双光气吸入染毒后大鼠肺泡Ⅱ型细胞变化的动态观察

本实验动态观察了双光气吸入染毒后大鼠肺泡Ⅱ型细胞的变化，分析了支气管肺泡灌洗液（ＢＡＬＦ）中碱性磷酸酶（ＡＫＰ）活性和总磷脂（ＴＰ）含量。结果表明，吸入双光气后大鼠ＢＡＬＦ中ＡＫＰ活性和ＴＰ含量的改变与肺泡Ⅱ型细胞的变化密切相关，并提示鼠肺对双光气所致肺损伤有很强的修复能力。     

双光气吸入染毒后大鼠肺泡Ⅱ细胞变化的动态观察

本实验动态观察了双光气吸入染毒后大鼠肺泡Ⅱ型细胞的变化，分析了支气管肺泡灌洗液（ＢＡＬＦ）中碱性磷酸酶（ＡＫＰ）活性和总磷脂（ＴＰ）含量。结果表明，吸入双光气后大鼠ＢＡＬＦ中ＡＫＰ活性和ＴＰ含量的改变与肺泡Ⅱ型型细胞的变化密切相关，并提示鼠肺对双光气所致肺损伤有很强的修复能力。     

PVC电缆失火烟雾吸入所致生肺损伤的实验观察

目的：深入了解吸入ＰＶＣ电缆失火烟雾致肺的生病理损伤及机理。方法：以１、３、５、７ｇ不同浓度的ＰＶＣ电缆燃烧烟雾进行大鼠吸入染毒实验。结果：除１ｇ染毒组未发现明显改变外，其余各组大鼠ＢＡＬＦ的细胞总数、中性白细胞以及肺巨噬细胞数，于染毒胡一过性降低，其后持续增高达２周。ＢＡＬＦ中ＬＤＨ，Ｆｎ及ＡＬ增高，磷脂组分改变。病理形态学观察可见肺出血、炎症浸润、间质水肿及肺水肿等改变。７ｇ染毒组尚可见肺泡上     

PVC电缆失火烟雾吸入所致急性肺损伤的实验观察

目的∶深入了解吸入ＰＶＣ电缆失火烟雾致肺的急性病理损伤及机理。方法∶以１、３、５、７ｇ不同浓度的ＰＶＣ电缆燃烧烟雾进行大鼠吸入染毒实验。结果∶除１ｇ染毒组未发现明显改变外，其余各组大鼠ＢＡＬＦ的细胞总数、中性白细胞数以及肺巨噬细胞数，于染毒早期有一过性降低，其后持续增高达２周。ＢＡＬＦ中ＬＤＨ、Ｆｎ及ＡＬ增高，磷脂组分改变。病理形态学观察可见肺出血、炎症浸润、间质水肿及肺水肿等改变。７ｇ染毒组尚可见肺泡上皮细胞增生及轻度的纤维化。结论∶ＰＶＣ失火烟雾吸入可致急性呼吸道损伤，表现为刺激性气道炎、肺泡炎及肺水肿，严重时可导致肺纤维化。     

豚鼠实验性铍肺病理及其BLAF中HA,FN及LM水平的变化

以１０ｇ／Ｌ高纯度氧化铍粉尘生理盐水混悬液经气管注入制成的豚鼠实验性铍肺模型，在病理上早期主要是支气管、肺的炎性改变，４及６周时肺内肉芽肿结节形成，１０周电镜下见肺间质有少量胶原增生。染毒后１、１０周时ＢＡＬＦ中ＨＡ、ＦＮ及ＬＭ水平测定结果见ＨＡ１周炎症水肿期明显增高，与对照组相比，着异有显著性，而ＬＭ水平在染毒组与对照组间差异无显著性。ＨＡ在反映肺间质疾病活动和上可能是较ＦＮ、ＬＭ更敏感的指标。     

