Dioxin Exposure in the Manufacture of Pesticide Production as a Risk Factor for Death from Prostate Cancer: A Meta-analysis (original) (raw)
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Cancer Causes & Control, 2015
Purpose The results of epidemiological studies about exposure to organochlorine pesticides (OCPs) and risk of prostate cancer (PC) are inconclusive. We conducted a meta-analysis to evaluate the association between exposure to specific OCPs and PC. Methods We searched PubMed, Scopus, and Web of science databases for case-control and cohort studies published till March 2015 that provided data about exposure to OCPs and PC. We also contacted authors and handsearched references of the included articles. We calculated pooled estimates using random effects model and explored heterogeneity between studies. Results We systematically reviewed 15 articles and based our meta-analysis on 10 articles covering nine case-control studies and a large prospective cohort study. Pooled estimates of PC for highest versus lowest exposed category to p,p 0-DDE was 1.02 (0.69-1.35), I 2 = 12.7 %, p = 0.333, trans-nonachlor, 0.88 (0.45-1.31), I 2 = 0.00 %, p = 0.892, oxychlordane, 0.91 (0.46-1.35), hexachlorobenzene, 0.88 (0.18-1.57), I 2 = 36.0 %, p = 0.210 from combining results of studies that applied serum OCPs measurements among the general population. For DDT, stratifying studies by exposed population revealed homogeneity, pooled estimate for serum level measurement for the highest exposed versus the lowest exposed of the general population was 0.81 (0.95-1.26), I 2 = 0.00 %, p = 0.400, and for occupational exposure 1.30 (0.94-1.67), I 2 = 13.4 %, p = 0.315. A positive but also insignificant association was obtained for pooling results for high exposure to lindane among farmers and pesticide applicators, 1.56 (0.82-2.29), I 2 = 41.7 %, p = 0.180. Conclusions The existing epidemiological data do not support the hypothesis that exposure to specific OCPs is associated with an increased incidence of PC in the general population.
Asian Pacific Journal of Cancer Prevention, 2014
Background: Chlorophenols (CPs) and related phenoxyacetic acids (PAs) are pesticide groups contaminated with highly toxic 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) during production. PAs and CPs exposure is associated with risk of cancer, but the situation regarding lung cancer has not been clearly defined. We proposed a meta-analysis of published researches to evaluate relationship between chronic exposure to PAs and CPs in pesticide production workplaces and the risk of lung cancer. Materials and Methods: After searching PubMed, Scopus, Scholar Google, Web of Sciences until August 2013, the association between chronic PAs and CPs exposure in production workplace and lung cancer was studied in 15 cohort studies. The standardized mortality rate (SMR) and 95% confidence intervals (CI) were collected from the papers. We used random or fixed-effects models, Egger test, funnel plot and meta regression in our analysis. Results: Five papers with six reports were included in the final analysis. The standardized mortality rate for lung cancer from the random model was 1.18 (95% CI: 1.03-1.35, p=0.014) with moderate heterogeneity. Publication bias was not found for included studies in meta-analysis (p=0.9). Conclusions: Our findings has strengthen the evidence of lung cancer from chronic exposure to chlorophenol related compounds (PAs, CPs).
Significant Issues Raised by Meta-analyses of Cancer Mortality and Dioxin Exposure
Environmental Health Perspectives, 2003
Scientific debate about the potential human carcinogenicity of dioxin-like compounds has been ongoing for nearly 25 years, and recent meta-analyses of data from three occupationally exposed cohorts have reached such different conclusions that the debate is certain to continue. The first meta-analysis [U.S. Environmental Protection Agency (U.S. EPA) 2000] produced an upper-bound estimate of the additional risk of death from any cancer of approximately 10-3 per picogram per kilogram per day for 2,3,7,8-tetrachlorodibenzop-dioxin (TCDD) intake, which the U.S. EPA generalized to all "dioxin-like" compounds via toxic equivalency factors (TEFs). This potency estimate implies that about 4,000 additional cancer deaths occur per year in the United States solely from background intake of dioxin-like compounds [about 1 pg toxic equivalents (TEQ)/kg/day], 95% of which comes from normal dietary sources, and only 10% of which is due to TCDD (U.S. EPA 2000). Subsequently, in 2001, I (Starr 2001) showed that the U.S. EPA's model did not fit the data adequately because it failed to account for a significant baseline elevation of all cancer mortality in the three cohorts; this meta-analysis demonstrated that "these data are entirely consistent with an intercept-only model, a model that has no slope component whatsoever in relation to estimated TCDD body burden," which implies zero additional human cancer deaths from any and all exposures to dioxin-like compounds. Finally, Crump et al. (2003), using updated data for the National Institute for Occupational Safety and Health (NIOSH) cohort (Steenland et al. 1999, 2001), concluded that their metaanalysis "provides some evidence that TEQ exposures near current background levels are carcinogenic." How is it possible for different investigators to reach such markedly different conclusions from similar analyses of essentially the same data? The answer lies in a) a failure to allow for causes of elevated cancer mortality other than dioxin exposure; b) differences in choices for a dose metric; c) selective use of different assumptions regarding the elimination half-life of TCDD in humans; and d) selective use of different assumptions regarding the impact on cancer mortality of the most recent 15 years of exposure. Resolution of the disparate conclusions will require detailed worker exposure data for TCDD and for direct-acting carcinogens, as well as a more general dose-response model that adequately reflects TCDD's characteristics as a promoter. Selection of a Dose Metric Average TCDD body burden. The U.S. EPA (2000) and I (Starr 2001) both employed average TCDD body burden as the dose metric. Fingerhut et al. (1991), in a study of the NIOSH cohort (5,172 workers from 12 U.S. plants), provided all cancer standardized mortality ratios (SMRs) for four exposure duration categories-< 1, 1 to < 5, 5 to < 15, and ≥ 15 years-all with at least 20 years elapsed since first exposure; SMRs [95% confidence intervals (CIs)] for these categories are 102
Use of Agricultural Pesticides and Prostate Cancer Risk in the Agricultural Health Study Cohort
American Journal of Epidemiology, 2003
The authors examined the relation between 45 common agricultural pesticides and prostate cancer incidence in a prospective cohort study of 55,332 male pesticide applicators from Iowa and North Carolina with no prior history of prostate cancer. Data were collected by means of self-administered questionnaires completed at enrollment (1993)(1994)(1995)(1996)(1997). Cancer incidence was determined through population-based cancer registries from enrollment through December 31, 1999. A prostate cancer standardized incidence ratio was computed for the cohort. Odds ratios were computed for individual pesticides and for pesticide use patterns identified by means of factor analysis. A prostate cancer standardized incidence ratio of 1.14 (95% confidence interval: 1.05, 1.24) was observed for the Agricultural Health Study cohort. Use of chlorinated pesticides among applicators over 50 years of age and methyl bromide use were significantly associated with prostate cancer risk. Several other pesticides showed a significantly increased risk of prostate cancer among study subjects with a family history of prostate cancer but not among those with no family history. Important family history-pesticide interactions were observed.
