Science and Uncertainty

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The Difficulties of Predicting the Effect of Exposure to Chemicals

John K. Pollak
Toxic Chemical Committee, Total Environment Centre, 88 Cumberland St, Sydney, NSW, 2000

Before discussing some of the difficulties of predicting the effects of chemicals on the environment and on public health, it must be pointed out that Homo sapiens is fundamentally a risk-taking animal and therefore the precautionary principle is mostly ignored. In addition the profit motive (either for personal gain or because of loyalty to shareholders) usually outweighs more responsible and precautionary attitudes. There are many examples of these attitudes within the manufacturing, chemical and also the pharmaceutical industry which illustrate this behaviour pattern (Pollak, 1993) One of the most blatant examples was the long phasing out period of the drug Enterovioform which continued to be produced for 50 years after it had been demonstrated that it caused undesirable health effects (Hanson, 1989) Hence the precautionary principle has to be supported by stringent legislation.

The current practice of testing the toxicity of chemicals, still depends mainly on the determination of the effects of individual chemicals. The acute and chronic toxic effects of individual chemicals are evaluated, using experimental animals. For the great majority of chemicals no tests for the interaction of chemicals and/or synergistic effects are carried out. For example, the latest Australian regulations for agricultural chemicals require only tests for the active principle (when only one active principle is present), even when a formulation contains a complex mixture of chemicals. On the other hand in the "real world", plants, animals and humans are exposed to the simultaneous or sequential presence of many chemicals.

The precautionary principle is quite openly ignored by pesticide registrars. The requirements for the clearance of agriculture and veterinary products in Australia demand that "Where two active constituents are formulated together, toxicity studies should be performed with the formulated product to investigate the possibility of synergism or potentiation...." (Anon. 1989), but pesticide registrars in N.S.W. and W.A. provide literature which recommends that different pesticide formulations can be mixed prior to application. Such mixtures therefore contain more than one active principle, many of these are known to be either 'probable' or 'possible' human carcinogens.

Other regulatory authorities also do not apply the precautionary principle, even when scientific information is available that synergistic interaction increases the toxicity of a particular mixture of chemicals. At a recent Workshop on the Health Risk Assessment and Management of Contaminated Land, sponsored by the Commonwealth Department of Health and the Commonwealth EPA, I was informed that synergistic actions of mixtures of chemicals cannot be considered, because this would be too difficult. Hence for the remediation of sites contaminated with complex mixtures of chemicals, the maximum residue level for any one chemical is determined as if it were the only chemical on the contaminated site, completely ignoring the synergistic interactions of the chemical mixture. This attitude is adopted in spite of the fact that such synergistic interactions have been studied and taken note of, in the U.S.A. by the EPA and other organisations (Simmons & Berman, 1989; Yang et al., 1989).

Furthermore, even when the detrimental effects of a chemical or a chemical mixture to public health and/or the environment are to be evaluated, the correct questions are often not asked. The investigations are usually concerned in trying to establish how toxic a given chemical is at a given concentration. But the more important question is really: "Can the deleterious effects of a particular chemical or chemical mixture on the environment or public health be evaluated with the knowledge that exists at the time?" Often the answer to this question is: "No". A classical example of this conundrum is DDT. Any testing procedure or evaluation of the toxicity of DDT, when it was first produced, would not have been able to predict the problems which biomagnification of DDT would cause to organisms on top of the food chain, because the concept of bioaccumulation and biomagnification did not exist at that time. The synergistic effects of DDT were also only discovered during its period of use, such as the synergistic effects of tumour promotion by DDT and TPA (12 teradeconoylphorboll-acetate) (Trosko, 1987).

At times medical practitioners observe in their patients symptoms and trends which suggest to them a correlation between the ill-health of a group of people in one location and/or the application or use of a particular chemical (Budd, 1993; McIntosh, 1993). When as a result of these observations, Health Authorities carry out an epidemiological study for a particular chemical (study factor) and for a particular disease (outcome factor) (e.g. cancer or birth defects), this is often negative, and therefore the use of the chemical is continued. It is still generally not understood by a significant proportion of the medical profession and also regulators, that chemicals which generate the formation of free radicals cause cellular toxicities. A vast number of chemicals including organochlorines and hydrocarbons do generate free radicals. As a result specific outcome factors (diseases) are not necessarily produced, but a condition of ill-health is produced, which depending on the genetic constitution and/or environmental factors leads to a great number of different diseases. Hence exposure to chemicals which give rise to free radicals are not really suitable to be analysed by epidemiological methods, but patients should be examined for cellular toxicity. Such methods are available, but are not used in Australia (Pollak, 1993).

Some of the diseases resulting from the action of free radicals and the subsequent peroxidation of lipids include atherosclerosis, liver diseases, diabetes, pre-eclampsia, cataract, retinopathy and lung fibrosis (Yagi, 1987).

During the last 60 years the production of organic chemicals has increased 500 times (Anon., 1988). Since a vast number (well in excess of 10,000) of these chemicals tend to generate free radicals, which may cause membrane and DNA damage, and therefore cellular toxicity, the precautionary principle demands that a decrease of the chemical load should be foremost in the mind of regulators concerned with care for the environment and public health.

In many instances science cannot provide 'definitive proof' for the toxic effects of chemicals, therefore it is all the more important that the following quote taken from the book "Managing the environmental crisis" by Henning and Mangun (1989) be adhered to by regulators and politicians alike.

~...environmental and natural resource managers should act continuously on behalf of the environmental public interest. They more than any other public administrators, must guard against public decisions that support short-term economic gain at the cost of substantial and potentially irreversible environmental losses in the long run "

REFERENCES

Anon. (1988). Hazardous Chemicals in Common Use; Need for Worldwide Endeavour to Protect Environment from Toxic Waste. New Perspectives 18: 24-26.

Anon,. (1989). Agricultural and Veterinary Chemical Section, Department of Primary Industry and Energy, Canberra, September 1989. Requirements for Clearance of Agricultural and Veterinary Products, First Edition, 1989, p. 82.

Budd, L. (1993) Childrens's Health and Chemicals: One Paediatrician's Experience. Proceedings of a Conference: The Toxic Chemical Load, Public Health and Environmental Issues. (p. 11), Toxic Chemicals Committee of Total Environment Centre, Inc. Sydney 1993.

Henning, D.H. & Mangun, W.R. (1989), Managing the Environment Crisis. Duke University Press, Durham, (p. 2).

Hanson, O. (1989) Inside Cibaleigy. International Organisation of Consumer Unions. Penang.


Ref: Precautionary Principle Conference papers, Institute of Environmental Studies, University of New South Wales, 20-21 September 1993.

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