Factors Affecting Student Decisions to Attend Selected BGSU Athletics Events

The purpose of this study was to determine the factors that increase and decrease the likelihood that students at Bowling Green State University will attend selected athletics events. Students were randomly selected to participate in a survey that featured the sports of football, hockey, volleyball, men’s basketball, and women’s basketball. It was concluded that the type of sport, free student admission, and the skill level of the opponent were to top factors that encouraged students at Bowling Green State University to attend athletic events while the time and date of the event, weather, and importance of the game were the factors that students claimed had the greatest impact on their decisions not to attend a game

Variable-temperature, variable-field magnetic circular dichroism spectroscopic study of NifEN-bound precursor and “FeMoco”

NifEN plays a key role in the biosynthesis of the iron–molybdenum cofactor (FeMoco) of nitrogenase. A scaffold protein that hosts the conversion of a FeMoco precursor to a mature cofactor, NifEN can assume three conformations during the process of FeMoco maturation. One, designated ΔnifB NifEN, contains only two permanent [Fe4S4]-like clusters. The second, designated NifENPrecursor, contains the permanent clusters and a precursor form of FeMoco. The third, designated NifEN“FeMoco”, contains the permanent [Fe4S4]-like clusters and a fully complemented, “FeMoco”-like structure. Here, we report a variable-temperature, variable-field magnetic circular dichroism spectroscopic investigation of the electronic structure of the metal clusters in the three forms of dithionite-reduced NifEN. Our data indicate that the permanent [Fe4S4]-like clusters are structurally and electronically conserved in all three NifEN species and exhibit spectral features of classic [Fe4S4]+ clusters; however, they are present in a mixed spin state with a small contribution from the S > ½ spin state. Our results also suggest that both the precursor and “FeMoco” have a conserved Fe/S electronic structure that is similar to the electronic structure of FeMoco in the MoFe protein, and that the “FeMoco” in NifEN“FeMoco” exists, predominantly, in an S = 3/2 spin state with spectral parameters identical to those of FeMoco in the MoFe protein. These observations provide strong support to the outcome of our previous EPR and X-ray absorption spectroscopy/extended X-ray absorption fine structure analysis of the three NifEN species while providing significant new insights into the unique electronic properties of the precursor and “FeMoco” in NifEN

Global estimates of mortality associated with long-term exposure to outdoor fine particulate matter.

Exposure to ambient fine particulate matter (PM2.5) is a major global health concern. Quantitative estimates of attributable mortality are based on disease-specific hazard ratio models that incorporate risk information from multiple PM2.5 sources (outdoor and indoor air pollution from use of solid fuels and secondhand and active smoking), requiring assumptions about equivalent exposure and toxicity. We relax these contentious assumptions by constructing a PM2.5-mortality hazard ratio function based only on cohort studies of outdoor air pollution that covers the global exposure range. We modeled the shape of the association between PM2.5 and nonaccidental mortality using data from 41 cohorts from 16 countries-the Global Exposure Mortality Model (GEMM). We then constructed GEMMs for five specific causes of death examined by the global burden of disease (GBD). The GEMM predicts 8.9 million [95% confidence interval (CI): 7.5-10.3] deaths in 2015, a figure 30% larger than that predicted by the sum of deaths among the five specific causes (6.9; 95% CI: 4.9-8.5) and 120% larger than the risk function used in the GBD (4.0; 95% CI: 3.3-4.8). Differences between the GEMM and GBD risk functions are larger for a 20% reduction in concentrations, with the GEMM predicting 220% higher excess deaths. These results suggest that PM2.5 exposure may be related to additional causes of death than the five considered by the GBD and that incorporation of risk information from other, nonoutdoor, particle sources leads to underestimation of disease burden, especially at higher concentrations

Ambient PM₂.₅, O₃, and NO₂ Exposures and Associations with Mortality over 16 Years of Follow-Up in the Canadian Census Health and Environment Cohort (CanCHEC)

