Short-term effects of air pollution on blood pressure.
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ABSTRACT:
SUBMITTER: Choi YJ
PROVIDER: S-EPMC6937254 | biostudies-literature | 2019 Dec
REPOSITORIES: biostudies-literature
Publications
Short-term effects of air pollution on blood pressure.
Choi You-Jung YJ Kim Sun-Hwa SH Kang Si-Hyuck SH Kim Sun-Young SY Kim Ok-Jin OJ Yoon Chang-Hwan CH Lee Hae-Young HY Youn Tae-Jin TJ Chae In-Ho IH Kim Cheol-Ho CH
Scientific reports 20191230 1
Elevated blood pressure (BP) has been proposed as a possible pathophysiological mechanism linking exposure to ambient air pollution and the increased risk of cardiovascular mortality and morbidity. In this study, we investigated the hourly relationship between ambient air pollutants and BP. BP measurements were extracted from the electronic health record database of the Seoul National University Bundang Hospital from February 2015 to June 2017. A total of 98,577 individual BP measurements were m ...[more]
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Project description:BackgroundExposure to air pollution has been consistently associated with cardiovascular morbidity and mortality, but mechanisms remain uncertain. Associations with blood pressure (BP) may help to explain the cardiovascular effects of air pollution.ObjectiveWe examined the cross-sectional relationship between long-term (annual average) residential air pollution exposure and BP in the National Institute of Environmental Health Sciences' Sister Study, a large U.S. cohort study investigating risk factors for breast cancer and other outcomes.MethodsThis analysis included 43,629 women 35-76 years of age, enrolled 2003-2009, who had a sister with breast cancer. Geographic information systems contributed to satellite-based nitrogen dioxide (NO2) and fine particulate matter (? 2.5 ?m; PM2.5) predictions at participant residences at study entry. Generalized additive models were used to examine the relationship between pollutants and measured BP at study entry, adjusting for cardiovascular disease risk factors and including thin plate splines for potential spatial confounding.ResultsA 10-?g/m(3) increase in PM2.5 was associated with 1.4-mmHg higher systolic BP (95% CI: 0.6, 2.3; p < 0.001), 1.0-mmHg higher pulse pressure (95% CI: 0.4, 1.7; p = 0.001), 0.8-mmHg higher mean arterial pressure (95% CI: 0.2, 1.4; p = 0.01), and no significant association with diastolic BP. A 10-ppb increase in NO2 was associated with a 0.4-mmHg (95% CI: 0.2, 0.6; p < 0.001) higher pulse pressure.ConclusionsLong-term PM2.5 and NO2 exposures were associated with higher blood pressure. On a population scale, such air pollution-related increases in blood pressure could, in part, account for the increases in cardiovascular disease morbidity and mortality seen in prior studies.
| S-EPMC4590742 | biostudies-literature
Project description:BackgroundRecent 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.ObjectivesWe 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.MethodsWe 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 μm (PM(2.5)) and ≤ 10 μm (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.ResultsAn interquartile increase in PM2.5 (2.4 μg/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.ConclusionsWe 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.
| S-EPMC3261981 | biostudies-literature
Project description:BackgroundLong-term exposure to air pollution has been hypothesized to elevate arterial blood pressure (BP). The existing evidence is scarce and country specific.ObjectivesWe investigated the cross-sectional association of long-term traffic-related air pollution with BP and prevalent hypertension in European populations.MethodsWe 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.ResultsIn 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.ConclusionsIn 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.
| S-EPMC4154218 | biostudies-literature
Project description:The association between air pollution and childhood respiratory disease is inconsistent. In the present study, we investigated a short-term effect of ambient air pollutants and daily childhood lower respiratory diseases (CLRD). Daily air pollutants, weather data, and CLRD data were collected from January 2014 to April 2015 (452 days) in Nanjing, China. Time-series regression and generalized additive models were used to assess the effects of air pollutants (PM10, PM2.5, NO2, SO2, O3, and CO) on CLRD. We observed that an interquartile range (IQR) increase in concentrations of PM10, NO2, and SO2 significantly increased the daily CLRD with 6 days cumulative effects (difference of estimates: 2.8%, 95% CI: 0.6-5.0%; 4.1%, 1.2-7.0%; 5.6%, 2.6-8.6%, respectively). However, no significant association was found in IQR concentrations of PM2.5, O3, and CO. Specifically, elevated PM10, PM2.5, NO2, and SO2 significantly increased the numbers of CLRD in cool season (3.6%, 1.5-5.7%; 2.4%, 0.3-4.5%; 4.9%, 2.9-7.0%; 6.3%, 3.7-9.0%, respectively). Additionally, the effect estimates of PM10, NO2, and SO2 in female and age >27 months were more pronounced than in male and age ≤27 months. This study suggested that short-term exposure to ambient PM10, NO2, and SO2 were associated with the increased CLRD numbers.
