2,4,5-T: Where is “proof of safety?”

Press, 27 October 1977, Page 21

2,4,5-T: Where is “proof of safety?”

The arguments over 2,4,5-T, and whether its use as a herbicidal spray causes birth defects in babies, have been a matter of grave public concern. OLIVER RIDDELL looks at the work the Health Department has been doing to reduce public alarm.

The accumulated data on 2,4,5-T and its “dioxin” contaminant are sufficient to give a very high assurance of safety in the normal use of this material. This belief is in accord with the concensus of world-wide scientific opinion. It is also the conclusion reached in a Health Department report into 2,4, 5-T and human birth defects. The report concludes that there is no evidence to implicate 2,4,5-T as a factor in human birth defects. The trouble is that, although this statement is scientifically correct, it is commonly misunderstood by the public and some scientists. The demand is usually for “proof of safety” — and a statement that there is no evidence for harm is unsatisfactory to many. According to the report, it must be faced that there is no way in which any substance, including common foodstuffs, can be proved absolutely safe. To achieve such a standard of proof would entail testing everv person with every substance at every conceivable exposure level in every imaginable circum* stance. Otherwise, there is always the possibility of

an individual somewhere who will react adversely under certain conditions. The best that can be achieved for any substance, the report says, is a high degree of “assurance” of safety based upon a rational and ex-

perienced scientific judgment of the available evidence. One of the scientists involved in the report was the department’s senior toxicologist, Michael Bates. Subsequently, he went on to report of 2,4, 5-T birth defects in some detail.

Recent publicity has implied that the herbicide is responsible for several clusters of related birth defects which have occurred in the North Island in recent years. Those include anencephaly (a defect in the development of the brain) and spina bifida (a variety of defects which often include an opening in the back through which the spinal cord may protrude). The herbicide 2,4,5-T is used mainly to control gorse and blackberry, and is the most widely used herbicide in New Zealand. It is one of a group of herbicides sometimes known as the “hormone” weed killers. It has been used since

1944 but it was not until about 1970 that it was found to cause an increase in the rate of abnormal offspring in rodents. Responsibility for these abnormalities was traced to a contaminant of 2,4,5-T — “dioxin” — present in the samples given to rodents at a concentration of about 30 ppm (parts per million). Since the original experimental production of birth defects, 2,4,5-T and dioxin have been investigated thoroughly to determine their effects on human health and the environment, Mr Bates says. A legal maximum limit of 0.1 PPM has been established for the dioxin content, and this is checked by periodic sample analysis by the D.S.I.R. It has been found that the dioxin content of the 2,4,5-T now used in New Zealand is usually not more than O.OSPPM and sometimes as low as 0.01 PPM. Also, the 2,4,5-T which is sprayed has been

diluted another 250-1000 times by the adding of water.

Mr Bates says there is no doubt that dioxin is an extremely toxic chemical, but that there is no more than one part of dioxin per 10M parts of 2,4,5-T. Depending on the species of animal tested, dioxin is between 5000 and 500,000 times more toxic than 2,4,5-T itself. For a person to consume a fatal dose of dioxin, he would have to take between 20 and 200 lethal doses of 2,4,5-T at one time. The herbicide itself is considered only mildly toxic.

The main area of concern is not so much toxicity in the ordinary sense but the fear that 2,4,5-T, specially its dioxin content, may cause birth defects.

All chemicals are capable of causing toxic effects in the developing embryo if they do not cause the death of the mother first. So the chem-

icals which are of most concern are those which are poisonous to the embryo at doses which have no’ effect on the mother. Thalidomide is a wellknown example of a chemical which causes effects poisonous to the embryo. The doses which caused birth defects were well below those which had any toxic effects on the mother. On the other hand, doses of dioxin or 2,4,5-T below the toxic level to the mother generally have little or no effect on the developing embryo. Many other chemicals, including aspirin or vitamin A, may cause malformations. Aspirin, for example, has caused, among other malformations, defects of the heart in monkeys which (from a reproductive point of view) are similar to man. Dioxin has not been shown to cause birth defects in monkeys. People often ask Mr Bates how he can be cer-

tain that humans are not far more sensitive to 2,4,5T than thalidomide. He cannot be absolutely certain, but this same uncertainty applies to every other chemical and foodstuff with which humans can come into contact. There is very little difference between the toxic level of dioxin for the mother and that for the embryo. If dioxin was causing human birth defects at least some women could be expected to suffer from the disfiguring chloracne, a characteristic acne-like reaction considered to be the initial sign of dioxin poisoning in humans. Chloracne has never been known to be caused by 2,4,5-T as it is used in New Zealand. A recent television programme implied that it was likely that 2,4,5-T was responsible for apparent clusters of birth defects in Whangarei, the Waikato and Opunake (Taranaki). The Health Department in-

vestigated these allegations. The actual frequency of birth defects has been associated with many causes — season, place, sex, ethnic group, social class, maternal age and the number of previous children. In spite of these associations, and numerous investigations, no causative environmental factor has ever been determined. It has been established, by analysing the incidence within the families, that inherited factors are involved. The current belief is that the inherited predisposition inter-acts with some probably relatively minor environmental factor which acts as a trigger. Mr Bates says it is important to note that for a birth defect to occur, any environmental factor which is responsible must exert its effect during the first four weeks of pregnancy. Four birth defects appeared in and near Opunake in south-west Taranaki in 1974-75. What attracted attention was that three of these infants were born to mothers living in the one (albeit long) road, while the remaining mother lived nearby.

The first 22 weeks of one pregnancy were spent in Hamilton in 1973, so it was excluded from the investigations. Of the remaining three, the father of one and the mother of another were brother and sister, strongly suggesting an inherited effect. So it seems probable that the clustering was accidental. This view was supported by statistical analysis which showed that in the three years in which the births occurred it would be expected that, by chance alone, 12 similar clusters of birth defects would occur in similarly sized population groups throughout New Zealand, said Mr Bates. From a statistical point of view the Northland incidence was no different from what might be expected to occur by chance, and the timing of the Waikato incidence was inconsistent with the suggestion that 2,4,5-T was the cause. Mr Bates maintains that no woman involved in the study was exposed to 2,4,5-T to any significant extent. The accumulated evidence shows a high order of safety for the 2,4,5-T used in New Zealand.