Effects of grain dust exposure and smoking on respiratory symptoms and lung function

In four groups of individually-matched subjects (nonsmoking grain workers, smoking grain workers, nonsmoking community controls, and smoking community controls) we measured pulmonary function variables from the spirogram, from the maximal expiratory flow-volume curve breathing air and helium, and from the single breath nitrogen test as well as symptom prevalences from a questionnaire in order to assess the relative effects of smoking and occupational exposure to grain dust in Saskatchewan country grain elevators. There were similar increased prevalences of respiratory symptoms and reductions in pulmonary function associated with either grain dust exposure or smoking, but the effects of smoking were slightly more pronounced. The combined effects of grain dust and smoking on lung function appeared to be additive except in the least exposed workers (five years or less) where a synergistic effect was observed in tests of peripheral airways dysfunction.     

Passive smoking and canine lung cancer risk.

A case-control study was conducted to determine whether household exposure to environmental tobacco smoke is associated with an increased risk for lung cancer in pet dogs. Lung cancer cases and controls with other forms of cancer were obtained from two veterinary teaching hospitals during 1985-1987. Exposures assessed included the number of smokers in the household, the amount smoked, and the proportion of time spent indoors by the pet. A weak relation was found for exposure to a smoker in the home (odds ratio = 1.6, 95% confidence interval 0.7-3.7), after controlling for confounding in stratified analyses. Strong evidence for a further increase in risk associated with more than one smoker in the home was not found, nor was a significant trend observed for increasing number of packs of cigarettes smoked per day or an exposure index based on number of smokers in each household, packs smoked per day, and the proportion of time the dog spent within the home. However, skull shape appeared to exert effect modification; the risk was restricted to breeds with short and medium length noses (odds ratio = 2.4, 95% confidence interval 0.7-7.8). Despite the inconclusive findings of the current study, epidemiologic studies in pet animals may add to our understanding of environmental tobacco smoke effects in human populations.     

吸烟、被动吸烟与肺癌发病风险的病例对照研究

目的 探讨吸烟、被动吸烟与肺癌的关联.方法 采用病例对照研究设计,面访肺癌新发病例1 303例和按性别、年龄(±2岁)频数匹配的健康对照1 303例.结果 吸烟是男性肺癌的重要危险因素(调整OR=4.974,95％ CI:3.933 ～6.291),随着开始吸烟年龄提前、吸烟年限延长、日吸烟量、吸烟包年以及吸烟深度的增加,患肺癌危险性增高,呈剂量反应关系(Ptrend＜0.001),戒烟≥10年患肺癌的危险性降低45.4％.男性吸烟患肺鳞癌的危险性比患肺腺癌大.被动吸烟是非吸烟者肺癌的危险因素(调整OR=1.912,95％CI:1.486～2.460),工作环境被动吸烟的男性非吸烟者患肺癌的调整OR为2.221(95％CI:1.361 ～3.625),家庭环境被动吸烟的女性非吸烟者患肺癌的调整OR为1.804(95％ CI:1.270～2.562).68.04％男性肺癌的发生可归因于吸烟,26.51％非吸烟者肺癌的发生可归因于被动吸烟.结论 吸烟是肺癌的重要危险因素,工作环境被动吸烟是男性非吸烟者肺癌的主要危险因素,家庭环境被动吸烟是女性肺癌的主要危险因素.戒烟具有重大的公共卫生学意义.     

