Pesticides

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Summary

TBD.

News Timeline

  • EPA releases estimates of U.S. pesticide use, WesternFarmPress.com, February 23, 2011.
  • EPA sued over pesticides, endangered species, Reuters, January 21, 2011.
    • Claims. "The EPA does a number of tests on pesticides but rarely discusses their effects with U.S. Fish and Wildlife officials, which the suit aims to force them to do, the Center for Biological Diversity said. "The ecological risk assessment does not consider the cumulative or synergistic effects posed by multiple pesticides on wildlife or the environment, nor does it address delayed effects of pesticides, referred to as 'lag effects,'" the suit filed in San Francisco federal court charges."

Studies and Reports

  • Mink P et al., Pesticides and prostate cancer: a review of epidemiologic studies with specific agricultural exposure information, Eur J Cancer Prev. 2008 Apr;17(2):97-110.
    • Abstract. "Prostate cancer is the most commonly diagnosed cancer in US men, and the second most commonly diagnosed cancer among men worldwide. Although pesticides have been implicated in studies of prostate cancer among farmers, meta-analyses have found heterogeneity across studies, and a number of exposures and lifestyle factors may be unique to farmers. The purpose of this paper is to review the epidemiologic literature to evaluate the hypothesis that agricultural exposure to pesticides is causally associated with prostate cancer risk. We analyzed the eight cohort studies and five case-control studies that quantified and/or evaluated agricultural exposure to particular pesticide classes or chemicals. Despite sporadic positive findings, these studies did not show consistently increased risks to support a causal association between agricultural pesticide use and prostate cancer. Studies using an 'external' comparison group must be interpreted in the context of confounding by differences in prostate-specific antigen screening intensity. Furthermore, most studies did not adjust for potential confounders other than age and time period. It is clearly not possible to exonerate any particular pesticide as a putative cause of prostate cancer - to do so would require an inverse empirical association with an upper confidence limit below the null value. Existing evidence does not point to any pesticide as satisfying widely used guidelines for establishing causation: a strong, exposure-dependent and demonstrably unconfounded, unbiased association, documented in several studies."
  • Li A et al., Evaluation of epidemiologic and animal data associating pesticides with Parkinson's disease, J Occup Environ Med. 2005 Oct;47(10):1059-87.
    • Abstract. "Exposure to pesticides may be a risk factor for developing Parkinson's disease (PD). To evaluate the evidence regarding this association in the scientific literature, we examined both analytic epidemiologic studies of PD cases in which exposure to pesticides was queried directly and whole-animal studies for PD-like effects after systemic pesticide exposure. Epidemiologic studies were considered according to study quality parameters, and results were found to be mixed and without consistent exposure-response or pesticide-specific patterns. These epidemiologic studies were limited by a lack of detailed and validated pesticide exposure assessment. In animal studies, no pesticide has yet demonstrated the selective set of clinical and pathologic signs that characterize human PD, particularly at levels relevant to human populations. We conclude that the animal and epidemiologic data reviewed do not provide sufficient evidence to support a causal association between pesticide exposure and PD."
  • Blair A et al., Mortality among participants in the agricultural health study, Ann Epidemiol. 2005 Apr;15(4):279-85.
    • Conclusion. "Several factors may contribute to the low mortality observed in this population (of licensed pesticide applicators and their spouses), including the healthy worker effect typically seen in cohorts of working populations (which may decline in future years), a short follow-up interval, and a healthier lifestyle manifested through lower cigarette use and an occupation that has traditionally required high levels of physical activity."
  • Burns C. Cancer among pesticide manufacturers and applicators, Scand J Work Environ Health. 2005;31 Suppl 1:9-17; discussion 5-7.
