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
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 (
Epidemiologic studies have shown that both air pollution and community noise are associated with cardiovascular disease mortality. Because road traffic is a major contributor to these environmental pollutants in metropolitan areas, it is plausible that the observed associations may be confounded by coexistent pollutants. As part of a large population-based cohort study to address this concern, we used a noise prediction model to assess annual average community noise levels from transportation sources in metropolitan Vancouver, Canada. The modeled annual average noise level was 64 (inter quartile range 60-68) dB(A) for the region. This model was evaluated by comparing modeled annual daytime A-weighted equivalent continuous noise levels (L(day)) with measured 5-min daytime A-weighted equivalent continuous noise levels (L(eq,day,5 min)) at 103 selected roadside sites in the study region. On average, L(day) was 6.2 (95% CI, 6.0-7.9) dB(A) higher than, but highly correlated (r=0.62; 95% CI, 0.48-0.72) with, L(eq,day,5 min). These results suggest that our model-based noise exposure assessment could approximately reflect actual noise exposure in the study region. Overall, modeled noise levels were not strongly correlated with land use regression estimates of traffic-related air pollutants including black carbon, particulate matter with aerodynamic diameter =2.5 µm (PM(2.5)), NO(2) and NO; the highest correlation was with black carbon (r=0.48), whereas the lowest correlation was with PM(2.5) (r=0.18). There was no consistent effect of traffic proximity on the correlations between community noise levels and traffic-related air pollutant concentrations. These results, consistent with previous studies, suggest that it is possible to assess potential adverse cardiovascular effects from long-term exposures to community noise and traffic-related air pollution in prospective epidemiologic studies.
Self-reported use of cigarettes generally underestimates the true cigarette exposure of smokers. Serum cotinine is considered the best biomarker to evaluate tobacco exposure. This study determined whether or not there were any significant differences in serum cotinine concentrations between men and women when they reported smoking the same number of cigarettes per day. We analyzed cotinine and tobacco consumption data on 680 women and 840 men, aged 20 years or older, who smoked at least 100 cigarettes during their lifetime and were still actively smoking at the time of the National Health and Nutrition Examination Surveys (1999-2002). Overall, compared with men, women reported smoking fewer cigarettes per day (16.1 vs. 18.7, p