Jonasson S, Wigenstam E, Koch B, Bucht A.

Early treatment of chlorine-induced

airway hyperresponsiveness and inflammation with corticosteroids. Toxicology and
Applied Pharmacology 2013;271(2): 168-174

Conclusion
This study points at the importance of early medical intervention following exposure to
Cl2 in order to prevent acute and long-term lung injuries. Both high-dose (100 mg/kg) and
relatively low-dose (10 mg/kg) of dexamethasone decreased the risk for developing delayed
effects such as persistent lung injuries, while only high-dose treatment could significantly
counteract acute-phase effects. Our data implicate the importance of early treatment with
corticosteroids in Cl2-induced lung injury in consistency with our previously published data in
a mouse model of alkylating mustard agent exposure. By using this mouse model, it is
possible to increase the understanding of how corticosteroids exert their therapeutic effect
in chemical-induced lung injuries, but the model is also of value in the search for
complementary pharmaceutical approaches targeting disease pathways other than
inflammation. The results provide a foundation for future studies aimed at identifying new
concepts for treatment of chemical-induced lung injury. In particular, studies addressing
combination of anti-inflammatory and anti-oxidant treatment are highly motivated.

Short term respiratory effects of acute

exposure to chlorine due to a
swimming pool accident
Abstract
OBJECTIVE Acute exposure to chlorine causes lung damage, and recovery may proceed slowly for several weeks.
The short term respiratory effects of acute chlorine inhalation during a swimming pool accident were examined.
METHODS A total of 282 subjects (134 children, aged <14 years) inhaled hydrogen chloride and sodium
hypochlorite during an accident caused by a malfunction of the water chlorinating system in a community pool in
Rome in 1998. Most people received bronchodilators and cortisone at the emergency room; five children were
admitted to hospital. A total of 260 subjects (92.2%) were interviewed about duration of exposure (<3, 35, >5
minutes), intensity of exposure (not at all or a little, a moderate amount, a lot), and respiratory symptoms. Lung
function was measured in 184 people (82 children) after 1530 days. The effects of exposure to chlorine were
analysed through multiple linear regression, separately in adults and in children.
RESULTS Acute respiratory symptoms occurred among 66.7% of adults and 71.6% of children. The incidences were
highest among those who had chronic respiratory disease and had a longer duration of exposure. In about 30% of the
subjects, respiratory symptoms persisted for 1530 days after the accident. Lung function levels were lower in those
who reported a high intensity of exposure than in those who reported low exposure, both in children and in adults
(mean (95% confidence interval (95% CI)) differences in forced expiratory volume in 1 second (FEV1,) were 109
(310 to 93) ml, and 275 (510 to 40) ml, respectively).
CONCLUSION Persistent symptoms and lung function impairment were found up to 1 month after the incident.
Although community pool accidents happen rarely, the medical community needs to be alerted to the possible clinical
and physiological sequelae, especially among susceptible people.

Chlorine is a highly irritating gas that, when inhaled, can damage larger
airways as well as distal lung structure. After massive acute chlorine
inhalation, pulmonary oedema, respiratory failure, and death have been
described both in laboratory animals and in humans.1 2 Acute accidental
inhalation of sublethal doses can be responsible for symptoms ranging
from upper airway irritation to more serious respiratory effects, such as
intense coughing, wheezing, and dyspnoea,3-8 together with lung
function decrements.5 6 9 10 Although most studies have shown that