    • Abstract. There are hundreds of studies of cancer and agriculture chemicals. However, few have focused on a single pesticide or class of pesticide. While cancer studies of nonspecific pesticide exposure among populations may provide hypotheses for additional testing, they contribute little to the understanding of the health risks of specific agricultural chemicals. This review concentrates on both the cancer findings and the exposure parameters in cohort studies of workers who manufacture or apply pesticides. Occupational studies of pesticide manufacturers and applicators provide important contributions to the causal assessment of the carcinogenicity of specific pesticides because the exposure is often longer, more intense, and better defined than for other study populations. Among the studies reviewed, there is little indication of increased cancer risk among pesticide manufacturers or sprayers. Limitations in sample size, exposure assessment, and the small number of studies make causal inference difficult. Additional methodological improvements with respect to exposure would contribute significantly to the understanding of the potential cancer risk from individual pesticides."
  • Alavanja M et al., Pesticides and lung cancer risk in the agricultural health study cohort, Am J Epidemiol. 2004 Nov 1;160(9):876-85.
    • Abstract. "The authors examined the relation between 50 widely used agricultural pesticides and lung cancer incidence in the Agricultural Health Study, a prospective cohort study of 57,284 pesticide applicators and 32,333 spouses of farmer applicators with no prior history of lung cancer. Self-administered questionnaires were completed at enrollment (1993-1997). Cancer incidence was determined through population-based cancer registries from enrollment through December 31, 2001. A lung cancer standardized incidence ratio of 0.44 (95% confidence interval: 0.39, 0.49) was observed overall, due in large part to a low cigarette smoking prevalence. Two widely used herbicides, metolachlor and pendimethalin (for low-exposed groups to four higher exposure categories: odds ratio (OR) = 1.0, 1.6, 1.2, 5.0; p(trend) = 0.0002; and OR = 1.0, 1.6, 2.1, 4.4; p(trend) = 0.003, respectively), and two widely used insecticides, chlorpyrifos and diazinon (OR = 1.0, 1.1, 1.7, 1.9; p(trend) = 0.03; and OR = 1.0, 1.6, 2.7, 3.7; p(trend) = 0.04, respectively), showed some evidence of exposure response for lung cancer. These excesses could not be explained by previously identified lung cancer risk factors. The usage levels in this cohort are considerably higher than those typically experienced by the general population. An excess risk among spouses directly exposed to pesticides could not be evaluated at this time."
  • Cantor K et al., Risk of non-Hodgkin's lymphoma and prediagnostic serum organochlorines: beta-hexachlorocyclohexane, chlordane/heptachlor-related compounds, dieldrin, and hexachlorobenzene, Environ Health Perspect. 2003 Feb;111(2):179-83.
    • Abstract. "Increases in non-Hodgkin's lymphoma (NHL) incidence and mortality rates during the past few decades remain largely unexplained. Studies suggest that organochlorine pesticides may contribute to an increased risk of NHL. In 1974, serum samples were obtained from 25,802 participants in the Campaign Against Cancer and Stroke in Washington County, Maryland (USA), and cryopreserved for future study. We measured prediagnostic levels of chlordane, lindane (gamma-hexachlorocyclohexane), beta-hexachlorocyclohexane, transnonachlor, heptachlor, heptachlor epoxide, oxychlordane, dieldrin, and hexachlorobenzene in serum samples of 74 cases of NHL and 147 matched controls. Previously, we found an association between NHL and serum levels of total PCBs (polychlorinated biphenyls), but not DDT (dichlorodiphenyltrichloroethane) and related compounds. In this instance, there was no evidence of an association between NHL risk and serum levels of any of the individual lipid- and recovery-corrected organochlorines that we evaluated, nor of the summed chlordane-related compounds (transnonachlor, heptachlor, heptachlor epoxide, oxychlordane). These findings do not support the hypothesis that the organochlorine compounds included in this study are strongly linked to the development of NHL. The possibility of a weak association cannot be excluded by these data."
  • Gammon M et al., Environmental toxins and breast cancer on Long Island. II. Organochlorine compound levels in blood, Cancer Epidemiol Biomarkers Prev. 2002 Aug;11(8):686-97.