铍病豚鼠BALF中纤维粘连蛋白,层粘连蛋白和磷脂的变化

以氧化铍（ＢｅＯ）气道染毒方法制备实验性豚鼠铍病模型。用间接酶免疫吸附法测定铍病豚鼠支气管肺泡灌洗液（ＢＡＬＦ）中纤维粘蛋白（ＦＮ）、层粘连蛋白（ＬＭ）水平的变化，结果表明染毒后１周豚鼠ＢＡＬＦ中ＦＮ明显升高，染毒后１０周ＬＭ有下降趋势。用高效液相色谱（ＨＰＬＣ）法测定染毒豚鼠ＢＡＬＦ中磷脂（ＰＬ）组分的变化，初期为ＰＩ和ＰＥ下降，尔后逐渐恢复。     

茶多酚对急性百草枯中毒大鼠治疗作用的实验研究

目的 探讨茶多酚（ｔｅａ ｐｏｌｙｐｈｅｎｏｌｓ,ＴＰ）对急性百草枯中毒的治疗作用方法 大鼠用百草枯（ｐａｒａｑｕａｔ,ＰＱ）灌胃（２５０ｍｇ／ｋｇ）染毒后３ｈ再经口灌注ＴＰ,分别测定染毒后８、２４、４８、７２ｈ大鼠血浆和支气管肺泡灌洗液（ＢＡＬＦ）中丙二醛（ＭＤＡ）含量及超氧化物歧化酶（ＳＯＤ）、谷胶基肽过氧化物酶（ＧＳＨ－Ｐｘ）的活力,并观察肺组织结构改变。结果 ＰＱ染毒后血浆及ＢＡＬＦ中ＭＤ     

豚鼠实验性铍肺病理及其BALF中HA、FN及LM水平的变化

以１０ｇ／Ｌ高纯度氧化铍粉尘生理盐水混悬液经气管注入制成的豚鼠实验性铍肺模型，在病理上早期主要是支气管、肺的炎性改变，４及６周时肺内肉芽肿结节形成，１０周时电镜下见肺间质有少量胶原增生。染毒后１、１０周时ＢＡＬＦ中ＨＡ、ＦＮ及ＬＭ水平测定结果见ＨＡ在１周炎症水肿期及１０周肺间质纤维化早期均显著增高，与对照组相比差异十分显著（Ｐ＜０．０１）。ＦＮ水平仅于炎症水肿期明显增高，与对照组相比，差异有显著性（Ｐ＜０．０５），而ＬＭ水平在染毒组与对照组间差异无显著性（Ｐ＞０．０５）。ＨＡ在反映肺间质疾病活动和进展上可能是较ＦＮ、ＬＭ更敏感的指标。     

还原型谷胱甘肽对急性百草枯中毒治疗作用的实验研究

探讨还原型谷胱甘肽对急性百草枯中毒的治疗作用。方法在大鼠用百草枯（Ｐａｒａｑｕａｔ,ＰＱ）灌胃（２５０ｍｇ／ｋｇ）染毒后不同时间腹腔注射还原型谷胱甘肽（ＧＳＨ）,分别测定染毒后８ｈ、２４ｈ、４８ｈ,７２ｈ大鼠血浆和支气管－肺泡灌洗液（ＢＡＬＦ）中丙二醛（ＭＤＡ）含量及超氧化物歧化酶（ＳＯＤ）、谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）的活力,并观察肺组织结构改变。结果ＰＱ染毒后血浆及ＢＡＬＦ中ＭＤＡ显著高     

支气管肺泡灌洗液成份分析与肺毒理学研究概况

在外源性化合物经呼吸道染毒对肺脏毒性作用的研究中 ,特别是动物实验研究 ,已越来越多地应用支气管肺泡灌洗 (ＢＡＬ)技术[1,2 ] 。可以通过对支气管肺泡灌洗液 (ＢＡＬＦ)中细胞、生化、肺表面活性物质等多种成份的分析 ,探讨外源性化合物对肺脏的毒作用机制。本文对肺毒理学研究中ＢＡＬＦ的成份变化及其意义作一综述。1　ＢＡＬＦ中细胞成份的变化及意义ＢＡＬＦ中细胞总数和分类计数 ,常用来评价外源性化合物对肺脏的毒性。正常ＢＡＬＦ中 95 %左右为肺泡巨噬细胞(ＰＡＭｓ) ,在毒物作用下 ,细胞成份主要改变为ＰＡＭｓ数目显著减少至…     

