Prostate Cancer and Ambient Pesticide Exposure in Agriculturally Intensive Areas in California

Department of Preventive Medicine, Keck School of Medicine, University of Southern California, 1441 Eastlake Avenue, Los Angeles, CA 90089-9175, USA.
American journal of epidemiology (Impact Factor: 5.23). 03/2011; 173(11):1280-8. DOI: 10.1093/aje/kwr003
Source: PubMed


In a population-based case-control study in California's intensely agricultural Central Valley (2005-2006), the authors investigated relations between environmental pesticide/fungicide exposure and prostate cancer. Cases (n = 173) were obtained from a population-based cancer registry, and controls (n = 162) were obtained from Medicare listings and tax assessor mailings. Past ambient exposures to pesticides/fungicides were derived from residential history and independently recorded pesticide and land-use data, using a novel geographic information systems approach. In comparison with unexposed persons, increased risks of prostate cancer were observed among persons exposed to compounds which may have prostate-specific biologic effects (methyl bromide (odds ratio = 1.62, 95% confidence interval: 1.02, 2.59) and a group of organochlorines (odds ratio = 1.64, 95% confidence interval: 1.02, 2.63)) but not among those exposed to other compounds that were included as controls (simazine, maneb, and paraquat dichloride). The authors assessed the possibility of selection bias due to less-than-100% enrollment of eligible cases and controls (a critical methodological concern in studies of this kind) and determined that there was little evidence of bias affecting the estimated effect size. This study provides evidence of an association between prostate cancer and ambient pesticide exposures in and around homes in intensely agricultural areas. The associations appear specific to compounds with a plausible biologic role in prostate carcinogenesis.

