Determination of nickel in lung specimens of thirty-nine autopsied nickel workers

Summary Lung specimens from 39 nickel refinery workers autopsied during the period from 1978 to 1984 were analyzed for nickel. Fifteen of the workers were employed in the Roasting and Smelting Department, where exposure to nickel was predominantly in the form of nickel-copper oxides, Ni₃S₂ and metallic dust. The remaining 24 men worked in the Electrolysis Department. Exposure in this group was considered to be mostly to the water-soluble compounds, NiSO₄ and NiCl₂, but also to a lesser degree to water-insoluble nickel compounds such as nickel-copper oxides and sulphides. The arithmetic mean ± SD for nickel concentration in lung tissues expressed in gg^–1 dry wt for the 39 workers was 150 ± 280. In the workers employed in the Roasting and Smelting Department, the average nickel concentration was 330 ± 380; for those who worked in the Electrolysis Department it was 34 ± 48. Lung tissue from 16 autopsied persons not connected with the refinery had an average nickel concentration of 0.76 ± 0.39. Statistical analysis based on log-normal distributions of the measured nickel concentrations allowed three major conclusions to be formulated: (1) nickel refinery workers exhibit elevated nickel levels in lung tissues at autopsy; (2) workers of the Electrolysis Department and the Roasting Smelting Department constitute distinct groups with respect to the accumulation of nickel in lung tissue; (3) workers who were diagnosed to have lung cancer had the same lung nickel concentrations at autopsy as those who died of other causes.     

镍化合物致人胚肺细胞转化及细胞周期的研究

目的 探讨镍化合物与职业性肺癌的关系。方法 用水不溶性氧化镍和二硫化三镍体外转化人胚肺细胞（ＭＲＣ－９和ＩＭＲ－９０）,并用流式细胞术分析这些转化细胞的细胞周期改变。结果 细胞在染毒３～５个月后,ＭＲＣ－９和ＩＭＲ－９０细胞均被诱发形态转化,包括转化灶的形成、无序重叠交叉生长和类上皮细胞化等。并且有的转化细胞能在软琼脂培养基中生长并形成集落。流式细胞术分析发现,转化细胞细胞周期发生改变。如未处理的     

扶正解毒汤对镍电解工人体内脂质过氧化的保护作用

目的研究从事镍电解工人体内镍负荷与自由基代谢变化的关系,并用扶正解毒汤干预体内脂质过氧化作用。方法自2010年7月—2011年7月,以100名镍电解作业人员为接触组,以80名无镍接触的健康人作为非接触组,分别测定两组人员血清中镍含量作为体内负荷;同时测定接触组服用扶正解毒汤1个月后血清中镍、丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)的水平。结果镍作业组血清中MDA含量明显升高;SOD活力、GSH含量明显下降,差异有统计学意义(P0.01),服用扶正解毒汤后镍、MDA含量明显下降;SOD活力、GSH含量明显升高,差异有统计学意义(P0.05),结论镍具有增加体内脂质过氧化产物、降低机体抗氧化能力的作用;扶正解毒汤对体内脂质过氧化有明显的保护作用。     

Risk of lung cancer in workers producing stainless steel and metallic alloys

Objectives: The mortality of workers involved in the production of stainless and alloyed steel from 1968 to 1992 was studied, in order to investigate the risk of lung cancer due to exposure to metals, i.e. iron oxides, chromium and/or nickel compounds. Methods: The study design was a historical cohort mortality study and a nested case-control study concerning lung cancer. Standardized mortality ratios (SMRs) were computed using regional mortality rates as an external reference for comparing observed and expected numbers of deaths, adjusting for age, sex and calendar time. Conditional logistic regression was used to estimate odds ratios (ORs). Occupational exposure was assessed through the complete job histories of cases and controls and a specific job-exposure matrix. Results: The cohort comprised 4,288 male and 609 female workers. The observed overall mortality was significantly lower than expected [649 deaths; SMR = 0.91; 95% confidence interval (CI) 0.84–0.98]. No significant SMR was observed for mortality from lung cancer (54 deaths; SMR = 1.19; CI 0.88–1.55). The case-control study was based on 54 cases and 162 individually matched controls. Smoking habits were available for 71%. No lung cancer excess was observed for exposure to (1) metals and/or their compounds, i.e. iron (OR = 0.94, CI 0.48–1.86), chromium and/or nickel (OR = 1.18, CI 0.62–2.25), and cobalt (OR = 0.64, CI 0.33–1.25), (2) acid mists (OR = 0.43, CI 0.17–1.10), and (3) asbestos (OR =  1.00, CI 0.54–1.86). With respect to exposure to polycyclic aromatic hydrocarbons (PAHs) and silica, which are often found together in workplaces, (1) high and statistically significant lung cancer excesses were observed, the ORs being 1.95 (CI 1.03–3.72) and 2.47 (CI 1.28–4.77) respectively, (2) quantitative exposure parameters revealed upward trends reaching statistical significance (P < 0.05), and (3) adjustments for tobacco consumption did not reveal any confounding factors from smoking. Conclusion: This study failed to detect any relationship between lung cancer and exposure to iron, chromium, nickel and/or their compounds. High and statistically significant relative risks, along with increasing trends, were observed for simultaneous exposure to PAHs and silica. Received: 12 April 1999 / Accepted: 2 October 1999     

