江苏省溧阳市2009-2013年主要肺部疾病死亡率及趋势分析

目的分析溧阳市肺癌、肺炎/支气管炎、肺心病及慢性阻塞性肺疾病(COPD)死亡率及变化趋势,为制定疾病防制措施提供依据。方法对溧阳市2009-2013年4种肺部疾病死亡病例以及人口数据进行统计分析,计算疾病粗死亡率、标化死亡率、年龄别死亡率、死亡率年度变化百分比(APC)及其95%CI等指标。结果肺癌、肺心病、肺炎/支气管炎及COPD年均粗死亡率分别为36.26/10万、22.62/10万、27.51/10万和29.92/10万;年均标化死亡率分别为16.34/10万、6.30/10万、7.39/10万和8.28/10万。5年间肺癌(APC=4.5%,95%CI:-5.3%~14.3%)和肺心病(APC=-10.0%,95%CI:-33.1%~13.1%)无明显变化趋势;肺炎/支气管炎(APC=20.1%,95%CI:9.4%~30.8%)及COPD(APC=69.3%,95%CI:41.5%~97.1%)逐年上升趋势。结论溧阳市COPD与肺炎支气管炎标化死亡率上升趋势明显,肺癌标化死亡率在高水平波动,肺心病死亡率稳中有降。     

中国人群肺癌发病危险因素的Meta分析

[目的]探讨中国人群肺癌发生的主要危险因素,为预防决策提供依据。[方法]利用Meta分析方法对我国1995～2007年间公开发表的有关肺癌危险因素病例对照研究的12篇文献资料进行定量综合分析。[结果]各因素合并OR值及95%CI分别为:吸烟OR=2.7820(2.3428～3.3035);油烟OR=2.6257(1.7312～3.9879);家族肿瘤史OR=1.8075(1.4745～2.2157);肺结核OR=2.6018(1.8946～3.5731);慢性支气管炎OR=2.3052(1.8013～2.9500);精神因素OR=2.2648(1.8364～2.7932);饮酒OR=1.4942(1.2491～1.7873);被动吸烟OR=1.7064(0.9109～3.1965);新鲜蔬菜OR=0.5376(0.4445～0.6503)。[结论]吸烟、饮酒、油烟、家族肿瘤史、肺结核、慢性支气管炎、精神因素是目前中国人群肺癌发病的危险因素;而多吃新鲜蔬菜是肺癌发生的保护性因素。     

DNA损伤结合蛋白2基因单核苷酸多态性相关的肺癌发病风险模型

[目的]研究DNA损伤结合蛋白2基因（DDB2基因）单核苷酸多态性位点rs3781620等位基因（nt23314 C〉G）多态与肺癌易感性的关系，并建立环境-遗传因素的肺癌发病风险模型。[方法]运用病例-对照研究，选择湖北省各地区医院经病理诊断确诊的原发性肺癌患者216例为病例组，社区人群448人为对照组，以Taqman探针基因分型的方法进行基因分型，采用多因素非条件Logistic回归后退法筛选肺癌相关危险因素并计算人群归因危险度百分比，绘制受试者工作特征曲线（ROC）。[结果]社区对照人群中DDB2基因的C和G两种等位基因分布频率分别为66．6％和33．4％。多因素分析结果表明与携带DDB2基因单核苷酸多态性位点rs3781620等位基因的野生型纯合子CC基因型者相比，携带CG或GG基因型的研究对象患肺癌危险度为OR=1．634（95％CI：1．104～2．420）；年长者（〉60岁）发生肺癌的危险度为OR=1．641（95％CI：1．110～2．426）；一级亲属家族有肿瘤史的危险度为OR=2．972（95％CI：1．452～6．084）；轻度和重度吸烟者分别为OR=1．649（95％CI：0．962～2．826）、OR=6．351（95％CI：3．978～10．139）；饮酒为OR=1．559（95％CI：1．034～2．349）；体育锻炼为OR=O．568（95％CI：0．383～0．844）。以上各因素的人群归因危险度百分比分别为11．27％、13．34％、7．16％、9．67％、44．90％、8．71％和-11．67％。Logistic回归模型ROC曲线下面积为0．786（95％CI：0．748-0．823）。[结论]遗传和环境因素在肺癌发病中起作用：一级亲属肿瘤家族史、DDB2基因单核苷酸多态性位点rs3781620 CG或GG基因型与肺癌易感性有关；不良的生活方式（吸烟、饮酒和缺乏锻炼）可增加肺癌的危险性。该模型对肺癌发病风险的评估能力中等。     

