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.
:
Thank you, Mr. Chairman and committee members, for the opportunity to speak to you today.
I would like to begin my remarks with some of the impartial findings of the International Joint Commission, the IJC. Many of you know the IJC was created under the Boundary Waters Treaty and they hold the Great Lakes Water Quality Agreement as a standing reference.
The binational treaty organization is responsible for oversight of government progress in restoring and maintaining the integrity of the waters of the Great Lakes basin ecosystem. To address toxic threats, they articulated a new approach that the governments of Canada and the United States committed to when they signed the revised agreement.
The IJC's position is that given the inherent complexities and limitations of evaluating chemicals in isolation from each other, in addition to the scientific uncertainties proving causal relationships between specific chemicals and corresponding health effects, society should eliminate the production and release of chemicals that can not be safely regulated.
The IJC identified a class of chemicals, called “persistent toxic substances”, that cannot be safely regulated. These chemicals include those that cause death, disease, behavioural abnormalities, cancer, genetic mutation, physiological or reproductive malfunctions, or physical deformities in an organism or its offspring. Please note that cancer is not the only end point that the commission was discussing; there are many other end points. It's also worth remembering that cancer is an end point that can take decades to emerge, and its etiology--its cause--can be even much longer to determine.
Article II, to which Canada committed with the United States, says in part that it is the policy of the parties that
the discharge of toxic substances in toxic amounts be prohibited, and the discharge of any or all persistent toxic substances be virtually eliminated.
In fact, in this entire annex that Canada committed to signing when they signed the Great Lakes Water Quality Agreement--annex 12, on persistent toxic substances--the general principle, the intent, of the program specific to this annex is to virtually eliminate the inputs of persistent toxic substances in order to protect human health and the continued health and productivity of aquatic living resources.
The list of chemicals also includes those that bioaccumulate--that become more concentrated as they work up the food chain--and chemicals that are persistent. “Persistent” is defined as a half-life greater than eight weeks in water, soil, or living things. If a chemical falls within these classifications, the IJC says it should be eliminated. The approach does not require exhaustive causal proof of harm; rather, decisions are based on a weight of evidence. When there is reasonable documentation that certain chemicals are linked to certain effects, this evidence is sufficient to trigger preventative measures to eliminate the toxic sources. For example, since many chlorinated chemicals studied to date exhibit one or many of these characteristics, the IJC recommended, in its 1992 biennial report, that these chemicals be eliminated from the Great Lakes ecosystem.
Let's turn to government, then. Governments typically regulate chemical releases in order to reduce the occupational, environmental, and public health threats of toxic chemicals. They do this assuming that there are acceptable levels of emissions. End-of-pipe control technology is now at odds with the more sustainable green chemistry that invests in innovative, clean production technologies that eliminate the use of toxic or unnecessary chemicals in the first place.
Further, typical government standard-setting and regulatory approaches to date have been based on risk assessment that evaluates chemicals in isolation from each other to determine the relative risk they pose to environment and health. This approach has allowed the continued production and use of thousands of chemicals, despite their potentially destructive impacts. We've heard approximately 70,000 to 85,000 different chemicals are now in commercial use; most have not been screened to learn whether they cause cancer or have any other effects on the nervous system, immune system, endocrine system, or reproductive system.
Based on quantitative structure activity relationships, which is the relationship between the structure of a chemical and its pharmacological action, one could predict that one chemical will act like another class of chemicals if they look similar in structure. For example, one would predict that the polybrominated diphenyl ethers would have properties very similar to those of PCBs. In fact, they're both highly stable at high temperatures. We understand the toxicity threats posed by PCBs and take measures to stop PCB production, so when the use of QSAR principles shows the likelihood they will behave like PCBs is high, why would we have to prove PBDE toxicity?
In my submission, which is more detailed, I actually present to you the structures of PCBs and PBDEs, and you'll see that they look very much alike.
So what's the European Union doing? Let's look elsewhere for some guidance.
The proposal on the new EU regulatory framework for the registration, evaluation, and authorization of chemicals, REACH, which some of you have heard of, was adopted in 2003. And I'll quote:
REACH aims to improve the protection of human health and the environment while maintaining the competitiveness and enhancing the innovative capability of the EU chemicals industry. A preventive and precautionary approach seeks to shift the burden of proof onto the chemical manufacturers to prove that a chemical is not hazardous to human health or the environment before it is introduced to commercial use, rather than wait for massive injury before any protective action is taken.
I want to come down to some terminology.
There's a lot of research and debate about the ability of certain chemical compounds to cause endocrine disruption at critical stages of fetal and childhood development. This kind of disruption fundamentally challenges the current policy assumptions that there is a safe threshold for exposure to toxic chemicals. It also challenges the regulatory paradigm of the last quarter of a century, which has evaluated chemicals on their ability to cause cancer. I frankly think we've learned a bit more since the sixteenth century about chemicals--the dose causes the disease.
