by Jonathan Latham, PhD
Piecemeal, and at long last, chemical manufacturers have begun removing the endocrine-disrupting plastic bisphenol-A (BPA) from products they sell. Sunoco no longer sells BPA for products that might be used by children under three. France has a national ban on BPA food packaging. The EU has banned BPA from baby bottles. These bans and associated product withdrawals are the result of epic scientific research and some intensive environmental campaigning. But in truth these restrictions are not victories for human health. Nor are they even losses for the chemical industry.
For one thing, the chemical industry now profits from selling premium-priced BPA-free products. These are usually made with the chemical substitute BPS, which current research suggests is even more of a health hazard than BPA. But since BPS is far less studied, it will likely take many years to build a sufficient case for a new ban.
But the true scandal of BPA is that such sagas have been repeated many times. Time and again, synthetic chemicals have been banned or withdrawn only to be replaced by others that are equally harmful, and sometimes are worse. Neonicotinoids, which the International Union for the Conservation of Nature (IUCN) credits with creating a global ecological catastrophe (1), are modern replacements for long-targeted organophosphate pesticides. Organophosphates had previously supplanted DDT and the other organochlorine pesticides from whose effects many bird species are only now recovering.
So the big and urgent question is this: if chemical bans are ineffective (or worse), what should anyone who wants to protect themselves and everyone else from flame retardants, pesticides, herbicides, endocrine disruptors, plastics and so on—but who doesn’t expect much help from their government or the polluters themselves—do?
What would an effective grassroots strategy for the protection of people and ecosystems from toxic exposures look like? Ought its overarching goal be a reduction in total population exposures and/or fewer chemical sales? Or should it aim for sweeping bans, such as of entire chemical classes? Or bans on specific usages (e.g. in all food or in all of agriculture)? Or on chemical use in particular geographic locations (e.g in/around all schools)? Or perhaps a better demand would be the dismantling (with or without replacement) of existing regulatory agencies, such as the culpable EPA? Or should chemical homicide be made a statutory crime? Or all of these together? And last, but not least, how can such goals be achieved given the finances and politics of our age?
The first task of chemical campaigning is to strip away the mythologies which currently surround the science of toxicology and the practice of chemical risk assessment. When we do this we find that chemical regulations don’t work. The chief reason, which is easy to demonstrate, is that the elementary experiments performed by toxicologists are incapable of generating predictions of safety that can usefully be applied to other species, or even to the same species when it exists in other environments or if it eats other diets. Numerous scientific experiments have shown this deficiency, and consequently that the most basic element of chemical risk assessment is scientifically invalid. For this reason, and many others too, the protection chemical risk assessments claim to offer is a pretense. As I will show, risk assessment is not a reality, it is a complex illusion.
This diagnosis may seem improbable and also depressing, but instead it reveals promising new political opportunities to end pollution and create a sustainable world. Because even in the world of chemical pollution, the truth can set you free.
The ensuing discussion, it should be noted, makes no significant effort to distinguish human health effects from effects on ecological systems. While these are often treated under separate regulatory jurisdictions, in practice, risks to people and ecosystems are difficult if not impossible to separate.
The story of the toxicological alarms surrounding BPA, which are diverse and scientifically extremely well substantiated, make an excellent starting point for this task.
Ignoring the full toxicity of BPA
According to the scientific literature, exposure to BPA in adulthood has numerous effects. It leads to stem cell and sperm cell defects (humans), prostate cancer (humans), risk of breast cancer (human and rats), blood pressure rises (humans), liver tumours and obesity (humans and mice) (Grun and Blumberg 2009; Bhan et al., 2014; Prins 2014). However, foetuses exposed to BPA suffer from a significantly different spectrum of harms. These range from altered organ development (in monkeys) to food intolerance (in humans) (Ayyanan et al., 2011; Menard 2014; vom Saal et al., 2014). Also in humans, early BPA exposures can lead to effects that are nevertheless delayed until much later in life, including psychiatric, social and behavioural abnormalities indicative of altered brain functions (Braun et al., 2011; Perera et al., 2012; Evans et al., 2014).
The above examples are just a representative handful. They are drawn from a much larger body of at least 200 publications (some have estimated a thousand publications) finding harms from BPA. The sheer quantity of results, the diversity of species tested, of consequences found, and of scientific methodologies used, represent a massive accumulation of scientific evidence that BPA is harmful (reviewed in Vandenberg et al., 2012). The evidence against BPA being safe, in short, is as close to unimpeachable as science can manage.
Nevertheless, such a large evidence base indicates that anti-BPA campaigning has been only partially successful. All the bans and the commercial withdrawals still ignore the implications of some of the most alarming scientific findings of all. For example, bans on baby bottles will not prevent foetal exposure. Nor will they prevent harms that result even from very low doses of BPA.
Ignoring the toxicity of BPS
The chemical most frequently used to make BPA-free products is called BPS. As its name implies, BPS is very similar in chemical structure to BPA (see Fig. 1). However, BPS appears to be absorbed by the human body significantly more readily than BPA and is already detectable in 81% of Americans (Liao et al., 2012).
