Shampoo Washes Neurons Down The Drain

An antimicrobial agent found in many shampoos and widely used in industrial applications inhibits the development of neuron structures that are essential for transmitting signals between cells, says a University of Pittsburgh study presented at the Cell Biology 2004 meeting.

Exposure to low levels of methylisothiazolinone (MIT) restricted growth of axons and dendrites of immature rat nerve cells in culture, apparently by disengaging the machinery of a key enzyme that is activated in response to cell-to-cell contact, and may have potentially damaging consequences to a developing nervous system, the researchers report. “Our results thus far suggest there is potential that everyday exposure to the chemical could also be harmful to humans. I would be particularly concerned about occupational exposure in pregnant women and the possibility of risk to the fetus,” said the study’s senior author Elias Aizenman, at the University of Pittsburgh School of Medicine.

As an antimicrobial agent, MIT and related compounds kill harmful bacteria that grow near moisture or water. As such, they often are found in personal care products, as well as in water-cooling systems and at factories that require water for manufacturing. Since learning about MIT, Dr. Aizenman has not found any published neurotoxicity reports, or data in any public documents filed with the Environmental Protection Agency. The first set of studies he and his team published in 2002 in The Journal of Neuroscience involved acute exposure to mature rat neurons. They reported that 10-minute exposure at a high concentration – roughly 100 times the dose used in their current study – was lethal to these cells.

For the current study, the researchers kept immature, developing neurons in a media solution containing low concentrations of MIT for 18 hours. In a standard culture, an immature neuron will in such time develop an axon, the extension from the cell body used for sending signals to other cells, and several dendrites, elaborate projections that receive incoming information. But after exposure to MIT, the cells had few, if any, axons and dendrites.

The researchers plan additional research to further understand the molecular mechanisms underlying MIT’s neurotoxic effect on cells, as well as studies involving whole animals. “This chemical is being used more and more extensively, yet there have been no neurotoxicity studies in humans to indicate what kind and at what level exposure is safe. I realize it’s a big leap to suggest there may be a parallel between environmental exposure and the noticeably higher rates of diagnosed childhood developmental disabilities, but I would caution that based on our data, there very well could be neurodevelopmental consequences from MIT,” concluded Dr. Aizenman.

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