Background: Few studies examining the associations between long-term exposure to ambient air pollution and mortality have considered multiple pollutants when assessing changes in exposure due to residential mobility during follow-up. Objective: We investigated associations between cause-specific mortality and ambient concentrations of fine particulate matter (≤ 2.5 μm; PM₂.₅), ozone (O₃), and nitrogen dioxide (NO₂) in a national cohort of about 2.5 million Canadians. Methods: We assigned estimates of annual concentrations of these pollutants to the residential postal codes of subjects for each year during 16 years of follow-up. Historical tax data allowed us to track subjects’ residential postal code annually. We estimated hazard ratios (HRs) for each pollutant separately and adjusted for the other pollutants. We also estimated the product of the three HRs as a measure of the cumulative association with mortality for several causes of death for an increment of the mean minus the 5th percentile of each pollutant: 5.0 μg/m³ for PM₂.₅, 9.5 ppb for O₃, and 8.1 ppb for NO₂. Results: PM₂.₅, O₃, and NO₂ were associated with nonaccidental and cause-specific mortality in single-pollutant models. Exposure to PM₂.₅ alone was not sufficient to fully characterize the toxicity of the atmospheric mix or to fully explain the risk of mortality associated with exposure to ambient pollution. Assuming additive associations, the estimated HR for nonaccidental mortality corresponding to a change in exposure from the mean to the 5th percentile for all three pollutants together was 1.075 (95% CI: 1.067, 1.084). Accounting for residential mobility had only a limited impact on the association between mortality and PM₂.₅ and O₃, but increased associations with NO₂. Conclusions: In this large, national-level cohort, we found positive associations between several common causes of death and exposure to PM₂.₅, O₃, and NO₂

Oxidative burden of fine particulate air pollution and risk of cause-specific mortality in the Canadian Census Health and Environment Cohort (CanCHEC)

Background: Fine particulate air pollution (PM2.5) is known to contribute to cardiorespiratory mortality but it is not clear how PM2.5 oxidative burden (i.e. the ability of PM2.5 to cause oxidative stress) may influence long-term mortality risk. Methods: We examined the relationship between PM2.5 oxidative burden and cause-specific mortality in Ontario, Canada. Integrated PM2.5 samples were collected from 30 provincial monitoring sites between 2012 and 2013. The oxidative potential (% depletion/µg) of regional PM2.5 was measured as the ability of filter extracts to deplete antioxidants (glutathione and ascorbate) in a synthetic respiratory tract lining fluid. PM2.5 oxidative burden was calculated as the product of PM2.5 mass concentrations and regional estimates of oxidative potential. In total, this study included 193,300 people who completed the Canadian long-form census in 1991 and who lived within 5 km of a site where oxidative potential was measured. Deaths occurring between 1991 and 2009 were identified through record linkages and Cox proportional hazard models were used to estimate hazard ratios (and 95% confidence intervals) for interquartile changes in exposure adjusting for individual-level covariates and indirect-adjustment for smoking and obesity. Results: Glutathione-related oxidative burden was associated with cause-specific mortality. For lung cancer specifically, this metric was associated with a 12% (95% CI: 5.0–19) increased risk of mortality whereas a 5.0% (95% CI: 0.1, 10) increase was observed for PM2.5. Indirect adjustment for smoking and obesity decreased the lung cancer hazard ratio for glutathione-related oxidative burden but it remained significantly elevated (HR=1.07, 95% CI: 1.005, 1.146). Ascorbate-related oxidative burden was not associated with mortality. Conclusions: Our findings suggest that glutathione-related oxidative burden may be more strongly associated with lung cancer mortality than PM2.5 mass concentrations.We would like to thank Farhan Mansoor for conducting the oxidative burden analysis and Christie McMann, Tim Shin, and Hongyu You for their help in compiling oxidative burden data. We would also like to thank Luc White (Environment Canada) and the Ontario Ministry of the Environment and Climate Change for their help in collecting PM2.5 filters for oxidative burden analyses. This work was funded by Health Canada

Low concentrations of fine particle air pollution and mortality in the Canadian Community Health Survey cohort

Background: Approximately 2.9 million deaths are attributed to ambient fine particle air pollution around the world each year (PM₂.₅). In general, cohort studies of mortality and outdoor PM₂.₅ concentrations have limited information on individuals exposed to low levels of PM₂.₅ as well as covariates such as smoking behaviours, alcohol consumption, and diet which may confound relationships with mortality. This study provides an updated and extended analysis of the Canadian Community Health Survey-Mortality cohort: a population-based cohort with detailed PM₂.₅ exposure data and information on a number of important individual-level behavioural risk factors. We also used this rich dataset to provide insight into the shape of the concentration-response curve for mortality at low levels of PM₂.₅. Methods: Respondents to the Canadian Community Health Survey from 2000 to 2012 were linked by postal code history from 1981 to 2016 to high resolution PM₂.₅ exposure estimates, and mortality incidence to 2016. Cox proportional hazard models were used to estimate the relationship between non-accidental mortality and ambient PM₂.₅ concentrations (measured as a three-year average with a one-year lag) adjusted for socio-economic, behavioural, and time-varying contextual covariates. Results: In total, 50,700 deaths from non-accidental causes occurred in the cohort over the follow-up period. Annual average ambient PM2.5 concentrations were low (i.e. 5.9 μg/m³, s.d. 2.0) and each 10 μg/m³ increase in exposure was associated with an increase in non-accidental mortality (HR = 1.11; 95% CI 1.04–1.18). Adjustment for behavioural covariates did not materially change this relationship. We estimated a supra-linear concentration-response curve extending to concentrations below 2 μg/m³ using a shape constrained health impact function. Mortality risks associated with exposure to PM₂.₅ were increased for males, those under age 65, and non-immigrants. Hazard ratios for PM₂.₅ and mortality were attenuated when gaseous pollutants were included in models. Conclusions: Outdoor PM₂.₅ concentrations were associated with non-accidental mortality and adjusting for individual-level behavioural covariates did not materially change this relationship. The concentration-response curve was supra-linear with increased mortality risks extending to low outdoor PM₂.₅ concentrations.Medicine, Faculty ofNon UBCPopulation and Public Health (SPPH), School ofReviewedFacult