Research into the toxicology of BPS is still at an early stage, but BPS is now looking likely to be even more toxic than BPA (Rochester and Bolden 2015). Like BPA, BPS has been found to interfere with mammalian hormonal activity. To a greater extent than BPA, BPS alters nerve cell creation in the zebrafish hypothalamus and causes behavioral hyperactivity in exposed zebrafish larvae (Molina-Molina et al., 2013; Kinch et al., 2015). These latter results were observed at the extremely low chemical concentrations of 0.0068uM. This is 1,000-fold lower than the official U.S. levels of acceptable human exposure. The dose was chosen by the researchers since it is the concentration of BPA in the river that passes their laboratory.
Chemical substitutions are business as usual
The substitution of one synthetic chemical for another, wherein the substitute later turns out to be hazardous, is not a new story. Indeed, a great many of the chemicals that environmental campaigners nowadays oppose (such as Monsanto’s best-selling herbicide Roundup) are still considered by many in their industries to be “newer” and “safer” substitutes for chemicals (such as 2,4,5-T) that are no longer widely used.
Thus, when the EU banned the herbicide atrazine, Syngenta replaced it with terbuthylazine. Terbuthylazine is chemically very similar and, according to University of California researcher Tyrone Hayes, it appears to have similar ecological and health effects.
The chemical diacetyl was forced off the market for causing “popcorn lung“. However, it has been largely replaced by dimers and trimers of the same chemical. Unfortunately, the safety of these multimers is highly dubious since it is believed that, in use, they break down into diacetyl.
The Bt pesticides produced inside GMO crops are considered (by farmers and agribusiness) to be safer substitutes for organochlorine, carbamate, and organophosphate insecticides. These chemicals replaced DDT, which was banned in agriculture following Rachel Carson’s Silent Spring. DDT was itself the replacement for lead-arsenate. Many other examples of what are sometimes called regrettable substitutions can be found.
Chemical bans (or often manufacturer withdrawals) that precede such substitutions are nevertheless normally celebrated as campaigning victories. But the chemical manufacturers know that substitution is an ordinary part of business. Because weeds and pests become resistant and patents run out, they are usually looking for substitutes irrespective of any environmental campaigning.
Manufacturers also know that, since approvals and permits initially rely primarily on data supplied by the applicant (and which is often anyway incomplete), problems with safety typically manifest only later, as independent data and practical experience accumulate. Given this current system it is almost inevitable that older (or more widely used) chemicals typically have a dubious safety record while newer ones are considered “safer”.
“Bad actors”: the rotten apple defence in toxicology
In these cycles, of substituting one toxin for another, BPA is likely to become a classic.
Environmental health non-profits become active participants in this toxic treadmill when they implicitly treat certain chemicals as rotten apples. Some even explicitly refer to particular chemicals as “bad actors“. The chemical “bad actor” framing strongly implies that the methods and institutions of chemical regulation are not at fault.
But we can ask the question, in what chemical or biological sense can BPA be termed a bad actor? Is there, for example, a specific explanation for how it slipped through the safety net?
The very short answer to this question is to recall the results noted above: BPA impairs mammalian hormonal and reproductive systems; it disrupts brain function; it impacts stem cell development; it causes obesity and probably cancer; it causes erectile dysfunction. Many hundreds of research papers attest that BPA’s harmful effects are numerous, diverse, prolonged, reproducible and found in many species. In short, they are easy to detect (e.g. vom Saal et al., 2014).
So while hundreds of scientists outside the regulatory loop have found problems, the formal chemical regulatory system has never flagged BPA, even though astonishingly, long before it was thought of as a plastic, BPA first came to the attention of science in specific searches for estrogen-mimicking (i.e. hormone-disrupting) compounds. And despite the overwhelming nature of the published evidence regulators still resist concluding that BPA is a health hazard. And so the clear answer to the “bad actor” question is that there is no special reason why BPA should have slipped through the regulatory process; instead, the case of BPA strongly implies not a series of bad actors but instead a dysfunctional regulatory system.
Framing the problem of pollution as being caused by a few “bad actor” chemicals is equally inconsistent with the facts in other cases too. Chemical regulatory systems initially approved but have sometimes later banned or restricted (and always under public pressure): atrazine, endosulfan, Roundup (glyphosate), lindane, methyl bromide, methyl iodide, 2,4,5-T, chlorpyrifos, DDT and others. Many other chemicals are strongly implicated as harmful by extensive and compelling independent scientific evidence that has so far not been acted on. And of course, chemical regulators have graduated whole classes of “bad actors”: the organophosphate pesticides, PCBs, organochlorine pesticides, chlorofluorocarbons, neonicotinoids, phthalates, flame retardants, perfluorinated compounds, and so on.
How many bad actors ought it to take before we instead indict the whole show?
Chemical regulation in theory and practice: the limits of toxicology
An alternative approach to judging regulatory systems by their results, is to analyse them directly and assess their internal logic and rigour. Thus one can ask what is known about the technical limitations of toxicology and the overall scientific rigour of chemical risk assessment? And, secondly, one can direct attention to the social and institutional practices of chemical regulation. Are chemical risk assessments, for example, being applied by competent and well-intentioned institutions?