Here's the precautionary principle, as defined right within CEPA, an internationally recognized principle for action that states:
where there are threats of serious or irreversible damage, lack of full scientific certainty shall not be used as a reason for postponing cost-effective measures to prevent environmental degradation;
Let's contrast this with sound science. Wikipedia offers the following definition of “sound science”, and I quote:
Sound science is a phrase often used by corporate business and industry public relations and by government agencies to describe the scientific research that is used to justify their political claims or positions, or to vilify research threatening their interests hence safeguarding their revenue. Sound science, however, has no specific scientific definition itself, so the phrase is used subjectively.
Wikipedia offers the following definition of “junk science”, which I rather like: “Junk science is a term used to derogate purportedly scientific data, research, analyses or claims which are driven by political, financial or other questionable motives.”
And then there's the really interesting phrase “scientific certainty”. I'm a scientist and I've never, ever encountered scientific certainty. So scientists could define “scientific certainty” as “being 95% sure that cause and effect have been correctly identified.” It is exceedingly rare for a large group of scientists to be 95% certain about anything, especially about anything as complex as environmental problems. When you're talking about living systems, great scientific uncertainty is the norm.
How is scientific uncertainty currently treated in environmental protection? Well, let's look at the classic case.
The classic case is the introduction of tetraethyl lead into gasoline. When chemical and automobile corporations announced that they were starting to put highly toxic tetraethyl lead into gas in 1922, numerous public health officials thought it was a bad idea and they urged delay and careful studies. The corporations argued that there was no scientific agreement about the threat, and in the absence of convincing evidence of widespread harm, which was impossible because they hadn't even taken the action yet, they insisted that they had the right to proceed. The consequences of that decision are now a matter of record: tens of millions of Canadians and Americans suffered brain damage, their IQs permanently diminished by exposure to lead dust.
Finally, I'd like to conclude with the Canada-Ontario agreement and come back to the Great Lakes Water Quality Agreement. The Canada-Ontario Agreement Respecting the Great Lakes Basin Ecosystem, COA, is a federal-provincial agreement aimed at enhancing and protecting Great Lakes basin ecosystems. The agreement outlines how the two governments will cooperate and coordinate their efforts. The most recent COA was signed in 2002. It expires in 2007. The agreement fundamentally has been helping Canada meet some of its commitments under the Great Lakes Water Quality Agreement.
The COA has an annex called harmful pollutants. Under the goals of the harmful pollutants annex are to virtually eliminate or reduce harmful pollutants in the Great Lakes. Of the ten expected results under the annex, six are focused on reductions of prioritized chemicals.
Let me note some of the principles in the 2002 COA--and these are included in more detail in my submission--I'll just name a few: adaptive management, openness, continuous learning, progress, improvement, pollution reduction, the precautionary principle, prevention, stakeholder engagement, and sustainability.
As we examine and currently witness the government's review of the Great Lakes Water Quality Agreement that's under way right now, it will become increasingly important to examine the current science policy and the emerging concepts in ecosystem protection and the protection of human health. The CEPA review is highly relevant to this review. It could set Canada's tone for addressing chemical insults for which the Great Lakes Water Quality Agreement contains many federal commitments.
Finally, most risk assessment and risk management methodologies consider that the greater the persistence of the chemical, the greater the potential risk to the ecosystem. I'd like for CEPA to consider that some pollutants arise from substances that are in use on a continual basis, high-production chemicals, chemicals that are in personal care products, pharmaceuticals that have value to society but are constantly introduced into the environment, and of which, for all intents and purposes, the supply is continuously replenished. Therefore, even substances that don't have long half-lives in the environment should be subject to scrutiny through CEPA.
To conclude, I recommend the precautionary principle of CEPA be not only upheld but applied vigorously to protect the most sensitive use; that debates that centre around sound science be excused as immaterial; and that scientific certainty is recognized to be a myth--as no such thing exists. I'm not arguing that toxic substances can derive from natural or man-made sources, there are toxic substances that are in use that the precautionary principle of CEPA needs to look at extremely carefully.
Thank you.
:
Thank you. I'm honoured to be invited to testify before this committee.
My name is Jack Weinberg. I'm a senior policy adviser to the International POPs Elimination Network, which is a network of non-governmental organizations in 70 countries. It started around the negotiation of the Stockholm Convention and now works more generally on chemical policy.
I got a call from colleagues on Monday—I live in Chicago—to come in on this, so I will try to shed as much light as I can. Although I've not been following your debates, I did prepare some notes.
Without talking about the study per se, although we can go into what I can share on it, my heart sank when I heard Dr. Schwarcz's comments, since I thought we had gone beyond some of those debates some time back. Let me give some examples, and then maybe I can go into more detail on how they might relate.
