Building-related symptoms and inflammatory potency of dust from office buildings

The aim was to investigate the association between building-related symptoms (BRS) in office buildings and the inflammatory potency of dust (PD). Furthermore, the association between dust potency and various building characteristics was investigated. Occupants of 22 office buildings received a retrospective questionnaire about BRS (2301 respondents). Dust was collected from groups of offices and building characteristics were recorded. The potency of a dust sample to induce interleukin-8 (IL-8) secretion from the lung epithelial cell line A549 was measured as the slope of the initial linear part of the concentration-response curve. Symptoms of the central nervous system (CNS) were associated with the potency of surface dust (OR = 1.4). This association may be due to an association between an index of CNS symptoms and dust potency in offices of 1-6 occupants (OR = 1.5). No single symptoms correlated with the potency of surface dust. The PD was not related to single building factors. The inflammatory PD may be used as an integrated proxy measure of biologically active compounds in dust, reflecting health relevant properties of the dust. PRACTICAL IMPLICATIONS: The potency of surface dust may be used as a crude measurement of the chemical and biological exposures present in the building, and being associated with the development of central nervous system symptoms. However, additional research is needed to establish the predictive value of the potency of surface dust.     

Effects of silica on human lung fibroblast in culture

Silica has been reported to directly stimulate cellular proliferation of human lung fibroblasts, and silica-treated macrophage supernatants induce fibroblast proliferation and some of their biosynthetic activities. Alveolar macrophages produce increased amount of tumour necrosis factor alpha (TNF-alpha) and transforming growth factor beta (TGF-beta). Lung fibroblasts are producers of interleukin-6 (IL-6). We investigated the capacity of lung fibroblasts obtained from normal and silicosis subjects to elaborate IL-6 in response to TNF-alpha and to TGF-beta. Our data show that TNF-alpha and TGF-beta are able to stimulate the proliferation of human lung fibroblasts in culture, to increase the collagen production of the cells and are both able to increase IL-6 production by lung fibroblasts of patients with silicosis. We hypothesise that silica is able to stimulate lung fibroblast both directly, increasing the cell proliferation, and indirectly stimulating the release of factors (as TNF-alpha and TGF-beta) from activated alveolar macrophages, that are able to increase proliferative and biosynthetic activities of fibroblast.     

Heating of indoor dust causes reduction in its ability to stimulate release of IL-8 and TNFalpha in vitro compared to non-heated dust

Dust is a major contaminant of the indoor air environment and may affect human health. Indoor dust accumulates on surfaces including heaters and light fixtures, and will be heated when these devices are used. Heat treatment of the dust may change its biologic properties and in this study we simulated the heat treatment with a dust-heating model (50-250 degrees C). The residual and the non-heated dust from seven samples were tested in cultures of fresh peripheral blood mononuclear cells and in A549 cell culture using the release of TNFalpha and IL-8, respectively, as effect indicators. The endotoxin-content and the particle size distribution of the residual and the non-heated dust suspensions were determined for some of the samples. We found that the residual dust had less ability to induce the release of TNFalpha and IL-8. The cytokine decline pattern was similar for all the dust tested and could partly be explained by the reduction in endotoxin content or possibly by inhibitory decomposition products. No correlation was found between the measured particle size distribution and the decreased cytokine levels. The results in this study suggest that the residual dust promotes reduced cytokine response and thereby a possibly lower inflammation reaction in the airways if suspended and inhaled compared with the non-heated dust. PRACTICAL IMPLICATIONS: Accumulation of indoor dust on electric heaters and light fixtures may produce a bad odor when switched on in the cold season and some people claim respiratory distress during such events. To investigate to what extent the residuals of heated indoor dust represent a health hazard, we measured the effect in cell cultures before and after heat treatment of the dust. The in vitro results imply that the residual dust will cause a lower proinflammatory response in the airways if suspended and inhaled compared with non-heated dust. This is partly explained by heat destruction of inflammatory components in the dust.     

