Impact of particulate matter exposition on the risk of ischemic stroke: epidemiologic evidence and putative mechanisms.
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ABSTRACT:
SUBMITTER: von Bornstadt D
PROVIDER: S-EPMC3915219 | biostudies-other | 2014 Feb
REPOSITORIES: biostudies-other
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Project description:BackgroundOutdoor air pollution is a known lung carcinogen, but research investigating the association between particulate matter (PM) and gastrointestinal (GI) cancers is limited.ObjectivesWe sought to review the epidemiologic literature on outdoor PM and GI cancers and to put the body of studies into context regarding potential for bias and overall strength of evidence.MethodsWe conducted a systematic review and meta-analysis of epidemiologic studies that evaluated the association of fine PM [PM with an aerodynamic diameter of ≤2.5μm (PM2.5)] and PM10 (aerodynamic diameter ≤10μm) with GI cancer incidence or mortality in adults. We searched five databases for original research published from 1980 to 2021 in English and summarized findings for studies employing a quantitative estimate of exposure overall and by specific GI cancer subtypes. We evaluated the risk of bias of individual studies and the overall quality and strength of the evidence according to the Navigation Guide methodology, which is tailored for environmental health research.ResultsTwenty studies met inclusion criteria and included participants from 14 countries; nearly all were of cohort design. All studies identified positive associations between PM exposure and risk of at least one GI cancer, although in 3 studies these relationships were not statistically significant. Three of 5 studies estimated associations with PM10 and satisfied inclusion criteria for meta-analysis, but each assessed a different GI cancer and were therefore excluded. In the random-effects meta-analysis of 13 studies, PM2.5 exposure was associated with an increased risk of GI cancer overall [risk ratio (RR)=1.12; 95% CI: 1.01, 1.24]. The most robust associations were observed for liver cancer (RR=1.31; 95% CI: 1.07, 1.56) and colorectal cancer (RR=1.35; 95% CI: 1.08, 1.62), for which all studies identified an increased risk. We rated most studies with "probably low" risk of bias and the overall body of evidence as "moderate" quality with "limited" evidence for this association. We based this determination on the generally positive, but inconsistently statistically significant, effect estimates reported across a small number of studies.ConclusionWe concluded there is some evidence of associations between PM2.5 and GI cancers, with the strongest evidence for liver and colorectal cancers. Although there is biologic plausibility for these relationships, studies of any one cancer site were few and there remain only a small number overall. Studies in geographic areas with high GI cancer burden, evaluation of the impact of different PM exposure assessment approaches on observed associations, and investigation of cancer subtypes and specific chemical components of PM are important areas of interest for future research. https://doi.org/10.1289/EHP9620.
| S-EPMC8890324 | biostudies-literature
Project description:Background and purposeAtrial fibrillation (AF) is a leading cause of cardioembolic stroke, but the relationship between AF and noncardioembolic stroke subtypes are unclear. Because AF may be unrecognized, and because AF has a substantial genetic basis, we assessed for predisposition to AF across ischemic stroke subtypes.MethodsWe examined associations between AF genetic risk and Trial of Org 10172 in Acute Stroke Treatment stroke subtypes in 2374 ambulatory individuals with ischemic stroke and 5175 without from the Wellcome Trust Case-Control Consortium 2 using logistic regression. We calculated AF genetic risk scores using single-nucleotide polymorphisms associated with AF in a previous independent analysis across a range of preselected significance thresholds.ResultsThere were 460 (19.4%) individuals with cardioembolic stroke, 498 (21.0%) with large vessel, 474 (20.0%) with small vessel, and 814 (32.3%) individuals with strokes of undetermined cause. Most AF genetic risk scores were associated with stroke, with the strongest association (P=6×10-4) attributed to scores of 944 single-nucleotide polymorphisms (each associated with AF at P<1×10-3 in a previous analysis). Associations between AF genetic risk and stroke were enriched in the cardioembolic stroke subset (strongest P=1.2×10-9, 944 single-nucleotide polymorphism score). In contrast, AF genetic risk was not significantly associated with noncardioembolic stroke subtypes.ConclusionsComprehensive AF genetic risk scores were specific for cardioembolic stroke. Incomplete workups and subtype misclassification may have limited the power to detect associations with strokes of undetermined pathogenesis. Future studies are warranted to determine whether AF genetic risk is a useful biomarker to enhance clinical discrimination of stroke pathogeneses.
