J

Issue 9 Winter/Spring 2013

OURNAL

U.S. Army Nuclear and Combating WMD Agency

Combating WMD
3 The Decision to Expand Biological threat 

Reduction Efforts into Africa

1 USANCA’s Senior Leaders Transition, the 7th Annual Combating WMD Conference, and Recent 

Army Documents on Capabilities for Countering WMD

10 Fukishima Daiichi Operating and Design 

Characteristics with Relevance to the Army 

Reactor Program

20 Toxin Weapons: What’s the Worry?

16 Using Google Earth and Primary Ray-Tracing to 

 ModelThermal Effects of a Surface Burst

 36 Regulating CBRN Survivability

14 ABCA-Optimizing CBRN Interoperability

28 Biotoxins Used As Warfare Agents – Part 2

25 Nuclear Targeting and the Nuclear Employment Augmentation Team (NEAT)

Ralph F. Kerr, PhD

COL Juan Cuadrado

Phil Shubert

Mitchell Wise, PhD

Mr. Matthew Jackson

Nicholas P. Haugen

LTC Michael S. Quinn

John S. Nordin, PhD

CW5 Bruce D. Brandes

 CW5 Stephen A. Gomes

Inside the Journal

COMBATING WMD

FROM THE ACTING DIRECTOR

SCIENCE and TECHNOLOGY

INTERNATIONAL

L
BIOGRAPHY

COLONEL JUAN ARIEL CUADRADO

Colonel Cuadrado commissioned in the US Army Field Artillery in 1984 and joined 

the Chemical Corps in 1987. Early career assignments include the 2-162nd Field 

Artillery Battalion (Puerto Rico); the1-39th Field Artillery Airborne Battalion (Fort 

Bragg); and the 18th Field Artillery Airborne Brigade in Fort Bragg, and Operations 

Desert Shield and Desert Storm. As an Army Functional Area 52 (Nuclear and 

Counterproliferation Officer), he served in a variety of technical and operational 

assignments including the Department of Chemistry and the Photonics Research 

Center in the United States Military Academy in West Point; Los Alamos National 

Laboratories; the Defense Threat Reduction Agency; United States Forces Korea; 

the National Nuclear Security Administration, Department of Energy; and the Office 

of Nuclear Deterrence Policy, Office of the Undersecretary of Defense for Policy in 

the Pentagon. Colonel Cuadrado holds a B.S. in Industrial Chemistry (University 

of Puerto Rico), a Masters in Analytical Chemistry (Florida State University), and 

a Masters in National Resource Strategy (Industrial College of the Armed Forces, NDU). Colonel Cuadrado currently 

serves as Deputy Director of the U.S. Army Nuclear and Combating WMD Agency (USANCA) in Fort Belvoir, Virginia.

Combating WMD JU.S. Army Nuclear and CWMD Agency

OURNAL

Published by the 

United States Army Nuclear and CWMD Agency 

(USANCA)

Acting Director

COL Juan Cuadrado

Editor

Mr. Glen Scott

Editorial Board

COL Juan Cuadrado, Chairperson 

Dr. Martin Moakler, Analysis Division 

Mr. Mark Fishback, Operations Division

COL Michael Bolluyt, Capabilities Division

Mr. Thomas Moore, Executive Officer

Design/Layout

Mr. Gerald Barrington

Mrs. Cassonya Gates

Disclaimer: Combating WMD Journal is published semi-annually by the 

United States Army Nuclear and CWMD Agency (USANCA). The views 

expressed are those of the authors, not the Department of Defense 

(DOD) or its elements. Combating WMD Journal’s contents does not 

necessarily reflect the official U.S. Army positions and does not supersede information in other official Army publications.

Distribution: U.S. Army organizations and activities with CBRN-related 

missions, to include all combat and materiel developers and units with 

chemical and nuclear surety programs, and FA52 officers. The Secretary of the Army has determined that the publication of this periodical is 

necessary in the transaction of the public business as required by law. 

Article Submission: We welcome articles from all U.S. Government 

agencies and academia involved with CBRN matters. Articles are reviewed and must be approved by the Combating WMD Journal Editorial 

Board prior to publication. Submit articles in Microsoft Word without automatic features, include photographs, graphs, tables, etc. as separate 

files, please call or email us for complete details. The editor retains the 

right to edit and select which submissions to print.

Mailing Address: 

Director, U.S. Army Nuclear and CWMD Agency (USANCA), 5915 16th 

Street Bldg 238 Fort Belvoir, VA 22060-0529.

Telephone: 703-806-7848, DSN 656-7848, Fax 703-806-7900

Electronic Mail: usarmy.belvoir.hqda-dcs-G-3-5-7.mail.usanca-mail- box@mail.mil

Subject line: ATTN: Editor, CWMD Journal (enter subject)

Distribution Statement A: Approved for public release; distribution is 

unlimited
USANCA’s Senior Leaders Transition, the 7th 

Annual Combating WMD Conference, and Recent 

Army Documents on Capabilities for Countering WMD

COL JUAN CUADRADO

Acting Director

U.S. Army Nuclear and CWMD Agency

1 ISSUE 9 Combating WMD Journal

hortly after the publication of the 

previous issue of the Combating 

Weapons of Mass Destruction 

(WMD) Journal, the USANCA Director, 

Mr. Peter Bechtel, accepted a new assignment as Director of the Capabilities 

Integration Directorate (DAMO-CI) in 

HQDA G-3/5/7. He appointed me Acting 

Director until a new SES was selected to 

serve in this challenging dual-hatted position as Deputy G-3/5 and USANCA Director. After a very exciting and rewarding six months I am pleased to announce 

that Mr. Daniel M. Klippstein has been 

appointed as Deputy Director for Plans 

and Policy, Office of the Deputy Chief of 

Staff, G-3/5/7 and will soon start his duty 

as the new SES-Director for USANCA.

In the last issue of the Combating 

WMD Journal, Mr. Peter Bechtel discussed the implications of recent strategic guidance and CBRN capabilities required for the Joint Force in the 

21st Century. As the Acting Director of 

USANCA, I see daily how this strategic guidance is influencing the Army to 

refocus from a COIN Centric position 

to a broader mission spectrum requiring new capabilities. In particular, as a 

result of recent strategic guidance, the 

Army is taking a new look at the Combating Weapons of Mass Destruction 

(CWMD) mission area and determining what new capabilities are required 

across DOTMLPF. I thought it might be 

useful to update you on the critical Army 

documents that have recently been published from our Army Leadership, which 

describe Army capabilities required for 

the future, to include countering WMD. 

Additionally, as USANCA recently 

hosted its 7th Annual Combating WMD 

Conference here at Fort Belvoir, I wanted to highlight the key take-aways from 

the conference and describe some of 

the common themes and challenges we 

S gathered from both senior Army leaders 

and CWMD Action Officers from across 

the Army, especially from the Army Service Component Commands (ASCCs). 

I trust that you, at the conclusion of this 

discussion, will see how the CWMD 

Community will continue to play a critical role in facilitating CWMD capability 

development and executing CWMD missions in both Army and Joint formations.

A tiered strategic plan framework 

headlined by The Army Plan informs 

the US Army’s CWMD strategy. The 

Army Plan consists of four sections; 

the Army Strategic Planning Guidance; 

the Army Planning Priorities Guidance; 

Army Programming Guidance Memorandum and the Army Campaign Plan. 

These documents describe and define the Army’s long range vision, set 

the priorities, level of effort, resource 

levels and synchronize the details.

Section I of the Army Plan is the Army 

Strategic Planning Guidance (ASPG). 

The ASPG outlines the Army’s vision 

and role as part of the Joint Force. 

The document also nests Army guidance within National, OSD and Joint 

Directives and provides Army leaders 

a vision, direction, and strategic objectives over the near, mid and long-term. 

Last year, USANCA in collaboration 

with HQDA G-3/5/7’s CWMD and Proliferation Policy Division (SSD) authored 

the first ever CWMD Appendix to the 

Army Campaign Support Plan. This appendix was designed to complement the 

US Government’s CWMD efforts and 

compliments the Guidance for Employment of Force (GEF), Joint Strategic 

Capabilities Plan (JSCP), the National 

Military Strategy for CWMD, and the 

DoD Global Campaign Plan for CWMD. 

The Appendix is designed to bridge 

the gap between National Strategy 

and Army Strategy and provide senior 

army leaders a framework for CWMD.

As an Army Staff Officer involved in 

CWMD issues you must understand 

how the Army is using these documents 

to develop capabilities for the Joint Force 

Commander to effectively counter WMD 

in their Area of Responsibility. Most importantly, you are the subject matter 

expert on your staff that must articulate 

how to integrate these capabilities with 

our General Purpose Forces (GPF). 

Countering WMD is not a specialist function only performed by CBRN forces or 

special operations forces. Rather, it is 

a military mission that requires maneuver formations, primarily BCTs, to understand how to plan/integrate CWMD 

Enablers into their formation in order 

to support CWMD mission areas. The 

topic of CWMD while conducting Unified Land Operations was the theme of 

our conference this year, and I would 

like to share with you some of the highlights resulting from our conference. 

This year we were fortunate to have 

key senior leaders from across the DoD 

CWMD Community share their insights 

with the conference attendees. The keynote speaker was MG Tucker, ADCS 

G-3/5/7, who recently commanded the 

2 ID in Korea and brought his insights as 

a Division Commander who had to plan 

on conducting Elimination Operations 

on the Korean Peninsula. MG Tucker 

voiced his concern that we must do 

much more to prepare and train GPFs to 

conduct WMD Elimination (WMD-E) and 

Interdiction. He asked “How does a BCT 

prepare and train to conduct CWMD 

mission sets?” MG Tucker stated that 

CWMD is a growth industry and with 

the establishment of Regionally Aligned 

Forces the Army needs to prepare for 

an increase in GCCs requirements for 

Army CWMD capabilities in the future.

he 

s 

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al 

 

 

h 
Combating WMD Journal ISSUE 9 2

Maj Gen Crabtree, Commander 

for SJFHQ-E at that time, discussed 

his organization’s mission, which is 

to plan and train to enable command 

and control for WMD-E, but cautioned 

that they have no forces assigned to 

do the WMD-E mission. This highlights 

again the critical role the Army plays 

in CWMD and especially WMD-E.

MG Smith, Commander 20th SUPCOM, presented an overview of the 

20th capabilities and recent activities. 

It was an impressive statement of how 

far the 20th has developed its capabilities and reach globally in a relatively 

short timeframe. Increasingly, the 20th 

is getting more involved with ASCCs to 

support opportunities to develop partner nation capacity to support CWMD, 

leveraging the expertise found only in 

the 20th SUPCOM. Of course the 20th 

is very engaged supporting planning 

and exercises on the Korean Peninsula.

The other speakers at our conference 

came from across the Army and the 

Intelligence Community. Of particular 

interest was hearing from all the ASCCs, 

who spoke to CWMD activities and challenges in their respective areas. It was 

a good opportunity to synchronize and 

coordinate activities across ASCCs, as 

well as exchange best practices and lessons learned. Consistent in all the briefings and discussion was recognition of 

an increasing Army role in nonproliferation and counterproliferation activities.

With an anticipated increase in WMD 

proliferation, the Army must enhance 

its WMD detection, identification, interdiction, exploitation, and forensics 

capabilities. Army CBRN formations 

will play a major role in future CWMD 

operations, but their capacity remains 

limited. As a result, GPF will be required 

to execute complimentary CBRN tasks. 

However, GPF currently lack the mission essential tasks, training and equipment to effectively conduct full-spectrum 

CWMD operations. The Army will need 

to incorporate sufficient training of its 

GPFs on WMD-related tasks to successfully execute all possible aspects 

of CWMD Unified Land Operations.

Where nations are less capable, it is 

critical to focus U.S. Army assistance on 

building indigenous capability to combat 

WMD threats. Building partner capacity 

(BPC) is essential to increasing barriers to WMD proliferation and use; improving the ability to identify, mitigate 

and defeat emerging WMD threats by 

developing an active layered defense. 

The National Military Strategy to Combat 

WMD (NMS-CWMD) highlights cooperation with security partners as a critical 

enabler, and it includes, as one of the 

eight key mission areas, “security cooperation and partner activities (SCPA).” 

These sentiments are reinforced in the 

Quadrennial Defense Review (QDR) 

BPC Roadmap and the Office of the 

Secretary of Defense (OSD) Guidance 

for Employment of the Force (GEF). The 

Joint Strategic Capabilities Plan requires 

Theater and CWMD Campaign Plans 

enunciating further guidance toward 

CWMD SCPA. Together, the aforementioned strategic guidance documents 

provide a strong impetus for the Army 

to identify and assess current partner 

capacity-building efforts, and to identify and address the most critical gaps. 

We are living in interesting times 

today in DoD as the Army refocuses 

after almost 12 years of combat operations. With the increasing awareness of the WMD threat, the Army will 

continue to develop and transform relevant capabilities to counter the WMD 

Threat world-wide. The Army’s cohort 

of FA52 Officers across the Army and 

Joint Force, especially at the strategic 

and upper operational levels, provide 

a unique nuclear and CWMD expertise to serve as a key player and advisor in these areas, complementing 

the equally relevant role of the CBRN 

Defense Officers. I ask you all to stay 

relevant by maintaining your technical 

skills required as a FA52 Officer and 

by staying current on strategic and operational guidance, such as The Army 

Plan discussed here. You are uniquely 

positioned to mesh strategic and operational guidance and tasks with technical nuclear and CWMD capabilities 

and policy, ensuring the Army is always 

ready for future threats and challenges.
The Decision to Expand Biological Threat Reduction 

Efforts into Africa

Ralph F. Kerr, PhD

3 ISSUE 9 Combating WMD Journal

fter many years of success reducing the threat of weapons 

of mass destruction (WMD) primarily in the former Soviet Union (FSU) 

via the Cooperative Threat Reduction 

(CTR) program, the United States Government (USG) expanded defense department measures to reduce biological 

threats in Africa. This expansion of the 

Biological Threat Reduction (BTR) program comes at a critical time as national 

security challenges appear to be shifting 

from Al Qaeda, Iraq and Afghanistan to 

global economics, cyber threats, China, 

and the Arab Spring.1 The expansion of 

BTR was sponsored by Senator Richard 

Lugar (R-Indiana) and this legislation 

appears to have glided through the legislative process. As one of the original 

sponsor’s of the CTR program, not to 

mention being the most senior Republican in the Senate and the Republican 

leader of the Senate Foreign Relations 

Committee at the time2, Senator Lugar 

appears to have welded much power 

which greatly assisted the passage 

of this legislation. Understanding the 

context of this issue and the process 

involved in approving the expansion of 

BTR into Africa will shed light on this 

important national security decision.

 

A Brief History of the CTR and BTR 

Programs

Congress initiated threat reduction efforts with the FSU in November 1991 

and in December 2011 the CTR program 

celebrated twenty years of success3. 

The program’s accomplishments to date 

are impressive and include the elimination of more than seven thousand nuclear warheads; almost eight hundred intercontinental ballistic missiles (ICBMs); 

nearly five hundred ICBM silos; close to 

two hundred ICBM mobile launchers; 33 

nuclear carrying submarines; and many 

other FSU WMDs4. Through this program thousands of chemical weapons 

were neutralized; fissile materials were 

secured and safeguarded; and weapA ons facilities were converted to peaceful purposes. Additionally, the work of 

many former weapons scientists and 

engineers was redirected to other useful purposes besides weapons research 

and development. The brainchild of 

former Senator Sam Nunn (D-Georgia) 

and Senator Lugar, this program was 

originally created to thwart “the nuclear 

security and proliferation risks emanating from the disintegrating Soviet state.” 

The CTR program initially focused on 

those former Soviet states (Ukraine, 

Kazakhstan and Belarus) that were left 

with nuclear weapons after the fall of the 

Soviet Union as well as Russia itself5. 

Ukraine, Kazakhstan and Belarus are 

now nuclear free countries and Russia 

has many less WMDs, WMD capabilities 

and WMD infrastructure than it did prior 

to the dissolution of the Soviet Union6. 

On the biological threat side, engagement with Russian officials proved to 

be more difficult at first than working 

on nuclear or chemical threat reduction 

issues7. In the late 1990s, as part of 

the CTR program, the US endeavored 

to reduce the threat of the FSU’s massive biological weapons (BW) complex8

by assisting Russian officials in what 

became known as the BTR program. 

These efforts primarily sought to improve safety and security at some of 

Russia’s BW sites and employ scientists 

in other-than-BW or “nonthreatening” research (e.g., biological sciences, public 

health and agriculture protection). To 

date, the US has helped Russia eliminate the infrastructure and equipment 

at numerous former BW research and 

production centers; enhance safe and 

secure storage and handling of biological pathogens; develop modern surveillance, warning, and response networks; 

and conduct cooperative research programs to increase transparency and 

thus discourage transfer of BW knowledge and expertise to other countries9

. 

But not all has gone as desired by US 

officials with the BTR program in Russia as several sites suspected of conducting BW research have remained 

off-limits (e.g., laboratories in Sergiev 

Posad, Yekaterinburg, and Kirov)10. So 

the question arises that if there is still 

work to be done in Russia to reduce 

biological threats, then why move on 

to someplace else, especially Africa?

Evolving Threat

The simple answer may be that the 

biological threat has evolved over time 

and therefore, expanding threat reduction efforts makes perfect sense. If that 

is the case, it also does not mean that 

the US has ‘cut and run’ from our efforts 

to curve biological threats in Russia. 

The Defense Threat Reduction Agency 

(DTRA) is the executing agency of the 

Department of Defense’s CTR work and 

a quick scan of the their Fiscal Years 

2011 and 2012 Budget Estimates for 

CTR reflect continued resourcing requests for BTR efforts in Russia11. Mr. 

Kenneth Myers, the Director of DTRA, 

also confirmed this point in testimony he 

provided on June 24, 2010 before the 

Senate’s Committee on Foreign Relations. “As these important efforts with 

our partners in the Former Soviet Union 

continue, we also are taking the knowledge and capabilities acquired through 

the Nunn-Lugar program implementation to new partners across the globe.”12 

Some of these newest partners are 

countries in east Africa. This is because 

“major infectious diseases known to 

have potential in biological warfare are 

endemic in eastern Africa”13 and senior 

USG officials are concerned that some 

of these disease samples may easily 

be obtained by terrorists. These officials believe pathogens could be stolen 

due to lax security at some laboratories 

where disease-causing bacteria and 

viruses are studied and samples are 

stored.14 Mr. Andrew Weber, the Assistant Secretary of Defense for Nuclear, 

Chemical and Biological Defense, who 
Combating WMD Journal ISSUE 9 4

accompanied Senator Lugar on trip to 

eastern Africa in November 2010 to look 

at some of these laboratories, described 

this dilemma as a “nexus between active 

terrorist groups, ungoverned spaces, 

and human and animal health laboratories working on endemic diseases, 

some of which are rare and exotic.” Mr. 

Weber explained that, “we want to make 

sure that the pathogens that could be 

used by terrorists are better secured and 

that there’s an enhanced capability to 

monitor infectious disease outbreaks.”15 

Two of the best examples of endemic 

disease causing pathogens that could 

be obtained in Africa and used against 

Americans may be anthrax and Ebola. 

These two diseases are considered by 

many experts in the biological counterproliferation field as significant threats 

because of their potential for causing 

death, the fear that their use may cause, 

and the economic losses that would 

result due to clean-up costs in the case 

of anthrax dissemination across a large 

area. In 1993, sixteen Aum Shinrikyo 

cult members went to Zaire (present 

day Democratic Republic of Congo) 

“to learn as much as possible about 

and, ideally, to bring back samples of 

Ebola virus.”16 This is the same cult 

that attacked the Tokyo subway with 

sarin gas in 1995 and that had also experimented with anthrax - cult members 

sprayed anthrax spores from the top of 

an eight-story building in eastern Tokyo 

attempting to cause a major biological 

emergency.17 Although the Aum cult’s 

attempts to develop and effectively use 

biological agents failed, the threat of 

others trying to use Ebola and/or anthrax from samples collected in Africa, 

or other diseases for that matter, still 

poses a serious biological threat risk. 

The rise of al Shabab, a powerful 

Islamist insurgent group that claimed 

responsibility for the deadly suicide 

bombings in Kampala, Uganda during 

the World Cup Finals in July 2010, has 

alarmed officials and refocused U.S. 

security interest and attention in the 

area.18 Al Qaeda, which sought to develop biological weapons in Afghanistan and considered by some experts 

to still be pursuing such efforts, has established cells in East Africa.19 These 

Al Qaeda linked cells, when combined 

with radicalization among sectors of the 

Muslim population, are the most serious threats in East Africa to the US and 

our allies according to Senator Lugar.20 

Mr. Myers (Director, DTRA) explained 

the evolution of the biological threat 

emanating from Africa in terms that 

may sound almost like a simple math 

equation. First is the fact that there 

are many disease pathogens being legitimately researched for their effects on 

humans, animals and plants; then there 

is the poor quality of security at many 

of these research laboratories; and this 

is happening in a region where terrorist cells appear to be growing. More 

simply stated, the combination of these 

factors: bioagents + quality (of security) 

+ quantity (of laboratories) + (terrorist) organizations = dangerous situation.21 This all adds up to a biological 

threat that should not be ignored. Adding weight to the dilemma this equation 

is the fact that history shows us that 

the Aum cult tried to collect samples 

of a bioagent (Ebola) from Africa. This 

is further compounded because many 

experts believe that the FSU obtained 

many of their samples for their biological 

warfare program from Africa as well.22 

National Security Concerns

There has been a consistent concern about biological terrorism within 

the executive and legislative levels of 

the USG for some time; in fact one 

may even speculate such concern 

goes back to when biological agents 

were first considered for use as military weapons.23 Against the backdrop 

of recent terrorist attacks including the 

World Trade Center bombing in 1993, 

the Oklahoma City bombing of the Alfred P. Murrah Federal Building on April 

19, 1995, and the sarin gas attack in 

the Tokyo subway by Aum Shinryko on 

March 20, 1995, President Bill Clinton 

released Presidential Decision Directive-39 (PDD-39), U.S. Policy on Counterterrorism, in June 1995. Regarding WMD in general, this policy stated: 

The United States shall give the highest 

priority to developing effective capabilities to detect, prevent, defeat and manage 

the consequences of nuclear, biological or 

chemical (NBC) materials or weapons use 

by terrorists. The acquisition of weapons 

of mass destruction by a terrorist group, 

through theft or manufacture, is unacceptable. There is no higher priority than 

preventing the acquisition of this capability or removing this capability from terrorist groups potentially opposed to the U.S.24

 

During the Clinton administration, 

Congress also passed the Nunn-LugarDomenici Defense against WMD Act of 

1996 that provided for the training of first 

responders to effectively handle WMD 

terrorist incidents. Funding was provided for the Department of Defense to train 

120 cities’ RAID (Rapid Assessment and 

Initial Detection) Teams to respond to 

chemical, biological, radiological and 

nuclear hazards. There were over two 

dozen findings in this act of which several specifically addressed concern of 

the WMD threat, to include bioterrorism:

- The problems of organized crime 

and corruption in the states of the 

former Soviet Union increase the potential for proliferation of nuclear, 

radiological, biological, and chemical weapons and related materials.

