Cardiovascular and Cerebrovascular Mortality Associated With Acute Exposure to PM2.5 in Mexico City.
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ABSTRACT:
SUBMITTER: Gutierrez-Avila I
PROVIDER: S-EPMC6091682 | biostudies-literature | 2018 Jul
REPOSITORIES: biostudies-literature
Publications
Cardiovascular and Cerebrovascular Mortality Associated With Acute Exposure to PM<sub>2.5</sub> in Mexico City.
Gutiérrez-Avila Iván I Rojas-Bracho Leonora L Riojas-Rodríguez Horacio H Kloog Itai I Just Allan C AC Rothenberg Stephen J SJ
Stroke 20180612 7
<h4>Background and purpose</h4>Acute exposure to particulate matter with aerodynamic diameter <2.5 μm (PM<sub>2.5</sub>) is associated with acute cardiovascular and cerebrovascular mortality. The aim of this study was to evaluate these associations with specific causes of cardiovascular and cerebrovascular mortality in Mexico City.<h4>Methods</h4>We obtained daily mortality records for Mexico City from 2004 to 2013 for cardiovascular and cerebrovascular causes in people ≥25 and ≥65 years old. Ex ...[more]
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Project description:Exposure to PM2.5 has been associated with the prevalence of obesity. In the Greater Mexico City Area (GMCA), both are ranked among the highest in the world. Our aim was to analyze this association in children, adolescents, and adults in the GMCA. We used data from the 2006 and 2012 Mexican National Surveys of Health and Nutrition (ENSANUT). Participants' past-year exposure to ambient PM2.5 was assessed using land use terms and satellite-derived aerosol optical depth estimates; weight and height were measured. We used survey-adjusted logistic regression models to estimate the odds ratios (ORs) of obesity (vs. normal-overweight) for every 10 µg/m3 increase in annual PM2.5 exposure for children, adolescents, and adults. Using a meta-analysis approach, we estimated the overall odds of obesity. We analyzed data representing 19.3 million and 20.9 million GMCA individuals from ENSANUT 2006 and 2012, respectively. The overall pooled estimate between PM2.5 exposure and obesity was OR = 1.96 (95% CI: 1.21, 3.18). For adolescents, a 10 µg/m3 increase in PM2.5 was associated with an OR of 3.53 (95% CI: 1.45, 8.58) and 3.79 (95% CI: 1.40, 10.24) in 2006 and 2012, respectively. More studies such as this are recommended in Latin American cities with similar air pollution and obesity conditions.
| S-EPMC7956483 | biostudies-literature
Project description:BackgroundThe association between fine particulate matter (PM2.5) and mortality widely differs between as well as within countries. Differences in PM2.5 composition can play a role in modifying the effect estimates, but there is little evidence about which components have higher impacts on mortality.MethodsWe applied a 2-stage analysis on data collected from 210 locations in 16 countries. In the first stage, we estimated location-specific relative risks (RR) for mortality associated with daily total PM2.5 through time series regression analysis. We then pooled these estimates in a meta-regression model that included city-specific logratio-transformed proportions of seven PM2.5 components as well as meta-predictors derived from city-specific socio-economic and environmental indicators.ResultsWe found associations between RR and several PM2.5 components. Increasing the ammonium (NH4+) proportion from 1% to 22%, while keeping a relative average proportion of other components, increased the RR from 1.0063 (95% confidence interval [95% CI] = 1.0030, 1.0097) to 1.0102 (95% CI = 1.0070, 1.0135). Conversely, an increase in nitrate (NO3-) from 1% to 71% resulted in a reduced RR, from 1.0100 (95% CI = 1.0067, 1.0133) to 1.0037 (95% CI = 0.9998, 1.0077). Differences in composition explained a substantial part of the heterogeneity in PM2.5 risk.ConclusionsThese findings contribute to the identification of more hazardous emission sources. Further work is needed to understand the health impacts of PM2.5 components and sources given the overlapping sources and correlations among many components.
