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CHLORINE See Occupational Exposure Standards Human Health Effects:
Evidence for Carcinogenicity: A4; Not classifiable as a human carcinogen.
Human Toxicity Excerpts: At autopsy, chlorine fatalities can
show sloughing of the bronchial columnar epithelium, purulent intraluminal
exudate, hyaline membranes in the alveolar spaces, thrombi in the pulmonary
vessels, and interstitial and alveolar pulmonary edema.
EXPOSURES TO ... 3-6 PPM ... STINGING OR BURNING SENSATION IN EYES, NOSE
& THROAT ... HEADACHE ... REDNESS & WATERING OF EYES, SNEEZING,
COUGHING, & HUSKINESS OR LOSS OF VOICE. ... MEN EXPOSED IN BLEACHING ROOMS TO CONCN OF THE ORDER OF (5 PPM) ...
SUFFER FROM DISEASE OF THE BRONCHI, & BECOME PREDISPOSED TO TUBERCULOSIS.
... IRRITATES SKIN CAUSING SENSATIONS OF BURNING OR PRICKLING, INFLAMMATION OR
EVEN BLISTER FORMATION. ACUTE EXPOSURE ... VOMITING. ... ANXIETY ... CHRONIC EXPOSURE. ... CONCN OF
0.8-1 PPM CAUSE PERMANENT, ALTHOUGH MODERATE, REDUCTION IN PULMONARY FUNCTION.
PATIENT HAD MYASTHENIA GRAVIS MANIFESTED BY LARYNGEAL STRIDOR AFTER
ACCIDENTAL EXPOSURE TO CHLORINE GAS.
DIAGNOSIS WAS ESTABLISHED BY CORRECTION OF ABNORMAL PULMONARY FUNCTION AFTER
INJECTION OF EDROPHONIUM CHLORIDE. PATIENT SUBSEQUENTLY HAD GENERALIZED
MYASTHENIA GRAVIS. Acute toxic levels: The extent of injury depends on the concn and duration of
exposure as well as the water content of the tissue involved and the presence of
underlying cardiopulmonary disease. ... Estimated clinical effects ... as
follows: ... 1-3 ppm: Mild mucous membrane irritation; ... 5-15 ppm: Moderate
irritation of upper resp tract; 30 ppm: Immediate chest pain, vomiting, dyspnea,
cough; 40-60 ppm: Toxic pneumonitis and pulmonary edema; 430 ppm: Lethal over 30
min; 1000 ppm: Fatal within a few min. Hypochlorite containing disinfectants or bleaching fluids, if inhaled, may
lead to life threatening poisoning through the immediate liberation of chlorine gas, if they are used together with
another cleansing fluid which is very acidic. /Hypochlorites/
Caution: Potential symptoms of overexposure are burning of eyes, nose and
mouth; lacrimation, rhinorrhea; coughing, choking and substernal pain; nausea,
vomiting; headache, dizziness; syncope; pulmonary edema; pneumonia; hypoxemia;
dermatitis; eye and skin burns. Corrosive effect and pulmonary effect: Complete destruction of skin or mucous
membrane. A concn of 3.5 ppm produces a detectable odor; 15 ppm causes immediate
irritation of the throat. Concn of 50 ppm are dangerous for even short
exposures; 1000 ppm may be fatal, even when exposure is brief.
... Reported prolongation of optical chronaxie in 3 subjects exposed to a
chlorine concn of 1.5 mg/cu m (0.52
ppm), but did not observed an appreciable effect at chlorine concn ranging from 0.6 to 1.0 mg/cu m
(0.21 to 0.34 ppm) (odor perception threshold: 0.8 mg/cu m). Approx 2-2.5 min
after cessation of exposure to the higher chlorine levels, the optical chronaxie
returned to baseline levels. In a series of 75 tests on 3 subjects, a chlorine concn of 1.5 mg/cu m (0.52 ppm)
elicited heightened light sensitivity, but exposure to a concn of 0.8 mg/cu m
(0.28 ppm) did not induce any effects. Changes in sensitivity to light became
evident only at, or above the odor perception threshold level.
