To the dismay of US and Vietnamese scientists, critics of the cooperative research project managed first to reduce the timeline for the proposed study from five to three years; then, they demanded that the project “be performed only as the US officials required.” And finally, they ended all funding for the research, blaming the Vietnamese government for the entire debacle and vowing never to approve a project for US scientists to perform research in Vietnam.14
In one section of his memorandum, “The Harms Allegedly Suffered by Plaintiffs,”
Judge Weinstein writes:
From April 1972 until the end of the Vietnam War in 1975, plaintiff Nguyen Van Guy served in the DRVN [Democratic Republic of Vietnam] army repairing communication lines at various southern Vietnam locations. He ingested food and water from areas that had been sprayed with herbicides. He periodically suffered from headaches, exhaustion and skin irritation while he was stationed in southern Vietnam; the skin irritation disappeared after he left Quang Ngai province in 1973 but the headaches and exhaustion continued, worsening over time. In 1983 his first wife’s pregnancy ended in stillbirth. They divorced. His spells of weakness and exhaustion worsened. His second wife, Plaintiff Vu Thi Loan, gave birth to two children, plaintiffs Nguyen Quang Trung and Nguyen Thi Thuy Nga, who were born developmentally disabled. In October 2003, Nguyen Van Guy was diagnosed with stomach cancer and liver damage and found to have fluid in the lung. It is alleged that these diseases conditions and birth defects were caused by his exposure to defendants’ [Dow, Monsanto, et al.] herbicides during the Vietnam War.15
And:
From 1964 to 1968, plaintiff Dr. Duong Quynh Hoa often traveled to the cities of Bien Hoa and Song Be, which became heavily contaminated with herbicides manufactured by the defendants. From 1968 to 1976, she resided in Tay Ninh province, where she was told several times to cover her head with plastic bags because US aircraft were spraying chemicals. In 1970, she gave birth to a son, Huynh Trug Son. He was born developmentally disabled and suffered from epileptic convulsions; he died from a convulsion at the age of eight months. She had two miscarriages, in July 1971 and January 1972. She was diagnosed with diabetes in 1985 and breast cancer, for which she underwent a mastectomy, in 1998. In 1999, a test revealed relatively high levels of dioxin in her blood. She attributes all these problems to exposure to herbicides manufactured by defendants.16
There is page after page detailing miscarriages, skin rashes, cancers, babies living only a few days, babies born with spina bifida, physically and mentally handicapped children, and high levels of dioxin in the blood of fathers and mothers who’d been exposed to Agent Orange/dioxin during and after the war.
One typical plaintiff, Ho Xuan Bat, was
active with the NLF in the Aluoi Valley and observed the spraying of herbicides on several occasions. Herbicides were stored, transferred and spilled at several military bases in the Aluoi Valley Region. In 1978, he married plaintiff Ho Thi Le and they continued to live in Aluoi Valley. They cultivated rice and vegetables for their own consumption and to sell in the local market, and consumed wild vegetables, fish and poultry. In 1980, Ho Thi Li gave birth to their first child, who died from a nose infection in 1982. In 1982, she gave birth to their second child, who died for unknown reasons after 16 days. Ho Xuan Bat’s health began to deteriorate: he experienced fatigue, headaches, coughing with blood, chest pain, loss of appetite and weight, fever, and other symptoms. In 2003, he was diagnosed with lung cancer and died from it a year later. Ho Thi Le [sic] attributes her miscarriage, the deaths of her two children and her husband’s death from lung cancer to their ingestion of food and water contaminated by herbicides by the defendants.17
The memorandum does not include reference to Dr. Wilbur McNulty’s research in 1982 at the Oregon Regional Primate Research Center in Portland, Oregon. Dr. McNulty’s research subjects were rhesus monkeys, human beings’ nearest relative (with the exception of chimpanzees) on the evolutionary scale. In the beginning, Dr. McNulty put what he thought were small quantities of dioxin in the monkeys’ food. “As fools rush in,” he confided, “the doses, in retrospect, were astronomical. They were in parts per billion instead of parts per trillion range, which is more relevant when it comes to food. I think the first level I used was twenty parts per billion in the diet, and that killed a young male rhesus monkey in twelve days…. A level of 2 parts per billion was lethal in seventy-six days. I discovered that monkeys are several times more sensitive to TCDD than mice, rats, rabbits, and dogs.”18
Dioxin turned out to be so toxic to his laboratory animals that McNulty decided to suspend all research with TCDD until the primate center could construct a special building with carefully controlled access, assigning the care of his monkeys to only one or two well-trained people in an effort to minimize the risk of contaminating other areas of the center.
“Dioxin,” said McNulty, “is the most toxic small man-made molecule we know of. It is less toxic on a per-gram basis than some biological toxins like botulin, but that’s a very large molecule. So molecule for molecule dioxin is probably the leader of the pack.”19
After consuming food containing minute amounts of TCDD, McNulty’s primates became very quiet, began losing weight, lost their appetite, grew progressively thinner and weaker, and then “just laid down and died.” Sometimes they would have episodes of retching and vomiting, but at much lower doses of dioxin a certain fraction of animals remained well for one to three or four months, and then suffered from an ailment characterized by failure of the elements of the bone marrow.
“They would have low white blood cell counts, very low platelet counts, so they suffered from hemorrhages and infections and were essentially carried away by bone marrow failure.”20
McNulty’s monkeys did not live in the jungles, mangrove forests, and rice paddies of Southeast Asia for years on end. They didn’t eat large quantities of food or drink from rivers and streams contaminated with TCDD-dioxin. They died painful deaths from the toxic effects of a poison that scientists have found to be teratogenic, fetotoxic, carcinogenic, and possibly mutagenic in laboratory animals.
Dioxin is a poison, says Harvard researcher Matthew Meselson, that works on laboratory animals by stopping cell division.
“Spermatogenesis stops, the replacement of red blood cells stops, the regeneration of the epithelial lining of the gut stops. After a few days or weeks without cell division the animals simply fall apart.”21
Weinstein writes,
It is contended that the acts of defendants adversely affecting plaintiffs constitute violations of the laws and customs of war, also known as war crimes, which prohibit: the employment of poison or poison weapons or other weapons calculated to cause superfluous injury or unnecessary suffering, the wanton destruction of cities, towns, villages or the natural environment, or devastation not justified by military necessity; the use of biological or chemical agents of warfare, whether gaseous, liquid or solid, employed because of their direct toxic effects on people, animals or plants; and the poisoning of food and water supplies in the course of war….
It is alleged that defendants’ actions have violated, and plaintiffs’ causes of action arise from, the following laws, treaties, conventions and resolutions, which constitute specific examples of the applicable law of nations or customary international law, as well as from domestic national and state laws. [See appendix 1.]