June 2023

Medical Mass Spectrometry Vol. 7 No. 1

Research Paper

HFC-152a (1,1-Diﬂuoroethane) inhalation causes a decreasein blood hemoglobin function
1,2

2,3,4

*, Ryoji Matoba2, Yasuhiro Kakiuchi3

Hiroshi Ochi , Kazuo Igarashi
1

Department of Legal Medicine, School of Medicine, Fujita Health University,
1‒98 Dengakugakubo, Kutsutake-cho, Toyoake, Aichi 470‒1192, Japan2
Department of Legal Medicine, Osaka University Graduate School of Medicine,2‒2 Yamadaoka, Suita, Osaka 565‒0871, Japan3
Department of Forensic Medicine, Kindai University Faculty of Medicine,2‒377 Ohnohigashi, Osakasayama, Osaka 589‒8511, Japan
4
Department of Research Development, Association of Medicinal Analysis,522‒417, 5‒1 Koyochonaka, Higashinada-ku, Kobe, Hyogo 658‒0032, Japan
Abstract 1,1-Diﬂuoroethane (HFC-152a) is widely used as a gas component of electronic and precision instrument propellant cleaners. Although HFC-152a has low toxicity, sudden deaths from the abusive inhalation of HFC-152a-containing
products have been observed globally. Two cases of HFC-152-related deaths have been reported as the forensic autopsy
case. Moreover, we investigated the biodistribution of HFC-152a in rats to elucidate the mechanism of action of HFC-152a.
Wistar Rats (n＝10) were exposed to the mixed gas (80% HFC-152a and 20% oxygen). They survived the 5-minute exposure but died from asphyxiation after the 10-minute exposure. No signiﬁcant diﬀerences were observed in the biodistribution of HFC-152a between these two groups. Total hemoglobin (tHb) and oxyhemoglobin saturation (O2Hb) were measured

to investigate the inﬂuence of HFC-152a on hemoglobin function. HFC-152a did not aﬀect tHb, whereas O2Hb was signiﬁcantly decreased by exposure to HFC-152a. Carbon monoxide (CO) is known as a typical toxic gas, and toxicity of CO is
known to reduce the oxygen-carrying capacity of blood by forming carboxyhemoglobin. Because similar phenomenon likeCO occurred when exposed to HFC-152a, it was suggested that the cause of sudden deaths due to HFC-152a inhalation was
asphyxia by decreased O2Hb level in blood.
Key words: 1,1-diﬂuoroethane, gas inhalation, GC-MS, oxyhemoglobin saturation, distribution of HFC-152a

Introduction

After the 1990s, Japanʼs most abused volatile substanceswere butane and propane canisters after the stricter regula-

Inhalant abuse is a prevalent form of substance abuse in

8,9)adolescents and young adults. The most common inhalanttions for organic solvents such as toluene

substances are aerosol sprays and dusters have been used totheir involvement is evidenced by secondary damage, such.

as explosions. However, deaths associated with inhalantabuse are sparsely reported in Japanese medical institu-

1‒7)

induce euphoria by inhaling their volatile components*Corresponding author. A hallmark oftions.

Kazuo Igarashi

Hydroﬂuorocarbons (HFCs) have been used as propellants for commercial and industrial aerosols. The organoﬂu-

Department of Research Development, Association of Medicinal Analysis, 522‒417, 5‒1 Koyochonaka, Higashinada-ku,

oride compound, 1,1-diﬂuoroethane (HFC-152a) is colorless, odorless and has a lower impact on ozone-depletion

Kobe, Hyogo 658‒0032, Japan
Tel/Fax: +81-78‒855‒8315

compared to other chloroﬂuorocarbons and hydrochloroﬂu10)
orocarbons (HFC-134a or HFCF-141b) . Moreover, HFC-

E-mail: kigarashi1868@hotmail.com
Received: January 6, 2023. Accepted: March 23, 2023.
Epub April 18, 2023.

152a is used as gas component of spray cleaner of elec-

DOI: 10.24508/mms.2023.06.008

tronic equipment and precision instrument. These HFCs,
71

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Medical Mass Spectrometry Vol. 7 No. 1

including HFC-152a, are also used apart from normal use
among people to induce euphoria by inhaling the gas com-

3(500 cm ). To avoid the possibility of suﬀocation due tohypoxia, the mixed gas consists of 80% of HFC-152a and11‒14)

ponents

20% of oxygen. This mixed gas was introduced to the expo-.

