Ambient Particulate Air Pollution and Blood Pressure in Peri-urban India.
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ABSTRACT:
SUBMITTER: Curto A
PROVIDER: S-EPMC6558270 | biostudies-literature | 2019 Jul
REPOSITORIES: biostudies-literature
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Ambient Particulate Air Pollution and Blood Pressure in Peri-urban India.
Curto Ariadna A Wellenius Gregory A GA Milà Carles C Sanchez Margaux M Ranzani Otavio O Marshall Julian D JD Kulkarni Bharati B Bhogadi Santhi S Kinra Sanjay S Tonne Cathryn C
Epidemiology (Cambridge, Mass.) 20190701 4
<h4>Background</h4>Evidence 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.<h4>Methods</h4>We studied 5531 participants from the Andhra Pr ...[more]
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Project description:BackgroundLimited evidence exists on the effect of particulate air pollution on blood glucose levels. We evaluated the associations of residential and personal levels of fine particulate matter (PM2.5) and black carbon (BC) with blood glucose and diabetic status among residents of 28 peri-urban villages in South India.MethodsWe used cross-sectional data from 5065 adults (?18?years, 54% men) included in the Andhra Pradesh Children and Parents Study. Fasting plasma glucose was measured once in 2010-2012 and prevalent prediabetes and diabetes were defined following the American Diabetes Association criteria. We estimated annual ambient PM2.5 and BC levels at residence using land-use regression models and annual personal exposure to PM2.5 and BC using prediction models based on direct measurements from a subsample of 402 participants. We used linear and logistic nested mixed-effect models to assess the association between exposure metrics and health outcomes. For personal exposures, we stratified analyses by sex.ResultsMean (SD) residential PM2.5 and BC were 32.9 (2.6) ?g/m3 and 2.5 (2.6) ?g/m3, respectively; personal exposures to PM2.5 and BC were 54.5 (11.5) ?g/m3 and 5.8 (2.5) ?g/m3, respectively. Average (SD) fasting blood glucose was 5.3 (1.3) mmol/l, 16% of participants had prediabetes, and 5.5% had diabetes. Residential PM2.5 and BC were not associated with higher blood glucose levels. Personal PM2.5 (20??g/m3 increase) and BC (1??g/m3 increase) were negatively associated with blood glucose levels in women (PM2.5: -1.93, 95%CI: -3.12, -0.73; BC: -0.63, 95%CI: -0.90, -0.37). In men, associations were negative for personal PM2.5 (-1.99, 95%CI: -3.56, -0.39) and positive for personal BC (0.49, 95%CI: -0.44, 1.43). We observed no evidence of associations between any exposure and prevalence of prediabetes/diabetes.ConclusionsOur results do not provide evidence that residential exposures to PM2.5 or BC are associated with blood glucose or prevalence of prediabetes/diabetes in this population. Associations with personal exposure may have been affected by unmeasured confounding, highlighting a challenge in using personal exposure estimates in air pollution epidemiology. These associations should be further examined in longitudinal studies.
