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J Siemiatycki

Publications and source records attributed to J Siemiatycki.

At least 19 recordsLinked to original sources
PubMed2005

Comparison of self-reported height and weight by cancer type among men from Montreal, Canada.

Among men there is epidemiological evidence for an association between obesity and increased risk of renal cell carcinoma, colon cancer and adenocarcinoma of the oesophagus. The evidence for other cancer sites remains inconsistent. We conducted a large population-based, multi-site, case-control study of environmental causes of cancer among males in Montreal, Canada. Among the many questionnaire items collected by interview were height and usual weight. We compared height, weight and body mass index (BMI) among individuals with 11 different cancer types (combined N=3016) and population-based controls (N=509). Linear regression was used to model the relationship of the disease status with each of three dependent continuous variables (height, weight and BMI), while adjusting for covariates. For most cancer groups, weight and BMI were lower than among population controls. Because of potential information bias and reverse causality bias, we focused on the comparisons among cancer types. The lowest BMI values were observed among men with squamous cell carcinoma of the oesophagus, lung and stomach cancers. The highest BMIs were reported by men with prostate and kidney cancers, and oesophageal adenocarcinoma. Inconsistencies in the epidemiological literature on obesity and cancer risk could be related to the difficulties in obtaining unbiased reports of pre-disease weight and to publication bias.

Adult↗
PubMed2004

A flexible modeling approach to estimating the component effects of smoking behavior on lung cancer.

OBJECTIVE: Despite the established causal association between cigarette smoking and lung cancer, the relative contributions of age started, duration, years since quitting, and daily amount smoked have not been well characterized. We estimated the contribution of each of these aspects of smoking behavior. STUDY DESIGN AND SETTING: A case-control study was conducted in Montreal on the etiology of lung cancer. There were 640 cases and 938 control subjects for whom lifetime smoking histories were collected. We used generalized additive models, incorporating cubic smoothing splines to model nonlinear effects of various smoking variables. We adopted a multistep approach to deal with the multicollinearity among time-related variables. RESULTS: The main findings are that (1) risk increases independently by daily amount and by duration; (2) among current smokers, lung cancer risk doubles for every 10 cigarettes per day up to 30 to 40 cigarettes per day and tails off thereafter; (3) among ex-smokers, the odds ratio decreases with increasing time since quitting, the rate of decrease being sharper among heavy smokers than among light smokers; and (4) absolute risks demonstrate the dramatic public health benefits of long-term smoking cessation. CONCLUSION: Our results reinforce some previous findings on this issue.

Adult↗
PubMed2003

Estimating the distribution of lag in the effect of short-term exposures and interventions: adaptation of a non-parametric regression spline model.

Information on the distribution of lag duration between exposure or intervention and the subsequent changes in risk can help in assessing the impact of exposure, predicting cost-effectiveness of intervention, and understanding the underlying biological mechanisms. Previous approaches focused more on optimizing the strength of the exposure-disease association than on directly estimating lag duration. We propose an alternative approach applicable to the analysis of the lagged effects of binary exposure variables. The density function of the distribution of lags is estimated based on flexible modelling of changes in hazard ratio of exposed versus unexposed subjects. The methodology is evaluated in a simulation study and is applied to the Framingham data to investigate the lagged effect of smoking cessation on coronary heart disease risk.

Biometry↗
PubMed2002

Consumption of non-alcoholic beverages and prostate cancer risk.

Our objective was to investigate the relations between the consumption of coffee, tea and carbonated beverages and the development of prostate cancer. The design was a population-based case-control study set in Montreal. The analysis was restricted to the subset of men, aged 45-70 years, who underwent interviews in which aspects of lifelong consumption of non-alcoholic beverages were ascertained. There were 399 incident cases of prostate cancer, 476 population controls and 621 cancer controls. There was no association between the consumption of either coffee or carbonated beverages and the development of prostate cancer. Among daily tea drinkers, the odds ratio associated with the highest tertile of cumulative consumption was 2.0 (95% confidence interval (CI) 1.3-3.0) when using population controls and 1.6 (95% CI 1.0-2.4) when using cancer controls. In conclusion, the consumption of coffee or carbonated beverages does not influence the risk of prostate cancer. Our findings provide no support to the hypothesis that tea consumption may be protective. While tea consumption may increase prostate cancer risk, we were unable to rule out alternative explanations for the positive association that we observed.

Aged↗
PubMed2001

A case-control study of the relationship between the risk of colon cancer in men and exposures to occupational agents.

