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Effects of work place carbon monoxide exposure on blood viscosity
Dikmenoğlu Neslihan1, Seringeç Nurten
1Department of Physiology, Hacettepe University Faculty of Medicine, Ankara, Turkey. nhdikmen@yahoo.com
Insights
Chronic low-level carbon monoxide (CO) exposure significantly increases plasma viscosity, a key factor in blood viscosity. This finding suggests a potential mechanism linking CO exposure to increased cardiovascular disease risk.
Area of Science:
- Cardiovascular Physiology
- Environmental Health Science
Background:
- Cardiovascular diseases (CVDs) are a significant global health concern.
- Both blood viscosity and exposure to carbon monoxide (CO) have been independently linked to CVDs.
Purpose of the Study:
- To investigate the impact of chronic low-level CO exposure on determinants of blood viscosity.
- To analyze effects on hematocrit, plasma viscosity, erythrocyte deformability, and erythrocyte aggregation.
Main Methods:
- Study included 10 men with occupational CO exposure (≥6 months) and 10 healthy controls.
- Plasma viscosity measured using a cone-plate viscometer.
- Erythrocyte deformability and aggregation assessed via laser-assisted optical rotational cell analyzer.
Main Results:
- Mean plasma viscosity was significantly higher in the CO-exposed group (1.4 ± 0.1 mPa·sn) compared to controls (1.2 ± 0.06 mPa·sn) (p < .05).
- Plasma fibrinogen levels were slightly elevated in the CO-exposed group (275 ± 11 mg/dL) versus controls (263 ± 14 mg/dL).
Conclusions:
- Chronic low-level CO exposure elevates plasma viscosity.
- Increased plasma viscosity may represent a mechanism contributing to the heightened risk of CVDs associated with CO exposure.
Abstract:
Both blood viscosity and carbon monoxide (CO) has been associated with cardiovascular diseases (CVDs). In order to investigate the effects of chronic low-level CO exposure on the determinants of blood viscosity (hematocrit, plasma viscosity, erythrocyte deformability, and erythrocyte aggregation), 10 men exposed to CO at work for at least 6 months and 10 healthy controls were included in the study. Plasma viscosity was determined by a cone-plate viscometer, erythrocyte deformability and erythrocyte aggregation by laser-assisted optical rotational cell analyzer. Mean plasma viscosity of the group exposed to CO (1.4 +/- 0.1 mPa.sn) was significantly higher than that of the controls (1.2 +/- 0.06 mPa.sn) (p < .05). Plasma fibrinogen level of the CO group (275 +/- 11 mg/dL) was slightly higher than that of the controls (263 +/- 14 mg/dL). The rise in plasma viscosity by chronic low-level CO exposure may be the mechanism of CO-induced increase in the risk for CVDs.
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