Sudden sniﬃng death syndrome death associated withsure chamber via a ﬂow meter at a ﬂow rate of 3 L/min. The

15‒22)

has occasionally been reported despite

opposite side of the exposure chamber had some holes tothe low toxicity of HFC-152a . There is no data on theacute toxicity of HFC-152a, any reports on the blood con-

allow mixed gas to ﬂow in one direction. After exposure,

centration of HFC-152a postmortem, and whether it was at
an intoxication level. We also report two fatal cases involv-

and tissue samples were collected. The collected samples

inhalant abuse

23)

rats were euthanized by cervical dislocation, whole blood
were stored at −80°
C until analyzed.

ing the inhalation of HFC-152a in our forensic laboratory.

Determination of 1,1-diﬂuoroethane (HFC-152a) in
biological samples

Carbon monoxide (CO) is a known toxic gas, and the
toxicity of CO is known to decrease the oxygen-carrying

Determination of HFC-152a was conducted using a
GC-MS headspace method. The working stock solution of

capacity of blood by forming carboxyhemoglobin (CO24)
Hb) . Post-mortem autopsy ﬁndings of CO poisonings are
surface of the decedentʼs body. It is currently unknown

HFC-152a was prepared by the water displacement method.
The standard HFC-152a gas was transferred into a sealed andwhether HFCs display a similar mechanism of action,
which may lead to reduced oxygen-carrying capacity inweighed glass vial containing 5 mL of distilled water. A ﬁnal
concentration of 0.3 mg/mL HFC-152a was prepared. This

humans after inhalant exposure. We hypothesize that theoxygen-binding may be aﬀected by HFC-152a exposure in

0.3 mg/mL working stock solution was used to create aneight-point calibration curve from 10 to 500μg/mL. This wasa similar manner.

accomplished by adding varying amounts of the working

This investigation aims to report the two fatal cases
involving HFC-152a inhalation in our laboratory and to

stock solution to a sealed 20 mL headspace vials containing
0.8 mL of water, 0.2 mL of negative-control whole blood orinvestigate the distribution of HFC-152a via animal experi-

0.2 g of negative-control tissue and 0.1 mL of 2,2,2-triﬂuo-

ments to elucidate their mechanism of action on hemoglobin.

roethanol (IS, 10 mg/mL aqueous solution). In addition, 2 gMaterials and Methodsof the glass bead (average diameter, about 2 mm) was
added to the headspace vial to homogenize tissue com-usually classiﬁed by asphyxiation and a pink hue on theChemicals and reagents

pletely. Gas-tight syringes were used to extract an exact
volume of HFC-152a from the vial for calibration. Samples

SynQuest Labs, Inc. (Alachua, FL, USA). For the inhalantexposure study, the air duster canister, Dust Blower (aero-(0.2 mL blood and 0.2 g of each tissue) obtained from thesol volume: 460 mL, constituent: ＞99% HFC-152a), was

20 mL headspace vials containing 1 mL of water, 0.1 mL ofobtained from ELECOM, Co. (Osaka, Japan). In addition,

IS aqueous solution and 2 g of the glass bead. Each vial was

oxygen (＞95%) as diluted gas of air duster was purchasedfrom GL Sciences, Inc. (Tokyo, Japan). The internal stan-

mixed for 1 min, heated at 70°
C for 20 min, and then 100μ
L of the headspace was injected into the GC-MS system.

dard (IS), 2,2,2-triﬂuoroethanol, was purchased from Wako

GC-MS system was a Shimadzu GCMS-QP2010 gas
chromatography-mass spectrometry (GC-MS) equipped

A standard of ＞99% HFC-152a was purchased fromdecedents or the sacriﬁced rats were also added to a sealed

Pure Chemical Industries, Ltd. (Osaka, Japan). All othersolvents and chemicals used were of analytical grade com-with a CP-PoraBOND Q fused silica column (Agilent Tech-mercially available.

nologies, CA, USA, 25 m×0.25 mm, i.d., thickness 3.0μm).

