橡胶职业暴露与多种疾病关系研究的死因别危险度职合分析模型

应用Ｃｏｘ回归风险度模型，进行了死因别（肺癌，肠癌和胰腺癌，及心脑血管疾病）联合分析，以便估计和检验橡化合物暴露对特定死因别的效应，以及死因间竞争性危险度。结果表明；心脑血管疾病可以对肺癌，肠癌和胰腺癌产生了竞争性死亡的效应。     

橡胶职业暴露与肺癌关系的前瞻性研究——Ⅲ肺癌危险因素联合作用方式

目的探讨橡胶工人中亚硝胺暴露、吸烟和经济收入低等主要危险因素对肺癌联合作用的模式。方法应用广义相对危险度模型拟合某橡胶厂队列随访资料。结果联合作用下,亚硝胺暴露与吸烟对肺癌危险度为相乘作用形式,亚硝胺暴露与经济收入为相加形式,吸烟与经济收入为相加形式。结论受样本限制,不同模型之间拟合优度的差别较小,但是,在公共卫生实践和生物学机理的认识方面,确定因素对疾病危险度的联合作用方式具有重要意义     

橡胶职业暴露与肠癌和胰腺癌关系的病例—队列研究

对上海某橡胶厂轮胎和胶鞋制造工人进行了２３年（１９７３～１９９５年）的随访调查。应用病例－队列方法，对橡胶职业暴露与肠癌和胰腺癌之间的关系进行了研究。准似然多因素分析表明，除内胎工种外，其它五类工种的肠癌相对危险度均升高，胶鞋和机修工种尤为明显，这种作用独立于与肠癌可能的非职业危险因素，如年龄、性别、饮茶、吸烟、饮酒、经济状况等。认为橡胶化合物中的亚硝胺（ＲＲ＝２．４３，９５％ＣＩ＝０．６５～９．１２）和碳黑（ＲＲ＝２．３０，９５％ＣＩ＝０．６４～８．２６）暴露可能与肠癌有关。与胰腺癌有关的橡胶化合物可能是溶剂（ＲＲ＝３．８４，９５％ＣＩ＝０．４６～３２．２０）和亚硝胺（ＲＲ＝２．７１，９５％ＣＩ＝０．６２～１１．９１）。结论认为，虽然本次研究的病例数较少，与职业相关变量的相对危险度增高未有统计学显著性，但所揭示的橡胶职业与这两种疾病的关系值得注意和进一步研究。     

橡胶职业暴露与肺癌关系的前瞻性研究

目的 探讨橡胶工人中亚硝胺暴露、吸烟和经济收低等主要危险因素对肺癌联合作用的模式。方法 应用广义相对危险度模型拟合某橡胶厂队列随访资料。结果 联合作用下，亚硝胺暴露与吸烟对肺癌危险度为相乘作用形式，亚硝胺暴露与经济收入为相加形式，吸烟与经济收为相加形式。结论受样本限制，不同模型之间拟合的差别较小，但是，在公共卫生实践和生物学机理的认识方面，确定地疾病危险度的联合作用方式具有重要意义。     

暴露剂量、时间和效应之间相互关系模型与多阶段致癌理论

目的 介绍分析暴露、时间和效应之间相互关系的模型在前瞻性队列研究中的应用。方法 应用Ｐoisson相乘模型和致癌多阶段理论分析了一个橡胶工人队列中亚硝胺暴露及与其有关的时间变量的肺癌危险度。结果 肺癌危险度随亚硝胺暴露年数增加而稳定升高,从暴露开始后经过一个潜隐期（大约２０～３０年）,肺癌危险度达到最高峰,然后迅速下降。结论 本资料中亚硝胺暴露对４肺癌危险度所显示的结果符合晚期阶段致癌原的特性。     

橡胶职业暴露与多种疾病间关系的分别分析

对某橡胶厂工人进行了２３年（１９７３￣１９９５）的随访调查,应用多因素分析方法,在控制可能的混杂因素下,分别估计了肺癌,肠癌,胰腺癌,缺血性心脏病和脑血管疾病的危险度。结果显示,亚硝胺的肺癌危险增高有统计学显著性（ＲＲ＝２．７１,９５％,ＣＩ＝１．３２￣５．５７）;与肠癌有关的橡胶化合物可能是亚硝胺（ＲＲ＝２．４３,９５％ＣＩ＝０．６５￣９．１２）和碳黑（ＲＲ＝２．３０,９５％ＣＩ＝０．６４￣８．     

亚硝胺暴露剂量、时间与肺癌效应关系和致癌多阶段模型的探讨

目的分析该橡胶工人队列中亚硝胺暴露及与其有关的时间变量的肺癌危险度。方法应用Ｐｏｉｓｏｎ相乘模型和致癌多阶段理论。结果肺癌危险度随亚硝胺暴露年数增加而稳定升高,从暴露开始后经过一个潜隐期（大约２０～３０年）,肺癌危险度达到最高峰,然后迅速下降。结论本资料中亚硝胺暴露对肺癌危险度所显示的行为符合晚期阶段致癌原的特性     

