COHb% as a marker of cardiovascular risk in never smokers: Results from a population-based cohort study

Hedblad, Bo; Engström, Gunnar; Janzon, Ellis; Berglund, Göran; Janzon, Lars

doi:10.1080/14034940600590523

Cited by 26 publications

(19 citation statements)

References 27 publications

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“…Thus, a consideration of environmental CO exposure and cardiovascular events as well as cerebral vascular events will be presented initially [28][29][30][31][32][33].…”

Section: Clinical Evidence That Co Is a Procoagulant And Antifibrinolmentioning

confidence: 99%

“…First, looking at the specific subject's degree of exposure, never smokers in the top quartile of observed circulating COHb (0.91%) were determined to have 3.7-fold the relative risk of cardiovascular events and 2.2-fold the relative risk of death compared to the quartile with the lowest COHb (0.43%) [28]. Increased environmental presence of CO in areas with significant [29] or low [30] air pollution was associated with increased incidence of stroke, and increased workplace exposure to CO [31] in nonsmokers was associated with a 1.97-fold increase in ischemic cardiac death.…”

Section: Clinical Evidence That Co Is a Procoagulant And Antifibrinolmentioning

confidence: 99%

“…Even more interesting, among tobacco smokers, the degree of increase in COHb was associated with increased cardiovascular events, stroke and death [32,33]. While supportive of the concept that CO may facilitate thrombophilia in these settings, it must be stressed that none of these settings [28][29][30][31][32][33] involved exposure to pure CO without exposure to other potential or actual products of combustion (e.g., fine particulate pollution, tobacco smoke).…”

Section: Clinical Evidence That Co Is a Procoagulant And Antifibrinolmentioning

confidence: 99%

“…There is evidence that excessive CO exposure may result in decreased in vivo and in vitro hemostasis in humans and rodents [4][5][6][7][8][18][19][20][21][22][23], potentially by inhibition of platelet aggregation [9][10][11][12][13]15,16,[20][21][22][23]. However, there is also evidence that increased CO exposure can enhance platelet activation [14,17] and cause enhanced coagulation/decreased fibrinolysis in humans and other mammalian species [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47][67][68][69][70]…”

mentioning

confidence: 99%

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Carbon monoxide: Anticoagulant or procoagulant?

Nielsen

Pretorius

2014

Thrombosis Research

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Within the past decade there have been several investigations attempting to define the impact of exogenous and endogenous carbon monoxide exposure on hemostasis.Critically, two bodies of literature have emerged, with carbon monoxide mediated platelet inhibition cited as a cause of in vitro human and in vitro/in vivo rodent anticoagulation. In contrast, interaction with heme groups associated with fibrinogen, α 2 -antiplasmin and plasmin by carbon monoxide has resulted in enhanced coagulation and decreased fibrinolysis in vitro in human and other species, and in vivo in rabbits. Of interest, the ultrastructure of platelet rich plasma thrombi demonstrates an abnormal increase in fine fiber formation and matting that are obtained from humans exposed to carbon monoxide.Further, thrombi obtained from humans and rabbits have very similar ultrastructures, whereas mice and rats have more fine fibers and matting present. In sum, there may be

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“…Thus, a consideration of environmental CO exposure and cardiovascular events as well as cerebral vascular events will be presented initially [28][29][30][31][32][33].…”

Section: Clinical Evidence That Co Is a Procoagulant And Antifibrinolmentioning

confidence: 99%

Section: Clinical Evidence That Co Is a Procoagulant And Antifibrinolmentioning

confidence: 99%

Section: Clinical Evidence That Co Is a Procoagulant And Antifibrinolmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Carbon monoxide: Anticoagulant or procoagulant?