- The conditions described in [the 

previous] paragraph have substantially increased the ability of potentially 

hostile nations, terrorist groups, and 

individuals to acquire WMD and related materials and technologies from 

within the states of the former Soviet 

Union and from unemployed scientists who worked on those programs.

- The acquisition or the development 

and use of WMD [are] well within the 

capability of many extremist and terrorist movements, acting independently 

from or as proxies for foreign states.

- The potential for the national security 

of the United States to be threatened by 

nuclear, radiological, chemical, or biological terrorism must be taken seriously.25

 

Although this last finding mentioned “national security,” the Act did not detail the 

national security interests threatened by 

WMD (or bioterrorism specifically). The 

only specific mention of a national security interest is found in finding 13 where 

it characterized the WMD threat posed a 

“significant and growing” to US citizens.26 

These actions during the Clinton administration - the establishment of official policy on WMD counterterrorism, 

funding to counter WMD, and working 

with Congress on the Defense against 
at laboratories and thus preventing the 

access to dangerous pathogens was a 

lot cheaper in the long run than trying to 

go after it and take pathogens away from 

terrorists after they already have them, 

or even worse, facing the consequences 

of a biological attack - i.e., treating casualties and paying for clean up and 

recovery operations.34 There has been 

a precedent from both the executive and 

legislative branches over several administrations to fund prudent, actionable 

measures to counter WMD threats. Examples included the RAID teams during 

the Clinton administration and the BioWatch program during the Bush administration, thus addressing this particular 

biothreat by expanding BTR into Africa 

was also considered prudent. Deciding to do this did not happen overnight. 

Dance and Decision

During the Bush administration, funding for the BTR program increased to 

incorporate expansion of efforts in Russia. The funding for BTR efforts in Fiscal 

Year (FY) 2004 was $54.2 million (M) 

requested and approved, but this met 

with some push back due to concern 

from House members wanting to restrict 

cooperative research at any site until 

it could be certified that no prohibited 

biological weapons (BW) research was 

taking place. House members were 

also concerned about the vulnerability 

of pathogens to theft or loss and they 

therefore permitted the use of up to 25% 

of the appropriated funds to address 

these issues (i.e., looking into cooperative research to ensure no BW research 

was taking place and conducting assessments of security at research laboratories). In FY 2005, of $55M authorized for the BTR, over half of the funds 

were shifted from cooperative research 

efforts to biosafety and biosecurity enforcement because of the Congressional concerns about possible biological 

weapons programs. Additionally, funding was approved for expanding BTR 

efforts into Kazakhstan, Uzbekistan and 

Georgia at this time also for biosecurity 

and biosafety efforts.35 Congress’ actions 

to fund biosafety and biosecurity measures via BTR during this time established a precedent that would continue. 

During the remainder of the Bush administration, funding for BTR efforts continued to grow with a significant expansion 

5 ISSUE 9 Combating WMD Journal

WMD Act were the beginning of a trend 

where USG officials sought to take prudent, actionable measures to counter 

the potential use of WMD that included 

biological threats. At the beginning of 

President George W. Bush’s administration and in the immediate aftermath 

of the Amerithrax27 attacks, additional 

measures were put in place by the White 

House and Congress to confront terrorism and the biological threat. This was 

due in a large part to speculation “that 

the next act that would be carried out by 

the Al Queda group in the United States 

would involve chemical and biological 

terrorism.”28 These concerns resulted 

with the promulgation of numerous national level strategies and directives29 to 

address the WMD threat, the consolidation of twenty some odd organizations in 

to the new Department of Homeland Security (DHS), and increased funding for 

more extensive biodefense measures. 

To address the biological threat directly, 

the Bush administration released Homeland Security Presidential Decision-10/

National Security Presidential Directive-33 (HSPD-10/NSPD-33), National 

Biodefense Strategy (often referred to 

as Biodefense for the 21st Century), in 

April 2004. This strategy specifically 

addressed the threat of biological terrorism to national security stating that 

attacks with biological weapons could:

- Cause catastrophic numbers of acute casualties, long-term disease and disability, 

psychological trauma, and mass panic;

- Disrupt critical sectors of our economy 

and the day-to-day lives of Americans; and

- Create cascading international effects by disrupting and damaging international trade relationships, potentially globalizing the impacts of 

an attack on United States soil.30 

Concerned that terrorists would aerosolize a biological agent that could result 

in thousands of casualties, the Bush 

administration established the BioWatch 

program. This program detects certain biological agents in the air through 

a comprehensive protocol of monitoring and laboratory analysis to provide 

warning of a potential bioterror event. 

BioWatch ‘sensors’ are located in approximately thirty metropolitan areas 

throughout the United States and provide continuous air monitoring. Where 

emplaced, this program can detect a 

biological agent within 36 hours of release thereby allowing time for federal, 

state and local officials to place in to 

effect response and recovery efforts.31 

Supporting the previous administration’s biodefense strategy and seeking 

to “encourage the alignment of global 

attitudes against the intentional misuse 

of the life sciences... to harm people, 

agriculture, or other critical resources,” 

President Barack Obama released the 

National Security Strategy for Countering Biological Threats in November 

2009.

32 This latest strategy also clearly 

articulates the threat to national security posed by biological agents. Paragraph four of the introduction states:

The effective dissemination of a lethal 

biological agent within an unprotected 

population could place at risk the lives 

of hundreds of thousands of people. The 

unmitigated consequences of such an 

event could overwhelm our public health 

capabilities, potentially causing an untold number of deaths. The economic 

cost could exceed one trillion dollars for 

each such incident. In addition, there 

could be significant societal and political 

consequences that would derive from 

the incident’s direct impact on our way of 

life and the public’s trust in government.33

Based on the clear threat to national 

security as articulated above in the Bush 

and Obama biodefense strategies; the 

fact that there are many endemic, deadly pathogens stored in numerous, poorly 

secured laboratories throughout Africa; and the possibility that samples of 

pathogens could end up in the hands of 

terrorists, then it only seemed prudent to 

try and take some measures to prevent 

this from happening. In looking at Mr. 

Myers equation of this situation: bioagents + quality (of security) + quantity (of 

laboratories) + (terrorist) organizations 

= dangerous situation, it seemed to 

make perfect sense to national leaders 

that if the quality (of security) could be 

improved at laboratories where pathogens are researched and stored, then 

samples of such pathogens ending up in 

the hands of terrorists might be thwarted. According to Mr. Myers, taking this 

approach was getting ‘the biggest bang 

for the buck.’ Paying to improve security 
Combating WMD Journal ISSUE 9 6

in FY 2008 appropriations ($144.5M) 

being approved by Congress due to 

growing concerns about the threat of biological weapons proliferation. Senator 

Lugar sought to add an additional $100 

million in Fiscal Year 2008 appropriations for additional expansion of BTR 

but the Senate reduced this amount to 

$50M.36 According to Mr. Myers, it was 

during this period (2006 - 2007) that 

Senator Lugar was seeking support to 

expand BTR efforts into other countries 

outside the FSU. When I asked him 

point blank if the BTR expansion received support because of the Senator’s 

influence, Mr. Myers said that Senator 

Lugar charted a path and worked as 

necessary with whomever he thought he 

needed to bring on the team to try and 

get this done. He characterized Senator Lugar as being patient, diplomatic, 

methodical, knowledgeable and not concerned about receiving credit.37 Not only 

were additional resources (i.e., funding) 

approved for the BTR program because 

of Senator Lugar’s efforts, the National 

Defense Authorization Acts of 2007 and 

2008 also directed the National Academy of Sciences to conduct studies on 

the proliferation of biological weapons. 

The first report released in 2007 primarily looked at BTR efforts within the FSU 

but included an astounding “concern” 

that received attention from nonproliferation experts and national leaders alike:

While this study did not address in 

depth facilities outside the FSU, committee members are aware of poor security 

conditions at some facilities in other regions of the world that handle dangerous 

pathogens. Their impressions concerning the lack of adequate security at facilities throughout South Asia, the Middle 

East, Africa, and Latin America are consistent with reports to the committee by 

U.S. government specialists who have 

visited a number of the facilities...Some 

vulnerable facilities are located in developing countries in Africa and Southeast Asia where reports suggest that 

there are safe havens for terrorist cells.38 

 

The second study report by the National Academies of Science was released in early 2009. Study members 

were asked to assess capabilities of 

developing countries to control dualuse technologies; assess approaches 

used in the FSU that could be employed in other countries; review international programs contributing to 

nonproliferation; and recommend USG 

integrated actions for programs outside 

the FSU.39 The first recommendation 

of the study was that “DoD should, 

within the U.S. government’s evolving 

global biological engagement strategy, 

promptly expand BTRP into selected 

developing countries beyond the FSU.”40 

As the process of funding BTR continued 

to increase through the end of the Bush 

administration ($184.5M requested and 

174.3M appropriated for FY 2009) there 

was an initial dip with the new Obama 

administration for FY 2010 in which 

$152M was requested and approved. 

For FY 2011, $209M was requested and 

approved, and for FY2012, $259.5M 

has been requested.41 In concert with 

the general increase of funding for BTR 

over that past few years, support for expanding to other countries also gained 

traction. This support was prominent 

amongst Congressional members and 

within the DoD where senior members 

from both Policy and Acquisition, Technology and Logistics (AT&L) offices, 

as well as DTRA, pulled together and 

aligned their efforts supporting BTR expansion. The combination of national 

strategies highlighting biological threat 

concerns, sustained resourcing over 

the life of the BTR program, studies by 

expert panels recommending expansion of BTR into Africa, and national 

leaders advocating for and supporting 

BTR expansion might be described as 

a dance of sorts that led to the decision to expand BTR efforts into Africa.

The above measures alone did not 

seal the deal, so to speak, and the dance 

needed additional synchronization and 

action. This synchronization and action 

included steps taken by senior leaders 

to bring this effort together. Although 

not every effort or ‘dance step’ of all 

the senior leaders involved in supporting and gaining the decision to expand 

BTR efforts into Africa is presented, the 

following dance steps helped tremendously in gaining this final decision and 

show how this decision came about. 

In support of Senator Lugar’s efforts 

seeking to expand the BTR program 

into other countries outside the FSU 

during the 2006 - 2007 timeframe, the 

defense department (who is overall in 

charge of executing this program) not 

only looked hard at this issue, but readily took the challenge on for action. Mr. 

Joseph Benkert’s testimony to the Senate Armed Services Subcommittee on 

Emerging Threats and Capabilities on 

April 2, 2008 may have been the first formal dance step that attests to this. His 

statement for the record reads in part:

- CTR advocates have been asking when CTR will “go global.” It is 

a good question, and we are looking at opportunities... I would offer 

the following thoughts in this regard. 

- CTR will always be ready to address 

stocks of WMD if they are found, and 

if applicable governments ask for our 

assistance to eliminate them. However, 

the WMD threat is no longer only about 

addressing WMD at its source. As we 

think about CTR in a global context, it 

must be in the way CTR has already 

been moving – increasing foreign institutional capacity to address WMD 

threats. The bio-security case is a 

good example. CTR’s biological threat 

reduction program was originally conceived to address the threat posed by 

the legacy of the Soviet Biopreparat 

– a complex of especially dangerous 

pathogens, infrastructure and scientific 

expertise. Biopreparat doesn’t exist 

outside the states of the former Soviet 

Union, although a bio-terrorism threat 

does exist. Our challenge is to make 

the original CTR bio-security model 

applicable to the global threat. This is 

going to focus much more on building 

foreign capacity than the infrastructure heavy work that was necessary 

to address the legacy of Biopreparat...

- With the forgoing in mind, I am happy to 

report that we are ready to move forward 

with CTR to address global threats.42 

Following Mr. Benkert’s testimony, 

action officers within the Office of the 

Secretary Defense for Policy began exploring options for expansion in concert 

with the recommendations from the two 

previously mentioned National Academies of Science study reports recommendations. 2010 was a busy year with 

regard to the efforts to expand BTR into 

Africa. On January 28, Senator Lugar 

gave a speech in Washington, D.C. on 

Nunn-Lugar and Arms Control declaring 

that, “The Nunn-Lugar program is well 
7 ISSUE 9 Combating WMD Journal

positioned to enter a new phase of global security engagement.”43 With specific regard to the BTR program, he said:

Biological threat reduction is an area 

ripe for the Global Security Cooperation 

I envision, particularly in view of what 

the President has proposed. [Note: I 

believe this is referring to the National Strategy for Countering Biological 

Threats – RFK.] The work of securing 

dangerous pathogens, building central 

reference laboratories and establishing 

disease surveillance and monitoring are 

all critically needed in many parts of the 

world. Nunn-Lugar biological engagement directly serves key U.S. interests, 

including safeguarding the welfare of 

our troops and detecting emerging infectious diseases and pandemics before 

they threaten the American people.44 

The next month after this speech 

(February 2010), DTRA submitted its 

budget request asking for funding to 

expand BTR efforts into select areas 

of Africa.45 And the Quadrennial Defense Review (QDR) was released 

highlighting this issue by directing:

Expand the biological threat reduction program. Countries that have the 

infrastructure and capability to report 

and track the spread of an outbreak of 

disease are able to save more lives. 

Detecting, diagnosing, and determining the origin of a pathogen will enable 

U.S. authorities to better respond to 

future disease outbreaks and identify whether they are natural or manmade. Accordingly, we are expanding 

the biological threat reduction program 

to countries outside the former Soviet 

Union in order to create a global network for surveillance and response.46 

This direction in the QDR to expand 

BTR codified the move for DoD to ‘go 

global’ and thus when Mr. Benkert’s successor testified before the same committee later that spring, he spoke directly 

about Africa. Dr. Michael Nacht told the 

Senate Armed Services Subcommittee 

on Emerging Threats and Capabilities 

on April 21, 2010, “The department is 

also considering expanding the [BTR] 

program into Sub-Saharan Africa...” 47 

And the dance continued into the summer with Mr. Myers testifying before the 

Senate’s Committee on Foreign Relations on June 24 in which he addressed 

expanding the BTR program.48 All these 

measures and the final congressional 

appropriations for DTRA’s expansion of 

BTR efforts into Africa sealed the deal. 

Conclusion

The decision to expand the BTR program into Africa was achieved over the 

course of several years (2007 – 2010) 

and included the convergence of advocacy and gentle prodding from an influential Senator, strategic vision from the 

White House, resourcing support from 

Congress, and willingness from senior 

DoD leaders to take this mission on and 

DTRA to execute. Expanding BTR into 

Africa did not happen out of the blue, but 

rather grew from the successes of the 

CTR program and precedents of other 

measures enacted by national leaders 

(e.g., RAID teams and BioWatch). The 

expansion of BTR into Africa to provide 

biosafety, biosecurity, and biosurveillance at laboratories where legitimate 

life sciences research is conducted is 

clearly in the interest of national security. These biosafety, biosecurity, and 

biosurveillance measures will go a long 

way toward thwarting the chances of 

dangerous disease pathogens ending 

up in the hands of those who wish to 

cause harm to us, our friends and allies. 

BIOGRAPHY

Dr. Kerr is a Senior Chemical, Biological, Radiological and Nuclear (CBRN) 

Analyst at the Joint Requirements 

Office for CBRN Defense in the J8 

Directorate of the Joint Staff. He holds 

a M.S. and Ph.D. in Biodefense from 

George Mason University, Virginia; a 

M.S. in National Security Strategy from 

the National War College, Fort McNair, Washington, D.C.; and a M.A. in 

Political Science from Jacksonville 

State University, Alabama. Dr. Kerr 

served as an Army Chemical Officer from 1982 - 2003.

ENDNOTES

1. Steve Andreasen and Samuel R. 

Berger, “The Final Failure,” Foreign 

Policy, op-ed, September 8, 2011, http:// 

www.nti.org/analysis/opinions/finalfailure/ (accessed January 14, 2012). 

See also Department of Defense, Sustaining U.S. Global Leadership: Priorities for the 21st Century Defense, 

January 2012, http://www.defense. 

gov/news/Defense_Strategic_Guidance.pdf (accessed January 10, 2012).

2. Richard G. Lugar – Biography, http://lugar.senate.gov/bio/ 

(accessed January 14, 2012). 

3. See webcast: “Lugar and Nunn in 

Conversation,” December 19, 2011, in 

which National Journal’s James Kitfield 

moderates a discussion with Senator Richard Lugar (R-IN) and former 

Senator Sam Nunn (D-GA) on the successes and challenges of the NunnLugar Cooperative Threat Reduction 

Program available at http://www.nti.

org/ (accessed January 14, 2012).

4. The Nunn-Lugar Scorecard, updated December 2011, available at http://

lugar.senate.gov/nunnlugar/ scorecard.html (accessed January 9, 2012).

5. Paul I. Berstein and Jason D. Wood, 

“The Origins of Nunn-Lugar and Cooperative Threat Reduction,” Case Study 

Series (3), Center for the Study of Weapons of Mass Destruction (Washington, 

DC: National Defense University Press, 

April 2009). See also National Research 

Council, Global Security Engagement: A 

New Model for Cooperative Threat Reduction (Washington, D.C.: The National 

Academies Press, 2009) and Defense 

Threat Reduction Agency, “Cooperative Threat Reduction Program,“ available at http://www.dtra.mil/missions/

NunLugar/GlobalCooperation Initiative.aspx (accessed January 9, 2012).

6. The Nunn-Lugar Scorecard, updated December 2011.

7. National Research Council, The 

Biological Threat Reduction Program 

of the Department of Defense: From 

Foreign Assistance to Sustainable 

Partnerships, Washington, D.C.: The 

National Academies Press, 2007, 17. 

8. For information about the FSU’s 

massive biological weapons complex, 

see Ken Alibek with Stephen Handelman, BIOHAZARD: The Chilling True 

Story of the Largest Covert Biological 

Weapons Program in the World – Told 

From Inside By The Man Who Ran It 

(New York: Random House, 1999); Michelle Stem Cook and Amy F. Woolf, 

“Preventing Proliferation of Biological Weapons: U.S. Assistance to the 

Former Soviet Union,” Congressional 

Research Service, Washington, D.C., 

April 10, 2002. http://www.fas.org/spp/
starwars/crs/RL31368.pdf (accessed 

January 21, 2012); and Milton Leitenberg and Raymond A. Zilinskas with 

Jens H. Kuhn, The Soviet Biological 

Weapons Program: A History (Cambridge, Massachusetts: Harvard, 2012). 

9. Amy F. Woolf, “Nonproliferation and 

Threat Reduction Assistance: U.S. 

Programs in the Former Soviet Union,” 

Congressional Research Service, 

Washington, D.C., April 26, 2011, 21 - 

22. http://www.pfas.org/sgp/crs/nuke/ 

RL31957.pdf (accessed January 21, 

2012) and National Research Council, 

The Biological Threat Reduction Program of the Department of Defense, 17.

10. National Research Council, The 

Biological Threat Reduction Program 

of the Department of Defense, 17. See 

also Defense Threat Reduction Agency, 

Fiscal Year 2012 Budget Estimate [for] 

Cooperative Threat Reduction, February 2011, (page) CTR 957. http://www.

comptroller.defense.gov/defbudget/ 

(accessed January 17, 2012). Note: 

The program is now called the Cooperative Biological Engagement Program 

(CBEP) but for the purpose of this paper, 

I will continue to refer to this as the Biological Threat Reduction (BTR) program 

due to the overwhelming amount of reference material and documents that 

refer to this original title of the program.

11. Defense Threat Reduction Agency, 

Fiscal Year 2011 and 2012 Budget Estimates [for] Cooperative Threat Reduction, February 2010 and 2011, respectively. http://www.comptroller.defense.gov/

defbudget/ (accessed January 17, 2012).

12. Kenneth A. Myers. Statement of 

Kenneth A. Myers III, Director, Defense 

Threat Reduction Agency and Director, U.S. Strategic Command Center for 

Combating Weapons of Mass Destruction on Implementation of New Strategic 

Arms reduction Treaty Inspection and 

Escort Provisions before the Committee on Foreign Relations, United States

Senate, June 24, 2010. http://www.

foreign.senate.gov/imo/media/doc/

Myers%20III,%20Kenneth %20A..

pdf (accessed January 14, 2012).

13. James Thuo Njuguna, “Evaluating the 

Threat of Biological Weapons in Eastern 

Africa,” African Security Studies Review, 

Volume 14, Number 1, 2005. http://

www.iss.co.za/pubs/ asr/14No1/FJnuguna.htm (accessed January 17, 2012). 

14. Kevin Wickel, “Cooperative Threat 

Reduction: Reducing Biological Risks 

in East Africa,” March 09, 2011, http://

www.stimson.org/spotlight/ (accessed 

January 9, 2012). See also Spencer 

Ackerman, “Pentagon Looks to Africa 

for Next Bio Threat,” February 23, 2011, 

http://www.wired.com/dangerroom/ (accessed January 9, 2012); Glenn Hess, 

“Biosecurity Efforts Expands to Africa: 

U.S. seeks to secure deadly pathogens 

to prevent their use in bioterror attacks,” 

Chemical & Engineering News, April 11, 

2011, Vol 89, No. 15, 30-32, http://pubs.

acs.org/ cen/government/89/8915gov1.

html (accessed January 12, 2012); 

Richard Lugar, “Nunn-Lugar Global: 

The African Mission – Countering More 

Threats, Faster,” November 2010, 1-5, 

http:www.lugar.senate.gov/nunnlugar/ 

AfricaTripReportFinal.pdf (accessed 

January 9, 2012); Mike Pflanz, “Why 

Senator Lugar is worried about bioterrorism in East Africa,” The Christian Science Monitor, 12 Nov 2010: 5, 

http://www.csmonitor.com/ World/Africa/2010/1112/ (accessed January 9, 

2012); and Paul Tinder, “Cooperative 

Threat Reduction set to expand,” April 

15, 2011, http:// www.bioprepwatch.

com.news/241516 (January 9, 2012).

