Smoking and lung cancer in Harbin, northeast China.

BACKGROUND: We studied the relationship between smoking and lung cancer risk in Harbin, Heilongjiang province, northeast China, an area with a very high baseline risk of lung cancer in both sexes, using data from a case-control study of lung cancer conducted between 1987 and 1990. PATIENTS AND METHODS: Cases were 218 patients with incident, histologically confirmed lung cancer and controls were 436 patients admitted to the same hospital with non-neoplastic and non-lung diseases. RESULTS: Compared with never-smokers, the multivariate odds ratio (OR) for current smokers was 3.47 [95% confidence interval (CI) 2.31--5.20], and for ex-smokers 1.53 (95% CI 0.81--2.87). Lung cancer risk increased by 20% (95% CI 14% to 28%) for an increment of 5 years in smoking duration, and by 29% (95% CI 15% to 45%) for an increment of five cigarettes per day. The OR for smokers reporting occupational exposure to selected known or likely lung carcinogens was 7.22, compared with non-smokers without occupational exposure. CONCLUSIONS: This study further confirms that cigarette smoking is a strong determinant of lung cancer also in this high-risk area of northeast China.     

Occupational Exposure to Vinyl Chloride, Acrylonitrile and Styrene and Lung Cancer Risk (Europe)

Several industry-based cohort studies have addressed the risk of lung cancer following exposure to vinyl chloride, acrylonitrile and styrene, with inconsistent results and usually without smoking adjustment. These exposures are addressed here in a large case-control study with full adjustment for smoking. Almost 6000 subjects were included in a case-control study conducted in seven European countries. For each job they held, local experts assessed the exposure to a number of occupational agents, including vinyl chloride, acrylonitrile and styrene, on the basis of detailed occupational questionnaires. Information on tobacco consumption and other risk factors was also collected. The odds ratio (OR) for ever exposure to vinyl chloride was 1.05 (95% confidence interval, CI: 0.68-1.62) and a modest, non-significant increase in the risk of lung cancer was found in the highest exposed subgroup. The OR for ever exposure to acrylonitrile was 2.20 (95% CI: 1.11-4.36) with a positive dose-response relationship between estimated cumulative exposure and lung cancer risk. No association between exposure to styrene and lung cancer risk was found. In conclusion, we cannot exclude a weak association between occupational exposure to vinyl chloride and lung cancer risk. Exposure to acrylonitrile was associated in our study with risk of lung cancer. Exposure to styrene does not seem to increase lung cancer risk.     

Lung cancer and occupation in New Mexico

The association between occupation and lung cancer risk was examined in a population-based, case-control study of 506 patients (333 males and 173 females) and 771 control (499 males and 272 females) subjects in New Mexico. A personal interview was used to obtain lifetime occupational and smoking histories and self-reported history of exposures to specific agents. High-risk jobs were identified in advance of data analysis and linked with industrial and occupational codes for hypothesis testing. For females, lung cancer risk was not associated with employment history, but power was limited. For males, elevated risks were found for the uranium mining industry [odds ratio (OR) = 1.9; 95% confidence internal (CI) = 0.8-4.9], underground miners (OR = 2.1; 95% CI = 1.1-3.7), painters (OR = 2.7; 95% CI = 0.8-8.9), and welders (OR = 3.2; 95% CI = 1.4-7.4). For self-reported exposure to any of 18 agents, only the OR for exposure to "other metals" was elevated. The population attributable risk in males was estimated as 14% for employment in any high-risk industry or occupation with an OR above 1 in this study.     