First of all, while the precautionary principle is embraced in most of the world, there is nowhere that it's embraced as a no-risk policy. The precautionary principle balances three important components. The first is that there is substantial reason to believe there's a cause-and-effect relationship—not necessarily definite proof, because that's almost impossible, but some substantial reason. The second is that the potential for harm is large-scale and irreversible. The third is a socio-economic consideration: what are the relative social implications and cost implications, and are alternatives available, and so forth.
A policy that's based on the precautionary principle, which CEPA has been and which it needs to continue to be, is a policy that balances in a proper way those three considerations and doesn't get stampeded by efforts to create scientific doubt and the whole manufacture of scientific uncertainty, which was begun with the public relations organizations supporting the tobacco industry, where the term “sound science” was first initiated.
The whole manufacture of doubt has become a large-scale industry. We've seen it with climate change. The cause and effect relationships in toxicology are much more complicated and the issues are much more individual, and therefore the manufacture of doubt is a much more lucrative industry and much easier to pursue.
I want to give an example of the kinds of things we heard that sound good on the surface but then fall apart. We talked about PBDEs. The study said there were 0.5 micrograms per litre in the blood, and since there are five litres of blood in a human body, we're talking about 2.5 micrograms in the human body. Well, that would make sense if blood were the main place where these pollutants are stored. But we know these pollutants are lipophilic; they're primarily stored in the fat. They only appear in the blood because there is some fat in the blood. So the kind of “sound science” that takes the only thing we know, which is what was found in somebody's blood, and therefore generalizes to a full-body burden of 2.5 micrograms in the body, is not sound science at all. It is public relations.
Let me give another example. We were told—and it's correct—that there are many forms of dioxin. The four-chlorine—the tetras, with a chlorine on the four corners—are the most toxic. That's well known. It's also well known that the octas, which are the common dioxin form—not the bichlorine, but the octas—are the really not highly.... But we've all known that for many years, and no place in the world that I know of regulates dioxin by individual congeners.
Scientists and policy people have come up with a notion of “toxic equivalency factors”, taking the tetras as one and then assigning all the other congeners a fraction; then, whenever you analyze for dioxin you come up with a toxic equivalency, the TEQ. All regulation on dioxin is based on TEQ, because there's recognition.
So again that was throwing smoke. That was not based on any real debate that's going on.
Also, as to this stuff about the apples and oranges, CEPA, I presume, like other chemical policy legislation, addresses anthropogenic toxic substances. It doesn't represent all chemicals; we're all made of chemicals. It's anthropogenic.
By anthropogenic, it's either things that are synthetic, things that are man-made, or since a lot of things that are man-made also exist in nature and because there are other ways of getting toxic materials into nature other than their manufacture, there are also toxic substances that are mobilized in nature, in the environment, by human activity in unnatural quantities. So it's anthropogenic toxic substances that we are talking about, not all chemicals.
The reason this is an important matter is that we started out, as you recall, when there was a hole in the ozone layer, and there was the question of the science, tying ozone-depleting substances to the stratospheric ozone depletion. That was debated for a while. It was opposed and the science was debated, but it was finally resolved.
Then we went through a much more bitter debate about greenhouse gases in the atmosphere. Again, the actual basic mechanism is extremely simple, so the manufacture of doubt was on all the actual climate science and the mechanisms and sinks, and all that sort of thing. So we lost a good decade, and maybe we'll lose more, in dealing with an extremely difficult problem that, once we recognize it, we'll find that the things we have in place are not sufficient to deal with it. It's a very serious problem to the world.
But the question before us today, anthropogenic toxic substances, is much more complicated. The stratosphere is a rather simple mechanism. For the atmosphere, the mechanism was simple but the climate models were difficult. Now we're talking about the biosphere--that is, humans and all living things evolved in a particular chemical environment, and everything about us is chemical.
Biochemistry is the miracle under which the fetus develops. We develop into full human beings. All our bodily functions are managed by a biochemical process.
We are now introducing a large number of anthropogenic toxic substances into this biosphere, and some of the impacts are known, and some are less known, but we cannot accept any longer....
We thought this was resolved with science that originated in the Great Lakes of U.S. and Canada in the 1980s and early 1990s. LD 500, where you see how much it takes to kill a fish, is not the be-all and end-all of toxicology. That's one aspect. That's for acute poison; that's what kills.
What we learn is in regard to what has been called endocrine disruption, but I think sometimes that gets confusing. So even though this is not the normal word, I prefer to call it signal disruption, because that's a more general term.
Most biological processes are managed through receptors on cells. Chemicals, then, are attached to that receptor, and they trigger some kind of activity. That's how development occurs. That's how bodies function. So that's receptors. It's very complicated. So you have a chemical information exchange system that goes on in the human body. It's also through smelling. Some animals exchange information that's necessary through hormones, but you have very complicated chemical information exchange systems.
