Acute cardiovascular health effects in a panel study of personal exposure to traffic-related air pollutants and noise in Toronto, Canada
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ABSTRACT:
SUBMITTER: Biel R
PROVIDER: S-EPMC7541521 | biostudies-literature | 2020 Jan
REPOSITORIES: biostudies-literature
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Project description:Traffic-related air pollution (TRAP) is increasing worldwide. Habitual physical activity is known to prevent cardiorespiratory diseases and mortality, but whether exposure to TRAP during exercise affects respiratory health is still uncertain. Exercise causes inflammatory changes in the airways, and its interaction with the effects of TRAP or ozone might be detrimental, for both athletes exercising outdoor and urban active commuters. In this Mini-Review, we summarize the literature on the effects of exposure to TRAP and/or ozone during exercise on lung function, respiratory symptoms, performance, and biomarkers. Ozone negatively affected pulmonary function after exercise, especially after combined exposure to ozone and diesel exhaust (DE). Spirometric changes after exercise during exposure to particulate matter and ultrafine particles suggest a decrease in lung function, especially in patients with chronic obstructive pulmonary disease. Ozone frequently caused respiratory symptoms during exercise. Women showed decreased exercise performance and higher symptom prevalence than men during TRAP exposure. However, performance was analyzed in few studies. To date, research has not identified reliable biomarkers of TRAP-related lung damage useful for monitoring athletes' health, except in scarce studies on airway cells obtained by induced sputum or bronchoalveolar lavage. In conclusion, despite partly counteracted by the positive effects of habitual exercise, the negative effects of TRAP exposure to pollutants during exercise are hard to assess: outdoor exercise is a complex model, for multiple and variable exposures to air pollutants and pollutant concentrations. Further studies are needed to identify pollutant and/or time thresholds for performing safe outdoor exercise in cities.
| S-EPMC7793908 | biostudies-literature
Project description:BackgroundEpidemiological evidence for the association between traffic-related noise and the incidence of major cardiovascular events such as acute myocardial infarction (AMI) and congestive heart failure (CHF) is inconclusive, especially in North America.ObjectivesWe evaluated the associations between long-term exposure to road traffic noise and the incidence of AMI and CHF.MethodsOur study population comprised ∼1 million people 30-100 years of age who lived in Toronto, Canada, from 2001 to 2015 and were free of AMI (referred to as the AMI cohort) or CHF (the CHF cohort) at baseline. Outcomes were ascertained from health administrative databases using validated algorithms. Annual average noise levels were estimated as the A-weighted equivalent sound pressure level over the 24-h period (LAeq24) and during nighttime (LAeqNight), respectively, using propagation modeling, and assigned to participants' annual six-digit postal code addresses during follow-up. We calculated hazard ratios (HRs) and 95% confidence intervals (CIs) for incident AMI and CHF in relation to LAeq24 and LAeqNight using random-effects Cox proportional hazards models adjusting for individual- and census tract-level covariates, including traffic-related air pollutants [e.g., ultrafine particles (UFPs) and nitrogen dioxide].ResultsDuring follow-up, there were 37,441 AMI incident cases and 95,138 CHF incident cases. Each interquartile range change in LAeq24 was associated with an increased risk of incident AMI (HR=1.07; 95% CI: 1.06, 1.08) and CHF (HR=1.07; 95% CI: 1.06, 1.09). Similarly, LAeqNight was associated with incident AMI (HR=1.07; 95% CI: 1.05, 1.08) and CHF (HR=1.06; 95% CI: 1.05, 1.07). These results were robust to various sensitivity analyses and remained elevated after controlling for long-term exposure to UFPs and nitrogen dioxide. We found near-linear relationships between noise and the incidence of AMI and CHF with no evidence of threshold values.ConclusionIn this large cohort study in Toronto, Canada, chronic exposure to road traffic noise was associated with elevated risks for AMI and CHF incidence. https://doi.org/10.1289/EHP5809.