Lung cancer risk and occupational exposure to meat and live animals

An increased risk of lung cancer has been reported for butchers and meat workers in several cohort studies, although confounding from tobacco smoking could not be ruled out in any of these studies. These exposures, as well as a potential risk associated with contact with live animals, are addressed here in a large case-control study with full adjustment for smoking. More than 5,900 subjects were included in a case-control study conducted in 7 European countries. For each job they employed local experts who assessed the exposure to a number of occupational agents, including (i) meat aerosols and (ii) live animals, on the basis of detailed occupational questionnaires. Information on tobacco consumption and other risk factors was also collected. A small increased risk of lung cancer was observed with exposure to meat aerosols, after adjusting for smoking, (odds ratio (OR)=1.27, 95% confidence interval (CI): 0.92, 1.75), which was most apparent for the upper tertile of cumulative exposure (OR=1.73, 95% CI: 1.03, 2.92). A similar overall effect was observed for exposure to live animals, with an increased risk observed for a high frequency of exposure, (OR=1.69, 95% CI: 1.21, 2.36) and a high intensity of exposure, (OR=1.85, 95% CI: 1.16, 2.94), with significant trends for increasing frequency (p=0.012), intensity (p=0.015) and cumulative exposure (p=0.024). In conclusion, this study provides evidence for an association between exposure to meat aerosols and lung cancer apparent in the highest tertile of exposure. The authors identified a more consistent association with exposure to live animals.     

Heating fuels and respiratory diseases in the risks of female lung cancer]

Recently, lung cancer has become the first cause of death in women of Harbin. Although 90% of this cancer in man could be attributed to smoking, the etiological factors for women lung cancer still remain obscure. A case-control study consisting of 418 female lung cancer patients and 398 controls was conducted from 1985-1987. The purpose of this study was to evaluate the relevancy of heating fuels and respiratory diseases in the development of lung cancer in women. After having adjusted for smoking, soft coal (OR = 2.26, 95% CI 1.53-3.33) and brazier (OR = 1.36, 95% CI 1.01-1.83) were found to increase the risk of female lung cancer. There was an obvious time-effect in the use of soft coal in relation to female lung cancer (TRND mean = 14.49, P less than 0.001). As to the past history of respiratory diseases, both pulmonary tuberculosis (OR = 1.81) and pulmonary emphysema (OR = 2.29) increased the risk of female lung cancer.     

Risk factors associated with lung cancer in Hong Kong

The purpose of this study was to investigate the risk factors associated with lung cancer in Hong Kong. Three hundred and thirty-one histologically or cytologically proven consecutive cases of lung cancer and the same number of in- and out-patients without cancer matched for age and sex were recruited for this study using a detailed questionnaire completed by a trained interviewer. Smoking was the most important risk factor associated with lung cancer but the attributable risk (AR) was estimated to be 45.8% in men and 6.2% in women, considerably lower compared with those estimated in early 1980s. In addition, among women, exposure to environmental tobacco smoke (ETS) at work+/-at home and lack of education, were independent risk factors for lung cancer with adjusted odds ratio (OR) 3.60, (95% confidence interval (CI) 1.52-8.51) and OR 2.41 (95% CI 1.27-4.55), respectively. Among men, exposure to insecticide/pesticide/herbicide, ETS exposure at work or at home, and a family history of lung cancer and were independent risk factors with adjusted OR 3.29 (95% CI 1.22-8.9, OR 2.43, 95% CI 1.24-4.76 and OR 2.37, 95% CI 1.43-3.94, respectively). Exposure to incense burning and frying pan fumes were not significant risk factors in both sexes. A moderate or high consumption of fat in the diet was associated with increased risk in men but decreased risk in women. The results of this study suggested that as the prevalence of smoking declined, the influence of smoking as a risk factor for lung cancer decreased even further. Moreover, the contribution of other environmental, occupational and socioeconomic factors may be more apparent as etiological factors for lung cancer in a population with relatively high lung cancer incidence but low AR from active smoking.     

