Toxic chemicals & health:
Dursban, the most widely used insecticide in the country, is also among the pesticides most hazardous to human health, according to scientific studies and the findings of the U.S. Environmental Protection Agency. This technical brief summarizes key points about Dursban.
Under the Food Quality Protection Act of 1996, the EPA was to review, by August 1999, pesticides that pose the highest risk to human health. One of these pesticides is Dursban.*
Dursban, which has been around for more than 35 years, is one of 37 similar organophosphate pesticides registered with the EPA, and designed specifically to poison the nervous system. The purpose of the EPA review was to make sure that existing Dursban uses meet the new Food Quality Protection Act health standard, which requires that all exposures pose "a reasonable certainty of no harm" to infants and children.
The EPA missed the August 1999 deadline for reviewing the riskiest pesticides, including Dursban. By October 1999 it had completed only a preliminary review of Dursban, and has taken no action to date. The EPA's draft review concluded that many uses of Dursban expose people, and especially children, to higher levels of the chemical than the agency considers safe. NRDC submitted detailed comments on the Dursban review to the EPA, ending with a call for a complete ban on Dursban. Below are some of the key reasons a ban is necessary.
* Note that the pesticide ingredient chlorpyrifos is known as Dursban in nonagricultural products, while in agriculture it is called Lorsban. For simplicity, we refer to chlorpyrifos in all cases as Dursban.
A Widely-Used Chemical
Extensive Use. All food and residential uses of Dursban now account for an estimated 15-24 million pounds applied annually.1Common in Homes and Schools. Dursban is the most common insecticide used in residential settings like homes, gardens, schools, hospitals, and daycare centers.2 Exterminator Favorite. Exterminators and other professionals use Dursban more than any other insecticide.3
High Risks, Especially to Children Unsafe Home Uses. The EPA's initial review of Dursban in October 1999 determined almost all household uses to be unsafe, meaning they exceed the agency's level of concern.4 The EPA also found all but one professional use of Dursban around the household or school unsafe for residents and students, especially young children.5 Children Are More Sensitive. Data from acute poisonings as well as animal studies suggest that children are more sensitive to Dursban than adults. Animal studies show that the nervous system in a fetus or very young animal may be more than 20 times more sensitive to Dursban than a mature adult nervous system.6,7,8 A Child's Developing Brain is More Vulnerable. Toxicology studies find that even low-dose exposures to Dursban during pregnancy or just after birth may decrease the manufacture of DNA and reduce the number of cells in certain parts of the brain. Combined with rodent studies of other organophosphates, the data suggest that low-level exposures to Dursban early in life may adversely affect the function of the nervous system later in life, with possible links to changes in normal learning and behavior.9
Acute Effects Reported Poisonings High. EPA estimates that Dursban alone accounted for about 6 percent, or 7,000, of all unintentional pesticide-related exposures reported to the American Poison Control Centers in 1996.10 Of these, 1,109 cases were judged to have health effects -- including one fatality -- related to the exposure. In 1994, the centers reported 2,348 unintentional exposures to Dursban among children under age 6. Poisonings Under-Reported. The true number of Dursban poisonings probably is higher than records indicate.11 Doctors and parents often fail to recognize symptoms of organophosphate poisonings in children.12 Mild or moderate symptoms of poisoning (such as headaches, nausea, and dizziness) can easily be mistaken for other illnesses. Even when correctly diagnosed, many cases of organophosphate pesticide poisoning treated in emergency rooms and doctors' offices don't get reported.13 Childhood Poisoning More Severe. Compared with children exposed to other pesticides, kids exposed to organophosphate insecticides like Dursban generally are three times more likely to be hospitalized, five times more likely to be admitted to a critical care unit, and four times more likely to die or suffer life-threatening illness or permanent disability.14
