Lymphocyte transformation test with nickel in hard metal asthma: another sensitizing component of hard metal.

To determine cell-mediated immunity to nickel, another matrix in hard metal besides cobalt, lymphocyte transformation tests (LTT) with nickel were carried out in seven hard metal asthma patients all of who had reacted to cobalt chloride in the bronchial provocation tests (BPT). Immunoallergic studies prior to the present study revealed that three of the seven generated a simultaneous positive reaction in the BPT with nickel and the allergosorbent test with nickel-conjugated human serum albumin (Ni-HSA). A stimulation index in LTT indicating a positive response was defined on the basis of results from the studies in the controls. Data revealed that two of the three who showed a combination of positive bronchial and immunological reactions with nickel had a positive LTT with nickel. In the other five, peripheral lymphocytes did not proliferate in response to nickel. Thus it is suggested that cell-mediated immunity to nickel as well as cobalt is implicated in some cases associated with hard metal asthma.     

Lymphocyte transformation with cobalt in hard metal asthma

Lymphocyte transformation tests with cobalt were done in 9 hard metal asthma patients diagnosed on the basis of a positive bronchial provocation test with cobalt. Positive lymphocyte proliferation in response to the metal was defined statistically from the results of 18 controls comprising 12 hard metal-exposed and 6 non-exposed controls. Out of the 4 patients who had been reported to have IgE antibody specific to cobalt, the lymphocytes of 2 proliferated with metal: one showed positive lymphocyte transformation to free cobalt, the other to both free cobalt and cobalt-conjugated human serum albumin. These results suggest that cobalt-sensitized lymphocytes play a role in some hard metal asthmatics. However, the mechanism underlying the hard metal asthma in the other 5 asthmatics who had neither cobalt-specific IgE antibody nor cobalt-sensitized lymphocytes remain to be elucidated.     

Cobalt-induced asthma in workers exposed to hard metal dust]

A case of 39 years old woman with asthma bronchiale associated with cobalt exposure is reported. Specific bronchial provocation tests in these patients supported the diagnosis of hard-metal-induced asthma and implicated cobalt as the agent responsible. The relevant literature data are reviewed.     

Respiratory hazards in hard metal workers: a cross sectional study.

A cross sectional study was conducted on 513 employees at three hard metal plants: 425 exposed workers (351 men, 74 women) and 88 controls (69 men, 19 women). Cough and sputum were more frequent in workers engaged in "soft powder" and presintering workshops compared with controls (12.5% and 16.5% v 3.5%). Spirometric abnormalities were more frequent among women in sintering and finishing workshops compared with control women (56.8% v 23.8%) and abnormalities of carbon monoxide test were more frequent in exposed groups than in controls; this difference was more pronounced in women (31.4% v 5.6%) than in men (18.5% v 13%). No significant correlation was observed between duration of exposure and age adjusted lung function tests. Slight abnormalities of chest radiographs (0/1, 1/1 according to ILO classification) were more frequent in exposed men than controls (12.8% v 1.9%) and mostly in soft powder workers. In subjects with abnormal chest radiographs FVC, FEV1 and carbon monoxide indices (fractional uptake of CO or CO transfer index or both) were lower compared with those with normal chest radiographs. Although relatively mild, the clinical, radiological, and functional abnormalities uncovered call for a regular supervision of workers exposed to hard metal dust.     

Clinical findings among hard metal workers.

In 1940, the first report appeared describing a pulmonary disorder associated with occupational exposures in the cemented tungsten carbide industry. The disease, known as "hard metal disease," has subsequently been characterised in detail and comprises a wide range of clinical signs and symptoms. In this report, clinical findings in a group of 41 hard metal workers employed until recently are described. A high prevalence of respiratory symptoms was found. Thirteen workers (31%) had abnormal chest radiographs indicative of interstitial lung disease. Fifty per cent of these had been employed in hard metal manufacturing for less than 10 years. Abnormalities of pulmonary function were also frequent and included a restrictive pattern of impairment and decrease in diffusing capacity (27%). Associations were found between diffusing capacity, chest radiographic abnormalities and right ventricular ejection fraction at exercise indicating cardiopulmonary effects. The findings show the continuous need to control excessive occupational exposures to prevent hard metal disease, the history of which now enters its sixth decade.     

Clinical findings among hard metal workers.

In 1940, the first report appeared describing a pulmonary disorder associated with occupational exposures in the cemented tungsten carbide industry. The disease, known as "hard metal disease," has subsequently been characterised in detail and comprises a wide range of clinical signs and symptoms. In this report, clinical findings in a group of 41 hard metal workers employed until recently are described. A high prevalence of respiratory symptoms was found. Thirteen workers (31%) had abnormal chest radiographs indicative of interstitial lung disease. Fifty per cent of these had been employed in hard metal manufacturing for less than 10 years. Abnormalities of pulmonary function were also frequent and included a restrictive pattern of impairment and decrease in diffusing capacity (27%). Associations were found between diffusing capacity, chest radiographic abnormalities and right ventricular ejection fraction at exercise indicating cardiopulmonary effects. The findings show the continuous need to control excessive occupational exposures to prevent hard metal disease, the history of which now enters its sixth decade.     

