Plastics that kill plants
Please note that this paper is now over 20 years old and the science of plastics has moved on, however this does not guarantee that the problems have totally disappeared
Plastics that kill plants - Plants grown in plastic shelters often sicken and die.
Despite a wealth of evidence, some manufactures still produce horticultural equipment made of the killer
plastic - By Richard Hardwick and Rosemary Cole
AT the Rockefeller Institute in 1949, Karl Maramorosch was studying certain viruses that are transmitted to plants by insects. To keep the insects from escaping, he grew each plant in its own transparent plastic cage, made of cellulose acetate. The plants grew badly. Their leaves developed spots, within two weeks most were dead. An American entomologist, F. W. Poos, had encountered similar problems with plant cages made of cellulose acetate. He changed to another plastic and never published his work. Maramorosch, however, persisted. Eventually he identified the cause of the damage, and in 1952 he published a paper in Science showing that vapours of a compound, di-ethyl phthalate used in the manufacture of certain grades of cellulose acetate, were toxic to plants such as clover, aster and tobacco. He also showed that di-ethyl phthalate dissolved in water was toxic to some animals. A piece of the plastic weighing three grams immersed in the water of a goldfish bowl killed a goldfish four centimetres long in 45 minutes.
In the late 1950s, a third group of American entomologists encountered the problem. This time Robert Kieckhefer and John Medler at the University of Wisconsin were using cages made of cellulose acetate. Broad beans and alfalfa grown in these cages died within two weeks. Like Maramorosch, Kieckhefer and Medler showed that the problem was due to a phthalate. They too showed that plastics containing phthalates were toxic to fish, as well as to plants, they too published their findings (in 1960). Their work too appears to have been forgotten. Phthalates continue to be manufactured, and their presence in plastics causes problems not only for laboratory scientists but also for growers and gardeners.
The problem is not confined to the US. In the late 1960s a postgraduate student, Terence Price, at Imperial College, London, was studying the mildew that attacks garden roses. He, too, decided to use transparent containers, and he, too, found that certain grades of transparent cellulose acetate were toxic to roses. A search of the literature disclosed the reports of the Americans work, and Price went on to show that his problem too was due to a phthalate, this time di-ethyl phthalate, in the cellulose acetate.
At about the same time, investigators at the National Vegetable Research Station (NVRS) were looking for plastic materials to cover early sown salad crops. They found a number of abnormalities in the leaves of lettuces that had been raised under plastic shelters. The shelters were made of certain grades of cellulose acetate. The formulation was changed and the symptoms disappeared. Nine years later we commissioned a new suite of growth cabinets. The story was repeated this time symptoms of damage to leaves appeared on brassica seedlings. Detective work showed the culprit to be plastic covered wire. The wiring was removed and replaced by wiring with a cotton-covered insulation, and the symptoms disappeared Plants showed mysterious signs of damage again in 1983, this time in glass houses, so we mounted a full-scale investigation. We now suspect that the earlier episodes at NVRS were due to vapours of a phthalate, probably di-butyl phthalate, emanating from plastic sheeting or wiring. At the time, the workers at NVRS simply reported the problem, solved it, and got on with the job in hand.
The solution depended on a way of testing the toxicity of suspect plastics. Many researches have since used the system developed at the NVRS. It is very simple, yet capable of precise results. A survey of common plastics for toxicity to plants would make good project for sixth-form science students (see simple test later).
In 1974 in Japan, Tokutaro Inden and Shoji Tachibana of Mie University published a paper on damage to growing crops caused by gases from plastic covering materials. Their paper shows that a number of plasticisers, including the molecular weight phthalates, are toxic to horticultural crops such as tomatoes, cucumbers, peppers and aubergines. They found that the less volatile di-ethyl-hexyl and di-decyl phthalates had no measurable effects. Inden and Tachibana site Japanese work going back to 1967, but they appear to have been unaware of the work that had already been reported in the West. Similarly, Inden and Tachibana's very thorough work, which was published in Japanese in 1975, seems to have been ignored in the West. But in Japan, companies such as Mitsubishi-Monsanto have for about the last 20 years banned di-butyl phthalate from any of their plastic items destined for use in horticulture - that is, from greenhouse covering material's, hose pipe and pots. They use di-ethyl-hexyl phthalate instead. Meanwhile, problems have continued to arise in the West. The next incident that we have traced happened in
West Germany in the 1970s, where the crops were damaged when grown in plastic tunnel greenhouses. The manufacturer of the plastic, BASF of Ludwigshafen, made alternative formulations and tested them. Its researchers found that some formulations caused no damage to plants, while others that contained di-butyl phthalate as the plasticiser seemed to damage the plants. Details of the horticulturally safe formulation reached at least some of their opposite numbers in Britain. But the story still goes on. Plastic items in houses or glass houses have recently damaged house plants in newly painted flats in Sweden (di-butyl phthalate is a constituent of some domestic paints) kohlrabi raised in glass houses in Germany (affected by plastic hose pipe) and tomatoes in east Lancashire (the plants were trained up strings held taut with a plastic device). Between 1981 and 1983 in Britain tomato and brassica plants in commercial glass houses were extensively damaged. The glass houses had concrete floors and unpainted frames of aluminium alloy, so at first it was not at all obvious why the plants grown in these houses sickened.