LPS诱发急性肺损伤中miR-16的表达及功能研究

目的观察脂多糖（LPS）诱发的急性肺损伤中microRNA-16（miR-16）的表达变化及其对炎症因子TNF-α等表达的调节。方法通过生物信息学分析不同物种间miR-16基因序列的保守性。通过小鼠气道向其肺内注入LPS（10 mg.kg-1）,构建小鼠急性肺损伤模型,采用实时荧光定量PCR分析miR-16、IL-6、TNF-α的表达水平;在培养的肺上皮细胞A549中采用miR-16 mi mic对miR-16进行过表达研究。结果 miR-16基因序列在斑马鱼、大鼠、小鼠和人中序列高度保守;miR-16在急性肺损伤病理过程中表达明显降低（P〈0.05）;A549细胞中miR-16的表达水平显著升高（P〈0.01）,相反,LPS诱导的炎症因子IL-6、TNF-α的表达水平显著降低（P〈0.05）。结论 miR-16在LPS诱发的急性肺损伤病理过程中的表达降低,miR-16过表达能够显著抑制LPS对炎症的诱发作用,表明miR-16在急性肺损伤的炎症发生过程中发挥着重要功能。     

既有建筑环境中甲醛浓度对小鼠肺组织及炎性细胞因子的作用

目的:研究既有建筑环境甲醛吸入对小鼠肺组织及炎性细胞因子表达的影响.方法:采用胶合板、粘合剂自制染毒室,染毒室甲醛平均浓度分别为0.28、0.73和1.21 mg/m3.染毒组小鼠每日染毒1次,每次4h,连续8d.8d后,取肺组织,HE染色,观察肺组织病理学改变,免疫组织化学方法观察肺组织TNF-α、IL-17、IL-6的阳性表达.结果:甲醛吸入组小鼠出现肺泡壁毛细血管扩张、充血,炎细胞浸润的病理改变;甲醛染毒组(0.28、0.73和1.21 mg/m3)小鼠肺组织TNF-α、IL-17表达明显高于正常对照组(P＜0.05);甲醛染毒组(0.73和1.21 mg/m3)小鼠肺组织IL-6表达较正常对照组明显增高(P＜0.01).结论:既有建筑环境甲醛可致小鼠肺组织病理损伤,炎性细胞因子TNF-α、IL-6、IL-17表达明显增强,提示炎性细胞因子参与了甲醛致肺组织损伤的病理发展过程.     

Induction of the imbalance of helper T-cell functions in mice exposed to diesel exhaust

Administration of diesel exhaust particles (DEP) increases antigen-specific IgE production and IgE-secreting cells, and induces Th2-type cytokine profiles in the airway in mice and humans. To determine the early effects of diesel exhaust (DE) inhalation on the cytokine production profile, BALB/c mice were exposed to 0 (controls) and 1.0 mg/m3 DE inhalation for 4 weeks. Intraperitoneal sensitization with ovalbumin (OVA) was conducted immediately before DE inhalation. Mice were treated with anti-CD4 or anti-CD8 mAb 1 day before and after the sensitization. On day 21, these mice were boosted with OVA and blood; bronchoalveolar lavage (BAL) fluid, and spleens were collected on day 28. In BAL fluid, both TNFalpha and IL-10 production in DE-exposed and control mice remained basically the same. IL-6 production in the anti-CD4 treatment group of DE-exposed mice, however, significantly increased compared with that of the controls. In vitro antigen-stimulated interleukin-4 (IL-4) and -10 (IL-10) production in spleen cells of exposed mice were not affected by low-dose DE inhalation. In vitro interferon (IFN)-gamma production in the anti-CD4 treated group of exposed mice decreased markedly. Although anti-OVA IgE production in the plasma of sham-treated mice exposed to DE was the same level as for controls, anti-CD4 mAb treatment in DE-exposed mice significantly reduced IgE production compared to controls. In anti-OVA IgG1 production, anti-CD4 or anti-CD8 mAb treatment in DE-exposed groups also significantly reduced. Anti-OVA IgG2a production was reduced by treatment with anti-CD4 mAb, but increased by anti-CD8 mAb treatment in DE-exposed mice. Low dose DE inhalation is thus shown to adversely affect the cytokine and antibody production in mice by altering CD4+ and CD8+ T-cell functions.     