    • Conclusions. "Whether environmental contaminants increase breast cancer risk among women on Long Island, NY, is unknown. The study objective is to determine whether breast cancer risk is increased in relation to organochlorines, compounds with known estrogenic characteristics that were extensively used on Long Island and other areas of the United States. Recent reports do not support a strong association, although there are concerns with high risks observed in subgroups of women. Blood samples from 646 case and 429 control women from a population-based case-control study conducted on Long Island were analyzed. No substantial elevation in breast cancer risk was observed in relation to the highest quintile of lipid-adjusted serum levels of p,p'-bis(4-chlorophenyl)-1,1-dichloroethene (DDE) [odds ratio (OR), 1.20 versus lowest quintile; 95% confidence interval (CI), 0.76-1.90], chlordane (OR, 0.98; 95% CI, 0.62-1.55), dieldrin (OR, 1.37; 95% CI, 0.69-2.72), the sum of the four most frequently occurring PCB congeners (nos. 118, 153, 138, and 180; OR, 0.83; 95% CI, 0.54-1.29), and other PCB congener groupings. No dose-response relations were apparent. Nor was risk increased in relation to organochlorines among women who had not breastfed or were overweight, postmenopausal, or long-term residents of Long Island; or with whether the case was diagnosed with invasive rather than in situ disease, or with a hormone receptor-positive tumor. These findings, based on the largest number of samples analyzed to date among primarily white women, do not support the hypothesis that organochlorines increase breast cancer risk among Long Island women."
  • Fleming L et al., Cancer incidence in a cohort of licensed pesticide applicators in Florida, J Occup Environ Med. 1999 Apr;41(4):279-88.
    • Abstract. "This study is a standardized incidence ratio (SIR) analysis of cancer incidence of licensed pesticide applicators in Florida, compared with that of Florida's general population. Through extensive data linkages, 33,658 applicators were assembled who had 1266 incident cancers and 279,397 person-years from January 1, 1975, to December 31, 1993. Disease risk from ethanol and tobacco use were significantly decreased. Among males, prostate cancer (SIR = 1.91; 95% confidence interval [CI], 1.72-2.13) and testicular cancer (SIR = 2.48; 95% CI, 1.57-3.72) were significantly elevated. No confirmed cases of soft tissue sarcoma (STS) were found, and the incidence of non-Hodgkin's lymphoma was not increased. There were few female applicators; nevertheless, cervical cancer incidence (SIR = 3.69; 95% CI, 1.84-6.61) was significantly increased, while the incidence of breast cancer was significantly decreased. Cancers that have been associated with estrogen disrupters were found in male, but not female, pesticide applicators. The lack of soft tissue sarcoma is at odds with prior literature associated with the use of phenoxy herbicides."
  • Fleming L et al., Mortality in a cohort of licensed pesticide applicators in Florida, Occup Environ Med. 1999 Jan;56(1):14-21.
    • Results and Conclusions. RESULTS: The pesticide applicators were consistently and significantly healthier than the general population of Florida. As with many occupational cohorts, the risks of cardiovascular disease and of diseases associated with alcohol and tobacco use were significantly lower, even in the subpopulations--for example, men, women, and licence subcategories. Among male applicators, prostate cancer mortality (SMR 2.38 (95% confidence interval (95% CI) 1.83 to 3.04) was significantly increased. No cases of soft tissue sarcoma were confirmed in this cohort, and non-Hodgkin's lymphoma was not increased. The number of female applicators was small, as were the numbers of deaths. Mortality from cervical cancer and breast cancer was not increased. Additional subcohort and exposure analyses were performed. CONCLUSIONS: Consistent with previous publications on farmers but at odds with current theories about the protective effects of vitamin D, prostate cancer was increased in these pesticide applicators. Female breast cancer was not increased despite theories linking risk of breast cancer with exposure to oestrogen disruptors--such as the organochlorines. The lack of cases of soft tissue sarcoma is at odds with previous publications associating the use of the phenoxy herbicides with an increased risk of these cancers."
  • Acquavella J et al., Cancer among farmers: a meta-analysis, Ann Epidemiol. 1998 Jan;8(1):64-74.
    • Conclusions. "The results do not suggest that farmers have elevated rates of several cancers. However, the known heterogeneity of exposures by type of farming, geographic area, time period, and other factors limits the informativeness of meta-analyses of these studies for assessing potential carcinogenic exposures in agriculture."
  • Ritter L, Report of a panel on the relationship between public exposure to pesticides and cancer. Ad Hoc Panel on Pesticides and Cancer. National Cancer Institute of Canada, Cancer. 1997 Nov 15;80(10):2019-33.
