這是henryhus找到的一份關於貧鈾的解說:
裡面的醫學專有名詞很多,改天henryhsu有空
再翻譯好了,大家可以跟致知之前貼的文章比較
就可以發現CHINA於貧鈾的描述有多離譜了
作者是 Prof Otto G Raabe PhD, CHP

Institute of Toxicology & Environmental Health
University of California

重點有二:

1:There is no known or expected leukemia risk
associated with small amounts of U-238 in the bone
because the marrow is no efficiently irradiated
---------U-238並不會增加白血病的風險,

2:, metallic lead has considerably higher toxicity than
metallic uranium.
---------鉛的毒性比U-238高多了

全文如下
-------------------------------------------------------------------------------------------------
There are several reports in the news about the implied toxicity of depleted uranium used for
projectiles and shielding material in modern warfare. It has been suggested to be a potent
carcinogen and leukemia inducer.

The toxicity of uranium has been under study for at least 50 years including life span studies in
small animals. Depleted uranium is only very weakly radioactive, and virtually all of the
observed or expected effects are from
nephrotoxicity associated with deposition in the kidney tubules and glomeruli damage at high
doses. The radiation doses from depleted uranium (specific activity only 15 Bq/mg)(U-238 has a
4.5 billion year half life) are very small compared to potential toxic effects from uranium ions in
the body (primarily damage to kidney tubules). The main route of potentially hazardous exposure
is inhalation since
gastrointestinal uptake is very small (<1/10,000).

Consider, for example the deposition of a respirable particle of depleted uranium dioxide in the
human lung. If that particle is approximately spherical and has a diameter of 1 micrometer
(aerodynamic diameter about 3 micrometer), it will emit an average of only one alpha particle
every 100 days. Meanwhile the cells of the lung are being irradiated in a milieu of even more
energetic alpha particles from natural radon and its decay products
that are present in all the air on the surface of the earth. The total radiation dose to the lung from
even relatively high exposures to airborne depleted uranium particles is not remarkable. The TLV
is 0.2 mg/cubic-meter based on chemical toxicity.

After inhalation, uranium will be slowly mobilized and enter the systemic circulation. The uranyl
ion is the form of mobile uranium within the body. It deposits at bone surfaces and remains in
the bone matrix with a half time of up to one year. It is slowly cleared to the blood and excreted
via the kidneys. While in the bone, alpha radiation is emitted, but with very low intensity since
depleted uranium is not very radioactive. The range of alpha radiation in the bone is about 30
micrometer and the radiation is very diffuse, so the bone marrow is not
effectively irradiated by uranium in the bone. Radiation induction of leukemia requires effective
high dose-rate irradiation of the bone marrow. There is no known or expected leukemia risk
associated with small amounts of U-238 in the bone because the marrow is not efficiently
irradiated. [The same is true for much more highly radioactive radium-226 and plutonium-239.]

As to its heavy metal toxicity, the closest analogy is lead. However, metallic lead has
considerably higher toxicity than metallic uranium. Compounds of lead are much more
hazardous than compounds of uranium since uranium tends to form relatively insoluble
compounds which are not readily absorbed into the body. Also, lead within the body affects the
nervous system and several biochemical processes
, while the uranyl ion does not readily interfere with any major biochemical process except for
depositing in the tubules of kidney where damage occurs if excess deposition occurs. Glomeruli
damage has been reported at high doses as well. The kidney damage is dosage dependent and
somewhat
reversible. Lead bullets are probably more dangerous than uranium bullets.

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阿幹 　於　2001/02/20 07:53
發表內容：

http://www.trustmed.com.tw/20010216023.html

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加拿大壁虎 　於　2001/02/24 13:06
發表內容：

在下對軍事是最近才開始有興趣﹐所以平常當隻壁虎。
但忝居國外多年﹐對閱讀英文文章已習以為常。若有網友對上
面那篇原文有興趣﹐在下可自告奮勇充當翻譯兵。

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小滬尾 　於　2001/02/24 13:22
發表內容：

加拿大壁虎兄﹐歡迎光臨
在此﹐小弟先謝謝老兄的好意。
Enjoy yourself here.

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Skywalker 　於　2001/02/24 18:45
發表內容：

加拿大壁虎兄
感謝閣下熱情支援，那日後就以此為筆名好了，別具風格！
P.S.
因為壁虎世界各國都不一樣，種類多！
抱歉！變成Discovery channel！

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強盜 　於　2001/02/24 22:04
發表內容：

大陸對貧鈾彈報道
美軍貧鈾彈難辭其咎
　
9月3日，歐洲核醫學協會在巴黎召開會議。面對眾多的核權威，美國前陸軍上校阿薩夫﹒杜拉科維克醫生語出驚人地宣稱，海灣戰爭綜合症的真正禍源是美軍所發射的大量貧鈾彈，“數萬名”美英海灣戰爭軍人正因貧鈾彈輻射而面臨死亡的危險！
　　
　　杜拉科維克現在是華盛頓喬治敦大學的一名核醫學教授，曾主管美國陸軍退伍軍人事務部駐達拉瓦醫院的核醫療工作。在3日的會議上，他表示，他領導的一個由美加科學家組成的聯合小組發現，在海灣戰爭結束九年后的今天，海灣戰爭軍人體內仍存在足以危及生命安全的超標准貧鈾。他們對其中17人所進行的檢測表明，這些人70％的尿液及骨頭中均發現有貧鈾。他們的結論是，參戰的軍人吸入了微小的鈾顆粒物。他們的發現首次解釋了，為什么患海灣戰爭綜合症的主要是隨軍的醫護人員和機械師。此前，有調查表明，那些專門在戰場上清除被貧鈾彈擊毀的坦克的機械師和在野戰醫院把傷亡伊軍衣服脫下來的醫護人員患病比例最高。
　　
　　貧鈾是對核反應堆進行處理后得到的一種副產品，又被稱為武器級鈾。貧鈾彈被美軍視為二十世紀九十年代的超級武器，有“銀彈”之稱，在海灣戰爭及去年的科索沃戰爭中都曾被大量使用。據估計，僅在海灣戰爭中，美英軍隊發射的貧鈾彈就達70至100萬枚，共有1400多輛伊軍坦克被擊毀。一枚120毫米口徑的反坦克貧鈾彈裝有4公斤固體貧鈾，殺傷力相當強。它能不費吹灰之力穿透堅固的裝甲，并在爆炸后燃燒，產生許多有毒及輻射性碎彈片和塵埃，其輻射的半衰期長達42億年之久。