Differences in inflammatory responses and cytotoxicity in RAW264.7 macrophages induced by Streptomyces Anulatus grown on different building materials

Streptomyces anulatus, an indicator microbe of mold in buildings, was grown on different building materials in order to study the impact of growth conditions on the ability of the spores of this microbe to induce toxicity and inflammatory responses. The microbes were grown for 2 months on sterilized and unsterilized wood, chipboard, concrete, plaster board and mineral wool in tight glass vessels under humid conditions. The highest microbial spore concentration was detected on the sterilized mineral wool followed by the sterilized plaster board and the unsterilized mineral wool. Mouse RAW264.7 macrophages were exposed in vitro for 24 h to the spores of S. anulatus and the production of the inflammatory mediators, nitric oxide (NO), tumor necrosis factor alpha (TNF alpha), interleukin-6 (IL-6), interleukin-10 (IL-10) and cytotoxicity, were measured. The dose equivalent to 5 x 10(5) spores/ml of medium was used to compare the different materials. The most intense production of NO (11.6 microM), TNF alpha (560 pg/ml) and IL-6 (2800 pg/ml) in macrophages was induced by the spores grown on sterilized plaster board. They also caused the greatest loss of cell viability (39%). The spores grown on sterilized concrete induced significant production of NO (1.5 microM) and decreased cell viability (22%), and the spores grown on unsterilized and sterilized mineral wool increased production of NO (4.1 microM and 0.8 microM, respectively). The spores did not stimulate production of the anti-inflammatory cytokine IL-10. These results indicate that the ability of S. anulatus to induce inflammatory responses and cytotoxicity in macrophages is dependent on the growth conditions provided by different building materials.     

乌司他丁在婴儿危重先天性心脏病术后的应用

目的探讨乌司他丁对婴儿危重先天性心脏病术后炎性反应的调节作用。方法将30例≤6个月、需手术纠治的危重先天性心脏病患儿按随机数字表法分为2组：试验组和对照组,每组15例。2组患儿均行先天性心脏病纠治手术。对照组术后仅给予常规治疗。在此基础上,试验组术后1 h即给予乌司他丁5 000 U.kg-1.次-1加入5%葡萄糖注射液10 mL中静脉滴注,8 h 1次,连用3 d。比较2组患儿性别、年龄、体质量及术中CPB时间、主动脉阻断时间等。检测2组患儿术后1（T1）、6（T2）、24（T3）、48（T4）、72（T5）h血浆白细胞介素6（interleukin-6,IL-6）、白细胞介素10（interleukin-10,IL-10）、肿瘤坏死因子α（tumor necrosis factor-α,TNF-α）、心肌肌钙蛋白Ⅰ（cardiactroponinⅠ,cTnⅠ）水平。结果 2组患儿在性别、年龄、体质量及术中CPB时间、主动脉阻断时间等方面比较差异均无统计学意义（均P〉0.05）。与对照组相比,试验组术后血浆cTnⅠ、IL-6、TNF-α水平的降低更早、更明显,试验组均在T5时点明显低于对照组（P〈0.05）。而血浆IL-10水平的降低却正好相反,试验组降低更慢,在T5时点明显高于对照组（P〈0.05）。对照组术后1例死于呼吸衰竭。试验组15例、对照组14例患儿随访3个月,均无心力衰竭、呼吸衰竭等严重并发症发生。结论乌司他丁在婴儿危重先天性心脏病术后应用可促进抑炎细胞因子IL-10的产生,抑制促炎细胞因子IL-6、TNF-α的释放,减轻心肌损伤。     

雷帕霉素预处理对大鼠肾缺血再灌注诱发肺损伤的影响

目的探讨雷帕霉素（RPM）预处理对大鼠肾缺血再灌注诱发肺损伤的影响及相关机制。方法采用随机数字表法将60只大鼠分为：假手术组（S组）、肾缺血再灌注组（I/R组）、RPM预处理组（R组）,每组20只。采用右肾切除和左肾缺血45 min行再灌注的方法制备肾缺血再灌注损伤模型。R组缺血前给予RPM（10 mg·kg^-1·d^-1）×3 d,最后1次术前2 h灌胃。再灌注6 h后经心脏采集血样,检测血清SOD活性、MDA、IL-1β、IL-6和TNF-α的水平;取肺组织,光镜下观察肺组织病理学结果,并测定肺组织湿干比重（W/D）。结果与S组比较：其他2组肺W/D、血清MDA、IL-1β、IL-6和TNF-α的水平明显升高（P〈0.05）,SOD活性明显降低（P〈0.05）;与I/R组比较：R组肺W/D、血清MDA、IL-1β、IL-6和TNF-α的水平明显降低,SOD活性明显升高,肺组织病理学损伤明显减轻（均P〈0.05）。结论 RPM预处理可减轻大鼠肾缺血再灌注诱发肺损伤,其机制可能与抗氧化应激和抗炎反应有关。     

