As researchers have recently reported, there has been an alarming increase in the concentration of PBDEs in breast milk over the past few years. Levels in Swedish women, for example, increased by 60 times from 1972 to 1997 while, in North America, they've increased by more than 200 times over a 25-year period (Lancet, 2007; 370: 1813-4).
Even more alarming, a nationwide study by the US non-profit Environ-mental Working Group (EWG) found unexpectedly high levels of PBDEsin the breast milk of every woman tested. Worse, the milk from several mothers had among the highest levels of these chemicals ever reported in humans worldwide (www. ewg.org/reports/mothersmilk).
PBDEs have also found their way into human blood and adipose (fat) tissue (Environ Health Perspect, 2004; 112: 1085-91), but their presence in breast milk is particularly unsettling. As the EWG points out, the chemicalsin breast milk are passed on not
only to the nursing infant but, more important, to the unborn fetus, which is especially vulnerable to the effects of noxious chemicals.
Precisely what impact PBDEs have on human health is not yet known, but more and more research is uncovering a litany of toxic effects associated with exposure to these poisonous agents. What's more, studies have found adverse effects at levels lower than those now detected in many women.
PBDEs have regularly been used in a range of everyday products since the 1970s, yet scientists have only now discovered just how hazardous these ubiquitous chemicals can be.
Although no human health studies have been done on PBDEs, studies in animals show nervous system, reproductive, developmen-tal and endocrine effects, as well as cancer in high-dose studies (J Occup Environ Med, 2005; 47: 199-211).
Many of the known health effects of PBDEs are thought to stem from their ability to disrupt thyroid-hormone balance and normal metabolism. Indeed, a mysterious epidemic of thyroid disease in cats may have been due to flame retardants, according to a small study by the US Environmental Protection Agency (EPA). They found extremely high levels of PBDEs in the cats, suggesting that the toxins could be behind common feline hyperthyroidism (overactive thyroid) (Environ Sci Technol, 2007; 41: 6350-6).
In addition, says the EWG, PBDEs may also cause hypothyroidism, or underactive thyroid. One study in mice found that serum T4 levels were significantly lower in those given a single dose as low as 0.8 mg/kg of body weight of a commercial PBDE mixture (Toxicology, 1994; 86: 49-61).
Another study in rats discovered that PBDEs reduced thyroid hor-mone levels at an even lower dose than that (Toxicology, 2007; 242; 80-90). Although these findings may not apply to humans, an occupational study did find higher rates of hypothyroidism among workers exposed to brominated fire retard-ants on the job (Environ Health Perspect, 2001; 109 [suppl 1]: 49-68).
An underactive thyroid can cause fatigue, depression, anxiety, unex-plained weight gain, hair loss and a low libido. Moreover, the effects of depressed thyroid-hormone levels on developing fetuses and infants can be devastating. Women with T4 levels
in the lowest 10 per cent of the population during the first trimester of pregnancy were almost three times as likely to have a child with an IQ of less than 85 (the lowest 20 per cent in the range of IQs) and five times as likely to have a child with an IQ of less than 70-in other words, 'mild retardation' (Clin Endocrinol, 1999; 50: 149-55).
As animal studies show, even short-term exposures to PBDEs can alter thyroid-hormone levels-and the effects are greater in fetuses and young animals than in adults. These results are worrying as human data suggest that pregnancy itself stresses the thyroid, and the developing fetus or infant lacks the thyroid reserves that adults have to protect them against systemic insults (Biochimie, 1999; 81: 563-70).
Thyroid hormones are important in neural development as they regulate numerous other hormones and growth factors in the brain. So, at least in rats, even short-term exposures to PBDEs at critical times can cause lasting harm (Toxicol Sci, 2005; 88: 172-80).
Indeed, small doses of PBDE mixtures administered to fetal or newborn mice and rats caused deficits in learning, memory and hearing, changes in behaviour, and delays in sensory motor develop-ment. Many of these effects became worse with age (Toxicol Sci, 2002; 67: 98-103; 104-7; Environ Health Perspect, 2001; 109: 903-8).
Although animal data may not necessarily apply to humans, the fact that they show significant neurol-ogical effects-which are inherently difficult to detect in rodents-raises concerns regarding human health.
Other adverse effects
As well as causing damage to the thyroid and nervous system, early exposure to PBDEs have also been linked to serious harm to the reproductive systems of both male and female rats. Observed effects included reduced levels of circulat-ing sex steroids, delayed onset of puberty, changes in ovarian cells, decreased weight of male rat reproductive organs and sperm count, and feminization of the male rats (Environ Health Perspect, 2006; 114: 194-201; Environ Health Perspect, 2005; 113: 149-54).
