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BACKGROUND: Evidence for an association between transportation noise and cardiovascular disease has increased; however, few studies have examined metabolic outcomes such as diabetes or accounted for environmental coexposures such as air pollution, greenness, or walkability. OBJECTIVES: Because diabetes prevalence is increasing and may be on the causal pathway between noise and cardiovascular disease, we examined the influence of long-term residential transportation noise exposure and traffic-related air pollution on the incidence of diabetes using a populationbased cohort in British Columbia, Canada. METHODS: We examined the influence of transportation noise exposure over a 5-y period (1994-1998) on incident diabetes cases in a populationbased prospective cohort study (n=380,738) of metropolitan Vancouver (BC) residents who were 45-85 y old, with 4-y of follow-up (1999-2002). Annual average transportation noise (Lden), air pollution [black carbon, particulate matter with aerodynamic diameter <2:5 lm (PM2.5), nitrogen oxides], greenness [Normalized Difference Vegetation Index (NDVI)], and neighborhood walkability at each participant's residence were modeled. Incident diabetes cases were identified using administrative health records. RESULTS: Transportation noise was associated with the incidence of diabetes [interquartile range (IQR) increase, 6.8 A-weighted decibels (dBA); OR=1:08 (95% CI: 1.05, 1.10)]. This association remained after adjustment for environmental coexposures including traffic-related air pollutants, greenness, and neighborhood walkability. After adjustment for coexposure to noise, traffic-related air pollutants were not associated with the incidence of diabetes, whereas greenness was protective. CONCLUSION: We found a positive association between residential transportation noise and diabetes, adding to the growing body of evidence that noise pollution exposure may be independently linked to metabolic health and should be considered when developing public health interventions. [ABSTRACT FROM AUTHOR]

BACKGROUND: Chikungunya virus (CHIKV) is a reemerging pathogen transmitted by Aedes aegypti and Aedes albopictus mosquitoes. The ongoing Caribbean outbreak is of concern due to the potential for infected travelers to spread the virus to countries where vectors are present and the population is susceptible. Although there has been no autochthonous transmission of CHIKV in Canada, there is concern that both Ae. albopictus and CHIKV will become established, particularly under projected climate change. We developed risk maps for autochthonous CHIKV transmission in Canada under recent (1981-2010) and projected climate (2011-2040 and 2041-2070). METHODS: The risk for CHIKV transmission was the combination of the climatic suitability for CHIKV transmission potential and the climatic suitability for the presence of Ae. albopictus; the former was assessed using a stochastic model to calculate R0 and the latter was assessed by deriving a suitability indicator (SIG) that captures a set of climatic conditions known to influence the ecology of Ae. albopictus. R0 and SIG were calculated for each grid cell in Canada south of 60°N, for each time period and for two emission scenarios, and combined to produce overall risk categories that were mapped to identify areas suitable for transmission and the duration of transmissibility. FINDINGS: The risk for autochthonous CHIKV transmission under recent climate is very low with all of Canada classified as unsuitable or rather unsuitable for transmission. Small parts of southern coastal British Columbia become progressively suitable with short-term and long-term projected climate; the duration of potential transmission is limited to 1-2 months of the year. INTERPRETATION: Although the current risk for autochthonous CHIKV transmission in Canada is very low, our study could be further supported by the routine surveillance of Ae. albopictus in areas identified as potentially suitable for transmission given our uncertainty on the current distribution of this species in Canada. [ABSTRACT FROM AUTHOR]