15. Mike Pflanz, “Why Senator Lugar is 

worried about bioterrorism in East Africa,” 12 Nov 2010. Note that these are 

direct quotes quoted in the reference.

16. Kyle B. Olsen, “Aum Shinrikyo: 

Once and Future Threat?”, Emerging 

Infectious Diseases, Vol. 5, No. 4, July-August 1999, 514, http://www.ncbi.

nlm.nih.gov/pmc/articles/PMC2627754/

pdf/10458955.pdf (accessed January 

9, 2012). See also Cole, The Eleventh Plague (New York: W.H. Freeman & Co., 1997), 2-3 and David E. 

Kaplan and Andrew Marshall, The 

Cult at the End of the World, (New 

York: Crown Publishers, 1996), 96-97.

17. Kaplan and Marshall, The Cult 

at the End of the World, 93-96 

and Olsen, “Aum Shrinrikyo,” 514.

18. Josh Kron, “Uganda Seen as a Front 

Line in the Bioterrorism Fight,” The New 

York Times, November 10, 2010, http://

www.nytimes.com/2010/11/11/world/

africa/11uganda.html (accessed January 9, 2012); and Wickel, “Cooperative 

Threat Reduction: Reducing Biological 

Risks in East Africa,” March 09, 2011.

19. Pflanz , “Why Senator Lugar is worried about bioterrorism in East Africa,” 

The Christian Science Monitor, 12 Nov 

2010: 5; Lugar, Speech of Senator 

Lugar, delivered in Madrid, Spain, November 8, 2010; and Wickel, “Cooperative Threat Reduction: Reducing Biological Risks in East Africa,” March 09, 2011.

20. Lugar, Speech of Senator Lugar, delivered in Madrid, Spain, November 8, 2010.

21. Interview with Mr. Kenneth Myers, Director, Defense Threat Reduction Agency on January 24, 2012.

22. Lugar, “Nunn-Lugar Global: The 

African Mission – Countering More 

Threats, Faster,” November 2010, 9.

23. Peter Lavoy, “What’s New in the 

New U.S. Strategy to Combat WMD?” 

Strategic Insights, Volume I, Issue 

10, December 2002, http://www.nps.

edu/Academics/centers/ccc/publications/OnlineJournal/2002/dec02/wmd.

html (accessed January 21, 2012). 

24. The White House, Presidential Decision Directive-39, U.S. Policy on Counterterrorism, http://www.fas.org/irp/ offdocs/

pdd/pdd-39.pdf (accessed January 17, 

2012). Italicization added for emphasis. 

25. Defense Against Weapons of 

Mass Destruction Act of 1996 (PL 

104-201), Appendix B, Threat Findings of the Nunn-Lugar-Domenici Act, 

September 23, 1996, http://www.rand.

org/content/dam/rand/pubs/monograph_ reports/MR1251/MR1251.

AppE.pdf (accessed January 17, 

2012). Italicization added for emphasis.

26. Ibid.

27. Federal Bureau of Investigation, 

Fact Sheet: Amerithrax or Anthrax Investigation, http://www.fbi.gov/aboutus/history/famous-cases/anthrax-amerithrax (accessed January 9, 2012).

28. Milton Leitenberg, “Biological Weapons and ‘Bioterrorism’ in the First Years 

of the 21st Century,” paper prepared 

for Conference on “The Possible Use 

of Biological Weapons by Terrorists 

Groups: Scientific, Legal, and International Implications,” Rome, Italy, 16 April 

2003, 22, http://www.fas.org/programs/

bio/resources/ documents/21centurybw.

pdf (accessed January 17, 2012).

29. See Office of Science and Technology Policy website on Biosecurity, 

available at http://www.whitehouse.gov/ 

administration/eop/ostp/nstc/biosecurity 

for a synopsis of “government policies 

related to the safe and secure conduct 

of biological research and the technologies arising out of the application of the 

life sciences” and executive strategies, 

directives and orders related to biosecurity (accessed January 10, 2012). 

Combating WMD Journal ISSUE 9 8
30. The White House, Homeland Security Presidential Decision-10, Biodefense for the 21st Century, http://

www.dhs. gov/xlibrary/assets/HSD10Biodefensefor21stCentury042804.

pdf (accessed January 17, 2012).

31. Ralph F. Kerr, “Biological Pathogens 

and Bureaucratic Pathologies: A Comparative Analysis of Two Federal Biodetection Programs” (PhD diss., George 

Mason University, 2010), 181-182.

32. National Security Council, National Strategy to Counter Biological 

Threats, November 2009, http://www.

white house.gov/sites/default/files/National_Strategy_for_Countering_BioThreats.pdf (accessed January 9, 2012).

33. Ibid.

34. Interview with Mr. Myers, Director, DTRA on January 24, 2012.

35. Amy F. Wolf, “Nonproliferation and Threat Reduction Assistance: U.S. Programs in the Former 

Soviet Union,” (Washington, D.C.: 

Congressional Research Service, 

April 26, 2011), 21-23. http://www. 

fas.org/sgp/crs/nuke/ RL31957.

pdf (accessed January 21, 2012).

36. Ibid.

37. Interview with Mr. Myers, Director, DTRA on January 24, 2012.

38. National Research Council, Committee on the Prevention of Proliferation of Biological Weapons, The 

Biological Threat Reduction Program of the Department of Defense: 

From Foreign Assistance to Sustainable Partnerships (Washington, DC: 

National Academies Press, 2007), 

21. Italicization added for emphasis.

39. National Research Council, Committee on the Prevention of Proliferation of Biological Weapons, Countering Biological Threats: Challenges for 

the Department of Defense’s Nonproliferation Program Beyond the Former Soviet Union (Washington, DC: 

National Academies Press, 2009), 1.

40. Ibid, 5.

41. Ibid.

42. Benkert, Joseph A. Statement for 

the Record, Joseph A. Benkert, Principal Deputy Assistant Secretary of Defense for Global Security Affairs, Senate 

Committee on Armed Services, Subcommittee on Emerging Threats and 

Capabilities, April 2, 2008. http://armedservices.senate.gov/statemnt/2008/

April/ Benkert%2004-02-08.pdf (accessed January 22, 2012). Italicization and bolding added for emphasis.

43. Senator Richard Lugar speech to the 

Conference on Strategic Weapons in the 

21st Century, given at the Ronald Reagan 

Building in Washington D.C, on Thursday, January 28, 2010, on Nunn-Lugar 

and Arms Control key to Future Nuclear 

and Biological Weapons Reductions. 

http://lugar.senate.gov/news/record.

cfm?id=321863 (accessed 21 Jan 2012).

44. Ibid.

45. Defense Threat Reduction 

Agency, Fiscal Year 2011 Budget Estimate, Cooperative Threat Reduction Program, February 2010, http://

comptroller.defense.gov/defbudget (accessed January 17, 2012).

46. Department of Defense, “Quadrennial Defense Review,” February 

2010, 36. http://www.defense.gov/

qdr/qdr %20as%20of%2029jan10%20

1600.PDF (accessed January 9, 2012). 

47. Statement of Dr. Michael Nacht Assistant Secretary of Defense for Global 

Strategic Affairs before the Senate Committee on Armed Services Subcommittee 

on Emerging Threats and Capabilities 

April 21, 2010. http://armed-services.

senate.gov/ statemnt/2010/04%20

April/Nacht%2004-21-10.pdf (accessed January 21, 2012).

48. Statement of Kenneth A. Myers 

III, Director, Defense Threat Reduction 

Agency and Director, U.S. Strategic Command Center for Combating Weapons of 

Mass Destruction on Implementation of 

New Strategic Arms reduction Treaty 

Inspection and Escort Provisions before 

the Committee on Foreign Relations, 

United States Senate, June 24, 2010. 

http://www.foreign.senate.gov/imo/

media/doc/Myers%20III,%20Kenneth 

%20A.pdf (accessed January 14, 2012).

9 ISSUE 9 Combating WMD Journal
Fukishima Daiichi Operating and Design Characteristics 

with Relevance to the Army Reactor Program

Phil Shubert

Army Reactor Program Manager, U.S. Army Nuclear and CWMD Agency

Combating WMD Journal ISSUE 9 10

asics of commercial nuclear power designs and how 

they applied to Fukishima

• Boiling Water Reactor (BWR) vs. 

Pressurized Water Reactor (PWR)

• Spent Fuel storage designs

• Emergency Core Cooling

• Emergency Power Supply configurations

• Design Basis Accidents

Figure 1. Fukushima Daiichi Nuclear 

Station

The March 2011 event in Japan has 

renewed international interest in nuclear events. The importance of nuclear 

events in our past and in our future 

cannot be minimized. Because of the 

enormous potential for both its benefits 

and the potential for disaster, nuclear 

has always generated great debate. 

Nuclear provides the promise of an 

abundant supply of “non greenhouse 

gas producing” energy while simultaneously posing severe dangers. For these 

reasons discussion on the future of nuclear uses is rarely unemotional. The 

sensational nature of nuclear events 

coupled with its technical complexity 

B has news reporting focused on the perilous and at times heroic circumstances 

surrounding these occurrences. This 

article discusses design features of currently operating power plants focusing 

on Fukishima Daiichi characteristics. 

The Fukushima Plants were Boiling Water Reactors (BWR). For water moderated plants in the U.S. there are two basic designs, Boiling Water Reactors and 

Pressurized Water Reactors (PWR).

Basic diagrams of these two types 

of Nuclear power plants are depicted 

below. (Figures 2 and 3 respectively)

The basic difference between these two 

types is that a pressurized water reactor 

has an extra set of major components, 

steam generators and a pressurizer. 

The pressurizer maintains pressure in 

the reactor side cooling water sufficient 

to prevent boiling. The steam generator 

is utilized to allow heat to be transferred 

from water that has been exposed to the 

nuclear core to circulating water in the 

steam cycle. By using a steam generator to transfer heat from the reactor 

side cooling system, the steam passing 

Figure 2. Pressurized Water Reactor

Figure 3. Boiling Water Reactor
11 ISSUE 9 Combating WMD Journal

through a turbine in a PWR does not get 

exposed to the Reactor fuel. A PWR design typically provides an environment 

outside of its primary containment walls 

free of radiological contamination, while 

a BWR typically has areas of contamination outside its primary containment.

The Boiling Water design does not 

have a pressurizer or steam generators. 

The core itself transfers enough heat to 

turn cooling water into steam. This is the 

type of design utilized in all of the plants 

at Fukishima Daiichi Nuclear station. 

Since there is steam exposed to the core 

in a BWR design, by its nature there is 

one less barrier to contamination when 

comparing a BWRS to a PWRS design.

Six BWR units at the Fukushima Nuclear 

Station:

Unit 1: 439 MWe BWR, 1971 (unit was 

in operation prior to event)

Unit 2: 760 MWe BWR, 1974 (unit was 

in operation prior to event)

Unit 3: 760 MWe BWR, 1976 (unit was 

in operation prior to event)

Unit 4: 760 MWe BWR, 1978 (unit was 

in outage prior to event)

Unit 5: 760 MWe BWR, 1978 (unit was 

in outage prior to event)

Unit 6: 1067 MWe BWR, 1979 (unit was 

in outage prior to event)

In addition to the core heat transfer 

designs, one of the additional design 

features to consider is the configuration of the pools that store spent fuel. 

Commercial power plants typically are 

designed to replace 1/3 of its core at 

each refueling with new fuel and to 

store 1/3 of its exposed fuel in a storage pool. Plants store the fuel in a 

pool with sufficient water to act as a 

barrier to radiation until the spent fuel 

has decayed to a level where it can be 

transferred to a cask for dry storage. 

The pool is also designed to have spacing the proper fuel and water chemistry to prevent inadvertent criticality.

One difference to note is the elevation 

difference between the refueling floor at 

Fukishima and other plants where the 

refueling floor is at the same or lower 

level from the reactor core. Many designs recognize that keeping a sufficient level over the spent fuel requires 

a greater head pressure to fill when 

the pool is elevated. Designs have to 

consider many ways of preventing the 

inadvertent draining or loss of level such 

as loop seal vents to prevent inadvertent siphoning. Plants also have to 

consider pool refill and residual heat 

removal to prevent evaporative losses 

from dropping pool levels. Typically 

8-10 feet over the fuel top is required 

but most plants keep 20 plus feet as a 

safety margin. According to The Nation, 

“Spent fuel pools at Fukushima were not 

equipped with backup water-circulation 

systems or backup generators for the 

water-circulation system they do have.”

It is important to note that in both PWR 

and BWR designs the fuel pools are 

normally outside the primary containments. Secondary containments can 

vary significantly in their construction. 

They range from sheet metal walls to 

reinforced concrete. They typically are 

not designed for increased pressures 

or ability to withstand explosions. The 

primary containments are much stronger and designed to specific pressure 

and missile damage requirements.

Reactor Control System Designs

In both PWR and BWR designs the 

control rods are designed to insert 

within 4 seconds from a trip or “scram” 

signal. They are failsafe in that a loss 

of power in either system causes the 

full insertion of rods. In a PWR their 

weight and springs act to drop the Control rods. In a BWR hydraulic pressure is applied to the rods, to insert 

from the bottom up, on loss of power. 

Figure 5. BWR Layout similar to Fukishima Daiichi

Figure 4. Typical PWR arrangement releative to Spent Fuel pool
Combating WMD Journal ISSUE 9 12

Emergency cooling systems

A PWR typically has high head injection pumps and old leg accumulators 

that are designed to automatically inject 

borated water into the core in case of 

an emergency. The high head injection pumps require electrical power, 

the cold leg accumulators are tanks 

at elevations higher than the core that 

can empty automatically if the reactor 

cooling system’s pressure drops below 

the head pressure of the accumulators. 

PWRs have a residual heat removal 

capability for long term heat removal 

from the core, but this system relies 

on electrical power for pump and valve 

operation. There are normally piping 

points where spool pieces can be installed to utilize other water sources 

to provide emergency water. These 

typically use water from other storage 

tanks or via pumps like high pressure 

fire pumps etc. Many times these 

are either gravity flow ( require reactor 

system pressures to be low ) or diesel 

powered pumps. For a complete loss 

of power, with no instrumentation or controls, offsite support would be required. 

The BWR is specifically designed to respond to pressure transients, having a 

“pressure suppression” type of design 

which vents overpressure using safety 

relief valves to below the surface of a 

pool of liquid water within the containment, known as the “wetwell” or “torus”. This is the large ring depicted in 

the illustration. BWRs, like the PWRs, 

would need electrical power to provide 

continued injection and residual heat 

removal should water inventory be lost. 

Like PWRs, there are normally piping points where spool pieces can be 

installed so that other water sources 

can provide emergency water. These 

typically use water from other storage 

tanks, or via pumps like high pressure 

fire pumps. Many times these are either 

gravity flow (requireing reactor system 

pressures to be low) or diesel powered 

pumps. In a complete loss of power situation with no instrumentation or controls, offsite support would be required.

What happened at Fukishima

On 11 March 2011, a magnitude 9 

earthquake generated a series of large 

tsunami waves that struck the east 

coast of Japan. The earthquake and 

tsunami created widespread devastation to the northeastern portions of Japan. Over 14,000 lives were lost and 

1000s more were missing or displaced.

The earthquake did affect several 

nuclear power plants: Tokai, Higashi 

Dori, Onaqawa, and TEPCO’s Fukushima Dai-ichi and Dai-ni. This article 

will discuss the most severe of these 

events at the Fukishima Dai-ichi Station.

The earthquake initiated a loss of offsite power at Dai-ichi and the automatic 

systems automatically inserted rods at 

its three operational reactors. Initiation of these automatic functions was 

based on detection of seismic activity. 

Diesel Generators onsite were in operation supplying shutdown power as 

designed. 46 minutes after the earthquake the first in a series of tsunami 

waves begin to strike the east coast 

of Japan. The Dai-ichi plant’s design 

basis accident was for a maximum 5.7 

meter wave. Waves that struck the 

Dai-ichi plant were estimated at greater than 14 meters. Only 1 D/G at unit 6 

( B train) remained on power. A/C power and batteries were not available, a 

long recognized event that is extremely 

challenging. US procedures have recognized for years that normal emergency procedures are inadequate to 

handle this situation and have required 

US plants to develop emergency contingency actions (ECAs) to assist operators in this situation. Much of the guidance in these ECAs direct the site staffs 

to pursue support from offsite sources 

while working to restore power. In the 

wake of severe emergency affecting so 

many lives outside of the station proper, the Japanese faced an emergency 

that taxed responders far beyond their 

planned resource levels. The magnitude of the impact to communication, 

transportation and emergency personnel for response to the general populace’s immediate needs compounded 

the difficulty in obtaining offsite support. The station operators have been 

lauded by many of the organizations 

that subsequently were marshaled to 

help in the effort. Operator’s efforts, 

heroic at time to restore ability to mitigate the event have been documented.

Following is a summary of the emergency response at the station as described by the Institute of Nuclear 

Power Operations.

With no core cooling to remove decay heat, core damage may have begun on Unit 1 on the day of the event. 

Steam-driven injection pumps were 

used to provide cooling water to the 

reactors on units 2 and 3, but these 

pumps eventually stopped working; and 

all cooling water to the reactors was lost 

until fire engines were used to restore 

water injection. As a result of inadequate core cooling, fuel damage also 

occurred in units 2 and 3. Challenges 

in venting containments contributed to 

containment pressures exceeding design pressure, which may have caused 

containment damage and leakage.

Hydrogen generated from the damaged fuel in the reactors accumulated 

in the reactor buildings either during 

venting operations or from other leaks 

and ignited, producing explosions in the 

Unit 1 and Unit 3 reactor buildings and 

significantly complicating the response. 

The hydrogen generated in Unit 3 may 

Figure 6. Overviews map showing evacuation and other zone progression 

and selected radiation levels.
13 ISSUE 9 Combating WMD Journal

have migrated into the Unit 4 reactor 

building, resulting in a subsequent explosion and damage. The loss of primary 

and secondary containment integrity resulted in ground-level releases of radioactive material. Following the explosion 

in Unit 4 and the abnormal indications 

on Unit 2 on the fourth day of the event, 

the site superintendent directed that 

all nonessential personnel temporarily evacuate, leaving approximately 70 

people on site to manage the event.

During releases, dose rates as high 

as 1,193 millirem per hour (mrem/hr) 

(11.93 mSv/hr) were measured at the 

site boundary, approximately 0.6 miles 

(1 km) from units 1&4. Windows for the 

emergency response center had to be 

covered with lead shielding to reduce 

dose rates in the center. Organized offsite radiation surveys began on March 

16. Radiation levels off site at that time 

ranged from 0.1 mrem/hr (1 μSv/hr) to 

20 mrem/hr (200 μSv/hr). Thirty-seven 

miles (60 km) northwest of the station, 

the dose rate was 0.8 mrem/hr (8 μSv/

hr). Water and soil samples indicated 

the presence of strontium, iodine, and 

cesium. Food and water restrictions 

were implemented in some areas as a 

result of radioactivity. People within the 

12.4 miles (20 km) surrounding the station were evacuated, and those living up 

to 18.6 miles (30 km) away were directed to shelter inside their homes as the 

releases of radioactive gases and materials increased as the event progressed 

and more fuel damage occurred. Potassium iodide tablets and powder were distributed to local governments beginning 

March 21. Because the evacuations had 

already been completed, the potassium 

iodide was not issued to the population to reduce radioactive iodine intake.

Radiation surveys of the on-site areas surrounding units 1and 3 showed 

dose rates as high as 13 rem/hr (0.13 

Sv/hr) in areas around units 2 and 3. 

More detailed surveys performed over 

the following weeks discovered localized dose rates greater than 1,000 

rem/hr (10 Sv/hr) around equipment 

and debris outside units 1 and 3.

Some personnel who responded to the 

event received high doses of radiation. 

Two control room operators received the 

highest doses a calculated internal and 

external dose of 67.8 rem (0.678 Sv) 

and 64.3 rem (0.643 Sv). The majority of 

dose received by these workers was internal (85-87 percent). Potassium iodide 

was provided to some station personnel 

on March 13. As of the end of March, approximately 100 workers had received 

doses of greater than 10 rem (0.1 Sv).

The Fukushima event was rated as 

a level 7 event on the International Nuclear and Radiological Event (INES) 

scale. The Nuclear Safety Commission 

of Japan estimated approximately 17 

million curies (6.3 E17 Bq) of iodine-131 

equivalent radioactive material was released into the air and 0.127 million 

curies (4.7 E15 Bq) into the sea between 

March 11 and April 5. The 1986 accident at Unit 4 of the Chernobyl nuclear 

power plant was the only other nuclear 

accident to have a level 7 INES rating.

Relevance to Army Reactor Program

The US Army’s decommissioned 

reactors and its operating Fast Burst 

Reactor do not have the catastrophic 

potential of the magnitudes experienced 

at the Japanese reactors. There are, 

however, underlying safety considerations that should be examined by all 

personnel with roles of responsibility 

related to sites under the Army Reactor 

Program’s umbrella. When developing 

safety analysis and evaluations, one 

should consider the potential for traditional events to exceed design basis. 

The principles that are ingrained in the 

Army’s nuclear culture include a conservative approach to operations, maintenance and engineering that seeks safety 

margins beyond just meeting design 

basis. This safety culture embodies a 

“Defense in Depth” approach that looks 

to ensure redundant safety features 

are second party verifications, be a 

part of the operating and maintenance 

procedures, safety analysis and design. 

This event shows how a common mode 

failure can create a situation where design basis conditions can be exceeded. 