pulmonary deficit after acute exposure to chlorine tends to disappear

after a few weeks,5 6 10 recent reports have documented long term
effects, such as asthmatic reactions, bronchial hyperresponsiveness,
and reduced lung function among exposed people both in the
general8 11 12 and in the work environment.13 14 Brooks et aldescribed
the reactive airway dysfunction syndrome as an asthma-like
occupational illness after an acute exposure to highly concentrated
respiratory irritants.15 Moreover, it has been suggested that a history of
asthma, bronchial hyperreactivity, and atopy can be associated with a
greater acute decrement in pulmonary function and more serious long
term pulmonary sequelae.12 16 17
The potential sources of exposure to chlorine are multiple and include
industrial operations18-20inappropriate mixing of household cleaning
agents,12 emissions during transport,11 and inhalation of fumes from
solid chlorine products.7 Due to the common use of chlorine and its
compounds for water disinfection, mishaps in the chlorinating of
swimming pools represent an important risk of exposure. However, the
health effects of chlorine inhalation after swimming pool accidents have
been documented in only few studies, and have concentrated on
pathophysiology, clinical presentation, and types of treatment.3 4 Early
physiological and clinical pulmonary alterations have rarely been
reported in accidents involving a few people.5 610
We have assessed the short term impact of an accidental acute
exposure to chlorine, which occurred in a swimming pool. The
respiratory health of 260 people has been studied and followed up with
spirometry within 1530 days from the accident.
Results
CHARACTERISTICS OF THE STUDY POPULATION
Table 1 shows the characteristics of the study population (134 children, 126 adults). Among children, 86.6% were
swimmers and 51.5% were engaged in physical exercise during the accident; a history of chronic respiratory disease
was present in 12.3%. Most adults were parents or pool personnel; 31.7% were current smokers. A total of 63.4%
vacated the pool in a few minutes, and 56.2% reported having been exposed not at all or a little.

Table 1

Characteristics of the study population exposed at the community pool accident in Rome, 1998

Children
n=134

Adult
s
n=126

Total
n=260

n %

n %

Sex:
Male

62

46.3

33

26.
2

95

Female

72

53.7

93

73.
8

165 63.5

Never

77

61.
1

77

61.1

Ex

6.3

6.3

Current

40

31.
7

40

31.7

36.5

Smoking habit:

History of chronic respiratory disease:

1-150

No

116

86.6

88.
112 9

228 87.7

Yes

18

13.4

14

11.1

32

12.3

Staff

11

8.7

12

4.6

Swimmer

116

86.6

2.4

119 45.8

Accompanying person

16

11.9

88.
111 1

127 48.8

Present at the pool as:

Engaged in physical exercise at the time of the

accident:
No

56

41.8

80.
101 2

157 60.4

Yes

69

51.5

3.2

73

28.1

<3

45

33.6

36

28.
6

81

31.1

35

44

32.8

40

31.
7

84

32.3

>5

34

25.4

49

38.
9

83

31.9

Not at all/a little

81

60.4

65

51.
6

146 56.2

A moderate amount

39

29.1

42

33.
3

81

31.2

A lot

10

7.5

19

15.
1

29

11.2

Time to vacate the pool (minutes):

Perception of exposure:

Totals may vary because of missing values.

1-150 Chronic respiratory disease includes asthma, bronchitis, emphysema.

ACUTE SYMPTOMS
Tables 2 and 3 show the incidences of acute symptoms among children and adults respectively. Among children, eye
irritation occurred in 50.0%, nose and throat problems in 54.5%, any respiratory symptoms (shortness of breath,
wheezing, cough) in 71.6%. The corresponding values among adults were 61.9, 73.0, and 66.7%. Among children,
the incidences of all symptoms tended to be higher among those who had a history of chronic respiratory disease
than among healthy people (nose and throat problems: 61.1v 53.5%), among those who were engaged in physical
exercise at the moment of the accident in comparison with those who were not (for respiratory symptoms:
84.1v 57.1%), among those who spent more time to vacate the pool (any respiratory symptoms: 91.2% for >5
minutesv 60.0% for <3 minutes), among those who reported having been exposed a lot compared with not at all or
a little (eye irritation: 80.0%v 38.3%). Similar results were found among adults. Furthermore, incidences were higher
among smokers and ex-smokers than among never smokers, and among the swimming pool personnel who spent
more time in the exposed area to help people.

Table 2
Incidences of acute symptoms for selected characteristics among children (n=134), Rome, 1998
Respiratory symptoms
Nose/throat
problems

Shortness Wheezing2of breath 150

Cough Total

50.0 54.5 7.5

2.2

70.2

71.6

Male

56.5 56.5 6.5

3.2

67.7

71.0

Female

44.4 52.8 8.3

1.4

72.2

72.2

Eye
irritation
Total
Sex:

History of chronic
respiratory disease:2-151
No

50.9 53.5 6.9

1.7

68.1

69.8

Yes

44.4 61.1 11.1 5.6

83.3

83.3

3.5

71.6

75.0

Present at the pool as:

Swimmer

52.6 56.9 65.5 71.6

Accompanying
person
31.3 37.5 68.8 68.8
Engaged in physical
exercise at the time of
the accident:
No