Chronic Effects Poisoning Leads to Long-term Problems. Sheldon Wagner, M.D., an EPA-funded medical consultant on more than 300 cases of pesticide poisoning, notes that patients complain most often about long-term effects from their acute exposures. For the last 10 years, Dursban has been the "number one source" of cases referred to Dr. Wagner.15 Persistent Effects. EPA scientists report that "chlorpyrifos has been associated with chronic effects in humans, including chronic neurobehavioral effects and multiple chemical sensitivity. Neurobehavioral effects reported include persistent headaches, blurred vision, unusual fatigue or muscle weakness, and problems with mental function including memory, concentration, depression, and irritability."16,17 Studies suggest that human health effects may occur even in the absence of measurable depression of the enzyme cholinesterase, which the EPA usually considers the most sensitive measure of exposure to organophosphates like Dursban.18 Some People Are More Sensitive. Around 10 percent of the population appears to be significantly more sensitive to chronic effects from Dursban poisoning. This is consistent with what is known about how people vary in their ability to produce key enzymes that metabolize organophosphates. In 1990, the Office of Technology Assessment reviewed case reports and studies of acute organophosphate poisoning among workers and concluded, "Case reports and studies of acute poisonings of agricultural and other workers indicate that 4 to 9 percent of the acutely poisoned individuals experienced delayed or persistent neurological and psychiatric effects .[including] depression, mood swings, anxiety, fatigue, lethargy, difficulty concentrating, and short-term memory loss."19 Links to Asthma. Dr. Wagner reports the case of a child with no history of allergy who developed new asthma that persisted after acute exposure to Dursban.20 In farmworkers, asthma has been associated with exposure to pesticides that, like Dursban, inhibit the enzyme cholinesterase. Dursban exposure also has been linked to an increase in atopy, or allergic sensitization. Researchers note that it is biologically plausible that exposure to organophosphate insecticides, like Dursban, relates to respiratory disease in children through disruption of cholinesterase-using nerves that control airways. 21 Prior to approving new pesticides, the EPA requires no core testing for effects on the developing nervous system or immune system function, including allergic sensitization.
Widespread Children's Exposure Most Children's Bodies Carry Traces. Organophosphates and their metabolites often are found in urine. As part of the National Health and Nutrition Examination Survey, around 1,000 adult volunteers had urine tested for various pesticides. TCP, the main breakdown product of Dursban, was found in the urine of 82 percent. Meanwhile, 92 percent of 89 Minnesota schoolchildren surveyed recently had measurable levels of TCP in their urine. (TCP is also a metabolite of the less-widely-used organophosphate chlorpyrifos methyl). Residues in Food. Using all relevant federal data on food consumption and pesticide residues on food, the Environmental Working Group concluded that nine of 10 American children age 6 months through 5 years ingest organophosphate insecticides in their food each day.22 In 1992, the EPA published a report finding Dursban residues in fish at over a quarter of sites tested.23 In 1999, the EPA said that this report "indicated that consumption of freshwater fish (i.e., by sport or subsistence fishermen and their families) could contribute to the dietary exposure to chlorpyrifos."24 Breast Milk Contamination. In a test of pregnant animals dosed with Dursban, breast milk concentrations of Dursban one and five days into the mother's lactation period were at least 10-fold greater than her blood concentrations of the chemical, regardless of the magnitude of the dose.25 To our knowledge, Dursban concentrations in human breast milk have not been measured.
Indoor Exposure.Carpets, furniture, and house dust have been identified as long-term reservoirs for pesticides. A study in Jacksonville, Florida, estimated detectable levels of Dursban would be found in indoor air in homes of at least 88 percent of the population across three seasons.26 Studies find Dursban levels in indoor air to be almost four times more concentrated at floor level, where small children play, than at two feet above the floor. Another study of household pesticide exposures found Dursban in the carpet dust of 67 percent of homes surveyed.27 Water Infiltration. In 1997, Dursban was found in over a quarter of surface waters sampled for pesticides by the U.S. Geological Survey. In 1994, Dursban was found in 65 percent of surface water samples from Georgia, Alabama and Florida. Elevated groundwater concentrations of Dursban have been linked to areas where it is used as a termiticide.
Dursban Is Just One of 37 Similar Chemicals
In the real world, children and others are exposed to multiple organophosphates -- in food, in drinking water, at home and school, in parks and on lawns. To date, the EPA has only reviewed Dursban's hazards in isolation, ignoring the fact that all organophosphate insecticides kill in a similar fashion, and people may be exposed to several of these insecticides every day. A consideration of the multiple exposures to organophosphates to which people are routinely subjected should only heighten concern about the risks from contact with Dursban alone.
