Associations between asthma emergency visits and particulate matter sources,including diesel emissions from stationary generators in Tacoma,Washington

The objective of this research was to evaluate the effect of particulate matter air pollution, including emissions from diesel generators, on visits to emergency departments for asthma. Daily asthma case data from participating hospitals in the greater Tacoma, Washington area were obtained. Daily asthma emergency room visit data were available from six Tacoma hospitals from January 3, 1998 to May 30, 2002. Only emergency visits where the primary discharge diagnosis was asthma were included in the analysis. Air pollution, daily temperature and relative humidity data were obtained from the Puget Sound Clean Air Agency. An association between daily PM2.5 and emergency department (ED) visits for asthma at lag days 2 and 3 was observed. The relative risk for lag day 2 was 1.04 (95% confidence interval[CI]: 1.01, 1.07) and for lag day 3 was 1.03 (1.0, 1.06). A significant association between ED visits for asthma and increased use of diesel generators was not detected. The use of low-sulfur diesel oil may have mitigated potential adverse health effects. These data indicate that air pollution in a medium-sized coastal city may be sufficient to have a public health impact on asthma.     

Lung cancer and diesel exhaust: an updated critical review of the occupational epidemiology literature

A recent review concluded that the evidence from epidemiology studies was indeterminate and that additional studies were required to support the diesel exhaust-lung cancer hypothesis. This updated review includes seven recent studies. Two population-based studies concluded that significant exposure-response (E-R) trends between cumulative diesel exhaust and lung cancer were unlikely to be entirely explained by bias or confounding. Those studies have quality data on life-style risk factors, but do not allow definitive conclusions because of inconsistent E-R trends, qualitative exposure estimates and exposure misclassification (insufficient latency based on job title), and selection bias from low participation rates. Non-definitive results are consistent with the larger body of population studies. An NCI/NIOSH cohort mortality and nested case-control study of non-metal miners have some surrogate-based quantitative diesel exposure estimates (including highest exposure measured as respirable elemental carbon (REC) in the workplace) and smoking histories. The authors concluded that diesel exhaust may cause lung cancer. Nonetheless, the results are non-definitive because the conclusions are based on E-R patterns where high exposures were deleted to achieve significant results, where a posteriori adjustments were made to augment results, and where inappropriate adjustments were made for the “negative confounding” effects of smoking even though current smoking was not associated with diesel exposure and therefore could not be a confounder. Three cohort studies of bus drivers and truck drivers are in effect air pollution studies without estimates of diesel exhaust exposure and so are not sufficient for assessing the lung cancer-diesel exhaust hypothesis. Results from all occupational cohort studies with quantitative estimates of exposure have limitations, including weak and inconsistent E-R associations that could be explained by bias, confounding or chance, exposure misclassification, and often inadequate latency. In sum, the weight of evidence is considered inadequate to confirm the diesel-lung cancer hypothesis.     

PGS-PLA共混材料的制备和性能

以聚癸二酸甘油酯（PGS）和聚乳酸（PLA）为原料在Haake转矩流变仪中密炼制备了不同配比的PGSPLA共混材料。研究了共混材料的转矩流变性能、热性能、力学性能及其共混形态。结果表明PGSPLA共混材料的转矩流变过程与PLA有很大差异,其熔融塑化过程大幅延长。DSC分析表明：随着PGS含量的增加,PGS-PLA共混材料的玻璃化温度、结晶温度和熔融温度降低,而结晶度提高;共混材料的冲击强度最大可以达到65.6 J/m,较纯PLA提高了447％;SEM观测表明PGS和PLA是分相的,且随PGS含量的提高     

The environmental carcinogen 3-nitrobenzanthrone and its main metabolite 3-aminobenzanthrone enhance formation of reactive oxygen intermediates in human A549 lung epithelial cells

The environmental contaminant 3-nitrobenzanthrone (3-NBA) is highly mutagenic and a suspected human carcinogen. We aimed to evaluate whether 3-NBA is able to deregulate critical steps in cell cycle control and apoptosis in human lung epithelial A549 cells. Increased intracellular Ca(2+) and caspase activities were detected upon 3-NBA exposure. As shown by cell cycle analysis, an increased number of S-phase cells was observed after 24 h of treatment with 3-NBA. Furthermore, 3-NBA was shown to inhibit cell proliferation when added to subconfluent cell cultures. The main metabolite of 3-NBA, 3-ABA, induced statistically significant increases in tail moment as judged by alkaline comet assay. The potential of 3-NBA and 3-ABA to enhance the production of reactive oxygen species (ROS) was demonstrated by flow cytometry using 2',7'-dichlorofluorescein-diacetate (DCFH-DA). The enzyme inhibitors allopurinol, dicumarol, resveratrol and SKF525A were used to assess the impact of metabolic conversion on 3-NBA-mediated ROS production. Resveratrol decreased dichlorofluorescein (DCF) fluorescence by 50%, suggesting a role for CYP1A1 in 3-NBA-mediated ROS production. Mitochondrial ROS production was significantly attenuated (20% reduction) by addition of rotenone (complex I inhibition) and thenoyltrifluoroacetone (TTFA, complex II inhibition). Taken together, the results of the present study provide evidence for a genotoxic potential of 3-ABA in human epithelial lung cells. Moreover, both compounds lead to increased intracellular ROS and create an environment favorable to DNA damage and the promotion of cancer.     

