scholarly journals Air pollution and cardiovascular disease: car sick

Author(s):  
Mark R Miller ◽  
David E Newby

Abstract The cardiovascular effects of inhaled particle matter (PM) are responsible for a substantial morbidity and mortality attributed to air pollution. Ultrafine particles, like those in diesel exhaust emissions, are a major source of nanoparticles in urban environments, and it is these particles that have the capacity to induce the most significant health effects. Research has shown that diesel exhaust exposure can have many detrimental effects on the cardiovascular system both acutely and chronically. This review provides an overview of the cardiovascular effects on PM in air pollution, with an emphasis on ultrafine particles in vehicle exhaust. We consider the biological mechanisms underlying these cardiovascular effects of PM and postulate that cardiovascular dysfunction may be implicated in the effects of PM in other organ systems. The employment of multiple strategies to tackle air pollution, and especially ultrafine particles from vehicles, is likely to be accompanied by improvements in cardiovascular health.

2016 ◽  
Vol 4 (1) ◽  
pp. 55-64 ◽  
Author(s):  
Jefferson L. Vieira ◽  
Guilherme V. Guimaraes ◽  
Paulo A. de Andre ◽  
Fátima D. Cruz ◽  
Paulo H. Nascimento Saldiva ◽  
...  

2014 ◽  
Vol 42 (4) ◽  
pp. 1006-1011 ◽  
Author(s):  
Mark R. Miller

Air pollution has been estimated to be responsible for several millions of deaths worldwide per year, the majority of which have been attributed to cardiovascular causes. The particulate matter in air pollution has been shown impair vascular function, increase blood pressure, promote thrombosis and impair fibrinolysis, accelerate the development of atherosclerosis, increase the extent of myocardial ischaemia, and increase susceptibility to myocardial infarction. The pathways underlying these effects are complex and poorly understood; however, particulate-induced oxidative stress repeatedly emerges as a potential mechanism in all of these detrimental cardiovascular actions. The present mini-review will use diesel exhaust as an example of a pollutant rich in combustion-derived nanoparticles, to describe the potential by which oxidative stress could drive the cardiovascular effects of air pollution.


ESC CardioMed ◽  
2018 ◽  
pp. 1075-1078
Author(s):  
Mark R. Miller ◽  
Anoop S. V. Shah ◽  
Nicholas L. Mills ◽  
David E. Newby

The air that we breathe remains a growing problem, with environmental air pollution generated by traffic, industry, and households continuing to be a serious public health issue. Increasing industrialization and the rapid expansion of urban environments across society mean that, for many, exposure to pollutants is unavoidable. Recent estimates suggest that air pollution is responsible for between 3 and 7 million deaths worldwide per year accompanied by high levels of morbidity (3.1% of global disability-adjusted life years) and associated economic risks (£16 billion per year in the United Kingdom alone). A recent report placed both indoor and outdoor air pollution within the top ten risk factors for all-cause disease, greater than that caused by risk factors such as sedentary lifestyle or high cholesterol. Importantly, the majority of deaths are caused by cardiovascular-related disease. This chapter provides an overview of how air pollution can have multiple detrimental effects on cardiovascular health.


2008 ◽  
Vol 115 (6) ◽  
pp. 175-187 ◽  
Author(s):  
Robert D. Brook

Air pollution is a heterogeneous mixture of gases, liquids and PM (particulate matter). In the modern urban world, PM is principally derived from fossil fuel combustion with individual constituents varying in size from a few nanometres to 10 μm in diameter. In addition to the ambient concentration, the pollution source and chemical composition may play roles in determining the biological toxicity and subsequent health effects. Nevertheless, studies from across the world have consistently shown that both short- and long-term exposures to PM are associated with a host of cardiovascular diseases, including myocardial ischaemia and infarctions, heart failure, arrhythmias, strokes and increased cardiovascular mortality. Evidence from cellular/toxicological experiments, controlled animal and human exposures and human panel studies have demonstrated several mechanisms by which particle exposure may both trigger acute events as well as prompt the chronic development of cardiovascular diseases. PM inhaled into the pulmonary tree may instigate remote cardiovascular health effects via three general pathways: instigation of systemic inflammation and/or oxidative stress, alterations in autonomic balance, and potentially by direct actions upon the vasculature of particle constituents capable of reaching the systemic circulation. In turn, these responses have been shown to trigger acute arterial vasoconstriction, endothelial dysfunction, arrhythmias and pro-coagulant/thrombotic actions. Finally, long-term exposure has been shown to enhance the chronic genesis of atherosclerosis. Although the risk to one individual at any single time point is small, given the prodigious number of people continuously exposed, PM air pollution imparts a tremendous burden to the global public health, ranking it as the 13th leading cause of morality (approx. 800000 annual deaths).


2019 ◽  
Vol 55 (4) ◽  
pp. 1901495 ◽  
Author(s):  
Denise J. Wooding ◽  
Min Hyung Ryu ◽  
Hang Li ◽  
Neil E. Alexis ◽  
Olga Pena ◽  
...  