Cancer risk among workers at a copper/nickel smelter and nickel refinery in Finland

Summary A total of 1388 workers employed for at least 3 months at a copper/nickel smelter and nickel refinery were followed up for cancer from 1953 to 1987 through the Finnish Cancer Registry. There were 1339 male and 49 female workers, making a total of 27130 and 706 person-years, respectively. All of the women worked in the refinery, which opened in 1960, the same year the smelting of nickel began. A total of 67 cancers were diagnosed among the men, the standardized incidence ratio for all cancers being 1.0. No cancer was found among the women (1.8 expected). The risk of cancer among men was analysed according to primary site, exposure to nickel, type of work, years since first exposure and age at diagnosis. In the subcohort of nickel refinery workers, one case of sinonasal cancer was observed, against 0.02 expected, but otherwise no significantly increased risks of cancer were found. In addition to the small size of the cohort, the non-positive finding concerning lung cancer might be related to the relatively low arsenic exposure and, perhaps, to the late commencement of nickel production.     

急性羰基镍中毒大鼠肺组织和细胞损伤的实验观察

目的 观察大鼠急性羰基镍中毒后肺细胞DNA损伤程度以及组织细胞病理变化。方法 SD大鼠静态分别吸人20、135和250 mg/m3羰基镍染毒30 min,另设250 mg/m3氯气染毒组和正常对照组在染毒后第1、2、3和7天取肺组织单细胞凝胶电泳试验检测肺细胞DNA损伤程度,同时观察大鼠肺组织病理变化和细胞超微结构改变。结果 不同浓度羰基镍染毒后不同时间,大鼠肺组织细胞均有损伤,以72 h DNA损伤最重,但损伤晚于氯气。不同浓度羰基镍染毒大鼠肺组织有炎性渗出和增生,部分细支气管破坏,黏膜坏死脱落;肺泡Ⅰ型细胞的细胞器肿胀,肺泡Ⅱ型细胞板层体减少且排空,胞质内空泡增多、线粒体肿胀,肺泡纵隔内胶原纤维增生。结论 急性羰基镍对大鼠肺组织细胞有明显的损伤作用,且存在剂量-效应关系和时间-效应关系。     

镍接触作业工人抗氧化能力的研究

目的探讨职业性镍接触对工人抗氧化能力的影响。方法根据生产工艺的不同,选取某钢铁企业镍接触工人男性炼钢工、轧钢工及钢渣处理工共181人作为镍接触组,同时选择该企业的男性水处理工55人为对照组。黄嘌呤氧化酶法、化学比色法和硫代巴比妥酸法分别测定两组人群血清中总超氧化物歧化酶(SOD)活力、谷胱甘肽过氧化物酶(GSH-Px)活力和丙二醛(MDA)含量。结果不同工种镍接触组总SOD活力、GSH-Px活力和MDA含量分别与对照组相比,差异均有统计学意义(P0.05);不同工龄组总SOD活力、GSH-Px活力和MDA含量分别与对照组相比,除0～5 a组总SOD活力、GSH-Px活力分别与对照组相比,差异无统计学意义(P0.05)外,其他各年龄组差异均有统计学意义(P0.05);不同工龄组MDA含量分别与对照组相比,差异均有统计学意义(P0.05)。结论镍接触对工人抗氧化能力有影响,抗氧化酶活力降低,脂质过氧化产物增加。     

