Depleted Uranium is Teratogenic

A Primer in the Art ofDeception

The Cult of Nuclearists, Uranium Weapons

and Fraudulent Science

by Paul Zimmerman

Copies of this book can be ordered at www.du-deceptions.comor by contacting the author at either [email protected]

or P.O. Box 145, Lyndonville, NY14098

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What follows is an excerpt from A Primer in the Art of Deception. The chapter in which itappears is entitled The Harlot of Babylon Unmasked: Fraudulent Science and the Cover-up of theHealth Effects of Depleted Uranium.

Depleted Uranium is Teratogenic

Being genotoxic, cytotoxic and mutagenic, depleted uranium can disrupt normalfetal development. It has the capacity to induce mutations in the male and female germ

T h e H a r l o t o f B a b y l o n U n m a s k e d : F r a u d u l e n t S c i e n c e

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cells prior to conception, and it can adversely affect the developing embryo/fetus at anytime between conception and birth. In experimental animals exposed to uranium com-pounds, uranium has been found to accumulate in the testes (ATSDR). Gulf War veteranswounded by DU shrapnel have elevated levels of uranium in their semen (Royal Society).In light of this discovery, the Royal Society cautions that this raises “the possibility ofadverse effects on the sperm from either the alpha-particles emanating from DU, chemicaleffects of uranium on the genetic material or the chemical toxicity of uranium.” Othershave postulated that an enhanced hazard to the DNA in sperm cells is created due to syn-ergistic effects between uranium’s alpha emissions and its chemically induced oxidativestress (Arfsten et al.; Domingo 2001). In experiments on female rats, it was discovered thaturanium crosses the placenta and concentrates in the tissue of the fetus (ATSDR; RoyalSociety; Albina et al. 2003). In experiments involving the implantation of DU pellets intopregnant female rats, it was observed that the amount of contamination to the mother wasdirectly related to the amount of contamination in the placenta and in the fetus (Arfsten etal.; Domingo 2001).

One little-known effect of the Gulf War was the statistically significant increase inthe incidence of birth defects among babies born to veterans. This conclusion came to lightin an epidemiological study performed by Araneta and her associates and published underthe title “Prevalence of Birth Defects Among Infants of Gulf War Veterans in Arkansas,Arizona, California, Georgia, Hawaii, and Iowa, 1989-1993.” The researchers investigat-ed the military records of 684,645 Gulf War veterans and 1,587,102 non-deployed veter-ans and the birth certificates of 2,314,908 babies born in states that conducted active caseascertainment of birth defects. From this information, they identified 11,961 infants bornto Gulf War Veterans and 33,052 infants born to non-deployed veterans. This data furtheridentified 450 infants born to mothers who had served in the Gulf War and 3966 infantsborn to non-deployed mothers. For infants conceived postwar to male veterans, a signifi-cantly higher prevalence of tricuspid valve insufficiency and aortic valve stenosis was dis-covered, compared to their non-deployed counterparts. Also, among Gulf War veterans,there was a higher incidence of aortic valve stenosis and renal agenesis [absent or imper-fect development of the kidney] or renal hypoplasia [underdevelopment of the kidney] ininfants born after service in the Gulf than among infants conceived prior to the war. Inaddition, this study confirmed that the incidence of hypospadias [an abnormal location ofthe opening of the urethra] was significantly higher among male infants conceived byfemale Gulf War veterans compared to male infants born to non-deployed women.

Under the best of circumstances, designing and successfully carrying out an epi-demiological study on the variables affecting birth outcomes presents a rigorous challenge.To produce meaningful results in any impoverished country ravaged by war is probably

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impossible. Limited access to health care, poor or nonexistent record keeping, travel restric-tions, an impoverished standard of living, hunger, stress, the list goes on and on, all worktogether to camouflage trends in birth outcomes and the incidence of neonatal deaths andcongenital malformations. A more suitably chaotic environment could not be envisionedfor allowing an aggressor to escape accountability in unleashing weapons that target repro-ductive health.

In the absence of definitive epidemiological studies which might define the terato-genic capacity of DU, what alternative sources of information are available to provideinsight into possible harm inflicted on developing embryos and fetuses in countries target-ed with DU weapons? The answer to this question, as if completing a large circle, bringsus back to the corrupted theory of radiation effects from internalized radioactive particlesand the political propaganda this false science has spawned. According to publication No.90 of the ICRP (2003), the threshold dose for radiation-induced teratogenic effects is 100mSv. And how was this number derived? You guessed it: from studies of the Japanesesurvivors of the atomic bombs dropped on Hiroshima and Nagasaki. And from amongstthis population, the only increased risks to fetuses, exposed to the threshold dose or above,was mental retardation and reduced head size (Schmitz-Feuerhake). According to theAtomic Bomb Casualty Commission, there was no increase in the incidence of birth defectsamong children whose parents were exposed to the blasts (Nakamura). No genetic effectswere ever detected among the offspring of survivors. Presently, no increased rates of mor-tality or cancer incidence in children born to exposed parents have yet been detected.(Nakamura).