　　貧鈾一旦被吸入進入人體，就會導致癌症、不可逆的腎損傷、免疫系統紊亂、影響生殖功能，甚至還有研究人員稱，貧鈾會從基因上改變細胞。后果可想而知。
　　
　　■一人當兵　全家遭殃
　　在海灣戰爭的地面行動中，北約軍隊和伊拉克的裝甲部隊展開激戰。美國陸軍第三裝甲師的杰里﹒維特當時是一名“布雷德利”裝甲運兵車駕駛員。在混戰中，他的“坐騎”先后兩次被擊中───不是被伊軍擊中，而是被自己的部隊擊中。不幸也正在這里，如果是被伊軍擊中的話，他今天就不會活得那么痛苦了。要知道，他當時并不知道擊中他的竟是美軍引以為豪、被五角大樓稱為“銀彈”的貧鈾彈。
　　
　　戰爭結束后，維特獲得了美軍頒發的“紫心”勛章。他帶著這枚勛章和仍嵌在體內的几枚彈片，離開部隊，回到了在新墨西哥州的家中。他以為從此可以過上平靜的生活了。但是，戰爭的魔影卻尾隨著他，讓他不得安寧，痛苦萬分。自從回到家后，他就一直感到莫名其妙地疼痛，關節、腹部、頭部等處經常不明不白地隱隱作痛。
　　
　　讓杰里﹒維特最為憤怒的是，貧鈾彈不僅讓他身患怪病，也連累了他一家人。
　　自從他回到家后，他家就發生了一連串的不幸：在他把那些在戰場上受輻射污染的東西帶回家后第二天，他的大兒子喬不明不白地因呼吸困難住進了醫院，而在此之前喬一直都是好端端的﹔戰后出生的小兒子德里克雙手長出了奇怪的水 ，連醫生也搞不明白是怎么回事﹔他妻子流了產﹔去年，維特肩上又長了個腫瘤。
　　
　　■五角大樓百般掩飾
　　越戰時，美軍在越南洒下了大量有毒的橙劑，并在越戰結束許多年后一直掩蓋事情真相。有人認為，美軍在海灣戰爭綜合症問題上與越戰同出一撤。
　　
　　迫于海灣戰爭老兵和公眾的壓力，五角大樓多次出面解釋說，導致海灣戰爭綜合症的原因可能是緊張、油井大火、伊軍進行的生化戰等。1994年美國國防科學委員會海灣戰爭健康影響特別調查小組就此進行了一次深入調查，結果發現患病者與生化武器制劑污染毫無關系。該特別小組由諾貝爾獎得主、生物學家喬舒亞﹒萊德伯格率領，成員是來自斯坦福大學、哈佛大學和約翰霍普金斯大學等知名學府的科學家，因此，其調查結果具有相當的權威性。萊德伯格說：“沒有任何証據能証明，（海灣戰爭）發生了任何程度的化學戰或生物戰，也沒有任何証據足以証明美軍人員暴露在生化戰制劑之中。”
　　
　　■兩份秘密備忘錄
　　道格﹒洛克也參加了海灣戰爭。當時他是美國陸軍醫療防治司令部一名中尉，率領一個陸軍醫療小組專門負責清理被貧鈾彈擊毀的受污染車輛。現在，他正在積極收集証據，以証明五角大樓事先就已知道貧鈾彈會威脅到他和其他參戰人員的健康。洛克說：“今天看來，很顯然，軍方是知道真相的，但他們沒有告訴任何人。

　　1991年3月開始清理被污染的裝備和傷亡人員時，我們曾收到兩份秘密備忘錄，其中一份被稱為洛斯阿拉莫斯備忘錄。”

　　據洛克介紹，洛斯阿拉莫斯備忘錄是由M﹒V﹒茲耶姆中校撰寫的，里面有這么一段話：“貧鈾彈對環境的影響一直受到關注，因此沒人能証明貧鈾彈在戰場上的有效性。在政治上，貧鈾彈可能不被接受并因此被禁止使用……望在撰寫戰后報告時，謹記住此秘密。”其言下之意就是告誡洛克等人，在寫報告或匯報他們的發現時，不能影響到貧鈾彈在未來的使用。
　　
　　第二份備忘錄是國防核研究局下發的。該備忘錄稱：“使用過的貧鈾彈所產生的阿爾法粒子（即氧化鈾塵埃）對健康的影響應予以關注，而彈片及完整貧鈾彈產生的貝塔粒子則會嚴重威脅健康……”洛克認為，這兩份備忘錄足以証明，美軍高層事先是知道貧鈾彈對環境及人體的影響的。
　　

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加拿大壁虎 　於　2001/02/25 08:37
發表內容：

謝謝小滬尾網主及Skywalker的支持（這地方氣氛真好﹐連對岸
的網友也能保持純討論的風度）。上面原文翻譯如下﹐若有用
詞不當的地方請告訴我一聲﹕
最近新聞裡有些文章提到近代武器所用的貧鈾的毒性。有些人
認為貧鈾具有很高的致癌性﹐尤其是血癌。

有關鈾毒性的研究已經進行最少五十年了﹐其中包括了小型動
物存活壽命的研究。貧鈾的放射性非常低﹐所以幾乎所有觀測
到的﹐對有生物的作用﹐都是基於它對腎臟功能的影響﹕在高
量攝取時會沉積在腎小管裡。鈾-238的半衰期雖有四十五億年
之久﹐但貧鈾微弱的放射性（每毫克的放射性比度只有15Bq）
對身體的毒性還遠不及鈾離子對腎功能的影響。又由於它很不
容易被腸胃吸收（若口服的只有不到萬分之一的量會被吸收）
﹐由粉狀吸入肺裡才識它對人體最有害的入侵途徑。

我們用吸入粉狀的氧化鈾來假設﹐若這些粉末為直徑一分釐的
球體（也就是其氣體動力直徑為三分釐）﹐它每一百天只會釋
出一顆α粒子。在這一百天內﹐我們從一般空氣吸入的氡氣及
其衰變產物所釋出的α粒子遠比這多很多﹐能量也要高很多。

[待續]

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加拿大壁虎 　於　2001/02/25 09:26
發表內容：

[接上]
所以﹐就算吸入不少貧鈾粉末﹐對肺的放射量也是微不足道的。
由純化學毒性來講﹐它的TLV [壁虎按﹕不知是不是指 Toxic Lethal
Volume]是每立方公尺0.2毫克。