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    • "Although epidemiological and toxicological studies provide important evidence for the role of environmental exposure in initiation or progression of degenerative diseases and cancer [1], [2], [3], [4], there is still a challenge to correlate exposure with disease prevalence. In fact, objectively verifiable, individual exposure data (and possible confounder levels) appear to be a major problem allowing to draw a link between the environmental exposure and the cause of disease. "
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    ABSTRACT: There is a need for a panel of suitable biomarkers for detection of environmental chemical exposure leading to the initiation or progression of degenerative diseases or potentially, to cancer. As the peripheral blood may contain increased levels of circulating cell-free DNA in diseased individuals, we aimed to evaluate this DNA as effect biomarker recognizing vulnerability after exposure to environmental chemicals. We recruited 164 individuals presumably exposed to halo-alkane-based pesticides. Exposure evaluation was based on human biomonitoring analysis; as biomarker of exposure parent halo-methanes, -ethanes and their metabolites, as well as the hemoglobin-adducts methyl valine and hydroxyl ethyl valine in blood were used, complemented by expert evaluation of exposure and clinical intoxication symptoms as well as a questionnaire. Assessment showed exposures to halo alkanes in the concentration range being higher than non-cancer reference doses (RfD) but (mostly) lower than the occupational exposure limits. We quantified circulating DNA in serum from 86 individuals with confirmed exposure to off-gassing halo-alkane pesticides (in storage facilities or in home environment) and 30 non-exposed controls, and found that exposure was significantly associated with elevated serum levels of circulating mitochondrial DNA (in size of 79 bp, mtDNA-79, p = 0.0001). The decreased integrity of mtDNA (mtDNA-230/mtDNA-79) in exposed individuals implicates apoptotic processes (p = 0.015). The relative amounts of mtDNA-79 in serum were positively associated with the lag-time after intoxication to these chemicals (r = 0.99, p<0.0001). Several months of post-exposure the specificity of this biomarker increased from 30% to 97% in patients with intoxication symptoms. Our findings indicate that mitochondrial DNA has a potential to serve as a biomarker recognizing vulnerable risk groups after exposure to toxic/carcinogenic chemicals.
    PLoS ONE 05/2013; 8(5):e64413. DOI:10.1371/journal.pone.0064413 · 3.23 Impact Factor
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    • "Residential exposure to pesticides has been linked to several adverse health outcomes, including adult cancers, such as non- Hodgkin lymphoma (Colt et al. 2006; Ward et al. 2009) and prostate cancer (Cockburn et al. 2011); childhood cancers, such as non- Hodgkin lymphoma, leukemia, and brain cancer (Infante-Rivard and Weichenthal 2007; Metayer and Buffler 2008; Van Maele- Fabry et al. 2011); and neurodevelopmental deficits (Bouchard et al. 2011; Engel et al. 2011; Rauh et al. 2011; Rosas and Eskenazi 2008). In epidemiologic studies of cancer, self-reported pesticide use is typically used to estimate residential pesticide exposure because of its low cost and participant burden (Ritz and Rull 2008). "
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    ABSTRACT: Background: Residential pesticide exposure has been linked to adverse health outcomes in adults and children. High-quality exposure estimates are critical for confirming these associations. Past epidemiologic studies have used one measurement of pesticide concentrations in carpet dust to characterize an individual’s average long-term exposure. If concentrations vary over time, this approach could substantially misclassify exposure and attenuate risk estimates. Objectives: We assessed the repeatability of pesticide concentrations in carpet dust samples and the potential attenuation bias in epidemiologic studies relying on one sample. Methods: We collected repeated carpet dust samples (median = 3; range, 1–7) from 21 homes in Fresno County, California, during 2003–2005. Dust was analyzed for 13 pesticides using gas chromatography–mass spectrometry. We used mixed-effects models to estimate between- and within-home variance. For each pesticide, we computed intraclass correlation coefficients (ICCs) and the estimated attenuation of regression coefficients in a hypothetical case–control study collecting a single dust sample. Results: The median ICC was 0.73 (range, 0.37–0.95), demonstrating higher between-home than within-home variability for most pesticides. The expected magnitude of attenuation bias associated with using a single dust sample was estimated to be ≤ 30% for 7 of the 13 compounds evaluated. Conclusions: For several pesticides studied, use of one dust sample to represent an exposure period of approximately 2 years would not be expected to substantially attenuate odds ratios. Further study is needed to determine if our findings hold for longer exposure periods and for other pesticides.
    Environmental Health Perspectives 05/2013; 121(5). DOI:10.1289/ehp.1205811 · 7.98 Impact Factor
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    • "The study by Sharpe et al. (2001) suggests that pesticide exposure might be more relevant among people exposed during leisure rather than when farming. Some studies indicate an increased risk of prostate cancer with occupational pesticide exposure (e.g., Strom, Yamamura, Flores-Sandoval, Pettaway, & Lopez, 2008), whereas others show no association (Cockburn et al., 2011; Fritschi, Glass, Tabrizi, Leavy, & Ambrosini, 2007; Kumar et al., 2010), and similarly in these studies specific occupational exposure was not defined. It is possible that subjects exposed to pesticides during leisure take fewer precautions than subjects who use pesticides in the workplace. "
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    ABSTRACT: Prostate cancer is the leading cancer type diagnosed in American men and is the second leading cancer diagnosed in men worldwide. Although studies have been conducted to investigate the association between prostate cancer and exposure to pesticides and/or farming, the results have been inconsistent. We performed a meta-analysis to summarize the association of farming and prostate cancer. The PubMed database was searched to identify all published case-control studies that evaluated farming as an occupational exposure by questionnaire or interview and prostate cancer. Ten published and two unpublished studies were included in this analysis, yielding 3,978 cases and 7,393 controls. Prostate cancer cases were almost four times more likely to be farmers compared with controls with benign prostate hyperplasia (BPH; meta odds ratio [OR], crude = 3.83, 95% confidence interval [CI] = 1.96-7.48, Q-test p value = .352; two studies); similar results were obtained when non-BPH controls were considered, but with moderate heterogeneity between studies (meta OR crude = 1.38, 95% CI = 1.16-1.64, Q-test p value = .216, I(2) = 31% [95% CI = 0-73]; five studies). Reported pesticide exposure was inversely associated with prostate cancer (meta OR crude = 0.68, 95% CI = 0.49-0.96, Q-test p value = .331; four studies), whereas no association with exposure to fertilizers was observed. Our findings confirm that farming is a risk factor for prostate cancer, but this increased risk may not be due to exposure to pesticides.
    American journal of men's health 09/2012; 7(2). DOI:10.1177/1557988312458792 · 1.15 Impact Factor
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