One example of a common mode event 

is the typical design of US plants to 

consider a 100 year flood level as design basis. Floods or Tsunamis like the 

Fukishima case can effect redundant 

trains of equipment and disrupt procedures that operating crews are trained 

to respond with. One can postulate 

some other common mode events that 

even though remote in possibility, could 

come to bear at sites under Army permits. Fire and security threats are examples where the “Defense in Depth” 

concepts we use would challenge redundant systems. The continuing professionalism by all in the Army Reactor 

Program to learn as much as possible 

about the challenges the Fukishima 

plant experienced in handling “Beyond 

Design Basis” events is crucial. The final chapter of the Fukishima saga has 

yet to be written. We will learn much 

from this event as we have in previous nuclear accidents. Introspection 

by those of us in the nuclear field has 

served us well and will serve us in this 

regard. Even though the same magnitudes of catastrophic potential do not 

exist for the Army Reactors, we still 

have the same professional requirements as the Fukishima nuclear workforce. We have the duty to uphold the 

public trust that has been placed upon 

us. The lessons learned from this event 

will be a valuable tool to address future 

considerations on handling events that 

exceed “design basis”, stay tuned.

BIOGRAPHY

Mr. Phil Shubert currently heads 

the Army’s Reactor Office. He is a 

Mechanical Engineering graduate 

from the University of Tennessee and 

served in the Navy as a Naval Flight 

Officer, with over 200 carrier landings 

on the USS Forrestal. He later served 

as a Senior Reactor Operator for the 

Tennessee Valley Authority (TVA), 

where he supervised the loading of 

the first fuel assembly at Watts Bar 

and was Unit Operating Supervisor 

for the initial critical for Watts Bar in 

1996. From 1997-2007 he served 

with the Joint Warfare Analysis Center 

(JWAC), a joint command located at 

Dahlgren Naval Base. From 2007- 

2011, he was a US manager for 

Alstom, which is a French multinational conglomerate. Phil returned 

to US government service in 2011 

as the Army Reactor Program manager under the US Army Nuclear and 

Combating WMD Agency (USANCA).
ABCA-Optimizing CBRN Interoperability

LTC Michael S. Quinn

CBRN Officer, U.S. Army Nuclear and CWMD Agency

he mission of the American, British, Canadian, Australian and 

New Zealand Armies’ Program 

(ABCA) is to optimize ABCA Armies’ 

interoperability in order to deliver successfullly coalition operations. Initiated 

in 1947 by America, Great Britain, and 

Canada, the program was a means to 

continue fostering the close cooperation that the countries had established 

during World War II. Australia jointed 

the program in 1964 and New Zealand 

in 2006, effectively forming today’s 

ABCA Armies Program which many 

may know as the “5 Eyes Community”.

Strategically guided by an executive 

council and overseen and directed by 

national directors, capability and support groups execute the daily activities 

of the Program. The Program consists 

of five capability groups: Command, 

Sense, Shield, Sustain and Act. Capability Group Shield is one of the two 

groups led by a US colonel. Over the 

last several years Capability Group 

Shield, similar to the US protect function, has focused on the interoperability of Counter IED and CBRN Combating /Countering WMD Operations.

The Shield CBRN sub group recently 

focused efforts on two interoperability 

topics: mass casuality decontamination 

operations during a WMD event and 

T national CBRN equipment capabilities. 

An ABCA Best Practices Guideline for 

Military Mass Casality Decontamination 

Operations During a Domestic Hazmat/

Weapons of Mass Destruction Incident 

Figure 1. ABCA Project Team conducting a critical analysis of national data 

gathered and submitted before the meeting.

Figure 2. UK soldiers and airmen, wearing the new GSR, rehearsing CBRN survey 

techniques at Winterbourne Gunner, UK.

Combating WMD Journal ISSUE 9 14
was published as ABCA Publication 

370 in Feb 2012 and is available on the 

ABCA web page. Driven by changes 

to technology, tactics, techniques, and 

procedures over the last 10 years, the 

most recent project, national CBRN 

equipment capabilities, analyzed four 

key functional areas: individual protective equipment; detection, identification and monitoring; decontamination; and medical countermeasures 

in order to reassess interoperability.

Following a four month information 

gathering period, the United Kingdom 

(UK) hosted the CBRN sub group project team at the UK’s Defence CBRN 

Center at Winterbourne Gunner, Salisbury, UK for a report writing and training 

observation week. (Figure 1) The report 

revealed several key points: first, both 

the US and UK are moving away from 

the NATO standard threaded protective 

mask canister filter with the fielding of the 

M50 series mask (US) and the General 

Service Respirator (UK) while Canada, 

Australia and New Zealand are maintaining the C-4 and S-10 protective masks 

respectively. Second, the US is introducing two new pieces of equipment: a 

low volatile hazard detection capability 

to the M256A1 kit which is being fielded 

as the M256A2 and an additional flag 

marker, “Toxic”, to the CBRN marking kit.

provided valuable insight to the UK’s 

CBRN transformation and training concepts, providing each ABCA nation better situational awareness when they 

address future interoperability issues.

For access to ABCA Publication 370, 

ABCA Best Practices Guideline for Military Mass Causality Decontamination 

Operations During a Domestic Hazmat/

Weapons of Mass Destruction Incident, 

and additional ABCA interoperability 

products, log on to www.abca-armies.

org. Once at the site, select “register” 

to submit a request for a password in 

order to view all ABCA documents.

BIOGRAPHY

LTC Michael S. Quinn is a CBRN Officer assigned to the US Army Nuclear 

and Combating WMD Agency’s Analysis Division. He has a BS in Chemistry from Auburn University and a MS 

in Health Sciences from Touro University. He was previously assigned as the 

Corps CBRN Officer, Allied Rapid Reaction Corps (NATO) and BN XO & S3, 

22nd Chemical BN (TE). His email address is michael.s.quinn@us.army.mil

On the surface, these two new pieces 

of equipment may appear minor, however the significance of highlighting 

both the M256A2 kit and flag marker 

are twofold: ABCA partners are made 

aware that these capabilities exist and 

are available through the national stock 

number system (NSN) and second, 

ABCA Standards require modification 

in order to define the new equipment 

for situational awareness and interoperability during coalition operations.

Understanding how each country 

equips, trains, and mans their CBRN 

force is critical function of the ABCA 

Shield team in order to enhance interoperability. The Royal Air Force (RAF) is 

the CBRN proponent for the UK military 

and as of April 2012, the RAF assumed 

total responsibility for the UK’s CBRN 

Regiment at RAF Honington. The UK’s 

former Joint CBRN Regiment was commanded by 1st Royal Tank Regiment 

with two army troops of Light Role (similar to Tech Escort CRT) and Fox Recon 

teams and two RAF squadrons of bio 

detection systems. The RAF now provides all CBRN specialist capability to 

the UK Army in support of operations. 

While at the Defence CBRN Center, 

the Project Team toured the instruction 

facilities, mask confidence exercise facility as well as observed soldiers and 

airmen conducting CBRN enhanced 

specialist training. (Figure 2) The visit 

Figure 3. Shield Project Team. (l-r) LTC M. Quinn (US), Mr. J. Pool (US), Mr. B. Parker (US), CSM P. Taylor (UK), 

WO3 J. Stinnett (USMC), MAJ M. Pettersen (NZ), MAJ M. Robertson (CA), LTC M. Boggs (NZ)

15 ISSUE 9 Combating WMD Journal
Combating WMD Journal ISSUE 9 16

Using Google Earth and Primary Ray-Tracing to

 Model Thermal Effects of a Surface Burst

Mr. Matthew Jackson

Nuclear Engineer, U.S. Army Nuclear and CWMD Agency

ntroduction and Limitations of 

Models

Most software tools that perform 

prompt calculations do not take terrain 

or line-of-sight effects into account. In 

the case of thermal effects for a nuclear 

explosion, this can prove to be a major limitation in an urban environment. 

Since the thermal radiation outpaces 

the blast wave, it will become incident on 

the surface of the structures/equipment 

before the blast wave can translate or 

collapse them. The more robust manner to address this would be to create 

3D grid, trace the rays from the point 

source, compute transmission coefficients for the ambient air and the materials forming the various structures, 

and compute primary and secondary 

rays. However to get a reasonably accurate solution, we could choose to only 

trace the primary ray, assume 100% 

absorption by the wall, which will give a 

rough picture of the effect of structures 

on thermal effects. For this purpose we 

can use a simplistic, circular, grid. Rays 

will be sent out from 0 to 360 degrees, 

any buildings intersecting these rays will 

be flagged, and their intersection point 

computed. In Google Earth it is relatively 

easy to draw in polygons to define a 

structure, with the limitation that all 3D 

structures will be modeled as prisms. 

Some of the primary limitations of 

the model are listed below. The model 

does not currently take terrain elevation into account; however this could 

readily be achieved by modeling key 

features as polygons, or by incorporating Digital Terrain Elevation Data. It is 

also assumed that all structures modeled as polygons are provided as a list 

of points in ordered pairs (as they would 

be if originating from Google Earth). 

The explosion is currently modeled 

as a point source and is implemented 

as a 2D solution. Rise and change in 

diameter of fireball is ignored as well.

I

Background Relations and Definitions

Let R be defined as the radius of effect, a radius defined by the user based 

on calculations gleaned from equations 

provided by EM-1 or similar resources. 

Let V1 represent the vector formed from 

the source to a node on the circumference of the effect radius and let V2 

represent the vector formed from two 

Figure 1. Thermal Effects Plot without Ray Tracing (©2011 Google, ©2011 

DigitalGlobe)

Figure 2. Example Grid

Figure 3. Definition of Vectors V11 V22

and R
17 ISSUE 9 Combating WMD Journal

points forming a segment of a structure.

Before delving into the details of the 

algorithm, several mathematic functions must be defined. As mentioned 

earlier, one of the assumptions of the 

code is that all polygons defined must 

be ordered pairs. In most grids, outer 

boundaries are oriented counterclockwise (CCW). Consider figure 3: the 

square block represents a structure, and 

the circle represents the desired thermal 

effect. The outer boundary must remain 

counterclockwise, yet upon removing 

the section of the circle blocked by the 

structure, the segment highlighted in red, 

while CCW relative to square polygon, is 

clockwise relative to the outer boundary. 

This means that when reading in the 

boundary points which define the building, they should be tested for orientation 

(counterclockwise or clockwise). The 

easiest way to do this is to take the cross 

product of the two vectors forming the 

points; if the cross product is less than 

zero, the points are ordered clockwise, 

otherwise they are CCW and their ordering must be reversed, or in mathematical 

terms segments are ordered CCW if:

For the purpose of ray-tracing, it is also 

necessary to determine whether one 

line intersects another, and if so, where 

that intersection point lies. There are a 

few ways to determine whether two lines 

intersect, but the easiest way is to simply 

take advantage of the CCW algorithm defined above. Following the methodology 

outlined by Dr. Jeff Erickson1, two line 

segments (Figure 4) intersect only when:

CCW(A,C,D) ≠ CCW(B,C,D) & 

CCW(A,B,C) ≠ CCW(A,B,D), (2)

Figure 4. Structure Blocking Thermal 

Rays 

V1 X V2 > 0 (1)

where CCW is defined in equation (1).

Equation 2 will be used to flag edges 

that intersect, but the intersection point 

also needs to be computed. Let two 

lines exist for the 4 coordinates 

(P1 -> P2, P3->P4):

L1=aV1+P1

L2=bV2+P3 (3)

The intersection point occurs where L1 

= L2:

aV1+P1= bV2+P3

a V1= bV2+(P3-P1 )

a(V1×V2 )= b (V2×V2 )+(P3-P1)×V2 

a(V1×V2 )= (P3-P1 )×V2

a((V1×V2 )∙(V1×V2 )=((P3-P1 )×V2)∙ 

(V1×V2)

Substituting (3) into equation (4) yields 

the intersection point P:

P=aV1+P1 (5)

In the scenario defined in figure 2, P1 

would represent the coordinate defining the location of the source, and P3 

the first coordinate of a line segment 

along a structure boundary.

When using latitude and longitude 

for coordinate pairs, it is necessary 

to take into account the coordinate 

system when computing the distance. Google Earth uses the WGS84 

coordinate system, which defines the 

a=

(((P3-P1 )×V2 )∙ (V1×V2 ))

((V1×V2)∙(V1×V2 ) )

(4)

following variables (all lat/lon should 

be converted to radians first)2:

a=6378137.0

b=6356752.3142

Using the spherical law of cosines, the 

distance between two latitude/longitude pairs { [lat1

,lon1],[lat2,lon2] } can 

be calculated:

d= arcsin(sin(lat1)*sin(lat2)+cos(lat1)* cos(lat2

 )*cos(lon2-lon1) )*R (7)

For this model, the outer boundary is 

defined by a circle (in theory it could 

be defined differently if a geometry for 

the outer boundary is more appropriate). To compute the coordinate at the 

outer radius of a circle at a given angle 

θ (assumed in radians), the following 

relations may be used:

Determining Location of Structures 

Relative to Source

Figure 6. Centroid of Unique Geometry

(6)

1-b2

 

a2

E= √

Rearth=

latcirc=latsrc+

loncirc=lonsrc+

[meters]

a(1-E2 )

(1-E2sin2(latitude) )1.5

180*Rsinθ

Rearth*π

π

180

180*Rcosθ

Rearth*π*cos(latsrc*

(8)
Combating WMD Journal ISSUE 9 18

Buildings are positioned in a plethora 

of orientations relative to the source. 

Ray tracing can be used to determine 

which buildings intersect a given ray, 

but has no inherent way of determining 

if one structure is shielded by another 

(see Building B in Figure 6). Fortunately, 

this can be accomplished by ranking 

the buildings by their distance from the 

source. There are at least two ways to do 

this: the most accurate would be to compute distances along the edges till the 

minimum length was found. A quicker, 

and for most cases, sufficiently accurate 

method, is to compute the distance from 

the centroid of structure to ground zero. 

For the purpose of simplicity, the latter 

was chosen. It is possible for unique geometries (figure 5) that a building with a 

more distant centroid (Building A) could 

be shielding a building with a less distant 

centroid (Building B). A computationally expensive way to correct this would 

be to loop through all structures, determine the closest point of intersection fk

for each building for a given angle θ:

for θ=0 to 2π

for j=0 to Number of Buildings

for i=0 to Number of Edges in Building j 

To gain some additional utility out 

of the process identified above, the 

edges on each building could also be 

reordered by distance from source, 

eliminating the need to loop through all 

edges for each angle where an edge 

is found to intersectV1.

Intersection Identification and Constructing the Boundaries of the New 

Polygon

In prior sections the methodology for 

identifying segments that intersect and 

their intersection point was discussed. 

Additionally, algorithms for computing 

the distance for lat/long pairs was discussed. The generic algorithm for draw-

 u={lonsrc+Reff cos(θ),latsrc+Reffsin(θ), 0}

if vi>intersection(edge i, u)

vi>intersection(edge i, u)

end if

end loop i,j

f

k

 ( θ)=min(vi )

end loop θ [A.1]

ing the thermal effects polygon would be:

 1. Read in building data (from kml 

or other source).

 a. Check whether elements are 

oriented clockwise or counterclockwise

 i. If counterclockwise, reverse directions of ordered pairs

 b. Compute centroid of building 

(or skip if using algorithm A.1)

 2. Rank buildings by distance, either using algorithm A.1 or by computing distance from source to centroid.

 3. Determine coarseness of mesh 

and construct array to hold angle, an 

integer value to flag angles that intersect a structure, as well as the {x,y,z} 

coordinates for the intersection of the 

structure and V1.

 4. Loop over all angles, compute 

V1.

 a. Loop over all buildings

 i. Loop over all building 

edges

 - Compute V2

 - If angle has not been 

already flagged as intersected by a 

building, check for intersection of V1, 

V2 (Eq. 2), and if true, compute intersection point (Eq.3-5).

 

 - Store intersection point 

with smallest distance from source in 

array constructed in step 3 (Eq. 6-7). 

 5. Create polygon array to store lat, 

lon coordinates of effect polygon.

 6. Construct polygon by looping 

over all angles

 a. If angle has been flagged as 

intersecting a building, store {x,y,z} 

intersection coordinate stored in array 

of step 3 in the array created in step 5.

 b. If not, compute the lat, lon at 

circumference using Eq. 8 and store in 

the array of step 5.

 7. Write file to kml (note kml 

expects coordinate pairs to be in the 

order {lon, lat, z}.

Results

A program was written using the algorithm outlined in the previous section. 

The program takes the source coordinates, HOB, radius of effect, and lat/

lon as inputs. As mentioned earlier, 

this initial implementation is only 2D, 

thus it would be invalid for HOB >> 0. 

At HOB above the average building 

heights the projection of shadowing 

onto the ground must be computed, as 

opposed to simply using the intersection point of the thermal ray with the 

building edge. 

 For the plot in figure 8, a hypothetical 

thermal effect with a radius of 100m was 

modeled. Rough outlines of buildings in 

the area were drawn in Google Earth 

and saved as a kml file, which was read 

by the algorithm outlined in the previous 

section, and used to compute the boundary of the effect polygon. At the beginning of this article, a thermal effect circle 

was drawn, ignoring all terrain and building interaction; but as seen in figure 7, a 

large area that was originally predicted 

to be within the thermal effect, was in 

fact a gross overestimate (excepting 

the upper right quadrant), while in other 

quadrants the presence of structures 

rendered the radius of effect largely a 

meaningless quantity. Thus by implementing this simple algorithm, it was 

possible to re-shape the area expected 

to be impacted by a given thermal effect

Future Work

The logical first step would be to 

extend the algorithm to three dimensions, and modify the code to support 

airbursts. This would primarily involve 

modifying the intersection code to project the results from the intersection 

point to the surface (or a fixed height 

above the ground). It would also be 

useful to determine a data source 

for altitude and use that to model the 

terrain as well as the buildings. Third, 

adding in support for translucent 

structures could potentially be used to 

model trees and other foliage which 

serve as a partial screen to incident 

rays. Finally, it would prove useful to 

utilize the delphic rise model to account for fireball shape and rise, which 

in turn would provide a more comprehensive model for the thermal footprint 

on a given landscape. 
19 ISSUE 9 Combating WMD Journal

BIOGRAPHY

Matthew Jackson is a nuclear engineer at the U.S. Army Nuclear and CWMD Agency, and can be 

reached at matthew.r.jackson3@us.army.mil or 703-806-7867 should any questions arise from this article.

Figure 7. Thermal Effects Program Input

Figure 8. 100m Thermal Effect with Ray Tracing (©2010 Google, ©2011 DigitalGlobe)
Combating WMD Journal ISSUE 9 20

oxins are poisonous metabolites 

produced by living organisms. 

Although classified as biological 

warfare agents by the 1972 Biological 

Warfare Convention they lack the ability 

to reproduce, as is the case with traditional biological agents like Bacillus 

anthracis (the causative agent of the 

disease anthrax). Thus, toxins are frequently claimed as chemical warfare 

agents as well as biological agents. 

However, the DoD classifies all toxins, 

including those produced by microorganisms or plants, as chemical agents. 

Owing to their complex structures, 

chemical synthesis of these agents is 

either not possible or impractical for production on an industrial scale. Many, if 

not most, toxins are formed as proteins 

or peptides (short chain length proteins) 

and are produced by representatives of 

all the major kingdoms of life. Mycotoxins are one exception to this general 

rule. These are structurally complex 

organic compounds produced by fungi.

Advances in biotechnology have further blurred the distinction between biology and chemistry. Genentech, a San 

Francisco area biotech firm created in 

1976, is a pioneer in the biotech industry. Scientists at Genentech successfully 

engineered a recombinant version of the 

human protein insulin into bacteria, an 

invention that has not only changed the 

life of millions of diabetics worldwide but 

has also heralded the industrial-scale 

manufacture of protein pharmaceuticals. 

It is now possible to produce thousands 

of pounds of insulin annually in a single 

plant. This technology is adaptable to 

virtually any protein and, similarly, to production of other complex biochemicals.

Small-scale toxin production does 

not require the sophisticated materials 

and engineering efforts necessary for 

chemical weapons production; indeed, 

crude preparations of small quantities 

of toxins are not beyond the capabilities 

of a Master of Science level biochemist 

Toxin Weapons: What’s the Worry?

Mitchell Wise, PhD

U.S. Army Nuclear and CWMD Agency

or microbiologist or even lay persons. 

There have been several instances in 

recent years where ricin, a toxin that can 

be extracted from beans of the castor 

oil plant, has been used or its use attempted by fringe terrorist groups in the 

US. However, on an industrial scale, biological toxins require a substantial input 

of technology. Converting these toxins 

into weapons capable of widespread 

dissemination to produce mass casualties requires financial support unlikely 

to be found at less than a State level.

This article will examine the potential 

development of toxins as weapons of 

mass destruction (WMD) and explore 

the rationales for such development. 

Although there are literally thousands of 

biological toxins known, the focus here 

will be on four that many experts believe 

have the greatest potential for weaponization: 1) botulinum (neuro) toxin 

(BoNT); 2) the mycotoxin T2; 3) ricin; and 

4) staphylococcal enterotoxin B (SEB). 

In examining the potential for toxins as WMD it might be worthwhile to 

first enumerate the quantities of these 

toxins required for battlefield employment. According to Franz 1

 it would 

take about 8 kg (kg = kilogram or 1,000 

grams) toxin per 100 m2 battlefield area 

for BoNT, the most potent toxin known 

to man, and about 800,000 kg per 100 

m2 for T2 toxin, the least potent of the 

toxins considered here, to effectively 

contaminate a battlefield. Even considering the advances in bioengineering, the production of these quantities 

is a daunting technological challenge.

Botulinum Toxin. BoNT is reputed 

to be the most toxic substance known (in 

theory a single gram could kill a million 

people). Intoxication by BoNT can occur 

by ingestion, inhalation or direct entry 

into the blood stream (through injection 

or an open wound). The estimated LD50 

for humans (lethal dose for 50% mortality rate) is about 1 ng toxin per kg body 

weight by intravenous (or intraperitoneal) injection and only slightly less, 3 ng 

toxin per kg, by inhalation2 (ng = nanogram or 1/billionth of a gram)3

. The time 

period after exposure is highly variable 

and depends on route of entry. Foodborne cases may present symptoms 

anywhere from 2 hours to 8 days but 

typically in 12 to 72 hours after ingestion. Inhalation cases occur in as little as 

12 hours in test monkeys administered 

high doses. The few known human cases of inhalation poisoning resulted in 

symptoms after 3 days 4. But, as these 

were laboratory accidents, they undoubtedly resulted from very low doses.