The EWG also found PBDE-associated impaired weight gain, enlarged livers and raised blood cholesterol in pregnant animals. Effects of exposures in utero on the fetus included limb and ureter malformations, enlarged hearts, bent ribs and delayed bone hardening. These malformations occurred at doses much lower than those that were harmful to the mouse mothers (www.ewg.org/reports/mothersmilk).
Even more alarming, one commercial PBDE mixture (deca) caused liver, thyroid and pancreas tumours at high doses when given to rats and mice (Natl Toxicol Program Tech Rep Ser, 1986; 309: 1-242). According to the Agency for Toxic Substances and Disease Registry (ATSDR) 2004 report, the US EPA has since classified deca-PBDE as a 'possible human carcinogen' (www.atsdr.cdc.gov/ toxprofiles/phs68-pbde. html#bookmark05).
Regulation in the future?
The growing evidence of serious health risks associated with PBDE exposure has prompted regulators across Europe and the US to ban certain forms of brominated fire retardants. And, happily, chemical fire retardants are not necessary for fire safety. Indeed, a number of manufacturers, including Ikea, Hewlett-Packard and Sony, have redesigned their products to be inherently less flammable without chemical treatments. For a PBDE-free manufacturer and product list, see www.ewg.org/pbdefree.
Sadly, however, PBDEs are still found in millions of homes world-wide, and only time will tell if we will succeed in getting rid of these nasty chemicals from our everyday lives.
How are we exposed?
PBDEs are thought to enter the human body via contaminated food, house dust and air, as well as through direct contact with certain consumer products. Also, as they don't fully bind to the products they are used in, they escape into the air and adhere to dust particles. Because people spend more than 80 per cent of their time indoors, indoor dust is a major route of exposure (Environ Sci Technol, 2005; 39: 925-31).
The food we eat is another major source of PBDE exposure. The highest levels are typically found in fish, an integral part of the diet for many people, particularly Europeans. Lower amounts are detected in meat and dairy products (Mol Nutr Food Res, 2007 [Epub ahead of print]; Chemosphere, 2002; 46: 635-40).
Children are especially exposed to these hazardous chemicals. As surveys indicate, while the adult dietary PBDE-intake range is 0.9-1.5 ng/kg/day, nursing infants receive up to 300 ng/kg/day via breast milk (Lancet, 2007; 370: 1813-4).
Exposure to PBDEs in household dust is again more prevalent in younger age groups than in adults because of greater hand-to-mouth contact. It's estimated that toddlers' exposure to the chemicals from household dust could be 100 times higher than that for adults (Lancet, 2007; 370: 1813-4).
Exposure to PBDEs can even occur before birth, as virtually any substance in the mother's body is transported to some extent into the womb via the placenta. Indeed, a Swedish study found a strong correlation between levels of PBDEs in maternal and cord blood, and breast milk samples (Environ Health Perspect, 2003; 111: 1235-41). This is troubling as the fetus-at this critical time of its development-is most vulnerable to toxic insults.
Minimizing the risks
According to the Environmental Working Group, exposure to brominated fire retardants is unavoidable. "Even if these toxic fire retardants were phased out immediately," it says, "our exposures to them would continue through the foods we eat or from the products in our households." Nevertheless, the EWG offers the following tips to parents and concerned consumers:
- Avoid degraded or crumbing foam that might contain fire retardants. Replace or cover couches, chairs and car seats that have exposed foam. Reupholster padded furniture in homes where children or pregnant women live.
- Be careful when removing and replacing the foam padding beneath your carpet. Remove old carpet padding from your home and clean up well afterwards.
- Buy products made with natural fibres (cotton and wool), which are naturally fire-resistant.
- Breastfeed your child. Although breastfed infants are exposed to higher levels of chemicals during the first few years of life, they still have fewer childhood and breast cancers, and other illnesses believed to be linked
to chemical exposures. Research on PCBs, chemicals similar to PBDEs, suggests that breastfeeding may well protect the developing brain or repair subtle deficits induced by prenatal chemical exposures (J Toxicol Clin Toxicol, 2002; 40: 467-75).
- Eat a varied diet that contains less meat and high-fat dairy products.
- Avoid fatty fish, which can be highly contaminated by PBDEs.
- Broil or grill food as much as possible, as this can reduce the amount of PBDEs per serving (Mol Nutr Food Res, 2007 [Epub ahead of print]).