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Development of a Novel Simulation Reactor for Chronic Exposure to Atmospheric Particulate Matter.

ABSTRACT: Epidemiological studies have shown that air pollution is associated with the morbidity and mortality from cardiopulmonary diseases. Currently, limited experimental models are available to evaluate the physiological and cellular pathways activated by chronic multi-pollutant exposures. This manuscript describes an atmospheric simulation reactor (ASR) that was developed to investigate the health effects of air pollutants by permitting controlled chronic in vivo exposure of mice to combined particulate and gaseous pollutants. BALB/c mice were exposed for 1?hr/day for 3 consecutive days to secondary organic aerosol (SOA, a common particulate air pollutant) at 10-150??g/m³, SOA (30??g/m³)?+?ozone (65?ppb) or SOA?+?ozone (65?ppb)?+?nitrogen dioxide (NO₂; 100?ppb). Daily exposure to SOA alone led to increased airway hyperresponsiveness (AHR) to methacholine with increasing SOA concentrations. Multi-pollutant exposure with ozone and/or NO₂ in conjunction with a sub-toxic concentration of SOA resulted in additive effects on AHR to methacholine. Inflammatory cell recruitment to the airways was not observed in any of the exposure conditions. The ASR developed in this study allows us to evaluate the chronic health effects of relevant multi-pollutant exposures at 'real-life' levels under controlled conditions and permits repeated-exposure studies.

SUBMITTER: Ye J

PROVIDER: S-EPMC5294446 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature

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Development of a Novel Simulation Reactor for Chronic Exposure to Atmospheric Particulate Matter.

Ye Jianhuai J Salehi Sepehr S North Michelle L ML Portelli Anjelica M AM Chow Chung-Wai CW Chan Arthur W H AW

Scientific reports 20170207

Epidemiological studies have shown that air pollution is associated with the morbidity and mortality from cardiopulmonary diseases. Currently, limited experimental models are available to evaluate the physiological and cellular pathways activated by chronic multi-pollutant exposures. This manuscript describes an atmospheric simulation reactor (ASR) that was developed to investigate the health effects of air pollutants by permitting controlled chronic in vivo exposure of mice to combined particul ...[more]

PMID: 28169367

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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.

Project description:BackgroundAmbient air pollution has been linked to the development of gestational diabetes mellitus (GDM). However, evidence of the association is very limited, and no study has estimated the effects of ozone.ObjectiveOur aim was to determine the association of prenatal exposures to particulate matter ≤ 2.5 μm (PM2.5) and ozone (O3) with GDM.MethodsWe used Florida birth vital statistics records to investigate the association between the risk of GDM and two air pollutants (PM2.5 and O3) among 410,267 women who gave birth in Florida between 2004 and 2005. Individual air pollution exposure was assessed at the woman's home address at time of delivery using the hierarchical Bayesian space-time statistical model. We further estimated associations between air pollution exposures during different trimesters and GDM.ResultsAfter controlling for nine covariates, we observed increased odds of GDM with per 5-μg/m3 increase in PM2.5 (ORTrimester1 = 1.16; 95% CI: 1.11, 1.21; ORTrimester2 = 1.15; 95% CI: 1.10, 1.20; ORPregnancy = 1.20; 95% CI: 1.13, 1.26) and per 5-ppb increase in O3 (ORTrimester1 = 1.09; 95% CI: 1.07, 1.11; ORTrimester2 = 1.12; 95% CI: 1.10, 1.14; ORPregnancy = 1.18; 95% CI: 1.15, 1.21) during both the first trimester and second trimester as well as the full pregnancy in single-pollutant models. Compared with the single-pollutant model, the ORs for O3 were almost identical in the co-pollutant model. However, the ORs for PM2.5 during the first trimester and the full pregnancy were attenuated, and no association was observed for PM2.5 during the second trimester in the co-pollutant model (OR = 1.02; 95% CI: 0.98, 1.07).ConclusionThis population-based study suggests that exposure to air pollution during pregnancy is associated with increased risk of GDM in Florida, USA.CitationHu H, Ha S, Henderson BH, Warner TD, Roth J, Kan H, Xu X. 2015. Association of atmospheric particulate matter and ozone with gestational diabetes mellitus. Environ Health Perspect 123:853-859; http://dx.doi.org/10.1289/ehp.1408456.

Dataset Information

Development of a Novel Simulation Reactor for Chronic Exposure to Atmospheric Particulate Matter.

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Development of a Novel Simulation Reactor for Chronic Exposure to Atmospheric Particulate Matter.

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