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Pesticide-Induced Diseases: Cancer

Bladder CancerBone CancerBrain CancerCervical CancerColorecatal CancerEye CancerGallbladder CancerKidney/Renal CancerLarynx CancerLeukemiaLip CancerLiver/Hepatic CancerLung CancerLymphomaMelanomaMouth CancerMultiple MyelomaNeuroblastomaOesophageal CancerOvarian CancerPancreatic CancerProstate CancerSoft Tissue SarcomaStomach CancerSinonasal Cancer ● Testicular CancerThyroid CancerUteran Cancer

The link between pesticides and cancer has long been a concern. While agriculture has traditionally been tied to pesticide-related illnesses, 19 of 30 commonly used lawn pesticides and 28 of 40 commonly used school pesticides are linked to cancer. Even with the growing body of evidence linking environmental exposures to cancer in recent years, a report released May 6, 2010 by the President’s Cancer Panel finds that the true burden of environmentally-induced cancer is greatly underestimated. The Panel’s report, Reducing Environmental Cancer Risk: What We Can Do Now, concludes that while environmental exposure is not a new front on the war on cancer, the grievous harm from carcinogenic chemical use has not been addressed adequately by the nation’s cancer program.

Bladder Cancer

  • Gene environment interaction in urinary bladder cancer with special reference to organochlorine pesticide: a case control study.
    Urinary bladder cancer (UBC) is a common disease worldwide with a higher incidence rate in developed countries. Organochlorine pesticides (OCPs), potent endocrine disrupters, are found to be associated with several cancers such as prostate, breast, bladder, etc. The present study was carried out in UBC subjects and healthy control subjects with an aim to determine the role of Glutathione S-transferase (GST) and GSTT1 polymorphism and its implication on the OCP detoxification or bioaccumulation which may increase the risk of UBC in humans. This study was also designed to identify the "gene-environment interaction" specifically between gene polymorphism in xenobiotic metabolizing genetic enzyme(s) and blood OCP levels. The results demonstrated a significant increase in frequency of GSTM1/GSTT1(null) genotype in UBC cases without interfering the distribution of other GSTT1/GSTM1 genotypes. Findings indicate that "gene-environment interaction" may play a key role in increasing the risk for UBC in individuals who are genetically more susceptible due to presence of GSTM1/GSTT1 null deletion during their routine encounter with or exposure to OCPs.
    [Sharma T, Jain S, Verma A et al. 2013. Cancer Biomark.13(4):243-51]
  • Cancer among farmers in central Italy
    A case-referent study of Italian farmers finds a possible relationship between fruit crops and colon and bladder cancer.
    [Forastiere, F, et al. 1993. Scand J Work Environ Health 19(6):382-389.]
  • Heterocyclic aromatic amine pesticide use and human cancer risk: results form the U.S. Agricultural Health Study
    A prospective cohort study of the Agricultural Health Study evaluated imazethapyr, a heterocyclic aromatic amine herbicide, finding significant trend in risk with increasing lifetime exposure for bladder cancer, limited to proximal cancers.
    [Koutros, S., et al. 2009. Int J Cancer 124(5):1206-1212.]
  • Geographical differences of cancer incidence in Costa Rica in relation to environmental and occupational pesticide exposure
    A study in Costa Rica finds heavy pesticide use in rural counties is associated with an increase risk for bladder cancer in males (OR 1.71).
    [Wesseling, C., et al. 1999. International Journal of Epidemiology 28:365-374.]

Bone Cancer

  • Geographical differences of cancer incidence in Costa Rica in relation to environmental and occupational pesticide exposure
    A study in Costa Rica finds heavy pesticide use in rural counties is associated with an increase risk for bone cancer in males (OR 1.81).
    [Wesseling, C., et al. 1999. International Journal of Epidemiology 28:365-374.
  • Occupational factors and risk of adult bone sarcomas: a multicentric case-control study in Europe
    A nuliticentric case-control study in 7 European countries finds that individuals that have ever used pesticides have over a two-fold increase risk of bone sarcoma (OR 2.33), yet the study finds that duration of use of pesticides showend no increase trend in the risk.
    [Merietti, F., et al. 2006. Int J Cancer 118(3):721-727.]
  • Risk of childhood cancers associated with residence in agriculturally intense areas in the United States
    An ecological study analyzing incidence data from U.S. children ages 0-14 years diagnosed with cancer between 1995 and 2001 and residence in a county with agricultural activity finds an elevated risk for malignant bone tumors (OR 2.3) and for subtype osteosarcoma (OR 2.7) at high agricultural activity (greater than 60% of county acreage devoted to farming). Also linked to Ewing’s sarcoma (OR 4.3) at high agricultural activity and for oat crop acreage and Ewing’s (OR 2.3)
    [Carrozza, S.E., et al. 2008. Environ Health Perspect 116(4):559-565.]
  • Ewing’s bone sarcoma, paternal occupational exposure, and other factors
    A study of Ewing’s bone sarcoma patients shows an elevated risk for children whose fathers are engaged in agricultural occupations during the period from six months prior to conception of the patient to the time of diagnosis (8.8 OR) and for children whose fathers had occupational exposure to herbicides, pesticides, or fertilizers (6.1 OR).
    [Holly, E.A., at al. 1992. Am J Epidemiol 135(2):122-129.]
  • Parental occupational exposures and Ewing’s sarcoma
    A NIH case-control study finds that although exposure to pesticides is not significantly associated with Ewing’s sarcoma, a higtory of household pesticide extermination is associated with ES among boy aged 15 years or younger (OR 3.0).
    [Moore, L.E., et al. 2005. Int J Cancer 114(3):472-478.]