Outdoor air pollution exposure increases chronic obstructive pulmonary disease (COPD) hospitalisations, and may contribute to COPD development. The mechanisms of harm, and the extent to which at-risk populations are more susceptible are not fully understood. Neutrophils are recruited to the lung following diesel exhaust exposure, a model of traffic-related air pollution (TRAP), but their functional role in this response is unknown. The purpose of this controlled human-exposure crossover study was to assess the effects of acute diesel exhaust exposure on neutrophil function in never-smokers and at-risk populations, with support from additional in vitro studies.18 participants, including never-smokers (n=7), ex-smokers (n=4) and mild–moderate COPD patients (n=7), were exposed to diesel exhaust and filtered air for 2 h on separate occasions, and neutrophil function in blood (0 h and 24 h post-exposure) and bronchoalveolar lavage (24 h post-exposure) was assessed.Compared to filtered air, diesel exhaust exposure reduced the proportion of circulating band cells at 0 h, which was exaggerated in COPD patients. Diesel exhaust exposure increased the amount of neutrophil extracellular traps (NETs) in the lung across participants. COPD patients had increased peripheral neutrophil activation following diesel exhaust exposure. In vitro, suspended diesel exhaust particles increased the amount of NETs measured in isolated neutrophils. We propose NET formation as a possible mechanism through which TRAP exposure affects airway pathophysiology. In addition, COPD patients may be more prone to an activated inflammatory state following exposure.This is the first controlled human TRAP exposure study directly comparing at-risk phenotypes (COPD and ex-smokers) with lower-risk (never-smokers) participants, elucidating the human susceptibility spectrum.


CommonHealth ◽  
2021 ◽  
Vol 2 (3) ◽  
pp. 122-133
Author(s):  
Lindsay Kraus ◽  
Heather Murphy

The effect of air pollution on health is listed as a significant cause of death worldwide. Slightly over 3 million deaths per year are due to outdoor air pollution. Studies have shown that short term increases in exposure to particulate matter have increased the risk of cardiovascular diseases such as myocardial infarction, stroke, and heart failure. However, less is known about the longer term effects of air pollution on various cardiovascular diseases. The American Heart Association formally recognized PM2.5 as a significant cardiovascular risk factor in 2010. Since then, more prolonged term exposure to air pollution has been suggested to cause chronic cardiometabolic and cardiovascular problems. The effects of long term (>3 years) air pollution are significant, but not as much is known about how location affects this exposure. Associations with cardiovascular diseases and their risk factors are often increased in urban settings, which is attributed to a higher concentrations of outdoor air pollution, independent of ethnic groups and seasonal changes. Potential causes of long term air pollution concentrations in cities or metropolitan areas come from traffic exposure and traffic intensity. The Environmental Protection Agency and United Nations have suggested changes in air quality standards, implementation plans, and ways to reduce vehicle emissions specifically to improve human health and reduce the adverse effects of air pollution; however, more work still needs to be done. This review assesses the impact of the global long term (>3 years) air pollution exposure, specifically in urban environments on cardiovascular health and disease.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Rita Biel ◽  
Coraline Danieli ◽  
Maryam Shekarrizfard ◽  
Laura Minet ◽  
Michal Abrahamowicz ◽  
...  

Abstract Urban populations are often simultaneously exposed to air pollution and environmental noise, which are independently associated with cardiovascular disease. Few studies have examined acute physiologic responses to both air and noise pollution using personal exposure measures. We conducted a repeated measures panel study of air pollution and noise in 46 non-smoking adults in Toronto, Canada. Data were analyzed using linear mixed-effects models and weighted cumulative exposure modeling of recent exposure. We examined acute changes in cardiovascular health effects of personal (ultrafine particles, black carbon) and regional (PM2.5, NO2, O3, Ox) measurements of air pollution and the role of personal noise exposure as a confounder of these associations. We observed adverse changes in subclinical cardiovascular outcomes in response to both air pollution and noise, including changes in endothelial function and heart rate variability (HRV). Our findings show that personal noise exposures can confound associations for air pollutants, particularly with HRV, and that impacts of air pollution and noise on HRV occur soon after exposure. Thus, both noise and air pollution have a measurable impact on cardiovascular physiology. Noise should be considered alongside air pollution in future studies to elucidate the combined impacts of these exposures in urban environments.


Land ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 184
Author(s):  
Javier Cárcel-Carrasco ◽  
Manuel Pascual-Guillamón ◽  
Fidel Salas-Vicente

Today, the design and remodeling of urban environments is being sought in order to achieve green, healthy, and sustainable cities. The effect of air pollution in cities due to vehicle combustion gases is an important part of the problem. Due to the indirect effect caused by the Covid-19 pandemic, political powers in Europe have imposed confinement measures for citizens by imposing movement restrictions in large cities. This indirect measure has given us a laboratory to show how the reduction in vehicle circulation affects in a short time the levels of air pollution in cities. Therefore, this article analyzes the effect in different European cities such as Milan, Prague, Madrid, Paris, and London. These cities have been chosen due to their large amount of daily road traffic that generates high levels of pollution; therefore, it can clearly show the fall in these pollutants in the air in the analyzed period. The results shown through this study indicate that the reduction in combustion vehicles greatly affects the levels of pollution in different cities. In these periods of confinement, there was an improvement in air quality where pollutant values dropped to 80% compared to the previous year. This should serve to raise awareness among citizens and political powers to adopt measures that induce sustainable transport systems.


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