Effects of Ambient Air Pollution on Blood Pressure Among Children and Adolescents: A Systematic Review and Meta-Analysis.
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SUBMITTER: Huang M
PROVIDER: S-EPMC8200690 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Maternal exposure to ambient air pollution has been associated with adverse birth outcomes such as preterm delivery. However, only one study to date has linked air pollution to blood pressure changes during pregnancy, a period of dramatic cardiovascular function changes.We examined whether maternal exposures to criteria air pollutants, including particles of less than 10 ?m (PM(10)) or 2.5 ?m diameter (PM(2.5)), carbon monoxide (CO), nitrogen dioxide (NO(2)), sulfur dioxide (SO(2)), and ozone (O(3)), in each trimester of pregnancy are associated with magnitude of rise of blood pressure between the first 20 weeks of gestation and late pregnancy in a prospectively followed cohort of 1684 pregnant women in Allegheny County, PA.Air pollution measures for maternal ZIP code areas were derived using Kriging interpolation. Using logistic regression analysis, we evaluated the associations between air pollution exposures and blood pressure changes between the first 20 weeks of gestation and late pregnancy.First trimester PM(10) and ozone exposures were associated with blood pressure changes between the first 20 weeks of gestation and late pregnancy, most strongly in non-smokers. Per interquartile increases in first trimester PM(10) and O(3) concentrations were associated with mean increases in systolic blood pressure of 1.88 mm Hg (95% CI=0.84 to 2.93) and 1.84 (95% CI=1.05 to 4.63), respectively, and in diastolic blood pressure of 0.63 mm Hg (95% CI=-0.50 to 1.76) and 1.13 (95% CI=-0.46 to 2.71) in non-smokers.Our novel finding suggests that first trimester PM(10) and O(3) air pollution exposures increase blood pressure in the later stages of pregnancy. These changes may play a role in mediating the relationships between air pollution and adverse birth outcomes.
| S-EPMC3656658 | biostudies-literature
Project description:BackgroundEvidence linking long-term exposure to particulate air pollution to blood pressure (BP) in high-income countries may not be transportable to low- and middle-income countries. We examined cross-sectional associations between ambient fine particulate matter (PM2.5) and black carbon (BC) with BP (systolic [SBP] and diastolic [DBP]) and prevalent hypertension in adults from 28 peri-urban villages near Hyderabad, India.MethodsWe studied 5531 participants from the Andhra Pradesh Children and Parents Study (18-84 years, 54% men). We measured BP (2010-2012) in the right arm and defined hypertension as SBP ≥130 mmHg and/or DBP ≥80 mmHg. We used land-use regression models to estimate annual average PM2.5 and BC at participant's residence. We applied linear and logistic nested mixed-effect models stratified by sex and adjusted by cooking fuel type to estimate associations between within-village PM2.5 or BC and health.ResultsMean (SD) PM2.5 was 33 µg/m (2.7) and BC was 2.5 µg/m (0.23). In women, a 1 µg/m increase in PM2.5 was associated with 1.4 mmHg higher SBP (95% confidence interval [CI]: 0.12, 2.7), 0.87 mmHg higher DBP (95% CI: -0.18, 1.9), and 4% higher odds of hypertension (95% CI: 0%, 9%). In men, associations with SBP (0.52 mmHg; 95% CI: -0.82, 1.8), DBP (0.41 mmHg; 95% CI: -0.69, 1.5), and hypertension (2% higher odds; 95% CI: -2%, 6%) were weaker. No associations were observed with BC.ConclusionWe observed a positive association between ambient PM2.5 and BP and hypertension in women. Longitudinal studies in this region are needed to corroborate our findings.
