The Relationships between Fitness Assessments, Fitness Levels and Coronary Heart Disease Risk Markers in Police Officers

Given the physical nature of a position in law enforcement, the assessment of cardiovascular (CV) health as well as muscular strength and endurance is paramount to ensuring the safety of these personnel and the citizens they serve. The present study retrospectively examined correlations between several markers of CV and muscular fitness for 65 local police officers (8 female, average age 35.6 ± 9.0 yrs, height 70.5 ± 2.8 in, weight 91.8 ± 18.7 kg, VO2 33.0 ± 5.3 mL/kg/min) taken from their annual screening including a graded exercise test (GXT; Bruce protocol), pushups completed in 1 minute, situps completed in 1 minute, handgrip strength, body composition (through DEXA and circumference measures) and bloodwork. Maximal oxygen uptake (VO2max) was estimated using the Foster equation. Coronary heart disease risk (CHD risk) was calculated using the online NIH 10-year heart attack risk calculator, which uses age, gender, total cholesterol, HDL cholesterol, smoking status, and blood pressure status in its algorithm. Significance was determined using an alpha level of 0.05. Interestingly, there was no significant correlation between VO2max and CHD risk (p = 0.1851). Apart from risk markers included in the risk calculation, CHD risk was significantly correlated with waist-hip ratio (r = 0.24739), and LDL cholesterol (r = 0.39117). VO2max was significantly negatively correlated with fat mass (r = -0.51849), body fat percentage (%BF; r = -0.64297), total cholesterol (TC; r = -0.3371), and LDL cholesterol (r = -0.267). Positive correlations were found between VO2max and other measures of fitness such as pushups (r = 0.54274), situps (r = 0.3282), and handgrip strength (r = 0.32041). As for body composition measures, %BF was significantly positively correlated with TC (r = 0.30188), systolic blood pressure (r = 0.28795), LDL cholesterol (r = 0.26533), and fasting glucose (r = 0.26536), but negatively correlated with fitness markers such as pushups (r = -0.58599), situps (r = -0.43604), and handgrip strength (r = -0.32393). Lean mass was significantly correlated with handgrip strength (r = 0.71835), though not pushups, situps or VO2max. Waist circumference was significantly negatively correlated with HDL cholesterol (r = -0.39202). Additionally, 62 of the participants (7 female) completed both a 1.5 mile run and GXT, allowing for a comparison of a submaximal to a maximal fitness assessment of CV fitness. Time to complete 1.5 miles was significantly correlated to GXT VO2max, with a Pearson correlation coefficient of -0.79593. Overall, relationships found between health markers, fitness, and CHD risk in this sample were in line with previous research on CHD risk factors and the assessment of CV and muscular fitness

Complex relationships between greenness, air pollution, and mortality in a population-based Canadian cohort

Background: Epidemiological studies have consistently demonstrated that exposure to fine particulate matter (PM 2.5 )is associated with increased risks of mortality. To a lesser extent, a series of studies suggest that living in greener areas is associated with reduced risks of mortality. Only a handful of studies have examined the interplay between PM 2.5 , greenness, and mortality. Methods: We investigated the role of residential greenness in modifying associations between long-term exposures to PM 2.5 and non-accidental and cardiovascular mortality in a national cohort of non-immigrant Canadian adults (i.e., the 2001 Canadian Census Health and Environment Cohort). Specifically, we examined associations between satellite-derived estimates of PM 2.5 exposure and mortality across quintiles of greenness measured within 500 m of individual's place of residence during 11 years of follow-up. We adjusted our survival models for many personal and contextual measures of socioeconomic position, and residential mobility data allowed us to characterize annual changes in exposures. Results: Our cohort included approximately 2.4 million individuals at baseline, 194,270 of whom died from non-accidental causes during follow-up. Adjustment for greenness attenuated the association between PM 2.5 and mortality (e.g., hazard ratios (HRs)and 95% confidence intervals (CIs)per interquartile range increase in PM 2.5 in models for non-accidental mortality decreased from 1.065 (95% CI: 1.056–1.075)to 1.041 (95% CI: 1.031–1.050)). The strength of observed associations between PM 2.5 and mortality decreased as greenness increased. This pattern persisted in models restricted to urban residents, in models that considered the combined oxidant capacity of ozone and nitrogen dioxide, and within neighbourhoods characterised by high or low deprivation. We found no increased risk of mortality associated with PM 2.5 among those living in the greenest areas. For example, the HR for cardiovascular mortality among individuals in the least green areas was 1.17 (95% CI: 1.12–1.23)compared to 1.01 (95% CI: 0.97–1.06)among those in the greenest areas. Conclusions: Studies that do not account for greenness may overstate the air pollution impacts on mortality. Residents in deprived neighbourhoods with high greenness benefitted by having more attenuated associations between PM 2.5 and mortality than those living in deprived areas with less greenness. The findings from this study extend our understanding of how living in greener areas may lead to improved health outcomes