染矽尘大鼠表面活性蛋白D和克拉拉细胞蛋白表达的变化

目的 探讨染矽尘大鼠肺组织和支气管肺泡灌洗液(BALF)表面活性蛋白-D(SP-D)和克拉拉细胞蛋白(CC16)表达的动态变化.方法 将80只大鼠随机分为对照组、染矽尘组(每组40只),采用气管暴露注入矽尘悬液法建立矽肺动物模型.染尘后在7、14、21、28和60 d时每组分别处死8只大鼠,取肺组织和BALF.免疫组化法检测不同时间点的肺组织SP-D和CC16在肺组织中的表达,并作定量分析;以Western Blot法检测BALF中SP-D和CC16含量,并作定量分析.结果 对照组大鼠肺泡Ⅱ型细胞和Clara细胞胞浆内有少量sP-D表达.染矽尘组染矽尘7d后肺组织SP-D表达明显升高,与对照组的差异有统计学意义(P＜0.01);14 d时达到高峰期,此后开始下降.在对照组细支气管周边的Clara细胞胞浆内CC16高表达,部分细胞核内也可见CC16表达.染矽尘大鼠7d后CC16表达明显减少,与对照组的差异有统计学意义(P＜0.01).随着染矽尘时间的延长,CC16表达逐渐减少,并且呈负相关性(t=-0.967,P＜0.01) 7、28 d染矽尘组BALF中SP-D含量均高于对照组,差异有统计学意义(P＜0.01);且28 d BALF中SP-D含量明显高于7 d染矽尘组,差异有统计学意义(P＜0.01).7、28 d染矽尘组BALF中CC16蛋白含量均低于对照组,差异有统计学意义(P＜0.01);且28 d明显低于7 d染矽尘组,差异有统计学意义(P＜0.01).结论 染矽尘能够导致大鼬市组织和BALF SP-D和CC16蛋白表达改变且与染矽尘时间有一定关系.     

稀土氧化钕粉尘对大鼠肺灌洗液中细胞总数变化和蛋白含量的影响

[目的]研究稀土氧化钕粉尘对大鼠肺灌洗液（BALF）中细胞总数和蛋白含量的动态变化。[方法]选用SPF级健康成年雄性SD大鼠195只,体重（200±16）g,采用气管非暴露插管灌注法染尘。不同染毒时间组分别采用100 mg/kg稀土氧化钕粉尘悬液0.8 mL和0.9%生理盐水0.8 mL一次性染尘,分别于第3、7、14、21、28天各处死15只实验组大鼠和10只对照组大鼠;不同剂量组按25、50、100、150 mg/kg剂量0.8 mL一次性染尘,在染毒第28天处死各实验组大鼠15只,对照组处死10只（由于实验组染毒时间均为28 d,所以设同一对照组为不同染毒剂量组中实验组对照）。取大鼠支气管肺泡灌洗液,用白细胞计数板在显微镜下对细胞总数进行计数。ELISA法分别测定不同染毒时间组和不同染毒剂量组大鼠BALF中上清液和巨噬细胞蛋白的含量。[结果]不同染毒时间组和不同染毒剂量组中实验组大鼠较对照组大鼠BALF中细胞总数均升高（P〈0.05）;且在各染毒时间组中细胞总数出现先增加后减少,在第14天达到最低值后又呈增加的变化趋势,但均高于对照组（P〈0.05）。在不同染毒剂量组中细胞总数随着染毒剂量增加而逐渐增多,细胞总数均高于对照组（P〈0.05）。不同染毒时间组中实验组大鼠较对照组大鼠BALF上清和巨噬细胞中的蛋白含量均明显增高（P〈0.01）。不同染毒剂量组中实验组大鼠较对照组大鼠BALF上清液和巨噬细胞中的蛋白含量均明显增高（P〈0.01）。不同染毒时间组大鼠BALF上清液和巨噬细胞蛋白含量出现先增加后减少,在第14天达到最低值后又呈增加的变化趋势,但均高于对照组（P〈0.05）。不同染毒剂量组中大鼠BALF上清液和巨噬细胞蛋白含量随着剂量增加而逐渐增多,蛋白含量均高于对照组（P〈0.05）。[结论]稀土氧化钕粉尘进入大鼠肺组织后,BALF中细胞总数以及上清液和巨噬细胞中蛋白含量     

