Comment submitted by B. Sachau

public comment on federal register of 5/2/07 vol 72 #84 pg 24198 40 cfr part 180 docket 2007 0036 ten toxic pesticides all lumped together when they should be examined separately by epa and not in a whole group - this long list of toxics just shows how easily epa approves everything that comes before them - lts almost l00% approval rate. chloroneb the only residue approved should be 0.000000000 instead of the high toxicity previously approved by epa. the following applies to chloroneb Aquatic Ecotoxicity All Toxic Effects for Organism Group Organism Group Effects Noted Fish Mortality Zooplankton Intoxication View All Aquatic Ecotoxicity Studies and References Summary of Acute Toxicity for Organism Group Organism Group Average Acute Toxicity Acute Toxicity Range Fish Moderately Toxic Moderate Toxicity View All Acute Summaries AS TO CYPERMETHRIN - NO RESIDUE SHOULD BE OVER 0.00000000. CYPERMETHRIN HAS EFFECTS SUCH AS Acute toxicity: Cypermethrin is a moderately toxic material by dermal absorption or ingestion [2,8]. Symptoms of high dermal exposure include numbness, tingling, itching, burning sensation, loss of bladder control, incoordination, seizures, and possible death (2,8). Pyrethroids like cypermethrin may adversely affect the central nervous system [2,8]. Symptoms of high-dose ingestion include nausea, prolonged vomiting, stomach pains, and diarrhea which progresses to convulsions, unconsciousness, and coma. Cypermethrin is a slight skin or eye irritant, and may cause allergic skin reactions [8]. The oral LD50 for cypermethrin in rats is 250 mg/kg (in corn oil) or 4123 mg/kg (in water) [2,8]. EPA reports an oral LD50 of 187 to 326 mg/kg in male rats and 150 to 500 mg/kg in female rats [8]. The oral LD50 varies from 367 to 2000 mg/kg in female rats, and from 82 to 779 mg/kg in mice, depending on the ratio of cis/trans- isomers present [2]. This wide variation in toxicity may reflect different mixtures of isomers in the materials tested. The dermal LD50 in rats is 1600 mg/kg and in rabbits is greater than 2000 mg/kg [2,8]. Chronic toxicity: Not Available Reproductive effects: No adverse effects on reproduction were observed in a three- generation study with rats given doses of 37.5 mg/kg/day, the highest dose tested [8]. Teratogenic effects: Cypermethrin is not teratogenic [2]. No birth defects were observed in the offspring of rats given doses as high as 70 mg/kg/day nor in the offspring of rabbits given doses as high as 30 mg/kg/day [8]. Mutagenic effects: Cypermethrin is not mutagenic, but tests with very high doses on mice caused a temporary increase in the number of bone marrow cells with micronuclei. Other tests for mutagenic effects in human, bacterial, and hamster cell cultures and in live mice have been negative [2]. Carcinogenic effects: EPA has classified cypermethrin as a possible human carcinogen because available information is inconclusive. It caused benign lung tumors in female mice at the highest dose tested (229 mg/kg/day); however, no tumors occurred in rats given high doses of up to 75 mg/kg/day [8]. Organ toxicity: Pyrethroids like cypermethrin may cause adverse effects on the central nervous system. Rats fed high doses (37.5 mg/kg) of the cis-isomer of cypermethrin for five weeks exhibited severe motor incoordination, while 20 to 30% of rats fed 85 mg/kg died 4 to 17 days after treatment began [2]. Long-term feeding studies have shown increased liver and kidney weights and adverse changes in liver tissues in test animals [8]. Pathological changes in the cortex of the thymus, liver, adrenal glands, lungs, and skin were observed in rabbits repeatedly fed high doses of cypermethrin [23]. Fate in humans and animals: In humans, urinary excretion of cypermethrin metabolites was complete 48 hours after the last of five doses of 1.5 mg/kg/day [2]. Studies in rats have shown that cypermethrin is rapidly metabolized by hydroxylation and cleavage, with over 99% being eliminated within hours. The remaining 1% becomes stored in body fat. This portion is eliminated slowly, with a half-life of 18 days for the cis-isomer . AS TO METHIDATHION - THERE SHOULD BE NO RESIDUE OVER 0.000000 AND NO EXEMPTIONS FOR THIS TOXIC PRODUCT. EFFECTS ARE Methidathion is a highly toxic compound that carries the signal word DANGER on its label. The acute oral LD50 for the compound ranges from 25 mg/kg in the mouse to 225 mg/kg in the chukar partridge. The oral LD50 for the compound to rats is between 25 mg/kg and 54 mg/kg (1). The compound is poisonous to humans, because of its capacity to interfere with enzymes related to breathing and other nervous system activities. Symptoms of acute methidathion poisoning may include nausea, vomiting, cramps, diarrhea, salivation, headache, dizziness, muscle