| S-EPMC6558270 | biostudies-literature
Project description:BackgroundChildhood exposure to air pollution contributes to cardiovascular disease in adulthood. Immune and oxidative stress disturbances might mediate the effects of air pollution on the cardiovascular system, but the underlying mechanisms are poorly understood in adolescents. Therefore, we aimed to identify immune biomarkers linking air pollution exposure and blood pressure levels in adolescents.MethodsWe randomly recruited 100 adolescents (mean age, 16 years) from Fresno, California. Using central-site data, spatial-temporal modeling, and distance weighting exposures to the participant's home, we estimated average pollutant levels [particulate matter (PM), polyaromatic hydrocarbons (PAH), ozone (O3), carbon monoxide (CO) and nitrogen oxides (NOx)]. We collected blood samples and vital signs on health visits. Using proteomic platforms, we quantitated markers of inflammation, oxidative stress, coagulation, and endothelial function. Immune cellular characterization was performed via mass cytometry (CyTOF). We investigated associations between pollutant levels, cytokines, immune cell types, and blood pressure (BP) using partial least squares (PLS) and linear regression, while adjusting for important confounders.ResultsUsing PLS, biomarkers explaining most of the variance in air pollution exposure included markers of oxidative stress (GDF-15 and myeloperoxidase), acute inflammation (C-reactive protein), hemostasis (ADAMTS, D-dimer) and immune cell types such as monocytes. Most of these biomarkers were independently associated with the air pollution levels in fully adjusted regression models. In CyTOF analyses, monocytes were enriched in participants with the highest versus the lowest PM2.5 exposure. In both PLS and linear regression, diastolic BP was independently associated with PM2.5, NO, NO2, CO and PAH456 pollution levels (P ≤ 0.009). Moreover, monocyte levels were independently related to both air pollution and diastolic BP levels (P ≤ 0.010). In in vitro cell assays, plasma of participants with high PM2.5 exposure induced endothelial dysfunction as evaluated by eNOS and ICAM-1 expression and tube formation.ConclusionsFor the first time in adolescents, we found that ambient air pollution levels were associated with oxidative stress, acute inflammation, altered hemostasis, endothelial dysfunction, monocyte enrichment and diastolic blood pressure. Our findings provide new insights on pollution-related immunological and cardiovascular disturbances and advocate preventative measures of air pollution exposure.
| S-EPMC7566149 | biostudies-literature
Project description: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 matched to the hourly levels of air pollutants. A generalized additive model was constructed for hour lags of 0-8 of air pollutants adjusting for age, sex, meteorological variables, and time trend. Systolic BP was shown to be significantly lower at 2-4?hours and 3-5?hours after increased levels of SO2 and CO, respectively (0.24?mmHg and 0.26?mmHg for an interquartile range, respectively). In contrast, O3 and NO2 were associated with significantly increased systolic BP at 3-5 lag hours and at 0-2 lag hours, respectively. BP elevation in association with O3 and NO2 was shown to be significantly greater in hypertensive patients than normotensive subjects. Our findings suggest that short-term exposure to air pollution may be associated with elevated BP.
| S-EPMC6937254 | biostudies-literature
Project description:ObjectiveTo investigate the role of air pollutants in risk of dementia, considering differences by study factors that could influence findings.DesignSystematic review and meta-analysis.Data sourcesEMBASE, PubMed, Web of Science, Psycinfo, and OVID Medline from database inception through July 2022.Eligibility criteria for selecting studiesStudies that included adults (≥18 years), a longitudinal follow-up, considered US Environmental Protection Agency criteria air pollutants and proxies of traffic pollution, averaged exposure over a year or more, and reported associations between ambient pollutants and clinical dementia. Two authors independently extracted data using a predefined data extraction form and assessed risk of bias using the Risk of Bias In Non-randomised Studies of Exposures (ROBINS-E) tool. A meta-analysis with Knapp-Hartung standard errors was done when at least three studies for a given pollutant used comparable approaches.Results2080 records identified 51 studies for inclusion. Most studies were at high risk of bias, although in many cases bias was towards the null. 14 studies could be meta-analysed for particulate matter <2.5 µm in diameter (PM2.5). The overall hazard ratio per 2 μg/m3 PM2.5 was 1.04 (95% confidence interval 0.99 to 1.09). The hazard ratio among seven studies that used active case ascertainment was 1.42 (1.00 to 2.02) and among seven studies that used passive case ascertainment was 1.03 (0.98 to 1.07). The overall hazard ratio per 10 μg/m3 nitrogen dioxide was 1.02 ((0.98 to 1.06); nine studies) and per 10 μg/m3 nitrogen oxide was 1.05 ((0.98 to 1.13); five studies). Ozone had no clear association with dementia (hazard ratio per 5 μg/m3 was 1.00 (0.98 to 1.05); four studies).ConclusionPM2.5 might be a risk factor for dementia, as well as nitrogen dioxide and nitrogen oxide, although with more limited data. The meta-analysed hazard ratios are subject to limitations that require interpretation with caution. Outcome ascertainment approaches differ across studies and each exposure assessment approach likely is only a proxy for causally relevant exposure in relation to clinical dementia outcomes. Studies that evaluate critical periods of exposure and pollutants other than PM2.5, and studies that actively assess all participants for outcomes are needed. Nonetheless, our results can provide current best estimates for use in burden of disease and regulatory setting efforts.Systematic review registrationPROSPERO CRD42021277083.