| S-EPMC7422718 | biostudies-literature
Project description:Background Exposure to road traffic noise has been linked to cardiometabolic complications, such as elevated blood pressure and glucose dysregulation. However, epidemiologic evidence linking road traffic noise to diabetes mellitus and hypertension remains scarce. We examined associations between road traffic noise and the incidence of diabetes mellitus and hypertension in Toronto, Canada. Methods and Results Using the Ontario Population Health and Environment Cohort, we conducted a retrospective, population-based cohort study of long-term residents of Toronto, aged 35 to 100 years, who were registered for provincial publicly funded health insurance, and were without a history of hypertension (n=701 174) or diabetes mellitus (n=914 607). Road traffic noise exposure levels were assessed by the equivalent continuous A-weighted sound pressure level (dBA) for the 24-hour day and the equivalent continuous A-weighted sound pressure level for the night (11 pm-7am). Noise exposures were assigned to subjects according to their annual residential postal codes during the 15-year follow-up. We used random-effect Cox proportional hazards models adjusting for personal and area-level characteristics. From 2001 to 2015, each interquartile range increase in the equivalent continuous A-weighted sound pressure level (dBA) for the 24-hour day (10.0 dBA) was associated with an 8% increase in incident diabetes mellitus (95% CI, 1.07-1.09) and a 2% increase in hypertension (95% CI, 1.01-1.03). We obtained similar estimates with the equivalent continuous A-weighted sound pressure level for the night (11 pm-7am). These results were robust to all sensitivity analyses conducted, including further adjusting for traffic-related air pollutants (ultrafine particles and nitrogen dioxide). For both hypertension and diabetes mellitus, we observed stronger associations with the equivalent continuous A-weighted sound pressure level (dBA) for the 24-hour day among women and younger adults (aged <60 years). Conclusions Long-term exposure to road traffic noise was associated with an increased incidence of diabetes mellitus and hypertension in Toronto.
| S-EPMC7335534 | biostudies-literature
Project description:AimsBlood biochemistry may provide information on associations between road traffic noise, air pollution, and cardiovascular disease risk. We evaluated this in two large European cohorts (HUNT3, Lifelines).Methods and resultsRoad traffic noise exposure was modelled for 2009 using a simplified version of the Common Noise Assessment Methods in Europe (CNOSSOS-EU). Annual ambient air pollution (PM10, NO2) at residence was estimated for 2007 using a Land Use Regression model. The statistical platform DataSHIELD was used to pool data from 144 082 participants aged ≥20 years to enable individual-level analysis. Generalized linear models were fitted to assess cross-sectional associations between pollutants and high-sensitivity C-reactive protein (hsCRP), blood lipids and for (Lifelines only) fasting blood glucose, for samples taken during recruitment in 2006-2013. Pooling both cohorts, an inter-quartile range (IQR) higher day-time noise (5.1 dB(A)) was associated with 1.1% [95% confidence interval (95% CI: 0.02-2.2%)] higher hsCRP, 0.7% (95% CI: 0.3-1.1%) higher triglycerides, and 0.5% (95% CI: 0.3-0.7%) higher high-density lipoprotein (HDL); only the association with HDL was robust to adjustment for air pollution. An IQR higher PM10 (2.0 µg/m3) or NO2 (7.4 µg/m3) was associated with higher triglycerides (1.9%, 95% CI: 1.5-2.4% and 2.2%, 95% CI: 1.6-2.7%), independent of adjustment for noise. Additionally for NO2, a significant association with hsCRP (1.9%, 95% CI: 0.5-3.3%) was seen. In Lifelines, an IQR higher noise (4.2 dB(A)) and PM10 (2.4 µg/m3) was associated with 0.2% (95% CI: 0.1-0.3%) and 0.6% (95% CI: 0.4-0.7%) higher fasting glucose respectively, with both remaining robust to adjustment for air/noise pollution.ConclusionLong-term exposures to road traffic noise and ambient air pollution were associated with blood biochemistry, providing a possible link between road traffic noise/air pollution and cardio-metabolic disease risk.
| S-EPMC5837618 | biostudies-literature
Project description:This study investigated the role of microenvironment on personal exposures to black carbon (BC), fine particulate mass (PM2.5 ), carbon monoxide (CO), and particle number concentration (PNC) among adult residents of Fort Collins, Colorado, USA. Forty-four participants carried a backpack containing personal monitoring instruments for eight nonconsecutive 24-hour periods. Exposures were apportioned into five microenvironments: Home, Work, Transit, Eateries, and Other. Personal exposures exhibited wide heterogeneity that was dominated by within-person variability (both day-to-day and between microenvironment variability). Linear mixed-effects models were used to compare mean personal exposures in each microenvironment, while accounting for possible within-person correlation. Mean personal exposures during Transit and at Eateries tended to be higher than exposures at Home, where participants spent the majority of their time. Compared to Home, mean exposures to BC in Transit were, on average, 129% [95% confidence interval: 101% 162%] higher and exposures to PNC were 180% [101% 289%] higher in Eateries.