吸入肺部後﹐鈾會逐漸以離子的形態進入血液循環。它會沉積在
骨頭表面而成為骨質的一部份。慢慢地（大約每一年有50%）會
重新進入血液循環而由腎排出體外。當它還是骨質的一部分時﹐
它會繼續釋出α粒子﹐但[像前面提過的]它的放射性很低﹐所以
釋出的放射線能量也很低。貧鈾在骨質裡釋出的α粒子的“射程
”只有三十分釐﹐所以骨髓受到的輻射量其實很低。要引發血癌
需要比那強很多很多的輻射量。總言之﹐從骨質裡少量的鈾-238
得到血癌幾乎是不可能的事。

至於鈾的“重金屬”毒性﹐應該和鉛類似。但金屬鉛的毒性要比
金屬鈾高太多了﹐因為鈾的化合物多不溶於水﹐而不易被人體吸
收。另外﹐鉛對神經系統及人體內的一些化學作用都有毒性﹐鈾
卻沒有。鈾對人體最大的影響還是腎功能﹐尤其是當吸收的量高
到它開始在腎小管沉積時。它對腎功能的影響跟吸收的量成正比
﹐而且不一定是永久的。所以﹐若以對人體的影響來看﹐鉛彈可
能比鈾彈更危險。

==============================
壁虎按﹕原文翻譯在此﹐若有用詞不當﹐請各看官踴躍指出。我
這是第一次翻譯這類文章﹐試了後才知比想像中費事很多……

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henryhus 　於　2001/02/25 09:57
發表內容：

感謝加拿大壁虎!!你翻的很好!!

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強盜 　於　2001/02/25 19:53
發表內容：

henryhus,大陸如何在貧鈾事件上詐騙世界?
指出來.

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強盜 　於　2001/02/25 21:26
發表內容：

我看了這篇文章想起原來美國各大煙草公司
採用金錢禮品收買一些醫學人士發表吸煙無害論
的文章的事來。
現在的醫學理論還未將人體研究得十分透徹，有些在純理論
上對人體無害的東西，人服下去卻有害。
如50年代西德的“反應停”，在當時醫學理論對人體無害，
但是卻造成了上萬計的“海豹兒”怪胎。
連藥都是如此，更何況一種真真切切帶有輻射性的東西？
對於這樣的事件，還是看一些理論帶事實研究的翔實文章
較爲準確。

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強盜 　於　2001/02/25 21:30
發表內容：

以下是一篇海牙和平會議上結合事實研究對貧鈾
較爲翔實的報告。

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強盜 　於　2001/02/25 21:32
發表內容：

Gulf War Veterans and Depleted Uranium

Prepared for the

Hague Peace Conference, May 1999

By Dr. Rosalie Bertell, Ph.D., G.N.S.H.

Source of Exposure:

Uranium metal is autopyrophoric and can burn spontaneously at room temperature in the presence of air, oxygen and water. At temperatures of 200-400 degrees Centigrade, uranium powder may self-ignite in atmospheres of carbon dioxide and nitrogen. Oxidation of uranium under certain conditions may generate sufficient energy to cause an explosion (Gindler 1973). Friction caused by bullet or missile entry into a tank or armored car, for example, can cause the uranium to ignite, forming a concentrated ceramic aerosol capable of killing most personnel in the vehicle. Depleted uranium was used extensively in place of tungsten for ordnance by the US and UK in the Gulf War.

There is no dispute of the fact that at least 320 tons of depleted uranium (DU) was lost in the Gulf war, and that much of that was converted at high temperature into an aerosol, that is, minute insoluble particles of uranium oxide, UO2 or UO3 , in a mist or fog. It would have been impossible for ground troops to identify this exposure if or when it occurred in war, as this would require specialized detection equipment. However, veterans can identify situations in which they were likely to have been exposed to DU. Civilians working at military bases where live ammunition exercises are conducted may also have been exposed.

Uranium oxide and its aerosol form are insoluble in water. The aerosol resists gravity, and is able to travel tens of kilometres in air. Once on the ground, it can be resuspended when the sand is disturbed by motion or wind. Once breathed in, the very small particles of uranium oxide, those which are 2.5 microns [ one micron = one millionth of a meter ] or less in diameter, could reside in the lungs for years, slowly passing through the lung tissue into the blood. Uranium oxide dust has a biological half life in the lungs of about a year. According to British NRPB [ National Radiation Protection Board ] experiments with rats, the ceramic or aerosol form of uranium oxide takes twice as long or about a two year biological half life in the lungs, before passing into the blood stream. [Stradling et al 1988]

Because of coughing and other involuntary mechanisms by which the body keeps large particles out of the lungs, the larger particles are excreted through the gastro-intestinal tract in feces. The uranium compounds which enter the body either through the wall of the gastro-intestinal tract or the lungs, can be broken down in the body fluids, and tetravalent uranium is likely to oxidize to the hexavalent form, followed by the formation of uranyl ions. Uranium generally forms complexes with citrate, bicarbonates or protein in plasma, and it can be stored in bone, lymph, liver, kidney or other tissues. Eventually this uranium which is taken internally is excreted through urine. Presence of depleted uranium in urine seven or eight years after exposure is sufficient evidence to substantiate long term internal contamination and tissue storage of this radioactive substance.

Uranium is both a chemical toxic and radioactive hazard: Soluble uranium is regulated because of its chemical toxicity, measured by damage to the kidney and tubules. Uranium is a heavy metal, known to cause uranium nephritis. Insoluble uranium, such as was released in the Gulf War, is regulated by its radiological properties, and not its chemical properties. Because of its slow absorption through the lungs and long retention in body tissues, its primary damage will be due to its radiological damage to internal organs rather than chemical damage to the renal system. Obviously, both types of damage occur simultaneously, therefore it is a matter of judgment which severe damage, radiological or chemical, occurs at the lowest dose level. However, with the lengthening of the time during which the contaminant resides in the body and the low overall dose, the risk of cancer death becomes greater than the risk of significant damage to the renal system.

Uranium decays into other radioactive chemicals with statistical regularity. Therefore, in its natural and undisturbed state, it always occurs together with a variety of other radioactive chemicals, some of the best known being thorium, radium, polonium and lead.

Natural uranium in soil is about 1 to 3 parts per million, whereas in uranium ore it is about 1,000 times more concentrated, reaching about 0.05 to 0.2 percent of the total weight. Depleted uranium concentrate is almost 100 percent uranium. More than 99 percent of both natural and depleted uranium consists of the isotope U-238. One gram of pure U-238 has a specific activity of 12.4 kBq, which means there are 12,400 atomic transformations every second, each of which releases an energetic alpha particle. Uranium 238 has a half life of 4.51 E+9 (or 4.51 times 10 to the 9thpower, equivalent to 4,510,000,000 years).