新发初治肺结核病人耐药情况及其发病的非生物学影响因素研究

[目的]研究广州市初治肺结核病人对利福平的耐药现况及其发病的非生物学影响因素,为结核病的防治提供科学依据.[方法]采用直接涂片检查法和培养法.对肺结核病人的痰液进行检查,阳性标本经抗酸染色镜检确认后,采用绝对浓度法的间接法进行耐药性测定;而非生物学影响因素的分折采用1∶1配对的病例一对照研究方法,统计分析应用单因素和多因素的Logistic回归分析法.[结果]131例初治肺结核病人痰标本中,直接涂片法检出阳性标本21例,阳性检出率为16.0%(21/131);培养法共检出阳性标本56例,阳性检出率为42.7%(56/131).培养法高于直接涂片法(P＜0.05).将培养阳性标本作利福平药物敏感性试验,其中有17株发生耐药,耐药率为30.4%(17/56);影响肺结核病人发病的非生物学因素的单因素分析显示:已婚(OR=8.0,OR95%CI=1.8～34.8)、未接种卡介苗(OR=5.5,OR95%CI=1.9～15.9)、流动人口(OR=8.3,OR95%CI=4.0～17.2)、农村人口(OR:37.5,OR95%CI=9.2～152.6)和贫穷(OR=8.0,OR95%CI=3.4～18.7)等因素与肺结核发病有明显的相关性;多元回归分析则显示,已婚(OR=16.4,OR95%CI=1.5～183.7)、农村人口(OR=18.6,OR 95%CI3.7～94.4)和贫穷(OR=6.2,OR95%CI=1.4～27.6)与肺结核病的发病密切相关.[结论]结核杆菌对利福平的初始耐药率仍处在较高水平,且已婚、农村人口和贫穷是影响肺结核发病的主要的非生物学因素.     

血清降钙素原和D-二聚体与肺癌的相关性及交互作用研究

目的 探讨降钙素原（procalcitonin,PCT）、血清D-二聚体与肺癌的相关性。方法 选取近两年来就诊的肺癌患者166例和同期健康患者或不患有肺部疾病患者166例,采用Spearman秩相关,Logistic剂量反应关系和交互作用研究它们之间的相关性。结果 年龄、降钙素原（procalcitonin,PCT）、癌胚抗原（carcinoembryonicantigen,CEA）、D-二聚体与肺癌存在相关性（r_s分别为0.289、0.262、0.387和-0.161）。年龄（≥ 60岁）（OR=2.53,95%CI:1.28~5.00,P=0.008）、PCT异常（OR=2.10,95%CI:1.07~4.14,P=0.032）、CEA异常（OR=11.68,95%CI:4.57~29.82,P=0.001）和D-二聚体异常（OR=1.43,95%CI:1.15~1.68,P=0.001）均是肺癌的影响因素。随着PCT和D-二聚体水平的增加,肺癌患者的危险性增高,呈现一定的剂量反应关系（均有P<0.05）。PCT与D-二聚体间对肺癌具有正相加模型的交互作用,同时作用时会增加肺癌的患病风险（交互作用指数=2.16,95%CI:1.08~5.43;交互作用超额相对危险度=1.29,95%CI:0.68~2.71;交互作用归因比=0.75,95%CI:0.37~1.42）。结论 PCT与D-二聚体偏高是肺癌患者的危险因素,且存在剂量反应关系。PCT与D-二聚体存在正相加模型的交互作用,同时偏高时会增加肺癌的患病风险。     

吸烟与饮酒对肺癌发病的影响及交互作用

目的探讨吸烟与饮酒及其交互作用对肺癌发病的影响。方法在肿瘤高发地区开展以人群为基础的病例对照研究,通过调查问卷收集主要人口学、吸烟和饮酒等相关信息,采用非条件logistic回归分析计算比值比(OR)及95%CI,并分析吸烟与饮酒在肺癌发病中的交互作用。结果调整相关因素(包括饮酒)后,与不吸烟者相比,吸烟者患肺癌的风险增加(P0.05),吸烟≥40年者患肺癌的风险是不吸烟者的4.79倍,每日吸烟≥20支者患肺癌的风险是不吸烟者的4.44倍,吸烟至肺部者患肺癌风险是不吸烟者的4.44倍(P值均0.001)。调整变量(包括吸烟)后,饮酒和饮酒年限与肺癌发病之间无统计学关联(P0.05)。吸烟和饮酒相乘交互作用的OR值(95%CI)为0.90(0.47~1.70)。吸烟和饮酒相加交互作用的超额相对危险度(RERI)值及其95%CI为0.36(-0.92~1.64),交互作用归因比(AP)值及95%CI为0.09(-0.22~0.40),交互作用指数(SI)值及95%CI为1.13(0.71~1.80)。结论吸烟是肺癌发病的主要危险因素,且该风险随吸烟年限、吸烟量、吸烟深度的增加而显著增加,现有证据并不支持饮酒与肺癌发病之间存在关联,吸烟和饮酒在肺癌发病中也未见交互作用。     

