冶炼厂烟尘PM_(2.5)复合污染探讨

目的　通过本研究确定 ,现有除尘设备是否还存在PM2 5复合污染。方法　通过化学、电子显微镜及电子能谱、GC MS等仪器对上述样品多种污染成分及粒径进行定性、定量测定。结果　上述复合污染成分 :水 2 2 % ,有机物 34 75 % ,无机物 4 3 75 %。无机物以Cu、C、Pb、Al为主 ,它们的粒径≤ 1 1μm ,有机污染物14 0多种 ,以酚类及PAHs为主 ,无机物中除铅、砷等重金属 ,还有砷酸、磷酸。结论　在现有除尘设备条件下的冶炼厂烟尘污染为多种重金属、酸性氧化物及几十种有机污染物 (酚类及PAHs)的复合污染 ,它们的粒径分布大多≤ 1 1μm。     

沙尘暴细颗粒物致大鼠肺泡巨噬细胞DNA损伤

[目的]探讨沙尘暴和正常天气细颗粒物(PM2.5)及其水提取物和有机提取物对大鼠肺泡巨噬细胞的细胞毒性和DNA的损伤作用。[方法]沙尘暴和正常天气PM2.5于2004年3月采集自甘肃省武威市和内蒙古自治区包头市。细胞毒性用四甲基偶氮唑盐(MTT)分析法观察,细胞DNA损伤用单细胞凝胶电泳(SCGE)技术检测。[结果]沙尘暴和正常天气PM2.5及其水提取物和有机提取物均对大鼠肺泡巨噬细胞产生一定的细胞毒性,且随剂量的增大而增强;然而,沙尘暴与正常天气之间除了包头沙尘暴PM2.5有机提取物之外,余差异均无显著性。正常天气PM2.5和沙尘暴PM2.5水提取物和有机提取物均可引起细胞DNA损伤,且随剂量增加而损伤增大;正常天气PM2.5比沙尘暴PM2.5水提取物和有机提取物对细胞DNA损伤作用更大。不论正常天气PM2.5还是沙尘暴PM2.5,其有机提取物对DNA的损伤作用均比水提取物作用更强,表明PM2.5中引起DNA损伤的主要化学物是有机化合物种类。武威与包头两城市工业水平不同,大气污染程度不同,但两地沙尘暴PM2.5及其水提取物和有机提取物对细胞DNA的损伤作用,在两地之间并无明显差异。[结论]正常天气PM2.5和沙尘暴PM2.5及其水提取物和有机提取物均可引起DNA损伤,且正常天气PM2.5的损伤作用更强;然而不同地方沙尘暴PM2.5毒性作用未见差异,推测其所含遗传毒性化学物可能类似。     

Assessment of intracellular cytokines and regulatory cells in patients with autoimmune diseases and primary immunodeficiencies — Novel tool for diagnostics and patient follow-up

Serum and intracytoplasmic cytokines are mandatory in host defense against microbes, but also play a pivotal role in the pathogenesis of autoimmune diseases by initiating and perpetuating various cellular and humoral autoimmune processes.     

PM2.5‐induced lung inflammation in mice: Differences of inflammatory response in macrophages and type II alveolar cells

Particulate matter 2.5 (<PM2.5 μm) leads to chronic obstructive pulmonary disease. In this study, biomarkers related to inflammation and oxidative stress in vitro and in vivo experiments were investigated to clarify the PM2.5‐induced lung inflammation mechanisms. In an in vitro study using RAW264.7 cells, PM2.5 caused phosphorylation of nuclear factor‐κB, p38 mitogen‐activated protein kinase and extracellular response kinases, an increase of proinflammatory gene and protein expressions (e.g. monocyte chemotactic protein‐1, tumor necrosis factor‐α). These biomarkers were substantially attenuated by polymyxin B (PMB). PM2.5 induced heme oxygenase‐1 (HO‐1) gene, which was attenuated by N‐ acetylcysteine (NAC). However, the suppressive effects of NAC on inflammatory biomarkers were very weak. In bone marrow‐derived macrophages (BMDMs) of wild‐type BALB/c mice, the effects of PMB and NAC on PM2.5‐induced inflammatory responses were similar to RAW264.7 cells. In BMDMs of MyD88^−/− mice, PM2.5‐induced proinflammatory mediators were substantially more attenuated. PM2.5 caused an increase of proinflammatory gene expressions (interleukin‐6, cyclooxygenase 2) and HO‐1 gene in MLE‐12 cells (mouse alveolar cell line). These biomarkers were substantially attenuated by NAC, but not by PMB. When BALB/c mice were exposed intratracheally to 0.2 mg PM2.5, PM2.5 caused severe lung inflammation, an increase of neutrophils along with proinflammatory mediators in bronchoalveolar lavage fluid. The inflammation was attenuated by NAC, particularly by NAC + PMB, but not by PMB alone. These results indicate that macrophages may act sensitively to lipopolysaccharide (LPS) present in PM2.5 and release proinflammatory mediators via the LPS/MyD88 pathway. However, type II alveolar cells may react sensitively to oxidative stress induced by PM2.5 and cause inflammatory response. Therefore, overall, PM2.5 may cause predominantly oxidative stress‐dependent inflammation rather than LPS/MyD88‐dependent inflammation in type II alveolar cell‐rich lungs. Copyright © 2017 John Wiley & Sons, Ltd.     

