Mortality–Air Pollution Associations in Low Exposure Environments (MAPLE): Phase 2
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PROVIDER: S-EPMC9556709 | biostudies-literature | 2022 Jan
REPOSITORIES: biostudies-literature
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| S-EPMC7334864 | biostudies-literature
Project description:Background pollution represents the lowest levels of ambient air pollution to which the population is chronically exposed, but few studies have focused on thoroughly characterizing this regime. This study uses clustering statistical techniques as a modelling approach to characterize this pollution regime while deriving reliable information to be used as estimates of exposure in epidemiological studies. The background levels of four key pollutants in five urban areas of Andalusia (Spain) were characterized over an 11-year period (2005-2015) using four widely-known clustering methods. For each pollutant data set, the first (lowest) cluster representative of the background regime was studied using finite mixture models, agglomerative hierarchical clustering, hidden Markov models (hmm) and k-means. Clustering method hmm outperforms the rest of the techniques used, providing important estimates of exposures related to background pollution as its mean, acuteness and time incidence values in the ambient air for all the air pollutants and sites studied.
| S-EPMC6018063 | biostudies-literature
Project description: Not available
| S-EPMC7300216 | biostudies-literature
Project description:BackgroundAir pollution exposures have been shown to adversely impact health through a number of biological pathways associated with glucose metabolism. However, few studies have evaluated the associations between air pollution and glycosylated hemoglobin (HbA1c) levels. Further, no studies have evaluated these associations in US populations or investigated whether associations differ in diabetic as compared to non-diabetic populations. To address this knowledge gap, we investigated the associations between airborne fine particulate matter (PM2.5) and nitrogen dioxide (NO2) and HbA1c levels in both diabetic and non-diabetic older Americans. We also examined the impact of PM2.5 and NO2 on prevalent diabetes mellitus (DM) in this cohort.MethodsWe used multilevel logistic and linear regression models to evaluate the association between long-term average air pollutant levels and prevalence of DM and HbA1c levels, respectively, among 4121 older (57+ years) Americans enrolled in the National Social Life, Health, and Aging Project between 2005 and 2011. All models adjusted for age, sex, body mass index, smoking status, race, household income, education level, neighborhood socioeconomic status, geographic region, urbanicity and diabetic medication use. We estimated participant-specific exposures to PM2.5 on a six-kilometer grid covering the conterminous U.S. using spatio-temporal models, and to NO2 using nearest measurements from the Environmental Protection Agency's Air Quality System. HbA1c levels were measured for participants in each of two data collection waves from dried blood spots and log-transformed prior to analysis. Participants were considered diabetic if they had HbA1c values≥6.5% or reported taking diabetic medication.ResultsThe prevalence of diabetes at study entry was 22.2% (n=916) and the mean HbA1c was 6.0±1.1%. Mean one-year moving average PM2.5 and NO2 exposures were 10.4±3.0μg/m3 and 13.1±7.0 ppb, respectively. An inter-quartile range (IQR, 3.9μg/m3) increase in one-year moving average PM2.5 was positively associated with increased diabetes prevalence (prevalence odds ratio, POR 1.35, 95% CI: 1.19, 1.53). Similarly, an IQR (8.6 ppb) increase in NO2 was also significantly associated with diabetes prevalence (POR 1.27, 95% CI: 1.10, 1.48). PM2.5 (1.8%±0.6%, p<0.01) and NO2 (2.0%±0.7%, p<0.01) exposures were associated with higher HbA1c levels in diabetic participants, while only NO2 was significantly associated with HbA1c in non-diabetic participants (0.8%±0.2%, p<0.01). Significant dose response relationships were identified for both pollutants in diabetic participants and for NO2 in non-diabetic participants.Conclusions/interpretationsIn a cohort of older men and women in the United States, PM2.5 and NO2 exposures were significantly associated with prevalence of DM and increased HbA1c levels among both non-diabetic and diabetic participants. These associations suggest that air pollution could be a key risk factor for abnormal glucose metabolism and diabetes in the elderly.
