Scott Weichenthal1, Eric Lavigne2, Marie-France Valois3, Marianne Hatzopoulou4, Keith Van Ryswyk5, Maryam Shekarrizfard4, Paul J Villeneuve6, Mark S Goldberg3, Marie-Elise Parent7. 1. Department of Epidemiology, Biostatistics, and Occupational Health and Gerald Bronfman Department of Oncology, McGill University, Montreal, Canada; Health Canada, Air Health Science Division, Ottawa, Canada. Electronic address: scott.weichenthal@mcgill.ca. 2. Department of Epidemiology, Biostatistics, and Occupational Health and Gerald Bronfman Department of Oncology, McGill University, Montreal, Canada; Department of Epidemiology, Public Health and Preventive Medicine, University of Ottawa, Ottawa, Canada. 3. Department of Medicine, McGill University, Montreal, Canada; Division of Clinical Epidemiology, Research Institute of the McGill University Hospital Centre. 4. Department of Civil Engineering, University of Toronto, Toronto, Canada. 5. Department of Epidemiology, Biostatistics, and Occupational Health and Gerald Bronfman Department of Oncology, McGill University, Montreal, Canada. 6. Department of Health Sciences, School of Mathematics and Statistics, Carleton University, Ottawa, Ontario, Canada. 7. INRS-Institut Armand-Frappier, University of Quebec, Montreal, Canada.
Abstract
BACKGROUND: Diesel exhaust contains large numbers of ultrafine particles (UFPs, <0.1µm) and is a recognized human carcinogen. However, epidemiological studies have yet to evaluate the relationship between UFPs and cancer incidence. METHODS: We conducted a case-control study of UFPs and incident prostate cancer in Montreal, Canada. Cases were identified from all main Francophone hospitals in the Montreal area between 2005 and 2009. Population controls were identified from provincial electoral lists of French Montreal residents and frequency-matched to cases using 5-year age groups. UFP exposures were estimated using a land use regression model. Exposures were assigned to residential locations at the time of diagnosis/recruitment as well as approximately 10-years earlier to consider potential latency between exposure and disease onset. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated per interquartile range (IQR) increase in UFPs (approximately 4000 particles/cm3) using logistic regression models adjusting for individual-level and ecological covariates. RESULTS: Ambient UFP concentrations were associated with an increased risk of prostate cancer (OR=1.10, 95% CI: 1.01, 1.19) in fully adjusted models when exposures were assigned to residences 10-years prior to diagnosis. This risk estimate increased slightly (OR=1.17, 95% CI; 1.01, 1.35) when modeled as a non-linear natural spline function. A smaller increased risk (OR=1.04, 95% CI: 0.97, 1.11) was observed when exposures were assigned to residences at the time of diagnosis. CONCLUSIONS: Exposure to ambient UFPs may increase the risk of prostate cancer. Future studies are needed to replicate this finding as this is the first study to evaluate this relationship. Crown
BACKGROUND: Diesel exhaust contains large numbers of ultrafine particles (UFPs, <0.1µm) and is a recognized human carcinogen. However, epidemiological studies have yet to evaluate the relationship between UFPs and cancer incidence. METHODS: We conducted a case-control study of UFPs and incident prostate cancer in Montreal, Canada. Cases were identified from all main Francophone hospitals in the Montreal area between 2005 and 2009. Population controls were identified from provincial electoral lists of French Montreal residents and frequency-matched to cases using 5-year age groups. UFP exposures were estimated using a land use regression model. Exposures were assigned to residential locations at the time of diagnosis/recruitment as well as approximately 10-years earlier to consider potential latency between exposure and disease onset. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated per interquartile range (IQR) increase in UFPs (approximately 4000 particles/cm3) using logistic regression models adjusting for individual-level and ecological covariates. RESULTS: Ambient UFP concentrations were associated with an increased risk of prostate cancer (OR=1.10, 95% CI: 1.01, 1.19) in fully adjusted models when exposures were assigned to residences 10-years prior to diagnosis. This risk estimate increased slightly (OR=1.17, 95% CI; 1.01, 1.35) when modeled as a non-linear natural spline function. A smaller increased risk (OR=1.04, 95% CI: 0.97, 1.11) was observed when exposures were assigned to residences at the time of diagnosis. CONCLUSIONS: Exposure to ambient UFPs may increase the risk of prostate cancer. Future studies are needed to replicate this finding as this is the first study to evaluate this relationship. Crown
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