Since part III of this series was devoted to the issue of non-ionizing radiation, largely derived from wireless devices such as cell phones, and its impact on health, I have not explored published information on the March 2011 disaster at the Fukushima Daiichi power plant since June. Interestingly, I feel that it was a good idea to wait this long to write an update since time is one of the best antidotes for the type of fear and panic that was so prevalent in this country right after the power plant disaster in March. As you may recall, many were predicting a massive and immediate influx of radioactive iodine (I131) into this country, leading to an epidemic of thyroid cancer and other thyroid-related diseases. These predictions then led to a literal stampede to every vendor of potassium iodide in the country, including Moss Nutrition, by masses of worried people who seemed to be convinced that immediate ingestion of sometimes substantial amounts of potassium iodide would protect them not only from I131-related thyroid dysfunction but from the adverse effects of every other radioactive isotope that was released into the environment by the disaster.
While we cannot say that, given the substantial time required for the development of I131-related thyroid dysfunction, all predictions of adverse effects in this country are incorrect, we can certainly say that, now that almost nine months have elapsed since the disaster, the many predictions of immediate apocalypse were somewhat exaggerated.
Ironically, given that potassium iodide supplementation is effective only with I131, it is interesting to note that current reports coming out of Japan point out that radioactive cesium is now the major environmental concern, as exemplified by the many reports during the first week of December about cesium134 and cesium137 contamination in Japanese baby formula. In addition, I found online a report from the November 18, 2011 edition of The Japan Times that states the following about radioactive cesium contamination in Japan:
“Radioactive cesium from the crippled Fukushima No. 1 nuclear plant probably reached as far as Hokkaido, Shikoku and the Chugoku region in the west, according to a recent simulation by an international research team based on data after March 20, a week after the hydrogen explosions.
Large areas of eastern and northeastern Japan were probably contaminated, with concentrations of cesium-137 exceeding 1,000 becquerels per kilogram of soil in some places, says the study, which was posted Monday on the website of the National Academy of Sciences.”
For information on units of measurement for ionizing radiation, including the becquerel, please see part I of this series.
Why is there more concern about radioactive cesium compared with radioactive iodine in Japan right now? In the recently published paper “Impacts of the Fukushima nuclear power plants on marine radioactivity” by Buesseler et al (1) the authors answer this question in two ways. The first answer relates to the specific nature of the explosion:
“Unlike Chernobyl, there was no large explosive release of core reactor material, so most of the isotopes reported to have spread thus far via atmospheric fallout are primarily the radioactive gases plus fission products such as cesium, which are volatilized at the high temperatures in the reactor core, or during explosions and fires.”
The second answer relates to the differences in half-life between I131 and radioactive cesium:
“There was considerable attention given to 131I releases due to its relatively high activities and tendency to accumulate in the human thyroid if ingested via land-based food supply or if bioconcentrated by seaweeds and consumed as part of the Japanese diet. We can see that the ocean release ratio of 131I/134Cs must have been relatively constant, with the highest measured activity ratios near 20-30 on March 22 followed by a predictable decrease due to the radioactive decay of 131I with its 8 day half-life.”
Of course, I realize that, given the health concerns relating to Cs137 exposure, what I have just described is not so much a comforting statement as it is a description of a classic “frying pan into the fire” scenario. Nevertheless, I feel it is important to state because it emphasizes a key clinical reality: Reflexive mass consumption of potassium iodide, driven by fear and panic, can yield results that are much lower than anticipated in terms of preventing radiation-induced dysfunction when non-iodine based isotopes are involved. Furthermore, as I will demonstrate in the next installment, the potential risks of reflexive mass consumption of potassium iodide, which may induce significant side effects, are potentially much higher than anticipated. In contrast, by examining the threat in a more detached logical manner, I feel we can more readily see that potassium iodide, while helpful, is far from a panacea for all forms of radiation. Furthermore, by “checking the fear and panic at the door,” so to speak, I feel it is easier to fully appreciate the many studies I will be reviewing in subsequent installments in this series on antioxidants that can assist in protecting us from damaging effects relating to several different radioactive isotopes, beyond I131.