The technical limitations of chemical risk assessment are rarely discussed in detail (but see Buonsante et al., 2014). A full discussion would be lengthy, but some of the most important limitations are outlined in the paragraphs below.
The standard assays of toxicology involve the administration (usually oral feeding) of chemicals in short term tests of up to 90 days to defined strains of organisms (most often rats or mice). These test organisms are of a specified age and are fed standardised diets.
The results are then extrapolated to other doses, other age groups and other environments. Such experiments are used to create estimates of harm. Together with estimates of exposure they form the essence of chemical risk assessment. When specific chemicals are flagged as being worthy of further interest, other techniques may be brought to bear. These may include epidemiology, cell culture experiments, and biological modeling, but the basis of risk assessment is always the estimation of exposure and the estimation of harm. To say that both estimates are prone to error, however, is an understatement.
Part I: limits to estimating chemical exposures
Fifty years ago no one knew that many synthetic chemicals would evaporate at the equator and condense at the poles, from where they would enter polar ecosystems. Neither did scientists appreciate that all synthetic fat-soluble compounds that were sufficiently long-lived would bio-accumulate as they rose up the food chain and thus reach concentrations inside organisms sometimes many millions of times above background levels. Nor until recently was it understood that sea creatures such as fish and corals would become major consumers of the plastic particles flushed into rivers. These misunderstandings are all examples of historic errors in estimating real world exposures to toxic substances.
A general and broad limitation of these estimates is that real world exposures are very complex. For instance, commercial chemicals are often impure or not well defined. Thus PVC plastics are a complex mixture of polymers and may be further mixed with Cadmium or Lead (in varied concentrations). One implication of this is that it is impossible for experiments contributing to risk assessment to be “realistic”. The reason is that actual exposures are always unique to individual organisms and vary enormously in their magnitude, duration, variability, and speed of onset, all of which influence the harm they cause. Whose specific reality would realism mimic?
Additionally, many regulatory decisions do not recognise that exposures to individual chemicals typically come from multiple sources. This failing is often revealed following major accidents or contamination events. Regulatory agencies will assert that actual accident-related doses do not exceed safe limits. However, such statements usually ignore that, because regulations function in effect as permits to pollute, many affected people may already be receiving significant exposures for that chemical prior to the accident.
Returning to the specific case of BPA, no one appreciated until 2013 that the main route of exposure to BPA in mammals is absorption through the mouth and not the gut. The mouth is an exposure route whose veinous blood supply bypasses the liver, and this allows BPA to circulate unmetabolised in the bloodstream (Gayrard et al. 2013). Before this was known, many toxicologists explicitly denied the plausibility of measurements showing high BPA concentrations in human blood. They had assumed that BPA was absorbed via the gut and rapidly degraded in the liver.
Part II: limits to estimating harms
Similarly significant obstacles are faced in estimating harm. Many of these obstacles originate from the obvious fact that organisms and ecosystems are enormously biologically diverse.
The solution adopted by chemical risk assessment is to extrapolate. Extrapolation allows the results of one or a few experiments to “cover” other species and other environmental conditions.
Most of the assumptions required for such extrapolations, however, have never been scientifically validated. Lack of validation is most obvious for species not yet discovered or those that are endangered. But in other cases they are actively known to be invalid (e.g. Seok et al., 2013).
For example, in their responses to specific chemicals, rats often do not extrapolate to humans. Indeed, they often do not extrapolate even to other rats. Thus individual strains of rats respond differently (which of course is why they get used); but also young and old rats give different responses. So do male and female rats (vom Saal et al., 2014). So too do rats fed non-standard diets (Mainigi and Campbell, 1981)
Even more extreme extrapolations are employed in ecological toxicology. For example, data on adult honey bees is typically extrapolated to every stage of the bee life cycle, to all other bee species, and sometimes to all pollinators, without the experimenters citing any supporting evidence. Such extrapolations may seem absurd but they are the primary basis of the claim that chemical risk assessment is comprehensive.
There are many other limits to estimating harm. Until it was too late, scientists were not aware that a human with an eighty-year lifespan could have a window of vulnerability to a specific chemical as short as four days. Neither was it known that the effects of chemicals could be strongly influenced by the time of day they are ingested.
Another crucially important limitation is that, for budgetary and practical reasons, toxicologists necessarily focus on a limited number of specific “endpoints”. An endpoint is whatever characteristic the experimenter chooses to measure. Typical endpoints are death (mortality), cancers, organism weight, and organ weights; but endpoints can even be more subtle measures like neurotoxicity. There is a whole politics associated with the choice of endpoints, which reflects their importance in toxicology, including allegations that endpoints are sometimes chosen for their insensitivity rather than their sensitivity; but the inescapable point is that no matter what endpoints are chosen, there is a much vaster universe of unmeasured endpoints. These typically include: learning defects, immune dysfunction, reproductive dysfunction, multigenerational effects, and so on. Ultimately, most potential harms don’t get measured by toxicologists and so are missing from risk assessments.