Signal disruption comes when chemicals that are synthetic or anthropogenic, either in their existence or in their quantities in the environment, which are different from the conditions under which these organisms evolved, are suddenly in the environment in quantities that are putting noise into a very complicated signaling system. That noise can take the form of a chemical that attaches to a receptor and triggers an action that's not supposed to be triggered. It can take the form of a chemical that attaches to a receptor and prevents it from reacting when it should react. Or in other ways it can interfere with the chemical before it reaches the reactor.
So a large number of health effects that began to be understood only in the 1980s and early 1990s, largely initiated by research in the Great Lakes, are mediated by these signal disruption mechanisms. Endocrine disruption is the mostly commonly discussed, but it's broad, and the dose equals the poison.
While it might have been adequate for the 16th century, science no longer addresses this. I think most scientists believe that for dioxin in the vicinity of zero, the dose response curve is linear to zero. I think that's been disproved, although there are many efforts to fudge it.
I think the dioxin dose response curve in the vicinity of zero.... But in large quantities of dioxin, as we saw, the prime minister to be of the Ukraine was poisoned with a large quantity of pure dioxin, and he didn't die. A lot of the signal-disrupting chemicals have very strange dose response curves. Some scientists have even been finding U-shaped dose response curves. Where it's close to zero, it's going up quite rapidly. Then not only does it taper off, but in larger doses it starts going down. This is because biological systems will respond to small doses as a signal of some kind, but when the dose gets large, that whole system shuts down, so as not to overreact the system.
We're not dealing with LD500s, and we're not dealing with how much will kill you and not much under that. We're dealing with a large number of effects that affect intelligence, learning ability, behaviour disorders, and a developing fetus. We're dealing with reproductive effects, such as the one that was mentioned from Servaso, and many other reproductive effects. We're dealing with immunological system dysfunctions that we still don't fully understand. Very likely, we're dealing with the prevalence of prostate cancer and other prostate problems in males of my age, caused by events that occurred when I was a fetus. It took all that time to develop.
These things were all discussed when I was following Great Lakes environmental issues ten years ago, and more. These are the problems that we have to address.
More was said in that presentation and in question and answer, but I'm sorry to say I'm not a trained toxicologist. I'm just a well-read layperson. I do admit to being an advocate.
I think those are very important questions, and I want to say a little, if I can conclude, about this committee.
:
I really hope that the debate over chemicals can become a good-faith debate and not a spin debate. To find one-sided sets of arguments from all kinds of places always tracing back to the same sources is discouraging.
Yes, they looked at blood, because you can't take a human body and cook out all the fat. Blood is the best. You can take a fat incision; you can do all kinds of medical procedures. That's why they looked at blood, but we know these are fat-loving content and we know the body burden exists in fat. I consider that to be just the manufacture of confusion to people who don't know this.
On the question of the dose response on dioxin, I remember that in the early 1990s there was a big conference. The industry then put out big press releases saying that this conference concluded the dose response was near zero, that it was not toxic; then, in Scientific American, all the scientific associations said those were not the conclusions, that was just a public relations spin on the conclusions.
Originally the U.S. EPA was going to reassess its dioxin based on those findings. Now it's been 15 years, and because they couldn't make that case, they haven't ever concluded that reassessment and have reached no conclusions, because either you'll reach the right conclusion or there's enough money and enough influence to keep you from reaching any conclusion.
Hormesis, though, is different. There's a dioxin curve. I only said “linear” in the vicinity of zero. The dioxin curve is not linear. In very small quantities it has profound impacts, but as those quantities go up--that's what Seveso and other things say, and this poisoning in Ukraine--when populations, whether people or animals, are exposed to small amounts, it disrupts a lot of the basic biochemistry, and particularly affects development.
We have studies on PCBs in the Great Lakes of children whose mothers ate Great Lakes fish. These are old studies now. Their children had substantial learning deficits relative to mothers who didn't eat Great Lakes fish. We knew this a long time ago, but the scientists who found that in studies eventually were intimidated, and all kinds of other things happened.
I think the discussion should be a discussion in good faith, in that we are really trying to not just look for all of the partial scientific factoids that support one particular case.
Chemical regulation is a complicated matter. I think it's very fortunate that CEPA is reviewed every five years; that allows a possibility of updating maybe every eight or nine or ten years. New things are found out. I think that CEPA is finally--and in your last review--starting to take up these chemicals for which there are very little data. I forget the name of the list, but you have a list of 23,000 chemicals that were originally grandfathered in, and you've now characterized them. I think that's a very important step. The question now is what's going to come next.
We think the European Union is moving in a good direction. They're actually starting to require the development of data on all these chemicals in more detail. Then they can move into regulatory decisions on them. If I understand, I believe your inherent toxicity criteria are still based on how many fish will die--the lethal dose 50--and do not take into account many of the other toxicological approaches.
