Adopted July 2, 1998
Background and General
Discussion
Pesticides have long
been used throughout the world in public health programs to control human
diseases transmitted by vectors or intermediate hosts as well as in agriculture
for crop protection. The use of
pesticides has increased dramatically in the past 50 years; for example, in
1939, there were 32 pesticide products registered with the U.S. Department of
Agriculture. By 1989, however, there
were 729 active-ingredient pesticide chemicals mixed with other ingredients and
formulated into 22,000 commercial products (1,2). In 1995, sales of pesticides in the United
States alone totaled 1.25 billion pounds of active ingredients and $10.4
billion (3).
With increased use of
pesticides comes the increased risk of both pesticide misuse and pesticide
poisoning. According to Grossman (4), in 1993, 140,000 pesticide
exposures, 93% of which involved home use, were reported to U.S. poison control
centers. Of the reported exposures,
25% involved pesticide poisoning
symptoms; over half of the exposures involved children under the age of 6.
Purpose
The purpose of this
position paper is to review current information on the status of pesticide use
and surveillance with particular emphasis on the implications for environmental
and public health. It is intended to be
used as a basis for initiating discussions on the topic among environmental and
public health practitioners and colleagues in related fields with policy makers
at all levels—local, state, national, and world-wide.
Problem Statement
According to the
United Nation’s Food and Agriculture Organization (5), a pesticide is “any substance or mixture of substances intended
for preventing, destroying, or controlling any pest, including vectors of human
or animal disease, unwanted species of plants or animals causing harm during,
or otherwise interfering with, the production, processing, storage, transport,
or marketing of food, agricultural conditions, wood and wood products, or
animal feedstuffs, or which may be administrant to animals for the control of
insects, arachnids, or other pest in their bodies.” According to Grossman (4),
over 70 million U.S. households make more than 4 billion pesticide applications
per year from a home arsenal averaging three to four pesticide products,
ranging from pest strips, bait boxes, and bug bombs to flea collars, pesticidal
pet shampoos, aerosols, granules, liquids, and dusts. In the United States, approximately 60-70% of pesticides used are
herbicides, 25-30% are insecticides, and 10-15% are fungicides; indeed,
approximately 75% of all cropland and 70% of livestock are treated with
pesticides, with almost 100% of some crops (corn, soybeans, cotton) treated
with herbicides (6).
Pesticides are
deliberately released into the environment to produce biological effects. Unfortunately, many pesticides cause
unintentional effects, including human toxicity. According to Weisenburger (6),
pesticide exposure may result in both acute and chronic health effects,
including acute and chronic neurotoxicity, organ and organ system damage,
irritation and chemical burns, and infant methemoglobinemia. In addition, a variety of cancers,
particularly hematopoietic cancers, immunologic abnormalities, and adverse
reproductive and developmental effects due to pesticide exposure have been
reported. Table 1 contains a listing of
human health effects seen following exposure to some common pesticides. In addition, although several sources of
pesticide poisoning information—such as poison control centers and emergency
rooms—exist, there is no comprehensive source for this information.
Also of concern are
current pesticide use and disposal practices.
Leftover products from home use, spray drift from application sites,
runoff from agricultural fields, accidental spills, and other
practices—including inappropriate or illegal use of pesticides or pesticide
formulations—have made pesticide contamination ubiquitous in the environment (7).
For example, in 1996 hundreds of homes were illegally sprayed with
methyl parathion, a cotton pesticide, by applicators in Mississippi, Louisiana
and Alabama resulting in the temporary relocation of over 1,100 persons. With respect to disposal, fully 6% of
American households simply do not dispose of pesticides because they do not
know how to safely. In a study of
pesticide labels, Lockwood et al., (8)
found that it requires an eleventh grade cognitive level to understand a
pesticide label, which means that 40-50% of the general population cannot read
and understand the directions on a pesticide product label, assuming they have
the 20/30 visual acuity to read the fine print. As of the late 1980's an estimated 1 million households still
stored products containing chlordane; 150,000 still had stored products with
DDT; 70,000 had heptachlor; and 85,000 stored Silvex, which is 2,4,5-T or the
herbicide that is known to contain 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as a contaminant (3).