| S-EPMC7438180 | biostudies-literature
Project description:Short-term changes in levels of fine ambient particulate matter (PM2.5) may increase the risk of acute ischemic stroke; however, results from prior studies have been inconsistent. We examined this hypothesis using data from a multicenter prospective stroke registry.We analyzed data from 9202 patients hospitalized with acute ischemic stroke, having a documented date and time of stroke onset, and residing within 50 km of a PM2.5 monitor in 8 cities in Ontario, Canada. We evaluated the risk of ischemic stroke onset associated with PM2.5 in each city using a time-stratified case-crossover design, matching on day of week and time of day. We then combined these city-specific estimates using random-effects meta-analysis techniques. We examined whether the effects of PM2.5 differed across strata defined by patient characteristics and ischemic stroke etiology.Overall, PM2.5 was associated with a -0.7% change in ischemic stroke risk per 10-?g/m increase in PM2.5 (95% confidence interval = -6.3% to 5.1%). These overall negative results were robust to a number of sensitivity analyses. Among patients with diabetes mellitus, PM2.5 was associated with an 11% increase in ischemic stroke risk (1% to 22%). The association between PM2.5 and ischemic stroke risk varied according to stroke etiology, with the strongest associations observed for strokes due to large-artery atherosclerosis and small-vessel occlusion.These results do not support the hypothesis that short-term increases in PM2.5 levels are associated with ischemic stroke risk overall. However, specific patient subgroups may be at increased risk of particulate-related ischemic strokes.
| S-EPMC3102528 | biostudies-literature
Project description:ImportanceAir pollution is associated with cardiovascular outcomes. Specifically, fine particulate matter measuring 2.5 μm or less (PM2.5) is associated with thrombosis, stroke, and myocardial infarction. Few studies have examined particulate matter and stroke risk in individuals with atrial fibrillation (AF).ObjectiveTo assess the association of residential-level pollution exposure in 1 year and ischemic stroke in individuals with AF.Design, setting, and participantsThis cohort study included 31 414 individuals with AF from a large regional health care system in an area with historically high industrial pollution. All participants had valid residential addresses for geocoding and ascertainment of neighborhood-level income and educational level. Participants were studied from January 1, 2007, through September 30, 2015, with prospective follow-up through December 1, 2017. Data analysis was performed from March 14, 2018, to October 9, 2019.ExposuresExposure to PM2.5 ascertained using geocoding of addresses and fine-scale air pollution exposure surfaces derived from a spatial saturation monitoring campaign and land-use regression modeling. Exposure to PM2.5 was estimated annually across the study period at the residence level.Main outcomes and measuresMultivariable-adjusted stroke risk by quartile of residence-level and annual PM2.5 exposure.ResultsThe cohort included 31 414 individuals (15 813 [50.3%] female; mean [SD] age, 74.4 [13.5] years), with a median follow-up of 3.5 years (interquartile range, 1.6-5.8 years). The mean (SD) annual PM2.5 exposure was 10.6 (0.7) μg/m3. A 1-SD increase in PM2.5 was associated with a greater risk of stroke after both adjustment for demographic and clinical variables (hazard ratio [HR], 1.08; 95% CI, 1.03-1.14) and multivariable adjustment that included neighborhood-level income and educational level (HR, 1.07; 95% CI, 1.00-1.14). The highest quartile of PM2.5 exposure had an increased risk of stroke relative to the first quartile (HR, 1.36; 95% CI, 1.18-1.58). After adjustment for clinical covariates, income, and educational level, risk of stroke remained greater for the highest quartile of exposure relative to the first quartile (HR, 1.21; 95% CI, 1.01-1.45).Conclusions and relevanceThis large cohort study of individuals with AF identified associations between PM2.5 and risk of ischemic stroke. The results suggest an association between fine particulate air pollution and cardiovascular disease and outcomes.
| S-EPMC7492916 | biostudies-literature
Project description:The incidence of perinatal stroke is high, similar to that in the elderly, and produces a significant morbidity and severe long-term neurologic and cognitive deficits, including cerebral palsy, epilepsy, neuropsychological impairments, and behavioral disorders. Emerging clinical data and data from experimental models of cerebral ischemia in neonatal rodents have shown that the pathophysiology of perinatal brain damage is multifactorial. These studies have revealed that, far from just being a smaller version of the adult brain, the neonatal brain is unique with a very particular and age-dependent responsiveness to hypoxia-ischemia and focal arterial stroke. In this review, we discuss fundamental clinical aspects of perinatal stroke as well as some of the most recent and relevant findings regarding the susceptibility of specific brain cell populations to injury, the dynamics and the mechanisms of neuronal cell death in injured neonates, the responses of neonatal blood-brain barrier to stroke in relation to systemic and local inflammation, and the long-term effects of stroke on angiogenesis and neurogenesis. Finally, we address translational strategies currently being considered for neonatal stroke as well as treatments that might effectively enhance repair later after injury.