Brain Cancer

Childhood Brain Cancer

Adult Brain Cancer

Breast Cancer

  • Environmental exposure and breast cancer among young women in Rio de Janeiro, Brazil
    A case series study in Brazil find an increased risk of breast cancer for residential use of pesticides during adulthood.
    [Ortega Jacome, G.P., et al. 2010. J Toxicol Environ Health A. 73(13-14):858-65.]
  • Pesticides and breast cancer risk: a comparison between developed and developing countries
    Literature review links DDT to breat cancer in the developing world. According to the authors, there is a dearth of studies in developing countries, which cannot be made up for generalizing the results from developed countries to the developing and third world.
    [Shakeel MK, George PS, Jose J, Jose J, Mathew A. 2010. Asian Pac J Cancer Prev. 2010;11(1):173-80.]
  • Reported residential pesticide use and breast cancer risk on  Long Island, New York
    A population based, case control study of Long Island, New York breast cancer cases finds an increased risk associated with: (a) lifetime residential pesticide use (OR 1.39); (b) application of lawn insecticides themselves (OR 1.56) and is higher if it is in liquid form (OR 1.77) or a combination of product type for outdoor plants (OR 1.83); (c) professional application of pesticides in a vegetable and fruit garden more than doubled (OR 2.29); and, (d) application of pesticides for insects or diseases on outdoor plants by self (OR 1.58) or by professional (OR 1.79).
    [Teitelbaum, S.L., et al. 2007. American Journal of Epidemiology 165(6):643-651.]
  • Breast cancer and serum organochlorine residues.
    The aim of this study was to compare the blood levels of total dichlorodiphenyltrichloroethane (DDT) and hexachlorobenzene (HCB) in samples collected at the time of breast cancer discovery, in order to avoid the potential consequences of body weight change (after chemotherapy or radiotherapy) on the pesticide residue levels. Blood levels of HCB and total DDT were compared in 159 women with breast cancer and 250 presumably healthy controls. Risk of breast cancer associated with organochlorine concentration was evaluated.Mean levels of total DDT and HCB were significantly higher for breast cancer patients than for controls. No differences in serum levels of total DDT or HCB were found between oestrogen receptor positive and oestrogen receptor negative patients with breast cancer.These results add to the growing evidence that certain persistent pollutants may occur in higher concentrations in blood samples from breast cancer patients than controls.
    [Charlier C, Albert A, Herman P, et al.2003. Occup Environ Med. 60(5):348-51.]
  • Breast cancer risk in Hispanic agricultural workers in California
    A registry-based case control study of breast cancer in farm labor union members in California finds risk of breast cancer to be associated with mushroom crops (OR 6.0) as well as the use of chlordane, malathion, and 2,4-D. According to the study, risk associated with chemical use is stronger in younger women and those with early-onset breast cancer.
    [Mills, P.K. and Yang, R. 2005. Int J Occup Environ Health 11(2):123-131.] Occupational histories of cancer patients in a Canadian cancer treatment center and the generated hypothesis regarding breast cancer and farming
    A Canadian study of newly diagnosed breast cancer patients and woman with other cancers finds that women 55 years and younger who had ever farmed has a significantly increased risk of breast cancer than any other type of occupation.
    [Brophy, J., et al. 2002. International Journal of Occupational and Environmental Health 8(4):346-353.]
  • Mammographic findings and occupational exposure to pesticides currently in use on Crete
    Women occupationally exposed to pesticides in Crete greenhouses have higher risks of incidence for number of breast tissue legions, which are risk markers for subsequent invasive breast cancer.
    [Dolapsakis, G., et al. 2001. Eur J Cancer 37(12):1531-1536.]
  • Identification of occupational cancer risks in British Columbia
    A population based case-control study of breast cancer cases in British Columbia finds excess risk for females in occupations as crop farmers and those in the fruit and vegetable industries.
    [Band, P.R., et al. 2000. J Occup Environ Med 42(3):284-310.]A population-based case-control study of farming and breast cancer in North Carolina
    A population based, case control study of North Carolina female farmers finds that while farmers in general tend to have lower breast cancer risk, for those women who reported being present in fields during or shortly after a pesticide application (OR 1.8) and for those who reported not using protective clothing while applying pesticides (OR 2.0) are at increased risk for breast cancer.
    [Duell, E.J., et al. 2000. Epidemiology 11(5):523-531.

