33 research outputs found

    Street-scale dispersion modelling framework of road-traffic derived air pollution in Hanoi, Vietnam

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    Traffic is an important source of air pollution in Vietnamese cities. The spatio-temporal variation of air pollution derived from traffic is poorly understood. Application of dispersion modelling can help but is hindered by the local scarcity of suitable input data. This study fills the data gap, by establishing a framework employing open-access global data to model emission from traffic activities in Hanoi. The outlined methodology explicitly defines road sources, calculates their emission, and employs background pollution profiles from Copernicus Atmospheric Monitoring Service (CAMS) to produce street-scale distribution maps for CO, PM10 and PM2.5. Pollution hotspots are found near major traffic flows with the highest hourly average CO, PM10 and PM2.5 concentrations at 1206, 87.5 and 61.5 μgm−3, respectively. The relationship between concentrations and properties of the road network is assessed. Motorcycles are the main emitters of the traffic sector. Emission from Heavy Good Vehicles dominate during the night, with contribution percentages increase as it gets further away from the city core. Modelled concentrations are underestimated mainly due to low vehicular emission factor. Adjusting emission factors according to vehicle quality in Vietnam greatly improves agreement. The presence of non-traffic emission sources contributes to the model underestimation. Results for comparisons of daily averaged PM values are broadly in agreement between models and observations; however, diurnal patters are skewed. This results partly from the uncertainties linked with background pollution levels from CAMS, and partly from non-traffic sources which are not accounted for here. Further work is needed to assess the use of CAMS's concentrations in Vietnam. Meteorological input contributes to the temporal disagreement between the model and observations. The impact is most noticeable with CO concentrations during morning traffic rush hours. This study recommends approaches to improve input for future model iterations and encourage applications of dispersion modelling studies in similar economic settings

    Disability, Home Physical Environment and Non-Fatal Injuries among Young Children in China

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    We compared the patterns of medically attended injuries between children with and without disabilities and explored the residential environment risks in five counties of Hubei Province in the People's Republic of China by a 1:1 matched case-control study based on the biopsychosocial model of the International Classification of Functioning, Disability and Health--ICF.1201 children aged 1-14 with disabilities and 1201 their healthy counterparts matched as having the same gender, same age, and lived in the same neighborhood were recruited in our study. Characteristics of injuries in the past 12 months were compared between children with and without disabilities. The associations among disability status, home environment factors and injuries were examined in logistic regression analysis taking into account sociodemographic factors.Children with disabilities had a significantly higher prevalence of injury than children without disabilities (10.2% vs. 4.4%; P<.001). The two groups differed significantly in terms of number of injury episodes, injury place and activity at time of injury. Falls were the leading mechanism of injury regardless of disability status. Most of the injury events happened inside the home and leisure activities were the most reported activity when injured for both groups. The univariate OR for injury was 4.46 (2.57-7.74) for the disabled children compared with the non-disabled children. Disabled children whose family raised cat/dog(s) were 76% more likely to be injured during the last 12 months (OR = 1.76; 95% CI = 1.02, 3.02), comparing with those whose family did not have any cat/dog. And for children without disabilities, those whose family had cat/dog(s) were over 3 times more likely to having injuries comparing with those whose family did not have any cat/dog.Children with disabilities had a significantly increased risk for injury. Interventions to prevent residential injury are an important public health priority in children with disabilities

    Zinc transporter gene expression is regulated by pro-inflammatory cytokines: a potential role for zinc transporters in beta-cell apoptosis?

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    <p>Abstract</p> <p>Background</p> <p>β-cells are extremely rich in zinc and zinc homeostasis is regulated by zinc transporter proteins. β-cells are sensitive to cytokines, interleukin-1β (IL-1β) has been associated with β-cell dysfunction and -death in both type 1 and type 2 diabetes. This study explores the regulation of zinc transporters following cytokine exposure.</p> <p>Methods</p> <p>The effects of cytokines IL-1β, interferon-γ (IFN-γ), and tumor necrosis factor-ι (TNF-ι) on zinc transporter gene expression were measured in INS-1-cells and rat pancreatic islets. Being the more sensitive transporter, we further explored ZnT8 (Slc30A8): the effect of ZnT8 over expression on cytokine induced apoptosis was investigated as well as expression of the insulin gene and two apoptosis associated genes, BAX and BCL2.</p> <p>Results</p> <p>Our results showed a dynamic response of genes responsible for β-cell zinc homeostasis to cytokines: IL-1β down regulated a number of zinc-transporters, most strikingly ZnT8 in both islets and INS-1 cells. The effect was even more pronounced when mixing the cytokines. TNF-ι had little effect on zinc transporter expression. IFN-γ down regulated a number of zinc transporters. Insulin expression was down regulated by all cytokines. ZnT8 over expressing cells were more sensitive to IL-1β induced apoptosis whereas no differences were observed with IFN-γ, TNF-ι, or a mixture of cytokines.</p> <p>Conclusion</p> <p>The zinc transporting system in β-cells is influenced by the exposure to cytokines. Particularly ZnT8, which has been associated with the development of diabetes, seems to be cytokine sensitive.</p
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