Short-Term Effects of Carbon Monoxide on Mortality: An Analysis within the APHEA Project

Samoli, Evangelia; Touloumi, Giota; Schwartz, Joel; Anderson, Hugh; Schindler, Christian; Forsberg, Bertil; Vigotti, Maria Angela; Vonk, Judith M.; Košnik, Mitja; Skorkovský, Jiří; Katsouyanni, Klea

doi:10.1289/ehp.10375

Cited by 100 publications

(77 citation statements)

References 31 publications

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“…36,52 PM air pollution was significantly associated with daily mortality counts for all-cause, cardiovascular, and respiratory mortality ( Table 2). Further analyses of the European data suggest that CVD deaths are also associated with exposure to NO 2 53 and CO. 54 A few new time-series studies have also confirmed similar increases in cardiovascular mortality related to short-term PM exposure in China [55][56][57] and Bangkok, Thailand. 42 Additional multicity studies have been conducted worldwide with analyses of CVD deaths (Table 2).…”

Section: Time-series and Related Studiesmentioning

confidence: 81%

Particulate Matter Air Pollution and Cardiovascular Disease

Brook¹,

Rajagopalan²,

Pope³

et al. 2010

Circulation

5,352

3,225

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Abstract-In 2004, the first American Heart Association scientific statement on "Air Pollution and Cardiovascular Disease" concluded that exposure to particulate matter (PM) air pollution contributes to cardiovascular morbidity and mortality. In the interim, numerous studies have expanded our understanding of this association and further elucidated the physiological and molecular mechanisms involved. The main objective of this updated American Heart Association scientific statement is to provide a comprehensive review of the new evidence linking PM exposure with cardiovascular disease, with a specific focus on highlighting the clinical implications for researchers and healthcare providers. The writing group also sought to provide expert consensus opinions on many aspects of the current state of science and updated suggestions for areas of future research. On the basis of the findings of this review, several new conclusions were reached, including the following: Exposure to PM Ͻ2.5 m in diameter (PM 2.5 ) over a few hours to weeks can trigger cardiovascular disease-related mortality and nonfatal events; longer-term exposure (eg, a few years) increases the risk for cardiovascular mortality to an even greater extent than exposures over a few days and reduces life expectancy within more highly exposed segments of the population by several months to a few years; reductions in PM levels are associated with decreases in cardiovascular mortality within a time frame as short as a few years; and many credible pathological mechanisms have been elucidated that lend biological plausibility to these findings. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM 2.5 exposure and cardiovascular morbidity and mortality. This body of evidence has grown and been strengthened substantially since the first American Heart Association scientific statement was published. Finally, PM 2.5 exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality. (Circulation. 2010;121:2331-2378.)

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Section: Time-series and Related Studiesmentioning

confidence: 81%

Particulate Matter Air Pollution and Cardiovascular Disease

Brook¹,

Rajagopalan²,

Pope³

et al. 2010

Circulation

5,352

3,225

View full text Add to dashboard Cite

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“…Then, in urban environments CO concentration usually varies from 2 to 40 ppm, but during heavy traffic or when peoples are exposed to secondhand cigarette smoke it may be as high as 170 ppm (Bevan, 1991, Stern et al, 1988, Wright et al, 1975. Although CO levels are relatively low in urban environment, data from the APHEA-2 project (Air Pollution and Health: A European Approach) studying the relation between air pollution and total cardiovascular mortality in 19 European cities, reported a significant association of CO with cardiovascular mortality (Samoli et al, 2007). 3. Regular exposure to low CO level and phenotypical remodelling of the heart 3.1 Acute low level CO exposure The acute effects of such low levels of CO on the myocardium are today few studied and results are contradictory and conflicting.…”

Section: Co In Urban Environmentmentioning

confidence: 99%

Carbon Monoxide Urban Air Pollution: Cardiac Effects

Meyer¹,

Tanguy²,

Obert³

et al. 2011

Advanced Topics in Environmental Health and Air Pollution Case Studies

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“…Epidemiological studies have reported effects such as heart failure, generation of cardiac arrhythmias and decreased heart rate variability [3,[5][6][7][8][9][10][11]. Experimental studies have shown that the Pb ++ blocks the L-type calcium channels [12].…”

Section: Introductionmentioning

confidence: 99%

Lead and Carbon Monoxide Effects on Human Atrial Action Potential. In Silico Study

Tobón

Pachajoa

Ugarte

et al. 2017

Computing in Cardiology Conference (CinC)

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Exposure to air pollutants like lead (Pb ++ ) and carbon monoxide (CO) IntroductionAir pollution is defined as the presence in the atmosphere of one or more substances in sufficient quantity to produce health alterations. Air pollution causes 4.3 million premature deaths annually [1]. In 2010, the economic cost of health impacts of air pollution in developing countries was around USD 1.7 billion [1].Lead (Pb ++ ) is a toxic agent that can exert adverse health effects in humans. According to the United States Environment Protection Agency (EPA), the Pb ++ is one of the most dangerous air pollutants, affecting multiple human body systems [2]. In general, more than 143.000 people die every year due to illnesses related to Pb ++ [3].Carbon monoxide (CO) is a toxic gas, from incomplete combustion. When people breath, the CO binds to hemoglobin and is significantly retained within the blood reducing the amount of oxygen that it can transport [4].Exposure to these air pollutants contributes to cardiovascular diseases [5]. Epidemiological studies have reported effects such as heart failure, generation of cardiac arrhythmias and decreased heart rate variability [3,[5][6][7][8][9][10][11]. Experimental studies have shown that the Pb ++ blocks the L-type calcium channels [12]. A decrease in Ltype calcium current (I CaL ) is an important mechanism that favors the generation of atrial arrhythmias [13]. Recently, it has been shown that chronic exposure to CO promotes a pathological phenotype of cardiomyocytes, where remodeling leads to an important reduction of the action potential duration (APD) in atrial myocardium increasing the risk of arrhythmias [9,10] and ischemia [14]. This study aims to assess the effects of the Pb ++ and CO at different concentrations on human atrial action potential, using computational simulation. Methods Human atrial cell modelThe Courtemanche-Ramirez-Nattel-Kneller [15,16] membrane formalism was implemented to simulate the electrical activity of human atrial cell. A 0.005 µM of acetylcholine concentration was simulated. The transmembrane voltage (V m ) is given by:where C m is the membrane capacitance (100 pF), I ion is the total membrane current, and I st is the external stimulus current. The model is considered under normal electrophysiological conditions. Model of Pb ++ and CO effects on I CaLWe developed concentration dependent equations to

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Short-Term Effects of Carbon Monoxide on Mortality: An Analysis within the APHEA Project

Cited by 100 publications

References 31 publications

Particulate Matter Air Pollution and Cardiovascular Disease

Particulate Matter Air Pollution and Cardiovascular Disease

Carbon Monoxide Urban Air Pollution: Cardiac Effects

Lead and Carbon Monoxide Effects on Human Atrial Action Potential. In Silico Study

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