Active and passive smoking and risk of renal cell carcinoma in Canada

This study aimed to assess the role of active and passive smoking in the development of renal cell carcinoma (RCC). Mailed questionnaires were completed by 1279 incident RCC cases and 5370 population controls between 1994 and 1997 in eight Canadian provinces. Data were collected on socio-economic status, smoking habits, diet and passive smoking status, as well as residential and occupational history. The study found an increased risk of RCC associated with active smoking. Elevated risk of RCC was also observed with passive smoking; compared with those never exposed to either passive or active smoking, men and women with 43 or more years of passive residential and/or occupational exposure had respective adjusted Odds Ratios (ORs) of 3.9 (95% Confidence Interval (CI) 1.4-10.6) and 1.8 (95% CI 1.0-3.3) (P=0.001 and P=0.09, respectively). Both active and passive smoking might play a role in the aetiology of RCC.     

Cigarette smoking and colorectal cancer risk in Germany: a population-based case-control study

Studies have shown fairly consistent positive relationships between smoking and risk of colorectal adenomas, but have yielded inconsistent results for colorectal cancer. Issues relating to the duration, cumulative dose of smoking and the effect of smoking cessation on colorectal cancer risk still need clarification. In a population-based case-control study in Germany, we recruited 540 incident cases of colorectal cancer and 614 controls matched to cases by sex, 5-year age groups and county of residence from January 2003 to June 2004. Subjects were aged>or=30 years, and provided information on risk factors of colorectal cancer, including lifetime cigarette smoking habits, in personal interviews. Odds ratios (OR) and 95% confidence intervals (CI) were computed using conditional logistic regression models, adjusting for potential confounders. Compared with nonsmokers, there was an increased risk for smoking for >or=30 years (OR: 1.25, 95% CI: 0.90-1.75) and a significant risk increase for >or=40 pack-years of smoking (OR: 1.92, 95% CI: 1.13-3.28). Stratification by sex yielded higher risk estimates among females than that among males, with adjusted ORs of 3.5 (95% CI: 1.29-9.52) and 1.15 (0.69-1.91) for women and men, respectively, following >or=30 pack-years of smoking (pinteraction=0.18). Among smokers, risk reduction was observed after >or=20 years of quitting smoking and was significant for >or=40 years (OR: 0.46; 95% CI: 0.21-0.98), when compared to current smokers (p for linear trend=0.05). This study supports the hypothesis that smoking for a long duration at a high cumulative dose increases the risk for colorectal cancer, particularly among women, and suggests that there is risk reduction after longterm smoking cessation.     

Risk factors for lung cancer among Canadian women who have never smoked

Risk factors for lung cancer among women who had never smoked were assessed in a case-control study of 161 newly diagnosed histologically confirmed cases and 483 population controls between 1994 and 1997 in eight Canadian provinces. Measurement included socio-economic status, smoking habits, alcohol use, diet, residential and occupational histories and exposure to environmental tobacco smoke (ETS). Dose-response associations were observed for consumption of tea, adjusted odds ratios (ORs) 0.6 (95% confidence interval (CI) = 0.3-0.9) for 1-7 cups per week and 0.4 (95% CI = 0.2-0.7) for > or = 8 cups per week (P = 0.0008), and smoked meat, adjusted ORs 1.3 (95% CI = 0.8-2.3) for 0.5 slice per week and 2.1 (95% CI = 1.1-4.0) for >0.5 slice per week (P = 0.02). Regular use of shortening in cooking was also related to lung cancer. Increased ORs with borderline significance were found for total consumption of meat, eggs or French fries and fried potatoes. Passive exposure to ETS at home (or at work) may be associated with lung cancer risk among never-smoker women; the adjusted ORs were 0.7 (95% CI = 0.2-2.3), 1.2 (95% CI = 0.4-3.2), 1.5 (95% CI = 0.5-4.0) for 1-16, 17-30, and 31 or more years of combined residential and/or occupational ETS exposure, respectively, with a similar pattern for smoker-years of ETS exposure.     

