicle engines have been shown to be proatherogenic in ApoE knockout mice and may constitute a major cardiovascular risk in humans. We posited that circulating nano-sized particles from traffic pollution sources induce vascular oxidative stress via JNK activation in endothelial cells. Diesel UFP were collected from a 1998 Kenworth truck. Intracellular superoxide assay revealed that these UFP dose-dependently induced superoxide (O(2)(-)) production in human aortic endothelial cells (HAEC). Flow cytometry showed that UFP increased MitoSOX red intensity specific for mitochondrial superoxide. Protein carbonyl content was increased by UFP as an indication of vascular oxidative stress. UFP also up-regulated heme oxygenase-1 (HO-1) and tissue factor (TF) mRNA expression, and pretreatment with the antioxidant N-acetylcysteine significantly decreased their expression. Furthermore, UFP transiently activated JNK in HAEC. Treatment with the JNK inhibitor SP600125 and silencing of both JNK1 and JNK2 with siRNA inhibited UFP-stimulated O(2)(-) production and mRNA expression of HO-1 and TF. Our findings suggest that JNK activation plays an important role in UFP-induced oxidative stress and stress response gene expression.

Differential cardiopulmonary effects of size-fractionated ambient particulate matter in mice
(Tong et al. 2010) in drop box
#UFP #cardiovascular #animal model #fractions of PM
A growing body of evidence from epidemiological and toxicological studies provides a strong link between exposure to ambient particulate matter (PM) of varying size and increased cardiovascular and respiratory morbidity and mortality. This study was designed to evaluate the cardiopulmonary effects of ambient coarse, fine, and ultrafine particles collected in Chapel Hill, NC. Mice were exposed to each size fraction by oropharyngeal instillation. Twenty-four hours later, pulmonary inflammation was assessed by bronchoalveolar lavage and cardiac injury was measured using a Langendorff cardiac perfusion preparation. Recovery of post-ischemic left ventricular developed pressure and infarct size were measured as indeces of cardiac ischemia/reperfusion injury. Coronary flow rate was measured before, during, and after ischemia. We demonstrate that coarse PM caused the most significant pulmonary inflammatory responses. In contrast, hearts from ultrafine-exposed mice had significantly lower post-ischemic functional recovery and greater infarct size, while hearts from coarse and fine PM-exposed mice had no significant responses to ischemia/reperfusion. The coronary flow rate was significantly reduced in the ultrafine PM group. This study shows that exposure of mice to coarse PM results in significant pulmonary toxicity while ultrafine PM appears to enhance cardiac ischemia/reperfusion injury.

Associations of long-term exposure to ambient PM1 with hypertension and blood pressure in rural Chinese population: The Henan rural cohort study
(Li et al. 2019) In dropbox
associatie studie tussen ultrafijnstof en hypertensie. Betreft 40.000 mensen!
ABSTRACT Background: The epidemiological evidence on relationships between long-term exposure to particulate matter and hypertension and blood pressure has been inconclusive. Limited evidence was available for particulate matter with an aerodynamic diameter ≤ 1 μm (PM1) in rural areas of developing countries. Objective: This study aimed to investigate the associations between long-term exposure to PM1 and hypertension and blood pressure among rural Chinese population. Methods: This study included 39,259 participants who had completed the baseline survey from Henan Rural Cohort. Participants’ exposure to PM1 was assessed by a satellite-based spatiotemporal model. The binary logistic regression model was used to examine the association between long-term PM1 exposure and hypertension, and multivariable linear regression model was used to investigate the associations between long-term PM1 exposure and systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP) and pulse pressure (PP). Moreover, we examined potential effect modifications by demographic, lifestyle and diet factors. Results: The mean concentration of PM1 for all participants during the 3-year before baseline survey was 59.98 μg/m3 . Each 1 μg/m3 increase in PM1 concentration was significantly associated with an increase of 4.3% [Odds ratio(OR) = 1.043, 95% confidence interval(CI): 1.033, 1.053] in odds for hypertension, an increase of 0.401 mm Hg (95% CI, 0.335, 0.467), 0.328 mm Hg (95% CI, 0.288, 0.369), 0.353 mm Hg (95% CI, 0.307, 0.399) and 0.073 mm Hg (95% CI, 0.030, 0.116) in SBP, DBP, MAP and PP, respectively. Further stratified analyses showed that the effect of PM1 on hypertension and blood pressure could be modified by sex, lifestyle and diet. Conclusions: This study suggests that long-term exposure to ambient PM1 increases the risk of hypertension and is associated with elevations in blood pressure in rural Chinese adults, especially in male and those with unhealthy habits.

