Hugh W. Davies

Association of Long-term Exposure to Community Noise and Traffic-related Air Pollution With Coronary Heart Disease Mortality

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 persons 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.

Long-Term Exposure to Traffic-Related Air Pollution and the Risk of Coronary Heart Disease Hospitalization and Mortality

Background Epidemiologic studies have demonstrated that exposure to road traffic is associated with adverse cardiovascular outcomes. Objectives We aimed to identify specific traffic-related air pollutants that are associated with the risk of coronary heart disease (CHD) morbidity and mortality to support evidence-based environmental policy making. Methods This population-based cohort study included a 5-year exposure period and a 4-year follow-up period. All residents 45–85 years of age who resided in Metropolitan Vancouver during the exposure period and without known CHD at baseline were included in this study (n = 452,735). Individual exposures to traffic-related air pollutants including black carbon, fine particles [aerodynamic diameter ≤ 2.5 μm (PM2.5)], nitrogen dioxide (NO2), and nitric oxide were estimated at residences of the subjects using land-use regression models and integrating changes in residences during the exposure period. CHD hospitalizations and deaths during the follow-up period were identified from provincial hospitalization and death registration records. Results An interquartile range elevation in the average concentration of black carbon (0.94 × 10−5/m filter absorbance, equivalent to approximately 0.8 μg/m3 elemental carbon) was associated with a 3% increase in CHD hospitalization (95% confidence interval, 1–5%) and a 6% increase in CHD mortality (3–9%) after adjusting for age, sex, preexisting comorbidity, neighborhood socioeconomic status, and copollutants (PM2.5 and NO2). There were clear linear exposure–response relationships between black carbon and coronary events. Conclusions Long-term exposure to traffic-related fine particulate air pollution, indicated by black carbon, may partly explain the observed associations between exposure to road traffic and adverse cardiovascular outcomes.

Correlation between co-exposures to noise and air pollution from traffic sources

Background: Both air and noise pollution associated with motor vehicle traffic have been associated with cardiovascular disease. Similarities in pollution source and health outcome mean that there is potential for noise to confound studies of air pollution and cardiovascular disease, and vice versa, or for more complex interactions to occur. Methods: The correlations between 2-week average roadside concentrations of nitrogen dioxide (NO2) and nitrogen oxides (NOX) and short term average noise levels (Leq,5min) for 103 urban sites with varying traffic, environment and infrastructure characteristics were examined. Results: The Pearson correlation coefficient for Leq,5min and NO2 was 0.53, and for Leq,5min and NOX , 0.64. Factors influencing the degree of correlation were number of lanes on the closest road, number of cars or trucks during noise sampling and presence of a major intersection. Conclusions: We recommend measurement of both pollutants in future studies of traffic-related pollution and cardiovascular disease to allow for more sophisticated analysis of this relationship.

Residential Greenness and Birth Outcomes: Evaluating the Influence of Spatially Correlated Built-Environment Factors

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 psychological mechanisms) may underlie associations between residential greenness and birth outcomes. Citation: Hystad P, Davies HW, Frank L, Van Loon J, Gehring U, Tamburic L, Brauer M. 2014. Residential greenness and birth outcomes: evaluating the influence of spatially correlated built-environment factors. Environ Health Perspect 122:1095–1102; http://dx.doi.org/10.1289/ehp.1308049

Changes in residential proximity to road traffic and the risk of death from coronary heart disease.

Background: 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. Methods: 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. Results: 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 (≤150 m from a highway or ≤50 m from a major road) had the greatest risk of CHD mortality (relative risk [RR] = 1.29 [95% confidence interval = 1.18–1.41]). By comparison, those who moved closer to traffic during the exposure period had less increased risk than those who were consistently exposed (1.20 [1.00–1.43]), and those who moved away from traffic had even less increase in the risk (1.14 [0.95–1.37]). All analyses were adjusted for baseline age, sex, pre-existing comorbidities (diabetes, chronic obstructive pulmonary disease, hypertensive heart disease), and neighborhood socioeconomic status. Conclusions: Living close to major roadways was associated with increased risk of coronary mortality, whereas moving away from major roadways was associated with decreased risk.

Impact of noise and air pollution on pregnancy outcomes.

Background: Motorized traffic is an important source of both air pollution and community noise. While there is growing evidence for an adverse effect of ambient air pollution on reproductive health, little is known about the association between traffic noise and pregnancy outcomes. Methods: We evaluated the impact of residential noise exposure on small size for gestational age, preterm birth, term birth weight, and low birth weight at term in a population-based cohort study, for which we previously reported associations between air pollution and pregnancy outcomes. We also evaluated potential confounding of air pollution effects by noise and vice versa. Linked administrative health data sets were used to identify 68,238 singleton births (1999–2002) in Vancouver, British Columbia, Canada, with complete covariate data (sex, ethnicity, parity, birth month and year, income, and education) and maternal residential history. We estimated exposure to noise with a deterministic model (CadnaA) and exposure to air pollution using temporally adjusted land-use regression models and inverse distance weighting of stationary monitors for the entire pregnancy. Results: Noise exposure was negatively associated with term birth weight (mean difference = −19 [95% confidence interval = −23 to −15] g per 6 dB(A)). In joint air pollution-noise models, associations between noise and term birth weight remained largely unchanged, whereas associations decreased for all air pollutants. Conclusion: Traffic may affect birth weight through exposure to both air pollution and noise.

Noise and health in vulnerable groups: A review

Vulnerable or susceptible groups are mentioned in most reviews and documents regarding noise and health. But only a few studies address this issue in a concrete and focused way. Groups at risk most often mentioned in the literature are children, the elderly, the chronically ill and people with a hearing impairment. The other categories encountered are those of sensitive persons, shiftworkers, people with mental illness (e.g., schizophrenia or autism), people suffering from tinnitus, and fetuses and neonates. The mechanism for this vulnerability has not been clearly described and relevant research has seldom focused on the health effects of noise in these groups in an integrated manner. This paper summarizes the outcomes and major conclusions of a systematic, qualitative review of studies over the past 5 years. This review was prepared for the 10 th Conference on Noise as a Public Health Problem (ICBEN, 2011). Evidence is reviewed describing effects, groups assumed to be at risk, and mechanisms pertaining to noise sensitivity and learned helplessness.

Noise exposure and children’s blood pressure and heart rate: the RANCH project

Background: Conclusions that can be drawn from earlier studies on noise and children’s blood pressure are limited due to inconsistent results, methodological problems, and the focus on school noise exposure. Objectives: To investigate the effects of aircraft and road traffic noise exposure on children’s blood pressure and heart rate. Methods: Participants were 1283 children (age 9–11 years) attending 62 primary schools around two European airports. Data were pooled and analysed using multilevel modelling. Adjustments were made for a range of socioeconomic and lifestyle factors. Results: After pooling the data, aircraft noise exposure at school was related to a statistically non-significant increase in blood pressure and heart rate. Aircraft noise exposure at home was related to a statistically significant increase in blood pressure. Aircraft noise exposure during the night at home was positively and significantly associated with blood pressure. The findings differed between the Dutch and British samples. Negative associations were found between road traffic noise exposure and blood pressure, which cannot be explained. Conclusion: On the basis of this study and previous scientific literature, no unequivocal conclusions can be drawn about the relationship between community noise and children’s blood pressure.

Exposure to occupational noise and cardiovascular disease in the United States: the National Health and Nutrition Examination Survey 1999–2004

Background Chronic exposure to occupational noise may be associated with increased risk of coronary heart disease (CHD) and hypertension. However, findings are inconsistent and many previous studies are limited by small sample size and inappropriate control for potential confounders. We used a nationally representative US sample to examine associations of self-reported exposure to occupational noise with CHD and hypertension. Methods This cross-sectional study included 6307 participants of the National Health and Nutrition Examination Survey 1999–2004, aged ≥20 years and employed at the time of interview. Noise exposure assessment was based on self-reported exposure to loud noise in the workplace. Results Compared with never exposed participants, subjects chronically exposed to occupational noise had a 2–3-fold increased prevalence of angina pectoris, myocardial infarction, CHD and isolated diastolic hypertension. After adjustment for various covariates, the odds ratios (95% CIs) for angina pectoris, CHD and isolated diastolic hypertension were 2.91 (1.35 to 6.26), 2.04 (1.16 to 3.58) and 2.23 (1.21 to 4.12), respectively. There were clear exposure–response relationships for the observed associations. Associations of noise exposure with angina pectoris, myocardial infarction and CHD were particularly strong for participants aged <50 years, men and current smokers. There was no significant increase in levels of cardiovascular biomarkers including blood lipids and circulating inflammatory mediators associated with noise exposure. Conclusions Chronic exposure to occupational noise is strongly associated with prevalence of CHD, especially for young male current smokers. This study suggests that excess noise exposure in the workplace is an important occupational health issue and deserves special attention.

Modeling population exposure to community noise and air pollution in a large metropolitan area

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.