The general population
may be exposed to pesticides in several ways, according to the route of
exposure, such as inhalation, ingestion of pesticides, or absorption through
the skin (via clothing or direct contact).
For example, residents living in proximity to farming areas may be
exposed to pesticide sprays in the air and in contaminated food or water;
people in urban areas may eat crops or animal products or drink water
contaminated with pesticide residues (9). For example, in 1993 USDA’s Agricultural
Marketing Service found that 39% of 7,328 samples tested had two or more
pesticide residues. During an average
day, most of us consume trace amounts of three to five pesticides. With respect to drinking water,
approximately 24 million people are exposed to herbicides, the most common
contaminant nationwide in drinking water, in the Midwest and Great Lakes Region
(3).
Additionally, there may be exposure via air, water, and food as a result
of the use of pesticides in public health programs aimed at killing disease
vectors in residential areas (9). Finally, in what has been termed the “circle
of poison,” pesticides manufactured in the U.S. and shipped out to other
countries may return on imported fruits and vegetables.
Most pesticide
formulations contain a small amount of the active ingredient, the pesticide,
and a much larger amount (up to 99+%) of other substances, referred to as
“inert ingredients.” Typically these
substances include carrier substances or solvents and compounds that improve
absorption; however, these substances are not usually included in any
discussion of the effects on health, even though their adverse effects may
exceed those of the active ingredients (9).
The adverse effects of pesticides may also be caused by impurities, such as
dioxins in certain phenoxyacid herbicides, ethylene thiourea in ethylene
bisdithiocarbamates, and isomalathion in malathion (9). According to Grossman (4), the EPA estimates that there are at
least 1,700 chemical compounds collectively listed under the rubric “inert
ingredients” on pesticide labels.
Unfortunately, inert ingredients are low priority, accounting for under
1% of the Office of Pesticide Programs budget, as the EPA still has many older
(pre-1972) active ingredients that need to be reregistered and evaluated for
health effects under the Federal Insecticide, Fungicide, and Rodenticide
Act (4). Also according to
Grossman (4), EPA has no specific
procedures or timeframes for ensuring that these inert substances are reviewed,
according to the EPA’s Office of the Inspector General.
Recommended Action
Many other authors
have developed recommendations that address pesticides (1-3,10,11); what follows is a listing of new, as well as a
compilation of old, recommendations.
1. Reduce pesticide use.
• Reduce
pesticide reliance, use, and risks.
• Discontinue
registration of new high-risk pesticides.
(Note: High-risk pesticides are those which fall within the “supertoxic”
range; that is, they have an oral LD50 of <5 mg/kg or have a dermal LD50 of
<20 mg/kg.)
• Make the
transition to biointensive integrated pest management (IPM) the goal of
national policy by encouraging the adoption of IPM on 75% of agricultural
cropland by the year 2000. (Note:
According to Benbrook et al. [3] “IPM
is a systems approach to pest management that is based on an understanding of
pest ecology. It relies on resistant
varieties and promoting plant health, crop rotation, disrupting pest
production, and the management of biological processes to diversify and build
populations of beneficial organisms.
Reduced risk pesticides should be used only as a last resort.”)
2. Develop a surveillance system.
• Require
mandatory reporting of all pesticide use, not just of pesticides classified for
restricted use (exclusive of typical household consumer use).
• Require
mandatory reporting of occupational pesticide-related incidents and illness.
• Make the
existing industrial data bases on health surveillance of pesticide-exposed
workers usable to the scientific community.
• Maximize
the use of routinely collected data, such as doctor’s reports for Workers’
Compensation, to supplement descriptive studies.