Now that, hopefully, I have established a firm basis for suggesting that the current threat of I131 from the Fukushima Daiichi disaster is not nearly as great as what was being suggested by the immediate panic in this country and the stampede for potassium iodide that followed soon after, I would like to explore in detail research on I131contamination of the environment from the one nuclear power plant disaster that truly did create an epidemic of I131-related illness, Chernobyl. In addition, I would like to explore research on the ways potassium iodide mitigated risk in this instance. Finally, I will review a paper that explores the physiology of potassium iodide supplementation when used to protect against I131-related illness caused by nuclear power plant accidents.
THYROID CANCER AND I131: THE CHERNOBYL EXPERIENCE
As I have been suggesting, fear and panic most often distort rational thought processes in a way that tends to over simplify. In the instance of the Fukushima Daiichi power plant disaster, fear and panic led many to believe that I131-related thyroid sickness could inevitably be incurred by almost anyone around the world, no matter what the level of exposure, and ingestion of potassium iodide would protect everyone without risk, no matter what the dose. As you will see in the papers I am about to present, risk of thyroid disease from I131 exposure is not exclusively dependent on the level of I131 exposure and the level of potassium iodide ingested. In contrast, other factors do come into play that can significantly modify risk, one of which is so simple to implement that it probably falls into the classification of common sense.
With that introduction in mind, consider the paper “Risk of thyroid cancer after exposure to 131I in childhood,” by Cardis et al (2). To begin this paper, the authors introduce the scenario and the nature of their study:
“After the Chernobyl nuclear power plant accident in April 1986, a large increase in the incidence of childhood thyroid cancer was reported in contaminated areas. Most of the radiation exposure to the thyroid was from iodine isotopes, especially 131I. We carried out a population-based case-control study of thyroid cancer in Belarus and the Russian Federation to evaluate the risk of thyroid cancer after exposure to radioactive iodine in childhood and to investigate environmental and host factors that may modify this risk.”
Before continuing, please note again what was pointed out above. The nature of the Fukushima Daiichi disaster was completely different than the Chernobyl disaster in terms of I131 release. In turn, there is every reason to believe that thyroid cancer rates related to the Fukushima Daiichi disaster should be less that what you will see in this review of the Cardis et al (2) paper, irrespective of the modifying environmental and host factors.
Next, the authors go into more detail on the increase in thyroid cancer that occurred as a consequence of the Chernobyl disaster:
“A very large increase in the incidence of thyroid cancer in young people was observed as early as 5 years after the accident in Belarus and slightly later in the Ukraine and the Russian Federation.”
“An increased incidence of thyroid cancer continues to be observed in this population as it ages into adolescence and young adulthood. The evidence that this increase is related to the fallout of radioactive iodine from the Chernobyl accident is compelling.”
However, as I suggested, there may have been another factor that modified risk that is so simple it is actually common sense in nature. Were any of the patients incurring thyroid cancer, due to the effects of the Chernobyl accident, deficient in iodine at the time of the explosion?:
“Questions remain, however, concerning the magnitude of the risk of thyroid cancer associated with these exposures and the role of iodine deficiency, which was present in most of the affected areas at the time of the accident and which has been postulated as a possible modifier of radiation-related thyroid cancer risk.”
To address these issues, Cardis et al (2) evaluated the following groups of people:
“We present risk estimates of thyroid cancer associated with exposure to 131I that are based on 276 case patients and 1300 control subjects who resided in the Gomel and Mogilev administrative regions (i.e., oblasts) of Belarus or the Tula, Orel, Kaluga, and Bryansk administrative regions of the Russian Federation and were aged younger than 15 years at the time of the Chernobyl accident. The case patients were diagnosed with histologically verified thyroid carcinoma between January 1, 1992 [to avoid overlap with a previous case-control study in Belarus], and December 31, 1998, and underwent surgery in Belarus or the Russian Federation.”