| S-EPMC6718580 | biostudies-literature
Project description:OBJECTIVE:Air pollution is a leading preventable risk factor for cardiovascular diseases. Previous studies mostly relied on concentrations at residence, which might not represent personal exposure. Personal air pollution exposure has a greater variability compared with levels of ambient air pollution, facilitating evaluation of exposure-response functions and vascular pathophysiology. We aimed to evaluate the association between predicted annual personal exposure to PM2.5 and black carbon (BC) and three vascular damage markers in peri-urban South India. METHODS:We analyzed the third wave of the APCAPS cohort (2010-2012), which recruited participants from 28 villages. We used predicted personal exposure to PM2.5 and BC derived from 610 participant-days of 24 h average gravimetric PM2.5 and BC measurements and predictors related to usual time-activity. Outcomes included carotid intima-media thickness (CIMT), carotid-femoral pulse wave velocity (cf-PWV) and augmentation index (AIx). We fit linear mixed models, adjusting for potential confounders and accounting for the clustered data structure. We evaluated nonlinear associations using generalized additive mixed models. RESULTS:Of the 3017 participants (mean age 38 years), 1453 (48%) were women. The average PM2.5 exposure was 51 µg/m3 (range 13-85) for men, and 61 µg/m3 (range 40-120) for women, while the average BC was 4 µg/m3 (range 3-7) for men and 8 µg/m3 (range 3-22) for women. A 10 ?g/m3 increase of PM2.5 was positively associated with CIMT (0.026 mm, 95% CI 0.014, 0.037), cf-PWV (0.069 m/s, 95% CI 0.008, 0.131) and AIx (0.8%, 95% CI 0.3, 1.3) among men. The exposure-response function for PM2.5 and AIx among men showed non-linearity, particularly within the exposure range dominated by tobacco smoking and occupational exposures. Both PM2.5 and BC were positively associated with AIx among women (0.6%, 95% CI 0.2, 1.0, per 10 ?g/m3 PM2.5; 0.5%, 95% CI 0.1, 0.8, per 2 ?g/m3 BC). CONCLUSIONS:Personal exposure to particulate matter was associated with vascular damage in a peri-urban population in South India. Personal exposure to particulate matter appears to have gender-specific effects on the type of vascular damage, potentially reflecting differences in sources of personal exposure by gender.
| S-EPMC7267772 | 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:Importance:Air pollution is a major threat to global health. Osteoporosis is responsible for a substantial burden of disease globally and is expected to increase in prevalence because of population aging. Few studies have investigated the association between air pollution and bone health, and their findings were inconclusive. Objective:To quantify the association between ambient and household air pollution and bone mass in a sample of the general population in peri-urban India. Design, Setting, and Participants:This was a population-based cross-sectional analysis of the Andhra Pradesh Children and Parents Study cohort, which recruited participants from 28 villages near Hyderabad, South India, during 2009 to 2012. Separate linear mixed models were fitted with nested random intercepts (household within villages) for each exposure-outcome pair and were sequentially adjusted for potential confounders. Data analysis was conducted between April 2019 and July 2019. Exposures:Annual mean ambient particulate matter air pollution less than 2.5 µm in aerodynamic diameter (PM2.5) and black carbon (BC) levels at the residence estimated by land-use regression and self-reported use of biomass cooking fuel. Main Outcomes and Measures:The primary outcome was bone mineral content (BMC) measured in grams, corrected by bone area at the lumbar spine and left hip, as measured by dual-energy x-ray absorptiometry. The secondary outcome was bone mineral density measured in grams per centimeters squared. Results:A total of 3717 participants were analyzed (mean [SD] age, 35.7 [14.0] years; 1711 [46.0%] women). The annual mean (SD) PM2.5 exposure was 32.8 (2.5) μg/m3, and the annual mean (SD) BC exposure was 2.5 (0.2) μg/m3; 57.8% of participants used biomass cooking fuels. In fully adjusted models, PM2.5 was associated with lower BMC in the spine (mean difference, -0.57 g per 3 μg/m3 increase in PM2.5; 95% CI, -1.06 to -0.07 g per 3 μg/m3 increase in PM2.5) and hip (mean difference, -0.13 g per 3 μg/m3 increase in PM2.5; 95% CI, -0.3 to 0.03 g per 3 μg/m3 increase in PM2.5). After confounder adjustment, exposure to PM2.5 was also associated with lower bone mineral density in the spine (mean difference, -0.011 g/cm2 per 3 μg/m3 increase in PM2.5; 95% CI, -0.021 to 0 g/cm2 per 3 μg/m3 increase in PM2.5) and hip (mean difference, -0.004 g/cm2 per 3 μg/m3 increase in PM2.5; 95% CI, -0.008 to 0.001 g/cm2 per 3 μg/m3 increase in PM2.5). Exposure to BC was associated with lower BMC in the spine (mean difference, -1.13 g per 1 μg/m3 increase in BC; 95% CI, -2.81 to 0.54 g per 1 μg/m3 increase in BC) and hip (mean difference, -0.35 g per 1 μg/m3 increase in BC; 95% CI, -0.96 to 0.25 g per 1 μg/m3 increase in BC), although the confidence intervals were wider. There was no association between biomass fuel use and spine BMC (mean difference, 0.12 g; 95% CI, -0.45 to 0.68 g). Conclusions and Relevance:In a cross-sectional analysis of a population-based cohort, ambient air pollution was associated with lower BMC in a young adult population in a peri-urban area of South India.
