85Operations Security, Site Security, and Terrorism In.docx

85
Operations Security, Site Security,
and Terrorism Incident Response
Paul M. Maniscalco
Hank T. Christen
• Discuss the definitions of operations security (OPSEC) and
site security.
• Describe the difference between OPSEC and site security.
• List the five critical component steps of OPSEC.
• Discuss and describe the intelligence cycle.
• Recognize how OPSEC integrates with the incident command
system.
• Discuss the challenges of implementing and sustaining site
security.
• Describe the integration of OPSEC and site security for
terrorism incident response.
• Recognize the importance of evidence preservation and the
role of responders in protecting evidence
for law enforcement agencies.
Objectives
7

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86 Homeland Security: Principles and Practice of Terrorism
Response
Introduction

When preparing organizations and individuals for re-
sponse to a high-impact/high-yield emergency incident,
some of the most often overlooked requirements are
OPSEC and site security.
Bound inextricably with coordination and integra-
tion strategies for response, OPSEC and site security are
often compromised in the heat of the battle. Responders,
with nothing but the best of intentions, converge on
the scene of an incident implementing strategies that,
pre-event, have failed to address these most important
aspects of the incident response and management strat-
egy. The discipline to apply the principles of OPSEC
and site security following a preestablished, organized,
and well-practiced plan is crucial given the nature of
the threat and the variety of conditions that may pre-
sent themselves. Failing to address these critical security
tenets prior to an event amounts to failing to protect the
protectors.
OPSEC
Terrorist attacks present the contemporary emergency
response manager or chief officer with more complex
challenges and greater probable risks. Site security and
OPSEC are multifaceted concepts, bringing together ele-
ments ranging from pre-event protection of information
concerning an organization’s activities, intentions, or
capabilities to operational issues such as scene access,
traffic control, and evidence protection. Due to the fact
that this involves so many different aspects of disaster
response, and because it cannot be completely achieved
without full integration of each of those aspects, site
security is best understood broadly. Robust control of
the incident and proximal areas should be the desired
goal. This includes maintaining command and control

over the human and material flow into, out of, and
around the site, providing for the security and safety
of responding personnel, providing these responders
with the ability to perform their jobs, ensuring per-
sonal accountability and the fulfillment of performance
requirements.
For an OPSEC program to be effective, personnel
must be aware of OPSEC concerns, implement OPSEC
countermeasures when appropriate, and be observant
of potential collection activities directed at their orga-
nization. This is possible only if the members of the
organization understand the range of threats affect-
ing their organization and actively support the OPSEC
program.
OPSEC Purpose
OPSEC as a formalized strategic concept was developed in
1988 under the provisions of National Security Decision
Directive 298, The National Operations Security Program.
OPSEC is a tool designed to promote operational effec-
tiveness by denying adversaries publicly available indica-
tors of sensitive activities, capabilities, or intentions. The
goal of OPSEC is to control information and observable
actions about an organization’s capabilities, limitations,
and intentions to prevent or control the exploitation of
available information by an adversary. The OPSEC pro-
cess involves five steps, which are discussed in greater
depth later in this section. These steps are:
1. Identification of critical information
2. Analysis of threats
3. Analysis of vulnerabilities
4. Assessment of risks
5. Application of appropriate countermeasures

The overarching OPSEC framework comences with
an assessment of the entire organization/activity in order
to determine and identify what exploiable but unclas-
sified evidence or classified or sensitive activities could
be acquired by an adversary through known collection
capabilities—human or technological.
Indication of sensitive activities is often the conse-
quence of publicly available information that can be found
via a variety of sources including agency Web sites, press
briefings, open house events, scheduled exercises, and de-
liberate probing of the 911 system by false alarm responses
or monitoring daily response actions. This information
can then be pieced together to develop critical informa-
tion and understanding of agency response tactics, tech-
niques, and procedures. Sensitive activities indicators can
originate routine administrative, logistics, or operational
activities, and if identified, these observations are analyzed
via known collection capabilities of an adversary to be
employed to exploit vulnerabilities and place responders
at risk. An agency chief officer, manager, or safety officer
uses this disciplined threat and vulnerability assessment
process to determine the current OPSEC state of affairs and
guide the agency through the selection and adoption of
countermeasures to diminish or eliminate the threat.
OPSEC Process
OPSEC considerations must be integral to the process of
planning for and integrated with all response doctrine
and standard operating procedures (SOP) irrespective
of whether they are sensitive operations or not. Similar
to the adaptation and adoption of safety principles and
engineering controls to keep responders safe, OPSEC
tenets should be an integral component of that strategic
process.

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CHAPTER 7: Operations Security, Site Security, and Terrorism
Incident Response 87
Early implementation of OPSEC in the agency
response planning process encourages and sustains a
heightened awareness by all personnel for maintaining

a protective posture for agency-critical information and
capabilities. In order to be effective in this arena, the
OPSEC planning process requires an unambiguous com-
prehension of the specific activity’s mission and agency
organizational and operational plans and doctrine. An ef-
fective OPSEC program should be seamlessly integrated
into an agency’s culture and reinforced by policy, SOPs,
and utility in all operational aspects.
The OPSEC planning process must identify and in-
corporate strategic/tactical countermeasures, where ap-
propriate and feasible, that are necessary to complement
physical, information, personnel, signals, computer, and
communications security measures. The synergy of the
OPSEC system provides an agency with total integra-
tion of security countermeasures to blunt vulnerabilities
and enhance safety of the responders. An agency might
implement OPSEC countermeasures including but not
limited to amendment of existing standard operating
administrative procedures; application of cover, con-
cealment, and deception techniques; and other OPSEC
measures that can degrade an adversary’s capability to
exploit vulnerabilities. Developing a sustainable and
cost-effective security countermeasures program that is
tailored to meet the identified threat is one of the central
benefits of an agency OPSEC program.
Even though the OPSEC system paradigm is often
described as a five-step process, the delineated steps were
never intended to be interpreted/implemented as an incre-
mental or sequential execution. The program strengths of
the OPSEC process are that it is structured to be dynamic
and flexible to facilitate an adaptive progression that meets
the specific and unique needs of an organization and the
operational environment of its jurisdiction. The global
strength of the OPSEC process is acknowledged in the

final report of the Joint Security Commission where the
commission identifies the tenets of OPSEC as the U.S.
government’s fundamental basis for risk management.
The five steps of the OPSEC process involve the
following:
1. Identification of critical information—Critical
information is factual data about an organiza-
tion’s intentions, capabilities, and activities that
the adversary needs to plan and act effectively
to degrade operational effectiveness or place the
potential for organizational success at risk. The
OPSEC process identifies critical information and
determines when that information may cease to
be critical in the life cycle of an operation, pro-
gram, or activity.
2. Analysis of threats—Threat analysis consists of
determining the adversary’s ability to collect, pro-
cess, analyze, and use information. The objective
of threat analysis is to know as much as possible
about each adversary and its ability to target the
organization. It is especially important to tailor
the adversary threat to the actual activity and, to
the extent possible, determine what the adver-
sary’s capabilities are with regard to the specific
operations of the activity or program.
3. Analysis of vulnerabilities—Vulnerability anal-
ysis requires that the OPSEC analyst adopt an
adversarial view of the activity requiring protec-
tion. The analyst attempts to identify weaknesses
or susceptibilities that are exploited by the ad-
versary’s collection capabilities. The vulnerabil-
ity analysis process must identify the range of

activities that can be observed by the adversary,
the type of information that can be collected, and
the specific organizational weaknesses that the
adversary can exploit. Based on this knowledge,
the OPSEC analyst determines what critical in-
formation the adversary can derive based on the
known threat and assessed vulnerabilities.
4. Assessment of risks—Risk assessment is the
heart of the OPSEC process. In a risk assessment,
threats and vulnerabilities are compared to deter-
mine the potential risk posed by adversary intel-
ligence collection activities targeting an activity,
program, or organization. When the level of vul-
nerability is assessed to be high and the adversary
threat is evident, then adversary exploitation is
expected, and risks are assessed to be high. When
the vulnerability is slight, and the adversary’s col-
lection ability is rated to be moderate or low,
the risk may be determined to be low, and no
protective measures are required. Based on the
assessed level of risk, cost/benefit measures can
be used to compare potential countermeasures
in terms of their effectiveness and cost.
5. Application of appropriate countermeasures—
In the final step, countermeasures are developed
to protect the activity. Ideally, the chosen coun-
termeasures eliminate the adversary threat, the
vulnerabilities that can be exploited by the adver-
sary, or the utility of the information. In assessing
countermeasures, the impact of the loss of critical
information on organizational effectiveness must
be balanced against the cost of implementing
corrective measures. Possible countermeasures
should include alternatives that may vary in terms

of feasibility, cost, and effectiveness. Based on the
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probability of collection, the cost effectiveness of

various alternatives and the criticality of the activ-
ity countermeasures are selected by the program
manager. In some cases, there may be no effective
means to protect information because of cost or
other factors that make countermeasure imple-
mentation impossible. In such cases, the manager
must decide to accept the degradation of effective-
ness or cancel the activity.
As described, threat analysis is the critical founda-
tion of the OPSEC process. Fundamentally, the assessed
threat level determines the extent of the agency’s vulner-
ability and risk. These findings provide agency leadership
with the requisite information to make informed deci-
sions relative to mitigating vulnerabilities as well as how
to select the most effective countermeasure strategies to
achieve the same. Subsequently, it is critical that threat
assessment findings truthfully reflect the entirety of the
intelligence collection effort that targets the agency.
The Intelligence Cycle
Intelligence is the product resulting from the collection,
collation, evaluation, analysis, integration, and interpre-
tation of collected information. The intelligence cycle
represents an investigation protocol by which informa-
tion is acquired, produced, analyzed, and then made
available to parties who have a direct need to know or
have access based upon specific and definitive agency
responsibility (such as the OPSEC officer or fusion center
liaison) or operational involvement in a specific matter
directly related to this intelligence product. This cycle
(FIGURE 7-1) is based upon five distinct functions that gov-
ern a critical component of this disciplined process. The
five functions are:

1. Planning and direction
2. Collection
3. Processing
4. Production
5. Dissemination
Each segment of the intelligence cycle has a spe-
cifically crafted function that provides valuable contri-
butions to the end product of the entire process. The
functions are described as follows:
1. Planning and direction—This step involves
the management of the entire intelligence effort,
from the identification of a need for data to the
final delivery of the intelligence product to the
consumer. The process consists of identifying,
prioritizing, and validating intelligence require-
ments; translating requirements into observables;
preparing collection plans; issuing requests for
information collection, production, and dissemi-
nation; and continuously monitoring the avail-
ability of collected data. In this step, specific
collection capabilities are tasked based on the
type of information required, the susceptibility of
the targeted activity to various types of collection
activity, and the availability of collection assets.
2. Collection—This step includes both acquiring
information and provisioning that information
to processing and production elements. The col-
lection process encompasses the management of
various activities, including developing collection
guidelines that ensure optimal use of available
intelligence resources. Intelligence collection re-
quirements are developed to meet the needs of

potential consumers. Based upon identified intel-
ligence, requirements collection activities are given
specific tasks to collect information. These tasks
are generally redundant and may use a number
of different intelligence disciplines for collec-
tion activities. Task redundancy compensates for
the potential loss or failure of a collection asset.
It ensures that the failure of a collection asset is
compensated for by duplicate or different assets
capable of answering the collection need. The use
of different types of collection systems contributes
to redundancy. It also allows the collection of dif-
ferent types of information that can be used to con-
firm or disprove potential assessments. Collection
operations depend on secure, rapid, redundant,
and reliable communications to allow for data
exchange and to provide opportunities for cross-
cueing of assets and tip-off exchanges between as-
sets. Once collected, information is correlated and
forwarded for processing and production.
3. Processing—This step involves the conversion
of collected information into a form suitable for FIGURE 7-1
Intelligence cycle.
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INTELLIGENCE CYCLE
Collection
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the production of intelligence. In this process,
incoming information is converted into formats
that can be readily used by intelligence analysts
in producing intelligence. Processing includes
such activities as translation and reduction of
intercepted messages into written format to per-
mit detailed analysis and comparison with other
information. Other types of processing include

video production, photographic processing, and
correlation of information collected by technical
intelligence platforms.
4. Production—This step is the process of analyz-
ing, evaluating, interpreting, and integrating raw
data and information into finished intelligence
products for known or anticipated purposes and
applications. The product may be developed from
a single source or from collection and databases.
To be effective, intelligence production must fo-
cus on the consumer’s needs. It should be ob-
jective, timely, and most importantly accurate.
As part of the production process, the analyst
must eliminate information that is redundant,
erroneous, or inapplicable to the intelligence re-
quirement. As a result of the analytical effort, the
analyst may determine that additional collection
operations are required to fill in gaps left by previ-
ous collection or existing intelligence databases.
The final intelligence product must provide the
consumer with an understanding of the subject
area and draw analytical conclusions supported
by available data.
5. Dissemination—This step is the conveyance of
intelligence to the consumer in a usable form.
Intelligence can be provided to the consumer in
a wide range of formats including verbal reports,
written reports, imagery products, and intelli-
gence databases. Dissemination can be accom-
plished through physical exchanges of data and
through interconnected data and communica-
tions networks.
An agency OPSEC manager must be familiar with

the intelligence cycle for three essential reasons. First,
awareness allows the OPSEC manager to assume a role
in the required intelligence production to effectively
support the agency OPSEC initiative. OPSEC managers
must be acutely aware of the range of threats confronting
the agency to ensure they implement effective counter-
measures that deny adversaries access to data that pro-
vide critical information.
Next, comprehension of the intelligence cycle
and associated functions provides the agency OPSEC
manager with the critical insight and threat perspec-
tive to develop protective measures in order to thwart
adversary collection activities that could undermine re-
sponse effectiveness and responder safety. The OPSEC
manager’s knowledge of an adversary’s collection
methods and patterns allows the program manager to
develop effective countermeasures that hide or distort
indicators that could be used against the agency and
its personnel.
Lastly, knowledge of the adversary’s analytical bi-
ases is used to develop deception programs that deceive
the adversary by confirming erroneous perceptions. For
example, expectations that agency credentials are ex-
ploitable to the point of personnel counterfeiting IDs, be-
lieving that official vehicles can be stolen from vendors,
or that uniform articles can be acquired without proper
credentials allow the adversary to exploit the public’s
trust and confidence in an agency by masquerading as
responders to launch an attack.
The importance of a coherent and seamlessly in-
tegrated OPSEC program in the contemporary public
safety and emergency response agencies’ SOPs cannot be

overstated. In the changing world, where emergency re-
sponders are no longer viewed as noncombatants and are
being targeted as part of the larger terrorist plot, adoption
and implementation of a robust, integrated OPSEC pro-
gram is an obligation, not a luxury. Organizations such
as the International Association of Emergency Medical
Services Chiefs (IAEMSC), International Association of
Fire Chiefs, and the International Association of Chiefs
of Police all have OPSEC and operations site security
best practice reference documents that one can access
and use when crafting one’s own agency protocols. An
example of the reference sheet from the IAEMSC is listed
herein for review (FIGURE 7-2).
This chapter segment does not presume to present
an exhaustive, comprehensive representation of intel-
ligence processes and OPSEC processes; however, it
does provide the learner with the opportunity to de-
velop a fundamental, analytical, historical, and theoreti-
cal understanding for further research on the general
subject of intelligence and OPSEC. Learners are encour-
aged to discuss these issues in greater detail with their
intelligence officer liaisons and local/regional fusion
center representatives. Additionally, information and
training on OPSEC can be obtained through a variety
of sources, including the Federal Law Enforcement
Training Center and the Interagency OPSEC Support
Staff at www.ioss.gov, or IOSS, 6411 Ivy Lane, Suite 400,
Greenbelt, MD 20770; (443) 479-4677.
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FIGURE 7-2 IAEMSC-recommended EMS agency operational
security measures.
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FIGURE 7-2 (Continued)
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FIGURE 7-2 (Continued)
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Incident Management/Unified Command as
the Foundation for Safety and Security
The framework that makes for effective and successful
deployment of OPSEC and site security strategies is the
incident management/unified command (IM/UC) struc-
ture as articulated in the National Response Framework
(NRF) and the National Incident Management System
(NIMS). Many OPSEC and site security issues are ad-
dressed by properly applying these disciplined and stan-
dard structures, practices, and protocols. For example,

interagency integration problems involving the establish-
ment of a chain of command, which produced many
of the issues that plagued security at the World Trade
Center site in the aftermath of the September 11, 2001,
terrorist attacks, could have been significantly amelio-
rated by the implementation of an effective IM/UC early
in the incident and the immediate establishment of a
workable security perimeter.
Simply restating the requirement for implementing
the IM/UC system, which has already been established
with the release of the NRF and the resulting NIMS, is
not the purpose here. Moreover, this chapter section
seeks to address the issue of the role OPSEC and site se-
curity plays in the response to a terrorist incident within
the framework of the IM/UC process.
Although it is in the blood of every individual who
chooses to devote his or her life’s work to respond-
ing when others are fleeing, we must resist the urge
to run in without fully understanding what we face
beyond a door, on the other side of a cloud of smoke,
or around a corner. Although this is easier said than
accomplished, in a terrorist event, our survival to fight
another day depends on projecting or knowing what
threats lie ahead.
The organizational protocol that is established by
IM/UC is simply the framework by which OPSEC/site
security is efficiently, effectively, and successfully es-
tablished; in other words, it is required but not self-
sufficient. While not a panacea, IM/UC implementation
is crucial for us to remediate the hard lessons learned
in the recent past, fixing the strategic and operational
problems inherent in past responses and implementing
standards for OPSEC and site security.

The adoption and implementation of the NIMS–IM/
UC framework addresses and corrects a large por-
tion of site security issues by the talents and service
provided via the law enforcement community at the
command post. It is important to note, however, that
not all of these issues are terrorism specific, and the
UC concept should be allied at most emergency
scenes.
Many of the difficulties inherent in the massive re-
sponse of multiple agencies are as prevalent in an earth-
quake as in a dirty bomb attack. What makes the issue
of OPSEC/site security so important and unique in the
context of terrorism is the particular nature of the threat.
The unpredictability of terrorism creates conditions that
are fluid, requiring speed and flexibility of thought and
action as well as thorough planning and preparation.
Furthermore, the targeting of responders and “soft tar-
gets” such as healthcare facilities and schools makes this
an even more complex matter to address and manage to
ensure one’s safety and the safety of those responders
who are being coordinated at the scene.
In analyzing many major recent terrorist attacks,
numerous areas of concern consistently emerge. By iden-
tifying each of these and focusing on the pitfalls of the
response at the time, as well as stating how the response
could have been improved, responders can learn lessons
and establish best practices for future incidents. These
concerns fall into two general categories. The first cat-
egory involves those concerns that are potentially pres-
ent in any sort of disaster and that are remedied by the
proper implementation of IM/UC. These include:
• Victim rescue in the immediate aftermath of an

incident
• Personnel needs including work shifts to en-
sure proper rest, adequate personal protective
equipment, and continuation of normal EMS/
law enforcement/fire services over the course of
the event
• Organizational integration/interoperability
communication issues
• Public relations, including providing informa-
tion to dignitaries, media, charities, and fami-
lies of victims/missing
• OPSEC/site security
• Staffing support for other elements
The second category of concern addresses those
concerns unique to terrorism that cannot be addressed
simply by the implementation of IM/UC, thereby requir-
ing further attention and creativity. These include:
• Search for secondary devices and hostile threats
to the scene and responders
• Perimeter establishment and access control
• Traffic and crowd control
• Evidence recovery and protection
OPSEC/Site Security—Challenges of a
General Nature
The importance IM/UC plays in enabling successful
OPSEC/site security cannot be overstated. Perhaps the
key component in OPSEC/site security is communication

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and coordination among responders, and the primary fo-
cus of IM/UC is just that. The following section addresses
each aspect of OPSEC/site security that is helped by the

implementation of IM/UC, including multiple examples
from recent terrorist attacks where such implementation
resulted in saved lives or property, and suggestions on
implementing site security at future incidents or events.
Victim Rescue
The first challenge to OPSEC/site security is victim res-
cue in the immediate aftermath of an incident (FIGURE
7-3). This is the initial and most dramatic problem faced
by all responders during and immediately following a
terrorist attack. As mentioned briefly before, a driving
characteristic that defines all responders is the natu-
ral instinct to rush forward, nobly doing whatever one
can to quickly save as many lives as possible. For the
safety of the responders and the victims, some restraint
and organization must be exercised, or the overall in-
cident outcome may become negative, and people may
die needlessly. The lasting images from the events of
September 11, 2001, are of the hundreds of first re-
sponder personnel rushing to the scene to help all who
were victimized by these horrible attacks. One striking
example in a day full of actions hampering, hindering,
and preventing all good intentions was the Shanksville,
Pennsylvania, plane crash site, which on September 11,
2001, was overwhelmed and severely congested due to
the phenomenon of response units, both on and off duty,
making their way to the scene either by self-dispatch
or by convincing dispatchers to send more help. The
resulting chaos clogged the scene, severely complicat-
ing command and control, and confusing perimeter
maintenance. Additionally, similar conditions emerged
in New York City after the mayor announced on televi-
sion that all available resources should be brought to
bear at the World Trade Center site. This resulted in

numerous well-meaning individuals self-dispatching to
the scene, creating an incredible problem with respect
to validation of personnel claiming to possess certain
capabilities, skills, certifications, and licenses, as well as
personal accountability for those operating on the scene
during the initial days postevent.
This area of OPSEC/site security primarily deals with
ensuring an effective response rather than an unorga-
nized, potentially dangerous, and surely less effective
response. Implementation of IM/UC could have dimin-
ished the reported congestion and ensuing confusion at
both events because it states that off-duty response per-
sonnel should not respond to an incident unless directed
to do so. Although operational doctrine dictates that you
man your post until otherwise directed, the reality is that
such a situation rarely exists. The instinct to respond is
powerful and is complicated by the “touch the plane”
phenomenon, in which people feel they have to be at
the disaster scene so they can tell others that they were
there when it happened. Therefore, it is incumbent on
the agency and organization leaders to stress and practice
operational discipline that demands coordination and
adherence to strict deployment protocol.
Another relevant example is the Bali bombing of
October, 2002. As with all responders, the Bali respond-
ers rushed in to help victims and save as many lives as
possible. However, OPSEC/site security was nonexistent,
and many more lives were in danger in the event of
coordinated secondary attack. Though it is difficult to
find fault with the selfless actions of such responders, it
is crucial that this emotional response be tempered by
reason and the knowledge that restraint and discipline
are not only necessary, but required to keep responders
safe and ensure that the investigation is not fouled by re-

sponder crime scene contamination thwarting attempts
to bring the perpetrators to justice.
Finally, there is the example of the brave responders
to the World Trade Center attacks. In their zeal to charge
into the scene and save as many people as possible, the
tunnel vision they experienced most likely contributed
to an ineffective assessment of the prevailing danger and
catastrophic structural failure of the towers. This is a
tremendously unique incident in our history with no
historical reference point, and the multiple planes em-
FIGURE 7-3 Victim rescue is an initial objective and a key
problem faced
by all responders during and after a terrorist attack.
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ployed in the attack were effective secondary devices of
significant proportion.
OPSEC/site security involves understanding the
situation to the greatest degree of accuracy possible,
including the possibility that attempting to rescue vic-
tims immediately may not be the wisest, safest, or most
appropriate course of action. Though it may seem that
delaying rescue efforts is tantamount to abandonment
of our duty to act and is contrary to the oath many of
us swear to, in the end, lives may be saved by taking the
time to fully assess the situation in a coherent fashion
prior to operational response execution.
Personnel Needs
The security needs of response personnel are a major
issue to be addressed in planning for response to a high-
impact/high-yield emergency incident. The needs are
varied and complex, complicated, and resource demand-
ing during and after a terrorist event. These demands are
further amplified given the dual threat of the likelihood
of hazardous materials being present and the active in-
tent of the terrorist(s) to hurt or kill as many people as

possible, including responders.
One good example of personnel needs was the 1997
sarin attacks in the Tokyo subway. Japanese medical
personnel lacked proper personal protective equipment;
more than 20% of the staff of St. Luke’s International
Hospital exhibited some sort of detrimental physical ef-
fects after treating victims of the attack. Had the hospital
planned properly and equipped the facility/personnel,
in addition to regularly training all employees, the in-
stances of secondary contamination would have been
greatly reduced.
The most recent and well-known example of re-
sponders lacking proper personal protective equipment
was the September 11, 2001, attacks. Early on in the re-
sponse, heavy particulate asbestos and other hazardous
materials contaminants, including Freon and cadmium,
were found at the site, yet there were responders with-
out proper protective equipment. This was attributed
to both poor planning and logistics acquisition prob-
lems, because there was simply not enough equipment
to go around—indicating that planners failed to grasp
the scope or even believe that an attack of that magni-
tude could occur—and on poor logistics management,
because some of the needed equipment was present (on-
scene) but was not distributed properly.
There is another critical aspect to protecting re-
sponders in a traditional sense; personnel rest and re-
habilitation are critical to the success and sustainability
of an operation. Although responders are often willing
to work to the point of exhaustion, doing so is danger-
ous to the responders, the victims, and the effectiveness
of the operation. Fatigue creates more victims through

poor decision making, increased stress, frustration, and
impaired judgment. The medical profession continues to
address the effects of sleep deprivation and fatigue due
to errors directly traced back to exhausted healthcare
providers. Several well-publicized studies that chronicle
the effects of long work hours in life-and-death, stressful
environments reveal that errors have produced increased
morbidity and mortality in the patients being cared for
by these well-meaning professionals. Studies conducted
over the last several years reveal that moderate sleep
deprivation produces impairments in cognitive and mo-
tor performance equivalent to illegal levels of alcohol
intoxication.
The last thing any coordinated response should have
to deal with is victims among the responding rescue
workers. To help prevent and ensure the equitable and
safe distribution of personnel, IM/UC has instituted
a system by which the incident commander assigns
shifts to the workers, thereby forcing rest on the weary,
whether they realize they need it at the time or not. The
final personnel issue to be addressed is the continuation
of public services, including EMS, medical, law enforce-
ment, and fire service, through the end of the incident
and into the recovery and mitigation stages.
Sustaining 911 response capacities for the entire
community must be a significant goal that all agencies
strive to achieve. Just because the agency is confronted
with a large disaster in the community does not allevi-
ate it from the obligation to ensure the best possible
planning efforts to at least attempt to provide appropri-
ate management of all emergencies in the community.
Clearly the fiscal implications of having a sustainable and
robust response system that can handle any and all 911
calls at all times are strictly cost prohibitive. The burden

sharing that has become widely accepted is the use of
mutual aid compacts between communities, regions, and
now states under the Emergency Management Assistance
Compact. The key to sustained successful operation is
embracing this concept and employing it on a regular
basis. Further, a review of response protocols for uni-
formity, ensuring interoperability, and having a shared
vision of application of OPSEC and site security tactics
are integral on “game day.”
Hospitals share the same concerns for their facili-
ties and staff. During the planning phase for respond-
ing to disasters, hospital planners must take the time
to consider a number of issues that previously did not
require their attention. Such matters include increased
security, physical management of patient flow, personal
protective equipment, decontamination strategies, staff
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training, and personnel support. One such hospital fail-
ure that resulted in much national media attention oc-
curred in Florida during the hurricane season of 2004.
In this case, Florida Hospital-Ormond Memorial fired
or suspended about 25 nurses for not working during
Hurricane Frances. Some nurses were fired for not call-
ing in, not showing up, or refusing to work, while others
were suspended for not completing a shift. The hospital
stated that under hospital policy, critical care employees
are required to work during a disaster. Some nurses
responded in media accounts alleging that they were
not trained to deal with these extreme scenarios and
also questioned who would protect their families. No
matter the reason, staffing rosters that were expected to
be populated based upon the internal disaster plan were
not, leaving the facility in a lurch to cover staff vacancies
and sustain operations.
Another unfortunate occurrence in the aftermath
of disasters is civil unrest and criminal activity. Police
presence is often distracted and concentrated at the site

of the disaster, coverage is weakened in the areas where
law enforcement officers would normally patrol or de-
ploy, and if the presence is weakened enough, citizens
might loot nearby houses, commercial districts, and in
some cases emergency response equipment. Examples
of this were found during and after countless disasters,
including Hurricane Charley’s landfall in Florida, and
there were unsubstantiated accusations of looting by the
responders themselves in the September 11, 2001, at-
tacks on New York City. In 2005, after Hurricane Katrina
hit New Orleans, there was considerable media attention
on allegations of emergency responder and law enforce-
ment involvement in looting. In 2009, there were still
grand jury investigations regarding numerous allegations
that were leveled at responders ranging from thefts to
abuse of authority and civil rights violations.
Community planners, responders, and emergency
services personnel must also consider the likelihood
of a situation where events have created a large scale
area that is too dangerous for anyone to enter or in
which to respond. Responders must ask themselves
two questions—and answer honestly. (1) In such a
given situation, what are the primary responsibilities
of responders in getting people out, keeping people
from entering, and making sure that the area remains
contained? (2) Are we currently prepared to evacu-
ate, relocate, secure, and effectively close a significant
portion of or an entire city as was necessary during
the 1986 Chernobyl nuclear power plant disaster or
Hurricane Katrina?
Proper and effective deployment of law enforce-
ment officers is a key aspect of incident management,
NIMS, and the NRF. With proper law enforcement

tactical implementation, the lion’s share of criminal
activity or any form of civil disorder can be mitigated.
The implementation strategy also provides for more ef-
fective coordination of responders at the scene, afford-
ing a higher level of coherence to ensure that security
of all personnel, integrated operations, investigatory
processes, and sustained evidentiary recovery can be
achieved.
A similar concern exists for fire services in the wake
of a disaster, specifically in fire-heavy disasters. The typi-
cal response for the fire service is to rush to the scene of a
major blaze, such as the World Trade Center, and engage
as quickly as possible to control the threat and resolve
the problem. One can only imagine the collateral dan-
gers if coincidental fires emerge in other parts of a city,
particularly in the event of a secondary terrorist attack.
The successes of mutual aid are clearly evident in the
various responses to a number of large-scale disasters,
but especially on September 11, 2001.
Emergency management professionals often speak
of the secondary attack. How many communities, agen-
cies, and/or organizations responsible for response and
recovery actually have plans in place for a controlled, co-
ordinated, organized deployment in the face of a growing
disaster? Can the existing response plans and operational
doctrine withstand a campaign event challenge?
Despite what most would believe, and as horrible
as the September 11, 2001, attacks were, the United
States has yet to experience a true mass casualty, mass
fatality event that overwhelms the capabilities of the
affected community and the country. As emergency
responders and leaders, we must revisit the pain and
shock we all felt on September 11, 2001, when almost

