Issue 29 – BFRs Explained

Issue 29, August 2010 (scroll down for this month’s articles): Flame retardants: Health concerns explained :: Multiplying the value of prevention with disease patterns :: Plus 5&5, a round-up of news and science highlights from last month.

Fire Safety Chemicals: Health Concerns Explained


BFRs were designed to make furniture and other household goods safer by making it more difficult for them to burn. But are they the safest way of doing so? (Image: Fastily, Wikimedia)

Brominated flame retardants are a controversial class of chemical. Several types of BFR have already been banned in Europe; this year the European Parliament has been considering whether or not BFRs should be banned entirely from electronics goods.

Manufacturers argue they are essential for saving lives; environment groups and manufacturers of non-halogenated fire retardants say they pose unnecessary environmental hazards and should be phased out in favour of greener alternatives.

Besides being endangered species, red panda, peregrine falcons, hooded seals and right whales have one thing in common: they all have traces of fire-safety chemicals in their bodies. Humans do too. It doesn’t matter from where you are, be it the pristine arctic or the most polluted city, you will almost certainly have brominated flame retardants (BFRs) in your blood.

As near-ubiquitous, persistent environmental pollutants, BFRs have come under increasing regulatory and scientific scrutiny. In Europe two classes of BFR, the PBDEs and PBBs, have already been banned. In the US, although PBDEs are still legal, they are the focus of a substantial research programme with a growing body of literature documenting potential health problems in people exposed to the chemicals.

Since PBDEs were banned in Europe, manufacturing has shifted to other brominated chemicals, mainly to the chemicals TBBPA (a brominated form of the polycarbonate additive BPA) and HBCD. Research into the “emerging” BFRs which are replacing PBDEs is still sporadic; although assumed by regulators to be safe, experimental data is lacking.

There is so little information about HBCD that no regulatory body has even been able to settle on a maximum limit for daily exposure. Nonetheless, HBCD is widely-used.

[Correction: We originally cited Harrad 2010, saying the paper suggests that 1 in 20 UK schoolchildren exceed an exposure limit on HBCD proposed in a Dutch paper (Bakker 2008) by a factor of 2. This is not correct: the Bakker limit is for BDE-99, not HBCD, and only a small number of children are likely to consume enough dust in the most-contaminated environments to be exposed at double the Bakker limit.]

TBBPA is considered to pose less of a risk to the environment and health because, unlike HBCD and the PBDEs, which are simply mixed into whatever they are meant to prevent burning, it is chemically bonded to polymers (except in some uses such as television casings). Although direct human exposure from household items should therefore be much lower, TBBPA is nonetheless being detected in people.

In one French study (Cariou 2008), 44% women tested had TBBPA in their breast milk. Analysis of umbilical cord blood from pregnant women in the study group revealed that, in some cases, levels of TBBPA were comparable to natural thyroxine levels.

Professor Barbara Demeneix, an expert in endocrinology from the Muséum National d’Histoire Naturelle in Paris, believes TBBPA poses a serious hazard to thyroid action: “Thyroid function is vital for neurogenesis. It is known that thyroid deficiency after birth is critical for development […] Further back in development subtle changes can potentially affect all sorts of outcomes, as thyroid function affects how every single cell in the body behaves.”

Other chemicals which are known to interfere with developmental thyroid function, such as PCBs, have also been shown to reduce children’s IQ (Stewart 2008). US researchers have found that increased prenatal exposure to several different PBDEs results in lower scores in neurodevelopmental tests in children (Herbstman 2010).

That different brominated compounds have similar and fundamental effects in the body has led for calls for a general ban on BFRs as a class of chemicals under the EU’s RoHS legislation, the EU’s electronics chemical safety regulation.

When it comes to organochlorines, the propensity for different molecules to behave in similar ways has already been explained in a 1994 systematic review of how the addition of chlorine atoms changes the behaviour of an organic molecule, by the German chemist Dietrich Henschler.

From his study, Henschler was able to articulate four general principles of organochlorine toxicity (Henschler 1994): firstly, that addition of chlorine usually increases toxicity of an organic molecule; secondly, that it produces new toxic effects; thirdly that the new molecules are likely to be mutagenic and/or carcinogenic; and finally, as a weaker generalisation, that the more chlorine atoms you attached to a molecule the more toxic it would be.