Animal experiment (inhalant exposure study)

The injector and detector temperatures were set at 150°
C
and 200°
C, respectively. The column temperature was ini-

All animal experiments were conducted following the
Guidelines for Animal Experimentation of Osaka Univer-tially held at 40°
C for 2 min, increased to 250°
C at a rate of
20°
C/min, and held at 250°
C for 1 min. A selected ion mon-sity Graduate School of Medicine. Adult male Wistar rats

itoring (SIM) of GC-MS was used for the quantitative
determination of HFC-152a. These ions used for SIM were

(weighing 250 g) were purchased from CLEA, Japan. Rats
were exposed to HFC-152a gas in the exposure chamber

m/z 51 for a fragment ion of HFC-152a (molecular weight72June 2023

Medical Mass Spectrometry Vol. 7 No. 1

Case 266) and m/z 61 for a fragment ion of IS (molecular weightA 27-year-old male was found dead on his bed by his

100).

friend. Extensive rigor mortis was reported and the body

Determination of total hemoglobin (tHb) and oxyhemoglobin (O2Hb) in blood

was transferred to the medical examinerʼs oﬃce for autopsy.

To determine total hemoglobin (tHb) and oxyhemoglobin(O2Hb) in blood samples after exposure to HFC-152a gas,Co., Japan), under his arm, four cans were present aroundThe decedent held an air duster, Dust Blower (ELECOM

AVOXimeter 4000 was used (Instrumentation Laboratory,

his bed and hundreds of empty cans were found on theporch. An autopsy was performed about 35 h after the dis-

MA, USA). Freshly drawn or anticoagulated whole blood

covery of the body. Findings at autopsy revealed signiﬁcantsamples were measured according to the manufacturerʼs
protocols. To investigate the eﬀect of HFC-152a on hemo-

cyanosis of the lips and face and lung congestions. Several
biological samples were collected during autopsy for toxi-

globin function in vivo, rats were exposed to HFC-152a gas

cological analysis and stored at −80°
C until analysis.

according to the abovementioned methods. The whole

Results

blood samples collected immediately after exposure was

GC-MS analysis of HFC-152a in biological samples

measured.
For an in vitro study, healthy adult venous blood wasused to investigate the eﬀect of HFC-152a on human hemo-

A quantitative determination for HFC-152a was undertaken using the SIM method of GC-MS analysis. The mass

globin function. This venous blood was anticoagulated bydipotassium

spectra of standard HFC-152a and IS, and a typical SIM
chromatogram of HFC-152a in a blood sample (case 1)(Merck, Germany). This blood containing the mixed gas(80% of HFC-152a and 20% oxygen) was tightly sealed

were shown in Fig. 1. The peaks of HFC-152a and IS had
retention times of 3.6 min and 7.2 min, respectively. More-and shaken gently at 37°
C. After a certain period of time,

over, there were no peaks that interfered with the measure-the incubated blood was used for measurement.

ments.

addingethylenediaminetetraacetic

acid

The linearity of the calibration curve using the spiked

Statistical analysis

blood and each tissue was observed from 0 to 500μg/mL

Kramer method was used to compare the signiﬁcance of(R ＝0.999). The lower limit of quantitation (LLOQ) was
about 0.1 μg/mL or μg/g. In addition, the accuracy of HFC-diﬀerences among all groups. All experimental data were152a measurement in the spiked samples was 93.8‒98.7%

expressed as means±standard deviation (SD). Results weresigniﬁcant at *p＜0.05 and **p＜0.01.

(data not shown). The coeﬃcient of variation (CV) for
HFC-152a measurement was lower than 5.7% at all QC lev-

A one-way analysis of variance followed by the Tukey‒

2els (data not shown). Using this method, HFC-152a levels

Case History

in biological samples obtained at autopsy were determined.

Case 1

A 39-year-old male was found on his bathroom ﬂoor by

When the HFC concentration in the sample exceeded thecalibration curve, the amount of the sample used for analy-

his housemate. An empty can of Dust Blower (ELECOM
Co., Japan, volume: 460 mL, constituent: HFC-152a) was

sis was appropriately changed and measured.
HFC-152a levels in biological samples obtained fromnext to his face. Although bradypnea was reported when he
was found, his breathing eventually stopped. He was trans-

two cases of sudden death after inhaling HFC-152a showed

ferred to the hospital but was dead on arrival. The house-case 2 were 295.1±2.8 and 509.6±2.2μg/mL, respectively.

mate had recalled seeing his roommate abuse inhalants forseveral years. An autopsy was performed approximately 18 h

Urine levels of case 1 and case 2 were 114.8±0.4 and 228.9±2.1μg/mL, respectively. Next, the levels of HFC-152a inafter death. Autopsy ﬁndings showed acute death fromcase 1 ranged from 39.5±0.3 μg/g in the liver to 138.5±

asphyxiation with lung congestion, lung edema, and an
enlarged spleen. Some biological samples were collected

0.5μg/g in the lungs. In case 2, ranged from 195.1±1.3μg/g
HFC-152a in the brain to 397.2±2.8μg/g in the lungs.

during autopsy for toxicological analysis and stored at

Other volatile compounds were not detected in all samples.

signiﬁcant variability (Table 1). Blood levels of case 1 and−80°
C until analysis.
73June 2023

Fig. 1.