Cervical Cancer

Colorectal Cancer

Eye Cancer

Gallbladder Cancer

Kidney/Renal Cancer

Larynx Cancer

Leukemia

Childhood Leukemia

  • Residential exposures to pesticides and childhood leukemia
    The aim of this study was to conduct a systematic review of published studies on the association between residential/household/domestic exposure to pesticides and childhood leukaemia, and to provide a quantitative estimate of the risk. Publications in English were searched in MEDLINE (1966-31 December 2009) and from the reference list of identified publications. Separate analyses were conducted after stratification for exposure time windows, residential exposure location, biocide category and type of leukaemia. Statistically significant associations with childhood leukaemia were observed when combining all studies. Exposure during and after pregnancy was positively associated with childhood leukaemia, with the strongest risk for exposure during pregnancy. Other stratifications showed the greatest risk estimates for indoor exposure, for exposure to insecticides as well as for acute non-lymphocytic leukaemia (ANLL). Outdoor exposure and exposure of children to herbicides (after pregnancy) were not significantly associated with childhood leukaemia. Findings support the assumption that residential pesticide exposure may be a contributing risk factor for childhood leukaemia but available data were too scarce for causality ascertainment. It may be opportune to consider preventive actions, including educational measures, to decrease the use of pesticides for residential purposes and particularly the use of indoor insecticides during pregnancy.
    [Van Maele-Fabry G, Lantin AC, Hoet P, Lison D. 2011. Environ Int. 37(1):280-91.]
  • Residential pesticides and childhood leukemia: a systematic review and meta-analysis
    A meta-analysis of 15 studies on residential pesticide use and childhood leukemia finds an association with exposure during pregnancy, as well as to insecticides and herbicides. An association is also found for exposure to insecticides during childhood.
    [Turner, M.C., et al. 2010. Environ Health Perspect 118(1):33-41]
  • Residential proximity to agricultural pesticide applications and childhood acute lymphoblastic leukemia
    A population based, case control study in California using residential histories and proximity to agricultural pesticide use shows an elevated risk of childhood ALL associated with moderate exposure, but not high exposure, to pesticides classified as organophosphates, chlorophenoxy herbicides, and triazines, and with agricultural pesticides used as insecticides or fumigants.
    [Rull, R.P., et al. 2009. Environ Res 109(7):891-9]
  • Pediatric acute lymphoblastic leukemia and exposure to pesticides.
    A case-control study of children diagnosed with ALL and their mothers in the Washington DC area finds an association between the development of childhood ALL and common household pesticides, as ALL child-mother pairs have elevated levels for the organophosphate metabolites diethylthiophosphate and diethyldithiophosphate and more case mothers (33%) than controls (14%) reported using insecticides in the home.
    [Soldin, O.P., et al. 2009. Therapeutic Drug Monitoring 31(4):495-501]
  • Risk of childhood cancers associated with residence in agriculturally intense areas in the United States
    An ecological study analyzing incidence data from U.S. children ages 0-14 years diagnosed with cancer between 1995 and 2001 and residence in a county with agricultural activity finds an elevated risk for AML at high agricultural activity (greater than 60% of county acreage devoted to farming).
    [Carrozza, S.E., et al. 2008. Environ Health Perspect 116(4):559-565]
  • Parental occupational exposure to pesticides and the risk of childhood leukemia in Costa Rica.
    In a Costa Rica population-based, case-control study, researchers find parental occupational exposure to pesticides increases the risk of childhood leukemia. Maternal pesticide exposure doubles offspring leukemia risk, whether before conception (OR 2.4), or during the first (OR 22) or second trimesters (OR 4.5) the risk is significant. Paternal pesticide exposure during the second trimester also increases risk (1.5 OR) in offspring. In regards to organophosphates, maternal exposure during the first trimester is three and a half times higher (OR 3.5). Exposure to benzimidazole pesticides during pregnancy also has twice the risk for childhood leukemia (OR 2.2)
    [Monge, P., et al. 2007. Scandinavian Journal of Work, Environment and Health 33(4):293-303]
  • Household exposure to pesticides and risk of childhood hematopoietic malignancies: The ESCALE study (SFCE).
    A French registry-based case-control study finds that children born to mothers living in households with pesticide use during pregnancy have over twice as much risk of acute leukemia.
    [Rudant, J., et al. 2007. Environmental Health Perspectives 115(12):1787-1793]
  • Association between prenatal pesticide exposures and the generation of leukemia-associated T(8;21)
    A study analyzing umbilical cord blood samples of infants whose meconium sample detected the pesticide propoxur, finds a two-fold increase incidence of t(8;21)(a22;a22), one of the most common cytogenetic abnormalities in childhood acute myeloid leukemia, suggesting that prenatal pesticide exposure is a factor in the generation of leukemia-associated chromosomal translocations.
    [Lafiura, K.M., et al. 2007. Pediatr Blood Cancer 48(5):624-628]
  • Household exposure to pesticides and risk of childhood acute leukaemia
    A study of household pesticide exposure and childhood acute leukemia finds an increased risk for maternal home insecticide use during pregnancy and during childhood, and with garden insecticide use and fungicide use during childhood. Pyrethroid and lindane lice shampoo treatment is also associated with childhood acute leukemia. The majority of the childhood cancers were acute lymphocytic leukemia.
    [Menegaux, F., et al. 2006. Occup Environ Med 63(2):131-134]
  • Child and maternal household chemical exposure and the risk of acute leukemia in children with Down's syndrome: a report from the Children's Oncology Group
    Children with Down’s syndrome have about a 20-fold increased risk for developing leukemia. A case-control study of acute leukemia in children with Down’s syndrome finds a positive association for acute lymphoblastic leukemia and maternal exposure to professional pest exterminations and to any pesticide.
    [Alderton, L.E., et al. 2006. American Journal of Epidemiology 164(3):212-221]
  • Agricultural pesticide use and childhood cancer in California.
    Looking at residential proximity to agricultural pesticides, a population-based case-control study of early childhood cancer, ages 0-4 years, in California finds an elevated risk for leukemia associated with probable and possible carcinogen use and with nearby agricultural applications of organochlorines and organophosphates during pregnancy (metam sodium OR 2.05 and dicofol OR 1.83)
    [Reynolds, P, et al. 2005. Epidemiology 16(1):93-100]
  • Critical windows of exposure to household pesticides and risk of childhood leukemia.
    A case-control study in California finds a significant increased risk of childhood leukemia to the use of professional indoor pesticide applications at any time from one year before birth to three years after. In addition, frequency of exposure to pesticides was also linked with increased risk
    [Ma, X., et al. 2002. Critical windows of exposure to household pesticides and risk of childhood leukemia. Environmental Health Perspectives 110:955-960]
  • Transplacental chemical exposure and risk of infant leukemia with MLL gene fusion
    A small case-control, population-based study finds a significant increase risk for infant acute leukemia for maternal exposure to insecticides (OR 9.68) during pregnancy, including the carbamate propoxur.
    [Alexander, F.E., et al. 2001. Cancer Res 61(6):2542-2546]
  • Risk of childhood leukemia associated with exposure to pesticides and with gene polymorphisms.
    A population-based case-control study of childhood ALL finds an increased risk for homeowner use of indoor insecticides and garden and interior plant pesticides, in particular with use during pregnancy and among carriers of the CYP1A1m1 and CYP1a1m2 gene mutations.
    [Infante-Rivard, C., et al. 1999. Epidemiology 10(5):481-487]
  • Childhood leukaemia and exposure to pesticides: results of a case-control study in northern Germany
    A population-based case-control study in Northern Germany finds a significant association for pesticide use in gardens and childhood leukemia.
    [Meinert, E., et al. 1996. Eur J Cancer32A(11):1943-1948]
  • Home pesticide use and childhood cancer: A case-control study
    A case-control study in Denver finds home use of pest strips containing dichlorvos is linked to childhood leukemia. The highest risk is found for exposure during the last 3 months of pregnancy, for exposure during the 2 years prior to diagnosis, and for exposure from birth through 2 years prior to diagnosis.
    [Leiss, J., et al. 1995. American Journal of Public Health 85:249-252]
  • Case-control study on the association between a cluster of childhood haematopoietic malignancies and local environmental factors in Aalsmeer, The Netherlands.
    A small case-control study of a flower cultivation community in the Netherlands finds an increase risk for childhood hematopoietic malignancies, such as leukemia, for parental occupational use of pesticides.
    [Mulder, Y.M., et al. 1994. Journal of Epidemiology and Community Health 48:161-165]
  • Epidemiological characteristics of childhood acute lymphocytic leukemia. Analysis by immunophenotype. The Childrens Cancer Group.
    A California study shows children’s exposure to insecticides is associated with a five-fold increase in childhood ALL.
    [Buckley, J.D., et al. 1994. Leukemia 8(5):856-864]
  • Parental occupation and other environmental factors in the etiology of leukemias and non-Hodgkin's lymphomas in childhood: a case-control study
    A hospital-based case-control study in Italy finds a positive association with paternal work as a farmer and childhood ALL
    [Magnani, C., et al. 1990. Tumori 76(5):413-419]
  • A population-based case-control study of childhood leukemia in Shanghai
    A population based case-control study in China of childhood leukemia cases finds an association between ALL with maternal occupational exposure to pesticides.
    [Shu, X.O., et al. 1988. Cancer 62(3):635-644]
  • Occupational Exposures of Parents of Children with Acute Nonlymphocytic Leukemia: A Report from the Childrens Cancer Study Group
    A case-control study finds a consistent pattern of association of AML, also known as acute nonlymphoblastic leukemia (ANLL), risk with paternal exposure to pesticides for jobs held longer than three years, which is substantially increased for children under age 6 at diagnosis. An elevated risk is also found for a child’s direct exposure to pesticides in the home and for maternal exposure to home pesticides at the time of pregnancy.
    [Buckley, J.D., et al. 1989. Cancer Research 49:4030-4037]
  • Environmental factors in childhood leukaemia.
    A small French case-control study finds paternal occupational exposures to pesticides as a risk factor for leukemia (12 cases versus 3 controls)
    [Laval, G. and Tuyns, A.J. 1988. British Journal of Industrial Medicine 45:843-844]
  • Childhood leukemia and parents' occupational and home exposures.
    A case-control study in California finds household pesticide use can more than triple the risk of childhood leukemia and that garden pesticides increase the risk to over six-fold.
    [Lowengart, R., et al. 1987. Journal of the National Cancer Institute 79(1):39-46]

Adult Leukemia

Lip Cancer

  • Pesticide sales and adult male cancer mortality in Brazil
    A study of pesticides sales different parts of Brazil and cancer mortality rates a decade later finds pesticide sales show statistically significant correlation with the mortality rates for several cancers, including cancer of the lip.
    [Chrisman, J.D., et al. 2008. Int J Hyg Environ Health. 212(3):310-21]
  • Swedish agricultural workers: A group with a decreased risk of cancer
    A Swedish study based on a cancer registry of agricultural workers finds an increased risk of cancer of the lip by a factor of greater than 2.
    [Wiklund, K. 1983. Cancer 51(3):566-568.]
  • Cancer mortality among Iowa farmers: recent results, time trends, and lifestyle factors (United States)
    Younger farmers (aged 20 to 64 years) had excess deaths for colon cancer (proportional mortality ratio 1.52) and skin melanoma (proportional mortality ratio 1.60), while older farmers (aged 65+ years) had excess deaths for cancers of the pancreas (proportional mortality ratio 1.18), lip (proportional mortality ratio 1.58), and leukemia (proportional mortality ratio 1.26).
    [Cerhan, J.R., et al. 1998. Cancer Causes Control 9(3):311-319]

