Long-term exposure to traffic-related air pollution associated with blood pressure and self-reported hypertension in a Danish cohort.
ABSTRACT: BACKGROUND: Short-term exposure to air pollution has been associated with changes in blood pressure (BP) and emergency department visits for hypertension, but little is known about the effects of long-term exposure to traffic-related air pollution on BP and hypertension. OBJECTIVES: We studied whether long-term exposure to air pollution is associated with BP and hypertension. METHODS: In 1993-1997, 57,053 participants 50-64 years of age were enrolled in a population-based cohort study. Systolic and diastolic BP (SBP and DBP, respectively) were measured at enrollment. Self-reported incident hypertension during a mean follow-up of 5.3 years was assessed by questionnaire. We used a validated dispersion model to estimate residential long-term nitrogen oxides (NO(x)), a marker of traffic-related air pollution, for the 1- and 5-year periods prior to enrollment and before a diagnosis of hypertension. We conducted a cross-sectional analysis of associations between air pollution and BP at enrollment with linear regression, adjusting for traffic noise, measured short-term NO(x), temperature, relative humidity, and potential lifestyle confounders (n = 44,436). We analyzed incident hypertension with Cox regression, adjusting for traffic noise and potential confounders. RESULTS: A doubling of NO(x) exposure during 1- and 5-year periods preceding enrollment was associated with 0.53-mmHg decreases [95% confidence interval (CI): -0.88, -0.19 mmHg] and 0.50-mmHg decreases (95% CI: -0.84, -0.16 mmHg) in SBP, respectively. Long-term exposure also was associated with a lower prevalence of baseline self-reported hypertension (per doubling of 5-year mean NO(x): odds ratio = 0.96; 95% CI: 0.91, 1.00), whereas long-term NO(x) exposure was not associated with incident self-reported hypertension during follow-up. CONCLUSIONS: Long-term exposure to traffic-related air pollution was associated with a slightly lower prevalence of BP at baseline, but was not associated with incident hypertension.
Project description:Long-term exposure to air pollution has been hypothesized to elevate arterial blood pressure (BP). The existing evidence is scarce and country specific.We investigated the cross-sectional association of long-term traffic-related air pollution with BP and prevalent hypertension in European populations.We analyzed 15 population-based cohorts, participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE). We modeled residential exposure to particulate matter and nitrogen oxides with land use regression using a uniform protocol. We assessed traffic exposure with traffic indicator variables. We analyzed systolic and diastolic BP in participants medicated and nonmedicated with BP-lowering medication (BPLM) separately, adjusting for personal and area-level risk factors and environmental noise. Prevalent hypertension was defined as ? 140 mmHg systolic BP, or ? 90 mmHg diastolic BP, or intake of BPLM. We combined cohort-specific results using random-effects meta-analysis.In the main meta-analysis of 113,926 participants, traffic load on major roads within 100 m of the residence was associated with increased systolic and diastolic BP in nonmedicated participants [0.35 mmHg (95% CI: 0.02, 0.68) and 0.22 mmHg (95% CI: 0.04, 0.40) per 4,000,000 vehicles × m/day, respectively]. The estimated odds ratio (OR) for prevalent hypertension was 1.05 (95% CI: 0.99, 1.11) per 4,000,000 vehicles × m/day. Modeled air pollutants and BP were not clearly associated.In this first comprehensive meta-analysis of European population-based cohorts, we observed a weak positive association of high residential traffic exposure with BP in nonmedicated participants, and an elevated OR for prevalent hypertension. The relationship of modeled air pollutants with BP was inconsistent.
Project description:BACKGROUND: Long-term exposure to traffic-related air pollution may increase blood pressure (BP) and induce hypertension. However, evidence supporting these associations is limited, and they may be confounded by exposure to traffic noise and biased due to inappropriate control for use of BP-lowering medications. OBJECTIVES: We evaluated the associations of long-term traffic-related air pollution with BP and prevalent hypertension, adjusting for transportation noise and assessing different methodologies to control for BP-lowering medications. METHODS: We measured systolic (SBP) and diastolic BP (DBP) at baseline (years 2003-2005) in 3,700 participants, 35-83 years of age, from a population-based cohort in Spain. We estimated home outdoor annual average concentrations of nitrogen dioxide (NO2) with a land-use regression model. We used multivariate linear and logistic regression. RESULTS: A 10-?g/m3 increase in NO2 levels was associated with 1.34 mmHg (95% CI: 0.14, 2.55) higher SBP in nonmedicated individuals, after adjusting for transportation noise. Results were similar in the entire population after adjusting for medication, as commonly done, but weaker when other methods were used to account for medication use. For example, when 10 mmHg were added to the measured SBP levels of medicated participants, the association was ? = 0.78 (95% CI: -0.43, 2.00). NO2 was not associated with hypertension. Associations of NO2 with SBP and DBP were stronger in participants with cardiovascular disease, and the association with SBP was stronger in those exposed to high traffic density and traffic noise levels ? 55 dB(A). CONCLUSIONS: We observed a positive association between long-term exposure to NO2 and SBP, after adjustment for transportation noise, which was sensitive to the methodology used to account for medication.
