Serum Troponin I Measurement of Subjects Exposed to the Taser X-26®

Christian M. Sloane MD
1. , a, Theodore C. Chan MDa, Saul D. Levine MDa, James V. Dunford MDa, Tom Neuman
MDa and Gary M. Vilke MDa
a

Department of Emergency Medicine, University of California, San Diego Medical Center, San
Diego, California
Received 9 February 2007;
revised 5 June 2007;
accepted 14 August 2007.
Available online 4 March 2008.

Abstract
The Taser® is a high-voltage, low-amperage conducted energy device used by many law
enforcement agencies as a less lethal force weapon. The objective of this study was to evaluate
for a rise in serum troponin I level after deployment of the Taser® on law enforcement training
volunteers. A prospective, observational cohort study was performed evaluating serum troponin I
levels in human subjects 6 h after an exposure to the Taser X-26®. Outcome measures included
abnormal elevation in serum troponin I level (> 0.2 ng/mL). There were 66 subjects evaluated.
The mean shock duration was 4.36 s (range 1.2–5 s). None of the subjects had a positive
troponin I level 6 h after exposure. It was concluded that human volunteers exposed to a single
shock from the Taser® did not develop an abnormal serum troponin I level 6 h after shock,
suggesting that there was no myocardial necrosis or infarction.
Keywords: Taser; cardiac; troponin I; CED (conductive energy/electrical device); myocardial
necrosis; less lethal weapon

Article Outline
Introduction
Materials and Methods
Study Design
Data Collection and Processing
Primary Data Analysis
Results

Discussion
Limitations
Conclusions
Acknowledgements
References

Introduction
The Taser® is a weapon that delivers high-voltage, low-amperage electricity in a pulsed
waveform and is representative of the group of less lethal weapons known as conducted energy
devices (CEDs). Although generally regarded as safe, there is little research on the effects of
these devices in the medical literature despite deaths reported in proximity to CED use. These
deaths have drawn wide media and lay public attention, raising questions regarding the overall
safety of CEDs as less lethal devices ([1], [2] and [3]).
Although deaths have been associated with the device's use (so-called “proximity deaths”), no
direct causal link has yet been identified. Recent studies have aimed to identify potential
physiologic consequences of a CED application (primarily in animals, but also in human trials)
([4], [5], [6], [7] and [8]). Because these devices deliver a high-voltage electrical discharge to the
body, some have suggested that CEDs may cause cardiac injury that could lead to sudden death
(9). Animal studies have drawn equivocal conclusions as to the cardiac effect of these devices
([5] and [6]). Our group has previously reported on the effect of CEDs in human subjects,
finding no significant cardiac dysrhythmias immediately after a CED application (8). For the
current study, we hypothesized that a Taser X-26® discharge would not result in myocardial
injury as measured by a rise in the cardiac enzyme troponin I 6 h post-activation in a population
of law enforcement training volunteers.

Materials and Methods

Study Design
This is a prospective cohort study performed with San Diego Police and San Diego County
Sheriff law enforcement officers undergoing training in the use of the Taser X-26® between
December 2005 and June 2006. As a component of training, officers were offered the
opportunity to experience the effects of the device. This strictly voluntary exposure was
delivered by either firing the Taser® dart at the subject from a distance of 10 feet or attaching
the subject to the device with two alligator clips. The maximum duration of shock delivered was
5 s, although one agency allowed that subjects could abort the deployment before the typical 5-s
standard firing duration. Duration is the only variable that can be adjusted. Each shock delivers
50,000 volts, 21 milliamps. This is constant and cannot be altered.
We enrolled only subjects who had previously volunteered to experience the Taser® exposure as
a part of their training. Those trainees who did volunteer were then approached and asked to
participate in our study. Informed consent was obtained from each subject. All subjects were
attached to a three-lead monitor both for safety and to determine the duration of the shock.
Subject inclusion criteria for study consisted of law enforcement personnel between the ages of
18 and 60 years who were willing to participate. There was only one shock delivered.
Exclusion criteria for our study, but not the voluntary exposure, included individuals who were
found to have a dysrhythmia before deployment of the Taser®, known or suspected history of
cardiac disease, individuals suspected to be under the influence of drugs, or inability to provide
informed consent. The police agencies did not exclude anyone who volunteered to get an
exposure.
Demographic data were not obtained from the subjects. The subjects as a group were typical
police officers, male and female, who were members of both the San Diego Police Department
and the San Diego County Sheriff's Office. The typical class consisted of 20–30 officers, of
whom anywhere from 1 to 8 volunteered for exposure. Of those who had volunteered for the
exposure, 90% agreed to participate in our study. The main reason given for declining our study
was aversion to a blood draw.
This study was approved by the UCSD Institutional Review Board.

