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Occup Environ Med 2007;64:60-65 doi:10.1136/oem.2006.027706
  • Original article

Occupational risk factors for prostate cancer and benign prostatic hyperplasia: a case–control study in Western Australia

  1. L Fritschi1,
  2. D C Glass2,
  3. J S Tabrizi3,
  4. J E Leavy4,
  5. G L Ambrosini4
  1. 1Western Australian Institute for Medical Research, Perth, Western Australia, Australia
  2. 2Centre for Occupational and Environmental Health, Department of Epidemiology and Preventive Medicine, Monash University, Victoria, Australia
  3. 3School of Population Health, University of Queensland, Brisbane, Queensland, Australia
  4. 4School of Population Health, University of Western Australia, Perth, Western Australia, Australia
  1. Correspondence to:
 Associate Professor
 L Fritschi, Laboratory for Cancer Medicine, Western Australian Institute for Medical Research, 5th Floor, Rear 50 Murray Street, Perth, Western Australia, Australia; fritschi{at}waimr.uwa.edu.au
  • Accepted 12 September 2006
  • Published Online First 3 October 2006

Abstract

Objective: To assess the association of selected occupational exposures with risk of prostate cancer and with risk of benign prostatic hyperplasia (BPH).

Methods: This population-based case–control study recruited 606 men with a diagnosis of confirmed prostate cancer, 400 men who had undergone their first prostatectomy for BPH and 471 male controls randomly selected from the electoral roll between 1 August 2001 and 1 October 2002 in Western Australia. χ2 tests and logistic regressions were used for univariate and multivariate analyses to investigate the association of the two outcomes with occupational exposure to pesticides, fertilisers, metals, wood dust, oils, diesel exhaust and polyaromatic hydrocarbons (PAHs).

Results: Exposure to toxic metals at a non-substantial level increased the risk of BPH (odds ratio (OR) 1.39, 95% confidence interval (CI) 1.1 to 1.84) and led to a non-significant excess risk of prostate cancer (OR 1.25, 95% CI 0.96 to 1.61). Non-significant excess risks were observed for prostate cancer after exposure to oils other than mineral oil (OR 1.54, 95% CI 0.95 to 2.51) and for BPH after exposure to PAHs (OR 1.20, 95% CI 0.91 to 1.58). A non-statistically significant protective effect for prostate cancer was seen after exposure to organophosphate pesticides (OR 0. 69, 95% CI 0.43 to 1.12). No other associations were found for either prostate cancer or BPH and no dose–response relationships were seen for the exposures investigated.

Conclusions: These results do not provide evidence that any of the occupational factors examined are risk factors for either prostate cancer or BPH.

Footnotes

  • Published Online First 3 October 2006

  • Funding: This study was supported by a Western Australian Health Promotion Foundation (Healthway) Research Project Grant and the BUPA Foundation. LF is supported by a Career Development Award from the National Health and Medical Research Council.

  • Competing interests: None.

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