Each atomic transformation produces another radioactive chemical: first, uranium 238 produces thorium 234, (which has a half life of 24.1 days), then the thorium 234 decays to protactinium 234 (which has a half life of 6.75 hours), and then protactinium decays to uranium 234 (which has a half life of 2.47E+5 or 247,000 years). The first two decay radioisotopes together with the U 238 count for almost all of the radioactivity in the depleted uranium. Even after an industrial process which separates out the uranium 238 has taken place, it will continue to produce these other radionuclides. Within 3 to 6 months they will all be present in equilibrium balance. Therefore one must consider the array of radionuclides, not just uranium 238, when trying to understand what happened when veterans inhaled depleted uranium in the Gulf War.

It should be noted that uranium 235, the more fissionable fraction which was partially removed in enrichment, makes up only 0.2 to 0.3 percent of the depleted uranium, whereas it was 0.7 percent of natural uranium. It is this deficit which enables one to use analytical methods to identify the uranium found in veterans urine as depleted and not natural uranium. The U 235 was extracted for use in nuclear weapons and nuclear reactor fuel. Depleted uranium is considered nuclear waste, a by-product of uranium enrichment.

The difference in radioactivity between natural and depleted uranium is that given equal quantities, depleted uranium has about half the radioactivity of the natural mixture of uranium isotopes. However, because of the concentration of the uranium in the depleted uranium waste, depleted uranium is much more radioactive than uranium in its natural state.

Uranium and all of its decay products, with the exception of radon which is a gas, are heavy metals. Unlike some other heavy metals which are needed in trace quantities by the human body, there is no known benefit to having uranium in the body. It is always a contaminant. Ingesting and inhaling some uranium, usually from food, is inescapable however, in the normal Earth environment, and we humans basically take in, on average, 5 Bq per year of uranium 238 in equilibrium with its decay products. This gives an effective radiation dose equivalent to the whole body of 0.005 mSv. Using a quantitative measure, we normally ingest about 0.000436 g a year.[UNSCEAR 1988, 58-59] This is a mixture of soluble and insoluble compounds, absorbed mostly through the gut.

Regulatory limits recommended by the International Commission on Radiological Protection [ICRP] assume that the maximum permissible dose for members of the public will be the one which gives the individual 1 mSv dose per year. This is in addition to the natural exposure dose from uranium in the food web. Assuming that this dose comes entirely from an insoluble inhaled uranium oxide, and using the ICRP dose conversion factor for uranium 238 in equilibrium with its decay products, one can obtain a factor of 0.84 mSv per mg, or a limit of intake of 1.2 mg (0.0012 g) per year for the general public. This would give an added radiation dose of 1.0 mSv from uranium, and an increase of almost 2.75 times the natural uranium intake level. Nuclear workers would be allowed by the ICRP maximum permissible level, to reach an annual dose of 20 mSv, comparable to an intake of 24 mg of uranium, 55 times the normal yearly intake.

The US has not yet conformed to the 1990 international recommendations which were used for this calculation, and it is still permitting the general public to receive five times the above general public amount, and the worker to receive 2.5 times the above occupational amount. The US may have used its domestic nuclear worker limits during the Gulf War, if it used any protective regulations at all. The military manual discusses the hazards of depleted uranium as less than other hazardous conditions on an active battle field!

The maximum dose per year from anthropogenic sources can be converted to the maximum concentration permissible in air using the fact that the adult male breathes in about 23 cubic metres of air in a day [ICRP 1977]. The maximum permissible concentration in air for the general public would be: 0.14 microgram per cu metre, and for workers: 2.9 micrograms per cu m assuming the Gulf War situation of continuous occupancy rather than a 40 hour work week, and an 8 hour day. It is common in the US and Canada to refer to 2000 pounds as a ton, whereas the British ton is 2240 pounds. Both are roughly 1000 kg. Just in order to understand the scale of the ceramic uranium released in Desert Storm, at least 300 million grams were lost, and breathing in only 0.023 g would be equivalent to the maximum permissible inhalation dose for a nuclear worker to receive in a year under the 1990 recommendations of ICRP.

Medical Testing for
Depleted Uranium Contamination:

Potential testing includes:

chemical analysis of uranium in urine, feces, blood and hair;

tests of damage to kidneys, including analysis for protein, glucose and non-protein nitrogen in urine;

radioactivity counting; or

more invasive tests such as surgical biopsy of lung or bone marrow.

Experience with Gulf War veterans indicates that a 24 hour urine collection analysis shows the most promise of detecting depleted uranium contamination seven or eight years after exposure. However, since this test only measures the amount of depleted uranium which has been circulating in the blood or kidneys within one or two weeks prior to the testing time, rather than testing the true body burden, it cannot be directly used to reconstruct the veterans dose received during the Gulf War. However, this seems to be the best diagnostic tool at this time, eight years after the exposure.

Feces tests for uranium are used for rapid detection of intake in an emergency situation, and in order to be useful for dose reconstruction, must be undertaken within hours or days of the exposure. Blood and fecal analysis are not advised except immediately after a known large intake of uranium.

Whole body counting for uranium, using the sodium iodide or hyper pure germanium detectors, is designed to detect the isotope uranium 235, the isotope of uranium partially removed from depleted uranium. For lung counting, again it is the uranium 235 which is detected, and the minimum detection limit is about 7.4 Bq or 200 pCi. Since normally humans take in only 5 Bq per year, this is not a very sensitive measure. Seven or eight years after the Gulf War exposure, this method of detection is most likely useless for veterans.

Routine blood counts shortly after exposure, or during a chelating process for decontamination of the body are useful. This is not a search for uranium in blood, but rather a complete blood count with differential. This is done to discover potentially abnormal blood counts, since the stem cells which produce the circulating lymphocytes and erythrocytes are in the bone marrow, near to where uranium is normally stored in the body. The monocyte stem cells in bone marrow are known to be among the most radiosensitive cells. Their depletion can lead to both iron deficient anemia, since they recycle heme from discarded red blood cells, and to depressed cellular immune system, since monocytes activate the lymphocyte immune system after they detect foreign bodies.