BACKGROUND: Climate change has increased the frequency and intensity of extremely hot weather. The health risks associated with extemely hot weather are not uniform across affected areas owing to variability in heat exposure and social vulnerability, but these differences are challenging to map with precision. OBJECTIVES: We developed a spatially and temporally stratified case-crossover approach for delineation of areas with higher and lower risks of mortality on extremely hot days and applied this approach in greater Vancouver, Canada. METHODS: Records of all deaths with an extremely hot day as a case day or a control day were extracted from an administrative vital statistics database spanning the years of 1998 -- 2014. Three heat exposure and 11 social vulnerability variables were assigned at the residential location of each decedent. Conditional logistic regression was used to estimate the odds ratio for a 1°C increase in daily mean temperature at a fixed site with an interaction term for decedents living above and below different values of the spatial variables. RESULTS: The heat exposure and social vulnerability variables with the strongest spatially stratified results were the apparent temperature and the labor nonparticipation rate, respectively. Areas at higher risk had values ≥ 34.4°C for the maximum apparent temperature and ≥ 60% of the population neither employed nor looking for work. These variables were combined in a composite index to quantify their interaction and to enhance visualization of high-risk areas. CONCLUSIONS: Our methods provide a data-driven framework for spatial delineation of the temperature -- mortality relationship by heat exposure and social vulnerability. The results can be used to map and target the most vulnerable areas for public health intervention. CITATION: Ho HC, Knudby A, Walker BB, Henderson SB. 2017. Delineation of spatial variability in the temperature -- mortality relationship on extremely hot days in greater Vancouver, Canada. Environ Health Perspect 125:66-75; http://dx.doi.org/10.1289/EHP224 [ABSTRACT FROM AUTHOR]

Background: Half the world’s population lives in urban areas. It is therefore important to identify characteristics of the built environment that are beneficial to human health. Urban greenness has been associated with improvements in a diverse range of health conditions, including birth outcomes; however, few studies have attempted to distinguish potential effects of greenness from those of other spatially correlated exposures related to the built environment. Objectives: We aimed to investigate associations between residential greenness and birth outcomes and evaluate the influence of spatially correlated built environment factors on these associations. Methods: We examined associations between residential greenness [measured using satellite-derived Normalized Difference Vegetation Index (NDVI) within 100 m of study participants’ homes] and birth outcomes in a cohort of 64,705 singleton births (from 1999–2002) in Vancouver, British Columbia, Canada. We also evaluated associations after adjusting for spatially correlated built environmental factors that may influence birth outcomes, including exposure to air pollution and noise, neighborhood walkability, and distance to the nearest park. Results: An interquartile increase in greenness (0.1 in residential NDVI) was associated with higher term birth weight (20.6 g; 95% CI: 16.5, 24.7) and decreases in the likelihood of small for gestational age, very preterm (< 30 weeks), and moderately preterm (30–36 weeks) birth. Associations were robust to adjustment for air pollution and noise exposures, neighborhood walkability, and park proximity. Conclusions: Increased residential greenness was associated with beneficial birth outcomes in this population-based cohort. These associations did not change after adjusting for other spatially correlated built environment factors, suggesting that alternative pathways (e.g., psychosocial and psych [ABSTRACT FROM AUTHOR]

Background: The risk of rheumatoid arthritis (RA) has been associated with living near traffic; however, there is evidence suggesting that air pollution may not be responsible for this association. Noise, another traffic-generated exposure, has not been studied as a risk factor for RA. Objectives: We investigated proximity to traffic, ambient air pollution, and community noise in relation to RA in the Vancouver and Victoria regions of British Columbia, Canada. Methods: Cases and controls were identified in a cohort of adults that was assembled using health insurance registration records. Incident RA cases from 1999 through 2002 were identified by diagnostic codes in combination with prescriptions and type of physician (e.g., rheumatologist). Controls were matched to RA cases by age and sex. Environmental exposures were assigned to each member of the study population by their residential postal code(s). We estimated relative risks using conditional logistic regression, with additional adjustment for median income at the postal code. Results: RA incidence was increased with proximity to traffic, with an odds ratio (OR) of 1.37 (95% CI: 1.11, 1.68) for residence ≤ 50 m from a highway compared with residence > 150 m away. We found no association with traffic-related exposures such as PM2.5, nitrogen oxides, or noise. Ground-level ozone, which was highest in suburban areas, was associated with an increased risk of RA (OR = 1.26; 95% CI: 1.18, 1.36 per interquartile range increase). Conclusions: Our study confirms a previously observed association of RA risk with proximity to traffic and suggests that neither noise levels nor traffic-related air pollutants are responsible for this relationship. Additional investigation of neighborhood and individual correlates of residence near roadways may provide new insight into risk factors for RA. [ABSTRACT FROM AUTHOR]