Role of smoking and diet in the cross-cultural variation in lung-cancer mortality: the Seven Countries Study. Seven Countries Study Research Group

We examined the role of smoking and diet in the cross-cultural variation in lung-cancer mortality, using aggregated data of the Seven Countries Study, a follow-up study comprising 12,763 middle-aged men in 16 cohorts in Europe, the United States and Japan, which started around 1960. Smoking habits were assessed with a standardised questionnaire. Dietary intake was collected in random sub-samples of each cohort by the dietary record method. Cohort-specific 25-year lung-cancer mortality among all men and among categories of smoking behaviour was related to smoking prevalence and population average dietary intake, respectively, using Poisson regression. Smoking prevalence was positively associated with lung-cancer mortality [risk ratio 1.47, 95% confidence interval (CI) 1.05-2.07, for an increase of 10 percentage points]. Lung-cancer mortality among smokers, which varied significantly among cultures, was positively associated with average fat intake, especially saturated fat intake (rate ratio 1.10, 95% CI 1.04-1.17, for an increase of 4.6 g) but not with unsaturated fat intake. Average fruit and vegetable intake were not related to lung-cancer mortality. Among never-smokers, the power to detect associations was low. In conclusion, both smoking prevalence and average fat intake, especially saturated fat, may play a role in the cross-cultural variation in lung-cancer mortality, either independently or by effect modification.     

Small cell lung cancer in women: risk associated with smoking, prior respiratory disease, and occupation

Small cell carcinoma of the lung (SCLC) occurs most frequently in heavy smokers, yet exhibits a lesser predominance among men than other smoking-associated lung cancers. Incidence rates have increased more rapidly in women than men and at a faster rate among women than other cell types. To investigate the importance of smoking and other risk factors, a case-control study of SCLC in women was conducted. A total of 98 women with primary SCLC and 204 healthy controls, identified by random-digit dialing and frequency matched for age, completed telephone interviews. Data collected include demographics, medical history, family cancer history, residence history, and lifetime smoking habits. Odds ratios (ORs) and 95% confidence intervals (95% CI) were calculated using logistic regression analysis. Risk for small cell carcinoma in women is strongly associated with current use of cigarettes. Ninety-seven of 98 cases had smoked cigarettes; 79% of cases were current smokers and 20% were former smokers at the time of diagnosis compared to 13% current and 34% former smokers among controls. The ORs associated with smoking are 108.7 (95% CI 14.8-801) for ever-use of cigarettes, 278.9 (95% CI 37.0-2102) for current smoking, and 31.5 (95% CI 4. 1-241) for former smoking. Risk increases steeply with pack-years of smoking and decreases with duration of smoking cessation. After adjusting for age, education, and lifetime smoking history, medical history of physician-diagnosed respiratory disease including chronic bronchitis, emphysema, pneumonia, tuberculosis, asthma, and hay fever is not associated with a significant increase in lung cancer risk. Employment in blue collar, service, or other high risk occupations is associated with a two to three-fold non-significant increase in risk for small cell carcinoma after adjusting for smoking.     

Gender differences in lung cancer risk by smoking: a multicentre case-control study in Germany and Italy

Several studies in the past have shown appreciably higher lung cancer risk estimates associated with smoking exposure among men than among women, while more recent studies in the USA report just the opposite. To evaluate this topic in a European population we conducted a case-control study of lung cancer in three German and three Italian centres. Personal interviews and standardized questionnaires were used to obtain detailed life-long smoking and occupational histories from 3723 male and 900 female cases and 4075 male and 1094 female controls. Lung cancer risk comparing ever-smokers with never-smokers was higher among men (odds ratios (OR) adjusted for age and centre = 16.1, 95% confidence interval (CI) 12.8-20.3) than among women (OR = 4.2, CI 3.5-5.1). Because the smoking habits of women were different from men, we conducted more detailed analyses using comparable levels of smoking exposure. After restriction to smokers and adjustment for other smoking variables, risk estimates did not differ appreciably between genders. The analysis of duration of smoking (0-19, 20-39, 40+ years) adjusted for cigarette consumption and time since quitting smoking revealed similar risk estimates in men (OR = 1.0, 3.3 [CI 2.6-4.2], 4.1 [CI 3.1-5.6]) and women (OR = 1.0, 2.7 [CI 1.7-4.1], 3.3 [CI 1.9-5.8]). The same was true of the analysis of average or cumulative smoking consumption, and also of analyses stratified by different histological types. We conclude that for comparable exposure to tobacco smoke, the risk of lung cancer is comparable in women and men.     

Air pollution and lung cancer mortality in the vicinity of a nonferrous metal smelter in Sweden

To evaluate the importance of exposure to ambient air pollution for lung cancer risk, we conducted a case-control study in the vicinity of a nonferrous metal smelter. The smelter started operations in 1930 and had very high emissions during the early decades, particularly of arsenic and SO(2). Among subjects deceased 1961-1990 in the municipality where the smelter is located and who had not worked at the smelter, 209 male and 107 female lung cancer cases were identified and matched by sex and year of birth to 518 and 209 controls, respectively. Information on smoking habits, occupations and residences was collected by questionnaire to next-of-kin and from registry data. Living close to the smelter was associated with a relative risk (RR) for lung cancer of 1.38 [95% confidence interval (CI) 0.89-2.14] among men, adjusted for smoking and occupational exposures. No clear difference in risk was detected for men deceased 1961-1979 compared to men deceased 1980-1990 (RR point estimates 1.42 and 1.29, respectively). There appeared to be an increased risk especially for men exposed in the beginning of the operations (RR = 1.51, 95% CI 0.90-2.54), in particular combined with exposure duration shorter than 20 years (RR = 2.52, 95% CI 0.89-7.11). For women, however, no overall increased risk for lung cancer was observed. Although not significant, our findings thus indicated an increased risk of lung cancer among men living close to the nonferrous smelter. This increase appeared to concern primarily men exposed during the early years of operations, when emissions were very high.     

Occupational exposure to metal compounds and lung cancer. Results from a multi-center case�Ccontrol study in Central/Eastern Europe and UK

Purpose

To study the association between occupational exposure to metals including chromium, cadmium, nickel, and arsenic compounds, within a population-based study design, while adjusting for confounding factors.

Methods

A population-based lung cancer case?Ccontrol study in Central/Eastern Europe and UK was conducted in 1998?C2003, including 2,853 cases and 3,104 controls. Exposure to 70 occupational agents was assessed by local expert-teams for all subjects. Odds ratios (OR) for exposure to dust and fumes/mist of chromium, nickel, cadmium, arsenic, as well as inorganic pigment dust and inorganic acid mist, were adjusting for smoking, age, center, sex, and exposure to other occupational agents including the metals under study.

Results

Exposure to arsenic (prevalence = 1.4%) was associated with an increased lung cancer risk ((OR) 1.65, 95% confidence interval (95% CI):1.05?C2.58). For chromium dust (prevalence = 4.8%, OR: 1.25, 95% CI: 0.95?C1.65), a linear upward trend for duration and cumulative exposure was observed. A weak association was observed for exposure to cadmium fumes (prevalence = 1.8%, OR: 1.19, 95% CI: 0.77?C1.82), which was strongest for the highest category of cumulative exposure (OR: 2.04, 95% CI: 1.07?C3.90). No increased risk was observed for inorganic acid mist, inorganic pigment dust, or nickel, after adjustment for other metals. An independent effect of nickel cannot be excluded, due to its collinearity with chromium exposure.

Conclusions

Occupational exposure to metals is an important risk factor for lung cancer. Although the strongest risk was observed for arsenic, exposure to chromium dust was most important in terms of attributable risk due to its high prevalence.     

Socio-economic status and lung cancer risk including histologic subtyping--a longitudinal study

We investigated prospectively the risk of lung cancer in relation to socio-economic status (SES) in 22,387 middle-aged individuals who attended a screening program in the city of Malm?, Sweden between 1974 and 1992. We also examined the relationship between SES and histologic subtype in smokers. By 2003, a total of 550 lung cancer cases had been identified. Relative risks (RR) were calculated with adjustment for age, current smoking, inhalation habits and marital status at baseline in the low SES group compared to high SES group. Among smokers, the RR (95% confidence interval (CI)) for lung cancer in the low SES group of men was 1.39 (1.11-1.73), and women 1.56 (1.04-2.34). Also among smokers, low SES was associated with an increased risk of squamous cell carcinoma in men; RR 1.89 (1.16-2.81) and women; RR 7.10 (1.63-30.86), and with an increased risk of mesothelioma in men RR 9.97 (1.29-76.96). We conclude that low SES groups run an increased risk of lung cancer despite accounting for smoking habits. Furthermore, low SES was positively associated with squamous cell carcinoma and mesothelioma. Our results suggest that the association between low SES and lung cancer could be mediated by unaccounted for smoking exposure, lifestyle or occupational hazards.     

Independent and combined effects of tobacco smoking,chewing and alcohol drinking on the risk of oral,pharyngeal and esophageal cancers in Indian men

Oral, pharyngeal and esophageal cancers are 3 of the 5 most common cancer sites in Indian men. To assess the effect of different patterns of smoking, chewing and alcohol drinking in the development of the above 3 neoplasms and to determine the interaction among these habits, we conducted a case-control study in Chennai and Trivandrum, South India. The cases included 1,563 oral, 636 pharyngeal and 566 esophageal male cancer patients who were compared with 1,711 male disease controls from the 2 centers as well as 1,927 male healthy hospital visitors from Chennai. We observed a significant dose-response relationship for duration and amount of consumption of the 3 habits with the development of the 3 neoplasms. Tobacco chewing emerged as the strongest risk factor for oral cancer, with the highest odds ratio (OR) for chewing products containing tobacco of 5.05 [95% confidence internal (CI) 4.26-5.97]. The strongest risk factor for pharyngeal and esophageal cancers was tobacco smoking, with ORs of 4.00 (95% CI 3.07-5.22) and 2.83 (95% CI 2.18-3.66) in current smokers, respectively. An independent increase in risk was observed for each habit in the absence of the other 2. For example, the OR of oral cancers for alcohol drinking in never smokers and never chewers was 2.56 (95% CI 1.42-4.64) and that of esophageal cancers was 3.41 (95% CI 1.46-7.99). Furthermore, significant decreases in risks for all 3 cancer sites were observed in subjects who quit smoking even among those who had quit smoking 2-4 years before the interview.     

Association of mesothelioma deaths with neighborhood asbestos exposure due to a large-scale asbestos-cement plant

A causal relationship between mesothelioma and occupational asbestos exposure is well known, while some studies have shown a relationship to non-occupational exposures. The aim of this study was to quantify the risk of mesothelioma death associated with neighborhood asbestos exposure due to a large-scale asbestos-cement (AC) plant in Amagasaki, Japan, adjusting properly risk factors including occupational exposures. We conducted a nested case-control study in which a fixed population of 143,929 residents who had been living in Amagasaki City between 1975 and 2002 were followed from 2002 to 2015. All 133 cases and 403 matched controls were interviewed about their occupational, domestic, household, and neighborhood asbestos exposures. Odds ratios (ORs) for mesothelioma death associated with the neighborhood exposure were estimated by a conditional logistic-regression model. For quantitative assessments for neighborhood exposure, we adopted cumulative indices for individuals' residential histories at each residence-specific asbestos concentration multiplied by the duration during the potential exposure period of 1957–1975 (crocidolite). We observed an increasing, dose-dependent risk of mesothelioma death associated with neighborhood exposure, demonstrating that ORs in the highest quintile category were 21.4 (95% confidence interval [CI] 5.8–79.2) for all, 23.7 (95% CI 3.8–147.2) for males, and 26.0 (95% CI 2.8–237.5) for females compared to the lowest quintile, respectively. A quantitative assessment for risk of mesothelioma deaths, adjusting for occupational and non-occupational exposures separately, showed a dose-dependent association with neighborhood exposure and no substantial gender differences in magnitude.     

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.     

Genetic polymorphisms in N-acetyltransferase-2 and microsomal epoxide hydrolase, cumulative cigarette smoking, and lung cancer.

N-acetyltrasferase-2 (NAT2) and microsomal epoxide hydrolase (mEH) are polymorphic genes that metabolize different tobacco carcinogens. Smaller studies found inconsistent relationships between NAT2 or mEH polymorphisms and lung cancer risk. To determine whether there is gene-environment interaction between NAT2 polymorphisms, alone or in combination with mEH polymorphisms, and cumulative smoking exposure in the development of lung cancer, we conducted a case control study of 1115 Caucasian lung cancer patients and 1250 spouse and friend controls. The results were analyzed using generalized additive models and logistic regression, adjusting for relevant covariates. There was no overall relationship between NAT2 genotype and lung cancer risk; the adjusted odds ratio (OR) of the rapid versus slow acetylator genotypes was 0.96 [95% confidence interval (CI), 0.79-1.16]. However, gene-environment interaction analyses revealed that the adjusted ORs increased significantly as pack-years increased. For nonsmokers, the fitted OR was 0.66 (95% CI, 0.44-0.99), whereas for heavy smokers (80 pack-years), the OR increased to 1.22 (95% CI, 0.89-1.67). When comparing the extreme genotype combinations of the NAT2 rapid acetylator, higher mEH activity genotype to the NAT2 slow acetylator, and very low mEH activity genotype, the corresponding ORs at 0 and 80 pack-years were 0.30 (95% CI, 0.14-0.62) and 2.19 (95% CI, 1.26-3.81), respectively. Results were similar with ORs derived from stratified models. In conclusion, NAT2 rapid acetylator genotypes are protective against lung cancer in nonsmokers but are risk factors in heavy smokers. The joint effects of NAT2 and mEH polymorphisms are consistent with an independent, additive effect of these two genes, modified by smoking history.     

Mortality Among Workers Employed in the Titanium Dioxide Production Industry in Europe

OBJECTIVES: To assess the risk of lung cancer mortality related to occupational exposure to titanium dioxide (TiO2). METHODS: A mortality follow-up study of 15,017 workers (14,331 men) employed in 11 factories producing TiO2 in Europe. Exposure to TiO2 dust was reconstructed for each occupational title; exposure estimates were linked with the occupational history. Observed mortality was compared with national rates, and internal comparisons were based on multivariate Cox regression analysis. RESULTS: The cohort contributed 371,067 person-years of observation (3.3% were lost to follow-up and 0.7% emigrated). 2652 cohort members died during the follow-up, yielding standardized mortality ratios (SMRs) of 0.87 (95% confidence interval [CI] 0.83-0.90) among men and 0.58 (95% CI 0.40-0.82) among women. Among men, the SMR of lung cancer was significantly increased (1.23, 95% CI 1.10-1.38); however, mortality from lung cancer did not increase with duration of employment or estimated cumulative exposure to TiO2 dust. Data on smoking were available for over one third of cohort members. In three countries, the prevalence of smokers was higher among cohort members compared to the national populations. CONCLUSIONS: The results of the study do not suggest a carcinogenic effect of TiO2 dust on the human lung.     

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.     

Oral cancer in southern India: the influence of smoking, drinking, paan-chewing and oral hygiene

Between 1996 and 1999 we carried out a case-control study in 3 areas in Southern India (Bangalore, Madras and Trivandrum) including 591 incident cases of cancer of the oral cavity (282 women) and 582 hospital controls (290 women), frequency-matched with cases by age and gender. Odds ratios (ORs) and 95% confidence intervals (CIs) were obtained from unconditional multiple logistic regressions and adjusted for age, gender, center, education, chewing habit and (men only) smoking and drinking habits. Low educational attainment, occupation as a farmer or manual worker and various indicators of poor oral hygiene were associated with significantly increased risk. An OR of 2.5 (95% CI 1.4-4.4) was found in men for smoking > or = 20 bidi or equivalents versus 0/day. The OR for alcohol drinking was 2.2 (95% CI 1.4-3.3). The OR for paan chewing was more elevated among women (OR 42; 95% CI 24-76) than among men (OR 5.1; 95% CI 3.4-7.8). A similar OR was found among chewers of paan with (OR 6.1 in men and 46 in women) and without tobacco (OR 4.2 in men and 16.4 in women). Among men, 35% of oral cancer is attributable to the combination of smoking and alcohol drinking and 49% to pan-tobacco chewing. Among women, chewing and poor oral hygiene explained 95% of oral cancer.     

