不同途径汞中毒对机体影响的分析研究

目的 研究不同接触途径所致汞中毒的临床特点。 方法 将33例患者按汞进入体内途径的不同分为3组,即呼吸道吸入中毒组、消化道摄入中毒组和皮肤吸收中毒组,分析其临床特点。 结果 3种不同接触途径所致汞中毒的临床表现各有特点,呼吸道吸入中毒组呼吸系统症状较突出,试排尿汞升高明显。皮肤吸收中毒组以亚急性中毒为主,无明显症状,多为肾病等,发病后检查发现尿汞升高;消化道摄入中毒者为急性起病,可伴有胃肠道症状,治疗后尿汞值最低。治疗前呼吸道吸入中毒组的平均尿汞值分别为消化道摄入中毒组、皮肤吸收中毒组的18.5倍和9.2倍;呼吸道吸入中毒组的试排平均尿汞水平高达5 838.2 μg/gCr。呼吸道吸入中毒组患者平均治疗3.91个疗程,其中58.3%患者超过5个疗程;消化道摄入中毒组患者平均治疗仅1.56个疗程,其中55.56%病例仅需治疗一个疗程;皮肤吸收中毒组患者平均治疗2.25个疗程,其中50%的患者超过5个疗程。3组患者治疗所用疗程比较,差异有统计学意义(F=8.98,P<0.05)。 结论 3种不同接触途径所致汞中毒临床表现不一,应强化汞中毒诊疗规范,以达到早期有效治疗,减少后遗症,降低死亡率。     

慢性汞中毒36例临床分析

目的：分析、探讨慢性汞中毒的临床表现特点。方法：对收治的36例慢性汞中毒病例进行分析总结。结果：慢性汞中毒的中毒方式多样，中毒可经呼吸道、消化道和皮肤；临床症状依侵入途径也呈多样，最常见为类神经症状，其次为精神症状和消化道症状，再次为手抖、心悸、腰背四肢酸痛和皮肤感觉异常、皮疹等；检查一般可有晨尿汞或驱排后尿汞增高。结论：慢性汞中毒时依侵入途径的不同，临床症状的多种多样，而且临床症状与尿汞高低不平行。     

急性、亚急性金属汞中毒32例的临床观察

本文总结我室历年来收治急性、亚急性金属汞中毒32例的临床资料。临床表现与慢性汞中毒相比有较大差别,急性期表现以周身中毒症状、口腔—牙龈炎症状及胃肠道症状为著,部分病人可有皮疹、呼吸道及肾脏受累,尿汞往往明显增高;而神经—精神症状和震颤多不明显。按接触情况可分为A(以温度计制造工为主)、B(溜金工)及C(误吸含汞偏方者)三组,其发病缓急与病情轻重亦有所不同。     

43例汞中毒患者临床特征

目的 分析总结确诊为汞中毒的43例患者的临床特点,旨在提高对汞中毒相关疾病的诊治水平。
方法 对43例汞中毒患者的接触途径、临床表现、实验室检查、治疗与转归等临床资料进行回顾性研究。
结果 职业性汞中毒均为金属汞以蒸气形式吸入,非职业性汞中毒主要经皮肤、呼吸道、消化道接触吸收。男性多因职业原因致中毒（占94.7%）,而女性除职业原因中毒（占58.3%）外,还有美白祛斑化妆品汞中毒。临床表现多样,急性中毒主要以全身症状为主,部分有皮肤及呼吸道受损,而慢性中毒则以神经-精神障碍、口腔症状、关节肌肉痛为主。经驱汞治疗,患者尿汞浓度降低,临床症状日趋缓解,其中以神经精神症状改善最为明显。4例汞中毒相关肾病综合征患者经驱汞治疗后,水肿症状消失。19例汞中毒患者出现同型半胱氨酸（homocysteine,Hcy）升高,且吸烟组Hcy升高发生率高于不吸烟组（P < 0.01）。
结论 汞中毒患者应尽早经驱汞治疗,尽早戒烟,改善预后。
     