Thanks to Nick Starkey of the Agricultural Development and Advisory Service, and Jack Hannay, of the Department of Applied Biology, Imperial College, we now know that sometime in the early 1980s there was a change in the formulation of the soft plastic strip that cushions the glass against the metal frame. The original formulation contained higher phthalates the new formulation contained di-butyl phthalate. Vapours of di-butyl phthalate from the strip diffused into the atmosphere and killed plants of sensitive species growing in the glasshouse (New Scientist, 16 June 1983, p 763). In the past few months, phthalates in PVC hose pipes, cellulose acetate pollination bags and polypropylene plant pots have killed plants. The last was unexpected it seems that di-butyl phthalate is present in some horticultural products without the manufacturer knowing it.
British industry has begun to tackle the problem. In March 1985, the British Plastics Federation advised manufacturers of plastic items for horticulture, that their products should not contain di-butyl phthalate or di- iso-butyl phthalate. The British Standards Institution is currently amending the wording of BS 3746 (PVC garden hose). So far as we know, PVC glazing strip produced in Britain no longer contains di-butyl phthalate. The less volatile di-decyl phthalate, or other non phthalate plasticisers, are used instead.
These episodes all concern either houseplants or glasshouse plants, which take in the phthalate vapour through their leaves. There is at present no evidence that phthalates are involved in the damage attributed to acid rain. Concern for the environmental effects of phthalates has been expressed in some countries, such as
Denmark, where much of the domestic waste is incinerated. When this waste contains plastics, plasticisers are volatilised and discharged into the air. Hans Lokke at the Danish Technical University, Lyngby, found that concentrations of phthalates in the air were too low to have any significant effects on field-grown crops. What about animal life? The original investigation by Karl Maramorosch showed that although phthalates are only slightly soluble in water, gross contamination by phthalate containing plastic could be lethal to goldfish. Some phthalates undoubtedly get into industrial and sewage effluents and hence into watercourses, where they may enter aquatic ecosystems. We now know that phthalates, unlike some other organic pollutants, resist breakdown by bacteria, and tend to accumulate at air-water interfaces. Recent work by Robert Metcalfe and Anders Sodegren of the University of Illinois suggests that phthalates may accumulate to toxic levels in the tissues of animals that feed at such interfaces.
By this time you may well be wondering if phthalates can kill plants in glass houses and goldfish in bowls, what do they do to humans? The first point is that even for plants, these compounds are not a universal poison. Indeed, only a relatively small number of species of plant seem to be sensitive to the effects of di-butyl phthalate, and many others appear to be completely immune. The second point is, that in the air of affected greenhouses, where the plants are dying or dead, the concentrations of phthalates are by any standards remarkably small. Put one hundredth of an ounce (200 milligrams) of di-butyl phthalate in an enclosure 100 metres long by 100 metres broad by 100 metres high, and stir well. The concentration of di-butyl phthalate in the atmosphere will be 200 pictograms per litre.
This figure is typical for the concentration in the air of a glasshouse affected by the chemical. The highest concentration we have recorded in an affected glass house was 750 pictograms per litre. These figures are three orders of magnitude below the maximum permitted levels set by the Health and Safety Executive for short-term exposure of humans. It seems that so far as sensitivity to phthalate vapours is concerned, plants have something that we have not. We suspect that free radicals may be involved in the toxicity and that the selectivity may be something to do with the nature of the waxes on the surface of the leaves of particular species. But no one knows why some plants are extremely sensitive to this rather simple molecule.
We know a great deal about the effects of liquid phthalates when they get into humans by, for example, the infusion of blood that has been stored in a plastic transfusion bag, or by eating foods packaged in plastic containers. The doses required for any noticeable effects are fairly massive, of the order of 25 grams per kilogram.
