With the exception of the flu pandemic years of 1918-1920, heart disease (HD) has been the leading cause of death in the United States since 1910,¹ with cancer and stroke among the 5 leading causes of death every year since 1924.² From 2000 to 2010, age-adjusted mortality decreased 30% for HD and 36% for stroke, but cancer mortality declined only 13%.³ Heart disease mortality approached that of cancer, suggesting that cancer might soon replace HD as the leading cause of death.

Background: Fine particulate matter <2.5 µm in diameter (PM _2.5 ) has known effects on cardiovascular morbidity and mortality. However, no study has quantified and compared the risks of incident myocardial infarction, incident stroke, ischemic heart disease (IHD) mortality, and cerebrovascular mortality in relation to long‐term PM _2.5 exposure. Methods and Results: We sought to quantitatively summarize studies of long‐term PM _2.5 exposure and risk of IHD and stroke events by conducting a review and meta‐analysis of studies published by December 31, 2019. The main outcomes were myocardial infarction, stroke, IHD mortality, and cerebrovascular mortality. Random effects meta‐analyses were used to estimate the combined risk of each outcome among studies. We reviewed 69 studies and included 42 studies in the meta‐analyses. In meta‐analyses, we found that a 10‐µg/m ³ increase in long‐term PM _2.5 exposure was associated with an increased risk of 23% for IHD mortality (95% CI, 15%–31%), 24% for cerebrovascular mortality (95% CI, 13%–36%), 13% for incident stroke (95% CI, 11%–15%), and 8% for incident myocardial infarction (95% CI, −1% to 18%). There were an insufficient number of studies of recurrent stroke and recurrent myocardial infarction to conduct meta‐analyses. Conclusions: Long‐term PM _2.5 exposure is associated with increased risks of IHD mortality, cerebrovascular mortality, and incident stroke. The relationship with incident myocardial infarction is suggestive of increased risk but not conclusive. More research is needed to understand the relationship with recurrent events.

A 2016 study reported a marked deceleration in the rate of decrease of heart disease (HD) mortality between January 1, 2011, and December 31, 2014, compared with the rate of decrease between January 1, 2000, and December 31, 2011,¹ and variability in this pattern by HD subtype.² This report examines the association between combined patterns of HD mortality subtypes and demographic changes in the population, especially the increase in the number of adults aged 65 years and older and the number of deaths associated with HD in the United States.

Low body mass index has been associated with increased mortality in severe COPD. The impact of body composition earlier in the disease remains unclear. We studied the impact of body composition on the risk of functional limitation in COPD. We used bioelectrical impedance to estimate body composition in a cohort of 355 younger adults with COPD who had a broad spectrum of severity. Among women, a higher lean-to-fat ratio was associated with a lower risk of self-reported functional limitation after controlling for age, height, pulmonary function impairment, race, education, and smoking history (OR 0.45 per 0.50 increment in lean-to-fat ratio; 95% CI 0.28 to 0.74). Among men, a higher lean-to-fat ratio was associated with a greater distance walked in 6 minutes (mean difference 40 meters per 0.50 ratio increment; 95% CI 9 to 71 meters). In women, the lean-to-fat ratio was associated with an even greater distance walked (mean difference 162 meters per 0.50 increment; 95% CI 97 to 228 meters). In women, higher lean-to-fat ratio was also associated with better Short Physical Performance Battery Scores. In further analysis, the accumulation of greater fat mass, and not the loss of lean mass, was most strongly associated with functional limitation among both sexes. Body composition is an important non-pulmonary impairment that modulates the risk of functional limitation in COPD, even after taking pulmonary function into account. Body composition abnormalities may represent an important area for screening and preventive intervention in COPD.

Some studies have linked long-term exposure to traffic related air pollutants (TRAP) with adverse cardiovascular health outcomes; however, previous studies have not linked highly variable concentrations of TRAP measured at street-level within neighborhoods to cardiovascular health outcomes. Long-term pollutant concentrations for nitrogen dioxide [NO2], nitric oxide [NO], and black carbon [BC] were obtained by street-level mobile monitoring on 30 m road segments and linked to residential addresses of 41,869 adults living in Oakland during 2010 to 2015. We fit Cox proportional hazard models to estimate the relationship between air pollution exposures and time to first cardiovascular event. Secondary analyses examined effect modification by diabetes and age. Long-term pollutant concentrations [mean, (standard deviation; SD)] for NO2, NO and BC were 9.9 ppb (SD 3.8), 4.9 ppb (SD 3.8), and 0.36 μg/m3 (0.17) respectively. A one SD increase in NO2, NO and BC, was associated with a change in risk of a cardiovascular event of 3% (95% confidence interval [CI] -6% to 12%), 3% (95% CI -5% to 12%), and − 1% (95% CI -8% to 7%), respectively. Among the elderly (≥65 yrs), we found an increased risk of a cardiovascular event of 12% for NO2 (95% CI: 2%, 24%), 12% for NO (95% CI: 3%, 22%), and 7% for BC (95% CI: -3%, 17%) per one SD increase. We found no effect modification by diabetes. Street-level differences in long-term exposure to TRAP were associated with higher risk of cardiovascular events among the elderly, indicating that within-neighborhood differences in TRAP are important to cardiovascular health. Associations among the general population were consistent with results found in previous studies, though not statistically significant.