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The association of traffic-related air and noise pollution with maternal blood pressure and hypertensive disorders of pregnancy in the HOME study cohort.
ABSTRACT: Traffic-related air and noise pollution may increase the risk for cardiovascular disorders, especially among susceptible populations like pregnant women. The objective of this study was to evaluate the association of exposure to traffic-related air pollution and traffic noise with blood pressure in pregnant women. We extracted systolic blood pressure (SBP) and diastolic blood pressure (DBP) at ?20?weeks gestation, as well as hypertensive disorders of pregnancy from medical records in the HOME Study, a prospective pregnancy and birth cohort from Cincinnati, OH (n?=?370). We estimated exposure to elemental carbon attributable to traffic (ECAT),1 a marker of traffic-related air pollution, at women's residences at ~20?weeks gestation using a validated land use regression model and traffic noise using a publicly available transportation noise model. We used linear mixed models and modified Poisson regression adjusted for covariates to examine associations of ECAT and traffic noise with blood pressure and hypertensive disorders of pregnancy risk, respectively. In adjusted models, we found a 1.6 (95% CI?=?0.02, 3.3; p?=?0.048) mm?Hg increase in SBP associated with an interquartile range increase in ECAT concentration; the association was stronger after adjusting for traffic noise (1.9?mm?Hg, 95%?=?0.1, 3.7; p?=?0.035). ECAT concentrations were not significantly associated with DBP or hypertensive disorders of pregnancy, and traffic noise was not associated with SBP, DBP, or hypertensive disorders of pregnancy. There was no evidence of a joint effect of traffic noise and ECAT on any outcome. In this cohort, higher residential traffic-related air pollution exposure at ~20?weeks gestation was associated with higher SBP in late pregnancy. It is important for future studies of traffic-related air or noise pollution to jointly consider both exposures and neighborhood characteristics given their correlation and potential cumulative impact on cardiovascular health.
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: Traffic noise has been associated with prevalence of hypertension, but reports are inconsistent for blood pressure (BP). To ascertain noise effects and to disentangle them from those suspected to be from traffic-related air pollution, it may be essential to estimate people's noise exposure indoors in bedrooms. OBJECTIVES: We analyzed associations between long-term exposure to indoor traffic noise in bedrooms and prevalent hypertension and systolic (SBP) and diastolic (DBP) BP, considering long-term exposure to outdoor nitrogen dioxide (NO2). METHODS: We evaluated 1,926 cohort participants at baseline (years 2003-2006; Girona, Spain). Outdoor annual average levels of nighttime traffic noise (Lnight) and NO2 were estimated at postal addresses with a detailed traffic noise model and a land-use regression model, respectively. Individual indoor traffic Lnight levels were derived from outdoor Lnight with application of insulations provided by reported noise-reducing factors. We assessed associations for hypertension and BP with multi-exposure logistic and linear regression models, respectively. RESULTS: Median levels were 27.1 dB(A) (indoor Lnight), 56.7 dB(A) (outdoor Lnight), and 26.8 ?g/m3 (NO2). Spearman correlations between outdoor and indoor Lnight with NO2 were 0.75 and 0.23, respectively. Indoor Lnight was associated both with hypertension (OR = 1.06; 95% CI: 0.99, 1.13) and SBP (? = 0.72; 95% CI: 0.29, 1.15) per 5 dB(A); and NO2 was associated with hypertension (OR = 1.16; 95% CI: 0.99, 1.36), SBP (? = 1.23; 95% CI: 0.21, 2.25), and DBP (??= 0.56; 95% CI: -0.03, 1.14) per 10 ?g/m3. In the outdoor noise model, Lnight was associated only with hypertension and NO2 with BP only. The indoor noise-SBP association was stronger and statistically significant with a threshold at 30 dB(A). CONCLUSION: Long-term exposure to indoor traffic noise was associated with prevalent hypertension and SBP, independently of NO2. Associations were less consistent for outdoor traffic Lnight and likely affected by collinearity.
