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STATEMENT OF
JAY FELDMAN, EXECUTIVE DIRECTOR
BEYOND PESTICIDES/NATIONAL COALITION
AGAINST THE MISUSE OF PESTICIDES

ON

S.B. 654, PESTICIDES – EDUCATION AND REPORTING
BEFORE THE
ECONOMIC AND ENVIRONMENTAL AFFAIRS COMMITTEE
MARYLAND SENATE
ANNAPOLIS, MARYLAND

MARCH 13, 2001

Mr. Chairman and members of the Committee.  I am Jay Feldman, Executive Director of Beyond Pesticides/National Coalition Against the Misuse of Pesticides (NCAMP), 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 that reduce or eliminate a reliance on pesticides. Our membership includes residents of Maryland and spans the 50 states and groups around the world.

We are here today in support of S.B. 654. The legislation will establish a statewide pesticide illness reporting system and advisory council, accompanied by training for health care providers.

The need for reporting

The issue of pesticide-induced illness, a serious public health question given the widespread use of pesticides in Maryland, is not currently evaluated by the state. In fact, state officials are unable to evaluate the health impact that pesticide use may be having in the state because pesticide poisoning is not a reportable medical or health event. This is not the case in eight states nationwide[1] where programs have been put in place by statutes that require the collection of this data.

The federal government has not collected this kind of information recently and is not expected to take on this function. The U.S. Environmental Protection Agency (EPA) did have a Pesticide Incident Monitoring System for over a decade, until 1981. Since that time, the federal government has been relying on states to conduct these programs to protect their residents and, in some cases, to assist in regulatory deliberations on pesticide safety. In fact, in a 1995 report the U.S. General Accounting Office (GAO) said, “According to EPA staff, data on incidents of exposure played a significant part in 19 instances in which the agency took measures to protect the public health between 1989 and 1994.”[2]

GAO clearly spells out the deficiencies in the federal data collection system and concludes, “Officials from these agencies that collect data on pesticide illnesses confirmed that a lack of comprehensive national data exists . . . for the general population. . .”[3] The report then explains the deficiencies associated with the range of databases that EPA uses to indicate the extent of acute pesticide incidents and illnesses. It cites four databases, including the American Association of Poison Control Centers, Section 6(a)(2) of the Federal Insecticide, Fungicide and Rodenticide Act, the National Pesticide Telecommunications Network, and the California Pesticide Illness Surveillance Program.

Partially in response to the lack of federal involvement in a critical public health issue and, in large measure due to a recognition of extensive pesticide use in their states. The state of Washington’ Pesticide Incident Reporting and Tracking (PIRT) Review Panel mission statement reads as follows:

The mission of the PIRT Panel is to monitor the activities of the state agencies responsible for pesticide regulation, to ensure timely response and adequate monitoring of pesticide use, protection of workers, the public and the environment from the effects of pesticide use and misuse.[4]

PIRT explains its goals and tasks as follows:

1. To reduce the risk from pesticide exposure to human health and the environment.

2. To reduce the overall incidence and severity of human pesticide exposures through timely incident investigation, education, and development of public health protection strategies for workers, and the public.

3. To ensure that appropriate legislation, rules, and guidelines are in place to provide adequate public health and environmental protection from pesticide use and misuse.

4. To ensure adequate reporting of health related or environmental incidents involving pesticides.

5. To provide the Governor, agency heads, the legislature, and the public with an annual report of PIRT activities and summary of agency pesticide incident investigations.[5]

PIRT explains its tasks as follows:

1. To review pesticide incidents of unusual complexity or those that cannot be resolved, as requested by the chair or any panel member.

2. To monitor the time periods required for response to reports of pesticide complaints or incidents as recorded by the Department of Agriculture, Ecology, Health and Labor and Industries.

3. To establish guidelines for centralizing the receipt of information relating to actual or alleged health and environmental incidents involving pesticides.

4. To review agency procedures for investigation of pesticide incidents and make recommendations for implementation by the appropriate agency.

5. To review and approve an annual report prepared by the Department of Health.[6]

Pesticides are toxic chemicals. Therefore, their use may result in adverse effects to human health and the environment. Passage of the Food Quality Protection Act (FQPA) in 1996 and the release of the National Academy of Sciences Report, Pesticides in the Diets of Infants and Children, in 1993 indicate that state lawmakers have reason to be concerned about pesticide exposure. Neither the federal nor the state laws provide adequate protection of public, according to the findings associated with both FQPA and the National Academy of Sciences. This legislation does not seek to regulate or legislate pesticide use. Instead, it seeks to provide better information with which the state of Maryland could take steps to protect the public, if necessary.