Project description:BACKGROUND: Recent studies have shown an association of short-term exposure to fine particulate matter (PM) with transient increases in blood pressure (BP), but it is unclear whether long-term exposure has an effect on arterial BP and hypertension. OBJECTIVES: We investigated the cross-sectional association of residential long-term PM exposure with arterial BP and hypertension, taking short-term variations of PM and long-term road traffic noise exposure into account. METHODS: We used baseline data (2000-2003) on 4,291 participants, 45-75 years of age, from the Heinz Nixdorf Recall Study, a population-based prospective cohort in Germany. Urban background exposure to PM with aerodynamic diameter ? 2.5 ?m (PM(2.5)) and ? 10 ?m (PM(10)) was assessed with a dispersion and chemistry transport model. We used generalized additive models, adjusting for short-term PM, meteorology, traffic proximity, and individual risk factors. RESULTS: An interquartile increase in PM2.5 (2.4 ?g/m(3)) was associated with estimated increases in mean systolic and diastolic BP of 1.4 mmHg [95% confidence interval (CI): 0.5, 2.3] and 0.9 mmHg (95% CI: 0.4, 1.4), respectively. The observed relationship was independent of long-term exposure to road traffic noise and robust to the inclusion of many potential confounders. Residential proximity to high traffic and traffic noise exposure showed a tendency toward higher BP and an elevated prevalence of hypertension. CONCLUSIONS: We found an association of long-term exposure to PM with increased arterial BP in a population-based sample. This finding supports our hypothesis that long-term PM exposure may promote atherosclerosis, with air-pollution-induced increases in BP being one possible biological pathway.
Project description:Atrial fibrillation is the most common sustained arrhythmia and is associated with cardiovascular morbidity and mortality. The few studies conducted on short-term effects of air pollution on episodes of atrial fibrillation indicate a positive association, though not consistently.The aim of this study was to evaluate the long-term impact of traffic-related air pollution on incidence of atrial fibrillation in the general population.In the Danish Diet, Cancer, and Health cohort of 57,053 people 50-64 years old at enrollment in 1993-1997, we identified 2,700 cases of first-ever hospital admission for atrial fibrillation from enrollment to end of follow-up in 2011. For all cohort members, exposure to traffic-related air pollution assessed as nitrogen dioxide (NO2) and nitrogen oxides (NOx) was estimated at all present and past residential addresses from 1984 to 2011 using a validated dispersion model. We used Cox proportional hazard model to estimate associations between long-term residential exposure to NO2 and NOx and risk of atrial fibrillation, after adjusting for lifestyle and socioeconomic position.A 10 ?g/m3 higher 10-year time-weighted mean exposure to NO2 preceding diagnosis was associated with an 8% higher risk of atrial fibrillation [incidence rate ratio: 1.08; 95% confidence interval (CI): 1.01, 1.14] in adjusted analysis. Though weaker, similar results were obtained for long-term residential exposure to NOx. We found no clear tendencies regarding effect modification of the association between NO2 and atrial fibrillation by sex, smoking, hypertension or myocardial infarction.We found long-term residential traffic-related air pollution to be associated with higher risk of atrial fibrillation. Accordingly, the present findings lend further support to the demand for abatement of air pollution. Citation: Monrad M, Sajadieh A, Christensen JS, Ketzel M, Raaschou-Nielsen O, Tjønneland A, Overvad K, Loft S, Sørensen M. 2017. Long-term exposure to traffic-related air pollution and risk of incident atrial fibrillation: a cohort study. Environ Health Perspect 125:422-427; http://dx.doi.org/10.1289/EHP392.
