室内空气污染对妇女非特异性免疫功能的影响

在不同空气污染的室内外环境下,选择45～60岁家庭妇女514人进行非特异性免疫功能唾液溶菌酶和SIgA的含量分析,发现唾液溶菌酶受下列因素影响,依次为室内燃煤、大气SO_2、大气IP和吸烟;而SIgA依次为室内燃煤、大气IP、大气SO_2,提示实行家庭燃料煤气化对保护妇女非特异性免疫功能有重要意义。     

大气污染物短期效应对上海市浦东新区居民肺癌死亡影响的病例交叉研究

目的 分析大气污染物与浦东新区居民每日肺癌死亡人数的相关性,为制定针对肺癌病人的保护措施提供依据。方法 采集浦东新区2005年1月1日至2019年12月31日之间的每日大气污染物浓度、气象因素以及居民肺癌死亡资料,利用时间分层-病例交叉设计并结合分布滞后非线性模型,探讨大气污染物短期暴露对浦东新区居民肺癌死亡的影响。结果 大气污染物(PM₁₀, SO₂, NO₂)浓度与浦东新区居民肺癌死亡风险呈正相关。PM₁₀, SO₂, NO₂浓度对居民肺癌死亡风险的影响均在累积8 d(Lag 0～7)最强。PM₁₀, SO₂, NO₂浓度上升10 μg/m³累积8 d(Lag 0～7)居民肺癌死亡风险分别上升1.09%(95%CI:0.35%～1.83%), 3.78%(95%CI:1.98%～5.61%)与2.76%(95%CI:1.10%～4.44%)。女性人群肺癌死亡对PM₁₀与NO₂的影响不敏感(P>0.05)。大气污染物对高龄人群与低文化水平人群肺癌死亡效应较强,人群间效应差异不显著。结论 大气污染物短期暴露可以升高浦东新区居民肺癌死亡风险,以累积8 d(Lag 0～7)效应最强。     

广东人群CYP1A1 MspⅠ基因多态性与肺癌易感性研究

目的：探讨广东人群CYP1A1 MspⅠ基因多态性与肺癌易感性的关系。方法：以病例-对照的研究方法，采用PCR技术，检测原发性肺癌患者、住院对照各91例及47名健康对照的CYP1A1 MspⅠ基因型，分析各基因型及与吸烟的交互作用和肺癌易感性的关系。结果：吸烟者的肺癌风险显著增加(0R＝1．87，95％CI：1．10—3．19)(P＜0．05)；MspⅠ突变型在病例组、对照组中各占39．56％、28．26％，其个体的肺癌风险增加(0R＝1．53，95％CI：0．81—2．88)，而杂合型则降低(0R＝0．83，95％CI：0．43--1．60)，携带一个以上突变基因的个体肺癌风险增加(0R＝1．15，95％CI：0．66—2．00)；分层分析发现，吸烟的突变型个体肺癌风险显著增加(0R＝2．56，95％CI：1．05—6．25)(P＜0．05)，而不吸烟对突变型(0R＝0．84，95％CI：0．11—6．21)，尤其是杂合型(0R＝0．27，95％CI：0．09—0．80)(P＜0．05)基因个体有明显的保护作用。结论：CYP1A1 MspⅠ突变型基因是吸烟者肺癌易感性的遗传标记，而杂合型基因可降低非吸烟者的肺癌风险。     

室内外空气污染与中风死亡分布的描述性研究

本文运用描述流行病学方法初步探讨了上海市不同空气污染条件下8个社区的中风死亡率(1978～1987)的时空分布及其与室内外空气污染的关系.结果表明中风死亡率与大气污染水平无明显关系,但发现在相同大气污染条件下,燃煤社区的中风死亡率明显高于燃气社区,提示燃煤型室内空气污染可能是中风的重要诱发因素之一.     