Those who have studied pesticide law find quickly that the standards of safety in the various statutes, whether FQPA or FIFRA are based on risk assessments or risk benefit equations that bring with them a high degree of uncertainty as to the adverse impacts that pesticide exposure will have on various population groups. There is no disagreement that children, for example, exhibit higher vulnerability than adults to pesticide exposure and that risk assessments for most of the pesticides in use do not take this fact into account. The “unreasonable adverse effects” standard of safety in FIFRA allows EPA to accept risk levels among the population. The “reasonable certainty of no harm” standard in FQPA is defined as “negligible risk,” which provides for a risk assessment calculation that may adopt inaccurate assumptions about exposure patterns, background levels, previous exposures, and more. None of these calculations look at synergistic effects. There is very little attention to contaminants and impurities that are contained in pesticide products.

All this means that government regulators need more and better information about adverse effects when pesticides are used. To assume adequate calculations in a laboratory or a government office and ignore the real world experience that could be gained from incident reporting is, in our belief, wrong.

Training is necessary for medical care providers


”Pesticide poisoning is a commonly under-diagnosed illness in America today,” according to the EPA published Recognition and Management of Pesticide Poisonings.”[7] The publication goes on to say,

Despite recommendations by the Institute of Medicine and others urging the integration of environmental medicine into medical education, health care providers generally receive a very limited amount of training in occupational and environmental health, and in pesticide-related illnesses, in particular.[8]

Because of this, S.B. 654 includes a provision to “educate health care providers in the state about the potential adverse effects of exposure to pesticides by residents of the state.” [Subtitle 15, (B)(1)] At the same time, recognizing the low degree of public awareness on this issue, the bill requires the development of a “program to educate residents of the state about pesticides and about risks associated with pesticides.” [Subtitle 15, (A)]

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.[9] Low levels of pesticide exposure can adversely affect a child’s neurological, respiratory, immune and endocrine system.

Our testimony today supports the adoption of the legislation before you, Child Care Facility – Pesticide Application – Prior Notification, in order to provide parental and day care center employee notification of pesticide use. We urge that this legislation be adopted to provide for universal, prior written notification when pesticides are used in child care facilities. Because of the ability of pesticide to drift or volatilize, it is important that this notification standard be applied in all cases when pesticides are used indoors, regardless of where the application takes place and the size of the area treated. The only way to insure proper notification in all cases is to require proper notification in all cases. Exceptions will only lead to an erosion of the program.

As we will show in this testimony, the registration of pesticides, and specifically the pesticides used in Maryland daycare facilities, is fraught with studies of 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. Full disclosure is a first and important step in the process.

Below we will take a look at some of the pesticides used in Maryland in an around daycare facilities and then provide an overview of the regulatory system behind the pesticides in use.

An overview of some of the pesticides used in Maryland in and around daycare facilities.

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.[10] 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.[11] Chlorpyrifos is linked to delayed peripheral neuropathy, degenerative lesions of sensory, motor or reflex nerves[12]. 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.[13] 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.[14] 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.[15]

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 carcinogen,[16] 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.[17] 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 used in Maryland’s school yards, 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.[18] 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.[19]  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.[20] Study conducted by the National Cancer Institute found elevated rates of canine lymphoma in dogs living in households where 2,4-D was used.[21]

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.[22] 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.[23]

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.

The growth in pesticide use is a troubling development in light of public exposure to hazardous pesticides that can cause cancer, toxic sensitization, neurological problems and a range of short term effects such as dizziness, headaches, rashes and mental disorientation.  In addition, most of the pesticides in use have not been fully tested for the range of possible adverse health effects.  This is true for both the active and inert ingredients.

While most of discussion focuses on active ingredients, pesticide formulations contain a majority so-called “inert” ingredients. Inert ingredients are often as toxic as the active ingredient, although the law defines these materials as secret because they are not added to the formulation to specifically kill the target pest. Inerts, often petrochemicals like benzene, toluene or xylene, are generally the largest percentage ingredient of a pesticide product. They form the solution, the dust, or the granule in which the active ingredient is mixed. According to a recent report, 209 inerts are considered hazardous air and water pollutants, 14 have been assessed as “extremely hazardous, 84 are reportable to the Toxic Chemical Release Inventory, 21 are known or suspected carcinogens, and 127 are regarded as occupational hazards.[24] Yet, when these materials are in pesticide products, they are not disclosed.