Specifically, what were the radiation doses received by the thyroid cancer patients? Consider the following, where the unit of measurement is the gray (Gy), which is a measurement of absorbed dose (For more information on units of radiation measurement, please see Part I of this series):
“The distribution of thyroid radiation doses was highly skewed for all subjects. The median radiation dose from all radiation types was estimated to be 365 mGy…in Belarus and 40 mGy…in the Russian Federation. The highest doses were about 10.2 Gy in Belarus and 5.3 Gy in the Russian Federation. Most of the dose was from 131I: The median dose from 131I in Belarus was 356 mGy and in the Russian Federation was 39 mGy…”
Next, Cardis et al (2) discuss doses specific to the thyroid gland:
“Individual estimated thyroid doses from external exposure ranged from close to 0 to 98 mGy…and from internal exposure from cesium ingestion up to 42 mGy…The total dose to the thyroid decreased with increasing age at exposure: the median doses were 400, 365, 124, and 43 mGy respectively, in the age groups of younger than 2, 2-4, 5-9, and 10-14 years.”
What were the findings from this study? First, as you might expect, there was a strong relationship between dose level and thyroid cancer incidence:
“A very strong dose-response relationship was observed in this study between radiation dose to the thyroid received in childhood and the risk of a subsequent thyroid cancer. This relation appears to be mainly related to exposure to 131I.”
However, there was another very important variable that impacted on thyroid cancer incidence that, as I have been suggesting, falls into the common sense category:
“Our results also indicate that iodine deficiency increases the risk of 131I-related cancer. Because no reliable population indicators of iodine-deficiency status at the time of the Chernobyl accident were available for all of the areas under study, soil iodine concentration in settlements of residence at the time of the Chernobyl accident was used as a surrogate marker for iodine status of study subjects.”
Did supplementation of potassium iodide play a positive role in reducing the risk of thyroid cancer? As you might expect, it did:
“Our findings also indicate that use of a dietary iodine supplement containing potassium iodide can reduce the risk of 131I-related thyroid cancer.”
Next, the authors go into more detail on the value of potassium iodide supplementation with this study group:
“Potassium iodide (which was administered to evacuated children in the days after the accident and continued to be given to some school children in the following years) alone, however, appears to reduce the risk of 131I-related thyroid cancer by a factor of approximately 3.”
Before continuing, please note again in this quote that benefit from potassium iodide supplementation in terms of reducing risk of I131-related thyroid cancer development was not only related to immediate supplementation, which, as I will show in my review of the paper that follows, is conventional wisdom. In contrast, potassium iodide supplementation conferred benefit even years after exposure.
The next quote provides more information on why potassium iodide supplementation might provide additional benefit in terms of preventing radiation-induced thyroid cancer in iodine deficient situations:
There are two mechanisms through which dietary iodine supplementation could be related to the incidence of thyroid cancer after exposure to radioiodines. First, stable iodine given shortly before, during, or immediately after exposure reduces the uptake of radioactive iodine by the thyroid and, therefore, reduces the radiation dose to the thyroid. However…no widespread systemic iodine administration occurred in the regions under study. Second, long-term dietary iodine supplementation reduces the size of the thyroid in iodine-deficient areas, and a reduction of thyroid growth, particularly in children, would be expected to be associated with reduced incidence of cancer.”
With these findings in mind, Cardis et al (2) conclude the following:
“Both iodine deficiency and iodine supplementation appear to be important and independent modifiers of the risk of thyroid cancer after exposure to 131I in childhood.”