10例非职业性汞中毒临床分析

职业性汞中毒多数是经呼吸道吸入所致，临床表现较相似，非职业性汞中毒由于中毒方式和侵人途径较多样，病情和处理办法也有区别，现将我院收治的10例病人分析如下。1临床资料1．l一般资料10例中男性6例，女性4例，年龄3～45岁。中毒方式：3例自股金属汞，（其中一例洗胃时把汞吸入肺部），2例小孩被他人多次诱服金属汞；5例用含汞化合物偏方治病（其中2例用以治癫病病，l例治性病，1例用含汞药捻近脚气，1例用含汞药粉涂擦头皮治头部“肿块”）。其中毒途径8例经消化道侵人，l例经呼吸道侵入，1例经皮肤侵入。1．2临床表现5例口服金属汞者…     

汞中毒16例临床误诊分析

本文通过对１６例汞中毒病例的临床分析，表明由于引起中毒的原因及中毒途径不同，临床表现各异，由呼吸道中毒者以神经精神症状为主，由消化道中毒者则肝肾损害更突出。若临床上不注意其职业史和毒物接触史，则极易造成误诊，漏诊。     

儿童汞中毒10例分析

[目的]加强对儿童汞中毒的认识,警示家长应防止儿童汞接触。[方法]收集临床病例进行分析。[结果]儿童汞中毒途径多样,可经呼吸道、皮肤和消化道等途径侵入,并因毒性蓄积而造成多脏器功能损害。[结论]加强对儿童汞中毒的关注,避免接触含汞物质及含汞环境。     

阿托品在有机磷农药局部损伤中的应用

有机磷农药足国内外应用最广泛的一种高效杀虫剂。具有品种多、杀虫力强、杀虫谱广、残留量低等特点。由于其毒性强，应用广，中毒发生率也较高。中毒途径可分为生产性中毒及使用性中毒，前者主要通过皮肤及呼吸道吸收造成中毒；后者主要为消化道和呼吸道途径吸收中毒。通过皮肤吸收中毒者，皮肤接触有机磷农药（尤其是敌敌畏乳油）后数小时，可出现局部瘙痒、烧灼感、红肿，甚至水疱、糜烂。     

急性甲醇中毒研究进展

急性甲醇中毒病情凶险。目前职业性中毒较为罕见,生活性中毒则较多见,其中大多数为饮用掺有甲醇的酒所致。近十多年来,甲醇中毒的毒理学和临床研究借助于检查手段提高取得一定进展。现简介如下: 一、代谢和中毒机理 (一)代谢 甲酸可经呼吸道、消化道和皮肤吸收。进入胃肠道的吸收高峰时间在30～60分钟。经皮吸收量可达0.192mg/cm~2/min。吸     

小儿急性汞吸入中毒6例报告(附1例尸解分析)

近年来 ,私人炼金者较多 ,由于采用家中煤炉烧炼蒸汞 ,故常危及家人健康。现就我院收治的 6例小儿急性汞中毒病例报告如下。1　一般资料6例患者 ,男 4例 ,女 2例 ,年龄 3个月至 4岁半。其中 5例为急性汞中毒 ,在接触汞蒸气 2～ 6 h后出现中毒症状。以汞中毒性肺炎为临床特征 ;1例为亚急性汞中毒 ,在接触汞蒸气 1 0 d后发病 ,以汞中毒性肾病为主要临床表现。2　临床表现其中 4例患儿以呼吸系统症状体征为主 ,尿汞明显增高 (6 5 0～ 2 5 0 0 nmol/L )。T:37.6～ 38.3℃。咳嗽、气促、恶心、呕吐、口唇青紫、精神萎靡 ,双肺可闻干、湿罗音或呼…     

急性硫丹中毒的临床研究

摘要：硫丹是一种高毒有机氯杀虫剂。主要通过消化道、呼吸道、皮肤吸收。中毒机制尚不清楚,临床表现为中枢神经系统症状合并多脏器损害。目前尚无特效解毒剂,治疗以清除毒物,控制脑水肿、肺水肿等对症治疗为主。     

3例叠氮化钠中毒病例临床分析

[目的]探讨叠氮化钠中毒的临床特点。[方法]对3例急性叠氮化钠中毒患者的临床表现、治疗情况等进行分析。[结果]叠氮化钠中毒可有不同临床表现,急性中毒表现有中毒性脑病、周围神经病变等。[结论]急性叠氮化钠中毒性脑病、周围神经病变目前尚无特效药物治疗,主要以激素、高压氧、维生素B12、运动疗法等对症支持治疗为主。     