... Discussed briefly the drying effects on the skin and hair of chlorinated
water. Swimmers have reported a bleaching effect of chlorine on their hair, some have developed
"green hair", and many a chemical conjunctivitis. There have also been
occasional reports of asthma precipitated by exposure to chlorinated water ... .
... (1935) Reported the outcome of 15 pregnancies among female workers at a
chlorine plant in the years 1932-33. Of
these, 13 births were normal and 2 were premature. In one of these 2 cases, a 6
1/2 month-old female fetus was stillborn; induced abortion was suspected. In the
other, the 4 1/2-month old fetus was macerated and no definitive cause was
established. No mention was made of possible congenital malformations. The
authors concluded that pregnancy, delivery, puerperium, and lactation were not
affected. In a series of in vitro experiments on a human lymphocyte culture system ...
(1971) reported that chlorine concn 2-20
times those normally found in drinking water induced chromatid and chromosome
breaks, translocations, dicentric chromosomes, and gaps.
... The effects of low concentrations of chlorine on pulmonary function in humans /was
studied/. Eighty healthy, unacclimated volunteers were exposed to chlorine gas at concentrations of 0.5 or 1
ppm, and several pulmonary function measurements were made. Comparisons were
made by paired t-tests between the percent change from base-line values obtained
at analogous times after a sham exposure. With the sham versus the 0.5 ppm
exposure, insignificant changes were observed. With the sham versus the 1 ppm,
there were many differences in percent change from base line that were
significant at the p < 0.05 level or better. These were in forced vital
capacity, forced expiratory volume at 1 second, peak expiratory flow rate,
forced expiratory flow rate at 50% and 25% vital capacity ... ,and airway
resistance. Most of the test results returned to normal by the next day. ... /It
was concluded/ that even though chlorine
does not produce any serious subjective symptoms at low concentrations, it
adversely affects pulmonary function transiently. ... /Authors/ reported on in-depth studies of 25 chloralkali plants. The
study involved 332 male workers on diaphragm cells matched with 382 workers not
exposed to chlorine. Air samples at
representative locations within each plant was done every 2 months throughout
the study year. TWA exposure data were calculated for each worker on an 8-hr
basis. All but 6 of the workers had exposures below 1 ppm, and 21 had TWAs above
0.52 ppm; the average concentration of chlorine ranged from 0.006 to 1.42 ppm with a
mean of 0.15 ppm. The average number of chlorine exposure years for all workers was
10.9. For these dosages (exposure concentration times years of employment),
medical histories showed no dose-response correlation between prevalence of
colds, dyspnea, palpitation, or chest pain. Chest X-rays, ventilatory capacity,
maximal ventilatory capacity, or forced expiratory volume at 3 seconds indicated
no evidence of permanent lung damage from chlorine at the exposures reported above.
However, of 329 electrocardiograms from 332 workers, 9.4% were abnormal compared
with 8.5% in the 382 controls. The incidence of fatigue was greater in those
exposed above 0.5 ppm but not below, and anxiety and dizziness showed a modest
correlation (p = 0.05) with exposure level. Leukocytosis (p = 0.05) and a lower
hematocrit (p = 0.017) showed some relation to exposure. No neoplasia or serious
pulmonary disease was reported.
Skin, Eye and Respiratory Irritations: ... Irritating to nose & throat at 5 ppm or above ...
... Highly irritating especially to the mucous membranes of the eyes and
respiratory tract. Caution: Potential symptoms of overexposure are burning of eyes, nose and
mouth; lacrimation, rhinorrhea; coughing, choking and substernal pain; nausea,
vomiting; headache, dizziness; syncope; pulmonary edema; pneumonia; hypoxemia;
dermatitis; eye and skin burns.
