Gateway Health and Environmental Effects Citations

1. EPA weight-of evidence category, "not classifiable as to human carcinogenicity", usually due to inadequate data. US EPA, 2005. Office of Pesticide Programs. List of Chemicals Evaluated for Carcinogenic Potential. September 30, 2018.

2. US EPA Office of Pesticide Programs. List of Chemicals Evaluated for Carcinogenic Potential. September 30, 2018.

3. International Agency for Research on Cancer, World Health Organization (IARC) category, the agent (mixture) is possibly carcinogenic to humans. November 2, 2018.

4. Extension Toxicology Network (EXTOXNET) Pesticide Information Profiles.

5. Illinois EPA, Endocrine Disruptors Strategy, February 1997.

6. Northwest Coalition for Alternatives to Pesticides (NCAP), Pesticide Factsheets.

7. Beyond Pesticides ChemWatch Factsheets. (Cited under factsheets on Beyond Pesticides Gateway)

8. US EPA, Office of Prevention, Pesticides and Toxic Substances, Reregistration Eligibility Decisions (REDs), Interim REDS (iREDs) and RED Factsheets.

9. Picloram causes birth defects when used in combination with 2,4-D (as is common in formulations), according to Reference #3.

10. EPA weight-of-evidence category, "possible human carcinogen." US EPA, 2004. Office of Pesticide Programs. List of Chemicals Evaluated for Carcinogenic Potential. July 29, 2004.

11. US EPA, 2000. Table 1: Toxicity Data by Category for Chemicals Listed under EPCRA Section 313. Toxic Release Inventory (TRI) Program.

12. EPA weight-of-evidence category, "Likely to be carcinogenic to humans (high dose); Not likely to be carcinogenic to humans (low doses)." US EPA, 2005. Office of Pesticide Programs. List of Chemicals Evaluated for Carcinogenic Potential. May 10, 2005.

13. Frazier, L. and M.L. Hage. 2001. Reproductive Hazards of the Workplace. Europe: Wiley. Table 10: Partial List of Reproductive Toxins.

14. Environmental Defense Fund, Scorecard Database.

15. EPA weight-of-evidence category, "Group B2 – Probable Human Carcinogen." US EPA, 2005. Office of Pesticide Programs. List of Chemicals Evaluated for Carcinogenic Potential. May 10, 2005.

16. EPA weight-of-evidence category, "Likely to be carcinogenic to humans." US EPA, 2005. Office of Pesticide Programs. List of Chemicals Evaluated for Carcinogenic Potential. May 10, 2005.

17. New Jersey Department of Health and Senior Services, Right to Know Hazardous Substances Fact Sheets. Available online at

18. Gosselin, R.E., R.P. Smith, and H.C. Hodge. 1984. Clinical Toxicology of Commerical Products, 5th edition. Baltimore, MD: Williams and Wilkins.

19. Tew, J.E. 1996. Protecting Honeybees from Pesticides. Ohio State University Cooperative Extension.

20. Briggs, S.A. 1992. Basic Guide to Pesticides: Their Characteristics and Hazards. Washington, DC: The Rachel Carson Council, 98.

21. California Environmental Protection Agency. Proposition 65: Chemicals Known to the State to Cause Cancer or Reproductive Toxicity. Office of Environmental Health Hazard Assessment. November 23, 2018.

22. US EPA, 2006. Hazard Assessment of the Organophosphates. Hazard ID Committee Report.

23. US EPA, 1995. Monosodium Methanearsonate and Disodium Methanearsonate; Toxic Chemical Release Reporting; Community Right-to-Know. Federal Register Environmental Documents.

24. US EPA. Integrated Risk Information System Database.

25. The Pesticide Management Education Program at Cornell University. Pesticide Active Ingredient Information.

26. EPA weight-of-evidence category, "Suggestive evidence of carcinogenicity but not sufficient to assess human carcinogenic potential." US EPA, 2005. Office of Pesticide Programs. List of Chemicals Evaluated for Carcinogenic Potential. May 10, 2005.

27. National Library of Medicine. TOXNET Hazardous Substances Database.

28. Colborn, T., et al. 1994. Developmental Effects of Endocrine-Disrupting Chemicals in Wildlife and Humans. Environmental Impact Assessment Review 14:469-489.

29. Agency for Toxic Substances and Disease Registry. ToxFAQs.

30. Colborn, T., D. Dumanoski, and J.P. Myers. 1996. Our Stolen Future: Are We Threatening Our Fertility, Intelligence, and Survival? New York: Dutton.

31. Feldman, J. and T. Shistar. 1997. Poison Poles: A Report About their toxic trail and the safer alternatives. National Coalition Against the Misuse of Pesticides.

32. Department of Pesticide Regulation (DPR), Endosulfan- Risk Characterization Document. California Environmental Protection Agency, 2007.