As examined elsewhere in this book, this data simply cannot be trusted. IngeSchmitz-Feuerhake from the Department of Physics at the University of Bremen,Germany, has this to say on the topic:

As was pointed out by different researchers, the Japanese datasuffer, however, from several restrictions which limit their suit-ability as a general base for deriving radiation risks. One pointis a probable and proven severe selection bias because of the cat-astrophic situation after the bombing. Another objection whichmust be stressed, especially considering perinatal effects, is thefact that the investigations of the Radiation Effects ResearchFoundation (RERF) in Hiroshima did not begin earlier than 5years after the catastrophe when the RERF research institutewas established there. The completeness of the data must there-fore be put into question (Schmitz-Feuerhake).

If we suspend belief in the reliability of the Hiroshima data, what other body of


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data exists that can provide knowledge of the teratogenic effects of radiation on popula-tions? Chernobyl! Numerous studies conducted throughout Europe testify that radiationreleased into the environment produced a wide spectrum of developmental malformationsat doses far below the threshold dose upheld by the ICRP. This explains one reason for thepropaganda campaign pursued by the radiation protection agencies that attempts to dismissthe Chernobyl accident as either poorly researched or of little consequence.

Many hundreds of scientific papers have been published in Russia and throughoutEurope on the catastrophic effects of Chernobyl on public health (ECRR 2006; IIRC). Anexcellent summary of this vast body of evidence was recently published by the EuropeanCommittee on Radiation Risk under the title Chernobyl: 20 Years On. The essays within thisvolume, written by respected authorities in their field, represent a first attempt to compilethe vast amount of data on the Chernobyl disaster that was originally published in lan-guages other than English. Pertinent to the present discussion is the article “Radiation-induced Effects in Humans After in utero Exposure: Conclusions from Findings After theChernobyl Accident.” The author, Inge Schmitz-Feuerhake, provides an overview ofdozens of studies which confirm that low levels of radiation present in many areas ofEurope after Chernobyl were responsible for a wide variety of birth defects. The data fromChernobyl are dangerous. It bears witness that the conclusions drawn from the atomicbomb survivors is fallacious, fraudulent and felonious. Further, it demonstrates that levelsof internal contamination deemed to be without consequence by the radiation protectionagencies could be responsible for producing the types of birth defects reported in Iraq andAfghanistan.

What follows is a summary of teratogenic effects documented after Chernobyl withcitations of where the research was published. This evidence, gathered by Schmitz-Feuerhake, demonstrates that plenty of scientific evidence exists of “nonmalignant” disor-ders produced by Chernobyl.

Observed increase of congenital malformations in utero after exposure bythe Chernobyl accident:

Belarus National Genetic Monitoring Registry-Anencephaly, spina bifida, cleft lip and/or palate, polydactyly, limb reduction defects, esophageal atresia, anorectal artesia, multiple malformation (Lazjuk et al. 1997)

Belarus highly exposed region of Gomel- Congenital malformations (Bogdanovich 1997; Savchenko 1995)


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Chechersky district of the Gomel region- Congenital malformations (Kulakov et al. 1993)

Mogilev region- Congenital malformations (Petrova et al. 1997)

Brest region-Congenital malformations (Shidlovskii 1992)

Ukraine, Polessky district of the Kiev region-Congenital malformations (Kulakov et al. 1993)

Lygyny region-Congenital malformations (Godlevsky and Nasvit 1998)

Turkey-Anencephaly, spina bifida (Akar et al. 1988/89; Calayan et al. 1990; Güvenc et al. 1993; Mocan et al. 1990)

Bulgaria, region of Pleven- Malformations of heart and central nervous system, multiple malformations (Moumdjiev et al. 1992)

Croatia-Malformations by autopsy of stillborns and cases of early death (Kruslin et al. 1998)

Germany, German Democratic Republic, Central Registry-Cleft lip and/or palate (Zieglowski and Hemprich 1999)

Bavaria- Cleft lip and/or palate, congenital malformations (Scherb and Weigelt 2004; Korblein 2003a, 2004; Scherb and Weigelt 2003)

West Berlin, Annual Health Report of 1987- Malformations in stillborns (Strahlentelex 1989)

City of Jena, Registry of Congenital Malfomations-Isolated malformation (Lotz et al. 1996)


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Observed increase of stillbirths, infant deaths, spontaneous abortions andlow birth weight after in utero exposure by the Chernobyl accident

Belarus, selected regions- Perinatal deaths (Petrova et al. 1997)

Chechersky District near Gomel- Perinatal deaths (Kulakov et al. 1993)

Gomel region- Perinatal deaths (Korblein 2003a, 2003b)

Ukraine, Polessky District near Kiev- Perinatal deaths, reduced birth rate, premature births (Kulakov et al. 1993)

Lygny region-Early neonatal deaths (Godlevsky and Nasvit 1998)

Zhitomir oblast, Kiev region, Kiev City-Perinatal deaths, reduced birth rate (Korblein 2003a, 2003b)

Europe: Greece, Hungary, Poland-Stillbirths (Scherb et al. 1999b, 2000b, 2003)

Sweden-Infant mortality (Korblein 2003a)

Poland-Spontaneous abortions (Ulstein et al. 1990)

Norway-Low birth weight (Czeisel 1988)

Hungary-Premature births among malformed children (Harjulehto et al. 1989)