Background: Exposure to wildfire smoke has been associated with cardiopulmonary health impacts. Climate change will increase the severity and frequency of smoke events, suggesting a need for enhanced public health protection. Forecasts of smoke exposure can facilitate public health responses. Objectives: We evaluated the utility of a wildfire smoke forecasting system (BlueSky) for public health protection by comparing its forecasts with observations and assessing their associations with population-level indicators of respiratory health in British Columbia, Canada. Methods: We compared BlueSky PM2.5 forecasts with PM2.5 measurements from air quality monitors, and BlueSky smoke plume forecasts with plume tracings from National Oceanic and Atmospheric Administration Hazard Mapping System remote sensing data. Daily counts of the asthma drug salbutamol sulfate dispensations and asthma-related physician visits were aggregated for each geographic local health area (LHA). Daily continuous measures of PM2.5 and binary mea­sures of smoke plume presence, either forecasted or observed, were assigned to each LHA. Poisson regression was used to estimate the association between exposure measures and health indicators. Results: We found modest agreement between forecasts and observations, which was improved during intense fire periods. A 30-μg/m3 increase in BlueSky PM2.5 was associated with an 8% increase in salbutamol dispensations and a 5% increase in asthma-related physician visits. BlueSky plume coverage was associated with 5% and 6% increases in the two health indicators, respectively. The effects were similar for observed smoke, and generally stronger in very smoky areas. Conclusions: BlueSky forecasts showed modest agreement with retrospective measures of smoke and were predictive of respiratory health indicators, suggesting they can provide useful information for public health protection. [ABSTRACT FROM AUTHOR]

Background: Adverse health effects associated with diesel exhaust (DE) are thought to be mediated in part by oxidative stress, but the detailed mechanisms are largely unknown. MicroRNAs (miRNAs) regulate gene expression post-transcriptionally and may respond to exposures such as DE. Objectives: We profiled peripheral blood cellular miRNAs in participants with mild asthma who were exposed to controlled DE with and without antioxidant supplementation. Methods: Thirteen participants with asthma underwent controlled inhalation of filtered air and DE in a double-blinded, randomized crossover study of three conditions: a) DE plus placebo (DEP), b) filtered air plus placebo (FAP), or c) DE with N-acetylcysteine supplementation (DEN). Total cellular RNA was extracted from blood drawn before exposure and 6 hr after exposure for miRNA profiling by the NanoString nCounter assay. MiRNAs significantly associated with DEP exposure and a predicted target [nuclear factor (erythroid-derived 2)-like 2 (NRF2)] as well as anti­oxidant enzyme genes were assessed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) for validation, and we also assessed the ability of N-acetylcysteine supplementation to block the effect of DE on these specific miRNAs. 8-hydroxy-2´-deoxyguanosine (8-OHdG) was measured in plasma as a systemic oxidative stress marker. Results: Expression of miR-21, miR-30e, miR-215, and miR-144 was significantly associated with DEP. The change in miR-144 was validated by RT-qPCR. NRF2 and its downstream antioxidant genes [glutamate cysteine ligase catalytic subunit (GCLC) and NAD(P)H:quinone oxidoreductase 1 (NQO1)] were negatively associated with miR-144 levels. Increases in miR-144 and miR-21 were associated with plasma 8-hydroxydeoxyguanosine 8-OHdG level and were blunted by antioxidant (i.e, DEN). Conclusions: Systemic miRNAs with plausible biological function are altered by acute moderate-dose DE exposure. Oxidative stress appears to mediate DE-associated changes in miR-144. [ABSTRACT FROM AUTHOR]