Twenty-Three Children Dead from Pesticide Poisoning in India

July 18th, 2013

Once again, we see schoolchildren victimized by the appearance of pesticide contamination in or around schools. This time, it was attributed to the luncheon served at a school in India as per this Reuter’s brief.

I’ve already pointed out the results of pesticide poisoning as it affects schools in New York City (my own law suit), an Afghani school for girls and now this incident. The author of this article, Ms. Annie Benerji, refers us to an important medical journal report published in 2008. There, a Dr. Eddleston (et. al.), tell us the huge numbers of individuals dying annually from ‘intentional’ poisoning in Asia alone. Knowing how repeated contact with organophosphate pesticides and other related poisons can lead to progressive damage from new contacts, I wrote the researcher as follows:

Dear Professor Eddleston,

Your name came up as I was researching this article from Reuters about the recent deaths of a large number of children from the ingestion of a school lunch, allegedly prepared with oils stored in a contaminated container. Referring back to your Lancet article of 2008, I wondered if you might convey a different message to the medical center in India that successfully identified the agent, if not the precise source, in this mass poisoning.

Your research concentrated upon ‘intentional’ loss of life from pesticides, i.e. suicide using these readily available poisons. Might these physicians identify ‘at risk’ individuals by taking baselines of blood cholinesterase levels (plasma and RBC) from people in the community at random? This might identify ongoing exposures currently unknown, or unreported, in the area. Since we know that schoolchildren in Afghanistan have fallen victim to OP fumes in past years, requiring evacuations of such programs, it is conceivable that these deaths were the byproduct of children already suffering from some degree of cholinesterase inhibition. By ingesting this food, it might easily push them over the edge into cardiac and respiratory arrest while others, not recently exposed to OP products, might fight off the sudden poisoning more effectively. Of course, we know that levels of PON I also affect the ability of individuals to combat this type of poisoning from the work of Clement Furlong. While this is variable in the population, repeated exposure may also deplete stores of this important physiological defense. Research appears more limited of this factor ‘in the field’, so to speak.

As a past victim of OP poisoning, I am aware of these matters and feel it requires some form of pro-active medical intervention. This would relieve the populations of vulnerable individuals in India and elsewhere (including the USA) from over-exposure.

Thank you for your most important efforts in this difficult area of science.

Barbara Rubin

Categories: Articles, commentary, Lancet, Letters

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