橡胶职业暴露与肺癌关系的前瞻性研究——Ⅱ巢式病例对照和病例队列设计

目的研究橡胶职业暴露、生活方式习惯、家庭环境和经济状况与肺癌之间以及因素相互之间的关系,并对本文应用的两种分析方法进行比较和评价。方法对队列在随访期间死亡的５１例病例及其对照用巢式病例－对照和病例－队列两种方法进行多因素分析。结果在控制非职业性危险因素条件下,亚硝胺暴露的危险度有显著增高（ＲＲ＝２．７１,９５％ＣＩ：１．３２～５．５７）,并发现亚硝胺暴露与肺癌间有明确的剂量－反应关系存在。结论（１）本文数据提示病例－队列分析因标准误较小、抽样更简便而优于巢式病例－对照研究方法;（２）亚硝胺暴露与肺癌之间有较确定的关系,但受到吸烟和经济状况等因素作用的修饰,需进一步研究     

橡胶职业暴露与肺癌关系的前瞻性研究

目的 研究橡胶职业暴露、生活方式习惯、家族环境和经济状况与肺癌之间以及因素相互之间的关系，并对本文应用的两种分析方法进行比较和评价。方法 对队列在随访死亡的５１例病人例及其对照组巢工病便－对照和病例－队列两种方法进行多因素分析。结果 在控制非职业性危险因素条件下，亚硝胺暴露的危险度有显著增高，（ＲＲ＝２．７１，９５％Ｃｌ：Ｌ１．３２－５．５７），并发现亚硝胺暴露与肺癌间有明确的剂量－反应关系存在。     

劳动卫生

99105,橡胶职业暴露与多种疾病间关系的前瞻性研究一标化死亡率分析/李克…//中国公共卫生学报一1998,17(l)一8~10 1973一1995年对某橡胶厂工人进行了随访调查,并应用标化死亡率分析方法研究疾病与特定暴露的关系。分析结果显示与普通人群相比较,队列人群的全死因死亡有轻微超额,为14%以下,相对危险度在。.98一1.14之间。与标准人群相比,队列人群中,男性的肺癌和膀胧癌有超额死亡,女性中脑血管病,食管癌和肺癌超额死亡,只有肺锡在两性中均有超额死亡。虽然在随访至不同年龄时某些疾病的SMR稍有变化,但总体上,一致性检验显示这种变化没有统…     

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     

肺癌病因研究中接尘量计算的真实性评价

为评价肺癌病例对照研究中接尘剂量估算方法的真实性,对广西锡矿病因研究对象进行了重新计算。广西锡矿队列发现男性肺癌死者１３０例,配对照６２７例。共７５７人。其中接法工人５７２名,发现各期矽肺共２４３例,根据在斩工业卫生监测资料估算所有接尘工人的累积总粉尘接触量,再计算不同接尘水平下矽肺的发病率。结果显示,随接尘水平上升,矽肺发病率升高,两者存在明显的接触剂量反应关系。完全符合矽肺发病特点。从而间接证     

Lung cancer and occupation in nonsmokers: a multicenter case-control study in Europe

BACKGROUND: Tobacco smoking is the main cause for lung cancer worldwide, making it difficult to examine the carcinogenic role of other risk factors because of possible confounding by smoking. Therefore, the present study aimed to investigate the association between lung cancer and occupation independent of smoking. METHODS: A case-control study of lung cancer was carried out between March 1998 and January 2002 in 16 centers from 7 European countries, including 223 never-smoking cases and 1039 controls. Information on lifestyle and occupation was obtained through detailed questionnaires. Job and industries were classified as entailing exposure to known or suspected carcinogens; in addition, expert assessment provided exposure estimates to specific agents. RESULTS: The odds ratio of lung cancer among women employed for more than 12 years in suspected high-risk occupations was 1.75 (95% confidence interval = 0.63-4.85). A comparable increase in risk was not detected for employment in established high-risk occupations or among men. Increased risk of lung cancer was suggested among individuals exposed to nonferrous metal dust and fumes, crystalline silica, and organic solvents. CONCLUSION: Occupations were found to play a limited role in lung cancer risk among never-smokers. Jobs entailing exposure to suspected lung carcinogens should receive priority in future studies among women. Nonferrous metal dust and fumes and silica may exert a carcinogenic effect independently from smoking.     