Hair tests need to be done very carefully since they tend to reflect the hair products used: shampoos, conditioners, hair coloring or permanent waves. Pubic hair would likely be the best material for analysis. I am not aware of good standards against which to test the Uranium content of hair, or how the analysis would differentiate between the various uranium isotopes.

Testing of lymph nodes or bone on autopsy would be helpful. However, invasive biopsies on live patients carry no benefit for the patient and are usually not recommended because of ethical considerations about experimentation on humans. If a veteran is recommended for bronchoscopy for medical reasons, it would be advisable to also take tissue samples for analysis for depleted uranium.

When chelation processes have been initiated the rate of excretion of uranium in urine will be increased and there is a risk of damage to kidney tubules. Therefore careful urine analysis for protein, glucose and non-protein nitrogen in important. Some researchers have also reported specifically finding B-2-microglobulinuria and aminoaciduria in urine due to uranium damage.

Relating Depleted Uranium Contamination
with Observed Health Effects in Veterans:

There are two ways of documenting the radiological health effects of a veterans exposure to depleted uranium. The first, and the one usually attempted in a compensation argument, would be to reconstruct the original dose and then appeal to regulatory limits or dose-response estimates available in the scientific literature. This methodology is not recommended for the Gulf War veterans, because the uranium excretion rate seven or eight years after exposure cannot be used to estimate the original lung and body burden of depleted uranium. Moreover, no dose-response estimates for the chronic health effects of such exposure are available from the literature, as will be seen later in this paper. Recognized dose-response estimates for radioactive materials are unique to fatal cancers (and even these are disputed). It is not clear whether regulatory limits for exposure to ionizing radiation apply in a war situation, or, if they do, whether the veteran should be considered to have been general public or a nuclear worker. Beyond this, the question of whether international or US standards should be used for a multinational situation needs to be addressed.

The second methodology would require ranking veterans on an ordinal scale for their original exposure, based on their current excretion rate of depleted uranium. This involves the reasonable assumption that the original contamination, although not precisely measurable, was proportional to the current excretion rate. The analysis of a 24 hour urine sample, for example, could be rated on a specific research scale as having high, medium or low quantities of the contaminate. By collecting detailed health and exposure data on each veteran, one can use biostatistical methods to determine firstly, whether any medical problems show an increase with the ordinal scale increase in exposure, determined through urine analysis; and secondly, whether there is a correlation between the descriptive accounts of potential depleted uranium exposure and the assigned ordinal scale determined on the basis of the urine analysis.

Using Non-Parametric Statistics one could determine the statistical significance of various medical problems being depleted uranium exposure related. This would undoubtedly eliminate some medical problems from consideration and highlight others. It could point to future research questions. It could also provide a fair method of dealing with the current suffering of the veterans using the best scientific methodology available at this time. Risk estimates based on radiation related cancer death are obviously unable to provide a reasonable response to current veteran medical problems.

Known Occupational Health Problems
Related to Uranium Exposure:

In Volume 2 of the Encyclopaedia of Occupational Health, under uranium alloys and compounds, page 2238, it reads:

Uranium poisoning is characterized by generalized health impairment. The element and its compounds produce changes in the kidneys, liver, lungs and cardiovascular, nervous and haemopoietic systems, and cause disorders of protein and carbohydrate metabolism.......

Chronic poisoning results from prolonged exposure to low concentrations of insoluble compounds and presents a clinical picture different from that of acute poisoning. The outstanding signs and symptoms are pulmonary fibrosis, pneumoconiosis, and blood changes with a fall in red blood count; haemoglobin, erythrocyte and reticulocyte levels in the peripheral blood are reduced. Leucopenia may be observed with leucocyte disorders (cytolysis, pyknosis, and hypersegmentosis).

There may be damage to the nervous system. Morphological changes in the lungs, liver, spleen, intestines and other organs and tissues may be found, and it is reported that uranium exposure inhibits reproductive activity and affects uterine and extra-uterine development in experimental animals. Insoluble compounds tend to be retained in tissues and organs for long periods.

Human and Animal Studies on Uranium Exposure:

In a study of uranium toxicity by the US Agency for Toxic Substances and Disease Registry [ATSDR 1998], released for public review and comments by 17 February 1998, exposure times were divided into three categories: acute, less than 15 days; intermediate, 15 to 365 days; and chronic more than a year. Most of the Gulf War Veterans would have had chronic duration exposure from the point of view of the length of time the material remained in the body. However, this ATSDR division was based of the duration of the presence of the external source of contamination, not its residence time in the body, therefore it would, in most cases be considered intermediate duration exposure. There is very little human research available to clarify the effects of intermediate duration exposure to humans.

It should not be assumed that lack of research implies lack of effect on that particular system. It should also be noted that although one or more papers may exist for acute and chronic duration exposures, these do not necessarily cover the questions which one might like to raise. No comments on the quality or extent of the research is implied by this table.

Health Effects which have been
associated with inhalation of uranium:

The more soluble compounds of uranium, namely, uranium hexafluoride, uranyl fluoride, uranium tetrachloride, uranyl nitrate hexahydrate, are likely to be absorbed into the blood from the alveolar pockets in the lungs within days of exposure. Although inhalation products also are transported through coughing and mucocilliary action to the gastro-intestinal tract only about 2 percent of this fraction is actually absorbed into the body fluids through the intestinal wall. Therefore all of the research papers on acute effects of uranium refer to these soluble uranium compounds via inhalation. The main acute effect of inhalation of soluble uranium compounds is damage to the renal system, and the main long term storage place of these compounds in the body is bone.

These research findings do not apply easily to the insoluble uranium compounds to which the Gulf Veterans were exposed when the depleted uranium ordnance was used in battle.

The uranium compound used for ordnance was uranium 238 and limited amounts of its decay products. Particles of these compounds smaller than 2.5 microns are usually deposited deep in the lungs and pulmonary lymph nodes where they can remain for years. According to research done in the UK by the NRPB, ceramic uranium is formed when uranium ignites through friction, as happened in the Gulf War. In this form, it is twice as slow to move from the lungs to the blood than would be the non-ceramic uranium. Of the portion of inhaled uranium which passes through the gastro-intestinal tract, only 0.2 percent is normally absorbed through the intestinal wall. This may be an even smaller portion for ceramic uranium. This fraction of the inhaled compound can, of course, do damage to the GI tract as it passes through because it emits damaging alpha particles with statistical regularity. The residence time of the insoluble uranium compounds in the GI tract (the biological half life) is estimated in years. [ibid.]

