Epidemiological studies have demonstrated associations between short-term increases in outdoor air pollution concentrations and adverse cardiovascular effects, including cardiac mortality and hospitalizations. One possible mechanism behind this association is that air pollution exposure increases the risk of developing a cardiac arrhythmia. To investigate this hypothesis, dates of implantable cardioverter defibrillator (ICD) discharges were abstracted from patient records in patients attending the two ICD clinics in Vancouver, BC, for the years 1997-2000. Daily outdoor air pollutant concentrations and daily meteorological data from the Vancouver region were obtained for the same 4-yr period. Generalized estimating equations were used to assess the association between short-term increases in air pollutant concentrations and ICD discharges while controlling for temporal trends, meteorology, and serial correlation in the data. Air pollution concentrations in the Vancouver region were relatively low from 1997 to 2000, as expected. In the 50 patients who resided within the Vancouver region and who experienced at least 1 ICD discharge during the period of follow-up, no significant associations between increased air pollution concentrations and increased ICD discharges were present. When the patient sample was restricted to the 16 patients who had at least 6 months of follow-up and experienced a rate of at least 2 days with ICD discharges per year, there was a statistically significant association between increased sulfur dioxide (SO(2)) concentration and ICD discharge 2 days after the SO(2) increase. When stratified by season, no associations between increased air pollutant concentrations and increased risk of ICD discharge were observed in the summer, although for several pollutants, concentration increases were associated with a decrease in ICD discharges. In the winter, increased SO(2) concentrations again were seen to be associated with increased risk of ICD discharge, at both 2 and 3 days following increases in SO(2) concentrations. These findings provide no compelling evidence that short-term increases in relatively low concentrations of outdoor air pollutants have an adverse effect on individuals at risk of cardiac arrhythmias. The findings regarding SO(2) are difficult to interpret. They may be chance findings. Alternatively, given the very low concentrations of SO(2) that were present in Vancouver, SO(2) may have been serving as a surrogate measure of other environmental or meteorological factors.
The concentration-response relationship between daily ambient inhalable particle (particulate matter less than or equal to 10 micro m; PM(10)) concentrations and daily mortality typically shows no evidence of a threshold concentration below which no relationship is observed. However, the power to assess a relationship at very low concentrations of PM(10) has been limited in studies to date. The concentrations of PM(10) and other air pollutants in Vancouver, British Columbia, Canada, from January 1994 through December 1996 were very low: the 50th and 90th percentiles of daily average PM(10) concentrations were 13 and 23 micro g/m(3), respectively, and 27 and 39 ppb, respectively, for 1-hr maximum ozone. Analyses of 3 years of daily pollution (PM(10), ozone, sulfur dioxide, nitrogen dioxide, and carbon monoxide) concentrations and mortality counts showed that the dominant associations were between ozone and total mortality and respiratory and cardiovascular mortality in the summer, and between nitrogen dioxide and total mortality in the winter, although some association with PM(10) may also have been present. We conclude that increases in low concentrations of air pollution are associated with increased daily mortality. These findings may support the notion that no threshold pollutant concentrations are present, but they also raise concern that these effects may not be effects of the measured pollutants themselves, but rather of some other factor(s) present in the air pollution-meteorology mix.
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Particulate air pollution is associated with cardiovascular morbidity. One hypothesized mechanism involves oxidative stress, systemic inflammation, and endothelial dysfunction.
To assess an intervention's impact on particle exposures and endothelial function among healthy adults in a woodsmoke-impacted community. We also investigated the underlying role of oxidative stress and inflammation in relation to exposure reductions.
Portable air filters were used in a randomized crossover intervention study of 45 healthy adults exposed to consecutive 7-day periods of filtered and nonfiltered air.
Reactive hyperemia index was measured as an indicator of endothelial function via peripheral artery tonometry, and markers of inflammation (C-reactive protein, interleukin-6, and band cells) and lipid peroxidation (malondialdehyde and 8-iso-prostaglandin F(2a)) were quantified. Air filters reduced indoor fine particle concentrations by 60%. Filtration was associated with a 9.4% (95% confidence interval, 0.9-18%) increase in reactive hyperemia index and a 32.6% (4.4-60.9%) decrease in C-reactive protein. Decreases in particulate matter and the woodsmoke tracer levoglucosan were associated with reduced band cell counts. There was limited evidence of more pronounced effects on endothelial function and level of systemic inflammation among males, overweight participants, younger participants, and residents of wood-burning homes. No associations were noted for oxidative stress markers.