Many pesticides affect the immune system, which can result in increased problems with allergies, asthma, hypersensitivity to chemicals and a reduced ability to combat infections and cancer.[25] Many insecticides, herbicides and fungicides are linked to cancer. As cited above, the commonly used weed killer 2,4-D has been linked to non-Hodgkin’s lymphoma in scientific studies of farmers and canine lymphoma in dogs. Studies show that children living in households where pesticides are used suffer elevated rates of leukemia, brain cancer and soft tissue sarcoma. The probability of an effect such as cancer, which requires a period of time to develop after exposure, is enhanced if exposure occurs early in life.

A U.S. General Accounting Office (GAO) review of pesticides, entitled Nonagricultural Pesticides: Risks and Regulation, found that, "The general public receives limited and misleading information on pesticide hazards."[26]  That was 1986 and nothing has changed in the intervening 13 years. While EPA offers virtually no public health warning to consumers who use or are exposed to the organophosphate insecticide, the agency does warn people to, "Wash immediately if automobiles are accidentally sprayed."

As evidence of public health and environmental effects associated pesticides mount, EPA claims that it regulates these toxic materials in compliance with a risk-benefit standard in the Federal Insecticide, Fungicide and Rodenticide Act (FIFRA).  In fact, in spite of the increasingly well-known risks, EPA often justifies the widespread use of poisons in pest control by referring to the "benefits" of their use.  The biggest difference in the way that pesticides, as opposed to other toxic substances, are regulated is that it is assumed that there are benefits to releasing pesticides in the environment.[27] Experience illustrates that alternative approaches to pest management that do not rely on toxic pesticides are quite effective.

Under FIFRA, EPA may register a pesticide after determining that it "will not generally cause unreasonable adverse effects on the environment," and may cancel the registration if it does cause unreasonable effects on the environment.  FIFRA defines "unreasonable adverse effects on the environment" to mean "any unreasonable risk to man or the environment, taking into account the economic, social and environmental costs and benefits of the use of any pesticide."[28]  Those who use a pesticide have a right to expect that they will receive a benefit commensurate with the risk they take, and to which they expose their families, neighbors, and environment.

While EPA has attempted to apply a partial benefits analysis to pesticides on the market which have exceeded risk criteria established by the agency, no analysis is conducted "up front," when the pesticide is registered.  The agency does not even pretend to do a benefit analysis.  Officials assume that if there were no benefits to using the pesticide, then there would be no market.  Therefore, barring evidence of extraordinary risks, EPA assumes that benefits outweigh the risks in the initial registration decision.  At the "tail end," EPA does an analysis of the "economic impact of cancellation."  EPA determines how the pesticide is used, how many acres are treated, and what is the most likely alternative to be used if the pesticide under consideration is cancelled.  The most likely alternative in EPA's analysis is generally the most commonly used alternative pesticide.

EPA has failed the public's confidence.  When it comes to non-agricultural pesticides, EPA has failed to comply with the most basic of benefits reviews.  Do pest problems justify exposure to carcinogens, neurotoxins and chemicals that cause birth defects, genetic damage, and toxic sensitization?  We do not think so, when there are less toxic alternatives.  Has EPA considered the range of alternative methods for pest management, which do not rely on toxic materials?  No it has not.  Is the agency out of compliance with the basic requirements of the law?  Yes, it is.

The threat to public health from pesticides is well documented in laboratory studies and victim reports.  The benefits do not outweigh the potential for additional, repetitive, and significant exposure to these toxins.  There are problems based on what is known as well as what is not known.  Lack of adequate data and public awareness on the full health and environmental consequences further argues for a change in use patterns and regulation pesticides.

I. Studies of Human Populations Offer Further Evidence of the Link Between Pesticide Exposure and Cancer

A. Elevated Cancer Rates Occur Among Occupationally Exposed Groups

In addition to the laboratory tests required in support of pesticide registration, evidence of the hazards posed by pesticide chemicals can be seen in human epidemiological studies.  These unfortunate observations indicate that human exposure to pesticides is partly responsible for cancer rates that have been on the rise since 1950.[29] 

           

B. Children, A Particularly Vulnerable Group, May Be At Serious Risk from Pesticide Exposures

Often the occupational setting offers the best opportunity to associate specific exposures with particular outcomes.  Numerous cancer mortality and case-control studies indicate that farmers, pesticide applicators, and pesticide plant workers suffer elevated rates of some cancer types, particularly lip, stomach, leukemia, lymphatic, multiple myeloma, and prostate.[30]