Interestingly, BoNT was the first toxin to be registered with the FDA as a 

therapeutic agent; originally used as 

a treatment for strabismus (crossed 

eyes), it has subsequently found application for additional neuromuscular disorders and, more famously, for 

cosmetic purposes. Thus, commercial 

production of the toxin is accomplished 

by fermentation of the bacterium Clostridium botulinum (Hall strain); improved 

efficiencies in large-scale production for 

this commercial product are inevitable. 

Fortunately, in terms of biodefense, 

the physicochemical properties of 

BoNTs render the toxins susceptible to 

chemical and environmental degradation. BoNTs are inactivated by disinfectants such as sodium hypochlorite 

(Clorox®) and they are denatured at 

elevated temperatures. The Centers for 

Disease Control (CDC) recommended 

protocol for inactivation of BoTN contamination of surfaces is 30 minutes exposure to sodium hypochlorite (> 0.1%) 

or sodium hydroxide (> 0.25 N). The 

CDC also reported that ozone treatment (> 2 mg per L) effectively inactivates BoTN in solution. The toxin is 

also destroyed by heating at 80oC for 

30 minutes or 100oC for 10 minutes. 

T
21 ISSUE 9 Combating WMD Journal

Although BoTN can be effectively inactivated by chemical or heat treatment, 

the thermal stability and bioavailability of 

BoNTs are also influenced by its purity 

and by associated (non-toxic) “neurotoxin-associated proteins” (NAPs)5

. Production of BoTN by C. botulinum typically involves concomitant production 

of these proteins which provide some 

protection against degradation by gastric acid and enzymes5

. Thus, a terrorist 

attack might well involve use of crude 

preparations of NAP containing BoTNs 

that would likely increase the potency of 

the toxin. Association with matrix proteins also affects the thermal stability of 

BoNTs and may be critical in detoxifying 

commercial food products or preventing 

terrorist attacks on the food system. 

BoNT (as well as spores of C. botulinum) can be decontaminated with gaseous formaldehyde at 0.3 to 0.6 g per ft3 

for 2 to 48 hours. Aqueous (seawater) 

solutions of formaldehyde were used for 

large-scale decontamination of Bacillus 

anthracis from areas of Gruinard Island, 

the location of biological warfare tests 

during World War II6. Decontamination 

of BoNT with ethylene oxide is not effective. It would be of interest to determine 

if ozone is an effective decontaminate.

The extreme toxicity and relative ease 

to aerosolize are characteristics of BoNT 

that make it attractive as a bioweapon. 

Efforts to weaponize this toxin, however, were abandoned by the US prior 

to termination of the biological weapons 

program in 1969 due to its instability. 

There is documented evidence that the 

Iraqis likewise pursued efforts to weaponize BoNT with similar difficulties7

. 

The prospect of terrorist employment 

of BoNT was recently modeled for contamination of the supply chain of milk 

and the efficacy of standard pasteurization for its decontamination. These 

investigators determined that 1 g of 

toxin could poison 100,000 individuals and that 10 g could affect 500,000 

people, most of whom would be children

8

. This analysis has, however, been 

disputed9. Highly sensitive and rapid 

detection methods for botulinum are currently available, such as the M1R electrochemiluminescence assay produced 

by BioVeris and deployed by the DoD10. 

Efforts to produce an effective vaccine for BoNT were initiated as early as 

1924. These early efforts were oriented 

around development of an immunogenic 

toxoid, i.e. a variant of the BoNT protein rendered non-toxic by treatment 

with formaldehyde. During World War 

II the Allies re-intensified efforts to produce a BoNT toxoid vaccine, succeeding in producing a reasonably effective 

bivalent vaccine (i.e. effective against 

two sero types (A and B) of the BoNT) 

shortly after the conclusion of WW II. 

In the 1970s, under contract with the 

DoD, the Michigan Department of Public 

Health (MDPH) developed a pentavalent vaccine providing immunity for up 

to a year against serotypes A through 

E. In recent years vaccines have been 

produced using recombinant protein 

fragments, i.e., a portion of the coding 

region of the BoNT gene that has been 

“cloned” into another microbe (either 

bacterium or yeast) to artificially produce 

high levels of the specific protein that 

retains the immunogenicity but not the 

toxicity of the BoNT. These cloned fragments can then be used, in the proper 

formulation, as vaccines11. Dynport 

announced in January 2012 successful completion of phase II clinical trials 

for their recombinant vaccine. This was 

timely because the CDC and Prevention 

terminated the use of the MDPH pentavalent vaccine in November 2011 for 

concerns about its loss in effectiveness 

due to storage for more than 30 years.

T2 Mycotoxins. At the other extreme 

of toxicity are the trichothecene (pronounced tri-kó-thee-seen) mycotoxins. 

In considering mycotoxins as potential 

weapons the history of their discovery 

is of some note. After several thousand citizens of the Soviet Union died 

as a result of consuming fungal contaminated wheat during WW II, Soviet 

scientists discovered mycotoxins as the 

likely cause. In the late 1970s and early 

1980s the Soviet Union was accused of 

employing weaponized T2, termed “Yellow Rain”, against isolated tribal peoples 

in South East Asia and Afghanistan. 

Although there is some evidence that 

T2 was employed, these allegations are 

hotly disputed by several reputable investigators. See J.B. Tucker12 for an excellent review of this controversy. Practical employment of T2 as a battlefield 

WMD is, nevertheless, questionable13. 

Although several related mycotoxins 

are known, T2 is one of the most toxic 

and, hence, most likely to be developed 

as a weapon. These metabolites are low 

molecular weight (250 to 500 Daltons), 

essentially non-volatile compounds 

produced by certain filamentous fungal 

species. While T2 is typically produced 

by species of Fusarium, trichothecenes 

are also produced by species of Cephalosporium, Myrothecium, Trichoderma 

and Stachybotrys. Unlike the other three 

toxins discussed here, trichothecenes 

can be absorbed through the skin and 

they are particularly stable to heat. Temperatures in excess of 200 oC may be 

required for their complete inactivation. 

The trichothecenes are derived from a 

group of natural compounds known as 

sesquiterpenes and are characterized 

by an epoxide ring at the C13-C14 position as well as an olefinic double bond 

at the C8 position (Fig 3). The highly 

reactive epoxide group is critical to their 

toxicity. The various trichothecenes are 

differentiated by substitutions around 

the trichothecin ring; these substitutions 

all contribute to one degree or another to the toxicity of the various forms. 

The trichothecenes are highly effective inhibitors of protein biosynthesis. 

In laboratory cellular assays T2 exerts 

its effect within 5 minutes. T2 also inhibits DNA synthesis in mice and rats, 

although to a lesser degree than protein 

synthesis2. The pathology in humans 

depends on both route and magnitude 

of exposure. Acute dermal exposure 

results in formation of severe irritation 

and blisters on the skin that may last 

for weeks. Respiratory exposure results in extreme irritation of the throat 

with coughing and deep chest pain.

As a condition that has been linked to 

Fusarium contaminated grain, alimentary toxic aleukia (ATA) results in necrotic 

lesions in the mouth, esophagus and 

stomach with accompanying leucopoenia (reduced white blood cell count) and 

frequently death. Putative victims of “yellow rain” also suffered severe gastrointestinal bleeding, diarrhea and death.

The estimated LD50 for T2 in humans 

is approximately 1,200 μg toxin per kg 

body weight by inhalation and approximately 25 to 50 μg per kg by ingestion 

(1μg = 1/millionthof a gram). In mice the 

LD50 for intravenous injection of T2 is 
Combating WMD Journal ISSUE 9 22

4.2 to 7.3 μg per kg, which approximates 

the LD50 (6.6 μg per kg) for dermal 

application. For monkeys the LD50 for 

dermal application of T2 in DMSO is 

>8.0 μg per kg 2. Thus, as a vesicant 

T2 is approximately 400 times more 

toxic than the chemical agent mustard2. 

As indicated previously T2 is particularly heat stable, thus the principle 

means of decontamination is through 

chemical treatment. Hypochlorite 

(household bleach), particularly in an 

alkaline solution, is regarded as an effective decontaminant. Although some 

reports have indicated that hypochlorite does not alter the epoxide ring, the 

combination of alkaline hydrolysis of 

side group bonds and oxidation by the 

hypochlorite appears to substantially 

reduce the toxicity of any resulting by 

products. One particularly innovative 

study demonstrated that aqueous ozone 

was an effective decontaminant. Ozone 

is highly reactive with carbon double 

bonds and appears to further react with 

the trichothecene degradation products 

to form smaller molecules not detected 

by the usual analytical methods (UV 

spectroscopy or mass spectrometry). 

The trichothecene compound deoxynivalenol, which is a common contaminant of wheat, barley, and maize, is also 

sensitive to aqueous sodium bisulfate. 

There are additional reports on enzymatic degradation of trichothecene mycotoxins. However, none of these enzymatic processes is currently practical for 

military applications. Physical methods 

such as gamma or microwave irradiation have only shown limited success. 

Effective decontamination of T2 or 

other trichothecenes should be easily accomplished with the current inventory of military decontaminates 

(DF-200, STB, DS-2), collateral material damage not withstanding. Direct 

experimental demonstration of these 

processes on representative surfaces 

such as chemical agent reactive coating (CARC) or the fabric in all purpose 

combat uniform (ACU) etc. is needed. 

Ricin. Ricin is a toxin derived from 

beans of the castor plant (Ricinus communis L.) and has been the subject of 

scientific study since the mid 19th century. Indian farmers have, for centuries, 

fed small amounts of seeds of the abrus 

plant (which makes abrin, a toxin similar 

to ricin) to calves as a crude means of 

immunizing them from toxic beans that 

could be ingested during grazing. Paul 

Ehrlich, a renowned immunologist of the 

early 20th century, used this same toxin in 

pioneering research on the mechanisms 

of humoral immunity and antibody action. 

Ricin is a dimeric glycoprotein (a protein chain with attached sugar residues) 

composed of A and B subunits with a 

reported molecular weight of approximately 64,000 kDa. The protein is translated from a single gene as a single 

protein which is subsequently cleaved 

within the plant cell into two separate 

proteins held together by a disulphide 

bond. The DNA coding sequence for 

ricin has been determined and both the 

A and the B subunits of ricin have been 

cloned and heterologously expressed in 

bacteria. The A subunit is responsible 

for the toxicity of ricin through its activity as a RNA glycosidase that inactivates ribosomes (molecular structures 

required for protein synthesis). The B 

subunit is a lectin which binds to carbohydrate residues on the exterior of 

target cells and facilitates entry of the 

A subunit into the interior of the cell.

Ricin can be absorbed into the body 

by inhalation, ingestion or injection into 

the circulatory system. Inhalation and 

injection are the most lethal routes, with 

an estimated LD50 for humans of 3 to 

5 μg per kg (based on animal studies). 

Death by inhalation involves hypoxia 

from pulmonary edema and alveolar 

(lung) flooding2. Intravenous administration results in intravascular coagulation and lesions of the kidneys and 

liver, with the exact cause of death not 

clearly understood. Rat toxicological 

response to ricin exposure by inhalation is delayed, with the onset of clinical symptoms appearing 8 to 12 hours 

after exposure. A similar delayed response was observed with primates2

. 

While ingestion of ricin can also induce toxicity, the toxic dose is approximately 100-fold greater than the dose 

for inhalation or injection toxicity. The 

toxin may be poorly adsorbed by or degraded in the digestive track. Nevertheless, it poses a potential threat from deliberate contamination of food sources.

Castor beans are abundant and used 

for the industrial production of castor oil 

which is used as a laxative and as an ingredient in numerous industrial products 

including lubrication oils, glues, detergents and dyes. The annual production 

of castor oil world-wide is in excess of 

1.2 million metric tons and, depending 

on the extraction process, the mash 

waste from castor oil production can 

also yield significant quantities of ricin. 

Interest in the use of ricin as a chemical agent by the US and other nations 

began during WW I. During WW II the 

US produced a weapon system capable 

of delivering aerosolized ricin, but it was 

never employed and subsequent efforts 

to improve the system were abandoned. 

Because the raw material for ricin is 

readily available and extraction of the 

toxin is relatively simple, there is concern that it can be employed as a terror 

weapon. There is evidence that Iraq 

attempted to weaponize ricin. Indeed 

there are numerous media reports of 

sundry radical groups attempting to use 

ricin in terrorist attacks. The August 12, 

2011 New York Times, for example, published an article describing efforts by the 

Yemeni branch of al-Qaida to produce 

significant quantities of ricin. According to the New York Times report these 

Islamic terrorists have been importing 

large quantities of castor beans and 

appear to be attempting to pack the extracted ricin with small explosives to produce an improvised toxin devise for employment in a confined space such as a 

shopping mall, airport or subway station. 

Ricin, like most proteins, is thermolabile. Although somewhat more 

stable than botulinum toxin, it is nevertheless denatured at temperatures 

above 80oC14. Decontamination of 

ricin on surfaces of militarily relevant 

materials (polycarbonate, butyl rubber, 

steel and Tyvek®) was demonstrated with hypochlorite (Chlorox®) and 

the commercial decontaminate Peridox®, a mixture of hydrogen peroxide, 

peroxyacetic acid and acetic acid15.

Animal studies demonstrated that ricin 

strongly induces an immune response 

and that both passive and active immunity can mediate the toxicity of ricin. 

In fact, Soligenix, a development stage 

pharmaceutical company, has recently licensed an experimental vaccine, 
23 ISSUE 9 Combating WMD Journal

RiVax, that was developed at the University of Texas Southwest Medical Center. 

RiVax contains the ricin A subunit that is 

genetically engineered to retain its immunogenicity thus providing protection 

while not possessing any toxic properties16. Phase I clinical trials proved 

successful and the company is currently 

seeking Food and Drug Adminstration 

(FDA) approval for status as an “orphan 

drug,” a classification designated for 

treatments of rare diseases allowing 

for various incentives from the FDA.

Because ricin is essentially untreatable and the course of its pathology 

irreversible by about 8 to 24 hours after 

inhalation and because vaccines for 

the general public are unlikely in the 

near term, post exposure treatments 

are being sought. Two approaches appear viable: (1) intervention with small 

molecule inhibitors of the A chain enzyme activity and (2) passive immunization with anti-ricin antibodies. Both 

these approaches are showing promise 

but are far from the clinical trial stage.

Like BoNT, ricin has found a place in 

the pharmacology arena. The notion 

of a “magic bullet” drug to specifically 

target and kill aberrant cells or tissues 

such as cancer was posited by Ehrlich 

at the turn of the 20th century. Over 

the last 40 years these magic bullets 

have been developed in the form of immunotoxins (IT). ITs are agents that 

combine an antibody or recombinant 

cell binding portion of an antibody to a 

toxic compound. Bacterial and plant 

toxins such as ricin have been extensively employed in ITs. Advances in understanding the molecular structure and 

function of these toxins as well as the 

biotechnology required to manipulate 

and produce large quantities of this protein have resulted in therapeutic application of ricin. From a bioweapons standpoint, research and development of ITs 

using ricin might be exploited to mask 

weapon development. Detection of ricin 

can be accomplished fairly rapidly (< 

15 min) by immunosorbent assays or 

electrochemiluminescence methods10.

Staphylococcal Enterotoxin B. Staphylococcal entertoxin B (SEB) is one of 

more than 20 serologically distinct proteins produced by strains of Staphylococcus aureus. These also include 

SEA, SEB, SEC1-3, SED-E, SEG-K, 

and SEU. Although the toxin is excreted from the producing organism and 

might rightly be termed an exotoxin, the 

“entero” term results from the fact that 

they are adsorbed through the gastrointestinal tract17. Based on the cDNA 

sequence of a cloned SEB, it is a 239 

amino acid protein, with a molecular 

weight of 28,300. Like botulinum toxin, 

SEB is expressed as a single peptide 

(without post-translational modification) 

that is highly susceptible to proteolytic 

cleavage by trypsin. The cleaved proteins remain associated through an internal disulphide bond and retain all the 

immunological and toxic properties of 

the parent protein. The enterotoxins, 

as well as other related exotoxins, are 

termed superantigens due to their ability 

to tightly bind major histocompatibility 

complex (MHC-II) receptors on antigen presenting white blood cells (e.g. 

macrophages,T-cells, etc). They also 

avidly bind T-cell antigen binding receptors. By executing both these activities simultaneously they circumvent the 

normal antigen recognition mechanism. 

 Up to one in five T-cells may thus be 

activated (compared to one in 10,000 in 

a normal immune response) resulting in 

massive up-regulation of various immunological regulatory factors (cytokines) 

such as: interferon gamma, interleukin-6 

and tumor necrosis factor-alpha2. Symptoms of SEB intoxication can be induced 

with as little as 30 ng, but the LD50 

for inhalation exposure is estimated to 

be 0.02 μg/kg, however an incapacitating dose is estimated at 0.0004 μg/

kg2. These estimates are highly variable 

between individuals, likely due to genetic variation in the MHC-II receptors. 

 Exposure results in fever, headache, 

myalgia, coughing, and nausea with 

vomiting and diarrhea through oral exposure. Symptoms, depending on dose, 

may occur in 2 to 12 hours after exposure. Although generally considered 

an incapacitating toxin, at high enough 

dose SEB can be lethal, typically as a 

result of pulmonary edema. Clinical 

diagnosis of SEB is likely to be difficult due to the generalized symptoms. 

Of the three protein toxins described 

in this report, SEB is considered the 

most stable to thermal denaturation. 

Because SEB is a serious threat in the 

food industry, numerous studies have 

been conducted on the thermal stability of the toxin in food products. Early 

investigations on the thermal stability of 

SEB resulted in some confusion. The 

protein seemed to actually be more resistant to denaturation at higher temperature (100oC ) than at lower temperatures (80oC). However, it was 

eventually demonstrated that SEB has 

a tendency to reactivate after initial heat 

treatment and that this reactivation occurred more readily with more rapid initial inactivation18. Aeration or mechanical agitation (stirring) circumvented this 

process; thus, it was determined that 

heat treatment at 100oC was, in fact, 

an effective decontamination process.

A 1986 study by Natick Laboratories 

evaluated the stability of botulinum toxin 

and SEA (a variant of SEB) on several 

surfaces. Immunological assays (ELISA 

and radioimmunoassay) were used to 

establish toxicity. On MRE (Meal, Ready 

to Eat) foil and BDU (Battle Dress Uniform) fabric, SEA was completely stable for up to two weeks at 30oC at a 

relative humidity ranging from 0 to 90 

%. At higher temperatures (37oC) on 

MRE foil SEB showed no loss of activity after two days but was degraded by 

84% in 14 days. At 45oC the toxin was 

80% degraded in two days and 94% 

degraded after 14 days. On glass under these conditions it was somewhat 

more stable. SEB was completely denatured with 5.25% Clorox® in 10 minutes. 

Efforts in the 1960s and 1970s to develop a vaccine against SEB focused on 

the creation of toxoids using dilute formaldehyde (as previously described with 

BoNT). Although unsuccessful, these 

efforts did demonstrate that SEB is susceptible to inactivation by formaldehyde. 

One major concern that cannot be 

ignored by the modern warfighter is the 

threat of contaminating limited volume 

water sources. Two recent studies have 

addressed this contingency. A 2009 

study by investigators at Edgewood 

Chemical and Biological Center and 

Temple University evaluated the stability 

of SEB and ricin in chlorinated water using polyacrylamide gel electrophoresis 

(PAGE), circular dichroism (CD) and 

liquid chromatography-mass spectrom-
Combating WMD Journal ISSUE 9 24

etry (LC-MS) to analyze the structural 

integrity of the toxins as well as a T-cell 

proliferation assay (a manifestation of 

its superantigen effect) for SEB and a 

murine 3T3 fibroblast cell toxicity assay for ricin. They found that after 30 

days at 25oC in a buffered solution neither toxin showed any adulteration in 

mass (PAGE, LC-MS), 3-D structure 

(CD) or toxicity (cellular assay). SEB 

was irreversibly denatured by heating 

to 95oC. After 5 days treatment at total 

free chlorine (TFC) to toxin molar ratios 

of 10:1 and 25:1 SEB retained 55% and 

16% activity respectively. At molar ratios 

above 50:1 no activity was detectable. 

(Ricin was completely inactivated at a 

TFC molar ratio of 100:1 in 24 hours.) 

Another study to determine the efficacy of hand held assays (HHAs), of the 

type used by the DoD to analyze BWA 

threats, in detecting SEB and ricin in water matrices it was found that the limit of 

detection increased from as low as 0.9-

12.5 ng/mL (depending on model tested) 

to values over 2,500 ng/mL in water 

treated with 1 or 2 mg/L cholorine (public 

drinking water generally ranges from 

0.3-1.0 mg/L). Examination of the toxin 

in treated vs. non-treated by PAGE and 

CD indicated that the toxin underwent 

substantial structural changes in the 

chlorine treated water. Thus, although 

toxicity was not directly evaluated, substantial denaturation of these toxins 

by chemical treatment likely occurred.

Conclusions. Advances in biotechnology over the past three and a half 

decades have considerably altered the 

potential for large scale production of 

toxins. Pharmaceutical grade proteins, 

such as insulin, are now produced on 

a massive scale. Although the mycotoxins, like T2, cannot, at present, be 

biosynthesized through genetic engineering, this limitation is only short 

term. The ability to produce paclitaxel, an anti-tumor drug derived from a 

similar biosynthetic pathway, through 

heterologous gene expression of the 

biosynthetic enzymes in bacteria, portents a similar capability for mycotoxins. But, even now, large scale production of T2 in a manner analogous to 

penicillin production is entirely possible. 

Toxins present several desirable characteristics as weapons. They are extremely toxic and in most cases curative 

treatment is not possible. However, with 

the exception of the mycotoxins, they 

are quite susceptible to denaturation. 

Ricin certainly represents a potential 

weapon. It was successfully weaponized by the US and has been deployed 

on numerous occasions by terrorists. 

Nevertheless, battlespace employment 

of toxin weapons against a sophisticated 

military is highly questionable. Protection can be afforded by current individual 

protective equipment and toxins are relatively easy to decontaminate. Because 

they are non-volatile, aerosolization is 

also difficult to achieve. And, even with 

current advances in biotechnology, their 

production remains quite expensive.