Occupation and smoking as risk determinants of lung cancer

The standardized incidence ratio (SIR) of lung cancer was determined for different occupational groups in Finland. The data on all cases of lung cancer diagnosed in Finland in age groups of 35-69 years in 1971-1975 were supplemented by information on occupation from the 1970 census (Central Statistical Office). The expected numbers of cases were based on the sex, age and occupation-specific numbers of person-years computed in the Central Statistical Office, and sex- and age-specific incidence rates of lung cancer among the economically active population (as defined 1 January 1971). Compared with the risk of the total economically active population, the relative risk of those not active (SIR) was 1.69 for men and 0.86 for women. Lower than expected relative risks were encountered among highly educated and white-collar male workers (religious, legal, pedagogical, medical, technical and administrative work), in sales work, transport service work and among farmers. High SIRs were found in mining and quarrying, forestry, woodworking (joiners), construction, painting and among unskilled workers. Among women the numbers of cases were small and only one significant SIR was obtained; the risk was lower than expected in farming. Data on the smoking habits of males in different main occupational categories in Finland show that variation between different occupational groups in the prevalence of smoking closely corresponds to that in the SIR for lung cancer (R = 0.96).     

Attributed risk to smoking for lung cancer,laryngeal cancer and esophageal cancer

OBJECTIVE: Lung, laryngeal and esophageal cancers have smoking as one of their main risk factors. The objective of this study was to evaluate the population attributed risk (PAR) of smoking for these forms of cancer. METHODS: The study was based in three case-control studies conducted in medium size cities in Brazil. Incident cases of lung cancer, laryngeal cancer and esophageal cancer seen at a hospital setting and diagnosed through biopsy were analyzed; controls were hospitalized patients with another diagnoses. Smoking was the exposure factor measured at three levels: non-smokers, former smokers and smokers, which were defined using a questionnaire applied by trained interviewers. For effect measure, odds ratio was used and the populational attributed risk for smoking was then calculated for a 95% CI. RESULTS: A total of 122 lung cancer cases and 244 controls, 50 cases of laryngeal cancer and 48 cases of esophageal cancer, and 96 controls for both of them were studied. The prevalence of smoking exposure was 34%, which is the overall prevalence of smoking in this city's adult population. Odds ratios (OR) for the PAR analysis were the adjusted OR for confounding variables from each study. Lung cancer PAR was 63% (95% IC, 0.58-0.68) for former smokers and 71% (95%IC, 0.65-0.77) for smokers. Larynx cancer PAR was 74% (95% IC, 0.70-0.78) and 86% (95%IC, 0.81-0.85) for former smokers and smokers, respectively. Esophageal cancer PAR was 54% (95%IC, 0.46-0.62) for smokers. CONCLUSION: Smoking is an avoidable risk factor and smoking cessation could be responsible for significant reductions in the incidence of these three forms of cancer.     

Examining the joint effect of multiple risk factors using exposure risk profiles: lung cancer in nonsmokers

Background

Profile regression is a Bayesian statistical approach designed for investigating the joint effect of multiple risk factors. It reduces dimensionality by using as its main unit of inference the exposure profiles of the subjects that is, the sequence of covariate values that correspond to each subject.

Objectives

We applied profile regression to a case–control study of lung cancer in nonsmokers, nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, to estimate the combined effect of environmental carcinogens and to explore possible gene–environment interactions.

Methods

We tailored and extended the profile regression approach to the analysis of case–control studies, allowing for the analysis of ordinal data and the computation of posterior odds ratios. We compared and contrasted our results with those obtained using standard logistic regression and classification tree methods, including multifactor dimensionality reduction.

Results

Profile regression strengthened previous observations in other study populations on the role of air pollutants, particularly particulate matter ≤ 10 μm in aerodynamic diameter (PM₁₀), in lung cancer for nonsmokers. Covariates including living on a main road, exposure to PM₁₀ and nitrogen dioxide, and carrying out manual work characterized high-risk subject profiles. Such combinations of risk factors were consistent with a priori expectations. In contrast, other methods gave less interpretable results.

Conclusions

We conclude that profile regression is a powerful tool for identifying risk profiles that express the joint effect of etiologically relevant variables in multifactorial diseases.     

