Thank you.
I think I was asked to come and speak to you here today because of an article I wrote in the National Post where I expressed some opinions on Environmental Defence's activities.
I direct an office at McGill called the Office for Science and Society, and our role is to educate. We don't tend to try to influence policy. We don't advocate, we educate. Let me give you a glimpse into what it is that we do and why I was asked to come here.
If you'd come with me just for a moment to the forest of South America and take a look around, you might see a monkey hanging from a tree and all of a sudden an arrow flies through the air and the animal is hit, but he jumps from one tree to the next tree and to the third tree before he collapses to the ground. He has been hit by what we call a three-tree poison. The substance was a chemical called tubocurarine. It's a substance that is isolated from a naturally occurring vine that grows on a tree. This same substance in 1942 was introduced into medicine by Dr. Harold Griffith, in Montreal actually, at the Queen Elizabeth Hospital, and it's made a tremendous impact on anesthesiology, because it reduces the force of contractions of the abdomen when a surgeon slices into it.
This makes several points: one is that the dosage is extremely important; two, that naturally occurring substances can be extremely toxic; and third, that a substance can be either used as a poison or as a drug, it all depends on how we go about it.
The same thing goes for synthetic substances. Consider an aspirin tablet. Many of us take a small dose every day to prevent heart disease, but if you swallow a whole bottle of aspirin, of course it is possibly lethal. So we ask the question whether or not aspirin is a toxic chemical, and to have an answer to that question we turn to the science of toxicology, which really is the study of the effects of chemicals on living organisms. It is a tremendously complicated area of study. The anthem of this area of study goes all the way back to Paracelsus in the 15th century, who gave us the term sola dosis facit venenum. For those of you who have forgotten your Latin, I'll translate that. It means “only the dose makes the poison”, and that indeed is the anthem of toxicology.
The main principle is that there's always a dose response curve, as you see here, in toxicology. With increasing dose, we see increasing effects. The question comes of what happens way down here at the bottom of the curve. Do the effects go to zero in a linear fashion, or is there some sort of a threshold below which we see no observable effects? I think most toxicologists would agree that there is a threshold.
We have a further nuance here, and that is a concept known as hormesis, which is getting a lot of attention in toxicological circles these days. It is that not only is there a threshold at very low levels, but in fact chemicals may behave dramatically different at low levels, and ndeed even have potentially a beneficial effect at trace levels, which of course goes on to be a detrimental effect as the dosage increases. Risk is basically a measure of toxicity and exposure. Every chemical has an inherent toxicity based on its molecular structure, and what we're interested in is the degree of exposure.
Of course, most of our concern these days is centred around the so-called synthetic chemicals. We hear of how we live in a chemically toxic soup, how we are surrounded by the 85,000 synthetic chemicals that permeate our life, which is, of course, true. That is roughly the number we are exposed to. It is also true that we do live in a chemical soup, but this chemical soup encompasses much more than the synthetic chemicals. It encompasses all of the substances in nature. If we had to have labels on an orange, for example, this is what it might look like, because there would be hundreds of different compounds naturally occurring in an orange.
There are about 20 million naturally occurring compounds that already have been investigated, and that is in contrast to the 85,000 synthetic ones that have been investigated. Indeed, the synthetic ones have been investigated far more thoroughly than the 20 million natural compounds.
If you were to look at this apple—or better yet, take a bite out of it—you might ask yourself what it is you are really sensing. You are really sensing this collage of chemicals, over 300 different compounds that have been isolated from an apple, things such as acetone, which you may recognize as nail polish remover, or furfural.
Furfural is a chemical that is known to be a carcinogen. When given to animals in a high dose, it triggers cancer, and that is the definition of a carcinogen. Not only is it found in apples, it is also found in grains and in sweet potatoes. And if you've had your cup of coffee today, you've ingested furfural along with benzene and styrene and other known carcinogens.
Obviously apples are not toxic. “An apple a day keeps the doctor away,” it has been said. Well, only if you throw it at him or her, actually, because there are no magical foods. But we don't worry about the furfural in an apple, because the dose really is so small.
We also, based upon our cooking process, expose ourselves to a large variety of potential carcinogens—benzopyrenes—in food that is cooked at a high temperature. These are known carcinogens.
Then, of course, we have all the environmental pollutants, the dioxin we hear so much about. Dioxin is spewed into our environment by various industries—not on purpose, but this so-called “most toxic man-made chemical” is a byproduct of industry. And indeed it is toxic; there is no question about it. But its toxicity depends on its structure.
Dioxin is not one compound. There are numerous compounds that fall into this category. When you have four chlorines on that molecule, it is extremely toxic, but when you only have two chlorines, it is far less toxic. So we have to pay attention to the structure of the molecule.
We also have to pay attention to the species we're investigating. The lethal dose of dioxin, based on milligrams per kilogram of body weight, depends on the species. It is indeed extremely lethal to guinea pigs, but far less lethal to hamsters. Where do humans come in? We don't know, because obviously it is not possible to do a controlled trial. It would not be ethical to do that.