Chemicals policy in a world where the environment of life is full of anthropogenic substances that are different from the chemical composition of life when things evolved is a very important responsibility on all of you. I believe that you need very sensitive legislation that goes for increased data and applies the precautionary principle--that is, a no-risk principle--but that also includes another principle that's different from the precautionary principle and that is also discussed and included in law in some places, a principle called the substitution principle. That is, if you have a substance, and it has hazardous properties that are well known but there are alternatives that do not have those hazardous properties or have less hazardous properties, if the economics and the utility are sufficiently compelling, there is sufficient reason to require substitution. You don't need to ban a chemical.
The final thing is, it's not the case that all chemicals can be safely managed. There are some chemicals that, if you produce them and they use them, end in the environment, particularly if they go into products, and so forth.
I very much hope you take a very close look at CEPA and continue to update it as the global debate on chemicals policy moves forward.
:
There's always a “but” in science. No matter what you look at, there always will be a “but”.
Science doesn't progress by giant leaps. It progresses by a series of very small steps. Of course, we're always trying to correct past errors. We hope that if we substitute a substance, it will be safer than the one before it. Obviously that's what the intent is, but it's not always easy to know that. You can't predict. And truly one of the main points I try to make is that one should never suggest that they have knowledge that actually doesn't exist. There's just way too much that we don't know about what the consequences are of regulating and substituting.
I'll give you an analogy, perhaps. Right now we're talking about PFOAs. It's been in the paper for the last couple of days because of the ban on certain perfluorinated compounds, especially the telomers that are used as stain removers. I think that this is a good thing. I think that we do have accumulating evidence of problems there, but there are going to be consequences. We use these products in order to resist stain. If that's not going to work, people will have more stains. They will go to the dry cleaner more often. Then we worry about the tricholoethylene that is used by dry cleaners. That's a very legitimate worry. Tricholoethylene is one of these persistent chemicals that I think we need to do something about.
Then we talk about replacing that maybe with liquid carbon dioxide. The manufacturing of liquid carbon dioxide is not a totally benign procedure either. There are other ways to make stain-resistant compounds. There are some very new technologies, including carbon nanotubes that you've probably heard about. This is all based on the buckyball technology, which is really quite fascinating, because it's essentially a discovery of a new form of carbon. Everyone knows about graphite and diamond as a form of carbon. Well, we have another form--these so-called buckyballs, after Buckminster Fuller, who was the architect who designed geodesic domes. These substances can be incorporated into fabrics in order to ward off stains.
We've already seen a demonstration in Chicago in which the demonstrators dropped their pants that they had purchased at Eddie Bauer, because Eddie Bauer was, according to them, using Teflon to keep off the stains. They weren't even using Teflon. What they were using was the buckyball technology, so they even got that part of it wrong. But in the next demonstration they had, they at least corrected that and they were demonstrating against the use of these nanoparticles in stain-resistant materials. Why? Because the suggestion is that we don't know what is going to happen if we expose the public to these nanotubes. The public, of course, has been sensitized to this because they read Michael Crichton's book, Prey, which suggests that these nanoparticles can somehow multiply or self-assemble and turn the world into toxic goo, as he calls it.
So there is always a “but”. Yes, we try to replace things with the new, and it doesn't always work better. We have to make some educated guesses on these things. We have to look at each class of chemicals very specifically. We have to look at the molecular structures. We have to look at the amounts. I think that there are thresholds, but obviously not everyone agrees with that.
Let me just address the first comment you made because of an interesting statement the interpreter made. You asked...when looking at my biography and the things that I do, because I give a lecture on the chemistry of love, and the interpreter said, “I thought I heard 'love', but it couldn't be that.” Well, it could, because I do do that.
The idea is that the world, of course, functions on chemicals, both natural and synthetic, and I try to emphasize that and explain it, including the fact that there are certain substances that are responsible for our falling in love. One that has been looked at is a chemical called phenylethylamine, which has been found in chocolates.
The press has made a big deal about that--chocolates being the classic gift of lovers on Valentine's Day--because you're saying, here, have some phenylethylamine and fall in love, hopefully, with the donor. It's a charming story but it's really chemical nonsense, because the phenylethylamine never goes through the blood-brain barrier, never goes to the brain. As we know, chocolates go directly to the hips without getting into the brain.
Those kinds of chemical subtleties are important, which addresses your next question about the mixture of chemicals. I don't have any answer to that and I don't think anyone has any answer to that because it's such an unbelievably complex mixture.
We can't possibly measure all the interactions. There certainly are some interactions that we know. We know, for example, that if you have iron and vitamin C together in your diet, the vitamin C enhances the absorption of iron. I mean, these kinds of things have been done. We know, for example, that if you take certain medications, you can't take them with grapefruit juice because it changes the blood chemistry, changes the level.
But these are unique interactions that have been measured. It just isn't possible to globally measure every possible interaction. What we do is we take a look at total exposure, doses, and the underlying chemistry, and based upon the knowledge that we have accumulated, we try to come to some sort of decision. It cannot be certain.