| S-EPMC6991311 | biostudies-literature
Project description:BackgroundEvidence linking ambient air pollution with atherosclerosis is lacking from low- and middle-income countries. Additionally, evidence regarding the association between household air pollution and atherosclerosis is limited. We evaluated the association between ambient fine particulate matter [particulate matter with an aerodynamic diameter of ?2.5 µm (PM2.5)] and biomass fuel use on carotid intima-media thickness (CIMT), a surrogate of atherosclerosis, in India.MethodsWe analysed the third follow-up of the Andhra Pradesh Children and Parent Study cohort (2010-2012), which recruited participants from 28 peri-urban villages. Our primary outcome was mean CIMT, measured using a standardized protocol. We estimated annual average PM2.5 outdoors at residence using land-use regression. Biomass cooking fuel was self-reported. We fitted a within-between linear-mixed model adjusting for potential confounders.ResultsAmong 3278 participants (48% women, mean age 38?years), mean PM2.5 was 32.7 [range 24.4-38.2] µg/m3, and 60% used biomass. After confounder adjustment, we observed positive associations between within-village variation in PM2.5 and CIMT in all participants [1.79%, 95% confidence interval (CI), -0.31 to 3.90 per 1 ?µg/m3 of PM2.5] and in men (2.98%, 95% CI, 0.23-5.72, per 1 ?µg/m3 of PM2.5). Use of biomass cooking fuel was associated with CIMT in all participants (1.60%, 95% CI, -0.46 to 3.65), especially in women with an unvented stove (6.14%, 95% CI, 1.40-10.89). The point-estimate for the PM2.5 association was larger in sub-groups with higher cardiometabolic risk profile.ConclusionsAmbient and household air pollution were positively associated with CIMT in a peri-urban population of India, although with limited precision for some estimates. We observed differences in the association between ambient and household air pollution and CIMT by gender.
| S-EPMC7124504 | biostudies-literature
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:Ambient particulate matter (PM) has been associated with mortality and morbidity for cardiovascular disease. MicroRNAs control gene expression at a posttranscriptional level. Altered microRNA expression has been reported in processes related to cardiovascular disease and PM exposure, such as systemic inflammation, endothelial dysfunction, and atherosclerosis. Polymorphisms in microRNA-related genes could influence response to PM.We investigated the association of exposure to ambient particles in several time windows (4-hour to 28-day moving averages) and blood leukocyte expression changes in 14 candidate microRNAs in 153 elderly males from the Normative Aging Study (examined 2005-2009). Potential effect modification by six single nucleotide polymorphisms (SNPs) in three microRNA-related genes was investigated. Fine PM (PM2.5), black carbon, organic carbon, and sulfates were measured at a stationary ambient monitoring site. Linear regression models, adjusted for potential confounders, were used to assess effects of particles and SNP-by-pollutant interaction. An in silico pathway analysis was performed on target genes of microRNAs associated with the pollutants.We found a negative association for pollutants in all moving averages and miR-1, -126, -135a, -146a, -155, -21, -222, and -9. The strongest associations were observed with the 7-day moving averages for PM2.5 and black carbon and with the 48-hour moving averages for organic carbon. The association with sulfates was stable across the moving averages. The in silico pathway analysis identified 18 pathways related to immune response shared by at least two microRNAs; in particular, the "high-mobility group protein B1/advanced glycosylation end product-specific receptor signaling pathway" was shared by miR-126, -146a, -155, -21, and -222. No important associations were observed for miR-125a-5p, -125b, -128, -147, -218, and -96. We found significant SNP-by-pollutant interactions for rs7813, rs910925, and rs1062923 in GEMIN4 and black carbon and PM2.5 for miR-1, -126, -146a, -222, and -9, and for rs1640299 in DGCR8 and SO4 for miR-1 and -135a.Exposure to ambient particles could cause a downregulation of microRNAs involved in processes related to PM exposure. Polymorphisms in GEMIN4 and DGCR8 could modify these associations.