Risk of lung cancer among former chromium smelter workers

Hexavalent chromium is a known carcinogen. Previous epidemiologic studies in the 1950s of United States workers from seven facilities producing chromium compounds from chromite ore have reported a markedly increased risk for dying from lung cancer. As part of a high risk notification project of workers from four of these facilities, a mortality study was performed. The cohort was assembled in 1990–1991 from the Social Security records of four former chromate producing facilities in northern New Jersey. The study subjects were known to have worked at these facilities some time between 1937 and 1971. Proportionate mortality and proportionate cancer mortality ratios (PCMR) were calculated. The overall risk for lung cancer was a PCMR of 1.51 (confidence limits [CL] 1.29–1.74) for white men and 1.34 (CL 1.00–1.75) for black men. These risks increased with increasing duration of employment and latency since time of first employment. The PCMR for greater than 20 years duration of work and more than 20 years since first exposure was 1.94 (CL 1.15–3.06) for white men and 3.08 (CL 1.13–6.71) for black men. The risk for lung cancer for white men remains elevated more than 20 years after exposure has ceased (PCMR, 1.29; CL 1.03–1.60). The PCMR for nasal cavity/sinus cancer was also found to be a significantly increased, 5.18 (CL 2.37–11.30). A cluster of bladder cancer was seen among black workers from one facility, (PCMR, 3.30; CL 1.42–6.51). Despite the cessation of exposure, former chromium workers remain at significantly increased risk of lung cancer. Although there have been case reports of nasal cavity/sinus cancer in association with chromium exposure, this is the first epidemiologic study to report a significant increase in these cancers. Limitations in this study include lack of exposure data and lack of information on smoking habits. The lack of increase in other smoking-related diseases besides lung cancer indicates that the increase in lung cancer cannot be attributed to cigarette smoking. The ongoing elevated risk of lung cancer after cessation of exposure emphasizes the need for developing early detection tests for lung cancer. © 1996 Wiley-Liss, Inc.     

Update of cancer incidence among workers at a copper/nickel smelter and nickel refinery

Objectives: To assess cancer risk among nickel-exposed workers. Methods: We updated cancer incidence among 1388 workers employed for at least 3 months at a copper/nickel smelter and nickel refinery in Harjavalta, Finland. There were 1155 workers exposed to nickel during the period 1960–1985 in the smelter (566 workers), repair shop (239 workers), or refinery (418 workers). Cancer incidence was followed through the files of the Finnish Cancer Registry up to 31 December 1995. For overall cancer and for a priori selected specific cancer types the ratio of observed to expected numbers of cases was computed as a standardized incidence ratio (SIR), controlled for age, gender, and calendar period and using the region-specific rates as a reference. Results: The overall cancer incidence among both nickel-exposed and unexposed subcohorts was at the expected level. A small increase in lung cancer incidence, which reached statistical significance among workers with a latency exceeding 20 years, was observed among the smelter workers exposed to insoluble nickel compounds. Among workers in the refinery, who were exposed primarily to nickel sulfate at levels below 0.5 mg/m³ as well as to low concentrations of other nickel compounds, there was an increased risk for nasal cancer (SIR 41.1, 95% CI 4.97–148), positively associated with latency and duration of employment, and an excess risk for stomach (SIR 4.98, 95% CI 1.62–11.6) and lung (SIR 2.61, 95% CI 0.96–5.67) cancers. Conclusions: Since elevated nasal and lung cancer risks were confined to the refinery, where the primary exposure was to nickel sulfate, it is likely that nickel sulfate is mainly responsible for the elevated respiratory cancer risk. We cannot rule out whether the excess stomach cancer risk is a chance finding, or related to the working environment. Received: 11 September 1997 / Accepted: 17 October 1997     

Biomonitoring of nickel and chromium in human pulmonary tissue

Nickel (Ni) and chromium (Cr) and some of its compounds may be able to induce cancer in the lungs as well as in the nose and paranasal sinuses after occupational exposure. Latency periods amount to 20 years and more. Therefore objective exposure data are not available in the most cases and expert evaluation of the causal connection is often difficult. Recent investigations have shown, that Ni and Cr can cumulate in human lung tissue after occupational exposure. For the evaluation of normal Ni- and Cr-values a total of 495 human lung tissue samples of 30 occupationally non-exposed persons were analysed by AAS including ZEEMAN-compensation after wet oxidative digestion. Additional samples of 10 deceased persons who have been occupationally exposed to nickel in previous times by nickel-refining and welding, especially flame spraying have been investigated. The median Ni- and Cr- concentrations in the lungs of the non-exposed persons ranged between 20–40 resp. 133–277 ng/g (wet weight). In nickel refinery workers Ni- concentrations were found which exceeded the normal range about 1,000. In welders, especially flame sprayers, also values more than 100 times higher could be analysed for Ni and Cr. Partially these concentrations were found years after the end of the inhalative exposure.     