体外循环对细胞因子的影响及干预研究

目的探讨体外循环（CPB）后细胞因子的变化及1,6-二磷酸果糖（FDP）在减少细胞因子释放中的作用。方法将63例先心病患儿按随机数字表法分为2组,观察组30例,在CPB前一次性在预充液中加入FDP200 mg.kg-1;对照组33例,预充液中不加FDP。2组分别于术前,CPB后3、48 h采集静脉血3 mL,采用ELE-SIA方法检测肿瘤坏死因子（TNF-α）、白介素6（IL-6）及白介素8（IL-8）水平的变化。结果 2组术前及CPB后48 h TNF-α、IL-6、IL-8水平变化比较差异无统计学意义（P〉0.05）;CPB后3 h对照组的TNF-α、IL-6及IL-8明显高于观察组（P〈0.01）。结论 CPB后细胞因子TNF-α、IL-6及IL-8明显升高,是导致全身炎症反应的重要因素,在预充液中加入FDP后,可以明显减少TNF-α、IL-6及IL-8等炎症介质的释放,减轻全身炎症反应。     

重症肺炎支原体肺炎肺泡灌洗液中TNF-α、IL-6、IL-8、IL-10水平观察

目的检测重症肺炎支原体肺炎患者支气管肺泡灌洗液（bronchial tube pul monary alveolus syringe fluid,BALF）中肿瘤坏死因子-α（Tumor necrosis factor-α,TNF-α）、白细胞介素-6（Interleukin-6,IL-6）、白细胞介素-8（In-terleukin-8,IL-8）白细胞介素-10（Interleukin-10,IL-10）浓度,探讨其临床意义。方法收住ICU的重症肺炎支原体肺炎患者36例,其CPIS评分〉6分为CPIS高分组共15例,CPIS评分〈6分为CPIS低分组共21例;正常对照组24例。取支气管肺泡灌洗液检测TNF-α、IL-6、IL-8、IL-10水平。结果重症肺炎支原体肺炎无论CPIS高分组和CPIS低分组支气管肺泡灌洗液中TNF-α、IL-6、IL-8、IL-10水平明显高于对照组,差异有统计学意义（P〈0.01）,CPIS高分组TNF-α、IL-6、IL-8水平高于CPIS低分组,差异有统计学意义（P〈0.01）,CPIS高分组IL-10水平稍高于CPIS低分组,差异无统计学意义（P〉0.05）。2组治疗后恢复期TNF-α、IL-6、IL-8、IL-10水平均明显下降（P〈0.01）。结论 TNF-α、IL-6、IL-8、IL-10在重症肺炎的发生发展中起重要作用,是重症肺炎支原体肺炎诊断的重要因素之一。利用支气管肺泡灌洗液检测TNF-α、IL-6、IL-8、IL-10水平变化对临床诊断治疗及预后有一定的临床价值。     

Rat IL-3 stimulates the growth of rat mucosal mast cells in culture

Rat mast cells with the properties of mucosal mast cells (MMC) proliferate in cultures of haemopoietic tissue in the presence of conditioned medium (CM) from antigen- or mitogen-activated T lymphocytes. The present study shows that recombinant rat interleukin-3 (rIL-3) both stimulated the development of MMC from bone marrow (BM) precursors and maintained the proliferation of rat MMC lines in an identical manner to that of CM. The content per cell of the MMC granule-specific proteinase RMCPII was similar in both IL-3- and CM-stimulated cultures. Passage of CM through DEAE-cellulose separated two active peaks that stimulated autologous MMC proliferation. The biochemical properties of peak 1 were similar to those of murine IL-3 and stimulated multi-potential stem cell development in soft agar cultures of BM cells from rats treated with 5-fluorouracil (which enriches for haemopoietic stem cells). RIL-3 was also active in this assay whereas peak 2 was not, demonstrating that peak 1 contained IL-3 activity. The presence of MMC in the majority of multi-potential colonies in the soft agar cultures confirmed the early stem cell origin of the MMC lineage. The cultured BM-derived mast cells in the rat are analogues of the MMC subset that is most readily observed proliferating in the gastrointestinal tract in response to helminth parasite infection. The demonstration that IL-3 is responsible for the development and proliferation of MMC should lead to a better understanding of the functional roles of these cells.     