On the other hand, like other bioweapons, it is relatively easy to present toxin 

weapon development under the aegis of 

biomedical research. Production facilities would be, for the most part, identical to pharmaceutical plants. Thus, 

state actors, desiring to avoid international scrutiny, could easily disguise research and development of more toxic 

forms and higher production levels as 

medical or pharmaceutical research.

Another desirable feature of toxin 

weapons is the element of plausible 

deniability. Toxins, because they 

are naturally occurring, can go unrecognized as the cause of mass 

casualties or can be attributed to 

natural causes. The Yellow Rain controversy clearly illustrates this potential. 

Utilization of toxin weapons by terrorist 

groups is of greater concern, although 

production of mass casualties on the 

scale of the attacks on the World Trade 

Center is unlikely. The use of toxins to 

contaminate food or drinking supplies 

could be psychologically devastating, 

especially if employed against children. 

The principle source of terrorism today 

is from Islamic inspired groups, these 

organizations have, so far, shown a far 

greater penchant for conventional high 

explosives. However, the pernicious creativity shown by these groups suggests 

that when it comes to inventing horror 

they have no limits. Collusion of oil rich 

states such as Iran, which possesses 

at least a modicum of technological sophistication, with terrorist organizations 

like Hezb’allah should not be ignored.

BIOGRAPHY

LTC Mitchell L. Wise is a Chemical Officer (IMA) with the US Army Nuclear and 

Combating Weapons of Mass Destruction Agency, Ft Belvoir, VA. He has a 

B.S. in Zoology from the University of 

Georgia, an M.S. in Fish Pathology from 

Auburn University, and a Ph.D. in Biochemistry and Biophysics from Oregon 

State University. He was previously assigned as the Chemical Officer for Headquarters, Multi-National Forces, Iraq.

His email address is mitchell.wise@us.army.mil

ENDNOTES

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Printing: Washington D.C., 1997; Vol. 3.

3. Gill, M. D. Microbio - logical Reviews 1982, 46, 86-94.

4. Amon, S. S.; Schechter, R.; 

V., T. I. Journal of the American Medi- cal Association 2001, 285, 1059-1070.

5. Cheng, L. W.; Onisko, B.; Johnson, E. A.; Reader, J. R.; Griffey, S. M.; Larson, A. 

E.; Tepp, W. H.; Stanker, L. H.; Brandon, D. L.; 

Carter, J. M. Toxicology 2008, 249, 123-129.

6. Manchee, R. J.; Broster, M. G.; 

Stagg, A. J.; Hibbs, S. E. Applied and Environ- mental Microbiology 1994, 60, 4167-4171.

7. Zilinskas, R. A. Journal of the Ameri- can Medical Association 1997, 278, 418-424.

8. Wein, L. M.; Liu, Y. Proceedings of the National Academy of Science, USA 2005.

9. Weingart, O. G.; Schreiber, T.; Mascher, C.; Pauly, D.; Corner, M. 

B.; Berger, T. F. H.; Egger, C.; Gessler, 

F.; Loessner, M. J.; Avondet, M.-A.; 

Dorner, B. G. Applied and Environmen- tal Microbiology 2010, 76, 3293-3300.

10. Wise, M. L.; Calomiris, J. J. 

Combating WMD Journal 2009, 3, 4-13.

11. Smith, L. A. Vac - cine 2009, 27, D33-D39.

12. Tucker, J. B. The Nonpro- lilferation Review 2001, 8, 25-42.

13. Stark, A.-A. Journal of Food 

Protection 2005, 68, 1285-1293.

14. Parker, D. T.; Parker, A. C.; 

RamachandranC.K. Joint C/B Tech- nical Data Source Book, Vol VI, 

Toxin Agents, Part 3 Ricin, 1996.

15. Rastogi, V. K.; Smith, L. S.; Wal- lace, L.; Shah, S. S. Edgewood Chemical Bi- ological Center, Technical Report 631, 2008.

16. Smallshaw, J. E.; Vitetta, 

E. S. Current Topics in Microbiology 

and Immunology 2012, 357, 259-272.

17. Muller-Alouf, H.; Carnoy, C.; Simon- et, M.; Alouf, J. E. Toxicon 2001, 39, 1691-1701.

18. Fung, D. Y. C.; Steinberg, D. H.; Miller, R. D.; Kurnantnick, M. J.; Murphy, T. 

F. Applied Microbiology 1973, 26, 938-942.
Nuclear Targeting and the 

Nuclear Employment Augmentation Team 

(NEAT)

CW5 Bruce D. Brandes and CW5 Stephen A. Gomes

Nuclear Targeting Officers

U.S. Army Nuclear and CWMD Agency

ver the years the Army has 

seen a rapid decrease in not 

only the number of nuclear 

munitions available to the inventory, but 

the ability of the Army to fight both offensively and defensively in a nuclear 

environment. As we start the transition from counter insurgency (COIN) 

operations and into full spectrum operations, our Soldiers require more 

training in basic defensive operations, 

while the Staff requires training on 

offensive nuclear weapons employment to include the integration and 

synchronization of these weapons 

into the Joint Force Land Component 

Commander’s scheme of maneuver. 

 Currently, there is a misunderstanding that precision airstrikes using conventional munitions can achieve desired 

effects on “deep targets” and thus nuclear weapons are not necessary. This 

presumes a number of planning factors 

favorable to the U.S. and its allies such 

as: air superiority, target access, and 

ability to destroy hard and deeply buried 

targets. The illustration depicted in Conventional versus Nuclear Figure 1., demonstrates the numerous conventional 

bombs needed to achieve the same destructive force as a nuclear weapon, and 

you can imagine the number of sorties 

required to deliver the conventional munitions. Offensive operations with nuclear weapons can significantly reduce 

combat losses of aircrew and aircraft.

 The Army’s premiere targeteers are 

its field artillery warrant officers. Trained 

as targeteers for life, the transition from 

a conventional targeting officer to a nuclear targeting officer can be a dramatic 

leap of faith. This is further compounded 

by the last 12 years of war, where the 

Army has focused in a COIN operating 

environment, targeting single high value individuals with conventional kinetic 

strikes. The U.S. Army has not trained 

to target large troop formations with nuclear weapons or plan nuclear strikes 

for terrain denial since the early 90s.

 As we continue into an era of not 

only fiscal austerity, but nuclear austerity, we must look again at the use of 

nuclear weapons in a tactical and even 

“precision strike” role. “Mutually assured 

destruction” and “missiles over the pole” 

are no longer likely scenarios. As we 

experience globalization of technology 

and resources, the ability of those who 

would wish to do harm to the United 

States and our allies are indeed high. 

Never before have political and economic sensitivities created such an impact 

on the capability to employ a weapon 

long considered taboo. As some nations 

seek to proliferate nuclear weapons, and 

other nations seek to increase the number of warheads in their current nuclear 

weapons stockpile, the U.S. Army must 

improve its ability to fight and survive in 

a nuclear environment. By understanding nuclear weapons effects, the Land 

Component Commander can synchronize targets and integrate nuclear operations into the scheme of maneuver.

 The Army left the nuclear weapons 

delivery business nearly 22 years ago. 

With the last of the 8 inch artillery units 

being pulled from Germany in 1990, the 

decline of the Army’s nuclear mission 

began. Yet the Army and Marine forces 

are the most likely of the Services to 

operate in a nuclear environment if a 

conflict should ever escalate to this point 

 In 1992, the Chief of Staff of the 

Army, GEN James Peay III, wanted to 

maintain nuclear expertise in the Army 

following President’s Bush’s Presidential Nuclear Initiative in 1991. GEN 

Peay III mandated that “Upon request 

by the supported Combatant Commander, the Department of the Army 

provide a U.S. Nuclear and CWMD 

Agency (USANCA) Nuclear Employment Augmentation Team (NEAT). 

 As directed by Army Regulation 

10-16, U.S. Army Nuclear and Combating Weapons of Mass Destruction 

Agency, the NEAT provides nuclear 

targeting expertise and assistance in 

analyzing the impact of offensive nuclear weapons on the friendly scheme 

of maneuver. This is further codified 

in the Joint Strategic Capabilities Plan 

(JSCP). To that end, we have always 

maintained offensive nuclear training, 

but certainly not at the levels of the Cold 

War. The Defense Threat Reduction 

Agency’s Theater Nuclear Operations 

Course (TNOC), a basic primer on theater nuclear operations, is conducted at 

the Defense Nuclear Weapons School 

at Kirtland AFB. While this course provides a familiarization with Nuclear Operations at the COCOM level, it does 

not provide the level of targeting proficiency to support adaptive planning in 

support of theater nuclear operations.

o

25 ISSUE 9 Combating WMD Journal
 The NEAT derives its guidance 

from military strategy, down to the Guidance for Employment of Forces, and 

the JSCP (Figure 2.). This guidance 

then directs the COCOM to develop 

numbered OPLANS. These plans incorporate the nuclear planning process 

for which COCOM staffs are neither 

trained nor resourced to conduct. One 

of the key components of the NEAT mission is planning support to OPLANS 

and exercises. In the direct support 

role, the NEAT deploys to supported 

commands to assist, advise and plan 

for crisis action and adaptive nuclear 

scenarios. In support of its NEAT mission, USANCA maintains 2-12 officer/

warrant officers/civilians to deploy in 

support of operations to include weeklong training events to full duration 

combat deployments. In this capacity, the NEAT becomes part of the COCOM staff in an OPCON relationship. 

 The NEAT composition is based upon 

the mission set. It is an “adhoc” team 

composed of officers and DA civilians 

tailored to the mission. The range and 

scope of the NEAT includes the following:

• Formal “on the-ground” theater 

nuclear support 

• The NEAT augments Joint Forces Land Component in theater

Figure 1. Conventional versus Nuclear

Figure 2. Guidance for Employment of Forces, and the JSCP

Combating WMD Journal ISSUE 9 26
• Supports the Army’s capability to plan for joint employment 

of nuclear weapons, conventional attacks on nuclear facilities, and friendly force vulnerability to nuclear weapons.

• Provide Pre-Strike Theater nuclear planning, prepare STRIKWARN 

messages, recommend movement of friendly forces and provide 

Post-Strike recommendations regarding operations/movement. 

• Support Army Planning efforts to counter WMD.

• Understand and communicate the 

impact of WMD effects on military 

operations – educate the force.

• Enhance force surviv -

ability in CBRN environments—manage the Army’s 

CBRN survivability program.

• Enhance interoperability of multinational forces 

in a nuclear environment

Figure 3. NEAT injects to the Joint Planning Cycle Figure 3. NEAT injects to the Joint Planning Cycle. 

NEAT Reach back/Resources/Expertise:

-Nuclear reactor operations

-High Altitude Electromagnetic

Pulse (HEMP) effects

-Nuclear medical science

 Integrating NEAT operations into 

the COCOM should be treated as any 

other War Fighting Function (WFF). 

Participation in the 6 step joint targeting 

process is the key to a successful integration of Nuclear and WMD operations. 

Keeping CWMD as a standalone entity 

will invariably de-synch nuclear operations with the scheme of maneuver. 

The NEAT participates in real world 

deployments and exercises, and continues to augment COCOM staffs for nuclear support. Until such time as a nuclear 

free world, USANCA’s NEATs remain 

prepared to deploy and assist any command in planning nuclear operations.

BIOGRAPHY

CW5 Bruce Brandes is a Nuclear 

Targeting Officer at USANCA, he 

has served as a targeting officer at 

all levels throughout his 30 years 

of active duty, and serves as an instructor for the Theater Nuclear Operations Course. His email address 

is bruce.d.brandes.mil@mail.mil

CW5 Stephen A. Gomes is a Nuclear 

Targeting Officer assigned at USANCA. 

He recently returned from a deployment in Kuwait as the ARCENT Command Electronic Warfare Officer. He 

is a graduate of the Theater Nuclear 

Operations Course (TNOC) and the 

Joint Targeting School, Dam Neck, VA. 

H i s e m a i l a d d r e s s i s 

stephen.a.gomes.mil@mail.mil

27 ISSUE 9 Combating WMD Journal
Combating WMD Journal ISSUE 9 28

Biotoxins Used As Warfare Agents – Part 2

John S. Nordin PhD

AristaTek, Inc.

his article is modified from a series of papers written by the same 

author for “The First Responder”, 

a newsletter of AristaTek, Inc., available 

at http://www.aristatek.com. Part 1, 

which presented an overview of Biotoxins and discussed Ricin as an example, 

was presented in the CMWD Journal. 

Review: What kind of Biotoxins 

Might Be Used as Warfare Agents?

A ‘biotoxin” is a poison produced by 

living organisms including certain bacteria, plants, algae, fungi, protozoa, reptiles, fish, mollusks, and insects. Over 

400 biotoxins have been identified and 

many more exist in nature. Roughly 

about 15 or 20 of these usually appear 

on various lists published by governmental agencies as having potential for 

use as warfare agents. Two natural 

biotoxins are classified as “Schedule 1 

Chemical Warfare Agents” under the 

United Nations agreement on biological 

weapons, e.g. the Chemical Weapons 

Convention in 1993 and earlier agreements. These are saxitoxin and ricin.

On June 12, 2002, President George 

W. Bush signed into law the Public 

Health and Safety Act of 2002 (PL 107-

188), which requires that the Department of Health and Human Services 

maintain a list of biological agents and 

toxins, which pose a severe treat to 

public safety. The list of biotoxins, 

as it appears in the August 23, 2002 

Federal Resister, (see also 42 CFR 

Part 72, Appendix A) is as follows: 

• Abrin 

• Botulinum neurotoxins 

• Clostridium perfringens epsilon 

toxin 

• Conotoxins 

• Diacetoxyscirpenol 

• Ricin 

• Saxitoxin 

• Shigatoxin and Shiga-like toxins 

• Staphylococcal enterotoxins 

• Tetrodotoxin 

• T-2 toxin

In addition, The Centers for Disease Control and Prevention website (http://www.bt.cdc.gov/agent/

biotoxins/) also lists the following 

biotoxins which do not appear in the 

Public Health and Safety Act of 2002:

Brevetoxin

Colchicne

Digitalis

Nicotine

Strychnine

Trichothecene

We will look at Saxitoxin, Brevetoxin, Arbin, Botulinum neurotoxins, and Clostridium perfrigens epsilon toxin in this article.

Saxitoxin and Brevetoxin

Saxitoxin and brevetoxin are both 

potent toxins produced by algae known 

as dinoflagellates. Saxitoxin is a potent toxin which if ingested (or injected) 

works as a selective sodium channel 

blocker in the nervous system resulting 

in rapid, incurable paralysis and death. 

Brevetoxins (there are more than one 

kind of Brevetoxin) bind to different sites 

than saxitoxin allowing an unchecked 

flow of sodium ions in and out of nerve 

cells. A dose of 0.2 milligram of saxitoxin is fatal to an average-weight human 

being. Brevetoxins are rarely fatal and 

patients usually recover, but the person 

may suffer permanent nerve damage 

and dementia. Saxitoxin is produced by 

“red-tide” algae, one of the algae species being“Alexandrium tamarense”. 

This algae species is found in marine 

waters throughout the world. The usual 

mode in which humans ingest this toxin 

is from eating contaminated shellfish 

(clams, mussels, oysters), which in turn 

have ingested (“filtered”) the algae at 

some previous time in their life, even 

though the “red tide” may have past 

and the waters look clean. Cooking 

the shellfish does not destroy the toxin.

In the 1950’s the CIA began experimenting with the biotoxin. Saxitoxin was 

produced and stockpiled in the United 

States as part of a chemical weapons 

program at Fort Detrick, MD using the 

code name Agent TZ. It is not clear what 

the CIA involvement was, but Internet 

sources1 suggest development of dart 

guns and manufacture of suicide tables 

for their agents if captured. Agent TZ is 

soluble in water and can be ingested or 

inhaled. If an intended victim is jabbed 

with a dart tip, death occurs quickly. The 

method used by the CIA at the chemical 

weapons program at Fort Detrick, MD 

involved harvesting a certain species 

of clam grown in “red tide” waters, and 

extracting the saxitoxin from the clams. 

President Nixon in 1969 ordered the 

CIA to destroy its entire stock collected 

over the years and not engage in addiT

Figure 1. Red Tide Algae, a Source 

of Saxitoxin Consumed by Shellfish 

which in Turn Is Eaten by Humans

Red tide off California coast, Noctiluca sp., photo by PJS Franks, from 

Woods Hole Oceanographic Institution photo gallery 

Figure 2. Red tide off New Zealand 

coast, photo by M. Godfrey, from 

NIWA Science website
29 ISSUE 9 Combating WMD Journal

tional covert research with saxitoxin. In 

1975, the CIA director revealed to Congress that they still possessed 10 grams 

of saxitoxin, in violation of the 1969 presidential order, which was then evenly 

distributed to scientists and medical 

researchers under the auspices of the 

National Institute of Health. Saxitoxin 

is useful in the study of nerve disorders 

because it selectively blocks only the sodium channels but does not affect potassium or calcium channels or the chloride 

ion count or acetylcholine response. 

In 1977, a paper was published in 

the open literature2 on the chemical 

synthesis of saxitoxin. The synthesis 

was modified by Jacobi3 published 

in 1984, and with another update in 

20064 yielding an optically pure product 

mimicking what is produced in nature. 

The Jacobi synthesis was carried at 

Wesleyan University in Connecticut. 

The three methods were reviewed in 

the open Internet by J. Baird5 in 2006.

Saxitoxin is said to be 1000 times 

more toxic than the nerve gas Sarin. 

The 0.2 milligram fatal dose for an average weight human is based on LD50 

mice studies (the lethal dose resulting in 

the death of 50% of the test animals in 

24 hours). The LD50 for mice is 8 microgram/kg, but humans are 4 times more 

sensitive to than mice to oral doses of 

saxitoxin because the human digestive 

track is longer and more saxitoxin is 

absorbed. The lethal oral dose for humans is 1 to 4 mg depending upon age 

and physical condition. Children are 

apparently more sensitive than adults. 

Alexandrium tamarense is not the only 

algae species that produce biotoxins. 

The causative algal species mostly belong in the general classification of dinoflagellates, which include Alexandrium 

tamarense, Alexandrium circinalis (a 

fresh water species), A. minutum, A. 

ostenfeldi, A. catenella (Pacific coast), 

A. fundyense (northeastern U.S. and 

Canadian coast), Gymnodinium catenatum, Karenia brevis (eastern Gulf 

of Mexico), various Dinophysis sp. (Europe, Asia, Japan), and Pyrodinium bahamense (Philippines and elsewhere). 

The affected waters may be red, grey, 

brown or other colors, e.g. “brown tide”, 

or the waters may not be noticeably 

colored. At least 12 different biotoxins 

are produced from various dinoflagellate species and have also been studied. The biotoxins fall under the general 

chemical classification of tetrahydropurines, of which saxitoxin is the first 

studied and best known. There are 

also other biotoxins besides tetrahydropurines produced from algae blooms. 

No human deaths have been directly 

attributed to direct contact to “red tide” 

algae, but people may experience respiratory irritation when winds blow aerosol 

onshore from waters containing “red 

tide” algae. Skin irritation and burning 

is possible when swimming in areas 

affected by “red tide” algae. Deaths of 

people and animals (including birds, fish, 

turtles, etc.) occur because of consumption of mollusks and other creatures, 

which feed on the algae; the mollusks 

concentrate the biotoxin in their flesh 

as the result of their filter feeding. The 

biotoxins have resulted in deaths of fish, 

marine animals, sea turtles, and birds. 

Generally, fish and shrimp caught in 

“red tide” waters are safe to eat at least 

in smaller quantities (check with the local health department/authorities to be 

sure). However, the 1987 deaths of 14 

humpback whales off Massachusetts 

in Cape Cod Bay were traced to the 

whales eating mackerel, which in turn 

had eaten smaller fish and zooplankton, 

which had consumed large amounts of 

Alexandrium tamarense. The saxitoxin 

was concentrated in the food chain. The 

1987 death of 700 bluenose dolphins 

was also similarly traced to bioaccumulation of neurotoxins in their fish diet. 

Four types of human shellfish 

poisoning have been identified: 

• Paralytic shellfish poisoning (PSP) 

• Amnesic shellfish poisoning (ASP) 

• Neurotoxic shellfish poisoning (NSP) 

• Diarrhetic shellfish poisoning (DSP) 

PSP description:

The onset of symptoms occurs within 

5 to 30 minutes after ingestion of contaminated shellfish. Initially there is a 

slight tingling progressing to numbness 

around the mouth, neck, and face. In 

severe cases, these symptoms spread 

to the extremities in coordination and 

respiratory difficulty. There may be 

difficulty swallowing, sense of throat 

constriction, speech incoherence, 

headache, dizziness, nausea, possible 

vomiting, and reduced eye pupil size. 

Biotoxin

Saxitoxin 

Brevetoxin 

(ere are 

several toxins) 

Domoic acid 

(CAS 14277-

97-5) 

Okadaic acid 

(CAS 78111-

18-8) 

0.2 mg for average weight 

human. 100% recovery from 

non-fatal doses without brain 

damage 

Deaths rare, but patients may 

suer dementia. Rat and human 

studies show brain damage. 

non-fatal doses without brain 

damage 

Deaths rare, but elderly patients 

experience memory loss. Large 

dose of okadaic acid from 

contaminated mussels results in 

permanent neurological 

sequelae. LC50 (mice, injected 

subcutaneously) 0.192 mg/kg 

Rat LD50 (injected subcutaneously) 0.33 mg/kg. In a 1987 

Canadian outbreak, of 145 patients 

studied, the three patients who 

died were elderly and showed 

severe damage to the hippocampus and other parts of the brain. 

For 10 cases, from mussel analysis, 

a 4.2 mg/kg oral dose of toxin 

resulted in severe neurological 

eects.

Alexandrium sp. 

and certain other 

dinoagellates 

Gymnodinium 

breve (Gulf of 

Mexico and 

Caribbean), Karenia 

sp. and other 

dinoagellites

Nitzchi pungens (a 

diatom) implemented in 1987 

Canadian 

outbreak. Also 

Pseudonitzschia sp. 