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

Risk estimates of mortality attributed to low concentrations of ambient fine particulate matter in the Canadian community health survey cohort

Background: Understanding the shape of the relationship between long-term exposure to ambient fine particulate matter (PM₂.₅) concentrations and health risks is critical for health impact and risk assessment. Studies evaluating the health risks of exposure to low concentrations of PM₂.₅ are limited. Further, many existing studies lack individual-level information on potentially important behavioural confounding factors. Methods: A prospective cohort study was conducted among a subset of participants in a cohort that linked respondents of the Canadian Community Health Survey to mortality (n = 299,500) with satellite-derived ambient PM₂.₅ estimates. Participants enrolled between 2000 and 2008 were followed to date of death or December 31, 2011. Cox proportional hazards models were used to estimate hazard ratios (HRs) for mortality attributed to PM₂.₅ exposure, adjusted for individual-level and contextual covariates, including smoking behaviour and body mass index (BMI). Results: Approximately 26,300 non-accidental deaths, of which 32.5 % were due to circulatory disease and 9.1 % were due to respiratory disease, occurred during the follow-up period. Ambient PM₂.₅ exposures were relatively low (mean = 6.3 μg/m³), yet each 10 μg/m³ increase in exposure was associated with increased risks of non-accidental (HR = 1.26; 95 % CI: 1.19-1.34), circulatory disease (HR = 1.19; 95 % CI: 1.07–1.31), and respiratory disease mortality (HR = 1.52; 95 % CI: 1.26–1.84) in fully adjusted models. Higher hazard ratios were observed for respiratory mortality among respondents who never smoked (HR = 1.97; 95 % CI: 1.24–3.13 vs. HR = 1.45; 95 % CI: 1.17–1.79 for ever smokers), and among obese (BMI ≥ 30) respondents (HR = 1.76; 95 % CI: 1.15-2.69 vs. HR = 1.41; 95 % CI: 1.04–1.91 for normal weight respondents), though differences between groups were not statistically significant. A threshold analysis for non-accidental mortality estimated a threshold concentration of 0 μg/m³ (+95 % CI = 4.5 μg/m³). Conclusions: Increased risks of non-accidental, circulatory, and respiratory mortality were observed even at very low concentrations of ambient PM₂.₅. HRs were generally greater than most literature values, and adjusting for behavioural covariates served to reduce HR estimates slightly.Medicine, Faculty ofNon UBCPopulation and Public Health (SPPH), School ofReviewedFacultyResearcherOthe

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

Additional file 2: Table S1. of Risk estimates of mortality attributed to low concentrations of ambient fine particulate matter in the Canadian community health survey cohort

Comparison of all variables (Pearson's correlation or ANOVA/T-Test). (XLSX 22 kb

Additional file 1:Figure S1. of Risk estimates of mortality attributed to low concentrations of ambient fine particulate matter in the Canadian community health survey cohort

Selection of Study Cohort.(PDF 88 kb