| S-EPMC5493680 | biostudies-literature
Project description:This paper assesses the effect of short-term exposure to particulate matter (PM) air pollution on human cognitive performance via a double cross over experimental design. Two distinct experiments were performed, both of which exposed subjects to low and high concentrations of PM. Firstly, subjects completed a series of cognitive tests after being exposed to low ambient indoor PM concentrations and elevated PM concentrations generated via candle burning, which is a well-known source of PM. Secondly, a different cohort underwent cognitive tests after being exposed to low ambient indoor PM concentrations and elevated ambient outdoor PM concentrations via commuting on or next to roads. Three tests were used to assess cognitive performance: Mini-Mental State Examination (MMSE), the Stroop Color and Word test, and Ruff 2 & 7 test. The results from the MMSE test showed a statistically robust decline in cognitive function after exposure to both the candle burning and outdoor commuting compared to ambient indoor conditions. The similarity in the results between the two experiments suggests that PM exposure is the cause of the short-term cognitive decline observed in both. The outdoor commuting experiment also showed a statistically significant short-term cognitive decline in automatic detection speed from the Ruff 2 and 7 selective attention test. The other cognitive tests, for both the candle and commuting experiments, showed no statistically significant difference between the high and low PM exposure conditions. The findings from this study are potentially far reaching; they suggest that elevated PM pollution levels significantly affect short term cognition. This implies average human cognitive ability will vary from city to city and country to country as a function of PM air pollution exposure.
| S-EPMC6546704 | biostudies-literature
Project description:BackgroundAir pollution exposure has been associated with increased blood pressure in adults.ObjectiveWe examined associations of antenatal exposure to ambient air pollution with newborn systolic blood pressure (SBP).MethodsWe studied 1,131 mother-infant pairs in a Boston, Massachusetts, area pre-birth cohort. We calculated average exposures by trimester and during the 2 to 90 days before birth for temporally resolved fine particulate matter (? 2.5 ?m; PM2.5), black carbon (BC), nitrogen oxides, nitrogen dioxide, ozone (O3), and carbon monoxide measured at stationary monitoring sites, and for spatiotemporally resolved estimates of PM2.5 and BC at the residence level. We measured SBP at a mean age of 30 ± 18 hr with an automated device. We used mixed-effects models to examine associations between air pollutant exposures and SBP, taking into account measurement circumstances; child's birth weight; mother's age, race/ethnicity, socioeconomic position, and third-trimester BP; and time trend. Estimates represent differences in SBP associated with an interquartile range (IQR) increase in each pollutant.ResultsHigher mean PM2.5 and BC exposures during the third trimester were associated with higher SBP (e.g., 1.0 mmHg; 95% CI: 0.1, 1.8 for a 0.32-?g/m3 increase in mean 90-day residential BC). In contrast, O3 was negatively associated with SBP (e.g., -2.3 mmHg; 95% CI: -4.4, -0.2 for a 13.5-ppb increase during the 90 days before birth).ConclusionsExposures to PM2.5 and BC in late pregnancy were positively associated with newborn SBP, whereas O3 was negatively associated with SBP. Longitudinal follow-up will enable us to assess the implications of these findings for health during later childhood and adulthood.
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Project description:Indonesia faces significant air quality issues due to multiple emissions sources, including rapid urbanization and peatland fires associated with agricultural land management. Limited prior research has estimated the episodic shock of intense fires on morbidity and mortality in Indonesia but has largely ignored the impact of poor air quality throughout the year on biomarkers of cardiovascular disease risk. We conducted a cross-sectional study of the association between particulate matter less than 2.5 microns in diameter (PM2.5) and blood pressure. Blood pressure measurements were obtained from the fifth wave of the Indonesian Family Life Survey (IFLS5), an ongoing population-based socioeconomic and health survey. We used the GEOS-Chem chemical transport model to simulate daily PM2.5 concentrations at 0.5° × 0.625° resolution across the IFLS domain. We assessed the association between PM2.5 and diastolic and systolic blood pressure, using mixed effects models with random intercepts for regency/municipality and household and adjusted for individual covariates. An interquartile range increase in monthly PM2.5 exposure was associated with a 0.234 (95% CI: 0.003, 0.464) higher diastolic blood pressure, with a greater association seen in participants age 65 and over (1.16 [95% CI: 0.24, 2.08]). For the same exposure metric, there was a 1.90 (95% CI: 0.43, 3.37) higher systolic blood pressure in participants 65 and older. Our assessment of fire-specific PM2.5 yielded null results, potentially due to the timing and locations of health data collection. To our knowledge, this is the first study to provide evidence for an association between PM2.5 and blood pressure in Indonesia.
| S-EPMC11217989 | biostudies-literature
Project description:Air pollution effects on cardiovascular hospitalizations in small urban/suburban areas have been scantly investigated. Such effects were assessed among the participants in the analytical epidemiological survey carried out in Pisa and Cascina, Tuscany, Italy (2009-2011). Cardiovascular hospitalizations from 1585 subjects were followed up (2011-2015). Daily mean pollutant concentrations were estimated through random forests at 1 km (particulate matter: PM10, 2011-2015; PM2.5, 2013-2015) and 200 m (PM10, PM2.5, NO2, O3, 2013-2015) resolutions. Exposure effects were estimated using the case-crossover design and conditional logistic regression (odds ratio-OR-and 95% confidence interval-CI-for 10 μg/m3 increase; lag 0-6). During the period 2011-2015 (137 hospitalizations), a significant effect at lag 0 was observed for PM10 (OR = 1.137, CI: 1.023-1.264) at 1 km resolution. During the period 2013-2015 (69 hospitalizations), significant effects at lag 0 were observed for PM10 (OR = 1.268, CI: 1.085-1.483) and PM2.5 (OR = 1.273, CI: 1.053-1.540) at 1 km resolution, as well as for PM10 (OR = 1.365, CI: 1.103-1.690), PM2.5 (OR = 1.264, CI: 1.006-1.589) and NO2 (OR = 1.477, CI: 1.058-2.061) at 200 m resolution; significant effects were observed up to lag 2. Larger ORs were observed in males and in subjects reporting pre-existent cardiovascular/respiratory diseases. Combining analytical and routine epidemiological data with high-resolution pollutant estimates provides new insights on acute cardiovascular effects in the general population and in potentially susceptible subgroups living in small urban/suburban areas.
| S-EPMC7908381 | biostudies-literature
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.
| S-EPMC4216159 | biostudies-literature
Project description:IntroductionAfrican Americans are disproportionately affected by high blood pressure, which may be associated with exposure to air pollutants, such as fine particulate matter and ozone.MethodsAmong African American Jackson Heart Study participants, this study examined associations between 1-year and 3-year mean fine particulate matter and ozone concentrations with prevalent and incident hypertension at Visits 1 (2000-2004, n=5,191) and 2 (2005-2008, n=4,105) using log binomial regression. Investigators examined associations with systolic blood pressure, diastolic blood pressure, pulse pressure, and mean arterial pressure using linear regression and hierarchical linear models, adjusting for sociodemographic, behavioral, and clinical characteristics. Analyses were conducted in 2017-2019.ResultsNo associations were observed between fine particulate matter or ozone concentration and prevalent or incident hypertension. In linear models, an IQR increase in 1-year ozone concentration was associated with 0.67 mmHg higher systolic blood pressure (95% CI=0.27, 1.06), 0.42 mmHg higher diastolic blood pressure (95% CI=0.20, 0.63), and 0.50 mmHg higher mean arterial pressure (95% CI=0.26, 0.74). In hierarchical models, fine particulate matter was inversely associated with systolic blood pressure (-0.72, 95% CI= -1.31, -0.13), diastolic blood pressure (-0.69, 95% CI= -1.02, -0.36), and mean arterial pressure (-0.71, 95% CI= -1.08, -0.33). Attenuated associations were observed with 1-year concentrations and at Visit 1.ConclusionsPositive associations were observed between ozone and systolic blood pressure, diastolic blood pressure, and mean arterial pressure, and inverse associations between fine particulate matter and systolic blood pressure, diastolic blood pressure, and mean arterial pressure in an African American population with high (56%) prevalence of hypertension. Effect sizes were small and may not be clinically relevant.
| S-EPMC10388406 | biostudies-literature