One reason why the introduction of chlorine atoms into organic compounds increases their toxicity is it makes them more lipophilic. Since the binding sites on many enzymes and hormone receptors are designed to receive lipophilic molecules, this increases the potential for chlorinated molecules to either be broken down into smaller chlorinated molecules or interfere with hormone signalling.

Lipophilic molecules are also more prone to bioaccumulation; if the molecules are also toxic, they can concentrate towards increasingly harmful levels as they move up the food chain.

The addition of chlorine also changes the reactivity of organic compounds. The result is unpredictable – reactivity can either be increased or decreased – however, neither is good. Increased stability means the molecules persist longer in the body and the environment, increasing the opportunities for and duration of toxic effects. Increased reactivity, on the other hand, means they are more likely to damage DNA or other essential molecules in the cell.

Brominated molecules show very similar behaviour as chlorinated molecules: they are lipophilic, are persistent, have been shown to bioaccumulate, and to interfere with hormone signalling such as thyroid function. It seems that, as with chlorine, the addition of bromine to a molecule can reasonably be expected to lead to a range of increased health hazards.

Dr Stuart Harrad, a researcher at the University of Birmingham (UK), says: “We don’t seem to have learned the lessons of using things like PCBs because we have ended up with compounds which are not dissimilar; perhaps we need to look more closely at whether or not we need them and if there are ways to get the fire safety benefits without the potential hazards.”

So is it possible to achieve fire safety without toxic chemicals? At a basic level, flame retardants are used because fire safety standards require a minimum time for something to ignite, for example from contact with a cigarette or candle, and once it has ignited, there is supposed to be a minimum rate at which an object burns.

BFRs are not essential for meeting these standards. The electronics company Nokia has eliminated all BFRs from its products. Sony Eriksson is doing likewise, and is also lobbying for BFRs and other hazardous compounds to be restricted under the forthcoming revisions to RoHS.

The space being vacated by BFRs is being filled with non-halogenated flame retardants, a growing market in Europe. Although they pose none of the problems associated specifically with halogen use, they are not perfectly benign. For example, organophosphates are finding increased use as flame retardants, in spite of being known neurotoxicants.

Richard Hull, Professor of Chemistry and Fire Science at the University of Lancashire (UK) says that fire safety is more complex than passing simple tests – tests which were predominantly designed to evaluate the 1970s technology of halogenated flame retardants – newer materials and char forming fire retardants offer cleaner routes to fire safety without needing to use environmentally persistent halogenated flame retardants.

Hull says that for furniture, in a published report of around 160 fabric/filler combinations, two-thirds passed ignition tests with no need for flame retardants at all: “The main reason BFRs are used is because they are cheap. If you add 20% flame retardant to a cushion, you know it’ll pass any flammability tests. What would be much better is if we thought more carefully about how we can prevent things igniting so we can avoid potentially hazardous chemicals altogether.”

Disease patterns: Multiplying the value of prevention

Disease patterns Venn diagram

Pattern of immune-related diseases. Entryway diseases shown in bold in each pattern. Comorbidities shared among diseases shown in intersections. Click to enlarge. (Image: Environmental Health Perspectives)

Rodney R Dietert, Professor of Immunotoxicology at Cornell University (USA), would like to make a very simple point: diseases are inter-related.

It might seem obvious that a patient manifesting one disease or condition is more likely, later on, to develop another, but Dietert says our medical and regulatory systems do not routinely recognise this – there simply is not a published literature on the subject.

As a result we are treating symptoms while failing to anticipate how a person’s health is likely to change in future, and we are underestimating the cost of environmental causes of illness.

In a paper published in this month’s Environmental Health Perspectives, Dietert argues for a new approach to both treating and preventing disease, based on mapping the relationships between different illnesses.

He argues that “illnesses such as type 1 diabetes and asthma are not only the end result of environmental exposures interacting with genetic background; they are the entryway into larger environmentally-associated health concerns”.

So far the only disease which is being interpreted in these terms is metabolic syndrome, where its relation to cardiovascular disease, diabetes and stroke is well-understood and incorporated into the rationale for both preventing and treating the illness.