twitching, difficulty breathing, blurred vision, and tightness in the chest (2). Acute exposure may cause intense breathing problems including paralysis of the respiratory muscles. The symptoms of acute methidathion poisoning are similar to acute exposure to parathion. The compound is also very highly toxic through exposure on the skin. The dermal LD50 in rabbits is about 200 mg/kg. The dermal LD50 is much higher (less toxic) to rats (1,546 mg/kg) (2). Methidathion is also highly toxic through inhalation (3) (based on studies with a product containing 40 percent methidathion). The technical product, a solid, has not been evaluated for inhalation toxicity. Methidathion is only a mild skin irritant and is non-irritating to the eyes (for rabbits). CHRONIC TOXICITY Beagle dogs fed small doses of the compound for two years experienced no compound related effects at or below the dose of 0.10 mg/kg/day. At doses above this amount (0.4 mg/kg/day and above) the dogs experienced enzymatic changes, and liver alterations. Inhibition of red blood cell cholinesterase, an enzyme, was observed only at the highest dose tested (1.6 mg/ kg/day) (3). Rats also have a low tolerance for the compound; the methidathion lifetime NOEL is 0.20 mg/kg/day. Compound related effects were first noted in the rats at doses of 2 mg/kg and above and included cholinesterase inhibition in the blood, brain and some nerve related effects (3). At the highest dose of 5 mg/kg, the rats ate more food but had less body weight gain. They also developed skin lesions and foam in their lungs. Rhesus monkeys fed small amounts of the compound developed changes in blood cholinesterase activity at doses of 1 mg/kg/day and above. Humans ingesting very small amounts of the compound (0.11 mg/kg/day) for six weeks, had no noticeable clinical effects (2). A study of exposure levels of mixer/loaders of methidathion (Supracide applications) in California showed that the greatest exposure potential to the compound was through the skin (dermal). The workers' clothing contained the greatest concentrations of the compound. Total amounts of the compound inhaled were between 13 ug/l and 21 ug/l per day of application activity. No estimates for total exposure were given owing to the difficulty in determining the amount of the compound being absorbed into the body through the skin (4). Reproductive Effects Moderate to low amounts of methidathion caused a number of adverse reproduction related effects. Male and female rats were fed low to moderate amounts of methidathion over two successive litters. The parents experienced tremors and decreased food consumption at 1.25 mg/kg. The low dose of 0.25 mg/kg disrupted mating behavior and also affected nursing offspring. At the highest dose tested (2.5 mg/kg), stillbirths and decreased pup survival was observed (3). Teratogenic Effects Small to moderate amounts of methidathion administered to pregnant rats and rabbits produced no birth defects in the offspring. The pregnant females experienced several compound related effects, most of which were typical of cholinesterase inhibition (3). The compound is unlikely to pose a significant developmental risk to humans exposed to small amounts. Mutagenic Effects Methidathion did not induce any genetic changes in a number of tests for gene mutation, chromosomal aberrations and DNA damage. The various gene mutation studies were conducted on hamster bone marrow cells, in mammalian cells, and on several species of bacteria (3). There is no evidence that the compound poses a genetic threat to organisms. Carcinogenic Effects Methidathion caused malignant and benign liver tumors in male mice. The tumors (adenomas) appeared in the mice fed 2.5 mg/kg/day for two years. Additional signs of cancer (carcinomas) were found in the male mice fed higher doses of the compound (5 mg/kg/day) for two years. This higher feeding level also produced numerous other signs of toxicity (3). The EPA has classified the compound as a possible human carcinogen. The committee stated that this one study constitutes only limited evidence of carcinogenicity because it induced common tumors in only one sex of one species and that the mutagenic tests were not supportive of a higher classification (3). Organ Toxicity In addition to the changes in relation to its carcinogenicity the compound can also affect liver weight, induce other liver changes, affect the gall bladder, and decrease ovary weights at moderate doses (3). Fate in Animals and Humans Methidathion is rapidly absorbed, broken down and eliminated in animals (2). The breakdown products of the parent compound are not of toxicological concern (3). Only very small amounts of various metabolic products of methidathion have been detected in milk from cows (8) and in chicken eggs (3). Following