Medical Surveillance: Medical histories should include sufficient detail to document the occurrence
of bronchitis, tuberculosis, or pulmonary abscesses. Recommended medical surveillance: ... A complete history and physical
examination: ... Examination of the eyes ... cardiac status, and teeth should be
stressed. The skin should be examined for evidence of chronic disorders. Simple
tests of olfactory ability should be carried out. 14" x 17" chest roentgenogram
... /along with respiratory function tests:/ FVC and forced expiratory volume (1
sec). ... Periodic medical exam: The above medical exam are to be repeated on an
annual basis, except that an X-ray is necessary only when indicated by the
results of pulmonary function testing or by signs and symptoms of resp disease.
Populations at Special Risk: ... Individuals with pulmonary disease, breathing /problems/, bronchitis, or
chronic lung conditions.
Probable Routes of Human Exposure: Dermal contact from handling chlorine
or its products in home and industry; inhalation from ambient air and workspace
exposure and ingestion of food and water treated with chlorine. Exposures most commonly result from either storage or transportation
accidents involving the pressurized liquid form. Other poisonings occur in
industrial accidents, school chemistry experiments, accidental release of chlorine from swimming pool operations, and
mixing of cleaning agents (adding acidic cleaning agents to hypochlorite bleach
releases chlorine gases).
Emergency Medical Treatment:
Emergency Medical Treatment:
Antidote and Emergency Treatment: Call for medical aid. ... Move to fresh air. If breathing has stopped, give
artificial respiration (but NOT mouth-to-mouth). If breathing is difficult, give
oxygen. ... Flush affected areas with plenty of water. Do not rub affected
areas. Inhalation: remove victim from source of exposure; call a doctor; support
respiration; administer oxygen. Eyes: flush with copious amounts of water for at
least 15 min. For immediate first aid: Ensure that adequate decontamination has been
carried out. If victim is not breathing, start artificial respiration,
preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket
mask as trained. Perform CPR if necessary. Immediately flush contaminated eyes
with gently flowing water. Do not induce vomiting. If vomiting occurs, lean
patient forward or place on left side (head-down position, if possible) to
maintain an open airway and prevent aspiration. Keep victim quiet and maintain
normal body temperature. Obtain medical attention. /Chlorine and related compounds/
For basic treatment: Establish a patent airway. Suction if necessary. Watch
for signs of respiratory insufficiency and assist ventilations if necessary.
Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary
edema and treat if necessary ... Monitor for shock and treat if necessary ...
For eye contamination, flush eyes immediately with water. Irrigate each eye
continuously with normal saline during transport ... Do not use emetics. For
ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution
if the patient can swallow, has a strong gag reflex, and does not drool. ...
Cover skin burns with dry sterile dressings after decontamination ... . /Chlorine and related compounds/
Animal Toxicity Studies:
Evidence for Carcinogenicity: A4; Not classifiable as a human carcinogen.
Non-Human Toxicity Excerpts: EXPOSURE OF CATS TO CONCN OF 900 MG/CU M (300 PPM) FOR 1 HR MAY CAUSE DEATH
AFTER A PERIOD DURING WHICH THE CONJUNCTIVA IS INFLAMED & THERE IS COUGHING
& DYSPNEA. ... DOGS RARELY DIE FOLLOWING 30 MIN EXPOSURE TO ... (650 PPM)
& NEVER TO A CONCN LESS THAN 280 PPM. RESPIRATORY RATE OF ANIMALS IS INCR
DURING EXPOSURE TO ... 200 TO 1000 PPM ... /AT/ CONCN OF 10000 OR MORE PPM ...
INSPIRATIONS OCCUR MORE SLOWLY & DEEPLY & ARE FINALLY ARRESTED. ...
PULSE RATE OF DOGS IS RETARDED DURING EXPOSURE TO CONCN OF 180-200 PPM OR MORE.