You also asked the question about the ozone layer. Just to give you a little bit of a history to that, the reason that the chlorofluorocarbons were introduced in the 1930s was because in those days refrigeration systems worked on ammonia or hydrogen sulphide. These are terribly toxic substances--terribly. There were all kinds of ammonia leaks. You may remember just a couple of years ago there was still some old ammonia system used in a hockey rink somewhere in Alberta and the ammonia leaked out and a number of people were very severely hurt.
There was a need to find a new chemical to replace the ammonia. The chlorofluorocarbons were great because they were chemically very unreactive. You could put them into a refrigerator and compress them, and when they expanded, they sucked the heat out of the fridge. Everyone thought that this was great.
Nobody at that time could ever have imagined that these chemicals could eventually have an impact on the ozone layer in the stratosphere. And how could they? Why would anyone have ever thought of that? There wasn't any knowledge about ozone destruction. It just wouldn't have come up. You had a problem that you wanted to solve, which was the problem of refrigeration. It was a tremendous breakthrough. It saved thousands of lives by introducing the freons instead of ammonia.
Then eventually we found that there was a problem with the ozone layer. Now we address that problem because we find that not all freons fall into the same category. It depends on exactly how many chlorines, how many fluorines we have in the molecule, and exactly how they are arranged.
Well, now we have freons that don't have an impact on the ozone layer. Will they have an impact on something else that we find out 30 years from now? Nobody really knows, but we have a pretty good base on which to make judgments, because since the 1930s we've accumulated a lot of toxicological information and I would say that the chance is that the freons we're introducing now have a minimal chance of having any type of untoward effect. But it always comes down to making the decision.
I'm not a proponent for industry. I don't care if industry does well or not. I'm an academic--all I'm interested in is the scientific method and good science--but I don't think that industry is bent on unleashing dangerous substances into the environment, because in the end it doesn't do them good either. What does them good is producing good products that the public will appreciate and benefit from with minimal hazard. But you can't always predict that a hazard will be minimal.
It comes down to making decisions, but the decisions should be made by people who have expertise in chemistry, toxicology, and physiology.
:
I'm not an expert on CEPA or the speed at which Parliament moves, although I gather it moves pretty slowly, whether it's on a CEPA issue or something else. From what I've read about CEPA, I think it is working as well as any such thing can work.
Yes, science progresses and things get out of date; what may be true today may not be true tomorrow. I encounter this regularly because I do a lot of public talks and I teach a lot of courses; the issue of today, yesterday, and tomorrow comes up all the time. I'll give you one example.
I had a former student at one of my public lectures ask me a question. I was talking about antioxidants and dietary supplements. She said, “You know, I remember having you as a prof at McGill 25 years ago”, which already is a bit unnerving. She said to me, “You know, at that time you were saying that there's really no need to take any kind of vitamin pill, but now you're suggesting that maybe a one-a-day vitamin is good. You see, you scientists--one day you say this, and the next day you say that. How can we trust you?”
Well, I would suggest that 25 years is not exactly one day this, next day that, and if I were saying the same thing today that I said 25 years ago, then I'd be really worried, because it would mean science hasn't progressed.
Certainly the story on phthalates has progressed dramatically. The original phthalate problem came up with something called diethylhexyl phthalate. That turned out to have environmental estrogenic consequences and various toxicity issues. Then they started to look at different molecules, because these phthalates were found in baby toys; that was a real concern because babies put their toys into their mouths.
It then turned out that when you rearranged the molecules somewhat so that you got something we call diisononyl phthalate, this doesn't have the estrogenic effects the same way.
Diisononyl phthalate was not used commonly until three or four years ago, so when you're talking about 2000, that probably was not part of the equation. Yes, I think the regulations tend to have a lag time there, but I don't know if there's any answer to that, because science keeps progressing. Maybe tomorrow we'll find another phthalate that is better, or maybe we'll find there's some problem with the diisononyl phthalate.
I think, especially as far as the public is concerned, it's very tough to get these issues across. I had a lady who called me up; she was really worried about her shower curtain. Why? It was because she had read the label on it, and the label said PVC, polyvinyl chloride. She had read somewhere that polyvinyl chloride is plasticized with phthalates, which is true; this is what makes it soft and pliable.
We used to have records--remember records? We used to put them on this machine; it turned around, and then you put an arm on it and music would play. Anyway, those black things were made of PVC, but they were very hard. The shower curtain is very soft because we add a plasticizer to it.
She was worried because she had heard about plasticizers and the phthalates. I don't know if she thought these were going to jump out of the shower curtain and attack, but she had toxicity concerns. I tried to explain to her that this was not a big issue, but she was going to change to a nylon shower curtain, not recognizing that there's an environmental concern there as well, because nylon production actually releases nitrous oxide into the environment, and nitrous oxide is a pretty potent greenhouse gas.