Air filtration was associated with improved endothelial function and decreased concentrations of inflammatory biomarkers but not markers of oxidative stress. Our results support the hypothesis that systemic inflammation and impaired endothelial function, both predictors of cardiovascular morbidity, can be favorably influenced by reducing indoor particle concentrations.
In metropolitan areas, road traffic is a major contributor to ambient air pollution and the dominant source of community noise. The authors investigated the independent and joint influences of community noise and traffic-related air pollution on risk of coronary heart disease (CHD) mortality in a population-based cohort study with a 5-year exposure period (January 1994-December 1998) and a 4-year follow-up period (January 1999-December 2002). Individuals who were 45-85 years of age and resided in metropolitan Vancouver, Canada, during the exposure period and did not have known CHD at baseline were included (n = 445,868). Individual exposures to community noise and traffic-related air pollutants, including black carbon, particulate matter less than or equal to 2.5 µm in aerodynamic diameter, nitrogen dioxide, and nitric oxide, were estimated at each person's residence using a noise prediction model and land-use regression models, respectively. CHD deaths were identified from the provincial death registration database. After adjustment for potential confounders, including traffic-related air pollutants or noise, elevations in noise and black carbon equal to the interquartile ranges were associated with 6% (95% confidence interval: 1, 11) and 4% (95% confidence interval: 1, 8) increases, respectively, in CHD mortality. Subjects in the highest noise decile had a 22% (95% confidence interval: 4, 43) increase in CHD mortality compared with persons in the lowest decile. These findings suggest that there are independent effects of traffic-related noise and air pollution on CHD mortality.
Ambient air pollution has been suggested as a risk factor for chronic obstructive pulmonary disease (COPD). However, there is a lack of longitudinal studies to support this assertion.
To investigate the associations of long-term exposure to elevated traffic-related air pollution and woodsmoke pollution with the risk of COPD hospitalization and mortality.
This population-based cohort study included a 5-year exposure period and a 4-year follow-up period. All residents aged 45-85 years who resided in Metropolitan Vancouver, Canada, during the exposure period and did not have known COPD at baseline were included in this study (n = 467,994). Residential exposures to traffic-related air pollutants (black carbon, particulate matter
A growing body of evidence links the built environment to physical activity levels, health outcomes, and transportation behaviors. However, little of this research has focused on cycling, a sustainable transportation option with great potential for growth in North America. This study examines associations between decisions to bicycle (versus drive) and the built environment, with explicit consideration of three different spatial zones that may be relevant in travel behavior: trip origins, trip destinations, and along the route between. We analyzed 3,280 utilitarian bicycle and car trips in Metro Vancouver, Canada made by 1,902 adults, including both current and potential cyclists. Objective measures were developed for built environment characteristics related to the physical environment, land use patterns, the road network, and bicycle-specific facilities. Multilevel logistic regression was used to model the likelihood that a trip was made by bicycle, adjusting for trip distance and personal demographics. Separate models were constructed for each spatial zone, and a global model examined the relative influence of the three zones. In total, 31% (1,023 out of 3,280) of trips were made by bicycle. Increased odds of bicycling were associated with less hilliness; higher intersection density; less highways and arterials; presence of bicycle signage, traffic calming, and cyclist-activated traffic lights; more neighborhood commercial, educational, and industrial land uses; greater land use mix; and higher population density. Different factors were important within each spatial zone. Overall, the characteristics of routes were more influential than origin or destination characteristics. These findings indicate that the built environment has a significant influence on healthy travel decisions, and spatial context is important. Future research should explicitly consider relevant spatial zones when investigating the relationship between physical activity and urban form.
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Residential proximity to road traffic is associated with increased coronary heart disease (CHD) morbidity and mortality. It is unknown, however, whether changes in residential proximity to traffic could alter the risk of CHD mortality.