42.9 41.1 5.4

1.8

57.1

57.1

Yes

57.9 66.7 10.1 2.9

81.2

84.1

60.0

60.0

Time to vacate the pool

(minutes):
<3

31.1 31.1 2.2

Respiratory symptoms
Eye
irritation

Nose/throat
problems

Shortness Wheezing2of breath 150

Cough Total

35

52.3 65.9 9.1

2.3

65.9

70.5

>5

67.7 73.5 11.8 5.9

91.2

91.2

Perception of
exposure:
Not at all/a little 38.3 39.5 3.7

66.7

67.9

A moderate
amount

69.2 79.5 7.7

5.1

71.8

74.4

A lot

80.0 90.0 40.0 10.0

100.0

100.0

Totals may vary because of missing values.

2-150 Wheezing includes shortness of breath with wheezing.

2-151 Chronic respiratory disease includes asthma and bronchitis.

Table 3
Incidences of acute symptoms for selected characteristics among adults (n=126), Rome, 1998
Respiratory symptoms
Eye
irritation
Total

Nose/throat Shortness Wheezing3

problems
of breath -150
Cough Total

61.9

73.0

17.5 7.1

61.1

66.7

Male

66.7

63.6

18.2 12.1 60.6

66.7

Female

60.2

76.3

17.2 5.4

61.3

66.7

Sex:

History of chronic
respiratory disease:3-151
No

61.6

71.4

17.9 7.1

62.5

67.0

Yes

64.3

85.7

14.3 7.1

50.0

64.3

Never

57.1

70.1

15.6 2.6

58.4

64.9

Ex

100.0 87.5

37.5 12.5 62.5

62.5

Current

62.5

75.0

17.5 15.0 65.0

70.0

75.0

33.3 33.3 83.3

91.7

Smoking habit:

Present at the pool as:

Staff

66.7

Swimmer

100.0 100.0 33.3

33.3

33.3

Accompanying
person

60.4

72.1

15.3 4.5

59.5

64.9

72.3

17.8 6.9

63.4

68.3

Engaged in physical
exercise at the time of
the accident:
No

61.4

Respiratory symptoms
Eye
irritation
Yes

50.0

Nose/throat Shortness Wheezing3

problems
of breath -150
Cough Total

75.0

50.0 25.0 100.0

100.0

Time to vacate the pool

(minutes):
<3

44.0

58.3

5.5

2.8

41.7

47.2

35

60.0

70.0

17.5 5.0

62.5

67.5

>5

77.6

87.8

26.5 12.2 75.5

81.6

Not at all/a
little

41.5

56.9

7.7

47.7

53.8

A moderate
amount

78.6

85.7

19.1 14.3 66.7

71.4

A lot

94.7

100.0 47.4 15.8 94.7

Perception of
exposure:

100.0

Totals may vary because of missing values.

3-150 Wheezing includes shortness of breath with wheezing.

3-151 Chronic respiratory disease includes asthma, bronchitis, emphysema.

RESPIRATORY SYMPTOMS AT 1530 DAYS

A total of 63 people (27% of the total) reported some respiratory symptoms at 1530 days after the accident (21.1%
of children and 32.7% of adults). Proportions of people with respiratory symptoms at 1530 days and some personal
characteristics of children and adults are shown in table 4. People who reported having been exposed a lot were
more likely to have respiratory symptoms at 1530 days than those exposed not at all or a little (42.9% v18.1% in the
entire sample). Adults who went to the emergency department, as well as those who received pharmacological
treatment either at the emergency department or at home, were more likely to have respiratory symptoms at 1530
days than those who did not (44.7v 24.2%, and 45.5v24.6%), but no significant differences were found among
children. In both age groups, those with a history of chronic respiratory disease had slightly higher rates of respiratory
symptoms at 1530 days than healthy people (34.5v 25.6%). Similarly, smokers and ex-smokers had a higher
probability of having respiratory symptoms at 1530 days than never smokers (40.6, 37.5, and 27.8% respectively).