Decreased risk of lung cancer in the cotton textile industry of Shanghai

The relationship between lung cancer risk and work in the cotton textile industry was investigated in a large population-based case-control study in urban Shanghai, where the industry is a major employer of men and women. Personal interviews obtained occupational, smoking, and other information from 1405 newly diagnosed lung cancer cases and 1495 controls. A significantly low risk of lung cancer was associated with cotton textile employment [odds ratio (OR) = 0.7,95% confidence interval (CI) = 0.6-0.9]. In men, the decreased risk was observed among both smokers (OR = 0.7, 95% CI = 0.5-1.1) and nonsmokers (OR = 0.3, 95% CI = 0.1-1.0). In women, the risk was also decreased regardless of smoking status (OR = 0.8, 95% CI = 0.4-1.6 among smokers; OR = 0.9, 95% CI = 0.6-1.2 among nonsmokers). In both sexes, the reductions in risk tended to be greater for lung cancer cell types other than adenocarcinoma. Low risks were found regardless of occupations within the cotton textile industry; the OR for workers in textile processing who potentially had greater dust exposure was 0.8 (95% CI = 0.6-1.2), whereas the OR for those in other industry jobs was 0.7 (95% CI = 0.4-1.0). There was little difference in risk according to self-reported exposure to textile dust, and no clear trend with duration of employment or dust exposure. Reasons for the reduced risk of lung cancer in cotton textile workers without a dose response are unclear, although several methodological explanations were considered. The findings, however, appear consistent with prior epidemiological studies and are interesting in light of speculation about tumor-inhibitory factors, such as bacterial endotoxins, that are found in dusts from cotton and other fiber crops.     

Risk factors for lung cancer in Iowa women: implications for prevention

BACKGROUND: Multiple risk factors possibly associated with lung cancer were examined as part of a large-scale residential radon case-control study conducted in Iowa between 1994 and 1997. We were particularly interested in stratifying risk factors by smoking status. Relatively little risk factor information is available for Midwestern rural women. METHODS: Four hundred thirteen female lung cancer cases and 614 controls aged 40-84, who were residents of their current home for at least 20 years, were included. Risk factors examined included cigarette smoking, passive smoking, occupation, chemical exposure, previous lung disease, family history of cancer, and urban residence. Multiple logistic regression analysis was conducted after adjusting for age, education, and cumulative radon exposure. RESULTS: As expected, active cigarette smoking was the major risk factor for lung cancer. While cessation of smoking was significantly associated with a reduced risk for lung cancer, the risk remained significantly elevated for 25 years. Among all cases, asbestos exposure was a significant risk. Among ex-smokers, pack-year history predominated as the major risk. Among never smokers, a family history of kidney or bladder cancer were significant risk factors (OR=7.34, 95% CI=1.91-28.18; and OR=5.02, 95% CI=1.64-15.39, respectively), as was a history of previous lung disease (OR=2.28, 95% CI=1.24-4.18) and asbestos exposure. No statistically significant increase in lung cancer risk was found for occupation or urban residence. CONCLUSIONS: Smoking prevention activities are urgently needed in rural areas of the United States. Relatives of individuals with smoking-related cancers are potentially at increased risk. Genetic risk factors should be more fully investigated in never smokers.     

Polymorphisms in the DNA repair genes XRCC1 and ERCC2, smoking, and lung cancer risk.

XRCC1 (X-ray cross-complementing group 1) and ERCC2 (excision repair cross-complementing group 2) are two major DNA repair proteins. Polymorphisms of these two genes have been associated with altered DNA repair capacity and cancer risk. We have described statistically significant interactions between the ERCC2 polymorphisms (Asp312Asn and Lys751Gln) and smoking in lung cancer risk. In this case-control study of 1091 Caucasian lung cancer patients and 1240 controls, we explored the gene-environment interactions between the XRCC1 Arg399Gln polymorphism, alone or in combination with the two ERCC2 polymorphisms, and cumulative smoking exposure in the development of lung cancer. The results were analyzed using logistic regression models, adjusting for relevant covariates. Overall, the adjusted odds ratio (OR) of XRCC1 Arg399Gln polymorphism (Gln/Gln versus Arg/Arg) was 1.3 [95% confidence interval (CI), 1.0-1.8]. Stratified analyses revealed that the ORs decreased as pack-years increased. For nonsmokers, the adjusted OR was 2.4 (95% CI, 1.2-5.0), whereas for heavy smokers (>/=55 pack-years), the OR decreased to 0.5 (95% CI, 0.3-1.0). When the three polymorphisms were evaluated together, the adjusted ORs of the extreme genotype combinations of variant alleles (individuals with 5 or 6 variant alleles) versus wild genotype (individuals with 0 variant alleles) were 5.2 (95% CI, 1.7-16.6) for nonsmokers and 0.3 (95% CI, 0.1-0.8) for heavy smokers, respectively. Similar gene-smoking interaction associations were found when pack-years of smoking (or smoking duration and smoking intensity) was fitted as a continuous variable. In conclusion, cumulative cigarette smoking plays an important role in altering the direction and magnitude of the associations between the XRCC1 and ERCC2 polymorphisms and lung cancer risk.     

