Statement of Jay Feldman, Executive Director
Beyond Pesticides/National Coalition Against the Misuse of Pesticides
at
Press Conference on the School Environment Protection Act
U.S. Senate
October 13, 1999

Good morning. I am Jay Feldman, Executive Director of Beyond Pesticides/National Coalition Against the Misuse of Pesticides, a national, grassroots, membership organization that represents community-based organizations and a range of people seeking to improve protections from pesticides and promote alternative pest management strategies which reduce or eliminate a reliance on pesticides. A key concern among our members is the impact of pesticides on children. Because of this, we are here today to endorse the School Environment Protection Act.

We are facing a national pesticide exposure crisis, the dimensions of which are not adequately calculated by the U.S. Environmental Protection (EPA). At the center of this crisis are our children. Children are especially vulnerable to pesticides. Children take in more pesticides relative to body weight than adults and are less able to detoxify toxic chemicals.1 Low levels of pesticide exposure can adversely affect a child’s neurological, respiratory, immune and endocrine system.

Studies of pesticides used in schools show adverse human health and environmental effects and uncertainties associated with effects on children and untested health outcomes. This is the reality we live with, one that cannot and should not be ignored by policy and decision makers. We believe that the only reasonable action to take is serious implementation of integrated pest management (IPM) that only uses synthetic pesticides as a last resort, accompanied by a full disclosure system that provides prior written notification when toxic materials are used.

A recent survey conducted by Beyond Pesticide/National Coalition Against the Misuse of Pesticides found that 30 states provide some level of protection from pesticides used in and around schools. Of those 30, only 16 states provide some level of protection from pesticides in school buildings. While some states have school integrated pest management (IPM) policies that include one or more of the provisions as set forth in SEPA, state protection is uneven and inadequate across the country, and children and staff continue to be harmed by pesticides in school.

Because there is no federal standard to protect children from pesticides while at school, the School Environment Protection Act (SEPA) is critically important. It will clearly define IPM with specific acceptable materials, ensure the development of an IPM plan, and, if pesticides are used, require prior notification and hazard information to all parents, students and staff. EPA will be required, with the assistance of a 12-member public advisory board, to phase out the most hazardous pesticides in schools. The goal, under the statute, is to provide for a safe learning environment.

We are here to tell you that this can be done. Those who argue that IPM requires an ability to spray pesticides immediately after identifying a pest problem are not describing IPM. Take for example the General Services Administration (GSA) and its definition of IPM, "a process for achieving long-term, environmentally-sound pest suppression through the use of a wide variety of technological and management practices. Control techniques in an IPM program extend beyond the application of pesticide to include structural and procedural modification that reduce the food, water, harborage, and access used by pests (GSA, Public Buildings Service, Specification No. BM-5-1, January, 1989, p.1). The IPM policy encourages the avoidance of pesticide use with the requirement: "The Contractor shall use non-pesticide methods of control wherever possible." The policy says that portable vacuums rather than pesticide sprays shall be used for initial cleanouts and that trapping devices rather than pesticide sprays shall be used for indoor fly control wherever appropriate. SEPA will bring all schools up to standard.

Children are at the heart of the issue. In terms of the legislation as it affects children, it should be recognized that our nation's most precious resource is our children. And yet, we as a nation allow the poisoning of our children. Sometimes the effects are vivid and dramatic, as captured by studies linking elevated arates of different types of childhood cancers to pesticide use in the home. In other instances, the effects may be more subtle and develop in the form of learning disabilities or problems with sexual physiological development.

The central problem is that we, as a nation, have not decided to protect the most vulnerable. Instead, we protect for the average. In the process we threaten future generations. The School Environment Protection Act recognizes that public policy can acknowledge and correct the situation in the schools. Children spend the majority of their days and developmental years in school, and therefore we must seek to create an environment in the schools that is conducive to good health.

An Overview of the Most Commonly Used Pesticides

Chlorpyrifos. One of the most commonly used insecticides used in schools, chlorpyrifos (Dursban) is a nervous system poison. It poisons children by reducing the body’s production of the enzyme cholinesterase, necessary to the transmission of nerve impulses, triggering a range of symptoms from nausea, dizziness, headaches, aching joints to disorientation and inability to concentrate.2 These symptoms are common to all organophosphate insecticides. The label for Dursban Plus states that “Repeated exposure to cholinesterase inhibitors may without warning, cause prolonged susceptibly to very small doses of any cholinesterase inhibitor. ” Unconsciousness, convulsions, and death can result with sufficient exposure.3 Chlorpyrifos is linked to delayed peripheral neuropathy, degenerative lesions of sensory, motor or reflex nerves.4 Chloryprifos, a chlorinated organophosphate insecticide, is linked to thousands of pesticide poisoning incidents around the country. Its half-life indoors is estimated to be 30 days.5 Various studies of different treatment methods show chlorpyrifos present up to eight years post application. A variety of different kinds of exposure to chlorpyrifos can cause acute toxicity. Direct skin contact with the insecticide either as a solid or in water can be toxic. Ingestion, breathing of vapors, or contact with chlorpyrifos-treated soil is also toxic.6 Laboratory tests have suggested that young children are more susceptible to chlorpyrifos than adults. A study of typical indoor application techniques showed that carpets act as a source of chlorpyrifos vapors following application, particularly for children. Air concentrations were up to five times higher in the infant-breathing zone.7

