June 10, 2003
The Honourable Anne McLellan
Minister of Health
0916A Brooke Claxton Building, 16th Floor
Dear Minister McLellan,
RE: Action Needed on PBDEs
As organizations devoted to public health, the health and safety of children, and the environment, we are writing to you today to urge that Canada take decisive and timely action on polybrominated diphenyl ethers (PBDEs), a group of toxic, persistent and bioaccumulative chemicals that are increasing in human tissue and in our environment. We are particularly concerned that these are similar in structure, activity, and persistence to PCBs – still considered hazardous years after banning - and known to be developmental neurotoxicants.
We are facing a rising crisis of lost human potential in Canada. The role of toxic chemicals in the etiologies of neurodevelopmental disorders has been largely ignored, though the evidence from both experimental animal and clinical research from the few neurotoxic chemicals that have been studied to date is compelling. Neurologically-based learning disabilities and related attentional disorders affect an estimated 15% of children. Last year Canada’s National Longitudinal Survey of Children and Youth (NLSCY) reported that the prevalence of behaviour problems in children ranged from 17- 21 %, while another 14-16% of children had low cognitive scores – the index suggests that 28.6 % of Canadian children were “vulnerable” . The consequences of these and other neurological, developmental and behavioural disorders are lifelong, often serious for both the child and his/her family, and costly for society. There is evidence the prevalence of ADHD , learning disabilities and autism are increasing in recent years.
PBDE formulations are produced and used in high volume in North America,
and used as flame retardant additives in the manufacture of
polyurethane foam; added to polymer in the manufacture of computer and TV boards
and housing at levels from 5- 20% (WHO). The EU risk assessment report for
Penta-BDE states that volatilization from the polymer matrix constitutes a
probable inhalation exposure route; breakdown and transformation by combustion
can form brominated dibenzo-p-dioxin and brominated dibenzofurans; and other
recycling practices may have the potential to release these toxicants into the
We have been aware for some time of the warnings from the scientific community about rising levels of the high-volume industrial chemicals - polybrominated diphenylethers (PBDEs) from every medium studied in the North American environment - in water, in fish, in our food, and in breast milk. PBDE levels in trout from the Great Lakes rose from non-detectable in 1975 to 60ng/gm in 1990 to 200 ng/gm in the year 2000 , and varying levels of PBDEs have been found in most commercial foods. These chemicals have been found to be persistent, bioaccumulative, highly lipophilic, developmentally neurotoxic, and disruptive to thyroid systems in experimental studies. The levels of these compounds in human tissue, such as breast milk, have been rising exponentially over the years of their use, especially in North America. A recent study by Petras et al. indicates that California women have levels 3-10 times higher than European women measured during the same period. Similarly a study by Alaee et al. comparing human milk samples from Vancouver, found that between 1992 and 2002 the median values for BDEs in milk have increased about fifteen fold. Levels in breast milk in Vancouver were ten times those of Swedish women – from a mean of 42.8 ng/g lipid weight to a maximum of 281.9 ng/g lipid.
The persistence of chemicals in the environment or in body tissues is a major factor for protracted health effects. The lipophilicity, or affinity to fat, of a chemical dictates its storage in adipose tissue and elimination in milk. The levels of PBDEs in North Americans appear to be doubling every two to five years. A study of PBDE levels in maternal and cord blood found relatively high levels, 15- 580 ng/g lipid in maternal serum and 14- 460 ng/g in fetal samples - far exceeding levels that moved Sweden to ban PBDEs in that country to protect the health and development of its citizens. The highest concentrations can be compared to the prenatal exposures to PCB concentrations (expressed in terms of the fat concentrations in maternal milk) reported by Jacobson and Jacobson as being associated with a 6.2 point deficit in full-scale IQ scores and effects related to memory and attention in the most highly exposed group (1250 ng/g or greater), and poorer word comprehension and overall reading comprehension and several other intellectual deficits in children born to mothers with milk concentrations of polychlorinated biphenyls of at least 1000 ng/g of fat. The authors reported that these PCB concentrations were only very slightly higher than those found in the general population in industrialized nations.
A study by Ericksson et al. linked exposure to tetraBDE and pentaBDE, the most common forms of PBDEs found in human samples, to permanent behavioral aberrations after a single dose on postnatal days 3, 10, or 19. These single exposures during brain development produced dose-related changes in spontaneous behavior in 2-4 month-old animals, increasing with age. In addition, neonatal exposure to PBDE 99 (pentaBDE) also affected learning and memory functions in these animals as adults. This study was replicated by Viberg et al. finding that mice at 6 months of age in both the low and high-dose groups treated on postnatal day 3 exhibited behavioral changes relative to controls.