Project description:INTRODUCTION: Experimental and epidemiological studies have reported associations between air pollution exposure, in particular related to vehicle exhaust, and cardiovascular disease. A potential pathophysiological pathway is pollution-induced pulmonary oxidative stress, with secondary systemic inflammation. Genetic polymorphisms in genes implicated in oxidative stress, such as GSTP1, GSTT1 and GSTCD, may contribute to determining individual susceptibility to air pollution as a promoter of coronary vulnerability. AIMS: We aimed to investigate effects of long-term traffic-related air pollution exposure, as well as variants in GSTP1, GSTT1 and GSTCD, on risk of acute myocardial infarction (AMI) and hypertension. In addition, we studied whether air pollution effects were modified by the investigated genetic variants. METHODS: Genotype data at 7 single nucleotide polymorphisms (SNPs) in the GSTP1 gene, and one in each of the GSTT1 and GSTCD genes, as well as air pollution exposure estimates, were available for 119 AMI cases and 1310 randomly selected population controls. Population control individuals with systolic blood pressure ?140 mmHg, diastolic blood pressure ?90 mmHg or on daily antihypertensive medication were defined as hypertensive (n = 468). Individual air pollution exposure levels were modeled as annual means of NO? (marker of vehicle exhaust pollutants) using central monitoring data and dispersion models, linking to participants' home addresses. RESULTS: Air pollution was significantly associated with risk of AMI: OR 1.78 (95%CI 1.04-3.03) per 10 µg/m³ of long-term NO? exposure. Three GSTP1 SNPs were significantly associated with hypertension. The effect of air pollution on risk of AMI varied by genotype strata, although the suggested interaction was not significant. We saw no obvious interaction between genetic variants in the GST genes and air pollution exposure for hypertension. CONCLUSION: Air pollution exposure entails an increased risk of AMI, and this risk differed over genotype strata for variants in the GSTP1, GSTT1 and GSTCD genes, albeit not statistically-significantly.
Project description:Air pollution causes hypertension, cardiovascular disease, and mortality. Asian dust (AD) reportedly induces asthma or acute myocardial infarction along with air pollution, but its impact on blood pressure (BP) is unknown. We investigated the association between short-term AD exposure and BP fluctuations in 300,952 individuals whose BP was measured during April 2005-March 2015 and divided them into AD and non-AD groups based on visitation for AD-related events. AD's occurrence, air pollutants' concentration (suspended particulate matter, SO2, NO2, photochemical oxidants), and meteorological variables (mean ambient temperature, relative humidity) were obtained from a monitoring station; AD events correlated with decreased visibility (< 10 km). We observed 61 AD days, with 3897 participants undergoing medical check-ups. Short-term AD exposure at lag day-0 was significantly associated with higher systolic BP (SBP), diastolic BP (DBP), and pulse rate (PR) risk (? = 1.85, 95% confidence interval (CI) 1.35-2.35 for SBP, ? = 2.24, 95% CI 1.88-2.61 for DBP, ? = 0.52, 95% CI 0.14-0.91 for PR) using multi-pollutant model. Population-attributable fractions exposed to AD were 11.5% for those with elevated SBP (SBP ? 120 mmHg) and 23.7% for those with hypertension (SBP ? 140 mmHg or DBP ? 90 mmHg). This study showed a strong association between short-term AD exposure and increased SBP and DBP.
Project description:Long-term exposure to particulate matter (PM) air pollution may increase blood pressure and the risk of hypertension. However, epidemiological evidence is scarce and inconsistent.We investigated the associations between long-term exposure to PM with an aerodynamic diameter <2.5?m (PM2.5), blood pressure, and incident hypertension in a large Taiwanese cohort.We studied 361,560 adults ?18y old from a large cohort who participated in a standard medical examination program during 2001 to 2014. Among this group, 125,913 nonhypertensive participants were followed up. A satellite-based spatiotemporal model was used to estimate the 2-y average PM2.5 concentrations at each participant's address. Multivariable linear regression was used in the cross-sectional data analysis with the 361,560 participants to investigate the associations between PM2.5 and systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse pressure (PP), and Cox proportional hazard regression was used in the cohort data analysis with the 125,913 participants to investigate the associations between PM2.5 and incident hypertension.Each 10-?g/m3 increment in the 2-y average PM2.5 concentration was associated with increases of 0.45?mmHg [95% confidence interval (CI): 0.40, 0.50], 0.07?mmHg (95% CI: 0.04, 0.11), and 0.38?mmHg (95% CI: 0.33, 0.42) in SBP, DBP, and PP, respectively, after adjusting for a wide range of covariates and possible confounders. Each 10-?g/m3 increment in the 2-y average PM2.5 concentration was associated with an increase of 3% in the risk of developing hypertension [hazard?ratio=1.03 (95% CI: 1.01, 1.05)]. Stratified and sensitivity analyses yielded similar results.Long-term exposure to PM2.5 air pollution is associated with higher blood pressure and an increased risk of hypertension. These findings reinforce the importance of air pollution mitigation strategies to reduce the risk of cardiovascular disease. https://doi.org/10.1289/EHP2466.