Another example of the difficulty of estimating real life harms is that organisms are exposed to mixtures of toxins (Goodson et al., 2015). The question of toxin mixtures is extremely important (Kortenkamp, 2014). All real life chemical exposures occur in combinations, either because of previous exposure to pollutants or because of the presence of natural toxins. Many commercial products moreover, such as pesticides, are only available as formulations (i.e. mixtures) whose principal purpose is to enhance the potency of the product. Risk assessments, however, just test the “active ingredient” alone (Richard et al., 2005).
Consider too that all estimates of harm depend fundamentally on the assumption of a linear (or at least simple) dose-response relationship for the effect of each chemical. This is necessary to estimate harms of doses that are higher, lower, or even in between tested doses. The assumption of a linear response is rarely tested, yet for numerous toxins (notably endocrine disrupting chemicals) a linear dose-response relationship has been disproven. Thus the question for any risk assessment is whether the assumption is reliable for the novel compound under review (reviewed in Vandenberg et al., 2012).
Replacing doubts with false certainty
To summarise, the process of chemical risk assessment relies on estimating real world exposures and their potential to cause harm by extrapolating from one or a few simple laboratory experiments. The resulting estimates come with enormous uncertainty. In many cases the results have been extensively critiqued and shown to be either dubious or actively improbable (Chandrasekera and Pippin, 2013). Yet extrapolation continues—even though we know that the various errors must multiply—because the alternative is to actually measure these different species, using different mixtures and under different circumstances. Given the challenges this would entail, the continued reliance on simplistic assumptions is understandable.
Nevertheless, one might have thought that such important limitations and assumptions would be frequently noted as caveats to risk assessments. They should be, but they are not. Following the UK’s traumatically disastrous outbreak of BSE (mad cow disease) in the 1980s, during which most of the UK population was exposed to infectious prions following highly questionable scientific advice, this exact recommendation was made in the Phillips report. Lord Phillips proposed that such caveats should be specifically explained to non-scientific recipients of scientific advice. In practice however, Phillips changed nothing.
When an unusual scientific document does discuss the limitations of chemical risk assessment (such as this description of the failure of interactions between pesticides to extrapolate between closely related species), it rapidly becomes obvious just how much the knowledge and understanding available to us are dwarfed by actual biological and system complexities. As any biologist ought to expect, the errors multiplied and the standard assumptions of risk assessment were overwhelmed even by ordinary life situations.
For good reason many scientific experts are therefore concerned about the number and quantity of man-made chemicals in our bodies. Recently, the International Federation of Gynecology and Obstetrics linked chemical exposure to the emergence of new diseases and disorders. They specifically mentioned obesity, diabetes, hypospadias and reproductive dysfunction and noted: “The global health and economic burden related to toxic environmental chemicals is in excess of millions of deaths” (Di Renzo et al., 2015). The Federation acknowledged this to be an underestimate. Nor does it count disabilities.
Conflicts of interest in chemical risk assessment
In addition to the technical difficulties, there is also the problem that the scientists who produce scientific knowledge often have financial (and other) conflicts of interest. Conflicts, we know, lead to biases that impact on science well before it is incorporated into risk assessment (e.g. Lesser et al., 2007).
A fascinating example of apparent unconscious bias comes from a recent survey of scientific publications on the non-target effects of pesticidal GMO (Bt) crops in outdoor experiments. It was commissioned by the Dutch government (COGEM 2014). The report observed that researchers who found negative consequences of GMO Bt crops were disregarding their own findings, even when these were statistically significant. Even more interesting to the Dutch authors, was that the rationales offered for doing so were oftentimes illogical. Typically, researchers were using experimental methods specialised for detecting ecotoxicological effects that were “transient or local”, but when such effects were found the researchers were dismissing the significance of their own results for being either transient or local. The COGEM report represented prima facie evidence that researchers within a whole academic discipline were avoiding conclusions that would throw doubt on the wisdom of using GMO Bt crops. Apparently the Bt researchers had a prior ideological commitment to finding no harm of the kind that scientists are supposed to not have.
Corporate capture and institutional dysfunctionality
Chemical regulation occurs primarily within a relatively small number of governmental or “independent” regulatory institutions.
Of these, the United States Environmental Protection Agency (EPA) is the most prominent and widely imitated example. The EPA has a variety of institutional and procedural defects that prevent it being an effective regulator. Perhaps the best known of these is to allow self-interested chemical corporations to conduct the experiments and provide the data for risk assessment. This lets them summarise (or even lie about) the results. As was once pointed out by Melvin Reuber, former EPA consultant, it is extraordinarily easy for an independent commercial testing operation to bias or fix the result of a typical toxicology study for the benefit of a client.
How the EPA first allowed corporations to generate and submit their own regulatory data is a story well worth knowing.
In the 1980s Industrial Bio-Test Laboratories (IBT) was the largest independent commercial testing laboratory in the United States. FDA scientist Adrian Gross discovered that IBT (and other testing companies) were deliberately, consistently, and illegally misleading both EPA and the FDA about their results. Aided by practices such as the hiring of a chemist from Monsanto, who manufactured them, to test PCBs, IBT created an illusion of chemical safety for numerous pesticides and other chemicals. Many are still in use. They include Roundup, atrazine and 2,4-D, all commonly used in US agriculture. Between them, Canadian regulators drew up a list of 106 questionable chemical registrations and FDA identified 618 separate animal studies as being invalid due to “numerous discrepancies between the study conduct and data.” Both regulators suppressed their findings.