A case-control study of employment experience and lung cancer among rubber workers

In this case-control study the detailed employment histories of 121 rubber plant employees who died of lung cancer from 1964 through 1973 were compared to those of 448 plant employees (controls) who died of other causes during the same calendar period. All subjects were white male hourly employees. Lung cancer cases and controls were matched individually on year of birth and year of first hire at the plant. Results of matched analyses indicated that there was no association between lung cancer mortality and employment in either rubber compounding and mixing jobs or curing jobs. Men who had worked for at least five years in rubber reclaim operations, where there was potentially heavy exposure to particulates and fumes, experienced a twofold increase in lung cancer risk. In addition, there was a 70% excess of lung cancer risk among men employed in making special products, where the primary production activity was fuel cell manufacturing. The latter two findings were marginally statistically significant.     

Exposure to titanium dioxide and risk of lung cancer in a population-based study from Montreal

OBJECTIVES: This study assessed the lung cancer risk from exposure to titanium dioxide, an important pigment with limited evidence of carcinogenicity in experimental animals but sparse data for humans. METHODS: The risk of lung cancer among residents in Montreal, Canada, was analyzed, including 857 histologically confirmed cases of lung cancer diagnosed during 1979-1985 among men aged 35-70 years and a group of referents comprising 533 randomly selected, healthy residents and 533 persons with cancer in organs other than the lung. Exposure to titanium dioxide and other titanium compounds was assessed by a team of industrial hygienists on the basis of a detailed occupational questionnaire. RESULTS: Thirty-three cases and 43 referents were classified as exposed to titanium dioxide. The odds ratio was 0.9 [95% confidence interval (95% CI) 0.5-1.5]. No trend was apparent according to the estimated frequency, level, or duration of exposure. The odds ratio was 1.0 (95% CI 0.3-2.7) for medium or high exposure for at least 5 years. Few subjects were classified as exposed to titanium dioxide fumes or to other titanium compounds, but the risk of lung cancer was nonsignificantly increased for exposure to these agents. CONCLUSIONS: Although misclassification of exposure and low exposure prevalence might have resulted in false negative results, this study does not suggest that occupational exposure to titanium dioxide increases the risk of lung cancer.     

Combustion of diesel fuel from a toxicological perspective

Epidemiological data and results of toxicity studies in experimental animals indicate the possible health risk of diesel exhaust exposure. Acute effects of this exposure include odor, eye irritations, lung function decrements, cardiovascular symptoms, and some non-specific effects. Most of these effects are reported among persons highly exposed to diesel exhaust. Lung function decrements are reported as chronic effects. Another chronic effect that has been studied extensively among occupationally exposed persons in lung cancer. In addition to lung cancer, but at a less frequent rate, an enhanced incidence of bladder cancer is reported. The carcinogenic action of diesel exhaust exposure is ascribed to effects of the soot particles, particle-associated organics, and/or gas phase compounds. Direct effects of the particle load may include retardation of lung clearance, inflammation, and increased cell proliferation. These effects were all demonstrated in rodents. The particles may also prolong the residence time of particulate organics or induce the generation of reactive oxygen species. These compounds are known to react with macromolecules, causing lipid peroxidation, DNA damage, and/or activation of other genotoxic substances such as polycyclic aromatic hydrocarbons (PAHs). However, these results have not yet been confirmed in mammals in vivo. A direct interaction of particles with lung tissue is also suggested as a cause of cancer but a mechanism for this interaction has not yet been proposed. Organics associated with the particles are known to contain genotoxic properties attributable to PAHs and their derivatives. A number of these compounds are also identified as carcinogens in animal studies. However, it is not clear whether parent PAHs, their nitro-, oxy-, alkylated, or heterocyclic derivatives, or possibly other compounds are principally responsible for inducing tumors in the lungs of animals after diesel exhaust exposure. Furthermore, the mechanism of the bioavailability of these organics is not completely understood. The effects of gas phase constituents on the carcinogenic properties of the particles and/or particle-associated organics either have not been investigated or the findings have been inconclusive.     

Mortality patterns from lung cancer and nonneoplastic respiratory disease among white males in the Beryllium Case Registry

Study was undertaken of mortality patterns among white males entered into the Beryllium Case Registry (BCR) while alive with a diagnosis of beryllium-related nonneoplastic respiratory symptoms or disease. Analyses demonstrate an excessive risk of lung cancer among those subjects in the BCR who had been previously diagnosed with acute chemical pneumonitis or bronchitis secondary to short-term beryllium exposure. In the evaluation of the excessive lung cancer risk in this population, consideration should be given to the competing effects from the high case fatality rate of nonneoplastic respiratory disease. This excessive risk of lung cancer could not be explained on the basis of cigarette smoking per se. The findings of the present study utilizing subjects in the BCR are consistent with results of animal studies that over 30 years ago first demonstrated beryllium to be a carcinogen and with numerous epidemiologic studies demonstrating an increased risk of lung cancer among workers occupationally exposed to beryllium and its compounds.