IN DOGS THAT INHALED AIR CONTAINING 800 PPM CHLORINE FOR 2-7 HR, A RAPIDLY INCR ACIDOSIS
OCCURRED. ... REPEATED EXPOSURE OF RABBITS TO CONCN ... FROM 2-5 MG/CU M
(0.7-1.7 PPM) OVER PERIODS UP TO 9 MO CAUSED A LOSS OF WT & AN INCR
INCIDENCE OF RESP DISEASE. IN GUINEA PIGS THE INHALATION OF SMALL QUANTITIES OF CHLORINE ACCELERATES THE COURSE OF
EXPERIMENTAL TUBERCULOSIS ... ... Exposures of 6 hr daily at 100 ppm repeated for 50 days caused only
slight unrest and irritation of the eyes and nose of rabbits, guinea pigs, and
pigeons. ... Twenty exposures, each of 6 hr, at the concn of 33 ppm caused no
harm to a monkey or to smaller animals. Repeated exposure at higher concn
resulted in a loss of wt that paralleled the severity of the exposure.
CHLORINE DISSOLVED IN WATER &
INJECTED INTO ANTERIOR CHAMBERS OF /EYES OF/ RABBITS ... CAUSING SEVERE
INFLAMMATION, CORNEAL OPACITY, IRIS ATROPHY, & INJURY OF LENS.
STRIPED BASS EGGS & PROLARVAE WERE EXPOSED TO INTERACTING TOTAL RESIDUAL
CHLORINE, CHANGE IN TIME, & EXPOSURE
TIME REPRESENTING CONDENSER ENTRAINMENT & EFFLUENT DISCHARGE CONDITIONS.
PROLARVAE SHOWED GREATER MORTALITY @ ALL LEVELS & UNEQUAL TIME INTERVALS FOR
36 HR AFTER EXPOSURE. LARVAL WHITE PERCH WERE SUBJECTED TO INTERACTING TOTAL RESIDUAL CHLORINE (0.00-0.30 MG/L), ELEVATED TEMP (2,
6, & 10 DEG C), & EXPOSURE TIME (0.08, 2.0, & 4.0 HR). LARVAE SHOWED
GREATER MORTALITY LEVELS AT 23 DEG C THAN AT 15 DEG C AT ALL TREATMENT LEVELS,
UP TO 96 HR AFTER EXPOSURE. Fifteen tons of chlorine escaped from
a chemical works and drifted downwind, covering 25 sq km. Cattle were most
severely affected, showing dyspnea, lacrimation, profuse nasal discharge and
depression, several animals dying within a day or two. Pigs showed salivation,
lacrimation, coughing, vomiting and anorexia. Horses suffered from frequent
urination and had cracking sounds in the lung; several were unthrifty and
dyspneic 6 months later. Rats were given 0, 1, 10, or 100 mg/l chlorine in drinking water. Blood glutathione
was significantly decreased after 6 months of treatment and this effect
persisted after 1 yr of treatment in the 10 and 100 mg/l groups. Treatment
groups showed an increase in blood osmotic fragility. The acute study revealed
that blood glutathione was significantly decr as early as 30 min after the admin
of 30 and 120 ug chlorine. The effect
was maintained up to 1 hr. However, the blood glutathione level returned to
control value by 2 hr. The osmotic fragility of red blood cells was increased
after an acute 15 min exposure and was without change after 30 min. The red
blood cell count & hematocrit were decr in the 100 mg/l group after 3 mo of
treatment. Chlorine administered
chronically in drinking water for 3 mo incr the incorporation of (3)H-thymidine
into nuclei of rat kidney and testes in the 100 mg/l group.