急性百草枯中毒大鼠氧化应激水平及二巯丙磺钠的作用

目的 观察急性百草枯(PQ)中毒大鼠体内氧化应激水平及二巯丙磺钠(Na-DMPS)的作用.方法 80只雄性SD大鼠随机分为正常对照组:8只;Na-DMPS对照组:8只;PQ染毒组:32只(腹腔注射质量分数为1%的PQ溶液20 mg/kg);Na-DMPS保护组:32只.正常对照组及Na-DMPS对照组于1 d处死,PQ组及NA-DMPS保护组于染毒后6h及1、3、7d处死,留取血清、肺泡灌洗液(BALF)及肺组织,检测血清、BALF及肺组织匀浆中丙二醛(MDA)含量、过氧化氢酶(CAT)活力,血清、BALF中谷胱甘肽(GSH)含量,反转录-聚合酶链反应(RT-PCR)检测肺组织Nrf2基因表达水平.结果 与正常对照组相比,PQ中毒组和Na-DMPS保护组血清、BALF、肺组织匀浆中MDA含量均升高,CAT活力和GSH含量均降低,差异有统计学意义(P<0.05或P<0.01);与相应时点PQ染毒组比较,Na-DMPS保护组6 h、1 d时血清、BALF及肺组织匀浆中MDA含量均明显降低,6 h及1、3 d时血清,1、3 d时BALF和肺组织匀浆中CAT活力明显增高,差异有统计学意义(P<0.05或P<0.01).与同时间点PQ染毒组比较,Na-DMPS保护组6 h、3 d时血清中GSH[(730.07±16.23)、(793.66±7.40)mg/L]和1、3 d时BALF中GSH[(609.75±6.74)、(631.83±12.03)mg/L]明显升高,差异均有统计学意义(P<0.05或P<0.01).1、3、7d时PQ染毒组Nrf2mRNA表达分别为(0.710±0.061)、(1.023±0.158)、(0.969±0.046),Na-DMPS保护组Nrf2mRNA表达分别为(1.005±0.060)、(1.464±0.166)、(1.066±0.191),明显高于对照组,差异有统计学意义(P<0.05或P<0.01);与PQ染毒组比较,1、3 d时Na-DMPS保护组Nrf2mRNA表达明显升高,差异有统计学意义(P<0.01).结论 Na-DMPS可降低PQ中毒大鼠体内MDA含量,增加的CAT活力,增加GSH含量及NRF2 mRNA的表达,促进体内氧化-抗氧化系统的平衡,具有保护作用.     

大鼠吸入氯甲酸三氯甲酯后肺损伤的形态学观察

将大鼠分别给予氯甲酸三氯甲酯静式染毒,取肺脏,通过光镜、扫描和透射电镜观察肺损伤情况。主要病变为6h出现细小支气管纤毛上皮细胞脱落,肺泡隔间质水肿,肺泡壁毛细血管内皮细胞肿胀、吞饮小泡增多、囊泡形成、破损,并呈进行性加重,Ⅰ型细胞破坏。24h出现明显的肺水肿,72hⅡ型细胞显著增生,到240h上述病变都有不同程度恢复。     