Urban greenness and mortality in Canada's largest cities: a national cohort study

Background: Findings from published studies suggest that exposure to and interactions with green spaces are associated with improved psychological wellbeing and have cognitive, physiological, and social benefits, but few studies have examined their potential effect on the risk of mortality. We therefore undertook a national study in Canada to examine associations between urban greenness and cause-specific mortality. Methods: We used data from a large cohort study (the 2001 Canadian Census Health and Environment Cohort [2001 CanCHEC]), which consisted of approximately 1·3 million adult (aged ≥19 years), non-immigrant, urban Canadians in 30 cities who responded to the mandatory 2001 Statistics Canada long-form census. The cohort has been linked by Statistics Canada to the Canadian mortality database and to annual income tax filings through 2011. We measured greenness with images from the moderate-resolution imaging spectroradiometer from NASA's Aqua satellite. We assigned estimates of exposure to greenness derived from remotely sensed Normalized Difference Vegetation Index (NDVI) within both 250 m and 500 m of participants' residences for each year during 11 years of follow-up (between 2001 and 2011). We used Cox proportional hazards models to estimate associations between residential greenness (as a continuous variable) and mortality. We estimated hazard ratios (HRs) and corresponding 95% CIs per IQR (0·15) increase in NDVI adjusted for personal (eg, education and income) and contextual covariates, including exposures to fine particulate matter, ozone, and nitrogen dioxide. We also considered effect modification by selected personal covariates (age, sex, household income adequacy quintiles, highest level of education, and marital status). Findings: Our cohort consisted of approximately 1 265 000 individuals at baseline who contributed 11 523 770 person-years. We showed significant decreased risks of mortality in the range of 8–12% from all causes of death examined with increased greenness around participants' residence. In the fully adjusted analyses, the risk was significantly decreased for all causes of death (non-accidental HR 0·915, 95% CI 0·905–0·924; cardiovascular plus diabetes 0·911, 0·895–0·928; cardiovascular 0·911, 0·894–0·928; ischaemic heart disease 0·904, 0·882–0·927; cerebrovascular 0·942, 0·902–0·983; and respiratory 0·899, 0·869–0·930). Greenness associations were more protective among men than women (HR 0·880, 95% CI 0·868–0·893 vs 0·955, 0·941–0·969), and among individuals with higher incomes (highest quintile 0·812, 0·791–0·834 vs lowest quintile 0·991, 0·972–1·011) and more education (degree or more 0·816, 0·791–0·842 vs did not complete high school 0·964, 0·950–0·978). Interpretation: Increased amounts of residential greenness were associated with reduced risks of dying from several common causes of death among urban Canadians. We identified evidence of inequalities, both in terms of exposures to greenness and mortality risks, by personal socioeconomic status among individuals living in generally similar environments, and with reasonably similar access to health care and other social services. The findings support the development of policies related to creating greener and healthier cities. Funding: None

Ambient PM2.5, O₃, and NO₂ Exposures and Associations with Mortality over 16 Years of Follow-Up in the Canadian Census Health and Environment Cohort (CanCHEC).