As an immunologist, Dietert sees similar opportunities for understanding the origins and consequences of disorders relating to immune dysfunction. Here, Dietert identifies five entryway conditions caused by insults to the developing immune system (see illustration, where entryway conditions are shown in bold).

Childhood asthma is one of the most important because of its entryway status in relation to three disease patterns relating to the body’s response to inflammation, allergy and infection.

Because childhood asthma is not, on Dietert’s terms, an isolated illness but a pattern of health risks across a lifetime, it means the benefits of preventing asthma multiply up far beyond the cost medicine days off work. Preventing the immune insults which lead to entryway diseases is therefore far more valuable than currently calculated.

To better understand the costs and health effects of the environmental risk factors which cause inflammatory dysfunction, it is necessary to test the developmental immunotoxicity of chemicals to which the foetus and infant are exposed.

This is not, however, currently a regulatory requirement. Instead, chemicals are tested on adult animals, from which potential toxicity to the infant extrapolated – even though effects on a developing immune system are known to bear little comparison to effects on a developed, adult immune system.

“We aren’t even measuring for developmental effects of chemicals,” says Dietert. “If asthma on its own isn’t enough, perhaps the additional risks of asthma plus everything else that might happen to a person as they are ageing up to 65 years old, makes these assessments valuable enough [for regulators].”

5&5: News and science highlights


Germany seeks EU ban on PAHs in consumer products: Germany has asked the European Commission to propose restrictions on eight polycyclic aromatic hydrocarbons (PAHs), which would effectively ban the compounds from all consumer products manufactured or imported into the EU.

Preventing Cancer – a Call to Action: Interesting reflections from Ted Schettler, MD MPH, on the meaning of the President’s Cancer Panel report in the context of the precautionary principle.

Dioxin Science Wars: Even after 20 years of study, the US EPA has yet to finally classify the most potent form of dioxin as a carcinogen. C&EN maps the controversies and reasons for delay, providing a detailed illustration of the conflicts in chemicals regulation.

Libraries adopt BPA-free paper: A short article on how libraries in Oregon, USA, have ditched BPA-laced thermal paper for BPA-free alternatives.

Health group sues FDA over antimicrobial soap: The US FDA is being sued over its delay in establishing safe conditions for the use of triclosan, used as an anti-microbial agent in soaps and detergents.


Diabetic symptoms in mothers and male offspring after short BPA exposure during pregnancy: Synopsis of animal study finding that brief and short-term BPA exposure causes symptoms of diabetes in mice mothers and male offspring.

Dietary Intake Is Associated with Phthalate Body Burden: Study finding an association between DEHP exposure and poultry consumption, and DEP exposure with potatoes and tomatoes. The study suggests diet is a significant exposure route to phthalates.

Tobacco’s Influence on the EU Treaty and Its Implications for Policy: In this study, the researchers sought to identify how and why the EU’s approach to Impact Assessment (IA) developed, that it had been influenced by British American Tobacco in its favour, and that IA is not a reliable tool for protecting health over economic interests.

Childhood Exposure to Phthalates May Limit Growth, Affect Thyroid Concentration: New study finding negative associations between urinary phthalate concentrations and thyroid hormones, IGF-I and growth in children.

Inflammatory Effects of Phthalates in Neonatal Neutrophils: New study finding that DEHP reduces the effectiveness of immune system cells that normally work to fight infections by promoting inflammation, especially in premature infants – those most likely, because of medical treatment, to be highly exposed to DEHP.


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  1. This is a very good overview of what is going on in the field of brominated flame retardants.The problem with these chemicals might be that they disrupt hormone transporters, these are proteins taking care of the transport of f.i. T4 and T3 over the membrane into the cell, where the hormones are used. An example is MCT 8 the transporter working in the hypothalamus, a deficiency of this transporter as is seen in genetically based disease, is severe mental retardation. It is on this moment very difficult to quantify the possibilities for compensation of the disruption, in general compensation mechanisms are good in thyroid hormone metabolism because of the negative feed back system, but when these transporters are negatively influenced we don’t know, what is happening.

  2. […] Issue 29 – BFRs Explained […]

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