• Modify and
use national surveys of acute health effects (including the National Center for
Health Statistics hospital survey, emergency room surveys, and the American
Association of Poison Control Centers poisoning survey) so that they include
standardized information on occupation, race, ethnicity, income, education, and
circumstances of pesticide-related incidents.
• Collect
information on occupation in emergency rooms at the time of the initial visit
for a specific problem.
3. Promote additional research.
• Encourage
additional research on pesticides and their health effects. (Note: It is quite obvious there is a dire need for all types of
properly-designed research---on children, seasonal workers, adults, exposure
scenarios/assessments, etc.)
• Accelerate
the testing of banned and restricted products that still pose a threat to humans
and wildlife because of their persistence and presence in human tissue.
• Assess the
quality of information on people of color in routinely collected vital and
medical records, census, and other data.
• Investigate
cancer and the potential neurodevelopmental and neurobehavioral effects of
pesticide exposure among children of farm workers, including leukemia,
lymphoma, and primary brain cancer.
• Design and
carry out studies that address reproductive outcomes in male and female workers
and their offspring who are exposed to pesticides.
• Investigate
the association, if any, between pesticide exposure and autoimmune disorders,
with emphasis on determining the role of specific classes and types of
pesticides.
• Develop
inexpensive, short-term screening techniques to test new and old products for
endocrine, nervous, and immune system disruptive capacity.
• Expand
toxicity testing in animals to include evaluation of toxicity to infant and
young animals.
4. Increase public awareness and
outreach.
• Increase
public awareness of inequities in exposures to pollution/act to reduce these
inequities.
• Teach IPM
in schools.
• Provide
both the public and workers with access to relevant and understandable
information on exposure to pesticides and the means of minimizing exposure
through the use of work practices, protective equipment, and simple hygiene
procedures, including soap and water.
• Develop
more innovative methods of delivering information to the public, employers, and
workers to promote the use of protective equipment and safer work
practices. The language, format, and
distribution of basic written information should assure that the materials are
culturally relevant and appropriate.
Heavy reliance on conventional written materials as the primary educational
tool in populations with limited reading skills is not particularly
effective. Use of standardized markings
is strongly encouraged.
• Release
exposure and health effects data to the public on public-use computer data
tapes.
• Disseminate
educational materials about resources for dealing with exposure through all
communities.
• Keep the
medical community better informed, so that clinicians are more alert to
pesticide-related illness.
5. Include susceptible populations in
setting tolerance levels.
• Establish
tolerances that protect children, taking into account the physiologic,
developmental, and dietary differences between children and adults.
• Consider
multiple routes of exposure when establishing tolerances.
• Consider
multiple pesticides that share a common mechanism of action and therefore may
be additive or synergistic in their effects when determining residue tolerance
levels.
6. Regulatory goals
• Make
reduction of pesticide use the primary goal of regulation.
• Enforce existing
regulations and require additional provisions for basic levels of personal
protection and washing facilities for all agricultural workers.
• Build the
infrastructure necessary to promote the use of IPM in all markets.
• Redesign
federal and state government programs to promote IPM.
• Promote
smarter, more efficient regulation; that is, make more high-risk chemical
pesticides more difficult to buy and more costly to use. In addition, federal regulations on
household pesticides should encourage the use of household hazardous waste
collection sites for disposal of used household pesticide containers.
• Extend the
Occupational Safety and Health Act (OSHA) coverage to farm and field workers.
• Identify
the specific obstacles and constraints on the EPA, the Department of Health and
Human Services, and the Department of Labor (OSHA) that prevent them from
conducting research, providing health services, and enforcing regulations to
alleviate environmental inequities in exposure to toxic substances.
• Require
industry to test all new products, their metabolites, intermediates, and
byproducts for a) multigenerational immune, endocrine, reproductive, and
nervous system effects in at least three animal species and b) their
environmental fate in all media.