Both tetra and commercial penta BDEs have been
found in experimental animal studies to reduce T4 in a dose-dependent manner, and to
increase TSH. Thyroid hyperplasia and goiter was also present. There was a lasting
effect on thyroxine production five months after the last dose. Learning and
behavioral effects have been noted from alterations in thyroid in experimental animal
studies, and from clinical studies of the effects of thyroid hormone deficiency
before birth, or beyond. Normal levels of maternal and fetal thyroid hormone are
necessary to initiate and orchestrate many time-sensitive processes to produce
the human brain. It has been known for some time that exposure to PCB
mixtures disrupts thyroid function, and longitudinal studies of children exposed to
PCBs as fetuses have found an association with reading deficits, lower IQ,
and attention at age eleven from exposures that were just at the high end of
the range found in the general population. Many other chemicals and compounds
have anti-thyroid actions, but these have not been studied for their
possible links to neurodevelopmental effects.
Despite their close relationships with PCBs, no dose-response testing to establish a NOEL (no-effect-level) for developmental neurotoxicity has been established for PBDEs. LDAC has urged that developmental neurotoxicity data to protect brain development should be required for priority chemicals for two decades. PBDEs are to be evaluated under the U.S. Voluntary Children’s Chemical Evaluation Program (VCCEP). However we are very concerned about several aspects of this program: the slow pace of first tier toxicity data collection; the fact that DNT testing is included only in the third and last tier of testing; and only if negotiated and triggered by results from the other two tiers. A tiered testing protocol runs counter to the response of the Scientific Advisory Panel to the USEPA’s Office of Pollution Prevention and Toxics Children’s Health Testing Program battery – which recommended that it was appropriate for the proposed battery of tests to be viewed as a single tier of studies. We cannot afford to wait the many years it will take for these data to be obtained, evaluated, and regulatory action taken.
The March 5, 2002 European Union Commission Recommendation regarding further the risk reduction strategies needed for PBDEs following the 1999 decision to ban, states:
“While the formal outcome of the human health risk assessment of the substance is that further information/testing is required, Member States noted the uncertainties regarding the risk characterization for infants exposed to the substance from milk. In particular there was concern about whether the concentration in human breast milk might increase during the time it would take to obtain the information needed to refine the risk characterization and to remove some of the uncertainties. Any risk reduction measures proposed for the substance must take account of the concerns about infants exposed via milk .”
An economic analysis by Muir et al. makes this point: “This analysis suggests that a business-as-usual scenario, where environmental concentrations of brominated flame retardants, such as PBDEs, are allowed to continue their increasing upward trend, especially in human mothers’ milk, has the potential for very large human health and economic costs and consequences. These costs dwarf any defensible estimate of the benefits of continuing to use BFRs. This result, together with our most basic scientific understanding of the physico-chemical properties of these compounds, strongly supports the idea that we do not need these compounds free in the environment, and calls for precautionary action to eliminate the problem.”
PBDEs are not yet on the CEPA Priority Substance List for risk assessment. However under provisions of CEPA, Ministers have authority to take timely action on substances that present a threat to the health of Canadians.
In November 1999, the European Union agreed to take precautionary action and to ban penta-BDE and octa-BDEs in this year, July 2003, and deca-BDE in January 2006. The California Assembly voted May 27th to ban, within five years, two brominated flame retardants found in the breast tissue of women
In conclusion our organizations recommend:
That timely action be taken under the Precautionary Principle –as mandated under CEPA 1999 , to ban the production and use of PBDEs in Canada to mitigate further exposures to the public from the penta, octa, and deca BDEs, as has been done by the European Union.
And in order to better understand and mitigate secondary exposure from lasting levels in the Environment, but not to wait for these data before action is taken:
1. That Health Canada conduct testing to establish a no-observable-effect-level (NOEL) for developmental neurotoxicity for the PBDEs.
2. That risk assessments include assessments of the cumulative neurotoxic and endocrine effects of low level environmental exposures to mixtures of various BDE congeners, PCBs, and dioxins and other dioxin-like chemicals in foods with a similar mode of action.
3. That a NOEL for thyroid hormone disruption be established, with associated neurodevelopmental effects in rodents, preferably mice, are carried out, and these studies should include the use of lower dose levels as well as iodine-deficient animals to better assess the risks to sensitive human populations.
We look forward to your response to these recommendations.
Barbara McElgunn RN
Health Policy Officer, Learning Disabilities Association of Canada
Ann Phillips PhD
South Riverdale Community Health Center
Jan Kasperski RN, MASC, CHE
Executive Director and CEO, Ontario College of Family Physicians
Executive Director, Pollution Probe
Researcher, Canadian Environmental Law Association.
cc: Dr. Kevin Keough
Chief Scientist, Health Canada
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