Monday, January 25, 2010

Yankee Swap: tritium contaminated water anyone?

First published in the Montague Reporter

First we hear about tens of thousands of picocuries* in the groundwater beneath Vermont Yankee Nuclear Power plant, next it’s over one hundred gallons of water contaminated with over 2 million picocuries in some sort of concrete trench. Oops. Besides sloppy practices, lax monitoring, shoddy construction, and obfuscation (what underground pipes?) what do these numbers mean? Should we worry about all that tritium? And what the heck is a picocurie anyway?

Tritium is a radioactive isotope of the element hydrogen. What sets apart the radioactive elements from the non-radioactive is their lack of stability. They can disintegrate spontaneously, sometimes changing into other elements over time. Uranium, for example, decays into lead (although it may take billions of years,) while it takes roughly a decade for tritium to decay into helium.

The difference between a radioactive element and a plain old element depends upon what’s in the nucleus. The nucleus of any atom consists of protons (positive elements), neutrons (neutral elements) and electrons (negative elements). While the chemical properties of an element mostly depend on the number of protons in the nucleus, the radioactive properties are determined by the number of neutrons and the balance amongst the protons, neutrons and electrons. An element like hydrogen and its radioactive twin, tritium, have the same number of protons (and so, the same chemical properties), but instead of a single neutron, tritium has three neutrons. Tritium occurs naturally in small amounts, in addition to being produced by man either purposefully for research and consumer products (ever wonder about that glowing watch dial or that luminous EXIT sign?), or as a by-product of the nuclear industry.

Because tritium is chemically similar to hydrogen it can and does take the place of hydrogen – when this happens in water tritiated water or radioactive water is formed.

The radiation released by tritium is referred to as a beta particle. Beta particles, or electrons, are a form of ionizing radiation capable stripping electrons from other atoms, causing a sort of chain reaction of destabilization, and breaking chemical bonds. Although the beta particles released by tritium are low energy, incapable of penetrating through barriers such as skin (unlike some other forms of radiation), should tritium enter the body through inhalation or umm…water, those emitted particles would then have full access to vulnerable tissues and molecules.

Tritiated water is particularly insidious. The tritiated water lurking below Vermont Yankee for example, could be absorbed by the root systems of nearby plants, or imbibed by unsuspecting animals. Once consumed, distributes rapidly throughout the body of plant or animal. Additionally, ingestion of tritiated water, can lead to incorporation of tritium into organic materials like DNA, proteins and amino acids. Only, unlike hydrogen, tritium will eventually decay, leaving behind an atom of helium and releasing a beta particle with enough energy to break nearby chemical bonds.

In the body, the making and breaking of the chemical bonds between atoms is a highly coordinated process, normal and essential to life. The “unscheduled” breaking of chemical bonds can cause permanent cell damage, damage to the cell’s DNA or cell death.

The human genome is contained within the DNA of our 46 chromosomes located in a cell’s nucleus. Replication of these chromosomes during cell division is a critical process, requiring a number of complex biochemical interactions including copying and construction of identical chromosomal pairs that are then split off into the newly divided cell. Because integrity of the genetic material is essential to life, not only are there biochemical systems involved in maintaining chromosomes during division, but there are also a number of mechanisms by which errors may be repaired.

Say a few molecules of tritium enter the cell and cozy up to nuclear DNA. At some point in their unstable life-time they will disintegrate, releasing their energized electrons. Should the cells’ chromosomes be in their pathway, the transfer of energy from electron to chromosome may be enough to break off a bit of chromosome. Sometimes, depending on conditions within the cell and location of the break, the broken pieces may rejoin the chromosome, leaving little or no evidence of damage; other times a broken piece remains separate, becoming a chromosomal deletion; or both the deleted piece and the damaged chromosome will be copied as if nothing happened, only it will be altered. Or, instead of direct interference with DNA, emitted electrons may interact with other molecules such as oxygen, causing “indirect” damage by creating highly reactive oxygen radicals.

Since DNA tends to be a target of ionizing radiation, tissues made up of cells that are rapidly dividing – such as blood forming organs constantly churning out cells – tend to be far more sensitive to radiation damage than say, brain cells. Similarly, embryos and fetal tissues are more susceptible to radiation damage than adult tissues.

There is some good news amidst all this havoc and destruction. That is, most if not all cells have some capacity for DNA repair. These include an array of enzymes and proteins that find and correct damaged DNA in addition to a number of antioxidants capable of disarming those reactive oxygen radicals. The presence of such repair mechanisms have led some to speculate that exposures to very low amounts of radiation may be a good thing, “priming” these repair systems and leading to greater protection with low levels of exposure – a phenomenon referred to as hormesis. However, a National Academy of Science report on The Health Effects of Low Level Ionizing Radiation, published in 2007, found no available evidence of radiation induced hormesis in mammals, and concluded that any single track of ionizing radiation (for example by a single ejected electron in the case of tritium) has the potential to cause cellular damage.

And, despite the capacity for repair, sometimes the system is overwhelmed, or sometimes the repair itself introduces a new error (think sloppy auto mechanic.) At this point the genetic damage has the potential to become permanent, or “fixed.” Permanent damage to DNA can result in the eventual development of cancerous cells, or a defect in an exposed fetus or as a mutation passed on to the next generation. While the evidence for carcinogenicity in human populations is strong for some radioactive isotopes like strontium-90, plutonium and radium, the health effects of tritium, a weak beta emitter are less clear.