1. USEPA, Pesticides Industry Sales and Usage: 1996 and 1997 Market Estimates, Office of Prevention Pesticides and Toxic Substances, November 1999.
3. U.S. Environmental Protection Agency, Chlorpyrifos incident review update, Memo by Jerome Blondell, Health Statistician, Health Effects Division, September 27, 1999 (hereinafter USEPA Memo, September 27, 1999).
4. U.S. EPA Memorandum, Occupational/Residential Handler and Postapplication Residential Risk Assessment, Office of Pesticides, Prevention and Toxic Substances. October 5, 1999 (hereinafter USEPA Memo, October 5, 1999).
5. Ibid. Risks fell within EPA's acceptable level for Dursban used in aerial and ground-based adult mosquitocide foggers, though decisions still pending on use of an additional margin of safety for children could affect this use as well.
6. Moser VC, Padilla S, Age- and gender related differences in the time course of behavioral and biochemical effects produced by oral chlorpyrifos in rats. Toxicol Appl Pharmacol 149: 107-109 (1998).
7. Chakraborti TK, Farrar JD, Pope CN, Comparative Neurochemical and Neurobehavioral Effects of Repeated Chlorpyrifos Exposures in Young and Adult Rats, Pharmacol Biochem Behav 46(1) 219-224 (1993).
8. Whitney KD, Seidler FJ, Slotkin TA, Developmental Neurotoxicity of Chlorpyrifos: Cellular Mechanisms, Toxicol Appl. Pharmacol 134:53-62 (1995).
9. Eskenazi B, Bradman A, Castorina R, Exposures of Children to Organophosphate Pesticides and Their Potential Adverse Health Effects, Environ. Health Perspect 107(Suppl. 3): June 1999.
11. USEPA Memorandum, Review of Poison Control Center Data for Residential Exposures to Organophosphate Pesticides, 1993-1996, Office of Prevention, Pesticides and Toxic Substances, February 11, 1999 (hereinafter USEPA Memo, February 11, 1999).
12. Solomon G, Trouble on the Farm: Growing up with Pesticides in Agricultural Communities, Natural Resources Defense Council, New York, NY, 1998
13. USEPA Memo, February 11, 1999.
15. USEPA Memo, September 27, 1999.
16. USEPA Memo, October 5, 1999.
17. USEPA, Cholinesterase Literature Review and Comment, Brian Dementi, Office of Pesticide Programs, Presented to EPA Scientific Advisory Panel Meeting of June 3-4, 1997. Arlington, Virginia.
19. U.S. Congress, Office of Technology Assessment, Neurotoxicity: Identifying and Controlling Poisons of the Nervous System, OTA-BA-436 (Washington, DC: U.S. Government Printing Office, April 1990), p. 287.
20. USEPA Memo, September 27, 1999.
21. Eskenazi et al., 1999.
22. Wiles R, Davies K, Campbell C, Overexposed: Organophosphate Insecticides in Children's Food, Environmental Working Group, Washington, DC, January 1998.
23. U.S. EPA Memorandum, Chlorpyrifos HED Preliminary Risk Assessment, Office of Prevention, Pesticides and Toxic Substances, October 18, 1999, p. 29.
24. Ibid., p. 29.
25. Makris S, Raffaele K, Sette W, Seed J, A Retrospective Analysis of Twelve Developmental Neurotoxicity Studies Submitted to the FIFRA Scientific Advisory Panel (SAP), available at http://www.epa.gov/scipoly/sap/1998/december/neuro.pdf, December 1998.
26. Whitemore RW, Immerman FW, Camann DE, Bond AE, Lewis RG, Schaum JL, Non-occupational exposures to pesticides for residents of two U.S. cities, Arch Environ Contam Toxicol, 26:47-59 (1994).
27. Camann DE, Buckley JD, Carpet Dust: An Indicator of Exposure at Home to Pesticides, PAHs, and Tobacco Smoke, ISEE/ISEA Joint Annual Conference, Research Triangle Park, NC, September 1994.
Last revised 5.9.00 by The Environmental Working Group