木尘与肺癌关系的队列研究

为进一步探讨木尘与肺癌的关系，我们进行了回顾性队列研究，暴露组为成都某木综厂工龄１年以上的接触木尘职工２３６２（男１７０７，女６５５）人，观察期１５年（１９７８年１月１日～１９９２年１２月３１日），观察了３３６７９人年。非暴露组为当地某煤矿工龄１年以上的男性职工２５８７人，观察期２１年（１９７２年１月１日～１９９２年１２月３１日），观察了５４０４０人年。结果显示：接触木尘职工肺癌的标化死亡率（ＳＭＲ）为７４．６２／１０５（ＲＲ＝４．０８，Ｐ＜０．０１），与当地居民死亡率比较，接尘职工的ＳＭＲ为２１８．６（９５％ＣＩ：１．４１～３．２３，Ｐ＜０．０１）。肺癌标准化死亡比例比（ＳＰＭＲ）为３４９．０，差异有非常显著意义（Ｐ＜０．０１）。提示：木尘可能与肺癌有关。     

接触不同沥青类型工人的肺癌流行病学研究

在回顾性队列研究基础上，对全国１５个省市２０个油毡厂工人肺癌发病情况继续进行前瞻性研究４年。结果表明，混合组和石油组肺癌显著超出对照人群和全国城市居民，ＳＭＲ分别为３．３３（Ｐ＜０．０１），１．７７（Ｐ＜０．０１）和３．４６（Ｐ＜０．０１），１．８８（Ｐ＜０．０１），接触不同种类沥青作业的油毡工人肺癌存在剂量－反应关系。接触人群中非吸烟者的肺癌也显著超量，其肺癌发病具有职业特点，是一种与职业有关的癌症。     

油毡工人癌症27年队列观察

本文对１２０名油毡工人癌症２７年队列观察，结果表明：接触组共死亡３８人，癌症死亡１１人，肺癌居全癌之首，与对照组和对照人群比较，肺癌均有明显超出量，ＳＭＲ分别为４．６３（Ｐ＜０．０１）和３．５１（Ｐ＜０．０５）。但按暴露至观察终点年数的肺癌ＳＭＲ随ｌａｔｅｎｃｙ增长的趋势不明显。肺癌死亡年龄较对照组提前６．８３年。吸烟对肺癌起协同作用，说明油毡工人肺癌无论与任何时期对照组和对照人群比较，均显示明显     

接触不同沥青类型工人的肺癌汉行病学研究

在回顾性队列研究基础上，对全国１５个省市２０个油毡厂工人肺癌发病情况继续进行前瞻性上，结果表明，混合组和石油组肺癌显著超出对照人群和全国城市居民，ＳＭＲ分别为３．３３（Ｐ〈０．０１），１．７７（Ｐ〈０．０１）和３．４６（Ｐ〉０．０１），１．８８（Ｐ〈０．０１），接触不同种类沥青作业的油毡工人肺癌存在剂量－反应关系。接触人君 中非吸烟乾的肺癌也显示超量，其肺癌发病具有职业特点，是一种有有关癌症。     

女性非吸烟者中被动吸烟与肺癌关系的探讨

为了探索非吸烟者中肺癌发病原因，采用病例对照的方法对北京市ＳＩＮＯ－ＭＯＮＩＣＡ项目监测人群中的肺癌病例进行了调查，分析结果显示被动吸烟与非吸烟女性患肺癌有一定阳性关联（ＯＲ＝２．５２，Ｐ＜０．０５），并随被动吸烟年支的增加而上升，当达２００年支以上时有显著统计学意义（Ｐ＜０．０５）。环境香烟烟雾（ＥＴＳ）诱发肺腺癌的可能性较大（ＯＲ＝２．３２，Ｐ＜０．０５），而与肺鳞癌似无关系（ＯＲ＝１．０４，Ｐ＜０．０５）。     

淄博矿区煤矿尘肺死亡回顾性队列研究

应用回顾性队列研究方法对淄博矿区１２个煤矿１９７７年１月１日在册的２０３７例煤矿尘肺的死因进行了调查。队列成员追访至１９８６年，共死亡４４３人，煤矿尘肺全死因死亡率为２４０８．８／１０万，与用山东省居民死亡率计算的期望值比较显著超高，ＳＭＲ＝２３５，９５％ＣＩ＝２１４～２５８。４非恶性呼吸道疾病（主要是尘肺病）死亡为全死因之首，占２５．１％，其次是恶性肿瘤、心血管疾病和肺结核。恶性肿瘤死亡明显超高，ＳＭＲ＝１９０，且主要集中于肺癌（占５９．２％，ＳＭＲ＝５５６），与呼吸道疾病相关的肺心病ＳＭＲ＝１９０，以及肺结核ＳＭＲ＝１００６的死亡率也明显超高。在掘进工和采煤工尘肺中，全死因、呼吸系疾病、恶性肿瘤、肺结核的死亡率显著增高，Ｐ＜０．０１。此外，在掘进工尘肺中心血管疾病，尤其是肺心病的死亡人数高于预期值（ＳＭＲ＝２７１，Ｐ＜０．０１）。     