| S-EPMC6435329 | biostudies-literature
Project description:Air pollution has increasingly been recognized as a major healthcare concern. Air pollution, particularly fine particulate matter (≤ 2.5 μm in aerodynamic diameter [PM2.5]) has demonstrated an increase in adverse cardiovascular events. This study aimed to assess the cardiovascular response to personal exposure to different levels of PM2.5. This prospective cohort study enrolled healthy volunteers aged ≥ 18 years with no cardiovascular disease. Study subjects carried personal exposure monitor of PM2.5, digital thermo-hygrometer for temperature and humidity, 24-h blood pressure monitor, and continuous electrocardiogram monitor. Measurements were repeated twice with an interval of 6-12 months. Statistical models consisted of generalized estimation equations to various repeated measures of each subject. A total of 22 subjects were enrolled in this study between July 2018 and January 2019. Measurement was performed twice in all participants, and a total of 36 data were collected except for insufficient data collection. The mean age of the study population was 41.6 years, and 95% of the subjects were females. No study subjects had hypertension or other cardiovascular diseases. The average systolic blood pressure increased with higher PM2.5 levels with marginal significance (0.22 mmHg [95% confidential intervals - 0.04 to 0.48 mmHg] per 10 μg/m3 of PM2.5). All parameters for heart rate variability significantly decreased with a higher level of PM2.5. In this study, we measured individual personal exposure to PM2.5 by using a portable device. We found that 24-h exposure to high levels of PM2.5 was associated with a significant decrease in heart rate variability, suggesting impaired autonomous nervous function.
| S-EPMC7538889 | biostudies-literature
Project description:Gene expression changes are linked to air pollutant exposures in in vitro and animal experiments. However, limited data are available on how these outcomes relate to ambient air pollutant exposures in humans. We performed an exploratory analysis testing whether gene expression levels were associated with air pollution exposures in a Los Angeles area cohort of elderly subjects with coronary artery disease. Candidate genes (35) were selected from published studies of gene expression-pollutant associations. Expression levels were measured weekly in 43 subjects (? 12 weeks) using quantitative PCR. Exposures included gaseous pollutants O3, nitrogen oxides (NOx), and CO; particulate matter (PM) pollutants elemental and black carbon (EC, BC); and size-fractionated PM mass. We measured organic compounds from PM filter extracts, including polycyclic aromatic hydrocarbons (PAHs), and determined the in vitro oxidative potential of particle extracts. Associations between exposures and gene expression levels were analyzed using mixed-effects regression models. We found positive associations of traffic-related pollutants (EC, BC, primary organic carbon, PM 0.25-2.5 PAH and/or PM 0.25 PAH, and NOx) with NFE2L2, Nrf2-mediated genes (HMOX1, NQO1, and SOD2), CYP1B1, IL1B, and SELP. Findings suggest that NFE2L2 gene expression links associations of traffic-related air pollution with phase I and II enzyme genes at the promoter transcription level.
| S-EPMC4495007 | biostudies-literature
Project description:Vehicles are major sources of air pollutant emissions, and individuals living near large roads endure high exposures and health risks associated with traffic-related air pollutants. Air pollution epidemiology, health risk, environmental justice, and transportation planning studies would all benefit from an improved understanding of the key information and metrics needed to assess exposures, as well as the strengths and limitations of alternate exposure metrics. This study develops and evaluates several metrics for characterizing exposure to traffic-related air pollutants for the 218 residential locations of participants in the NEXUS epidemiology study conducted in Detroit (MI, USA). Exposure metrics included proximity to major roads, traffic volume, vehicle mix, traffic density, vehicle exhaust emissions density, and pollutant concentrations predicted by dispersion models. Results presented for each metric include comparisons of exposure distributions, spatial variability, intraclass correlation, concordance and discordance rates, and overall strengths and limitations. While showing some agreement, the simple categorical and proximity classifications (e.g., high diesel/low diesel traffic roads and distance from major roads) do not reflect the range and overlap of exposures seen in the other metrics. Information provided by the traffic density metric, defined as the number of kilometers traveled (VKT) per day within a 300 m buffer around each home, was reasonably consistent with the more sophisticated metrics. Dispersion modeling provided spatially- and temporally-resolved concentrations, along with apportionments that separated concentrations due to traffic emissions and other sources. While several of the exposure metrics showed broad agreement, including traffic density, emissions density and modeled concentrations, these alternatives still produced exposure classifications that differed for a substantial fraction of study participants, e.g., from 20% to 50% of homes, depending on the metric, would be incorrectly classified into "low", "medium" or "high" traffic exposure classes. These and other results suggest the potential for exposure misclassification and the need for refined and validated exposure metrics. While data and computational demands for dispersion modeling of traffic emissions are non-trivial concerns, once established, dispersion modeling systems can provide exposure information for both on- and near-road environments that would benefit future traffic-related assessments.