Fractionation of nickel species from airborne aerosols: practical improvements and industrial applications

Presently recommended methods for fractionation of airborne nickel dusts are laborious and time-consuming. A new method has been developed based on existing procedures of leaching nickel fractions from sample filters, and based on the principles of flow-injection analysis. A special sample filter holder has been constructed to be used in conjunction with the flow-injection system. In this system, soluble nickel compounds are extracted from the filter with ammonium citrate buffer, sulphidic nickel by peroxycitric acid, and metallic nickel by CuCl₂/KCl. The final dissolution of the filter by HNO₃/HCl results in the oxidic fraction. Endpoint determination of these fractions is performed by use of graphite-furnace atomic absorption spectrometry (GF-AAS). The analytical criteria of this method have been established, and the suitability of the method for application in the practice of industrial hygiene has been demonstrated. Received: 28 July 1999 / Accepted: 20 November 1999     

Investigations on the quantitative determination of nickel and chromium in human lung tissue

Summary Nickel (Ni) and some of its relatively insoluble compounds as well as chromates may be able to induce cancer in the region of the lungs, as well as in the nose and paranasal sinuses after occupational exposure. Latency periods may amount to 20 years and more. The results of recent investigations have shown that these metals cumulate in the lung tissue after inhalation of relatively insoluble chromium and nickel compounds. The quantitative detection of these heavy metals in samples of pulmonary tissue hence permits the amount of past exposure to be estimated. To establish the normal values, samples of pulmonary tissue from 30 normal subjects were investigated for chromium and nickel content. The samples were taken from different segments and lobes of the lungs, taking topographical anatomical criteria into consideration. In addition, 15 persons who had formerly been exposed to nickel and/or chromium (11 nickel refinery workers, of whom 10 had died of lung cancer, 2 stainless steel welders, 1 foundry worker, 1 electrical technician) were also investigated. From the results of 495 tissue samples from the normal group, median chromium concentrations between 130 and 280 ng/g were calculated, with median nickel concentrations of 20–40 ng/g (wet weight). If these values are related to the nickel concentrations measured in refinery workers, values 112-5,860 times higher were found. The concentrations were about 500 times higher than normal for nickel, and about 60 times higher than normal for chromium in the stainless steel welders. For the foundry workers who died of lung cancer, chromium and nickel concentrations in the normal range were calculated, with the exception of the nickel concentrations in the upper and lower lobes of the right lung. The very high nickel concentrations found in the samples of lung tissue from former nickel refinery workers should be regarded as a guideline with regard to the appraisal of the causal relationship between lung cancer and occupational exposure to relatively insoluble nickel compounds. This result is also supported by epidemiological investigations on this subgroup and must thus be considered etiologically conclusive. For the welders, chromium and nickel concentrations were found that were markedly above normal, but as yet there is no epidemiologically reliable verification for the increased occurrence of malignancies in this occupational group. On the basis of present scientific knowledge, no indications were found of relevant chromium and/or nickel exposure of the lung tissue that might be able to induce lung cancer in either foundry workers or for electric technicians.Dedicated to Professor V. Becker on his 65th birthday     

Cancer morbidity in nitrate fertilizer workers

Summary A cohort of 2,131 male nitrate fertilizer workers was evaluated for cancer morbidity from 1963 to 1986. No significant increase in total cancer, stomach cancer (5 actual vs 6.7 expected cases), or lung cancer (13 vs 13 expected) was found. On the other hand, 26 actual cases of prostate cancer were observed vs 16 expected cases (standardized morbidity ratio, SMR = 161; 95%, confidence interval, CI = 107–239). This risk increase however, was, not enhanced by applying at least a 10-year latency period. In a cohort of 1,148 male fertilizer workers who had never been exposed to nitrate, there was an increased incidence of lung cancer (SMR = 151,95% CI = 103–220) but not of stomach cancer or prostate cancer. There was no association between airborne nitrate exposure dose and total cancer, stomach cancer, lung cancer or prostate cancer, respectively.     