Mice and rats were exposed to chlorine gas at their respective RD50 concn
(approx 9-11 ppm) for 6 hr/day for 1, 3, or 5 days (The RD50 concn is that concn
which reduces respiratory rate by 50%). Lesions were observed in the nasal
passages of all exposed groups and were of similar severity and character in
rats and mice. The most severe changes were found in the olfactory mucosa of the
anterior portion of the dorsal meatus and consisted of partial to complete
degeneration of olfactory sensory cells, with olfactory sustentacular cells
being more resistant to chlorine
exposure. Lesions in the respiratory epithelium were located primarily on the
free margins of the naso- and maxilloturbinates and adjacent nasal septum. The
respiratory epithelium exhibited loss of cilia and cellular exfoliation,
primarily on naso- and maxilloturbinates. Eurasian watermilfoil was exposed to various chlorine concn on a continuous or an
intermittent basis in 96 hr toxicity studies. Continuous exposure to chlorine concn as low as 0.05 mg/l total
residual chlorine depressed shoot and
total plant dry wt approx 30% relative to controls. Shoot length was depressed
approx 16% at this concn. Chlorophyll-a was depressed 25% at 0.1 mg/l total
residual chlorine.
Long term exposure of chlorine to
channel catfish /(concentration not specified) was found to/ drastically reduce
blood pressure and heart rate. Low level chlorination has been found to lead to significant shifts in the
species composition of marine phytoplankton communities. These shifts depend on
(a) the composition of the communities at the time of stress and (b)
morphological and systematic characteristics of the species, thus exhibiting
different sensitivities to chlorine.
Chlorine has an impact similar to that
demonstrated with other pollutants: a decrease in the predominance of centric
diatoms and subsequent success of pennate diatoms and micro flagellates. Very
low concentrations of chlorine (0.05 -
0.15 mg/l) have caused changes in species composition.
The toxicity of total residual chlorine in freshwater environments was ... a
function of the relative abundance of free residual chlorine in discharged effluents. The higher
the percentage of free residual chlorine, the more toxic the effluent.
Increased pH resulted in decreased total residual chlorine toxicity. ... Salinity affected the
biological response to exposure to chlorine additions under marine and estuarine
conditions. The toxicity of chlorinated effluents increased with increasing
temperature in fresh water environments. Vertebrates and invertebrates responded
differently to exposure to chlorinated effluents in both the freshwater and
marine-esturine habitats. ... Estuarine water was chlorinated to 10 mg/l, aged 10-35 days and then used as
growth medium for three phytoplankton species, Thalassiosira pseudonana,
Dunaliella species, Isochrysis galbana. Total residual chlorine compounds were undetectable in the
chlorinated water; two species did not grow even after the water had been aged
35 days. A more resistant species grew in chlorinated water aged 23 or 35 days
but did not grow in water aged 10 days. All three species grew well in the same
water that had not been chlorinated. Elemental chlorine is /SRP: a general
biocidal agent/ ... germicidal ... fungicidal, protozoacidal, and virucidal.
... COXSACKIE VIRUS A2 WAS INACTIVATED MORE SLOWLY BY CHLORINE @ PH 9 THAN AT PH 7, & MORE
SLOWLY @ 3-6 DEG C THAN @ 27-29 DEG C. ... INACTIVATION RATE ALSO DEPENDED ON
CONCN OF FREE CHLORINE ...
A purified prepn of the simian rotavirus SA-11 containing mostly single
virion particles and a prepn of cell associated SA-11 virions were tested for
their resistance to inactivation by chlorine. Both virus prepn were inactivated
more rapidly at pH 6 than 10. The presence of carcinogenic and mutagenic chemicals in the effluent of a
wastewater treatment plant was indicated by papilloma development in caged
bullhead catfish (Ictalurus melas), hepatic enzyme induction in exposed fish,
and Ames test mutagenicity of organic extracts of wastewater. ... Mutagenic and
carcinogenic chemicals were not identified in the wastewater, but chlorination
was implicated as a factor contributing to the induction of papillomas. The
prevalence of papillomas on wild black bullheads exposed to the effluent
decreased from 73 to 23% after the amount of residual chlorine in the effluent leaving the chlorine contact chamber was reduced from
1.3-3.1 mg/l to 0.25-1.2 mg/l. Rats were fed ground beef which had been treated with aqueous chlorine. Results of the hematologic
evaluations demonstrated almost no effects associated with the feeding of rats
with chlorine treated meat for 92 days.