Project description:Living near major roadways has been associated with increased risk of cardiovascular morbidity and mortality, presumably from exposure to elevated levels of traffic-related air and/or noise pollution. This association may potentially be mediated through increased risk of incident hypertension, but results from prior studies are equivocal. Using Cox proportional hazards models we examined residential proximity to major roadways and incident hypertension among 38,360 participants of the Women's Health Initiative (WHI) Clinical Trial cohorts free of hypertension at enrollment and followed for a median of 7.9 years. Adjusting for participant demographics and lifestyle, trial participation, and markers of individual and neighborhood socioeconomic status, the hazard ratios for incident hypertension were 1.13 (95% CI: 1.00, 1.28), 1.03 (0.95, 1.11), 1.05 (0.99, 1.11), and 1.05 (1.00, 1.10) for participants living ?50, >50-200, >200-400, and >400-1000 m vs >1000 m from the nearest major roadway, respectively (ptrend=0.013). This association varied substantially by WHI study region with hazard ratios for women living ?50 m from a major roadway of 1.61 (1.18, 2.20) in the West, 1.51 (1.22, 1.87) in the Northeast, 0.89 (0.70, 1.14) in the South, and 0.94 (0.75, 1.19) in the Midwest. In this large, national cohort of post-menopausal women, residential proximity to major roadways was associated with incident hypertension in selected regions of the U.S. If causal, these results suggest residential proximity to major roadways, as a marker for air, noise and other traffic-related pollution, may be a risk factor for hypertension.
Project description:BACKGROUND:Two recent case-control studies in Italy reported that long-term exposure to particulate air pollution or living near major traffic roads was associated with an increased risk of deep vein thrombosis (DVT). No prospective evidence exists on the possible association between long-term traffic-related air pollution and incident venous thromboembolism (VTE). OBJECTIVES:To examine the association between long-term traffic exposure and incident VTE in a population-based prospective cohort study. METHODS:We studied 13,143 middle-aged men and women in the Atherosclerosis Risk in Communities Study without a history of DVT or pulmonary embolism at baseline examination (1987-1989). The Geographical Information System-mapped traffic density and distance to major roads in the four study communities served as measures of traffic exposure. We examined the association between traffic exposure and incident VTE with proportional hazards regression models. RESULTS:A total of 405 subjects developed VTE in 2005. Traffic density was not significantly associated with VTE. Relative to those in the lowest quartile of traffic density, the adjusted hazard ratios across increasing quartiles were 1.18 (95% confidence interval [CI] 0.88-1.57), 0.99 (95% CI 0.74-1.34) and 1.14 (95% CI 0.86-1.51) (P-value for trend across quartiles = 0.64). For residents living within 150 m of major roads, as compared with subjects living further away, the adjusted hazard ratio was 1.16 (95% CI 0.95-1.42, P = 0.14). CONCLUSIONS:This first prospective study in the general population does not support an association between air pollution exposure or traffic proximity and risk of DVT. More data may be needed to clarify whether traffic or air pollution influences the risk of VTE.
Project description:The Ghana Randomized Air Pollution and Health Study (GRAPHS) is a community-level randomized-controlled trial of cookstove interventions for pregnant women and their newborns in rural Ghana. Given that household air pollution from biomass burning may be implicated in adverse cardiovascular outcomes, we sought to determine whether exposure to carbon monoxide (CO) from woodsmoke was associated with blood pressure (BP) among 817 adult women.Multivariate linear regression models were used to evaluate the association between CO exposure, determined with 72 hour personal monitoring at study enrollment, and BP, also measured at study enrollment. At the time of these assessments, women were in the first or second trimester of pregnancy.A significant positive association was found between CO exposure and diastolic blood pressure (DBP): on average, each 1 ppm increase in exposure to CO was associated with 0.43 mmHg higher DBP [0.01, 0.86]. A non-significant positive trend was also observed for systolic blood pressure (SBP).This study is one of very few to have examined the relationship between household air pollution and blood pressure among pregnant women, who are at particular risk for hypertensive complications. The results of this cross-sectional study suggest that household air pollution from wood-burning fires is associated with higher blood pressure, particularly DBP, in pregnant women at early to mid-gestation. The clinical implications of the observed association toward the eventual development of chronic hypertension and/or hypertensive complications of pregnancy remain uncertain, as few of the women were overtly hypertensive at this point in their pregnancies.