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Rückerl, Regina; Phipps, Richard P.; Schneider, Alexandra; Frampton, Mark W.; Cyrys, Josef; Oberdörster, G.; Wichmann, Heinz‐Erich; Peters, Annette

doi:10.1186/1743-8977-4-1

Cited by 173 publications

(73 citation statements)

References 55 publications

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“…Likewise, positive associations be tween sCD62P (our most sensitive biomarker) or sCD40L and particulate matter have been reported in previous studies. 6,7,45 These platelet activation marker associations with pollutant changes in the previous 24 hours provide an explanation for previously reported triggering of myocardial infarction by ambient particulate matter. 46-51 …”

Section: Commentsupporting

confidence: 59%

Association Between Changes in Air Pollution Levels During the Beijing Olympics and Biomarkers of Inflammation and Thrombosis in Healthy Young Adults

Rich¹,

Kipen²,

Huang³

et al. 2012

JAMA

345

271

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Section: Commentsupporting

confidence: 59%

Association Between Changes in Air Pollution Levels During the Beijing Olympics and Biomarkers of Inflammation and Thrombosis in Healthy Young Adults

Rich¹,

Kipen²,

Huang³

et al. 2012

JAMA

345

271

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“…In conjunction with the prothrombotic effect caused by short-term exposure to WPS, we found a significant decrease in platelet numbers in WPS-exposed mice compared with air-exposed ones, this is indicative of platelet activation in vivo . A decrease of platelet numbers following pulmonary exposure to pollutant particles has been reported from experimental and clinical studies [18,25]. The numbers of platelet were found slightly but insignificantly increased in mice exposed to WPS for 1 month [14].…”

Section: Discussionmentioning

confidence: 96%

Short-Term Nose-Only Water-Pipe (Shisha) Smoking Exposure Accelerates Coagulation and Causes Cardiac Inflammation and Oxidative Stress in Mice

Yuvaraju

Beegam

Ali

2015

Cell Physiol Biochem

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Background/Aim: Water-pipe smoking (WPS) has acquired worldwide popularity, and is disseminating particularly rapidly in Europe and North America. However, little is known about the short-term cardiovascular effects of WPS. Methods: Presently, we assessed the short-term cardiovascular effects of nose-only exposure to mainstream WPS in BALB/c mice for 30 min/day for 5 consecutive days. Control mice were exposed to air. At the end of the exposure period, several cardiovascular endpoints were measured. Results: WPS did not affect the number of leukocytes and the plasma concentrations of C-reactive protein, tumor necrosis factor α (TNFα) and interleukin-6 (IL-6). Likewise, plasma levels of lipid peroxidation (LPO), reduced glutathione (GSH) and catalase were not affected by WPS. By contrast, WPS aggravated in vivo thrombosis by shortening the thrombotic occlusion time in pial arterioles and venules. The number of circulating platelets was reduced by WPS suggesting the occurrence of platelet aggregation in vivo. Elevated concentrations of fibrinogen and plasminogen activator inhibitor-1 were seen after the exposure to WPS. Blood samples taken from mice exposed to WPS and exposed to adenosine diphosphate showed more platelet aggregation. The heart concentrations of IL-6 and TNFα were augmented by WPS. Likewise, heart levels of LPO, reactive oxygen species and the antioxidants catalase and GSH were increased by WPS. However, the systolic blood pressure and heart rate were not affected by WPS. Conclusion: It can be concluded that short-term exposure to WPS exerts procoagulatory effects and induce cardiac inflammation and oxidative stress. At the time point investigated, there was no evidence for blood inflammation or oxidative stress.

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“…A marker of platelet activation (sCD40L) has been reported to be increased in association with ultrafine and accumulation mode PM in subjects with coronary artery disease (Ruckerl et al 2007b). An association was also observed between PM and increased platelet aggregation in healthy individuals (Rudez et al 2009).…”

Section: Cardiovascular Diseasementioning

confidence: 99%

Air pollution and health: emerging information on susceptible populations

OʼNeill

Breton

Devlin

et al. 2011

Air Qual Atmos Health

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Outdoor air pollution poses risks to human health in communities around the world, and research on populations who are most susceptible continues to reveal new insights. Human susceptibility to adverse health effects from exposure to air pollution can be related to underlying disease; demographic or anthropometric characteristics; genetic profile; race and ethnicity; lifestyle, behaviors, and socioeconomic position; and location of residence or daily activities. In health research, an individual or group may have an enhanced responsiveness to a given, identical level of pollution exposure compared to those who are less susceptible. Or, people in these different groups may experience varying levels of exposure (for example, a theoretically homogeneous population whose members differ only by proximity to a road). Often the information available for health research may relate to both exposure and enhanced response to a given dose of pollution. This paper discusses the general direction of research on susceptibility to air pollution, with a general though not an exclusive focus on particulate matter, with specific examples of research on susceptibility related to cardiovascular disease, diabetes, asthma, and genetic and epigenetic features. We conclude by commenting how emerging knowledge of susceptibility can inform policy for controlling pollution sources and exposures to yield maximal health benefit and discuss two areas of emerging interest: studying air pollution and its connection to perinatal health, as well as land use and urban infrastructure design.

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Untitled

Cited by 173 publications

References 55 publications

Association Between Changes in Air Pollution Levels During the Beijing Olympics and Biomarkers of Inflammation and Thrombosis in Healthy Young Adults

Association Between Changes in Air Pollution Levels During the Beijing Olympics and Biomarkers of Inflammation and Thrombosis in Healthy Young Adults

Short-Term Nose-Only Water-Pipe (Shisha) Smoking Exposure Accelerates Coagulation and Causes Cardiac Inflammation and Oxidative Stress in Mice

Air pollution and health: emerging information on susceptible populations

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