Fine particulate matter air pollution plus ozone impairs vascular function and raises diastolic blood pressure. We aimed to determine the mechanism and air pollutant responsible. The effects of pollution on heart rate variability, blood pressure, biomarkers, and brachial flow-mediated dilatation were determined in 2 randomized, double-blind, crossover studies. In Ann Arbor, 50 subjects were exposed to fine particles (150 μg/m ³ ) plus ozone (120 parts per billion) for 2 hours on 3 occasions with pretreatments of an endothelin antagonist (Bosentan, 250 mg), antioxidant (Vitamin C, 2 g), or placebo. In Toronto, 31 subjects were exposed to 4 different conditions (particles plus ozone, particles, ozone, and filtered air). In Toronto, diastolic blood pressure significantly increased (2.9 and 3.6 mm Hg) only during particle-containing exposures in association with particulate matter concentration and reductions in heart rate variability. Flow-mediated dilatation significantly decreased (2.0% and 2.9%) only 24 hours after particle-containing exposures in association with particulate matter concentration and increases in blood tumor necrosis factor α. In Ann Arbor, diastolic blood pressure significantly similarly increased during all of the exposures (2.5 to 4.0 mm Hg), a response not mitigated by pretreatments. Flow-mediated dilatation remained unaltered. Particulate matter, not ozone, was responsible for increasing diastolic blood pressure during air pollution inhalation, most plausibly by instigating acute autonomic imbalance. Only particles from urban Toronto additionally impaired endothelial function, likely via slower proinflammatory pathways. Our findings demonstrate credible mechanisms whereby fine particulate matter could trigger acute cardiovascular events and that aspects of exposure location may be an important determinant of the health consequences.

Daily changes in levels of ambient fine particulate matter (PM) air pollution (PM <2.5 μm in diameter [PM_2.5]) have been associated with higher risk of acute cardiovascular events, excess hospitalizations, and deaths.¹ These cardiovascular effects of PM_2.5 appear to be mediated through a combination of autonomic, hemostatic, inflammatory, and vascular endothelial disturbances with consequent changes in cardiac and vascular function.^2-7 Relying on the current evidence, the US Environmental Protection Agency (EPA) regulates mean daily and annual PM_2.5 levels. Whether the current regulatory standards are sufficient to protect public health remains controversial.⁸

Background and Purpose— The association between short-term elevations in ambient air particles and increased cardiovascular morbidity and mortality is well documented. Ambient particles may similarly increase the risk of stroke. Methods— We evaluated the association between daily levels of respirable particulate matter (aerodynamic diameter ≤10 μm, PM ₁₀ ) and hospital admission for ischemic and hemorrhagic stroke among Medicare recipients (age ≥65 years) in 9 US cities using a 2-stage hierarchical model. In the first stage, we applied the time-stratified case-crossover design to estimate the effect of PM ₁₀ in each city. We used a 3-day unconstrained, distributed lag model to simultaneously estimate the effect of PM ₁₀ 0 to 2 days before the admission day and controlled for meteorological covariates in all of the models. In the second stage, we used random-effects metaanalytic techniques to combine the city-specific effect estimates. Results— Ischemic (n=155 503) and hemorrhagic (19 314) stroke admissions were examined separately. For ischemic stroke, an interquartile range increase in PM ₁₀ was associated with a 1.03% (95% CI, 0.04% to 2.04%) increase in admissions on the same day only. Similar results were observed with CO, NO ₂ , and SO ₂ . For hemorrhagic stroke, no association was observed with any pollutant 0 to 2 days before admission. Conclusions— These results suggest that elevations in ambient particles may transiently increase the risk of ischemic, but not hemorrhagic, stroke. Studies with more accurate assessment of timing of stroke onset are necessary to confirm or refute these findings.

Background: Heat-wave frequency, intensity, and duration are increasing with global climate change. The association between heat and mortality in the elderly is well documented, but less is known regarding associations with hospital admissions. Objectives: Our goal was to determine associations between moderate and extreme heat, heat waves, and hospital admissions for nonaccidental causes among Medicare beneficiaries ≥ 65 years of age in 114 cities across five U.S. climate zones. Methods: We used Medicare inpatient billing records and city-specific data on temperature, humidity, and ozone from 1992 through 2006 in a time-stratified case-crossover design to estimate the association between hospitalization and moderate [90th percentile of apparent temperature (AT)] and extreme (99th percentile of AT) heat and heat waves (AT above the 95th percentile over 2–8 days). In sensitivity analyses, we additionally considered confounding by ozone and holidays, different temperature metrics, and alternate models of the exposure–response relationship. Results: Associations between moderate heat and hospital admissions were minimal, but extreme heat was associated with a 3% (95% CI: 2%, 4%) increase in all-cause hospital admissions over the subsequent 8 days. In cause-specific analyses, extreme heat was associated with increased hospitalizations for renal (15%; 95% CI: 9%, 21%) and respiratory (4%; 95% CI: 2%, 7%) diseases, but not for cardiovascular diseases. An added heat-wave effect was observed for renal and respiratory admissions. Conclusion: Extreme heat is associated with increased hospital admissions, particularly for renal causes, among the elderly in the United States. Citation: Gronlund CJ, Zanobetti A, Schwartz JD, Wellenius GA, O’Neill MS. 2014. Heat, heat waves, and hospital admissions among the elderly in the United States, 1992–2006. Environ Health Perspect 122:1187–1192; http://dx.doi.org/10.1289/ehp.1206132