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Project description:UNLABELLED:Geostatistical interpolation methods to estimate individual exposure to outdoor air pollutants can be used in pregnancy cohorts where personal exposure data are not collected. Our objectives were to a) develop four assessment methods (citywide average (CWA); nearest monitor (NM); inverse distance weighting (IDW); and ordinary Kriging (OK)), and b) compare daily metrics and cross-validations of interpolation models. We obtained 2008 hourly data from Mexico City's outdoor air monitoring network for PM10, PM2.5, O3, CO, NO2, and SO2 and constructed daily exposure metrics for 1,000 simulated individual locations across five populated geographic zones. Descriptive statistics from all methods were calculated for dry and wet seasons, and by zone. We also evaluated IDW and OK methods' ability to predict measured concentrations at monitors using cross validation and a coefficient of variation (COV). All methods were performed using SAS 9.3, except ordinary Kriging which was modeled using R's gstat package. Overall, mean concentrations and standard deviations were similar among the different methods for each pollutant. Correlations between methods were generally high (r=0.77 to 0.99). However, ranges of estimated concentrations determined by NM, IDW, and OK were wider than the ranges for CWA. Root mean square errors for OK were consistently equal to or lower than for the IDW method. OK standard errors varied considerably between pollutants and the computed COVs ranged from 0.46 (least error) for SO2 and PM10 to 3.91 (most error) for PM2.5. OK predicted concentrations measured at the monitors better than IDW and NM. Given the similarity in results for the exposure methods, OK is preferred because this method alone provides predicted standard errors which can be incorporated in statistical models. The daily estimated exposures calculated using these different exposure methods provide flexibility to evaluate multiple windows of exposure during pregnancy, not just trimester or pregnancy-long exposures. IMPLICATIONS:Many studies evaluating associations between outdoor air pollution and adverse pregnancy outcomes rely on outdoor air pollution monitoring data linked to information gathered from large birth registries, and often lack residence location information needed to estimate individual exposure. This study simulated 1,000 residential locations to evaluate four air pollution exposure assessment methods, and describes possible exposure misclassification from using spatial averaging versus geostatistical interpolation models. An implication of this work is that policies to reduce air pollution and exposure among pregnant women based on epidemiologic literature should take into account possible error in estimates of effect when spatial averages alone are evaluated.
| S-EPMC4670782 | biostudies-literature
Project description:BACKGROUND:Most large, prospective studies of the effects of diabetes on mortality have focused on high-income countries where patients have access to reasonably good medical care and can receive treatments to establish and maintain good glycemic control. In those countries, diabetes less than doubles the rate of death from any cause. Few large, prospective studies have been conducted in middle-income countries where obesity and diabetes have become common and glycemic control may be poor. METHODS:From 1998 through 2004, we recruited approximately 50,000 men and 100,000 women 35 years of age or older into a prospective study in Mexico City, Mexico. We recorded the presence or absence of previously diagnosed diabetes, obtained and stored blood samples, and tracked 12-year disease-specific deaths through January 1, 2014. We accepted diabetes as the underlying cause of death only for deaths that were due to acute diabetic crises. We estimated rate ratios for death among participants who had diabetes at recruitment versus those who did not have diabetes at recruitment; data from participants who had chronic diseases other than diabetes were excluded from the main analysis. RESULTS:At the time of recruitment, obesity was common and the prevalence of diabetes rose steeply with age (3% at 35 to 39 years of age and >20% by 60 years of age). Participants who had diabetes had poor glycemic control (mean [±SD] glycated hemoglobin level, 9.0±2.4%), and the rates of use of other vasoprotective medications were low (e.g., 30% of participants with diabetes were receiving antihypertensive medication at recruitment and 1% were receiving lipid-lowering medication). Previously diagnosed diabetes was associated with rate ratios for death from any cause of 5.4 (95% confidence interval [CI], 5.0 to 6.0) at 35 to 59 years of age, 3.1 (95% CI, 2.9 to 3.3) at 60 to 74 years of age, and 1.9 (95% CI, 1.8 to 2.1) at 75 to 84 years of age. Between 35 and 74 years of age, the excess mortality associated with previously diagnosed diabetes accounted for one third of all deaths; the largest absolute excess risks of death were from renal disease (rate ratio, 20.1; 95% CI, 17.2 to 23.4), cardiac disease (rate ratio, 3.7; 95% CI, 3.2 to 4.2), infection (rate ratio, 4.7; 95% CI, 4.0 to 5.5), acute diabetic crises (8% of all deaths among participants who had previously diagnosed diabetes), and other vascular disease (mainly stroke). Little association was observed between diabetes and mortality from cirrhosis, cancer, or chronic obstructive pulmonary disease. CONCLUSIONS:In this study in Mexico, a middle-income country with high levels of obesity, diabetes was common, glycemic control was poor, and diabetes was associated with a far worse prognosis than that seen in high-income countries; it accounted for at least one third of all deaths between 35 and 74 years of age. (Funded by the Wellcome Trust and others.).