Silicosis and smoking strongly increase lung cancer risk in silica-exposed workers

It remains controversial whether silica is a human lung carcinogen. In this study, we estimated the relative risks of lung cancer due to silica and silicosis by meta-analysis. We collected papers published from 1966-2001 which epidemiologically reported on the relationship between silica/silicosis and lung cancer. We removed papers which did not exclude the effects of asbestos and radioactive materials including radon. We selected the most recent one if some papers were based on the same cohort. Based on the selected papers, we summarized the lung cancer risks from silica, silicosis and non-silicosis with exposure to silica, by meta-analysis using a random effects model. The pooled relative risks were 1.32 (95% confidence interval (CI), 1.23-1.41) for silica, 2.37 (95% CI, 1.98-2.84) for silicosis and 0.96 (95% CI, 0.81-1.15) for non-silicosis with exposure to silica. Since some papers on silica did not exclude silicosis, the risk due to silica itself may be smaller than 1.32. It was less possible that silica exposure directly increases lung cancer risk. On the other hand, the relative risk, 2.37 for silicosis suggested that silicosis increases lung cancer risk. Meta-analysis also revealed that cigarette smoking strongly increased the lung cancer risk in silicotic patients (relative risk, 4.47; 95% CI, 3.17-6.30). Thus, the present study suggested the great importance of preventing silicosis and smoking cessation in reducing lung cancer incidence in silica-exposed workers.     

吸烟对慢性阻塞性肺疾病及呼吸道症状的影响

  目的   探讨吸烟对慢性阻塞性肺疾病(chronic obstructive pulmonary disease, COPD)及呼吸道症状的影响。   方法   利用多阶段分层整群随机抽样的方法在安徽5个COPD监测点抽取≥40岁调查对象, 并对其进行问卷调查、身体测量和肺功能检测。利用复杂抽样Logistic回归分析模型分析吸烟对COPD及呼吸道症状的影响。   结果   ≥30包年的吸烟者在总人群中占13.9%(95% CI:10.3%~17.5%, P < 0.001), ≥40年的吸烟者在总人群中占8.5%(95% CI:6.7%~10.3%, P < 0.001)。吸烟者平均吸烟年数为32.4 (95% CI:31.2~33.5)年, 吸烟者日均吸烟量为21.1 (95% CI:19.6~22.7)支/天。调整混杂因素后, COPD和呼吸道症状的患病风险均随吸烟包年和吸烟年数的增加而呈上升趋势(均有P_trend < 0.001)。   结论   吸烟增加COPD及呼吸道症状的患病风险, 吸烟包年和吸烟年数越多, 慢阻肺和呼吸道症状的患病风险越大。     

Design issues in studies of radon and lung cancer: implications of the joint effect of smoking and radon.

Many case-control studies have been undertaken to assess whether and to what extent residential radon exposure is a risk factor for lung cancer. Nearly all these studies have been conducted in populations including smokers and nonsmokers. In this paper, we show that, depending on the nature of the joint effect of radon and tobacco on lung cancer risk, it may be very difficult to detect a main effect due to radon in mixed smoking and nonsmoking populations. If the joint effect is closer to additive than multiplicative, the most cost-effective way to achieve adequate statistical power may be to conduct a study among never-smokers. Because the underlying joint effect is unknown, and because many studies have been carried out among mixed smoker and nonsmoker populations, it would be desirable to conduct some studies with adequate power among never-smokers only.     

Involuntary smoking and lung cancer

Involuntary smoking contains human carcinogens. Exposure prevalence among adults is on the order of 40%. A meta-analysis of epidemiologic studies on lung cancer and exposure to involuntary smoking from the spouse included 51 studies. The overall relative risk (RR), based on 7369 cases of lung cancer, was 1.25 [95% confidence interval (95% CI) 1.15-1.37]. No evidence existed of an RR difference between the two genders, and study design had no influence on the results. The summary RR was lower for adenocarcinoma than for other histological types. In the largest studies cumulative exposure suggested a dose-response relationship with a unit risk of similar magnitude. The summary RR was 1.17 (95% CI 1.04-1.32) for workplace exposure. Several sources of bias may lead to both overestimation and underestimation of true association, and the most plausible interpretation favors a causal association. Even if excess risk from exposure to involuntary smoking is small, its large prevalence makes it an important environmental carcinogen.     