Table 4
Personal characteristics of children and adults who underwent clinical examination after 2 weeks and proportion (%)
of respiratory symptoms at 1530 days, Rome, 1998

Respiratory symptoms4-151 at 1530 days

Children
n=123
n

Adult
s
n=113

Total
n=236

n %

n %

Time to vacate the pool

(minutes):
<3

37

13.5

29

24.1

66

18.2

35

44

15.9

38

28.9

82

21.9

>5

31

41.94-150

45

42.2

76

42.14150

Perception of exposure:
Not at all/a little

73

12.3

54

25.9

127 18.1

A moderate
amount

38

36.8

41

34.1

79

35.4
42.94-

A lot

10

4-150

30.0

18

50.0

23.6

66

24.2

28

160

Visit to the emergency

department:
No

55

44.7
Yes
Treatment:

68

19.1

47

150

68

20.6

69

24.6

121 23.9
4-

115 29.6

4-152

No

45.5

137 22.6
4-

150

99

10
0

31.0

207 25.6

13

46.1

29

Never

72

27.8

Ex

37.5

Current

32

40.6

Yes

55

21.8

44

No

107 20.6

Yes

16

32.3

History of chronic
respiratory disease:

25.0

34.5

Smoking habit:

4-150 p<0.05;

4-160 p<0.005.

4-151 Respiratory symptoms include shortness of breath, wheezing, and cough.

4-152 Treatment=pharmacological treatment either at the emergency department or at home.

Totals may vary because of missing values.

LUNG FUNCTION MEASUREMENTS AT 1530 DAYS

The relation between exposure (perception of exposure) and spirometric indices at 1530 days after the accident is
shown in table5. In both age groups, FVC, FEV1, and FEF2575tended to be lower among those people with the
highest exposure, although the results from linear regression analysis were significant only for FEV1. For this
variable, in the entire sample, we found a reduction of 178 ml (95% confidence interval (95% CI) 334 to 22) for
people who reported having been exposed a lot versus not at all or a little. The corresponding values were 109
(310 to 93) ml among children and 275 (510 to 40) ml among adults. In both age groups there was no effect
modification of the relation between exposure and lung function either by the visit to the emergency department, by
pharmacological treatment, or by history of chronic respiratory disease. On the contrary, the effect of exposure on
lung function tended to be higher among smokers and ex-smokers than among never smokers (mean (95% CI)
FEV1 ml adjusted difference beteween exposed and unexposed people was 499 (1049 to 51) for smokers, 338
(1528 to 849) for ex-smokers, 165 (449 to 117) for never smokers). Oxyhaemoglobin saturation was normal in all
people (SatO2 96%).

Table 5
Association between exposure to chlorine and lung function (adjusted ml difference, 95% CI) at 1530 days, Rome,
1998
Children

Parameter
FVC
150

5-

Perception of
exposure

Adults

Total

ml
difference5n

151

Not at all/a
little
44 Reference

ml
difference5- 95%
151
CI

95% CI

4
7

Referenc
e

91 Reference

A fair
amount

27 56

65 to177

3
8

204

434
to 26

65 49

175
to 76

A lot

300 to 80

1
7

204

502
to 95

25 140

315
to 35

4
7

Referenc
e

49 to 207

3
8

156

336
to 25

310 to 93

1
7

275

510
to
40

4
7

Referenc
e

110

FEV15- Not at all/a

150
little
44 Reference
A
moderate
amount

A lot

27 79

109

FEF25 Not at all/a

5-150
little
44 Reference
75
A
moderate
amount

27 23

A lot

78

310 to 356

3
8

594 to 438

91 Reference

65 17

130
to 95

25 178

334
to
22

91 Reference

24

495
to
543

65 27

272
to
326

245

904

25 165

574

ml
difference5- 95%
n 151
CI

Children

Parameter

Perception of
exposure

Adults

ml
difference5n

151

95% CI
7

Total

n
to
415

ml
difference5- 95%
151
CI

ml
difference5- 95%
n 151
CI

to
243

5-150 The mean (SD) FVC, FEV1, and FEF2575in the reference groups were respectively: 1902 (624) ml,
1654 (524) ml, 2037 (826) ml among children; 3662 (938) ml, 2978 (727) ml, 2948 (1320) ml among adults;
2819 (1191) ml, 2344 (919) ml, 2503 (1191) ml in the whole sample.

5-151 Difference (ml) in lung function variables between exposed people and the reference groups after
adjustment for age, sex, height, BMI, history of chronic respiratory disease, instrument, physician, number of
days since the accident and smoking among adults.