A case of sarcoidosis that developed three years after the onset of hard metal asthma

A 23-year-old man who worked at a hard metal factory from 1988 had developed bronchial asthma in 1990. He was diagnosed as having bronchial asthma by inhalation challenge with cobalt. He never developed a severe attack after that by avoiding inhalation of cobalt. In 1993, he developed iridocyclitis, and his chest radiograph showed bilateral hilar lymph node swelling. He was diagnosed as having sarcoidosis with pathological certainty and an increased serum angiotensin-converting enzyme (ACE) level. On second admission, an inhalational challenge with cobalt resulted in no significant decrease of FEV₁. Cobalt is well known to cause occupational asthma and other interstitial lung diseases. Although we could not get clear evidence suggesting an association between the sarcoidosis and his history of cobalt exposure, there is a possibility that changes in the immune reaction to cobalt might explain the improvement of asthma followed by sarcoidosis in this case. Am. J. Ind. Med. 33:379–383, 1998. © 1998 Wiley-Liss, Inc.     

哮喘患者气道反应性的流行病学分析

６４１个哮喘核心家系的资料分析结果显示，利用乙酰甲胆碱（ＭＴＣＨ）激发试验测定的气道高反应性，做为哮喘诊断标准的灵敏度和特异度分别是７２％、７０％。气道反应阳性者患哮喘的危险性是气道反应阴性者的５．０１倍，其中，男女患哮喘的危险性分别是４．９７倍和５．０６倍，都具有高度显著性意义。患哮喘的危险性随着气道反应性的增强而增大。同一ＭＴＣＨ剂量激发的气道反应阳性者，患哮喘的危险性随着年龄的增加而增加，且有明显的线性趋势（Ｐ＜０．０１）。无论是临床还是预防医学，气道反应性的测定都具有重要意义     

Decreased ventilatory function in hard metal workers.

OBJECTIVES: To study individual effects on pulmonary function of exposure to hard metal including cobalt. METHODS: All of the workers in a hard metal company (583 men and 120 women) were examined for smoking, respiratory symptoms, ventilatory function, occupational history of exposure to hard metal, and present exposure to airborne cobalt. The ventilatory function indices (forced vital capacity (FVC), forced expiratory volume in one second (FEV1), forced expiratory volume in one second per cent (FEV1%), peak expiratory flow (PEF), mid-maximal flow (MMF), forced expiratory flow at 50% vital capacity (V50), forced expiratory flow at 25% vital capacity (V25)) were standardised for height and age and expressed as a percentage of predicted values. RESULTS: Two way analysis of variance of indices of ventilatory function showed that an interaction of hard metal exposure and smoking decreased %V50 for both men and women. Among the currently exposed men, those with asthmatic symptoms (defined as reversible dispnoea with wheeze) had significantly lower %FVC, %FEV1%, %PEF, %MMF, %V50, and %V25 than did workers without asthma. The ventilatory disfunction did not differ between exposed and non-exposed workers with asthmatic symptoms. Even among the men without asthmatic symptoms, %V50 was significantly lowered by the interaction of hard metal exposure and smoking. The multilinear regression analysis of indices of ventilatory function for all of the subjects on sex, smoking (Brinkman index), exposure to hard metal, and asthmatic symptoms showed that asthmatic symptoms and smoking had significant effects on all variables and that the decrease in %V25 was associated with hard metal exposure. In the currently exposed and non-exposed workers, multilinear regression analysis applying indices for cobalt exposure (mean cobalt concentration, duration of exposure, and cumulative dose) showed that not only asthmatic symptoms or smoking but also duration of exposure had significant decreasing effects on %FVC, %MMF, and %V25. CONCLUSIONS: Occupational exposure to hard metal probably causes impairment of ventilatory function in a dose dependent manner.     

Effect of hard metal dust on ventilatory function.

The effect of hard metal dust generated in shaping on ventilatory function has been studied, in particular, the relation between levels of exposure to cobalt and changes in ventilatory function. In 15 healthy young men a significant decrease in FVC occurred after a six hour exposure to hard metal dust containing cobalt at a mean concentration of 38 micrograms/m3 (range 14-76 micrograms/m3). No dose-effect relation could be discerned between the decrease in FVC and the hard metal concentration or the cobalt concentration. All the subjects complained of irritation of the airways. On the other hand, in 42 shaping workers exposed to cobalt at an average concentration of 85 micrograms/m3 no significant decreases in ventilatory function were detected after seven hour exposures to hard metal, although in 42 shapers, who had been exposed to cobalt at a mean concentration of 126 micrograms/m3, the FEV1% was significantly decreased compared with matched controls. This finding suggests that hard metal dust containing cobalt at a mean concentration of 126 micrograms/m3 causes chronic bronchial obstruction.     