It's tough to get this kind of information across, but it is always evolving. In the case of nylon, there are new green chemical processes being implemented now that will not release nitrous oxide into the environment, so if I were asked this question in six months, I might have an answer different from the one I'm giving you now. Science is an evolving discipline.
:
Mr. Chairman, I do have five minutes and then unfortunately I have a flight.
The CEPA process is very good in principle. I think the fundamental guts of the documents, in my opinion, are sound. The problem comes with its implementation. It's heavily based on risk assessment and risk communication, risk management, not on risk reduction, and very little evidence of the application of the precautionary principle, on which it's based. So there's a lot of risk communication, and a previous member asked again whether the public is adequately informed.
It's very frustrating to speak to some of the individuals associated with trying to implement actions under CEPA when one hears that a predominant strategy for risk reduction is risk communication. It's not actually reducing exposure. It's not actually implementing a precaution. It's just communicating to people that there are dangers associated with exposure to certain substances.
“Relative risk” is a term that's extremely confusing. One must remember what risk is voluntary and what risk is involuntary. So when we hear about relative risk, we hear, well, what's the risk of exposure to this substance in a product compared to the risk of flying or crossing the street, which are voluntary actions.
The risk of exposure to a chemical in a product is a problematic area for CEPA. Some of the substances we've been talking about today are in products. Mercury is in thermometers. Mercury is highly neuro-toxic. But under CEPA, you can't regulate the mercury in thermometers because it's a product.
Synthetic musks that are in all the stuff that you used today when you got up and took your shower, such as the soaps that have no purpose except cosmetic--some of which are endocrine disrupters, and others may be carcinogens--have no function. Yet we can't regulate them under CEPA because it's in products. So regulation of chemicals in products is something CEPA needs to grapple with.
And there are actual pollution prevention actions and initiatives that demonstrate adherence to the precautionary principle.
Those would be three major areas.
Finally, on the monitoring piece, which the previous member had asked about, monitoring does need to be improved. I know that the health ministry would probably welcome the appropriate level of investment in monitoring and toxicological studies to understand what the threats to human health are and what the trends in body burns are over time.
First of all, let me say that PCBs were originally identified for phase-out in the 1970s, and I think that it's quite amazing that in the U.S. and Canada large stockpiles still remain untreated. And part of the reason that they remain untreated is the debate over incineration and the fact that communities don't want them incinerated, for very good reasons. At the same time, when they are stored perpetually, they continue to leak to the environment many of the same pollutants that people are worried about from incinerators, such as what we called earlier the toxic equivalency of dioxin. PCBs also express the same toxic equivalency, so you can get the same effect by not incinerating them.
It turns out that quite a while ago Canadian scientists and entrepreneurs developed some very excellent technologies for destroying PCBs. The one I'm most familiar with is gas-phase chemical reduction. It was a former Environment Canada scientist who developed the GPCR technology. The company went out of business, not because it didn't work--every time it was tried it worked brilliantly, it's the one technology that NGOs all over the world really liked—but because the incinerator industry was so strong that they were always able to basically monkey-wrench any effort to move away from incineration.
So GPCR is a very good alternative. There are others. I'm less confident in some of the others. There's something that sometimes is called base-catalyzed dechlorination and sometimes is called base-catalyzed decomposition. They changed their name somewhere along the way. In some of the early applications there were problems, and I'm told that some of the more recent applications have had fewer problems. There may be some others, but those are the two.
If you have purely liquid PCBs and that's all you're dealing with, the BCD might be cheaper, although I don't know. I'm more partial to the GPCR technology, although the Canadian company that was vending it has gone out of business and we don't know if somebody is going to pick up the intellectual property and go forward.
So, yes, things like PCBs need to be addressed. Transportation is a big problem. Storage is a big problem because these are semi-volatile compounds. So if you transport it and then you move it around and you store it and then you put it into the incinerator, you can have as much toxic pollution of the environment coming from the transportation, storage, and handling as you would have come from the incinerator.
All these things have to be taken into account, but I believe incinerators are the wrong technology for this. I believe the right technology is there. But the fact that both Canada and the U.S. have sat on their PCB stockpiles, and therefore the people who develop new technologies could never make a profit out of them, not because they didn't work, but because they didn't get business, is a problem.
I don't know what it has to do with CEPA, but I think that's a very important issue and I believe there are good solutions. I believe they've just been monkey-wrenched over the years because there's a very mature industry that builds and operates incinerators, but also that operates and sells all the flue gas cleaning equipment that goes along with it. They've been very politically effective, and the start-up industries that had better ways of doing this just didn't have a chance.
Thank you.
My understanding, if my information is correct, is that Health Canada is apparently planning a national study in which about 5,000 people will be monitored for toxic substances over a two-year period starting 2007 to 2009.
When I first became aware of that I was wondering--I've got three questions, and this first one would be along these lines--is that long enough? At first blush I would think it might take a longer-term period of time to gauge the effect, but there are maybe some things I don't understand about the study. Mr. Glover might have to comment in respect to that, but I'd appreciate if Dr. Schwarcz or also Mr. Weinberg would respond on that.