Senior IBT managers were jailed, but what the scandal had revealed was that whenever results showed evidence of harm—which was often—, misleading regulators was standard practice.
More remarkable even than the scandal was EPA’s response. Instead of bringing testing in-house, which would seem the logical response to a system-wide failure of independent commercial testing, EPA instead created a Byzantine system of external reporting and corporate summarising. The resulting bureaucratic maze ensures that no EPA employee ever sets eyes on the original experiments or the primary data, and only a handful can access even the summarised results. This system has the consequence of excluding any formal possibility that whistleblowing on the part of Federal employees or FOIA requests (from outsiders) might reveal fraudulent or otherwise problematic tests. EPA calculatedly turned a blind eye to any potential future wrongdoing in the full knowledge that the chemical regulatory system it oversaw was systemically corrupt.
Probably more familiar to readers is what is called “regulatory capture.” This takes many forms, from the offering to public servants of favours and future jobs, to the encouragement of top-down political interference with regulatory agencies. The culminating effect is to ensure that political will within agencies to protect the public is diluted or lost.
Regulatory capture can become a permanent feature of an institution. For example, OECD member countries have an agreement called the Mutual Acceptance of Data (MAD). MAD is appropriately named. It has the effect of explicitly excluding from regulatory consideration most of the peer-reviewed scientific literature (Myers et al., 2009a). The purported goal of MAD was to elevate experimental practices by requiring certification via Good Laboratory Practice (GLP) which was a procedure introduced after the IBT scandal (Wagner and Michaels, 2004). GLP is a mix of management and reliability protocols that are standard in industrial laboratories but rare in universities and elsewhere. However, the consequence of accepting MAD has been to specifically exclude from regulatory consideration evidence and data not produced by industry.
The MAD agreement explains much of the regulatory inaction over BPA. Because of MAD, FDA (and also its European equivalent the European Food Safety Authority) have ignored the hundreds of peer-reviewed BPA studies—since they are not GLP— in favor of just two by industry. These two industry studies, whose credibility and conclusions have been publicly challenged by independent scientists, showed no ill effects of BPA (Myers et al., 2009b).
Whistleblowing at the EPA
Various EPA whistleblowers have described in detail the specifics of their former organisation’s capture by branches of the chemical industry.
Whistleblower William Sanjour has described how regulatory failure was ensured by the organisational structure imposed on the EPA at its Nixon-era inception. The structure of EPA is inherently conflicted since it has the dual functions of both writing and and enforcing regulations. Unwillingness to enforce high standards led his superiors to order Sanjour to write deliberate loopholes into those regulations. More recently, the EU’s EFSA was similarly caught proposing loopholes for new regulations on endocrine disrupting chemicals. Inserting loopholes is standard practice in the writing of chemical safety regulations.
In the same article, Sanjour also proposed that since corporate capture renders them useless, the public would be better off with no regulatory agencies. In a similar vein, former EPA pesticide scientist Evaggelos Vallianatos called his former employer, at book length, the “polluter’s protection agency.” Another EPA whistleblower, David Lewis, this time at EPA’s Office of Water, has shown in court-obtained documents that EPA scientists buried evidence and even covered up deaths so as to formulate regulations that would permit land application of sewage sludge. This sludge was routinely contaminated with pathogens, heavy metals, industrial chemicals, pharmaceuticals, flame retardants, and other known hazardous substances. The corruption around sewage sludge regulations extended well beyond the EPA. It encompassed other federal agencies, several universities, the National Academy of Science, and municipalities. David Lewis eventually obtained a legal judgement that the City of Augusta, Ga, had “fudged” the toxicity testing of its own sewage sludge in order to meet EPA guidelines. The city had done so at the request of EPA.
In another recent case, DeSmogBlog obtained, through a Freedom of Information Act request (FOIA), internal documents showing how EPA offered access to its fracking study plans:
“[Y]ou guys are part of the team here,” one EPA representative wrote to Chesapeake Energy as they together edited study planning documents in October 2013, “please write things in as you see fit.”
Even more recently, EPA whistleblower and chemist Dr Cate Jenkins and the non-profit Public Employees for Environmental Responsibility (PEER) successfully sued EPA for suppressing information about toxic effects on 9/11 first responders. The case ended with a judgement showing that EPA had, among numerous egregious acts, created fake email accounts (including for EPA head Lisa Jackson) to evade accountability. According to Judge Chambers, EPA:
“Failed, and failed miserably, over an extended course of time in complying with its discovery obligations and…Court discovery orders”
Judge Chambers also found that EPA worked a “fraud on the Court” through numerous “false claims” and inaccurate claims of privilege which upon examination applied to “none of the documents provided”. The judge also found that EPA deliberately and illegally destroyed an unknown number of documents which should have been under a litigation hold.
