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ObjectivesTo investigate the dose–response association of aerobic physical activity (PA) and muscle-strengthening exercise (MSE) with all-cause mortality.MethodsNational Health Interview Survey data (1997–2014) were linked to the National Death Index through 2015, which produced a cohort of 416 420 US adults. Cox proportional-hazard models were used to estimate HRs and 95% CIs for the associations of moderate aerobic PA (MPA), vigorous aerobic PA (VPA) and MSE with mortality risk. Models controlled for age, sex, race-ethnicity, income, education, marital status, survey year, smoking status, body mass index and chronic conditions.ResultsRelative to those who engaged in no aerobic PA, substantial mortality risk reduction was associated with 1 hour/week of aerobic PA (HR: 0.85, 95% CI: 0.83 to 0.86) and levelled off at 3 hours/week of aerobic PA (0.73, 0.71 to 0.75). Similar results were observed for men and women and for individuals younger and older than 60 years. MSE conferred additional mortality risk reduction at 1 time/week (0.89, 0.81 to 0.97) and appeared no longer beneficial at 7 times/week (0.99, 0.94 to 1.04).ConclusionThe minimum effective dose of aerobic PA for significant mortality risk reduction was 1 hour/week of MPA or VPA, with additional mortality risk reduction observed up to 3 hours/week. For older adults, only small decreases in mortality risk were observed beyond this duration. Completing MSE in combination with aerobic PA conferred additional mortality risk reduction, with a minimum effective dose of 1–2 times/week.

Background Several studies suggest that living in areas of high surrounding greenness may be associated with a lower cardiopulmonary mortality risk. However, associations of greenness with specific causes of death in cancer patients and survivors has not been examined and it is unknown whether this relationship is affected by area levels of fine particulate matter air pollution (PM2.5). This study evaluated associations between greenness and PM2.5 on causes of death in a large, U.S.-based cohort of cancer patients and survivors. Methods Surveillance, Epidemiology and End Results (SEER) data were used to generate a cohort of 5,529,005 cancer patients and survivors from 2000 to 2016. Census-tract Normalized Difference Vegetation Index (NDVI) during May-October from 2003 to 2016 was population-weighted to act as a county-level greenness measure. County-level PM2.5 exposure was estimated from annual concentrations averaged from 1999 to 2015. Cox Proportional Hazards models were used to estimate the association between greenness, PM2.5, and cause-specific mortality while controlling for age, sex, race, and other individual and county level variables. Findings An IQR increase in greenness was associated with a decrease in cancer mortality for cancer patients (Hazard ratio of 0.94, 95% CI: 0.93–0.95), but not for cardiopulmonary mortality (0.98, 95% CI: 0.96–1.00). Inversely, an increase in 10 μg/m3 PM2.5 was associated with increased cardiopulmonary mortality (1.24, 95% CI: 1.19–1.29), but not cancer mortality (0.99, 95% CI: 0.97–1.00). Hazard ratios were robust to inclusion of PM2.5 in models with greenness and vice versa. Although exposure estimates were constant over most stratifications, greenness seemed to benefit individuals diagnosed with high survivability cancers (0.92, 95% CI: 0.90–0.95) more than those with low survivability cancers (0.98. 95% CI: 0.96–0.99). Interpretation Higher levels of greenness are associated with lower cancer mortality in cancer patients. The evidence suggests minimal confounding between greenness and PM2.5 exposures and risk of mortality.