Finland-Reduced birth rate (Harjulehto et al. 1991), Stillbirths (Scherb and Weigelt 2003)


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Germany- Total FRG + GDRPerinatal deaths (Korblein and Kuchenhoff 1997; Scherb et al. 2000a, 2003)

Southern Germany-Early neonatal deaths (Lüning et al. 1989)

Bavaria- Perinatal deaths, stillbirths (Grosche et al. 1997; Scherb et al. 1999a, 2000a, 2003)Reduced birth rate (Korblein 2003a)

Increase of Down’s syndrome after in utero exposure by the Chernobyl accident

Belarus, National Genetic Monitoring Registry-Excess 1987-1994 ca. 17% (Lazjuk et al. 1997)

Western Europe-Beginning one year after the accident, reaching 22% within 3 years (Dolk et al. 1999)

Sweden- “Slight” excess in most exposed areas (30%) (Ericson and Kallen 1994)

Scotland, Lothian Region (0.74 million inhabitants)-Excess peak in 1987 (2-fold significant) (Ramsay et al. 1991)

South Germany-Investigations of amniotic fluid (Sperling et al. 1991)

Berlin West-Sharp increase after 9 months (Sperling et al. 1991, 1994)

Observed health defects in children after in utero exposure by theChernobyl accident apart from malformations and Down’s syndrome

Belarus, Selected Regions-Mental disorders (Kondrashenko et al. 1996)Speech-language disorders, mental retardation (Kolominsky et al. 1999)


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Chechersky District near Gomel-Diseases of respiratory organs, blood, circulation, etc. (Kulakov et al. 1993)

Stolin District in Brest region-Diseases of respiratory organs, glands, blood, circulation, digestive organs (Sychik and Stozharov 1999a, 1999b)

Belarus, Ukraine, Russia-Mental retardation and other mental disorders (Kozlova et al. 1999)

Ukraine, Polessky District near Kiev- Diseases of respiratory organs, blood, circulation etc. (Kulakov et al. 1993)

Ukraine, Rovno Province- Childhood morbidity (Ponomarenko et al. 1993)

Immigrants to Israel from contaminated areas- Asthma (Kordysh et al., 1995)

The evidence of the teratogenic impact of Chernobyl is overwhelming. Yet, asSchmitz-Feuerhake observes, this evidence is ignored by the international radiation protec-tion committees. These experts retreat from the evidence by fielding the stale argumentthat doses of radiation, estimated from environmental monitoring of cesium isotopes, aremuch too low to be responsible for the purported effects. According to these estimates, themean effective lifetime exposure for people dwelling in large regions of Europe and Turkeywas below 1.2 mSv (UNSCEAR 1988). The highest average dose to a population in thefirst year after the accident occurred in Belarus and was estimated at 2.0 mSv. The arrayof observed teratogenic effects at these doses scream out that the current science of radia-tion effects is deeply flawed. As to the problem, take your pick: (1) Environmental moni-toring of cesium is a useless tool in estimating the “dose” to a population in the aftermathof a radiation release. (2) The people in Europe received much higher “doses” fromChernobyl than estimated. (3) Teratogenic effects can be induced by internal emitters atmuch lower “doses” than the corrupted Hiroshima data upheld by the radiation protectionagencies would suggest. The spin-masters are pinned to the wall by this bind. Whateveroption they choose, the masquerade disguising Chernobyl effects crumbles!

To navigate the morass of untruths and deceptions, Schmitz-Feuerhake proposesthat biological dosimetry should be utilized to give more accurate dose estimates than thephysical dosimetry of measuring environmental cesium:


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Investigations of unstable and stable chromosome aberrations inthe lymphocytes of persons in the contaminated regions havebeen carried out by a variety of research groups in rather largecollectives directly after the accident or some years later.Dicentric chromosomes can be considered as radiation-specificand most sensitive because of their very low and nearly constantrate in unexposed persons (Hoffmann and Schmitz-Feuerhake,1999).

It is generally found that the observed rates of dicentric chromo-somes after Chernobyl are considerably higher — by 1 or 2orders of magnitude — than would be expected from physical-ly derived dose estimates. This evaluation is possible althoughthe dose-effect relationships in cases of incorporated radioactiv-ity are not known. For low dose homogenous exposure by lowLET irradiation the rate of dicentrics can be considered asdose-proportional which follows from studies in the range ofbackground exposure. In European countries, far from theChernobyl site, the exposure of the tissues, except the thyroid,is assumed to be mainly generated by Cs137 and Cs134 whichdistribute homogeneously inside the body. The whole-bodydoubling dose for dicentrics by homogeneous low LET radia-tion is about 10 mSv (Hoffmann and Schmitz-Feuerhake,1999). Elevations of dicentrics in persons which are higher than2-fold would therefore mean that the whole-body dose exceeds10 mSv. Such elevations have been found manifold afterChernobyl. A remarkable finding in many of the chromosomestudies is that they report an overdispersion of the dicentrics andthe occurrence of multi-aberrant cells (Bochkov and Katosova1994; Hille et al. 1995; Salomaa et al. 1997; Scheid et al. 1993,Sevan`kaev et al. 1993; Stephan and Oestreicher 1989;Verschaeve et al. 1993). This is an indication of a relevant con-tribution of incorporated alpha-activity which is not consideredadequately in the physical dose estimates.