Project description: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:Background:Early-life exposure to traffic-related air pollution may decrease fetal growth and increase childhood obesity risk. Our objective was to evaluate the relationship of early-life exposure to traffic-related air pollution with birthweight in term newborns and obesity at age 7-8 years in two prospective birth cohorts in Cincinnati, OH (the Health Outcomes and Measures of the Environment (HOME) Study and Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS)). Methods:We estimated elemental carbon attributable to traffic (ECAT) exposure at residential addresses during pregnancy with a validated land use regression model. We assessed birthweight among term infants using birth records or parent report (HOME Study n= 333 and CCAAPS n=590). We measured children's weight and height at 7-8 years, and calculated age- and sex-specific BMI z-scores (HOME Study n= 198 and CCAAPS n=459). Using multivariable linear regression, we estimated the difference in term birthweight and BMI z-score per interquartile range (IQR) increase in ECAT concentrations in each cohort separately and in the pooled sample. Results:In adjusted models, ECAT exposure was not associated with lower birthweight (pooled sample ?: 30g; 95% CI: -6, 66), or with higher BMI z-score (pooled sample ?: -0.04; 95% CI: -0.15, 0.08). Infant sex modified the association between ECAT and birthweight (p=0.05). Among male newborns, higher ECAT concentrations were associated with higher birthweight (?: 61g; 95% CI: 9, 113), but we observed no association among female newborns (?: -9g; 95% CI: -58, 41). Conclusions:In contrast to some prior studies, early-life traffic-related air pollution exposure was not associated with lower birthweight or increased childhood adiposity in these two cohorts.
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.
Project description:Associations between road traffic noise and hypertension have been repeatedly documented, whereas associations with rail or total road, rail, and air (RRA) traffic noise have rarely been investigated. Moreover, most studies of noise in the environment have only taken into account the residential neighborhood. Finally, few studies have taken into account individual/neighborhood confounders in the relationship between noise and hypertension. We performed adjusted multilevel regression analyses using data from the 7,290 participants of the RECORD Study to investigate the associations of outdoor road, rail, air, and RRA traffic noise estimated at the place of residence, at the workplace, and in the neighborhoods around the residence and workplace with systolic blood pressure (SBP), diastolic blood pressure (DBP), and hypertension. Associations were documented between higher outdoor RRA and road traffic noise estimated at the workplace and a higher SBP [+1.36 mm of mercury, 95% confidence interval (CI): +0.12, +2.60 for 65-80 dB(A) vs 30-45 dB(A)] and DBP [+1.07 (95% CI: +0.28, +1.86)], after adjustment for individual/neighborhood confounders. These associations remained after adjustment for risk factors of hypertension. Associations were documented neither with rail traffic noise nor for hypertension. Associations between transportation noise at the workplace and blood pressure (BP) may be attributable to the higher levels of road traffic noise at the workplace than at the residence. To better understand why only noise estimated at the workplace was associated with BP, our future work will combine Global Positioning System (GPS) tracking, assessment of noise levels with sensors, and ambulatory monitoring of BP.
Project description:BACKGROUND:Studies on the hypertensive effect of long-term air pollution exposure were inconclusive and showed scarce evidence from rural areas in developing countries. In this context, we examined the associations of air pollution exposure with hypertension and blood pressure, and their effect modifiers in rural Chinese adults. METHODS:We studied 39,259 participants from a cohort established in five rural regions of central China. Individual exposures to PM2.5 and PM10 (particulate matter with an aerodynamic diameter less than or equal to 2.5 ?m and 10 ?m) and nitrogen dioxide (NO2) was evaluated using satellite-based spatiotemporal models. Mixed-effect regression models were applied to examine the associations of long-term exposure to air pollution with hypertension and four blood pressure component measurements, including systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP) and pulse pressure (PP). Several potential effect modifiers related to demographic and behavioral factors were also examined. RESULTS:The results showed that for each 1 ?g/m3 increase in PM2.5, PM10 and NO2, the adjusted odds ratio of hypertension was 1.029 (95%CI: 1.001,1.057), 1.015 (95%CI: 1.001, 1.029) and 1.069 (95%CI: 1.038, 1.100), respectively. These three air pollutants were also associated with increased SBP (except for PM10), DBP and MAP. The hypertensive effects of air pollution were more pronounced among males, smokers, drinkers, individuals with a high-fat diet, and those with high-level physical activity. CONCLUSION:Long-term exposure to PM2.5, PM10 and NO2 was associated with increased blood pressure and hypertension in rural Chinese adults, and the associations were modified by several behavioral factors.