Medical Mass Spectrometry Vol. 7 No. 1

EI mass spectra of HFC-152a and I.S. (2,2,2-triﬂuoroethanol) and typical SIM chromatogram of HFC-152a in bloodobtained from autopsy sample (case 1).

Table 1.

HFC-152a levels in body ﬂuids and various tissues obtained from postmortem samples

Biological samples

Case 1Case 2

Heart blood

295.1±2.8 μg/mL

509.6±2.2 μg/mL

Urine

114.8±0.4 μg/mL

228.9±2.1 μg/mL

Gastric content

220.0±1.4 μg/mL

382.0±4.8 μg/mL

Brain

85.1±0.3 μg/g

195.1±1.3 μg/g

Heart42.2±0.3 μg/g

224.3±1.8 μg/g

Lung138.5±0.5 μg/g

397.2±2.8 μg/g

Liver39.5±0.3 μg/g

234.7±1.3 μg/g

Kidney108.7±0.8 μg/g

230.8±1.4 μg/g

±2μg/g (adipose tissue). In the death group, the average
concentrations of HFC-152a were 361±14μg/mL (blood),239±1μg/g (brain), 175±9μg/g (heart), 104±1μg/g (lung),
122±3μg/g (liver), 168±7μg/g (spleen), 234±9μg/g (kidney), 297±1μg/g (adipose tissue). There were no signiﬁcant diﬀerences in HFC-152a levels between two groups.
For this reason, it was considered that rats in the survivalgroup were placed under a normal typical breathing environment immediately after exposure to HFC-152a, and theiractivity state returned to the original state with progress.

The data showed the means±SD of three determinations.

Change with time of distribution of HFC-152a levels
in rats

Distribution of HFC-152a in rats after inhalant exposure

To investigate the change in time distribution of HFC-

152a levels after inhalation exposure, rats were exposed to

To investigate the biodistribution of HFC-152a after

the mixed gas for 5 min. After certain periods of time (0, 10

inhalant exposure, rats were exposed to mixed gas accord-and 30 min), rats were euthanized by cervical dislocation

ing to the methods described above. They were alive during

and biological samples were collected (survival group). In

the ﬁrst 5 min of exposure but died at 10 min of exposure.
We compared the distribution of HFC-152a levels in these

addition, we also investigated the postmortem change ofHFC-152a levels. In survival group, their activities were

two groups (survival and death).

low for 10 min, whereas these activities recovered to nor-In the survival group, the average concentrations of
HFC-152a were 377±2μg/mL (blood), 215±5μg/g (brain),

mal about 30 min later.
HFC-152a concentrations in collected biological samples

166±2μg/g (heart), 111±5μg/g (lung), 146±12μg/g

were shown in Fig. 2. HFC-152a concentrations in blood at(liver), 178±1μg/g (spleen), 257±3μg/g (kidney), and 309

10 and 30 min after exposure decreased signiﬁcantly in the74June 2023

Medical Mass Spectrometry Vol. 7 No. 1

Fig. 2.

Changes with time of HFC-152a distribution after exposure.

Rats were exposed to mixed gas (80% HFC-152a and 20% oxygen). The survival means rats that placed under normal breeding environment
just after exposure. The death means that rats are euthanized just after exposure and placed under normal breeding environments. After certain period time, biological samples were collected. GC/MS methods quantitated the HFC-152a levels in collected samples. All results wereshown as mean±SE (n＝10). The statistical signiﬁcances were shown as ** (p＜0.01) compared with HFC-152a levels at same sampling time.

survival group, but not in the death group. HFC-152a levelsin blood samples obtained from the survival group at 0, 10

of exposure, while the concentration of HFC-152aremained constant after post-mortem exposure. HFC-152aand 30 min were 338.1±9.9μg/mL, 54.5±16.5μg/mL, andconcentrations in various tissues obtained from the survival

15.0±6.9 μg/mL, respectively. On the other hand, in thedeath group, HFC-152a levels at 0, 10 and 30 min were±0.3 μg/g and 3.9±1.1 μg/g in the liver, respectively, togroup at 0, 10 and 30 min ranged from 93.1±6.8 μg/g, 14.3