Data Collection and Processing
Six hours after application of the CED, a single 5-mL sample of venous blood was obtained from
all subjects using standard blood draw technique and analyzed for troponin I levels. Samples
from the initial 9 subjects were analyzed using a Biosite (San Diego, CA) “Triage Meter” pointof-care assay. Due to an improved cost profile, all subsequent samples were analyzed at the
UCSD Medical Center chemistry laboratory using the Advia Centaur Immunoassay System
(Siemens Healthcare Diagnostics, Tarrytown, NY).

Primary Data Analysis
Laboratory results were recorded as positive (troponin I $ 0.2 ng/mL) or negative (troponin I <
0.2 ng/mL). After the results were obtained, all blood samples were subsequently destroyed.
The primary endpoint was a positive troponin I. The duration of each CED application was also
recorded. Data were entered into an Excel spreadsheet (Microsoft Corporation, Redmond, WA)
and confidence intervals calculated.

Results
A total of 66 subjects volunteered and underwent a Taser X-26® shock delivery. A total of 47
experienced a 5-s discharge. No patients were excluded from participation based on an abnormal
baseline rhythm strip and none was excluded based on a history of cardiac disease.
The mean duration of discharge was 4.36 s (median 5 s, range 1.2–5 s). Six-hour troponin I
results were negative (troponin I # 0.2 ng/mL) in all subjects (95% confidence interval 0–5.4%).

Discussion
Both the San Diego Police Department and San Diego Sheriff's Department purchased the
Taser® X26, and it was estimated that more than 1000 units were placed into service by the end
of 2006. The training procedure for both agencies includes a multi-day course including how to
operate the device, safety, and tactics. Officers are also provided an opportunity to actually
experience the deployment of the Taser® but are under no pressure or obligation to do so. No
firm numbers were recorded, but in our observation, approximately 10% of all officers
participating in the CED training over the study period volunteered to experience the Taser®
shock.
The Taser® is designed to be deployed up to 7 meters (21 feet) from the subject. By pulling the
trigger, a compressed nitrogen cartridge device deploys two, approximately 2-cm-long barbtipped darts at 160 feet per second that are attached to the gun by thin, 7-meter (21-foot) copper
wires through which the electrical shock is delivered. The Taser® delivers energy as a sequence
of dampened sine-wave current pulses, each lasting about 11 ms. This energy is reportedly
neither pure alternating current (AC) nor pure direct current (DC), but akin to rapid-fire, lowamplitude DC shocks (10). The power output of the device is 26 watts, with an average 2.1 mA
of current and a maximum of 50,000 volts. A pulse of 5 s duration is automatically delivered
through the wires to incapacitate the subject by causing involuntary tonic-clonic muscular
contractions. An officer may repeat the delivery of electricity by pulling the device trigger again.
When used in demonstrations, an alligator clip adaptor permits electrical discharge without
actual deployment of dart. The manufacturer states that thousands of law enforcement volunteers
have received shocks without harm, although many of these uses employed only 0.5-s discharges
(11).

Although the potential for adverse effects of the Taser® are not well understood, the device
generally has been regarded as safe ([5], [11] and [12]). However, deaths have been reported in
individuals in the field after a CED deployment. The vast majority of deaths reported in
“tasered” subjects are associated with illicit drug use, especially phencyclidine in the 1980s (13).
There are some reported deaths of “tasered” subjects found not to be under the influence of
drugs, although these cases generally involve subjects with other co-morbid factors presenting in
a state of excited delirium ([13], [14] and [15]).
There are a number of animal studies investigating the physiologic effects of Taser® and CEDs.
A 1989 study on earlier “stun-gun” models (with higher energy output) demonstrated the ability
to induce deadly cardiac rhythms, including asystole and ventricular fibrillation, in a swine
model (6). Subsequent studies directly stimulating porcine hearts using the newer Taser® failed
to induce cardiac dysrhythmia (5). In a swine model using much more aggressive and prolonged
CED exposures consisting of 5 s on, 5 s off for 3 min, Jauchem et al. showed that neither
troponin T nor troponin I became elevated when measured at 60 min post-exposure (4).
Research on human subjects is more limited. Our group recently reported on human subjects
who were monitored electrocardiographically before and after a Taser® deployment. In this
study of 120 subjects, there were no significant rhythm disturbances other than an increase in
sinus tachycardia after a Taser X-26® (8).
The next logical step for us was to assess whether there is any cardiac damage as a result of a
CED application. We measured serum troponin I levels 6 h after the shock in our human
volunteers. Troponin I is a standard marker with excellent sensitivity and specificity at 6 h for
myocardial ischemia, infarction, and necrosis ([16] and [17]). In fact, troponin I is routinely used
in emergency departments to assess patients with chest pain for myocardial infarction ([16] and
[18]). We hypothesized that if the Taser® is directly injuring heart muscle as a result of
electrical current, this should be apparent by 6 h, as the release of troponin I is typically
measurable as soon as 4 h after cardiac injury. Our study demonstrates that there is no significant
injury to cardiac myocytes measured by troponin I as a result of a Taser® shock.
Manufacturer-sponsored studies have reported similar results to our study. Ho et al. measured
troponin I levels in 66 human subjects measured immediately after a 5-s Taser X26® application
in resting human subjects, then again at 16 and 24 h after Taser® application (7). All values were
negative except for one subject who had a slight troponin I elevation at 24 h. This patient had a
complete cardiac evaluation including cardiac stress test, which was normal. No cause for the
elevated troponin was identified. A repeat level 8 h later was negative. Possible explanations
given by the authors for the elevated troponin were laboratory error, delayed physiologic
clearance, or idiopathic. The subject suffered no complications (7).