Low Dietary Inorganic Phosphate Stimulates Lung Tumorigenesis Through Altering Protein Translation and Cell Cycle in K-ras LA1 Mice

Recent surveys indicate that Pi intake has increased steadily as Pi-containing foods have increased. Our previous study demonstrated that high dietary Pi strongly stimulated lung tumorigeneis. In order to answer the issue whether low Pi may be chemopreventive, we examined the effects of low Pi on lung cancer. Eighteen 5-wk-old male K-ras ^LA1 lung cancer model mice were randomly allocated to 2 groups. One group was fed a normal diet (0.5% Pi) and other group was fed low Pi (0.1% Pi) diet for 4 wk. Lung cancer development was evaluated by histopathological examination, Western blot, kinase assay, and immunohistochemistry. Low Pi increased the expression of sodium-dependent phosphate co-transporter 2b, and activated Akt signal with decreased PTEN expression in the lungs of K-ras ^LA1 mice. Low Pi increased the Akt/mTOR-mediated protein translation through upregulating the phosphorylation of p70S6K and 4E-BP1. In addition, low Pi stimulated cell cycling as evidenced by altered cell cycle regulators such as cyclin D1 and D3. Finally, low Pi increased lung tumorigenesis in K-ras ^LA1 mice compared to the normal diet group. Our results clearly demonstrated that low Pi also promoted lung tumorigenesis, thus suggesting that an appropriate intake of dietary Pi may be critical for lung cancer prevention as well as treatment.     

Long-term concentrations of ambient air pollutants and incident lung cancer in California adults: results from the AHSMOG study.Adventist Health Study on Smog.

The purpose of this study was to evaluate the relationship of long-term concentrations of ambient air pollutants and risk of incident lung cancer in nonsmoking California adults. A cohort study of 6,338 nonsmoking, non-Hispanic, white Californian adults, ages 27-95, was followed from 1977 to 1992 for newly diagnosed cancers. Monthly ambient air pollution data were interpolated to zip code centroids according to home and work location histories, cumulated, and then averaged over time. The increased relative risk (RR) of incident lung cancer in males associated with an interquartile range (IQR) increase in 100 ppb ozone (O3) was 3.56 [95% confidence interval (CI), 1.35-9.42]. Incident lung cancer in males was also positively associated with IQR increases for mean concentrations of particulate matter <10 microm (PM10; RR = 5.21; CI, 1.94-13.99) and SO2 (RR = 2.66; CI, 1.62-4.39). For females, incident lung cancer was positively associated with IQR increases for SO2 (RR = 2.14; CI, 1.36-3.37) and IQR increases for PM10 exceedance frequencies of 50 microg/m3 (RR = 1.21; CI, 0.55-2.66) and 60 microg/m3 (RR = 1.25; CI, 0.57-2.71). Increased risks of incident lung cancer were associated with elevated long-term ambient concentrations of PM10 and SO2 in both genders and with O3 in males. The gender differences for the O3 and PM10 results appeared to be partially due to gender differences in exposure.     

沈阳市可吸入尘(IP)与其它因素的相关分析

为了探讨北方城市ＩＰ（可吸入尘）和ＴＳＰ（总悬浮颗粒）之间的关系,在沈阳市内３个能代表不同大气污染水平的地区,定点同时连续测定ＴＳＰ、ＩＰ和ＳＯ２共９０天。分别在春秋两季。同时收集当天气象资料（气温、气湿、风速、风向）。相关、回归和主因素分析结果表明,ＩＰ与ＴＳＰ虽呈非常显著相关,但其比例受季节、风速的影响很大。春天季风使ＴＳＰ中含扬尘比例很大,ＩＰ显示为一个更稳定的指标。ＳＯ２与气温呈非常显著负相关,说明它是煤烟污染的主要代表。主因素分析显示沈阳大气污染有３个主要来源。首位是煤烟。分析得出ＩＰ与ＴＳＰ关系的２个回归方程,分别代表春秋两季     

二氧化硫和二氧化氮混合气体对豚鼠气道反应的作用

目的 探讨二氧化硫（SO2）和二氧化氮（NO2）混合气体对豚鼠气道反应的影响。方法 40只成扯豚鼠平均分为4组吸入不同浓度SO2和NO2混合气体（A组：SO214.3mg /m^3 NO23.1mg/m^3 空气;B组：SO228.6mg/m^3 NO26.1mg/m^3 空气;C组：SO242.9mg/m ^3 NO210.3mg/m^3 空气;对照组吸入空气）,分别于0、5、1、15min测定气道内压（IP）,另外用组织胺进行气道反应激发试验。结果 吸入三组不同浓度SO2和NO2混合气体5minIP升高,15min时,A、B组下降,差异均无显著性（P＞0.05）,组胺激发后三组PC20值与对照组相比差异显著（P＜0.05）。结论 短时吸入混合SO2和NO2气体可使豚鼠气道反应性增高。     