The chemical action of all isotopic mixtures of uranium (depleted, natural and enriched) is identical. Current evidence from animal studies suggests that the chemical toxicity is largely due to its chemical damage to kidney tubular cells, leading to nephritis.

The differences in toxicity based on the solubility of the Uranium compound (regardless of which uranium isotope is incorporated in the compound) are more striking: water soluble salts are primarily renal and systemic chemical toxicants; insoluble chemical compounds are primarily lung chemical toxicants and systemic radiological hazards. Once uranium dioxide enters the blood, hexavalent uranium is formed, which is also a systemic chemical toxicant.

It is important to note that there is no scientific evidence which supports the US Veteran Administration claim that the insoluble uranium to which the Gulf War Veterans were exposed will be primarily a renal chemical toxicant. Yet this is the criteria which the VA proposes for attributing any health problems of the Veteran to depleted uranium. Intermediate and chronic exposure duration to insoluble uranium is regulated in the US by its radiological property. The slow excretion rate of the uranium oxide allows for some kidney and tubule repair and regeneration. Moreover, because of the long biological half life, much of the uranium is still being stored in the body and has not yet passed through the kidneys. The direct damage to lungs and kidneys by uranium compounds is thought to be the result of the combined radiation and chemical properties, and it is difficult to attribute a portion of the damage to these separate factors which cannot be separated in life.

There is human research indicating that inhalation of insoluble uranium dioxide is associated with general damage to pulmonary structure, usually non-cancerous damage to alveolar epithelium. With acute duration exposure this can lead to emphysema or pulmonary fibrosis (Cooper et al, 1982; Dungworth, 1989; Saccomanno et al, 1982; Stokinger 1981; Wedeen 1992). Animal studies demonstrate uranium compounds can cause adverse hematological disturbances (Cross et al. 1981 b; Dygert 1949; Spiegel 1949; Stokinger et al 1953).

Important information from a chart developed by ATSDR [referenced earlier] is reproduced here, the reader will find all of this information and the references in the original document.

Availability of Human or Animal Data

for the Presence of a Particular Health Effect

after Exposure via Inhalation to Insoluble Uranium

Effect on body system studied: Effects of acute duration exposure (less than 15 days) Effects of intermediate duration exposure (15 days to 1 year) Effects of chronic duration exposure (more than 1 year)

Respiratory Human Studies:
rales, slight degeneration in lung epithelium; hemorrhagic lungs [1]
Animal Studies:
severe nasal congestion, hemorrhage; gasping in 100 percent [2]
Animal Studies:
slight degenerative changes in lung;[3] pulmonary edema; hemorrhage; emphysema; inflamation of the brochi; bronchial pneumonia; alveoli and alveolar interstices; edematous alveoli; hyperemia and atelectasis.; lung lesions; minimal pulmonary hyaline fibrosis and pulmonary fibrosis. [2] Animal Studies:
minimal pulmonary fibrosis [3] Lung cancer in dog [3]

Hepatic
Animal Studies:
moderate fatty livers in 5 of 8 animals that died; focal necrosis of liver.[3] Animal Studies:
increased bromo-sulfalein retention [2]

Hematological Animal Studies:
increased macrophage activity; increased plasma prothrombin and fibrinogen.[3] A (increased percentage myeloblasts and lymphoid cells in bone marrow; decreased RBC; increased plasma prothrombin and fibrinogen; increased neutrophils ; decreased lymphocytes) Animal Studies:
lengthened blood clotting time, decreased blood fibinogen [2]

Gastro-intestinal Human Studies:
anorexia, abdominal pain, diarrhea, tenesmus or ineffective straining, and pus and blood in stool [1] Animal Studies:
anorexia; vomited blood; ulceration of caecum.[1],[6]

Renal Human Studies:
proteinuria, elevated levels of NPN, aminoacid nitrogen/creatinine, abnormal phenol-sulfonphthalein excretion. Increased urinary catalase; diuresis.[1]
Animal Studies:
Proteinuria, glucosuria and polyuria; severe degeneration of renal cortical tubules 5-8 days post exposure. [2]
Animal Studies:
diuresis, mild degeneration in glomerulus and tubules. [3] proteinuria, increased NPN.[3] minimal microscopic lesions in tubular epithelium [1] Animal Studies:
slight azotemia [4] slight degenerative changes [3] minimal microscopic lesions [1], [5],[6] tubular necrosis and regeneration [6]

Cardiovascular

Musculo-skeletal Animal Studies:
severe muscle weakness; lassitude [3 with F].

Endocrine

Metabolic

Dermal

Ocular Animal Studies:
conjunctivitis [2] Animal Studies:
eye irritation [2]

Body Weight Animal Studies:
26 percent decrease inMetabolicght; 14 percent decrease at 22 mg / cu m air; [1], [3] 12 percent decrease at 2.1 mg/cu m air.[2] 2.9 to 27.9 percent decreased body weight guinea pig [6]

Other Systemic Animal Studies:
weakness and unsteady gate, [1] minimal lymph node fibrosis.[3] rhinitis [1] Animal Studies:
minimal lymph node fibrosis [3] lung cancer (dog) [3]

Mortality Animal Studies:
20 percent for dogs at 2 mg per cu. m air [2] Animal Studies:
10 percent rat and guinea pig [4] 17 percent dog [4] 60 percent rabbits [3] 67 percent rabbits [4] Animal Studies:
4.5 percent mortality dog [3]

Uranium tetrafluoride, UF4 , insoluble in water.

Uranium hexafluoride, UF6 , soluble in water, highly chemically toxic.

Uranium dioxide, UO2 , insoluble in water, highly toxic and spontaneously flammable, used in ordnance in place of lead in the Gulf War. (Also called uranium oxide.)

Uranium trioxide, UO3 , insoluble in water, poisonous, decomposes when heated. (Also called uranium oxide.)

Uranyl Chloride, UO2Cl2 , uranium oxide salt.

Uranium Nitrate, UO2(NO3)2.2H2O , soluble in water, toxic and explosive.

--------------------------------------------------------------------------------

With respect to ORAL exposure, there is no human data but a great deal of animal data. This was not as likely a pathway in the Gulf War as was inhalation, but possible contamination of food and water can not be totally ignored.

DERMAL exposure was researched in humans only in the acute duration of exposure case. Animal studies on dermal exposure include acute, intermediate and chronic duration of exposure, and immunologic/lymphoreticular and neurologic effects.