Liver/Hepatic Tumors

  • Global DNA methylation screening of liver in piperonyl butoxide-treated mice in a two-stage hepatocarcinogenesis model.
    To identify key molecules in piperonyl butoxide (PBO)-induced hepatocarcinogenesis, study searched hypermethylated genes using CpG island (CGI) microarrays in non-neoplastic liver cells as a source of proliferative lesions at 25 weeks after tumor promotion with PBO using mice. The study further performed methylation-specific polymerase chain reaction (PCR), real-time reverse transcription PCR, and immunohistochemical analysis in PBO-promoted liver tissues. Ebp4.1, Wdr6 and Cmtm6 increased methylation levels in the promoter region by PBO promotion, although Cmtm6 levels were statistically non-significant.Results suggest that PBO promotion may cause altered epigenetic gene regulation in non-neoplastic liver cells surrounding proliferative lesions to allow the facilitation of hepatocarcinogenesis. Both Wdr6 and Cmtm6 showed decreased expression in non-neoplastic liver cells in contrast to positive immunoreactivity in the majority of proliferative lesions produced by PBO promotion. These results suggest that both Wdr6 and Cmtm6 were spared from epigenetic gene modification in proliferative lesions by PBO promotion in contrast to the hypermethylation-mediated downregulation in surrounding liver cells. Considering the effective detection of proliferative lesions, these molecules could be used as detection markers of hepatocellular proliferative lesions and played an important role in hepatocarcinogenesis.
    [Yafune A, Kawai M, Itahashi M, et al. 2013. Toxicol Lett. 222(3):295-302]
  • Geographical differences of cancer incidence in Costa Rica in relation to environmental and occupational pesticide exposure
    A study in Costa Rica finds heavy pesticide use in rural counties is associated with a two-fold increase risk for liver cancer in females (OR 2.20).
    [Wesseling, C., et al. 1999. International Journal of Epidemiology 28:365-374.]
  • Mortality in a cohort of pesticide applicators in an urban setting: sixty years of follow-up
    A mortality cohort study in Rome of urban pesticide applicators finds an increased risk for cancer of the liver.
    [Giordano, F., et al. 2006. Int J Immunopathol Pharmacol 19(Suppl 4):61-65.]
  • Risk of childhood cancers associated with residence in agriculturally intense areas in the United States
    An ecological study analyzing incidence data from U.S. children ages 0-14 years diagnosed with cancer between 1995 and 2001 and residence in a county with agricultural activity finds an elevated risk for hepatic tumors (OR 3.3) and for subtype hepatoblastoma (OR 4.0) at high agricultural activity (greater than 60% of county acreage devoted to farming).
    [Carrozza, S.E., et al. 2008. Environ Health Perspect 116(4):559-565.]