3,000 people were murdered. Three thousand sounds
like an unimaginable number, but to our enemies,
based upon their stated intent to inflict harm, 3,000 is
a training exercise.
Integration
Integration issues are a central consideration in any
emergency response, but they are critical for a large-
scale incident. The most obvious example of this is in
the immediate aftermath of the September 11, 2001,
attacks on the World Trade Center in New York City.
Lack of interoperability between fire and police radios
was found to be a major problem during the response
to the 1993 bombing of the World Trade Center, and
unfortunately, the same problem reared its ugly head on
September 11, 2001. Due to this failure and overloaded
radio equipment, fire fighters in World Trade Center
tower 1 were unaware of reports of the imminent col-
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lapse of the tower from a New York Police Department
(NYPD) helicopter and therefore did not initiate their
own evacuation. This lack of communication resulted
in an increased number of casualties that might have
been avoided. The proper implementation of IM/UC,
which stresses both horizontal and vertical information
sharing, would have required interoperable radios, and
the NYPD helicopter in the air above the World Trade
Center would have been able to relay the information
regarding the collapse directly to the fire department,
allowing fire fighters to have a fuller depth of under-
standing for the events and begin evacuating.
The Moscow theater siege of October 2002 is an-
other tragic example of the cost of lives lost when agen-
cies are not integrated. Chechen terrorists took over the
theater, claimed the patrons as hostages, and were killed
when Russian commandos pumped a toxic gas into the
theater, which rendered both terrorists and hostages
unconscious, in some cases killing them. The refusal

and delay by Russian authorities to release information
regarding the type of gas used to subdue and incapaci-
tate the Chechen terrorists rendered medical personnel
unable to properly diagnose and treat the nearly 650
hostage victims of the gas, 117 of whom perished in
the rescue. The unfortunate reality is that authorities
in the Spetsnaz (Russian Special Forces, who carried out
the raid) did not involve the medical community or on-
site medical responders. If the Spetsnaz had coordinated
the assault and included a medical component in tacti-
cal operations, the critical medical communication and
coordination would have positioned the rescue attempt
for greater success, saving additional lives because the
medical knowledge, treatment, and response capabili-
ties would have been on scene and poised to effectively
intervene when called upon.
The Press and Dignitaries
Public relations is an important aspect of OPSEC/site
security because outside factors such as the media and
the victims’ families can seriously complicate a response
or errantly alter public understanding and perception of
the response actions and effectiveness. An example of
the lack of OPSEC/site security with respect to the media
causing major problems was evident during the Beltway
sniper shootings of October 2002. The sniper pair left
notes for the police with specific instructions not to be
relayed to the press, and allegedly made numerous re-
quests for the media not to be involved in the interaction
between the sniper and police. The press obtained this
information through the notorious unnamed source and
went public with information that not only jeopardized
the investigation, but also put many lives in danger. The
resulting lack of trust between the snipers and the po-

lice impeded communication between investigators and
the perpetrators, slowing the investigation as authorities
shifted focus toward damage control.
The media is a valuable asset when responding to an
incident, provided relations take place in a controlled,
efficient manner. An example of the positive and negative
role the media can play in responding to an event was
during the sarin attacks in Tokyo. The most common
and frustrating problem during any response is a lack of
information and communication. In the Tokyo incident,
personnel at local hospitals had no idea what type of haz-
ardous material or contaminant was creating their medical
problems. The hospital personnel dealing with the un-
known became aware of the substance from watching the
local television broadcasts. Coincidently, physicians who
had experience with sarin and the effects on humans were
also watching. The resultant communication between the
physicians viewing the news coverage and the hospitals
correctly identified the culprit substance. Concurrently,
the media was criticized for filming while people suffered
and died instead of helping them to the hospital.
Media coverage of terrorist events can be a double-
edged sword, and it is up to planners to ensure that the
benefits of having the media present are not outweighed
by the disadvantages. This entails having a public infor-
mation officer (PIO) who is trained prior to an incident
on the successful discharge of the PIO duties that are
integrated into the command structure to assist with
response information dissemination and management
of the media (FIGURE 7-4). The PIO must work closely
FIGURE 7-4 The public information officer is trained prior to
an incident
on the successful discharge of the PIO duties integrated into the

command
structure and can therefore assist with response information
dissemina-
tion and management of the media.
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with the OPSEC officer to determine what information
is shared with the media so that the released information
does not compromise the integrity of the investigation
or the safety of responders operating at the scene.
In the event of a major disaster, it is common prac-
tice for government officials of all levels to visit the site to
offer reassurance, including governors visiting the areas
devastated by disaster in their states and the president
coming to the scene of a disaster to lend support and wit-
ness the operations in person, such as after September 11,
2001. It is necessary to have strict OPSEC/site security
to maintain the safety of these dignitaries. Concurrently,
OPSEC/site security is also structured to ensure the dig-
nitaries or their entourages do not disrupt operations,
disturb the scene, or hinder investigations. While the
visit of these dignitaries is important to reassure the pub-
lic, it must not come at the cost of successfully executing
the local or state recovery efforts or the strategies in the
NRF. As has been stated, planning cannot take place in
a vacuum; plans to deal with the onslaught of media and
dignitaries must be a part of the ongoing community
response to any event that may overwhelm a commu-
nity’s ability to operate under normal daily conditions.
Therefore, meet, greet, and planning meetings must be
conducted with all involved parties to include the lo-
cal media representatives with the primary goal that all
participants have a job to do and planning prior to the
worst case scenario will allow for the completion of the
mission in a safe and cooperative manner. All egos, pre-
conceived assumptions, and negative relationships must
be checked at the door.
OPSEC/Site Security Demands for

Off-Site Operations
OPSEC personnel must also take into account the issue
of security and staffing support for elements of the re-
sponse not located directly at the event site, such as joint
or regional operation centers, joint or regional informa-
tion centers, multiagency coordination centers, morgues,
food distribution, and donation reception sites. While
these sites may not be physically located inside the inci-
dent perimeter, they are likely targets. These critical ar-
eas are vulnerable to being compromised or attacked by
a variety of means including, but not limited to physical
attacks with arms, explosives, criminal acts, and hazard-
ous material dispersal.
Law enforcement officials, such as federal marshals
or local police or security forces, must be present to
ensure protection and sustained operation of these vital
services. It is vital to the success and continuation of
the response that community planners, local, city, and
county emergency managers and responders (career and
volunteer) meet on a regular basis prior to a catastrophic
emergency to promulgate prudent operational response
doctrine, to ensure OPSEC and site security, and lastly to
test planning strategies through comprehensive robust
exercising activities.
OPSEC/Site Security for a Terrorist Incident
It isn’t enough simply to adopt and fully implement
the NIMS–IM/UC framework in order to control and
overcome the majority of OPSEC/site security issues,
although it is important to note that the majority of con-
cerns, challenges, and problems faced by EMS, medical
personnel, law enforcement, security personnel, and fire

service are not unique to terrorism/weapons of mass de-
struction events. The implementation of a plan and/or a
system to alleviate identified problems and to avoid new
problems is only as good as the training that is provided
to familiarize all those who will utilize the plan and/or
system. It is impossible and may border on negligence
to expect that people, agencies, departments, and com-
munities will be able to utilize plans designed to place
everyone on the same sheet of paper without coherent
and comprehensive ongoing training and exercising.
In the case of a natural disaster, for example, the
difficulties inherent in the massive response of multiple
agencies remain. The logistics involved in mobilizing
personnel, equipment, and resources coupled with emo-
tions, hungry, tired victims, and those nefarious few who
are bent on taking advantage of victims in need creates
circumstances that will derail the best laid plans. Now,
add to that a situation where these very same people are
asked to respond, faced with all the normal obstacles,
but have had little or no time to be acquainted with the
new plan and even less time being trained on the plan’s
usefulness, purpose, and operational guidance. You now
have the current scenario in place; add to this already
chaotic, stressful, and incredibly frustrating event the
current severity and the particular nature of the threats
we face in the post–September 11, 2001, era.
The unpredictability of terrorism presents condi-
tions that are highly fluid and subject not only to the
whims of nature or the physics of a damaged building
but to the advanced plans and suicidal determination of
well-trained terrorists. Additionally, a garden variety ter-
rorist does not abide by Occupational Safety and Health
Administration requirements, does not apply for permits,
does not worry about the adequacy of financial support,

does not follow labor laws and/or legal restraints pre-
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venting action, and the list goes on and on. The terrorist

groups that have been identified, and most likely those
we have yet to uncover, commit, plan, train, and act in
an organized, efficient, and effective manner.
An organizational structure adequate to deal with
such an elusive threat, represented by NIMS–IM/UC,
only provides the means by which proper measures
can be successfully implemented. This is not a ques-
tion of whether a strategy will be properly followed,
but what the strategy entails. The plan in no way pro-
vides implementation funding, training and educational
funding, staffing backfill, or overtime funding, allowing
comprehensive training and education, equipment ac-
quisition, and maintenance. Any plan is only as good
as the assumptions it is based on, and a plan certainly
is useless when those utilizing the plan have yet to see
the plan, be familiar with it, and receive training in plan
implementation.
The critical issue is the priority that must be given
to OPSEC/site security at all incidents, not just those
eventually identified as terrorism related. Adoption of
this position creates a familiarity with OPSEC and site
security for all responders and becomes institutional-
ized into the way we do business 24 hours a day, 7
days a week.
The after action reports from numerous major ter-
rorism incidents clearly reveal shortcomings in OPSEC/
site security that warrant significant emphasis and close
attention by agencies developing their terrorism/WMD
response plans in concurrence with NIMS–IM/UC.
There is a striking convergence of properties that
characterizes this second group of OPSEC/site security
concerns: that they cannot be solved by organizational

reform alone, and that they are all particularly pertinent
in a terrorist attack. This highly interconnected list for
scene management includes perimeter establishment,
access and egress control, personal accountability, evi-
dence protection and chain of custody, and the search for
secondary devices and threats. Solving the inadequacies
in these areas requires not just that the organizational
structure exists, but that it be imbedded in a prominent
position within the incident command structure.
Establishing a Perimeter
The effective establishment of a perimeter is often a cru-
cial aspect of gaining control over the scene of an attack.
Establishing a perimeter has ramifications in all aspects
of maintaining OPSEC/site security. Force protection
cannot be assured, evidence cannot be protected, chain
of custody cannot be guaranteed, and access to the scene
cannot be controlled with a porous or haphazard cre-
ation of a perimeter.
The overall response to the 1995 terrorist bombing
of the Alfred P. Murrah Federal Building in Oklahoma
City, Oklahoma, is an excellent model of what was
right and what was wrong. There were three layers of
perimeters quickly established by morning on the day
after the bombing; the inner perimeter was designed to
provide limited access to only those personnel autho-
rized to participate in the rescue/recovery work and the
criminal investigation, a staging area that also served as
a buffer for workers, and a limited traffic access cordon.
Unfortunately, an effective perimeter was not established
immediately and the site quickly became overwhelmed
with hundreds of well-meaning people who wanted to
help in any way they could. The problem was that no

control existed over any area of the dangerous site and
one convergent responder—a nurse—was killed early
on due to falling debris.
The eventual establishment of an effective perimeter
was accomplished by close coordination of disparate
agencies and proper utilization of their abilities along
with the securing and construction of fencing. At the
World Trade Center site on September 11, 2001, in
admittedly more trying circumstances, “Perimeter se-
curity was not adequately established, allowing large
numbers of unnecessary personnel to enter” (McKinsey
& Company) due in large part to a 5-day delay in the
creation of an adequate credentialing system and
the construction of a fence. It took an extra 4 days
at the World Trade Center to establish security even
approaching the perimeter set up at the Murrah Federal
Building. The potential repercussions for this sort of
inattention are massive.
Another example of the need for perimeter secu-
rity is the case of a 1997 bombing of a women’s clinic
in suburban Atlanta, where Eric Rudolph is alleged to
have planted a secondary explosive device timed
to detonate upon the arrival of personnel responding to
the initial explosive event. A CNN camera crew filming
an interview with a witness of the initial blast caught
the nearby second explosion on film; both media and
civilians were endangered because they were allowed
access to an area surrounding the scene, which should
have been secured.
The uncontrolled scene increases the potential and
likelihood that individuals not involved in the initial
catastrophic event will become victims as a result of a
secondary attack, the hazardous material (if present) will

be spread to a wider area, and the criminal investigation
will be hampered or evidence destroyed. Ground zero at
a terrorist attack, therefore, demands special attention to
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the formation of perimeters as a necessary prerequisite
to full OPSEC/site security implementation.
The cooperation and discipline required to ensure
security and safety does not and will not happen over-
night or because it is the right thing to do. All aspects of
scene control must be carefully planned, practiced, and
exercised on an ongoing basis. It is impossible to expect
two completely divergent disciplines to come together
and cooperate without the right training and education.
A vital perspective to understand in this matter is the
doctrinal conflict that this creates—attribution versus
intervention. One large group of responders is running
in to tear the scene apart to look for victims and survivors
and to treat the injured (intervention). The other large
response group requires the meticulous preservation of
evidence and maintaining the site just as it was found
(attribution).
There is no question that each group has a vital
and important role and responsibility—none more im-
portant than the other. It is naïve and irresponsible for
any responding person, agency, group, or department
to expect these two parallel forces to eventually meet
in the middle without long-term focused efforts aimed
at settling the differences and ensuring that both jobs
are completed efficiently and timely. A mutual respect
must be achieved through policy and reinforced through
exercising if the contemporary emergency response and
public safety professions realistically expect to bridge
the intervention–attribution gap. This can only be ac-
complished well before the incident response through
regular meetings, educational sessions, training, and ef-
fective exercising opportunities. Failure to address this
coordination factor pre-event will result in a response that

resembles a cacophony—not the desired symphony.
Scene Evidence Preservation
As previously stated, ensuring the preservation of evi-
dence is another fundamental aspect of OPSEC/site se-
curity in the event of a terrorist attack. Consider the
Oklahoma Department of Civil Emergency Management
after action report, which outlines the problems that
presented themselves because of the large number of
volunteers who were incorporated into rescue operations
without being registered or identified. “Since the site was
a crime scene, all our volunteers were required to be
critically screened before they could work at the bomb
site” (Oklahoma Department of Civil Emergency).
Fortunately, authorities implemented this system
to rectify the unimpeded access people were afforded;
about 30 unauthorized convergent responder volun-
teers were evicted from one floor alone. This was not
handled as well at the site of the 2002 Bali bombings.
There, “the crime scene was seemingly ruined and un-
protected” (Pastika) due, in addition to unavoidable cir-
cumstances involved in the response, to “the public’s
curiosity,” (Pastika) which was apparently allowed to
hinder the investigation despite the fact that a police
line had been set up.
The removal, addition, destruction, or alteration
of material, whether intentional, unintentional, or sim-
ply the product of an inexperienced volunteer seeking
a souvenir, could be a major hindrance to the proper
conduct of the criminal investigation and identification
of those responsible. Even the most minute and seem-
ingly unimportant pieces of evidence often prove to be
irreplaceable in these situations, and they cannot afford

to be compromised. To the untrained eye, the aftermath
of a terrorist attack is a pile of debris or a chaotic mass of
humanity. To the trained criminal investigator, the scene
is a roadmap that tells the complete story of the circum-
stances leading up to the event and the event itself. As
noted previously, the control of access to the site of a
terrorist incident through well-guarded and protected
perimeters and a secure credentialing system that does
not allow for forgeries is the only way to guarantee the
integrity of the crime scene.
The Influence of Traffic and Crowd Control upon
an Incident Scene
Traffic and crowd control make up an extremely impor-
tant aspect of scene OPSEC/site security, especially in
the wake of a terrorist attack. With this aspect, OPSEC/
site security takes on a much broader impact subse-
quent to the flow of people and materials in and out of
the site itself, and the city or general area in which the
attack has occurred is impacted by activity elsewhere.
The frightening nature of terrorism, especially for cases
in which chemical, biological, radiological, or nuclear
(CBRN) substances are implicated either by fact or by
speculation, could result in mass hysteria and chaos. In
the absence of accurate, timely information from au-
thorities, rumor mongering can take root, leading to
potentially disastrous public panic. Something in the
vein of an uncontrolled, large-scale attempt to flee a
city in the midst of reports of a CBRN incident could
freeze attempts to contain the attack or worse, prompt
more people into the affected area, and risk exposure to
a greater slice of the population.
Consider the description of the evacuation of coastal
Florida at the approach of Hurricane Floyd in 1999:
“Even many of those not in evacuation zones fled at the

sight of satellite images on the news, which depicted a
monstrous Floyd larger than the entire state of Florida
… the result was a transportation nightmare” (Kriner).
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The Florida public, frightened by memories of 1992’s
Hurricane Andrew, is akin to today’s nationwide mem-
ory of September 11, 2001; combined with sensational-
izing factors such as talk of a hurricane engulfing a state
or the imminent citywide release of a chemical agent,
they can easily produce wholesale disorder. Full control
of the site of a terrorist incident area requires that the
information being disseminated from a scene be released
in multiple media and methods of communication to
dispel rumors, with an eye to directing the public to the
proper course of action. Emergency response managers
and chief officers cannot lose sight of the fact that our
communities are made up of cultures that interpret the
same information in different ways. Keeping in mind the
cultural, language, and educational barriers that make
up each community requires extensive preparations to
ensure a complete information sharing plan of action.
Concurrently, traffic and crowd control of the entire
surrounding area must be fused with information con-
trol to ensure that on-site efforts receive proper support
and aid.
Control of human traffic also has great importance
in its localized form. In the rush to leave a scene to avoid
injury or seek medical attention, it is very possible that
citizens will unintentionally carry hazardous substances,
particularly CBRN material, with them. Depending on
the nature of the agent that has been introduced, the
failure to contain contaminated people or other material
could lead to secondary contamination of individuals
or property.
The 1995 sarin nerve agent attack on the Tokyo sub-
way system is an example of the difficulties and effects
associated with the uncontrolled vector of contaminated

victims. In that incident, over 4,000 affected victims,
some contaminated and off-gassing, sought medical
treatment without official transport. This means that
a very large number of people who either came into
contact or had a good chance of coming into contact
with sarin were moving freely throughout the city. It
is fortunate that the toxicity of the sarin used in the at-
tacks was not potent enough to kill many more and the
associated off-gassing that occurred resulted in illness
and not death.
Citizens seeking medical assistance were not treated
by responders prepared with on-scene decontamination
assets, causing a high rate of secondary exposure among
the medical staff at unspecialized facilities. Containment
of the incident area includes, therefore, the ability to
bring specialized treatment to the site, because “agent
absorbed by cloth may be released as a vapor by the
cloth for 30 minutes or more after exposure” (CBWinfo.
com). Again, because the sarin was put together quickly
and was only 30% pure, the agent did not lead to any
serious injuries to people not in direct contact with the
dispersal device. However, it is startling that such an
impure chemical mixture was able to affect over 20% of
the hospital workers treating victims who hadn’t been
in direct contact with the sarin dispersal device and had
been transported from the scene over an extended period
of time. The lesson is clear—in responding to an attack
in which biological, chemical, or radiological weapons
are suspected, establishing control of the traffic of people
both in and out of the area is crucial for the protection
of the scene victims and those would-be victims in the
surrounding communities.
Secondary Devices or Threats

Perhaps the most pressing and worrying element of con-
cern is that of secondary devices and threats targeting
responders and evacuating civilians. Terrorism poses
a distinct, highly dangerous hazard and challenge in
itself, but the potential for secondary attacks and fall-
out aimed at even more casualties to responders further
complicates the big picture and attempts to control the
aftermath. Terrorism aims to cause as much damage
or harm to as many people as possible, so a follow-up
attack should be a primary consideration, not merely
considered a marginal possibility.
The previously mentioned example of Eric Rudolph
and his involvement in abortion clinic bombings is rel-
evant here as well. The detonation of a bomb outside of
an Atlanta night club 1 week after the women’s clinic
blast where a secondary attack was successful provided
responders with enough warning to suspect a similar
tactic in the Atlanta night club bombing. Fortunately, the
responders remained diligent, and the secondary device
that Rudolph allegedly planted was located and ren-
dered safe before it killed or injured responders. Similar
terror tactics were used extensively by several interna-
tional terrorist organizations, most notably the Real Irish
Republican Army and the Colombian paramilitary gue-
rilla group known as the Revolutionary Armed Forces
of Colombia. Real Irish Republican Army guerilla forces
“have operated a two-bomb strategy, hoping secondary
devices ‘catch’ security forces rushing to the scene of
the first” (CNN). The adoption of such tactics by the
enemies of the United States, given their resourcefulness
and excellent access to information, should certainly not
be discounted.
Regardless of the recent elevated concerns and atten-
tion given to this phenomenon, preparation for such a

scenario was lacking. In the aftermath of the collapse of
the World Trade Center towers, the initial rescue phase
was followed by a massive recovery effort. Within a day
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or so after the two towers collapsed, there were already
thousands of workers on the scene. Following the at-
tacks, estimates placed the number of volunteers and
workers from all disciplines at ground zero at 30,000
to 40,000. At the same time, however, “risk of second-
ary attack was not made a priority as the rescue effort
was vigorously pursued” (Senay). The buildings in the
immediate vicinity were not searched for 4 days; it took
months to clear all structures properly. There was no
standard procedure for obtaining resources such as mili-
tary aid to augment this task and expeditiously proceed
with the search and clearance process.
Failure to secure a perimeter immediately and
control site access, as just mentioned, left avenues
open through which to strike. In addition, the ma-
jority of the nation’s federal response and leadership
to the disaster was housed in two Manhattan hotels
surrounded by response vehicles brightly decorated
with a wide variety of responding agencies’ logos,
decals, and identifying placards. The worst kept se-
cret in the city of New York was where all the federal
responders were resting, recuperating, and spending
their down time. There is no question that a well-
planned or even a last-minute secondary attack would
have produced a very high number of casualties due
to the large number of vulnerable personnel in the
area. Such an attack would have crippled the New
York response, but more importantly, the secondary
attack at that particular time would have crippled the
nation due to the message it sent to those not directly
affected by the events in New York and Washington,
DC, elevating the appearance of capacity and potency
of the terrorist attackers.

Numerous tactics could be applied in a secondary
attack. The potential for snipers to receive training and
apply it with startling effect was demonstrated by the
killing spree undertaken by the Beltway snipers, John
Allen Muhammad and Lee Boyd Malvo. Powerful and ac-
curate weapons such as shoulder-fired rocket-propelled
grenades and American-made Stinger missiles, in addi-
tion to heavily proliferated small arms, are obtainable
through the international black market and have been
proven to be deadly in small-scale guerilla conflicts in
Africa, the Middle East, and across the globe. Suicide
attacks come in many forms, including vehicle-borne
improvised explosive devices and explosives strapped on
or secreted in the body of an individual; both tactics have
proven to render devastating effects. It is clear, therefore,
that there is both a real threat and a worrisome example
in which this threat was not prepared for sufficiently.
The NYPD report makes this apparent: “NYPD lacked
systematic intelligence and threat assessment function
and had difficulty assessing risk of further terrorist at-
tack in weeks after 9/11” (McKinsey & Company). But
given this historical perspective and embracing a desire
to enhance response safety, readiness, and capacity, the
contemporary emergency response leader can use these
events and context as a platform for moving ahead with
refinement of existing plans to address gaps that might
exist to afford their communities and responders a better
degree of safety.
Chapter Summary
Operational security and site security are the most im-
portant concepts that are engaged through a conscien-
tious, comprehensive effort to protect and secure vital
infrastructure before, during, and after a catastrophic

event. To ensure that OPSEC and site security is a con-
cept that is embraced and promoted, dialogue with all
traditional and nontraditional response agencies should
occur on an ongoing basis prior to “game day.” These
meet-and-greet-and-break-bread gatherings require the
checking of egos at the door and the establishment of
a real goal-oriented working session. Where possible,
agencies should assign, support, and fund the position
of OPSEC officer to address and coordinate these respon-
sibilities. This requirement also includes the creation
of memoranda of understanding detailing the roles, du-
ties, and responsibilities of all agencies and responders
assisting in the development of long-term working
relationships all aimed at security, safety, and preserva-
tion of life.
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103
Wrap Up
Chapter Questions
1. List and discuss the definitions of OPSEC and site
security.
2. Discuss the differences between OPSEC and site
security.
3. List and discuss the five steps of the OPSEC
process.
4. Diagram and subsequently discuss the compo-
nents of the intelligence cycle.
5. Identify what agency is charged with fostering
widespread adoption of OPSEC at the national,
state, tribal, territorial, and local agency levels.
What support does it provide to these constituent
agencies?
6. Discuss why site security is an important strategic
and tactical consideration at emergency response
scenes.