We used a population-based cohort study with a 5-year exposure period and a 4-year follow-up period to explore the association between changes in residential proximity to road traffic and the risk of CHD mortality. The cohort comprised all residents aged 45-85 years who resided in metropolitan Vancouver during the exposure period and without known CHD at baseline (n = 450,283). Residential proximity to traffic was estimated using a geographic information system. CHD deaths during the follow-up period were identified using provincial death registration database. The data were analyzed using logistic regression.
Compared with the subjects consistently living away from road traffic (>150 m from a highway or >50 m from a major road) during the 9-year study period, those consistently living close to traffic (
Recent evidence suggests that chronic exposure to high levels of ambient particulate matter (PM) is associated with decreased pulmonary function and the development of chronic airflow obstruction. To investigate the possible role of PM-induced abnormalities in the small airways in these functional changes, we examined histologic sections from the lungs of 20 women from Mexico City, a high PM locale. All subjects were lifelong residents of Mexico City, were never-smokers, never had occupational dust exposure, and never used biomass fuel for cooking. Twenty never-smoking, non-dust-exposed subjects from Vancouver, British Columbia, Canada, a low PM region, were used as a control. By light microscopy, abnormal small airways with fibrotic walls and excess muscle, many containing visible dust, were present in the Mexico City lungs. Formal grading analysis confirmed the presence of significantly greater amounts of fibrous tissue and muscle in the walls of the airways in the Mexico City compared with the Vancouver lungs. Electron microscopic particle burden measurements on four cases from Mexico City showed that carbonaceous aggregates of ultrafine particles, aggregates likely to be combustion products, were present in the airway mucosa. We conclude that PM penetrates into and is retained in the walls of small airways, and that, even in nonsmokers, long-term exposure to high levels of ambient particulate pollutants is associated with small airway remodeling. This process may produce chronic airflow obstruction.
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Evidence suggests that air pollution exposure adversely affects pregnancy outcomes. Few studies have examined individual-level intraurban exposure contrasts.
We evaluated the impacts of air pollution on small for gestational age (SGA) birth weight, low full-term birth weight (LBW), and preterm birth using spatiotemporal exposure metrics.
With linked administrative data, we identified 70,249 singleton births (1999-2002) with complete covariate data (sex, ethnicity, parity, birth month and year, income, education) and maternal residential history in Vancouver, British Columbia, Canada. We estimated residential exposures by month of pregnancy using nearest and inverse-distance weighting (IDW) of study area monitors [carbon monoxide, nitrogen dioxide, nitric oxide, ozone, sulfur dioxide, and particulate matter
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Here we compare PM(2.5) (particles with aerodynamic diameter less than 2.5 microm) mass and filter absorbance measurements with elemental carbon (EC) concentrations measured in parallel at the same site as well as collocated PM(2.5) and PM(10) (particles with aerodynamic diameter less than 10 microm) mass and absorbance measurements. The data were collected within the Traffic-Related Air Pollution on Childhood Asthma (TRAPCA) study in Germany, The Netherlands and Sweden. The study was designed to assess the health impact of spatial contrasts in long-term average concentrations. The measurement sites were distributed between background and traffic locations. Annual EC and PM(2.5) absorbance measurements were at traffic sites on average 43-84% and 26-76% higher, respectively, compared to urban background sites. The contrast for PM(2.5) mass measurements was lower (8-35%). The smaller contrast observed for PM(2.5) mass in comparison with PM(2.5) absorbance and EC documents that PM(2.5) mass underestimates exposure contrasts related to motorized traffic emissions. The correlation between PM(10) and PM(2.5) was high, documenting that most of the spatial variation of PM(10) was because of PM(2.5). The measurement of PM(2.5) absorbance was highly correlated with EC measurements and suggests that absorbance can be used as a simple, inexpensive and non-destructive method to estimate motorized traffic-related particulate air pollution. The EC/absorbance relation differed between countries and site type (background/traffic), supporting the need for site-specific calibrations of the simple absorbance method. While the ratio between PM(2.5) and PM(10) mass ranged from 0.54 to 0.68, the ratio of PM(2.5) absorbance and PM(10) absorbance was 0.96-0.97, indicating that PM(2.5) absorbance captures nearly all of the particle absorbance.