Several cohort studies suggest greenness is associated with decreased mortality risk. Potential confounding by or interactions between physical activity and air pollution remains unclear. This study evaluates associations of greenness, air pollution, and physical activity with mortality risk and investigates confounding and effect modification across these key risk factors. National Health Interview Survey (NHIS) data covering 1997–2014 were linked to the National Death Index to generate a cohort of 403,748 individuals with 39,528 deaths. Greenness, represented by census-tract Normalized Difference Vegetation Index (NDVI) for the seasonal period of May-October, was averaged over the years 2003–2016. Air pollution was estimated by census-tract level PM(2.5) concentrations from 1999–2015. Cox Proportional Hazard Models were used to estimate hazard ratios (HR) for differences in greenness, air pollution, and physical activity. Alternative models that evaluated potential confounding and stratified models that evaluated effect modification were examined. Mortality risks were associated with PM(2.5) (HR = 1.14, 95% CI: 1.09–1.19 per 10 μg/m(3)) and physical inactivity (1.49, 1.44–1.54 relative to sufficiently active), but not with greenness (1.01, 0.99–1.03 per IQR). The PM(2.5)-mortality association was mitigated at high levels of greenness (1.05, 0.91–1.22). There was no strong evidence of confounding between air pollution, physical activity, and greenness. However, stratified analysis suggested effect modification for PM(2.5) and NDVI by physical activity. A significant protective greenness-mortality association was observed for only highly active individuals (0.91, 0.86–0.96). Also, relatively high PM(2.5)-mortality HRs were observed for more physically active individuals (1.25, 1.12–1.40). PM(2.5) air pollution and physical inactivity are robustly associated with mortality risk. Greenness may be most beneficial and air pollution relatively harmful to highly active individuals. This analysis provides evidence that, in addition to not smoking, being physically active and living in a clean, green environment contributes to improved health and reduced risk of mortality.

The purpose of this study was to estimate cardiopulmonary mortality associations for long-term exposure to PM2.5 species and sources (i.e., components) within the U.S. National Health Interview Survey cohort. Exposures were estimated through a chemical transport model for six species (i.e., elemental carbon [EC], primary organic aerosols [POA], secondary organic aerosols [SOA], sulfate [SO4], ammonium [NO3], nitrate [NH4]) and five sources of PM2.5 (i.e., vehicles, electricity generating units [EGU], non-EGU industrial sources, biogenic sources [bio], “other” sources). In single-pollutant models, we found positive, significant (p < 0.05) mortality associations for all components, except POA. After adjusting for remaining PM2.5 (total PM2.5 minus component), we found significant mortality associations for EC (hazard ratio [HR] = 1.36; 95% CI: [1.12, 1.64]), SOA (HR = 1.11; 95% CI: [1.05, 1.17]), and vehicle sources (HR = 1.06; 95% CI: [1.03, 1.10]). HRs for EC, SOA, and vehicle sources were significantly larger than for remaining PM2.5 (per unit μg/m3). Our findings suggest that cardiopulmonary mortality associations vary by species and source, with evidence that EC, SOA, and vehicle sources are important contributors to the PM2.5 mortality relationship. With further validation, these findings could facilitate targeted pollution regulations that more efficiently reduce air pollution mortality., Cardiopulmonary Mortality and Fine Particulate Air Pollution by Species and Source in a National U.S. Cohort Zachari A. Pond, Carlos S. Hernandez, Peter J. Adams, Spyros N. Pandis, George R. Garcia, Allen L. Robinson, Julian D. Marshall, Richard Burnett, Ksakousti Skyllakou, Pablo Garcia Rivera, Eleni Karnezi, Carver J. Coleman, and C. Arden Pope III Environmental Science & Technology 2022 56 (11), 7214-7223 DOI: 10.1021/acs.est.1c04176

We use newly digitized individual-level death certificate data with detailed information on the location, date and cause of death to investigate the effects of city-level non-pharmaceutical interventions (NPIs) on mortality during the 1918 influenza pandemic. We collect information on the timing and nature of NPIs for cities in Ohio and Massachusetts with populations over 25,000 and focus on four cities that did not adopt any NPIs during the height of the pandemic. Using a synthetic control design to compare death rates in these cities with a composite of other similar cities who did implement NPIs, we find that the pneumonia and influenza (P&I) death rate was more than twice as high during the fall of 1918 in the no-intervention cities as in the comparison cities.