七氟烷和丙泊酚对单肺通气下行食管癌根治术患者炎症反应及肺功能的影响

目的研究单肺通气下行食管癌根治术中使用丙泊酚和七氟烷对患者炎症反应及肺功能的影响。方法选择2012年1月²014年6月在我院接受食管癌根治手术的患者92例作为研究对象。根据数字法将患者随机分成丙泊酚组(A组,46例)与七氟烷组(B组,46例)。对比两组患者在不同时间点的肺泡-动脉氧分压差(PA-a O2)、氧合指数(OI)及呼吸指数(RI)水平,两组患者在不同时间点的血浆IL-1及NF-k B DNA结合活性水平以及两组患者在围手术期发生感染的情况。结果与T0相比,B组T2、T3及T4的PA-a O2水平均增加;与T0相比,两组T22014年6月在我院接受食管癌根治手术的患者92例作为研究对象。根据数字法将患者随机分成丙泊酚组(A组,46例)与七氟烷组(B组,46例)。对比两组患者在不同时间点的肺泡-动脉氧分压差(PA-a O2)、氧合指数(OI)及呼吸指数(RI)水平,两组患者在不同时间点的血浆IL-1及NF-k B DNA结合活性水平以及两组患者在围手术期发生感染的情况。结果与T0相比,B组T2、T3及T4的PA-a O2水平均增加;与T0相比,两组T2⁵的OI水平均下降;与T0相比,A组T25的OI水平均下降;与T0相比,A组T2⁵的RI及B组T25的RI及B组T2⁶的RI水平均增加;与B组相比,A组T36的RI水平均增加;与B组相比,A组T3⁷的RI水平均降低,差异均有统计学意义(均p<0.05)。与T0相比,两组T3及T6的血浆IL-1水平均显著升高;与T0相比,B组T7的血浆IL-1水平上升;与B组相比,A组T2、T3、T6及T7的血浆IL-1水平显著降低;与T0相比,两组T6及T7的NF-k B DNA结合活性水平显著上升;与B组相比,A组T1及T7的NF-k B DNA结合活性水平显著下降,差异均有统计学意义(均p<0.05)。两组围手术期的感染率对比,差异无统计学意义(p>0.05)。结论单肺通气下实施食管癌根治手术时应用丙泊酚麻醉对患者的炎性反应以及肺功能的影响更小。     

Effect of short-term exposure to low levels of SO2 and NOx on pulmonary function and methacholine and allergen bronchial sensitivities in asthmatic children

Air pollution is an inevitable consequence of industrialization. Continuous exposure to air pollution may cause or trigger respiratory allergic diseases. This study was designed to evaluate whether short-term, 5-min exposures to low levels of sulfur dioxide (SO2) and nitrogen oxides (NOx) influence pulmonary function and increase bronchial sensitivity to methacholine and specific allergens. Five male and 1 female mite-sensitive asthmatic children (mean age 12 y) were studied during symptom-free periods. Pulmonary function tests were conducted after breathing 5, 15, 35, 65, and 105 breaths of compressed polluted air, which was collected from the Lin-Sun S. Road tunnel in Taipei city. Concentrations of SO2 and NOx were 70-120 ppb and 450-500 ppb, respectively, and were 6-fold and 20-fold, respectively, higher than those of ambient air. Methacholine and mite allergen bronchial challenges were completed after 105 breaths of polluted air were inhaled. No difference in pulmonary function was noted after polluted air and ambient air were inhaled, and the methacholine and allergen sensitivities of airways were not increased after polluted air was inhaled. The authors concluded that short-term exposures to low concentrations of SO2 and NOx did not affect the lung function and did not increase bronchial sensitivity to methacholine and allergen.     

