磁铁矿工人的肺癌流行病学研究

对磁铁矿井下采矿工人的肺癌进行了回顾性队列研究，队列由２４１０名男性工人组成。观察期为１９８０年１月１日至１９８９年１２月３１日，在此１０年期间共累积２１４３３人年。以１９８７年全国城市男性居民人口的死因别、年龄别死亡率为标准，求算各项死因的标化率比（ＳＲＲ）。磁铁矿全体采矿工人的肺癌未显示超量发生（ＳＲＲ＝１．１４，Ｐ＞０．０５）。但当把该人分为矽肺与非矽肺两群组分析时，矽肺组的肺癌超量发生（Ｓ     

不同类型厂矿接尘工人肺癌病因学研究──矽尘或矽肺与肺癌的关系

为评价游离二氧化硅（简称矽尘或ＳｉＯ２）是否致肺癌？矽肺是否是肺癌前变基础？选择四类接尘厂矿进行队列和队列内病例对照研究。队列对象６８２８５人。有矽肺６４８７例，肺癌３３０例（男３１９，女１１），配对照１３５８例。根据厂矿历年工业卫生记录和近期对已知致癌物监测结果，定量评估了每个对象的接尘水平及每个病例对照的累积接触量。研究对象追访到１９８９年底，死亡６１９２人。与全国居民死亡平均数计算的期望值近似。全死因中癌症是第一死因，但全癌低于国家居民死亡率。分析结果说明：（１）矽尘单独存在时不是肺致癌剂。肺癌不超高，与接尘关系不明显；（２）在６４８７名矽肺队列中，肺癌相对危险度仅比非矽肺高０．２２倍，主要反应在铜铁矿工人中（Ｒ＝２．２），而矽肺患病率最严重的钨矿工人，其肺癌危险度反而随接尘水平上升而下降，再则肺癌死亡率与矽肺期别不呈正比；形态学上观察也不支持肺癌病变与矽肺纤维化病变相关。本研究结果难以支持矽尘或矽肺与肺癌病因学相关的假说。     

冶金行业矽肺患者肺癌流行病学研究

对全国冶金系统４７个厂矿１９８０年１月１日以前确诊并生存的４３７２例矽肺患者的肺癌进行了回顾性队列研究，观察期从１９８０年１月１日至１９８９年１２月３１日共１０年。研究结果表明：矽肺患者的全死因、全癌（主要为肺癌）、慢支－肺炎－肺心病和肺结核显著超出全国对照组。全癌中以肺癌为主，ＳＭＲｓ为２３７。当将矽肺人群分成包括铁矿、烧结、耐火、冶炼和铸造等不同作业类型后，除铸造（ＳＭＲｓ＝１５７，Ｐ＞０．０１）外所有作业类型的肺癌均显著超出全国对照组（ＳＭＲｓ均在２００以上，Ｐ＜０．０１）。肺癌的这种超出未显示出同矽尘的累计接尘年数和Ｌａｔｅｎｃｙ有相关趋势，且不论是吸烟（ＳＭＲｓ＝２５７，Ｐ＜０．０１）或非吸烟组（ＳＭＲｓ＝２０９，Ｐ＜０．０１）同全国对照组比较均有极显著超出。     

铸造工人肺癌死亡队列研究

以三个工厂３ ２７９名铸钢、铸铁工为暴露组, 以同厂１ １７６ 名机加、修机工为非暴露组, 对１９７２ 年１ 月１ 日在册的队列成员进行了回顾性队列研究。观察期自１９７２ 年１ 月１ 日至１９９２ 年１２ 月３１ 日。结果表明, 铸造工肺癌粗死亡率４６－４４／１０ 万, 占恶性肿瘤死亡的３０－１０ ％ , 在恶性肿瘤死亡中居首位。以一般人群作参比标准时, 铸工标化死亡比（Ｓｔａｎｄａｒｒｉｚｅｄ Ｍｏｒｔａｌｉｔｙ Ｒａｔｉｏ, ＳＭＲ） 为１－５６ , １－８３ （ Ｐ＜ ０－０５）。男性尘肺患者肺癌死亡率高于男性非尘肺患者, ＳＭＲ 为２－１５ （χ２ ＝ ６－９２） , 相对危险度（ＲＲ） 为３－４０ （χ２ ＝ ６－９６） , 年龄分层处理后总的相对危险度（Ｒｅｌａｔｉｖｅ Ｒｉｓｋ Ｔｏｔａｌ ＲＲＴ） 为１－６９ （χ２ＭＨ＝ １－１９）。结果表明,该队列铸造工肺癌死亡超量, 尘肺患者尤为明显。     