Akdur O, Durukan P, Ikizceli I, Ozkan S, Avsarogullari L. A rare complication of

chlorine gas inhalation: pneumomediastinum. Emerg Med J 2006;23:e59

A rare complication of chlorine gas inhalation: pneumomediastinum

Abstract
Chlorine gas is frequently produced from a homemade mixture of diluted hypochlorite with
hydrochloric acid. Lowconcentration household bleach alone is regarded as a chemical irritating
the mucous membranes, but when it is mixed with hydrochloric acid to clean the floor of
bathrooms and toilets, chlorine is produced.1Chlorine gas is a potent pulmonary irritant that
causes acute damage in both the upper and lower respiratory tract.2 Such cleaning mixtures are
commonly used in Turkey. This article describes pneumomediastinum, a rare complication of
chlorine gas inhalation.
Discussion
Chlorine gas inhalation cases are usually mild to moderate; death is rare.2 Patients who need
medical care after a minor exposure to chlorine gas may experience burning of the eyes or throat,
consistent with irritation of their mucous membranes. Patients with major exposure to chlorine
gas may also have cough, shortness of breath, chest tightness or other symptoms referable to the
lungs.3 This patient also described violent coughing and shortness of breath just after the
inhalation. So, it may be accepted as a moderate to severe case of chlorine gas inhalation.
In 1944, Macklin and Laenec4 described the pathophysiological mechanism of the spontaneous
pneumomediastinum, and their description is still valid today. Trigger factors have been
described as all those noniatrogenic factors contributing to an increase in the pressure gradient
between the alveoli and the interstitium. So, rupture of marginal alveoli as a result of increased
intraalveolar pressure and dissection of the air along the pulmonic vascular sheaths into the
mediastinum is seen.5 It may follow severe strain or cough, and has been described with various
conditions such as parturition, bronchial asthma, certain respiratory tract infections, foreign body
aspiration and pulmonary embolism.1 This is also the probable mechanism of
pneumomediastinum in our patient,which was precipitated after violent coughing.
Spontaneous pneumomediastinum has a good prognosis, subsiding in a week without any
treatment.1 Our patient also recovered rapidly, without intervention other than oxygen, and her
chest radiograph returned to normal after 5days.
Cases of exposure to chlorine gas because of household mixing products are usually mild. But
clinicians must be aware of complications such as pneumomediastinum. This case presentation
draws attention to this easytotreat, but potentially dangerous complication.

Jones R, Wills B, Kang C. Chlorine Gas: An Evolving Hazardous Material Threat and
Unconventional Weapon. West J Emerg Med. 2010; 11(2):151-156

Chlorine Gas: An Evolving Hazardous Material Threat and Unconventional

Weapon
INTRODUCTION
Once used as a chemical weapon in the World War I, chlorine gas has long been known for its
pulmonary irritant properties. Many chlorine exposures are the result of accidents at swimming
pools and mixing of household agents. However, recent events in the Iraq war, the war on terror
and large-scale industrial incidents have demonstrated that chlorine represents a persistent
hazardous material (HAZMAT) threat. Massive quantities of chlorine are stored and transported
across the United States with minimal security. Chlorine has been successfully used as an
unconventional weapon in Operation Iraqi Freedom. In this article, we will review the domestic
threats of chlorine exposure, discuss its use as an unconventional weapon, review toxicologic
principles, and examine treatment of chlorine-related casualties. We will also discuss some
pertinent disaster management aspects of chlorine-related mass casualty (MASCAL) incidents.
Industrial production of chlorine in the U.S. exceeds 15 million tons annually. It is used in
numerous industrial practices, including the manufacturing of paper, plastic and chemical
products. It is also widely used in the municipal treatment of sewage and drinking water. Since
chlorine production occurs in fewer than 20 states, it must be transported in large quantities to
metropolitan centers. This large-scale transport and storage close to urban centers could make it
an attractive target for extremist organizations. The use of chlorine could allow terrorists to
deploy a chemical weapon in a highly populated area without having to manufacture or transport
it themselves.1 An intentional release of chlorine by terrorists, bombing of storage vessels, or an
unintentional release from an industrial incident could produce thousands of casualties. In fact an
intentional release of chlorine, included as one of the Department of Homeland Securitys 15
National Planning Scenarios, could result in over 17,000 fatalities and 100,000 injuries if it
occurred in a highly populated area2,3. Despite this, many at-risk communities are unaware of the
volume of chlorine that is transported through their area. The following events document recent
incidents involving chlorine releases and highlight some of the risks posed by chlorine gas.
General Toxicology