BACKGROUND: We conducted a population-based case-control study in Montreal, Canada, to explore associations between hundreds of occupational circumstances and several cancer sites, including colon. METHODS: We interviewed 497 male patients with a pathologically confirmed diagnosis of colon cancer, 1514 controls with cancers at other sites, and 533 population-based controls. Detailed job histories and relevant potential confounding variables were obtained, and the job histories were translated by a team of chemists and industrial hygienists into a history of occupational exposures. RESULTS: We found that there was reasonable evidence of associations for men employed in nine industry groups (adjusted odds ranging from 1.1 to 1.6 per a 10-year increase in duration of employment), and in 12 job groups (OR varying from 1.1 to 1.7). In addition, we found evidence of increased risks by increasing level of exposures to 21 occupational agents, including polystyrene (OR for "substantial" exposure (OR(subst)) = 10.7), polyurethanes (OR(subst) = 8.4), coke dust (OR(subst) = 5.6), mineral oils (OR(subst) = 3.3), polyacrylates (OR(subst) = 2.8), cellulose nitrate (OR(subst) = 2.6), alkyds (OR(subst) = 2.5), inorganic insulation dust (OR(subst) = 2.3), plastic dusts (OR(subst) = 2.3), asbestos (OR(subst) = 2.1), mineral wool fibers (OR(subst) = 2.1), glass fibers (OR(subst) = 2.0), iron oxides (OR(subst) = 1.9), aliphatic ketones (OR(subst) = 1.9), benzene (OR(subst) = 1.9), xylene (OR(subst) = 1.9), inorganic acid solutions (OR(subst) = 1.8), waxes, polishes (OR(subst) = 1.8), mononuclear aromatic hydrocarbons (OR(subst) = 1.6), toluene (OR(subst) = 1.6), and diesel engine emissions (OR(subst) = 1.5). Not all of these effects are independent because some exposures occurred contemporaneously with others or because they referred to a group of substances. CONCLUSIONS: We have uncovered a number of occupational associations with colon cancer. For most of these agents, there are no published data to support or refute our observations. As there are few accepted risk factors for colon cancer, we suggest that new occupational and toxicologic studies be undertaken focusing on the more prevalent substances reported herein.

Adult↗
PubMed2001

Case-control study of alcohol consumption and prostate cancer risk in Montréal, Canada.

OBJECTIVES: to estimate the risk of prostate cancer associated with alcohol consumption. METHODS: Between 1979 and 1985 a population-based case-control study was carried out in Montréal, which accrued over 4000 men in total, including cases of prostate cancer, other cancers, and population controls. The present analysis was restricted to the subset, aged 45-70 years. who underwent face-to-face interviews, in which aspects of lifelong alcohol consumption were ascertained. The cancer control series was further restricted to men whose tumor types were considered unrelated to alcohol consumption. There were 399 incident cases of prostate cancer, 476 population controls, and 674 cancer controls. RESULTS: When using the population controls, risk increased with increasing cumulative consumption of alcohol. There was no decrease in risk after quitting. Risk was particularly high among those who reported having started before age 15 years (odds ratio = 3.8; 95% confidence interval: 1.6-9.3). The results obtained using the cancer controls were less pronounced, but still indicated an excess risk associated with alcohol consumption. Beer was the most prevalent type of alcohol consumed in this population and showed the strongest association with prostate cancer. CONCLUSIONS: The results are consistent with an increase in the risk of prostate cancer due to alcohol consumption.

Adult↗
PubMed2001

Joint effects of smoking and body mass index on prostate cancer risk.

Between 1979 and 1985, a population-based case-control study of cancer at multiple sites was carried out in Montréal. A total of 399 cases with histologically confirmed prostate cancer and 476 population controls, 45-70 years of age, gave face-to-face interviews and provided adequate smoking histories. We analyzed the effects of smoking cigarettes only and of smoking cigars, or pipes, or both, with or without cigarettes, on the risk of prostate cancer. Overall, the associations between smoking cigarettes and prostate cancer were weak and compatible with no effect; the associations with cigar and pipe smoking were stronger. Among men with high body mass index, however, we found appreciable associations between cigarette smoking and prostate cancer risk. A history of ever smoking daily was associated with an odds ratio of 2.31 (95% confidence interval = 1.09-4.89). Risk increased with the amount smoked per day and with the duration of smoking. Taken together, the findings of increased risk associated with cigar and pipe smoking and the findings of increased risk associated with cigarette smoking among obese men suggest that tobacco smoking may be a risk factor for prostate cancer.

Aged↗
PubMed2001

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

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

Adult↗
PubMed2001

Activities and exposures during leisure and prostate cancer risk.