Of course, while those of us in the clinical nutrition community might think a relationship between I131-induced thyroid cancer and iodine deficiency is common sense and a statement of the obvious, many others, as indicated by the editorial by John Boice, Jr (3) entitled “Radiation-induced thyroid cancer – What’s new?” that accompanied the Cardis et al study (2), never considered that this issue might be crucial. Boice, Jr. (3) begins his editorial by stating:
“After 50 years of research, it was known that the thyroid gland of children, but not adults, was especially sensitive to the carcinogenic action of ionizing radiation, that a straight line adequately represented the relationship between dose of radiation and effect…”
However, the findings from the Cardis et al (2) study introduced another variable that, as I suggested, had not been considered:
“The findings from Cardis et al., however, newly suggest that diets deficient in stable iodine potentiate the risk of radiation-induced thyroid cancer and that continued use of dietary supplements containing potassium iodide substantially reduces the risk of radiation-induced thyroid cancer, even if taken many months or years after the exposure occurred.”
The next set of quotes from the Boice, Jr (3) editorial provide much more detail as to why dietary deficiency of iodine could play a major role in creating increased susceptibility to thyroid cancer development after I131 exposure:
“Conceivably, the elevated radiation risk reflects an interaction with a dysfunctional thyroid gland…”
I feel this quote is particularly significant because it highlights a key foundational concept of functional medicine; that illness occurs not just as a function of being exposed to stressful and/or harmful environmental stimuli but also as a function of host resistance. As I mentioned, while the idea of this relationship is old news to us, it appears, based on the Boice, Jr. (3) commentary, that the radiation-induced thyroid cancer research community has not considered it previously.
The next quote I would like to present provides more detail on why iodine deficiency increases the risk of I131-induced thyroid cancer:
“The thyroid glands of children living in areas of iodine deficiency are also more active and undergo more cellular proliferation and growth than in areas of iodine sufficiency, and it may be that this enhanced cellular activity is related to the enhanced risk observed. Thus, the growing thyroid glands of children coupled with an abnormal growth potential related to iodine deficiency may enhance the expression of cellular damage induced by radiation. It is then noteworthy that children who may have had normal functioning thyroid glands because of residing in the areas of highest iodine soil content and who subsequently took potassium iodide supplements were not at a statistically significantly increased risk of developing thyroid cancer after radiation exposures.”
Next, Boice, Jr. (3) comments on the idea that potassium iodide supplementation conferred benefit in terms of thyroid cancer prevention even years after initial I131 exposure, which goes against conventional thinking:
“It is somewhat remarkable that potassium iodide administered months after exposure would reduce risk at all because the radioactive iodines would have already been absorbed and because there would be no blockage in uptake that would have reduced thyroid dose. Yet a threefold reduction in risk was observed in children given potassium iodide as a dietary supplement compared with those without such an administration. The authors speculate that the continued administration of this potassium iodide supplement reduced the size of the thyroid gland in these areas of iodine deficiency and that this reduction in cellular proliferation resulted in a reduced thyroid cancer risk.”
Why has it traditionally been assumed that only immediate ingestion of potassium iodide supplements can provide protection against I131-induced thyroid cancer? One reason may be that previous research has been conducted on survivors from atomic bomb exposure which, as I have been suggesting, is very different from the type of radiation exposure that occurs with reactor accidents where much, if not most of the exposure is comparatively long-term and occurs via ingestion of contaminated food and drink. Boice, Jr. (3) states:
“Studies of other populations exposed to fallout from weapons testing in the South Pacific could not evaluate an independent effect for 131I because the contributions of the other radioactive iodines and of external radiation were substantial.”
Interestingly, another example of why data from atomic bomb explosions cannot be extrapolated to reactor accidents in terms of thyroid cancer incidence can be seen in the following quote from the Boice, Jr. (3) editorial:
“Studies of radioactive fallout from the Nevada test site indicated a lower contribution of the shorter-lived radioactive iodines, and the risk of thyroid cancer was not statistically significantly increased.”