Which brings us to concentration. How much is too much? What does it mean that the groundwater has over 200,000 picocuries of tritium per liter of water, or that there are “troughs” with over 2 million picocuries per liter? A curie (named in honor of radiation pioneers Pierre and Marie Curie) is a quantity of radionuclide in which there are 37 billion disintegrations a second. That’s a lot of disintegration and in the case of tritium would be a lot of beta particles whizzing about. But the amounts drawn from the ground water were measured in picocuries per liter – or one millionth of a millionth of a curie. So, every second, until all the tritium has disintegrated to helium (the half-life for tritium is 12.5 years) there would be roughly 7,400 electrons winging about in a liter of Vermont Yankee groundwater.

As a result of the current hypothesis that exposure to any amount of ionizing radiation carries with it some risk of cancer, the U.S. EPA’s Maximum Contaminant Level Goal for all radionuclides in drinking water, a goal which aims for “zero-risk” to public health, is zero picocuries per liter. Unfortunately, achieving “zero risk” is not only wishful thinking but currently unenforceable and, because there is some naturally occurring tritium impracticable. Instead, EPA has developed Maximum Contaminant Levels (MCL) for drinking water. While the MCLs are enforceable, they are calculated considering best available technology and economic feasibility. For tritium, the derived** MCL is 20,000 picocuries per liter, while the derived MCL for strontium 90, a more powerful beta emitter associated with bone cancer and leukemia, is 8 picocuries.

Here’s the thing. Right now we’re talking two wells and a trench (where, incidentally, a small amount of radioactive cobalt has turned up as well.) While current concentrations in the ground water (the trench is another story) may not present an immediate health risk, who knows what a more comprehensive analysis - currently underway - might reveal?

*As of Feb 10, 2010 over 2 million pCi was measured in test wells around the plant.

For more see: http://www.rutlandherald.com/article/20100205/NEWS04/2050349/1003/NEWS02

**The MCL for beta emitters is based on a dose of 4mrem/year to the total body and assumes ingestion of 2L a day – the picocurie concentrations are derived for each specific beta emitting isotope depending on their strength. Over the years, there has been discussing of using different calculations for tritium that would dramatically reduce the MCL.

Thursday, January 07, 2010

Evolution of the Toxic Response: In the beginning there were chemicals....

The following is what I intend to be the first in a series of essays on the Evolution of the Toxic Response – a topic which piqued my interest after what could either be called a disastrous flirtation with the publishing world, or an invaluable lesson in pursuing your passion. The disaster was allowing myself to be duped into thinking the content and style of this blog would actually make an engaging book (wrong,) the passion was in realizing that writing primarily about toxicants of interest to the consumer (and in the style that would be most appealing to mass market publishers) has caused me to lose my way as a toxicologist and a scientist.

There is no doubt that some toxicants are, well, toxic. But there is always the question of exposure, dose, and potency. Topics often lost in breezy articles meant to engage a reader – rather than inform about the complexities not only of toxicology but science in general. Unfortunately the publishing world seems to have no confidence in its mass readership. Readers are attracted by alarmism, so hype it up. They’ll doze if there is too much science, so keep it simple. They just want to be told what’s best for them, so just tell them. But after whipping off one light and fluffy page after another about dangerous toxicants hidden away our homes and gardens (along with a few good toxins in our ‘fridges) all in preparation for my failed Book Proposal, a request by the local news paper to write about bisphenol A or BPA resulted in a nearly visceral reaction at the thought of writing yet one more article for consumer consumption about chemicals consumed by consumers.

But after the storm, and the lull where I could barely bring myself to write another word about chemicals, came the passion. I was attracted to toxicology because I was fascinated by chemicals that screwed up the normal processes of life. But that was back in a time long long ago when toxicology meant PCBs, lead, mercury, dioxin, and assorted pesticides. These were obvious chemicals in concentrations that couldn’t hide within the peaks and valleys of the chemists’ printout. But science has come a long way since then. Now, we know far more about the minute amounts of a myriad of chemicals contaminating our water, air and food than we do about the way they might interact with our lung cells, or livers, or brains. We know that our bodies sequester the smallest amounts of these chemicals in our bones, brains, and fat cells.

Many of these chemicals will stick around on earth at least for our lifetimes, and those of our children. What will be the consequences of these chemical exposures – if any? What do we really mean when we say that these chemicals are toxic? At what point does a contaminant become a toxicant? Given all the synthetic and naturally occurring chemicals entering and exiting our bodies with virtually every breath – some of which by now are unavoidable, others we might choose to inhale and ingest, and still others have been with us for eons, how can I, as toxicologist better understand the collective impact?

This was when I remembered I’ve inherited more than my big ears, hazel eyes and dry skin from my ancestors. I’ve inherited a whole system of toxic defense mechanisms, because really, well before the first animal ventured onto land, well before the first single-celled organism respired oxygen, life on earth relied upon chemical defense mechanisms of one sort or another.

And to some extent, we owe our lives -- as do all life forms -- from bacteria, to plants and all animals -- to these toxic detoxification processes.

Yet are they enough to protect life from the steady rain of natural and synthetic chemicals experienced by life on earth today?

That is the question I intend to explore in this upcoming series of essays, so stay tuned if you dare.

Also if you are a toxicologist, chemist, geologist etc. and would like to discuss the topic further please don't hesitate to contact me at emonosson@verizon.net I'd love to begin a virtual journal group on this topic.