Additive effect of smoking and cotton dust exposure on respiratory symptoms and pulmonary function of cotton textile workers

One hundred and sixty-nine and 175 cotton textile workers (CTWs) were enrolled in the first (1991) and second (1996) surveys to investigate the prevalence of byssinosis. The synergistic effect of smoking on cotton dust exposure was also evaluated. Although the difference in prevalence of abnormal pulmonary function between the first (38.5%) and second study (38.9%) was not statistically significant, smokers had significantly higher frequency than nonsmokers in both surveys. A significant trend existed between the cotton dust levels and the frequency of abnormal lung function. The significant trend was also noted in both smokers and nonsmokers. The frequency of respiratory symptoms and the prevalence of severe byssinosis in the second survey (14.9% and 12.6%, respectively) were significantly lower than that in the first survey (39.7% and 21.9%, respectively). The reduction of symptoms was due to remodeling of this old cotton mill. The prevalences of respiratory symptoms and byssinosis in smokers being significantly higher than in nonsmokers only found in the first survey, but not found in the second survey. These results indicate that smoking potentiates the effect of cotton dust exposure on respiratory symptoms and byssinosis. The second study reveals high prevalence of byssinosis still existed in Taiwanese cotton mill, although the prevalence was declining. Smoking was found to show an additive effect on cotton dust exposure. Anti-smoking campaign, occupational health program to reduce the dust exposure, and periodical medical examination are measures to prevent from byssinosis.     

The effect of domestic factors on respiratory symptoms and FEV1

This study was conducted to determine whether indoor air pollution factors affected respiratory function and symptoms in 1357 non-smoking Caucasian children. Interviews were conducted to determine: exposure to pets and to gases, vapours and dusts from hobbies; the use of gas stoves; fireplaces, air conditioners and humidifiers; type of heating systems; and the number of residents, and the number of smokers in the home. The forced expiratory volume in one second (FEV1) was obtained from maximum expiratory flow volume curves, and symptoms from the application of a standardized questionnaire. Indoor pets and the use of fireplaces and humidifiers had no consistent relationships with FEV1 when considered individually or in combination with the other factors. Hobbies, the use of gas stoves, the absence of air conditioning, the use of hot water heating, crowded homes, and the presence of smokers in the home all had negative relationships with FEV1. The largest effect on lung function was observed in children from homes with hot water heating systems, whereas the smallest effect was observed in children with smokers in the home. Children who lived in homes with hot water heating systems with no air conditioning had mean FEV1 of up to 0.4 litres lower than did their counterparts who lived in homes with forced air heating and air conditioning. Pets, heating systems, cooking fuel, crowding and passive smoking showed no consistent effects on the reporting of any of the symptoms. Girls who were exposed to the emissions from indoor hobbies reported more phlegm, wheeze and dyspnoea.     

吸烟和健康饮食评分在文化程度与肺癌发病风险关联中的中介效应研究

目的 探讨吸烟和健康饮食评分在文化程度与肺癌发病风险关联中的中介效应。方法 基于英国生物银行（UKB）前瞻性队列研究数据,剔除文化程度信息缺失及基线患有癌症的个体后,最终纳入446 772名研究对象。采用Cox比例风险回归模型估计文化程度与肺癌发病风险的关联以及吸烟和健康饮食评分与肺癌发病的关联,采用中介效应模型分析吸烟和健康饮食评分在文化程度和肺癌风险关联中的中介效应。结果 在7.13年的中位随访时间内,新发肺癌1 994例。受教育年数每增加一个标准差（5年）,肺癌风险降低12%（HR=0.88,95%CI：0.84~0.92）。根据UKB自我报告的最高学历转换为国际教育代码分类标准（ISCED）中对应的1~5级,级数越大代表文化程度越高。与ISCED-1者相比,ISCED-2、ISCED-3、ISCED-4和ISCED-5人群的肺癌发病HR值（95%CI）依次为0.83（0.72~0.94）、0.67（0.53~0.85）、0.76（0.65~0.89）和0.72（0.64~0.80）。文化程度与吸烟呈负相关（β=-0.079,95%CI：-0.081~-0.077）,与健康饮食评分呈正相关（β=0.042,95%CI：0.039~0.045）。中介效应分析显示,吸烟与健康饮食评分在文化程度与肺癌的关联中存在中介效应,中介比例分别为38.952%（95%CI：31.802%~51.659%）和1.784%（95%CI：0.405%~3.713%）。结论 吸烟和健康饮食评分可能介导文化程度对肺癌发病的影响,这表明提高文化程度可能通过改变吸烟和饮食等生活方式降低肺癌发病风险。     

The risk of lung cancer with increasing time since ceasing exposure to asbestos and quitting smoking

Objectives

To examine if the risk of lung cancer declines with increasing time since ceasing exposure to asbestos and quitting smoking, and to determine the relative asbestos effect between non‐smokers and current smokers.

Methods

A cohort study of 2935 former workers of the crocidolite mine and mill at Wittenoom, who responded to a questionnaire on smoking first issued in 1979 and on whom quantitative estimates of asbestos exposure are known. Conditional logistic regression was used to relate asbestos exposure, smoking category, and risk of lung cancer.

Results

Eighteen per cent of the cohort reported never smoking; 66% of cases and 50% of non‐cases were current smokers. Past smokers who ceased smoking within six years of the survey (OR = 22.1, 95% CI 5.6 to 87.0), those who ceased smoking 20 or more years before the survey (OR = 1.9, 95% CI 0.50 to 7.2), and current smokers (<20 cigarettes per day (OR = 6.8, 95% CI 2.0 to 22.7) or >20 cigarettes per day (OR = 13.2, 95% CI 4.1 to 42.5)) had higher risks of lung cancer compared to never smokers after adjusting for asbestos exposure and age. The asbestos effect between non‐smokers and current smokers was 1.23 (95% CI 0.35 to 4.32).

Conclusion

Persons exposed to asbestos and tobacco but who subsequently quit, remain at an increased risk for lung cancer up to 20 years after smoking cessation, compared to never smokers. Although the relative risk of lung cancer appears higher in never and ex‐smokers than in current smokers, those who both smoke and have been exposed to asbestos have the highest risk; this study emphasises the importance of smoking prevention and smoking cessation programmes within this high risk cohort.     

The interaction of asbestos and smoking in lung cancer: a modified measure of effect

OBJECTIVES: The ratio of the relative risk of lung cancer due to asbestos exposure in non-smokers to that in smokers has been termed the relative asbestos effect (RAE). In a review, Liddell [Liddell FDK (2001) Ann Occup Hyg; 45: 341-56] estimated that the RAE was approximately 2. This measure is satisfactory when there is an appreciable relative risk due to asbestos but does not generalize to lower levels of exposure. A modified measure is proposed to overcome this difficulty. The modified measure, RAEm, is defined as the ratio of the excess relative risk (RR - 1) in non-smokers to that in smokers. METHODS: The cohort studies combined in Liddell's 2001 analysis have been used to give a combined estimate of the modified measure. RESULTS: The combined value of RAEm is 3.19 with 95% confidence interval 1.67-6.13. CONCLUSION: The excess relative risk of lung cancer from asbestos exposure is about three times higher in non-smokers than in smokers. The modified measure has been placed within a more versatile model of interaction. If interaction is present the relative risk from asbestos exposure changes only slightly between light and heavy smokers, but is higher in very light smokers and non-smokers. The relative risk estimated from epidemiological studies of a mixed population of non-smokers and smokers applies to smokers.