Secondly, if I understood correctly what Mr. Weinberg said regarding these many “fat-loving chemicals”--and I don't know what percentage of chemicals out there are “fat-loving chemicals”-- where then does the dangerous reading come? The “total body burden” I think was the term used. It's the matter of how much there is in the fat of the body, if you will.
With that question, then, are we off the mark when we're doing testing--biomonitoring, if you will--by way of people's blood and urine, when in some of these cases it's more that the detrimental effect is picked up in terms of the fat of the human body? That's where the dangerous readings would be detected. So I have that question. I don't know if it was PBDE that was the one referenced there--possibly--but that is my second question.
And lastly is that it intrigued me a little bit--and it's nothing novel, it's been said by lots of people and it was remarked here a few times--Mr. Weinberg, when you commented about things like a “predisposition” to prostate cancer caused when you were a fetus or pre-born.
Are we really way, way too late in terms of a lot of our testing then, and should we be getting some sense earlier on? The gig is up, so to speak, if most of this effect and the predisposition is already caused by pre-birth, at the fetal time. Are we way behind the eight ball on that? And as I said, in effect the gig is up when most of the damage....
I have a son who is 12 years old and he has Asperger syndrome. This will be an interesting debate, I guess, over the years ahead. There seems to be a rapid increase of these childhood...autism and so on. Are these caused in the pre-birth period of time? Maybe we're way, way too late in terms of any of the biomonitoring and testing. Should we be doing it at the fetal stage?
Those are my three complicated questions that could take some long time in response, I'm sure.
:
I appreciate the opportunity to participate here and to witness the debate today.
I would like to bring back to the committee members what CEPA does in terms of many of the issues you have heard, because I think that is fundamentally the task before you. So I will remind you of what CEPA does and doesn't do and where we, as departments, stand on that last question with respect to biomonitoring.
As I've reported in previous meetings with you, we do think biomonitoring is a tool to measure progress, to identify trends, to help us set priorities and to interpret the results of the actions we've taken. Are these actions doing enough? Do we need to do more? It is not a silver bullet, but it's an important piece of the equation to help us measure success.
I would also like to point out that not everything can be measured through biomonitoring. Yes, the persistent bioaccumulative substances matter. There are some things that are highly reactive and that change when they get into the body; those make us sick, and there are ways to look for them. Those also matter because of their impact on human health and the illnesses they create, so we need a system that deals with all of those.
In terms of the other question with respect to measuring success, CEPA has three basic goals: pollution prevention, environmental protection, and human health protection. If you summarize CEPA, that's what it does. The key is, what are the measures for measuring success against those three criteria? As administrators of the act, I think the greater the clarity there is on how we will be measured in the future, the easier it will be to make sure we're putting the tools in place to answer that question in the future. So CEPA has three basic goals, and the question is the criteria we use to measure those, and that, obviously, is very challenging.
We have heard about precaution, we have heard about risk-based.... Just to remind members, CEPA is both. As I reported in previous appearances, it is risk-based, which is how we do our work...hazard and exposure in order to understand risk. But it also is precaution, as is inherent in the act, allowing us to act in the absence of certainty. So CEPA does have both of those elements right in the act, which you've heard debated. They are tools within the act for us to use, and we try very hard to do that. You have heard comments about our ability to implement, but I would just point out that both of those elements are there in the act today—risk-based and precaution.
The other thing is that we've heard about the burden of reverse onus, and putting the burden of proof on industry. CEPA does allow us to do that. On the new substances side, that's required; companies have to come forward and provide us that data. It starts off with that burden of proof for new substances. For existing substances, we are allowed through section 71 to demand data from industry; we can put the onus on them. Those tools are also within the act.
Finally, to sum up, we heard about REACH. I'd just like to point out that REACH has not yet passed in Europe; it is and has been subject to significant debate, and has been amended. That's not to say we should not to look at it, but Canada does have, in my opinion, a solid piece of legislation, and the categorization piece that we are going to complete by this September is world-leading. No other jurisdiction has done what we're about to complete, to go through every one of our existing substances and ask, are they persistent, bioaccumulative, and inherently toxic; what is the potential for exposure to humans; and are they hazardous to humans? We will then be able to set priorities that are far ahead of any other jurisdiction's, as we move forward, in terms of what we assess, how we assess it, what we choose to risk-manage, how we choose to risk-manage, and what burdens we want to put on industry in terms of information or action.
With the number of substances that are in use in any country, it will always be important to prioritize, whether it's the Europeans with REACH, or the Americans with their stewardship programs in the high-production, high-volume challenges. CEPA does have within it that categorization, which will help us as a country to set priorities for where we go with the next round of things. I think that's an important element, as we measure success. We are ahead of most of the world in terms of our existing substances.
Thank you.