AUTOIMMUNE THYROID DYSFUNCTION AND I131: THE CHERNOBYL EXPERIENCE
As we all know, today’s world of health care tends to think in “all or none” terms. Therefore, if no thyroid cancer occurs with I131 exposure, we are “home free.” However, as we also all know and, as is demonstrated in the study I am about to review, there are many “shades of gray” to consider when dealing with chronic illness. Therefore, even if we see no clinically detectable disease, we know that dysfunction can still exist that can be ascertained via laboratory testing. In “Thyroid autoantibodies and thyroid function in subjects exposed to Chernobyl fallout during childhood: Evidence for a transient radiation-induced elevation of serum thyroid antibodies with an increase in thyroid autoimmune disease” by Agate et al (4), this functional medicine aspect of thyroid exposure to I131 is considered. To introduce their paper, the authors state the following:
“Besides thyroid carcinoma, it has been suggested that radiation exposure from the Chernobyl accident might also be responsible for an increased incidence of other thyroid diseases, particularly autoimmune thyroid disease (AITD). In keeping with this notion, some years ago we showed a significant increase of serum antithyroperoxidase antibody (TPOAb) prevalence in a cohort of Belarusian children and adolescents exposed to Chernobyl fallout, but not in an unexposed control group.”
To further explore this issue, the following study was conducted:
“We measured the antithyroglobulin (TgAbs) and antithyroperoxidase (TPO-Abs) antibodies and TSH in 1433 sera collected between 1999 and 2001 from 13- to 17-yr-old adolescents born between January 1982 and October 1986 in paired contaminated and noncontaminated villages of Belarus, Ukraine, and Russia. A total of 1441 sera was collected from age- and sex-matched controls living in Denmark and Sardinia (Italy). Free T4 and free T3 were measured when TSH was abnormal.”
What were the findings from this study? The authors state:
“A significantly higher prevalence of TPOAb was found in radiation-exposed Belarusian subjects 13-15 yr after the Chernobyl accident. This finding confirms, although at a lower level of significance…the results of our previous study performed in 1998 in a cohort or radiation-exposed Belarusian children.”
As suggested in the previously discussed paper, could iodine deficiency have played a role, in addition to I131exposure, in creating the higher prevalence of TPOAb reported in the above quote? Agate et al (4) state:
“Iodine deficiency as a possible environmental factor was not specifically addressed in this study. However, it has been previously demonstrated that the risk of post-Chernobyl radiation-related cancer was three times higher in iodine-deficient areas than elsewhere, and we cannot exclude a favoring role of iodine deficiency in the development of a thyroid autoimmune phenomenon.”
With the above in mind, the authors conclude:
“In conclusion, the present study indicates that 13-15 yr after the Chernobyl nuclear accident, the prevalence of TPOAb in Belarusian adolescents exposed during childhood to radioactive fallout is still increased when compared with that of unexposed subjects, but the difference is remarkably less evident that that found in a contaminated Belarusian village 6-8 yr after the accident. No clear radiation effect on thyroid autoantibody prevalence is found in Ukraine and Russia, where the estimated radiation exposure was lower than in Belarus. This suggests that the thyroid autoimmune reaction elicited by radiation was transient with no effect on thyroid function after 13-15 yr. However, because it was shown that autoimmune hypothyroidism can naturally occur over decades, we cannot exclude that thyroid dysfunctions related to radiation exposure may develop in a later period.”
