Archive for the ‘Children’ Category

Coexposure of neonatal mice to a flame retardant PBDE 99 (2,2′,4,4′,5-pentabromodiphenyl ether) and methyl mercury enhances developmental neurotoxic defects

Wednesday, January 28th, 2009

http://www.ncbi.nlm.nih.gov/pubmed/17982161?dopt=AbstractPlus

Coexposure of neonatal mice to a flame retardant PBDE 99 (2,2′,4,4′,5-pentabromodiphenyl ether) and methyl mercury enhances developmental neurotoxic defects

Fischer C, Fredriksson A, Eriksson P.
Department of Environmental Toxicology, Uppsala University, Norbyvägen 18A, S-752 36 Uppsala, Sweden.

Toxicol Sci. 2008 Feb;101(2):275-85. Epub 2007 Nov 2.

Epidemiological studies indicate that exposure to environmental pollutants during early human development can have deleterious effects on cognitive development. The interaction between environmental pollutants is suggested as one reason for the observed defective neurological development in children from the Faeroe Islands as compared to children from the Seychelles. We have previously seen in mice that polychlorinated biphenyls (PCBs) can interact together with methyl mercury (MeHg), as well as PCB together with polybrominated diphenyl ether (PBDE 99) to exacerbate developmental neurotoxic effects when present during a critical period of neonatal brain development. PBDEs are a new class of global environmental contaminants. The present study shows that neonatal coexposure to PBDE 99 (0.8 mg/kg body weight) and MeHg (0.4 or 4.0 mg/kg body weight) can exacerbate developmental neurotoxic effects. These effects are manifested as disrupted spontaneous behavior, reduced habituation, and impaired learning/memory abilities. This is seen in the low dose range, where the sole compounds do no give rise to developmental neurotoxic effects. The effects seen are more than just additive. Furthermore, a significant effect of interaction was seen on the cholinergic nicotinic receptors in the cerebral cortex and hippocampus. This suggests that a mechanism for the observed cognitive defects is via the cholinergic system. Furthermore, PBDE can interact with MeHg causing developmental neurotoxic effects similar to those we previously have observed between PCB 153 + MeHg and PCB 52 + PBDE 99. This is of vital importance, as the levels of PBDEs are increasing in mother’s milk and in the environment generally.

PMID: 17982161 [PubMed - indexed for MEDLINE]

The legal failure to prevent subclinical developmental toxicity.

Monday, January 26th, 2009

My experience suggests that clinical effects as well as subclinical ones are not being prevented. The rise in autism is a case in point. –Dr. Larry Plumlee

http://www.ncbi.nlm.nih.gov/pubmed/18226082?dopt=AbstractPlus
Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):267-73. Links

The legal failure to prevent subclinical developmental toxicity.

Cranor C.

Department of Philosophy, University of California, Riverside, CA 92521, USA. carl.cranor@ucr.edu

Legal systems appear to function poorly to identify and prevent subclinical developmental toxic effects in children that can lead to long-term harm. In the USA, the vast majority of substances enter commerce without any legally required testing (under so-called ‘post-market’ laws). In 1984, less than 20% of all substances had been subject to pre-market testing and there has been little change since. Once substances are suspected of contributing to harm, an administration agency has the burden to show risks or harms and their causes, an increasingly difficult demonstration. Post-market laws tend to produce no data prior to exposures and any protections result after some harm may have occurred. Pre-market screening laws such as the US Toxic Substances Control Act provide little data or protection. Pre-market testing and approval laws, analogous to US drug and pesticide laws, offer better approaches for identifying and eliminating toxicants before they result in harm, but do not apply to many products and rarely include concerns for developmental toxicity. The Registration, Evaluation, Authorization and Restriction of Chemicals legislation in the European Union has greater promise for the identification of new or existing toxicants. However, the potential for serious, subtle subclinical developmental effects provides reasons to pursue a more precautionary approach to identifying potential toxicants and forestalling harms. This paper sketches a more robust precautionary law and a more substantial departure from existing laws that would treat chemical invasions as trespasses. The scientific community can assist legal efforts by credibly publicizing the seriousness of subclinical developmental effects.

PMID: 18226082 [PubMed - in process]