| S-EPMC4199035 | biostudies-literature
Project description:BACKGROUND: Traffic noise has been associated with prevalence of hypertension, but reports are inconsistent for blood pressure (BP). To ascertain noise effects and to disentangle them from those suspected to be from traffic-related air pollution, it may be essential to estimate people's noise exposure indoors in bedrooms. OBJECTIVES: We analyzed associations between long-term exposure to indoor traffic noise in bedrooms and prevalent hypertension and systolic (SBP) and diastolic (DBP) BP, considering long-term exposure to outdoor nitrogen dioxide (NO2). METHODS: We evaluated 1,926 cohort participants at baseline (years 2003-2006; Girona, Spain). Outdoor annual average levels of nighttime traffic noise (Lnight) and NO2 were estimated at postal addresses with a detailed traffic noise model and a land-use regression model, respectively. Individual indoor traffic Lnight levels were derived from outdoor Lnight with application of insulations provided by reported noise-reducing factors. We assessed associations for hypertension and BP with multi-exposure logistic and linear regression models, respectively. RESULTS: Median levels were 27.1 dB(A) (indoor Lnight), 56.7 dB(A) (outdoor Lnight), and 26.8 ?g/m3 (NO2). Spearman correlations between outdoor and indoor Lnight with NO2 were 0.75 and 0.23, respectively. Indoor Lnight was associated both with hypertension (OR = 1.06; 95% CI: 0.99, 1.13) and SBP (? = 0.72; 95% CI: 0.29, 1.15) per 5 dB(A); and NO2 was associated with hypertension (OR = 1.16; 95% CI: 0.99, 1.36), SBP (? = 1.23; 95% CI: 0.21, 2.25), and DBP (??= 0.56; 95% CI: -0.03, 1.14) per 10 ?g/m3. In the outdoor noise model, Lnight was associated only with hypertension and NO2 with BP only. The indoor noise-SBP association was stronger and statistically significant with a threshold at 30 dB(A). CONCLUSION: Long-term exposure to indoor traffic noise was associated with prevalent hypertension and SBP, independently of NO2. Associations were less consistent for outdoor traffic Lnight and likely affected by collinearity.
| S-EPMC4216159 | biostudies-literature
Project description:BackgroundLong-term exposure to air pollution and noise is detrimental to health; but studies that evaluated both remain limited. This study explores associations with natural and cause-specific mortality for a range of air pollutants and transportation noise.MethodsOver 4 million adults in Switzerland were followed from 2000 to 2014. Exposure to PM2.5, PM2.5 components (Cu, Fe, S and Zn), NO2, black carbon (BC) and ozone (O3) from European models, and transportation noise from source-specific Swiss models, were assigned at baseline home addresses. Cox proportional hazards models, adjusted for individual and area-level covariates, were used to evaluate associations with each exposure and death from natural, cardiovascular (CVD) or non-malignant respiratory disease. Analyses included single and two exposure models, and subset analysis to study lower exposure ranges.ResultsDuring follow-up, 661,534 individuals died of natural causes (36.6% CVD, 6.6% respiratory). All exposures including the PM2.5 components were associated with natural mortality, with hazard ratios (95% confidence intervals) of 1.026 (1.015, 1.038) per 5 µg/m3 PM2.5, 1.050 (1.041, 1.059) per 10 µg/m3 NO2, 1.057 (1.048, 1.067) per 0.5 × 10-5/m BC and 1.045 (1.040, 1.049) per 10 dB Lden total transportation noise. NO2, BC, Cu, Fe and noise were consistently associated with CVD and respiratory mortality, whereas PM2.5 was only associated with CVD mortality. Natural mortality associations persisted < 20 µg/m3 for PM2.5 and NO2, < 1.5 10-5/m BC and < 53 dB Lden total transportation noise. The O3 association was inverse for all outcomes. Including noise attenuated all outcome associations, though many remained significant. Across outcomes, noise was robust to adjustment to air pollutants (e.g. natural mortality 1.037 (1.033, 1.042) per 10 dB Lden total transportation noise, after including BC).ConclusionLong-term exposure to air pollution and transportation noise in Switzerland contribute to premature mortality. Considering co-exposures revealed the importance of local traffic-related pollutants such as NO2, BC and transportation noise.
| S-EPMC10041702 | biostudies-literature