The chart on the following page is reproduced from the Schmitz-Feuerhake article.It clearly demonstrates that “official” dose estimates for people living in certain areas ofEurope are woefully inaccurate when compared to the biological dosimetry of chromosomeaberrations in lymphocytes. Such a discrepancy once again casts doubt on the scientificintegrity of those organizations who are supposedly protecting the world from radioactivepollution. The science speaks for itself: the population in many areas of Europe receivedmuch higher doses from Chernobyl than generally accepted and birth defects were inducedfrom much smaller doses than suggested by ICRP science.


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In the article “The Chernobyl Catastrophe — 20 Years After (a meta-review),”Alexey V. Yablokov of the Russian Academy of Sciences summarizes the extensive researchthat has been carried out on the health effects from the accident. The congenital malfor-mations which increased in frequency after 1986 included cleft lip and/or palate (“harelip”), doubling of kidneys, polydactyly (extra fingers or toes), anomalies in the developmentof nervous and blood systems, amelia (limb reduction defects), anencephaly (defectivedevelopment of the brain), spina bifida, Down’s syndrome, esophageal and anorectal atre-sia, and multiple malformations occurring simultaneously. In 15 heavily contaminated dis-tricts in Belarus, the frequency of congenital malformations increased between 200% and300% between the years 1982-1985 and 1987-1989. In a study of 30 areas with low levelsof contamination, less than one curie per cubic kilometer, significant increases in the ratesof many of the aforementioned congenital malformations were observed (Lazjuk et al.1999).

The evidence from Chernobyl must be considered when assessing the hazards ofdepleted uranium. Low levels of environmentally dispersed radionuclides from the acci-

Chromosome aberrations in lymphocytes of persons living in WestEuropean regions contaminated by Chernobyl releases;

(dics = dicentric; cr = centric rings)

Region Sample Date ofStudy

Method Results(mean

elevation)

Reference Remarks

Salzburg,Austria

17 adulsts 1987 dics + cr Ca. 4-fold Pohl-Rüling etal. 1991

Germany:southernregions

29 chilrden+ adults

1987-1991 dics + cr Ca. 2.6-fold Stephan,Oestreicher

1993

physical dose estimate <0.5

mSv

Norway:selected regions

44 reindeerSamis, 12

sheep farmers

1991 dics + cr 10-fold Brogger et al.,1996

physical dose estimate 5.5

mSv


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dent produced congenital malformations. This fact glaringly highlights that the main-stream science of radiation effects, which denies that such malformations could haveoccurred, is wrong. The pronouncements of the official mouthpieces simply cannot betrusted. The whole enterprise is in disrepair. Scientists of integrity must step forward andfinally put their house in order, for the reigning science is phony and the layperson can nolonger buy into the lies.

Complementing the data from Chernobyl are other studies which have proven thatlow levels of radiation in the environment produce birth defects. One study was publishedby Padmanabham et al. under the title “Heritable Anomalies Among the Inhabitants ofRegions of Normal and High Background Radiation in Kerala: Results of a Cohort Study1988-1994.” Although not a study of depleted uranium exposure, this research is pertinentto the discussion because it demonstrates that exposure to low levels of background radia-tion can influence pregnancy outcomes. The authors conducted a genetic epidemiologicaland fertility survey of 70,000 people in the region around Kerala, India. Part of the studypopulation lived in regions where they received annual exposure to normal levels of back-ground radiation, 85 to 100 mR/yr. (estimated from measurements taken 10 centimetersabove the soil). The remainder dwelt in regions of significantly higher levels of backgroundradiation produced by a high concentration of the mineral monazite in the soil which con-tains thorium, uranium and their radioactive daughters. Their estimated annual exposureaveraged 563 to 735 mR/yr. (based on measurements taken 10 and 100 centimeters abovethe soil). Contrary to the propaganda matrix which insists that doses this low cannot pos-sibly produce birth defects, this research revealed that those living in areas of high back-ground radiation had a statistically significant increase in congenital malformations includ-ing Down’s syndrome, autosomal dominant anomalies and multifactorial diseases. Thesefindings were not an isolated occurrence. In their article, the authors mention similar stud-ies conducted in areas of high background radiation which, on the whole, supported theirfindings:

A cytogenetic study in the Brazilian HBRR [high backgroundradiation region] with background radiation of 640 mR/yr.showed a significant increase in chromosome aberrations(Barcinsky et al.). Wei and colleagues reported a higher inci-dence of Down syndrome, chromosomal aberrations, and reac-tivity of T lymphocytes in Yanjiang County of China. Gopal-Ayengar and colleagues (1970) observed a higher incidence ofcytological abnormalities and pollen sterility in four species ofwild plants from the Kerala HBRR. However, Gruneberg andassociates (1966) found no difference in musculoskeletal abnor-malities in rats (Rattus rattus I.) from the HBRR and NRR [nor-


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mal-radiation region]. In a cytogenetic study of 1,482 adultsand infants from the Kerala HBRR and NRR, there was a 50percent excess of aberrations among the subjects from theHBRR (George 1983, Cheriyan 1983). Nevertheless, in a sur-vey of 2,381 couples from the HBRR and NRR, Gopal-Ayengar and colleagues (1972) did not find any difference inrates of fertility, mortality, and twinning. Kochupillai and col-leagues (1976) reported a higher incidence of Down syndromeand severe mental retardation in the Kerala HBRR. Georgeand co-workers (1989) did not find any significant increase ofDown syndrome and other congenital anomalies in 3,000infants born to parents from the HBRR.