There was a slight prolongation of the prothrombin time in all male groups fed
the chlorine treated meat. This
prolongation was most pronounced in the rats fed ground beef treated with 600
ppm and was significant (p< 0.05) when compared with the control males. In
the absence of any other hematologic evidence, it is not possible to attribute
the prolonged prothrombin time to the administration of the test compound.
Prothrombin times of females did not differ significantly. The clinical
chemistry and urine analysis yielded results wherein the values for the control
and test rats are consistent with reported values for rats under standard
laboratory conditions. On the basis of these hematologic and clinical data,
there were no adverse effects on male or female rats fed ground beef treated
with up to 600 ppm aqueous chlorine.
Studies on the acute toxic effects of chlorine on lab animals show that single
exposures to concn of more than 360 mg/cu m for 30-60 min are lethal for various
animal species. Single exposures to concn of 29-87 mg/cu m for several hr are
associated with an incr mortality in rodents. Repeated exposures to chlorine concn of 3-26 mg/cu m for a period of
several wk or months induced dose related pulmonary and other adverse effects.
Chlorine does not appear to be a
carcinogenic or tumor-promoting agent in lab animals.
Chlorine is considered to be
phytotoxic ... acute injury of chlorine
on vegetation is ... defoliation with no leaf symptoms. Single effects of chlorine on higher forms of plants incl
spotting of the leaves at concn above 1.5 mg/cu m and marginal and interveinal
injury of the plant at higher concn (150-300 mg/cu m). ... Chlorine does appear to retard the germination
of seeds. Life cycle tests have been conducted with two freshwater invertebrate species
and one freshwater fish species. ... Two 2 week tests beginning with 16 to 24 hr
old Daphnia magna /were conducted/. Flow through tests were conducted with
nominal sewage concentrations of 1.2 to 20%; untreated Lake Superior water was
the dilution water. The secondary sewage was chlorinated just before entering
the diluter systems, and the probable predominant form of total residual chlorine was monochloramine. The total
residual chlorine concentrations ranged
from control to 114 ug/l in one test and control to 136 ug/l in the second.
Daphnids did not survive the 2 week exposure to the three highest chlorinated
effluent concentrations (14 to 114 ug/ l in the first test and 7 to 136 ug/l in
the second). Daphnids that survived to adulthood reproduced successfully. In the
first test, therefore, the lowest unacceptable concentration was 4 ug/l,
resulting in a chronic value 7.483 ug/l for that test. The results of the second
test are more difficult to interpret. At the test concentration of 7 ug/l, all
daphnids died in seven days in both test chambers. At the next lower
concentration of 2 ug/l, all daphnids died in one test chamber in seven days,
but 50% of the daphnids in the duplicate chamber survived and reproduced
successfully. Two of the four controls from both tests had survival as low as 70
percent. The influence of different treatment processes on the mutagenic activity
(Ames test) and some chemical parameters in water were investigated in a few
waterworks. Application of a chlorine
treatment generally increased the direct and promutagenic activity, but the
extent of the increase depended on the type of water chlorinated.