7. Outline the critical components of establishing
and sustaining site security operations and how
they integrate into the incident command system
process.
8. Discuss the importance of evidence protection
and the value emergency responders afford law
enforcement when responders take protective
measures to recognize and preserve suspected
evidence at the scene of an incident.
9. Identify and discuss the importance of personal
accountability at the scene of an incident and
how OPSEC and site security can augment this
process. Additionally, describe what measures
for personnel authentication can be employed
by integrating OPSEC and site security into local
response policy and operational doctrine.
Chapter Project I
Develop a sample OPSEC policy for your agency that
addresses each of the five steps in the OPSEC process.
Remember to allow for integration of mutual aid re-
sponse assets into the protocol.
Chapter Project II
Review a past large-scale incident, examining the re-
sponse for site security compliance. Discuss the pros
and cons of the response and how you would improve/
enhance the site security operation.
Vital Vocabulary

Intelligence The product resulting from the collection,
collation, evaluation, analysis, integration, and interpre-
tation of collected information.
OPSEC A tool designed to promote operational effec-
tiveness by denying adversaries publicly available indica-
tors of sensitive activities, capabilities, or intentions.
Public information officer (PIO) The position within
the incident command system responsible for providing
information about the incident. The PIO functions as a
point of contact for the media.
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105
Weapons of Mass Effect—
Chemical Terrorism
and Warfare Agents
Paul M. Maniscalco
Dr. Christopher P. Holstege
Dr. Frederick R. Sidell
• Understand the importance of preparedness for a chemical
attack.
• Recognize the characteristics of nerve agents.
• Outline victim treatment procedures for nerve agent exposure.
• Outline treatment procedures for cyanide exposure.
• Define vesicants and list the symptoms for exposure to
specific vesicants.
• Recognize the symptoms of exposure to pulmonary agents.
• Define the common riot control agents.
• Recognize the importance of triage in mass victim incidents.
Objectives
8
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Introduction
Chemical warfare agents are chemical substances that
were developed for use on the battlefield to kill, injure,
or incapacitate. For 79 years, from their first use in 1915
in World War I until 1993, the intentional use of these

chemicals to kill, injure, or incapacitate was limited to
battlefield use. The requisite tactics and necessary tech-
nology for chemical terrorism events are unmistakably
notable from using chemical weapons designed to meet
military needs. Chemical terrorism can be defined as
an asymmetric warfare tactic employed by nonmilitary
actors against noncombatant (civilian) targets.
At the first World Trade Center attack in New York
City in 1993, the attackers integrated cyanide into the
construct of the explosive device they manufactured.
Fortunately, the expected dissemination did not effi-
ciently occur with the violent explosion; the explosion
rapidly consumed the integrated product, rendering
the tactic ineffective. In June 1994, the religious cult
Aum Shinrikyo disseminated one of these agents, sarin,
throughout an apartment complex in Matsumoto, Japan,
with the intent of causing widespread harm or death to
people. In March 1995, the same group released sarin
on the Tokyo subways, causing injuries in over 1,000
people and death in 12. Terrorists had a new weapon—a
chemical weapon.
Rogue individuals and organizations continue to
possess or have access to these weapons. There are prob-
ably several dozen countries with the capacity to manu-
facture these chemicals, and some of these countries
are known to be sponsors of terrorist groups and acts
of terrorism. In addition, instructions for the synthesis
of these agents are widely available to terrorist groups
and rogue individuals in books, on the Internet, and in
other places such as militia newsletters.
Some very toxic chemicals are regularly manufac-
tured in large amounts in this country and are trans-
ported daily on our highways and railways. Chemicals

such as cyanide, phosgene, and chlorine, all of which
were once military agents, are widely used in large
amounts (CP FIGURE 8-1). Many commonly used pesticides
have very similar properties to nerve agents.
With the ever-increasing number of toxic chemicals
in the world and the existence of rogue organizations
that are willing to use them to further their causes, it is
essential that communities and emergency response or-
ganizations prepare to confront the challenges presented
by a chemical terrorist event.
Terrorist incidents involving military chemical
agents are, from an individual victim treatment founda-
tion level, not much different from a regular hazardous
materials incident; victim care is the same. The criti-
cal differences are: (1) it is a deliberate release and (2)
most likely it is a high-impact/high-yield incident with
numerous victims.
Overall, there are differences between an accidental
spill of a toxic chemical and a deliberate release of the
same chemical. Probably the most important difference
is the fear and anxiety generated in the community and
among the emergency responders who must deal with
unknown factors. This fear and anxiety may be present
in possible victims, who do not know and who can-
not be immediately reassured that they have not been
harmed, or it might be present in responders who fear
a secondary hostile device at the scene designed to in-
jure them. Many more agencies become involved in a
deliberate release incident, including emergency medi-
cal services (EMS), fire/rescue, emergency management,
law enforcement, and all levels of government that will
converge on the scene in an effort to assist. The site of a

deliberate incident is a crime scene, a chemical hot zone,
a biological hot zone, and in most cases a high-impact/
high-yield multiple casualty incident. These events result
in EMS and the medical community playing a significant
lead role in consequence management. Between delayed
onset of symptoms, decontamination practices, victim
tracking, and other relevant activities, EMS and hospitals
must remain attentive to victim signs and symptoms that
may indicate a sentinel event of an attack.
Delivery/Dissemination
Chemical agents are disseminated in many ways. Bombs,
rockets, mines, and other explosive devices are used by
the military. When these explode, some of the agent
remains as liquid, some immediately evaporates to form
vapor, and some will exist as small droplets of the agent
suspended in air, or an aerosol. These small droplets
eventually evaporate and become a vapor. The result is
a hazard from the liquid agent, both as the original liq-
uid and as the aerosol droplets (which neither remain
long nor travel far) and a hazard from agent vapor. Agents
can also be sprayed from airplanes during battlefield
use, as some agents were during the Vietnam War.
Liquid chemical agents might be employed with an
explosive device by nonmilitary users. The user would
have to make the device, which is not without hazard,
and then detonate it in the right place at the right time.
The emergency response community must be prepared
for a consequence response to a chemical attack.
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CHAPTER 8: Weapons of Mass Effect—Chemical Terrorism
and Warfare Agents 107
Other means of disseminating the agent are more likely.
Insecticides are sprayed from airplanes and helicopters in
both crop dusting (FIGURE 8-1) and mosquito eradication.
This is an obvious and expensive way to disseminate an
agent, but it is effective for spreading it over a large area
providing the weather and winds are favorable. Vehicle-
mounted spray tanks can be driven through the streets

of a target area to disseminate an agent. For example,
in Matsumoto, the agent was spread from the back of
a vehicle in which a container of agent was heated (to
help it to evaporate), and the vapor was blown through
the street by a fan. Indoor areas might be attacked by
putting an agent in the air system, and rooms could be
thoroughly and quickly contaminated by the use of a
common aerosol spray can. There are other methods of
disseminating liquids.
Nerve Agents
Nerve agents are toxic materials that produce injury
and death within seconds to minutes. The signs and
symptoms caused by nerve agent vapor are characteristic
of the agents and are not difficult to recognize with a
high index of suspicion. Very good antidotes that will
save lives and reduce injury if administered in time are
available.
Nerve agents are a group of chemicals similar to,
but more toxic than, commonly used organophosphate
insecticides such as Malathion. Nerve agents were de-
veloped in Germany during the 1930s for wartime use,
but they were not used in World War II. They were
used in the Iran–Iraq war. They were also used by the
religious cult Aum Shinrikyo in Japan on two occa-
sions; the first use injured about 300 people and killed
seven in Matsumoto in June 1994; the second killed
12 and injured over 1,000 in the Tokyo subways in
March 1995.
The common nerve agents are tabun (GA), sarin
(GB), soman (GD), GF, and VX (GF and VX have no
common names) (CP FIGURE 8-2).

The nerve agents are liquids (not nerve gases) that
freeze at temperatures below 0°F and boil at tempera-
tures above 200°F (CP FIGURE 8-3). Sarin (GB), the most
volatile, evaporates at about the rate of water, and VX,
the least volatile, is similar to light motor oil in its rate
of evaporation. The rates of evaporation of the oth-
ers lie in between. In the Tokyo subway attack, sarin
leaked out of plastic bags and evaporated. Serious injury
was minimized because the rate of evaporation of sarin
is not rapid, so the amount of vapor formed was not
large. If the sarin had evaporated more rapidly (e.g.,
like gasoline or ether), much more vapor would have
been present, and more serious injury in more people
would have occurred.
Nerve agents produce physiological effects by in-
terfering with the transmission between a nerve and the
organ it innervates or stimulates, with the end result
being excess stimulation of the organ. Nerve agents
do not actually act on nerves. Instead, they act on the
chemical connection of the nerve to the muscle or organ.
Normally, an electrical impulse travels down a nerve,
but the impulse does not cross the small synaptic gap
between the nerve and the organ. At the end of the nerve,
the electrical impulse causes the release of a chemical
messenger, a neurotransmitter, which travels across the
gap to stimulate the organ. The organ may be an exocrine
gland, a smooth muscle, a skeletal muscle, or another
nerve. The organ responds to the stimulus by secret-
ing, by contracting, or by transmitting another message
down a nerve. After the neurotransmitter stimulates the
organ, it is immediately destroyed by an enzyme so that
it cannot stimulate the organ again. Nerve agents inhibit
or block the activity of this enzyme so that it cannot de-
stroy the neurotransmitter or chemical messenger. As a
result, the neurotransmitter accumulates and continues

to stimulate the organ. If the organ is a gland, it contin-
ues to secrete; if it is a muscle, it continues to contract;
or if it is a nerve, it continues to transmit impulses. There
is hyperactivity throughout the body.
FIGURE 8-1 Crop dusting is an obvious and expensive way to
disseminate
an agent, but it is effective for spreading it over a large area
providing the
weather and winds are favorable.
Remember that it does not take an explosive device
to disseminate chemical agents. There are multiple
methods of disseminating chemical agents over a wide
area.
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Nerve agents perform the following actions within
the human body:
• Block the activity of an enzyme (called acetyl-
cholinesterase)
• Cause too much neurotransmitter to accumu-
late (acetylcholine)
• Cause too much activity in many organs,
glands, muscles, skeletal muscles, smooth mus-
cles (in internal organs), and other nerves
In the presence of nerve agent poisoning, exocrine
glands secrete excessively. These glands include the tear
glands (tearing), the nasal glands (rhinorrhea or runny
nose), the salivary glands (hypersalivation), and the
sweat glands (sweating). In addition, the glands in the
airways (bronchorrhea) and in the gastrointestinal tract
secrete excessively in the presence of nerve agents.
The clinically important smooth muscles that re-
spond are those in the eye (to produce small pupils, or

miosis), in the airways (to cause constriction), and in
the gastrointestinal tract (to cause vomiting, diarrhea,
and abdominal cramping).
Skeletal muscles respond initially with movement
of muscle fibers (fasciculations, which look like rip-
pling under the skin), then twitching of large muscles,
and finally weakness and a flaccid paralysis as the mus-
cles tire.
Nerve agents affect the following:
• Lacrimal glands (tearing)
• Nose (rhinorrhea)
• Mouth (salivation)
• Sweat glands (diaphoresis)
• Bronchial tract (in airways causing wheezing)
• Gastrointestinal tract (cramps, vomiting, diar-
rhea)
• Skeletal muscles
Fasciculations, twitching, weakness, paraly- –
sis
• Smooth muscles
Airways (constriction) –
• Central nervous system
Loss of consciousness –
Convulsions –
Cessation of breathing –
Among the nerve-to-nerve effects are stimulation of
autonomic ganglia to produce adrenergic effects such
as hypertension (high blood pressure) and tachycardia
(rapid heart rate). The exact mechanisms in the central

nervous system are less well defined, but the result is
loss of consciousness, seizures, cessation of breathing
(apnea) because of depression of the respiratory center,
and finally death. Early effects also include stimulation
of the vagus nerve, which causes slowing of the heart
(bradycardia), or stimulation of the sympathetic system
to cause tachycardia.
The effects that occur depend on the route of
exposure and the amount of exposure. The initial ef-
fects from a small amount of vapor are not the same as
those from a small droplet on the skin, and the initial
effects from a small amount of vapor are not the same
as those from a large amount of vapor. Exposure to nerve
agent vapor produces effects within seconds of contact.
These effects will continue to worsen as long as the victim
is in the vapor atmosphere but will not worsen signifi-
cantly after the victim is removed from the atmosphere.
Exposure to a small concentration of vapor will
cause effects in the sensitive organs of the face that come
into direct contact with the vapor—the eyes, the nose,
and the mouth and lower airways. Miosis (small pupils)
is the most common sign of exposure to nerve agent
vapor. Reddened, watery eyes may accompany the
small pupils, and the victim may complain of blurred
and/or dim vision, a headache, and nausea and vomiting
(from reflex mechanisms). Rhinorrhea (runny nose) is
also common, and after a severe exposure the secre-
tions might be quite copious. Increased salivation may be
present. Agent contact with the airways will cause con-
striction of the airways and secretions from the glands
in the airways. The victim will complain of shortness
of breath (dyspnea), which, depending on the amount
of agent inhaled, may be mild and tolerable or may be

very severe. These effects will begin within seconds after
contact with the agent. They will increase in severity
while the victim is in the vapor, but will maximize within
minutes after the victim leaves the vapor.
Sudden exposure to a large concentration of vapor,
or continuing exposure to a small amount, will cause
loss of consciousness, seizures, cessation of seizures with
cessation of breathing and flaccid paralysis, and death.
After exposure to a large concentration, loss of con-
sciousness occurs within seconds, and effects progress
rapidly to cessation of breathing within 10 minutes.
Vapor Exposure
Small Concentration
• Miosis (red eyes, pain, blurring, nausea)
• Runny nose
• Shortness of breath
• Effects start within seconds of contact.
Large Concentration
• Loss of consciousness
• Convulsions
• Cessation of breathing
• Flaccid paralysis
• Effects start within seconds of contact.
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A very small, sublethal droplet of agent on the skin
causes sweating and muscular fasciculations in the area
of the droplet. These may begin as long as 18 hours
after agent contact with the skin and generally will not
be noticed by either the victim or medical personnel. A
slightly larger, but still sublethal droplet will cause those
effects and later cause gastrointestinal effects, such as
nausea, vomiting, diarrhea, and cramps. The onset of
these are also delayed and may start as late as 18 hours
after exposure. A lethal-sized droplet causes effects much

sooner, usually within 30 minutes of contact. Without
any preliminary signs, there will be a sudden loss of
consciousness and seizures followed within minutes by
cessation of breathing, flaccid paralysis, and death.
Effects from skin contact with a liquid droplet will
occur even though the droplet was removed or decon-
taminated within minutes after contact. Rapid decon-
tamination will decrease the illness but will not prevent
it. Nerve agent liquid on skin will cause effects that begin
many minutes to many hours after initial contact. After
the effects begin they may worsen because of continued
absorption of agent through the skin.
Liquid on Skin
Very Small Droplet
• Sweating, fasciculations
• Can start as late as 18 hours after contact
Small Droplet
• Vomiting, diarrhea
• Can start as late as 18 hours after contact
Lethal-Sized Droplet or Larger
• Loss of consciousness
• Convulsions
• Cessation of breathing
• Flaccid paralysis
• Usually starts without warning within 30
minutes
Management of a nerve agent casualty consists of

removing the agent from the victim (decontamination)
or the victim from the agent, administration of anti-
dotes, and ventilation if needed. EMS providers must
have proper personal protective equipment during these
operations.
For the antidotes to be effective, the victim must be
removed from the contaminated area and/or the agent
must be removed from the victim’s skin. Although the
antidotes are quite effective, they cannot overcome the
effects of the agent while the victim is continuing to
breathe the agent or while the agent is still being ab-
sorbed through the skin. Skin decontamination will
not remove an agent that has been absorbed into the
skin. Even if the agent is not yet through the skin,
effects may start as long as several hours after skin
decontamination.
Removing the victim from the area of contamination
or the vapor area should be rather simple in a normal
hazardous materials incident, but the complexities of
a mass casualty terrorism event present some unique
challenges. If the agent was released inside a building or
other enclosed space, moving the victims outside should
suffice. If the agent was released outside, victims should
be removed and triaged far upwind.
Removal of the agent from the skin must be done
as early as possible. It is unlikely that you will see a liv-
ing victim with visible amounts of nerve agent on his
skin. However, if this occurs, remove it (the substance)
as quickly as possible. Flushing with large amounts of
water or wiping it off with dirt or any other convenient
substance will help. If clothing is wet, suggesting agent
exposure, remove the clothing as quickly as possible.

This should be done in the hot zone before the victim
reaches the decontamination site in the warm zone.
Although the agent is removed from the surface of the
skin, the agent that has already penetrated into the skin
cannot be removed, and absorption will continue; the
victim may worsen despite antidotes.
The antidotes for nerve agent poisoning are atro-
pine and an oxime, 2-pyridoxime chloride or 2-PAMCl
(Protopam). They act by different mechanisms. Atropine
blocks the excess neurotransmitter and protects the site
on the organ that the neurotransmitter stimulates. As
a result, the glands dry and the smooth muscles stop
contracting (such as those in the airways and gastroin-
testinal tract). However, atropine has little effect on the
skeletal muscles, and these muscles may continue to
twitch despite an adequate dose of atropine.
The initial dose of atropine is 2 mg to 6 mg. This
dose might seem high to those accustomed to admin-
istering it for cardiac or other purposes, but it is the
amount necessary to overcome a total-body excess of
the neurotransmitter. After the initial dose, a dose of
2 mg should be administered every 5 to 10 minutes
until (1) the secretions have diminished considerably,
and (2) breathing has improved or airway resistance has
decreased (if the victim is being ventilated). Tachycardia
(rapid heart rate) is not a contraindication to atropine
Treatment for nerve agent exposure involves decontami-
nation, administration of antidotes, and ventilation.
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use in these victims. Atropine can be administered by
an intramuscular (IM) route, an intravenous (IV) route,
or by an endotracheal route. Atropine administered by
IV to animals hypoxic from nerve agent poisoning has
caused ventricular fibrillation, so good advice is not to
administer it by this route until ventilation has begun.

The oxime, 2-PAMCl, attacks the complex of the
agent bound to the enzyme and removes the agent
from the enzyme. As a result, the enzyme can resume
its normal function of destroying the neurotransmit-
ter. Despite the fact that this drug sounds like a very
effective antidote, it does not reverse the effects seen
clinically in the glands and smooth muscle. It does re-
duce the skeletal muscle twitching and weakness. It is
almost totally ineffective when used against poisoning
from one nerve agent, soman (GD), but it is unlikely
that identification of the agent will be made before the
initial therapy, and use of the oxime in the usual doses
will do no harm.
The initial dose of 2-PAMCl is 1 gram given slowly
(over 20 minutes or longer) in an IV drip. More rapid
administration will cause hypertension (which can tran-
siently be reversed by phentolamine). The 2-PAMCl
should not be titrated with the victim’s condition as
atropine is, but it should be administered at hourly in-
tervals for a total of three doses.
A third drug, diazepam (Valium) or a similar benzo-
diazepine anticonvulsant, should be used for any convul-
sions and as rapidly as possible.
The military originally had an autoinjector device
called the MARK I with two spring-powered injectors,
one containing atropine (2 mg) and the other 2-PAMCl
(600 mg) (CP FIGURE 8-4). The latest iteration of this
countermeasure is a single unit autoinjector with two
chambers called the “antidote treatment—nerve agent,
autoinjector” (ATNAA). The ATNAA provides atropine
injection and pralidoxime chloride injection in separate
chambers as sterile, pyrogen-free solutions for intramus-
cular injection. The ATNAA is a specially designed unit

for automatic self-administration or buddy administra-
tion by military personnel. When activated, the ATNAA
sequentially administers atropine and pralidoxime chlo-
ride through a single needle. There is a civilian version of
the ATNAA that is called the DuoDote, manufactured by
Meridian Medical Technologies, which is intended as an
initial treatment of the symptoms of organophosphorus
insecticide or nerve agent poisonings (CP FIGURE 8-5).
The autoinjector is a very effective and fast way to
administer the antidotes, and use of this causes the drugs
to be absorbed faster. Instructional material for both
the ATNAA and DuoDote can be found in the reference
section of this text.
When treating an unconscious victim severely af-
fected by nerve agent poisoning, gasping for air or not
breathing, seizing or postictal, the responder should take
care of the airway, breathing, and circulation first. When
an airway is inserted and ventilation is attempted in a
severe nerve agent victim, the airway resistance will be
so great that most devices used for ventilation will not be
effective, making ventilation impossible. It might be best
to IM administer the antidotes first. This ensures that
some air will be moved when ventilation is attempted.
A victim might be exposed to vapor only and be out
of the vapor environment and be walking and talking
when first seen. This victim might be relatively asymp-
tomatic or may be very uncomfortable from shortness of
breath but generally is in no danger of loss of life. There
may be miosis with red, watery eyes, rhinorrhea, a head-
ache or eye pain, nausea and vomiting, and shortness of
breath with auscultatory sounds of airway constriction
and secretions. Atropine (2 mg, IM or IV) will reduce or
eliminate the shortness of breath and most of the rhinor-

rhea, but not the eye effects (miosis, pain) or the nausea
and vomiting. The responder should start 2-PAMCl (1
gram, slow IV drip).
Initial Antidote Use
Vapor Exposure
• Miosis and/or runny nose—no antidotes unless
eye pain is severe (eye drops)
• Shortness of breath—2 or 4 mg of atropine de-
pending on severity; 2-PAMCl by slow drip
• Unconscious, convulsions, severe breathing
difficulty; moderate to severe effects in two or
more systems—6 mg of atropine IM; 2-PAMCl
by slow drip; ventilation
Liquid on Skin
• Local sweating, fasciculations—2 mg of atro-
pine; 2-PAMCl by slow drip
• Vomiting, diarrhea—2 mg of atropine;
2-PAMCl by slow drip
• Unconscious, convulsing, severe breathing
difficulty; moderate to severe effects in two or
more systems—6 mg of atropine IM; 2-PAMCl
by slow drip; ventilation
In all cases, follow with 2 mg of atropine every 5 to
10 minutes until improvement occurs using the amount
of wheezing (bronchospasm) as an indicator of when to
administer subsequent doses.

Systemic atropine (IM, IV, and endotracheally) has
almost no effect on the eyes unless large amounts are
administered. If eye pain/headache or nausea and vomit-
ing are severe, these are relieved by topical application
of atropine or homatropine eye ointment. These medi-
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cations will cause severe blurring of vision for about 24
hours, and it is best not to administer them unless the
pain or vomiting is severe. The slight reduction in vision
(dimness, slight blurring) caused by the agent is less
than that caused by the medications. Miosis by itself
(without pain or nausea) should not be treated.
If dyspnea is more than moderate and if the victim
is still capable of walking and talking, the initial dose of
atropine should be 4 mg. Whether the initial amount is
2 mg or 4 mg, an additional 2 mg should be adminis-
tered in 5 to 10 minutes if there is no improvement in
the victim’s condition. More should be given at similar
intervals if necessary, but in most instances the initial 2
mg will reduce the symptoms.
A more severely affected victim will be unable to
walk or talk. He will be unconsciousness with severe
breathing difficulties or not breathing, perhaps convuls-
ing or postictal with copious secretions and muscular
twitching. A severely affected victim may also be one
who has moderate or severe signs in two or more organ
systems (respiratory, gastrointestinal, muscular, and
central nervous systems). The eyes and nose are not
considered in this evaluation. This victim should ini-
tially be given 6 mg of atropine (IM, not IV), and an IV
drip containing 1 gram of the oxime should be started.
Ventilation begins after the antidotes are administered.
Diazepam or a similar anticonvulsant should be admin-
istered. Atropine should be continued at 5- to 10-minute
intervals until there is improvement.
A small liquid droplet on the skin will cause sweat-

ing and fasciculation at the site, and if this is noted, the
victim should receive atropine (2 mg, IM) and 2-PAMCl
(1 gram in a slow IV drip). A slightly larger droplet
initially will cause gastrointestinal effects (nausea,
vomiting, diarrhea, cramps), and a victim with these
symptoms should receive the same drugs in the same
amounts. A victim with either the small droplet or the
larger droplet might worsen, and atropine should be
continued at intervals. The onset of these effects may
be as long as 18 hours after contact with the agent. Any
victim suspected of contacting a liquid agent should be
kept under observation for 18 hours.
A large, lethal-sized droplet of agent will cause sud-
den loss of consciousness followed by seizures, cessation
of breathing, flaccid paralysis, and death. These effects
begin within 30 minutes of contact with the agent, and
there are usually no preliminary effects before the loss
of consciousness. Management is the same as for severe
vapor exposure, with early decontamination if therapy
is to be successful.
You can save a victim with a heartbeat by timely
and adequate therapy. Occasionally an arrested victim
can also be saved. One victim from the Tokyo subway
incident had no heartbeat when he was taken into the
hospital, but he was adequately treated. He walked out
of the hospital several days later.
Cyanide
Cyanide, like the nerve agents, can cause serious illness
and death within minutes. Cyanide was not successful
as a warfare agent in World War I for several reasons,
including: (1) it is volatile and tended to evaporate and

be blown away by a breeze; (2) it is lighter than air and
will not stay close to the ground where it can do dam-
age; and (3) the dose to cause effects is relatively large,
and, unlike other agents, it causes few effects at lower
doses.
Some forms of cyanide are gases under temperate
conditions (hydrogen cyanide, cyanogen chloride), and
other forms are solids (sodium, potassium, or calcium
cyanide). Hundreds of thousands of tons of cyanide are
manufactured, shipped, and used worldwide annually.
It is used in the manufacture of certain synthetic prod-
ucts, paper, and textiles; in tanning; in ore extraction; in
cleaning jewelry; in printing; and in photography. It is
in the seeds of some foods and is in the cassava plant—a
staple in certain parts of the world. It is produced when
synthetic materials (e.g., plastics) burn. Cyanide has
been associated with killing. For centuries it has been
used for assassinations and is used in the gas chamber for
executions. People sometimes ingest cyanide with sui-
cidal intent. It was taken by the followers of the Reverend
Jim Jones for suicide and was illicitly placed in Tylenol
bottles in the Chicago area years ago.
The human body has a means of detoxifying or
neutralizing small amounts of cyanide, and this is very
effective until the system is overwhelmed. The body
combines cyanide with a form of sulfur, and the nontoxic
product is excreted. When the body runs out of sulfur,
effects appear.
Cyanide causes biological effects by combining with
an enzyme that is in cells, and stopping or inhibiting
its activity. This enzyme normally metabolizes oxygen
in the cell so that the cell can function. When cyanide
stops the activity of this enzyme, the cell cannot func-

tion and dies. There is plenty of oxygen available in the
blood, but the cell cannot use it so it does not take it
from the blood.
The effects of exposure to a small concentration of
vapor or the initial effects from drinking cyanide are
relatively nonspecific. They include a brief period of
rapid onset, gasping respiration, tachycardia, anxiety,
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altered mental status, seizures, hypotension, dysrhyth-
mias, chest palpations/tightness, tachypnea, diaphoresis,
low pulse oximetry even with presence of oxygen, skin
pale to slightly reddish color, deep breathing, feelings of
anxiety or apprehension, agitation, dizziness, a feeling of
weakness, nausea with or without vomiting, and muscu-
lar trembling. As more cyanide is absorbed, conscious-
ness is lost, respiration decreases in rate and frequency,
and seizures, cessation of breathing, and disturbances in
heart rate and rhythm follow. After inhalation of a high
concentration of vapor, seizures can occur within 30
seconds, and cessation of breathing and disturbances of
cardiac rhythm follow. Death occurs in 6 to 10 minutes
after exposure.
Large Amount by Inhalation
Hyperventilation: 15 seconds
Convulsions: 30 seconds
Cessation of breathing: 3–5 minutes
Cessation of heartbeat: 6–10 minutes
Management
Hydroxocobalamin 5g IV
or
Amyl nitrite pearl
Sodium nitrite IV (10 mL; 300 mg)
Sodium thiosulfate IV (50 mL; 12.5 g)
and

Ventilation with oxygen
Correction of acidosis
Cyanogen chloride causes the effects of cyanide as
listed previously. However, it is very irritating (similar to
the riot control agents) and will produce burning of the
eyes, the nose, and airways. It has a pungent odor.
There are few findings on physical examination. The
skin is said to be cherry red (because of the red, oxygen-
ated venous blood), but this is not always present. The
pupils are normal in size or slightly large, secretions are
relatively normal, and there are no muscular fascicula-
tions, all of which serve to distinguish cyanide poisoning
from nerve agent poisoning.
In the laboratory, cyanide can be measured in blood.
Also, there will be more than the normal amount of
oxygen in venous blood, and there may be a metabolic
acidosis. Management consists of removing the victim
from the contaminated atmosphere (or by removing the
poison from the victim), and administering antidotes
and oxygen.
Hydroxocobalamin
Hydroxocobalamin, a vitamin B12 precursor, is now
available in multiple countries as an antidote for cyanide
poisoning. In 2006, it was approved by the U.S. Food
and Drug Administration. Hydroxocobalamin com-
plexes cyanide, forming cyanocobalamin (vitamin B12).
One molecule of hydroxocobalamin binds one molecule
of cyanide. The U.S.-approved adult starting dose is 5 g
administered by IV infusion over 15 minutes. Depending
upon the severity of the poisoning and the clinical re-

sponse, a second dose of 5 g may be administered by IV
infusion for a total dose of 10 g. Hydroxocobalamin has
few adverse effects, which include allergic reaction and
a transient reddish discoloration of the skin, mucous
membranes, and urine. No hemodynamic adverse ef-
fects other than a potential mild transient rise of blood
pressure are observed.
The Cyanide Antidote Kit
The cyanide antidote kit (CP FIGURE 8-6) contains the fol-
lowing three components: (1) amyl nitrite; (2) sodium
nitrite; and (3) sodium thiosulfate. Amyl nitrite is avail-
able in a pearl. This should be broken and placed in
a breathing bag for the victim to inhale. Instructions
state that this should be held under the victim’s nose for
him or her to breathe. Sodium nitrite is packaged in an
ampule containing 300 mg in 10 mL for IV administra-
tion. Amyl nitrite should be used only until the sodium
nitrite can be administered by IV. The third component
is a sulfur compound, sodium thiosulfate. When this
is administered, the body can resume the normal pro-
cess of tying up cyanide with sulfur to form a nontoxic
substance. An ampule contains 12.5 g in 50 mL for IV
administration. These three antidotes should be given
sequentially to a victim who is unconscious and/or not
breathing. Oxygen should be administered, even though
the oxygen content of blood is normal. The acidosis
should be corrected.
Vesicants
Vesicants are agents that cause vesicles or blisters. They
may be of animal, vegetable, or mineral origin, such
as some types of sea creatures, poison ivy, and certain
chemicals. Other things, such as sunlight, can produce

blisters. Vesicants have been used as chemical warfare
agents. Several have been developed for this purpose, but
only one—sulfur mustard (CP FIGURE 8-7)—has been used.
The other major chemical warfare vesicant is lewisite.
Cyanide antidotes are: hydroxocobalamin or amyl ni-
trites, sodium nitrite, and thiosulfate.
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Sulfur mustard was first synthesized in the early
1800s and was first used on the battlefield in World War
I. During that war it caused more chemical casualties
than any other agent; however, only about 3 percent of
these casualties died. Iraq used it extensively during its
war with Iran, and pictures of some casualties were in
the media during that period. Its use has been alleged
in some other conflicts over the past 80 years.
In the early 1940s, nitrogen mustard (developed
for military use), a close relative of sulfur mustard, was
used in the treatment of cancer, the first chemical to be
used for that purpose.
Sulfur mustard (mustard) is a light yellowish to
brown oily liquid that smells like garlic, onions, or mus-
tard (the reason for its name). Its boiling point is over
200°F, and it freezes at 58°F. The low freezing point
hinders its battlefield use in cool weather, and it is often
mixed with another chemical to lower the freezing point.
It does not evaporate very quickly, but large amounts
of mustard, particularly in warm weather, produce a
vapor hazard.
Mustard causes cellular damage and death with sub-
sequent tissue damage. The mechanism by which it does
this has not been entirely clear, but the best evidence
suggests that it damages DNA, which then prevents
further cellular functioning and leads to cellular death.
Although its best-known effects are those on the tissues,
the agent directly contacts the skin, the eyes, and the

airways. When it is absorbed into the body in adequate
amounts, mustard damages many tissues such as bone
marrow, lymphoid tissue, and the gastrointestinal tract.
Its effects are similar to those caused by radiation, and
it is a radiomimetic agent.
Once liquid or vapor mustard is in contact with
an epithelial surface, the skin, the eye, or the mucosa
of the airways, it penetrates that surface quite rapidly,
and enough is absorbed within a minute to cause cel-
lular damage. Decontamination after a minute will not
prevent tissue damage, but it will reduce the amount of
ensuing damage. Once into tissue, the chemical reactions
within the cell that eventually result in clinical effects
begin. Once mustard touches a body surface, irreversible
damage is done in cells within minutes.
Upon contact with the skin, the eyes, or the airways,
mustard causes no immediate clinical effects. There is no
immediate pain, redness, or blister formation. The victim
usually does not know he or she has been exposed. The
itching and pain of erythema, the irritation of the con-
junctiva, or the irritation and discomfort in the upper
airways do not appear until many hours later. The period
without signs or symptoms is called the latent period,
and it can range from 2 to 24 hours after contact. Com-
monly these effects begin in 4 to 8 hours after contact.
At the site of an incident or spill involving mus-
tard, there will be no victims with signs and symptoms
of mustard exposure. Hours later, the pain, irritation,
and discomfort will start, and the victims will seek
medical care.
The initial effects in the eyes after exposure to mus-

tard vapor are irritation or burning, and the victim will
complain of grittiness in his eyes. The eyes will be red,
similar to the appearance of eyes with sand or dust in
them. This may progress to a severe conjunctivitis,
swelling of the lids, and even corneal edema (seen as
an irregular light pattern on the cornea). The victim
will complain of pain, irritation, and sensitivity to light.
He may also complain of inability to see. This is usu-
ally because the lids are shut, either because of swelling
or because of involuntary contracture of the muscles
around the eye. Rarely, a droplet of mustard will get into
the eyes, and this may cause more severe damage to the
cornea, including ulceration and perforation.
Mustard contact with skin will initially cause redness,
or erythema, which is similar to sunburn with burning
and itching. If the contact was to a low concentration
of vapor, this may be the extent of the injury, but more
commonly small blisters develop around the edges of the
redness. These gradually coalesce to form larger blisters,
which are generally no worse than second degree burns.
Third degree burns are very uncommon and require
exposure to a large amount of liquid agent.
Mustard vapor, when inhaled, damages the mucosa
or inner layer of the airways. The damage begins at the
upper part of the airways (the nose) and descends to
the lowermost portion, the terminal bronchioles. The
amount of damage depends on the amount of mustard
inhaled, which, in turn, depends on the concentration
of the vapor and exposure time. The initial effects
are in the nose and sinuses with burning, irritation,
and perhaps some nasal bleeding. Pharyngitis, with a
sore throat and a nonproductive cough, may appear,
followed by laryngitis with hoarseness or complete
lack of voice. Mustard damage in the lower airways

causes shortness of breath and a cough productive of
inflammatory and necrotic material as the agent de-
stroys the inner lining of these small airways. Severe
damage provides an ideal setting for infection 4 or 5
days later.
Vesicants cause vesicles or blisters.
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Initial Effects
There are no immediate effects of contact with sulfur
mustard; effects start potentially hours after contact.
Skin
• Redness (erythema) with burning and itching
• Blisters
Eye
• Redness with burning and itching
Airways
• Nasal and sinus pain
• Sore throat, nonproductive cough
Large amounts of absorbed mustard severely damage
the precursor cells in the bone marrow, with a decrease
in the white cells, red cells, and platelets in the blood.
This usually happens four or more days after exposure
in a severely exposed victim. The lining of the gastroin-
testinal tract is also severely damaged after absorption of
a large amount of mustard with subsequent loss of fluid
and electrolytes starting days after exposure. This effect
is similar to that seen after radiation exposure.
Immediate decontamination—within a minute—
should be performed to minimize the damage, but re-
sponders will not be on the scene that quickly. Skin

damage will be reduced by decontamination of the con-
tact site on the skin if done within 30 minutes, but not
beyond that time.
A victim returning hours after the incident with
red skin (erythema) needs no immediate care, although
soothing lotions (e.g., calamine) can be applied to re-
duce the burning and itching. Later, areas of blistering
or denuded skin must be irrigated frequently, with the
application of topical antibiotics three or four times a
day to these areas. Fluids do not need to be replaced in
large amounts as they do after thermal burns, because
mustard burns do not cause the amount of fluid loss seen
in thermal burns. Care must be taken not to overhydrate
victims. They will not need significant fluid replacement
unless they are dehydrated from other causes.
A victim with red eyes (conjunctivitis) who is com-
plaining of burning or irritation in the eyes should have
his or her eyes washed out and a soothing ophthalmic
ointment or drops applied. Because the lesion appears
hours after contact with the agent, the agent is no longer
in the eye because of absorption and evaporation, and
the purpose of eye irrigation is to wash out inflammatory
debris. Later eye care consists of regular application of a
topical antibiotic and a mydriatic (to prevent future ad-
hesions between lens and iris). Petroleum jelly should be
applied regularly to the edges of the lids (to prevent ad-
hesions). Some believe that topical steroids used within
the first 24 hours only will reduce inflammation, but
application should be done by an ophthalmologist.
A suggestion of airway involvement by the agent,
such as nasal or sinus irritation or a sore throat with a
dry hacking cough, may occur. Laryngeal damage with

voice changes or hoarseness accompanied by signs of
beginning lower airway damage is an indication for the
immediate insertion of an endotracheal tube. Later, more
severe damage will necessitate assisted ventilation in-
cluding positive end-expiratory pressure and frequent
sputum examinations for infecting organisms.
Bone marrow depression and severe gastrointestinal
damage occur days after the initial exposure in an already
severely ill victim.
All victims must be decontaminated before they
enter a medical facility. When signs and symptoms
appear hours after the initial agent contact, the agent
will be gone from exposed surfaces by evaporation or
by absorption. Later decontamination will not prevent
further injury to the victim. However, liquid may be in
clothing or the agent (liquid or condensed vapor) may
be in hair.
Lewisite
Lewisite was developed late in World War I but was not
used in that war. Japan possibly used it against China
in the late 1930s; otherwise it has not been used on the
battlefield. Some countries are known to have military
stockpiles of lewisite.
Lewisite is an oily liquid with the odor of gerani-
ums. Its freezing point is below 0°F, it boils at 190°F, it
contains arsenic, a heavy metal, and it is more volatile
than mustard.
Lewisite participates in many biological reactions,
but the mechanism of cellular injury is unknown. It
damages cells causing cellular death, and its biological

effects are similar to those of mustard with topical dam-
age to eyes, skin, and airways (CP FIGURE 8-8). It does not
damage marrow, the gastrointestinal tract, or lymphoid
tissue, but it does damage systemic capillaries allowing
leakage of intravascular volume. This can culminate in
hypovolemic shock in severe cases.
An important initial clinical distinction between
lewisite and mustard is that lewisite vapor causes imme-
diate irritation of eyes, skin, and upper airways. Lewisite
Immediate decontamination is very important with
mustard exposure.
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liquid causes pain or burning on whatever surface it con-
tacts within seconds. The victim is alerted to its presence
and will leave the area or remove the liquid. Mustard
causes no clinical effects until the lesions develop, hours
after contact.
Lewisite causes topical damage to eyes (conjunc-
tivitis and more severe damage), skin (erythema and
blisters), and airways (damage to the lining or mucosa)
similar to that of mustard. Severe lewisite exposure may
cause pulmonary edema, which is very uncommon after
mustard exposure. Generally, the lesions from lewisite
are deeper with more tissue damage than those from
mustard.
Management of a victim with lewisite exposure is
similar to the management of a victim with mustard
exposure. The victim will usually self-decontaminate
quickly because of the pain or irritation. In addition to
the measures recommended for mustard lesions, there
is a specific antidote for the systematic (nontopical) ef-
fects of lewisite. This is British antilewisite, a drug used
for several other types of heavy metal poisoning, and is
for hospital use only.

Pulmonary Agents
Pulmonary agents are chemicals that produce pul-
monary edema (fluid in the lung), with little damage
to the airways or other tissues. The best known and
most studied of these is phosgene (carbonyl chloride),
although other chemicals (e.g., chlorine) behave in this
manner.
Phosgene and chlorine were major agents in World
War I until the use of mustard. Their usefulness as war-
fare agents has diminished since then, and now they are
not considered important militarily. However, both are
important in industry, and large amounts of both are
manufactured and shipped annually.
After inhalation of phosgene, the carbonyl part of
the molecule causes damage in the thin wall between the
blood vessels (capillaries) and the air sac (alveolus). As a
result of this damage, the watery part of the blood leaks
into the alveoli. When these become filled with fluid,
air cannot enter to deliver oxygen to the blood, oxygen
cannot be delivered to other tissues, and the victim suf-
focates in a sense. This fluid in the lungs is similar to
that seen in drowning. Damage by these agents is some-
times called “dry-land drowning.” Another name for this
is noncardiac pulmonary edema, which is pulmonary
edema (fluid in the lung tissue) caused by something
other than heart failure.
A high concentration of phosgene causes an immedi-
ate irritation in the eyes, nose, and upper airways. This
is usually transient and is followed later by pulmonary
edema. An extremely high concentration will cause la-
ryngeal edema and death within a short period of time,

but this is very uncommon. The usual circumstance is
that the victim inhales phosgene without immediate ef-
fects. Anywhere from 2 to 24 hours later, the victim
begins to become short of breath. Initially, he or she
notices the shortness of breath only with walking or
other exertion, but as time passes, it is present at rest.
A cough brings up clear, frothy sputum—the fluid that
leaked into the lungs. If the symptoms begin late, after
6 or 8 hours, the damage is usually not severe enough to
cause death, but if the effects begin early, from an hour to
6 hours after exposure, the lung damage is often severe
enough to cause death despite medical care.
Initial Effects
Initial effects of pulmonary agents include the following:
• Shortness of breath with exertion, later at rest
• Cough, later with production of frothy sputum
A responder at the site may see few symptomatic
victims, except possibly some with irritation of the eyes
and upper airways or some exposed to extremely high
concentrations who will soon have laryngeal edema.
Most casualties will be minimally symptomatic, and the
tendency might be to discharge them from care. This
could well be a mistake. Symptoms can start suddenly,
and if they begin within the first several hours, death
may occur within the next several hours. Anyone who
has been exposed to one of these agents must be kept
under medical observation for at least 6 hours.
A victim exposed to a pulmonary agent will have two
major problems for hospital management. The first is
the fluid in the lungs (pulmonary edema) with resulting
lack of oxygen (hypoxemia). The second is loss of fluid
from the intravascular space (hypovolemia), which may

lead to hypotension, shock, and organ damage.
Initial management of victims is twofold. The first
and hardest thing to remember is that anyone possibly
exposed to one of these agents should be kept at abso-
lute rest with absolutely no exertion. The victim must
be carried, not walked, to the ambulance. It is hard to
tell a healthy person at the site of a spill or incident who
has no symptoms that he or she cannot walk, but it must
be done. World War I experience with these casualties
Lewisite causes eye and upper airway irritation and
pain on contact.
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Response
shows that a victim breathing comfortably in bed might
collapse and die if allowed to walk down the hall to the
bathroom.
The second and more obvious part of managing a
pulmonary agent victim is to provide oxygen to anyone
who is short of breath. This usually will not happen
while the responder is on the scene initially, but may
happen when the responder provides transport later.
Riot Control Agents
Most people are familiar with riot control agents,
otherwise known as tear gas or irritants. Three are in
common use in this country. CS (or 2-chlorobenzal-
malononitrile—also called o-chlorobenzylidene ma-
lononitrile) is used by law enforcement agencies and
the military; phenacyl chloride—also called Mace—was
used in World War I and is now in small spray devices
carried for self-protection; and pepper spray, which is
replacing the others for both law enforcement and mili-
tary use and for self-protection.
Unlike other agents that are liquids, these are solids.
The powdery particles are suspended in liquids when

they are in spray devices. These agents have much in
common. Their effects begin within seconds of contact,
the effects last only a few minutes after the person is in
fresh air, they are effective in small concentrations, and
the lethal concentration is thousands of times higher
than the effective concentration, which means that ac-
cidentally producing an overdose is very unlikely.
These agents cause irritation, pain, or burning on
surfaces they contact, including the eyes, the nose, the
mouth and airways, and the skin. Eye effects include
burning, tearing, redness, and an initial involuntary
temporary closing of the eyes (blepharospasm). While
the eyes are closed, the victim cannot see and might be
considered incapacitated. The interior of the nose burns,
and there are secretions from the nose. There are secre-
tions from the mouth, and the interior of the mouth
burns. If the agent is inhaled, there will be coughing
and perhaps a feeling of shortness of breath. There is an
initial burning or tingling on the skin accompanied by a
mild redness. Sometimes a high concentration will cause
retching or gagging. The effects will gradually recede in
15 to 30 minutes after exposure has ceased.
There are potential complications that seem to be
rare. If the face is close to the agent when it is dispersed
with force (e.g., a spray device), the force may drive the
particles into the eye. This necessitates flushing with
copious amounts of water or manual removal of the
particle by an ophthalmologist. The agent might pre-
cipitate a severe reaction in a person with chronic lung
disease (chronic obstructive pulmonary disease, asthma,
etc.) including hyperactive airways. The use of oxygen,
assisted ventilation, and bronchodilators might be in-
dicated. A person exposed to a high concentration in a
hot and humid environment might develop a delayed

dermatitis beginning about 6 hours after contact, with
erythema developing into blisters.
People can develop tolerance to these agents. With
continued exposure, the effects lessen and the exposed
people can open their eyes and function relatively
normally.
Triage
Triage is an ongoing process that begins with the first
person to see the victim and continues through hospi-
tal management. The responder will triage at several
places, including in the hot zone, in the cold zone after
the victim has been decontaminated, and possibly in
between. In the hot zone, the responder is encumbered
with protective clothing and victim examination is not
ideal. The following triage categories are generally used:
immediate, delayed, and minimal.
An immediate victim is one who is in danger of loss
of life unless there is intervention within a short period
of time. Intervention generally has to do with airway,
breathing, and circulation (the ABCs), and to this the
administration of antidotes should be added. A delayed
victim is one who can wait for intervention, and this
wait will not affect the outcome of care. The victim is
stable but will require further care. A minimal victim is
one who requires care for a relatively minor injury. The
care can be done quickly, the injury is not life threat-
ening, and the victim is unlikely to require long-term
care (i.e., hospitalization). An expectant victim is one
who cannot be saved with the resources available or
resources cannot be made available within the time the
victim needs them.

Treatment for exposure to pulmonary agents is oxygen
and immediate rest (no exertion).
Effective triage of chemically exposed victims is crucial
in mass victim events.
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Nerve Agents
An immediate victim is one who (1) is unconscious,
is apneic or struggling to breathe, is convulsing or has
convulsed, and has muscular twitching or is flaccid; or
(2) has moderate or severe signs in two or more organ
systems (respiratory, gastrointestinal, muscular, and
central nervous system). This victim should be given 6
mg of atropine—IM, not IV—and a 20- to 30-minute
drip of 1 g of 2-PAMCl.
A delayed victim is one who is recovering from mod-
erate or severe effects or from the effects of several doses
of antidote.
A minimal victim is one who is walking and talking.
That person may be severely short of breath or vomiting,
but still has muscle strength and control and can under-
stand the spoken word enough to respond. Generally,
this victim should be given 2 mg of atropine with a drip
of 2-PAMCl. If the victim is extremely short of breath,
4 mg of atropine should be administered. Despite the
shortness of breath, this victim is not immediate.
An expectant victim is one who is not breathing and
is without a heartbeat. However, if he or she has been
without cardiac activity for a very brief period of time,
every attempt should be made to resuscitate the victim.
Cyanide
Cyanide victims can die within minutes after inhaling a
large concentration of the agent. Those who are uncon-
scious and not breathing but who still have a heartbeat
should be classified as immediate, and the antidotes

should be given as soon as possible. If a victim is con-
scious, he or she will be minimal and will not need anti-
dotes. An expectant victim is one who has been without
a heartbeat for many minutes.
Vesicants
Almost all vesicant victims will be delayed. They will
need no immediate care, but they will need further care
for their eye, skin, or airway injuries. An exception is a
victim with moderate to severe airway effects including
shortness of breath. He or she is immediate and needs
intensive pulmonary care.
Pulmonary Agents
Although shortness of breath, the major symptom from
these agents, can be faked, anyone complaining of short-
ness of breath within 6 hours of exposure should be
classified as immediate for intensive pulmonary care. A
victim with shortness of breath beginning later than 6
hours postexposure will also need care and monitoring.
A victim with severe shortness of breath and copious
frothy sputum within an hour after exposure is expect-
ant, although an attempt should be made to provide
maximum care.
Riot Control Agents
Victims of riot control agents will be usually classified
as minimal with the exception of a victim who has a se-
vere airway reaction to these agents or a polypharmacy
scenario where underlying conditions are exacerbated
and possibly require immediate care.
Early Recognition
When first responders in protective gear first enter the
hot zone, they usually will not know what the toxic agent

is and usually will not have a detector to tell them. They
must quickly evaluate the victims based on what is seen
and heard and take appropriate action. Early therapeutic
intervention is needed for only two types of agents—nerve
agents and cyanide. A victim exposed to a large concentra-
tion of a pulmonary agent may be in severe respiratory
distress, but there is nothing that can be done in the hot
zone; if the effects started before the responder arrived,
probably nothing can be done elsewhere.
In most chemical mass casualty situations, the vic-
tims will exhibit a spectrum of effects. Some victims’
conditions will be quite severe, and others will have
minor effects, and the responder must quickly evaluate
this spectrum. For example, if some victims are convuls-
ing or are unconscious and appear to be postictal, the
responder should look at other victims. The presence
of miosis, runny noses, and shortness of breath or any
one or two of these strongly suggests that nerve agents
were the offending substance. If the conscious victims
are relatively normal with a few nonspecific complaints,
cyanide should be considered. If all victims are conscious
with no complaints, the responder should consider that
(1) no chemical agent was present, or it was present in
concentrations too low to produce effects, or (2) the
agent was one that produces delayed effects only, such
as mustard or the pulmonary agents.
If many victims are complaining of irritation or
burning in the eyes and nose, on the mucous membranes
of the mouth, and on the skin, one might consider the
following:
1. Riot control agents (in which case the victims will
improve with fresh air)

2. Phosgene (the effects will improve, but there will
be later, more severe ones)
3. Cyanogen chloride (the irritation will gradually
decrease, and if the victim is conscious when help
arrives it is unlikely that a lethal concentration
was present)
4. Lewisite (the effects will worsen)
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Response
Refer to TABLE 8-1 for a summary of signs, symptoms,
and decontamination procedures for chemical agents.
Chapter Summary
Chemical agents are not new, and terrorist organizations
have access to these substances as demonstrated by the
use of sarin in a Tokyo subway attack in 1995. Many
industrial chemicals such as chlorine, cyanide, phosgene,
and pesticides are readily available in large quantities.
It is essential that response agencies be prepared
for a chemical attack. Effective planning must include
protective equipment, decontamination procedures, and
antidotes. A deliberate incident is a crime scene, usually
with mass numbers of victims.
Nerve agents are toxic materials that produce injury
or death in seconds to minutes. Nerve agents are similar
to insecticides but are more toxic.
Very good antidotes are available for nerve agents,
but they must be administered quickly. Common nerve
agents include tabun (GA), sarin (GB), soman (GD), and
GF and VX. Effects from nerve agents show very quickly.
Management of nerve agent exposure consists of decon-
tamination, administration of antidotes, and ventilation.
The antidotes for nerve agent poisoning are atropine

and an oxime, PAMCl (Protopam). Atropine blocks the
excess neurotransmitters. PAMC1 removes the nerve
agent from enzymes, allowing the enzymes to block the
neurotransmitters. Benzodiazepines (i.e., diazepam) can
be used as anticonvulsants.
Cyanide can cause serious illness and death within
minutes. Cyanide affects the ability of the cells to me-
tabolize oxygen. Treatment of cyanide poisoning can in-
clude hydroxocobalamin or using the cynanide antidote
kit (amyl nitrite pearl or sodium nitrite IV and sodium
thiosulfate IV). Victims should be ventilated with oxygen
and acidosis should be corrected.
Vesicants are agents that cause vesicles or blisters.
The most common vesicant agents are sulfur mustard
and lewisite. Mustard does not cause an immediate ef-
fect; the common latent period is 4 to 8 hours after
contact. Inhaled vapor causes damage to the airway and
bronchioles. Victims must be decontaminated immedi-
ately and the eyes irrigated.
Lewisite produces instant effect on contact. The
symptoms include immediate pain, eye damage, and
airway injury.
Pulmonary agents produce pulmonary edema. The
best-known agents are phosgene and chlorine. The ef-
fects of these agents are not immediate, but shortness
of breath followed by pulmonary edema follows hours
after exposure. Exposed victims with no symptoms must
be kept under medical observation for at least 6 hours.
Initial victim treatment includes keeping the victim at
rest and administering oxygen.

Riot control agents are known as tear gas and ir-
ritants. They include tear gas, Mace, and pepper spray.
Effects begin in seconds but last only a few minutes
after the victim is removed to fresh air. These agents
cause pain, burning, and irritation to the contact body
surfaces. The use of oxygen is indicated.
Triage is an ongoing process in a chemical exposure
incident. The triage categories are immediate (critical),
delayed, and minimal (walking wounded). A critical
victim is one who is unconscious, apneic, or convuls-
ing. Almost all vesicant victims will be delayed. Most
riot control victims will be in the minimal or walking
wounded category.
Early responders must quickly evaluate the scene.
Rapid therapeutic intervention is needed only for nerve
agents and cyanide. If a victim shows severe pulmonary
distress from a pulmonary agent, nothing can be done
in the prehospital setting.
The use of positive pressure ventilation and albuterol
nebulizers has been shown to improve the noncardiac
pulmonary edema condition. The extent of treatment
offered by a responder is dependent upon the type of
incident, number of victims and your local treatment and
MCI protocols. The learner is encouraged to review the
guidance documents provided by local authorities.
In mass casualty incidents, victims will exhibit a
spectrum of effects. Responders must quickly don pro-
tective equipment and triage all victims to determine
treatment categories.
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TABLE 8-1 Chemical Agents: Symptoms and Treatment
Agent Signs and symptoms Decontamination
Immediate treatment/
management

Nerve agents (GA,
GB, GD, GF, VX)
Vapor: Small exposure—
Miosis, rhinorrhea, and mild
dyspnea. Large exposures—
Sudden loss of consciousness,
convulsions, apnea, flaccid
paralysis, copious secretions,
and miosis. Liquid on skin:
Small to moderate exposure—
Localized sweating, nausea,
vomiting, and feeling of weak-
ness. Large exposure—Sudden
loss of consciousness, convul-
sions, apnea, flaccid paralysis,
and copious secretions.
Large amounts of water
with a hypochlorite
solution.
Administration of atropine
and pralidoxime chloride
(2-PAMC1); diazepam in
addition if casualty is
severe; ventilation and
suction of airway for
respiratory distress.
Mustard (HD, H) Asymptomatic latent period
(hours). Erythema and
blisters on the skin, irritation,
conjunctivitis, corneal
opacity, and damage in the

eyes; mild upper respiratory
signs, marked airway damage;
also gastrointestinal effects
and bone marrow stem cell
suppression.
with a hypochlorite
solution.
Decontamination
immediately after
exposure is the only way
to prevent/limit injury/
damage. Symptomatic
management of lesions.
Lewisite (L) Lewisite causes immedi-
ate pain or irritation of skin
and mucous membranes.
Erythema and blisters on
the skin and eyes and airway
damage similar to those seen
after mustard exposure
develop later.
with a hypochlorite
solution.
Immediate decontami-
nation; symptomatic
management of lesions
the same as for mustard
lesions; a specific antidote
British antilewisite (BAL)

will decrease systemic
effects.
Phosgene oxime (CX) Immediate burning and
irritation followed by
wheal-like skin lesions and eye
and airway damage.
Large amounts of water. Immediate decontami-
nation; symptomatic
management of lesions.
Cyanide (AC, CK) Initially may have dyspnea,
weakness, and dizziness.
Skin decontamination
is usually not neces-
sary because agents
are highly volatile. Wet,
contaminated cloth-
ing should be removed
and the underlying skin
decontaminated with
water or other standard
decontaminates.
Antidote: intravenous
sodium nitrite and sodium
thiosulfate. Supportive
care: oxygen and correct
acidosis.
Pulmonary agents
(CG)
Eye and airway irritation,

dyspnea, chest tightness, and
delayed pulmonary edema.
Vapor: fresh air. Liquid:
copious water irrigation.
Termination of exposure,
ABCs of resuscitation,
enforced rest and
observation, oxygen
with or without positive
airway pressure for signs
of respiratory distress,
other supportive therapy
as needed.
(continues)
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TABLE 8-1 Chemical Agents: Symptoms and Treatment
(continued)
Agent Signs and symptoms Decontamination
Immediate treatment/
management
Riot control agents
(CS, CN)
Burning and pain on exposed
mucous membranes and
skin, eye pain and tearing,
burning nostrils, respiratory
discomfort, and tingling of the
exposed skin.
Eyes: thoroughly flush
with water, saline, or
similar substance.
Skin: flush with copious

amounts of water,
alkaline soap and
water, or a mildly
alkaline solution (sodium
bicarbonate or sodium
carbonate). Generally,
decontamination is not
required if wind is brisk.
Usually none is necessary;
effects are self-limiting.
Source: Medical management of chemical casualties handbook,
2nd ed. (1995). Aberdeen Proving Ground, MD: Chemical
Casualty Care Office, United
States Army Medical Research Institute of Chemical Defense.
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121
Wrap Up
Chapter Questions
1. Discuss several reasons why your community
should be prepared for a terrorist chemical attack.
2. What are the methods of disseminating a chemi-
cal agent?
3. Define nerve agents. How do they act on the
body?
4. List five common nerve agents.
5. What are the symptoms of nerve agent expo-
sure?
6. What is the treatment for nerve agent exposure?
Name three antidotes.
7. Discuss the symptoms of cyanide poisoning.
What are the antidotes for cyanide exposure?
8. What are vesicants? What are the signs of vesicant

exposure? What is the treatment?
9. Define lewisite. How does lewisite exposure differ
from mustard exposure?
10. What are pulmonary agents? What is the treat-
ment for severe exposure?
11. List three riot control agents. What are the symp-
toms and treatment for exposure?
12. What are the triage categories in a chemical attack
with mass victims? Describe typical symptoms of
a victim in each category.
Chapter Project
You are an EMS training officer in an organization that
has no chemical attack training program. Your goal is to
develop guidelines for first response fire units and EMS
units. Develop a written chemical response guideline
that includes the following key elements:
• Categories of chemical agents
• Symptoms at onset and long-term symptoms
• Advanced life support care for each type of
agent including antidotes
• Basic life support treatment procedures
• Safety guidelines
• Triage categories and related symptoms
Vital Vocabulary
Cyanide A toxic material, like the nerve agents, can

cause serious illness and death within minutes, but is
also volatile and lighter than air.
Hydroxocobalamin A vitamin B12 precursor that is now
available in multiple countries as an antidote for cyanide
poisoning.
Lewisite An oily liquid with the odor of geraniums that
contains arsenic and a heavy metal and is more volatile
than sulfur mustard.
Nerve agents Toxic materials that produce injury and
death within seconds to minutes.
Pulmonary agents Chemicals that produce pulmonary
edema (fluid in the lung), with little damage to the air-
ways or other tissues.
Riot control agents Solids suspended in liquids as
powdery particles; often used in spray devices and used
commonly in the United States.
Sulfur mustard (mustard) A light yellowish to brown
oily liquid that smells like garlic, onions, or mustard
and causes cellular damage and death with subsequent
tissue damage.
Vesicants Agents that cause vesicles or blisters.
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123
Weapons of Mass Effect—
Biological Terrorism
Dr. Charles Stewart
Paul M. Maniscalco
Hank T. Christen
• Define the concept of biological warfare.
• Know the history of biological warfare.
• Understand and be able to apply the concepts of biological
threat assessment.
• Define the importance of biological protective equipment.
• Outline the types of biological agents including the chemical
effects, detection, and prophylaxis/treat-

ment of botulinum toxins, Clostridium toxins, ricin, saxitoxin,
staphylococcal enterotoxin, tetrodotoxin,
and trochothecene mycotoxins.
Objectives
9
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Response
Introduction
The uses of biological substances as weapons pose a
unique problem for the emergency response and pub-
lic health communities. Unlike the consequences of a
chemical attack or an explosion, which are essentially
readily identifiable, in-your-face events, biological ter-
rorism creates a slow-motion riot that builds with each
hour after the event. The inability to quickly and im-
mediately identify what has occurred allows the threat
maturation process to continue while increasing the risk
to a vulnerable population.
Biological terrorism is the use of etiological agents
(disease) to cause harm or kill a population, food, and/or
livestock. Biological terrorism includes the use of organ-
isms such as bacteria, viruses, and the use of products
of organisms—toxins.
Biological terrorism has recently become more
threatening to the world. One only needs to consider
the current state of technology, the future possibilities
of biotechnologies, and what appears to be a readiness
on the part of some individuals/countries to utilize this
technology as a weapon.
Successful genetic engineering has arrived, and ad-
vances are being achieved almost daily. It requires a
relatively easy process and only crude technology to
manufacture a lethal organism/toxin in sufficient quan-
tities. Some are specifically designed to be resistant to

antibiotics for use as a horrible weapon. It has been
said that “if you can make beer, you can make bugs
(biological weapons).” This is an oversimplification, but
it provides a vivid picture of what a motivated person
with modern technology is capable of achieving. A recent
phenomenon has emerged with the availability of equip-
ment and the reduced costs associated with acquiring
the same; it is referred to as “garage science.” A simple
Internet search easily reveals the extent of experimen-
tation and activities that are associated with aspiring
biology hobbyists. You can find individuals hacking
DNA while others are conducting a variety of organic
experiments—all interesting—but highly illustrious of
the fact that technology can be exploited to help and hurt
if the players are nefarious. Do-it-yourself biotechnology
is now happening and encouraged by forums like DIY
Bio, Biopunk, and others.
Biological weapons (BWs) have the potential to
wreak considerable havoc and death among humans,
resulting in a medical disaster. Moreover, should BWs
be employed against livestock or vegetation, the results
would be an economic disaster.
BWs are more deadly and financially efficient,
pound for pound and dollar for dollar, than chemical
agents or even nuclear weapons. It has been estimated
that 10 grams of anthrax could kill as many people as
a metric ton of the nerve agent sarin. BWs are relatively
inexpensive and easy to manufacture, and dispersal
devices can be disguised as agricultural or pest-control
sprayers. A human carrying the disease is also a disper-
sal agent. Unfortunately for the law-abiding world, it
is very difficult, if not impossible, for an intelligence
service to detect research, production, or transporta-

tion of these agents for rogue intentions. It is equally
hard to defend against these agents once they have
been employed due to the inability to readily recognize
delivery.
History of Biological Agents as Weapons
The use of biological agents as a warfare weapon has a
long and deadly past. In fact, history has shown us that
use of BWs occurred more than 2,000 years ago. Some
examples of its employment include:
1. In the 6th century B.C., Assyrians poisoned enemy
wells with rye ergot (U.S. Army, 1996); Solon
used the purgative hellebore during the siege of
Krissa (U.S. Army).
2. Persian, Greek, and Roman authors quote the
use of animal cadavers to contaminate water
supplies. In 1155, Barbarossa used the bodies of
dead soldiers to poison the wells at the battle of
Tortona.
3. The Scythian archers would dip their arrows in
blood mixed with manure or in decomposing
cadavers.
4. The Mongols in the 1300s catapulted plague vic-
tim corpses into the city of Kaffa to infect the
defenders (U.S. Army). The besieged town was
rapidly devastated by disease.
5. British and early American settlers gave American
Indians blankets used by victims of smallpox.
The resultant infection decimated the defenseless
American Indian tribes.

6. In 1941, the Allies tested anthrax on Gruinard
Island off the shore of Scotland (Bernstein, 1987).
Starting in 1986, a determined effort was made
to decontaminate the island, with 280 tons of
formaldehyde solution diluted in seawater being
sprayed over all 520 acres (2 km²) of the island,
and the worst-contaminated topsoil around the
dispersal site being removed. A flock of sheep was
then placed on the island and remained healthy.
On April 24, 1990, after 48 years of quarantine,
junior defense minister Michael Neubert visited
the island and announced its safety by removing
the warning signs (Harrison, 2001).
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CHAPTER 9: Weapons of Mass Effect—Biological Terrorism
125
7. During World War II, the Allies administered
235,000 doses of antitoxin to Allied troops and
deliberately leaked this information to the Nazis.
Simultaneously, they told the Nazis that the Allies
were prepared to use BWs if they were employed
in the war (Mobley, 1995).
8. During World War II, on the Pacific front, the
Japanese tested BWs on prisoners of war in China,
killing more than 1,000 people. In fact, it has
been reported that the Japanese had “stockpiled
400 kilograms of anthrax to be used in specially
designed fragmentation bombs” (U.S. Army,
1996).
9. Unclassified information from Central Intelligence
Agency and Defense Intelligence Agency docu-
ments indicates that several rogue states such as
Iran, Libya, and North Korea have or are pursuing
BW programs (Horrock, 1997).
10. In September and October of 1984, followers of
the Bhagwan Sri Rajneesh contaminated restau-
rant salad bars in Oregon. More than 750 people
were intentionally infected with Salmonella.

11. In 1994, a Japanese sect of the Aum Shinrikyo
cult attempted an aerosolized release of anthrax
from the tops of buildings in Tokyo.
12. In 1995, two members of a Minnesota militia
group were convicted of possession of ricin,
which they had produced themselves for use in
retaliation against local government officials.
13. In 1996, an Ohio man attempted to obtain bu-
bonic plague cultures through the mail.
14. In 2001, anthrax was delivered by mail to U.S.
media and government offices (FIGURE 9-1A, 9-1B,
and 9-1C). There were five deaths. The first victim,
Robert Stevens, worked at American Media Inc., in
Boca Raton, Florida. Two were distribution clerks
in the Brentwood postal facility in Washington,
DC. Joseph P. Curseen, 47, died at the Southern
Maryland Hospital Center in Clinton, Maryland,
and Thomas L. Morris Jr., 55, died at the Greater
Southeast Community Hospital in Washington,
DC. Kathy Nguyen, 61, died October 31, 2001.
She was a New York hospital worker who con-
tracted inhalation anthrax. The last victim, Ottilie
Lundgren, 94, died November 21, 2001, at Griffin
Hospital in Derby, Connecticut.
In recent times, the military examined the possibil-
ity of biological actions against the United States. In
the 1950s, Serratia and Bacillus species were released
from ships in the San Francisco Bay area and caused
at least one death (Cole, 1988). In the 1960s, military
researchers introduced B. subtilis into New York City

subway ventilator shafts. Both passengers and security
guards were oblivious to the danger (Cole, 1985). The
bacteria were rapidly spread to the ends of the subway
system, successfully demonstrating the ability to exploit
that environment with these substances.
The U.S. Office of Technology Assessment has
estimated that a small private plane with 220 pounds
of anthrax spores, flying over Washington, DC, on a
FIGURE 9-1A Anthrax letter sent to Tom Brokaw.
FIGURE 9-1B Anthrax letter sent to Senator Tom Daschle.
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windless night, could kill between 1 and 3 million peo-
ple and render the city uninhabitable for years.
Other countries are certainly continuing to develop
biowarfare capabilities. The Soviets and their allies em-
ployed a trichothecene mycotoxin dubbed “yellow rain”
in Laos, Cambodia, and Afghanistan, and the former
USSR and Iraq have independently developed anthrax
species. In 1979, an outbreak of inhalational anthrax oc-
curred in Sverdlovsk, Russia. This outbreak resulted from
an accident at a Soviet biowarfare research facility.
Treaties
The Geneva Convention (1925) prohibited the use
of biological and chemical warfare. In 1972, the
United Nations Convention on the Prohibition of
the Development, Production and Stockpiling of
Bacteriological (Biological) and Toxin Weapons and
on Their Destruction (a.k.a. the Biological and Toxin
Weapons Convention) was executed with an imple-
mentation date of March 26, 1975. By June 2005, there
were 171 signatories, and 155 of these had ratified
the convention to stop development, production, and
stockpiling of chemical and bacteriological (biologi-

cal) weapons. Research for defensive purposes is still
allowed and continues across the globe.
Treaties and multilateral agreements cannot com-
pletely rid the world of chemical weapons and BWs,
which are simple, inexpensive, and produced by widely
available technology. Nor will they fully eradicate the
threat of individuals who fervently desire to acquire
and use them as weapons. Here are some recent ex-
amples:
Paris police, in 1984, raided a suspected safe house
for the German Red Army Faction. During the search they
found documentation and a bathtub filled with flasks
containing Clostridium botulinum (Douglas, 1987).
Russia’s biological warfare technology may be vul-
nerable to leakage to third parties through either theft or
outright sale (like nuclear materials), as a result of the fi-
nancial crises that exist. Open-source intelligence reports
that army personnel and scientists have been known to
sell off military equipment to get money to feed their
families. In some cases, reports have been received that
these individuals, in critical and sensitive positions, have
not been paid in months, making them vulnerable to
recruitment by rogue organizations or nations.
The Aum Shinrikyo cult members (famous for
the sarin gas attack in Tokyo subways) were found to
have anthrax and botulinum cultures when the Japanese
national police conducted their raid of the Aum base
camp at the foot of Mount Fuji. They had constructed
dedicated laboratories and had purchased a helicopter
equipped with a spraying apparatus. The Aum had also
visited Zaire during the Ebola outbreak to collect speci-

mens of Ebola virus (Flanagin & Lederberg, 1996).
In the town of The Dalles, Oregon, in 1984, more
than 750 people became sick after eating in four differ-
ent restaurants. The illness was traced to the Bhagwan
Sri Rajneesh sect, which had spread salmonella on salad
bars in the four restaurants (Cole, 1996). The intention
of this group was to sicken many of the community
to prevent them from going to the polls, thus interfer-
ing with the political process and manipulating a local
election.
A U.S. microbiologist named Larry Wayne Harris
fraudulently ordered three vials of bubonic plague cul-
tures by mail in 1995 (Horrock, 1997). The ease with
which he obtained these cultures prompted new legis-
lation to ensure that biological materials are destined
only for legitimate medical and scientific purposes. These
products are often shipped via commercial delivery com-
panies such as UPS and FedEx, which is perfectly legal.
In December 2002, six terrorist suspects were ar-
rested in Manchester, England; their apartment was serv-
ing as a ricin laboratory. Among them was a 27-year-old
chemist who was producing the toxin.
On October 15, 2003, a ricin-laced letter, addressed
to the Department of Transportation in Washington,
FIGURE 9-1C Anthrax letter sent to the New York Post.
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DC, U.S.A., was intercepted at a mail sorting facility in
Greenville, South Carolina. The letter, which threatened
future ricin attacks if the government didn’t pass pend-
ing trucking legislation, was signed by Fallen Angel.
On February 3, 2004, three U.S. Senate office build-
ings were closed after the toxin ricin was found in the
mailroom that serves Senate Majority Leader Bill Frist’s

office.
Threat Assessment
Although the conclusion that the United States is very
vulnerable to a biowarfare attack or terrorism is indis-
putable, the BW programs of the 1950s and 1960s were
appropriately criticized for the unethical exposure of
unwitting test subjects. Despite the escalating BW threats
and the experiences of the anthrax attacks of 2001, our
level of preparedness is still insufficient given the po-
tential harm and disruption that could be realized in the
aftermath. With limited capacity to anticipate a biologi-
cal attack, little or no ability to detect one if it occurs
(unless the perpetrators decide to announce the release
and take credit for their demonic acts), and a dimin-
ished ability to effectively manage the consequences if
attacked, this problem poses a series of complex issues
that need immediate review. There are a number of rea-
sons for this unpreparedness, which will be discussed
in the following sections.
Intelligence
When a BW manufacturing facility can be constructed
in the area of a large garage, law enforcement/intelli-
gence services are confronted with great difficulty in
locating it. Accessing cultures is not nearly as expen-
sive or tracked as well as nuclear material. BW culture
processing requires equipment that would be consid-
ered suitable for a well-equipped hospital laboratory
or academic research facility and is thus easily ordered
and diverted. If this does not sound credible, please
take some time to research the many events of missing
samples from labs, black market activities, and incidents
where individuals have exploited loopholes in the system
to acquire samples under fraudulent terms (Harris &

Paxman, 1982).
As the threat of terrorism has evolved over the years,
so has the role of EMS in support of interagency opera-
tions. The importance of seamlessly integrating EMS
representation into intelligence functions such as state,
regional, and local intelligence fusion centers is a critical
requirement to ensure the vertical and horizontal flow
of essential information. For instance, tying in to the
911 dispatch data system to monitor call volume and
activity with the ability to drill down on data from past
years to quickly conduct a correlative analysis of activi-
ties for aberrancy is an important data node. Given that
most EMS systems operate and staff on the margins, the
sensitivity of call volume and the fragility of the system
provide a source for rather quick alerts that something
is not right. Drawing those EMS data along with emer-
gency department activity data into a central location
for the EMS representative to coordinate and collaborate
on the end operations analysis with the public health
representative could be that single, important clue that
provides a community early notification of an incident.
In the end, that early alert could mean the difference
between quick response and control or expansion into
a citywide/regional problem or worse.
Detection
Detection of biological agents occurs most often after a
release. Quite simply, presently there are limited tech-
nologies that can detect the deployment of a bacterial
agent in the civilian community under normal operat-
ing procedures. The only truly accurate means of de-
tection is through the clinical presentation of patients,
and that will be retrospective for most of the casual-
ties. Some limited battlefield detection devices exist,

but these are unusable in the majority of U.S. cities.
These devices can be effective for special events such
as the Olympics, a presidential inauguration, or where
crowds are moderately constrained, but due to cost and
availability, they have limited benefit to local emergency
response organizations. When threat assessments are
quite high and advance notice of the threat exists, use
of these items through the National Guard civil support
teams or through the Department of Defense is highly
recommended.
Biological warfare agents are almost undetectable
during transit. Likewise, there is no mechanism us-
ing routine customs, immigration, drug scan, or bomb
search procedures to identify the agent. The only way
to find it would be a physical search by a very well-
trained and very lucky searcher (Mayer, 1995). Indeed,
the agent could be simply sent using FedEx or a similar
overnight carrier from one point to another. Even in
an event where a package is broken and the product is
leaked, law enforcement may have a high index of sus-
picion, but identification of the agent will usually take
place at a laboratory, not in the field.
A bioterrorism threat might not be directly concen-
trated on actual humans. Livestock, crops, and water
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supply are strategic targets and vulnerable to attack. As
an example, it is not inconceivable that a rogue indi-
vidual or group could attempt to destroy all pork and
pork products in the United States. Although this would
not be a fatal blow for the United States on the whole,
it would certainly not help the U.S. economy to have a
porcine plague. Detection of this plague would be very
difficult indeed prior to symptoms in a substantial num-
ber of the affected animals. (While they should for a
number of strategic reasons, few communities include
veterinarians in their biological surveillance plans.)

Control of Supplies
A military commander maintains the luxury of knowing
that his troops are under threat of attack. The civilian
emergency response chief does not usually have this
warning and the targets for introduction of a biologi-
cal agent are almost unlimited. To a large extent, the
battlefield commander controls the food and water
supply of his troops. To institute such control in the
civilian sector would mean martial law, and this is un-
acceptable in a free society. This level of freedom is
not without cost and it creates vulnerability for rogue
groups to exploit.
Personal Protective Equipment
Biological terrorism is most likely to be executed co-
vertly, and sick individuals may be the initial detector
that an attack has occurred. If a biological agent is de-
livered effectively, a large number of casualties can be
generated in a relatively short period of time depending
on the etiologic agent utilized. In the midst of treating the
casualties, the emergency responder and organization
must not only provide effective care, but also protect
themselves and their members.
This will be difficult most of the time due to the
unknowing responders believing that they are operat-
ing at another sick job. After the release of a bioagent,
there is an incubation period in the new host prior to
its clinical manifestation. In some cases, this period may
be more than 72 hours, and from some agents, it is 2
weeks or more.
One of the limiting factors of personal protective
equipment (PPE) is that military issued gear is not certified
by the Occupational Safety and Health Administration
(OSHA). OSHA certification is a standard requirement

for civilian use of any PPE. It has been only recently that
some of this equipment is being considered for civil-
ian use or “technology transfer,” hence some testing for
OSHA standard compliance is taking place (see Chapter
13, “Personal Protective Equipment”).
Regardless, much of the civilian PPE that is available
for bioagents is designed for use in the static environ-
ment of the laboratory and not the street. This, too,
is another issue that will require a cooperative public/
private working arrangement. Clearly, with the threat
to the civilian responder escalating, continuing research
for better and more functional PPE should be expected
with the expertise of military, Homeland Security science
and technology, academia, and private industry pooling
talent and resources to create a successful resolution of
this operational conundrum.
Even if the military or the Centers for Disease
Control and Prevention (CDC) provide gear, it must
be prepositioned and issued after either a significant
threat or after the first casualties have been identified.
In either case, there is a significant risk that many of the
emergency services (including emergency physicians,
nurses, paramedics, and EMTs) will be exposed and
become unknowing casualties prior to the arrival of pro-
tective gear. Worst-case scenario is that these responders
become additional disease vectors, further complicating
the overarching response strategies.
Prophylaxis
The U.S. General Accounting Office found that at the
beginning of the Gulf War in 1991, the U.S. Army’s
stockpiles of vaccine for anthrax and botulism had
fallen far short of what was needed to protect U.S.
troops. Indeed, the General Accounting Office felt

that at least 20 percent and perhaps 40 percent of
the military’s biowar budget was not directed at dis-
eases or toxins that were identified as threats by the
military’s own intelligence agencies (Horgan, 1994).
Recently, heated discussions have again taken place
at the Pentagon and in the media about the need to
provide vaccinations to all uniformed service members
as a provision of force protection in the face of these
BW threats.
Protecting the armed forces against a biological at-
tack is less challenging and complex than protecting
the civilian population. Military personnel are a captive
audience who have little choice regarding whether they
will receive an immunization.
At present, we do not have sufficient emergency
providers with enough immunizations to provide care
for the population of a U.S. city (if attacked) without
additional harm coming to the rescuers. These pro-
viders will be at the highest risk if an active agent
is employed. On the positive side of this discussion,
with recent advances in vaccinology, depending upon
the threat being confronted, promising countermea-
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sures are starting to be identified as is the ability to
administer countermeasures after the exposure has
occurred.
Training
Emergency responders might be called upon to know
treatments for exotic diseases that they are unlikely to
have ever encountered. Emergency service members
must be aware of symptoms and epidemiological pat-
terns that may indicate a biological attack, but many
have never been taught these techniques of pattern
identification. This creates a heavy reliance upon the
expertise of the EMS medical director, the public health
director, and the EMS training chief for guidance on next

steps and real-time training.
EMS, the fire service, police, and even hospitals
must purchase PPE and train employees for work in
protective gear that has been found only in the mili-
tary and specialized hazardous materials teams.
Emergency service organizations must realize that they
are significant targets for primary/secondary attacks
and should conduct their routine operations appropri-
ately while ensuring that the proper security measures
are implemented.
Interagency Coordination and Public Perception
It is always difficult to balance the perceived needs
of multiple population groups. Drawing the fine line
between antiwar protesters who feel any research into
biowar techniques should be forbidden and those who
look for a threat around any corner is always diffi-
cult. When given the choice of where to spend defense
money, it is easier to put it into real and visible tools
such as guns, planes, and troops, playing the CNN
factor to the max. In the past, cruise missiles shown
on CNN are easier to sell to a congressional committee
than protective garments for use in Bloomfield, New
Jersey. Even in this post-September 11, 2001 world,
we see reluctance on the part of some in Congress
about really making the necessary sustainable invest-
ments in EMS, medical, public health, and other re-
sponder readiness. Hopefully, the momentum that has
been attained regarding community bioterrorism and
pandemic preparedness will continue to grow, and
this view will change so a sustainable capacity can be
achieved.
Likewise, control of a program that will spend mil-
lions of dollars brings a smile to many bureaucrats’ faces.

Will infighting between bureaucratic agencies dissipate
any real effort to protect the United States? These issues
require policy decisions with requisite directives to be
issued in an effort to set the tone, from the top, ensuring
that the process does not become mired in rivalry and
competition. Perhaps we can start with a reexamination
of the National Response Framework and refine this doc-
trine to incorporate an emergency support function that
specifically addresses EMS and critical care medicine,
while concurrently creating an agency that will have the
responsibility for the same and be held accountable for
seeing that readiness for this vital function is sustainably
accomplished.
When a bioterrorism incident occurs, who will be in
charge? Will it be local EMS, fire, police, or emergency
management personnel? Will it be medical authorities
from state, county, or local departments of health? Will
it be medical authorities from the Department of Health
and Human Services, CDC, or even military specialists
from one of the biowar development centers at Dugway
Proving Ground in Utah or Fort Detrick in Maryland?
Will the Federal Bureau of Investigation attempt to as-
sume control of the scene to preserve evidence? Will
the Federal Emergency Management Agency attempt
to usurp control of the incident? Will martial law be
declared with the military in control of a city? With the
recent H1N1 pandemic (2009) it was the secretary of
the Department of Homeland Security who was front
and center in the management of the federal response
coordination. Even with the issuance of Presidential
Decision Directive 39, these questions have not been
fully and adequately answered.
Command and control issues are always best an-

swered in advance of the incident, rather than during the
emergency. Having a comprehensive emergency action
annex to the existing community emergency manage-
ment plan for bioterrorism incidents is strongly encour-
aged. Determination of issues such as these should be
accomplished before “game day,” not on the field of play.
The latter will contribute to the chaos one can expect at
this type of incident.
Deniability
The existence of naturally occurring or endemic agri-
cultural pests or diseases and outbreaks will permit an
adversary to anonymously use bioterrorism with com-
pletely plausible deniability. Such biological warfare
attacks could be against the food supply or crops. The
effects of such biological and economic warfare could
bring devastation to the affected nation. The Russian
wheat aphid has caused over $1 billion in losses in
the western United States since it was first discovered/
identified in Texas in 1986. What would a focused and
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deliberate release of a BW agent mean to the economics
of the United States?
Response Time
Even if an astute emergency physician notes that an
unusual number of patients brought in by EMS or as
emergency department walk-ins have certain symptoms
and contacts the CDC for help, and the crisis is imme-
diately recognized as a bioterrorism event, and help is
dispatched immediately, the lag time may be unwieldy.
With some of the agents that have been identified, there
is an incubation period that exceeds 3 days from time of
agent distribution until the first cases occur and some
agents carry as much as a 20-day period. A patient may
be contagious during much of this incubation period
with emergency personnel and hospital staff unaware of
the jeopardy they are in. Some of the agents have mor-
tality rates that approach 100 percent when symptoms

go unrecognized.
Given an absolute best-case scenario from notifica-
tion, it will take at least 2 hours for a qualified team
of predesignated physicians and prehospital providers
(paramedics and EMTs) to assemble (this best-case sce-
nario occurs only if a community has had the foresight
to convene a team prior to the event), ready gear, and
respond to the deployment assembly point. It will take
another few hours to assess the situation, draw appro-
priate clinical samples, and formulate an idea of what
illness or toxin was employed. During this time, others
will be exposed and potential carriers may be leaving
the city, bound for other destinations.
When casualties exceed the available medical re-
sources, additional resources must be identified and
summoned, and either the patients must be transported
to them or the providers and equipment transported to
the patients. This scenario will warrant the deployment
of federal assets in the form of National Disaster Medical
System disaster medical action teams and military units
such as the deployable medical teams, if available. All
of this will take many hours or days.
If news services broadcast any warning, one can
expect a panic-stricken response that may cause gridlock
on the roads and further complicate any response team’s
travel to the area (and cause a spike in the standard 911
call volume). Essentially, we are looking at a regional,
if not national or international emerging health crisis.
This statement is very real. Consider the fact that in a
conventional weapon attack such as the 1993 World
Trade Center bombing, patients were tracked as far
west as Pennsylvania and as far north as New Haven,
Connecticut.

Response Strategies
In addition to the requisite response doctrine for pro-
tecting responders are support networks for responders’
families and operational response and logistic sustain-
ment tactics that the contemporary emergency response
chief or executive must employ in response to a biologi-
cal event. Given that the prevailing mantra for response
to an infectious event is “social distancing and adminis-
tration of countermeasures,” we need to briefly examine
the reality of this intervention.
The contemporary disaster response/planning doc-
trine involves bringing lots of people and resources to
a location where an event has transpired and working
our way out of it as quickly as possible. In the event
of a bioterrorism incident or a pandemic, the reality
of this strategy effectively being employed is ques-
tionable due to a number of issues, including but not
limited to the scope of the event, limited resources,
numbers of people affected, and the large geographic
area that could be involved. Currently, conventional
wisdom dictates that a social distancing response that
is often bantered about translates into a concept we
are all familiar with—shelter in place. It is important
to note here that sheltering in place is a temporary,
limited-duration tactic designed to protect individuals
from an immediate pending event such as a gas leak,
extreme inclement weather, or other hostile environ-
ment. Generally, these events can last a few hours to
a day. As discussed previously, given that conven-
tional responses and structures are neither designed
nor configured to support hundreds if not thousands
of individuals staying at home and servicing all of
the affected people in disparate locations, the opera-
tionalization of the social distancing strategy becomes

a complex problem that must be addressed sooner
rather than later. Basically, we conduct emergency
response operations daily in a “price club” manner,
while the social distancing strategy will require us to
refine and realign our response patterns and capacity
to be more like Meals on Wheels—a retail approach
rather than the standard wholesale scheme we utilize
to conduct routine operations and run-of-the-mill di-
saster response.
It is important that the empowerment of the citizenry
to become prepared for a disaster is achieved. Failure
to take the necessary steps to create this environment
could result in spontaneous and unnecessary evacua-
tions of communities and failed or ineffective emergency
response capacity.
Although highways leading from an attacked met-
ropolitan area are most certainly attractive for citizens
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who feel they need to take matters into their own hands,
they will likely be roads to nowhere, leaving citizens
trapped and vulnerable. In most cases, remaining in
homes or other safe havens in the community will pro-
vide the greatest personal security. This is true in terms
of physical and emotional safety, because people make
their best decisions when they are in stable, familiar
environments, and make their worst decisions when in
unstable, unfamiliar environments. A strategic concept
and operational framework to address the emerging is-
sues revolving around extended social distancing re-
quirements has been developed out of the University
of Virginia’s Critical Incident Analysis Group. The pre-
senting model is best described as “shelter in place on
steroids” and looks at the series of complex and at times
daunting requirements posed by needing to implement
a coherent and supported social distancing strategy that
will protect and support citizens.

Community shielding is a unique opportunity to
engage individuals, communities, and government in a
unified response to future acts of terrorism, in particu-
lar bioterrorism. The concept envisions an integrated,
facilitated form of sheltering, wherein individuals and
groups within a community employ a self-imposed iso-
lation, or quarantine, within their natural and famil-
iar surroundings, for a temporary period of time until
a threat or danger abates. The success of community
shielding depends upon the development of partner-
ships among government, business, the media, and the
public, creating an integrated social infrastructure that
facilitates a shelter-in-place response by providing es-
sential resources to augment individual preparation for
natural or unnatural catastrophic events.
Community shielding allows individuals to remain
in their homes and communities, rather than evacuat-
ing an affected area in an attempt to avoid a threat or
danger. Both a government-ordered, mandatory evacu-
ation and a spontaneous evacuation of citizens in the
absence of instructions to leave an area usually result
in a chaotic response, mass movement of citizens on
congested roadways to nowhere, and the entrapment
of vulnerable citizens suffering from illness or in need
of medical care. Gridlock of transportation systems
in an affected area also hampers local first responders
from reaching those most in need. By contrast, com-
munity shielding fosters empowerment and resilience
in American citizens to remain at home in their com-
munities and fight, rather than to flee, delivering a
strong response to defeat the terrorist objective of dis-
rupting and destroying American lives and the normal
functioning of our society.
Just as individual cells in the body are nourished

within organs, so too must places of refuge be sup-
ported through community shielding, a wider form
of sheltering. When communities are deployed to
provide necessary strategic support for sheltering in
place, there is less chance for first responders to be
overwhelmed by unnecessary and dangerous evacu-
ation attempts.
A variety of survey outcome data sources demon-
strates a significant increase in the willingness of citi-
zens to participate in a community shielding strategy
if their sheltering in place is augmented by the provi-
sion of resources until it is safe to leave their homes
or communities (i.e., delivery of food, water, medica-
tions, and medical treatment; dissemination of reli-
able information as to the crisis, its duration, and the
safety and well-being of family members; and a means
to communicate within and outside the affected com-
munity). These findings strongly suggest that if local
communities’ emergency preparedness and response
plans include bringing food, water, medications, and
other necessities directly to citizens’ homes and work-
places and providing assurances as to the safety and
well-being of family members from whom they are
separated, citizen response would be favorable and in
support of community shielding.
Implementation of community shielding as part of
emergency preparedness planning/response to future
events will require continued efforts toward a national
initiative to increase awareness of the concept and
to gain support from key government and commu-
nity leaders, as well as the American public. Public
education will be necessary to enlist the citizens as
significant participants in preparing for such future
events, including the dissemination of information as

to what steps to take to prepare, how notification of
events will be provided, and how communication will
be maintained during a crisis. Moreover, the funda-
mentals of how to respond to these challenges should
be analyzed by the contemporary emergency response
chief or executive now in order to allow for realign-
ment of planning, training, and operational paradigms
to effectively respond to a community in need with
shielding implemented.
Realities and Costs
It is unlikely that a rational foreign government would
risk potential military reprisals and the political/eco-
nomic sanctions that overt use of biological warfare
against the United States would bring (Lebeda, 1997).
Covert action or deniable independent rogue factions
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and transnational terrorist organizations do not have the
same constraints. Terrorist organizations operating in a
civilian environment have freedom of movement and
the ability to use commercially available equipment for
development and discharge of their weapon. They are
not constrained by a need for precise targeting or pre-
dictable results. A determined transnational organization
or rogue individual may not be deterred, may escape
detection and intelligence-gathering activities, and may
succeed in releasing a biological agent in a susceptible
target area. Lastly, transnational terrorist groups gener-
ally are not affiliated with one country or organization,
and as such they have no return address, making a mili-
tary retaliation very complicated if not impossible.
The effects of a bioterrorism incident are cata-
strophic. In a paper by researchers at the CDC, the
projected economic impact alone ranges from $477
million per 100,000 people exposed to brucellosis to
$26.2 billion in the case of anthrax (Kaufmann, Meltzer,
& Schmid, 1997). Over 30,000 deaths were predicted
if anthrax was used as the biological agent. The paper

consistently used the lowest possible expense for all fac-
tors that affected costs, including the virulence of the
disease. Costs of both preparedness and intervention
were significant. It is clear that this would not be the
case in a real disaster of this magnitude. Even so, the
researchers concluded that reducing preventable losses
has a significantly greater impact than reducing the prob-
ability of an attack through intelligence gathering and
prevention strategies.
The authors also noted that the best possible mea-
sures to decrease both costs and deaths were those that
would enhance rapid response to an attack. “These mea-
sures would include developing and maintaining EMS
response operation and hospital critical care capacities,
laboratory capabilities for both clinical diagnostic test-
ing and environmental sampling, developing and main-
taining drug medical counter-measure stockpiles, and
developing and practicing response plans at the local
level” (Kaufmann et al., 1997).
Possible Biotoxins
Until recently, toxins were of interest only to the toxi-
cologist, the rare patient who ingested or was exposed
to these toxins, and the even rarer writer who discussed
toxicological environmental emergencies. Unfortunately,
several simultaneous political and scientific events have
moved these toxins to a more prominent medical and
social position.
Discovery that some of these toxins have been used
as agents in warfare or have been stockpiled to use in
warfare has given the medical community an impetus
to learn more about the effects and production of toxins
for biological warfare. New uses for old toxins include

botulinum therapy for spastic muscles and dystonia. For
an overview of biological symptoms and treatments,
refer to TABLE 9-1.
Botulinum Toxins
Botulinum neurotoxin is among the most potent toxins
known. The mouse lethal dose is less than 0.1 nano-
gram per 100 grams. It is over 275 times more toxic
than cyanide.
Mueller (1735–1793) and Kerner (1786–1862) in
Germany first described botulism. They associated the
disease with ingestion of insufficiently cooked blood
sausages and described death by muscle paralysis and
suffocation. In the early 1900s, botulism occurred com-
monly in the United States and nearly destroyed the
canned-food industry (Meyer, 1956).
The major source of botulinum toxin is the organism
Clostridium botulinum. There are seven serotypes pro-
duced by clostridia species. These serotypes are similar
but do not cross-react to immune reactions. They are
released as a single polypeptide chain of about 150,000
daltons, which is cleaved to generate two disulfide-linked
fragments. The heavy fragment (histone 100,000 daltons)
is involved in cell binding and penetration, while the light
chain is responsible for the toxic intracellular effects.
Clinical Effects
Two natural types of poisoning occur. In the first type,
food tainted with clostridia species is stored or processed
in a way that allows the anaerobic organisms to grow and
multiply. As they grow, they produce and release toxin.
If the food is not subsequently heated to destroy the
toxin, clinically significant amounts can be consumed.

The toxin passes through the gut into the general cir-
culation and is distributed throughout the body. In the
second type, usually found in infants, the organisms
colonize and produce their toxin in the gut. The clinical
effects of the two types of botulism are the same.
After ingestion with botulinum toxin, the victim will
develop diplopia and ptosis (difficulty speaking and swal-
lowing), decreased bowel function, and muscle weakness
that can progress to a flaccid paralysis. The patient will
generally be awake, oriented, and afebrile. Development
of respiratory failure may be quite rapid after initial symp-
toms develop. The hallmark sign is progressive, bilateral
descending paralysis, which occurs usually within 24
hours of ingesting a contaminated product.
1/20/10 10:29:43 AM1/20/10 10:29:43 AM
DISTRIBUTION.
F
O
S
T
E
R
,
C
E
D
R
I
C

1
6
9
2
T
S
133
TA
B
LE
9
-1
B
io
lo
gi
ca
l A
ge
nt
s:
S

ym
pt
om
s
an
d
Tr
ea
tm
en
t
S
ig
n
s
a
n
d
s
y
m
p
to
m

s
D
ia
g
n
o
s
is
T
re
a
tm
e
n
t
P
ro
p
h
y
la
x
is
D
e

c
o
n
ta
m
in
a
ti
o
n
A
n
th
ra
x
In
cu
b
a
ti
o
n
p
e
ri

o
d
is
1
–6
d
a
y
s.
F
e
v
e
r,
m
a
la
is
e
,
fa
ti
g

u
e
, c
o
u
g
h
, a
n
d
m
il
d
ch
e
st
d
is
co
m
fo
rt
a

re
fo
ll
o
w
e
d
b
y
s
e
v
e
re
re
sp
ir
a
to
ry
d
is

tr
e
ss
w
it
h
d
y
sp
n
e
a
, d
ia
p
h
o
re
si
s,
st
ri

d
o
r,
a
n
d
c
y
a
n
o
si
s.
S
h
o
ck
a
n
d
d
e
a

th
o
cc
u
r
w
it
h
in
3
6
h
o
u
rs
o
f
se
v
e
re
sy
m

p
to
m
s.
P
h
y
si
ca
l f
in
d
in
g
s
a
re
n
o
n
sp
e
ci

fi
c.
P
o
ss
ib
le
w
id
e
n
e
d
m
e
d
ia
st
in
u
m
.
D

e
te
ct
a
b
le
G
ra
m
s
ta
in
o
f
th
e
b
lo
o
d
a
n
d
b

y
b
lo
o
d
cu
lt
u
re
in
t
h
e
c
o
u
rs
e
o
f
il
ln
e

ss
.
A
lt
h
o
u
g
h
u
su
a
ll
y
n
o
t
e
ff
e
ct
iv
e
a

ft
e
r
sy
m
p
to
m
s
a
re
p
re
se
n
t,
h
ig
h
-d
o
se
a

n
ti
b
io
ti
c
tr
e
a
tm
e
n
t
w
it
h
p
e
n
ic
il
li
n

, c
ip
ro
fl
o
x
a
ci
n
,
o
r
d
o
x
y
cy
cl
in
e
s
h
o
u
ld

b
e
u
n
d
e
rt
a
k
e
n
. S
u
p
p
o
rt
iv
e
th
e
ra

p
y
m
a
y
b
e
n
e
ce
ss
a
ry
.
A
li
ce
n
se
d
v
a
cc

in
e
f
o
r
u
se
in
t
h
o
se
c
o
n
si
d
e
re
d
a
t
ri

sk
f
o
r
e
x
p
o
su
re
. V
a
cc
in
e
sc
h
e
d
u
le
is
0

, 2
, a
n
d
4
w
e
e
k
s
fo
r
in
it
ia
l s
e
ri
e
s,
fo
ll

o
w
e
d
b
y
b
o
o
st
s
a
t
6
,
12
, a
n
d
1
8
m
o
n

th
s,
a
n
d
th
e
n
a
y
e
a
rl
y
b
o
o
st
e
r.
S
e
cr

e
ti
o
n
a
n
d
le
si
o
n
p
re
ca
u
ti
o
n
s
sh
o
u
ld

b
e
p
ra
ct
ic
e
d
. A
ft
e
r
a
n
in
v
a
si
v
e
p
ro

ce
d
u
re
o
r
a
u
to
p
sy
is
p
e
rf
o
rm
e
d
,
th
e
in
st

ru
m
e
n
ts
a
n
d
a
re
a
u
se
d
s
h
o
u
ld
b
e
t
h

o
ro
u
g
h
ly
d
e
co
n
ta
m
in
a
te
d
w
it
h
a
sp
o

ri
ci
d
a
l a
g
e
n
t
su
ch
a
s
io
d
in
e
o
r
ch
lo
ri
n
e

.
B
o
tu
li
n
u
m
t
o
x
in
s
P
to
si
s,
g
e
n
e
ra
li
ze

d
w
e
a
k
n
e
ss
, d
iz
zi
n
e
ss
, d
ry
m
o
u
th
a
n
d

t
h
ro
a
t,
b
lu
rr
e
d
v
is
io
n
a
n
d
d
ip
lo
p
ia
,

d
y
sa
rt
h
ri
a
, d
y
sp
h
o
n
ia
, a
n
d
d
y
sp
h
a
g

ia
f
o
ll
o
w
e
d
b
y
sy
m
m
e
tr
ic
a
l d
e
sc
e
n
d

in
g
fl
a
cc
id
p
a
ra
ly
si
s
a
n
d
d
e
v
e
lo
p
m
e

n
t
o
f
re
sp
ir
a
to
ry
f
a
il
u
re
.
S
y
m
p
to
m
s
b

e
g
in
a
s
e
a
rl
y
a
s
2
4
h
o
u
rs
, b
u
t
m
a
y

ta
k
e
s
e
v
e
ra
l d
a
y
s
a
ft
e
r
in
h
a
la
ti
o
n

o
f
a
t
o
x
in
.
C
li
n
ic
a
l d
ia
g
n
o
si
s;
n
o
ro
u

ti
n
e
la
b
o
ra
to
ry
fi
n
d
in
g
s.
B
io
te
rr
o
ri
sm
/

w
a
rf
a
re
s
h
o
u
ld
b
e
su
sp
e
ct
e
d
if
n
u
m
e

ro
u
s
co
ll
o
ca
te
d
c
a
su
a
lt
ie
s
h
a
v
e
p
ro
g

re
ss
iv
e
d
e
sc
e
n
d
in
g
b
u
lb
a
r,
m
u
sc
u
la
r,

a
n
d
re
sp
ir
a
to
ry
w
e
a
k
n
e
ss
.
In
tu
b
a
ti
o

n
a
n
d
v
e
n
ti
la
to
ry
a
ss
is
ta
n
ce
fo
r
re
sp
ir

a
to
ry
f
a
il
u
re
.
T
ra
ch
e
o
st
o
m
y
m
a
y
b
e

re
q
u
ir
e
d
. A
d
m
in
is
tr
a
ti
o
n
o
f
b
o
tu
li
n

u
m
a
n
ti
to
x
in
(I
n
v
e
st
ig
a
ti
o
n
a
l N
e
w

D
ru
g
[
IN
D
]
p
ro
d
u
ct
)
m
a
y
p
re
v
e
n
t
o

r
d
e
cr
e
a
se
p
ro
g
re
ss
io
n
t
o
r
e
sp
ir
a
to
ry

fa
il
u
re
a
n
d
h
a
st
e
n
re
co
v
e
ry
.
P
e
n
ta

v
a
le
n
t
to
x
o
id
(t
y
p
e
s
A
, B
, C
, D
, a
n
d
E
)

is
a
v
a
il
a
b
le
a
s
a
n
I
N
D
p
ro
d
u
ct
f
o
r

th
o
se
a
t
h
ig
h
ri
sk
o
f
e
x
p
o
su
re
.
H
y
p
o

ch
lo
ri
te
(
0
.5
%
f
o
r
10
–1
5
m
in
u
te
s)
a
n
d
/o
r

so
a
p
a
n
d
w
a
te
r.
T
o
x
in
is
n
o
t
d
e
rm
a
ll
y

a
ct
iv
e
a
n
d
s
e
co
n
d
a
ry
a
e
ro
so
ls
a
re
n

o
t
a
h
a
za
rd
f
ro
m
p
a
ti
e
n
ts
.
C
h
o
le
ra
In

cu
b
a
ti
o
n
p
e
ri
o
d
is
1
–5
d
a
y
s.
A
sy
m
p
to

m
a
ti
c
to
s
e
v
e
re
w
it
h
s
u
d
d
e
n
o
n
se
t.

V
o
m
it
in
g
,
a
b
d
o
m
in
a
l d
is
te
n
ti
o
n
,
a
n

d
p
a
in
w
it
h
li
tt
le
o
r
n
o
f
e
v
e
r
fo
ll
o
w

e
d
ra
p
id
ly
b
y
d
ia
rr
h
e
a
.
F
lu
id
lo
ss
e
s
m

a
y
e
x
ce
e
d
5
–1
0
li
te
rs
p
e
r
d
a
y
.
W
it
h

o
u
t
tr
e
a
tm
e
n
t,
d
e
a
th
m
a
y
r
e
su
lt
f
ro

m
se
v
e
re
d
e
h
y
d
ra
ti
o
n
,
h
y
p
o
v
o
le
m

ia
, a
n
d
s
h
o
ck
.
C
li
n
ic
a
l d
ia
g
n
o
si
s.
W
a

te
ry
d
ia
rr
h
e
a
a
n
d
d
e
h
y
d
ra
ti
o
n
. M
ic
ro

sc
o
p
ic
e
x
a
m
o
f
st
o
o
l s
a
m
p
le
s
re
v
e
a

ls
f
e
w
o
r
n
o
r
e
d
o
r
w
h
it
e
c
e
ll
s.
C
a

n
b
e
id
e
n
ti
fi
e
d
in
s
to
o
l b
y
d
a
rk
f
ie
ld

o
r
p
h
a
se
co
n
tr
a
st
m
ic
ro
sc
o
p
y
a
n
d
c

a
n
b
e
g
ro
w
n
o
n
a
v
a
ri
e
ty
o
f
cu
lt
u
re
m

e
d
ia
.
F
lu
id
a
n
d
e
le
ct
ro
ly
te
re
p
la
ce
m
e
n

t.
A
n
ti
b
io
ti
cs
s
u
ch
a
s
te
tr
a
cy
cl
in
e
, a
m
p

ic
il
li
n
,
o
r
tr
im
e
th
o
p
ri
m
-
su
lf
a
m
e
th
o
x
a

zo
le
w
il
l
sh
o
rt
e
n
t
h
e
d
u
ra
ti
o
n
o
f
d
ia
rr
h

e
a
.
A
li
ce
n
se
d
, k
il
le
d
v
a
cc
in
e
is
a
v
a
il

a
b
le
b
u
t
p
ro
v
id
e
s
o
n
ly
a
b
o
u
t
5
0
%

p
ro
te
ct
io
n
t
h
a
t
la
st
s
n
o
m
o
re
t
h
a
n
6

m
o
n
th
s.
V
a
cc
in
a
ti
o
n
s
ch
e
d
u
le
is
a
t

0
a
n
d
4
w
e
e
k
s
w
it
h
b
o
o
st
e
r
d
o
se
s

e
v
e
ry
6
m
o
n
th
s.
P
e
rs
o
n
a
l c
o
n
ta
ct
ra

re
ly
c
a
u
se
s
in
fe
ct
io
n
;
h
o
w
e
v
e
r,
e
n
te
ri

c
p
re
ca
u
ti
o
n
s
a
n
d
c
a
re
fu
l
h
a
n
d
w
a
sh

in
g
s
h
o
u
ld
b
e
fr
e
q
u
e
n
tl
y
e
m
p
lo
y
e

d
.
B
a
ct
e
ri
ci
d
a
l s
o
lu
ti
o
n
s
su
ch
a
s
h
y
p

o
ch
lo
ri
te
w
o
u
ld
p
ro
v
id
e
a
d
e
q
u
a
te
d

e
co
n
ta
m
in
a
ti
o
n
.
(c
o
n
ti
n
u
e
s)
1/20/10 10:29:43 AM1/20/10 10:29:43 AM
DISTRIBUTION.
F

O
S
T
E
R
,
C
E
D
R
I
C
1
6
9
2
T
S
Response
TA
B
LE
9
-1
B

io
lo
gi
ca
l A
ge
nt
s:
S
ym
pt
om
s
an
d
Tr
ea
tm
en
t
(c
o
n
ti

n
u
e
d
)
S
ig
n
s
a
n
d
s
y
m
p
to
m
s
D
ia
g
n
o
s

is
T
re
a
tm
e
n
t
P
ro
p
h
y
la
x
is
D
e
c
o
n
ta
m
in
a
ti

o
n
P
la
g
u
e
P
n
e
u
m
o
n
ic
p
la
g
u
e
:
In
cu
b

a
ti
o
n
p
e
ri
o
d
is
2
–3
d
a
y
s.
H
ig
h
f
e
v
e

r,
c
h
il
ls
,
h
e
m
o
p
ty
si
s,
t
o
x
e
m
ia
,
p
ro
g

re
ss
in
g
r
a
p
id
ly
t
o
d
y
sp
n
e
a
, s
tr
id
o
r,
a

n
d
cy
a
n
o
si
s.
D
e
a
th
r
e
su
lt
s
fr
o
m
r
e
sp

ir
a
to
ry
f
a
il
u
re
,
ci
rc
u
la
to
ry
c
o
ll
a
p
se
, a
n

d
b
le
e
d
in
g
d
ia
th
e
si
s.
B
u
b
o
n
ic
p
la
g
u

e
:
In
cu
b
a
ti
o
n
p
e
ri
o
d
is
2
–1
0
d
a
y
s.
M

a
la
is
e
, h
ig
h
f
e
v
e
r,
a
n
d
t
e
n
d
e
r
ly
m

p
h
n
o
d
e
s
(b
u
b
o
e
s)
; m
a
y
p
ro
g
re
ss
sp
o

n
ta
n
e
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a
n
d
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is
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n

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t
6
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n
d
18
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s,
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p
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cr
e

ti
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t,
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s.
1/20/10 10:29:44 AM1/20/10 10:29:44 AM
DISTRIBUTION.
F
O
S
T
E
R
,

C
E
D
R
I
C
1
6
9
2
T
S
135
S
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a
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m
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(c
o
n
ti
n
u
e
s)
1/20/10 10:29:44 AM1/20/10 10:29:44 AM
DISTRIBUTION.

F
O
S
T
E
R
,
C
E
D
R
I
C
1
6
9
2
T
S
Response
TA
B
LE
9
-1

B
io
lo
gi
ca
l A
ge
nt
s:
S
ym
pt
om
s
an
d
Tr
ea
tm
en
t
(c
o
n

ti
n
u
e
d
)
S
ig
n
s
a
n
d
s
y
m
p
to
m
s
D
ia
g
n

o
s
is
T
re
a
tm
e
n
t
P
ro
p
h
y
la
x
is
D
e
c
o
n
ta
m
in

a
ti
o
n
S
ta
p
h
y
lo
co
cc
a
l
e
n
te
ro
to
x
in
B
F
ro
m

3
–1
2
h
o
u
rs
a
ft
e
r
a
e
ro
so
l e
x
p
o
su
re
, s
u
d

d
e
n
o
n
se
t
o
f
fe
v
e
r,
c
h
il
ls
,
h
e
a
d
a

ch
e
, m
y
a
lg
ia
, a
n
d
n
o
n
p
ro
d
u
ct
iv
e
c
o
u

g
h
.
S
o
m
e
p
a
ti
e
n
ts
m
a
y
d
e
v
e
lo
p
s

h
o
rt
n
e
ss
o
f
b
re
a
th
a
n
d
r
e
tr
o
st
e
rn
a
l

ch
e
st
p
a
in
. F
e
v
e
r
m
a
y
la
st
2
–5
d
a
y
s,
a

n
d
c
o
u
g
h
m
a
y
p
e
rs
is
t
u
p
t
o
4
w
e
e

k
s.
P
a
ti
e
n
ts
m
a
y
a
ls
o
p
re
se
n
t
w
it
h
n

a
u
se
a
, v
o
m
it
in
g
,
a
n
d
d
ia
rr
h
e
a
if
t
h
e

y
sw
a
ll
o
w
t
h
e
t
o
x
in
. H
ig
h
e
r
e
x
p
o
su

re
le
v
e
ls
c
a
n
le
a
d
to
s
e
p
ti
c
sh
o
ck
a
n
d

d
e
a
th
.
C
li
n
ic
a
l d
ia
g
n
o
si
s.
P
a
ti
e
n
t
p

re
se
n
ts
w
it
h
a
f
e
b
ri
le
re
sp
ir
a
to
ry
s
y
n
d

ro
m
e
w
it
h
o
u
t
ch
e
st
X
-r
a
y
a
b
n
o
rm
a

li
ti
e
s.
L
a
rg
e
n
u
m
b
e
rs
o
f
p
a
ti
e
n
ts

p
re
se
n
ti
n
g
w
it
h
t
y
p
ic
a
l
sy
m
p
to
m
s
a
n

d
s
ig
n
s
o
f
st
a
p
h
y
lo
co
cc
a
l
e
n
te
ro
to
x
in

B
p
u
lm
o
n
a
ry
e
x
p
o
su
re
w
o
u
ld
s
u
g
g
e

st
a
n
in
te
n
ti
o
n
a
l a
tt
a
ck
w
it
h
th
is
t
o
x

in
.
T
re
a
tm
e
n
t
is
li
m
it
e
d
t
o
su
p
p
o
rt
iv

e
c
a
re
. A
rt
if
ic
ia
l
v
e
n
ti
la
ti
o
n
m
ig
h
t
b
e

n
e
e
d
e
d
f
o
r
v
e
ry
s
e
v
e
re
ca
se
s
a
n

d
a
tt
e
n
ti
o
n
t
o
fl
u
id
m
a
n
a
g
e
m
e
n
t

is
e
ss
e
n
ti
a
l.
U
se
o
f
p
ro
te
ct
iv
e
m
a
sk
.

T
h
e
re
is
c
u
rr
e
n
tl
y
n
o
v
a
cc
in
e
a
v
a
il
a

b
le
t
o
p
re
v
e
n
t
st
a
p
h
y
lo
co
cc
a
l
e
n
te

ro
to
x
in
B
in
to
x
ic
a
ti
o
n
.
H
y
p
o
ch
lo
ri
te

(
0
.5
%
f
o
r
10
–1
5
m
in
u
te
s)
a
n
d
/o
r
so
a
p
a

n
d
w
a
te
r.
D
e
st
ro
y
a
n
y
f
o
o
d
t
h
a
t
m

a
y
h
a
v
e
b
e
e
n
c
o
n
ta
m
in
a
te
d
.
T
ri
ch

o
th
e
ce
n
e
m
y
co
to
x
in
s
(T
2
)
E
x
p
o
su
re
c

a
u
se
s
sk
in
p
a
in
, p
ru
ri
tu
s,
r
e
d
n
e
ss
,
v
e

si
cl
e
s,
n
e
cr
o
si
s,
a
n
d
sl
o
u
g
h
in
g
o
f
e

p
id
e
rm
is
.
E
ff
e
ct
s
o
n
t
h
e
a
ir
w
a
y
in
cl

u
d
e
n
o
se
a
n
d
t
h
ro
a
t
p
a
in
, n
a
sa
l d
is
ch
a

rg
e
,
it
ch
in
g
, s
n
e
e
zi
n
g
, c
o
u
g
h
,
d
y
sp
n

e
a
, w
h
e
e
zi
n
g
, c
h
e
st
p
a
in
, a
n
d
h
e
m
o

p
ty
si
s.
T
h
e
t
o
x
in
a
ls
o
p
ro
d
u
ce
s
e
ff
e

ct
s
a
ft
e
r
in
g
e
st
io
n
o
r
e
y
e
c
o
n
ta
ct
. S

e
v
e
re
p
o
is
o
n
in
g
r
e
su
lt
s
in
p
ro
st
ra
ti

o
n
, w
e
a
k
n
e
ss
,
a
ta
x
ia
, c
o
ll
a
p
se
, s
h
o
ck
,

a
n
d
d
e
a
th
.
S
h
o
u
ld
b
e
s
u
sp
e
ct
e
d
if

a
n
a
e
ro
so
l a
tt
a
ck
o
cc
u
rs
in
t
h
e
f
o
rm
o

f
y
e
ll
o
w
r
a
in
w
it
h
d
ro
p
le
ts
o
f
y
e
ll
o

w
f
lu
id
co
n
ta
m
in
a
ti
n
g
c
lo
th
e
s
a
n
d
t
h

e
e
n
v
ir
o
n
m
e
n
t.
C
o
n
fi
rm
a
ti
o
n
r
e
q

u
ir
e
s
te
st
in
g
o
f
b
lo
o
d
, t
is
su
e
,
a
n
d
e
n

v
ir
o
n
m
e
n
ta
l
sa
m
p
le
s.
T
h
e
re
is
n
o
s
p
e

ci
fi
c
a
n
ti
d
o
te
. S
u
p
e
ra
ct
iv
e
ch
a
rc
o
a
l s

h
o
u
ld
b
e
g
iv
e
n
o
ra
ll
y
if
s
w
a
ll
o
w
e
d
.

T
h
e
o
n
ly
d
e
fe
n
se
is
t
o
w
e
a
r
p
e
rs
o
n

a
l p
ro
te
ct
iv
e
e
q
u
ip
m
e
n
t
d
u
ri
n
g
a
n

a
tt
a
ck
. N
o
s
p
e
ci
fi
c
im
m
u
n
o
th
e
ra
p
y
o
r

ch
e
m
o
th
e
ra
p
y
is
a
v
a
il
a
b
le
fo
r
u
se
in
t

h
e
f
ie
ld
.
O
u
te
r
g
a
rm
e
n
ts
s
h
o
u
ld
b
e

r
e
m
o
v
e
d
, a
n
d
e
x
p
o
se
d
s
k
in
s
h
o
u

ld
b
e
d
e
co
n
ta
m
in
a
te
d
w
it
h
s
o
a
p
a
n

d
w
a
te
r.
E
y
e
e
x
p
o
su
re
sh
o
u
ld
b
e
t
re
a

te
d
b
y
co
p
io
u
s
sa
li
n
e
ir
ri
g
a
ti
o
n
.
O
n

ce
d
e
co
n
ta
m
in
a
ti
o
n
is
co
m
p
le
te
, i
so
la
ti
o

n
is
n
o
t
re
q
u
ir
e
d
.
1/20/10 10:29:44 AM1/20/10 10:29:44 AM
DISTRIBUTION.
F
O
S
T
E
R
,
C
E
D

R
I
C
1
6
9
2
T
S
137
S
ig
n
s
a
n
d
s
y
m
p
to
m
s

D
ia
g
n
o
s
is
T
re
a
tm
e
n
t
P
ro
p
h
y
la
x
is
D
e
c
o

n
ta
m
in
a
ti
o
n
T
u
la
re
m
ia
U
lc
e
ro
g
la
n
d
u
la

r
tu
la
re
m
ia
p
re
se
n
ts
w
it
h
a
lo
ca
l u
lc
e
r
a
n

d
r
e
g
io
n
a
l
ly
m
p
h
a
d
e
n
o
p
a
th
y
, f
e
v

e
r,
ch
il
ls
, h
e
a
d
a
ch
e
, a
n
d
m
a
la
is
e
. T
y

p
h
o
id
a
l o
r
se
p
ti
ce
m
ic
t
u
la
re
m
ia
p
re
se
n

ts
w
it
h
f
e
v
e
r,
h
e
a
d
a
ch
e
, m
a
la
is
e
,
su

b
st
e
rn
a
l d
is
co
m
fo
rt
,
p
ro
st
ra
ti
o
n
, w
e
ig
h
t

lo
ss
,
a
n
d
a
n
o
n
p
ro
d
u
ct
iv
e
co
u
g
h
.
C

li
n
ic
a
l d
ia
g
n
o
si
s.
P
h
y
si
ca
l f
in
d
in
g
s
a

re
u
su
a
ll
y
n
o
n
sp
e
ci
fi
c.
C
h
e
st
X
-r
a
y
m

a
y
re
v
e
a
l p
n
e
u
m
o
n
ic
p
ro
ce
ss
, m
e
d
ia

st
in
a
l
ly
m
p
h
a
d
e
n
o
p
a
th
y
, o
r
p
le
u
ra
l e

ff
u
si
o
n
. R
o
u
ti
n
e
cu
lt
u
re
is
p
o
ss
ib
le
b
u

t
d
if
fi
cu
lt
. T
h
e
d
ia
g
n
o
si
s
ca
n
b
e
e
st
a
b

li
sh
e
d
b
y
se
ro
lo
g
y
.
A
d
m
in
is
tr
a
ti
o
n

o
f
a
n
ti
b
io
ti
cs
w
it
h
e
a
rl
y
tr
e
a
tm
e
n
t

is
v
e
ry
e
ff
e
ct
iv
e
.
A
li
v
e
, a
tt
e
n
u
a
te
d

v
a
cc
in
e
is
a
v
a
il
a
b
le
a
s
a
n
in
v
e
st
ig

a
ti
o
n
a
l n
e
w
d
ru
g
.
It
is
a
d
m
in
is
te
re
d
o
n

ce
b
y
sc
a
ri
fi
ca
ti
o
n
. A
2
-w
e
e
k
co
u
rs
e
o
f

te
tr
a
cy
cl
in
e
is
e
ff
e
ct
iv
e
a
s
p
ro
p
h
y
la
x

is
w
h
e
n
g
iv
e
n
a
ft
e
r
e
x
p
o
su
re
.
S
e
cr

b
e
p
ra
ct
ic
e
d
. S
tr
ic
t
is
o
la
ti
o
n
o
f
p
a

ti
e
n
ts
is
n
o
t
re
q
u
ir
e
d
.
O
rg
a
n
is
m
s
a
re

r
e
la
ti
v
e
ly
e
a
sy
t
o
r
e
n
d
e
r
h
a
rm
le
ss

b
y
h
e
a
t
a
n
d
d
is
in
fe
ct
a
n
ts
.
V
e
n
e
zu

e
la
n
e
q
u
in
e
e
n
ce
p
h
a
li
ti
s
S
u
d
d
e
n

o
n
se
t
o
f
il
ln
e
ss
w
it
h
g
e
n
e
ra
l m
a
la
is
e

,
sp
ik
in
g
f
e
v
e
rs
, r
ig
o
rs
,
se
v
e
re
h
e
a
d
a

ch
e
,
p
h
o
to
p
h
o
b
ia
, a
n
d
m
y
a
lg
ia
s.
N
a

u
se
a
,
v
o
m
it
in
g
, c
o
u
g
h
, s
o
re
th
ro
a
t,
a

n
d
d
ia
rr
h
e
a
m
a
y
fo
ll
o
w
. F
u
ll
r
e
co
v
e
ry

t
a
k
e
s
1–
2
w
e
e
k
s.
C
li
n
ic
a
l d
ia
g
n
o
si
s.

P
h
y
si
ca
l f
in
d
in
g
s
a
re
u
su
a
ll
y
n
o
n
sp
e

ci
fi
c.
T
h
e
w
h
it
e
b
lo
o
d
c
e
ll
co
u
n
t
o

ft
e
n
s
h
o
w
s
a
st
ri
k
in
g
le
u
k
o
p
e
n
ia
a
n

d
ly
m
p
h
o
p
e
n
ia
. V
ir
u
s
is
o
la
ti
o
n
m
a
y

b
e
m
a
d
e
fr
o
m
s
e
ru
m
, a
n
d
in
so
m
e
c
a

se
s
th
ro
a
t
sw
a
b
sp
e
ci
m
e
n
s.
S
u
p
p
o
rt

iv
e
t
h
e
ra
p
y
o
n
ly
.
A
li
v
e
, a
tt
e
n
u
a
te
d

v
a
cc
in
e
is
a
v
a
il
a
b
le
a
s
a
n
in
v
e
st
ig
a

ti
o
n
a
l n
e
w
d
ru
g
. A
s
e
co
n
d
, f
o
rm
a
li
n
-
in

a
ct
iv
a
te
d
k
il
le
d
v
a
cc
in
e
is
a
v
a
il
a
b
le

f
o
r
b
o
o
st
in
g
a
n
ti
b
o
d
y
t
it
e
rs
in
t
h

o
se
in
it
ia
ll
y
r
e
ce
iv
in
g
t
h
e
li
v
e
v
a
cc

in
e
.
B
lo
o
d
a
n
d
b
o
d
y
f
lu
id
p
re
ca
u
ti
o

n
s
(b
o
d
y
su
b
st
a
n
ce
is
o
la
ti
o
n
)
sh
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It is sometimes difficult to distinguish organophos-
phate nerve agent poisoning from botulism. The copious
secretions of the nerve agent will be the significant clue
to the differential. Isolated cases have a wider differential
diagnosis including Guillain-Barré syndrome, myasthe-
nia gravis, and tick paralysis.
Botulinum toxin penetrates into the cell and blocks
release of acetylcholine, preventing neuromuscular trans-
mission and leading to muscle weakness and paralysis
(Jankovic & Brin, 1991). Botulinum toxin is thought to
preferentially affect active neuromuscular fibers and has
been shown in rats to have a greater affinity when nerve
activity is greater (Hughes & Whaler, 1962). It may also
affect the central nervous system (Hallett, Glocker, &
Deuschl, 1994). The local injection of botulinum toxin
has been used clinically to treat involuntary focal muscle
spasms and involuntary dystonia.
Botulinum toxin was used to assassinate Reinhard
Heydrich, a Nazi leader and probable successor to
Hitler. The Czechoslovakian underground used a gre-
nade impregnated with botulinum toxin made by English
researchers in Porton Down near Wiltshire, England.
Although Heydrich’s wounds were relatively minor, he
died unexpectedly several days after the attack (Mobley,
1995). Botulinum is a highly effective weapon of isolated
assault. It is a one-shot weapon that is neither commu-

nicable or transmittable, but for assignation it can be
highly effective.
Detection
Detection of botulinum may be done by mouse bioassay
or by liquid chromatography. Uses of radioimmunoas-
say and radioreceptor assays have also been reported. A
DNA probe has been designed for detection of botulinum
toxin, which would markedly expedite diagnosis. An
immunoassay has been developed by Environmental
Technologies Group, Incorporated, in Baltimore,
Maryland, to detect this toxin, ricin, and staphylococ-
cal enterotoxin.
Survivors will probably not develop an antibody
response due to the small amount of toxin required for
lethality.
Prophylaxis and Treatment
Botulinum toxoid vaccine is available (Hanson, 1994;
Hatheway, 1995; Wiener, 1996). The CDC provides
a pentavalent vaccine that gives protection from toxin
types A, B, C, D, and E but provides no protection
against the F and G type toxins. The military believes that
F and G type toxins are unlikely to be used in warfare
because the strains of Clostridium botulinum that produce
toxins F and G are difficult to grow in large quantities.
If new techniques allow production of toxins F and G
in large quantities, the pentavalent vaccine will be use-
less. A heptavalent antitoxin against types A through G
is available in limited supply at the U.S. Army Medical
Research Institute of Infectious Diseases in Fort Detrick,
Frederick, Maryland.

Treatment is supportive. Respiratory failure will
require prolonged (weeks to months) ventilatory sup-
port. If ventilatory support is available, fatalities are
likely to occur in less than 5 percent of the exposed
population.
An equine antitoxin is available and may be of some
help in both food-borne and aerosol botulism. This is
available from the CDC and protects against A, B, and E
toxins. It has been used for treating ingestion botulism
and should be given as soon as the diagnosis is made. It is
not without its own risks and it does not reverse paralysis,
but does prevent progression of the disease. There is no
human-based antitoxin currently available, but human-
based antitoxin testing is now in progress. Obviously, it
will not help in types C and D intoxication.
Although penicillin has been recommended, it is
controversial because it may increase the release of
toxin in the gut and may worsen neurological symp-
toms through lysis of bacterial cells in the gut or wound
(Hatheway, 1995). It is also assumed to be ineffective if
the toxin were to be inhaled in a direct toxin release.
Clostridium Toxins
Tetanus neurotoxin is secreted by Clostridium species
in similar fashion to botulinum. The toxin is a single
150,000-dalton polypeptide that is cleaved into two pep-
tides held together by disulfide and noncovalent bonds.
The intoxication occurs at extremely low concentrations
of toxin, is irreversible, and, like botulism, affects the
activity of the nerve cell when toxicity occurs.
Clostridium perfringens also secretes at least 12 toxins
and can produce gas gangrene (clostridial myonecrosis),

enteritis necroticans, and clostridium food poisoning.
One or more of these toxins could be produced as a
weapon. The alpha toxin is a highly toxic phospholipase
that could be lethal when delivered as an aerosol.
Clinical Effects
Where botulinum toxin causes a flaccid paralysis, tetanus
causes spastic paralysis. The tetanus neurotoxin migrates
retroaxonally (up the nerve fiber) and by transcytosis, it
reaches the spinal inhibitory neurons, where it blocks
neurotransmitter release and thus causes a spastic pa-
ralysis. Despite the seemingly different actions of tetanus
and botulism, the toxins act in a similar way at the ap-
propriate cellular level. The clinical effect in humans is
well documented and includes twitches, spasms, rictus
sardonicus, and convulsions.
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Clostridium perfringens alpha toxin would cause
vascular leaks, pulmonary damage, thrombocytopenia,
and hepatic damage. In the case of an inhaled clostrid-
ium perfringens, severe respiratory distress would occur
rapidly.
Detection
If C. perfringens is suspected, acute serum and tissue
samples should be collected for further testing. Specific
immunoassays are available for both C. perfringens and
C. tetani species. As with most of these toxins and dis-
eases, specific laboratory findings may be too late to be
of clinical use.
C. perfringens and tetanus are generally sensitive to
penicillin, and this is the current drug of choice. There
are some data that indicate treatment with either clin-
damycin or rifampin may decrease C. perfringens toxin

production and give better results.
Every medical provider is aware of the schedule for
tetanus immunizations. It is unlikely that there will be
any use of this toxin in the United States due to wide-
spread tetanus immunization (Lebeda, 1997).This may
not be true in other countries, and in the United States
there has been no published program about clinical
syndromes of overwhelming amounts of tetanus toxin.
Although the U.S. military apparently discounts this
toxin, it is so easy to make and spread and so lethal that
it would make a useful biological toxin.
There is no specific prophylaxis against most of the
C. perfringens toxins. Some toxoids for enteritis necroti-
cans are available for humans. Veterinary toxoids are
in wide use.
Ricin
Ricin is a type II ribosome inactivating protein produced
by the castor bean plant and secreted in the castor seeds
(CP FIGURE 9-1). The toxin is a 576 amino acid protein
precursor weighing 65,000 daltons. Once inside the cell,
ricin depurinates an adenine from rRNA and thereby
inactivates the ribosome, killing the cell.
Ricin is available worldwide by simple chemical pro-
cess of the castor bean. Although ricin is only a natural
product of the castor bean plant, ricin has been produced
from transgenic tobacco using gene transfer principles.
Large amounts of toxin could not be produced easily
by this transgenic method (Sehnke, Pedrosa, & Paul,
Frankel, & Ferl 1994).
Clinical Effects

The clinical picture of ricin poisoning depends on the
route of exposure. Castor bean ingestion causes rapid
onset of nausea, vomiting, abdominal cramps, coughing
up blood, seizure activity, and severe diarrhea followed
by vascular collapse. Death usually occurs on the third
day. Inhalation of ricin will cause nonspecific weakness,
cough, fever, hypothermia, and hypotension, followed
by cardiovascular collapse about 24 to 36 hours after
inhalation. Death will occur about 36 to 48 hours after
inhalation. High doses by inhalation appear to produce
severe enough pulmonary damage to cause death.
At least one fatality has been documented as a di-
rect result of ricin employed in biowarfare. In 1978,
ricin-impregnated pellets were fired from an umbrella
at Georgi Markov and Vladimir Kostov. The pellets were
coated with wax designed to melt at body temperature
and release the ricin. Markov died as a result of the
ricin attack, but Kostov survived. At least six other as-
sassinations have used the same technique, according
to intelligence sources.
Detection
Enzyme-linked immunosorbent assay for blood or his-
tochemical analysis may be useful in confirming ricin
intoxication. Ricin causes marked immune response and
sera should be obtained from survivors for measurement
of antibody response. An immunoassay technique has
been developed by Environmental Technologies Group
for ricin.
Standard laboratory tests are of little help in diag-
nosis of ricin intoxication. The patient may have some
leukocytosis with neutrophil predominance. The pleo-

morphic picture of ricin intoxication would suggest
many respiratory pathogens and may be of little help
in diagnosis.
There is no approved immunologic treatment or chemo-
prophylaxis for ricin poisoning at this time. Respiratory
protection will prevent inhalation exposure and is the
best prophylaxis currently available. Ricin has no dermal
activity and is not transported through the skin.
There is ongoing effort to produce both active im-
munization and passive antibody prophylaxis suitable for
humans. These techniques have been used in animals.
Treatment is supportive and includes both respira-
tory support and cardiovascular support as needed. If
oral ingestion is suspected, lavage followed by charcoal
is appropriate.
Saxitoxin
Saxitoxin is a dinoflagellate toxin responsible for para-
lytic shellfish poisoning. It is also found in several species
of puffers and other marine animals and was originally
discovered in 1927 (Sato et al., 1997). The toxin is very
soluble in water, is heat stable, and is not destroyed by
1/20/10 10:29:45 AM1/20/10 10:29:45 AM
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cooking. The lethal dose is 1 to 2 mg. There are multiple
related toxins with substitutions at key positions.
Clinical Effects
Saxitoxin is similar in effects and treatment to tetrodo-
toxin. Onset of symptoms is within minutes of exposure.
Death may occur within 24 hours. If the patient survives,
normal functions are regained within a few days.
Detection

A mouse unit is the minimum amount of saxitoxin that
will kill a 20-gram mouse within 15 minutes. There is a
standardized mouse assay for routine surveillance, and
immunoassays are available.
There is no antidote for saxitoxin, so symptomatic treat-
ment is appropriate. Antibodies for tetrodotoxin will
frequently protect against saxitoxin (Kaufman, Wright,
Ballou, & Monheit, 1991).
Staphylococcal Enterotoxin
Staphylococcal food poisoning is familiar to most emer-
gency practitioners. Although the disease is changed
when the enterotoxin is delivered via aerosol, it will result
in the common food poisoning syndrome. The organism
that produces this agent is readily available and could be
tailored to produce large quantities of the toxin.
Clinical Effects
Staphylococcal food poisoning begins 1 to 6 hours after
exposure with the sudden onset of fever, chills, head-
ache, myalgias, and a nonproductive cough. The cough
may progress to dyspnea and substernal chest pain. In
severe cases, pulmonary edema may be found. Nausea,
vomiting, and diarrhea are common (as in the poisoning
familiar to emergency physicians). The only physical
finding of note is conjunctival injection.
In food-borne staphylococcal enterotoxin B, fever
and respiratory involvement are not found, and the
gastrointestinal symptoms predominate. Sickness may
last as long as 2 weeks and severe exposures may cause

fatalities.
Detection
The lab is not helpful in diagnosing staphylococcal en-
terotoxin poisoning. Erythrocyte sedimentation rate
may be elevated, but this is a nonspecific finding. A
chest X-ray is usually normal, but it may have increased
interstitial markings and possibly pulmonary edema. An
immunoassay has been developed by Environmental
Technologies Group from Baltimore, Maryland, that is
cost efficient and usable in the field environment.
There is no significant treatment regimen available for
staphylococcal enterotoxin. Therapy is entirely support-
ive. There is no current prophylaxis available, although
experimental immunization has been reported.
Tetrodotoxin
Tetrodotoxin is a potent neurotoxin produced by fish,
salamanders, frogs, octopus, starfish, and mollusks, no-
tably the puffer (also called the globefish or blowfish)
(Lange, 1990).The dangers of tetrodotoxin poisoning
were known by the ancient Egyptians (2400 to 2700
B.C.). All organs of the freshwater puffer are toxic with
the skin having the highest toxicity followed by gonad,
muscle, liver, and intestine. In saltwater puffers, the liver
is the most toxic organ. The lethal dose of tetrodotoxin
is only 5 micrograms per kilogram in the guinea pig.
Puffer intoxication is a serious public health problem
in Japan, and over 50 people each year are intoxicated.
Raw puffer fish, commonly called fugu, is a delicacy

in several Southeast Asian countries including Japan.
Consumption of fugu causes mild tetrodotoxin intoxi-
cation with a pleasant peripheral and perioral tingling
sensation. Improperly prepared fugu may contain a le-
thal quantity of tetrodotoxin. Fatalities have gradually
decreased because of the increased understanding of
the toxin and careful preparation of the puffer for food
(Laobhripatr et al., 1990). Cooking the food will not
dissipate the toxin. Tetrodotoxin is heat stable.
There are several microbial sources of tetrodotoxin
including Pseudomonas, Vibrio, Listonella, and Alteromonas
species. Although there is only one known bacteria that
has produced tetrodotoxin toxicity in humans, there is
a significant potential for genetic alteration of common
species of bacteria to produce tetrodotoxin (Nozue et
al., 1990).
Tetrodotoxin is well known for its ability to inhibit
neuromuscular function by blocking the axonal sodium
channels (Tambyah, Hui, Gopalakrishnakone, & Chin,
1994). Mortality from tetrodotoxin is thought to be due
to hypoxic brain damage from prolonged respiratory
paralysis.
Clinical Effects
The clinical symptoms and signs of tetrodotoxin poi-
soning are similar to those of the acetylcholinesterase
poisons (Mackenzie, Smalley, Barnas, & Park, 1996).
Clinical symptoms include nausea, vomiting, vertigo,
perioral numbness, unsteady gait, and extremity numb-
ness. Clinical symptoms begin within 30 minutes of in-
gestion. The speed of onset depends on the quantity of
the toxin ingested. The symptoms progress to muscle
weakness, chest tightness, diaphoresis, dyspnea, chest

pain, and finally paralysis. Hypotension and respira-
tory failure are seen in severe poisonings. Patients will
frequently complain of a sensation of cold or chilliness.
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Paresthesias spread to the extremities with symptoms
often more pronounced distally. Death can occur within
17 minutes after ingestion of tetrodotoxin.
Detection
Detection of tetrodotoxin is by mouse bioassay (Yasumoto,
1991) or by liquid chromatography. Use of radioimmu-
noassay and radioreceptor assays has also been reported.
An in vitro colorimetric cell assay against a rabbit an-
tiserum has been developed and may be more rapid
than older methods, but it is not yet publicly available
(Kaufman et al., 1991).
At present, there is no known antidote for tetrodotoxin
intoxication. There are numerous anecdotal treatments
of survivors with supportive therapy alone. Certainly
respiratory support and airway management will be life-
saving for a majority of these patients. Gastric lavage
will remove unabsorbed toxin from the gut and is used
in puffer fish intoxication. Activated charcoal has been
reported to effectively bind the toxin and may be em-
ployed in ingestions.
4-Aminopyridine has been used to treat tetrodotoxin
intoxication in laboratory animals (Chang et al., 1996).
4-Aminopyridine is a potent potassium channel blocker
and enhances impulse evoked acetylcholine release from
presynaptic motor terminals. There have been no hu-
man studies of its use as an antidote. 4-Aminopyridine
can cause muscle fasciculation and seizures in a dose-
dependent phenomenon.

Naloxone has been proposed as a possible antidote
against tetrodotoxin intoxication, because the opiates
and tetrodotoxin have similar molecular configurations
(Sims & Ostman, 1986). There are no reports of this in
either laboratory or clinical use.
Active and passive immunization against tetrodotoxin
has been demonstrated in laboratory animals, although
there is no known available human immunization for tet-
rodotoxin (Fukiya & Matsumura, 1992). Tolerance does
not develop on repeated puffer fish exposure. Monoclonal
antibodies have been produced and protected laboratory
animals against lethal doses of tetrodotoxin (Matsumura,
1995; Rivera, Poli, & Bignami, 1995).
Trichothecene Mycotoxins
The trichothecene mycotoxins are produced by fungi
and achieved fame in the 1970s as the best candidates for
the infamous yellow rain found in Laos, Cambodia, and
Afghanistan. Naturally occurring trichothecenes have
caused moldy corn toxicosis in animals.
Trichothecene mycotoxins are potent inhibitors of
protein synthesis, inhibit mitochondrial respiration, im-
pair DNA synthesis, and destroy cell membranes.
Clinical Effects
Consumption of trichothecenes causes weight loss,
vomiting, bloody diarrhea, and diffuse hemorrhage.
The onset of the illness occurs within hours, and death
occurs within 12 hours. Inhalation adds respiratory dis-
tress and failure to the picture. Survivors have reported
a radiation-sickness-like disease. This has included fe-
ver, nausea, vomiting, leukopenia, diarrhea, bleeding,
and finally sepsis. Painful skin lesions also occur in

survivors.
Detection
There is no readily available diagnostic test for trichoth-
ecenes, although reference laboratories may be able to
help with gas-liquid chromatography. There are some
polyclonal and monoclonal antibodies for detection in
liquid or solid samples. Urine samples are most useful
for this purpose because the metabolites can be detected
as long as 28 days after exposure to the agent.
Ascorbic acid has been proposed to decrease the lethal-
ity of trichothecenes. This has been studied in animals
only, but because ascorbic acid has few side effects and
is cheap, it should be used in all suspected cases.
Dexamethasone (1 to 10 mg intravenously) has also
been shown to decrease lethality as late as 3 hours after
exposure to these toxins.
In ingestions, charcoal or superactivated charcoal
will absorb remaining toxin and decrease lethality.
Possible Live Bacteriological Warfare Agents
Possible live bacteriological warfare agents include
only a few diseases that have been researched. Much
of the information that is known to those in the field
was obtained from The United States Army Field Manual
8–9; Handbook on the Medical Aspects of NBC Defensive
Operations (FM 8–9) (U.S. Army, 1996; also available
on the Internet at http://www.nbc-med.org/FMs). Other
diseases have been proposed and researched as a result

of multiple sessions with interested colleagues and this
author’s travels to the city of Sverdlovsk in the Union of
Soviet Socialist Republics.
Although these diseases have been proposed by
the U.S. military and others as possible biological war-
fare agents, there is no question that the list is neither
exhaustive nor all-inclusive. Other diseases that have
been considered include typhoid fever, Ebola virus,
melioidosis, Rift Valley fever, epidemic typhus, Rocky
Mountain spotted fever, scrub typhus, coccidiomyco-
sis, histoplasmosis, Chikun-Gunya fever, Crimean-
Congo fever, Lassa fever, dengue fever, eastern equine
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encephalitis, western equine encephalitis, Venezuelan
encephalitis, Omsk hemorrhagic fever, Korean hemor-
rhagic fever, and many others (at least 60). The astute
reader can recognize the potential for biowarfare in
almost any disease that can possibly afflict humans.
Numerous other diseases could be used as biowarfare
agents against selected crops or livestock.
With the current level of gene manipulation, it is
easy to foresee a chimera-tailored bacteria or rickett-
sia that has characteristics of one disease, with tailored
resistance to all usual antibiotics, yet responsive to an
unusual antibiotic that the designer has stockpiled. It
is equally easy to think of a tailored virus that has un-
usual mortality for white Anglo-Saxon males, but has
little mortality for Asian or African American people.
One does not have to imagine an increase in lethality
in order to find substantial biowarfare applications. A
rapidly spreading upper respiratory illness—the com-
mon cold—that merely causes 3 days of cough, fever,
rhinorrhea, and malaise could be incapacitating if an
entire army caught it simultaneously. A city’s police force
would be unable to deal with terrorists effectively if over
three-fourths of the entire city’s population had uncon-
trollable diarrhea for a 2- or 3-day course.

Anthrax
Anthrax is caused by Bacillus anthracis. Under usual
(nonwartime) conditions, humans become infected by
contact with an infected animal or contaminated ani-
mal by-products. Anthrax is also known as wool-sorter’s
disease. This refers to the sheep shearers of the United
Kingdom who frequently get the cutaneous form of the
disease as part of the wool production process. There
are three forms of anthrax: cutaneous, inhalation, and
gastrointestinal. Almost all naturally occurring cases of
anthrax are cutaneous or gastrointestinal.
Anthrax was proposed and investigated as a bio-
weapon by both the Allies in World War II and the
Communists in the former Union of Soviet Socialist
Republics. Indeed, an epidemic that caused 96 cases
of human anthrax in the city of Ekatrinburg (formerly
Sverdlosvk) in the spring of 1979 has been traced to
an escaped Russian BW strain of anthrax. In these pa-
tients, the pathogen was airborne. Although medical
records were confiscated by the Soviet State Security
Committee known as the KGB, investigators have pieced
together the epidemiology and the source of the epi-
demic (Meselson et al., 1994). Following the epidemic,
thousands of citizens were immunized against anthrax,
the exteriors of the buildings and trees were washed
by local fire brigades, and several unpaved streets were
asphalted. Notably absent in the public health response
was a military component. In 1992, Russian President
Boris Yeltzin admitted that the military was the source
of the outbreak. Perestroika and the downfall of the
former Communist empire has led to greater release of
information, but the staff of city hospital number 40,
where the victims were cared for, remains quite sensitive

in discussions about this event (Maniscalco, 2001).
In the case of weaponization of anthrax, it is likely
to be disseminated as an aerosol of the very persistent
spores. The incubation time is from 1 to 6 days, but as
the Ekatrinburg incident showed, anthrax may have a
prolonged incubation period of up to 2 months. The
longer incubation periods are seen most frequently when
partial treatment has been given. The spores can be quite
stable, even in the alveolus, and as such frequently re-
main dormant, but very much alive for up to 3 months.
The duration of the disease is between 2 and 5 days.
Presentation
The inhalation form of anthrax is particularly uncom-
mon and particularly lethal. In its early presentation,
inhalation anthrax could be confused with a plethora of
viral or bacterial respiratory illnesses. The disease pro-
gresses over 2 to 3 days acting much like a common flu
and then suddenly develops respiratory distress, shock,
and death within 36 hours. Widening of the mediasti-
num on chest radiograph is common in the later stages
of the disease and is due to the swollen and engorged
lymph nodes within the mediastinum. Unfortunately the
radiographic evidence is a late finding and does not bode
well for survival of the patient. Evidence of infiltrates
on the chest X-ray are uncommon. Other suggestive
findings include chest wall edema, hemorrhagic pleural
effusions, and hemorrhagic meningitis.
Diagnosis
Diagnosis can be made by culture of blood, pleural fluid,
or cerebrospinal fluid. The blood culture is most often
positive. In fatal cases, impressions of mediastinal lymph

nodes or spleen will be positive. Anthrax toxin may be
detected in blood by immunoassay.
The cases in Ekatrinburg were diagnosed on autopsy
by a pathologist who noted a peculiar “cardinal’s cap”
meningeal inflammation typical in anthrax. Inhalational
anthrax may be diagnosed at autopsy by the mediastinal
inflammation that can also be observed on computerized
tomography scan of the chest in the living patient.
Environmental Technologies Group, Incorporated,
has developed an immunoassay for anthrax.
Therapy
Penicillin is considered the drug of choice for treatment
of naturally occurring anthrax. However, penicillin-
resistant strains do exist, and one could expect that
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anthrax used for a BW would be developed as peni-
cillin resistant. Tetracycline and erythromycin have
been used for patients who are allergic to penicillin.
Induction of resistance to these antibiotics is an easy
exercise for genetic manipulation, and warfare strains
should be presumed to be resistant to these antibiotics
until proven otherwise. Chloramphenicol, gentamycin,
and ciprofloxacin would be appropriate choices for ini-
tial therapy. The U.S. military recommends oral cipro-
floxacin or intravenous doxycycline for initial therapy
(U.S. Army, 1996). This therapy is not appropriate for
those under 18 years of age or for pregnant females.
Supportive therapy for airway, shock, and fluid volume
deficits is appropriate.
Prophylaxis
Two types of anthrax vaccine for human use are avail-
able in the United States and United Kingdom, albeit
in totally insufficient quantities for a civilian biological

warfare challenge. Both are based on the partially puri-
fied protective antigen of the Bacillus anthracis adsorbed
to an aluminum adjuvant. The usual immunization se-
ries is six 0.5 mL doses over a span of 18 months. The
military feels that a primary series of three 0.5 mL doses
(at 0, 2, and 4 weeks) will be protective against both
cutaneous and inhalation anthrax for about 6 months
after the primary series. These immunizations were
given to many coalition troops during the Gulf War in
anticipation of Saddam Hussein’s employment of this
agent. Large quantities of antigen are presumed to be
stockpiled for military use because this agent has been
a recurring threat. Unless civilian immunizations start
about 1 month prior to a terrorist attack, EMS and medi-
cal providers will be essentially unprotected.
Although minor reactions to the anthrax vaccine
are common (occurring in 6 percent of the immunized
population), major reactions are uncommon. Obviously,
the vaccine is contraindicated for those who are known
to be sensitive to it and for those who have already had
clinical anthrax. The choice between immunization and
some allergic reaction and no immunization in the face
of a serious biowarfare threat presents a difficult clinical
dilemma.
Live anthrax vaccine is used in Russia to immunize
both livestock and human beings. It is a spore vaccine
with both STI-1 and strain 3 mixtures. The Russians feel
that this vaccine is superior at stimulating cell-mediated
immunity (Shlyakhov & Rubinstein, 1994). There would
be considerable resistance to use of the Russian vaccine
in Western countries because of concerns over purity
and residual virulence of a live vaccine.
There is no available evidence that these vaccines

will adequately protect against an aerosol challenge. New
vaccines with a highly purified protective antigen or
designer attenuated strains have both been used in labo-
ratories but are not commercially available (Coulson,
Fulop, & Titball, 1994; Ivins et al., 1995).
Antibiotic prophylaxis with ciprofloxacin (500 mg
orally twice day), or doxycycline (100 mg orally twice a
day) is also recommended by the U.S. military for an im-
minent attack by a BW. Should the attack be confirmed
as anthrax, then antibiotics should be continued for 4
weeks for all who are exposed. Those exposed should
also be started on antianthrax vaccine with the standard
schedule (if it is available) if they have not been previ-
ously immunized. Those who have received fewer than
three doses of vaccine prior to exposure should receive
a single booster injection. If vaccine is not available, an-
tibiotics should be continued until patients can be safely
and closely observed when the antibiotics are discon-
tinued. Inhaled spores are not destroyed by antibiotics
and may persist beyond the course of recommended
antibiotics.
Brucellosis
Brucellosis is a zoonotic disease caused by small non-
motile coccobacilli. The natural reservoir is domestic
herbivores such as goats, sheep, cattle, and pigs. There
are four species: Brucella melitensis, B. abortus (cattle),
B. suis (pigs), and B. canis (dogs). Humans become in-
fected when they ingest raw infected meat or milk, inhale
contaminated aerosols, or make contact with their skin.
Human infection is also called undulant fever. Human-
to-human transmission can occur only if serum is passed
from an infected patient to another human, so it is ex-
tremely rare.

Brucella species have been long considered as bio-
logical warfare agents because of the stability, persis-
tence, and ease of infection without human-to-human
transfer. Brucellosis can be spread by aerosol spray or
by contamination of food supply (sabotage). There is a
long persistence in wet ground or food.
Presentation
The incubation period for brucellosis is about 8 to 14
days, but may be considerably longer. Clinical disease
is a nonspecific febrile illness with headache, fatigue,
myalgias, anorexia, chills, sweats, and cough. The fe-
ver can reach up to 105°F. The disease may progress
and include arthritis, lymphadenopathy, arthralgias,
osteomyelitis, epididymitis, orchitis, and endocarditis.
Disability is pronounced, but lethality is only about
5 percent or less in usual cases. The disease may be
followed by recovery and relapse. The duration of the
disease is usually a few weeks, but brucellosis can last
for years.
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Diagnosis
Diagnosis of brucellosis is by blood culture, by bone
marrow culture, or by serology. There are no other
laboratory findings that contribute to a diagnosis of
brucellosis.
Therapy
To treat brucellosis, the U.S. military recommends doxy-
cycline (100 mg twice a day) plus rifampin (900 mg/day)
for 6 weeks. These antibiotics are generally available
in sufficient quantities in the United States. Alternative
proposed therapy has been doxycycline (100 mg twice a
day) for 6 weeks and streptomycin (1 g/day) for 3 weeks.
Trimethoprim/sulfamethoxazole has been given for 4 to

6 weeks but is thought to be less effective. Relapse and
treatment failure is common.
Prophylaxis
There is no information available about chemoprophy-
laxis for brucellosis. Human vaccines are not routinely
available in the United States, but they have been devel-
oped by other countries. A variant of B. abortus, S19-BA,
has been used in the former Union of Soviet Socialist
Republics to protect occupationally exposed groups.
Efficacy is limited and annual revaccination is needed. A
similar vaccine is available in China. Neither of these two
vaccines would meet Western requirements for safety
and effectiveness (Corbel, 1997).
Cholera
Cholera is a well-known diarrheal disease caused by
Vibrio cholerae acquired in humans through ingestion
of contaminated water. The organism causes a pro-
found secretory rice-water diarrhea by elaborating an
enterotoxin.
Although cholera can be spread by aerosols, more
likely terrorist or military employment would be con-
tamination of food or water supplies. There is negligible
direct human-to-human transmissibility. The bacterium
does not have long persistence in food or pure water and
is not persistent when applied by aerosols, thereby mak-
ing it an ineffective bioweapon for mass distribution.
Presentation
Cholera can cause a profuse, watery diarrhea that
causes hypovolemia and hypotension. Without treat-
ment, cholera can rapidly kill adults and children alike

from severe dehydration and resultant shock. The in-
cubation period is 1 to 5 days and the course of the
illness is about 1 week.
A patient with cholera may have vomiting early in
the illness. There is little abdominal pain associated with
the disease. The hallmark of the disease is rice-water
diarrhea.
Diagnosis
Gram staining of the stool sample of a person with
cholera will show few or no red or white cells. Renal
failure may complicate severe dehydration. Electrolyte
abnormalities are common with the profound fluid loss;
generally hypokalemia predominates.
Rotavirus, Escherichia coli, and toxic ingestions such
as staphylococcal food poisoning, Bacillus cereus, and
even clostridia species can cause similar watery diar-
rhea. Bacteriological diagnosis of cholera diarrhea has
been well studied for decades. Vibrio species can be seen
and identified readily with dark field or phase contrast
microscopes. Culture will prove the diagnosis but is not
necessary for the treatment.
Therapy
Treatment of cholera is mostly supportive. Although
most U.S. emergency physicians are used to treating
significant hypovolemia with intravenous fluid re-
placement, it is unlikely to be readily available if an
epidemic of cholera is caused by terrorist or enemy
action. The World Health Organization (WHO) oral
rehydration formula is appropriate but generally not
stocked in sufficient quantities in most cities. Pedialyte

and sport drinks such as Gatorade will provide interim
oral hydration. If a cholera epidemic develops, intra-
venous fluids should be reserved for those patients
who are vomiting and cannot tolerate oral rehydration,
patients who have more than 7 liters per day of stool,
and patients who have extensive hypovolemia and are
in clinical shock.
Tetracycline and doxycycline have both been found
to shorten the course of the diarrhea. Other effective
drugs include ampicillin (250 mg every 6 hours for 5
days) and trimethoprim/sulfamethoxazole (1 tablet every
12 hours). Appropriate alteration of dosages should be
used for pediatric patients.
Prophylaxis
The currently available vaccine for cholera is a killed sus-
pension of V. cholerae. It provides incomplete protection
and lasts for no longer than 6 months. It requires two
injections with a booster dose every 6 months. Improved
vaccines are being tested but are not yet available.
Ebola Virus
The Ebola virus is a member of a family of RNA viruses
known as filoviruses commonly referred to as viral hem-
orrhagic fever (VHF) (CP FIGURE 9-2). When magnified
several thousand times by an electron microscope, these
viruses have the appearance of long filaments or threads.
Ebola virus was discovered in 1976 and was named
for a river in Zaire, Africa, where it was first detected
(CDC, 2009).
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Ebola virus has been covered significantly in the pop-
ular literature and in several books and movies (including
Outbreak). Members of the Aum Shinrikyo cult visited
Zaire to collect Ebola. This virus is highly contagious and
easily spread by body fluids, particularly blood. It is quite
dangerous for the healthcare provider because human-

to-human contact will rapidly spread the disease. Ebola
and all of the VHFs are capable of being aerosolized.
Use of this virus (with greater than 90 percent le-
thality) would be considered a doomsday operation by
the military. There is no guarantee that this virus would
be able to be contained if spread to a modern city. The
persistence is low, but the transmissibility is so high that
this is immaterial.
For example, the distribution of the virus might be
effective by simply putting an infected individual on a
plane that flies around the world and ensuring that he
coughs repeatedly. The effect of this distribution plan
could be extraordinary because the incubation period
for overt illness is upwards of 14 days.
Presentation
Ebola virus is a viral hemorrhagic fever. It can be spread
by blood and blood products, secretions, and by drop-
let nuclei or aerosol transmission ( Jaax et al., 1995).
It is highly lethal (more than 90 percent) with a rapid
course.
Diagnosis
A diagnosis is made by detection of Ebola antigens, anti-
body, or genetic material, or by culture of the virus from
these sources. Diagnostic tests are usually performed on
clinical specimens that have been treated to inactivate
(kill) the virus. Research on Ebola virus must be done
in a special, high-containment laboratory to protect sci-
entists working with infected tissues.
Therapy

Therapy is supportive only and involves extensive critical
care medicine including artificial ventilation. A release of
Ebola would significantly tax the overall healthcare sys-
tem and require tremendous resources for each patient.
Even then it is important that everyone understand that
there is no known therapy for this disease.
Prophylaxis
There is no known prophylaxis for Ebola virus. Sera
from survivors have been obtained, and it is possible
that passive protection could be developed. A recent
accidental exposure to live Ebola virus was successfully
treated with convalescent antisera.
Plague
Plague is a zoonotic disease caused by Yersinia pestis.
It is naturally found on rodents and prairie dogs and
their fleas. Under normal conditions, the following three
syndromes are recognized: inhalational (pneumonic),
septicemic, and bubonic. Usually an initial infection is
in the form of bubonic plague.
In 1994 defectors revealed that the Russians had
conducted research on Yersinia pestis, the plague bac-
terium, to make it more virulent and stable in the
environment. The plague can retain viability in water
for 2 to 30 days, in moist areas for up to 2 years, and
in near freezing temperatures for several months to
a year.
Plague could be spread by either infected vectors
such as fleas or by an aerosol spray. Person-to-person
transmissibility is high and the bacterium is highly in-

fective. The persistence is low, but the transmissibility
is so high that this is immaterial.
Presentation
In bubonic plague, the incubation period is from 2 to 10
days. The onset is acute with malaise, fever (often quite
high), and purulent lymphadenitis. The lymphadenitis
is most often inguinal, but cervical and axillary nodes
can also be involved, depending on where the flee bites
occurred (CP FIGURE 9-3A and CP FIGURE 9-3B). As the
disease
progresses, the nodes become tender, fluctuant, and fi-
nally necrotic. The bubonic form may progress to the
septicemic form whereby the plague bacterium infects
the major organ systems systemically. Involvement of the
lungs results in the pneumonic form and the patient be-
comes contagious through coughing and droplet nuclei.
The course of the disease is 2 to 3 days, and the disease
has a high mortality rate.
In primary pneumonic plague, the incubation pe-
riod is 2 to 3 days. The onset is acute and fulminant with
malaise, fever, chills, cough with bloody sputum, and
toxemia. The pneumonia progresses rapidly to respira-
tory failure with dyspnea, stridor, and cyanosis.
In untreated patients, the mortality is over 50 percent
for the bubonic and septicemic forms. In the pneumonic
form, the mortality approaches 100 percent. The termi-
nal events in septicemic plague are circulatory collapse,
hemorrhage, and peripheral thrombosis. In pneumonic
plague, the terminal event is often respiratory failure as
well as circulatory collapse.
Diagnosis

A presumptive diagnosis of plague can be made by find-
ing the typical safety pin bipolar staining organisms in
Giemsa-stained specimens. Appropriate specimens are
lymph node aspirate, sputum, or cerebral spinal fluid.
Immunofluorescent staining is available and helpful if
readily accessible. Y. pestis can be readily cultured from
any of these sources.
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Environmental Technologies Group, Incorporated,
has developed an immunoassay for plague.
Therapy
Plague is readily contagious and strict isolation of patients
is essential. Streptomycin, tetracycline, and chloram-
phenicol are all useful if they are given within the first
24 hours after symptoms of pneumonic plague begin.
Supportive therapy of complications is essential.
Prophylaxis
Plague vaccine is available but has not been shown to
be effective against an aerosol exposure and subsequent
pneumonic plague. The plague vaccine is a whole cell
formalin-killed product. The usual dose is 0.5 mL given
at 0, 1, and 2 weeks.
Plague vaccines providing protection against aerosol
exposure are not yet available but are under develop-
ment (Oyston et al., 1995). Current whole-cell plague
vaccines stimulate immunity against the bubonic form
but are probably not effective for the pneumonic form
(Meyer, 1970; Russel et al., 1995).
Q Fever
Q fever is a rickettsial zoonotic disease caused by Coxiella
burnetii. The usual animals affected are sheep, cattle, and
goats. Human disease is usually caused by inhalation of

particles contaminated with Coxiella.
Presentation
Q fever is a self-limiting febrile illness of 2 days to 2
weeks. The incubation period is about 10 to 20 days.
The patient is visually ill, but uneventful recovery is the
rule. Q fever pneumonia is a frequent complication and
may be noted only on radiographs in most cases. Some
patients will have nonproductive cough and pleuritic
chest pain. Other complications are not common and
may include chronic hepatitis, endocarditis, meningitis,
encephalitis, and osteomyelitis.
The value of this disease as a BW is in disruption
of society. Mass distribution of the C. burnetii would
cause significant societal disruption by overloading the
healthcare system, creating fear, and causing mass social
distancing, thereby disrupting the economy.
Diagnosis
Q fever’s presentation as a febrile illness with an atypical
pneumonia (characterized by a dry cough) is similar to
a host of other atypical pneumonias, including myco-
plasma, legionnaire’s disease, chlamydia pneumonia,
psittacosis, or hantavirus.
The diagnosis can be confirmed serologically and
other laboratory findings are unlikely to be helpful. Most
patients with Q fever will have slightly elevated liver
enzymes. It is difficult to isolate rickettsia, and Q fever
is no exception.
Therapy

As with other rickettsial diseases such as Rocky
Mountain spotted fever, the treatment of choice for
Q fever is tetracycline, doxycycline, or erythromycin.
Although not tested, azithromycin and clarithromycin
would be expected to be effective.
Prophylaxis
A formalin-inactivated whole cell vaccine is available as
an investigational drug in the United States and has been
used for those who are at risk of occupational infection
with Q fever (Ackland, Worswick, & Marmion, 1994).
One dose will provide immunity for an aerosol challenge
within 3 weeks.
Skin testing is required to prevent a severe local reac-
tion in previously immune individuals. A live attenuated
strain (M44) has been used in the former Union of Soviet
Socialist Republics (Genig, 1965).
Smallpox
Smallpox was used as a BW in the United States during
the French and Indian War. Smallpox is an orthopox
virus that affects primates, particularly man. The disease
was declared eradicated in the world in 1977, and the
last reported human case occurred in a laboratory in
1978. Theoretically, the virus exists in only two labo-
ratories in the world, one in the United States and one
in Russia. The virus can be transmitted by face-to-face
contact, droplet nuclei, secretions, and aerosols. It is a
durable virus and can exist for long periods outside the
host. It is remotely possible that it is still living outside of
the repository labs. A very closely related disease, mon-
keypox, cannot be easily distinguished from smallpox
without significant evaluation of its RNA. A major con-

cern of disaster medicine planners is/was the develop-
ment of this virus as a war weapon by the former Soviet
Union and the unknown amount of product produced
at the time.
Release of this virus would have massive and ex-
treme societal effects. Although much of world was vac-
cinated in the 1960s and 1970s, it is unknown whether
those vaccinations would in fact protect an individual.
Given that vaccinations were stopped by WHO in 1985,
it is supposed that an entire generation could be totally
unprotected and thus suffer massive mortality from the
disease if it were to be released. Because of the virus’s
communicability, only one person need be infected to
distribute this virus on an unsuspecting and unprotected
world.
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Presentation
Smallpox has a long incubation period of about 10 to
17 days. The illness has a prodrome of 2 to 3 days with
malaise, fever, headache, and backache. Over the next
7 to 10 days, all of the characteristic lesions erupt, prog-
ress from macules to papules to vesicles to pustules and
then crust and scarify (CP FIGURE 9-4). The lesions are
more numerous on the extremities and face than on the
trunk. The disease is fatal in about 35 percent of cases.
Some patients will develop disseminated intravascular
coagulopathy. Other complications include smallpox
pneumonia, arthritis (a person who had smallpox may
have permanent joint deformities), and keratitis (which
may cause blindness).
Diagnosis
Like many viral diseases, the diagnosis of smallpox is
best made by clinical impression. Routine labs are not
helpful, although leukopenia is frequent. Clotting factors
may be depressed and thrombocytopenia may be found.

Diagnosis may be made with immunofluorescence, elec-
tron microscopy, or culture.
Clinical presentation would allow the diagnosis to
occur rapidly in most healthcare settings. Much has
been written and distributed about smallpox since the
failed vaccination program of 2003. As a result, it is
likely that any person presenting to most any healthcare
clinic or emergency department would be identified
rapidly.
Therapy
Therapy for smallpox is entirely supportive. Use of
several antiviral medications has been proposed as
possible amelioration treatment, but this is untested.
It is understood by science that administration of
the vaccination post–disease development will likely
lessen the disease process and as a rule would be given
to all patients, unless they are pregnant or immuno-
compromised.
Prophylaxis
Prophylaxis against smallpox has been available since
the early 1800s when Dr. Edward Jenner developed a
vaccine and is well documented. Because smallpox is
presumed to have been eradicated worldwide, there is
no recommendation or requirement for routine vacci-
nation. Adequate stocks of smallpox vaccine are prob-
ably not available for exposure of large portions of the
population. It is anticipated that if an outbreak were
to occur, institution of a ring vaccination plan (similar
to what eradicated the disease) would be immediately
instituted, and this would limit the spread.

Objects in contact with a contaminated patient need
to be cleansed with live steam or sodium hypochlorite
solution.
Tularemia
Tularemia or rabbit fever is caused by Francisella tularen-
sis, a gram-negative bacillus. Humans can contract this
disease by handling an infected animal or by the bites of
ticks, mosquitoes, or deerflies. The natural disease has a
mortality rate of 5 to 10 percent. As few as 50 organisms
can cause disease if inhaled.
Presentation
Like plague, tularemia has an ulceroglandular form, a
pneumonic form, and a septicemic form. Two addi-
tional forms also occur with tularemia. Oculoglandular
tularemia occurs when the inoculum is in the eye.
Gastrointestinal tularemia occurs when tularemia bacilli
are ingested. It may also infect the oropharynx.
The septicemic form can occur in 5 to 15 percent of
natural cases. The clinical features include fever, prostra-
tion, and weight loss.
The pneumonic form may occur by inhaling con-
taminated dusts or by a deliberate aerosol. The resulting
pneumonia is atypical and may be fulminant. Fever,
headache, malaise, substernal discomfort, and cough are
prominent. The cough is often nonproductive. A chest
X-ray may or may not show a pneumonia.
Diagnosis
As noted, the diagnosis of pneumonic tularemia will be
difficult clinically, with several types of atypical pneumo-

nia as differential diagnoses. The laboratory is unhelpful
early in this disease.
Therapy
Human-to-human spread of pneumonic tularemia is
unusual and isolation is not required.
Treatment is streptomycin or gentamycin for 10
to 14 days. Tetracycline and chloramphenicol are also
useful, but the military reports that there has been a
significant relapse rate.
Prophylaxis
A live vaccine strain is available to U.S. military personnel.
This vaccine is delivered intradermally and provides pro-
tection to an aerosol challenge by the third week postim-
munization. Protection is dependent on the inhaled dose
of tularemia, and inhalation of massive quantities of bac-
teria may overwhelm the protective effects of the vaccine
(Hornick & Eigelsbach, 1966). Protection falls after 14
months, suggesting that a booster dose is appropriate.
This vaccine is not available for civilian use.
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Chapter Summary
As the emergency service community continues to be
subjected to reports of escalating bioterrorism threats,
the increase of media attention on the biothreat results
in heightened fears and public questions of readiness.
Events such as the West Nile virus outbreak immediately
result in the press and public fearing that the event was a
deliberate act rather than a naturally occurring event.
While the probability of a high-impact or wide-
spread attack using BWs is low, the yield from such an
event could be devastating. It is for this reason that be-
ing prepared to respond to the aftermath of a biological

attack is critical. As highlighted in this chapter, there
are many complex issues that nonmilitary responders
are not familiar with that accompany the planning and
response phases of a bioterrorism event. We strongly
recommend that this matter be given the attention it
deserves so that your members can be protected and
the response effectiveness to your community can be
maintained.
Remember that this type of incident can rapidly
swell to a level that will overwhelm your EMS system
as well as local healthcare resources. Incorporating the
talents of your public health and hospital officials in
the planning process will provide you with the ability
to develop comprehensive and cohesive contingency
plans.
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Wrap Up
Chapter Questions
1. Define biological warfare. How is a biological at-
tack different from other, more traditional forms
of terrorism?
2. Briefly discuss the history of biological terrorism.
3. What are the major steps in a biological threat
assessment?
4. What types of PPE are necessary for emergency
responders in a biological event?
5. Discuss the clinical effects, detection, and
prophylaxis/treatment for the following biologi-
cal toxins:
a. Ricin
b. Botulinum toxin
c. Clostridium toxin

6. Discuss the clinical effects and treatments for:
a. Anthrax
b. Ebola virus
c. Tularemia
d. Q fever
Chapter Project
Develop a comprehensive outline of a biological threat as-
sessment for your jurisdiction or region. Consider key as-
sessment elements from this chapter including detection,
control of supplies, PPE, training, and prophylaxis.
Vital Vocabulary
Biological terrorism The use of etiological agents (dis-
ease) to cause harm or kill a population, food, and/or
livestock.
Community shielding An effective and unique pre-
paredness strategy to engage individuals, communi-
ties, and government in a unified response to disasters
and future acts of terrorism, in particular bioterrorism.
Originating from the University of Virginia’s Critical
Incident Analysis Group, this strategy is being adopted
widely as a means of community and organizational
resilience.
Enzyme-linked immunosorbent assay An immuno-
logical immunoassay technique for accurately measur-
ing the amount of a substance, for example, in a blood
sample.
Erythrocyte sedimentation rate Also called the sedi-
mentation rate or Biernacki reaction, it is the rate at

which red blood cells precipitate in a period of one
hour; a common hematology test which is a nonspe-
cific measure of inflammation. Anticoagulated blood
is placed in an upright tube, known as a Westergren
tube, and the rate at which the red blood cells fall is
measured and reported in mm/h.
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and later.)
>>
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>>
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>>
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>>
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>> setpagedevice
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>>
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>>
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/SVE
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and later.)
>>
/Namespace [
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<<
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>>
<<
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>>
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>>

]
<<
/PageSize [684.000 855.000]
>> setpagedevice

85Operations Security, Site Security, and Terrorism In.docx

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