| S-EPMC10498344 | biostudies-literature
Project description:Exposure to traffic-related air pollution (TRAP) may contribute to increased prevalence of hypertension and elevated blood pressure (BP) for residents of near-highway neighborhoods. Relatively few studies have investigated the effects of reducing TRAP exposure on short-term changes in BP. We assessed whether reducing indoor TRAP concentrations by using stand-alone high-efficiency particulate arrestance (HEPA) filters and limiting infiltration through doors and windows effectively prevented acute (ie, over a span of hours) increases in BP. Using a 3-period crossover design, 77 participants were randomized to attend three 2-hour-long exposure sessions separated by 1-week washout periods. Each participant was exposed to high, medium, and low TRAP concentrations in a room near an interstate highway. Particle number concentrations, black carbon concentrations, and temperature were monitored continuously. Systolic BP (SBP), diastolic BP, and heart rate were measured every 10 minutes. Outcomes were analyzed with a linear mixed model. The primary outcome was the change in SBP from 20 minutes from the start of exposure. SBP increased with exposure duration, and the amount of increase was related to the magnitude of exposure. The mean change in SBP was 0.6 mm Hg for low exposure (mean particle number and black carbon concentrations, 2500 particles/cm3 and 149 ng/m3), 1.3 mm Hg for medium exposure (mean particle number and black carbon concentrations, 11 000 particles/cm3 and 409 ng/m3), and 2.8 mm Hg for high exposure (mean particle number and black carbon concentrations, 30 000 particles/cm3 and 826 ng/m3; linear trend P=0.019). There were no statistically significant differences in the secondary outcomes, diastolic BP, or heart rate. In conclusion, reducing indoor concentrations of TRAP was effective in preventing acute increases in SBP.
| S-EPMC7878425 | biostudies-literature
Project description:Several reviews have assessed the relationship between exposure to ambient air pollution and adverse birth outcomes during pregnancy, but the results remain controversial. The objective of this study was to assess this correlation quantitatively and to explore sources of heterogeneity. We included all published case-control or cohort studies that evaluated the correlation between ambient air pollution and low birth weight (LBW), preterm birth (PTB), and small for gestational age (SGA). Analytical methods and inclusion criteria were provided on the PROSPERO website (CRD42018085816). We evaluated pooled effects and heterogeneity. Subgroup analyses (grouped by exposure period, study settings, study design, exposure types, data source, Newcastle-Ottawa quality score (NOS), and adjustment for smoking or meteorological factors) were also conducted and publication bias was examined. The risk of bias in systematic reviews (ROBIS) tool was used to evaluate the overall risk of bias in this review. Forty studies met the inclusion criteria. We observed pooled odds ratios (ORs) of 1.03-1.21 for LBW and 0.97-1.06 for PTB when mothers were exposed to CO, NO2, NOx, O3, PM2.5, PM10, or SO2 throughout their pregnancy. For SGA, the pooled estimate was 1.02 in relation to NO2 concentrations. Subgroup analysis and sensitivity analysis decreased the heterogeneity to some extent, such as the subgroups of continuous measures (OR=0.98 (0.97-0.99), I2=0.0%) and NOS>7 (OR=0.98 (0.97-0.99), I2=0.0%) in evaluating the association between PTB and NO2. This review was completed with a low risk of bias. High concentrations of air pollution were significantly related to the higher risk of adverse birth outcomes. However, the sources of heterogeneity among studies should be further explored.