女怀非吸烟者中被动吸烟与肺癌关系的探讨

为了探索非吸烟中肺癌发病原因，采用病例对照的方法对北京市ＳＩＮＯ＿ＭＯＮＩＣＡ则人群中的肺癌病例进行了调查，分析结果显示动吸吸烟与非吸烟女性患肺癌有一定的阳性关联（ＯＲ＝２．５２，Ｐ〈０．０５），并随被动吸烟年支的增中而上升，当达２００年支以上时有显统计学意义（Ｐ〈０．０５）。环境香烟烟雾（ＥＴＳ）诱发肺腺癌的可能性较大（ＯＲ＝２．３２，Ｐ〈０．０５），而与肺鳞似无关系（ＯＲ＝１．０４，Ｐ〈０     

人肺癌组织耐药基因（MDR1）表达及意义

应用ＰＣＲ定量分析技术对１０４例肺癌患者的ＭＤＲ１基因进行了前瞻性研究，结果发现，初治患者６９％（５５／８０）有ＭＤＲ１基因表达增高，而经过治疗的患者１００％（２４／２４）有ＭＤＲ１基因表达增高，其中小细胞肺癌（ＳＣＬＣ）的增高有显著意义（Ｐ＜０．０１），在没有经过治疗的患者，２１％（１８／８０）ＭＤＲ１表达量处于高水平，而经过治疗的患者，７５％（１８／２４）ＭＤＲ１表达量较高（Ｐ＜０．０１）。ＭＤＲ１基因高表达的患者化疗有效率明显低于ＭＤＲ１不表达或低表达的患者，其中以ＳＣＬＣ患者最为明显（Ｐ＜０．０１）。结果表明，检测肺癌患者尤其是ＳＣＬＣ患者的ＭＤＲ１基因的表达情况，对临床指导化疗非常重要。     

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。     

油毡工肺癌病因学研究

对全国１５个省市２０家油毡厂工人的肺癌发病作了连续１７例的队列研究。结果表明，男性油毡人工肺癌发病率超出对照人群和全国城市居民，ＳＭＲ分别为３３７和１８１。按工作场所沥青烟浓度平均为０．８８ｍｇ．ｍ＾３，９６ｎｇ／ｍ＾３，６．２８ｍｇ／ｍ＾３，分成低、中、高３层接触水平后，与对照人群肺癌相比的ＳＭＲ为１９９（Ｐ〉０．０５），３１９（Ｐ〈０．０１），４１５（Ｐ〈０．０１）；与全国城市居民相比的ＳＭＲ     

冶金系统13个耐火材料厂矽肺患者死亡的流行病学研究

本文对冶金系统１３个火材料厂１９８０年１月１日以前确诊并生存的男性矽肺患者１２８４例进行了队列研究来观察１０年（１９８０．１￣１９８９．１２）期间矽肺队列成员的职业变动情况、死亡情况及死亡原因。研究结果表明：耐火行业矽肺患者的平均寿命比煤矿短，比铁矿长、与陶瓷行业近似。矽肺确诊越早其死亡年龄越小，全癌为矽肺患者的首位死因，其次为慢性支气管肺炎，肺心病，肺结核和脑血管病，全癌中以肺癌的死亡率为最高。     

耐火材料厂矽尘作业工人肺癌流行病学研究

本文对冶金系统十一个耐火材料厂的矽砖、粘土砖制造工人的肺癌进行了回顾性队列研究。队列由６２６６名男性工人组成，观察期为１９６３年１月１日至１９８５年１２月３１日，在此２３年期间共累积１３０７３０人年。以全国不同地区的十个大、中型钢铁企业的钢坯初轧厂１１４７０名男性职工在１９７１年至１９８５年间的年龄别、死因别死亡率为标准，计算各项死因的标化率比（ＳＭＲ）。矽尘作业人群的肺癌显示超量发生（ＳＲＲ为１     

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     

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.     

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     

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.     

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.     

Does occupational exposure to silica cause lung cancer?

Silica is not generally considered to be a carcinogen, however, occupations characterized by high exposure to crystalline silica have excessive rates of lung cancer mortality. Respiratory cancer excesses have been reported from North America and from Europe for the following dusty trades in which exposure to silica is a common factor: iron and steel foundry workers, steel casting workers, sand blasters, metal molders, non-uranium miners, and ceramic workers. These findings have been reinforced by two reports from the Swedish Pneumoconiosis Register and the Ontario Ministry of Labor indicating that silicotics have statistically significant risks of lung cancer mortality. Animal studies suggest that silica can be an initiating carcinogen or can act as a cocarcinogen or promoter when combined with benzo(a)pyrene. We propose three candidate hypotheses and two pathways for silicocarcinogenesis.     

Mortality among workers exposed to cutting oil mist: update of previous reports

BACKGROUND: Earlier reports of the mortality experience of this cohort of automotive workers followed from 1938 to 1967 who were exposed to cutting oil mist noted an excess of gastrointestinal cancer. The present report describes the mortality experience of these workers followed for mortality through 1980. METHODS: Cause-specific standardized mortality ratios were calculated by comparing the observed number of deaths to the expected numbers based on rates for the U.S. male population. RESULTS: The SMRs for liver and biliary tract, and testicular cancers were significantly elevated. Among the subset of workers with heavy oil mist exposure, SMRs were significantly elevated for cancers of the lung and testis, and for Hodgkin's disease. The risk of death due to lung cancer was greatest among workers with heavy exposure to oil mist employed for 15 or more years. Mortality due to stomach cancer was in excess among workers with heavy exposure to oil mist who were employed for 5 or more years. There were significant excesses of deaths due to asthma and emphysema. CONCLUSIONS: Further studies with information on the presence of contaminants and additives in oil mists will help elucidate the relationship between oil mist exposure and cancer.     

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.