AIR POLLUTION INFLUENCES ON EXHALED NITRIC OXIDE AMONG PEOPLE WITH TYPE II DIABETES.

OBJECTIVE: In a population with type 2 diabetes mellitus (T2DM), we examined associations of short-term air pollutant exposures with pulmonary inflammation, measured as fraction of exhaled pulmonary nitric oxide (FeNO). METHODS: Sixty-nine Boston Metropolitan residents with T2DM completed up to 5 bi-weekly visits with 321 offline FeNO measurements. We measured ambient concentrations of particle mass, number and components at our stationary central site. Ambient concentrations of gaseous air pollutants were obtained from state monitors. We used linear models with fixed effects for participants, adjusting for 24-hour mean temperature, 24-hour mean water vapor pressure, season, and scrubbed room NO the day of the visit, to estimate associations between FeNO and interquartile range increases in exposure. RESULTS: Interquartile increases in the 6-hour averages of black carbon (BC) (0.5 µg/m3) and particle number (PN) (1,000 particles/cm3) were associated with increases in FeNO of 3.84% (95% CI 0.60% to 7.18%) and 9.86 % (95% CI 3.59% to 16.52%), respectively. We also found significant associations of increases in FeNO with increases in 24-hour moving averages of BC, PN and nitrogen oxides (NOx). CONCLUSION: Recent studies have focused on FeNO as a marker for eosinophilic pulmonary inflammation in asthmatic populations. This study adds support to the relevance of FeNO as a marker for pulmonary inflammation in diabetic populations, whose underlying chronic inflammatory status is likely to be related to innate immunity and proinflammatory adipokines.

Brachial artery responses to ambient pollution, temperature, and humidity in people with type 2 diabetes: a repeated-measures study.

BACKGROUND: Extreme weather and air pollution are associated with increased cardiovascular risk in people with diabetes. OBJECTIVES: In a population with diabetes, we conducted a novel assessment of vascular brachial artery responses both to ambient pollution and to weather (temperature and water vapor pressure, a measure of humidity). METHODS: Sixty-four 49- to 85-year-old Boston residents with type 2 diabetes completed up to five study visits (279 repeated measures). Brachial artery diameter (BAD) was measured by ultrasound before and after brachial artery occlusion [i.e., flow-mediated dilation (FMD)] and before and after nitroglycerin-mediated dilation (NMD). Ambient concentrations of fine particulate mass (PM2.5), black carbon (BC), organic carbon (OC), elemental carbon, particle number, and sulfate were measured at our monitoring site; ambient concentrations of carbon monoxide, nitrogen dioxide, and ozone were obtained from state monitors. Particle exposure in the home and during each trip to the clinic (home/trip exposure) was measured continuously and as a 5-day integrated sample. We used linear models with fixed effects for participants, adjusting for date, season, temperature, and water vapor pressure on the day of each visit, to estimate associations between our outcomes and interquartile range increases in exposure. RESULTS: Baseline BAD was negatively associated with particle pollution, including home/trip-integrated BC (-0.02 mm; 95% CI: -0.04, -0.003, for a 0.28 µg/m3 increase in BC), OC (-0.08 mm; 95% CI: -0.14, -0.03, for a 1.61 µg/m3 increase) as well as PM2.5, 5-day average ambient PM2.5, and BC. BAD was positively associated with ambient temperature and water vapor pressure. However, exposures were not consistently associated with FMD or NMD. CONCLUSION: Brachial artery diameter, a predictor of cardiovascular risk, decreased in association with particle pollution and increased in association with ambient temperature in our study population of adults with type 2 diabetes. CITATION: Zanobetti A, Luttmann-Gibson H, Horton ES, Cohen A, Coull BA, Hoffmann B, Schwartz JD, Mittleman MA, Li Y, Stone PH, de Souza C, Lamparello B, Koutrakis P, Gold DR. 2014. Brachial artery responses to ambient pollution, temperature, and humidity in people with type 2 diabetes: a repeated-measures study. Environ Health Perspect 122:242-248; http://dx.doi.org/10.1289/ehp.1206136.

Opposing effects of particle pollution, ozone, and ambient temperature on arterial blood pressure.

BACKGROUND: Diabetes increases the risk of hypertension and orthostatic hypotension and raises the risk of cardiovascular death during heat waves and high pollution episodes. OBJECTIVE: We examined whether short-term exposures to air pollution (fine particles, ozone) and heat resulted in perturbation of arterial blood pressure (BP) in persons with type 2 diabetes mellitus (T2DM). METHODS: We conducted a panel study in 70 subjects with T2DM, measuring BP by automated oscillometric sphygmomanometer and pulse wave analysis every 2 weeks on up to five occasions (355 repeated measures). Hourly central site measurements of fine particles, ozone, and meteorology were conducted. We applied linear mixed models with random participant intercepts to investigate the association of fine particles, ozone, and ambient temperature with systolic, diastolic, and mean arterial BP in a multipollutant model, controlling for season, meteorological variables, and subject characteristics. RESULTS: An interquartile increase in ambient fine particle mass [particulate matter (PM) with an aerodynamic diameter of ≤ 2.5 µm (PM2.5)] and in the traffic component black carbon in the previous 5 days (3.54 and 0.25 µg/m3, respectively) predicted increases of 1.4 mmHg [95% confidence interval (CI): 0.0, 2.9 mmHg] and 2.2 mmHg (95% CI: 0.4, 4.0 mmHg) in systolic BP (SBP) at the population geometric mean, respectively. In contrast, an interquartile increase in the 5-day mean of ozone (13.3 ppb) was associated with a 5.2 mmHg (95% CI: -8.6, -1.8 mmHg) decrease in SBP. Higher temperatures were associated with a marginal decrease in BP. CONCLUSIONS: In subjects with T2DM, PM was associated with increased BP, and ozone was associated with decreased BP. These effects may be clinically important in patients with already compromised autoregulatory function.