Children rarely fall prey to cancer, yet there are few more tragic events than cancer striking a young person. Epidemiological studies of childhood cancer lend very disturbing evidence that exposure to pesticides at home may be an important risk factor.  Childhood tumors and blood disorders have been linked with substantial prenatal or environmental exposure to specific insecticides by Infante, et al.[31] while Gold, et al. report that children with brain cancer are more likely than normal controls to be exposed to insecticides in the home.[32]  A study sponsored by the National Cancer Institute indicates that household and garden pesticide use can increase the risk of childhood leukemia as much as seven-fold.[33]

II. Gaps in the Toxicity Database of Pesticides Make It Impossible to Assess the Full Extent of the Hazard They Pose.

The limited toxicity and epidemiological information which exists makes it clear that many of these chemicals pose a real and unnecessary hazard.  Yet there is a great deal of information which we lack.  Gaps in the toxicity data of the vast majority of pesticides in use today, which have been cited by numerous reports and studies by the General Accounting Office (GAO)[34] and National Academy of Sciences (NAS),[35] make it impossible to fully assess the long-term health hazard that pesticides pose.  Since the overhaul of FIFRA in 1972 and EPA's mandate to bring pesticides into full compliance with modern safety standards, EPA is now about half way through its task. In its Pesticide Reregistration Progress Report for 1997, EPA announced it has completed 171 reviews, with 210 more to do. It should be pointed out that the eligibility reviews that EPA is counting here still does not mean a registration has been completed with a full data set for health and enviornmetnal effects. Many reregistration eligibility documents (REDs) contain requirements for testing, or outstanding data. Also, as lawn care chemicals fall under the category of terrestrial nonfood use pesticides, the toxicity data requirements are less rigorous.  The battery of chronic toxicity data including the potential to cause cancer, birth defects, and reproductive effects are not required of lawn pesticides if they do not also have food or feed uses.  While 26 of the 33 most commonly used lawn pesticides do also have food or feed uses, as mentioned above this does not guarantee the existence of complete toxicity information.  Finally, EPA does not require testing for immune system effects or chronic neurotoxicity, despite increasing scientific concern and evidence that pesticides adversely affect the immune and nervous system.[36]  Currently, EPA's required neurotoxicity testing is limited to an acute delayed paralytic effect caused by some members of a distinct group of pesticides. 

III. EPA Does Not Adequately Assess the Public's and Children's Exposure to Pesticides.

While it is the responsibility of the EPA to assess the risks associated with each pesticide's use in order to ensure adequate public protection, their internal memoranda acknowledges that the information necessary to assess public exposure to lawn care pesticides is lacking.[37]  The agency has virtually no data on two major routes of public exposure to lawn pesticides, through inhalation and skin absorption.  The memo reveals, "In order to provide meaningful exposure estimates for homeowners and other individuals who may be exposed to pesticides via contact with treated lawns, the Exposure Assessment Branch would need dislodgeable residue data."  Children, with their playing habits, may be subject to the greatest levels of exposure.  This is of serious concern as they are also at special risk to carcinogenic or neurotoxic pesticides which are particularly harmful to immature and developing systems[38].

A study published by Fenske, et al. In the American Journal of Public Health, examined health risks associated with pesticide residues in air and on surfaces. Chlorpyrifos, (DursbanTM), the commonly used organophosphate insecticide, was applied accoridng to normal broadcast application techniques. Substanitally ihger chlorpyrifos concentrations were measured in the infant breathing zone, which is closer to the floor compared to the adult breathing zone. Moreover, ventilation had far less impact on decreasing infant breathing zone levels than adult breathing zone levels. The study concluded that exposures to organophosphate insecticides "following properly conducted broadcast applications could result in doses at or above the threshold of toxicological response in infants, and should be minimized through appropriate regulatory policy and public education."[39]

IV. Chemical Sensitivity Is Increasing and Could Become a Large Problem with Significant Economic Consequences Related to the Disablement of Productive Members of Society.

A medical problem that is receiving increasing attention and which deserves special consideration is the non-specific, debilitating syndrome of chemical sensitivity.  Often (but perhaps not always) the result of some acute or traumatic exposure, victims suffer the triggering of symptoms and observed sensitivities at very low levels of chemical exposure.  A report to the New Jersey State Department of Health by Dr. Claudia Miller at the University of Texas Health Science Center and Dr. Nicholas Ashford at the Massachusetts Institute of Technology contains the most comprehensive study of this topic to date, and concludes that "existing evidence does suggest that chemical sensitivity is increasing and could become a large problem with significant economic consequences related to the disablement of productive members of society

V. Parents and the Public Need Full Information to Make Responsible Decisions

Given the adverse health impact of pesticides, people have a right to full notification and disclosure when they are being exposed to these toxic materials so that they can take precaution and avoid exposure for their children. Unfortunately, neither the federal or state regulatory system currently provide adequate protection. As a result, the proposed legislation is necessary to address a tremendous gap in protection.

