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Within-city Spatial Variations in Ambient Ultrafine Particle Concentrations and Incident Brain Tumors in Adults.

ABSTRACT: BACKGROUND:Ambient ultrafine particles (UFPs, <0.1 µm) can reach the human brain, but to our knowledge, epidemiologic studies have yet to evaluate the relation between UFPs and incident brain tumors. METHODS:We conducted a cohort study of within-city spatial variations in ambient UFPs across Montreal and Toronto, Canada, among 1.9 million adults included in multiple cycles of the Canadian Census Health and Environment Cohorts (1991, 1996, 2001, and 2006). UFP exposures (3-year moving averages) were assigned to residential locations using land-use regression models with exposures updated to account for residential mobility within and between cities. We followed cohort members for malignant brain tumors (ICD-10 codes C71.0-C71.9) between 2001 and 2016; Cox proportional hazards models (stratified by age, sex, immigration status, and census cycle) were used to estimate hazard ratios (HRs) adjusting for fine particle mass concentrations (PM2.5), nitrogen dioxide (NO2), and various sociodemographic factors. RESULTS:In total, we identified 1,400 incident brain tumors during the follow-up period. Each 10,000/cm increase in UFPs was positively associated with brain tumor incidence (HR = 1.112, 95% CI = 1.042, 1.188) after adjusting for PM2.5, NO2, and sociodemographic factors. Applying an indirect adjustment for cigarette smoking and body mass index strengthened this relation (HR = 1.133, 95% CI = 1.032, 1.245). PM2.5 and NO2 were not associated with an increased incidence of brain tumors. CONCLUSIONS:Ambient UFPs may represent a previously unrecognized risk factor for incident brain tumors in adults. Future studies should aim to replicate these results given the high prevalence of UFP exposures in urban areas.

SUBMITTER: Weichenthal S

PROVIDER: S-EPMC7004474 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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Within-city Spatial Variations in Ambient Ultrafine Particle Concentrations and Incident Brain Tumors in Adults.

Weichenthal Scott S Olaniyan Toyib T Christidis Tanya T Lavigne Eric E Hatzopoulou Marianne M Van Ryswyk Keith K Tjepkema Michael M Burnett Rick R

Epidemiology (Cambridge, Mass.) 20200301 2

<h4>Background</h4>Ambient ultrafine particles (UFPs, <0.1 µm) can reach the human brain, but to our knowledge, epidemiologic studies have yet to evaluate the relation between UFPs and incident brain tumors.<h4>Methods</h4>We conducted a cohort study of within-city spatial variations in ambient UFPs across Montreal and Toronto, Canada, among 1.9 million adults included in multiple cycles of the Canadian Census Health and Environment Cohorts (1991, 1996, 2001, and 2006). UFP exposures (3-year mov ...[more]

PMID: 31714401

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Project description:BackgroundThe metabolomic signatures of short- and long-term exposure to PM2.5 have been reported and linked to inflammation and oxidative stress. However, little is known about the relative contribution of the specific PM2.5 species (hence sources) that drive these metabolomic signatures.ObjectivesWe aimed to determine the relative contribution of the different species of PM2.5 exposure to the perturbed metabolic pathways related to changes in the plasma metabolome.MethodsWe performed mass-spectrometry based metabolomic profiling of plasma samples among men from the Normative Aging Study to identify metabolic pathways associated with PM2.5 species. The exposure windows included short-term (one, seven-, and thirty-day moving average) and long-term (one year moving average). We used linear mixed-effect regression with subject-specific intercepts while simultaneously adjusting for PM2.5, NO2, O3, temperature, relative humidity, and covariates and correcting for multiple testing. We also used independent component analysis (ICA) to examine the relative contribution of patterns of PM2.5 species.ResultsBetween 2000 and 2016, 456 men provided 648 blood samples, in which 1158 metabolites were quantified. We chose 305 metabolites for the short-term and 288 metabolites for the long-term exposure in this analysis that were significantly associated (p-value < 0.01) with PM2.5 to include in our PM2.5 species analysis. On average, men were 75.0 years old and their body mass index was 27.7 kg/m2. Only 3% were current smokers. In the adjusted models, ultrafine particles (UFPs) were the most significant species of short-term PM2.5 exposure followed by nickel, vanadium, potassium, silicon, and aluminum. Black carbon, vanadium, zinc, nickel, iron, copper, and selenium were the significant species of long-term PM2.5 exposure. We identified several metabolic pathways perturbed with PM2.5 species including glycerophospholipid, sphingolipid, and glutathione. These pathways are involved in inflammation, oxidative stress, immunity, and nucleic acid damage and repair. Results were overlapped with the ICA.ConclusionsWe identified several significant perturbed plasma metabolites and metabolic pathways associated with exposure to PM2.5 species. These species are associated with traffic, fuel oil, and wood smoke. This is the largest study to report a metabolomic signature of PM2.5 species' exposure and the first to use ICA.

Project description:Epidemiology studies have linked exposure to pollutant particles to increased cardiovascular mortality and morbidity, however, the mechanism remains unknown. In this study, we hypothesized that the ultrafine fraction of ambient pollutant particles would cause endothelial cells dysfunction. We profiled gene expression of human pulmonary artery endothelial cells (HPAEC) exposed to ultrafine Chapel Hill particles (UFP) (100μg/ml) or vehicle for 4h with Affymetrix HG U133 Plus 2.0 chips (N = 4 each). Using an unpaired t-test (p <0.01, 5% false discovery rate) we found 426 unique genes to be differentially expressed with 320 upregulated genes and 106 downregulated genes. Among these genes, we noted upregulation of genes related to coagulation-inflammation circuitry including tissue factor (F3), coagulation factor II receptor-like 2 (F2RL2, PAR3), interleukin (IL)-6 and IL-8. Upregulation of these genes were independently confirmed by RT-PCR and/or protein release. Genes related to the CXC chemokine family that have been implicated in the pathogenesis of vascular disease were upregulated, including MCP-1 (2.60 fold), IL-8 (2.47 fold), CXCL1 (1.41 fold), CXCL2 (1.95 fold), CXCL3 (2.28 fold) and CXCR4 (1.30 fold). In addition, genes related to clotting independent signaling of F3 were also differentially expressed, including FOS, JUN and NFKBIA. Treatment of HPAEC with UFP for 16 hours increased the release of IL6 and IL8 by 1.9-fold and 1.8-fold respectively. Pretreatment of HPAEC with a blocking antibody against F3 attenuated IL6 and IL8 release by 30% and 70% respectively. Thus using gene profiling, we uncovered that UFP may induce vascular endothelial cells to express genes related to clotting and angiogenesis. These results provide a novel hypothesis that PM may cause cardiovascular adverse health effects via induction of tissue factor in vascular endothelial cells which then triggers clotting dependent and independent downstream signaling. Keywords: particle treatment

Dataset Information

Within-city Spatial Variations in Ambient Ultrafine Particle Concentrations and Incident Brain Tumors in Adults.

Publications

Within-city Spatial Variations in Ambient Ultrafine Particle Concentrations and Incident Brain Tumors in Adults.

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