| S-EPMC3977338 | biostudies-literature
Project description:BackgroundThe systematic evaluation of the results of time-series studies of air pollution is challenged by differences in model specification and publication bias.MethodsWe evaluated the associations of inhalable particulate matter (PM) with an aerodynamic diameter of 10 ?m or less (PM10) and fine PM with an aerodynamic diameter of 2.5 ?m or less (PM2.5) with daily all-cause, cardiovascular, and respiratory mortality across multiple countries or regions. Daily data on mortality and air pollution were collected from 652 cities in 24 countries or regions. We used overdispersed generalized additive models with random-effects meta-analysis to investigate the associations. Two-pollutant models were fitted to test the robustness of the associations. Concentration-response curves from each city were pooled to allow global estimates to be derived.ResultsOn average, an increase of 10 ?g per cubic meter in the 2-day moving average of PM10 concentration, which represents the average over the current and previous day, was associated with increases of 0.44% (95% confidence interval [CI], 0.39 to 0.50) in daily all-cause mortality, 0.36% (95% CI, 0.30 to 0.43) in daily cardiovascular mortality, and 0.47% (95% CI, 0.35 to 0.58) in daily respiratory mortality. The corresponding increases in daily mortality for the same change in PM2.5 concentration were 0.68% (95% CI, 0.59 to 0.77), 0.55% (95% CI, 0.45 to 0.66), and 0.74% (95% CI, 0.53 to 0.95). These associations remained significant after adjustment for gaseous pollutants. Associations were stronger in locations with lower annual mean PM concentrations and higher annual mean temperatures. The pooled concentration-response curves showed a consistent increase in daily mortality with increasing PM concentration, with steeper slopes at lower PM concentrations.ConclusionsOur data show independent associations between short-term exposure to PM10 and PM2.5 and daily all-cause, cardiovascular, and respiratory mortality in more than 600 cities across the globe. These data reinforce the evidence of a link between mortality and PM concentration established in regional and local studies. (Funded by the National Natural Science Foundation of China and others.).
| S-EPMC7891185 | 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:Elevated ambient pollution exposure is potentially linked to thromboembolism. However, the mechanisms by which particulate matter (PM) interferes with the balance of hemostatic system remain unclear. This study investigates PM-mediated hemostatic changes in individuals across unique seasonal variations of ambient pollution. This prospective study was conducted between February and July 2020 during alterations in ambient pollution in Chiang Mai, Thailand. Blood tests from 30 healthy subjects were assessed at four-week intervals, four times in total. Various coagulation tests, including prothrombin time (PT), activated partial thromboplastin time (aPTT), von Willebrand factor (vWF), platelet count, and platelet functions, were evaluated. A mixed-effects model was used to analyze the impact of high PM2.5 and PM10 on hemostatic parameters. Thirty male subjects with mean age of 38.9 ± 8.2 years, were included. High levels of PM2.5 and PM10 were significantly associated with PT shortening, with no such effect observed in aPTT. PM2.5 and PM10 values also positively correlated with vWF function, while vWF antigen levels remained unchanged. Soluble P-selectin showed a strong positive association with PM2.5 and PM10 levels. Platelet function analysis revealed no correlation with PM values. Short-term exposure to elevated PM2.5 and PM10 concentrations was linked to shortened PT and enhanced vWF function in healthy individuals. Exploring the impact of these changes on clinically relevant thrombosis is crucial. Additional studies on the pathogenesis of pollution-related thrombosis are warranted for maintaining good health.
| S-EPMC11292950 | biostudies-literature