Particulate air pollution is associated with an acute phase response in men. Results from the MONICA–Augsburg Study

Peters, Annette; Fröhlich, Margit; Döring, Angela; Immervoll, T; Wichmann, H. E.; Hutchinson, Winston L.; Pepys, Mark B.; Köenig, Wolfgang

doi:10.1053/euhj.2000.2483

Cited by 374 publications

(258 citation statements)

References 33 publications

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“…We did not find a DE-associated increase in CRP, as anticipated by an epidemiological model [19]. One explanation for this is that PM-associated increases in CRP found in the epidemiological study were due to PM components other than those generated from DE.…”

Section: Discussioncontrasting

confidence: 46%

Coagulation markers in healthy human subjects exposed to diesel exhaust

Carlsten

Kaufman

Peretz

et al. 2007

Thrombosis Research

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Background-Ambient particulate matter (PM) is associated with cardiovascular morbidity and mortality. It has been proposed that PM induces a pro-thrombotic process, increasing the risk of cardiovascular events, with some support from epidemiological and laboratory-based models. Diesel exhaust is a major contributor to urban PM, and we conducted a controlled human exposure of diesel exhaust in healthy subjects.

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Section: Discussioncontrasting

confidence: 46%

Coagulation markers in healthy human subjects exposed to diesel exhaust

Carlsten

Kaufman

Peretz

et al. 2007

Thrombosis Research

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“…The link between air pollution and adverse respiratory and cardiovascular health is substantial (Dockery, 2001;Kim et al, 2004;Lin et al, 2005;McConnell et al, 2003;Peters et al, 2001;Pope et al, 1991;Romieu et al, 1996). Acute pulmonary responses to short-term particulate matter (PM) exposure (Atkinson et al, 2001;Oberdorster et al, 1995) as well as decrements in resting lung function associated with chronic PM exposure have been reported (Gauderman et al, 2004;Rundell, 2004).…”

mentioning

confidence: 99%

“…Current investigations suggest that PM toxicity is highly influenced by number concentration and/or particle surface area (Oberdorster, 1996), while ambient particulate matter with median aerodynamic diameter less than 2.5 µm (PM 2.5 ) has been associated with lung damage (Gauderman et al, 2004;Kim et al, 2004;McConnell et al, 2003) and cardiovascular events (Burnett et al, 1995;Peters et al, 2001;Ware, 2000). The most common source of PM 2.5 is found in combustion emissions of fossil-fueled automobiles and diesel-powered trucks, with over 90% of the particle count from diesel aerosol having an aerodynamic diameter of <30 nm (Kittelson et al, 2004).…”

mentioning

confidence: 99%

Vehicular Air Pollution, Playgrounds, and Youth Athletic Fields

Rundell

Caviston

Hollenbach

et al. 2006

Inhalation Toxicology

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In spite of epidemiological evidence concerning vehicular air pollution and adverse respiratory/cardiovascular health, many athletic fields and school playgrounds are adjacent to high traffic roadways and could present long-term health risks for exercising children and young adults. Particulate matter (PM 1 ,0.02-1.0 µm diameter) number counts were taken serially at four elementary school athletic/playground fields and at one university soccer field. Elementary school PM 1 measurements were taken over 17 days; measurements at the university soccer field were taken over 62 days. The high-traffic-location elementary school field demonstrated higher 17-day [PM 1 ] than the moderate and 2 low traffic elementary school fields (48,890 ± 34,260, 16,730 ± 10,550, 11,960 ± 6680, 10,030 ± 6280, respective mean counts; p < .05). The 62-day mean PM 1 values at the university soccer field ranged from 115,000 to 134,000 particles cm −3 . Lowest mean values were recorded at measurement sites furthest from the highway (∼34,000 particles cm −3 ) and followed a second-order logarithmic decay (R 2 = .999) with distance away from the highway. Mean NO 2 and SO 2 levels were below 100 ppb, mean CO was 0.33 ± 1.87 ppm, and mean O 3 was 106 ± 47 ppb. Ozone increased with rising temperature and was highest in the warmer afternoon hours (R = .61). Although the consequence of daily recess play and athletic activities by school children and young athletes in high ambient [PM 1 ] conditions has not yet been clearly defined, this study is a critical component to evaluating functional effects of chronic combustion-derived PM exposure on these exercising schoolchildren and young adults. Future studies should examine threshold limits and mechanistic actions of real-world particle exposure.

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“…Several important cardiovascular effects have been documented, including disruption of autonomic nervous system activity by decreased heart rate variability, 9,10 arterial vasoconstriction, 11 cardiac arrhythmias in patients with implantable defibrillators, 12 cardiac events including myocardial infarction 5 that required hospitalization, 3 and exacerbation of ST-segment changes in experimental models of myocardial infarction. 6 A significant role has been suggested for increases in inflammatory mediators, as evidenced by C-reactive protein, increased white cell counts, and plasma viscosity, [13][14][15][16] arising as a result of cytokine production linked to deposition of particulate matter in the airways and alveoli. The potential involvement of inflammatory mediators is central to the concept of plaque vulnerability in the occurrence of acute cardiovascular events.…”

mentioning

confidence: 99%

“…Furthermore, other factors may play a role in pollution-induced changes in oxygen supply and myocardial perfusion. The candidate mechanisms include changes in plasma viscosity, 15 hemostatic factors, 13,14 and alterations in endothelial function, 11,18 which could occur as a result of oxidant stress 16 or disruption due to inflammatory consequences of air pollutants.…”

mentioning

confidence: 99%