(east and west 

coast of U.S. and 

Gulf of Mexico) 

Dinophysis sp.; 

also Prorocentrum 

lima 

PSP

NSP 

ASP 

DSP 

Algae species Poisoning Fatal dose 

Type 

Table 1. Example Biotoxins from Eating Shellfish
Combating WMD Journal ISSUE 9 30

In severe cases, within 2 to 12 hours, 

there is complete paralysis and death 

from respiratory failure in the absence 

of ventilatory support. Without artificial respiration, up to 75% of severely 

affected patients, die within 12 hours. 

Gastric lavage and administration of 

activated charcoal or dilute bicarbonate 

solution is also recommended. Benzedrine is effective in aiding artificial 

respiration. The PSP symptoms mimic 

acute organophosphorous pesticide or 

nerve gas Sarin poisoning, but the use 

of anticholinesterase agents is not recommended for PSP patients and may 

do more harm than good. After about 12 

hours, if death has not occurred, patients 

start to recover gradually and are without residual symptoms after a few days. 

Cooking the shellfish does not destroy 

the biotoxin. 

It is imperative to obtain samples of 

the shellfish tissue and their source 

so that diagnosis can be made. The 

mouse bioassay of the food extract is 

the usual diagnostic method. Radioimmunoassay and indirect enzymelinked immunoabsorbent assay have 

been developed for saxitoxin, but not 

all of the biotoxins, which cause PSP. 

HPLC analysis methods have been 

developed for all of the PSP toxins. 

NSP description:

There are several different kinds of 

brevetoxin (given names such as brevetoxin A, brevetoxin B, and other names). 

Brevetoxins act by disrupting the flow of 

sodium ions in nerve cells. They bind 

to the sites near the nerve cells allowing 

an unchecked flow of sodium ions in and 

out of the cells (in contrast to saxitoxin 

which binds different sites and blocks 

sodium ions from passing through the 

sodium channel). Brevetoxin poisoning rarely results in death, and patients 

recover within a few days, but permanent nerve damage and dementia can 

occur. Symptoms include false temperature sensations, muscular aches, 

dizziness, and anxiety. These are 

usually accompanied by vomiting, diarrhea, and abdominal pain. Cooking the 

shellfish does not destroy the biotoxin. 

ASP description:

Much of what is known is the result 

of investigation of 153 cases of acute 

intoxication, which were reported in 

1987 as the result of individuals eating 

mussels harvested from Prince Edward 

Island, Canada. The onset of symptoms 

varied between 15 minutes to 38 hours 

after eating. Many of the patients were 

elderly and suffered gastrointestinal 

distress and also neurological effects 

that included memory loss and dementia. Younger patients seemed to have 

more digestive problems. Twenty-three 

(23) patients required intensive care 

because of seizures, coma, profuse respiratory secretions, or unstable blood 

pressure. Three patients died. The 

cause of death was coma, encephalopathy, convulsions, and cardiovascular collapse. In the mouse bioassay, mice were 

given intraperitioneal injections of extracts from the mussels. The mice soon 

exhibited an uncontrolled scratching of 

both shoulders with their hind legs, and 

most of the mice died within 3.5 hours 

after injection. Further research demonstrated that the toxin was domoic acid, 

an amino acid with a molecular weight 

of 311. The involved mussels contained 

between 31 and 128 mg of domoic acid 

per 100 grams of mussel tissue. The 

toxin was produced by an algae (diatom) 

called Nitzschi pungen, which in turn 

was ingested by the mussels during 

their normal filter feeding. In ten patients studied, there was a clear dose response between amount of domoic acid 

in mussels consumed and neurological 

effects. Further tests using monkeys 

using mussel extracts gave similar dose 

response to the ten patients studied. 

Later research demonstrated the presence of domoic acid in anchovies in 

California, and razor clams and crabs off 

British Columbia. Domoic acid caused 

the death of large numbers of Brown pelicans and cormorants in 1991 and over 

400 sea lions in 1998, both incidents 

off the California coast. The anchovies 

in California had been eating the diatom, Pseudonitzschia australis that produced the domoic acid; the seabirds that 

died in 1991 in turn ate the anchovies. 

In the brain, domoic acid damages the 

hippocampus and amygdaloid nucleus. 

It damages neurons by activating AMPAS and kainatic receptor causing an 

influx of calcium. The uncontrolled increase of calcium causes the nerve cells 

to degenerate. When the hippocampus 

is damaged, long-term memory loss occurs. There is no antidote for domoic acid. 

Cooking the mussels does not destroy 

domoic acid. 

DSP description: 

Acute high-dose exposure to okadaic acid, which accumulates in certain 

clams and some crabs, is the underlying cause of human DSP. Symptoms 

occur between 30 minutes to 12 hours 

after eating contaminated shellfish. 

Symptoms include diarrhea, nausea, 

vomiting, abdominal cramps, and chills. 

Gastrointestinal bleeding and hiccups 

have occurred. Full recovery is usually experienced within a few days, 

but death can occur especially in elderly patients due to coma, seizures, 

and/or pulmonary edema. DSP mostly 

occurs in Europe, Japan, and South 

America. Over 5000 people experienced DSP in Spain in 1981. Okadaic 

acid (and/or its esters) primarily affects 

the cells lining the intestinal gut; the 

exact mechanism is not clear, but the 

chemical is thought to stimulate phosphorylation that controls sodium secretion by intestinal cells and also affects 

calcium ion transport in general across 

cell membranes in the body. Patients 

over 50 years old may also experience 

neurological effects including memory loss, severe anterograde amnesia, 

and motor or sensorimotor neuropathy. 

Cooking the shellfish does not destroy 

the biotoxin. 

Abrin

Abrin is a potent toxin extracted from 

the seeds of the Jequirity Pea (Abrus 

precatorius) plant. The adult fatal 

dose for abrin is about 0.0026 mg if 

ingested, or about 0.04 micrograms 

per kilogram (μg/kg) of body weight. 

The fatal dose can vary between individuals. Its toxicity is roughly 75 

times that of ricin. It is also fatal by 

inhalation or by absorption through 

sensitive skin areas as in the eyes. 

Like ricin, the toxin acts by inhabitation of body protein synthesis. Initial 

symptoms by ingestion include watery 

diarrhea at first, later nausea, vomiting, abdominal cramps, and chills. The 

vomiting and diarrhea becomes bloody. 

Severe dehydration may result followed 

by low blood pressure. Other symptoms 

may include hallucinations, seizures, 

and blood in the urine. Within days, the 

person’s liver, spleen, and kidneys may 
31 ISSUE 9 Combating WMD Journal

stop working. Death could take place 

within 36 to 72 hours of exposure. If 

death has not occurred within 5 days, 

the person usually recovers but may 

suffer long-term organ damage. There 

is no specific antidote. If abrin powder is inhaled, pulmonary edema and 

hemorrhaging can result. Abrin dust in 

air can result in blindness or at minimum severe eye irritation. There have 

also been reports6 of people who have 

ingested the seeds and slipped into a 

coma, a condition called “acute demyelinating encephalitis” , resulting in death. 

The plant itself goes by many names, 

including: Rosary Pea, Jequirity Pea, 

Jequirity Bean, Crab’s Eye, Deadly 

Crab’s Eye, Precatory pea, Precatory 

bean, Roseary Pea, Abrus seed, Jumble 

beans, Ratti seeds, Prayer beads, Tentos de America, Tentos dos mundos, 

Jequirite, Aivoeiro, Buddist rosary bead, 

Ruti, Indian bead, and Wild liquorice. 

The plant itself is a vine which grows up 

to 10 feet tall and has clusters of rose 

pink or purplish flowers about 0.5 to 0.8 

inches long. The flowers produce brown 

seedpods with shiny red and black 

seeds about 5 to 8 mm long. The plant 

itself is grown in tropical and subtropical 

areas and has been planted in warmer 

parts of the United States. The red and 

black seeds are sometimes used in 

necklaces and other decorative items. 

One seed if chewed can kill, especially 

a child. All parts of the plant are toxic 

to some degree, but the seed, which 

contains abrin, is especially toxic. If 

the dried seed is swallowed whole, it 

is less toxic but some of the toxic elements can still leach out by the digestive enzymes. Sucking on the seeds 

can release some of the toxic contents. 

Immature seeds are poisonous if ingested even whole. If holes are drilled 

in the seed as in a necklace and the 

seed is ingested, the toxic contents 

will leach out by intestinal secretions. 

Five glycoproteins have been purified 

from the seeds, four of which (abrin a, b, 

c, and d) are extremely toxic. The other 

glycoprotein is “abrus agglutinin” which 

is a powerful hemagglutinator but is relatively non-toxic to animal cells; its molecular weight is approximately 134,900. 

Arbin (a, b, c, and d) are the toxic 

parts. The molecular weight is between 63,000 and 67,000. Abrin has 

been given CAS# 1393-62-0. Purified arbin is a yellowish-white powder. Most of its toxicity is destroyed if 

heated to 80oC (176oF) for 30 minutes. 

The U.S. Department of Health 

and Human Services – Centers for 

Disease Control (CDC) Website provides a summary table (Table 2).

As far as we have been able to determine from an Internet search, Abrin 

is not known (to date) to have been 

used in any wars or terrorist attacks. 

Abrin also has potential medical uses 

such as in treatment to kill cancer cells. 

Botulinum neurotoxins One of the 

most toxic biotoxins known is botulinum neurotoxin, with an estimated human lethal dose of 0.001 micrograms 

per kilogram of body weight (μg/kg) by 

inhalation, or 1 μg/kg if ingested. The 

poisoning is called botulism. There 

are actually seven types of botulinum neurotoxins recognized, labeled 

serotypes A through G, with type A 

being the most toxic and types B and 

E causing less severe toxicity to humans. The botulinum neurotoxins are 

produced primarily by a spore-forming 

bacterium known as Clostridium botulinum and to a lesser extent by sporeforming bacteria Clostridium baratii 

and Clostridium butyricum. Clostridium sporogenes does not produce 

the neurotoxin. These bacteria and 

its spores are found worldwide in soil, 

ponds, coastal waters, sediments, the 

intestinal tracks of fish and mammals, 

and in shellfish. 

Human botulism is primarily caused 

by types A, B, E, and F neurotoxin. 

Types C and D most commonly affect 

fowl, birds, cattle, and horses and do not 

affect humans. Type E typically occurs 

from eating contaminated fish. Type G, 

isolated from a soil in Argentina, has 

not yet been linked to any outbreak. 

All of them are single polypeptide chains 

(molecular weight about 150,000) that 

work by blocking the release of acetylcholine from peripheral cholinergic 

nerve endings. What this means is 

that the nerve terminals are blocked, 

and the muscles do not work, usually 

starting at the eyes and face, then the 

throat, chest, and extremities. When 

the diaphragm and chest muscles become fully involved, respiration is in 

hibited and death occurs. There are 

differences on how the different types 

interact with nerve endings and block

Figure 2. Illustrations of Jequirity Pea
Combating WMD Journal ISSUE 9 32

the release of acetylcholine, which is 

the reason why some types are more 

toxic than others or are more toxic to 

bird or animal species or to humans. 

The neurotoxin itself is destroyed if 

heated to 80oC (176oF) for 10 minutes 

or longer. If heated to 100oC (212oF), 

destruction occurs quicker. However, 

cooking food containing spores does 

not destroy the spores at 100oC (212oF). 

When canning food, the spores must be 

destroyed by moist heat at temperatures 

of at least 121oC (250oF). The spores if 

ingested normally do not prorogate and 

produce neurotoxin in adult humans 

because gut conditions are too acidic, 

but the spores can colonize and produce neurotoxin in the intestinal tracks 

of infants under 12 months of age. 

Four different kinds of botulism 

poisoning are recognized: 

1. Inhalation botulism. This 

kind does not occur naturally and 

could mean that a terrorist has released the toxin as an aerosol. 

2. Food borne botulism. This is usually the result of ingestion of food that 

has been inadequately processed or inadequately cooked before being eaten. 

If food is contaminated with Clostridium 

botulinum spores, and the bacteria allowed to grow under anaerobic conditions, the neurotoxin will be produced. 

If not cooked properly to destroy the 

toxin, botulism food poisoning will 

occur. The most common source is 

home-canned foods. There have been 

incidences of poisoning in commercial 

products. Neurological symptoms usually appear within 6 hours to 8 days of 

ingestion of the food, the shorter time 

associated with more severe poisoning.

3. Infant (intestinal) botulism. This 

results from ingestion of bacteria spores 

which germinate in the intestinal gut and 

produce the toxin. This can happen as 

the result of food, soil, or dust contaminated with the spores. The infant gut is 

most susceptible to spore germination, 

but adult infections can occur if acidic 

conditions are not maintained in the gut. 

This is the most common incidence of 

botulism poisoning reported to the CDC 

in the United States. Pediatricians do 

not recommend feeding honey to infants 

as the honey could contain the spores.

4. Wound botulism. This happens 

when wounds become contaminated 

with dirt containing botulism spores. 

This is especially a problem with chronic 

injection drug users. The incubation 

period is between 4 and 14 days since 

contamination, the shorter time corresponding to the more severe infection. 

Neither the spores nor the neurotoxins are able to penetrate intact skin. 

About 110 cases of U.S. botulism poisoning are reported to the CDC annually. 

Confirmation of botulism poisoning 

is done by either detection of botulinum toxin or by isolation of Clostridium 

botulinum in a clinical specimen and the 

patient also displays clinical symptoms 

of botulism poisoning. The specimen 

could be a person’s stool sample in the 

case of infant or food borne botulism or 

Table 2. CDC Emergency Preparedness and Response for Abrin7

Exposure 

Inhalation 

Skin 

Eyes 

Ingestion 

Pressure demand, self-contained breathing 

apparatus (SCBA) (SCBA CBRN, if 

available) is recommended in response to 

non-routine emergency situations. 

Breath Response (pressure demand) 

HEPA PAPR. 

Remove contaminated clothes. 

Rinse skin with plenty of water 

or shower (and soap if 

available). 

Seek medical attention immediately. 

Rinse mouth. Do not induce 

vomiting. Use slurry of 

activated charcoal. In the 

event of vomiting, lean patient 

forward or place on le side 

(head-down position, if 

possible) to maintain open 

airway and prevent aspiration. 

Early and aggressive IV uid 

and electrolyte replacement. 

Seek medical attention 

immediately. 

Immediately ush with large 

amounts of tepid water for at 

least 15 minutes. 

Seek medical attention 

immediately. 

Irritation (see ingestion 

for other symptoms) 

Potential for allergic skin 

reaction; redness, blisters, 

pain. 

May be absorbed 

Tearing, swelling of the 

eyelids, pain, redness, 

corneal injury. 

Cardiovascular (heart and 

blood circulation) shock 

from severe dehydration, 

life-threatening low blood 

pressure, fast heart rate 

(tachycardia) and irregular heart rhythms 

(arrhythmias). 

Central Nervous System 

(brain) - drowsiness, 

disorientation, hallucinations, seizures, coma. 

Gastrointestinal (stomach 

and intestines) - burning 

pain in the mouth, 

abdominal pain, nausea, 

vomiting, diarrhea, 

bleeding and swelling of 

the lining of the GI tract, 

liver cell damage and 

death. 

Genitourinary (kidneys 

and urine) - blood in 

urine, low or no urinary 

output, kidney cell 

damage and death. 

Musculoskeletal - muscle 

weakness, tremors, and 

muscle spasm (tetany)

Eyes - dilated pupils and 

bleeding in the back of the 

eye (retinal hemorrhage) 

Skin - blue skin (cyanosis) 

and redness (ushing) 

Symptoms delayed 1-3 

days. 

May be fatal.

Tychem® BR or Responder® CSM 

protective clothing. Eyes should be 

protected when possible. 

Goggles with respiratory protection or full 

face-piece respirator. 

Do not eat, drink, or smoke during work. 

Wash hands before eating

Symptoms Personal Protective Equipment First Responder Response 

Fresh air, rest, half-upright 

position. Perform CPR if 

necessary. Seek medical attention 

immediately. 
33 ISSUE 9 Combating WMD Journal

Toxin 

Botulinum toxin A 0.0012 

0.0012 

0.0011 

0.0012 

0.0004 

0.0011 

0.0025

LD50 (μg/kg) 

Botulinum toxin B

Botulinum toxin C1

Botulinum toxin C2

Botulinum toxin D

Botulinum toxin E

Botulinum toxin F

a serum sample, or a food sample. The 

standard test for botulinum toxin testing is the mouse neutralization test. A 

more sensitive test8 published in 2006 

is an amplified enzyme-linked immunosorbent assay (ELISA) test applicable for botulinum neurotoxin in foods. 

Antitoxin therapy is available and is 

administrated to adult patients with food 

borne or wound or inhalation botulism. 

The antitoxin must be administrated early. It is not administrated to infants. The 

CDC must release and approve its use. 

The antitoxin is a horse serum product 

and may cause serum sickness in approximately 20% of treated persons. 

A human-derived antitoxin product for 

infants is or has been under evaluation9 in California. Also, the decision 

to administer the antitoxin often can’t 

wait for confirmation by testing for the 

toxin or bacteria, and must be made 

on the basis of display of symptoms 

especially if a suspect food is identified or there is evidence of a wound 

which may have been contaminated. 

The patient’s serum should be collected 

before administration of the antitoxin. 

The specific antitoxins availa b l e f r o m t h e C D C a r e 

• Licensed Bivalent Anti-AB 

equine antitoxin, Aventis-Pasteur

• IND Univalent Anti-E equine 

antitoxin, Aventis-Pasteur

• IND Heptavalent despeciated 

(Fab’2) equine Anti-ABCDEFG antitoxin, U.S. Army California Dept. 

of Health Services, Infant Botulism 

Treatment and Prevention Program

• Licensed Anti-AB human antitoxin for infant botulism “Baby-BIG”

The classic symptoms of botulism poisoning include double vision, blurred 

vision, drooping eyelids, slurred speech, 

difficulty swallowing, dry mouth, and 

muscle weakness. Infants appear lethargic, feed poorly, are constipated, have a 

weak cry, and have a poor muscle tone. 

If untreated, these symptoms may progress to cause paralysis of the arms, legs, 

trunk, and respiratory muscles. (according to the CDC website). Because of 

respiratory failure, the patient may need 

to be on a breathing machine (ventilator) 

for weeks. If severe, the person may 

require intensive medical and nursing 

care for months. The person affected 

by botulism poisoning is not infectious. 

Several countries are reported10 to 

have produced botulinum neurotoxins as weapons. The United States 

once produced botulinum neurotoxin 

under military code name X. The entire stockpile of botulinum neurotoxin 

was ordered destroyed by President 

Nixon (1969) along with other biological agents. The former Soviet Union 

continued their biological weapons research program. In April 1992, President 

Boris Yeltsin declared that his country 

had continued a massive offensive biological warfare buildup which included 

botulinum warfare buildup. In 1995, 

Iraq admitted to the United Nations Special Commission inspection team that it 

had produced 19,000 liters of botulinum 

neurotoxin concentrate for use in specially designed missiles and sprayers, 

including approximately 10,000 liters 

loaded in military weapons. In 1990, 

Iraq deployed 13 missiles with a 600 

km range containing botulinum toxin. 

Fortunately, botulinum neurotoxins 

are unstable in the environment. Therefore the range of an aerosol attack out 

in the open is limited. The neurotoxin 

would be expected to degrade in the 

environment within one or two days. 

Contaminated surfaces can be cleaned 

with a 0.1% chlorine bleach solution.

Clostridium perfrigens epsilon toxin 

Clostridium perfrigens is the name of 

the microorganism and epsilon toxin is 

one of several biotoxins that it produces. 

Gas gangrene results from wound contamination by this microorganism, which 

grows in the wound and produces biotoxins. In addition, Clostridium perfringens can cause food poisoning. Clinical 

symptoms resulting from food poisoning include intense abdominal cramps 

and diarrhea which begins between 8 

to 24 hours after eating food containing these bacteria. The toxins are a 

particular problem with farm animals, in 

particular, goats, sheep, young caves, 

and pigs. Theoretically, a person could 

also become poisoned by inhalation of 

dust containing the microorganism or 

its toxin. The toxins can be transmitted in contaminated food, water, or as 

an aerosol. Specific information on human poisoning by the epsilon toxin is 

minimal, but farm animals are affected. 

There are 5 different strains of Clostridium perfringens (labeled Types A, 

B, C, D, and E) and perhaps at least 20 

toxins (labeled alpha, beta, beta2, etc, 

epsilon, iota, etc.; some sources cite 12 

toxins). The toxins vary in toxicity and 

in their effect on animals and people. 

The epsilon toxin (which is produced 

by strains B and D) is singled out as 

being the most toxic, based primarily 

on intervenous injection of the toxin to 

test animals. The LD50 value (lethal 

dose resulting in death of 50% of the 

test animals) for the epsilon toxin using a mouse as the test animal is 0.78 

nanograms (0.1 μg/kg of body weight), 

(ref: Iowa State University, Center for 

Food Security and Public Health website). Goats and lambs injected with the 

epsilon toxin develop severe pulmonary 

edema (fluid in their lungs) and show 

neurological symptoms. Rats injected 

(intraperitionally) develop cerebral edema. Onset of neurological symptoms by 

intervenous injection may occur anywhere from 2 minutes to one hour in test 

calves to 0.5 hours to 3 hours for goats 

and lambs. The epsilon toxin works by 

causing potassium and fluid leakage 

from body cells. Neurological symptoms 

include stupor (mild poisoning) to coma 

and death (more severe poisoning). 

About one-third of the incidences 

of food poisoning in the United States 

is caused by Clostridium perfringens, 

mostly from the type A strain producTable 3. LD50 values for Botulinum 

Toxins11
Combating WMD Journal ISSUE 9 34

Toxin 

Clostridium perfringens epsilon toxin 0.1 

0.4 

3 

5 

13 to 16 

81 

1500

LD50 (μg/kg) 

Clostridium perfringens beta toxin 

Clostridium perfringens lechithinase toxin 

Clostridium perfringens delta toxin 

Clostridium perfringens perfringolysis O 

Clostridium perfringens enterotoxin 

Clostridium perfringens kappa toxin 

Table 4. LD50 Values for Clostridium perfringens Toxins11 

Figure 3. Photos of Clostridium botulinum bacteria

tives. When cooking meat, it is also 

important to cool the meat product down 

quickly and refrigerate if consumed 

at a later time. More details are in a 

paper published by the University of 

Wisconsin, Food Research Institute12.