Chlorine is element number 17 on the periodic table. It exists as a yellow-green gas at

temperatures above 34C. Because this gas has a density greater than air, it tends to settle along
the ground.15 All irritant gases have the potential to cause pulmonary injury, which is principally
related to the duration of exposure. Irritant gases with high water solubility (e.g. ammonia)

interact with oral, nasal and ocular mucosa rapidly causing discomfort. This warning property
allows people to leave an area of exposure, limiting contact and thus reduces the likelihood of
significant pulmonary damage. Irritant gases with low water solubility (e.g. phosgene) generate
damaging caustic and oxidizing byproducts more slowly, resulting in very little warning
properties. The absence of robust warning properties may result in prolonged exposures,
allowing these agents to reach distal airways and produce greater pulmonary injury. Chlorine gas
has an intermediate solubility, which gives it some warning properties, but may also allow for
prolonged exposure and pulmonary damage.16,17 At 1-3 parts per million (PPM), chlorine starts to
cause irritation of the mucus membranes. Pulmonary symptoms begin at exposures greater than
15 PPM, and concentrations greater than 430 PPM are fatal within 30 minutes (Table 1).18,19 In
comparison, the Occupational Safety and Health Administration (OSHA) has set the permissible
exposure limit (PEL) for an eight-hour time period at 1 PPM.20

Table.
Symptoms of chlorine exposure by concentration level
Pathophysiology

Chlorines toxic effects are due primarily to the production of hypochlorous and hydrochloric
acid that occurs when elemental chlorine (Cl2) reacts with water. These two acids then further
react to produce oxygen free radicals (Figure 1). In large exposures, the acids and free radicals
then damage cell walls and interact with sulfhydryl groups on various amino acids and enzyme
systems.16,18 Histologic findings of this damage include bronchial edema, desquamation of
epithelial cells, erosions and localized necrosis.2,21

Figure.
Chlorine and water interact forming acid and oxidant byproducts
Clinical Effects

Local irritation from acid results in an inflammatory response of the upper and lower airways
leading to bronchospasm, cough and dyspnea. Disruption of cell membranes and proteins by the
acids and free radicals results in death of alveolar cells and endothelial cells of adjacent

capillaries. Clinical manifestations of this damage include pulmonary edema and Acute
Respiratory Distress Syndrome (ARDS).16,22 Fortunately, most patients with mild to moderate
exposures will have resolution of their acute symptoms within three to five days and will have
normal pulmonary function tests after several months.15,23 Some patients, however, will have
chronic respiratory problems, such as reactive airway disease (RAD). While there is no way to
predict which patients will develop long term complications, patients with a history of smoking
or a prior history of RAD may be at increased risk..18
Although the most serious clinical effects of chlorine toxicity tend to be pulmonary, it can also
cause skin and eye injuries. While dermal manifestations include irritation and pain, in severe
exposures, chemical burns, including blister formation, can take place. Ocular complications
include irritation and conjunctivitis. Severe cases can result in corneal defects.24 Chlorine also
causes other non-specific symptoms, such as nausea, vomiting, rhinorrhea and headache.25
MANAGEMENT STRATEGIES OF CHLORINE EXPOSURE
Pre-hospital and Personal Protective Measures

The most important aspect of managing a chlorine release is identification of the prevailing wind
direction in order to stage upwind while establishing scene safety. Personal protective equipment
(PPE) for all first responders is paramount. The incident in Tacoma resulted in pre-hospital
provider injuries due to limited utilization of PPE and an unexpected shift in wind direction. This
event illustrates the importance of the use of appropriate PPE for all responders, which should
include self-contained respirators as well as eye and skin protection.19 According to OSHA
standards, all personnel moving into high-risk areas must be issued positive pressure ventilation
systems.26 This level of protection best corresponds to OSHA level A or level B PPE since both
consist of positive pressure self-contained breathing apparatuses with full face plates as well as
protective over garments.26 Per OSHA standard 910.120, if this type of system is not initially
used, those conducting the preliminary assessment must be issued an escape breathing apparatus
capable of operation for at least five minutes.26 Military personnel working in a contaminated
area or working on the decontamination line should be outfitted in mission-oriented protective
posture (MOPP) level 4 equipment.27 MOPP level 4 is roughly equivalent to OSHA level C PPE
because it uses a chemical protective mask instead of a positive pressure breathing system. While
this level of protection is insufficient to enter areas of high concentration, such as near a leaking
chlorine tank, it does provide adequate protection for perimeter duty and work on the
decontamination line. MOPP level 4 also represents the highest level of PPE that all U.S. soldiers
are trained to use. Experience with higher levels of PPE, such as positive pressure respiratory
systems, is reserved for specialized military HAZMAT teams.