中国非吸烟人群环境烟草烟雾暴露与肺癌发生关联的Meta分析

目的：采用Meta分析方法综合评价中国非吸烟人群环境烟草烟雾（ETS）暴露与肺癌发生危险的关系。方法以“肺癌/肺肿瘤”、“非吸烟”、“病例对照”、“危险因素”、“环境烟草烟雾/被动吸烟”、“lung cancer/lung neoplasm”、“non-smoking/non-smoker”、“China/Chinese”、“case-control/case control”、“risk factor”、“environmental tobacco smoke/passive smoking”为检索词,检索中国生物医学文献数据库、中国学术期刊全文数据库、万方知识服务平台、中国科技期刊全文数据库、PubMed和Web of Science数据库,系统收集1999年1月至2013年12月公开发表的有关中国非吸烟人群ETS暴露与肺癌发生关联的病例-对照研究,共检索到相关文献129篇。采用RevMan 5.2软件进行分析,计算合并OR（95%CI）值。结果最终纳入18篇文献,累计肺癌病例6145例,对照8132例。合并分析结果显示,中国非吸烟人群ETS暴露可增加肺癌发病的风险,合并OR（95%CI）值为1.52（1.42~1.64）;分层分析显示,ETS暴露与非吸烟女性及男性肺癌发生的关联均有统计学意义,合并OR（95%CI）值分别为1.58（1.42~1.75）和1.34（1.08~1.65）;来源于家庭及工作环境的ETS暴露均可增加患肺癌的风险,合并OR（95%CI）值分别为1.48（1.20~1.82）和1.38（1.13~1.69）;儿童期及成年期ETS暴露与肺癌发生的关联无统计学意义,合并OR（95%CI）值分别为1.37（0.98~1.91）和1.34（0.97~1.85）。结论 ETS暴露是中国非吸烟人群肺癌发病的重要危险因素。     

慢性肺部疾患与肺癌关系的病例对照研究

为了探讨慢性肺部疾患与肺癌的联系性,1991～1993年以医院为基础对249例新发原发性肺癌患者进行了1:1配对的病例对照研究.单因素分析结果表明:慢支、肺结核、肺气肿与肺癌发病有关,经用吸烟调整后的OR分别为5.39、4.74、3.65;Logistic回归模型拟合结果显示,肺癌与慢支和肺结核有关,回归系数分别为1.802和1.700.     

女性激素替代治疗、口服避孕药与女性肺癌关系的Meta分析

目的探讨女性激素替代治疗(HRT)与口服避孕药(OCs)对女性肺癌的影响。方法搜索Medline等计算机数据库,系统收集相关文献。采用固定模型或随机效应模型(研究结果存在异质性)计算合并OR。结果纳入Meta分析的文献共12篇,其中3篇为队列研究,9篇为病例对照研究。Meta分析HRT与肺癌合并OR值为0.88(95%CI:0.77～1.01)。按是否吸烟进行分层分析,吸烟者与非吸烟者中HRT的合并OR值分别为0.76(95%CI:0.61～0.95)和0.78(95%CI:0.64～0.95)。口服避孕药与女性肺癌无统计学关联(OR=0.95;95%CI:0.83～1.20)。结论HRT可能降低女性肺癌发生的危险度,其结果还需要进一步深入研究来验证。     