Research on the teratogenic effects of depleted uranium in animals provides a the-oretical basis for the possibility that such effects may also occur in humans. Domingo andcolleagues, working at the University of Barcelona in Spain, have published a number ofanimal studies on the reproductive effects of DU in mice. Their work has demonstratedthat the administration of UO2

++ to female mice, both orally and subcutaneously, leadsto decreased fertility, embryonic and fetal toxicity, including reduced growth and malforma-tions (cleft palate and skeletal defects), and developmental ossification variations (Hindin etal.). As interpreted by Domingo and his group, these aberrations were induced by urani-um’s chemical toxicity working on many levels: the molecular level (damaging DNA andRNA), at the cellular level, and/or at the organ level, affecting organs including the testes,placenta and embryo/fetus (Hindin et al.).

Other animal studies have demonstrated the teratogenic capacity of uranium. In “AReview of the Effects of Uranium and Depleted Uranium Exposure on Reproduction andFetal Development,” Arfsten, Still and Ritchie offer the following observations:

Based on a review of the pertinent literature, there are severallines of evidence to suggest that DU exposure could potentiallyaffect reproductive function and development in rodents. Atthis time, information on the reproductive and developmentaleffects of DU alloy in rodents is limited. However, existing dataindicate that implanted DU translocates to the rodent testes andovary, the placenta and fetus (Benson 1998; Pellmar et al. 1999a).DU has been shown to be genotoxic in in vitro cell model systems(Miller et al. 1998a) and possibly carcinogenic in rats (Hahn et al.2002) suggesting that DU alloy could potentially disrupt or dam-age rapidly dividing cell populations in the fetus and the adultrat.


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Studies of the effects of natural uranium provide additional evi-dence that DU could have an adverse effect on rodent reproduc-tion and development. Dosing of rodents with uranium hasbeen shown to cause testicular toxicity, maternal toxicity, feto-toxicity, increased developmental variations and growth retarda-tion independent of maternal toxic response (Domingo 2001).Intratesticular injection of enriched uranium compoundsincreased the incidence of cytogenic damage in developingmouse sperm (Hu and Zhu 1990). In vitro studies showed thaturanium is both cytotoxic and genotoxic to Chinese hamsterovary (CHO) cells (Lin et al. 1993) and reduces cell number indeveloping mouse embryos in culture (Kundt et al. 2000).

The Toxicological Profile for Uranium has this to say on the toxic effect of uranium onfetal development:

Because uranium can cross the placenta into the fetus, it is pos-sible that uranium may have adverse effects on fetal develop-ment, especially metallotoxicity to the embryonic kidneys or thebrain (Domingo et al. 1989b, 1989a; Paternain et al. 1989). Thepotential for teratogenicity and general developmental toxicityof uranium was demonstrated by results from oral animal stud-ies in which the following were reported in mice: increased fetalmortality, reduced survivability, reduced growth (Paternain et al.1989), reduced fetal body weight and length, an increased inci-dence of stunted fetuses, increased external and skeletal malfor-mations and developmental variations, an increased incidenceof cleft palate, underdeveloped renal papillae, and bipartitesternebrae, reduced or delayed ossification of the hind limb, forelimb, skull and tail, an increase in the relative brain weight ofthe offspring, a reduced viability and lactation index (Domingoet al. 1989a), and embryotoxicity (Paternain et al. 1989). Theseeffects have not been observed or documented in any humanstudy (ATSDR)

“In aggregate, the human epidemiological evidence is consistent with increased riskof birth defects in offspring of persons exposed to DU.” This is the conclusion of Hindin,Brugge and Pannikkar in their article “Teratogenicity of Depleted Uranium Aeerosols: AReview From an Epidemiological Perspective.” Their assessment that DU is a teratogenefollows from two “compelling strands of evidence.” First, plausibility has been amplydemonstrated by the numerous in vitro and in vivo studies which confirm that uranium is


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genotoxic, cytotoxic and mutagenic. Second, this theoretical evidence is finding humanexpression in the documented cases of birth defects in areas of Iraq which suffered theheaviest DU contamination. When data gathered prior to 1990 on birth defects in south-ern Iraq are compared to data gathered after the environment was contaminated with DU,an upward trend in the rate of incidence exists for a number of different types of congen-ital malformations.

Hindin and her colleagues report on data gathered by a clinical epidemiologyresearch team operating out of one of the three major maternity hospitals in Basra (Al-Sadoon et al.; Fasy). Since 1989, this group has maintained a congenital malformationsregistry which contains information on the health of all newborns assessed prior to dis-charge from the facility. The data gathered in 1990 is used as a baseline, representing apopulation unexposed to depleted uranium. In the years 1991 to 2001, the population wasdwelling in contaminated lands. The annual birth rate ranged between 9,845 and 13,905.In 1990, the number of congenital malformations recorded in the registry was 37, repre-senting an incidence rate of 3.04 per 1000 births. For the period 1991 through 1997, thenumber of congenital malformations hovered around the same rate, ranging from a low of1.31/1000 to a high of 4.56/1000. But starting in 1998, an alarming trend began to beobserved. That year, 79 babies were born with congenital malformations, a rate of7.76/1000. In 1999, 136 malformed babies were born (9.78/1000). In 2000, 221 babiessuffered congenital defects (17.6/1000). In 2001, the number rose to 254 (22.19/1000).