Toxin identification in humans and animals can be done using the mouse neutralization test (MNT) or enzyme-linked 

immunosorbent assay test (ELISA) 

on clinical samples (e.g. feces, intestinal fluids). Another test is the polymerase chain reaction assay test (PCR). 

Clostridium perfringens gram Tissue smear showing Clostridium perfringens

positive bacterial stain, anaerobic, rod-shaped 

ing the alpha toxin, or enterotoxin. A 

more serious form is the type C strain 

producing the beta2 toxin. Other strains 

besides type A produce the alpha toxin. Symptoms (from the alpha toxin) of 

food poisoning include diarrhea, nausea, severe abdominal cramps, and 

bloating but rarely vomiting or fever. 

The symptoms appear 8 to 24 hours 

after ingestion of contaminated food. 

Patients generally recover within a day 

or two, although the elderly can take 

longer. Deaths are rare. However, the 

type C strain producing the beta2 toxin 

can cause sloughing of the mucosa off 

the intestines and intestinal perforation, 

and severe infection, often resulting in 

death. Symptoms include a bloody stool 

and probably vomiting and fever in addition to type A symptoms. Intervention 

including removal of part of the intestine 

with prolonged antibiotic treatment and 

intravenous fluid replacement may be 

necessary. This type of food poisoning 

may be called “necrotizing enteritis” or 

“pig-bel disease”. The beta2 toxin is 

usually associated with enteritis in pigs, 

therefore the name “pig-bel disease.” 

Information on human food poisoning 

from the epsilon toxin is sketchy and is 

complicated by proper identification of 

the strain and maybe more than one toxin can be produced. Fluid replacement 

including electrolyte monitoring is part of 

treatment as potassium loss is a feature 

of epsilon toxin poisoning. Limited information available on the Internet seems 

to suggest that the symptoms are similar to that produced by the alpha toxin. 

The purified alpha toxin can be lethal by inhalation as an aerosol, 

causing acute pulmonary disease, 

vascular leak, hemolysis, thrombocytopenia, and liver damage. 

The toxins including the epsilon toxin 

can be destroyed by heat. Thorough 

cooking of food is required. The vegetative form of the bacteria can be 

destroyed at 70oC (158oF), but much 

higher temperatures and prolonged 

heating is required to kill the spores. 

The high temperatures required to kill 

all of the spores also compromise the 

nutritional value of the product, and 

sometimes food processors use a combination of gamma irradiation treatment 

and heat, or add salt or other preservaAn Internet search failed to turn up 

evidence that Clostridium perfringens 

epsilon toxin has been weaponized. 

The South African biological weapons 

program between 1981 and 1984 developed the bacteria as a potentially lethal 

agent to resemble food poisoning. In 

1991, Iraq representatives informed the 

United Nations Special Commission inspection team that Iraq had researched 

the offensive use of Clostridium perfringens as a potentially lethal agent, and 

had produced 90 gallons of the bacteria. 
35 ISSUE 9 Combating WMD Journal

Presumably the toxin can be manufactured by fermentation of Clostridium 

perfringens or more likely by another 

microorganism expressing the cloned 

gene for the toxin. The microorganism. E. coli has already been cloned to 

produce the epsilon toxin for the production of a vaccine for inoculation of farm 

animals. The purified toxin or even the 

crude material could be released as an 

aerosol. A person inhaling the material would be expected to suffer severe 

pulmonary edema (fluid buildup in the 

lungs) in addition to vascular leak, organ 

damage, and neurological problems including cerebral edema, as the result of 

potassium leakage from body cells. The 

alpha toxin is also a potentially lethal 

agent when dispersed as an aerosol. 

BIOGRAPHY

Dr. Nordin received his PhD degree in 

biochemical engineering from the University of Minnesota and has worked 

with several engineering firms and 

with the not-for-profit Western Research Institute on environmental and 

public safety problems. He is currently 

a co-owner of AristaTek Inc 

ENDNOTES

1. Globalsecurity.org, http://www.

globalsecurity.org/wmd/intro/bio_saxitoxin.htm.

2. Tanino, H, T. Nakata, T. Kanrko, 

and Y. Kisshi. “A stereospecific total 

synthesis of dl-saxitoxin”. Journal 

American Chemical Society. 99(8) pp 

2818-2819. (1977).

3. Jacobi, P.A.; M.J. Martinelli, and 

S. Polanc. “Total synthesis of (.+-.)-saxitoxin”. Journal American Chemical Society 106(19) pp. 5594-5598 (1984)

4. Felming, J.J.; J. Du Bois. Journal American Chemical Society 128(12) 

pp3926-3927 (2006)

5. Baird, John. “Total Synthesis of 

Saxitoxin” . 

 http://www.scs.illinois.edu/

denmark/presentations/2006/gm-2006-

04n11.pdf.

6. Sahni, V.; SK Agarwai, NP 

Singh, and S. Sikdar. “Acute demyelinating encephalitis after jequirity pea 

ingestion (Abrus precatorius). Clin. 

Toxicol. (Phila), 45(10: 77-9. See 

 http://www.ncbi.nlm.nih.gov/

pubmed/17357388.

7. U.S. Department of Health and 

Human Services – Centers for Disease 

Control (CDC) Website (http://www.

bt.cdc.gov/agent/abrin/erc1393-62-0.

asp)

8. S.K. Sherma, J. L Ferreira, B.S. 

Eblen, and R.C. Whiting, “Detection of 

Type A, B, E, and F Clostridium botulism Neurotoxins in Foods by Using an 

Amplified Enzyme-linked Immunosorbent Assay with Digoxigenin-Labeled 

Antibodies”, Applied and Environmental 

Microbiology, 72(2), Feb. 2006, p. 1231-

1238.

9. World Health Organization Poisons Information Monograph 858, Clostridium botulinum. See

http://www.who.int/csr/delibepidemics/

clostridiumbotulism.pdf.

10. “The Comprensive Sourcebook 

of Bacterial Protein Toxins” (book), edited by J.E. Alouf and M.R. Popoff, 3rd 

edition, Academic Press, 2006.

11. Univ. of Florida, citing D.M. 

Gill, Microbiological Reviews 46: 86-94. 

(1982) and other sources. See http://

www.ehs.ufl.edu/programs/bio/toxins/.

12. Food Research Institute, “Survival and Growth of Clostridium perfringens during the Cooling Step of Thermal 

Processing of Meat Products”. (2002). 

University of Wisconsin. See 

http://www.wisc.edu/fri/briefs/cperfsurvivgrow.pdf.

Most of the information presented on 

shellfish poisoning came from (1) a paper prepared by Charles Baier, University of Idaho, December 2000, “Red Tide 

and Shellfish Poisoning: Toxic Products 

of Marine Algae” which is available at 

http://www.agls.uidaho.edu/etox/resources/case_studies/REDTIDE2.PDF 

and (2) from the United States National Library of Medicine TOXNET at 

http://toxnet.nlm.nih.gov/

c g i - b i n / s i s / h t m l g e n ? H S D B . 

Additional information on biotoxins may be found at the website, 

http://www.globalsecurity.org under Weapons of Mass Destruction.
Regulating CBRN Survivability

Nicholas P. Haugen

U.S. Army Nuclear and CWMD Agency

rogram Managers (PMs) responsible for developing military systems 

work to implement requirements 

defined by Capabilities Development 

Documents (CDDs) and Capabilities Production Documents (CPDs). 

These documents are approved by the 

Joint Requirements Oversight Council 

(JROC), a four-star level panel established by law. The JROC, as its name 

makes clear, is a “joint.” It is chaired by 

the Vice Chairman of the Joint Chiefs of 

Staff and has representatives from each 

of the Services. If it finds a capability 

being developed by a Service to be of 

joint interest, it can assume responsibility for the CDDs and CPDs that define 

the system’s requirements. The JROC 

is also a military organization. Its members are military officers, and its work is 

managed by the Joint Staff. As the joint 

nature of the JROC prevents Services 

from working on redundant efforts or at 

cross purposes, the military nature of the 

JROC helps to ensure that systems are 

being developed to satisfy user needs.

 

One of the key ways that the JROC 

manages requirements is to define critical requirements as Key Performance 

Parameters (KPPs). If a PM cannot 

get his system to meet a KPP, then his 

program will fail unless the JROC reduces the KPP requirement. Below the 

level of a KPP is a Key Systems Attribute (KSA). According to Chairman 

of the Joint Chiefs of Staff guidance, 

“Attributes or characteristics considered essential to achieving a balanced 

solution/approach to a system, but 

not critical enough to be designated 

a KPP” should be designated KSAs.1 

A KPP is often a grouping of multiple 

KSAs. A KSA can also stand alone 

independent of an overarching KPP. 

There are six mandatory KPPs for all 

CDDs and CPDs. These are mandatory 

in the sense that the CDD or CPD writer 

must either include each one or justify its 

exclusion. They are Force Protection, 

Survivability, Sustainment, Net-Ready, 

Training, and Energy. This article argues that for relevant Army systems, 

CBRN survivability should be a mandatory KSA under the Survivability KPP.2 

What are you talking about?

The official DoD definition of CBRN 

survivability is “The capability of a system to avoid, withstand, or operate during and/or after exposure to a CBR environment (and relevant decontamination) 

or a nuclear environment, without losing 

the ability to accomplish the assigned 

mission.”3 Meanwhile, “The intent of 

the Survivability KPP includes reducing 

a system’s likelihood of being engaged 

by hostile fire...reducing system’s vulnerability if hit by hostile fire...and allowing the system to survive and continue 

to operate in a CBRN environment, if 

required.”4 Of note, survivability refers 

to a system’s ability to survive, not its 

ability to protect its occupants. In the 

case of the mandatory KPPs, a system’s 

ability to protects its occupants is addressed by the Force Protection KPP. 

In the world of CBRN environments, a 

large system will protect its occupants 

with a collective protection system 

or other passive defense measures. 

The logical link between the Survivability KPP and CBRN survivability is 

specifically authorized by DoD guidance. DODI 3150.09, the CBRN Survivability Policy, states “For CBRN 

mission-critical systems, the CBRN 

survivability performance attribute(s) 

will be evaluated to determine KPP or 

KS0 designation. They may be combined with the force protection, survivability, or net-ready KPP, if appropriate.”5

 

De-conflicting Current Regulation

The most important reason why the 

Army should implement a requirement 

for a mandatory KSA for CBRN survivability is that doing so would de-conflict 

and clarify existing regulatory requirements. There is currently a disconnect 

between DoD guidance, which tells 

a Program Manager (PM) he doesn’t 

need to make his system survivable, and 

Army guidance, which tells him he must.

Department of Defense acquisition 

guidance tells PMs that if something 

is not listed as part of a KPP, then that 

requirement is in the PM’s trade space. 

The exact language reads, “Performance requirements that do not support the achievement of KPP thresholds 

shall be limited and considered part of 

the engineering trade space during development.”6

 Most Army CDDs and 

CPDs list CBRN survivability requirements in the additional performance 

attributes section of a CDD or CPD. 

So an Army PM would reasonably 

conclude that he has the authority to 

trade away the CBRN survivability requirements defined in his CDD or CPD.

However, Army regulation tells him otherwise. Army Regulation 70-75, Survivability of Army Personnel and Materiel, states:

“If an item is designated as mission 

critical/mission essential or is a critical component of one or more mission 

critical end items, it will be nuclear and 

[Chemical Biological, and Radiological 

(CBR)] contamination survivable. If this 

critical item or component is electronic 

equipment, at a minimum, it will be survivable to high-altitude electromagnetic 

pulse (HEMP). If this critical item is a 

weapon system...it will also survive the 

initial nuclear weapons effects of blast, 

thermal radiation, initial nuclear radiation, and source region electromagnetic 

pulse (REMP)....waiver processes exp

Combating WMD Journal ISSUE 9 36
37 ISSUE 9 Combating WMD Journal

ist for nuclear survivability criteria and 

(CBR) contamination criteria...This waiver process does not change the need 

to meet the survivability requirement.”7

One might argue that requirements 

like this exist elsewhere in regulation 

and that does not automatically elevate 

the requirement to a KSA. However, 

the fact that the regulation establishes 

a waiver process for systems that need 

relief, and that even that waiver process 

only allows for alternative methods of 

achieving CBRN survivability, makes 

clear that the intent of the Army is to 

have this requirement met in all cases.

One might also argue that, while 

AR 70-75 creates a unique threshold 

somewhere above additional performance attribute, it is not appropriate 

to raise it to a KSA. Joint guidance 

tells the developer that he should not 

make an attribute a KSA unless he is 

“willing to consider restructuring the

program if the attribute is not met?”8

In other words, because a system fails 

to meet its CBRN survivability requirements does not necessarily mean that 

the Army should end the program.

This argument is based on a shortsighted understanding of the world’s 

threats. If one compares a list of states 

with nuclear weapon development 

programs, or of states that have not 

signed the Chemical Weapons Convention, one is likely to see a list of potential adversaries. Indeed, some of 

these states are potential adversaries 

precisely because of their possession 

or development of weapons of mass 

destruction. If we create a situation 

where our weapons systems cannot 

survive in a CBRN environment, we are 

presenting an easily exploitable vulnerability to our most likely adversaries. 

Enforcement Mechanisms

Currently, if an Army system fails 

to meet a Key Systems Attribute, the 

first place the program will go is the 

Army Requirements Oversight Council 

(AROC). This is the General Officerlevel body that manages Army requirements. Documents and requirements 

validated by the AROC are passed to 

the JROC. The responsibilities of the 

AROC include making resource decisions based on military need and risk 

and program affordability. Its principal 

members include the Vice Chief of Staff 

of the Army, the Deputy Chief of Staff 

(DCS)/G-3/5/7, the DCS G-1, the DCS 

G-2, the DCS G-4, the CIO/G-6, the 

DCS G-8, the principal military deputy to 

the ASA(ALT), and a representative from 

U.S. Army Training and Doctrine command (TRADOC).9

 If a future system 

were to fail to meet its CBRN survivability KSA, this is the body that would 

approve a reduction in its requirements.

Now consider the Nuclear and Chemical Survivability Committee (NCSC). 

This is the body that currently approves 

waivers of CBRN survivability criteria. 

In doing so, it considers military need 

and risk and program affordability. Its 

membership includes representatives 

of the ASA(ALT) the DCS G-2, DCS 

G-3, the DCS G-4, the DCS G-8, Army 

Materiel Command, TRADOC, Army 

Test and Evaluation Command, and 

U.S. Army Research, Development, 

and Engineering Command.10 Making CBRN survivability a mandatory 

KSA for appropriate systems would 

transfer the responsibility for reducing 

requirements from the NCSC to the 

AROC. With the redundancy of membership and responsibility, this would 

be a rational consolidation of functions.

Some might argue that the AROC 

should not be burdened with evaluating requests in this specialized area. 

They might be surprised to learn that 

the AROC has already done so. In 2011 

the AROC met and considered the reduction of CBRN survivability requirements as part of a scope reduction of 

M109 Family of Vehicles requirements 

reduction. CRBN survivability was 

considered alongside KPP and KSA requirements on the grounds that Army 

regulation took it out of the PM’s trade 

space. The AROC, meeting at the GO 

level, decided to reduce nuclear survivability requirements from a threshold to an objective requirement, and to 

retain HEMP and CBR contamination 

survivability requirements as threshold. 

While this was a disappointing outcome 

from the perspective of an advocate 

for nuclear survivability, it was a decision made along the lines one would 

expect of a serious decision: senior

leaders representing all relevant 

perspectives within the Army, taking into account relevant information on cost, military risk, and impacts on the development timelines.

 

What Systems Are Relevant?

Whether or not a mandatory KSA for 

CBRN survivability is an appropriate policy response depends to a great deal on 

which systems it is applied to. According to the AR 70-75 quotation above, 

current CBRN survivability policy is to be 

applied to all “mission critical systems.” 

This term is defined broadly in both DoD 

and Army policy. Indeed, its definition 

is so loose that it can be applied almost 

arbitrarily. Naturally, this is not a good 

situation. For one thing, it allows different combat developers to come to different conclusions about what systems are 

Mission Critical, even within the same 

Center of Excellence. For another, It 

turns the question of “is my system mission critical” into “do I want my system to 

have CBRN survivability requirements.” 

A wiser policy should attach more 

specific guidance to whether or not a 

system requires CBRN survivability 

requirements. It should also account 

for the fact that HEMP, other nuclear 

weapons effects such as blast, and 

CBR contamination are three distinct 

threats. The only distinctions made in 

the current policy is that mission critical systems with electronics should be 

HEMP survivable (in addition to being CBR contamination survivable), 

and a mission critical system that is a 

weapon should also be survivable to 

nuclear weapons effects besides HEMP.

Taking each CBRN environment in 

turn, one can make much more specific determinations about what systems 

need to be survivable. In the case of 

CBR contamination, the threat that can 

create this is a state actor with chemical weapons. A terrorist or insurgent 

may acquire or produce enough agent 

to destroy the occasional platform, but 

would be just as able to do so with a 

conventional munition. To destroy an 

operationally significant number of vehicles through CBR contaminiation, an 

enemy would need to have a very large 

quantity of weapons and military forces 

equipped and trained to employ them on 

the battlefield. The case of Iraq before 
the first Gulf War is a good case. What 

sorts of formations are required to face 

enemies of this sort? Those designed 

for high intensity conflict. Besides vehicle of the Heavy Brigade Combat Team, 

we also need to make equipment that 

supports the operations of ports and 

airfields survivable, as these operational 

chokepoints would be natural targets 

for an enemy with chemical weapons.

In the case of nuclear weapons effects 

besides HEMP, these are generated by 

tactical nuclear weapons. Like chemical weapons, these are the weapons of 

the same states capable of fighting us 

in a high-intensity conflict. If a terrorist 

were to acquire a nuclear weapon, he 

would most likely have only one or a 

very few, and would not want to “waste” 

it on a deployed U.S. Army formation. 

Why take out ten tanks when you can 

kill tens of thousands of people? In the 

case of these weapons, we can also 

choose to skip the hardening of equipment that supports the operations of 

ports and airfields. If a nuclear weapons 

were to hit a port or airfield, the port or 

airfield itself is likely to be unusable.

Finally, in the case of HEMP, the 

requirement must be applied broadly. 

HEMP is an attractive option for an 

adversary, and a HEMP can impact a 

broad geographic area. HEMP is an 

attractive option because, unlike making a significant impact with tactical 

nuclear weapons, which requires many 

weapons, generating a HEMP requires 

only one weapon plus a ballistic missile capability. Generally speaking, the 

larger the weapon, all other factors being equal, and the higher up it can be 

detonated, the broader the area that can 

be impacted. Within that area, systems 

with electronics that are powered on 

are susceptible to upset and destruction. Also, due to its wide ranging impact, one must assume that resupply 

and repair systems will not be up and 

running for a significant period of time. 

To ensure that the proper equipment is 

made survivable to HEMP, the requirement should be applied to any piece of 

equipment, the instantaneous and permanent loss of which throughout a theater of war, would prevent an the Army 

from completing its mission within that 

theater. This would prevent systems 

like trucks from being developed without 

HEMP hardening as happens today.

Next Steps

The proper place to codify these requirements is Army Regulation 71-9, 

Warfighting Capabilities Determination. That document serves as the 

Army’s supplement to the JCIDS guidance provided by the Joint Staff, so 

any Army-unique requirements would 

best be captured there. It establishes 

the AROC and lays out its responsibilities and functions, so the proposal that 

the AROC consider KSAs for CBRN 

survivability would be codified in it.

In closing, it is worth noting that this 

proposal is not a radical departure from 

what the Army does today. The Army 

already takes CBRN survivability out of 

the PMs trade space, it just does so in a 

way that is confusing. The Army already 

calls together GO-level representatives 

to consider failures to meet CBRN survivability standards, it just does so in 

a body that is redundant to the AROC. 

The Army already imposes this requirement on “mission critical systems,” but 

does not provide meaningful guidance 

about what mission critical means. This 

proposal to impose a mandatory KSA for 

CBRN survivability is a call to rationalize the way the Army does business

BIOGRAPHY

Mr. Haugen is the CBRN Survivability Manager at USANCA. Previously, 

he worked for DTRA, SAIC, Inc., and 

Pacific Northwest National Laboratory, and served on active duty in the 

U.S. Army. He is a graduate of the 

U.S. Military Academy, Georgetown 

University, and the U.S. Naval War 

College. He is currently enrolled as 

a master’s candidate with University 

of Maryland University College, where 

he is studying Cybersecurity Policy.

ENDNOTES

1. Joint Capabilities Integration 

and Development System Manual, 19 January 2012, p. B-A-1.

2. JCIDS Manual, B-A-2.

3. Department of Defense Instruction 3150.09, the CBRN Survivability Policy, 17 August 2009, p. 23.

4. JCIDS Manual, B-A-2.

5. Department of Defense Instruction 3150.09, the CBRN Survivability Policy, 17 August 2009, p. 16.

6. Department of Defense Instruction 5000.2, 2 December 2008, p. 20.

7. Army Regulation 70-75, Survivability of Army Personnel and Materiel, 

2 May 2005, p. 2. Emphasis added.

8. JCIDS Manual, B-A-4.

9. Army Regulation 71-9, Warfighting Capabilities Determination, 28 December 2009, pp 14-15.

10. AR 70-75, pp. 2-4.

Combating WMD Journal ISSUE 9 38
Highlighted Courses available at the 

Defense Nuclear Weapons School (DNWS)

 and 

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Theater Nuclear Operations Course (TNOC)

TNOC is the only course offered by a Department of 

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support staff, targeteers, and staff nuclear planners for joint 

operations and targeting. The course provides overview of 

nuclear weapon design, capabilities and effects to include 

U.S. nuclear policy, and joint nuclear doctrine. TNOC meets 

U.S. Army qualification requirements for the additional skill 

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Next class availability:

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or call the Registrar at 505 846-5666 DSN 246-5666.

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Correction:

2010 CWMD Journal article by Dr. Timothy Joseph, 

The Mission that Drove World History - The Manhattan 

Project, was incorrectly labeled as a nuclear detonation 

occurring over Hiroshima vice Nagasaki.”

Combating WMD Resource Page

39 ISSUE 9 Combating WMD Journal
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