Particulate air pollution, coronary heart disease and individual risk assessment: a general overview

Hassing, Carlijne; Twickler, Marcel Th B; Brunekreef, Bert; Cassee, Flemming R.; Doevendans, Pieter A.; Kastelein, John J.P.; Cramer, Maarten J.

doi:10.1097/hjr.0b013e32831de25d

Cited by 26 publications

(16 citation statements)

References 74 publications

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“…In real-world conditions, air pollution is inhaled either acutely or chronically (Hassing et al 2009;Pope et al 2002Pope et al , 2006. Herein, we used a model that simulated acute exposure to PM at very high concentration.…”

Section: Discussionmentioning

confidence: 99%

Myocardial Mitochondrial Injury Induced by Pulmonary Exposure to Particulate Matter in Rats

Golomb

Matza

Cummings³

et al. 2012

Toxicol Pathol

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Exposure to air pollution has been associated with acute myocardial ischemia, impaired myocardrial function, and ST-segment depression. Particulate matter (PM)-associated metals, especially vanadium and nickel, have been implicated in observed cardiovascular impairments. We aimed to assess the effect of single intratracheal pulmonary exposure to vanadium-rich respirable oil combustion PM (HP-10) on the intrinsic myocardial ischemic tolerance and mitochondrial integrity in rats. The authors subjected isolated heart tissue slices derived from saline or PM-exposed rats to low glucose low oxygen induced ischemia followed by oxygenated condition with glucose supplementation. Mitochondrial structural integrity was determined by TEM (transmission electron microscopy) and functionality by the 3-(4, 5 dimethylthiazol-2yl)-2, 5 diphenyltetrazolium bromide (MTT) assay. Rats exposed to PM exhibited no apparent inhibition of mitochondrial dehydrogenase activity in oxygenated conditions at 24 or 48 hr post-PM exposure. However, in conditions of simulated ischemia/reoxygenation, these heart slices showed a delayed but consistent and significant decrease in dehydrogenase activity compared to controls at 48 hr after exposure to PM. Electron microscopy revealed significant myocardial mitochondrial injury upon exposure to PM characterized by mitochondrial swelling and fusion. The authors conclude that exposure to soluble vanadium-rich PM induces mitochondrial functional impairment and structural abnormality, which compromises mitochondrial respiration and results in decreased tolerance to ischemia/reoxygenation in rats.

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Section: Discussionmentioning

confidence: 99%

Myocardial Mitochondrial Injury Induced by Pulmonary Exposure to Particulate Matter in Rats

Golomb

Matza

Cummings³

et al. 2012

Toxicol Pathol

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“…Direct evidence via a controlled inhalation study is lacking (Cassee et al, 2010) and the potentially harmful effects of emissions may not be suitably predicted by studies using cells or healthy animals. The association between exposure to urban PM and cardiovascular disease is well established and pose a serious problem (Araujo and Nel, 2009; Brook, 2008; Mills et al, 2007; Hassing et al, 2009). Therefore, technologies that alter PM and co-pollutants require testing in models of cardiovascular disease.…”

Section: Introductionmentioning

confidence: 99%

The biological effects of subacute inhalation of diesel exhaust following addition of cerium oxide nanoparticles in atherosclerosis-prone mice

Cassee

Campbell

Boere

et al. 2012

Environmental Research

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BackgroundCerium oxide (CeO2) nanoparticles improve the burning efficiency of fuel, however, little is known about health impacts of altered emissions from the vehicles.MethodsAtherosclerosis-prone apolipoprotein E knockout (ApoE−/−) mice were exposed by inhalation to diluted exhaust (1.7 mg/m3, 20, 60 or 180 min, 5 day/week, for 4 weeks), from an engine using standard diesel fuel (DE) or the same diesel fuel containing 9 ppm cerium oxide nanoparticles (DCeE). Changes in hematological indices, clinical chemistry, atherosclerotic burden, tissue levels of inflammatory cytokines and pathology of the major organs were assessed.ResultsAddition of CeO2 to fuel resulted in a reduction of the number (30%) and surface area (10%) of the particles in the exhaust, whereas the gaseous co-pollutants were increased (6–8%). There was, however, a trend towards an increased size and complexity of the atherosclerotic plaques following DE exposure, which was not evident in the DCeE group. There were no clear signs of altered hematological or pathological changes induced by either treatment. However, levels of proinflammatory cytokines were modulated in a brain region and liver following DCeE exposure.ConclusionsThese results imply that addition of CeO2 nanoparticles to fuel decreases the number of particles in exhaust and may reduce atherosclerotic burden associated with exposure to standard diesel fuel. From the extensive assessment of biological parameters performed, the only concerning effect of cerium addition was a slightly raised level of cytokines in a region of the central nervous system. Overall, the use of cerium as a fuel additive may be a potentially useful way to limit the health effects of vehicle exhaust. However, further testing is required to ensure that such an approach is not associated with a chronic inflammatory response which may eventually cause long-term health effects.

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“…Besides, the temperature of a specified geographic area may not accurately represent the actual individual temperature exposure, which is influenced by personal behaviors. Furthermore, data on concomitant air pollution, known to have negative effects on various cardiopulmonary parameters 12,35 were not available. However, the studied zone is free from heavy industries, and the major air pollutant is car traffic, thus minimizing the effect of this parameter.…”

Section: European Journal Of Cardiovascular Prevention and Rehabilitatimentioning

confidence: 99%

Effects of ambient temperature, humidity, and other meteorological variables on hospital admissions for angina pectoris

Abrignani

Corrao

Biondo

et al. 2011

Eur J Prev Cardiolog

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Background: Seasonal peaks in cardiovascular disease incidence have been widely reported, suggesting weather has a role. Design The aim of our study was to determine the influence of climatic variables on angina pectoris hospital admissions. Methods: We correlated the daily number of angina cases admitted to a western Sicilian hospital over a period of 12 years and local weather conditions (temperature, humidity, wind force and direction, precipitation, sunny hours and atmospheric pressure) on a day-to-day basis. A total of 2459 consecutive patients were admitted over the period 1987-1998 (1562 men, 867 women; M/F -1:8).Results: A seasonal variation was found with a noticeable winter peak. The results of Multivariate Poisson analysis showed a significant association between the daily number of angina hospital admission, temperature, and humidity. Significant incidence relative ratios (95% confidence intervals/measure unit) were, in males, 0.988 (0.980-0.996) (p ¼ 0.004) for minimal temperature, 0.990 (0.984-0.996) (p ¼ 0.001) for maximal humidity, and 1.002 (1.000-1.004) (p ¼ 0.045) for minimal humidity. The corresponding values in females were 0.973 (0.951-0.995) (p < 0.017) for maximal temperature and 1.024 (1.001-1.048) (p ¼ 0.037) for minimal temperature. Conclusions: Environmental temperature and humidity may play an important role in the pathogenesis of angina, although it seems different according to the gender. These data may help to understand the mechanisms that trigger ischemic events and to better organize hospital assistance throughout the year.

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Particulate air pollution, coronary heart disease and individual risk assessment: a general overview

Cited by 26 publications

References 74 publications

Myocardial Mitochondrial Injury Induced by Pulmonary Exposure to Particulate Matter in Rats

Myocardial Mitochondrial Injury Induced by Pulmonary Exposure to Particulate Matter in Rats

The biological effects of subacute inhalation of diesel exhaust following addition of cerium oxide nanoparticles in atherosclerosis-prone mice

Effects of ambient temperature, humidity, and other meteorological variables on hospital admissions for angina pectoris

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