Pesticide exposure and cancer: an integrative literature review
Saúde em Debate
We conducted an integrative literature review of published studies on pesticide and cancer exposure, focusing on farmers, rural population, pesticide applicators, and rural workers. The Medline/PubMed was used as searching database. After the retrieval, 74 articles were selected according to pre-established criteria, which design involved 39 case-controls, 32 cohorts, 2 ecological ones, and 1 cross-sectional. Among them, 64 studies showed associations between pesticides and cancer while 10 did not find any significant association. The studies found 53 different types of pesticides significantly associated with at least one type of cancer and 19 different types of cancers linked to at least one type of pesticide. Although few studies presented contradictory results, the sole fact of being a farmer or living near crops or high agricultural areas have also been used as a proxy for pesticide exposure and significantly associated with higher cancer risk. The literature well illustrates t...
American journal of …, 1997
The authors examined cancer mortality in a historical cohort study of 21,863 male and female workers in 36 cohorts exposed to phenoxy herbicides, chlorophenols, and dioxins in 12 countries. Subjects in this updated and expanded multinational study coordinated by the International Agency for Research on Cancer were followed from 1939 to 1992. Exposure was reconstructed using job records, company exposure questionnaires, and serum and adipose tissue dbxin levels. Among workers exposed to phenoxy herbicides contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or higher chlorinated dioxins, mortality from soft-tissue sarcoma (6 deaths; standardized mortality ratio (SMR) = 2.03, 95% confidence interval (CO 0.75-4.43) was higher than expected from national mortality rates. Mortality from all malignant neoplasms (710 deaths; SMR = 1.12, 95% Cl 1.04-1.21), non-Hodgkin's lymphoma (24 deaths; SMR = 1.39,95% Cl 0.89-2.06), and lung cancer (225 deaths; SMR = 1.12,95% Cl 0.98-1.28) was slightly elevated. Risks for all neoplasms, for sarcomas, and for lymphomas increased with time since first exposure. In workers exposed to phenoxy herbicides with minimal or no contamination by TCDD and higher chlorinated dioxins, mortality from all neoplasms (398 deaths; SMR = 0.96, 95% Cl 0.87-1.06), non-Hodgkin's lymphoma (9 deaths; SMR = 1.00), and lung cancer (148 deaths; SMR = 1.03) was similar to that expected, and mortality from soft-tissue sarcoma was slightly elevated (2 deaths; SMR = 1.35). In a Poisson regression analysis, workers exposed to TCDD or higher chlorinated dioxins had an increased risk for all neoplasms (rate ratio = 1.29,95% Cl 0.94-1.76) compared with workers from the same cohort exposed to phenoxy herbicides and chlorophenols but with minimal or no exposure to TCDD and higher chlorinated dioxins. These findings indicate that exposure to herbicides contaminated with TCDD and higher chlorinated dioxins may be associated with a small increase in overall cancer risk and in risk for specific cancers.
Environmental Health Perspectives, 1998
The authors studied noncancer mortality among phenoxyacid herbicide and chlorophenol production workers and sprayers included in an international study comprising 36 cohorts from 12 countries followed from 1939 to 1992. Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin or higher chlorinated dioxins (TCDD/HCD) was discerned from job records and company questionnaires with validation by biologic and environmental measures. Standard mortality ratio analyses suggested a moderate healthy worker effect for all circulatory diseases, especially ischemic heart disease, among both those exposed and those not exposed to TCDD/HCD. In Poisson regression analyses, exposure to TCDD/HCD was not associated with increased mortality from cerebrovascular disease. However, an increased risk for circulatory disease, especially ischemic heart disease (rate ratio [RRI 1.67, 95% confidence interval [Cl] 1.23-2.26) and possibly diabetes (RR 2.25, 95% Cl 0.53-9.50), was present among TCDD/HCD-exposed workers. Risks tended to be higher 10 to 19 years after first exposure and for those exposed for a duration of 10 to 19 years. Mortality from suicide was comparable to that for the general population for all workers exposed to herbicides or chlorophenols and was associated with short latency and duration of exposure. More refined investigations of the ischemic heart disease and TCDD/HCD exposure association are warranted. -Environ Health Perspect 106(Suppl 2):645-653 (1998). http.//ehpnetl.niehs.nih.gov/docs/1998/Suppl-2/645-653vena/abstract.html