| S-EPMC5215048 | biostudies-literature
Project description:Human exposure to fine particles can have significant harmful effects on the respiratory and cardiovascular system. To investigate daily exposure characteristics to PM2.5 with ambient concentrations in an urban environment, a personal exposure measurements were conducted for school children, office workers and at their residents, in the city of Taj 'Agra', India. In order to account for all the sources of particulate matter exposure, measurements on several different days during December 2013 to February 2014 were carried out. Personal environment monitors (PEM) and APM 550 were used to measure PM2.5 concentration. The research findings provide insight into possible sources and their interaction with human activities in modifying the human exposure levels.
| S-EPMC4716460 | biostudies-literature
Project description:Few epidemiologic studies have investigated health effects of water-soluble fractions of PM2.5 metals, the more biologically accessible fractions of metals, in their attempt to identify health-relevant components of ambient PM2.5.In this study, we estimated acute cardiovascular effects of PM2.5 components in an urban population, including a suite of water-soluble metals that are not routinely measured at the ambient level.Ambient concentrations of criteria gases, PM2.5, and PM2.5 components were measured at a central monitor in Atlanta, Georgia, during 1998-2013, with some PM2.5 components only measured during 2008-2013. In a time-series framework using Poisson regression, we estimated associations between these pollutants and daily counts of emergency department (ED) visits for cardiovascular diseases in the five-county Atlanta area.Among the PM2.5 components we examined during 1998-2013, water-soluble iron had the strongest estimated effect on cardiovascular outcomes [R?R=1.012 (95% CI: 1.005, 1.019), per interquartile range increase (20.46ng/m3)]. The associations for PM2.5 and other PM2.5 components were consistent with the null when controlling for water-soluble iron. Among PM2.5 components that were only measured during 2008-2013, water-soluble vanadium was associated with cardiovascular ED visits [R?R=1.012 (95% CI: 1.000, 1.025), per interquartile range increase (0.19ng/m3)].Our study suggests cardiovascular effects of certain water-soluble metals, particularly water-soluble iron. The observed associations with water-soluble iron may also point to certain aspects of traffic pollution, when processed by acidifying sulfate, as a mixture harmful for cardiovascular health. https://doi.org/10.1289/EHP2182.
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Project description:We use individual-level data to estimate the effects of long- and short-term exposure to air pollution (PM2.5) on the probability of dying from COVID-19. To the best of our knowledge, our study is the first to look at this relationship using individual-level data. We find that for Mexico City there is evidence of a positive relationship between pollution and mortality that significantly grows with age and that appears to be mostly driven by long- rather than short-term exposure. By using a rich set of individual- and municipal-level covariates we are able to isolate the effect of exposure to pollution from other crucial factors, thus alleviating endogeneity concerns related to selection. Our results provide yet another reason for the need to implement environmental strategies that will reduce the exposure to air pollution: it is a key element to improve the general population's health. In addition, and considering that at this moment we do not know when the pandemic will stop or if SARS-CoV-2 will become a recurrent threat, the relationship that we uncovered suggests that financial resources should be allocated to improve medical services in those areas where PM2.5 concentrations tend to be high.
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Project description:BackgroundStudies on the extent to which long-term exposure to ambient particulate matter (PM) with aerodynamic diameter ≤2.5μm (PM2.5) contributes to adult mortality in India are few, despite over 99% of Indians being exposed to levels that the World Health Organization (WHO) considers unsafe.ObjectiveWe conducted a retrospective cohort study within the Million Death Study (MDS) to provide the first-ever quantification of national mortality from exposure to PM2.5 in India from 1999 to 2014.MethodsWe calculated relative risks (RRs) by linking a total of ten 3-y intervals of satellite-based estimated PM2.5 exposure to deaths 3 to 5 y later in over 7,400 small villages or urban blocks covering a total population of 6.8 million. We applied using a model-based geostatistical model, adjusted for individual age, sex, and year of death; smoking prevalence, rural/urban residency, area-level female illiteracy, languages, and spatial clustering and unit-level variation.ResultsPM2.5 exposure levels increased from 1999 to 2014, particularly in central and eastern India. Among 212,573 deaths at ages 15-69 y, after spatial adjustment, we found a significant RR of 1.09 [95% credible interval (CI): 1.04, 1.14] for stroke deaths per 10-μg/m3 increase in PM2.5 exposure, but no significant excess for deaths from chronic respiratory disease and ischemic heart disease (IHD), all nonaccidental causes, and total mortality (after excluding stroke). Spatial adjustment attenuated the RRs for chronic respiratory disease and IHD but raised those for stroke. The RRs were consistent in various sensitivity analyses with spatial adjustment, including stratifying by levels of solid fuel exposure, by sex, and by age group, addition of climatic variables, and in supplementary case-control analyses using injury deaths as controls.DiscussionDirect epidemiological measurements, despite inherent limitations, yielded associations between mortality and long-term PM2.5 inconsistent with those reported in earlier models used by the WHO to derive estimates of PM2.5 mortality in India. The modest RRs in our study are consistent with near or null mortality effects. They suggest suitable caution in estimating deaths from PM2.5 exposure based on MDS results and even more caution in extrapolating model-based associations of risk derived mostly from high-income countries to India. https://doi.org/10.1289/EHP9538.