Method of
Implementation
Upon adoption, the
National Environmental Health Association should disseminate this paper as
widely as possible by release to the membership, publication in the Journal of Environmental Health,
provision of copies of this paper to affiliates to share with their members,
and provision of copies of this paper to similar professional associations for
their review. Affiliates and members
should be encouraged to provide comments to legislators based upon the
information contained herein, or by providing a copy of this document as
augmentation to comments provided.
References
1. Moses
M, Johnson ES, Anger WK, Burse VW, Horstman SW, Jackson RJ, et al.
Environmental equity and pesticide exposure. Toxicol Ind Health 1993;9(5):913‑59.
2. Maroni
M, Fait A. Health effects in man from
long‑term exposure to pesticides. A review of the 1975‑1991
literature. Toxicol 1993;78(1‑3):1‑180.
3.
Benbrook
CM, Groth E, Halloran JM, Hansen MK, Marquardt S. Pest management at the crossroads. New York: Consumers Union, 1996.
4.
Grossman
J. What’s hiding under the sink:
dangers of household pesticides.
Environ Health Perspect 1995;103(6):550-4.
5. FAO
International Code of Conduct on the Distribution and Use of Pesticides. Food and Agriculture Organization of the
United Nations, Rome, 1986;28.
6.
Weisenburger
DD. Human health effects of
agrichemical use. Hum Pathol
1993;24:571-6.
7. Wolfe
MF, Seiber JN. Environmental activation
of pesticides. Occup Med 1993;8(3):561‑73.
8.
Lockwood
JA, Wangberg JK, Ferrell MA, Hollon JD.
Pesticide labels: proven protection or superficial safety?. J Am Optometric Assoc 1994;65(1):18‑26.
9. Al-Saleh
IA. Pesticides: a review article. J Environ Pathol Toxicol Oncol
1994;13(3):151-61.
10. Reigart JR. Pesticides and children.
Ped Ann 1995;24(12):663-8.
11. Colborn T. Pesticides—how research has succeeded and failed to translate
science into policy: endocrinological effects on wildlife. Environ Health Perspect 1995;103(Suppl 6):81-6.
12. Extoxnet. Extension Toxicology
Network. 1993. Http://ace.ace.orst.edu/info/extoxnet/
13. Foster WG. The reproductive toxicology of Great Lakes contaminants. Environ Health Perspect 1995;103(9):63-9.
14. Vial T, Nicolas B, Descotes J. Clinical immunotoxicity of pesticides. J Toxicol Environ Health 1996;48:215-29.
15. Lu FC.
A review of the acceptable daily intakes of pesticides assessed by
WHO. Reg Toxicol Pharmacol
1995;21:352-64.
16. Fleming LE, Timmeny W. Aplastic anemia and pesticides—an etiologic
association? JOM 1993;35(11):1106-16.
17. Murphy SD. Toxic effects of pesticides.
In: Klassen CD, Amdur MO, Doull J, eds.
The basic science of poisons.
Casarett and Doull’s Toxicology, New York: Macmillan, 1986:519-81.
18. Sittig M. Handbook of toxic and hazardous chemicals and carcinogens. Park Ridge, NJ: Noyes Publications, 1985.
19. Arena JM, Drew RH, eds. Poisoning: toxicology, symptoms,
treatments. Springfield, IL: Charles C.
Thomas, Publisher, 1986.
(Original paper prepared by Ginger L. Gist, Ph.D., DAAS, Senior Environmental Health Scientist, Agency for Toxic Substances and Disease Registry)
Fiscal Impact
The committee foresees
the only fiscal impact on NEHA with the adoption of this paper to be the cost
of making and mailing copies. The fiscal
impact of the problem will be felt mainly by state and federal authorities with
responsibilities in pesticide regulation.