Associations between cigarette smoking and the risk of four leading cancers in Miyagi Prefecture, Japan: a multi-site case-control study

Although cigarette smoking is a well-known risk factor of lung cancer, associations of cigarette smoking with the risk of other sites have not been fully elucidated in Japan. To simultaneously evaluate the associations of cigarette smoking with the risks of cancers of the stomach, lung, colon, and rectum, which have been the leading cancer sites in recent years in Miyagi Prefecture, Japan, we conducted a hospital-based case-control study. Study subjects consisted of 614 stomach, 515 lung, 324 colon, and 164 rectal cancer cases and 2444 hospital controls admitted to a single hospital in Miyagi Prefecture from 1997 to 2001. Information on smoking habit and other lifestyle factors was collected using a self-administered questionnaire. Distributions of referral base among cases and controls were also investigated. For each site, odds ratios (ORs) and 95% confidence intervals (95% CIs) for smoking habit were estimated with adjustment for age, year of survey, history of alcohol drinking, family history of index cancer, and occupational history, respectively, using an unconditional logistic regression model. Cigarette smoking (ever vs. never) was associated with an increased risk of stomach (OR = 1.62; 95% CI 1.20-2.19) and lung (OR = 3.82; 95% CI 2.49-5.86) cancer among males and lung cancer among females (OR = 2.02; 95% CI 1.28-3.18). For female stomach cancer, the association with cigarette smoking was uncertain (OR = 0.65, P = 0.1533). For rectal cancer, a significant increased risk was observed in both-sex-combined analysis. There was no association between cigarette smoking and the risk of colon cancer. Detailed analysis showed that the association of cigarette smoking with cancer risk might be modified by the patient referral pattern, i.e., screened or not screened. The present results indicate that the association of cigarette smoking with cancer risk may differ among sites and sexes. In terms of the population attributable risk, a large proportion of leading cancers in males appears to be related to cigarette smoking.     

Case-control study of oropharyngeal cancer

BACKGROUND: In order to test some hypotheses of risk factors for oropharyngeal cancer (neoplasm of base of tongue, palate and tonsils) matched case-control study was conducted in Belgrade, Serbia and Montenegro, during the period 1998-2000. METHODS: Study comprised 100 incidence cases with oropharyngeal cancer and 100 controls with some non-malignant diseases of head and neck. RESULTS: According to multivariate analysis, ever smoking, interaction between smoking and alcohol consumption, and occupational exposure to wood dust were found to be independent risk factors for oropharyngeal cancer (odds ratio-OR=5.10 95% confidence intervals-95% CI=1.70-15.27, OR=2.61 95% CI=1.54-4.41, and OR=4.16 95% CI=1.45-11.91, respectively). CONCLUSION: The results of the present study are in line with other authors' findings showing that smoking and alcohol consumption are the main risk factors for oropharyngeal cancer. The effect of occupational exposure to wood dust warrants further investigation.     

控烟是预防肺癌的主要措施——记太原市肺癌病例对照流行病学调查

背景 与目的:山西省太原市空气污染常较为严重.了解各种类型肺癌的危险因素,以采取有效的预防措施.方法:2005年3月—2007年9月,山西省太原市396例肺癌新发病例和465名健康对照者纳入本研究.利用太原市肿瘤医院病理学检查确诊的肺癌病例,配以人群为基础、随机选择的对照,进行病例对照询问调查和环境监测.分析时注意排除...     

