Dataset Information

Risk of nonaccidental and cardiovascular mortality in relation to long-term exposure to low concentrations of fine particulate matter: a Canadian national-level cohort study.

ABSTRACT:

Background

Few cohort studies have evaluated the risk of mortality associated with long-term exposure to fine particulate matter [? 2.5 ?m in aerodynamic diameter (PM(2.5))]. This is the first national-level cohort study to investigate these risks in Canada.

Objective

We investigated the association between long-term exposure to ambient PM(2.5) and cardiovascular mortality in nonimmigrant Canadian adults.

Methods

We assigned estimates of exposure to ambient PM(2.5) derived from satellite observations to a cohort of 2.1 million Canadian adults who in 1991 were among the 20% of the population mandated to provide detailed census data. We identified deaths occurring between 1991 and 2001 through record linkage. We calculated hazard ratios (HRs) and 95% confidence intervals (CIs) adjusted for available individual-level and contextual covariates using both standard Cox proportional survival models and nested, spatial random-effects survival models.

Results

Using standard Cox models, we calculated HRs of 1.15 (95% CI: 1.13, 1.16) from nonaccidental causes and 1.31 (95% CI: 1.27, 1.35) from ischemic heart disease for each 10-?g/m(3) increase in concentrations of PM(2.5). Using spatial random-effects models controlling for the same variables, we calculated HRs of 1.10 (95% CI: 1.05, 1.15) and 1.30 (95% CI: 1.18, 1.43), respectively. We found similar associations between nonaccidental mortality and PM2.5 based on satellite-derived estimates and ground-based measurements in a subanalysis of subjects in 11 cities.

Conclusions

In this large national cohort of nonimmigrant Canadians, mortality was associated with long-term exposure to PM(2.5). Associations were observed with exposures to PM(2.5) at concentrations that were predominantly lower (mean, 8.7 ?g/m(3); interquartile range, 6.2 ?g/m(3)) than those reported previously.

SUBMITTER: Crouse DL

PROVIDER: S-EPMC3346774 | biostudies-literature | 2012 May

REPOSITORIES: biostudies-literature

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Publications

Risk of nonaccidental and cardiovascular mortality in relation to long-term exposure to low concentrations of fine particulate matter: a Canadian national-level cohort study.

Crouse Dan L DL Peters Paul A PA van Donkelaar Aaron A Goldberg Mark S MS Villeneuve Paul J PJ Brion Orly O Khan Saeeda S Atari Dominic Odwa DO Jerrett Michael M Pope C Arden CA Brauer Michael M Brook Jeffrey R JR Martin Randall V RV Stieb David D Burnett Richard T RT

Environmental health perspectives 20120207 5

<h4>Background</h4>Few cohort studies have evaluated the risk of mortality associated with long-term exposure to fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM(2.5))]. This is the first national-level cohort study to investigate these risks in Canada.<h4>Objective</h4>We investigated the association between long-term exposure to ambient PM(2.5) and cardiovascular mortality in nonimmigrant Canadian adults.<h4>Methods</h4>We assigned estimates of exposure to ambient PM(2.5) derived ...[more]

PMID: 22313724

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Project description:Cohort studies in North America and western Europe have reported increased risk of mortality associated with long-term exposure to fine particles (PM2.5), but to date, no such studies have been reported in China, where higher levels of exposure are experienced.We estimated the association between long-term exposure to PM2.5 with nonaccidental and cause-specific mortality in a cohort of Chinese men.We conducted a prospective cohort study of 189,793 men 40 y old or older during 1990-91 from 45 areas in China. Annual average PM2.5 levels for the years 1990, 1995, 2000, and 2005 were estimated for each cohort location using a combination of satellite-based estimates, chemical transport model simulations, and ground-level measurements developed for the Global Burden of Disease (GBD) 2013 study. A Cox proportional hazards regression model was used to estimate hazard ratios (HR) for nonaccidental cardiovascular disease (CVD), chronic obstructive pulmonary disease (COPD), and lung-cancer mortality. We also assessed the shape of the concentration-response relationship and compared the risk estimates with those predicted by Integrated Exposure-Response (IER) function, which incorporated estimates of mortality risk from previous cohort studies in western Europe and North America.The mean level of PM2.5 exposure during 2000-2005 was 43.7??g/m3 (ranging from 4.2 to 83.8??g/m3). Mortality HRs (95% CI) per 10-?g/m3 increase in PM2.5 were 1.09 (1.08, 1.09) for nonaccidental causes; 1.09 (1.08, 1.10) for CVD, 1.12 (1.10, 1.13) for COPD; and 1.12 (1.07, 1.14) for lung cancer. The HR estimate from our cohort was consistently higher than IER predictions.Long-term exposure to PM2.5 was associated with nonaccidental, CVD, lung cancer, and COPD mortality in China. The IER estimator may underestimate the excess relative risk of cause-specific mortality due to long-term exposure to PM2.5 over the exposure range experienced in China and other low- and middle-income countries. https://doi.org/10.1289/EHP1673.

Project description:BackgroundAir pollution, especially fine particulate matter (PM), can cause brain damage, cognitive decline, and an increased risk of neurodegenerative disease, especially alzheimer's disease (AD). Typical pathological findings of amyloid and tau protein accumulation have been detected in the brain after exposure in animal studies. However, these observations were based on high levels of PM exposure, which were far from the WHO guidelines and those present in our environment. In addition, white matter involvement by air pollution has been less reported. Thus, this experiment was designed to simulate the true human world and to discuss the possible white matter pathology caused by air pollution.Results6 month-old female 3xTg-AD mice were divided into exposure and control groups and housed in the Taipei Air Pollutant Exposure System (TAPES) for 5 months. The mice were subjected to the Morris water maze test after exposure and were then sacrificed with brain dissection for further analyses. The mean mass concentration of PM2.5 during the exposure period was 13.85 μg/m3. After exposure, there was no difference in spatial learning function between the two groups, but there was significant decay of memory in the exposure group. Significantly decreased total brain volume and more neuronal death in the cerebral and entorhinal cortex and demyelination of the corpus callosum were noted by histopathological staining after exposure. However, there was no difference in the accumulation of amyloid or tau on immunohistochemistry staining. For the protein analysis, amyloid was detected at significantly higher levels in the cerebral cortex, with lower expression of myelin basic protein in the white matter. A diffuse tensor image study also revealed insults in multiple white matter tracts, including the optic tract.ConclusionsIn conclusion, this pilot study showed that even chronic exposure to low PM2.5 concentrations still caused brain damage, such as gross brain atrophy, cortical neuron damage, and multiple white matter tract damage. Typical amyloid cascade pathology did not appear prominently in the vulnerable brain region after exposure. These findings imply that multiple pathogenic pathways induce brain injury by air pollution, and the optic nerve may be another direct invasion route in addition to olfactory nerve.

Dataset Information

Risk of nonaccidental and cardiovascular mortality in relation to long-term exposure to low concentrations of fine particulate matter: a Canadian national-level cohort study.

Background

Objective

Methods

Results

Conclusions

Publications

Risk of nonaccidental and cardiovascular mortality in relation to long-term exposure to low concentrations of fine particulate matter: a Canadian national-level cohort study.

Similar Datasets

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