‘Water is life,’ so central to human life, yet over one billion people across the world have no access to safe drinking water. Of late, there has been increasing global attention focused on resolving water quality problems especially in developing countries, as the lack of access to clean water denies the most essential of all rights, the right to life. The latest estimates suggest that around 200 million people, from among 25 nations the world over, are under the dreadful fate of fluorosis. India and China, the two most populous countries of the world, are the worst affected. India is plagued with numerous water quality problems due to prolific contaminants mainly of geogenic origin and fluoride stands first among them. The weathering of primary rocks and leaching of fluoride-containing minerals in soils yield fluoride rich groundwater in India which is generally associated with low calcium content and high bicarbonate ions. The unfettered ground water tapping exacerbates the failure of drinking water so...

Fluoride in Drinking Water: A Review on the Status and Stress Effects

Molecular mechanisms of fluoride toxicity

Polybrominated diphenyl ethers (PBDEs) are a class of flame retardants used in a variety of consumer products. In the past 25 years, PBDEs have become ubiquitous environmental contaminants. They have been detected in soil, air, sediments, birds, marine species, fish, house dust, and human tissues, blood and breast milk. Diet and house dust appear to be the major sources of PBDE exposure in the general population, though occupational exposure can also occur. Levels of PBDEs in human tissues are particularly high in North America, compared to Asian and European countries, and have been increasing in the past 30 years. Concentrations of PBDEs are particularly high in breast milk, resulting in high exposure of infants. In addition, for toddlers, dust has been estimated to account for a large percentage of exposure. PBDEs can also cross the placenta, as they have been detected in fetal blood and liver. Tetra-, penta- and hexaBDEs are most commonly present in human tissues. The current greatest concern for potential adverse effects of PBDEs relates to their developmental neurotoxicity. Pre- or postnatal exposure of mice or rats to various PBDEs has been shown to cause long-lasting changes in spontaneous motor activity, mostly characterized as hyperactivity or decreased habituation, and to disrupt performance in learning and memory tests. While a reduction in circulating thyroid hormone (T4) may contribute to the developmental neurotoxicity of PBDEs, direct effects on the developing brain have also been reported. Among these, PBDEs have been shown to affect signal transduction pathways and to cause oxidative stress. Levels of PBDEs causing developmental neurotoxicity in animals are not much dissimilar from levels found in highly exposed infants and toddlers.

Developmental neurotoxicity of polybrominated diphenyl ether (PBDE) flame retardants

Since the 1970s, an increasing number of regulations have expanded the use of brominated and chlorinated flame retardants. Many of these chemicals are now recognized as global contaminants and are associated with adverse health effects in animals and humans, including endocrine and thyroid disruption, immunotoxicity, reproductive toxicity, cancer, and adverse effects on fetal and child development and neurologic function. Some flame retardants such as polybrominated diphenyl ethers (PBDEs) have been banned or voluntarily phased out by manufacturers because of their environmental persistence and toxicity, only to be replaced by other organohalogens of unknown toxicity. Despite restrictions on further production in some countries, consumer products previously treated with banned retardants are still in use and continue to release toxic chemicals into the environment, and the worldwide use of organohalogen retardants continues to increase. This paper examines major uses and known toxic effects of commonly-used organohalogen flame retardants, replacements for those that have been phased out, their combustion by-products, and their effectiveness at reducing fire hazard. Policy and other solutions to maintain fire safety while reducing toxicity are suggested. The major conclusions are: (1) Flammability regulations can cause greater adverse environmental and health impacts than fire safety benefits. (2) The current options for end-of-life disposal of products treated with organohalogens retardants are problematic. (3) Life-cycle analyses evaluating benefits and risks should consider the health and environmental effects of the chemicals, as well as their fire safety impacts. (4) Most fire deaths and most fire injuries result from inhaling carbon monoxide, irritant gases, and soot. The incorporation of organohalogens can increase the yield of these toxic by-products during combustion. (5) Fire-safe cigarettes, fire-safe candles, child-resistant lighters, sprinklers, and smoke detectors can prevent fires without the potential adverse effects of flame retardant chemicals. (6) Alternatives to organohalogen flame retardant chemicals include using less flammable materials, design changes, and safer chemicals. To date, before evaluating their health and environmental impacts, many flame retardant chemicals have been produced and used, resulting in high levels of human exposure. As a growing literature continues to find adverse impacts from such chemicals, a more systematic approach to their regulation is needed. Before implementing new flammability standards, decision-makers should evaluate the potential fire safety benefit versus the health and environmental impacts of the chemicals, materials, or technologies likely to be used to meet the standard. Reducing the use of toxic or untested flame retardant chemicals in consumer products can protect human and animal health and the global environment without compromising fire safety.

Halogenated flame retardants: do the fire safety benefits justify the risks?

Conclusions: The results support the possibility of an adverse effect of high fluoride exposure on children’s neurodevelopment. Future research should include detailed individual-level information on prenatal exposure, neurobehavioral performance, and covariates for adjustment.

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Developmental fluoride neurotoxicity: a systematic review and meta-analysis

Dose-effect relationship between drinking water fluoride levels and damage to liver and kidney functions in children.

2,2',4,4'-Tetrabromodiphenyl ether (PBDE-47) causes developmental neurotoxicity in animal studies, but the mechanism remains poorly understood. This paper investigates the mechanism by studying the effects of oxidative stress, DNA damage, and apoptosis induced by PBDE-47 in cultured primary rat hippocampal neurons at different PBDE-47-concentrations (0, 2.06, 20.6, and 41.2 microM). The results showed that reactive oxygen species (ROS) level, percentage of apoptosis, malondialdehyde (MDA) content, the glutathione peroxidase (GSH-Px) level and the lactic dehydrogenase (LDH) leakage rate were affected by exposure of cells to 41.2 microM PDBE-47 (P<0.05), but not to the lower concentrations tested (20.6 and 2.06 microM). Reduced glutathione (GSH), superoxide dismutase (SOD), and increased DNA damage (tested by a comet assay) were affected at all concentrations tested in a dose-related manner (P<0.05). These results suggested that PBDE-47 could induce oxidative stress, DNA damage, and apoptosis in primary rat hippocampal neurons. Whether or not this concentration response pattern indicates that ROS leads to DNA damage and/or apoptosis must be confirmed with further experiments.

Aiguo Wang

Papers

Dose-effect relationship between drinking water fluoride levels and damage to liver and kidney functions in children.

PBDE-47-induced oxidative stress, DNA damage and apoptosis in primary cultured rat hippocampal neurons

Effects of fluoride on DNA damage, S-phase cell-cycle arrest and the expression of NF-κB in primary cultured rat hippocampal neurons

Effects of fluoride on the expression of NCAM, oxidative stress, and apoptosis in primary cultured hippocampal neurons

Effects of Fluoride on Lipid Peroxidation, DNA Damage and Apoptosis in Human Embryo Hepatocytes