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.     

Environmental factors in relation to breast cancer characterized by p53 protein expression.

Findings from studies of cigarette smoking and low-dose ionizing radiation exposure and breast cancer are unclear. Laboratory studies indicate that both exposures can cause DNA damage, potentially increasing cancer risk if such mutations occur in growth control genes, such as p53. We examined the potential etiologic heterogeneity of breast cancer by evaluating whether associations between cigarette smoking and low-dose ionizing radiation and breast cancer differed by p53 protein expression status. Data were obtained from the Carolina Breast Cancer Study, a population-based, case-control study conducted among African-American and white women ages 20-74 years. Questionnaire data were available from 861 women with incident, primary invasive breast cancer and 790 community-based controls. p53 immunostaining was performed on tissue from 683 women with breast cancer; 46% were classified as p53+. Two separate unconditional logistic regression models were used to calculate odds ratios (ORs) for p53+ and p53- breast cancer, as compared with controls, in relation to smoking and low-dose ionizing radiation exposure. Smoking was not differentially associated with p53+ or p53- breast cancer, even when duration, dose, and passive smoking status were considered. Exposure to individual sources of radiation did not differ for p53+ and p53- breast cancers. However, ORs for combined exposure to chest X-rays and occupational radiation were higher for p53+ [OR, 2.2; 95% confidence interval (CI), 1.0-5.3] than p53- breast cancer (OR, 1.2; 95% CI, 0.5-3.4). Combined exposure to radiation from other medical sources as well as occupational exposure was also higher for p53+ (OR, 3.7; 95% CI, 0.8-16.8) than for p53- breast cancer (OR, 1.7; 95% CI, 0.3-10.5). Although preliminary, our results suggest that exposure to multiple sources of low-dose ionizing radiation may contribute to the development of p53+ breast cancer.     

Semi-Quantitative Exposure Assessment of Occupational Exposure to Wood Dust and Nasopharyngeal Cancer Risk

Occupational exposure to wood dust is one cause of nasopharyngeal cancer (NPC); however, assessing thisexposure remains problematic. Therefore, the objective of this study was to develop a semi-quantitative exposureassessment method and then utilize it to evaluate the association between occupational exposure to wood dust andthe development of NPC. In addition, variations in risk by histology were examined. A case-control study wasconducted with 327 newly diagnosed cases of NPC at the National Cancer Institute and regional cancer centersin Thailand with 1:1 controls matched for age, gender and geographical residence. Occupational informationwas obtained through personal interviews. The potential probability, frequency and intensity of exposure towood dust were assessed on a job-by-job basis by experienced experts. Analysis was performed by conditionallogistic regression and presented in odds ratio (ORs) estimates and 95% confidence intervals (CI). Overall, a nonsignificant relationship between occupational wood dust exposure and NPC risk for all subjects was observed(ORs=1.61, 95%CI 0.99-2.59); however, the risk became significant when analyses focused on types 2 and 3 ofNPC (ORs = 1.62, 95%CI 1.03-2.74). The significant association was stronger for those exposed to wood dust for> 10 year (ORs=2.26, 95%CI 1.10-4.63), for those with first-time exposure at age > 25 year (ORs= 2.07, 95%CI1.08-3.94), and for those who had a high cumulative exposure (ORs=2.17, 95%CI 1.03-4.58) when compared withthose considered unexposed. In conclusion, wood dust is likely to be associated with an increased risk of type 2or 3 NPC in the Thai population. The results of this study show that semi-quantitative exposure assessment issuitable for occupational exposure assessment in a case control study and complements the information fromself-reporting.