| S-EPMC5580354 | biostudies-literature
Project description:The World Health Organization (WHO) recently released new guidelines for outdoor fine particulate air pollution (PM2.5) recommending an annual average concentration of 5 μg/m3. Yet, our understanding of the concentration-response relationship between outdoor PM2.5 and mortality in this range of near-background concentrations remains incomplete. To address this uncertainty, we conducted a population-based cohort study of 7.1 million adults in one of the world's lowest exposure environments. Our findings reveal a supralinear concentration-response relationship between outdoor PM2.5 and mortality at very low (<5 μg/m3) concentrations. Our updated global concentration-response function incorporating this new information suggests an additional 1.5 million deaths globally attributable to outdoor PM2.5 annually compared to previous estimates. The global health benefits of meeting the new WHO guideline for outdoor PM2.5 are greater than previously assumed and indicate a need for continued reductions in outdoor air pollution around the world.
| S-EPMC9519036 | biostudies-literature
Project description:BackgroundRecent studies have indicated long-term effects on mortality of particulate and sulphur dioxide (SO(2)) pollution, but uncertainties remain over the size of any effects, potential latency and generalisability.MethodsA small area study was performed across electoral wards in Great Britain of mean annual black smoke (BS) and SO(2) concentrations (from 1966) and subsequent all-cause and cause-specific mortality using random effect models within a Bayesian framework adjusted for social deprivation and urban/rural classification. Different latencies and changes in associations over time were assessed.ResultsSignificant associations were found between BS and SO(2) concentrations and mortality. The effects were stronger for respiratory illness than other causes of mortality for the most recent exposure periods (shorter latency times) and most recent mortality period (lower pollutant concentrations). In pooled analysis across four sequential 4 year mortality periods (1982-98), adjusted excess relative risk for respiratory mortality was 3.6% (95% CI 2.6% to 4.5%) per 10 microg/m(3) BS and 13.2% (95% CI 11.5% to 14.9%) per 10 ppb SO(2), and in the most recent period (1994-8) it was 19.3% (95% CI 5.1% to 35.7%) and 21.7% (95% CI 2.9% to 38.5%), respectively.ConclusionsThese findings add to the evidence that air pollution has long-term effects on mortality and point to continuing public health risks even at the relatively lower levels of BS and SO(2) that now occur. They therefore have importance for policies on public health protection through regulation and control of air pollution.
| S-EPMC2094283 | biostudies-literature
Project description:Chronic exposure to ambient particulate matter (PM) increases the risk of cardiovascular disease (CVD). One proposed mechanism linking PM exposure and CVD is the induction of low-grade systemic inflammation that underlies disease progression. However, the intermediaries that relay signals from the proximal sites of inflammation to the periphery remain unknown. We have previously shown that fine PM (PM2.5) alter red blood cell distribution width. Therefore, the overall goal of this study was to elucidate how PM exposure impacts the spleen and splenic macrophages which are primarily responsible for the turnover of aged and damaged red blood cells.
2024-12-02 | GSE262906 | GEO
Project description:In this study, we modeled early life air pollution exposure using C57BL/6J male mice on a controlled chow diet, exposed to real-world inhaled concentrated PM2.5 (~10x ambient level/ ~60-120g/m3) or filtered air (FA) over 14 weeks. We investigated PM2.5 effects on phenotype, transcriptome and chromatin accessibility, compared the effects with a prototypical high-fat diet (HFD) stimulus, and examined the effects of cessation of exposure on reversibility of phenotype/genotype.
2020-11-05 | GSE145840 | GEO
Project description:Menopause is a significant milestone in a woman's life, characterized by decreasing estradiol (E2) and increasing follicle-stimulating hormone (FSH) levels. Growing evidence suggests that air pollution may affect reproductive health and disrupt hormone profiles, yet the associations in women undergoing menopausal transition (MT) remains underexplored. We examined the associations between annual air pollutant exposures and repeated measures of E2 and FSH in 1365 women with known final menstrual period (FMP) date from the Study of Women's Health Across the Nation. Air pollution was calculated as the annual averages of 24-h average PM2.5 levels, daily one-hour maximum NO2 levels, and daily 8-h maximum O3 levels. Linear mixed models with piece-wise linear splines were used to model non-linear trajectories of E2 and FSH in three distinct time periods: up to 2 years before the FMP (early MT), within 2 years before and 2 years after FMP (transmenopause), and >2 years post-FMP (postmenopause). In the transmenopausal period, an interquartile (5 μg/m3) increase in PM2.5 was associated with a significant decrease in E2 levels (-15.7 %, 95 % CI: -23.7, -6.8), and a 10 ppb increase in NO2 was associated with a significant decrease in E2 levels (-9.2 %, 95 % CI: -16.2, -1.7). A higher PM2.5 was also associated with an accelerated rate of decline in E2. Regarding FSH, a 10 ppb increase in NO2 was associated with decline in FSH levels (-11.7 %, 95 % CI: -21.8, -0.1) in the early MT and accelerated rates of decline in the postmenopause (-1.1 % per year, 95 % CI: -2.1, -0.1). Additionally, inverse associations between O3 and FSH were observed in the transmenopause and postmenopause. Our study suggests that increases in PM2.5, NO2, and O3 exposures are linked to significant declines in E2 and FSH levels across menopausal stages, suggesting the detrimental impact of air pollutants on women's reproductive hormones.