Lung Cancer

Lymphoma

Hodgkin's Lymphoma

Non-Hodgkin's Lymphoma

Melanoma

Mouth Cancer

Multiple Myeloma

Neuroblastoma

Oesophageal Cancer

Ovarian Cancer

Pancreatic Cancer

Prostate Cancer

  • Risk of total and aggressive prostate cancer and pesticide use in the Agricultural Health Study.
    Because pesticides may operate through different mechanisms, the authors studied the risk of prostate cancer associated with specific pesticides in the Agricultural Health Study (1993-2007). With 1,962 incident cases, including 919 aggressive prostate cancers among 54,412 applicators, this is the largest study to date. Three organophosphate insecticides were significantly associated with aggressive prostate cancer: fonofos, malathion and terbufos. The organochlorine insecticide aldrin was also associated with increased risk of aggressive prostate cancer. This analysis has overcome several limitations of previous studies with the inclusion of a large number of cases with relevant exposure and detailed information on use of specific pesticides at 2 points in time. Furthermore, this is the first time specific pesticides are implicated as risk factors for aggressive prostate cancer.
    [Koutros S, Beane Freeman LE, Lubin JH, et al. 2013. Am J Epidemiol. 177(1):59-74]
  • Pesticide exposure and inherited variants in vitamin d pathway genes in relation to prostate cancer.
    Vitamin D and its metabolites are believed to impede carcinogenesis by stimulating cell differentiation, inhibiting cell proliferation, and inducing apoptosis. Certain pesticides have been shown to deregulate vitamin D's anticarcinogenic properties.Study hypothesizes that certain pesticides may be linked to prostate cancer via an interaction with vitamin D genetic variants. Study evaluated interactions between 41 pesticides and 152 single-nucleotide polymorphisms (SNP) in nine vitamin D pathway genes among 776 prostate cancer cases and 1,444 male controls in a nested case-control study of Caucasian pesticide applicators within the Agricultural Health Study.Five significant interactions displayed a monotonic increase in prostate cancer risk with individual pesticide use in one genotype and no association in the other. These interactions involved parathion and terbufos use and three vitamin D genes (VDR, RXRB, and GC). In this study, genetic variations in vitamin D pathway genes, particularly GC rs7041, an SNP previously linked to lower circulating vitamin D levels, modified pesticide associations with prostate cancer risk. Because this study is the first to examine this relationship, additional studies are needed to rule out chance findings.
    [Karami S, Andreotti G, Koutros S, Barry KH, et al. 2013.Cancer Epidemiol Biomarkers Prev. 22(9):1557-66]
  • Genetic susceptibility loci, pesticide exposure and prostate cancer risk.
    Uncovering SNP (single nucleotide polymorphisms)-environment interactions can generate new hypotheses about the function of poorly characterized genetic variants and environmental factors, like pesticides. Authots evaluated SNP-environment interactions between 30 confirmed prostate cancer susceptibility loci and 45 pesticides and prostate cancer risk in 776 cases and 1,444 controls in the Agricultural Health Study. Among men carrying two T alleles in EH domain binding protein 1 (EHBP1) SNP, the risk of prostate cancer in those with high malathion use was 3.43 times those with no use. Among men carrying two A alleles in TET2, the risk of prostate cancer associated with high aldrin use was 3.67 times those with no use. In contrast, associations were null for other genotypes. Although additional studies are needed and the exact mechanisms are unknown, this study suggests known genetic susceptibility loci may modify the risk between pesticide use and prostate cancer.
    [Koutros S, Berndt SI, Hughes Barry K et al. 2013. PLoS One. 8(4):e58195]
  • Farming, reported pesticide use, and prostate cancer.
    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. This study performed a meta-analysis to summarize the association of farming and prostate cancer. Prostate cancer cases were almost four times more likely to be farmers compared with controls with benign prostate hyperplasia. Reported pesticide exposure was inversely associated with prostate cancer, 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.
    [Ragin C, Davis-Reyes B, Tadesse H, et al. 2013. Am J Mens Health.7(2):102-9]
  • Chronic chlorpyrifos exposure does not promote prostate cancer in prostate specific PTEN mutant mice.
    Environmental factors are likely to interact with genetic determinants to influence prostate cancer progression. The Agricultural Health Study has identified an association between exposure to organophosphorous pesticides including chlorpyrifos, and increased prostate cancer risk in pesticide applicators with a first-degree family history of this disease. Authors used bioluminescence imaging and histopathological analyses to test whether chronic exposure to chlorpyrifos in a grain-based diet for 32 weeks was able to promote prostate cancer development. Chronic exposure to chlorpyrifos in the diet did not promote prostate cancer development in mice despite achieving sufficient levels to inhibit acetylcholinesterase activity in plasma. The mechanistic basis of pesticide-induced prostate cancer may be complex and may involve other genetic variants, multiple genes, or nongenetic factors that might alter prostate cancer risk during pesticide exposure in agricultural workers.
    [Svensson RU, Bannick NL, Marin MJ, et al. 2013. J Environ Pathol Toxicol Oncol.32(1):29-39]
  • Environmental exposures and prostate cancer.
    Many malignancies have been linked to specific environmental exposures. Several environmental and occupational factors have been studied for an association to prostate cancer (CaP) risk. These include Agent Orange exposure, farming and pesticides, sunlight/ultraviolet radiation, as well as trace minerals used in tire and battery manufacturing. This manuscript reviews the literature on these environmental exposures and CaP.
    [Mullins JK, Loeb S. 2012. Urol Oncol. 30(2):216-9]
  • Prostate cancer and toxicity from critical use exemptions of methyl bromide: environmental protection helps protect against human health risks.
    Authors performed a systematic review of the literature, including in vitro toxicological and epidemiological studies of occupational and community exposure to the halogenated hydrocarbon pesticide methyl bromide. Study focused on toxic (especially chronic) or carcinogenic effects from the use of methyl bromide, on biomonitoring data and reference values. Out of the 542 peer reviewed publications between 1990-2011, 91 referring to toxicity of methyl bromide and 29 using the term "carcinogenic", "neoplastic" or "mutagenic". Overall, exposure to methyl bromide is associated with an increased risk of prostate cancer. Two epidemiological studies have analyzed environmental, non-occupational exposure to methyl bromide providing evidence for its health risk to the general public. Both the epidemiological evidence and toxicological data suggest a possible link between methyl bromide exposure and serious health problems, including prostate cancer risk from occupational and community exposure. The environmental risks of methyl bromide are not in doubt, but also its health risks, especially for genetically predisposed subjects, should not be underestimated.
    [Budnik LT, Kloth S, Velasco-Garrido M, Baur X. 2012. Environ Health.11:5]
  • Genetic variation in base excision repair pathway genes, pesticide exposure, and prostate cancer risk.
    Authors evaluated interactions between 39 pesticides and 394 tag single-nucleotide polymorphisms (SNPs) for 31 BER genes among 776 prostate cancer cases and 1,444 male controls in a nested case-control study of white Agricultural Health Study (AHS) pesticide applicators. The interaction between fonofos and rs1983132 in NEIL3 [nei endonuclease VIII-like 3 (Escherichia coli)], which encodes a glycosylase that can initiate BER, was the most significant overall. Fonofos exposure was associated with a monotonic increase in prostate cancer risk among men with CT/TT genotypes for low and high use compared with no use, whereas fonofos was not associated with prostate cancer risk among men with the CC genotype. These findings regarding fonofos is consistent with previous AHS findings of increased prostate cancer risk with fonofos exposure among those with a family history of prostate cancer. Although requiring replication, our findings suggest a role of BER genetic variation in pesticide-associated prostate cancer risk.
    [Barry KH, Koutros S, Berndt SI, Andreotti G, et al. 2011. Environ Health Perspect. 119(12):1726-32]
  • Prostate cancer risk and exposure to pesticides in British Columbia farmers.
    Several epidemiologic studies have reported an increased risk of prostate cancer among farmers. The aim of this study was to assess the risk of developing prostate cancer in relation to exposure to specific active compounds in pesticides. A case-control approach was used with 1,516 prostate cancer patients and 4,994 age-matched internal controls consisting of all other cancer sites excluding lung cancer and cancers of unknown primary site. Lifetime occupational history was obtained through a self-administered questionnaire and used in conjunction with a job exposure matrix to estimate the participants' lifetime cumulative exposure to approximately 180 active compounds in pesticides. The significant association between prostate cancer risk and exposure to DDT, simazine, and lindane is in keeping with those previously reported in the literature. Authors also observed a significant excess risk for several active ingredients that have not been previously reported in the literature such as dichlone, dinoseb amine, malathion, endosulfan, 2,4-D, 2,4-DB, and carbaryl. Some findings in this study were not consistent with those reported in the literature, including captan, dicamba, and diazinon. It is possible that these findings showed a real association and the inconsistencies reflected differences of characteristics between study populations.
    [Band PR, Abanto Z, Bert J, et al.2011. Prostate. 71(2):168-83]
  • Prostate cancer and ambient pesticide exposure in agriculturally intensive areas in California.
    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. 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 and a group of organochlorines) but not among those exposed to other compounds that were included as controls (simazine, maneb, and paraquat dichloride).
    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.
    [Cockburn M, Mills P, Zhang X, et al. 2011. Am J Epidemiol. 173(11):1280-8]
  • Xenobiotic-metabolizing gene variants, pesticide use, and the risk of prostate cancer.
    Researchers evaluated pesticide-SNP interactions between 45 pesticides and 1913 XME SNPs with respect to prostrate cancer among 776 cases and 1444 controls in the Agricultural Health Study. A positive monotonic interaction was observed between petroleum oil/petroleum distillate use and rs1883633 in the oxidative stress gene glutamate cysteine ligase; men carrying at least one variant allele (minor allele) experienced an increased prostate cancer risk. Among men carrying the variant allele for thioredoxin reductase 2 (TXNRD2) rs4485648, microsomal epoxide hydrolase 1 (EPHX1) rs17309872, or myeloperoxidase (MPO) rs11079344, an increased prostate cancer risk was observed with high, compared with no, petroleum oil/petroleum distillate, or terbufos use. Researchers observed several pesticide-SNP interactions in oxidative stress and phase I/II enzyme genes and risk of prostate cancer. Additional work is needed to explain the joint contribution of genetic variation in XMEs, pesticide use, and prostate cancer risk.
    [Koutros S, Andreotti G, Berndt SI, et al. 2011. Pharmacogenet Genomics. 21(10):615-23]
  • An update of cancer incidence in the Agricultural Health Study.
    The objective was to reevaluate cancer incidence among Agricultural Health Study participants. A significant excess of prostate cancer was seen for private and commercial applicators. Excesses were observed for lip cancer and multiple myeloma among private applicators from North Carolina and for marginal zone lymphoma among Iowa spouses. Although lower rates of smoking and increased physical activity probably contribute to the lower overall cancer incidence, agricultural exposures including pesticides, viruses, bacteria, sunlight, and other chemicals may increase risks for specific cancer sites.
    [Koutros S, Alavanja MC, Lubin JH, et al. 2010. J Occup Environ Med. 52(11):1098-105]
  • Pesticide use modifies the association between genetic variants on chromosome 8q24 and prostate cancer.