The chronic effects of chlorine on
rhesus monkeys at concentrations of 0, 0.1, 0.5, and 2.5 ppm of chlorine in the environment were studied. Four
monkeys per sex were assigned to each concentration group and they were exposed
for 6 hr/day, 5 days/wk for one yr. There were no exposure related differences
among groups in body weight, pulmonary diffusing capacity, distribution of
ventilation, elevated neurologic parameters, electrocardiographic parameters,
clinical chemistry, hematology, or urinalysis parameters. After 6 wk of high
level exposure, ocular irritation was observed during the daily exposures. At
the end of the exposure, conjunctival irritation was observed in the group
exposed to 2.5 ppm, but there was no evidence of chronic changes in the
conjunctiva nor were the corneas affected. Respiratory epithelial hyperplasia of
the nasal passages of both sexes exposed to 2.5 ppm was observed in some
animals: It was present only in its mildest form at lower exposure
concentrations. Tracheal epithelial lesions were associated with a loss of cilia
and goblet cells in the affected areas. ... Studied the effects on lung function in rabbits given a single, 30-min
exposure to a chlorine concn of 145,
290, or 580 mg/cu m (50, 100, or 200 ppm). Respiratory volumes, flow rates,
pressure measurements, and pulmonary compliance were used for evaluating lung
function, prior to exposure, and 30 min, 3, 14, and 60 days after exposure.
Respiratory flow rates decr initially after exposure to concn of 580 or 290
mg/cu m ... but returned to normal within 60 days of exposure. Rabbits exposed
to 145 mg/cu m ... did not exhibit any significant change in respiratory flow
rates. A decr in pulmonary compliance was noted initially in rabbits exposed to
chlorine levels of 145, 290, or 580
mg/cu m ... . During the post-exposure phase, pulmonary compliance returned to
normal in rabbits exposed to 145 mg/cu m ... but there was a subsequent
compensatory incr in pulmonary compliance in rabbits exposed to a chlorine concn of 290 or 580 mg/cu m ...
Pathological exam of the lungs of rabbits exposed ... /at/ 580 or 290 mg/cu m
... revealed initial hemorrhage and edema, followed by chronic inflammation,
which receded during the post-exposure phase. The lungs of rabbits exposed to
145 mg/cu m ... did not show the pathological changes attributed to the higher
exposures ... . ... Mice exposed to chlorine in concn
of 14.5 and 7.3 mg/cu m (5.0 and 2.5 ppm) for 8 hr/day for 3 consecutive days
showed a loss in body weight, and microscopic exam of the lungs of mice exposed
to 14.5 mg/cu m ... yielded findings similar to these following lethal or near
lethal short-term exposures. ... Rats were exposed to chlorine
concn of 0, 2.9, 8.7, or 26 mg/cu m (0, 1, 3, or 9 ppm) for 6 hr/day, 5 days/wk,
for 6 wk. Some mortality occurred in female rats exposed to 26 mg/cu m ... and
smaller gains in body weight were noted in females exposed to 2.9, 8.7, or 26
mg/cu m ... and in males exposed to 8.7 or 26 mg/cu m ... Clinical signs of
ocular and upper respiratory tract irritation, such as lacrimation, hyperemia of
the conjunctiva, and nasal discharge occurred in rats exposed to 8.7 or 26 mg/cu
m ... rats exposed to 2.9 mg/cu m ... showed occasional slight indication of
irritation. All groups of rats ... had urinary staining of the perineal fur, and
the urinary specific gravity was elevated in females at all ... levels and in
males at levels of 8.7 and 26 mg/cu m ... Pathological exam of the rats exposed
... /at/ 26 mg/cu m ... revealed inflammation of the upper and lower respiratory
tract. Focal to multifocal mucopurulent inflammation of the nasal turbinates and