多壁碳纳米管致大鼠肺损伤效应的研究

[目的]探讨多壁碳纳米管（multi-wall carbon nanotubes,MWCNTs）对大鼠的肺损伤效应。[方法]Wistar大鼠160只,随机分成5组：生理盐水对照组、脱氧核苷酸钠盐（deoxyribonucleic acid sodium salt,DNA钠盐）组、DNA钠盐-MWCNTs 2.0、10.0、20.0mg/mL3组（低、中、高染毒组）,并用DNA钠盐提高MWCNTs的分散度。采用气管滴注的方法染毒,一次滴注量为每kg体重1.5mL,每天1次,连续滴注3d,分别于滴注结束后24h、7d、28d、90d时间段,每实验组各处死8只动物,测定肺灌洗液中总蛋白（TP）、乳酸脱氢酶（LDH）、谷胱甘肽（GSH）和超氧化物歧化酶（SOD）等细胞毒性及细胞氧化损伤指标及大鼠体重,并观察动物肺组织病理学改变情况。[结果]MWCNTs染毒结束后24h,各染毒组大鼠进食及饮水量均有所下降。染毒结束后7、28、90d时,大鼠体重与滴注前体重相比有不同程度的升高,但染毒剂量越高,体重增加幅度越小。中、高剂量染毒组灌洗液中TP和LDH含量随着染毒浓度的增加而升高;灌洗液中GSH和SOD有不同程度的下降,但随时间的延长有不同程度的升高。电镜下,MWCNTs染毒后7d可观察到大鼠肺组织细胞核膜发生肿胀,核固缩,单位膜结构不清楚;内质网扩张,线粒体发生肿胀,嵴断裂等病理改变。[结论]MWCNTs可引起肺组织损伤和氧化损伤,对大鼠具有肺毒性作用。     

不同粒径二氧化硅纳米颗粒对大鼠肺组织的急性毒性研究

目的 观察不同粒径二氧化硅颗粒对大鼠肺组织的急性毒性.方法 将105只大鼠随机分为7组,每组15只,分别给予20、50、80、140、280、800 nm SiO2颗粒,浓度为400mg/m3.对照组不给予粉尘颗粒,各组动物在相同条件下静态吸入染尘2 h后,在24、48、72 h后处死大鼠测定肺泡灌洗液(BALF)中细胞总数、总蛋白含量和乳酸脱氢酶(LDH)活力,并进行肺组织病理观察.结果 与对照组[(0.08±0.02)g/g]比较,800 nm组除72 h总蛋白含量[(0.25±0.01)g/L]明显升高,差异有统计学意义(P<0.05)外,其他各时间各指标差异均无统计学意义(P>0.05).280mm组各时间细胞总数、总蛋白含量和LDH活力均明显高于对照组,差异有统计学意义(P<0.05).140nm组染尘后72 h细胞总数和总蛋白含量及各时点LDH活力明显高于对照组,差异有统计学意义(P<0.05).20、50、80 nm组24 h细胞总数、各时间总蛋白含量和LDH活力均明显高于对照组,差异有统计学意义(P<0.05).染尘大鼠肺组织肺泡间隔增厚,伴炎症细胞浸润.结论 在该实验条件下,较小粒径SiO2颗粒引起肺部损伤有更严重的趋势.随着染尘后时间的延长,大鼠肺部损伤均有不同程度的改善.     

Comparative toxicity of standard nickel and ultrafine nickel in lung after intratracheal instillation

A comparison was made of the bronchoalveolar lavage fluid (BALF) response to ultrafine nickel (Uf-Ni) and standard-sized nickel (Std-Ni). Rats were intratracheally instilled with 0, 0.1, 0.5, 1 and 5 mg Uf-Ni and Std-Ni, respectively. At 3 d after instillation, the body weight and wet lung weight were determined. At the same time, BALF was analyzed for lactate dehydrogenase (LDH), total protein (TP), tumor necrosis factor-alpha (TNF-alpha), and total cell and differential cell counts. The results showed that indicators of lung injury and inflammation in BALF were markedly raised with increased Uf-Ni and Std-Ni for each from 0 to 1 mg, and there were no differences in the indices between instillation of Uf-Ni at 1 mg and 5 mg. The results also showed that the effects of Uf-Ni on the indices were significantly higher than those of Std-Ni. Additional groups of rats were intratracheally instilled with 1 mg of Uf-Ni or Std-Ni, and wet lung weight and BALF profiles were analyzed at 1, 3, 7, 15 and 30 d later. The effect of Uf-Ni and Std-Ni on indices that can be presumed to reflect epithelial injury and permeability (LDH or TP), and release of proinflammatory cytokine (TNF-alpha) were increased throughout the 30 d post-exposure and the effects of Uf-Ni on these indices were significantly higher than those of Std-Ni from 1 to 30 d after instillation. Moreover, the number of neutrophils and LDH activity in BALF of rats after exposure to Uf-Ni were significantly greater than those of Std-Ni-exposed rats up to 30 d after instillation. Our findings suggest that Uf-Ni has a much more toxic effect on the lung than St-Ni, but the mechanism remains to be elucidated.     

