 Why was the chest acceleration formerly introduced as injury criterion?
 It was the only meaningful thorax measurement available for the Hybrid II dummy
 Digges, 1999: “The chest injury criteria for frontal impacts was initially based on the resultant chest acceleration measured on the Hybrid II dummy. This early dummy did not have the capability of measuring chest deflection.
Consequently, acceleration was the preferred tolerance measurement“
 Prasad, 1999: “Recognizing that the test device in the regulation was the
Hybrid II dummy, which had a very stiff and non-biofidelic thorax design, chest acceleration was the only possible injury response that was meaningful to control.
“
 Note: Introduction of the Hybrid III dummy in 1984
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 How was the 60 g-threshold defined?
 It was based on volunteer tests of non-injurious level
 Kent et al., 2003: “This tolerance level was not, however, based on the
attainment of severe thoracic soft tissue injuries in living humans.
Rather, this level is approximately 30% greater than the acceleration level at which human volunteers began sustaining hyphema, other soft tissue trauma, and became unwilling to continue to higher levels“
 Digges, 1999: “This acceleration limit was based on voluntary
exposures in early rocket-sled tests conducted by Col. J.P. Stapp. Stapp himself was exposed to 40G’s for 100msecs without injury. Another subject had undergone 45G’s for 44msec.“
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 Is 60 g a realistic limit for chest acceleration?
 No, the actual human acceleration tolerance is substantially greater than 60 g for 3 ms
 Kent et al., 2003: “Melvin et al. (1998) measured peak chassis acceleration levels exceeding 60 g in approximately 1/3 of the cases and some cases of acceleration over 125 g with the 60 g threshold exceeded for nearly 20ms.
They estimated that the chest acceleration experienced by the occupant was greater (by approximately a factor of 1.5) than the chassis acceleration, which would result in chest acceleration levels over three times the 60 g
limit. Despite these acceleration levels, no serious thoracic soft tissue injuries were sustained.“
 Forman et al., 2005: “... the cadaver tests presented here provide additional data supporting the contention that the tolerance limit for inertially induced intrathoracic vascular or organ trauma is above the currently accepted 60g limit.
“
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 The introduction of chest acceleration based criteria was not based on scientific findings from biomechanics
 Today's knowledge show that a 60 g tolerance level is not valid
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 Chest acceleration does not predict thorax injuries
 PMHS sled tests
 Fayon et al., 1975: “Plotting then the maximum resultant chest
accelerations thus measured against injuries, one can see no clear correlation ”
 Indy Car drivers
 Melvin et al., 1998: “Specifically, it does not appear that chest
acceleration-based criteria for injury prediction, as currently required for injury assessment in federally regulated crash testing, have validity .“
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 Chest acceleration does not predict hard tissue thorax injuries
 PMHS sled tests
 Kent et al., 2001: “Peak acceleration and the average spinal acceleration measured at the first and eighth or ninth thoracic vertebrae are shown to be
unrelated to the presence of injury “
 Matched PMHS-Hybrid III sled tests
 Kent et al. 2000: “These differences in measured acceleration raise
questions about the validity of using T1 acceleration to develop injury criteria which are then applied using ATD chest CG acceleration to evaluate restraint system performance .“
 Kent et al. 2001:
“A statistical analysis is performed to evaluate the injurypredictive efficacy of the dummy-based maximum chest deflection, maximum chest acceleration, and CTI. Consideration of the maximum chest acceleration, either as an independent covariate or as part of CTI, is found to weaken the injury model .“
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 Chest acceleration does not predict aortic ruptur
 Impactor tests
 Hardy et al., 2008: “Deformation of the thorax is required for TRA
(traumatic rupture of the aorta)“
 Sled tests
 Forman et al., 2008: “The sled tests resulted in sustained mid-spine accelerations of up to 80 g for 20 ms with peak mid-spine accelerations
of up to 175 g, and maximum chest deflections lower than 11% of the total chest depth. No macroscopic injuries to the thoracic aorta resulted from these tests.“
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 Chest acceleration does not predict thorax injuries from blunt impact
 Impactor tests
 Neathery et al., 1975: “It has thus been demonstrated from cadaver data, from dummies with thoracic biofidelity as specified by Kroell, from dummies without this biofidelity, and from a mathematical simulation which satisfies these biofidelity requirements for blunt frontal impact that both a 3 ms
acceleration of 60 g and a severity index of 1000 based on spinal acceleration are grossly in error and completely misleading in predicting injury under these blunt frontal impact conditions .”
 Neathery et al., 1975: “ Current methods of evaluation of occupant protection
(severity index or 3 ms level of thoracic spinal acceleration or chest load level) should not be used when significant blunt frontal chest impact occurs .“
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 Low chest acceleration is a consequence of localized chest loading (e.g. pure belt loading)
 Localized chest loading increases the injury risk
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 Thorax compression (deflection) by external force, is the major mechanism of thorax injury
Injury Mechanism
Sternum
Fracture
11%
Flail Chest
9%
Aorta 3%
Vena Cava 3%
Heart Injury 9%
Compression
⇒
Deflection
Lung Contusion
20%
Multi Rib
Fracture 34 %
Hemothorax
11 %
■ ■■ Ribs ■ ■ Lung ■ ■ ■ Other organs
Fig. Break down into type of thoracic injury(AIS2+)
※ Reference ： JSAE 20115636 “Analysis of Thoracoabdominal Injury based on Japanese Trauma Data Bank and In-depth accident study” Tominaga et al.
Viscous
Injury
⇒
V*C
Internal
Organ kinematics
⇒
Chest G
Fig. Mechanism and it’s supposed criteria for thorax injury