Hindin, Brugge and Panikkar created a redacted presentation of the data from theBasra Registry. The periods examined were 1990, 1991-94, 1995-98, 1999-2000. In addi-tion, they classified the total number of congenital malformations into distinct diagnoses.By this means, progressive increases in the rates of several disorders were easily recognized.Among these were births with multiple congenital malformations, congenital heart diseases,cleft lip and palate, and phocomelia (an unusual skeletal malformation in which the limbsare abnormally short). An increasing trend in neural tube defects was also noted. (Themost common types of NTDs are: anencephalia1, hydrocephalus, spina bifida andmeningomyelocele2. The overall incidence worldwide is 2.6 per 1000 total single births).Hindin reports this:

Between 1990 and 1999–2000 the incidence of anencephalyrose from 2.5 to 17.4 per 10,000 births and of meningomyelo-cele from 7.0 to 11.3 per 10,000. The relative risk of these twoNTDs among births in the study hospital for the years 1991–94,1995–98, 1999–2000, in comparison to 1990, were 0.74, 1.31,and 2.91. By 1999–2000, the combined prevalence rate ofanencephaly and meningomyelocele in the study hospital hadreached 29/10,000.


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In a separate study conducted by Al-Shammosy at the Diwaniah maternal and chil-dren’s hospital north and east of Basra, the incidence of neural tube defects in 2000 was8.4 cases per 1000. The types of defects noted included anencephaly, meningocele (protru-sion of the membranes of the brain or spinal cord through a defect in the skull or spinalcolumn), meningomyelocele and encephalocele (a congenital gap in the skull with hernia-tion of brain substance.) In yet another study reported by Al-Taha at the Iraqi CongenitalAbnormalities Clinic, a comparison was made of stillborns and children under two years ofage born before and after the Gulf War. Among 1038 children examined in 1989-1990compared to 945 children seen in 1992-1993, the incidence rate of anencephaly or hydro-cephalus rose from 0.5% to 1.1% and the percentage of patients seen with skeletal abnor-malities rose from 2.8% to 4.6%.

This quotation from an article in the Guardian Unlimited entitled “Victims of a WarThey Never Saw” paints a grim picture of the reality behind these statistics:

For the past three months Dr. Zenad has been monitoring thebirth defects in their delivery room, where 20 to 30 babies areborn daily. She keeps her findings in a hard-backed grey note-book. She has divided the page into columns, in which shewrites the sexes, dates of birth and weights of the babies. In afourth column, she logs their deformities. She begins: “August -we had three babies born with no head. Four had abnormallylarge heads.

In September we had six with no heads, none with large headsand two with short limbs. In October, one with no head, fourwith big heads and four with deformed limbs or other types ofdeformities.”

These reports from Iraq give added credibility to a small study conducted in NewMexico which suggested a possible relationship between DU exposure and the frequencyof hydrocephalus. Rural and sparsely populated, Socorro County is located downwind ofa DU-weapons testing site, the Terminal Effects Research and Analysis division of the NewMexico Institute of Mining and Technology. On average, 250 births occur yearly in thecounty. An investigation by a community activist revealed that between 1984 and 1986,five infants were born with hydrocephalus. (The normal rate of hydrocephalus is one casein every 500 live births). According to the demonstrably incomplete State of NewMexico’s passive birth defects registry, between 1984 and 1988, 19 infants were bornstatewide with the condition, three of these within Socorro county. Regardless of whichaccounting is correct, the results are disturbing given that Socorro contains less than 1%of the state’s population.


The impact of uranium on the developing fetus has not been thoroughly investigat-ed. Due to uranium’s affinity for bone, there are concerns that it may adversely affect skele-tal development. In light of the observation that uranium crosses the placenta and is trans-ferred from mother to fetus, the Royal Society has stated: “The effects of maternal expo-sure to DU on skeletal development in the fetus also need to be considered.” Such cautionis warranted in light of the fact that experiments on rats have demonstrated that both acuteand chronic intakes of uranium can cause damage to bones (Makhijani, Smith and Thorne2006). Often science finds disturbing echoes in peoples’ lives. In September 2004, the NewDaily reported the experience of Gerald Darren Matthew who served in the 719thTransportation company based in Harlem. Following deployment in the Gulf, he begansuffering migraines, fatigue and a burning sensation while urinating. Undergoing properdiagnostic testing, he was found to be contaminated with DU. When his daughter, VictoriaClaudette, was born, she was missing three fingers (Rose).

