Endothelial Function and Chronic Exposure to Air Pollution in Normal Male Subjects

Abstract

Abstract-Exposure to urban air pollution, ultrafine particles or gases, is associated with acute cardiovascular mortality and morbidity. We investigated the effect of ambient air pollution on endothelial function in 40 healthy white male nonsmokers spontaneously breathing ambient air in Paris, France. Air pollutant levels (nitrogen, sulfur and carbon oxides, and particulate matter) were averaged during the 5 days preceding arterial measurements. Brachial artery endothelium-dependent flow-mediated dilatation and reactive hyperemia induced by hand ischemia and endotheliumindependent glyceryl trinitrate dilatation were measured using a radiofrequency-based echo-tracking device at 2-week intervals. Flow-mediated dilatation was independently and negatively correlated with the average levels of sulfur dioxide (PϽ0.001) and nitrogen monoxide (PϽ0.01). Sulfur dioxide levels explained 19% of the variance of flow-mediated dilatation. An increase in gaseous pollutants, 2 weeks apart, was significantly associated with a decreased in flow-mediated dilatation. No association was found between air pollutants and glyceryl trinitrate-induced vasodilatation. Reactive hyperemia was significantly and positively correlated with particulate matter with aerodynamic diameters Ͻ10 m and Ͻ2.5 m (PϽ0.0001 and PϽ0.001, respectively) and nitrogen dioxide (PϽ0.01). An increase in particulate matter, 2 weeks apart, was significantly correlated with an increase in reactive hyperemia. Endothelial function was impaired by ordinary levels of pollution in healthy young males, in an urban area, and may be reduced by 50% between the least and the most polluted day. Gaseous pollutants affect large artery endothelial function, whereas particulate matter exaggerates the dilatory response of small arteries to ischemia. (Hypertension. 2007;50:970-976.)

Particulate Matter Air Pollution and Cardiovascular Disease

“…Daily changes in ambient gaseous pollutants (SO 2 and NO x ) in Paris, France, have also been associated with impaired endothelium-dependent vasodilation among nonsmoking men. 197 197 or microvascular 178 endothelial function in all studies. Even when the few negative studies are considered, the overall evidence supports the concept that ambient PM is capable of impairing vascular function, particularly among higher-risk individuals (eg, those with diabetes) and after traffic-related exposure (Table 6).…”

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

“…Goldberg et al (2008) found positive and statistically significant associations of SO 2 with reduced oxygen saturation and increased pulse rate in congestive heart failure patients. Briet et al (2007) (not considered by the EPA) found that 5-day average SO 2 reduced endothelium-dependent brachial artery flow-mediated dilatation in healthy male subjects along with nitric oxide, but not with other pollutants, such as NO 2 and PM.…”

Particulate Matter, Hypertension, and the Metabolic Syndrome

“…PM 2.5 has previously been shown to regulate ROS generation through an NADPH oxidase -dependent mechanism in a variety of cell types and may represent an important upstream pathway by which PM 2.5 may potentiate effects of AII (Brook, 2007 ;Mills et al, 2007 ;Dvonch et al, 2009 ). Since AII is well known to regulate NADPH oxidases, this may well represent an important upstream pathway by which PM 2.5 exerts additive effects on AII -mediated BP and CV remodeling (Briet et al, 2007 ;Choi et al, 2007 ). In addition, PM 2.5 may have direct effects on AII receptor subtype 1 signaling that could partly explain our fi ndings.…”