IS THYROID DISEASE INDUCED BY I131 AN IODINE DEFICIENCY DISORDER? A HYPOTHESIS
Of course, the short answer to this question is no. There is no question, as noted in the above studies, that I131exposure can act independently to create thyroid disease. However, can any environmental factor or intervention reduce the risk of incurring I131-related thyroid disease besides ingestion of large doses of potassium iodide, as is commonly believed by both the general population and the medical and scientific community? As the papers discussed above strongly suggest, the answer to this question is an emphatic “Yes.” There is a very good chance, particularly in areas where exposure to I131 from nuclear power plant accidents is relatively low, such as what appears to have happened in the United States after the Fukushima Daiichi power plant accident, that risk of subsequent thyroid disease, even in highly susceptible populations such as children, can be substantially reduced by corrections of iodine deficiency either by improvements in diet and/or modest levels of iodine supplementation. Of course, it is certainly true that certain levels of I131 exposure create a high enough level of health risk to make the potential benefit of large doses of potassium iodide much higher than the potential risks. At what point, when I131exposure occurs, does high dose potassium iodide supplementation have a higher potential for benefit than for risk? I will answer this question with a review of three papers that specifically address the issue of high levels of I131exposure and treatment with potassium iodide supplements. The first will be presented in the next section and the other two will be presented in the next installment of this series. However, it appears very likely that risk from low levels of exposure can be substantially reduced by simple correction of iodine deficiency.
Right after the Fukushima Daiichi disaster, as I mentioned, I received several calls from panic-stricken people living primarily on the east coast about how to avoid the thyroid apocalypse that was inevitably coming our way. My reply was certainly not what they anticipated but, as I am suggesting, was highly accurate. What was my suggestion? I pointed out that the best advice I could give is to take the same action that should have been taken before the disaster; calmly and methodically determine, as best as possible, if iodine deficiency exists. If it does exist, take reasonable, low risk actions to correct it via changes in diet and, if necessary, supplementing with modest levels of potassium iodide.
WHEN SIGNIFICANT EXPOSURE TO I131 OCCURS, WHAT SPECIFICALLY IS HAPPENING PHYSIOLOGICALLY AND HOW CAN POTASSIUM IODIDE SUPPLEMENTATION REDUCE THE NEGATIVE IMPACT?
Up to this point, my goal in this newsletter has been to define, using observational data, the realities of I131 exposure from nuclear power plant accidents in terms of disease risk to the general population and show that high risk interventions are very often not needed to substantially reduce disease risk. Now, though, I would like to review some papers that go into more detail on the physiology of I131 exposure and the impact of potassium iodide supplementation from both positive and negative standpoints. The first paper is “Physiological basis for the use of potassium iodide as a thyroid blocking agent – logistic issues in its distribution,” by Becker (5). To begin this paper, Becker points out how exposure occurs:
“In the event of release of radioiodines into the atmosphere, their primary pathway of early entry into the body would be through inhalation, although iodine can also enter through ingestion in the food chain (particularly in milk and water) and can be absorbed through the skin. When the thyroid is exposed to iodide, it is rapidly taken into the gland and used to synthesize thyroid hormones.”
What are the best methods of protection? Becker (5) points out:
“Proposed methods of protection include air filtration (the use of air masks and sheltering), food and milk control, and population evacuation. All have varying effectiveness and practicality. However, pharmacologic thyroid blockade seems the most efficient, and this is best achieved by the oral administration of large amounts of nonradioactive iodide in the form of potassium iodide (KI). Its speed of action is rapid as is its excretion from the body when it is no longer administered.”
What exactly happens to potassium iodide once it is ingested?
“Potassium iodide is absorbed rapidly into the circulation and by the thyroid. In larger amounts it acts immediately to block further uptake of iodide by several means, particularly by saturating the iodide transport mechanisms of the thyroid, by inhibiting the intrathyroidal organification of iodide, and by simple dilution. If sufficient iodide is given with or before radioiodine exposure, thyroid uptake of radioiodine can be reduced to almost zero.”
The next quote defines the level of protection of KI supplementation as a function of when it is ingested:
“If KI is given simultaneously with the radioiodine, the protective effect is about 97%, which means that only 3% is taken into the thyroid. If the KI is given 12 hours before radioiodine administration or exposure, protection is still excellent, approximately 90%. Even 24 hours before radioiodine exposure, the protective effect is about 70%.”