VI. An Expansion of Current Law Is Needed To Protect Children in Daycare Facilities.

This committee and now the state of Maryland recognized last year the importance of providing children with an extra measure of protection from pesticides while they are in school. We applaud you for that. This bill extends the disclosure protection from the law to daycare facilities that care for children during the period of their lives when they are most sensitive to environmental toxins. Providing parents with full information on the use of pesticides in daycare facilities enables them to make informed decisions.

We urge passage of this legislation. Thank you for your consideration or our remarks.



[1] The states operating pesticide incident monitoring systems include Arizona, California, Florida, Michigan, New Mexico, New York, Oregon, and Washington.

[2] Pesticides: EPA’s Efforts to Collect and Take Action on Exposure Incident Data, GAO/RCED-95-163, July, 1995, p.5.

[3] Pesticides: Improvements Needed to Ensure the Safety of Farmworkers and Their Children, GAO/RCED-00-40, March 2000, p.11.

[4] PIRT Summary to the 2000 Legislature: Pesticide Incident Reporting and Tracking Review Panel, Washington State Department of Health, Environmental Health Programs, December, 1999, p.2.

[5] Ibid.

[6] Ibid.

[7] Recognition and Management of Pesticide Poisonings, Fifth Edition, EPA, March, 1999, p.2.

[8] Ibid. p.2.

[9] 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.

[10] 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.

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

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

[13] 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.

[14] Racke, K.D., “Environmental Fate of Chlorpyrifos,” Rev. Environ. Contam. Toxicol., 1311-150, 1993.

[15] 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.

[16] 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.

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

[18] 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.

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

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

[21] 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).

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

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

[24] Northwest Coalition for Alternatives to Pesticides, Worst Kept Secrets: Toxic Inert Ingredients in Pesticides, 1998.

[25] Paigen, B., “Children and Toxic Chemicals,” Journal of Pesticide Reform, Northwest Coalition for Alternatives to Pesticides, Summer, 1986.

[26]U.S. General Accounting Office (GAO), Nonagricultural Pesticides: Risks and Regulation, Washington, D.C., GAO/RCED-86-97.

Shistar, T., National Coalition Against the Misuse of Pesticides, The Benefit Side of Risk-Benefit Analysis, 1990.

[28]Federal Insecticide, Fungicide and Rodenticide Act (FIFRA), as amended, 1972.

    [29]Epstein, S., M.D., "Losing the War Against Cancer," The Ecologist, 17(2): 91-99, 1987.

[30]Statement of Leon F. Burmeister, Professor, Department of Preventive Medicine and Environmental Health, University of Iowa, before the Subcommittee on Department Operations, Research, and Foreign Agriculture, Committee on Agriculture, U.S. House of Representatives, May 21, 1985.

[31]P.F. Infante, et al., "Blood Dyscrasias and Childhood Tumors and Exposure to Chlordane and heptachlor," Scandinavian Journal of Work and Environmental Health, 4: 137-150, 1975.

[32]E. Gold, et al., "Risk Factors for Brain Tumors in Children," American Journal of Epidemiology, 109(3): 30-9-319, 1979.

[33]R. Lowengart, et al., "Childhood Leukemia and Parents' occupational and Home Exposures," Journal of the National Cancer Institute, 79: 39, 1987.

[34]U.S. General Accounting Office, Lawn Care Pesticides: Risks Remain Uncertain While Prohibited Safety Claims Continue, RCED-90-134,  (1990), Pesticides: EPA's Formidable Task to Assess and Regulate Their Risks, RCED-86-125, 1986; U.S. General Accounting Office, Nonagricultural Pesticides: Risks and Regulation, RCED-86-98, 1986.

[35]National Research Council, National Academy of Sciences, Toxicity Testing: Strategies to Determine Needs and Priorities, 1984.

[36]C.D. Klaassen, et al. (eds), "Toxic Effects of Pesticides," Cassarett and Doull's Toxicology, Macmillan Publishing Company, New York, NY, 1986.

[37]U.S. Environmental Protection Agency, Lawn Pesticide Policy Group Briefing Paper, January, 1988.

[38]E.J. Calabrese, Age and Susceptibility to Toxic Substances, John Wiley & Sons, 1986.

[39] 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.