338.1±9.9 μg/mL, 266.9±19.0 μg/mL and 329.9±38.8 μg/

333.2±44.6 μg/g, 189.8±15.3 μg/g and 148.6±8.3 μg/g inadipose, respectively. In contrast, in death group, HFC-152a

mL, respectively.
HFC-152a concentrations in various tissues obtainedlevels at 0, 10 and 30 min ranged from 93.1±6.8, 94.8±23.6

from the survival group decreased signiﬁcantly after 30 min

and 127.1±10.7 μg/g in the liver, respectively, to 333.2±
75

June 2023

Fig. 3.

Medical Mass Spectrometry Vol. 7 No. 1

Inﬂuence of HFC-152a on tHb and O2Hb levels in
rat blood after exposure.

(A and B) Rats were exposed to mixed gas (80% of HFC-152a and
20% of oxygen) for 5 min (survival) or 10 min (death). In addition,
rats were exposed to artiﬁcial air (80% of nitrogen and 20% of oxygen) for 10 min (cont.). After exposure, whole blood was collected
and total hemoglobin (tHb) and oxyhemoglobin saturation (O2Hb)
were measured by AVOXimeter. All results were shown as mean±
SE (n＝10). The statistical signiﬁcances were shown as follows: n.s.;
not signiﬁcant, **; p＜0.01 compared with levels of dead.

Fig. 4.

Inﬂuence of HFC-152a on tHb and O2Hb levels inhuman blood.

(A and B) The anticoagulated human whole blood was incubatedwith mixed gas (80% of HFC-152a and 20% of oxygen) for certain
period of time. The tHb and O2Hb of incubated blood were measured by AVOXimeter. All results were shown as mean±SE (n＝10). The statistical signiﬁcances were as follows: n.s.; not signiﬁcant, **; p＜0.01 compared with levels at 10 min.

44.6, 289.3±35.8 and 307.1±49.3 μg/g in adipose, respectively.

with other groups (survival and control).
Next, we investigated whether a similar inﬂuence

Inﬂuence of HFC-152a to hemoglobin function

occurred on human hemoglobin in vitro. The anticoagulated

The total hemoglobin (tHb) and oxyhemoglobin saturation (O2Hb) in collected samples were measured by AVOX-

human whole blood was mixed with the gas were shaken

imeter according to the methods mentioned above. Then, toinvestigate the inﬂuence of HFC-152a to hemoglobin func-

samples were used for the measurement of tHb and O2Hb.

tion, rats were exposed to the mixed gas for 5 min (survival

respectively. The tHb score did not recognize remarkablegroup) and 10 min (death group). Rats exposed to artiﬁcialchange derived from the diﬀerence in incubation time.

air (80% of nitrogen and 20% of oxygen) for 10 min were

However, O2Hb score signiﬁcantly decreased depending on

applied as a control group. In both groups, whole blood was

incubation time.

collected from the heart after being euthanized. In the deathgroup, whole blood was collected after exposure to HFC-

Discussion

152a. In Fig. 3(A) and 3(B), levels of tHb and O2Hb inblood collected after exposure to HFC-152a were shown,

Our autopsy cases observed remarkable diﬀerences in
HFC-152a levels in postmortem samples. As the cause ofrespectively. No signiﬁcant diﬀerence in tHb score was rec-these diﬀerences between the two cases, we assumed thatognized among these three groups. However, the O2Hb

the death process diﬀered. The victim in case 1 was alivescore signiﬁcantly decreased in the death group comparedwhen he was found, whereas the victim in case 2 wasgently at 37°
C for a certain period. The incubated blood
The tHb and O2Hb were shown in Fig. 4(A) and 4(B),76June 2023

Medical Mass Spectrometry Vol. 7 No. 1

already dead when he was found. Generally, the blood con-logical features have been found in terms of the biodistribu-

centration of toxicants has been used as a diagnostic index
of poisoning. In our autopsy cases, HFC-152a levels in thetion of HFCs.

heart blood of case 1 and case 2 were 295.1 μg/mL andmany poisoning cases due to CO inhalation occur every
29)
year . The toxicity of CO was known to decrease the oxy-

