Ambient particulate matter air pollution exposure and mortality in the NIH-AARP diet and health cohort

BACKGROUND: Outdoor fine particulate matter (≤ 2.5 μm; PM2.5) has been identified as a global health threat, but the number of large U.S. prospective cohort studies with individual participant data remains limited, especially at lower recent exposures. OBJECTIVES: We aimed to test the relationship between long-term exposure PM2.5 and death risk from all nonaccidental causes, cardiovascular (CVD), and respiratory diseases in 517,041 men and women enrolled in the National Institutes of Health-AARP cohort. METHODS: Individual participant data were linked with residence PM2.5 exposure estimates across the continental United States for a 2000–2009 follow-up period when matching census tract–level PM2.5 exposure data were available. Participants enrolled ranged from 50 to 71 years of age, residing in six U.S. states and two cities. Cox proportional hazard models yielded hazard ratio (HR) estimates per 10 μg/m3 of PM2.5 exposure. RESULTS: PM2.5 exposure was significantly associated with total mortality (HR = 1.03; 95% CI: 1.00, 1.05) and CVD mortality (HR = 1.10; 95% CI: 1.05, 1.15), but the association with respiratory mortality was not statistically significant (HR = 1.05; 95% CI: 0.98, 1.13). A significant association was found with respiratory mortality only among never smokers (HR = 1.27; 95% CI: 1.03, 1.56). Associations with 10-μg/m3 PM2.5 exposures in yearly participant residential annual mean, or in metropolitan area-wide mean, were consistent with baseline exposure model results. Associations with PM2.5 were similar when adjusted for ozone exposures. Analyses of California residents alone also yielded statistically significant PM2.5 mortality HRs for total and CVD mortality. CONCLUSIONS: Long-term exposure to PM2.5 air pollution was associated with an increased risk of total and CVD mortality, providing an independent test of the PM2.5–mortality relationship in a new large U.S. prospective cohort experiencing lower post-2000 PM2.5 exposure levels. CITATION: Thurston GD, Ahn J, Cromar KR, Shao Y, Reynolds HR, Jerrett M, Lim CC, Shanley R, Park Y, Hayes RB. 2016. Ambient particulate matter air pollution exposure and mortality in the NIH-AARP Diet and Health cohort. Environ Health Perspect 124:484–490; http://dx.doi.org/10.1289/ehp.150967

Obesity and Metabolic Syndrome Influences on the Risk of Air Pollution Related Asthma Hospital Admission

Background: Asthma is a growing epidemic in the U.S. Obesity, and more recently metabolic syndrome, has been shown to be associated with increased prevalence of asthma morbidity prevalence. Air pollution exposure, meanwhile, is associated with increased risk of acute asthma exacerbation. However, it is unclear the extent to which co-morbidities, specifically obesity and metabolic syndrome, increase the risk of air pollution related asthma morbidity. Methods: Data for 105,914 unscheduled asthma hospital admissions with a primary diagnosis of asthma in New York City (NYC) during 2003–2006, were obtained from the New York State Department of Health Statewide Planning and Research Cooperative Survey. Daily monitored pollutant concentrations from NYC-area monitors were averaged to determine daily exposure estimates for pollutants, including fine particulate matter (PM2.5), nitrogen dioxide (NO2), sulfur dioxide (SO2), and ozone (O3). A Poisson, generalized linear model was utilized to assess the association of these acute air pollution exposures with daily asthma hospital admissions among children (ages 1–17), adults (ages 18–64), and older adults (ages 65 and older). Analyses stratified by secondary diagnoses were then performed to determine whether obesity or metabolic syndrome co-morbid conditions modified the associations of air pollution and asthma hospital admissions in these age subpopulations. Results: Asthma hospital admissions among children, adults, and older adults were significantly associated with acute air pollutant exposures. Children with obesity had significantly higher risk ratios for asthma hospital admissions vs. children without obesity for associations with PM2.5 and NO2, especially among girls with obesity and during the warm season of the year. While the individual co-morbidities corresponding to metabolic syndrome (i.e., hypertension, diabetes, obesity, and hyperlipidemia) were not observed to significantly modify the associations of air pollutants and asthma hospital admissions, adults and older adults with multiple secondary diagnoses corresponding to metabolic syndrome had significantly higher risk ratios for asthma hospital admissions vs. those without metabolic syndrome. Conclusions: Obesity in children, and metabolic syndrome in adults, significantly increased the risk of air pollution related asthma hospital admissions in NYC. This information may enhance the consideration of susceptibility to air pollution in government policymaking, as well as inform physicians advising at-risk patients