    • Conclusions. "The Panel concluded that it was not aware of any definitive evidence to suggest that synthetic pesticides contribute significantly to overall cancer mortality. The Panel also concluded that it did not believe that any increased intake of pesticide residues associated with increased intake of fruits and vegetables poses any increased risk of cancer. The Panel further concluded, among other things, that tobacco use continues to be the most important preventable cause of cancer and premature mortality and thus is an appropriate focus for cancer control strategy."
  • Dich J et al., Pesticides and cancer, Cancer Causes Control. 1997 May;8(3):420-43.
    • Abstract. "Epidemiologic evidence on the relationship between chemical pesticides and cancer is reviewed. In animal studies, many pesticides are carcinogenic, (e.g., organochlorines, creosote, and sulfallate) while others (notably, the organochlorines DDT, chlordane, and lindane) are tumor promoters. Some contaminants in commercial pesticide formulations also may pose a carcinogenic risk. In humans, arsenic compounds and insecticides used occupationally have been classified as carcinogens by the International Agency for Research on Cancer. Human data, however, are limited by the small number of studies that evaluate individual pesticides. Epidemiologic studies, although sometimes contradictory, have linked phenoxy acid herbicides or contaminants in them with soft tissue sarcoma (STS) and malignant lymphoma; organochlorine insecticides are linked with STS, non-Hodgkin's lymphoma (NHL), leukemia, and, less consistently, with cancers of the lung and breast; organophosphorous compounds are linked with NHL and leukemia; and triazine herbicides with ovarian cancer. Few, if any, of these associations can be considered established and causal. Hence, further epidemiologic studies are needed with detailed exposure assessment for individual pesticides, taking into consideration work practices, use of protective equipment, and other measures to reduce risk."
  • Amoateng-Adjepong Y et al., Mortality among workers at a pesticide manufacturing plant, J Occup Environ Med. 1995 Apr;37(4):471-8.
    • Abstract. "This study evaluated the mortality experience of 2384 workers at a plant in Colorado that produced aldrin, azodrin, vapona, and other pesticides. Subjects were followed up for a median of 29 years, from 1952 through 1990. Comparisons of the cohort's mortality rates with those of the Colorado population indicated that observed and expected numbers of deaths were similar for all causes (465 observed/473 expected) and for all cancers (113/106). Standardized mortality ratios were elevated for hepatobiliary cancer (5/2.0; standardized mortality ratio, 249, 95% confidence interval, 81 to 581), due to an excess of biliary duct/gall bladder cancer, and for pneumonia (20/13; standardized mortality ratio, 150, 95% confidence interval, 92 to 232). These increases were limited to white men in hourly jobs but were not limited to any particular production unit and did not display duration-response trends. It is unlikely that these excesses are due to occupational exposures at the plant."
  • Boyle C et al., Proxy respondents and the validity of occupational and other exposure data. The Selected Cancers Cooperative Study Group, Am J Epidemiol. 1992 Sep 15;136(6):712-21.
    • Abstract. "As part of a multicenter cancer case-control study conducted in 1984-1988, a proxy interview was attempted for all cases who were initially interviewed for the study but who died during the 4-year data collection period. To assess the validity of using wives, other relatives, or other informants to obtain information about a subject, the authors compared occupational and other exposure data obtained from 270 male cancer cases and their proxy respondents. The primary focus of the case-control study was on Vietnam military service and exposure to phenoxy herbicides, but cases and their proxy respondents were also asked about occupational and other exposures relevant to the cancers. The accuracy of reporting for specific occupational exposures (e.g., asbestos and formaldehyde) and specific occupations (e.g., dry cleaning and meat packing or processing) was poor, although the latter improved somewhat when only case-spouse pairs were examined. Similarly, there was poor sensitivity in the reporting of herbicide exposure information in farming and other related occupations. In contrast, the reporting of certain demographic characteristics, childhood history characteristics, and use of alcohol and cigarettes was relatively good, and was even better when only case-spouse pairs were examined. The poor quality of proxy information for detailed exposure information suggests the need for careful use and interpretation of proxy information in epidemiologic studies."

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