Organic mercury compounds: human exposure and its relevance to public health

Humans may be exposed to organic forms of mercury by either inhalation, oral, or dermal routes, and the effects of such exposure depend upon both the type of mercury to which exposed and the magnitude of the exposure. In general, the effects of exposure to organic mercury are primarily neurologic, while a host of other organ systems may also be involved, including gastrointestinal, respiratory, hepatic, immune, dermal, and renal. While the primary source of exposure to organic mercury for most populations is the consumption of methylmercury-contaminated fish and shellfish, there are a number of other organomercurials to which humans might be exposed. The antibacterial and antifungal properties of organomercurials have resulted in their long use as topical disinfectants (thimerosal and merbromin) and preservatives in medical preparations (thimerosal) and grain products (both methyl and ethyl mercurials). Phenylmercury has been used in the past in paints, and dialkyl mercurials are still used in some industrial processes and in the calibration of certain analytical laboratory equipment. The effects of exposure to different organic mercurials by different routes of exposure are summarized in this article.     

Some aspects of arsenic toxicity and carcinogenicity in living organism with special regard to its influence on cardiovascular system,blood and bone marrow

This paper gathers data on the most current aspects of arsenic action, especially its influence on the cardiovascular system, blood and bone marrow. A potential carcinogenic mechanism of arsenic is also discussed. Arsenic is a potent toxicant that may exist in several valencies and in a number of inorganic and organic forms. Most cases of arsenic-induced toxicity in humans are due to exposure to inorganic arsenic, and there is an extensive database on the human health effects of common arsenic oxides and oxyacids. Exposure of humans living near hazardous waste sites may involve inhalation of arsenic dusts in the air, ingestion of arsenic in water, food or soil, or dermal contact with contaminated soil or water. The exposure to arsenic via the inhalation route is responsible for the increased risk of lung cancer, although respiratory irritation, nausea and skin effects may also occur. The oral route of exposure to arsenic predominates in the general population. The most common effects of arsenic ingestion are gastrointestinal irritation, peripheral neuropathy, vascular lesions, anemia, skin diseases, including skin cancer and other cancers of the internal organs like bladder, kidney, liver or lung. Relatively little information is available on the effects of direct dermal contact with inorganic arsenicals, but several studies indicate local irritation and dermatitis as the major ones.     

Toxicology of toluene diisocyanate

In studies on animals, toluene diisocyanate (TDI) was a contact and respiratory sensitizer, was not toxic by the oral or dermal routes, but was irritating, and toxic by inhalation. The respiratory tract was the target in acute, subchronic, and chronic exposure studies. Typically, at concentrations of above 0.1 ppm (parts per million), clinical signs of nasal irritation were evident, and histopathological investigations revealed rhinitis and epithelial hyperplasia of nasal passages. With increasing concentration, effects were more severe; affected the larynx, trachea, and lung; and, eventually, affected body weight and survival. The carcinogenicity of TDI to rats and mice was investigated. By inhalation, there was no treatment-related increase in tumor incidence in either species at the highest concentration tested (0.15 ppm). Effects of TDI were seen as rhinitis in nasal turbinates of both species, and as reduced body weight gain in mice. Through oral administration of TDI dissolved in corn oil to rats and mice (up to 120 mg/kg/day), increased incidence of a number of tumor types was seen. This route is of questionable relevance to occupational exposure. The dosing solutions were known to have degraded, and TDI would hydrolyze to diaminotoluene in the acidic stomach environment. Several in vitro tests for genotoxicity gave positive results, which can be ascribed to degradation of TDI by solvents. In properly conducted assays, in vivo TDI was negative for genotoxicity. In a two-generation reproduction study in rats, there were no effects on reproductive indices at the highest exposure concentration of 0.3 ppm TDI, which elicited toxicity in both generations. In a developmental toxicity study in rats, there was evidence of minimal fetotoxicity in the presence of maternal toxicity at 0.5 ppm, with no effects at 0.1 ppm. No treatment-related embryotoxicity or teratogenicity was observed.     