矽肺对肺癌及总死亡影响的回顾性队列研究

目的 利用香港矽肺患者队列的资料进行分析,探讨矽尘、矽肺与肺癌的关系.方法 选择1981年1月1日至1998年12月31日期间在香港尘肺诊所登记的2789例男性矽肺病例为研究对象,取用同时期一般男性人群作为对照.用人年的方法估计各死因的标化死亡比(SMR),用Axelson's法间接调整吸烟的混杂影响.矽尘与肺癌的剂量-效应关系采用多因素p-spline平滑法模型来拟合最佳风险模型.结果 该组研究队列人数为2789,共观察24 992.6人年,失访率仅为2.9%.该队列主要工种为建筑工人(5 1.09%)和地下沉箱操作工人(37.54%).队列总死亡人数为853人,平均死亡年龄为(63.8±10.27)岁,整个队列中86例死于肺癌.全死因及全癌的SMR均明显上升,首位死因是呼吸道疾病,肺癌的5MR明显增加(SMR:1.69,95%CI:1.35～2.09).去除年龄、时期和吸烟的混杂因素的影响,矽肺对肺癌的相对危险度下降到1.12(95%CI:0.89～1.38).间接调整吸烟的混杂影响后建筑工人及地下沉箱工人肺癌的相对危险度分别为1.09(95%CI:0.82～1.42)和1.56(0.98～2.36).多因素p-spline平滑法风险模型分析显示,肺癌与累积呼吸性矽尘总量或平均矽尘浓度的关系无剂量-效应关系.结论 队列研究未发现接触矽尘或矽肺能增加肺癌死亡的危险,平滑法模型拟合的风险模型并不支持矽尘与肺癌死亡之间存在剂量-效应关系.     

焦炉工人肺癌病例对照研究

本文进行了一项队列内病例对照研究，病例来自于１６个焦化厂１５年期间（１９７１年１月１日－１９８５年１２月３１日）死亡的１２９１名焦炉工人中死于肺癌的１４５例患者。按照１：１的配对原则，余下的死亡者中取与病例同一工厂、相同性别和年龄的死亡者做为对照，共匹配成１３９对。通过相对危险度（ＲＲ）和逻辑回归分析，结果表明：焦化厂炼焦工作区的肺癌有超量发生（ＲＲ为２．９８，Ｐ＜０．０１）。并具有职业特片，其Ｒ     

煤工尘肺死亡的回顾性队列研究

为探索煤工尘肺病人的主要死因以及煤工尘肺与恶性肿瘤死亡之间的关系，采用流行病学回顾性队列研究方法对开滦矿务局１９５２～１９９５年诊断的３２２８例煤工尘肺患者（全部为男性）的结局进行了调查。队列观察从１９７０年１月１日开始，至死亡病例的死亡日期或１９９５年１２月３１日终止，以全国男性人群为参照。用标化死亡比（ＳＭＲ）作为统计指标，并计算９５％可信区间（９５％ＣＩ）。结果：全死因ＳＭＲ较全国人群高１１％（ＳＭＲ＝１．１１，９５％ＣＩ：１．０４～１．１８）。其中肺心病死亡（ＳＭＲ＝５．９７，９５％ＣＩ：５．２３～６．７７）、肺结核死亡（ＳＭＲ＝３．６８，９５％ＣＩ：３．０１～４．４６）均高于全国人群。全癌死亡低于全国人群（ＳＭＲ＝０．８１，９５％ＣＩ：０．７１～０．９２），但肺癌死亡高于全国人群（ＳＭＲ＝１．３６，９５％ＣＩ：１．１０～１．６６）。按不同死亡年代及粉尘种类进一步分析，均发现肺癌高发。结果表明：煤工尘肺病人的全死因死亡比稍高于全国人群，其中，肺心病和肺结核有明显的超额死亡。煤工尘肺病人中肺癌死亡超高。提示：煤工尘肺与肺癌的发生有关。     

铁合金作业工人癌症的流行病学研究

本文对吉林，重庆等６个铁合金厂１９８０年１月份工资在册的４８３１名男性铁合金作业工人以同铁俣金厂在地理位置上近的四个钢坯初轧厂同期５２６０名工人做对照进行了为期１０年（１９８０年１月１日－１９８９年１２月３１日）的回顾性队列研究。     

接触焦炉逸散物工人肺癌的流行病学研究

对１６个焦化厂１８５０６名男职工在原１１年回顾性队列研究基础上继续观察４年，使观察期延长到１５年（１９７１年１月１日－１９８５年１２月３１日），进一步研讨焦炉焦炉作业人群肺癌与焦炉逸散物的联系。研究结果表明：焦化厂的炼焦工作区人群肺癌是超量高发的癌症，超出量特别大，而肺癌在其它工作区均无显著超出。在炼焦工作区人群内，肺癌ＳＲＲ按非焦炉、炉侧、炉顶作业的顺序上升形成梯度：２．３８＜３．５５＜５．５６     

某厂铸造工人恶性肿瘤死亡的队列研究

对哈尔滨某厂铸钢、铸铁车间１９７１年１月１日在册的全部职工进行了回顾性队列研究，观察期为１９７１年１月１日至１９９２年１２月１３日，结果表明，不论以哈尔滨市７０年代还是８０年代一般男性人群为参比，该厂铸造工人恶性肿瘤和肺癌都超量，提示肺癌的超量与职业因素有关，研究结果支持粉尘，尘肺与肺癌有联系的观点。     

Is silicosis required for silica-associated lung cancer?

BACKGROUND: Abundant epidemiologic and experimental evidence supports the 1997 International Agency for Research on Cancer classification of crystalline silica as a human lung carcinogen. Nonetheless, there remains uncertainty about whether excessive lung cancer occurs exclusively among workers with silicosis. METHODS: A review was performed of published occupational epidemiologic literature directly pertinent to the interrelations among silica exposure, silicosis, and lung cancer. RESULTS: The association between silica and lung cancer is generally, but not uniformly, stronger among silicotics than nonsilicotics. However, the existing literature is ambiguous due to incomplete or biased ascertainment of silicosis, inadequate exposure assessment, and the inherently strong correlation between silica exposure and silicosis which hinders efforts to disentangle unique contributions to lung cancer risk. CONCLUSIONS: Until more conclusive epidemiologic findings become available, population-based or individually-based risk assessments should treat silicosis and lung cancer as distinct entities whose cause/effect relations are not necessarily linked.     

铁矿工人肺癌回顾性队列研究

对１５个铁矿采矿工人的肺癌进行了回顾性队列研究。队列由１６９５１名１９７１年前入放的男职工组成,观察期从１９８０年至１９８９年,失访７６０人（４．５％）,队列内非接尘人群是接尘人群各群的对照人群。接尘人群及其井下、露天、赤铁矿、磁铁矿各舸矿各组中癌均无明显超量。但接尘人群分为非矽肺和矽肺两群时组,矽肺患者人群的肺癌显示超量。赤铁矿、磁铁矿、井下矿、吴矿各群组都再分为非矽肺和矽肺两群组时,除露天采矿     

Silicosis and lung cancer in U.S. metal miners

The association between silicosis and lung cancer mortality was estimated in 9,912 (369 silicotics and 9,543 nonsilicotics) white male metal miners. These miners were examined by the U.S. Public Health Service during 1959-1961 and were followed through 1975. Miners were excluded from this study if they were employed in a mine during 1959-1961 that used diesel equipment underground. The ores that were mined consisted of copper, lead-zinc, iron, mercury, lead silver, gold and gold-silver, tungsten, and molybenum. The standardized mortality ratio (SMR, U.S. white male rates) for lung cancer was 1.73 (95% CI: .94-2.90) in silicotics and 1.18 (95% CI: .98-1.42) in nonsilicotics. Additionally, SMRs were higher in silicotics than in nonsilicotics, even in most subgroups stratified by cigarette smoking habit, type of ore mined, years of service in an underground job, radon exposure group, or year of hire. When lung cancer mortality between silicotics and nonsilicotics was compared, the age-adjusted rate ratio (95% CI) was 1.56 (.91-2.68), and the age- and smoking-adjusted rate ratio was 1.96 (.98-3.67). Corresponding figures for miners who were employed in mines with low levels of radon exposure were 1.90 (.98-3.67) and 2.59 (1.44-4.68), respectively. These findings indicate that lung cancer mortality risk was increased in silicotics, and this probably did not result from chance or bias. However, confounding from radon exposure could not be ruled out. The findings indicate that further follow-up of this cohort is needed.     

Mortality of workers compensated for silicosis during the period 1959-1963 in the Veneto region of Italy

After reports appeared from other countries indicating an excess risk of lung cancer among silicotics, a cohort of workers compensated for silicosis during the period 1959-1963 in the Veneto region of Italy was constructed and followed for mortality through 1984. The results of the study showed a large mortality excess for infectious diseases (180 observed versus 9.5 expected), due to silicotuberculosis, and for diseases of the respiratory system (270 observed versus 33.5 expected) due to silicosis. An elevated standardized mortality ratio of 239 (70 observed versus 29.3 expected) from lung cancer was also detected. An increasing pattern was observed with time since first exposure, while the relationship with employment category and duration of exposure was less clear-cut. The lung cancer excess was also strongly associated with cigarette smoking, there being a dose-response relationship with daily cigarette consumption. The study confirms the results from other epidemiologic studies on silicotics which show this pathological condition to be associated with increased lung cancer mortality.     

Mortality of a cohort of men in a silicosis register: further evidence of an association with lung cancer

Lung cancer mortality from 1980 to 1986 was studied in a cohort of 1,419 men in a silicosis register who had no previous exposure to asbestos and polyaromatic hydrocarbons. The 28 deaths from lung cancer were statistically in excess of expected (SMR 2.03; 95% CI 1.35-2.93). Excess risks of lung cancer were found in both underground workers (SMR 3.41; 95% CI 1.10-7.97; based on 5 deaths) and surface workers (SMR 1.87, 95% CI 1.18-2.81; based on 23 deaths). All lung cancer deaths were smokers. There was an increase in SMRs with longer latency periods and years of exposure, with the greatest risk found in those who had worked for 30 or more years after more than 30 years since first exposed (SMR 3.07, based on 16 deaths). The risk for lung cancer was higher in those with tuberculosis (SMR 2.52; 95% CI 1.52-3.94) and showed an increasing trend with severity of silicosis, from category 1 to 3 and from category A to C, with highest risk in those with tuberculosis and category 3 (SMR 4.44 based on 3 deaths) or tuberculosis and category C (SMR 7.63 based on 7 deaths). Most of the excess lung cancer risk in silicotics is due to smoking, but a synergistic effect between smoking and silica/silicosis on the risk of lung cancer is also likely. In particular, a possible role of silicosis and tuberculosis as the fibrotic seedbed for malignant growth in the lung is strongly supported.     