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 Chest acceleration is not linked to any thorax injury mechanism – neither to skeletal injury nor to organ injury
 The use of chest acceleration for restraint design is counterproductive – it leads to higher injury risks
 Chest deflection is a better predictor of thorax injuries than chest acceleration
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 Localized chest loading can lower chest accelerations
 Distributed loading is beneficial according to injury biomechanics
 Chest acceleration criterion will mislead restraint design
Chest deflection:
RodPot measuring sternum deflection
Chest acceleration:
Accelerometer firmly attached to thoracic spine
Load transfer via elastic ribs:
The more ribs engaged/loaded the more load transferred a
≈
F = f ( defl , n ribs
)
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 Influence of arm movement
 Direct load path from wrist to spine box
 Possible contact of the arm or hand with the interior may have a nonbiofidelic effect of up to 12% on the measured chest acceleration .
Red curves show T1 acceleration without any hand or arm contact
Light blue curve and dark blue curve show T1 acceleration with a hand or arm contact
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 Thoracic spine acceleration is a function of load from lumbar spine
Shear Force from lumbar spine increases according to forward displacement of the chest.
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 Thoracic spine acceleration is a function of load from lumbar spine
 Non-biofidelic stiff connection between thoracic and lumbar spine
 Masuda (JAMA/Toyota), 2013: “Predominant factor of the Chest G is internal force from lumbar spine, it’s depend on the relative forward displacement between pelvis and thorax. >> Even if, external force on the thorax is
decreased by belt load limiter.etc, the relative displacement and Chest G increases .“
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 Unfavorable localized loading of the dummy thorax can reduce the chest acceleration measurement
 A contact of the dummy hand or arm with the interior leads to unrealistic chest acceleration
 Lower thorax loading can result in increased chest acceleration
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 USNCAP update 2007
 National Highway Traffic Safety Administration, Department of Transportation
(DOT): Consumer Information; New Car Assessment Program, Docket No.
NHTSA-2006-26555:
“However, unlike the current NCAP program which uses chest acceleration to assess thoracic injury risk, the new frontal program will focus instead on peak chest deflection instead. We believe that
the inclusion of chest deflection into frontal NCAP will encourage development of restraint systems that will further reduce the risk of thoracic injuries.
”
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
Digges, 1999: Injury measurements and criteria, Models for Aircrew Safety Assessment: Uses, Limitations and
Requirements
 Fayon et al., 1975: Thorax of 3-Point Belt Wearers During a Crash (Experiments with cadavers), Stapp Car Crash
Journal

Forman et al. 2005: An Experimental Investigation of Acceleration as a Mechanism of Aortic Injury, SAE Technical
Paper Series
 Forman et al., 2008: Posterior acceleration as a mechanism of blunt traumatic injury of the aorta, J. Biomech.
 Gehre, 2013: Contacts between arm and dashboard – change of the chest acceleration, PDB report
 Hardy et al., 2008: Mechanisms of Traumatic Rupture of the Aorta and Associated Peri-isthmic Motion and
Deformation, Stapp Car Crash Journal
 Kent et al. 2000: Driver and right-front passenger restraint system interaction, injury potential, and thoracic injury prediction, AAAM

Kent et al., 2001: The Influence of Superficial Soft Tissues and Restraint Condition on Thoracic Skeletal Injury
Prediction, Stapp Car Crash Journal
 Kent et al., 2001: Restrained Hybrid III dummy based criteria for thoracic hard-tissue injury prediction, IRCOBI
 Kent et al., 2003: The Hybrid III dummy as a discriminator of injurious and non-injurious restraint loading, AAAM

Prasad, 1999: Biomechanical basis for injury criteria used in crashworthiness regulations, IRCOBI

Masuda (Jama/Toyota), 2013: Chest Acc Criteria, presented at OICA webmeeting

Melvin et al. 1998: Biomechanical Analysis of Indy Race Car Crashes, Stapp Car Crash Journal
 Neathery et al., 1975: Prediction of Thoracic Injury from Dummy Responses, Stapp Car Crash Journal
 National Highway Traffic Safety Administration, Department of Transportation (DOT): Consumer Information; New Car
Assessment Program, Docket No. NHTSA-2006-26555
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