室内燃煤与大气污染对儿童肺功能的交互影响

目的 研究室内燃煤与大气污染对儿童肺功能的交互作用影响。方法 1995—1996年间在中国4城市的城区和郊区的8所小学对6～12岁的儿童进行肺功能的队列测试,每年分冷、暖两季进行。通过3步回归过程进行统计分析。结果 室外空气颗粒物与儿童第1秒最大呼气量(FEV1)、用力肺活量(FVC)和FEV1／FVC都有显著的负相关关系。家庭燃煤与TSP对FEV1和FVC有较显著的交互作用。家庭燃煤与PM10对肺功能的交互作用较弱,但有加重颗粒物对肺功能产生不利影响的趋势。未发现室内燃煤与SO2和NOx对肺功能有显著的交互影响作用。结论 家庭燃煤这种室内污染因素加重了环境空气颗粒物污染,特别是TSP对儿童肺功能的不利影响。     

Ⅰ、Ⅱ相代谢酶基因多态性与肺癌易感性关系的研究

目的探讨Ⅰ相代谢酶CYPlA1、2E1、2D6和Ⅱ相GSTM1基因多态性与肺癌遗传易感性的关系及吸烟与基因之间的交互作用。方法 采用病例对照研究和聚合酶链反应-限制性片段长度多态性等技术,检测217例肺癌患者和200例对照CYPlA1、2E1、2D6和GSTM1基因型频率分布以及与吸烟的关系。结果 肺癌组GSTM1缺陷型频率为58.5％,与对照组(47.5％)比较差异有统计学意义(P=0.02);CYPlA1、2E1、2D6在肺癌组和对照组分布差异无统计学意义(P>0.05)。吸烟与GSTM1有协同作用,与CYPlA1、2E1、2D6未见明显的协同作用。结论 吸烟和GSTM1缺陷型均是肺癌的危险因素,GSTM1缺陷型有吸烟行为的人更易患肺癌,是肺癌的高危人群。     

Mortality from lung cancer in workers exposed to sulfur dioxide in the pulp and paper industry

Our objective in this study was to evaluate the mortality of workers exposed to sulfur dioxide in the pulp and paper industry. The cohort included 57,613 workers employed for at least 1 year in the pulp and paper industry in 12 countries. We assessed exposure to SO(2) at the level of mill and department, using industrial hygiene measurement data and information from company questionnaires; 40,704 workers were classified as exposed to SO(2). We conducted a standardized mortality ratio (SMR) analysis based on age-specific and calendar period-specific national mortality rates. We also conducted a Poisson regression analysis to determine the dose-response relations between SO(2) exposure and cancer mortality risks and to explore the effect of potential confounding factors. The SMR analysis showed a moderate deficit of all causes of death [SMR = 0.89; 95% confidence interval (CI), 0.87-0.96] among exposed workers. Lung cancer mortality was marginally increased among exposed workers (SMR = 1.08; 95% CI, 0.98-1.18). After adjustment for occupational coexposures, the lung cancer risk was increased compared with unexposed workers (rate ratio = 1.49; 95% CI, 1.14-1.96). There was a suggestion of a positive relationship between weighted cumulative SO(2) exposure and lung cancer mortality (p-value of test for linear trend = 0.009 among all exposed workers; p = 0.3 among workers with high exposure). Neither duration of exposure nor time since first exposure was associated with lung cancer mortality. Mortality from non-Hodgkin lymphoma and from leukemia was increased among workers with high SO(2) exposure; a dose-response relationship with cumulative SO(2) exposure was suggested for non-Hodgkin lymphoma. For the other causes of death, there was no evidence of increased mortality associated with exposure to SO(2). Although residual confounding may have occurred, our results suggest that occupational exposure to SO(2) in the pulp and paper industry may be associated with an increased risk of lung cancer.     

2012-2017年辽宁地区城市居民肺癌筛查结果分析

目的 分析2012-2017年辽宁省城市癌症早诊早治项目肺癌筛查结果,评价癌症早诊早治对居民预防肺癌的意义。方法 于2012-2017年,采用整群抽样方法对辽宁地区城市中40~74岁居民进行防癌风险问卷调查,对评估为肺癌高风险人群进行低剂量螺旋CT 扫描。采用x2检验方法比较组间高风险率、筛查率及检出率差异。结果 共收集人群调查问卷200249份,评估为肺癌高风险者39669人,高风险率为19.81%。高风险者中实际完成低剂量螺旋CT 检查13133人,筛查率为33.11%,女性筛查率（39.63%）高于男性（27.07%）（x2=705.967,P＜0.001）,50~59岁年龄组筛查率最高（34.03%）（x2=11.339,P＜0.001）。检出肺内结节1062人,检出率为8.09%,随着年龄增长肺内阳性结节检出率增高,差异有统计学意义（x2=46.499,P＜0.001）;检出疑似肺癌病人75例,检出率为0.57%,且随着年龄增加而增加,40~49岁组,50~59岁组,60~69岁组,70~74岁组检出率分别为0.25%、0.40%、0.95%和3.47%,差异有统计学意义（x2=40.261,P＜0.001）。结论 辽宁城市地区肺癌筛查参与率较低,肺内结节及可疑肺癌检出率较低。     