The objective of this study was to identify activities and exposures during leisure that might be associated with the development of prostate cancer. We analyzed data derived from a population-based case-control study that was carried out in Montreal between 1979 and 1985. Men (>4000) were interviewed, including cases of prostate cancer, other cancers, and population controls. The present analysis was restricted to the subset, aged 45-70 years, who underwent face-to-face interviews in which aspects of activities and exposures during leisure were ascertained. There were 400 incident cases of prostate cancer and 476 population controls. We calculated odds ratios (OR) for prostate cancer, adjusted for age, ethnic origin, respondent status, family income, body mass index, cigarette smoking, and alcohol consumption. Home or furniture maintenance was associated with an increased risk [OR, 1.4; 95% confidence interval (CI), 1.0-1.9], as was painting, stripping, or varnishing furniture (OR, 2.1; 95% CI, 0.7-6.7). Exposure during leisure to metal dust was associated with prostate cancer (OR, 3.2; 95% CI, 1.0-9.9), as was exposure to lubricating oils or greases (OR, 2.2; 95% CI, 1.2-3.7) and exposure to pesticides or garden sprays (OR, 2.3; 95% CI, 1.3-4.2). These findings are consistent with results derived from studies of occupational exposures.

Activities of Daily Living↗
PubMed2000

Rectal cancer and occupational risk factors: a hypothesis-generating, exposure-based case-control study.

In 1979, a hypothesis-generating, population-based case-control study was undertaken in Montreal, Canada, to explore the association between occupational exposure to 294 substances, 130 occupations and industries, and various cancers. Interviews were carried out with 3, 630 histologically confirmed cancer cases, of whom 257 had rectal cancer, and with 533 population controls, to obtain detailed job history and data on potential confounders. The job history of each subject was evaluated by a team of chemists and hygienists and translated into occupational exposures. Logistic regression analyses adjusted for age, education, cigarette smoking, beer consumption, body mass index, and respondent status were performed using population controls and cancer controls, e.g., 1,295 subjects with cancers at sites other than the rectum, lung, colon, rectosigmoid junction, small intestine, and peritoneum. We present here the results based on cancer controls. The following substances showed some association with rectal cancer: rubber dust, rubber pyrolysis products, cotton dust, wool fibers, rayon fibers, a group of solvents (carbon tetrachloride, methylene chloride, trichloroethylene, acetone, aliphatic ketones, aliphatic esters, toluene, styrene), polychloroprene, glass fibers, formaldehyde, extenders, and ionizing radiation. The independent effect of many of these substances could not be disentangled as many were highly correlated with each other.

Adult↗
PubMed2000

Occupational risk factors for renal cell carcinoma in Montreal.

BACKGROUND: Little is known about the role of workplace exposures on the risk of renal cell cancer. METHODS: A population-based case-control study was undertaken in Montreal to assess the association between hundreds of occupational circumstances and several cancer sites, including the kidney. A total of 142 male patients with pathologically confirmed renal cell carcinoma, 1900 controls with cancer at other sites and 533 population-based controls were interviewed. Detailed job histories and relevant data on potential confounders were obtained. A group of chemists-hygienists evaluated each job reported and translated them into a history of occupational exposures using a checklist of 294 substances. Multivariate logistic regression models using either population, cancer controls, or a pool of both groups were used to estimate odds ratios. RESULTS: There were some indications of excess risks among printers, nursery workers (gardening), aircraft mechanics, farmers, and horticulturists, as well as in the following industries: printing-related services, defense services, wholesale trade, and retail trade. Notwithstanding the low precision of many of the odds ratio estimates, the following workplace exposures showed some evidence of excess risk: chromium compounds, chromium (VI) compounds, inorganic acid solutions, styrene-butadiene rubber, ozone, hydrogen sulphide, ultraviolet radiation, hair dust, felt dust, jet fuel engine emissions, jet fuel, aviation gasoline, phosphoric acid and inks. CONCLUSIONS: For most of these associations there exist no, or very little, previous data. Some associations provide suggestive evidence for further studies.

Adult↗
PubMed2000

Occupational risks for lung cancer among nonsmokers.

We conducted a case-control study in 12 European study centers to evaluate the role of occupational risk factors among nonsmokers. We obtained detailed occupational histories from 650 nonsmoking cases (509 females/141 males) and 1,542 nonsmoking controls (1,011 females/531 males). On the basis of an a priori definition of occupations and industries that are known (list A) or suspected (list B) to be associated with lung carcinogenesis, we calculated odds ratios (ORs) for these occupations, using unconditional logistic regression models and adjusting for sex, age, and center effects. Among nonsmoking men, an excess relative risk was observed among those who had worked in list-A occupations [OR = 1.52; 95% confidence interval (C) = 0.78-2.97] but not in list-B occupations (OR = 1.05; 95%), CI = 0.60-1.83). Among nonsmoking women, there was an elevation of risk for list-A occupations (OR = 1.50; 95% CI = 0.49-4.53), although this estimate was imprecise, given that less than 1% of cases and controls were exposed. Exposure to list-B occupations was associated with an increase in relative risk (OR = 1.69; 95% CI = 1.09-2.63) in females, but not in males. Women who had been laundry workers or dry cleaners had an OR of 1.83 (95% CI = 0.98-3.40). Our findings confirm that certain occupational exposures are associated with an increased risk for lung cancer among both female and male nonsmokers; however, knowledge on occupational lung carcinogens is biased toward agents to which mainly men are exposed.