Project description:BACKGROUND:While air pollution has been associated with depression and anxiety in adults, its impact on childhood mental health is understudied. OBJECTIVE:We examined lifetime exposure to traffic-related air pollution (TRAP) and symptoms of depression and anxiety at age 12 years in the Cincinnati Childhood Allergy and Air Pollution Study cohort. METHODS:We estimated exposure to elemental carbon attributable to traffic (ECAT), a surrogate of diesel exhaust, at birth, age 12 years, and average exposure throughout childhood, using a validated land use regression model. We assessed depression and anxiety at age 12 years by parent report with the Behavior Assessment System for Children-2, and by child report with the Child Depression Inventory-2 (CDI-2) and the Spence Children's Anxiety Scale (SCAS). Associations between TRAP at birth, age 12 years, and childhood average and mental health outcomes were estimated using linear regression models adjusting for covariates including parent depression, secondhand smoke exposure, race, household income, and others. RESULTS:Exposure to ECAT was not significantly associated with parent-reported depression or anxiety. However, exposure to ECAT at birth was associated with increased child-reported depression and anxiety. Each 0.25?µg/m3 increase in ECAT was associated with a 3.5 point increase (95% CI 1.6-5.5) in CDI-2 scores and 2.3 point increase (95% CI 0.8-3.9) in SCAS total anxiety scores. We observed similar associations between average childhood ECAT exposures but not for concurrent exposures at age 12. CONCLUSIONS:TRAP exposure during early life and across childhood was significantly associated with self-reported depression and anxiety symptoms in children. The negative impact of air pollution on mental health previously reported among adults may also be present during childhood.
Project description:Objective To investigate the relation between exposure to both air and noise pollution from road traffic and birth weight outcomes.Design Retrospective population based cohort study.Setting Greater London and surrounding counties up to the M25 motorway (2317 km2), UK, from 2006 to 2010.Participants 540?365 singleton term live births.Main outcome measures Term low birth weight (LBW), small for gestational age (SGA) at term, and term birth weight.Results Average air pollutant exposures across pregnancy were 41 ?g/m3 nitrogen dioxide (NO2), 73 ?g/m3 nitrogen oxides (NOx), 14 ?g/m3 particulate matter with aerodynamic diameter <2.5 ?m (PM2.5), 23 ?g/m3 particulate matter with aerodynamic diameter <10 ?m (PM10), and 32 ?g/m3 ozone (O3). Average daytime (LAeq,16hr) and night-time (Lnight) road traffic A-weighted noise levels were 58 dB and 53 dB respectively. Interquartile range increases in NO2, NOx, PM2.5, PM10, and source specific PM2.5 from traffic exhaust (PM2.5 traffic exhaust) and traffic non-exhaust (brake or tyre wear and resuspension) (PM2.5 traffic non-exhaust) were associated with 2% to 6% increased odds of term LBW, and 1% to 3% increased odds of term SGA. Air pollutant associations were robust to adjustment for road traffic noise. Trends of decreasing birth weight across increasing road traffic noise categories were observed, but were strongly attenuated when adjusted for primary traffic related air pollutants. Only PM2.5 traffic exhaust and PM2.5 were consistently associated with increased risk of term LBW after adjustment for each of the other air pollutants. It was estimated that 3% of term LBW cases in London are directly attributable to residential exposure to PM2.5>13.8 ?g/m3during pregnancy.Conclusions The findings suggest that air pollution from road traffic in London is adversely affecting fetal growth. The results suggest little evidence for an independent exposure-response effect of traffic related noise on birth weight outcomes.
Project description:Previous studies suggested associations between prenatal exposure to air pollution and hypertensive disorders of pregnancy. We explored the associations between ambient concentrations of five major air pollutants during preconceptional and prenatal periods and three hypertensive disorders of pregnancy in Seoul, Korea, using a population-representative cohort.We obtained heath and demographic data of pregnant women residing in Seoul for 2002-2013 from the Korean National Health Insurance Service-National Sample Cohort. For mother's individual exposures to air pollution, we computed concentrations of particulate matter ?10 ?m in diameter (PM10), nitrogen dioxide (NO2), carbon monoxide (CO), sulfur dioxide (SO2), and ozone (O3) during 1, 3, 6, and 12 months to birth using regulatory monitoring data in Seoul. The associations between air pollution and hypertensive disorders were explored by using logistic regression models after adjusting for individual confounders.Among 18,835 pregnant women in Seoul, 0.6, 0.5, and 0.4% of women developed gestational hypertension, preeclampsia, and preeclampsia requiring magnesium sulfate (Mg-preeclampsia), respectively. Although most odds ratios (ORs) were not statistically significant, we found increasing risk gradients with disease severity depending on the pollutant. There was the association between PM10 during 6 months to birth and gestational hypertension (OR for an interquartile range increase?=?1.68 [95% confidence interval?=?1.09-2.58]). NO2 and ozone during 12 and 1 month, respectively, before birth were associated with Mg-preeclampsia (1.43 [1.01-2.03], 1.53 [1.03-2.27]).We observed positive associations of exposure to some air pollutants before and during pregnancy with hypertensive disorders of pregnancy among the Korean general population. Future studies with refined exposure metrics should confirm our findings.