Mortality Within 30 Days of Exposure:

The lowest acute duration lethal dose observed, with exposure to the soluble uranium hexafluoride, was 637 mg per cu metre of air. No acute dose deaths were found using insoluble compounds. Since there were acute deaths in the Iraqi tanks in persons not directly hit, one can assume concentrations of uranium aerosol were greater than this amount. It should also be noted that it was the radiation protection units of the military which designated these contaminated tanks off bounds. They were acting because of radiological (not chemical) properties of the aerosol.

The intermediate duration exposure, 15 to 365 days, dose level for mortality with insoluble uranium oxide, was 15.8 mg per cu metre of air. With soluble uranium hexachloride it was much lower, 2 mg per cu metre air.

The dose resulting in lung cancer in the dog study, with chronic duration inhalation of the insoluble uranium oxide, was 5.1 mg per cu metre air, for 1 to 5 years, 5 day a week and 5.4 hours a day.

Systemic Damage:

Damage to body organs occurred with intermediate or chronic exposure at doses as low as 0.05 mg per cu metre air. A generally sensitive indicator of exposure seems to be loss of body weight. However this finding is somtimes attributed to the unpleasant taste of the uranium laced food given to animals. There is also damage to the entrance portals: respiratory and gastro-intestinal systems; and the exit portals: intestinal and renal systems. Uranium oxide was associated with fibrosis and other degenerative changes in the lung. It was also associated with proteinuria, and increased NPN (non-protein nitrogen) and slight degenerative changes in the tubules. The more severe renal damage was associated with the soluble compounds uranium tetrafluoride and uranium hexafluoride (not thought to have been used in the Gulf War ordnance).

Focal necrosis of the liver was only associated with uranium oxide. This may be a clue to one of its storage places in body tissue. Uranium oxide is also associated with hematological changes, lymph node fibrosis, severe muscle weakness and lassitude at intermediate or chronic dose rates in 0.2 to 16 mg per cu metre air. None of the uranium research dealt with the synergistic, additive or antagonistic effects potentially present in the Gulf War mixture of iatrogenic, pathological, toxic chemical and electromagnetic exposures.

Potential US Government administration of
radio-protective substances to combat military:

It is obvious that the US had some expectation of the health effects related to using depleted uranium ordnance in the Gulf War. This is evident based on military research and manuals. They would also have had access to information on chemical and biological agents which could protect against some of the harmful side effects. These agents might also confuse the toxicology of this exposure. Some potential radio-protective agents are thiols (also called mercaptans, these are organosulfur compounds that are derivatives of hydrogen sulfide), nitroxides (used as a food aerosol and an anesthetic), cytokines (non-antibody proteins released by one cell population, e.g T-lymphocytes, generating an immune response), eicosanoids (biologically active substances derived from arachidonic acid, including the prostaglandins and leukotrienes), antioxidants and modifiers of apoptosis (fragmentation of a cell into small membrane bound particle which are then eliminates by phagocytes).

Just in case this is the reality and not merely a suspicion, it would be good to examine the after effects of exposure to ceramic depleted uranium in Iraqi veterans and in the survivors of the El Al crash at Shipol Airport, Amsterdam. It is unlikely that these two populations were given any protective agents.

Proposal for assisting the Gulf War veterans:

In keeping with the above findings, it is proposed to undertake an analysis of both questionnaire and clinical data for a sample of each of the following populations: US, Canadian and British Gulf War veterans or civilian base workers exposed to DU; US, Canadian and British military personnel not exposed to DU; Iraqi Veterans exposed to DU; Iraqi Veterans not exposed to DU; and firemen and civilians exposed to the El Al crash.

Sampling strategy and sample size to be determined:

Each participant should complete a questionnaire [See draft questionnaire in Appendix A] covering general background variables, exposure profile and medical problems and symptoms. Each participant will agree to collect a 24 hour urine sample for analysis, and to take 500 mg blue-green algae (Spirulina) 48 hours before beginning the collection. This is a mild chelating agent. Each participant will agree to the analysis of this data for the benefit of all exposed persons, and to the release of the results of the analysis without identifying characteristics for individuals.

All questionnaire data will be entered into computer using Epi Info Software (WHO) and transferred on disc to the Biostatistical Support Unit of the University of Toronto for analysis.

Research Hypotheses to be tested:
(to be written as a null hypothesis)

There will be a high correlation between the questionnaire exposure estimates and the level of depleted uranium found in urine. Medical problems related to damage of the blood and/or hepatic systems will show an association with exposure data and urine sample analysis for depleted uranium.

Preliminary work to be accomplished:

Identification of principal investigators for each identified study group.

Development of a Grant Proposal, including the null hypotheses and protocols.

Development of a budget for each population study group.

Agreement of the Research team to undertake the study.

Raising of funds or assignment of costs for the study.

Identification and training of data entry processors for each group.

Benefits for Participants:

In addition to the general benefits to be obtained by clarifying the health effects of exposure to this toxic material, especially in the ceramic form experienced in the Gulf War, each participant testing positive for DU in a urine analysis will be assisted to enter a chelating process to remove as much as possible of the contaminant from the body.

References:

ATSDR 1998: Toxicological Profile for Uranium Draft for Public Comment, US Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Ragistry, September 1997.

Cooper JR, Stradling GN, Smith H, et al 1982. The behaviour of uranium 233 oxide and uranyl 233 nitrate in rats. International Journal of Radiation Biology and Related Studies in Physics, Chemistry and Medicine. Vol 41(4): 421-433.

Cross FT, Palmer RF, Busch RH et al, 1981. Development of lesions in Syrian golden hamsters following exposure to radon daughters and uranium dust. Health Physics Vol 41:1135-153.

Dungworth DL. 1989 Non-carcinogenic responses of the respiratory tract to inhaled toxicants. In: Concepts in Inhalation Toxicology. Editors: McClellan RO, and Henderson RF. Hemisphere Publ. Corp. New York NY.

Dygert HP 1949. Pharmacology and Toxicology of Uranium Compounds. Pages: 647-652, 666-672, and 673-675. McGraw Hill Books Inc.

Encyclopaedia of Occupational Health and Safety, Third (Revised) Edition. Technical Editor: Dr. Luigi Parmeggiani, published by the International Labour Organization in 1983 (ISBN: 92-2--103289-2) Geneva, Switzerland.

Gindler JE, 1973. Physical and Chemical Properties of Uranium. In: Uranium, Plutonium and Transplutonic Elements Editors: Hodge et al. New York NY: Springer Verlag; 69-164.

ICRP 1991: Recommendations of the International Commission on Radiological Protection. Publication, accepted in 1990 and reported in Publication 60. Pergamon Press, UK.