exposure to the compound, the majority of it is lost as a breakdown product through the lungs as carbon dioxide indicating complete metabolism (3, 8). Between 30 and 50 percent of the ingested amount is eliminated (as breakdown products) in urine. Half of the initial amount of the compound is removed from mammals within six hours. The compound does not significantly accumulate in rat tissue. ECOLOGICAL EFFECTS Methidathion is highly toxic to birds following acute exposure. The LD50 for the compound ranges from 23 mg/kg to 33 mg/kg in mallards, 8.41 in Canadian geese, 33.2 mg/kg in the ring-necked pheasant and 225 mg/kg in the chukar partridge (3, 8). When the mallards were fed methidathion in their diets, the compound was moderately toxic. The compound is highly acutely toxic to all aquatic organisms (vertebrates and invertebrates) and thus can pose substantial risk to these populations if the compound gets into surface water through actions like pesticide drift, in surface water run-off or by entry into the sewer system. Methidathion is potentially hazardous to freshwater and saltwater species because it is highly toxic to both. In addition, tests on lobsters indicated that the combination of methidathion and another organophosphate insecticide, phosphamidon, was more toxic than either compound separately or than would be expected if the toxicities were added together (2). The LC50 of the compound is 0.01 mg/l (rainbow trout) and 0.002 mg/l (bluegill sunfish). Methidathion is highly toxic to honey bees and products containing the compound require cautionary labeling to that effect (2, 3). honey bees are vanishing from the united states. certainly any product that kills honey bees needs to be taken OFF THE MARKET. this is an organaphosphate which also harms. tebuthiuron - no residue should be over 0.000000 and no exemptions should exist for this product which should be phased off the market. effects are ACUTE TOXICITY Skin, eye or clothing contact with the herbicide should be avoided (8). It is classified as a moderately poisonous herbicide. Symptoms of tebuthiuron poisoning in rodents include lack of energy, loss of appetite, muscular incoordination and death. Vomiting occurred in cats and dogs (2, 11). Tebuthiuron has high acute oral toxicity in experimental animals. The amount of the herbicide that causes death to one-half (50%) of test animals to which it is given is referred to as its lethal dose fifty, or LD50. The oral LD50 for tebuthiuron is 644 mg/kg in rats, 57.9 mg/kg in mice, and 286 mg/kg in rabbits. The dermal LD50 for tebuthiuron in rabbits is greater than 5,000 mg/kg. Neither skin irritation nor general overall intoxication were produced in rabbits that had 200 mg/kg of the material applied to their skin (2, 3, 8). 67 mg of the herbicide in the eye of rabbits produced short-term conjunctivitis, inflammation of the lining of the eye, but no irritation to other eye parts, the cornea and iris (8). The inhalation by animals of 3.7 g/m3 technical tebuthiuron for 4 hours did not cause death or toxicity. Tebuthiuron did not induce allergic reactions when tested on the skin of guinea pigs. CHRONIC TOXICITY Decreases in body weight gain and red blood cell counts, along with minor effects on the pancreas were seen in rats fed 125 mg/k/g/day for three months (2). Exposure of rats to dietary doses of tebuthiuron as high as 80 mg/kg for 2 years was well tolerated with no indication of cumulative toxicity or serious effects. Similarly, no toxic effects were observed in mice exposed to doses as high as 200 mg/kg for most of their lifetime, or in dogs given doses of 25 mg/kg for one year (8). The EPA has established a Lifetime Health Advisory (LHA) level of 500 micrograms per liter (ug/l) for tebuthiuron in drinking water. This means that EPA believes that water containing tebuthiuron at or below this level is acceptable for drinking every day over the course of one's lifetime, and does not pose any health concerns. However, consumption of tebuthiuron at high levels well above the LHA level over a long period of time has been shown to cause excessive weight loss and damage to the pancreas in animals studies (14). thiabendazole - no exemptions should be given for this product and no residue should be over 0.00000. this product should not be sold or manufactured. effects are Thiabendazole is classified as a slightly toxic pesticide and carries the signal word CAUTION on the label. Effects of acute overexposure to the fungicide include dizziness, anorexia, nausea, and vomiting. Other symptoms such as itching, rash, chills, and headache occur less frequently. The symptoms are brief and are related to the dose level (8). The rat oral LD50 is 3,100-3,600 mg/kg, mouse oral LD50 1,395-3,810 mg/kg and the rabbit oral LD50 is