CYP1A1基因多态性与肺癌个体易感性研究

[目的 ]探讨CYP1A1Msp1和Ile/Val多态性单独或联合作用 ,对肺癌易感性的影响。 [方法 ]以病例一对照研究的方法 ,采用PCR扩增限制酶切法 (PCR -RFLP)和等位基因特异性扩增 (Allele SpecificAmplification ,ASA)检测 92例肺癌病人 (病例组 )和 98例非肿瘤病人 (对照组 )CYP1A1基因Msp1和Ile/Val基因型。 [结果 ]Msp1多态性位点 :具有B和C基因型者患肺癌的危险性是A基因型者的 1 85倍 (χ2 =4 3 6,P <0 0 5 ,OR =1 85 ,95 %CI 1 0 4～ 3 3 0 )。Ile/Val多态性位点 :Val/Val基因型者患肺癌的危险性是Ile/Ile基因型者的 3 3倍 (χ2 =4 12 ,P <0 0 5 ,OR =3 3 ,95 %CI 1 0 2～10 72 )。Ile/Val基因型联合B基因型、C基因型或Val/Val基因型联合C基因型与Ile/Ile基因型联合A基因型相比 ,患肺癌的危险性增加 ,其相对危险度分别为 3 0 9(χ2 =5 81,P <0 0 5 ,95 %CI 1 7～ 9 96) ;4 74(χ2 =4 74,P <0 0 5 ,95 %CI1 11～ 2 0 9) ;5 5 (χ2 =4 42 ,P <0 0 5 ,95 %CI 1 2 7～ 2 3 6)。 [结论 ]CYP1A1基因的B、C和Val/Val基因型可能是肺癌的易感基因型 ,两种易感基因型同时存在 ,更增加对肺癌的易感性     

Previous pulmonary diseases and risk of lung cancer in Gansu Province, China

BACKGROUND: Although active smoking is well established as the main cause of lung cancer, there is accumulating evidence that history of prior lung diseases may be an independent risk factor for lung cancer. METHODS: A population-based case-control study in Gansu Province, China identified 886 lung cancer cases (656 male, 230 female) diagnosed between January 1994 and April 1998. A standardized interview collected information on a variety of potential risk factors including a history of physician-diagnosed non-malignant lung diseases (pulmonary tuberculosis, chronic bronchitis/emphysema, asthma, pneumonia), age and year in which each condition was first diagnosed, and any therapy or hospitalization received. RESULTS: Pulmonary tuberculosis (odds ratio [OR] = 2.1, 95% CI : 1.4-3.1) and chronic bronchitis/emphysema (OR = 1.4, 95% CI : 1.1-1.8) were associated with increased risk of lung cancer, after adjustment for active smoking and socioeconomic status. The OR for asthma (OR = 1.4, 95% CI : 0.9-2.1) and pneumonia (OR = 1.5, 95% CI : 1.0-2.3) were also elevated. The risk of lung cancer remained significant for pulmonary tuberculosis and chronic bronchitis/emphysema when analysis was limited to the pathologically confirmed cases and self-responders. CONCLUSIONS: This study provides additional evidence that previous pulmonary tuberculosis and chronic bronchitis/emphysema are causally related to lung cancer, although the precise mechanism is still unclear. The results for asthma and pneumonia, while suggestive of a positive association, did not reach the traditional level of statistical significance and should be interpreted with caution.     

Preexisting lung disease and lung cancer among nonsmoking women.

Preexisting lung disease was examined as a risk factor for lung cancer in a population-based, case-control study of nonsmoking women in Missouri conducted between June 1, 1986, and April 1, 1991. A history of lung disease was reported by approximately 41% of 618 cases and 35% of 1,402 controls (odds ratio (OR) = 1.2; 95% confidence interval (Cl) 1.0-1.5. The risk was more pronounced when next-of-kin interviews were excluded (OR = 1.5). Previous lung disease was significantly related both to adenocarcinoma (OR = 1.4), which accounted for 62% of the cancers, and to all other cell types of lung cancer combined (OR = 1.8). Despite having discontinued smoking for more than 15 years, long-term ex-smokers were at a 2.2-fold risk of lung cancer compared with lifetime nonsmokers. Among lifetime nonsmokers, significant risks were noted for asthma (OR = 2.7) and pneumonia (OR = 1.5). Emphysema (OR = 2.6) and tuberculosis (OR = 2.0) were also significantly related to lung cancer, but only among former smokers. Chronic bronchitis was linked to elevated risks of nonadenocarcinomas only (OR = 2.3). Pleurisy was not reported more frequently by cases than by controls. Approximately 16% of all lung cancers among nonsmoking women could be attributed to previous lung diseases, most notably asthma, pneumonia, emphysema, and tuberculosis.     