Synthetic Pyrethroids. Synthetic pyrethroids are the synthetic analogues of naturally occurring pyrethrins, yet have an improved stability to light, yielding longer residence times. The family of pyrethroid insecticides are neurotoxins. These chemicals are available in a variety of formulations, some combined with additional pesticides, including highly toxic organophosphates and carbametes. Some of the pyrethroids are suspect carcinogens, including cypermethrin which EPA considers a possible human carcinogen8, and permethrin which has accumulated some evidence of tumorigencity. Cypermethrin has also been known to cause gastrointestinal problems. Permethrin’s mode of action to kill pests is similar to that of the organochlorine insecticide DDT.9 Permethrin containing pesticides products effect the immune and reproductive systems and can be irritating to both eyes and skin. Other symptoms include tremors,incoordination, elevated body temperature, increased aggressive behavior and disruption in learning.

Diazinon. One of the insecticides commonly used on lawns, diazinon, is a nervous system poison. It poisons children by reducing the body’s production of the enzyme cholinesterase, necessary to the transmission of nerve impulses, triggering a range of symptoms from nausea, dizziness, headaches, aching joints to disorientation and inability to concentrate.10 EPA’s now defunct Pesticide Incident Monitory System (PIMS) reported 903 diazinon-related human poisonings between 1966 and 1980.

2,4-D. Most studies have been unable to associate specific types of pesticides with specific types of disease. However, exposure to phenoxy herbicides (2,4-D, mecoprop, MCPA, all which are major lawn pesticides) have been linked with increased risk of specific cancers of the lymphatic and blood systems. For example, a 1986 National Cancer Institute study of Kansas farmers reports that those exposed to 2,4-D for 20 or more days per year were six times more likely to develop non-Hodgkins lymphoma than nonfarmers. Even higher risk was found for farmers who frequently mixed or applied the herbicide themselves.11 Women workers exposed to atrazine, another major lawn herbicide, were nearly three times more likely to suffer ovarian cancer according to a recently published study by Donna et al, 1989.12 Study conducted by the National Cancer Institute found elevated rates of canine lymphoma in dogs living in households where 2,4-D was used.13

2,4-D is also an endocrine disruptor. This means that miniscule exposure to the chemical during fetal development can effect adverse health outcomes later in life, causing cancer, infertility (reduced sperm count) and changes to sexual traits. The chemical acts as an estrogen mimic and disrupts the normal functioning of hormones and the message center of the body, causing long-term effects. Hormones get into the developing cell and bind to receptors. Depending on the types of hormones that are there, you can get genes permanently turned on and permanently turned off -not by virtue of the presence or absence of a hormone, but by just changing the amount of the hormone. It is not that males have just testosterone and no estradial or that females have just estradial and not testosterone, it is the relative amounts of these hormones, the maintenance of a regulated internal environment and the determination for which genes end up being active. Very, very subtly, in the smallest possible amounts, hormones can lead to very dramatic changes in how active these genes are and the way these cells function for the rest of the life of an individual. This is what is referred to as genetic imprinting. What hormone mimics like 2,4-D do that is different from the natural hormones is that they appear at the wrong times. They can interact in very complex synergistic fashion with unpredictable outcomes in terms of which genes are going to be turned on and which genes are going to be turned off. The EPA regulatory apparatus has only begun to think about considering these issues and testing requirements in this area are not even due out until August of this year.

Glyphosate (Roundup/Rodeo). The adverse effects associated with glyphosate were documented by doctors in Japan between June, 1984 and March, 1986 in cases associated with gastrointestinal, respiratory, cardiovascular, and central nervous system damage caused by ingestion.14 At the time, the doctors identified the surfactant in the pesticides, POEA, as the cause of the adverse effects. This raises serious concerns about the product formulation, most of which is usually not disclosed on the product label, but protected as trade secret information.

A recent review identifies serious adverse effects associated with glyphosate’s so-called inert ingredients. Inert is a term of art because it can include chemicals that are both chemically and biologically active. (See below.) Glyphosate products have been reported to contain ammonium sulfate, benziothiazolone, 3-iodo-2-propynyl butylcarbamate (IPBC), isobutane, methyl pryrrolidionone, pelargonic acid, polyethoxylated tallowaine (POEA), potassium hydroxide, sodium sulfite and sorbic acid. These chemicals are associated with a range of acute effects, including eye irritation, nausea, diarrhea, respiratory reactions, miscarriages in laboratory tests, skin reactions, weight loss. The California Department of Pesticide Regulation, 1998, in an unpublished report attributes the following adverse effects to glyphosate exposure: eye irritation, painful eyes, burning eyes, blurred vision, swollen eye, face, joints, facial numbness, coughing, headaches skin rash, heart palpitations, elevated blood pressure, chest pains and more.15