燃煤烟气对实验动物潜隐性损害的研究

目的　探讨燃煤烟气 (主要是SO2 )对健康的潜在危害作用。方法　将实验家兔分别喂养在燃烧固硫煤、普通煤及不烧煤 (空白对照 )环境中 ,连续观察 90d ,监测 3种实验环境中SO2 的浓度 ;实验前、实验中 (45d)、实验后 (90d) 3次测定家兔的外周血淋巴细胞的DNA损伤情况 (彗星试验 ) ;实验结束时 ,作支气管和肺的病理切片观察。结果　普通煤组 2 4hSO2 平均浓度为 13 0 4mg/m3 ,是固硫煤组的 4 86倍(2 6 8mg/m3 ) ,是空白对照组的 31 80倍 (0 4 1mg/m3 )。普通煤组和固硫煤组家兔的淋巴细胞DNA损伤率有随时间和SO2 浓度增加而逐渐增加的趋势 ,实验 90d后 ,彗星细胞阳性率普通煤组为 10 36 % ,固硫煤组为 5 4 2 % ,空白对照组仅为 1 73% ,彗星细胞阳性率与SO2 浓度存在一定的非线性剂量 -效应关系(R2 =0 784 ,P <0 0 1)。病理结果表明 ,普通煤组有 1例家兔支气管上皮重度鳞形化生伴不典型增生细胞。结论　燃煤烟气能引起细胞DNA损伤 ,对机体具有潜在致癌的可能性     

1999 - 2018年黔南州居民肺癌发病年龄变化趋势分析

目的 了解1999 - 2018年黔南州居民肺癌发病年龄趋势,为黔南州开展肺癌的防治工作提供依据。方法 基于1999年1 月1 日至2018年12 月31 日间黔南州具有连续数据的新发肺癌数据,按照肺癌病例出生年份计算1929 - 1998年出生队列发病率,并按照肺癌发病年龄计数年龄别发病率等统计指标。采用国际Segi's标准人口进行年龄结构标化,利用线性回归模型分析平均发病年龄变化趋势。结果 1999 - 2018年黔南州男性30～39岁、40～49岁组发病率呈下降变化,50～59岁、60～69岁组发病率呈上升变化,70～79岁、80岁～组发病率变化不大,男性发病率不同年龄、不同出生队列变化较为接近;女性除0～29岁以外,其余年龄组发病率随组内出生年份增加而增加。1999 - 2018年黔南州肺癌平均发病年龄下降,男性由1999年的66.99岁下降到2018年的66.05岁,女性由1999年的65.87岁下降到2018年的65.32岁。同时,2018年60岁～年龄发病率构成比占74.04%,低于1999年（占76.21%）。结论 1999 - 2018年黔南州肺癌平均发病年龄有所下降。     

燃煤对儿童免疫功能的影响研究

目的：探讨不同生活燃料对儿童免疫功能的影响。方法：配对选择燃煤和燃气各41名小学生作为研究对象,监测不同燃料导致的室内空气污染水平,同时对研究对象进行了免疫功能7项指标包括IgA、IgG、IgM、补体C3、血清溶菌酶和CD4、CD8的检测.结果：燃煤家庭的室内SO2、CO2、NO2及IP均显著高于燃气家庭,但两组儿童的各项免疫指标未见显著性差异。结论：南方由于住房结构尤其是通风状况,导致燃料所产生的室内空气污染物扩散稀释速度快,在室内停留时间短,儿童实际暴露水平低,因此未见明显的免疫功能损害。     

Ruminant-produced trans-fatty acids raise plasma total and small HDL particle concentrations in male Hartley guinea pigs