| S-EPMC9472672 | biostudies-literature
Project description:BackgroundParticulate matter ≤10 μm in aerodynamic diameter (PM10) and diet quality are risk factors for systemic inflammation, which is associated with preterm birth (PTB). PM10 and a pro-inflammatory diet (assessed by the Dietary Inflammatory Index [DII®]) have been individually evaluated as causes of PTB and differences by offspring sex have been reported for the DII. However, additional studies are needed to evaluate joint effects of these associations to inform intervention efforts.ObjectivesTo evaluate the independent and joint effects of PM10 and energy-adjusted DII (E-DII) on PTB risks.MethodsPM10 estimates were generated from daily citywide averages for 1216 pregnant women from three subcohorts of the Early Life Exposures in Mexico to Environmental Toxicants study using data from the Mexico City Outdoor Air Monitoring Network. Among a subset of participants (N = 620), E-DII scores were calculated using a validated food frequency questionnaire. Cox Proportional Hazards models were run for select periods during pregnancy and entire pregnancy averages for E-DII and PM10. We assessed for potential non-linear associations using natural splines.ResultsIn adjusted models, PM10 exposure was associated with increased risks of PTB for a range of values (58-72 μg/m3) during the second trimester, while negative associations were seen during the second (≥74 μg/m3) and third trimesters (55-65 μg/m3). Analyses conducted using distributed lag models for periods closer to delivery (max lag = 90) did not show negative associations between PM10 exposure and preterm birth, and indeed positive significant associations were observed (estimates and figures). E-DII was not associated with PTB and there was no evidence of effect modification by infant sex. There was no evidence of interaction between PM10 and E-DII and the risk of preterm birth.DiscussionAssociations between PM10 and PTB in Mexico City varied over time and across levels of PM10. Our findings of negative associations in the second and third trimesters, which are contrary to the hypothesized relationship between PM10 and PTB, may be due to a number of factors, including live birth bias and the exposure period evaluated. Differences in results for the periods evaluated suggest that PM10 from shorter exposure windows may play a more proximal role in initiating preterm labor.
| S-EPMC7525039 | biostudies-literature
Project description:BackgroundAmbient air pollution is a modifiable risk factor for cardiovascular disease, yet uncertainty remains about the size of risks at lower levels of fine particulate matter (PM2.5) exposure which now occur in the USA and elsewhere.MethodsWe investigated the relationship of ambient PM2.5 exposure with cause-specific cardiovascular disease mortality in 565 477 men and women, aged 50 to 71?years, from the National Institutes of Health-AARP Diet and Health Study. During 7.5 x 106 person-years of follow up, 41 286 cardiovascular disease deaths, including 23 328 ischaemic heart disease (IHD) and 5894 stroke deaths, were ascertained using the National Death Index. PM2.5 was estimated using a hybrid land use regression (LUR) geostatistical model. Multivariate Cox regression models were used to estimate relative risks (RRs) and 95% confidence intervals (CI).ResultsEach increase of 10 ??g/m3 PM2.5 (overall range, 2.9-28.0? ?g/m3) was associated, in fully adjusted models, with a 16% increase in mortality from ischaemic heart disease [hazard ratio (HR) 1.16; 95% CI 1.09-1.22] and a 14% increase in mortality from stroke (HR 1.14; CI 1.02-1.27). Compared with PM2.5 exposure <8? ?g/m3 (referent), risks for CVD were increased in relation to PM2.5 exposures in the range of 8-12? ?g/m3 (CVD: HR 1.04; 95% CI 1.00-1.08), in the range 12-20? ?g/m3 (CVD: HR 1.08; 95% CI 1.03-1.13) and in the range 20+ ?g/m3 (CVD: HR 1.19; 95% CI 1.10-1.28). Results were robust to alternative approaches to PM2.5 exposure assessment and statistical analysis.ConclusionsLong-term exposure to fine particulate air pollution is associated with ischaemic heart disease and stroke mortality, with excess risks occurring in the range of and below the present US long-term standard for ambient exposure to PM2.5 (12? µg/m3), indicating the need for continued improvements in air pollution abatement for CVD prevention.
| S-EPMC7124502 | biostudies-literature