Effects of Personal Exposure to Particulate Air Pollution on Diabetic Patients-Changes in Cardiovascular System and Biomarkers of Inflammation and Oxidative Stress

Abstract

P-036 Abstract: Daily variations in exposure to particulate air pollution have been associated with cardiovascular morbidity and mortality. Some studies have suggested that people with diabetes mellitus are vulnerable to cardiovascular health effects associated with exposure to air pollution. We hypothesized that a short-term exposure of diabetic patients in Windsor Ontario Canada to elevated levels of particulate matter (PM10) was associated with impaired cardiovascular function, and increased blood pro-inflammatory cytokines and oxidative stress markers. Non-smoking diabetics (n = 25, twenty one of them were type II diabetics, and 15 were females), age 27–67 years (mean 46.2) were recruited for the study. Patients were followed for 7 weeks, total of 171 visits. One day before each visit, patients were given a personal PM10 monitor to wear for approximately 24 hours. Upon visiting the clinic, brachial artery diameter, flow-mediated vasodilation (FMD), heart rate and blood pressure were measured, and blood samples were drawn to determine the concentrations of C-reactive protein (CRP), thiobarbituric acid reactive substances (TBARS, an oxidative stress marker), tumor necrosis factor-α (TNF-α), and interleukin-6. To analyze the associations between personal exposure to PM10 and health outcomes, mixed-effects models were used assuming random slopes and random intercepts. Ambient temperature, glucose, and study time were adjusted when needed. Subjects were also stratified into groups of body mass index (BMI) <29 and ≥29 (the 50th percentile), with and without cardiovascular medication use, and with and without high blood pressure and/or high cholesterol. The 24-hour median concentration of PM10 was 25.5 μg/m3 (5th–95th percentile 9.8–133 μg/m3). FMD was negatively associated with high BMI (p = 0.022) and high blood pressure and/or high cholesterol (p = 0.078), indicating a relationship between the brachial artery narrowness and these cardiovascular risk factors. PM10 was significantly associated with a decrease in basal brachial artery diameter (p = 0.006), and an increase in CRP (p = 0.086) and TBARS (p = 0.001), the latter two having been linked to reduced endothelial relaxation factor nitric oxide. These changes occurred only in subjects not taking cardiovascular medication. In this sub-group, PM10 was also associated with elevated diastolic blood pressure (p = 0.027). PM10 did not have an adverse impact on FMD, heart rate, TNF-α, or interleukin-6. In conclusion, our results suggest that daily exposure to particulate air pollution may be linked to an impaired basal arterial dilatation in diabetic patients, possibly attributable to a reduced nitric oxide-mediated vasodilation associated with oxidative stress and an influx of CRP.