    In the Agricultural Health Study, a prospective study of licensed pesticide applicators,authors observed increased prostate cancer risk with specific pesticide use among those with a family history of prostate cancer. Thus, study evaluated the interaction among pesticide use, 8q24 variants, and prostate cancer risk. The authors estimated odds ratios (OR) and 95% confidence intervals (95% CI) for interactions among 211 8q24 variants, 49 pesticides, and prostate cancer risk in 776 cases and 1,444 controls. Authors observed a significant interaction among variants on chromosome 8q24, pesticide use, and risk of prostate cancer. Insecticides, particularly organophosphates, were the strongest modifiers of risk, although the biological mechanism is unclear. This is the first report of effect modification between 8q24 and an environmental exposure on prostate cancer risk.
    [Koutros S, Beane Freeman LE, Berndt SI, et al. 2010. Cancer Res. 70(22):9224-33]
  • Coumaphos exposure and incident cancer among male participants in the Agricultural Health Study (AHS).
    Previous research in the Agricultural Health Study (AHS) cohort observed a positive association between coumaphos and prostate cancer in men with a family history of prostate cancer. This study was performed to determine the association between coumaphos and other major cancer sites and to explore the consistency of the association with prostate cancer early (1993-1999) and later (2000-2005) in AHS follow-up. This study included 47,822 male licensed pesticide applicators.
    Approximately 8% of applicators reported use of coumaphos; 8.5% reported a family history of prostate cancer. Cumulative exposure to coumaphos was not associated with cancer risk overall or with any major cancer site including prostate. In men with a family history of prostate cancer, we observed a positive association between ever use of coumaphos and prostate cancer in both early periods of follow-up. Across all years, this association was statistically significant. Coumaphos was not associated with any cancer evaluated here. In men with a family history of disease, there was evidence of an association between coumaphos and prostate cancer, possibly due to genetic susceptibility.
    [Christensen CH, Platz EA, Andreotti G, et al. 2010. Environ Health Perspect. 118(1):92-6]
  • Occupational exposure to terbufos and the incidence of cancer in the Agricultural Health Study.
    Study investigated associations between use of terbufos and the incidence of cancer. The Agricultural Health Study is a prospective cohort study of 57,310 licensed pesticide applicators from Iowa and North Carolina. Detailed information about 50 pesticides, including terbufos, and potential confounders was obtained from self-administered questionnaires. Overall cancer risk was slightly increased among terbufos users. Suggestive associations were observed between terbufos use and cancers of the prostate and lung and leukemia and non-Hodgkin's lymphoma, although the exposure-response gradients were non-monotonic and p for trends were not significant. However, cautious interpretation of these results is warranted by the lack of existing experimental and epidemiologic evidence to support carcinogenic effects of terbufos.
    [Bonner MR, Williams BA, Rusiecki JA, et al. 2010. Cancer Causes Control. 21(6):871-7]
  • Chlordecone exposure and risk of prostate cancer.
    Study analyzed the relationship between exposure to chlordecone and the risk of prostate cancer. Researchers investigated 623 men with prostate cancer and 671 controls. Exposure was analyzed according to case-control status. Study found a significant increase in the risk of prostate cancer with increasing plasma chlordecone concentration and for cumulative exposure index. Stronger associations were observed among those with a positive family history of prostate cancer and among those who had lived in a Western country. The rs3829125 and rs17134592 allele variants were in complete linkage disequilibrium and were found at low frequency (0.04). Among subjects with plasma chlordecone concentrations above the LD, carriers of the allele variants had a higher risk of prostate cancer.
    [Multigner L, Ndong JR, Giusti A, et al. 2010. J Clin Oncol. 28(21):3457-62]
  • Does exposure to agricultural chemicals increase the risk of prostate cancer among farmers?
    Several studies suggest that farmers may be at increased risk of prostate cancer. The present analysis, based on a large population-based case-control study conducted among men in the Montreal area in the early 1980's, aim at identifying occupational chemicals which may be responsible for such increases. The original study enrolled 449 prostate cancer cases, nearly 4,000 patients with other cancers, as well as 533 population controls. The present analysis was restricted to a study base of men who had worked as farmers earlier in their lives. There were a total of 49 men with prostate cancers, 127 with other cancers and 56 population controls. There was evidence of a two-fold excess risk of prostate cancer among farmers with substantial exposure to pesticides, as compared to unexposed farmers. There was some suggestion, based on few subjects, of increased risks among farmers ever exposed to diesel engine emissions. The results for pesticides are particularly noteworthy in the light of findings from previous studies. Suggestions of trends for elevated risks were noted with other agricultural chemicals, but these are largely novel and need further confirmation in larger samples.
    [Parent ME, Désy M, Siemiatycki J. 2009. Mcgill J Med. 12(1):70-7]
  • Cancer mortality among Iowa farmers: recent results, time trends, and lifestyle factors (United States)
    A cancer mortality study of Iowa farmers shows an excess of deaths for cancers of the prostate (1.26 PMR).
    [Cerhan, J.R., et al. 1998. Cancer Causes Control 9(3):311-319.]
  • Mortality among white and nonwhite farmers in North Carolina, 1976-1978
    A mortality study of farmers in North Carolina finds an increased frequency of prostate cancer among white decedents under 65 years of age (PMR 1.6).
    [Delzell, E., and Grufferman, S. 1985. Am J Epidemiol 121(3):391-402.]
  • Cancer among farmers in central Italy
    A case-referent study of Italian farmers finds a possible relationship between wheat crops and prostate cancer.
    [Forastiere, F, et al. 1993. Scand J Work Environ Health 19(6):382-389.]
  • Meta-analyses of prostate cancer and farming
    A meta-analyses of prostate cancer and farming studies between 1983 and 1994 finds a positive association between prostate cancer and farming, which the study authors attribute to exposure to hormonally active agricultural chemicals.
    [Keller-Byrne, J.E., et al. 1997. Am J Ind Med 31(5):580-586.]
  • Use of agricultural pesticides and prostate cancer risk in the Agricultural Health Study cohort
    A prospective cohort study of Iowa and North Carolina male pesticide applicators finds that the two highest exposure scenarios (OR 2.73 and 3.47) significantly increase risk for prostate cancer. Significant interaction odds ratios occurred among persons who used butylate (OR 1.93); four organophosphorothioate insecticides including coumaphos (OR 2.58), fonofos (OR 2.04), chlorpyrifos (OR 1.65), and phorate (OR 1.64); and a pyrethroid, permethrin (for animal use) (OR 2.31).
    [Alavanja, M., et al. 2003. American Journal of Epidemiology 157:800-814.]
  • Cancer incidence in a cohort of licensed pesticide applicators in Florida
    A standardized incidence ratio anaylsis (SIR) of licensed pesticide applicators in Florida, compared with Florida’s general population, finds an increased incidence rate for prostate cancer (SIR 1.91).
    [Fleming, L., et al. 1999. Journal of Occupational and Environmental Medicine 41(4):279-288.]
  • A case-control study of farming and prostate cancer in African-American and Caucasian men
    A population-based case-control study in South Carolina finds farming is associated with increase risk of prostate cancer in Caucasians (OR 1.8) but not African-Americans. The study also finds that farmers who mixed or applied pesticides have a greater risk (OR 1.6); and, the increased risk is found only for those farming less than 5 years. The authors conclude that the racial difference “may be explained by different farming activities or different gene-environment interactions by race.” [Meyer, T.E., et al. 2007. Occup Environ Med 64(3):155-160.]
  • Proportionate mortality study of golf course superintendents
    A mortality study of a cohort of 686 deceased U.S. male golf course superintendents from the finds elevated levels for prostate cancer (PMR 293).
    [Kross, B.C., et al. 1996. Am J Ind Med 29(5):501-506.]
  • Pesticide sales and adult male cancer mortality in Brazil
    A study of pesticides sales in different parts of Brazil and cancer mortality rates a decade later finds pesticide sales show statistically significant correlation with the mortality rates for several cancers, including prostate cancer (r=0.69; p=0.019).
    [Chrisman, J.D., et al. 2008. Int J Hyg Environ Health. 212(3):310-21]
  • Prostate cancer risk in California farm workers
    Hispanic farmworkers are found to be at an increased risk for prostate cancer when exposed to relatively high levels of certain organochlorines, organophosphates, fumigants and triazine herbicides.
    [Mills, P.K. and Yang, R. 2003. J Occup Environ Med  45(3):249-258.]
  • Occupation and prostate cancer
    Occupational exposures to pesticides including farmers, forestry workers or horticulturists finds a slight increased risk among farmers, speculating that certain pesticides act as hormone modifiers and influence the prostate cancer risk.
    [Parent, M. and Siemiatycki, J. 2001. Epidemiologic Reviews 23(1):138-143.]
  • Prostate cancer and exposure to pesticides in agricultural settings
    Individuals that have worked in agriculture is associated with a 40% increased risk of prostate cancer (OR 1.4)
    [Settimi, L., et al. 2003. Int J Cancer 104(4):458-461.]
  • Cancer incidence among triazine herbicide manufacturing workers
    Workers at a triazine manufacturing plant are found to have an elevated number of prostate cancer cases.
    [MacLennan, P.A., et al. 2002. J Occup Environ Med 44(11):1048-1058.]
  • Occupation and prostate cancer risk in Sweden
    Swedish stuy shows significantly elevated standardized incidence ratio are found in farmers and ceratin occupations and industries with exposures to herbicides and fertilizers. Results suggest that farmers; certain occupations and industries with exposures to cadmium, herbicides, and fertilizers; and men with low occupational physical activity levels have elevated prostate cancer risks.
    [Sharma-Wagner, S., et al. 2000. J Occup Environ Med 42(5):517-525.]
  • Prostate cancer in pesticide applicators in Swedish agriculture
    A cohort of over 20,000 licensed agriculture pesticide applicators in Sweden finds a statistically significant increased risk of prostate cancer.
    [Dich, J., and Wiklund, K. 1998. Prostate 34(2):100-112.]
  • Farming and prostate cancer among African-Americans in the Southeastern Untied States
    A study looking at African-American farmers shows further support that prostate cancer risk is associated with farming occupations.
    [Dosemeci, M., et al. 1994. Journal of the National Cancer Institute 86(22):1718-1719.]
  • Farming and prostate cancer mortality
    A restrospective cohort study of male farmers find an increased risk associationed with acres of farmland sprayed with herbicides and dying from prostate cancer. No other farm activity examined in the study was associated with any detectable pattern of increased or decreased risk.
    [Morrison, H., et al. 1993. American Journal of Epidemiology 137(3):270-280.]
  • Correlation analysis of pesticide use data and cancer incidence rates in California counties
    An ecological study in California analyzing data on pesticide use and cancer incidence finds a correlation between black males diagnosed with prostate cancer and atrazine and captan.
    [Mills, P.K. 1998. Arch Environ Health 53(6):410-413.]
  • Agent Orange exposure, Vietnam War veterans, and the risk of prostate cancer
    Twice as many Vietnam veterans exposed to Agent Oragne were identified with prostate cancer (239 vs 124 unexposed men, respectively; (OR 2.19). Individuals who were exposed to Agent Orange had an increased incidence of prostate cancer; developed the disease at a younger age, and had a more aggressive variant than their unexposed counterparts.
    [Chamie, K., deVere White, R. W., Lee, D., Ok, J. and Ellison, L. M. 2008. Cancer, 113: 2464–2470.]
  • Use of Agricultural Pesticides and Prostate Cancer Risk in the Agricultural Health Study Cohort
    Using Agriculutral Health Study data, researchers evaluated the role of 45 pesticides and found that a few of them showed evidence of a possible association with prostate cancer among pesticide applicators. Methyl bromide was linked to the risk of prostate cancer in the entire group, while exposure to six other pesticides -chlorpyrifos, coumaphos, fonofos, phorate, permethrin, and butylate- was associated with an increased risk of prostate cancer among men with a family history of the disease.
    [Alavanja MC, et al. 2003. Am J Epidemiol 157(9):800-14.]

Sinonasal cancer

Soft Tissue Sarcoma

Stomach Cancer

  • Methyl bromide exposure and cancer risk in the Agricultural Health Study.
    Study used Poisson regression to calculate rate ratios (RR) and 95 % confidence intervals (CI) for associations between methyl bromide use and all cancers combined, as well as 12 specific sites, among 53,588 Agricultural Health Study pesticide applicators with follow-up from 1993 to 2007. A total of 7,814 applicators (14.6 %) used methyl bromide, predominantly before enrollment. Based on 15 exposed cases, stomach cancer risk increased monotonically with increasing methyl bromide use for low and high use compared with no use. No other sites displayed a significant monotonic pattern. Results provide little evidence of methyl bromide associations with cancer risk for most sites examined; however, study observed a significant exposure-dependent increase in stomach cancer risk. Small numbers of exposed cases and declining methyl bromide use might have influenced our findings. Further study is needed in more recently exposed populations to expand on these results.
    [Barry KH, Koutros S, Lubin JH, et al. 2012. Cancer Causes Control. 23(6):807-18]
  • Associations between stomach cancer incidence and drinking water contamination with atrazine and nitrate in Ontario (Canada) agroecosystems, 1987-1991
    Drinking water contaminated with atrazine below the maximum allowable limits (50ng/l to 649ng/l) is associated with stomach cancer incidence.
    [Van Leeuwen, J.A., et al. 1999. International Journal of Epidemiology 28:836-840.]
  • Agricultural exposures and gastric cancer risk in Hispanic farm workers in California
    Occupation in the citrus industry (OR 2.88) and in areas with high 2,4-D use (OR 1.85), and use of acaricide propargite (OR 2.86) or triflurin (OR 1.69) are associated gastric cancer.
    [Mills, P.K., and Yang, R.C. 2007. Environ Res 104(2):282-289.]
  • Cancer among farmers in central Italy
    A case-referent study of Italian farmers finds a significantly increased risk of stomach cancer among farmers with greater than 10 years experience and among licensed pesticides users with greater than 10 years’ experience.
    [Forastiere, F, et al. 1993. Scand J Work Environ Health 19(6):382-389.]

Testicular Cancer

  • Occupational and environmental exposures associated with testicular germ cell tumours: systematic review of prenatal and life-long exposures.
    Testicular germ cell tumours (TGCT) are the most common cancers in men aged between 15 and 44 years and the incidence has increased steeply over the past 30 years. The rapid increase in the incidence, the spatial variation and the evolution of incidence in migrants suggest that environmental risk factors play a role in TGCT aetiology. The purpose of this review was to summarise the current state of knowledge on occupational and environmental factors thought to be associated with TGCT. After exclusion of duplicate reports, 72 relevant articles were selected; 65 assessed exposure in adulthood, 7 assessed parental exposures and 2 assessed both. Associations with occupation was reported for agricultural workers, construction workers, firemen, policemen, military personnel, as well as workers in paper, plastic or metal industries. Electromagnetic fields, PCBs and pesticides were also suggested. However, results were inconsistent and studies showing positive associations tended to had lower quality ranking using the assessment scale. Current evidence does not allow concluding on existence of any clear association between TGCT and adulthood occupational or environmental exposure. The limitations of the studies may partly explain the inconsistencies observed. The lack of association with adulthood exposure is in line with current hypotheses supporting the prenatal origin of TGCT. Future research should focus on prenatal or early life exposure, as well as combined effect of prenatal and later life exposure. National and international collaborative studies should allow for more adequately powered epidemiological studies. More sophisticated methods for assessing exposure as well as evaluating gene-environment interactions will be necessary to establish clear conclusion.
    [Béranger R, Le Cornet C, Schüz J, Fervers B. 2013. PLoS One. 8(10):e77130]
  • Pesticide exposure and serum organochlorine residuals among testicular cancer patients and healthy controls.
    The incidence of testicular cancer (TC) has been increasing worldwide during the last decades. The reasons of the increase remains unknown, but recent findings suggest that organochlorine pesticides (OPs) could influence the development of TC. A hospital-based case-control study of 50 cases and 48 controls was conducted to determine whether environmental exposure to OPs is associated with the risk of TC, and by measuring serum concentrations of OPs, including p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE) isomer and hexachlorobenzene (HCB) in participants. A significant association was observed between TC and household insecticide use. Crude and adjusted ORs for TC were also significantly associated with higher serum concentrations of total OPs in cases compared with controls. These findings give additional support to the results of previous research that suggest that some environmental exposures to OPs may be implicated in the pathogenesis of TC.
    [Giannandrea F, Gandini L, Paoli D, et al. 2011. J Environ Sci Health B. 46(8):780-7]
  • Cancer incidence in a cohort of licensed pesticide applicators in Florida
    Cancer incidence among licensed pesticide applicators in Florida is elevated for testicular cancer (SIR 2.48) and cervical cancer (SIR 3.69).
    [Fleming, L., et al. 1999. Journal of Occupational and Environmental Medicine 41(4):279-288.]
  • Correlation analysis of pesticide use data and cancer incidence rates in California counties
    An ecological study in California analyzing data on pesticide use and cancer incidence finds a correlation between Hispanic males diagnosed with testicular cancer and atrazine.
    [Mills, P.K. 1998. Arch Environ Health 53(6):410-413.]
  • Testicular cancer associated with employment in agriculture and oil and natural gas extraction
    A hospital-based case-control study find an increased risk for testicular cancer in men who work in the agricultural industry.
    [Mills, P.K., et al. 1984. Lancet 1(8370):207-210.]

Thyroid Cancer

  • Risk factors of thyroid tumors: role of environmental and occupational exposures to chemical pollutants.
    The rising incidence of thyroid cancer observed during the last few decades in most western countries is explained in large part by increasing numbers of diagnoses due to changes in medical screening practices. However, beside radiation exposure, exposure to environmental chemicals may also play a role in thyroid cancer etiology and in the increased incidence. This paper presents the main chemicals suspected to induce thyroid tumorigenesis, and epidemiological results on the association between chemical exposure and thyroid tumors.This review found that environmentally abundant chemicals may disrupt thyroid function and/or play a role in tumorigenesis through a variety of mechanisms. Epidemiological results provide insufficient evidence of a causal link between exposure to environmental chemicals and thyroid tumors, but raise the hypothesis of an increased risk of thyroid neoplasm for workers in the leather, wood, and paper industries, and those exposed to certain solvents and pesticides.
    [Leux C, Guénel P. 2010. Rev Epidemiol Sante Publique.58(5):359-67]
  • Nitrate intake and the risk of thyroid cancer and thyroid disease
    Study finds an increased risk of thyroid cancer with higher average nitrate levels in public water supplies (nitrate is a contaminant of drinking water in agricultural areas) and with longer consumption of water exceeding 5 mg/L nitrate-N (for >or=5 years at >5 mg/L, relative risk = 2.6).
    [Ward MH, et al. 2010. Epidemiology. 21(3):389-95].
  • Thyroid disruption: mechanism and clinical implications in human health.
    Exposure to specific environmental toxins, including polychlorinated biphenyls, dioxins, phthalates, polybrominated diphenyl ethers (PBDEs), and other halogenated organochlorines, has been shown to interfere with the production, transportation, and metabolism of thyroid hormones by a variety of mechanisms. A broad range of chemicals, with structural similarity to thyroid hormone, have been shown to bind to thyroid receptors with both agonist and antagonist effects on thyroid hormone signaling. The incidence of thyroid disease in the United States, particularly for thyroid cancer and thyroid autoimmune disease, is increasing substantially. The evidence for the significant effects of background levels of thyroid-disrupting chemicals, the known pathways for thyroid disruptors, and the evidence and implications for neurodevelopmental damage due to thyroid-disrupting chemicals is reviewed.
    [Patrick L. 2009. Altern Med Rev. 14(4):326-46]
  • Mechanism of trifluralin-induced thyroid tumors in rats.
    Trifluralin has been reported to cause a significant increase in thyroid follicular cell tumors in male Fischer 344 rats. This study was designed to determine the mechanism of thyroid hyperactivity after trifluralin exposure. A group of 15 male Fischer 344 rats were exposed to trifluralin-fortified (6500 ppm) diet for 2 weeks. In the trifluralin treated rats, the serum T3 and T4 levels decreased by 17% and 90%, respectively and TSH increased by 37% more than the control rats. The decrease in total serum T3 and T4 levels in the trifluralin treated rats was due to enhanced peripheral metabolism and an increase in bile flow that results in a compensatory increase in TSH synthesis and secretion. The increased levels of TSH with chronic exposure to trifluralin would exert a continuous stimulation of the thyroid gland leading to cellular hypertrophy and proliferation predisposing to the development of follicular cell tumors in rats.
    [Saghir SA, Charles GD, Bartels MJ, et al. 2008. Toxicol Lett.180(1):38-45]
  • Risk of childhood cancers associated with residence in agriculturally intense areas in the United States
    An ecological study analyzing incidence data from U.S. children ages 0-14 years diagnosed with cancer between 1995 and 2001 and residence in a county with moderate to high agricultural activity finds statistically significantly elevated risk for thyroid carcinomas (OR 3.0) at high agricultural activity (greater than 60 percent of the total county acreage is devoted to farming). An increased risk is also found for thyroid carcinomas and oat crop acreage (OR 2.0).
    [Carrozza, S.E., et al. 2008. Environ Health Perspect 116(4):559-565.]
  • A mode of action for induction of thyroid gland tumors by Pyrethrins in the rat.
    Prolonged treatment with high doses of pyrethrins results in thyroid gland tumors in the rat. To elucidate the mode of action for tumor formation, the effect of pyrethrins on rat thyroid gland, thyroid hormone levels and hepatic thyroxine UDPglucuronosyltransferase activity was investigated. Treatment with pyrethrins and NaPB increased hepatic microsomal thyroxine UDPglucuronosyltransferase activity and serum thyroid stimulating hormone levels (TSH), but reduced serum levels of either thyroxine (T4) and/or triiodothyronine (T3). The effects of pyrethrins in female rats were dose-dependent, with 100 ppm being a no-effect level, and on cessation of treatment were essentially reversible in both sexes. The concordance between the effects of pyrethrins and NaPB suggests that the mode of action for Pyrethrins-induced rat thyroid gland tumors is similar to that of some other non-genotoxic inducers of hepatic xenobiotic metabolism.
    [Finch JM, Osimitz TG, Gabriel KL, et al. 2006. Toxicol Appl Pharmacol.214(3):253-62]

Uteran Cancer

  • An endocrine-disrupting chemical, fenvalerate, induces cell cycle progression and collagen type I expression in human uterine leiomyoma and myometrial cells.
    Fenvalerate (Fen), widely used for its high insecticidal potency and low mammalian toxicity, is classified as an endocrine-disrupting chemical. Recently, Fen has received great attention for its adverse effects on human reproductive health. In this study, we found that Fen (10 microM) had a stimulatory effect on the growth of both cell lines at 24 h compared with controls by MTS (p < 0.01) and BrdU (p < 0.01) assays in hormonally responsive uterine leiomyoma (UtLM) cells and normal uterine smooth muscle cells (UtSMC). Data shows that Fen can stimulate the growth of both UtLM cells and UtSMC, which involves a combination of enhanced cell cycle progression and inhibition of apoptosis. Also this compound can increase collagen I expression, at both mRNA and protein levels. Results also indicate that Fen exposure could be considered a novel risk factor for uterine fibroids through molecular mechanisms that do not directly involve the ERs.
    [Gao X, Yu L, Castro L, Moore AB, et al. 2010. Toxicol Lett. 196(3):133-41]
  • Geographical differences of cancer incidence in Costa Rica in relation to environmental and occupational pesticide exposure
    A study in Costa Rica finds heavy pesticide use in rural counties is associated with an increase risk for cancer of the corpus uteri (OR 1.78).
    [Wesseling, C., et al. 1999. International Journal of Epidemiology 28:365-374.]