33. Californians for Alternatives to Toxics (CATs). Toxicological Profiles.

34. Insecticide Resistance Action Committe (IRAC) eClassification of Chemical Mode of Action

35. Registry of Toxic Effects of Chemical Substances (RTECS).

36. European Commission. Endocrine Disruptors: Study on Gathering Information on 435 Substances with Insufficient Data. Final Report. EU DG Environment: B4-3040/2001/325850/MAR/C2. BKH Consulting Engineers: M0355037. November 2002.

37. U.S. Geological Survey, Pesticides in the Nation's Streams and Ground Water, 1992-2001.

38. Thurman, E.M. and A.E. Cromwell. 2000. Atmospheric Transport, Deposition, and Fate of Triazine Herbicides and Their Metabolites in Pristine Areas at Isle Royale National Park. Environmental Science and Technology 34:3079-3085.

39. U.S. EPA, Office of Prevention, Pesticides and Toxic Substances, New Active Ingredients Factsheets:

40. Mineau, P., A. Baril, B.T. Collins , J. Duffe, G. Joerman, R. Luttik. 2001. Reference values for comparing the acute toxicity of pesticides to birds. Reviews of Environmental Contamination and Toxicology 170:13-74.

41. Arctic Monitoring and Assessment Programme. 2009. AMAP Assessment 2009: Human Health in the Arctic.

42. Hageman, et al. 2006. Atmospheric Deposition of Current-Use and Historic-Use Pesticides in Snow at National Parks in the Western United States. Environ. Sci. Technol., 2006, 40 (10), pp 3174–3180.

43. Pesticide Action Network Pesticide Database.

44. Federal Register. September 5, 2008.

45. Federal Register. March 21, 2003.

46. Fluoride Action Alert Pesticide Project Factsheets.

47. EPA docket ID EPA-HQ-OPP-2010-0324. August 17, 2011.

48. USDA/Forest Service. Dinotefuran: Human Health and Ecological Risk Assessment Final Report. April 24, 2009.

49. U.S. Department of Energy Bonneville Power Administration. 2000. Halosulfuron: Herbicide Fact Sheet

50.IUPAC Agrochemical Information.

51. Federal Register. Fenbuconazole Pesticide Tolerance. January 15, 2002.

52. California Department of Pesticide Regulation, Public Reports on New Active Ingredients

53. EPA Pesticide Registration Review Status

54. National Toxiocology Program. 14th Report on Carcinogens. Nov 3, 2016.

55. University of California Statewide Integrated Pest Management Program. Pesticide Information.

56. PAN Pesticide Database.

57. Yueh, MF et al. 2014. The commonly used antimicrobial additive triclosan is a liver tumor promoter. PNAS doi: 10.1073/pnas.141911911. Triclosan promotes liver cancer cell development and proliferation in mice through pathways common to humans.

58. Kim, J et al. 2017. Triclosan affects axon formation in the neural development stages of zebrafish embryos (Danio rerio). Environmental Pollution doi: 10.1016/j.enjvpol.2017.12.110.

59. Lassen et al. 2016. Prenatal Triclosan Exposure and Anthropometric Measures Including Anogenital Distance in Danish Infants. Environmental Health Perspectives doi: 10.1289/ehp.1409637. Prenatal triclosan exposure associated with reduced head circumference, a trait linked to cognitive impairment.

60. Stuart, M et al. 2012. Review of risk from potential emerging contaminants in UK groundwater. Science of the Total Environment 416, 1-21. UK Environment Agency detected triclosan in groundwater 22 times in 22 sites over the period 1992-2009, at a maximum concentration of 2.11 µg/L.

61. Karnjanapiboonwong, A et al. 2011. Occurrence of PPCPs at a Wastewater Treatment Plant and in Soil and Groundwater at a Land Application Site. Water, Air, & Soil Pollution 216(1-4), 257-273. Triclosan detected in 5 out of 7 groundwater samples from a West Texas Land Application Site, at concentrations ranging 12-53 ng/L.

62. Parenti, CC et al. 2018. Environmental concentrations of triclosan activate cellular defence mechanism and generate cytotoxicity on zebrafish (Danio rerio) embryos. Science of the Total Environment 650, 1752-1758. Triclosan levels commonly found in the environment invoke oxidative stress immune responses and cause high levels of cell death in zebrafish embryos.

63. Lee, HR et al. 2014. Progression of Breast Cancer Cells Was Enhanced by Endocrine-Disrupting Chemicals, Triclosan and Octylphenol, via an Estrogen Receptor-Dependent Signaling Pathway in Cellular and Mouse Xenograft Models. Chemical Research in Toxicology doi: 10.1021/tx5000156.

64. Riad, M et al. 2017. Reproductive toxic impact of subchronic treatment with combined butylparaben and triclosan in weanling male rats. J Biochem Mol Toxicol doi: 10.1002/jbt.22037. Treatment with triclosan alone causes testicular oxidative stress and DNA damage, leading to a marked reduction in sperm count and sperm motility.

65. Jurewicz, J et al. 2017. Environmental levels of triclosan and male fertility. Environmental Science and Pollution Research 25(6), 5484-5490. Men with higher urinary concentrations of triclosan have poorer semen quality, exhibiting a greater percentage of sperm with abnormal morphology as compared to men with lower triclosan levels.

66. Kang, D. et al., 2008. Cancer incidence among pesticide applicators exposed to trifluralin in the Agricultural Health Study. Environmental Research, 107(2), 271-276. Regression analysis of pesticide exposures and cancer incidence across a cohort of 50,127 private and commercial pesticide applicators show that above-average levels of trifularlin exposure significantly predict incidence of colon cancer, controlling for lifestyle factors and other agricultural exposures.

67. Kılıç, Z.S., Aydın, S., Bucurgat, Ü.Ü. and Başaran, N., 2018. In vitro genotoxicity assessment of dinitroaniline herbicides pendimethalin and trifluralin. Food and Chemical Toxicology, 113, 90-98. Trifluralin exposure at concentrations as low as 1.7 ppb causes significant damage to DNA and chromosomes in human peripheral lymphocytes, demonstrating genotoxicity as a mechanism of carcinogenicity. 

68. Saghir, S.A., Charles, G.D., Bartels, M.J., Kan, L.H., Dryzga, M.D., Brzak, K.A. and Clark, A.J., 2008. Mechanism of trifluralin-induced thyroid tumors in rats. Toxicology Letters, 180(1) 38-45. Trifluralin treatment increased the conjugation and excretion of thyroid hormones (TH), thereby increasing pituitary production of thyroid stimulating hormone (TSH) and causing thyroid tumor development. The mode of action for tumor promotion by trifluralin has relevance to human health, as increased bile excretion coupled with decreased functioning of a shared class of thyroid hormone binding agents would be expected to cause similar effects in humans.

69. Emmerson, J.L., Pierce, E.C., McGrath, J.P., 1980. The chronic toxicity of compound 36352 (trifluralin) given as a compound of the diet to the Fischer 344 rats for two years. StudiesR-87 andR-97 (Elanco Products Co., Division of Eli Lilly and Co., Indianapolis, IN). Cited in Reregistration Eligibility Decision (RED) on trifluralin, USEPA, Office of Prevention, Pesticides and Toxic Substances. EPA 738-R-95-040, April 1996. Chronic exposure to trifluralin causes thyroid tumor development in rats.

70. Zhang, L., Rana, I., Taioli, E., Shaffer, R.M. and Sheppard, L., 2019. Exposure to Glyphosate-Based Herbicides and Risk for Non-Hodgkin Lymphoma: A Meta-Analysis and Supporting Evidence. Mutation Research/Reviews in Mutation ResearchMeta-analysis of every available published human study on NHL and glyphosate, including the most recently updated data from the ongoing U.S. Agricultural Health Study, published in 2018. Statistical analysis revealed a 41% increased risk of NHL resulting from high exposure to glyphosate-based herbicide.

71. EFSA, 2018. Peer review of the pesticide risk assessment of the active substance variant florpyrauxifen-benzyl:

72. Khanam, S., 2017. Effect of Carbaryl on Hemoglobin and Hematocrit Values of Broiler Chicks. Malaysian Journal of Medical Research, 1(2), pp.38-40.

73. Hussain R, Ali F, Rafique A, Ghaffar A, Jabeen G, Rafay M, Liaqat S, Khan I, Malik R, Khan MK, Niaz M, Akram K and Masood A, 2019. Exposure to sub-acute concentrations of glyphosate induce clinicohematological, serum biochemical and genotoxic damage in adult cockerels. Pak Vet J, 39(2): 181-186.

74. Neto da Silva, K., Garbin Cappellaro, L., Ueda, C.N., Rodrigues, L., Pertile Remor, A., Martins, R.D.P., Latini, A. and Glaser, V., 2020. Glyphosate-based herbicide impairs energy metabolism and increases autophagy in C6 astroglioma cell line. Journal of Toxicology and Environmental Health, Part A, pp.1-15.

75. Rappazzo, K.M., Warren, J.L., Davalos, A.D., Meyer, R.E., Sanders, A.P., Brownstein, N.C. and Luben, T.J., 2019. Maternal residential exposure to specific agricultural pesticide active ingredients and birth defects in a 2003–2005 North Carolina birth cohort. Birth defects research, 111(6), pp.312-323.

76. Ledoux, M.L., Hettiarachchy, N., Yu, X., Howard, L. and Lee, S.O., 2019. Penetration of glyphosate into the food supply and the incidental impact on the honey supply and bees. Food Control, p.106859.

77. Zgurzynski, M.I. and Lushington, G.H., 2019. Glyphosate Impact on Apis mellifera Navigation: A Combined Behavioral and Cheminformatics Study. EC Pharmacology and Toxicology, 7, pp.806-824.

78. Rendón-von Osten, J. and Dzul-Caamal, R., 2017. Glyphosate residues in groundwater, drinking water and urine of subsistence farmers from intensive agriculture localities: a survey in Hopelchén, Campeche, Mexico. International journal of environmental research and public health, 14(6), p.595.