Limitations
Our subjects were healthy resting volunteers without coexisting use of stimulant drugs or excited
delirium. We also excluded subjects with significant cardiac disease. These are potentially the
patients who would be the most likely to show a rise in troponin if one were to occur. However,
due to ethical limitations and institutional review board policies, this is an area of study that
simply cannot be done in humans at present.
Whereas the majority of our subjects (47 of 66; 71%) were exposed to a full 5-s shock, a small
number of subjects did abort the shock after a shorter duration. As we found no abnormal
elevation in either group (full 5-s shock or those who stopped before the full 5-s discharge), it is
unclear what effect this may have had on our results.
As this was an initial study, we delivered only one shock to each volunteer. This may not always
be the case in field deployments. In our study in humans, we found no troponin elevation after a
single shock, but the effect of multiple sequential shocks remains to be determined.
Finally, we measured only a 6-h troponin I level and did not measure subsequent troponin I
levels. However, as discussed previously, we believe the 6-h assessment was appropriate to
assess for direct myocardial injury as a result of electrical current.

Conclusions
In human volunteers who received a single Taser X-26® activation, there was no evidence of
myocardial injury as measured by serum troponin I at 6 h post-activation. This finding suggests
that there is no cardiac injury in healthy subjects who receive a single 5-s CED shock. This study
adds to the growing body of literature on human subjects that assesses the physiologic result of a
CED application on human subjects.

Acknowledgments
The authors thank the San Diego Police Department and the San Diego County Sheriff's
Department volunteers who participated in this study. Additionally, the authors thank Biosite
Incorporated for an unrestricted Educational Grant.

References

1 A. Berenson, As police use of Tasers soars, questions over safety emerge: The New York
Times (2004) July 18.

2 R. Anglen, 101 cases of death following stun-gun use: The Arizona Republic (2005) March 4.

3 M. Silverstein and M. Barton, “Nonlethal” force can kill http://www.acluco.org/news/pressrelease/release_tasers081806.htm Accessed September 19, 2006.

4 J.R. Jauchem, C.J. Sherry, D.A. Fines and M.C. Cook, Acidosis, lactate, electrolytes, muscle
enzymes, and other factors in the blood of Sus scrofa following repeated TASER exposures,
Forensic Sci Int 161 (2006), pp. 20–30
5 W.C. McDaniel, R.A. Stratbucker, M. Nerheim and J.E. Brewer, Cardiac safety of
neuromuscular incapacitating defensive devices, Pacing Clin Electrophysiol 28 (Suppl) (2005),
pp. S284–S287. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (48)

6 O. Roy and A. Podgorski, Tests on a shocking device—the stun gun, Med Biol Eng Comput 27
(1989), pp. 445–448. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus
(15)
7 J.D. Ho, J.R. Miner and D.R. Lakireddy et al., Cardiovascular and physiologic effects of
conducted electrical weapon discharge in resting adults, Acad Emerg Med 13 (2006), pp.
589–595. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (48)
8 S. Levine, C. Sloane, T. Chan, J. Dunford and G. Vilke, Cardiac monitoring of subjects
exposed to the taser, Prehosp Emerg Care 10 (2006), p. 130.
9 D.J. O'Brien, Electronic weaponry—a question of safety, Ann Emerg Med 20 (1991), pp.
583–587. Abstract | View Record in Scopus | Cited By in Scopus (18)
10 G.J. Ordog, J. Wasserberger, T. Schlater and S. Balasubramanium, Electronic gun (Taser)
injuries, Ann Emerg Med 16 (1987), pp. 73–78. Abstract | View Record in Scopus | Cited By
in Scopus (48)
11 Taser International, Advanced Taser M26 field use statistics [Taser International web site]
http://www.taser.com/facts/stats.htm Accessed September 11, 2006.
12 J.D. Ho, R.F. Reardon and W.G. Heegaard, Deaths in police custody: an 8 month surveillance
study [abstract], Ann Emerg Med 46 (Suppl) (2005), p. S94.

13 R.N. Kornblum and S.K. Reddy, Effects of the Taser in fatalities involving police
confrontations, J Forensic Sci 36 (1991), pp. 434–438.
14 J. Strote and H.R. Hutson, Taser use in restraint-related deaths, Prehosp Emerg Care 10
(2006), pp. 447–450