| S-EPMC6421124 | biostudies-literature
Project description:Hypertensive disorders of pregnancy (HDP, including gestational hypertension, preeclampsia, and eclampsia) have a substantial public health impact. Maternal exposure to high levels of air pollution may trigger HDP, but this association remains unclear. The objective of our report is to assess and quantify the association between maternal exposures to criteria air pollutants (ozone, carbon monoxide, nitrogen dioxide, sulfur dioxide, and particulate matter ≤ 10, 2.5 μm) on HDP risk. PubMed, EMBASE, MEDLINE, Current Contents, Global Health, and Cochrane were searched (last search: September, 2013). After a detailed screening of 270 studies, 10 studies were extracted. We conducted meta-analyses if a pollutant in a specific exposure window was reported by at least four studies. Using fixed- and random-effects models, odds ratios (ORs) and 95% CIs were calculated for each pollutant with specific increment of concentration. Increases in risks of HDP (OR per 10 ppb = 1.16; 95% CI, 1.03-1.30) and preeclampsia (OR per 10 ppb = 1.10; 95% CI, 1.03-1.17) were observed to be associated with exposure to NO2 during the entire pregnancy, and significant associations between HDP and exposure to CO (OR per 1 ppm = 1.79; 95% CI, 1.31-2.45) and O3 (OR per 10 ppb = 1.09; 95% CI, 1.05-1.13) during the first trimester were also observed. Our review suggests an association between ambient air pollution and HDP risk. Although the ORs were relatively low, the population-attributable fractions were not negligible given the ubiquitous nature of air pollution.
| S-EPMC4166571 | biostudies-literature
Project description:The available evidence on the effects of ambient air pollution on cardiovascular diseases (CVDs) has increased substantially. In this umbrella review, we summarized the current epidemiological evidence from systematic reviews and meta-analyses linking ambient air pollution and CVDs, with a focus on geographical differences and vulnerable subpopulations. We performed a search strategy through multiple databases including articles between 2010 and 31 January 2021. We performed a quality assessment and evaluated the strength of evidence. Of the 56 included reviews, the most studied outcomes were stroke (22 reviews), all-cause CVD mortality, and morbidity (19). The strongest evidence was found between higher short- and long-term ambient air pollution exposure and all-cause CVD mortality and morbidity, stroke, blood pressure, and ischemic heart diseases (IHD). Short-term exposures to particulate matter <2.5 μm (PM2.5 ), <10 μm (PM10 ), and nitrogen oxides (NOx ) were consistently associated with increased risks of hypertension and triggering of myocardial infarction (MI), and stroke (fatal and nonfatal). Long-term exposures of PM2.5 were largely associated with increased risk of atherosclerosis, incident MI, hypertension, and incident stroke and stroke mortality. Few reviews evaluated other CVD outcomes including arrhythmias, atrial fibrillation, or heart failure but they generally reported positive statistical associations. Stronger associations were found in Asian countries and vulnerable subpopulations, especially among the elderly, cardiac patients, and people with higher weight status. Consistent with experimental data, this comprehensive umbrella review found strong evidence that higher levels of ambient air pollution increase the risk of CVDs, especially all-cause CVD mortality, stroke, and IHD. These results emphasize the importance of reducing the alarming levels of air pollution across the globe, especially in Asia, and among vulnerable subpopulations.
| S-EPMC9310863 | biostudies-literature
Project description:Given health threats of climate change, a comprehensive review of the impacts of ambient temperature and ar pollution on suicide is needed. We performed systematic literature review and meta-analysis of suicide risks associated with short-term exposure to ambient temperature and air pollution. Pubmed, Scopus, and Web of Science were searched for English-language publications using relevant keywords. Observational studies assessing risks of daily suicide and suicide attempts associated with temperature, particulate matter with aerodynamic diameter ≤10 μm (PM10) and ≤2.5 mm (PM2.5), ozone (O3), sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO) were included. Data extraction was independently performed in duplicate. Random-effect meta-analysis was applied to pool risk ratios (RRs) for increases in daily suicide per interquartile range (IQR) increase in exposure. Meta-regression analysis was applied to examine effect modification by income level based on gross national income (GNI) per capita, national suicide rates, and average level of exposure factors. In total 2274 articles were screened, with 18 studies meeting inclusion criteria for air pollution and 32 studies for temperature. RRs of suicide per 7.1 °C temperature was 1.09 (95% CI: 1.06, 1.13). RRs of suicide per IQR increase in PM2.5, PM10, and NO2 were 1.02 (95% CI: 1.00, 1.05), 1.01 (95% CI: 1.00, 1.03), and 1.03 (95% CI: 1.00, 1.07). O3, SO2, and CO were not associated with suicide. RR of suicide was significantly higher in higher-income than lower-income countries (1.09, 95% CI: 1.07, 1.11 and 1.20, 95% CI: 1.14, 1.26 per 7.1 °C increased temperature, respectively). Suicide risks associated with air pollution did not significantly differ by income level, national suicide rates, or average exposure levels. Research gaps were found for interactions between air pollution and temperature on suicide risks.
| S-EPMC8303705 | biostudies-literature