DOGS AND EXPOSURE TO HERBICIDE 2,4-D By Jean Cottam (Article)

DOGS AND EXPOSURE TO HERBICIDE 2,4-D
By K. Jean Cottam, PhD

“On December 8, 2003 Nova, my two-year-old puppy, was diagnosed with lymphoma,” wrote Adrienne Beattie, “which came on quickly and aggressively, causing her spleen and liver to become enlarged, the development of anemia, a loss of weight, fatigue, weakness, coughing, sore joints, growth on abdomen, intestines, lungs, and liver, as well as swollen lymph nodes. Nova became weak and died on December 30, 2003.”(1)

It seems that a pet’s risk of developing lymphoma doubles with exposure to pesticides, especially when 2,4-D is used. Sweden banned 2,4-D in 1988. Consequently Swedish dogs live longer and canine cancer rates are lower than in the past. (2)

My dog’s exposure to this herbicide had a happy ending. More than three years following the onset of rare, cutaneous lymphoma as a result of inadvertent dermal exposure to a sprayed grass in my condominium in early August 2002 Trixie is alive and well. At the time I didn’t realize that the half life of 2,4-D could be as much as ten days, otherwise, I would have continued to walk her away from the grounds of my condominium for another week or so. Two independent pathologists in Guelph diagnosed Trixie’s cutaneous lymphoma. She had a tiny tumour in her side which I discovered when running my hand against it.

Trixie’s veterinarian took many tests and determined that the lymphoma was localized. In fact my dog had no adverse symptoms apart from her tumour which was immediately removed. Had she developed the disease prior to our lawn spraying in late July, and I discovered it, as I did, in early September, by that time her lymphoma undoubtedly would have spread. So she wouldn’t have survived for more than about three months following the diagnosis, even if subjected to chemotherapy. On the other hand, it is highly unlikely that she would developed the lymphoma in August independently of our herbicide application.

In his letter of November 18, 2002 Trixie’s veterinarian states, among other things, “that the case was very unusual in a sense that primary cutaneous lymphoma is rare and direct skin contact with the herbicide could be the cause.” (3) This undermines the argument that 2,4-D is not harmful to dogs, put forward by Donald Page of the Industry Task Force II on 2,4-D Research Data. Page is notorious as the No. 1 watchdog of the industry. Trixie’s case as described in my Letter to the Ottawa Citizen dated November 14 was noticed by Page, who is in the habit of immediately reacting to any adverse comment made about 2,4-D worldwide. He contacted me by phone and subsequently faxed his written responses both to my veterinarian and myself. In his letter to the Ottawa Citizen published on November 18 he argued that there was no evidence that 2,4-D is carcinogenic. On February 5, 2003 Page wrote to Dr. Alan Meek, Dean, Ontario Veterinary College, University of Guelph, in which he condemned the findings of Dr. H.M. Hayes et al, authors of the famous US National Cancer Institute (NCI) study (1991) which determined a direct correlation between numbers of exposures and CML (Canine Malignant Lymphoma). The study claimed that dogs whose owners used 2,4-D on their lawns four times a year or more were twice as likely to develop CML as dogs whose owners did not use 2,4-D. The only study that refutes these findings, at Michigan State University’s School of Veterinary Medicine, was industry-funded and was based on the assumption that dogs are exposed to pesticides by ingesting them, whereas most cancers are in fact contracted through inhalation or dermal exposure. (4)

Back in April 30, 2002 Page had also written to Dr. Darcy Shaw, DVM, President of the Canadian Veterinary Medical Association, based in Ottawa, condemning the 1991 NCI study. A copy of his letter was addressed to Dr. Lorne H. Hepworth, DVM, President of Crop Life, a chemical industry lobby. (Hepworth is a former veterinarian who practised in rural Saskatchewan.) It is noteworthy that the letter admitted that the NCI study was government funded, i.e. independent, whereas the Michigan State University’s review of Hayes’ et al findings was apparently funded by the industry. (5)

In a 1995 report HM Hayes, RE Tarone and KP Cantor produced a detailed analysis of the data in response to critical objections by industry sponsored reviewers. Industry critics complained that there could have been “recall bias” (greater tendency to remember using pesticides) among the owners of dogs with cancer. However, Hayes et al had used separate control groups: dogs with cancers other than lymphoma and dogs without cancer. There was no significant difference between the two control groups, showing that recall bias regarding cancer in general was not an issue. This report included data showing the geographic location of cases and controls, use of pesticides other than 2,4-D, multiple pesticide use and owner application vs. application of the pesticides by a lawn care company or professional landscaper. “The authors conclude that there is no evidence of inappropriate bias in their work and that while no one epidemiological study can prove causation, ‘until additional studies are undertaken...the higher risk we found in dogs...would, at the very least, argue for prudence in the pursuit of a perfect lawn.’” (6)

The findings of Hayes et al concerning canine lymphoma were supported by a study undertaken by PM Reynold, JS Reif, HS Ramsdell and JD Tessari in 1994. To determine whether dogs absorb 2,4-D and excrete it though their urine after their owners have applied lawn herbicides, the authors tested the urine of 44 dogs which had recently been exposed to herbicides on their home lawns and 15 dogs which had not. Findings showed a clear correlation between recent application of lawn herbicides and the presence of 2,4-D in the dogs’ urine. Some dogs whose owners had not recently applied herbicides had small amounts of 2,4-D in the urine, indicating that they might have been exposed to the chemical at parks or by contact with pesticides applied to neighbours’ lawns.(7)