Adult↗
PubMed2000

Workplace exposures and oesophageal cancer.

OBJECTIVES: To describe the relation between oesophageal cancer and many occupational circumstances with data from a population based case-control study. METHODS: Cases were 99 histologically confirmed incident cases of cancer of the oesophagus, 63 of which were squamous cell carcinomas. Various control groups were available; for the present analysis a group was used that comprised 533 population controls and 533 patients with other types of cancer. Detailed job histories were elicited from all subjects and were translated by a team of chemists and hygienists for evidence of exposure to 294 occupational agents. Based on preliminary results and a review of literature, a set of 35 occupational agents and 19 occupations and industry titles were selected for this analysis. Logistic regression analyses were adjusted for age, birthplace, education, respondent (self or proxy), smoking, alcohol, and beta-carotene intake. RESULTS: Sulphuric acid and carbon black showed the strongest evidence of an association with oesophageal cancer, particularly squamous cell carcinoma. Other substances showed excess risks, but the evidence was more equivocal-namely chrysotile asbestos, alumina, mineral spirits, toluene, synthetic adhesives, other paints and varnishes, iron compounds, and mild steel dust. There was considerable overlap in occupational exposure patterns and results for some of these substances may be mutually confounded. None of the occupations or industry titles showed a clear excess risk; the strongest hints were for warehouse workers, food services workers, and workers from the miscellaneous food industry. CONCLUSIONS: The data provide some support for an association between oesophageal cancer and a handful of occupational exposures, particularly sulphuric acid and carbon black. Many of the associations found have never been examined before and warrant further investigation.

Adult↗
PubMed1998

Nonoccupational exposure to chrysotile asbestos and the risk of lung cancer.

BACKGROUND: Heavy industrial exposure to asbestos causes lung cancer and mesothelioma, but it remains unknown whether much lower environmental exposure to asbestos also causes these cancers. Nevertheless, regulatory agencies, including the Environmental Protection Agency (EPA), have assessed the risk of lung cancer by extrapolating known risks from past industrial exposure to asbestos to today's much lower environmental asbestos levels (roughly 100,000 times lower). We also tested the EPA's model for predicting the risk of asbestos-induced lung cancer in a population of women with relatively high levels of nonoccupational exposure to asbestos. METHODS: Mortality among women in 2 chrysotile-asbestos-mining areas of the province of Quebec was compared with mortality among women in 60 control areas, and age-standardized mortality ratios were derived. With the help of an expert panel, we estimated past exposure to asbestos among women in the mining areas and used these data with the EPA's model to predict the relative risk of lung cancer. We then compared this prediction with the observed mortality ratios. RESULTS: On the basis of the estimated exposure in the asbestos-mining areas, a relative risk of death due to lung cancer of 2.1 was predicted by the EPA's model, amounting to about 75 excess deaths from lung cancer in this population. By contrast, we calculated a standardized mortality ratio of 1.0 and a standardized proportionate mortality ratio of 1.1 (P> 0.05), suggesting that there were between 0 and 6.5 excess deaths from lung cancer among the women with nonoccupational exposure to asbestos. Seven deaths from pleural cancer were observed (relative risk=7.63; P<0.05). CONCLUSIONS: We found no measurable excess risk of death due to lung cancer among women in two chrysotile-asbestos-mining regions. The EPA's model overestimated the risk of asbestos-induced lung cancer by at least a factor of 10.

Adult↗
PubMed1998

Associations between several sites of cancer and occupational exposure to benzene, toluene, xylene, and styrene: results of a case-control study in Montreal.

BACKGROUND: Except for the leukemogenic effects of benzene, there is inadequate or sparse evidence on the carcinogenicity of the most common monocyclic aromatic hydrocarbons. The purpose of this study was to generate hypotheses on associations between exposure to benzene, toluene, xylene, and styrene and various common types of cancer. METHODS: In the context of a population-based case-control study carried out in Montreal, 3,730 cancer patients (15 types of cancers, not including leukemia) and 533 population controls were interviewed, and their job histories were translated by a team of experts into occupational exposures, including benzene, toluene, xylene, and styrene. In the present analysis, exposure to these substances was compared between each case series and a control group pooling selected cancer patients and population controls, using logistic regression analysis. RESULTS: Exposure levels were low for most exposed subjects, and there was a high correlation between exposure to benzene, toluene and xylene. For most sites of cancer there was no evidence of excess risk due to these substances. However, limited evidence of increased risk was found for the following associations: esophagus-toluene, colon-xylene, rectum-toluene, rectum-xylene and rectum-styrene. CONCLUSIONS: These latter observations warrant further investigation.

Adult↗