greater than 3,850 mg/kg. The lethal dose in sheep is 1,200 mg/kg. Thiabendazole is not a skin irritant or a sensitizer. CHRONIC TOXICITY Rats force-fed 200 mg/kg/day or less showed little or no growth effects. At higher levels (400 mg/kg) there was growth suppression. Death occurred in a few days at 1,200 mg/kg and 30% mortality occurred within 30 days at 800 mg/kg. A decrease of active bone marrow at high doses was also noted (3). At doses somewhat below the LD50, mice had liver, spleen, and intestinal effects. In dogs, high daily doses (200 mg/kg) for two years produced few effects other than occasional attacks of vomiting and persistent anemia. Sheep experience toxic depression and anorexia at very high doses (800-1,000 mg/kg). Studies on cattle, sheep, goats, swine, horses and zoo animals have shown few chronic symptoms at low doses (8). Reproductive Effects A three-generation study in rats showed no adverse effects on reproduction at 20- 80 mg/kg. However, four times this rather low therapeutic dose produced serious pregnancy-related disorders (eclampsia) in sheep (3). Mice studied for five generations showed no effects at 10 mg/kg, decreased weanling weights at 50 mg/kg, and decreased weanling weight and size at 250 mg/kg. i consider this far too serious a risk to human and other life on this planet. thidiazuron - this should be banned totally from all products and especially from cotton. As consumers, we don't often think that cotton, the "fabric of our lives," will wind up in the food we eat or the milk we drink. In fact, only 40% of the plant -- the boll -- is used for the fiber, while the remaining 60% goes for seed oil and other byproducts. And that's how cotton enters the food chain. In the U.S. alone, half a million tons of cottonseed oil are used annually as an ingredient in processed foods, such as snack foods and salad dressings. Another three million tons of raw cottonseed are fed to beef and dairy cattle, which, depending on the state, may also consume cotton "gin trash" in their feed. When we eat these animal products, we're eating cotton. Why should we care? Cotton is the most intensively sprayed field crop in the world, accounting for more than 10% of the pesticides used worldwide and 25% of the pesticides used in the U.S. Yet despite cotton's role in the food chain, chemicals that are banned for use on food crops are used on cotton. The accepted wisdom is that most pesticides break down before harvest, or get removed during processing. But that's not always the case, as residues from pesticides, such as the toxic defoliant tribuphos (DEF), frequently appear on scans of cottonseed and other byproducts. Cottonseed oil, however, is rarely tested for pesticide residues. During a recent round of tests on milk, the U.S. Department of Agriculture did not look for DEF and other toxic cotton pesticides. Finally, cotton is increasingly genetically engineered (GE) -- 61% of the U.S. cotton crop this year. But cotton food products, like all GE foods, are not required to be labeled as such. This is of concern to all consumers who want to eat as naturally as they can. the only residue allowed should be 0.000000000. nitrapyrin -there seem to be data gaps on this product. were the following tests and follow up done? 6 months: product identity and composition, physical and chemical characteristics, avian subacute dietary and freshwater fish toxicity, acute freshwater invertebrate toxicity. - 9 months: hydrolysis, photodegradation, acute dermal and inhalation toxicity, primary eye irritation and dermal sensitization, gene mutation (Ames). - 12 months: preliminary analysis of product samples, leaching and adsorption/desorption, structural chromosomal aberration, acute toxicity to estuarine and marine organisms. - 15 months: teratology (2 species). - 18 months: animal metabolism and residues. - 24 months: plant metabolism, storage stability, analytical methods and stability of residues under storage, crop residue studies for corn, sorghum, strawberries, wheat, and cottonseed, general metabolism. - 27 months: aerobic aquatic metabolism, field dissipation (soil) and dissipation aquatic (sediment). - 39 months: rotational crops (confined), irrigated crops, reproduction (2-generation). - 50 months: chronic feeding (2 species), oncogenicity (2 species), rotational crops (field). until all tests are done, this product should not be sold or manufactured i think the risk assessment set by epa is far too low and allows far too much risk to be taking place on american citizens bodies. 481 chemicals are NOW in americans bodies - we need a brake on this full speed ahead approval of toxics by this agency. i cannot believe the negligence exhibited by this agency in regard to health in america. b. sachau 15 elm st florham park nj 07932