Search

Background The association between fine particulate matter and cardiovascular disease has been convincingly demonstrated. The role of traffic-related air pollutants is less clear. To better understand the role of traffic-related air pollutants in cardiovascular disease development, we examined associations between NO 2 , carotid atherosclerotic plaque, and cardiometabolic disorders associated with cardiovascular disease. Methods and Results Cross-sectional analyses were conducted among 2227 patients (62.9±13.8 years; 49.5% women) from the Stroke Prevention and Atherosclerosis Research Centre (SPARC) in London, Ontario, Canada. Total carotid plaque area measured by ultrasound, cardiometabolic disorders, and residential locations were provided by SPARC medical records. Long-term outdoor residential NO 2 concentrations were generated by a land use regression model. Associations between NO 2 , total carotid plaque area, and cardiometabolic disorders were examined using multiple regression models adjusted for age, sex, smoking, and socioeconomic status. Mean NO 2 was 5.4±1.6 ppb in London, Ontario. NO 2 was associated with a significant increase in plaque (3.4 mm 2 total carotid plaque area per 1 ppb NO 2 ), exhibiting a linear dose-response. NO 2 was also positively associated with triglycerides, total cholesterol, and the ratio of low- to high-density lipoprotein cholesterol ( P <0.05). Diabetes mellitus mediated the relationship between NO 2 and total carotid plaque area ( P <0.05). Conclusions Our results demonstrate that even low levels of traffic-related air pollutants are linked to atherosclerotic plaque burden, an association that may be partially attributable to pollution-induced diabetes mellitus. Our findings suggest that reducing ambient concentrations in cities with NO 2 below current standards would result in additional health benefits. Given the billions of people exposed to traffic emissions, our study supports the global public health significance of reducing air pollution.

Background: This work aimed to explore whether different forms of a simple isometric exercise test could be used to predict the blood pressure (BP)-lowering efficacy of different types of isometric resistance training (IRT) in healthy young adults. In light of the emphasis on primary prevention of hypertension, identifying those with normal BP who will respond to IRT is important. Also, heightened BP reactivity increases hypertension risk, and as IRT reduces BP reactivity in patients with hypertension, it warrants further investigation in a healthy population., Methods: Forty-six young men and women (24 ± 5 years; 116 ± 10/ 68 ± 8 mm Hg) were recruited from 2 study sites: Windsor, Canada (n = 26; 13 women), and Northampton, United Kingdom (n = 20; 10 women). Resting BP and BP reactivity to an isometric exercise test were assessed prior to and following 10 weeks of thrice weekly IRT. Canadian participants trained on a handgrip dynamometer (isometric handgrip, IHG), while participants in the UK trained on an isometric leg extension dynamometer (ILE)., Results: Men and women enrolled in both interventions demonstrated significant reductions in systolic BP (P < 0.001) and pulse pressure (P < 0.05). Additionally, test-induced systolic BP changes to IHG and ILE tests were associated with IHG and ILE training-induced reductions in systolic BP after 10 weeks of training, respectively (r = 0.58 and r = 0.77; for IHG and ILE; P < 0.05)., Conclusions: The acute BP response to an isometric exercise test appears to be a viable tool to identify individuals who may respond to traditional IRT prescription., (© American Journal of Hypertension, Ltd 2017. All rights reserved. For Permissions, please email: journals.permissions@oup.com)

Background: Laboratory studies suggest that exposure to fine particulate matter (≤2.5 μm in diameter) (PM2.5) can trigger a combination of pathophysiological responses that may induce the development of hypertension. However, epidemiological evidence relating PM2.5 and hypertension is sparse. We thus conducted a population-based cohort study to determine whether exposure to ambient PM2.5 is associated with incident hypertension., Methods and Results: We assembled a cohort of 35 303 nonhypertensive adults from Ontario, Canada, who responded to 1 of 4 population-based health surveys between 1996 and 2005 and were followed up until December 31, 2010. Incident diagnoses of hypertension were ascertained from the Ontario Hypertension Database, a validated registry of persons diagnosed with hypertension in Ontario (sensitivity=72%, specificity=95%). Estimates of long-term exposure to PM2.5 at participants' postal-code residences were derived from satellite observations. We used Cox proportional hazards models, adjusting for various individual and contextual risk factors including body mass index, smoking, physical activity, and neighbourhood-level unemployment rates. We conducted various sensitivity analyses to assess the robustness of the effect estimate, such as investigating several time windows of exposure and controlling for potential changes in the risk of hypertension over time. Between 1996 and 2010, we identified 8649 incident cases of hypertension and 2296 deaths. For every 10-µg/m(3) increase of PM2.5, the adjusted hazard ratio of incident hypertension was 1.13 (95% confidence interval, 1.05-1.22). Estimated associations were comparable among all sensitivity analyses., Conclusions: This study supports an association between PM2.5 and incident hypertension.

Background: Laboratory studies suggest that fine particulate matter (≤ 2.5 µm in diameter; PM(2.5)) can activate pathophysiological responses that may induce insulin resistance and type 2 diabetes. However, epidemiological evidence relating PM2.5 and diabetes is sparse, particularly for incident diabetes., Objectives: We conducted a population-based cohort study to determine whether long-term exposure to ambient PM(2.5) is associated with incident diabetes., Methods: We assembled a cohort of 62,012 nondiabetic adults who lived in Ontario, Canada, and completed one of five population-based health surveys between 1996 and 2005. Follow-up extended until 31 December 2010. Incident diabetes diagnosed between 1996 and 2010 was ascertained using the Ontario Diabetes Database, a validated registry of persons diagnosed with diabetes (sensitivity = 86%, specificity = 97%). Six-year average concentrations of PM2.5 at the postal codes of baseline residences were derived from satellite observations. We used Cox proportional hazards models to estimate the associations, adjusting for various individual-level risk factors and contextual covariates such as smoking, body mass index, physical activity, and neighborhood-level household income. We also conducted multiple sensitivity analyses. In addition, we examined effect modification for selected comorbidities and sociodemographic characteristics., Results: There were 6,310 incident cases of diabetes over 484,644 total person-years of follow-up. The adjusted hazard ratio for a 10-µg/m(3) increase in PM(2.5) was 1.11 (95% CI: 1.02, 1.21). Estimated associations were comparable among all sensitivity analyses. We did not find strong evidence of effect modification by comorbidities or sociodemographic covariates., Conclusions: This study suggests that long-term exposure to PM2.5 may contribute to the development of diabetes.