The ultimate effect of these institutional defects is that chemical risk assessments in the US and the EU have a safety bar for approval that is so low that regulators virtually never decline to approve a chemical. In contrast, the exact same institutions use standards for taking any chemical off the market that are so high that such an event nearly never happens. Yet if both standards were based purely on science, as they claim to be, both bars would be the same height.
This double standard represents the overwhelming bias in the system. At every stage of chemical risk assessment—from the funding of research to the ultimate decision to approve a chemical—the process is dominated by commercial concerns and not by science (as was recently shown yet again).
Beyond any conceivable doubt, inappropriate external influences swamp the scientific content and protective mission of chemical risk assessment.
Chemical risk assessment: can the show be salvaged?
It therefore seems clear that to frame individual chemicals as “bad actors” is incorrect. Chemical risk assessments themselves are the problem. Thus we can perfectly explain why approved chemicals accumulate red flags when exposed to the scientific process but also why those that replace them are no less harmful. Specific chemicals like BPA are thus the messengers and shooting them one by one is not only pointless, it is counterproductive. It distracts and detracts from the infinitely more important truth, that the institutions, the methods, and thus the entire oversight of chemical regulation is failing in what it claims to do, which is to protect from us from harm.
Importantly, chemical regulatory systems are not just broken, they are unfixable. Even with the best intentions, such as the full cooperation of all the institutions mentioned here and of the entire academic research community, remedying the technical problems would be a task that is beyond Herculean.
Consider just one of these–the testing of a chemical in combination with others. The testing of mixtures is an improvement often suggested by NGOs and thousands of scientific studies show that this is an important consideration. The pesticide Chlordecone, for example, increases the toxicity of an “otherwise inconsequential” dose of the common contaminant carbon tetrachloride by 67-fold in rats (Curtis et al., 1979).
To test mixtures properly, however, would be astonishingly expensive and also enormously costly towards experimental animals. According to the US National Toxicology Program, standard 13 week studies of the interactions between just 25 chemicals would require 33 million experiments costing $3 trillion. This is because each chemical needs to be tested against all possible combinations of the others. To study mixtures of all 11,000 chlorinated chemicals in commerce would require 103311 experiments. This is more experiments than there are atoms in the universe. Our entire planet would have to devote itself to animal experimentation and the work would still not be done by the end of time itself (Yang 1994). Even then we would only know the toxicity of organochlorines towards a single test species. Would the results be extrapolable to any other species? Well, we could buy another planet and test it!
Imagine also that an adequate test for synthetic chemicals were devised and it was run by competent institutions. Would any chemical pass? The multiple harms of the single chemical BPA, plus the frequency with which chemical substitutes turn out later to be harmful, and plenty of other data, suggests it is possible that few chemicals would pass. This conclusion, of course, contradicts the presumption of innocence that underlies all chemical regulation. But we should be clear that the presumption is arbitrary and therefore may be wrong. What is so unbelievable, after all, about proposing that all man-made chemicals cause dysfunction at low doses in a significant subset of all the biological organisms on earth?
Strategising for success
Obviously, the implications of this knowldge are many, but the one of specific importance to environmental health campaigners, is that organising for a ban on a specific hazardous chemical, such as the herbicide atrazine, is likely to be a strategic error. If chemical risk assessment is ineffective then demanding a ban is pointless because achieving it will result only in the substitution of a chemical that is no better. But even worse, if chemical risk assessment is ineffective, such campaigns undermine the wider cause because they falsely imply that chemical regulations protect the public and limit pollution.
Messaging is extremely important. If the public learned that chemical regulations were effective only from the chemical industry they probably would disbelieve it. However, since they hear it from the entire environmental movement then chemical risk assessment acquires credibility. Why, they no doubt reason, would the environment movement pretend chemical testing was effective if it wasn’t? And indeed the environment movement traditionally reinforces this message still further whenever it calls for more testing.
In the light of this understanding, if they accept the accumulated scientific evidence, environmental and public health advocates who campaign for bans or restrictions on single chemicals have an opportunity to substantively rethink their strategies and reframe their activities. This doesn’t necessarily mean abandoning any discussion of individual chemicals, but at the very least it does mean explicitly framing those specific chemicals not as “bad actors” but as symptoms of a much bigger problem of incompetent and dysfunctional regulation, with all that implies.
This challenge is also a tremendous opportunity. Having facts that are more stark and analysis that is more scientific and more rigorous creates a superior and more powerful basis upon which to organise and strategise. Thus it brings more ambitious environmental health goals within reach. Advocates can choose from a broader range of possible approaches and engage a broadened segment of the population. They can place clear and obvious intellectual distance between their own realistic strategies for protecting the public and the planet and contradt them with the plainly inadequate views of the chemical industry. For example, it is surely easier to explain to a layperson the generic absurdities of chemical risk assessment (and thus gain their support) than it is to explain the toxicological niceties of glyphosate (Roundup) or 2,4-D, especially one chemical (of 80,000) at a time. They say the truth can set you free, but in the world of toxic campaigning it is a strategy that has hardly been tried yet. I am optimistic, therefore, that the tide can be turned.