| S-EPMC4050239 | biostudies-other
Project description:suspended particulate matter Raw sequence reads
| PRJNA423140 | ENA
Project description:Particulate matter PM2.5 Raw sequence reads
| PRJNA772531 | ENA
Project description:Although peripheral blood mRNA and micro-RNA change after ischemic stroke, any role for long noncoding RNA (lncRNA), which comprise most of the genome and have been implicated in various diseases, is unknown. Thus, we hypothesized that lncRNA expression also changes after stroke.lncRNA expression was assessed in 266 whole-blood RNA samples drawn once per individual from patients with ischemic stroke and matched with vascular risk factor controls. Differential lncRNA expression was assessed by ANCOVA (P<0.005; fold change>|1.2|), principal components analysis, and hierarchical clustering on a derivation set (n=176) and confirmed on a validation set (n=90). Poststroke temporal lncRNA expression changes were assessed using ANCOVA with confounding factor correction (P<0.005; partial correlation with time since event >|0.4|). Because sexual dimorphism exists in stroke, analyses were performed for each sex separately.A total of 299 lncRNAs were differentially expressed between stroke and control males, whereas 97 lncRNAs were differentially expressed between stroke and control females. Significant changes of lncRNA expression with time after stroke were detected for 49 lncRNAs in men and 31 lncRNAs in women. Some differentially expressed lncRNAs mapped close to genomic locations of previously identified putative stroke-risk genes, including lipoprotein, lipoprotein(a)-like 2, ABO (transferase A, ?1-3-N-acetylgalactosaminyltransferase; transferase B, ?1-3-galactosyltransferase) blood group, prostaglandin 12 synthase, and ?-adducins.This study provides evidence of altered and sexually dimorphic lncRNA expression in peripheral blood of patients with stroke compared with that of controls and suggests that lncRNAs have potential for stroke biomarker development. Some regulated lncRNA could regulate some previously identified putative stroke-risk genes.
| S-EPMC5127755 | biostudies-literature
Project description:Patient readmission for ischemic stroke significantly strains the healthcare and medical insurance systems. Current understanding of the risk factors associated with these readmissions, as well as their subsequent impact on mortality within China, remains insufficient. This is particularly evident in the context of comprehensive, contemporary population studies. This 4-year retrospective cohort study included 125 397 hospital admissions for ischemic stroke from 838 hospitals located in 22 regions (13 urban and 9 rural) of a major city in western China, between January 1, 2015 and December 31, 2018. The Chi-square tests were used in univariate analysis. Accounting for intra-subject correlations of patients' readmissions, accelerated failure time (AFT) shared frailty models were used to examine readmission events and pure AFT models for mortality. Risk factors for patient readmission after ischemic stroke include frequent admission history, male gender, employee's insurance, advanced age, residence in urban areas, index hospitalization in low-level hospitals, extended length of stay (LOS) during index hospitalization, specific comorbidities and subtypes of ischemic stroke. Furthermore, our findings indicated that an additional admission for ischemic stroke increased patient mortality by 16.4% (P < .001). Stroke readmission contributed to an increased risk of hospital mortality. Policymakers can establish more effective and targeted policies to reduce readmissions for stroke by controlling these risk factors.
| S-EPMC10966977 | biostudies-literature
Project description:PurposeDiffusion MRI offers insight into ischemic stroke progression in both human and rodent models. However, diffusion MRI to evaluate therapeutic application of mesenchymal stem cells is limited. Robust analytical techniques are required to identify potential physiological changes as a function of cell therapy in stroke. Here, we seek to establish Neurite Orientation Dispersion and Density Imaging (NODDI) as a feasible method in evaluating stroke evolution in response to cell-based therapeutics.MethodsDiffusion MRI data at 21.1T were acquired from 16 male rats. Rats were grouped randomly: naïve (baseline, N = 5), stroke with injections of phosphate buffered saline (N = 6), stroke with injection of 2D human mesenchymal stem cells (hMSC, N = 5). Data were acquired on days 1, 3, 7, and 21 post-surgery. DTI and NODDI maps were generated, with regions of interest placed in the ischemic hemisphere external capsule and striatum. Diffusion parameters were compared between groups each day, and within groups across hemispheres and longitudinally. Behavioral characterizations were on days 0 (pre-surgery), 3, 7, 14, and 21.ResultsThe 2D hMSC preserved diffusional restriction in the external capsule compared to saline (day 1: MD, P = .4060; AD, P = .0220). NODDI indicates that hMSC may have preserved intracellular volume fractions (ICVF: day 1, P = .0086; day 3, P = .0021; day 21, P = .0383). Diffusion metrics of hMSC treated animals were comparable to naïve for the external capsule.ConclusionsNODDI compliments DTI metrics, enhances interpretation of tissue outcome in ischemic stroke following hMSC application, and may be useful in evaluating or predicting therapeutic response.
| S-EPMC9290760 | biostudies-literature