House dust‐mite allergen exposure is associated with serum specific IgE but not with respiratory outcomes

Exposure to house dust has been associated with asthma in adults, and this is commonly interpreted as a direct immunologic response to dust‐mite allergens in those who are IgE sensitized to house dust‐mite. Mattress house dust‐mite concentrations were measured in a population‐based sample of 2890 adults aged between 27 and 56 years living in 22 centers in 10 countries. Generalized linear mixed models were employed to explore the association of respiratory symptoms with house dust‐mite concentrations, adjusting for individual and household confounders. There was no overall association of respiratory outcomes with measured house dust‐mite concentrations, even in those who reported they had symptoms on exposure to dust and those who had physician‐diagnosed asthma. However, there was a positive association of high serum specific IgE levels to HDM (>3.5 kU_A/l) with mattress house dust‐mite concentrations and a negative association of sensitization to cat with increasing house dust‐mite concentrations. In conclusion, there was no evidence that respiratory symptoms in adults were associated with exposure to house dust‐mite allergen in the mattress, but an association of house mite with strong sensitization was observed.     

溶血磷脂酸对人肺成纤维细胞I型胶原合成的影响

目的探讨溶血磷脂酸（lysophosphatidic acid,LPA）对人肺成纤维细胞（HFL-1）I型胶原（procollagentype I,PCOL I）合成的影响。方法将HFL-1培养后置于6孔板中,随机分为6组：对照组,LPAI、Ⅱ、Ⅲ组（用1umol．L-1。的LPA刺激6、12、24h后收集细胞）,IL-13组（用100ug·L-1的IL-13作用48h后收集细胞）,LPA＋IL-13组（用1umol·L-1的LPA刺激12h、100ug·L-1的IL-13刺激48h后收集细胞）,每组3孔。用RT—PCR方法检测PCOLImRNA的表达;用免疫组化方法检测PCOLI蛋白的表达。结果免疫组化与RT—PCR方法均显示LPA刺激后,PCOLI的表达降低,IL-13刺激后,PCOLI的表达增高,且LPA＋IL-13组PCOLI表达比LPA组较高,比IL-13组较低。结论LPA可以下调HFL-1PCOLI的合成。     

Suppression of IL-6 level in human peripheral blood mononuclear cells stimulated with PHA/LPS after occupational exposure to chromium

The toxic metals alter the immune response of animals as well as humans. In addition to the well documented and numerous toxic effect of chromium on various target organs, number of studies shown that acute and chronic exposure to inorganic chromium may result in impairment of immune functions in the experimental systems. Immunosuppression appears to be more subtle effect of exposure to heavy metals. Therefore, we have taken two different groups of chromium exposed individuals. These were leather tanning workers and chromeplaters. These groups of individuals were regularly exposed to chromium. All the leather tanning workers were highly exposed to chromium having a mean of 96.60+/-113.95 mg/dl (range 12.4-417.21 mg/dl). A suspension of exposed and unexposed human PBMC (0.5x10(6) cells/ml) prepared and cultured in RPMI-1640 supplemented with 10% FCS for 18 h in the presence or absence of PHA (5 microg/ml) and LPS (10 ng/ml) which used for stimulation of IL-2, IL-4, TNF-alpha, IL-10 and IL-6, respectively. The levels of Th1/Th2 cytokine: IL-2, IL-4, TNF-alpha, IL-10 and IL-6 were evaluated in the sera and PHA/LPS stimulated culture supernatant of human PBMCs of chromium exposed workers. In these workers the level of IL-6 was 543.95+/-123.75 pg/ml and 388.40+/-61.24 pg/ml in PHA/LPS stimulated culture supernatant of normal individuals and highly chromium exposed workers, which was significant (P<0.05). This observation suggests that IL-6 levels were suppressed in chromium exposed groups as compared to unexposed healthy volunteers. Although the level of IL-2 in PHA stimulated culture supernatant of PBMCs was suppressed in chromium exposed individuals but it was not significant, IL-4 and IL-10 could not be detected. However, there was no difference in TNF-alpha levels in sera samples as well as unstimulated culture supernatant of h-PBMCs of chromium exposed individuals as compared to control.     