We're also hearing this being described as the most potent carcinogen ever tested on animals. We don't contest that; that indeed is correct. If you take the case of a rat, you can provoke a liver tumour with a daily intake of 10 nanograms per kilogram of body weight. That's a very small number. We also know that at one nanogram there is no effect. But of course what we're really interested in is what the human exposure is, and the human exposure is about 0.002 nanograms, which is 1/500 of the no-effect dose in animals.
So numbers matter. In science we're always talking quantitatively as well as qualitatively. We also look at epidemiology, and we have a lot of this for dioxin, which was a contaminant in Agent Orange. In Operation Ranch Hand, air force personnel were exposed to fantastic amounts of Agent Orange. Numerous papers have been written on its effects, and researchers still debate whether or not there has been any consequence of dioxin to people who were essentially immersed in it.
We also had a terrible accident in 1976 in Seveso, Italy, when a herbicide manufacturer released a huge amount of dioxin. We've been following the consequences of that in the population of the area, and the only thing that has come to light is that there has been, interestingly enough, a disproportionate number of girls being born to men who were exposed.
This is something we have some indication is happening in North America as well; the area around Sarnia apparently has given rise to the same kind of problem. So there is a possible hormonal connection to dioxin, which is quite distinct from its carcinogenic potential.
Of course, what we're really interested in, and the reason I've been asked to come here, is what we do about the chemicals that are present in our blood, as Environmental Defence has found.
For example, polybrominated diphenyl ethers, which are flame retardants and certainly save lives because of that activity, are present. In the Environmental Defence study, one subject had 0.5 micrograms per litre in the blood. That is a large amount of polybrominated diphenyl ether, but let's put it into context. It means, because we have roughly 5 litres of blood, 2.5 micrograms in the body. The no-effect dose in rodents is about 2,500 micrograms. That's quite a bit larger.
So what do we really do with this number? Does it mean that it has an effect on humans? The fact is that we don't know, but we do have to keep in mind that all of these carcinogens fall into a relatively small percentage in terms of premature cancer risks. An unbalanced diet is responsible for about 35%, and all of the industrial products, depending on opinion, may be 1% to 5%, but they're in the bottom range. So where are we going to put our emphasis and where will we put our money to try to improve people's diets with a chance of reducing cancer rates very significantly?
Tobacco, infections, sexual behaviour, we can do a lot there. We can do a great deal on occupational exposure as well. So whether or not all the attention being paid to the 1% is warranted has to be regarded in light of everything else.
I'd like to leave you with a couple of points that I try to get across to our students, and to the public as well, when we talk about chemicals and potential toxicity.
There are no good or bad chemicals; there are only safe or dangerous ways to use chemicals, and in fact there are safe ways to use dangerous chemicals.
Effects depend on molecular structure. We have to be very specific. People talk about phthalates--let's ban phthalates--which are plasticizing agents used in shower curtains, for example, to make them soft and pliable. Well, they're also used in children's toys, but there are many different kinds of phthalates and they have a huge range of toxicities. It makes no sense to lump them all into the same category, the same way that it makes no sense to lump all the dioxins into one category. In all probability in toxicity there are thresholds below which there is no observable effect.
High-dose animal studies may not reflect human risk properly, because the dosage itself imparts negative effects on top of what the chemical is. I think it would be far better to take a look at what the maximum human exposure is, put in a safety factor perhaps of 100, and test that dose in animals, rather than test the maximum tolerated dose in animals.
Our bodies don't handle natural or synthetic chemicals differently. We have various protective mechanisms. We have enzyme systems that handle small doses of chemicals, and only when these are overburdened do we run into problems. Small doses are not necessarily a problem, and the presence of a chemical does not equate the presence of a risk. Indeed, if we do a proper analysis of our blood, we would find thousands of different chemicals, most of them coming from natural sources but some of those would have toxicities comparable to the synthetics.
Science can never prove that there's no risk associated with a chemical. We hear a great deal about the precautionary principle. We're asked, as scientists, to show that there is no possible risk before we unleash a chemical upon the unsuspecting public. This is a criterion that scientists can never meet. You can never prove that a negative effect is possible.
I could not prove to you that reindeer cannot fly. I suspect we would all agree that they cannot, but I couldn't prove it. I could take one reindeer up to the top of the Peace Tower and nudge it off, and if there ever was a moment that the reindeer would want to fly, that would be it. I don't think it would. We'd have a mess, but all I would have proven is that the reindeer or its confrères, on that given day, could not or did not wish to fly. You cannot prove a negative.
Risk cannot be eliminated. It has to be evaluated with respect to benefits. We talk about eliminating bisphenol A, for example, which is a potential estrogenic compound but is also used to fix our teeth. We hear a great deal that people who have poor dental care are more prone to heart disease. Well, bisphenol A is found in the composites that are used there. It is used by policemen, to shield them from bullets. It is used to make unbreakable bottles. We have to make decisions.
It is always a question of risk and benefit, and that's where judgments come in, but that's where toxicological knowledge also has to come in.
I leave you with one final thought, and that is that not taking any risk is also a risk, in and of itself. So I thank you for listening to me, and if there are any questions that come up after, obviously I would be very happy to try to answer those.