Washington, DC–(ENEWSPF)–July 6, 2015. With the release of its Tier 1 screening results for the first 52 pesticide chemicals (active and inert ingredients) evaluated under the Endocrine Disruptor Screening Program (EDSP), the U.S. Environmental Protection Agency (EPA) is at odds with a large body of scientific evidence worldwide that identifies many of these chemicals, most notably the herbicides 2,4-D and atrazine, as interacting with the endocrine system or acting as endocrine disruptors. Independent scientific data has shown these chemicals to interfere with the hormone system.
EPA’s EDSP is a multi-step process used to ensure that exposure to chemicals does not result in adverse human health and environmental effects that can occur from the disruption of hormones. The two-tiered screening and testing system requires that EPA identify which chemicals are able to interact with the endocrine system, specifically with three hormonal pathways – estrogen, androgen, and thyroid – in Tier 1. Tier 2 is designed to go one step further, requiring EPA to determine endocrine effects across taxa (e.g. mammals, birds, amphibians, and invertebrates) as well as potential effects on non-endocrine systems (e.g. neurological, immunological, hepatic, and renal). According to EPA, Tier 1 screening data are the best way to determine whether a chemical has the potential to interact with the endocrine system and requires more thorough testing. However, there are concerns as to whether or not EPA is recognizing effects at doses below their currently established “points of departure” and about the lack of testing for non-monotonic dose-responses (indicating a potential for harmful responses that are greater at lower doses).
EPA found that there was no evidence for potential interaction with any of the endocrine pathways for 20 chemicals. For 14 chemicals that the agency said did show potential interaction, EPA stated that it “already has enough information to conclude that they do not pose risks.” Of the remaining 18 chemicals, EPA found that all showed potential interaction with the thyroid pathway, 17 of them with the androgen (male hormones) pathway, and 14 also potentially interacted with the estrogen (female hormones) pathway. While most of the chemicals were not recommended for additional testing, some, such as captan, cypermethrin, dimethoate, and linuron, were recommended for specific Tier 2 tests. A comparative thyroid assay was recommended by the agency for four chemicals that showed interaction with the thyroid pathway in mammals, a medaka one-generation reproductive test was recommended for 13 chemicals that showed interaction with the estrogen or androgen pathways in wildlife, and a larval amphibian growth and development assay was recommended for five chemicals that showed interaction with the thyroid pathway in wildlife. Chemicals identified to show interactions with two or more pathways include , iprodione, linuron, MGK 264, simazine, and tebuconazole. Despite these findings, some of these chemicals were not recommended for additional testing for reasons that include the lack of expectation of impact on current EPA-established regulatory endpoints on human health and ecological risk assessment.
When EPA says, “there was no evidence,” it does not mean “no evidence.” It means that EPA may have evidence for interaction, but has decided that it is outweighed by evidence against it, or that the only evidence is something that occurs in the presence of overt toxicity, or that they can find some other explanation. When EPA says it has “enough information to conclude that they do not pose risks,” that means that the dose that has been associated with the endocrine effects is as high or higher than that associated with known toxic effects (including safety factors.) Thus, EPA is applying a threshold model to endocrine disruption, pointing to a major deficiency in EPA’s risk-assessment process used to evaluate the effects of chemicals on human health and the environment. A threshold model is not appropriate for hormonally-active substances, which often show opposite effects at higher or lower doses.
For atrazine in particular, the agency found interaction with both the estrogen and androgen pathways, but did not recommend it for Tier 2 testing, stating that it is not “expected to impact current EPA-established regulatory endpoints for human health or ecological risk assessment.” EPA’s conclusion is surprising, especially in light of the developmental effects on frogs that have been documented under current use conditions. Hormonal impacts of atrazine which have been well documented by regulators and scientists, including University of California, Berkeley, biologist Tyrone Hayes, Ph.D., and the European Union’s classification of atrazine as a category 1 endocrine disruptor (evidence of disruption in a living organism). Dr. Hayes’ research has found that frogs exposed to atrazine – in concentrations within federal standards – can become so completely feminized that they can mate and lay viable eggs. According to Dr. Hayes, this “chemical castration” is not limited to amphibians, but has been repeated in fish, reptiles, birds, and mammals by other researchers studying atrazine. In addition to causing severe harm to endangered species, atrazine has been linked to a myriad of health problems in humans. It has also been linked to increased incidences of both the congenital disorder gastroschisis and choanal atresia in areas where the chemical is more widely used. Along with atrazine, propazine and simazine, also in the traizine class of chemicals, have been linked to developmental and reproductive toxicity, are highly soluble in water and are the most frequently detected pesticides found at concentrations at or above one or more benchmarks in over half of sites sampled. Like atrazine, EPA also found interaction of simazine with the estrogen and androgen pathways.
2,4-D, another chemical not recommended for additional Tier 2 testing, was not judged by EPA to have interactions with any of the three endocrine pathways. While EPA found a number of thyroid and developmental effects in animals treated with 2,4-D, these were dismissed because the doses were judged to cause overt toxicity. Additionally, in EPA’s extended one-generation reproduction test (EOGRT), the agency found no treatment-related thyroid effects in males or females. In contrast to these conclusions, however, studies have found a direct correlation of urinary levels of 2,4-D with elevated levels of the luteinizing hormone (LH) – responsible for stimulating the production of testosterone in males and regulating the menstrual cycle and ovulation in females – which suggests a direct effect on hormonal levels by the chlorophenoxy herbicide. Others have observed abnormal sperm and higher rates of birth defects in farmers with long-time exposure to 2,4-D, as well as effects on the thyroid and gonads, documented in Beyond Pesticides’ comments to EPA. Studies have also found that 2,4-D promotes the proliferation of androgensensitive cells by acting synergistically with its main metabolite, 2,4-dichlorophenol (DCP), also known for its endocrine disrupting effects.
Congress passed the Food Quality Protection Act (FQPA) and the Safe Drinking Water Act (SDWA) Amendments in 1996 requiring that EPA screen pesticide chemicals for their potential to produce effects similar to those produced by the female hormones in humans and giving EPA the authority to screen certain other chemicals and to include other endocrine effects. Based on recommendations from an advisory committee, EPA expanded the EDSP to include male hormones and the thyroid system, and to include effects on fish and wildlife. However, delays and criticisms from scientists have highlighted inadequacies of the overall program. After the FQPA set a 1999 deadline for EPA to develop a battery of assays with which pesticide manufacturers were required to screen their products as possible endocrine disrupters, EPA repeatedly pushed back the deadline for over a decade. Moreover, critics of EDSP have said that EPA’s testing protocol is outdated, failing to keep pace with the science.
For more information, read more about endocrine disruptors at the Pesticide-Induced Diseases Database page.
Sources: EPA, www.beyondpesticides.org
All unattributed positions and opinions in this piece are those of Beyond Pesticides