镍冶炼工人肺癌流行病学研究

对四个接镍作业厂矿进行了肿瘤回顾性队列调查。观察组全死因、恶性肿瘤粗死亡率与相对应对照组相比差异无显著性。镍精炼厂男性肺癌粗死亡率６１．９１／１０万，其ＳＭＲ以不同参比标准，可达２５３．１７～４５１．１３，且有统计学意义。某镍矿肺癌粗死亡率为２４．６０／１０万，以全国及当地一般人群作参比标准时ＳＭＲ分别为２８９．８６，９７５．６１（Ｐ〈０．０１）。镍精炼、冶炼工肺癌死亡危险度增高在我国也得到了证实     

Mortality in lung and gastrointestinal cancer among shipyard workers

Summary The risk of shipyard workers acquiring lung cancer and gastrointestinal cancer was investigated retrospectively by analysing the mortality pattern of 365 deceased shipyard workers. Instead of using the proportional mortality ratio (PMR), the odds ratio (OR) was determined according to a method proposed by Axelson, Miettinen and Der Wang. The pattern of causes of death among Swedish males was used as a reference. The OR was 2.3 for lung cancer and 1.4 for gastrointestinal cancer, using death in cancers of other sites (ICD 170–209) as reference diseases. There was a heavy exposure to asbestos, which is the probable cause of the increased risk of lung cancer in this population.     

Mortality study among workers producing chromate pigments in France

In a follow-up study of 294 men who had worked for at least 6 months in a chromate-producing factory in France between 1958 and 1987, only 16 were lost to follow-up and the number of person-years in the study was 5207. Occupational data were provided by the administration of the plant. The causes of deaths were ascertained from hospital and general practitioners' records. The observed numbers of deaths were compared with the expected numbers based on local rates with adjustment for age, sex and calendar time (standardized mortality ratio, SMR). The overall mortality did not differ significantly from that expected (SMR = 1.20, 95% CI = 0.98–1.47), whereas mortality due to lung cancer was in significant excess (SMR = 3.60, 95% CI = 2.13–5.68). Significantly higher lung cancer SMRs were found for workers whose duration of employment was more than 10 years. A non-significant excess was observed for all forms of digestive tract cancer (SMR = 1.30, 95% CI = 0.60–2.47). There were two cases of brain cancer when 0.24 was expected (SMR = 8.44, 95% CI = 1.02–30.49). No previous report has mentioned an association of brain cancer with chromate pigments; however, because of the small numbers involved, a chance excess should be considered.     

Pulmonary nodules in workers exposed to urban stressor

By multilayer spiral low-dose computed tomography (LD-CT) of the chest this study assesses the early detection of lung lesions on a sample of 100 traffic policemen of a big Italian city professionally exposed to urban pollutants and 100 controls non-occupationally exposed to urban pollutants matched by sex, age, length of service and cigarette smoking habit. Exposure to urban pollutants in traffic policemen was characterized using the annual average concentrations of PM₁₀, NO₂ and benzene in the period 1998-2008 measured by fixed monitoring stations located in different areas of the city. A significant and increasing number of suspicious lung nodules with diameters between 5 and 10 mm was observed: in traffic policemen (including smokers and non-smokers) vs. controls (including smokers and non-smokers); in total smokers (including traffic policemen and controls) vs. total non-smokers (traffic policemen and controls); in smoker traffic policemen vs. smoker controls and vs. non-smoker traffic policemen; in non-smoker traffic policemen vs. non-smoker controls. The RR of finding cases with at least one lung nodule with diameters between 5 and 10 mm in traffic policemen (including smokers and non-smokers) compared to controls (including smokers and non-smokers) is 1.94 (CI 1.13-3.31); in total smokers vs. non-smokers the RR is 1.96 (CI 1.20-3.19). The comparison between the interaction exposure and smoking shows an increase in smoker traffic policemen than in smoker controls (RR=2.14; CI 1.02-4.52). The RR for smoker traffic policemen was higher than in non-smoker traffic policemen (RR=2.09; CI 1.19-3.66). The results of our study show that: (1) while smoker workers have a higher risk for developing solid suspicious lung nodules, the simple routinely exposure to urban pollutants is unable to produce the same kind of increased risk; (2) the interaction of smoking and exposure to urban pollutants greatly increases the risk for the development of solid suspicious lung nodules. In conclusion, the use of chest LD-CT in workers at risk helps identify suspicious solid lung nodules at early stage.     

氧化镍生产厂的劳动卫生学调查

在某镍业公司氧化镍生产厂进行了劳动卫生状况调查，测定了空气中有害物质浓度和部分接镍人员指导甲中镍含量。结果表明，该厂主要职业危害因素是空气镍浓度高，焙烧车间部分受检工人指甲镍含量全部超过健康成人指甲镍正常上限值。这说明该人群体内镍负荷增高，需积极采取措施降低接镍水平。