Particulate matter air pollution and ambient temperature: opposing effects on blood pressure in high-risk cardiac patients.

OBJECTIVE: Fine particulate matter air pollution (PM2.5) and extreme temperatures have both been associated with alterations in blood pressure (BP). However, few studies have evaluated their joint haemodynamic actions among individuals at high risk for cardiovascular events. METHODS: We assessed the effects of short-term exposures during the prior week to ambient PM2.5 and outdoor temperature levels on resting seated BP among 2078 patients enrolling into a cardiac rehabilitation programme at the University of Michigan (from 2003 to 2011) using multiple linear regression analyses adjusting for age, sex, BMI, ozone and the same-day alternate environmental factor (i.e. PM2.5 or temperature). RESULTS: Mean PM2.5 and temperature levels were 12.6 ±â€Š8.2 µg/m and 10.3 ±â€Š10.4°C, respectively. Each standard deviation elevation in PM2.5 concentration during lag days 4-6 was associated with significant increases in SBP (2.1-3.5 mmHg) and DBP (1.7-1.8 mmHg). Conversely, higher temperature levels (per 10.4°C) during lag days 4-6 were associated with reductions in both SBP (-3.6 to -2.3 mmHg) and DBP (-2.5 to -1.8 mmHg). There was little evidence for consistent effect modification by other covariates (e.g. demographics, seasons, medication usage). CONCLUSION: Short-term exposures to PM2.5, even at low concentrations within current air quality standards, are associated with significant increases in BP. Contrarily, higher ambient temperatures prompt the opposite haemodynamic effect. These findings demonstrate that both ubiquitous environmental exposures have clinically meaningful effects on resting BP among high-risk cardiac patients.

Higher fine particulate matter and temperature levels impair exercise capacity in cardiac patients.

OBJECTIVE: Fine particulate matter (PM2.5) air pollution and variations in ambient temperature have been linked to increased cardiovascular morbidity and mortality. However, no large-scale study has assessed their effects on directly measured aerobic functional capacity among high-risk patients. METHODS: Using a cross-sectional observational design, we evaluated the effects of ambient PM2.5 and temperature levels over 7 days on cardiopulmonary exercise test results performed among 2078 patients enrolling into a cardiac rehabilitation programme at the University of Michigan (from January 2003 to August 2011) using multiple linear regression analyses (controlling for age, sex, body mass index). RESULTS: Peak exercise oxygen consumption was significantly decreased by approximately 14.9% per 10 µg/m(3) increase in ambient PM2.5 levels (median 10.7 µg/m(3), IQR 10.1 µg/m(3)) (lag days 6-7). Elevations in PM2.5 were also related to decreases in ventilatory threshold (lag days 5-7) and peak heart rate (lag days 2-3) and increases in peak systolic blood pressure (lag days 4-5). A 10°C increase in temperature (median 10.5°C, IQR 17.5°C) was associated with reductions in peak exercise oxygen consumption (20.6-27.3%) and ventilatory threshold (22.9-29.2%) during all 7 lag days. In models including both factors, the outcome associations with PM2.5 were attenuated whereas the effects of temperature remained significant. CONCLUSIONS: Short-term elevations in ambient PM2.5, even at low concentrations within current air quality standards, and/or higher temperatures were associated with detrimental changes in aerobic exercise capacity, which can be linked to a worse quality of life and cardiovascular prognosis among cardiac rehabilitation patients.

Exploration of the composition and sources of urban fine particulate matter associated with same-day cardiovascular health effects in Dearborn, Michigan.

The objective was to explore associations of chemical components and source factors of ambient fine particulate matter (aerodynamic diameter ≤ 2.5 µm; PM2.5) with cardiovascular (CV) changes following same-day exposure to ambient PM2.5. Twenty-five healthy adults living in rural Michigan were exposed to ambient air in an urban/industrial community for 4 to 5 h daily for five consecutive days. CV health outcomes were measured 1-2 h post exposure. Contributing emission sources were identified via positive matrix factorization. We examined associations between PM2.5 mass, composition and source factors, and same-day changes in CV outcomes using mixed-model analyses. PM2.5 mass (10.8 ± 6.8 µg/m(3)), even at low ambient levels, was significantly associated with increased heart rate (HR). Trace elements as well as secondary aerosol, diesel/urban dust and iron/steel manufacturing factors potentially explained the HR changes. However, trace element analysis demonstrated additional associations with other CV responses including changes in blood pressure (BP), arterial compliance, autonomic balance and trends toward reductions in endothelial function. Two factors were related to BP changes (diesel/urban dust, motor vehicle) and trends toward impaired endothelial function (diesel/urban dust). This study indicates composition of PM2.5 and its sources may contribute to CV health effects independently of PM2.5 mass.