Non-malignant respiratory diseases and lung cancer among Chinese workers exposed to silica

The objective of this study was to explore whether a medical history for non-malignant respiratory disease contributes to an increased lung cancer risk among workers exposed to silica. We analyzed data from a nested case-control study in 29 dusty workplaces in China. The study population consisted of 316 lung cancer cases and 1356 controls matched to cases by facility type and decade of birth who were alive at the time of diagnosis of the index case and who were identified in a follow-up study of about 68,000 workers. Age at first exposure and cigarette smoking were accounted for in the analysis. Smoking was the main risk factor for both lung cancer and chronic bronchitis. Lung cancer risk showed a modest association with silicosis and with cumulative silica exposure, which did not vary by history of previous pulmonary tuberculosis. Among subjects without a medical history for chronic bronchitis or asthma, lung cancer risk was associated with silicosis (odds ratio [OR], 1.6; 95% confidence interval [CI], 1.1 to 2.2), and it was increased in each quartile of cumulative silica exposure. However, risk was not elevated in the highest quartile (OR, 1.3, 1.6, 1.8, 1.4). Among subjects with a medical history for chronic bronchitis or asthma, lung cancer risk was associated with neither silicosis (subjects with chronic bronchitis: OR, 0.6; subjects with asthma: OR, 0.4) nor with silica exposure. In this study population, we observed a modest association of both silicosis and cumulative exposure to silica with lung cancer among subjects who were not previously diagnosed with chronic bronchitis or asthma, but not among subjects who had a medical history for either disease. Risk of lung cancer associated with silicosis or cumulative exposure to silica did not vary by previous medical history of pulmonary tuberculosis.     

Opposing effects of emphysema, hay fever, and select genetic variants on lung cancer risk

The authors compared histories of nonmalignant respiratory diseases (asthma, bronchitis, emphysema, hay fever, and pneumonia) in 1,553 lung cancer patients and 1,375 healthy controls enrolled in a Texas case-control study from 1995 to 2003. They incorporated data on two biologically relevant polymorphic genes, matrix metalloproteinase-1 and myeloperoxidase. Emphysema was associated with a statistically significant increased lung cancer risk (odds ratio (OR) = 2.87, 95% confidence interval (CI): 2.20, 3.76), while hay fever had a significant protective effect (OR = 0.58, 95% CI: 0.48, 0.70). Odds ratios were consistent after exclusion of respiratory disease diagnoses made up to 10 years before interview. There was little association between other respiratory diseases and lung cancer risk. Among carriers of "protective" genotypes, emphysema was associated with a 1.7-fold increased risk (95% CI: 0.84, 3.50), as compared with the substantially higher risk for persons possessing one (OR = 4.98, 95% CI: 2.94, 8.44) or two (OR = 4.23, 95% CI: 1.84, 9.73) "adverse" genotypes. For hay fever, significantly decreased risks were evident with one (OR = 0.32, 95% CI: 0.21, 0.50) or two (OR = 0.35, 95% CI: 0.19, 0.66) protective genotypes as compared with none (OR = 0.69, 95% CI: 0.30, 1.59). The biologic role of respiratory disease in lung cancer is unclear. Further study may yield new insights for identification of susceptible subgroups.     

Psychological distress and depressed mood in employees with asthma, chronic bronchitis or emphysema: A population-based observational study on prevalence and the relationship with smoking cigarettes

OBJECTIVES: To evaluate if employees with asthma, chronic bronchitis or emphysema can be characterized as a population of patients with a high prevalence of psychological distress and/or depressed mood. Above all, we wanted to examine the influence of smoking status on the relationship between chronic disease and psychological distress/depressed mood. METHODS: A postal survey was conducted among 12,103 employees participating in the Maastricht Cohort Study. RESULTS: Smoking employees, who reported having asthma, chronic bronchitis or emphysema were more likely to report suffering from depressed mood compared to smokers with no long-lasting disease (prevalence rate, PR: 29.3 and 9.0%, respectively; OR for depressed mood = 4.04; 95% CI: 2.56-6.39) and when compared to smoking employees with a history of heart disease, hypertension or myocardial infarction (PR: 18.1%; OR: 1.99; 95% CI: 1.07-3.68), or rheumatoid arthritis (PR: 20.1%; OR: 1.73; 95% CI: 0.96-3.11). CONCLUSION: These findings provide health care professionals with additional evidence regarding the importance for including the assessment of psychological distress and depressed mood in the routine evaluation of the patient with asthma, chronic bronchitis or emphysema, especially with regard to smoking cessation.     