Ambient Particulate Matter Air Pollution Exposure and Mortality in the NIH-AARP Diet and Health Cohort.

BackgroundOutdoor fine particulate matter (≤ 2.5 μm; PM2.5) has been identified as a global health threat, but the number of large U.S. prospective cohort studies with individual participant data remains limited, especially at lower recent exposures.ObjectivesWe aimed to test the relationship between long-term exposure PM2.5 and death risk from all nonaccidental causes, cardiovascular (CVD), and respiratory diseases in 517,041 men and women enrolled in the National Institutes of Health-AARP cohort.MethodsIndividual participant data were linked with residence PM2.5 exposure estimates across the continental United States for a 2000-2009 follow-up period when matching census tract-level PM2.5 exposure data were available. Participants enrolled ranged from 50 to 71 years of age, residing in six U.S. states and two cities. Cox proportional hazard models yielded hazard ratio (HR) estimates per 10 μg/m3 of PM2.5 exposure.ResultsPM2.5 exposure was significantly associated with total mortality (HR = 1.03; 95% CI: 1.00, 1.05) and CVD mortality (HR = 1.10; 95% CI: 1.05, 1.15), but the association with respiratory mortality was not statistically significant (HR = 1.05; 95% CI: 0.98, 1.13). A significant association was found with respiratory mortality only among never smokers (HR = 1.27; 95% CI: 1.03, 1.56). Associations with 10-μg/m3 PM2.5 exposures in yearly participant residential annual mean, or in metropolitan area-wide mean, were consistent with baseline exposure model results. Associations with PM2.5 were similar when adjusted for ozone exposures. Analyses of California residents alone also yielded statistically significant PM2.5 mortality HRs for total and CVD mortality.ConclusionsLong-term exposure to PM2.5 air pollution was associated with an increased risk of total and CVD mortality, providing an independent test of the PM2.5-mortality relationship in a new large U.S. prospective cohort experiencing lower post-2000 PM2.5 exposure levels.CitationThurston GD, Ahn J, Cromar KR, Shao Y, Reynolds HR, Jerrett M, Lim CC, Shanley R, Park Y, Hayes RB. 2016. Ambient particulate matter air pollution exposure and mortality in the NIH-AARP Diet and Health cohort. Environ Health Perspect 124:484-490; http://dx.doi.org/10.1289/ehp.1509676

Many Labs 4:Failure to replicate mortality salience effect with and without original author involvement

Interpreting a failure to replicate is complicated by the fact that the failure could be due to the original finding being a false positive, unrecognized moderating influences between the original and replication procedures, or faulty implementation of the procedures in the replication. One strategy to maximize replication quality is involving the original authors in study design. We (N = 21 Labs and N = 2,220 participants) experimentally tested whether original author involvement improved replicability of a classic finding from Terror Management Theory (Greenberg et al., 1994). Our results were non-diagnostic of whether original author involvement improves replicability because we were unable to replicate the finding under any conditions. This suggests that the original finding was either a false positive or the conditions necessary to obtain it are not yet understood or no longer exist. Data, materials, analysis code, preregistration, and supplementary documents can be found on the OSF page: https://osf.io/8ccnw