胞浆内线粒体 DNA 在脂多糖诱导肺泡巨噬细胞炎症反应时的变化简

目的：观察胞浆内线粒体 DNA（mitochondrial DNA,mtDNA）在脂多糖（lipopolysaccharide,LPS）诱导的NR8383肺泡巨噬细胞炎症反应时的动态变化,以初步探讨胞浆内 mtDNA在肺泡巨噬细胞炎症反应中的作用。方法将体外培养的大鼠肺泡巨噬细胞（NR8383）用终浓度为1μg·mL-1的 LPS刺激0、3、6、12和24 h后收集细胞培养上清液及细胞,采用差速离心法分离胞浆中的mtDNA,实时荧光定量聚合酶链反应（real-time PCR）检测胞浆中mtDNA表达情况,采用酶联免疫吸附法（ELISA）检测细胞培养上清液中 IL-1β蛋白水平。结果 LPS刺激后3、6、12和24 h IL-1β及胞浆中mtDNA的含量均显著高于0 h组（P＜0．01）。结论 LPS刺激肺泡巨噬细胞后,胞浆中mtDNA含量升高,推测其可能参与了肺泡巨噬细胞的炎症反应。     

Antigen-independent activation of cytotoxic T cells by lymphokines

Supernatants from phorbol myristate acetate (PMA)-stimulated EL4.IL2 cells (EL4.PMA), but not recombinant IL-2 (rIL-2), induced the production of cytotoxic T lymphocytes (CTL) in low density murine spleen cell cultures. CTL induction in these cultures was completely abrogated by treatment with anti-Thy-1 or anti-Lyt-2 antibody plus complement but not by anti-L3T4 antibody plus complement. Fractionation of EL4.PMA on a Sephadex G-150 column demonstrated that the CTL-inducing activity in EL4.PMA eluted with an apparent molecular weight of about 44,000 and was partially separated from IL-2. This 44,000 MW material was shown to contain insignificant amounts of PMA. Following a 3-day culture period with the partially purified factor, C57BL/6J thymocytes could proliferate and differentiate into cytotoxic cells in response to rIL-2, whereas there was no proliferation or generation of cytotoxic cells when the thymocytes were cultured in rIL-2 alone. The number of IL-2 receptor-positive cells in C57BL/6J thymocytes also increased from 1.1% to 22.8% after 3 days of culture in the partially purified factor. Recombinant IL-4 (BSF-1) and IL-5 (TRF), when used alone or in combination with rIL-2, were unable to induce a cytotoxic response under similar culture conditions. These findings are consistent with the interpretation that EL4.PMA contains a novel lymphokine that directly, or indirectly, induces the expression of IL-2 receptors on resting CTL precursors without intentional stimulation by specific antigen. In the presence of IL-2, these precursors may then differentiate into effector CTL.     