地塞米松预处理对大鼠光气吸入性肺损伤基质金属蛋白酶-9表达的影响

目的 探讨地塞米松对大鼠光气吸入性急性肺损伤(ALI)基质金属蛋白酶-9(MMP-9)表达的影响.方法 将SD大鼠随机分为3组:正常对照组(吸入与光气染毒组同等流量的空气)、光气染毒组(吸入8.33 mg/L的光气)、地塞米松预处理组(尾静脉注入2.5 mg/kg地塞米松1 h后,吸入8.33 mg/L的光气).染毒2 h后,收集支气管肺泡灌洗液(BALF)测定中性粒细胞细胞数、蛋白含量和肺湿/干重比(W/D).用放射免疫法测定各组血清和BALF中MMP-9水平.进行肺组织的病理学检查,用免疫组化法和实时定量聚合酶链反应(PCR)测定MMP-9表达的变化.结果 与染毒组比较,预处理组大鼠肺W/D、BALF中中性粒细胞数和蛋白含量明显降低,差异有统计学意义(P＜0.01).与染毒组[血清:(9.439±0.100)μg/L、BALF:(20.640±0.446)μg/L]比较,预处理组MMP-9含量[血清(4.799±0.043)μg/L、BALF:(15.052±0.029)μg/L]明显降低,差异有统计学意义(P＜0.01).与染毒组(2.789±0.282)比较,预处理组MMP-9mRNA的表达量(1.183±0.260)明显降低,差异有统计学意义(P＜0.01).染毒组肺泡壁明显充血、增厚,肺泡壁和肺间质内可见较多白细胞浸润以及肺泡结构破坏;预处理组肺泡结构较为清晰,肺泡壁稍增厚,伴少量炎性细胞浸润.正常对照组大鼠肺、支气管组织中MMP-9蛋白表达呈弱阳性,染毒组MMP-9蛋白表达呈强阳性,预处理组肺、支气管组织中MMP-9蛋白表达明显减弱.结论 地塞米松能有效地保护大鼠光气吸入性ALT,可能通过抑制MMP-9表达而达到肺保护作用.

Abstract：

Objective To investigate the effects of dexamethasone on expression of matrix metalloproteinase-9 (MMP-9) in rats with acute lung injury induced by phosgene. Methods The rats were randomly divided into 3 groups: normal control group that consists of the rats with air exposure, phosgene group that consists of the rats with phosgene exposure and dexamethasone group that consists of the rats with phosgene exposure after 2.5 mg/kg dexamethasone being injected. Wet and dry ratio of the lung (W/D) was calculated, and leukocyte count and total protein content of bronchoalveolar lavage fluid (BALF) were recorded at 2 h after exposure. The concentrations of MMP-9 in the serum and BALF were measured by enzyme-linked immunosorbent assay. The pathologic changes of lung tissues were observed under light microscopy. The immunohistochemistry and the RT-PCR were used to detect the contents of MMP-9 in the lung tissue. Results Compared with phosgene group, the lung W/D, protein content and WBC count in of BALF dexamethasone group was significantly decreased (P＜0.01). MMP-9 levels of the serum and BALF in dexamethasone group were (4.799±0.043) μg/L and (15.052±0.029) μg/L, respectively, which were significantly lower than those [(9.439±0.100) and (20.640±0.446) μg/L] in phosgene group (P＜0.01). Compared with phosgene group (2.789±0.282), the expression level(1.183±0.260) of lung M MP-9 mRNA in dexamethasone group was significantly lower than that in phosgene group (P＜0.01).Histological experimental results showed the marked hyperemia and thickening of alveolar wallsand stroma cells infiltrating and more visible alveolar structure damage of alveolar walls in phosgene group while the alveolar structure and the alveolar walls were clear and slightly thickened with inflammatory cells in dexamethasone group. Immunohistochemical results showed that MMP-9 protein expression levels of lung and brochus tissues in normal control group and dexamethasone group were weakly positive, which in phosgene group were strongly positive. Conclusion Dexamethasone has a beneficial effects on acute lung injury induced by phosgene in rats due to the inhibiting MMP-9.     