Outbreak of fatal arsenic poisoning caused by contaminated drinking water

An outbreak of subacute poisoning occurred among nine members of a family; eight were ill with gastrointestinal symptoms, four developed encephalopathy, and two died. Abnormal liver function tests and leukopenia were common laboratory findings. Epidemiologic and environmental investigations traced the source of arsenic exposure to a farm well with water containing 108 ppm arsenic. The soil adjacent to the well was also contaminated with arsenic, possibly from waste pesticide. Presumably, arsenic gained access to the well through obvious leaks in the well's casing. To our knowledge, this is only the second reported outbreak of fatal arsenic poisoning from contaminated drinking water and one of few instances where illness followed exposure to a toxic substance which was disposed of, or possibly disposed of, in an indiscriminate manner.     

病毒唑加庆大霉素雾化吸人联合开瑞坦治疗亚急性咳嗽的临床观察

目的观察病毒唑加庆大霉素雾化吸入联合开瑞坦治疗亚急性咳嗽临床疗效。方法选择上呼吸道感染后的亚急性咳嗽患者101例随机分为治疗组51例和对照组50例。治疗组给予病毒唑加庆大霉素雾化吸入联合开瑞坦口服治疗;对照组给予常规抗生素联合开瑞坦口服的经验治疗。治疗5～7d后观察并比较2组临床疗效和不良反应。‘结果治疗组总有效率为94．12％,高于对照组的78％,且疗程短,临床症状改善快,不良反应少,差异有统计学意义（P〈0．05）。结论病毒唑加庆大霉素雾化吸入联合开瑞坦用于上感后亚急性咳嗽疗效显著。     

Endosulfan-induced hepatotoxicity is route of exposure independent in rats

Endosulfan is an important hepatotoxic agent that generates free oxygen radicals in liver. With the widespread use of endosulfan in agriculture, human beings are most likely to be exposed to it by eating food contaminated with endosulfan, exposure to its low levels by skin contact with contaminated soil, smoking cigarettes made from tobacco that has endosulfan residues on it, or by nose and whole body inhalation exposure in the farms during its application. Since endosulfan is a frequently used pesticide, and the incidence of toxic injury to the liver tissue in relation to its widespread use reported in the literature, we considered it necessary to investigate whether endosulfan-induced liver injury could be route of exposure dependent. Eighteen mature male albino Wistar rats, weighing between 180 and 220 g, were used in this study. The hepatotoxic effects of oral administration of endosulfan (5 mg/kg body weight) daily for 30 days, and 30 days whole body inhalation exposure to ungraded concentration of endosulfan were investigated in rats using serum liver enzymes and histopathological assay. At the end of the experimental period, serum alanine aminotransferase, aspartate amino transferase, alkaline phosphatase, and creatine kinase activities obtained for the group of rats exposed orally to endosulfan were not significantly different (p ≥ 0.05) from the activities obtained for rats exposed by whole body inhalation. However, the activity of these enzymes obtained for the rats exposed to endosulfan by both oral and inhalation routes were significantly increased (p ≤ 0.05) compared, respectively, to the control. Also, on microscopic examination, the liver tissues of experimental groups exhibited severe damage histopathologically. The results of the enzyme and histological analyses showed that both oral and whole body inhalation exposure to endosulfan may cause liver tissue damage in rats. The exposure to endosulfan in rats caused liver tissue damage independent of the route of exposure.     

中生菌素可湿性粉剂的大鼠急性毒性研究

目的 研究质量分数为3%的中生菌素可湿性粉剂不同染毒途径染毒的大鼠急性毒性。方法 每组10只大鼠(雌雄各半),经口、经皮均采用一次性大剂量染毒方式,剂量分别为5 000 mg/kg和2 000 mg/kg。呼吸道以悬浮液经气溶胶发生装置雾化后染毒2 h,每组10只大鼠,剂量为1 126 mg/m³、2 031 mg/m³、2 501 mg/m³、3 539 mg/m³、4 464 mg/m³。连续观察大鼠毒性症状和体征14 d,并对吸入毒性实验大鼠的肺部进行组织学检查。结果 经口、经皮染毒大鼠未见明显中毒症状;经呼吸道染毒引起呼吸系统症状为主的毒性反应,大体剖检显示肺脏充血、出血,体积增大;病理检查发现肺组织结构破坏、肺泡隔大小不一,肺泡壁增粗、断裂,肺间质大量中性粒细胞浸润及红细胞外渗,可见血管内皮细胞增生;肺组织病理半定量评分提示染毒剂量越高引起的肺损伤越明显。结论 中生菌素可湿性粉剂的悬浮液经呼吸道吸入,可引起大鼠肺脏损伤。