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From April 17, 2006                                                                                                        

Renowned Scientist Warns Pesticide Regulation Is Inadequate
(Beyond Pesticides, April 17, 2006) Theo Colborn, Ph.D., director of the Endocrine Disruption Exchange, Inc., which and co-author of Our Stolen Future, warns in an article published in Environmental Health Perspectives (Vol. 114, No. 1) that the current pesticide regulatory system does not adequately protect the public from the neurodevelopmental effects of pesticides.

The following are excerpts from the discussion section of “A Case for Revisiting the Safety of Pesticides: A Closer Look at Neurodevelopment,” by Theo Colborn, Ph.D., published in the January 2006 issue of Environmental Health Perspectives (Vol. 114, No. 1). See ehp.niehs.nih.gov/members/2005/7940/7940.html for the full article. Dr. Colborn will be honored and will speak at Beyond Pesticides' upcoming 25th Anniversary Gala and National Pesticide Forum.

There is a great deal of uncertainty about the neurodevelopmental effects of pesticides among the human studies presented [in this article]. Exposure has become too complex because of the hundreds of pesticide active ingredients on the market, confounded by background exposure to industrial chemicals that share similar effects. In addition, functional changes are expressed over a continuum, making it difficult to document the damage, which often is expressed as more than one lesion and at different intervals or stages of development.

Although the information is available, EPA has rarely used open literature in its risk assessments, generally using only data submitted by manufacturers. Industry continues to use traditional toxicologic protocols that test for cancer, reproductive outcome, mutations, and neurotoxicity, all crude end points in light of what is known today about functional end points. EPA should accept non-guideline, open literature to determine the toxicity of a chemical. For example, Brucker-Davis published a comprehensive review of the open literature in which she found 63 pesticides that interfere with the thyroid system. Yet, to date, EPA has never taken action on a pesticide because of its interference with the thyroid system.

The amazing litany of diverse mechanisms discovered in the series of chlorpyrifos studies raises serious questions about the safety of not only chlorpyrifos and the other organophospahates (OPs), but all pesticides in use today. Most astounding is the fact that a large part of chlorpyrifos toxicity is not the result of cholinesterase inhibition, but of other newly discovered mechanisms that alter the development and function of a number of regions of the brain and central nervous system. These findings send a warning that even though an OP pesticide like CPF may have a very high EC50 for acute toxicity as a result of cholinesterase inhibition, it may have other toxic strategies that are far more egregious than cholinesterase inhibition.

The knowledge gained from a decade of [chlorpyrifos and 2,4-D brain studies] not only demonstrates the insidious nature of chlorpyrifos and 2,4-D exposure, but it also demonstrates the weaknesses in current standard practices for determining the safety of a pesticide or any other synthetic chemical. Even an EPA analysis of developmental neurotoxicity studies stated that EPA’s current developmental neurotoxicologic testing protocol is “not a sensitive indicator of toxicity to the offspring” and urged EPA “to further consider if it will use literature data.” In the case of CPF and 2,4-D, it appears that those who reviewed the data failed to understand its significance or had other reasons to ignore it. EPA needs to convene a panel of independent experts to review these studies for applicability to determine if and how they can be used for registration.

In most animal studies pesticides are administered at high oral or subcutaneous doses orally, not reflecting that, for most humans and wildlife, exposure could in many instances be dermal or via inhalation and, in many cases, over a long period of time at low doses. EPA currently requires chronic toxicity studies, but it is locked into using high doses to elicit effects and has not overcome the difficulty of detecting effects from chronic or ambient exposure or low doses. In addition, the human pharmacokinetics of pesticide exposure can either enhance or reduce the health impacts depending on individual variations.

In the future, the most efficient, comprehensive assays will take advantage of the fact that most chemicals have more than one effect in one system. Cross-disciplinary teams will be required to design these assays so that every organ system is carefully screened for damage. And most important, this will reduce by thousands the numbers of animals needed for testing. However, improved neurodevelopmental tests with laboratory animals will not fulfill their greatest potential if they are not backed up by better batteries of tests to detect functional disabilities in children.

To protect human health, a new regulatory approach is also needed that takes into consideration this vast new knowledge about the neurodevelopmental effects of pesticides, not allowing the uncertainty that accompanies scientific research to serve as an impediment to protective actions.