Cigar and pipe smoking and lung cancer risk: a multicenter study from Europe

BACKGROUND: Because limited information is available on the quantitative association between consumption of tobacco products other than cigarettes and lung cancer risk, we undertook a case-control study of this relationship. METHODS: We investigated lung cancer risk among smokers of cigars and/or cigarillos only and of pipes only and compared these risks with the risk of smokers of cigarettes only in a case-control study conducted in seven European areas. Our study population consisted of 5621 male case patients with lung cancer and 7255 male control subjects. Each subject or his proxy was interviewed with respect to the subject's smoking history and other risk factors for lung cancer. RESULTS: The odds ratio (OR) for smoking cigars and cigarillos only was 9.0 (95% confidence interval [CI] = 5.8-14.1), based on 43 exposed case patients and 77 exposed control subjects, and the OR for smoking a pipe only was 7.9 (95% CI = 5.3-11.8), representing 61 case patients and 129 control subjects. The OR for smoking cigarettes only was 14.9 (95% CI = 12.3-18.1), based on 4204 case patients and 3930 control subjects. A dose-response relationship was present for duration of use and cumulative consumption both for cigars and cigarillos and for pipe tobacco. An effect was also suggested for inhalation of cigar and cigarillo smoke. The dose-response relationships between lung cancer risk and either duration of smoking or average and cumulative consumption were similar for cigar and cigarillo smoking, pipe smoking, and cigarette smoking. CONCLUSION: Our results suggest that smoking of European cigars, cigarillos, and pipe tobacco might exert a carcinogenic effect on the lung comparable to that of cigarettes.     

Occupational X-ray examinations and lung cancer risk

Occupational X-ray examination programs have been conducted in many countries to screen for occupational and nonoccupational respiratory diseases, resulting in widespread exposure to X-radiation. We conducted a multicentre case-control study of lung cancer in the Czech Republic, Hungary, Poland, Romania, Russia and Slovakia, including 2,589 cases and 2,859 controls enrolled during 1998-2002. We collected detailed information on occupational X-ray examinations, occupations and tobacco smoking. We calculated odds ratios of lung cancer via multiple logistic regression after adjustment for age, sex, center and tobacco smoking. Among controls 24.9% reported no X-ray examination, 62.9% reported 1-30 examinations and 12.2% reported more than 30 examinations. When we chose individuals with no examination as the reference group, the odds ratios of lung cancer were 1.21 (95% confidence interval [CI] 0.99-1.48), 1.33 (95% CI 1.08-1.64), 1.49 (95% CI 1.18-1.87), 1.52 (95% CI 1.17-1.99) and 2.15 (95% CI 1.50-3.08) for 1-10, 11-20, 21-30, 31-40 and more than 40 examinations, respectively (p-value of test for linear trend <0.0001). The association between X-ray examinations and lung cancer risk was strong in countries with low prevalence of exposure and absent in countries with high prevalence of exposure. Odds ratios for X-ray examinations were lower among smokers than among nonsmokers. The magnitude of the increased risk observed is higher than expected on the basis of other studies of radiation-exposed populations. Although the association we detected between X-ray examinations and lung cancer risk may reflect a carcinogenic effect of repeated exposure to low-level ionizing radiation, reporting bias and particularly uncontrolled confounding by occupational exposure to carcinogens are also likely explanations of the results.     

Association between the risk for lung adenocarcinoma and a (-4) G-to-A polymorphism in the XPA gene.

Polymorphisms of genes coding for DNA repair can affect lung cancer risk. A common single nucleotide (-4) G-to-A polymorphism was identified previously in the 5' untranslated region of the XPA gene. In a case-control study in European Caucasians, the influence of this polymorphism on primary lung cancer risk overall and according to histologic subtypes was investigated. Four hundred sixty-three lung cancer cases (including 204 adenocarcinoma and 212 squamous cell carcinoma) and 460 tumor-free hospital controls were investigated using PCR amplification and melting point analysis of sequence-specific hybridization probes. Odds ratios (OR) were calculated by multiple logistic regression analysis adjusting for age, gender, smoking habits, and occupational exposure and showed a slightly enhanced risk for all lung cancer cases as well as for squamous cell carcinoma and adenocarcinoma cases. Gene-environment interactions were analyzed with respect to smoking and occupational exposure. A nearly 3-fold increased risk for adenocarcinoma associated with the XPA AA genotype was observed for occupationally exposed individuals (OR, 2.95; 95% confidence interval, 1.42-6.14) and for heavy smokers (OR, 2.52; 95% confidence interval, 1.17-5.42). No genotype-dependent increase in OR was found for nonexposed individuals or those smoking <20 pack-years. The significant effect of the XPA polymorphism in heavy smokers and occupationally exposed individuals suggests an important gene-environment interaction for the XPA gene. The underlying mechanisms as to why AA homozygotes are predisposed to lung adenocarcinoma and which specific carcinogens are involved remains to be determined.     

Lifetime residential and workplace exposure to environmental tobacco smoke and lung cancer in never-smoking women, Canada 1994-97

Although the risk of lung cancer among never-smokers living with a spouse who smokes has been extensively studied, the impact of lifetime residential and workplace environmental tobacco smoke has received less attention. As part of a large population-based case-control study of lung cancer, we collected lifetime residential and occupational passive smoking information from 71 women with lung cancer and 761 healthy control subjects, all of whom reported being lifetime nonsmokers. The adjusted odds ratio (OR) for lung cancer associated with residential passive exposure only was 1.21 (95% confidence interval [CI] 0.5-2.8). Although more years of and more intense residential passive smoke exposure tended to be associated with higher risk estimates, no clear dose-response relationship was evident. The OR for women with passive exposure as a child and as an adult was 1.63 (95% CI 0.8-3.5) and for those only exposed as an adult 1.20 (95%CI 0.5-3.0). Exposure to environmental tobacco smoke only in the workplace was associated with an adjusted OR of 1.27 (95% CI 0.4-4.0). Risks associated with increasing occupational exposure year tertiles were 1.24, 1.71 and 1.71. Total smoker-years of residential and occupational exposure combined resulted in a statistically significant trend (linear test for trend p = 0.05) with ORs for tertiles of exposure of 0.83, 1.54 and 1.82. Our results are consistent with the literature suggesting that long-term, regular exposure to either residential or occupational environmental tobacco smoke is associated with increased lung cancer risk in never-smoking women.     

Gender, smoking, glutathione-S-transferase variants and bladder cancer incidence: a population-based study

OBJECTIVE: Male gender, tobacco smoking and occupational exposure to arylamines and polycyclic aromatic hydrocarbons are the primary risk factors for bladder cancer. Emerging, and consistent data indicate that risk may be modified by polymorphisms in carcinogen metabolism genes, including those involving the glutathione-S-transferases. Recent work further suggests that susceptibility to the carcinogenic effects of tobacco on the bladder may differ among men and women. METHOD: We investigated the gender specific risk of bladder cancer associated with glutathione-S-transferase M1 (GSTM1) and T1 (GSTT1) polymorphisms in a population-based case-control study of 354 bladder cancer cases and 542 controls. RESULTS: We found an increased risk of bladder cancer associated with GSTM1 null genotype among women (OR 1.7; 95% CI 1.0-3.0), but not men (OR 0.9; 95% CI 0.7-1.3). Among women, the GSTM1 null genotype was associated with an elevated bladder cancer risk only among smokers (OR 2.3; 95% CI 1.1-4.5 in ever smokers versus OR 0.9; 95% CI 0.3-2.5 in never smokers). There was no apparent association between bladder cancer and the GSTT1 null polymorphism in either men or women, and we did not detect evidence of any GSTT1-smoking or GSTT1-GSTM1 gene-gene interaction. CONCLUSION: Our data suggest that a subset of women may be particularly susceptible to tobacco-induced bladder cancer.     

Blood cadmium may be associated with bladder carcinogenesis: the Belgian case-control study on bladder cancer

BACKGROUND: The aim of this study was to assess the relationship between exposure to cadmium and bladder cancer risk. METHODS: We conducted a case-control study in Belgium and measured the blood levels of cadmium in 172 bladder cases and 359 population controls. The data were analyzed as tertiles after logarithmic transformation. Cut-off points were based on the levels among the controls. Logistic regression was performed to calculate odds ratios (ORs) for bladder cancer occurrence with corresponding 95% confidence intervals (95% CI). RESULTS: After adjustment for sex, age, and occupational exposure to PAHs or aromatic amines, the OR for cadmium was 8.3 (95% CI 5.0-13.8) comparing the highest to the lowest tertile (p for trend <0.001). Additional adjustment for smoking (current cigarette smoking status, years of cigarette smoking and number of cigarettes smoked per day) decreased the OR, however it remained strongly significant (OR: 5.7; 95% CI 3.3-9.9). CONCLUSION: Our study suggests that individuals with increased exposure to cadmium have an increased risk of bladder cancer. Future studies should expand on this investigation by studying a larger number of bladder cancer patients and by collecting extensive information on the lifetime occupational, residential, and environmental exposures to clarify the role of cadmium in bladder cancer.     

Association between glutathione S-transferase p1 polymorphisms and lung cancer risk in Caucasians: a case-control study

Glutathione transferases (GSTs), a multiple gene family of phase II enzymes, catalyze detoxifying endogenous reactions with glutathione and protect cellular macromolecules from damage caused by cytotoxic and carcinogenic agents. Glutathione S-transferase p1 (GSTP1), the most abundant GST isoform in the lung, metabolizes numerous carcinogenic compounds including benzo[a]pyrene, a tobacco carcinogen. Previous studies suggest that genetic polymorphisms of GSTP1 exon 5 (Ile105Val) and exon 6 (Ala114Val) have functional effects on the GST gene product resulting in reduced enzyme activity. Individuals with reduced GST enzymatic activity may be at a greater risk for cancer due to decreased detoxification of carcinogenic and mutagenic compounds. Utilizing a hospital-based case-control study, we investigated the association between GSTP1 polymorphisms at exons 5 and 6 with lung cancer risk. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay was used to successfully genotype the GSTP1 exons 5 and 6 polymorphism in 582 Caucasian lung cancer cases and 600 frequency matched Caucasian controls. There was no association between the exon 5 variant genotypes (A/G+G/G) and overall lung cancer risk (OR=1.09; 95% CI 0.82-1.45) nor when stratified by age, gender, and smoking status. However, the exon 6 variant genotypes (C/T+T/T) were associated with a statistically significant elevated lung cancer risk (OR=1.40; 95% CI 1.06-1.92). Additionally, there was an increase in lung cancer risk for the exon 6 variant genotypes in younger individuals (<62 years) (OR=1.63; 95% C.I. 1.07-2.49) but no effect in older individuals (OR=1.14; 95% CI 0.72-1.81). A statistically significant increased risk of lung cancer was also observed for the exon 6 variant genotypes among men (OR=2.17; 95% CI 1.41-3.33), but not among women (OR=0.80; 95% CI 0.51-1.28). Among ever smokers, the exon 6 variant genotypes were associated with an elevated lung cancer risk (OR=1.58; 95% CI 1.14-2.19), which was not evident for never smokers (OR=0.53; 95% CI 0.21-1.33). These data demonstrate that the GSTP1 exon 6 polymorphism, but not the exon 5 polymorphism, is associated with lung cancer risk that is especially evident in men, younger individuals, and ever smokers.     

Bladder cancer risk in relation to occupations held in a nationwide case-control study in Iran

Globally, bladder cancer has been identified as one of the most frequent occupational cancers, but our understanding of occupational bladder cancer risk in Iran is less advanced. This study aimed to assess the risk of bladder cancer in relation to occupation in Iran. We used the IROPICAN case-control study data including 717 incident cases and 3477 controls. We assessed the risk of bladder cancer in relation to ever working in major groups of the International Standard Classification of Occupations (ISCO-68) while controlling for cigarette smoking, opium consumption. Logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CI). In men, decreased ORs for bladder cancer were observed in administrative and managerial workers (OR 0.4; CI: 0.2, 0.9), and clerks (OR 0.6; CI: 0.4, 0.9). Elevated ORs were observed in metal processors (OR 5.4; CI: 1.3, 23.4), and workers in occupations with likely exposure to aromatic amines (OR 2.2; CI: 1.2, 4.0). There was no evidence of interactions between working in aromatic amines-exposed occupations and tobacco smoking or opium use. Elevated risk of bladder cancer in men in metal processors and workers likely exposed to aromatic amines aligns with associations observed outside Iran. Other previously confirmed associations between high-risk occupations and bladder cancer were not observed, possibly due to small numbers or lack of details on exposure. Future epidemiological studies in Iran would benefit from the development of exposure assessment tools such as job exposure matrices, generally applicable for retrospective exposure assessment in epidemiological studies.