In the late 1990s Greenpeace USA adopted the novel campaigning position that all chlorinated hydrocarbons should be banned, in part on the grounds that every one so far investigated had proven toxicologically problematic. In doing so they took chemical campaigning to a new level. Greenpeace was threatening thousands of products of the chemical industry with a strategic goal that had a realistic chance of significantly enhancing the quality of our environment. If they had succeeded neonicotinoids would not now be ubiquitous in the environment, DDT would never have been allowed. Nor would 2,4-D, but it is unlikely that your material standard of living would be lower, it might even be higher.
Greenpeace was hit by a campaign of corporate espionage. Their offices were bugged and their computers were hacked, they were infiltrated by phony volunteers and more. The chemical industry was spooked. Greenpeace eventually backed off, but by raising the stakes and making their case with science, they had shown a way.
The book Pandora’s Poison elaborates on the some of the ambitious ideas for eradicating pollution that Greenpeace tried but never in the end adequately road tested. It is time to learn the lessons of the past and move chemical safety campaigning outside of the comfort zone of the chemical industry, which is where it belongs.
1) The IUCN full reference for neonicotinoids is: Worldwide Integrated Assessment of the Impact of Systemic Pesticides on Biodiversity and Ecosystems.
Ayyanan A, O. Laribi, S. Schuepbach-Mallepell, C. Schrick, M. Gutierrez, T. Tanos, G. Lefebvre, J. Rougemont, O. Yalcin-Ozuysal, Brisken C. Perinatal Exposure to Bisphenol A Increases Adult Mammary Gland Progesterone Response and Cell Number. Molecular Endocrinology, 2011; DOI: 10.1210/me.2011-1129
Buonsante, Vito A., Muilerman H, Santos T, Robinson C, Tweedale AC (2014) Risk assessment׳s insensitive toxicity testing may cause it to fail. Environmental Research 135: 139–147
Bae S., Hong Y-C. (2014). Exposure to Bisphenol A From Drinking Canned Beverage Increases Blood Pressure: Randomized Crossover Trial. Hypertension 10.1161/HYPERTENSIONAHA.114.04261
Bhan A, Hussain I, Ansari KI, Bobzean SAM, Perrotti LI, Mandal SS (2014) Bisphenol-A and diethylstilbestrol exposure induces the expression of breast cancer associated long noncoding RNA HOTAIR in vitro and in vivo. The Journal of Steroid Biochemistry and Molecular Biology 141: 160.
Braun JM, Kalkbrenner AE, Calafat AM, Yolton K, Ye X, Dietrich KN, Lanphear BP (2011) Impact of Early Life Bisphenol A Exposure on Behavior and Executive Function in Children. Pediatrics, 128: 873-882.
Chandrasekera PC, Pippin JJ (2013). Of rodents and men: species-specific glucose regulation and type 2 diabetes research. ALTEX 31:157-176.
Curtis LR, Williams W.Lane, Harihara M. (1979) Potentiation of the hepatotoxicity of carbon tetrachloride following preexposure to chlordecone (Kepone) in the male rat. Toxicology and Applied Pharmacology Volume 51: Pages 283-293.
Evans SF, Kobrosly RW, Barrett ES, Thurston SW, Calafat AM, Weisse B, Stahlhut R, Yolton K, Swan SH (2014) Prenatal bisphenol A exposure and maternally reported behavior in boys and girls. NeuroToxicology 45: 91–99.
Gayrard V, Lacroix MZ, Collet SH, Viguié C, Bousquet-Melou A, Toutain P-L, and Picard-Hagen N (2013) High Bioavailability of Bisphenol A from Sublingual Exposure. Environ Health Perspect. 121: 951–956.
Goodson et al. (2015) Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead. 36: Supplement 1, S254–S296.
Kinch C, Ibhazehiebo K, Jeong J-H, Habibi HR, and Kurrasch DM (2015) Low-dose exposure to bisphenol A and replacement bisphenol S induces precocious hypothalamic neurogenesis in embryonic zebrafish. PNAS doi: 10.1073/pnas.1417731112
Kortenkamp, A (2014) Low dose mixture effects of endocrine disrupters and their implications for regulatory thresholds in chemical risk assessment. Current Opinion in Pharmacology Volume 19, December 2014, Pages 105–111.
Lesser, LI Ebbeling CB , Goozner M, Wypij D, Ludwig DS (2007) Relationship between Funding Source and Conclusion among Nutrition-Related Scientific Articles. PLOS DOI: 10.1371/journal.pmed.0040005
Liao C, Liu F, Alomirah H, Duc Loi V, Ali Mohd M, Moon H-B, Nakata H, and Kannan K (2012) Bisphenol S in urine from the United States and seven Asian countries: occurrence and human exposures. Environ. Sci. Technol. 46: 6860–6866.
Mainigi, KD. and T.C Campbell (1981) Effects of low dietary protein and dietary aflatoxin on hepatic glutathione levels in F-344 rats. Toxicology and Applied Pharmacology 59: 196–203.