| S-EPMC11639416 | biostudies-literature
Project description:Zinc (Zn) is a major elemental component of respirable ambient particulate matter (PM) detected often at alarming levels in urban air. Exposure to PM has been widely associated with increased cardiovascular morbidity and mortality, however, it is not known what components or sources of PM are causative. We recently demonstrated that long-term episodic inhalation of combustion PM, having similar amount of Zn found in urban PM, caused myocardial lesions in rats. We further demonstrated that a single pulmonary exposure to Zn at high concentration is associated with disturbances in cardiac mitochondrial function, ion channel regulation, calcium homeostasis, and cell signaling. Therefore, in this study we investigated the role of PM-associated Zn in cardiac injury using multiple exposure scenarios. Male Wistar-Kyoto (WKY) rats of 12-14 wks age were intratracheally exposed (once per wk x 8 or16 wks) to either (1) saline (control); (2) PM having no soluble Zn; (3) combustion PM suspension containing 14.5 ug/mg water-soluble Zn at high and (4) low dose levels, (5) the aqueous fraction of this suspension devoid of solid insoluble particulate fraction (14.5 ug/mg soluble Zn), or (6) Zn sulfate. Zn concentrations were identical in groups 3, 5 and 6. Pulmonary toxicity was apparent in all exposure groups when compared to saline as determined by recovery of cells in bronchoalveolar lavage fluid. Long-term exposure to PM with or without soluble Zn, or Zn sulfate caused distinct myocardial lesions characterized by subepicardial and randomly distributed myocardial inflammation, degeneration, and fibrosis. The lesion severity was higher in those groups receiving Zn PM. Because cardiac mitochondria are likely the primary target of inhaled metal or other absorbed PM components, we analyzed mitochondrial DNA damage using QPCR and found that all exposure groups except those exposed to PM without Zn caused variable degree of damage. Aconitase activity, sensitive to inhibition by oxidative stress was inhibited slightly but significantly in rats receiving zinc sulfate. Although modest, microarray (Affymetrix) analysis revealed expression changes in the heart reflective of effects on cell signaling, inflammation/oxidative stress, mitochondrial fatty acid metabolisms and cell cycle regulation in rats exposed to zinc sulfate. However, these changes were minimal following exposure to PM devoid of soluble metals. We demonstrate that episodic subchronic pulmonary exposure to zinc sulfate causes cardiac injury and mitochondrial DNA damage. Thus, water-soluble PM-associated zinc may be one of the PM components responsible for cardiovascular morbidity. Experiment Overall Design: Group 1 received Saline to serve as a control. Group 2 received Mount St. Helenâs ash, which does not contain any water-soluble zinc or other metals such that we can delineate any cardiac effect secondary to pulmonary deposition of these particles as these fine mode particles themselves are not likely to translocate to the heart. Group 3 received whole saline suspension of the same fugitive oil combustion particle sample used in the previous study, which contained insoluble components plus water-soluble zinc (Kodavanti et al., 2003; 14.5 ug/mg zinc) and also a small amount of water-soluble nickel (3.0 µg/mg). Elemental composition of this PM is comparable to Ottawa urban PM (Kodavanti et al., 2003). Group 4 also received same particle sample but at half the dose than group 3. Group 5 received saline-soluble or leachable fraction of PM-HD devoid of any solid material but contained soluble components including zinc and nickel. And, group 6 received zinc sulfate at concentration that was present in groups 3 or 5. This design allowed us to test if cardiac injury in rats was due to leached of zinc or solid particles. There were 4 replicates per treatment group.
2008-06-14 | E-GEOD-6541 | biostudies-arrayexpress