Although trans-fatty acid (tFA) intake has been positively associated with coronary heart disease (CHD), the relative effect of consuming industrially produced (IP)- compared with ruminant-produced (RP)-tFA on CHD risk factors is unclear. This study was designed to examine the effects of feeding partially hydrogenated vegetable oil (PHVO), IP-tFA source, and butter oil (BO), RP-tFA source, on the development of atherosclerosis and risk factors associated with CHD. Forty-eight male Hartley guinea pigs were fed a hypercholesterolemic diet containing (9% by weight) PHVO, BO, coconut oil (CO; positive control), or soybean oil (SO; negative control) for 8 or 12 wk (n = 6/group). Morphological analysis revealed that none of the groups developed atherosclerosis. Plasma and hepatic lipids did not differ between the tFA groups, but total and small HDL particles were significantly higher in the BO group than in the PHVO group and mean HDL particle size was significantly smaller in the BO group than in the PHVO group. Compared with the other treatment groups, the SO treatment resulted in significantly lower total cholesterol (TC) and LDL cholesterol in plasma, whereas hepatic TC was significantly higher in the SO group than in the other treatment groups. Plasma and hepatic cholesterol concentrations did not differ between the tFA and CO treatments. These results demonstrate that when fed at a high dose, IP- and RP-tFA had the same effect on established CHD risk factors in male Hartley guinea pigs. The effects of RP-tFA on HDL particle sizes and concentrations warrant further investigation.     

人参瓜蒌莪术汤对小鼠lewis肺癌细胞凋亡的影响

目的探讨人参瓜蒌莪术汤对lewis肺癌模型小鼠的治疗作用及机制。方法建立小鼠Lewis肺癌移植瘤模型,分为模型对照组（NS组）,环磷酰胺对照组（CP组）,人参瓜蒌莪术汤高剂量组（RGEH组）、中剂量组（RGE组）、低剂量组（RGEL组）。在计算抑瘤率的基础上,运用TUNEL法原位检测瘤组织细胞凋亡。结果人参瓜蒌莪术汤对小鼠Lewis肺癌表现出明显的抑制作用,中剂量组效果最为明显,抑瘤率可达47．88％;人参瓜蒌莪术汤低、中、高剂量组均能明显诱导瘤组织细胞凋亡（P〈0．01）。中、高剂量组诱导细胞凋亡作用强于环磷酰胺阳性对照组（P〈0．05）。结论人参瓜蒌莪术汤具有抑制小鼠Lewis肺癌生长的作用,其作用机制可能与诱导肿瘤组织细胞调亡有关。     

Measurement of acidic aerosol species in eastern Europe: implications for air pollution epidemiology.

A large number of studies have indicated associations between particulate air pollution and adverse health outcomes. Wintertime air pollution in particular has been associated with increased mortality. Identification of causal constituents of inhalable particulate matter has been elusive, although one candidate has been the acidity of the aerosol. Here we report measurements of acidic aerosol species made for approximately 1.5 years in Erfurt, Germany, and Sokolov, Czech Republic. In both locations, the burning of high-sulfur coal is the primary source of ambient air pollution. Twenty-four-hour average measurements were made for PM10, [particulate matter with an aerodynamic diameter (da) < or = 10 microns], as well as fine particle (da < 2.5 microns) H+ and SO4(2-) for the entire study. Additionally, separate day and night measurements of fine particle H+, SO4(2-), NO3-, and NH4+ and the gases, SO2, HNO3, HONO, and NH3 were collected with an annular denuder/filter pack system over a 7-month (late winter-summer) period with additional measurements during pollution episodes the following winter. At both sites, 24-hr SO2 (mean concentrations of 52 micrograms/m3, with peak levels of > 585 micrograms/m3) and PM10 (mean concentration 60 micrograms m3) concentrations were quite high. However, aerosol SO4(2-) concentrations (mean concentration of approximately 10 micrograms/m3) were not as great as expected given the high SO2 concentrations, and acidity was very low (mean concentration of < 1 microgram/m3, with peak levels of only 7 micrograms/m3). Low acidity is likely to be the result of NH3 neutralization and slow conversion of SO2 to SO4(2-).(ABSTRACT TRUNCATED AT 250 WORDS)