Decontamination

Treatment of patients in the pre-hospital setting consists principally of decontamination and

supporting the patients breathing. Decontamination, as with most chemical exposures, involves
evacuation of the patient from the area of exposure, removing clothing, and irrigating with
copious amounts of water. Although the duration of decontamination has not been conclusively
identified, three to five minutes of rinse time has been advocated.19 While 0.5% chlorine solution
is recommended for the decontamination of undifferentiated chemical exposures,27 it is not
expected to be relevant in cases of chlorine-related casualties. Patients complaining of ocular
irritation should undergo copious eye irrigation. Contact lenses should be removed to ensure
proper irrigation.15,16 Unlike people exposed to liquid chlorine, patients exposed to only chlorine
vapor represent no significant risk of contaminating rescue workers (off gasing).24 Patients
exposed to gaseous chlorine probably will not require any decontamination other than removal of
the clothing. However, if they are experiencing ocular or dermal symptoms, they should undergo
decontamination.2
Treatment

Pre-hospital support of respiratory injuries involves removing patients from the source of
exposure, providing supplemental oxygen, and administering inhaled beta-agonists for patients
with bronchospasm. For patients in extreme respiratory distress, rapid sequence intubation (RSI)
should be considered, but this type of resource-intensive procedure may not be feasible if there
are multiple casualties and limited resources cannot support such an intervention. The use of a
standardized triage system can help to sort patients based on the severity of their injuries and to
guide resource allocation in such a situation.
ED care of patients is supportive. However, it is very important that the ED be prepared to
decontaminate patients who arrive via private vehicles since these patients may not have been
decontaminated prior to arrival. During the disaster in Graniteville, over 95% of the patients
arrived via private vehicle.4 After appropriate decontamination, skin wounds should be treated
like other chemical burns, including: irrigation, tetanus prophylaxis, local wound care and
analgesia. Eye irritation should prompt copious lavage and evaluation for corneal defects. Severe
eye injuries, including any that result in a corneal defect, require ophthalmology consultation. If
ophthalmologic consultation is not immediately available, patients with corneal defects should
receive topical antibiotic prophylaxis to prevent bacterial superinfection. These patients also
require ophthalmologic follow-up within the next few days.
Mild respiratory symptoms and bronchospasm can be treated with aerosolized beta-agonists. If a
patient has a persistent cough but no respiratory distress, nebulized lidocaine (4 mL of a 4%
solution) may provide symptomatic relief.28 For patients with severe respiratory distress, RSI

should be considered. Patients may develop ARDS, with its characteristic bilateral infiltrates on
chest x-ray and hypoxia that does not improve with increased inspired oxygen concentration.
Therefore, when a patient is intubated after a chlorine exposure, low tidal volumes (58 mL/kg
ideal body weight) are recommended.29 The patients inspired oxygen concentration and peak
expiratory end pressure (PEEP) can then be adjusted to maintain the patients oxygen saturation.
There is no specific antidote for chlorine exposures. Several studies have suggested that inhaled
or parenteral steroids are effective at decreasing respiratory complications after chlorine
exposure.30,31 The proposed mechanism is decreased recruitment of inflammatory mediators and
immune cells, as well as increased stimulation of surfactant producing pneumocytes.32 One
animal model showed a benefit of inhaled budesonide if administered within 30 minutes of
exposure. This same study showed a significant decrease in improvement if treatment was
delayed to 60 minutes, which suggests that steroids should be administered soon after an
exposure when feasible.33 Nebulized sodium bicarbonate may be another adjunctive treatment for
chlorine pulmonary exposures. Theoretically, inhaled bicarbonate can neutralize hypochlorous
and hydrochloric acids, decreasing severity of lung injury. One non-randomized, placebocontrolled study of chlorine exposure reported improved pulmonary function tests (PFT), but
patient-oriented benefits and long-term outcomes were not determined.34 Another study
examining nebulized sodium bicarbonate revealed improved subjective symptoms, with no
reported adverse effects.35 In both studies patients received concomitant inhaled beta-agonists
and intravenous steroids. Another case series utilized bicarbonate without beta-agonists or
steroids in patients with mild chlorine exposures. All three patients subjectively improved after
treatment with a 3.75% sodium bicarbonate nebulizer and no adverse effects were reported.36 The
utility of nebulized bicarbonate has not been firmly established, and the optimal dose has also not
been delineated. A reasonable dose is 3.755% nebulized over 20 minutes and may be repeated.
A 3.5% solution can be prepared by taking 2 mL of a 7.5% intravenous preparation of sodium
bicarbonate solution (the concentration found in most cardiac crash carts) and combining with
2 mL of normal saline. Because precipitates can form if combined, it is important that nebulized
sodium bicarbonate be administered separately from nebulized albuterol sulfate.37 Another
theoretical treatment is the administration of an anti-oxidant such as N-acetyl cysteine (NAC).
Although some data from animal models exists, there is currently not enough information to
support the use of anti-oxidants in a clinical setting.32,38
Some patients will present with minimal or no symptoms. A small percentage who are minimally
symptomatic on presentation may go on to develop delayed pulmonary edema over a period of
several hours.4 Therefore, patients with mild symptoms should be observed for eight to 24 hours
for delayed onset of respiratory complications.17 Patients who are asymptomatic after their
exposure can be discharged after six hours of observation, but must be counseled on symptoms
that should prompt a return for further care.