吉林市0~14岁儿童支气管哮喘流行病学调查

目的 了解吉林省吉林市0~14岁儿童哮喘的流行现状、临床特征以及影响因素,为地区儿童哮喘防治和管理提供流行病学依据。 方法 2010年采用随机整群抽样法,在吉林市四个行政区抽取调查对象7 650名,首先对调查对象填写初筛表,再对确诊对象进行详细调查。 结果 吉林市0~14岁儿童哮喘累积患病率为2.94%,近1年现患率为1.70%。0~6岁哮喘的患病人数占总患病数的60%,其中1岁和3岁是两个患病年龄的高峰,上呼吸道感染、湿疹、过敏性鼻炎以及遗传因素等与儿童哮喘发病有关。 结论 2010年吉林市0~14岁儿童哮喘的患病率高于2000年全国儿童哮喘平均水平,多种因素可增加儿童哮喘的发病危险,4岁以下儿童,尤其是托幼儿童是哮喘高风险人群,应重视过敏体质高危儿呼吸道疾病的综合管理。     

Respiratory diseases in hard metal workers: an occupational hygiene study in a factory.

A hygiene study of a hard metal factory was conducted from 1981 to 1984. All workers exposed to hard metal were medically examined and their exposure to cobalt measured. Eighteen employees had occupational asthma related to exposure to hard metal, a prevalence rate of 5.6%. Nine had a positive bronchial provocation test to cobalt and reactions of the immediate, late, or dual type were elicited. Exposure measurements suggest that asthma may be caused by cobalt at a mean time weighted average concentration below 0.05 mg/m3. Only two of the nine individuals with cobalt asthma had a positive patch test to cobalt. Chest radiographs of three workers showed diffuse shadows of category 1 or over. X ray microanalysis of lung biopsy specimens from two of these three workers showed the presence of tungsten, titanium, cobalt, nickel, and some minerals. One of the two was diagnosed as having pneumoconiosis due to exposure to silica in a steel industry and the other was suspected of having pulmonary fibrosis caused by dust generated from the carborundum wheels used to grind hard metal. There were no cases with interstitial pneumonitis in the factory.     

Respiratory hazards in hard metal workers: a cross sectional study

A cross sectional study was conducted on 513 employees at three hard metal plants: 425 exposed workers (351 men, 74 women) and 88 controls (69 men, 19 women). Cough and sputum were more frequent in workers engaged in "soft powder" and presintering workshops compared with controls (12.5% and 16.5% v 3.5%). Spirometric abnormalities were more frequent among women in sintering and finishing workshops compared with control women (56.8% v 23.8%) and abnormalities of carbon monoxide test were more frequent in exposed groups than in controls; this difference was more pronounced in women (31.4% v 5.6%) than in men (18.5% v 13%). No significant correlation was observed between duration of exposure and age adjusted lung function tests. Slight abnormalities of chest radiographs (0/1, 1/1 according to ILO classification) were more frequent in exposed men than controls (12.8% v 1.9%) and mostly in soft powder workers. In subjects with abnormal chest radiographs FVC, FEV1 and carbon monoxide indices (fractional uptake of CO or CO transfer index or both) were lower compared with those with normal chest radiographs. Although relatively mild, the clinical, radiological, and functional abnormalities uncovered call for a regular supervision of workers exposed to hard metal dust.     

Inorganic particulates in pneumoconiotic lungs of hard metal grinders.

Data from the analysis of lung dust in 16 metal grinders who had been exposed to hard metals between five and 44 years is reported. The mean latent time between the first exposure and analysis in biopsy or necropsy specimens was 33.6 years. Mineralogical and elementary analysis by a variety of techniques showed small or trace amounts of hard metal in all lungs. Many specimens, however, did not contain all hard metal components, cobalt, for example, being detected in four cases only. All the lungs contained quartz and silicates and in most of the necropsy cases carborundum and corundum could also be shown. Histologically no specific pattern was found. The appearances included mixed dust nodular pneumoconiosis, diffuse interstitial lung fibrosis, and foreign body and sarcoid like granulomatous changes. In view of the mixed dust exposure of the hard metal grinders and the variable histological appearance we think that the term "mixed dust pneumoconiosis in hard metal grinders" is more appropriate than "hard metal lung" to describe this condition.     