A further unknown exists as to the effect of uranium incorporated into bone on thebone marrow and the production of blood cells. Research conducted in 2004 heightens thisconcern. Arruda-Neto and colleagues exposed young beagle dogs to daily doses of uranylnitrate and discovered that uranium accumulated in the marrow as much as in the bone.This was contrary to the results obtained from single, acute doses. If the marrow of theembryo likewise concentrates uranium, this raises concern about the possibility of urani-um-induced leukemia. Further, it suggests a possible mechanism for damage to the immunesystem given that stem cells developing in the bone marrow are precursors to the varioustypes of cells making up the immune system.

Another possible concern about uranium contamination in the fetus is its negativeimpact on the developing brain. As observed by Makhijani et al.: “uranium’s primarychemical form in the body is as the uranyl cation (UO2

2+) which is a toxic heavy metalchemically analogous to the lead cation (Pb2+) [Lemercier et al. 2003; Domingo 2001].Thus, the known neurotoxicity of lead suggests that uranium may produce similar chemi-cal effects. Similar to lead, uranium’s chemical actions induce oxidative stress in the body,adversely affecting cellular structure and function. Further, like lead, uranium is known tocross the blood-brain barrier. When this is taken into consideration, along with uranium’sradioactivity, warning flags go up that uranium may adversely affect the brain of the devel-oping fetus.

There is some evidence to show that uranium may adversely affect hormone func-tion. Whish and colleagues report that uranyl nitrate mimics estrogen activity in vivo and invitro. In addition, some have postulated that uranium in the fetus may create hormonal orenzymatic disruption (Arfsten et al.; Domingo 2001). This possibility is mentioned by

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Makhijani, Smith and Thorne in their article “Science for the Vulnerable: SettingRadiation and Multiple Exposure Environmental Health Standards to Protect Those Mostat Risk”:

The potential for uranium to affect the hormonal systems is sug-gested by research on exposures to lead which shares chemicalsimilarities with uranium in the body (Lemercier et al. 2003).Recent research has shown that both “prenatal and postnatalexposure to lead is associated with growth restriction in labora-tory animals and humans” and that exposure to lead can alsoalter sex hormone production and delay puberty in rats (Selevanet al. 2003). An epidemiological study published in 2003 foundthat even relatively low average levels of lead caused a measur-able delay in puberty in African-American and Mexican-American girls, whereas no statistically significant delay in non-Hispanic White girls was found. The observed effect on thegirls’ sexual development was tentatively attributed, at least inpart, to potential “alterations in endocrine function (Selevan etal. 2003).” Many questions as to how lead caused the observeddelay and whether or not the children had been exposed to high-er levels in the past before the study’s screening began remainunanswered. Nonetheless the potential for uranium to play ananalogous role in affecting hormonally mediated processes indeveloping children could add further to its list of health con-cerns and could also add significant new avenues for potentialsynergisms with its other chemical and radiological healtheffects. This research also raises the question of the combinedeffects of exposure to uranium and hormonally active com-pounds. This is an area requiring further study.

A mysterious medical condition emerged from the Gulf War that may be related tothe teratogenicity of depleted uranium. Upon returning home, a small number of veter-ans reported feeling a burning sensation after contact with their own semen. The wives ofthese men reported vaginal pain, swelling and burning after intercourse. Semen in contactwith their skin produced such reactions as redness, burning, swelling, rashes and blood blis-ters. These were symptoms suffered by women in the general population who had local-ized or systemic seminal plasma hypersensitivity, an allergy to proteins found in semen.This condition has been linked to specific immunoglobulin E antibody which is triggeredby seminal plasma protein antigens. Symptoms typically begin between five and 30 min-utes after intercourse and can last from hours to days. In severe cases, a systemic reactioncan occur involving breathing troubles/wheezing, hives, itching, dizziness, and in rare cases,


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vascular collapse or anaphylactic shock. Diagnosis of this condition relies on determiningwhether or not relief of symptoms occurs by use of a condom, preventing skin contact withsemen, and presence of the specific IgE antibodies. With perhaps the odd exception in thegeneral population, men do not have allergic reactions to their own semen.

In an attempt to determine whether “burning semen syndrome” was identical toseminal plasma hypersensitivity, Jonathan Bernstein and colleagues at the University ofCincinnati College of Medicine undertook research on the subject. Included in their inves-tigation was a posting on the internet of a screening questionnaire which was completed by211 respondents. Approximately 75 percent (159 of 211) of those who participated in theGulf War found the questionnaire through internet web pages that publicized the investi-gation to veterans throughout the United States and Canada. The remaining members ofthe study group answering the questionnaire were referred for evaluation by physiciansfrom United States Veterans hospitals. Eighty-nine percent (188 of 211) of the respondentshad either personally experienced burning after contact with their own semen or had a sex-ual partner who felt burning sensations after contact with their semen. As a control group,the questionnaire was distributed to 1073 women in the general population who suspectedthey had symptoms of localized and/or systemic seminal plasma hypersensitivity. Of these,12 percent fulfilled the diagnostic criteria.

Of the 211 people filling out the questionnaire, only seven percent (15 of 211)reported having symptoms of burning semen syndrome prior to being dispatched to theGulf. By contrast, 48 percent (101 of 211) developed symptoms immediately after theirfirst sexual contact upon returning home. Fewer than 50 percent (97 of 211) of the GulfWar couples reported relief of symptoms by use of a condom. For women suffering fromseminal plasma hypersensitivity in the general population, 100% report complete reliefafter condom use.