Disaster and Mass Casualty (MASCAL) Considerations

Personnel moving into areas of higher concentration or prolonged exposure time will need
appropriate HAZMAT equipment for respiratory and skin protection. First responders must be
equipped with and trained to use this PPE prior to a major chlorine release. Because of the
potential for large numbers of exposed patients who may require treatment and monitoring, a
hospital can become overwhelmed. It is important that hospitals and municipalities have mutualaid agreements that coordinate the transfer of medications, equipment and personnel to the areas
they are most needed. Especially important is respiratory support equipment. During the
previously mentioned event in South Carolina, 10% of the hospitalized patients required
intubation and mechanical ventilation.3 Additionally, incident command must help coordinate
patient triage and transportation to appropriate medical facilities. Equitable distribution of
patients based on each hospitals surge capacity can minimize the strain on individual hospitals.
Triage is an ongoing process, and must be repeated as patients move through the levels of
decontamination. The initial level of decontamination is the hot zone, which is typically the
actual incident location. The warm zone is geographically distant from the incident and is
frequently the entry point to decontamination. This area can restrict patient flow and may be an
appropriate time to re-triage. As patients complete the decontamination process, they pass from
the warm zone to the cold zone. Upon reaching this area, patients may need to be re-triaged
again, then directed to the appropriate level of care.39
A critical challenge to MASCAL incident command is maintaining clear and regular
communication. People working or living in areas being evacuated must be notified of the need
to leave, as well as safe evacuation routes that avoid exposure. The general population must be
notified of signs and symptoms of chlorine exposure and then directed to triage and care areas
for the walking wounded. Hospitals nearest the incident scene must be prepared to receive
most of the walking wounded, as well as the most critical patients. There must also be a point
of contact for friends and families seeking missing loved ones. The best mechanism for the
spread of such information will vary, depending on the size and demographics of a given
community.
In addition to the occult HAZMAT threat, the intentional use of chlorine as an unconventional
weapon is now occurring. Large chlorine stores in the U.S. are vulnerable and lack adequate
security. Operation Iraqi Freedom has demonstrated multiple events of successful use of
weaponized chlorine transport vehicles, resulting in hundreds of casualties. Successful
management of a chlorine MASCAL incident requires increased awareness and planning. As for
all HAZMAT responses, proper equipment and training for first responders and a network of
supporting medical facilities are needed to provide adequate care. Management of chlorine
exposure involves decontamination and treatment of potential pulmonary injuries. Beta-agonists

can be helpful for bronchospasm. Nebulized bicarbonate may decrease symptoms and prevent
lung injury. Early corticosteroid use may play a role in treating lung inflammation and, possibly,
preventing post-injury scarring. Severe cases may require endotracheal intubation and
mechanical ventilation. While all these measures may prove useful in the treatment of patients
after a chlorine exposure, further research is needed to delineate the optimal treatment regimen.
Recognizing the evolving threat posed by chlorine, both in the form of an accidental release as
well as an unconventional weapon, is an important first step to being prepared for this type of
incident.