Melzer D; Nicholas J. Osborne; William E. Henley; Ricardo Cipelli; Anita Young; Cathryn Money; Paul Mccormack; Robert Luben; Kay-Tee Khaw; Nicholas J. Wareham; Tamara S. Galloway (2012) Urinary Bisphenol: A Concentration and Risk of Future Coronary Artery Disease in Apparently Healthy Men and Women. Circulation 125: 1482-1490.
Menard S. , L. Guzylack-Piriou, M. Leveque, V. Braniste, C. Lencina, M. Naturel, L. Moussa, S. Sekkal, C. Harkat, E. Gaultier, V. Theodorou, E. Houdeau. (2014) Food intolerance at adulthood after perinatal exposure to the endocrine disruptor bisphenol A. The FASEB Journal 28: 4893-4900.
Molina-Molina J-M, Esperanza Amaya, Marina Grimaldi, José-María Sáenz, Macarena Real, Mariana F. Fernández, Patrick Balaguer, Nicolás Olea (2013) In vitro study on the agonistic and antagonistic activities of bisphenol-S and other bisphenol-A congeners and derivatives via nuclear receptors. Toxicology and Applied Pharmacology 272: 127–136.
Myers JP et al (2009a) Why Public Health Agencies Cannot Depend on Good Laboratory Practices as a Criterion for Selecting Data: The Case of Bisphenol A. Environ Health Perspect 117:309–315.
Myers JP, Zoeller TH and vom Saal F (2009b) A Clash of Old and New Scientific Concepts in Toxicity, with Important Implications for Public Health. Environ Health Perspect 117: 1652–1655.
Perera F, Julia Vishnevetsky, Julie B Herbstman, Antonia M Calafat, Wei Xiong, Virginia Rauh and Shuang Wang (2012) Prenatal Bisphenol A Exposure and Child Behavior in an Inner-City Cohort. Environ. Health Perspect. 120: 1190–1194.
Prins, Wen-Yang Hu, Guang-Bin Shi, Dan-Ping Hu, Shyama Majumdar, Guannan Li, Ke Huang, Jason Nelles, Shuk-Mei Ho, Cheryl Lyn Walker, Andre Kajdacsy-Balla, and Richard B. van Breemen (2014) Bisphenol A Promotes Human Prostate Stem-Progenitor Cell Self-Renewal and Increases In Vivo Carcinogenesis in Human Prostate Epithelium. Endocrinology doi.org/10.1210/en.2013-1955.
Richard S, Moslemi S, Sipahutar H, Benachour N, and Seralini G-E (2005) Differential Effects of Glyphosate and Roundup on Human Placental Cells and Aromatase. Environ Health Perspect. 113: 716–720.
Seok et al (2013) Genomic responses in mouse models poorly mimic human inflammatory diseases. Proc Natl Acad Sci U S A. 110: 3507–3512.
Tarapore P, Jun Ying, Bin Ouyang, Barbara Burke, Bruce Bracken, Shuk-Mei Ho. (2014) Exposure to Bisphenol A Correlates with Early-Onset Prostate Cancer and Promotes Centrosome Amplification and Anchorage-Independent Growth In Vitro. PLoS ONE DOI: 10.1371/journal.pone.0090332
Rubin B S, M K Murray, D A Damassa, J C King, and A M Soto (2001) Perinatal exposure to low doses of bisphenol A affects body weight, patterns of estrous cyclicity, and plasma LH levels. Environ Health Perspect. 109: 675–680.
Vandenberg Laura N. , Theo Colborn, Tyrone B. Hayes, Jerrold J. Heindel, David R. Jacobs, Jr., Duk-Hee Lee, Toshi Shioda, Ana M. Soto, Frederick S. vom Saal, Wade V. Welshons, R. Thomas Zoeller, and John Peterson Myers (2012) Hormones and Endocrine-Disrupting Chemicals: Low-Dose Effects and Nonmonotonic Dose Responses. Endocrine Reviews DOI: http://dx.doi.org/10.1210/er.2011-1050
Rochester and AL Bolden (2015) Bisphenol S and F: A Systematic Review and Comparison of the Hormonal Activity of Bisphenol A Substitutes. Environmental Health Perspectives
vom Saal F., Catherine A. VandeVoort, Julia A. Taylor, Wade V. Welshons, Pierre-Louis Toutain and Patricia A Hunt. (2014) Bisphenol A (BPA) pharmacokinetics with daily oral bolus or continuous exposure via silastic capsules in pregnant rhesus monkeys: relevance for human exposures. Reproductive Toxicology 45: 105–116.
Wagner, Wendy, and David Michaels. (2004) “Equal Treatment for Regulatory Science: Extending the Controls Governing the Quality of Public Research to Private Reseach.” Am. JL & Med. 30 : 119.
Yang RSH (1994) Toxicology of chemical mixtures derived from hazardous waste sites or application of pesticides and fertilizers. In Yang RSH, ed: Toxicology of Chemical Mixtures. Academic Press 99-117.
Yuan Z, S Courtenay, RC Chambers, I Wirgin (2006) Evidence of spatially extensive resistance to PCBs in an anadromous fish of the Hudson River. Environmental Health Perspectives 114. 77-84.