Diesel exhaust particles enhance T-cell activation in severe asthmatics

Prevalence of asthma is increasing in westernized countries. Epidemiological studies showed the impact of traffic pollution on the triggering of asthma symptoms and exacerbations, and this effect is mainly attributed to the polycyclic aromatic hydrocarbon core of diesel exhaust particles (DEP). However, although DEP induce IgE synthesis, little is known of their role on T-cell activation, the main cells orchestrating asthma inflammation. We assessed the effect of DEP on T-cell activation in severe uncontrolled asthmatics during (n = 13) and outside (n = 19) exacerbations. Results were compared with data obtained in healthy controls (n = 14). Peripheral blood mononuclear cells were cultured in the presence of low-dose DEP. T-cell activation markers, CD69 and CD25, interleukin-4 (IL-4) and interferon (IFN)-gamma production and T-cell proliferation were assessed by flow cytometry. DEP exposure increased the proportion of CD3+CD69+ T cells in all subjects. The proportion of CD25+ T cells increased under DEP stimulation in the exacerbation group only. IFN-gamma- and IL-4-producing T cells increased in both asthmatic groups, especially during exacerbations, but not in controls. This effect was more pronounced for IL-4. In response to DEP stimulation, T-cell proliferation increased in higher proportion in asthmatics compared with controls. These results show that DEP activate T cells in asthmatics only, with a higher effect during exacerbations. This is in keeping with epidemiological data which demonstrated that DEP trigger respiratory symptoms in asthmatics but not in controls. The higher effect of DEP in exacerbated asthmatics suggests that uncontrolled asthma is a risk factor for aggravation under exposure to traffic pollutants.     

玄参的毛细管电泳指纹图谱研究

目的建立玄参药材的毛细管电泳指纹图谱（CEFP）。方法采用毛细管区带电泳法,以50 mmol.L-1硼砂为背景电解质,运行电压12.1 kV,检测波长280 nm,重力进样20 s（高度8.5 cm）,以10个不同产地药材的电泳图谱建立了玄参CEFP。用＂中药色谱指纹图谱超信息特征数字化评价系统3.0＂软件获得相关指纹峰特征参数,用双定性相似度（SF与S′F）和双定量相似度（C与P）分别评价。对玄参CEFP进行了破坏性试验考察并考察了大峰和小峰分别缺失时4个相似度指标变化特征。结果以哈巴俄苷峰为参照物峰,按共有峰出现率100%确定10个共有指纹峰,建立了玄参CEFP。采用DQDQS法评价出3批质量完全合格,4批含量明显偏低,3批含量明显偏高。破坏性试验结果表明玄参CEFP指纹在碱性条件下极易降解,其次在酸性条件和氧化作用下也发生降解。采用混批勾兑技术按含量相似度105%计算了两类含量高低不同样品的勾兑系数。结论由SF与S′F和C与P构成的双定性双定量相似度（DQDQS）法能同时监测大峰和小峰的变动和缺失,能准确的解决色谱指纹图谱的宏观定性和定量评价的关键问题,所建立的CEFP为玄参药材质量控制提供了新方法。     

Soy biodiesel emissions have reduced inflammatory effects compared to diesel emissions in healthy and allergic mice

Abstract

Toxicity of exhaust from combustion of petroleum diesel (B0), soy-based biodiesel (B100), or a 20% biodiesel/80% petrodiesel mix (B20) was compared in healthy and house dust mite (HDM)-allergic mice. Fuel emissions were diluted to target fine particulate matter (PM_2.5) concentrations of 50, 150, or 500?μg/m³. Studies in healthy mice showed greater levels of neutrophils and MIP-2 in bronchoalveolar lavage (BAL) fluid 2?h after a single 4-h exposure to B0 compared with mice exposed to B20 or B100. No consistent differences in BAL cells and biochemistry, or hematological parameters, were observed after 5?d or 4 weeks of exposure to any of the emissions. Air-exposed HDM-allergic mice had significantly increased responsiveness to methacholine aerosol challenge compared with non-allergic mice. Exposure to any of the emissions for 4 weeks did not further increase responsiveness in either non-allergic or HDM-allergic mice, and few parameters of allergic inflammation in BAL fluid were altered. Lung and nasal pathology were not significantly different among B0-, B20-, or B100-exposed groups. In HDM-allergic mice, exposure to B0, but not B20 or B100, significantly increased resting peribronchiolar lymph node cell proliferation and production of T_H2 cytokines (IL-4, IL-5, and IL-13) and IL-17 in comparison with air-exposed allergic mice. These results suggest that diesel exhaust at a relatively high concentration (500?μg/m³) can induce inflammation acutely in healthy mice and exacerbate some components of allergic responses, while comparable concentrations of B20 or B100 soy biodiesel fuels did not elicit responses different from those caused by air exposure alone.