Nielsen

Pretorius

2014

Thrombosis Research

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show abstract

“…Nevertheless, relationships have been shown previously between COHb levels and the degree of urbanization (Radford and Drizd, 1982), and between COHb levels in donated blood and urban average ambient CO levels (Lipfert, unpublished memorandum). Further, Hart et al (2006) showed that COHb was associated with all-cause mortality even after controlling for self-reported smoking, and Hedblad et al (2005Hedblad et al ( , 2006 showed that high levels of COHb are associated with cardiovascular risk factors and mortality. However, Bono et al (2007) found that smoking effects dominated COHb findings in urban traffic policemen.…”

Section: Biomarkers and Personal Exposures It Is Widely Recognizedmentioning

confidence: 99%

On exposure and response relationships for health effects associated with exposure to vehicular traffic

Lipfert

Wyzga

2008

J Expo Sci Environ Epidemiol

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This work examines various metrics and models that have been used to estimate long-term health effects of exposure to vehicular traffic. Such health impacts may include effects of air pollution due to emissions of combustion products and from vehicle or roadway wear, of noise, stress, or from socioeconomic effects associated with preferred residential locations. Both categorical and continuous exposure metrics are considered, typically for distances between residences and roadways, or for traffic density or intensity. It appears that continuous measures of exposure tend to yield lower risk estimates that are also more precise than categorical measures based on arbitrary criteria. The selection of appropriate exposure increments to characterize relative risks is also important in comparing pollutants and other agents. Confounding and surrogate variables are also important issues, since studies of traffic proximity or density cannot identify the specific agents related to traffic exposures that might be responsible for the various health endpoints that have been implicated. Studies based on ambient air quality measurements are necessarily restricted to species for which data are available, some of which may be serving as markers for the actual agents of harm. Studies based on modeled air quality are limited by the accuracy of mobile source emission inventories, which may not include poorly maintained (high emitting) vehicles. Additional exposure modeling errors may result from precision limitations of geocoding methods. Studies of the health effects of traffic are progressing from establishing the existence of relationships to describing them in more detail, but effective remedies or control strategies have generally not yet been proposed in the context of these epidemiological studies. Resolution of these dose-response uncertainties is important for the development of effective public health strategies for the future.

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Differential effects of patient-related factors on the outcome of radiation therapy for rectal cancer

et al. 2016

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Objective The objective of this study was to investigate whether cancer specific survival in rectal cancer patients is affected by patient-related factors, conditional on radiation treatment. Methods 359 invasive rectal cancer patients who consented and provided questionnaire data for a population-based case-control study of colorectal cancer in Metropolitan Detroit were included in this study. Their vital status was ascertained through to the population-based cancer registry. Hazard ratios (HR) for cancer specific and other deaths and 95% confidence intervals (CIs) were calculated according to selected patients' characteristics, stratified by radiation status, using joint Cox proportional hazards models. Results A total of 159 patients were found to be deceased after the median follow-up of 9.2 years, and 70% of them were considered to be cancer specific. Smoking and a history of diabetes were associated with an increased probability of deaths from other causes (HR 3.20, 95% CI 1.72–5.97 and HR 2.02, 95% CI 0.98–4.16, respectively), while regular use of non-steroidal anti-inflammatory drugs (NSAIDs) was inversely correlated with cancer-specific mortality (HR 0.50, 95% CI 0.30–0.81). Furthermore, the associations of smoking and NSAIDs with the two different types of deaths (cancer vs others) significantly varied with radiation status (P-values for the interactions= 0.014 for both). In addition, we observed a marginally significantly reduced risk of cancer specific deaths in the patients who had the relative ketogenic diet overall (HR=0.49, 95% 0.23–1.02). Conclusion Further research is warranted to confirm these results in order to develop new interventions to improve outcome from radiation treatment.

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COHb% as a marker of cardiovascular risk in never smokers: Results from a population-based cohort study

Cited by 26 publications

References 27 publications

Carbon monoxide: Anticoagulant or procoagulant?

Carbon monoxide: Anticoagulant or procoagulant?

On exposure and response relationships for health effects associated with exposure to vehicular traffic

Differential effects of patient-related factors on the outcome of radiation therapy for rectal cancer

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