Lung cancer in motor exhaust-related occupations

The association between employment in motor exhaust-related occupations and the risk for lung cancer was examined in 2,291 male cases of lung cancer and 2,570 controls in data pooled from three U.S. case control studies carried out by the National Cancer Institute between 1976 and 1983. Most analyses were limited to subjects providing direct, in-person interviews, including 1,444 cases and 1,893 controls. For those providing direct interviews and employed 10 years or more in motor exhaust-related (MER) occupations, the age, smoking, and study area adjusted odds ratio (OR) for lung cancer was 1.5 (95% CI = 1.2-1.9). Risk was elevated for truck drivers (OR = 1.5; 95% CI = 1.1-1.9) and for other MER occupations (OR = 1.4; 95% CI = 1.1-2.0). The odds ratios associated with MER employment of 10+ years were 1.6 (95% CI = 1.2-2.1) for whites and 1.4 (95% CI = 0.9-2.1) for nonwhites; 1.2 (95% CI = 0.7-2.0) [corrected] for those with possible exposure to other recognized or reported lung carcinogens; and 1.6 (95% CI 1.2-2.1) for those without such exposure. The 50% excess risk for lung cancer associated with employment in motor exhaust-related occupations could not be explained by greater use of cigarettes or by other occupational exposures among these workers.     

Pesticide use and chronic bronchitis among farmers in the Agricultural Health Study

BACKGROUND: Farmers have increased risk for chronic bronchitis. Few investigators have considered pesticides. METHODS: We evaluated pesticides as risk factors for chronic bronchitis using the Agricultural Health Study enrollment data on lifetime pesticide use and history of doctor-diagnosed chronic bronchitis from 20,908 private pesticide applicators, primarily farmers. RESULTS: A total of 654 farmers (3%) reported chronic bronchitis diagnosed after age 19. After adjustment for correlated pesticides as well as confounders, 11 pesticides were significantly associated with chronic bronchitis. Heptachlor use had the highest odds ratio (OR=1.50, 95% Confidence Interval (CI)=1.19, 1.89). Increased prevalence for chronic bronchitis was also seen for individuals who had a history of a high pesticide exposure event (OR=1.85, 95% CI=1.51, 2.25) and for those who also applied pesticides in off-farm jobs (OR=1.40, 95% CI=1.04, 1.88). Co-morbid asthma and current farm activities did not explain these results. CONCLUSIONS: These results provide preliminary evidence that pesticide use may increase chronic bronchitis prevalence.     

Risk factors for community-acquired pneumonia in German adults: the impact of children in the household

The objective of this case-control study was to identify the main risk factors for community-acquired pneumonia (CAP) in a German adult population. A self-administered questionnaire was given to CAP cases provided by the German competence network CAPNETZ and population-based, randomly selected controls (sex- and age-matched). Multivariate analysis showed that in addition to known risk factors such as previous CAP [odds ratio (OR) 1.6, 95% confidence interval (CI) 1.3-2.1], more than one respiratory infection during the previous year (OR 3.6, 95% CI 2.9-4.5), chronic pulmonary diseases (OR 2.3, 95% CI 1.7-3.0), number of comorbidities (OR 1.6, 95% CI 1.4-1.9), and number of children in the household (2 children: OR 2.2, 95% CI 1.5-3.4; > or = 3 children: OR 3.2, 95% CI 1.5-7.0) were independent risk factors for CAP. This was pronounced in particular in people aged < or = 65 years. The most likely explanation for this finding is higher exposure to infectious agents.     

鞍钢工人的肿瘤危险度——肺癌病例-对照研究

对鞍钢男工中６１０例肺癌新发病例及９５９例对照进行了访问调查。经吸烟、其他肺疾患、家族肿瘤史、食用水果等非职业因素调整后，岗位工龄等于或超过１５年的下列工人的肺癌危险度显著增高：冶炼工和轧钢工（ＱＲ＝１．５，９５％ＣＩ＝１．１～２．２），耐火砖厂工（ＯＲ＝２．９，９５％ＣＩ＝１．４～５．９），装卸工（ＯＲ＝２．５，９５％ＣＩ＝１．０～６．１），焦炉工（ＯＲ＝３．４，９５％ＣＩ＝１．４～８．５）。各种粉尘和Ｂ［ａ］Ｐ暴露与肺癌危险性呈显著的剂量－反应关系，但与粉尘的特殊成分未见此种关联。长期暴露于污染物的钢铁工人的肺癌的危险度增加４０％。