Carbon monoxide (CO) is a known toxic gas. In Japan,

509.6 μg/mL, respectively. These blood levels were higher
1‒4,16,17)

than previously reported autopsy cases

gen-carrying capacity of blood by forming abnormal
24)
CO-Hb , eventually leading various poisoning symptoms. Moreover,the cause of death obtained from these autopsy cases has
been estimated to be asphyxiation or fatal cardiac arrhyth2,25,26)

mia

by reduced oxygen partial pressure. Therefore, we investigated whether HFC-152a has similar eﬀects to CO. Rats

. However, the actual mechanism of death due toinhalation of HFC-152a is still unknown.

were exposed to HFC-152a for 5 min (survival group) or

Therefore, the biodistribution of HFC-152a was preliminarily investigated by animal experiments. First, we exam-

10 min (death group). For control group, rats were exposed
to artiﬁcial air for 10 min. As the result, no signiﬁcant dif-ined ratsʼ HFC-152a levels in the blood after inhalant exposure, but no statistical diﬀerence in HFC-152a levels inference in tHb score was recognized among these 3 groups.

blood was found between survival and death groups. These

group compared with other groups (survival and control).

results suggest that it is diﬃcult to use the blood level of
HFC-152a as an index of HFC-125a poisoning and that a

Moreover, human whole blood samples incubated with
HFC-152a did not show any signiﬁcant change in tHb. In

new index is needed.

contrast, the O2Hb score signiﬁcantly decreased depending

However, O2Hb score signiﬁcantly decreased in the death

Next, the changes in HFC-152a distribution after inhala-on incubation time. From these results, it was revealed that
HFC-152a was able to reduce O2Hb in vivo and in vitro.

tion exposure were investigated. Rats survived the 5 min
exposure to HFC-152a, and their locomotion recovered

Therefore, the likely mechanism of action of HFC-152aover time. In these survival groups, the immediate decreaseof HFC-152a levels was shown in all collected samples

was thought to be asphyxia by decreasing the O2Hb level.
HFC-152a likely has a high binding aﬃnity to hemoglobin

except for adipose. However, no signiﬁcant changes wereas the number of O2Hb decreases, which contributes toasphyxia. In addition, the possibility of abnormal HFC-Hbobserved in all samples collected in the death group, which
was euthanized after 5 min exposure to HFC-152a. In addi-

formation by HFC-152a inhalation was beyond the scope oftion, there was a tendency for HFC-152a levels to increase

this study that should be investigated in future reports.

slightly even 30 min after exposure in the liver, brain, heart,and kidney. Regarding this point, the possibility of redistri-, blood levels of
According to the previous reports
HFC 152a in fatal cases vary from 83.5 to 546 μg/mL. The

bution of HFCs among tissues is considered, but it is notclear. These ﬁndings suggested that HFC-152a was rapidly

present blood levels in two cases were within those in pre-1‒4,15‒22)

viously reported fatal cases and then it was considered that
HFC-152a levels in blood were lethal. The diﬀerences ineliminated via respiration. Therefore, it was thought that
HFC-152a levels in postmortem samples were diﬃcult to

HFC-152a levels were observed between both cases. HFC152a levels of case 1, which was transferred to the emer-

use as an index of HFC-152a poisoning. Furthermore, therapid elimination of HFC-152a by respiration may accountgency unit immediately after discovery, were signiﬁcantly

for the diﬀerences in HFC-152a levels observed between

lower than case 2, which was found dead on. It has been
9,18)
rapidly eliminates HFC-152a.
reported that exhalation

our autopsy cases.

Therefore, it is considered that lower HFC-152a levels of

The distribution of inhaled HFC-152a has been reported
27)

28)

and humans . It has been reported that repeatedexposure of HFC-152a to rats tended to accumulate in car-in ratscase 1 result from the elimination by exhalation.

Conclusion

diac tissue. In addition, according to inhalation experimentsof HFC-152a in humans, HFC-152a tends to be stored inUsing an animal exposure model, we demonstrated thatasphyxia due to decreased O2Hb was likely the toxic mech-adipose tissue. Our inhalation experiments in rats also

anism of HFC-152a inhalation. Therefore, the evaluation of
HFC-152a poisoning should be carried out by O2Hb score,

showed no signiﬁcant reduction in adipose tissue, althoughother tissues showed rapid reduction after 30 min. Based on
the previous reports, including ours, it seems that no toxico-

and it is diﬃcult to evaluate the HFC-152a poisoning by77

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Medical Mass Spectrometry Vol. 7 No. 1

HFC-152a levels in the blood or other tissue sample. In
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