Cardiovascular disease and long-term occupational exposure to ultrafine particles: A cohort study of airport workers
(Moller et al. 2020)
#UPF aircraft negative study #Copenhagen follow up #Cardio Vascular #Occupational exposure #Brain
AIM: To investigate if ischemic heart disease (IHD) and cerebrovascular disease is associated with long-term occupational exposure to ultrafine particles (UFP) outdoors at an airport. METHODS AND RESULTS: This is a register-based follow-up study based on a cohort comprising an exposed group of 6515 men employed in unskilled work at Copenhagen Airport and a reference group of 61,617 men in unskilled work in other firms in greater Copenhagen during 1990-2012. The exposure was assessed from information on proportion of time spent on the airport apron for each calendar year (apron-years) and the primary exposure measure was cumulated apron-years. The cohort was merged to the National Patient Register that includes data on all contacts to public and private hospitals in Denmark and the Register of Causes of Death. Risk estimates were provided by Poisson regression and adjusted for age, calendar year and educational level. We found no associations between cumulative apron-years and IHD (IRR, 1.00; 95%CI, 0.97-1.03) or cerebrovascular disease (IRR, 1.00; 0.98-1.02) when adjusted for confounders. CONCLUSION: In this large cohort study, we found no association between outdoor occupational exposure to UFP and IHD and cerebrovascular disease.

Ambient particulate pollutants in the ultrafine range promote early atherosclerosis and systemic oxidative stress
(Araujo et al. 2008) in dropbox (high impact)
#UFP versus PM2.5 #atherosclerosis
Air pollution is associated with significant adverse health effects, including increased cardiovascular morbidity and mortality. Exposure to particulate matter with an aerodynamic diameter of <2.5 microm (PM(2.5)) increases ischemic cardiovascular events and promotes atherosclerosis. Moreover, there is increasing evidence that the smallest pollutant particles pose the greatest danger because of their high content of organic chemicals and pro-oxidative potential. To test this hypothesis, we compared the proatherogenic effects of ambient particles of <0.18 microm (ultrafine particles) with particles of <2.5 microm in genetically susceptible (apolipoprotein E-deficient) mice. These animals were exposed to concentrated ultrafine particles, concentrated particles of <2.5 microm, or filtered air in a mobile animal facility close to a Los Angeles freeway. Ultrafine particle-exposed mice exhibited significantly larger early atherosclerotic lesions than mice exposed to PM(2.5) or filtered air Exposure to ultrafine particles also resulted in an inhibition of the antiinflammatory capacity of plasma high-density lipoprotein and greater systemic oxidative stress as evidenced by a significant increase in hepatic malondialdehyde levels and upregulation of Nrf2-regulated antioxidant genes. We conclude that ultrafine particles concentrate the proatherogenic effects of ambient PM and may constitute a significant cardiovascular risk factor.

Inhaled Nanoparticles Accumulate at Sites of Vascular Disease
(Miller et al. 2017)
#translocation UFP #UPF #cardio #human #animal
The development of engineered nanomaterials is growing exponentially, despite concerns over their potential similarities to environmental nanoparticles that are associated with significant cardiorespiratory morbidity and mortality. The mechanisms through which inhalation of nanoparticles could trigger acute cardiovascular events are emerging, but a fundamental unanswered question remains: Do inhaled nanoparticles translocate from the lung in man and directly contribute to the pathogenesis of cardiovascular disease? In complementary clinical and experimental studies, we used gold nanoparticles to evaluate particle translocation, permitting detection by high-resolution inductively coupled mass spectrometry and Raman microscopy. Healthy volunteers were exposed to nanoparticles by acute inhalation, followed by repeated sampling of blood and urine. Gold was detected in the blood and urine within 15 min to 24 h after exposure, and was still present 3 months after exposure. Levels were greater following inhalation of 5 nm (primary diameter) particles compared to 30 nm particles. Studies in mice demonstrated the accumulation in the blood and liver following pulmonary exposure to a broader size range of gold nanoparticles (2–200 nm primary diameter), with translocation markedly greater for particles <10 nm diameter. Gold nanoparticles preferentially accumulated in inflammation-rich vascular lesions of fat-fed apolipoproteinE-deficient mice. Furthermore, following inhalation, gold particles could be detected in surgical specimens of carotid artery disease from patients at risk of stroke. Translocation of inhaled nanoparticles into the systemic circulation and accumulation at sites of vascular inflammation provides a direct mechanism that can explain the link between environmental nanoparticles and cardiovascular disease and has major implications for risk management in the use of engineered nanomaterials.