What happens when KI is given after exposure? As you will see, Becker’s statement significantly differs from the actual data reported in the Boice, Jr (3) paper discussed above:
“After radioiodine exposure however, the situation is strikingly different because effectiveness in blocking falls rapidly. If the KI is given one hour after radioiodine, protection is only 85%, and by three hours the protective effect is down to about 50%. Giving KI six hours after radioiodine exposure as negligible protective effect.”
How can these different positions be explained? My theory would be that Becker is considering the situation from more of a theoretical pharmaceutical perspective, not allowing for the reality that actual disease occurrence is determined by both the biochemical blocking effect of pharmaceutical levels of KI supplementation plus overall health of the thyroid based on optimal physiologic levels of iodine ingestion that, ideally, has been occurring long before the radioiodine exposure.
The next quote I would like to present discusses optimal doses of KI:
“…data from Sternthal et al has been recalculated in terms of the index ‘protective effect.’ 10 mg will provide about 35% protective effect. In other words, it would have reduced the uptake by 65%. However, doses of 30 mg or more will provide more than 95% percent protection. However, doses of 30 mg or more will provide more than 95% protection. Although 100 mg is no more protective than 30 mg, a larger dose has pharmacologic advantage in that the blood level of iodide, which determines its blocking effectiveness is higher and lasts longer.”
Based on the data from the Sternthal et al study, Becker states the following about the impact of KI supplementation in the doses mentioned above on serum thyroid hormone measurements:
“It is assumed that in a reactor emergency KI will be taken for a minimum of several days and for a maximum of 10 days. In this study, most of those who received more than 30 mg a day for eight days had a significant decline in serum thyroid hormone levels, and three of the five patients who received 100 mg a day had significantly elevated thyroid stimulating hormone levels and biochemical hypothyroidism. Considerable variation in individual response was found, suggesting that there may be a population particularly susceptible to this iodide effect.”
For more discussion on the idea that iodine supplementation will have variable effects on thyroid function in different populations, please see my iodine newsletter series that can be found on the Moss Nutrition website (click here).
The next quote I would like to present emphasizes what I have stated before; KI only protects against radioactive iodine. It has no affect whatsoever on other radioactive species such as cesium or plutonium:
“It must be made clear that KI will protect only against radioiodines in the plume and does not protect against any other sources of radiation such as the noble gases which may be released in large quantities in an accident.”
In concluding the paper, Becker discusses concerns relating to side effects of KI that might occur with inappropriate use:
“There are difficult problems with inappropriate and premature ingestion, particularly in a population that might be frightened or panicked and would feel that it would be ‘safer’ to take KI at the first rumor and before any official announcement. There are also those who feel that if the recommended dose will protect them, extra safety will be ensured by taking more than the recommended dose. There is also the problem of accidental ingestion and poisoning.”
In the next installment of this series I will review papers that both discuss optimal use of KI with radiation accidents and the risks inherent with recommendations of mass use.
Moss Nutrition Report #242 – 12/01/2011 – PDF Version
- Buesseler K et al. Impacts of the Fukushima nuclear power plants on marine radioactivity. Environmental Sci Tech. 2011;45(23):9931-5.
- Cardis E, Kesminiene A, Ivanov V, Malakhova I, Shibata Y, Khrouch V, et al. Risk of Thyroid Cancer After Exposure to 131I in Childhood. JNCI Journal of the National Cancer Institute. 2005;97(10):724-32.
- Boice Jr. J. Radiation-induced thyroid cancer – What’s new? Journal of the National Cancer Institute. 2005;97(10):703-5.
- Agate L et al. Thyroid autoantibodies and thyroid function in subjects exposed to Chernobyl fallout during childhood: Evidence for a transient radiation-induced elevation of serum thyroid antibodies without an increase in thyroid autoimmune disease. J Clin Endocrinol Metab. 2008;93(7):2729-36.
- Becker DV. Physiological basis for the use of potassium iodide as a thyroid blocking agent – logistic issues in its distribution. Bull NY Acad Med. 1983;59(10):1003-8.