Effects of 0.60 PPM nitrogen dioxide on circulating and bronchoalveolar lavage lymphocyte phenotypes in healthy subjects

Nitrogen dioxide (NO2) is a common oxidant air pollutant. Animal studies have suggested that NO2 exposure causes a decrease in the numbers of some splenic lymphocyte subtypes and impairs lymphocyte-dependent immune responses. To investigate whether ambient levels of NO2 alter circulating and bronchoalveolar lavage fluid (BALF) human lymphocytes, we studied five healthy nonsmoking adult volunteers. In each subject, blood and bronchoalveolar lavage fluid was obtained and then, more than 2 weeks later, volunteers were exposured to 0.60 ppm NO2 for 2 hr with intermittent light to moderate exercise on 4 separate days within a 6-day period. We measured standard tests of pulmonary function (airway resistance, thoracic gas volume, maximal expiratory flow) and had the subjects rate the severity of respiratory symptoms before and after each NO2 exposure. Circulating and BALF lymphocytes were labeled with fluorochrome-conjugated monoclonal antibodies to human lymphocyte antigens and a flow cytometer was used to count lymphocyte subtypes. Neither any single day's exposure nor all four exposures caused a change in symptoms or in the results of tests of pulmonary function. The total number of circulating lymphocytes obtained after NO2 exposure was slightly greater than at baseline (1792 +/- 544 vs 1598 +/- 549 cells/mm3 at baseline; P = not significant) but the proportions of lymphocyte subtypes did not differ. In the BALF obtained after NO2 exposure and in the baseline state, the total number of lymphocytes and the percentages of T cells (CD 3), B cells (CD 20), T cytotoxic-suppressor cells (CD 8), T helper-inducer cells (CD 4), and large granular lymphocytes (CD 57) also did not differ after NO2 exposure. A slightly but significantly greater proportion of natural killer cells (CD 16) was found in the BALF obtained after NO2 exposure (7.2 +/- 3.1 vs 4.2 +/- 2.4% of total lymphocytes). We conclude that repeated exposures of healthy nonsmoking adults to 0.60 ppm NO2 are not associated with clinically significant symptoms, changes in airway caliber, or alterations in circulating and BALF lymphocyte subtypes. We suggest that brief, daily exposures to NO2 at levels higher than those achieved in urban atmosphere are unlikely to provoke acute respiratory impairment in healthy, nonsmoking adults.     

Glutaraldehyde-induced occupational asthma: BALF components and BALF and serum Clara cell protein (CC16) changes due to specific inhalatory provocation test

OBJECTIVES: The purpose of this study was to evaluate bronchoalveolar lavage fluid (BALF) components and Clara cell protein (CC16) concentration in serum and BALF in patients with glutaraldehyde (GA)-induced asthma, before and after a specific inhalatory provocation test (SIPT) with GA, in comparison to atopic asthmatics and healthy individuals. METHODS: Spirometry and bronchoalveolar lavage were performed before and after SIPT. The serum and BALF concentrations of CC16 and cytogram content in BALF were evaluated. RESULTS: In GA-sensitized asthmatics, the level of CC16 in BALF and serum was significantly lower at 24 h after SIPT in comparison with the values recorded prior to the experiment. There was a significant increase in the proportion of eosinophils, basophils and lymphocytes in BALF of GA-sensitized asthmatics obtained after SIPT. CONCLUSIONS: The determination of CC16 either in serum or in BALF is a non-invasive test to detect Clara cell damage.