The influence of soil remediation on lead in house dust

Lead in house dust has long been recognized as a principal source of excess lead absorption among children at the Bunker Hill Superfund Site (BHSS) in northern Idaho. House dust lead concentration from homeowner's vacuum cleaner bags has been monitored since the epidemic of childhood lead poisoning in 1974. Geometric mean house dust lead concentrations decreased from >10000 mg/kg in 1974 to approximately 4000 mg/kg in 1975, in response to air pollution control initiatives at the defective primary lead smelter. After smelter closure, 1983 mean dust lead concentrations were near 3000 mg/kg and were most dependent on soil sources. Following emergency soil removals from public areas and roadsides and fugitive dust control efforts in the mid-1980s, house dust lead decreased by approximately 40-60% to 1200-1500 mg/kg. In 1992, a cleanup goal of 500 mg/kg dust lead community average, with no individual home exceeding 1000 mg/kg, was adopted. This goal was to be achieved by a combination of contaminated soil removals and fugitive dust control efforts throughout the 21 square mile BHSS. Continual reductions in house dust lead concentrations have been noted throughout the residential area soil cleanup. Geometric mean house dust lead concentrations averaged approximately 500-600 mg/kg from 1996 to 1999 and dropped below 500 mg/kg in 2000. Analysis of these data indicates that approximately 20% of the variance in dust lead concentrations is attributed to yard, neighborhood, and community soil lead concentrations. Since 1996, dust lead concentrations and dust and lead loading rates have also been measured by dust mats placed at entryways into the homes. Neighborhood soil lead concentrations, household hygiene, the number of adults living in the home, and the number of hours a child spends outdoors in summer explain approximately 26% of the variance in mat dust lead loading rates. It is estimated that post-remedial house dust lead concentrations will stabilize at 400-500 mg/kg, as compared to approximately 200 mg/kg in socio-economically similar background communities; the difference possibly attributed to residual soil concentrations (3-6 times background), recontamination of rights-of-way, tracking of non-residential mining district soils and dusts, fugitive dusts associated with the remediation, and residual structural or carpet dusts.     

Interaction between ozone and airborne particulate matter in office air

This study investigated the hypotheses that humans are affected by air pollution caused by ozone and house dust, that the effect of simultaneous exposure to ozone and dust in the air is larger than the effect of these two pollutants individually, and that the effects can be measured as release of cytokines and changes of the respiratory function. Experimental exposures of eight atopic but otherwise healthy subjects were performed in a climate chamber under controlled conditions. The three controlled exposures were about 75 microg/m3 total suspended particulate matter, 0.3 p.p.m. ozone, and the combination of these. The exposure duration was 3 h. The outcome measures were interleukins and cells in nasal lavages (NAL), respiratory function, bronchial metacholine responsiveness, rhinometry symptoms and general well-being in a questionnaire and time course of general irritation on a visual analogue scale. Indications of interactions between exposure types were demonstrated for peak expiratory flow (PEF) (P<0.05) and for discomfort symptoms (P<0.03). Non-significant interactions were found for the concentration of interleukin-8 in NAL. The combined exposure was found to cause significantly more effects than either ozone exposures or dust exposures. This is interpreted as indications of a potentiation caused by the combined exposures to dust and ozone. The findings in this study are based on a limited number of subjects and thus should not be over-interpreted. However, they support the hypothesis that ozone at relatively high concentrations interacts with dust exposures to cause decrements in PEF and increase in discomfort measures. PRACTICAL IMPLICATIONS: If confirmed at lower ozone and dust concentrations this finding could help to explain many problems with indoor air quality reported in offices throughout the world.     

依达拉奉对脓毒血症大鼠急性肺损伤的保护机制研究

目的：探讨依达拉奉对脓毒血症致急性肺损伤（ALI）的保护机制。方法将60只雄性SD大鼠随机分3组：对照组（NS组）、模型组（LPS组）及依达拉奉治疗组（ED组）,每组20只。LPS和ED组采用尾静脉注射LPS（10mg·kg-1）建立ALI模型,ED组随后立即尾静脉注射依达拉奉（5mg·kg-1）。LPS注射6h后抽取动脉血行血气分析测氧分压（PaO2）、二氧化碳分压（PaCO2）、氧合指数（PaO2/FiO2）,提取肺组织测定干/湿重比值（D/W）,观察肺组织病理改变,测定血浆中肿瘤坏死因子-α（TNF-α）、白细胞介素6（IL-6）含量。结果与NS组比较,LPS组肺组织D/W、动脉血气测得PaO2、PaCO2、PaO2/FiO2显著下降,肺损伤病理评分及血浆TNF-α、IL-6升高（P＜0．05）。与LPS比较,ED组肺组织D/W、动脉血气测得PaO2、PaCO2、PaO2/FiO2升高,肺损伤病理评分及血浆TNF-α、IL-6明显下降（P＜0.05）,但仍高于NS组（P＜0．05）。结论依达拉奉对急性肺损伤具有保护作用,其机制可能是通过清除肺内氧自由基,减少炎性细胞因子TNF-α、IL-6产生。