My veterinarian’s oncology manual refers to the Hayes et al study and its conclusions. “A case-control study found that dogs with lymphoma were exposed to 2,4-D more frequently than were control dogs. In addition, the risk of a dog developing lymphoma increased two-fold if the owner applied 2,4-D to the lawn four or more times per year.”(8) Furthermore, untreated lymphoma progresses rapidly, with 1-2 months from presentation to terminal stages. (9) Cats were found to have a higher incidence of lymphoma than do dogs or humans. Lymphoma accounts for approximately 90% of the hematopoietic tumours in dogs and cats. (10)

About 200 newspapers across Canada and the United States discussed the NCI study, which proved controversial because it conflicted with the animal feeding studies database of private laboratories.(11) However, the usual route of canine exposure to the chemicals is dermal or via the lungs and/or nasal passages. This distinction is important because the 2,4-D used in the feeding studies could be “technical acid” or “research grade”, which may well be a purer form of 2,4-D, not contaminated by variable amounts of dioxins. Also these feeding studies are unlikely to include the usual carrier (inert) products which usually prove to be more toxic than the “active” chemical and may well be co-acting with the “ active” chemical in a synergism that produces an even more toxic total effect on the organism. It is reasonable to discount all oral exposure/feeding studies, as their design is fundamentally flawed. (12)

A recent article in the Journal of the American Veterinary Medicine Association (April 15, 2004) reported that Purdue University researchers had surveyed 83 owners of Scottish terriers diagnosed with bladder cancer. “The risk ... was found to be between four and seven times more likely in exposed animals,” said Larry Glickman, professor of epidemiology and environmental medicine in Purdue’s School of Veterinary Medicine. Glickman and his colleagues earlier established that Scotties are about 20 times more likely to develop bladder cancer than other breeds. The researchers hoped to determine which of the many lawn chemicals were involved. It is noteworthy that humans and animals often share genes that can predispose them to cancer. Glickman’s team intends to survey children, as well as dogs, who have been exposed to lawn pesticides, comparing the chemicals in their urine samples with those from households with untreated lawns. (13)

In the fact sheet of the National Pesticide Telecommunication Network sponsored cooperatively by Oregon State University and the U.S. Environmental Protection Agency (EPA) it is stated that “data presented through NPTN documents are based on selected authoritative and peer-reviewed literature” which do not replace regulatory requirements. In the document statements such as “many pesticide products are beneficial” as well as citing a period of “24 hours or longer” during which pets ought to be kept off the treated area seem controversial and insufficiently restrictive. (14)

END NOTES (1)Beattie, Adrienne. “Killer in a bottle: A dog’s cancer death.” Fast Forward Weekly. June 10, 2004. (2)Ibid. (3)Dr. Robert Ostrowski, DVM, Letter, November 18, 2002. (4)Page, Donald L. Letter to the Ottawa Citizen, dated November 18, 2002; Letter to Dr. Alan Meek, Dean, Ontario Veterinary College, University of Guelph, dated February 5, 2003; Hayes HM et al. 1991. “A case-Control Study of Canine Malignant Lymphoma: Positive Association with Dog Owners’ Use of 2,4-D Herbicides,” Journal of National Cancer Institute 83:1226-1231. (5)Page, Donald L. Letter to Dr. Darcy Shaw, DVM, President, The Canadian Veterinary Medical Association, April 30, 2001. (6)Hayes HM, Tarone RE, Cantor KP. “On the Association Between Canine Malignant Lymphoma and Opportunity for Exposure to 2,4-dichlorophenoxyacetic Acid.” Environmental Research. August 1995. 70(2): 119-125. (7)Reynolds PM, Reif JS, Ramsdell HS, Tessar JD. April-May 1994. “Canine Exposure to Herbicide-Treated Lawns and Urinary Excretion of 2,4-D Acid.” Cancer Epidemiol Biomarkers Prev 3(3):233-237. (8)Ogilvie, Gregory K. DVM and Anthony S. Moore, MVSc. Managing the Veterinary Cancer Patient: A Practice Manual. Trenton, NJ: Veterinary Learning Systems Co. Inc., 1995. Reprinted 1996, pp. 229-230. (9)Ibid., p. 230. (10)Ibid., p. 249. (11)2,4-D and Cancer in Dogs. Industry Task Force II on 2,4-D Research Data web site: www.24d.org/dogs.html. (12)Peggy Land to Jean Cottam, e-mail of November 18, 2002; Cox, Caroline. “Insecticide Fact Sheet: Imidacloprid.” Journal of Pesticide Reform. Spring 2003. 21(1): 16; Pesticide Information Profile: 2,4-D. Dioxin Contamination. Web site: pmep.cce.cornell.edu/profiles/extoxnet/24d–captan/24d-ext.html. (13)Journal of the American Veterinary Medicine Association, April 15, 2004. (14)Pets and Pesticide Use, NPTN, January 1998.

K. Jean Cottam

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