Saccamanno G, Thun MJ, Baker DB, et al 1982. The contribution of uranium miners to lung cancer histogenesis renal toxicity in uranium mill workers. Cancer Research Vol. 82 43-52.

Spiegel CJ, 1949. Pharmacology and Toxicology of Uranium Compounds. McGraw Hill Book Co.Inc.

Stokinger HE, Baxter RC, Dygent HP, et al 1953. In: Toxicity Following Inhalation for 1 and 2 Years. Editors: Voegtlin C and Hodge HC.

Stokinger HE, 1981. Uranium. In: Industrial Hygiene and Toxicology. Vol 2A, 3rd Edition. Editors:Clayton CD and Clayton FE. John Wiley and Sons, New York NY, 1995-2013.

Stradling GN, Stather JW, Gray SA, et al. The metabolism of Ceramic Uranium and Non-ceramic Uranium Dioxide after Deposition in the Rat Lung. Human Toxicology 1988 Mar 7; Vol 7 (2): 133-139.

UNSCEAR: United Nations Scientific Committee on the Effects of Atomic Radiation reports to the UN General Assembly.

Wedeen RP, 1992. Renal diseases of Occupational Origin. Occupational Medicine Vol 7 (3):449.

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henryhus 　於　2001/02/26 08:32
發表內容：

強盜;
---我看了這篇文章想起原來美國各大煙草公司
採用金錢禮品收買一些醫學人士發表吸煙無害論
的文章的事來。
------------------------------------------------------------------------
你這是很不恰當的比喻!!我們可以說那些專家被煙草公司
收買,是因為他們的研究與大多數其他醫生的研究相反
而且有很多自己沒辦法合理解釋的漏洞,更重要的是與
一些已知的醫學理論不合!!但是貧鈾上恰恰相反:
一些與貧鈾相關報導根本違反目前已知的關於貧鈾
的性質!!這些paper並不是在貧鈾事件後才被收買後寫下
而是遠在此事件前就已確認的!hneryhsu以前在大學時念
toxiology,radiobiology時就已經唸過了,尤其是最奇怪的一點是
只要是貧鈾的報導,一定會刻意強調白血病!!這根本是違反
醫學的基本關唸!!!其中包括who(世界衛生組織)的專家
都出面反對!!反倒是這些所謂的反貧鈾人士的動機相當可疑
---

--------------------------------------------------------------------------------

henryhus 　於　2001/02/26 08:33
發表內容：

強盜;
---我看了這篇文章想起原來美國各大煙草公司
採用金錢禮品收買一些醫學人士發表吸煙無害論
的文章的事來。
------------------------------------------------------------------------
你這是很不恰當的比喻!!我們可以說那些專家被煙草公司
收買,是因為他們的研究與大多數其他醫生的研究相反
而且有很多自己沒辦法合理解釋的漏洞,更重要的是與
一些已知的醫學理論不合!!但是貧鈾上恰恰相反:
一些與貧鈾相關報導根本違反目前已知的關於貧鈾
的性質!!這些paper並不是在貧鈾事件後才被收買後寫下
而是遠在此事件前就已確認的!hneryhsu以前在大學時念
toxiology,radiobiology時就已經唸過了,尤其是最奇怪的一點是
只要是貧鈾的報導,一定會刻意強調白血病!!這根本是違反
醫學的基本關唸!!!鈾-238不會引起白血病這在醫學是基本常識
這其中包括who(世界衛生組織)的專家都出面反對!!反倒是這些
所謂的反貧鈾人士的動機相當可疑
---

--------------------------------------------------------------------------------

henryhus 　於　2001/02/26 09:03
發表內容：

再者Prof Otto G Raabe 是醫學界相當受人敬重的專家
如果他所言不實,早就被美國醫學界群起而攻之了!

--------------------------------------------------------------------------------

henryhus 　於　2001/02/26 18:05
發表內容：

強盜:
1HENRYHUS倒滿好奇的,你看的懂你貼的東東嗎???
2:你貼的實在毫無義意,根本沒有實質的DATA---

--------------------------------------------------------------------------------

henryhus 　於　2001/02/26 18:09
發表內容：

=======================================
以下是一篇海牙和平會議上結合事實研究對貧鈾
較?翔實的報告。
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HENRYHSU是完全不會去看這種東西的-----

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henryhus 　於　2001/02/26 18:09
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以下是一篇海牙和平會議上結合事實研究對貧鈾
較?翔實的報告。
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HENRYHSU是完全不會去看這種東西的-----

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Skywalker 　於　2001/02/26 22:29
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Henryhus
閣下是否是被趕出全防討論區的那一位！

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henryhus 　於　2001/02/27 11:25
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SKYWAKER:
是!!實在莫名其妙!!

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Skywalker 　於　2001/02/27 19:47
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那邊快要淪為中華人民共和國網友的一言堂，根本就已經淪陷了！故咱們這些DIIC老網友在小滬尾兄經營的網站停留時間越來越長，閣下實話實說確遭驅逐的遭遇，值得同情！

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henryhus 　於　2001/02/27 20:44
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skywalker:
該網管居然說我假冒你之名 貼帖子,真是
奇怪!!!

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Skywalker 　於　2001/02/27 20:57
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敝人記得www.diic.com.tw未設置網管，怎會冒出一個網管？

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路過的人 　於　2001/02/28 13:23
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最近的〝自然〞雜誌 (Nature)有一篇探討這題材的短文...
(Nature Vol. 409, p121, Jan 11, 2001)
文中並不認為有足夠証據顯示
uranium shells與leukaemia有密切相關！

文中並引述德國政府核能研究實驗室的領導人
Manfred Paschke 所言：

If anything, we would expect depleted uranium to
cause lung or bone cancer, rather than leukaemia.

另外，小弟提供一則反駁性的文章...

http://www.llrc.org/durs.htm
(小弟不貼原文啦...長的嚇人，沒興趣的會看到發瘋！)

有興趣的網友可自行查閱參考本文...

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henryhus 　於　2001/02/28 16:01
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路過的人:
你講到重點了,---根據以前的研究,
U-238可能跟 LUNG OR BONE CANCER
有關,但不會導致白血病這是很多研究很早就證
實了!!

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henryhus 　於　2001/02/28 16:29
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路過的人:
好長啊!!不過總算看完了,這是一篇滿典型
用一大堆專業術語嚇唬外行人的文章

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henryhus 　於　2001/02/28 16:48
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