BackgroundFew studies examining the associations between long-term exposure to ambient air pollution and mortality have considered multiple pollutants when assessing changes in exposure due to residential mobility during follow-up.ObjectiveWe investigated associations between cause-specific mortality and ambient concentrations of fine particulate matter (≤ 2.5 μm; PM2.5), ozone (O3), and nitrogen dioxide (NO2) in a national cohort of about 2.5 million Canadians.MethodsWe assigned estimates of annual concentrations of these pollutants to the residential postal codes of subjects for each year during 16 years of follow-up. Historical tax data allowed us to track subjects' residential postal code annually. We estimated hazard ratios (HRs) for each pollutant separately and adjusted for the other pollutants. We also estimated the product of the three HRs as a measure of the cumulative association with mortality for several causes of death for an increment of the mean minus the 5th percentile of each pollutant: 5.0 μg/m3 for PM2.5, 9.5 ppb for O3, and 8.1 ppb for NO2.ResultsPM2.5, O3, and NO2 were associated with nonaccidental and cause-specific mortality in single-pollutant models. Exposure to PM2.5 alone was not sufficient to fully characterize the toxicity of the atmospheric mix or to fully explain the risk of mortality associated with exposure to ambient pollution. Assuming additive associations, the estimated HR for nonaccidental mortality corresponding to a change in exposure from the mean to the 5th percentile for all three pollutants together was 1.075 (95% CI: 1.067, 1.084). Accounting for residential mobility had only a limited impact on the association between mortality and PM2.5 and O3, but increased associations with NO2.ConclusionsIn this large, national-level cohort, we found positive associations between several common causes of death and exposure to PM2.5, O3, and NO2.CitationCrouse DL, Peters PA, Hystad P, Brook JR, van Donkelaar A, Martin RV, Villeneuve PJ, Jerrett M, Goldberg MS, Pope CA III, Brauer M, Brook RD, Robichaud A, Menard R, Burnett RT. 2015. Ambient PM2.5, O3, and NO2 exposures and associations with mortality over 16 years of follow-up in the Canadian Census Health and Environment Cohort (CanCHEC). Environ Health Perspect 123:1180-1186; http://dx.doi.org/10.1289/ehp.1409276

HystadPerryPublicHealthHumanSciAmbientPM2.5NO2Exposures(SupplementalMaterial).pdf

Background: Few studies examining the associations between long-term exposure to ambient air pollution and mortality have considered multiple pollutants when assessing changes in exposure due to residential mobility during follow-up. Objective: We investigated associations between cause-specific mortality and ambient concentrations of fine particulate matter (≤ 2.5 μm; PM₂.₅), ozone (O₃), and nitrogen dioxide (NO₂) in a national cohort of about 2.5 million Canadians. Methods: We assigned estimates of annual concentrations of these pollutants to the residential postal codes of subjects for each year during 16 years of follow-up. Historical tax data allowed us to track subjects’ residential postal code annually. We estimated hazard ratios (HRs) for each pollutant separately and adjusted for the other pollutants. We also estimated the product of the three HRs as a measure of the cumulative association with mortality for several causes of death for an increment of the mean minus the 5th percentile of each pollutant: 5.0 μg/m³ for PM₂.₅, 9.5 ppb for O₃, and 8.1 ppb for NO₂. Results: PM₂.₅, O₃, and NO₂ were associated with nonaccidental and cause-specific mortality in single-pollutant models. Exposure to PM₂.₅ alone was not sufficient to fully characterize the toxicity of the atmospheric mix or to fully explain the risk of mortality associated with exposure to ambient pollution. Assuming additive associations, the estimated HR for nonaccidental mortality corresponding to a change in exposure from the mean to the 5th percentile for all three pollutants together was 1.075 (95% CI: 1.067, 1.084). Accounting for residential mobility had only a limited impact on the association between mortality and PM₂.₅ and O₃, but increased associations with NO₂. Conclusions: In this large, national-level cohort, we found positive associations between several common causes of death and exposure to PM₂.₅, O₃, and NO₂

HystadPerryPublicHealthHumanSciAmbientPM2.5NO2Exposures.pdf

Background: Few studies examining the associations between long-term exposure to ambient air pollution and mortality have considered multiple pollutants when assessing changes in exposure due to residential mobility during follow-up. Objective: We investigated associations between cause-specific mortality and ambient concentrations of fine particulate matter (≤ 2.5 μm; PM₂.₅), ozone (O₃), and nitrogen dioxide (NO₂) in a national cohort of about 2.5 million Canadians. Methods: We assigned estimates of annual concentrations of these pollutants to the residential postal codes of subjects for each year during 16 years of follow-up. Historical tax data allowed us to track subjects’ residential postal code annually. We estimated hazard ratios (HRs) for each pollutant separately and adjusted for the other pollutants. We also estimated the product of the three HRs as a measure of the cumulative association with mortality for several causes of death for an increment of the mean minus the 5th percentile of each pollutant: 5.0 μg/m³ for PM₂.₅, 9.5 ppb for O₃, and 8.1 ppb for NO₂. Results: PM₂.₅, O₃, and NO₂ were associated with nonaccidental and cause-specific mortality in single-pollutant models. Exposure to PM₂.₅ alone was not sufficient to fully characterize the toxicity of the atmospheric mix or to fully explain the risk of mortality associated with exposure to ambient pollution. Assuming additive associations, the estimated HR for nonaccidental mortality corresponding to a change in exposure from the mean to the 5th percentile for all three pollutants together was 1.075 (95% CI: 1.067, 1.084). Accounting for residential mobility had only a limited impact on the association between mortality and PM₂.₅ and O₃, but increased associations with NO₂. Conclusions: In this large, national-level cohort, we found positive associations between several common causes of death and exposure to PM₂.₅, O₃, and NO₂