Nonetheless in the USA, the industrial monitoring agency has placed a limit of 5 milligrams per cubic decimetre on di-butyl phthalate and di-ethyl hexyl phthalate.
Italy withdrew approval for di-octyl phthalate as a precautionary measure two years ago. A committee of the Ministry of Agriculture, Fisheries and Food in Britain is currently considering the question of plasticisers in food-wrapping films. Films manufactured in this country contain di-octyl adipate, but some foreign manufacturers use di-octyl phthalate. Phthalates can diffuse out of the film into the food if it is fatty in nature (for example, bacon or butter). We do not yet know how much phthalate finds its way into the British diet.
Research on the effects of phthalates in the diet on animals is interesting. Sharat Gangolli at the British Industrial Biological Research Association has shown that in rats, daily doses of 500 grams per kilogram in food cause their testicles to atrophy. Phthalates seem to cause this atrophy by interfering with the metabolism of zinc in those organs. J. M. Ward at the National Cancer Institute, Maryland, showed that 3000 parts per million of di-ethyl phthalate in the diet could make other chemicals more effective in inducing liver cancer in mice. K Shiota and H. Nishimura find that massive doses of phthalate given orally to pregnant mice cause birth defects among the offspring. Again the researchers suggest that a perturbation in the metabolism of zinc has caused the abnormalities.
Finally, researchers at the US National Toxicology Program have shown that in some strains of rats, massive doses of phthalates infused into the blood cause cancer of the liver. In all these cases phthalates may disturb the activity of the peroxisomes. Peroxisomes detoxify reactive forms of oxygen - singlet oxygen, and free radicals of oxygen. These highly active, and potentially destructive, forms of oxygen arise as a by-product of electron transport chains. Cells of animals and plants have evolved chemical defences against reactive oxygen because it can quickly destroy the cell. In animal cells, massive doses of phthalates may interfere with these defences.
When we discovered the medical literature on phthalates, we were immediately excited, phthalates were thought to act in animal systems in much the way that we had postulated they act in plants (see below).
The major difference, it seems, is one of degree. Researchers working with animals deal in doses of milligrams and grams, while we were working in pictograms. But the same mechanism may underlie the responses of rats and cauliflower's to phthalates. None of the research councils in Britain is funding research into toxicity to plants due to phthalates. Yet the world produces more than five million tonnes a year, and much of this escapes into the atmosphere phthalates have been found from the waters of the Gulf of Mexico to the air over Japan. Some of the plastic samples that have been sent to us at NVRS do injure plants but appear not to contain phthalates. Thus we suspect that phthalates may not be the only causes of phytotoxicity in glass houses. But we have not been able to pursue this suggestion. The most worrying aspect is perhaps that we can now see that botanical research was duplicated and even triplicated before the problem received widespread attention. Even with sophisticated computer searches, many of the more obscure, but nonetheless important, references reached us only in the old-fashioned way, by correspondence from scientists who had read one of our papers.
We would be glad to hear from people who have evidence for possible deleterious effects of plastics on plants.
Dr Richard Hardwick and Dr Rosemary Cole work at the National Vegetable Research Station, Wellesbourne, Warwick, UK.
How Phthalates might wreak havoc in the cells of animals and plants!
Phthalates are clear oily liquids, used as carriers of pigments and catalysts and, in quantities of up to 50% by weight, to give flexibility to items made of plastic, such as cellulose acetate or poly vinyl chloride (PVC) Rosemary Cole, Richard Hardwick and Tom Fyfield at the National Vegetable Research Station noted that phthalates are easily hydrolysed to the alcohol and phthalic acid, and that the two carboxyl (-COOH) groups on phthalic acid can chelate a divalent cation of zinc or copper, such as Zn2+ or Cu2+
They suggested that di-butyl phthalate might interfere with the active centres of certain key enzymes such as a ascorbic acid oxidase and super oxide oxidase. These enzymes both have Zn2+ or Cu2+ in their active centres, They detoxify various reactants. Without these enzymes, the reactants would accumulate, puncturing cell membranes and killing cells.
A test for plastics that kill
A simple test can evaluate the toxicity of plastics to plants. Raise seedlings of the test plant (for example cabbage seedlings one variety, Derby Day, is particularly sensitive) in pots of soil or compost, and cover with a glass jar. Suspend a piece of the suspect plastic over the seedlings. A number of control enclosures should contain plants grown under standard conditions, but with no plastics. Glassware must also be washed and dried in an oven after each experiment - vapours of phthalates can adhere to the glass sides of the enclosures and contaminate subsequent tests. If the plastic is toxic to plants, they will show the signs of damage in two to three weeks. End of article: