Exposure to road traffic and railway noise and associations with blood pressure and self-reported hypertension: a cohort study

<p>Abstract</p> <p>Background</p> <p>Epidemiological studies suggest that long-term exposure to transport noise increases the risk for cardiovascular disorders. The effect of transport noise on blood pressure and hypertension is uncertain.</p> <p>Methods</p> <p>In 1993-1997, 57,053 participants aged 50-64 year were enrolled in a population-based cohort study. At enrolment, systolic and diastolic blood pressure was measured. Incident hypertension during a mean follow-up of 5.3 years was assessed by questionnaire. Residential long-term road traffic noise (L_den) was estimated for 1- and 5-year periods preceding enrolment and preceding diagnosis of hypertension. Residential exposure to railway noise was estimated at enrolment. We conducted a cross-sectional analysis of associations between road traffic and railway noise and blood pressure at enrolment with linear regression, adjusting for long-term air pollution, meteorology and potential lifestyle confounders (N = 44,083). Incident self-reported hypertension was analyzed with Cox regression, adjusting for long-term air pollution and potential lifestyle confounders.</p> <p>Results</p> <p>We found a 0.26 mm Hg higher systolic blood pressure (95% confidence intervals (CI): -0.11; 0.63) per 10 dB(A) increase in 1-year mean road traffic noise levels, with stronger associations in men (0.59 mm Hg (CI: 0.13; 1.05) per 10 dB(A)) and older participants (0.65 mm Hg (0.08; 1.22) per 10 dB(A)). Road traffic noise was not associated with diastolic blood pressure or hypertension. Exposure to railway noise above 60 dB was associated with 8% higher risk for hypertension (95% CI: -2%; 19%, P = 0.11).</p> <p>Conclusions</p> <p>While exposure to road traffic noise was associated with systolic blood pressure in subgroups, we were not able to identify associations with hypertension.</p

Particulate air pollution, systemic oxidative stress, inflammation, and atherosclerosis

Air pollution has been associated with significant adverse health effects leading to increased overall morbidity and mortality of worldwide significance. Epidemiological studies have shown that the largest portion of air pollution-related mortality is due to cardiovascular diseases, predominantly those of ischemic nature. Human studies suggest an association with atherosclerosis and increasing experimental animal data support that this association is likely to be causal. While both gasses and particles have been linked to detrimental health effects, more evidence implicates the particulate matter (PM) components as major responsible for a large portion of the proatherogenic effects. Multiple experimental approaches have revealed the ability of PM components to trigger and/or enhance free radical reactions in cells and tissues, both ex vivo as well as in vivo. It appears that exposure to PM leads to the development of systemic prooxidant and proinflammatory effects that may be of great importance in the development of atherosclerotic lesions. This article reviews the epidemiological studies, experimental animal, and cellular data that support the association of air pollutants, especially the particulate components, with systemic oxidative stress, inflammation, and atherosclerosis. It also reviews the use of transcriptomic studies to elucidate molecular pathways of importance in those systemic effects

Exposure to fine particulate matter and acute effects on blood pressure: effect modification by measures of obesity and location

BACKGROUND: Observational studies and controlled experiments have provided evidence that airborne particulate matter (PM) is capable of acutely increasing blood pressure (BP) in certain scenarios. The goal of this study was to evaluate whether and to what extent obesity and community location affect relationships between fine particulate matter (PM(2.5)) and blood pressure (BP) measures. METHODS: Using data from a stratified random sample survey of adults conducted in 2002–3 in Detroit, Michigan, we tested body mass index (BMI) and waist circumference (WCIR) in separate models as effect modifiers of the relationship between PM(2.5) exposure and BP. We also tested interactions with community location. Models were adjusted for covariates with established prohypertensive effects. RESULTS: PM(2.5) exposure was positively associated with increased pulse pressure (PP) for those categorised as obese (BMI≥30) across lags 2 (β 4.16, p<0.05) and 3 days (μ 2.55, p<0.05) prior to BP measure. WCIR similarly modified the effect of exposure to PM(2.5) on PP (β 4.34, p<0.003). The observed effects were enhanced in the community with closer proximity to local emissions of PM(2.5), and for residents classified as obese (BMI≥30) or with WCIR above high-risk cuts points. CONCLUSIONS: This community-based study suggests that positive associations between PM(2.5) exposure and PP and systolic BP are enhanced in areas proximate to sources of PM (2.5) emissions. These patterns were observed for all residents, but were more visible and consistent among those who were obese. Research is needed to examine the mechanistic pathways by which air particles interact with obesity and location to affect BP, and inform community interventions to reduce the population burden of hypertension and related co-morbidities

Relational pathways between socioeconomic position and cardiovascular risk in a multiethnic urban sample: complexities and their implications for improving health in economically disadvantaged populations

BACKGROUND: The study was designed to provide evidence of a cascade effect linking socioeconomic position to anthropometric indicators of cardiovascular disease (CVD) risk through effects on psychosocial stress, psychological distress and health-related behaviours, and consider implications for disease prevention and health promotion. METHODS: A cross-sectional stratified two-stage probability sample of occupied housing units in three areas of Detroit, Michigan, was used in the study. 919 adults aged ≥25 years completed the survey (mean age 46.3; 53% annual household income <$20 000; 57% non-Hispanic black, 22% Latino, 19% non-Hispanic white). Variables included self-report (eg, psychosocial stress, depressive symptoms, health behaviours) and anthropometric measurements (eg, waist circumference, height, weight). The main outcome variables were depressive symptoms, smoking status, physical activity, body mass index and waist circumference. RESULTS: Income was inversely associated with depressive symptoms, likelihood of current smoking, physical inactivity and waist circumference. These relationships were partly or fully mediated by psychosocial stress. A suppressor effect of current smoking on the relationship between depressive symptoms and waist circumference was found. Independent effects of psychosocial stress and psychological distress on current smoking and waist circumference were found, above and beyond the mediated pathways. CONCLUSIONS: The results suggest that relatively modest improvements in the income of economically disadvantaged people can set in motion a cascade of effects, simultaneously reducing exposure to stressful life conditions, improving mental well-being, increasing health-promoting behaviours and reducing anthropometric risks associated with CVD. Such interventions offer important opportunities to improve population health and reduce health disparities

Acute Effects of Ambient Particulate Matter on Blood Pressure Differential Effects Across Urban Communities

Recent studies have suggested a link between exposure to ambient particulate matter <2.5μm in diameter (PM(2.5)) and adverse cardiovascular outcomes. The objective of this study was to examine the effects of differing community-level exposure to PM(2.5) on daily measures of blood pressure (BP) among an adult population. During the period May 2002 through April 2003, BP was examined at two time points for 347 adults residing in three distinct communities of Detroit, MI. Exposure to PM(2.5) was assessed in each community during this period, along with multivariate associations between PM(2.5) and BP. In models combining all three communities, PM(2.5) was significantly associated with systolic pressure (SP); a 10 μg/m(3) increase in daily PM(2.5) was associated with a 3.2 mm Hg increase in SP (p=0.05). However, in models that added a location interaction, larger effects were observed for SP within the community with highest PM(2.5) levels; a 10 μg/m(3) increase in daily PM(2.5) was associated with a 8.6 mm Hg increase in SP (p=0.01). We also found young age (<55 years) and not taking BP medications to be significant predictors of increased BP effects. Among those taking BP medications, the PM(2.5) effect on BP appeared to be mitigated, partially explaining the age effect, as those participants less than 55 years were less likely to take BP medications. Short-term increases in exposure to ambient PM(2.5) are associated with acute increases in BP in adults, especially within communities with elevated levels of exposure