A study on lung toxicity of respirable hard metal dusts in rats

The aetiology of hard metal lung disease has not been clarified so far. The pulmonary toxicity of respirable dusts collected in a hard metal factory was studied in vivo in rats. The effect of the samples was examined 1, 4, 7 and 30 days after single intratracheal injection. Lactate dehydrogenase (LDH), acid phosphatase (AP), protein and phospholipid were determined in cellfree bronchoalveolar lavage (BAL) and lung tissue. The lungs and regional lymph nodes were processed histologically. Lung toxicity of the samples collected during hard metal production varied. Samples containing considerable amount of cobalt dissolved upon acid treatment were found to induce inflammation. It has been established that the biological effect of samples of identical composition is changed by heat treatment and pre-sintering. Our examinations seem to prove that cobalt plays a prominent role in the development of pathological alterations.     

0～14a儿童支气管哮喘流行病学调查

目的 了解安徽省合肥市0～14a儿童哮喘的流行现状、分布及影响因素，以及儿童哮喘的临床特征。方法 采用整群随机抽样的方法，在合肥市中市区和西市区共抽取调查对象10105人，先对所有调查对象填写初筛表进行筛查，然后再对确诊对象进行详细调查。结果 合肥市0～14a儿童哮喘累计患病率为6．06％，现患率为3．90％，其中男、女儿童的现患率分别为4．76％和2．99％。性别比为1．59：1。在年龄分布上，0～4a期间随年龄的增加哮喘的发病也增加。发病季节以秋冬季发作为主。性别、家中饲养宠物、个人过敏史及遗传因素与哮喘发病有关。哮喘发病的诱因以感冒、运动、天气变化等为主。结论 合肥市0～14a儿童哮喘的患病率高于全国平均水平，男童高于女童，多种因素可以增加哮喘的发病危险。     

连云港市城区儿童哮喘流行病学调查

目的 调查连云港市城区3～14岁儿童支气管哮喘(简称哮喘)的流行现状。方法 整群随机抽样9 612名儿童,发放初筛调查问卷,可疑对象予确诊,采用SPSS 19.0软件统计分析结果。结果 连云港城区3～14岁儿童哮喘患病率为4.2%,其中男5.01%,女3.28%,天气变化或接触冷空气是本地区儿童哮喘恶化的主要原因。哮喘组中家具合成板为主以及父亲吸烟的几率明显大于对照组(P＜0.05)。哮喘诊断前β内酰胺类使用率达80.60%。仅47.01%的家庭表示完全能够承受治疗费用,33.58%的患儿每年影响学习时间超过10d,5.97%的患儿从不参加体育活动。结论 连云港地区3～14岁儿童哮喘患病率高于全国水平,生活环境及方式有待改善,及时诊断、合理用药和规范治疗是防治关键。     

开封市市区0～14岁儿童哮喘流行病学调查

目的　调查分析开封市区儿童哮喘患病率、危险因素及治疗状况与卫生经济学的关系。方法　用随机整群抽样方法 ,对开封市市区 110 0 0名 0～ 14岁儿童进行哮喘流行病学调查。采用回顾性询问填表法初筛出可疑对象 ,并按全国统一诊断标准逐个体格检查 ,明确诊断 ,填写统一调查表 ,并进行统计学处理。结果　①患病率为 1.16 % (现患率为 0 .91% ) ,男女比为 1.72∶1;各年龄组患病率差异有非常显著性 (P <0 .0 0 1) ,以 3～ 5岁组患病率最高。工业区儿童患病率明显高于居民区 ,比值比 (OR)为 2 .13∶1(P <0 .0 0 1)。②相关因素分析 :以过敏性疾病史、上呼吸道感染史、家族史为主要因素 ;与民族类别和狗、猫接触史差异无显著性 (0 .0 5

相似文献   

Evaluation of right and left ventricular function in hard metal workers.

Ingested cobalt has previously been associated with the development of a congestive cardiomyopathy. Despite occasional reports of cardiomyopathy after industrial exposure to cobalt, this association remains controversial. In a study of 30 cemented tungsten carbide workers with a mean duration of exposure to cobalt of 9.9 +/- 5.3 years radionuclide ventriculography was performed to study right and left ventricular ejection fractions at rest and exercise. For the entire group, rest and exercise biventricular function was normal. There was, however, a weak but significant inverse correlation between duration of exposure and resting left ventricular function (r = -0.40, p less than 0.03). Workers with abnormal chest x ray findings (9/30) had relatively lower exercise right ventricular ejection fractions (45% +/- 6 v 52% +/- 7, p less than 0.02). An inverse relation was also found between rest and exercise right ventricular ejection fraction and severity of parenchymal abnormalities on x ray examination (r = -0.44, p less than 0.01 and r = -0.41, p less than 0.02). Diminished right ventricular reserve was probably due to fibrotic lung disease and early cor pulmonale. Although overt left ventricular dysfunction was not present, prolonged exposure to industrial cobalt may be a weak cardiomyopathic agent with unknown long term significance.