2020—2021年芜湖市主城区大气PM2.5中多环芳烃污染特征及健康风险评估

目的 调查芜湖市主城区大气 PM2.5中多环芳烃（PAHs）污染特征及其人群健康风险。方法 2020年6月至2021年5月，每月10至16日采集芜湖市主城区大气PM2.5样品，检测和分析其中16种优先控制PAHs浓度及组成特征，并利用特征比值法和物质结构判断PM2.5中PAHs来源，采用US EPA健康风险模型评估其人群健康风险。结果 大气PM2.5浓度均值为49.2μg/m³，范围为7~151μg/m³；16种PAHs均有不同程度检出，总浓度均值为6.85ng/m³，范围为0.13~31.62ng/m³；PM2.5与16种PAHs各月份日均浓度变化存在相关性（R=0.867，P<0.001）；16种PAHs季节变化为冬季＞秋季＞春季＞夏季，构成均以4~6 环为主；大气PM2.5中PAHs主要来源为机动车排放和燃煤。PM2.5中16种PAHs的总致癌风险值（Risk）为2.20×10^-7，低于1×10^-6，致癌风险可忽略；非致癌风险危害商值（HQ）为0.49，小于1，非致癌健康风险低。结论 芜湖市主城区大气PM2.5中PAHs污染较轻，无明显健康风险。     

Roles of MAPK pathway activation during cytokine induction in BEAS-2B cells exposed to fine World Trade Center (WTC) dust

The World Trade Center (WTC) collapse on September 11, 2001 released copious amounts of particulate matter (PM) into the atmosphere of New York City. Follow-up studies on persons exposed to the dusts have revealed a severely increased rate for asthma and other respiratory illnesses. There have only been a few studies that have sought to discern the possible mechanisms underlying these untoward pathologies. In one study, an increased cytokine release was detected in cells exposed to WTC fine dusts (PM_2.5 fraction or WTC_2.5). However, the mechanism(s) for these increases has yet to be fully defined. Because activation of the mitogen-activated protein kinase (MAPK) signaling pathways is known to cause cytokine induction, the current study was undertaken to analyze the possible involvement of these pathways in any increased cytokine formation by lung epithelial cells (as BEAS-2B cells) exposed to WTC_2.5. Our results showed that exposure to WTC_2.5 for 5?hr increased interleukin-6 (IL-6) mRNA expression in BEAS-2B cells, as well as its protein levels in the culture media, in a dose-dependent manner. Besides IL-6, cytokine multiplex analyses revealed that formation of IL-8 and -10 was also elevated by the exposure. Both extracellular signal-regulated kinase (ERK) and p38, but not c-Jun N-terminal protein kinase, signaling pathways were found to be activated in cells exposed to WTC_2.5. Inactivation of ERK signaling pathways by PD98059 effectively blocked IL-6, -8, and -10 induction by WTC_2.5; the p38 kinase inhibitor SB203580 significantly decreased induction of IL-8 and -10. Together, our data demonstrated activation of MAPK signaling pathway(s) likely played an important role in the WTC_2.5-induced formation of several inflammatory (and, subsequently, anti-inflammatory) cytokines. The results are important in that they help to define one mechanism via which the WTC dusts may have acted to cause the documented increases in asthma and other inflammation-associated respiratory dysfunctions in the individuals exposed to the dusts released from the WTC collapse.     

轻中度癌痛患者的回顾性记忆与前瞻性记忆功能损害的临床研究

目的 探讨轻中度癌痛患者的回顾性记忆（RM）与前瞻性记忆（PM）功能，了解癌痛对记忆功能的影响。方法 收集轻中度癌痛患者和健康对照者各37例，进行总体认知评估及RM和PM问卷调查。结果癌痛组简易精神状态量表得分为24.19±3.20，低于健康对照组的27.54±1.83（P＜0.01）；PM得分为14.76±4.53，高于健康对照组的9.59±1.38（P＜0.01）；癌痛组RM得分略低于健康对照组（12.78±4.27 vs. 12.91±5.12），差异无统计学意义（P＞0.05）。结论 轻中度癌痛患者存在总体认知功能的损害，以记忆功能损害较为明显，其中以PM损害为主。     

Environmental Inequality in Exposures to Airborne Particulate Matter Components in the United States

Background: Growing evidence indicates that toxicity of fine particulate matter ≤ 2.5 μm in diameter (PM_2.5) differs by chemical component. Exposure to components may differ by population.Objectives: We investigated whether exposures to PM_2.5 components differ by race/ethnicity, age, and socioeconomic status (SES).Methods: Long-term exposures (2000 through 2006) were estimated for 215 U.S. census tracts for PM_2.5 and for 14 PM_2.5 components. Population-weighted exposures were combined to generate overall estimated exposures by race/ethnicity, education, poverty status, employment, age, and earnings. We compared population characteristics for tracts with and without PM_2.5 component monitors.Results: Larger disparities in estimated exposures were observed for components than for PM_2.5 total mass. For race/ethnicity, whites generally had the lowest exposures. Non-Hispanic blacks had higher exposures than did whites for 13 of the 14 components. Hispanics generally had the highest exposures (e.g., 152% higher than whites for chlorine, 94% higher for aluminum). Young persons (0–19 years of age) had levels as high as or higher than other ages for all exposures except sulfate. Persons with lower SES had higher estimated exposures, with some exceptions. For example, a 10% increase in the proportion unemployed was associated with a 20.0% increase in vanadium and an 18.3% increase in elemental carbon. Census tracts with monitors had more non-Hispanic blacks, lower education and earnings, and higher unemployment and poverty than did tracts without monitors.Conclusions: Exposures to PM_2.5 components differed by race/ethnicity, age, and SES. If some components are more toxic than others, certain populations are likely to suffer higher health burdens. Demographics differed between populations covered and not covered by monitors.