Triclopyr (Garlon, Turflon). Garlon can cause permanent impairment of vision. Effects include severe conjunctival irritation, moderate internal redness, and moderate to severe corneal injury. Washing is not effective in prevention these effects. Subchronic and chronic feeding laboratory studies found kidney and liver effects in dogs. In soils with low biological activity trichlopyr remained for more than two years. Faftors such as organic matter, pH, temperature and water content influenced the decomposition rate. Triclopyr is mobile and leaches readily into surface run off waters. In October, 1998, EPA issued a label change under its reregistration process which establishes, “Homeowner reentry is restricted until sprays have dried and dusts have settled.” The agency is requiring additional product chemistry and acute toxicity studies.

Oryzalin (Surflan). Oryzalin is a possible human carcinogen, classified by EPA as a Class C carcinogen. According to a 1987 EPA registration standard, oryzalin causes a “significantly elevated incidence of thyroid gland tumors and three different categories of skin tumors in male and female rats.” Benign liver tumors are seen in male rats at high doses, and benign mammary tumors in femals. Anti-thyroid pesticides similar to oryzalin, depress formation of thyroxin by the throid gland, stimulating the pituitary by a feedback mechanisms to circulate thyroid stimulating hormone (TSH), which then stimulates the thyroid to make more thyroxin. Overstimulation of the gland results in hyperplasia, and later, tumors. Oryzalin was found to be fetotoxic.

END NOTES

(1) National Research Council, National Academy of Sciences, Pesticides in the Diets of Infants and Children, Washington, DC: National Academy Press, 1993; Calabreses, E.J., Age and Susceptibility to Toxic Substances, John Wiley & Sons, 1986; Natural Resources Defense Council, Intolerable Risk: Pesticides in Our Children’s Food, February, 1989; Spyker, J.M. and D.L. Avery, “Neurobehaviroal Effects of Prenatal Exposure to the Organophosphate Diasinon in Mice, “ Journal of Toxicology and Environmental Health 3:989-1002, 1977; Paigen, B., “Children and Toxic Chemicals,” Journal of Pesticide Reform, Summer 1986.

(2) Bushnell, P.J. et al., “Behaviorial and Neurochemical Effects of Acute Chlorpyrifos in Rats: Tolerance to Proloned Inhibition of Chloinesterase,” Journal of Pharmacology Exper. Thera. 266(2):1007-1017, 1993.

(3) Morgan, D.P., Recognition and Management of Pesticide Poisonings, Washington, DC: US EPA, Office of Pesticide Programs, Health Effects Division, 4th ed., 1989.

(4) Lotti, M., “The Pathogenesis of Organophosphate Polyneuropathy,” Critical Review of Toxicology 21(6):465-487, 1992.

(5) California Dept. of Health Services, Hazard Evaluation Section, Office of Environmental Health Hazard Assesssment, “Hazards of indoor-use pesticides under investigation, Tox-Epi Review, Berkely, CA: September 1987.

(6) Racke, K.D., “Environmental Fate of Chlorpyrifos,” Rev. Environ. Contam. Toxicol., 1311-150, 1993.

(7) Fenske, R.A., et. al., “Potential exposure and health risks of infants following indoor residential pesticide applications,” American Journal of Public Health 80(6):689-693, 1990.

(8) Memo from W.L. Burnam, Helath Effects Division, to Health Effects Division branch chiefs, et al., U.S. EPA, Office of Pesticide Programs list of chemicals evaluated for carcinogenic potential,Washington, D.C., Feb. 19, 1997.

(9) Vijverberg, H.P., et al., “Neurotociological effects and the mode of action of synthetic pyrethroids,”Critical Review of Toxicology, 21:105-126, 1990.

(10) Volberg, D.I., et al., Pesticides in Schools: Reducing the Risks, Attorney General of New York State, New York State Department of Law, Environmental Protection Bureau, New York, March 1993.

(11) S.K. Hoar, et al., "Agricultural Herbicide Use and Risk of Lymphoma and Soft-Tissue Sarcoma," Journal of the American Medical Association, 256(9): 1141-1147, 1986.

(12) A. Donna, et al., "Triazine Herbicides and Ovarian Epithelial Neoplasms," Scandinavian Journal of Work and Environmental Health, 15: 47-53, 1989.

(13) Hayes, H.M., et al., “Case-Control Study of Canine Malignant Lymphoma: Positive Association With Dog Owner’s Use of 2,4-Dichlorophenoxyacetic Acid Herbicides,” Journal of the National Cancer Institute, 83 (17):1226-1231 (1991).

(14) Sawada, Y., “Probable Toxicity of Surface-Active Agent in Commercial Herbicide Containing Glyphosate,” The Lancet, p. 299 (1988).

(15) Caroline Cox, Herbicide Factsheet: Glyphosate (Roundup), Journal of Pesticide Reform, Northwest Coalition for Alternatives to Pesticides, 1998.

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