Bernstein and his colleagues summarize the results of their research as follows:

The common denominator of Gulf War burning semen syn-drome and seminal plasma hypersensitivity in the general pop-ulation are the symptoms of localized vaginal burning and painimmediately after contact with semen. However, the initialquestionnaire survey and subsequent clinical evaluationrevealed cogent differences. In seminal plasma hypersensitivityoccurring in the general population, the man is typically asymp-tomatic, and skin test responses to homologous semen are neg-ative. Symptoms experienced by women invariably disappearafter use of a condom. In contrast, male partners in the Gulf


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War burning semen syndrome often complain of burning aftercontact with their own ejaculates, and several of the men in thisstudy also exhibited positive skin tests to their own seminal plas-ma proteins. Moreover, less than half of the Gulf War femalepartners experienced relief of symptoms if partners used con-doms correctly. The questionnaire survey revealed that manyGulf War couples with burning semen syndrome exhibitedother features of the Gulf War syndrome, which tended to com-plicate the clinical evaluation and ultimate diagnosis of burningsemen syndrome. When Gulf War veterans were divided into“healthy” and “unhealthy” groups, a significant correlationbetween post-traumatic stress disorder and the “unhealthy”group was established. For this reason, Gulf War veterans whodid not have irrelevant concomitant somatic/psychologic com-plaints and their sexual partners were preferentially selected forthe treatment phase of this project to evaluate responses to ther-apy exclusive of these possible confounders.

In general, both women from the general population andfemale partners of Gulf War veterans exhibited specific IgGand IgE antibody responses to whole seminal plasma. However,as previously reported, the results of this study demonstratedthat IgE-mediated skin testing, with or without confirmatory invitro specific IgE antibody responses, was the best predictor ofsuccessful outcome after seminal plasma protein desensitizationin either the general population or Gulf War female partners.The combination of specific IgE skin tests to seminal plasmaprotein and successful therapeutic responses to rapid desensiti-zation in three of these Gulf War couples indicates that burn-ing semen syndrome is induced by an IgE-mediated mechanismin a subpopulation of Gulf War couples presenting with thisproblem. The cause(s) of non-IgE mediated burning semensyndrome remains to be determined.

Several Gulf War and male subjects from the general popula-tion were noted to also produce low levels of specific IgG andIgE antibody to their own seminal plasma protein. Indeed,three of four Gulf War men also demonstrated IgE-mediatedskin test reactivity. The significance of these findings isunknown but could represent either exogenous cross-reactivitybetween common environmental proteins or immunologicmimicry resulting in autoantibodies to one or more seminal


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plasma protein antigenic determinants in men. One or both ofthese possibilities is suggested by the fact that the vast majorityof patients claiming to have burning semen syndrome by histo-ry did not have these symptoms before the Gulf War exposure.Further work is necessary to determine whether antibodyresponses in male subjects have a functional role in the underly-ing immunologic phenomena associated with seminal plasmahypersensitivity and burning semen syndrome.

Simply stated, the results of Bernstein’s group demonstrate that the symptoms expe-rienced by a portion of Gulf War couples can be explained as an expression of seminalplasma hypersensitivity. However, the remainder are suffering symptoms as a result ofexposure to some noxious agent during service in the Gulf. Obviously, further research iswarranted. Given that depleted uranium is known to be deposited in the testes and hasbeen found in the semen of veterans, it is a prime candidate for study. As of this writing,there are no reports in the published literature that semen from veterans experiencing burn-ing semen syndrome has been subjected to isotopic analysis of uranium.

To put a human face on this topic, the experience of Terry Riordon and his wife,Susan, is very moving. Terry was a captain in the Canadian Armed Forces. Prior to hisservice in the first Gulf War, he was a cross-country skier and a marathon runner. Afterserving for two months in the Gulf, he returned home in February 1991. At that time, hecould barely walk. He had documented loss of motor control, chronic fatigue, respiratorydifficulties, chest pain, difficulty breathing, sleep problems, short-term memory loss, testiclepain, body pains, aching bones, diarrhea and depression (www.umrc.net). After his deathin April 1999, an autopsy was performed. Tests confirmed the presence of depleted ura-nium in his lungs and his bones.

In an article published in Vanity Fair in 2004, Susan Riordon offered these poignantmemories:

At first, Terry merely had the usual headaches, body pain, ooz-ing rash, and other symptoms. But later he began to suffer fromanother symptom which afflicts some of those exposed to DU:burning semen. “If he leaked a little lubrication from his penis,it would feel like sunburn on your skin. If you got to the pointwhere you did have intercourse, you were up and out of that bedso fast — it actually causes vaginal blisters that burst and bleed.”“It hurt [Terry] too. He said it was like forcing [semen] throughbarbed wire,” Riordon says. “It seemed to burn through con-


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doms; if he got any on his thighs or his testicles, he was in hell.”In a last, desperate attempt to save their sex life, says Riordon,“I used to fill condoms with frozen peas and insert them [aftersex] with a lubricant.” That, she says, made her pain just aboutbearable. Perhaps inevitably, he became impotent. “And thatwas like our last little intimacy gone” (Rose).

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Depleted Uranium is Teratogenic