Exposures to silica mixed dust and cohort mortality study in tin mines: exposure-response analysis and risk assessment of lung cancer

BACKGROUND: Mineral dusts that contain crystalline silica have been associated directly or indirectly with the development of pneumoconiosis or silicosis, non-malignant respiratory diseases, lung cancer, and other diseases. The health impacts on workers with silica mixed dust exposure in tin mines and dose-response relationships between cumulative dust exposure and the mortality from lung cancer are investigated. METHODS: A cohort of 7,837 workers registered in the employment records in 4 Chinese tin mines between 1972 and 1974 was identified for this study and the mortality follow-up was traced through 1994. Of the cohort, the cause of death was ascertained for 1,061 (97%) of the 1,094 deceased workers. Standardized mortality ratios (SMRs) were calculated for all workers, non-exposed workers, and dust-exposed workers with different exposure levels, silicotics, and non-silicotics based on Chinese national rates. RESULTS: The mortality from all causes in four tin mines was nearly the same as the national mortality. Malignant neoplasm, cerebrovascular disease, and cardiovascular disease accounted for 68.6% of all deaths. Mortality excess from lung cancer, liver cancer, all malignant diseases, and non-malignant respiratory diseases was observed among dust-exposed workers; a 50-fold excess of pneumoconiosis was observed. There was an upward trend for SMRs of lung cancer was noted from no exposure to low, medium, and high exposure levels (SMRs=1.29, 2.65, 2.66, 3.33). The shape of the exposure-response curve for risk of lung cancer at high exposure levels was inconsistent in these four mines. CONCLUSIONS: The findings indicated a positive dose-response relation between exposure to cumulative dust and the mortality of lung cancer. High arsenic content in dust particles, together with crystalline silica, may play an important role in causing increased mortality from lung cancer.     

Long-term effect of occupational dust exposure

In 1950-1960, a cohort of dust-exposed workers and a cohort of multiple matched unexposed subjects was set up from the files of preventive medical checkups performed in 1,089 Viennese plants. Male workers with a history of long-term exposure to nonfibrous particulates in different industries (metal, ceramics, brick, glass, stone etc.) aged greater than or equal to 40, and male workers without dust exposure (matched for residency, start of observation, age, and smoking) were followed up to 1980 or death (48,960 person yr). By life table methods, dust-exposed workers compared to unexposed workers showed a reduced survival of age 60 (p less than 0.0001), due to lung cancer (123 exposed, 87 controls, p = 0.001), stomach cancer (48/27, p = 0.003), silicosis (40/0), emphysema, bronchitis and asthma (41/23, p = 0.007). No difference in mortality from cardiovascular diseases was observed (p greater than 0.50). We concluded that heavy and long term exposure to respirable particulates is related to increased lung cancer mortality after age 60. A comparison of 2,212 deaths among Austrian silicotics, with deaths in the corresponding population showed a relation between lung cancer and silicosis (p less than 0.001), fairly independent of age and time-period. The estimated relative lung cancer risk of Austrian silicotics in the period 1955-79 averaged 1.41 (95% confidence 1.21-1.64).     

Retrospective mortality cohort study of Italian workers compensated for silicosis

Objectives

To estimate cause specific mortality in a large cohort of Italian workers compensated for silicosis.

Methods

The cohort included 14 929 subjects (14 098 men and 831 women) compensated for silicosis between 1946 and 1979, alive on 1 January 1980, and resident in Tuscany (a region of central Italy with 3 547 000 inhabitants). Mortality follow up ranged from 1980 to 1999. Vital status and the causes of death were determined by linkage with the regional mortality registry and with the national mortality database. The cohort mortality rates were compared to the rates of the local reference population. SMRs and their 95% confidence intervals were computed assuming a Poisson distribution of the observed deaths. Specific SMR analyses were performed according to the level of disability, the year of compensation assignment, and the job type.

Results

A significant excess mortality was observed in male silicotics for cancer of the lung, trachea, and bronchus and cancer of the liver, respiratory diseases (silicosis, asbestosis, antracosilicosis, and other pneumoconiosis), and for tubercolosis. Statistically significant mortality excess was observed in female silicotics for respiratory diseases (specifically silicosis and other pneumoconiosis) and tuberculosis. Analyses for period of compensation assignment showed a twofold increased SMR for biliary tract cancer among female workers and for liver cancer among male workers compensated before 1970.

Conclusions

The excess mortality from respiratory tract cancers and respiratory tract diseases detected in Italian compensated silicotics are in agreement with previous epidemiological studies. Although the twofold increased risk for liver cancer among males is suggestive of a possible association with silica dust exposure, the finding needs to be confirmed.