(July 1, 1998)
Table 1.—Health
effects of selected pesticides (1,12-19).
|
Pesticide |
Evidence of Health Effects |
Produces
Malformations in Pregnancy |
Alters
Fertility |
Potentially
Immunotoxic |
Potential
Endocrine Disrupter |
|
|
|
Known |
Suspected |
|
|
|
|
|
2,4-D |
Chloracne (TCDD) |
Cancers: soft-tissue sarcoma, lymphatic and
hematopoietic, stomach, colon, prostate; liver dysfunction; teratogenesis |
Yes |
|
Yes |
Yes |
|
2,4,5-T |
Chloracne; porphyria |
Cancers: soft-tissue sarcoma, lymphatic and
hematopoietic, stomach, colon, prostate; liver dysfunction; teratogenesis |
Yes |
|
|
Yes |
|
Aldrin |
Neurotoxic effects |
Cancer |
Yes |
Yes |
|
Yes |
|
Arsenicals |
Lung cancer; liver disease; pancytopenia;
arsenical keratoses; peripheral neuropathy |
Aplastic anemia |
|
|
|
|
|
Captan |
|
Cancer |
Possibly |
Yes |
|
|
|
Carbaryl |
Neurotoxic effects |
Chromosome aberrations; cancer; kidney damage |
Yes |
Possibly |
Yes |
Yes |
|
Chlordane/ Heptachlor |
Neurotoxic effects; liver damage; kidney
damage |
Myelolymphoproliferative disorders; brain
cancer; liver cancer |
|
Yes |
Possibly |
Yes |
|
Chlordecone (Kepone) |
Neurotoxic effects |
Liver disease; liver cancer |
|
Yes |
|
Yes |
|
Diazinon |
Neurotoxic effects |
|
Yes |
|
|
|
|
Dibromo- chloropropane |
Cancer; liver disease; kidney failure |
|
|
Yes |
|
Yes |
|
Dichlorvos |
Neurotoxic effects |
Cancer; lung damage; liver damage |
Possibly |
Possibly |
Yes |
|
|
DDT |
Chloracne; cerebral dysfunction; liver damage;
kidney damage |
Chromosome aberrations; high cholesterol and
triglyceride levels; tremors, muscular weakness; pancreatic cancer; aplastic
anemia; thyroid damage |
|
Yes |
Yes |
Yes |
|
Dieldrin |
Neurotoxic effects |
Cancer |
Yes |
Yes |
Yes |
Yes |
|
Diquat dibromide |
Corrosive; gastrointestinal tract damage;
kidney damage; liver damage; neurotoxic effects; cataracts |
|
|
Possibly |
Yes |
|
|
Endrin |
CNS depression |
|
Yes |
|
Yes |
|
|
Ethylene dibromide |
CNS depression; severe eye and skin
irritation; cancer; lung damage |
|
Possibly |
Yes |
|
|
|
Hexachloro-
benzene |
Porphyria |
Liver cancer; thyroid cancer; neurotoxic
effects; lung damage |
Yes |
Possibly |
Yes |
|
|
Lindane |
Aplastic anemia; heart damage; neurotoxic
effects |
Liver cancer; liver damage; leukemia; kidney
damage |
|
Yes |
Yes |
Yes |
|
Maneb |
Hemolytic anemia; kidney damage; irritant;
heart damage |
Cancer; thyroid hyperplasia |
Yes |
Yes |
Yes |
Yes |
|
Methyl parathion |
Neurotoxic effects |
Liver damage; inflammation of the stomach;
respiratory stress |
Yes |
Possibly |
Yes |
|
|
Mirex |
|
Liver cancer |
|
Yes |
Yes |
Yes |
|
Paraquat |
Lung damage; kidney failure; liver damage;
skin, eye, and mucosal irritant; damage to the heart, adrenal glands, and
digestive system |
Parkinson’s disease; cancer |
Yes |
Possibly |
Yes |
|
|
Pentachloro-
phenol |
Liver damage; kidney damage; neurotoxicity;
chloracne |
Aplastic anemia; cancer |
Possibly |
Possibly |
Yes |
Yes |