necrotic erosions of the mucosal epithelium were observed. Inflammation and
epithelial hyperplasia in the trachea and bronchiolar areas and epithelial
hyperplasia and hypertrophy of the respiratory bronchioles and alveolar ducts
accompanied by inflammation were also observed. The alveolar sacs contained incr
numbers of alveolar macrophages and secretory material. Focal necrosis,
hypertrophy, and hyperplasia of the alveolar epithelial cells adjacent to the
alveolar ducts was found together with areas of atelectasis and interstitial
inflammation in the lungs. Long-term exposure to chlorine
accelerated the evolution of tuberculosis in guinea pigs injected with a
virulent strain of human tuberculosis. ... Guinea pigs were exposed to a chlorine level of 5 mg/cu m (1.69 ppm) for 5
hr/day, for 47 days prior to or after the injection. The average survival rate
was lower in guinea pigs exposed to chlorine before injection with tuberculosis
than in either guinea pigs exposed after injection, or in control animals, which
were injected but not exposed to chlorine. The potential cocarcinogenicity of chlorine was studied ... A benzpyrene solution
was applied to the shaved skin of NMRI mice twice/wk for 10 wk, with a total
dose per animal of 750 ug or 1500 ug benzpyrene applied ... Some groups were
also treated with a 1% solution of sodium hypochlorite (NaOCl), applied either
before, during, or after the benzpyrene treatment. After 128 wk of observation,
it appeared that pre-treatment with the chlorine solution retarded tumor development
and markedly reduced total tumor rates in the groups give either 750 or 1500 ug
of benzpyrene. Treatment with the chlorine solution after application of
benzpyrene also retarded tumor development in the group give 750 ug of
benzpyrene. The number of carcinomas was reduced by about 40% by the chlorine solution applications, independent of
the method of treatment or the dose of benzpyrene.
Non-Human Toxicity Values: LC50 MOUSE INHALATION 137 PPM/1 HR LC50 Rat male 299 (260-344) ppm/1 hr Under Haber's Rule: C x t = 7500 for chlorine gas on cats /where the amount (C)
present in one cubic meter of air is expressed in mg and multiplied by the time
(t) in minutes necessary for the experimental animal inhaling this air to obtain
a lethal effect/. LC50 mouse 368 mg/cu m/30 min (95% C.I., 307-441 mg/cu m)
Ecotoxicity Values: LC50 DAPHNIA MAGNA (WATER FLEA) 0.097 MG/L/30 MIN /CONDITIONS OF BIOASSAY NOT
SPECIFIED/ LC50 DAPHNIA MAGNA (WATER FLEA) 0.063 MG/L/60 MIN /CONDITIONS OF BIOASSAY NOT
SPECIFIED/ LC50 GAMBUSIA AFFINIS 1.59 MG/L/30 MIN /CONDITIONS OF BIOASSAY NOT SPECIFIED/
LC50 GAMBUSIA AFFINIS 0.84 MG/L/60 MIN /CONDITIONS OF BIOASSAY NOT SPECIFIED/
TLm Grass shrimp 0.22 mg/l/96 hr. /Conditions of bioassay not specified/
TLm Ocean spot 0.14 mg/l/24 hr; toxic effect: stress. /Conditions of bioassay
not specified/ LC50 Daphnia magna (water flea) 0.017 mg/l/46 hr. /Conditions of bioassay not
specified/ LC50 Oncorhynchus kisutch (coho salmon) 208 ug/l/1 hr /Conditions of bioassay
not specified/ LC100 Larval clam 0.5 mg/l/100 hr. /Conditions of bioassay not specified/
TL50 Keratella cochlearis 0.019 mg/l/4 hr. /Conditions of bioassay not
specified/ LC50 Daphnia pulex 0.49 mg/l/96 hr. /Conditions of bioassay not specified/
LC50 Yellow perch 0.88 mg/l/1 hr. /Conditions of bioassay not specified/
LC50 Micropterus salmoides (largemouth bass) 0.74 mg/l/1 hr. /Conditions of
bioassay not specified/ TLm Salmo gairdnerii (rainbow trout) 0.08 mg/l/168 hr. /Conditions of
bioassay not specified/ TLm Carassius auratus (goldfish) 0.17 mg/l/24 hr, intermittent chlorination,
at 17-25.5 deg C. /Conditions of bioassay not specified/
LC50 Lepomis macrochirus (bluegill sunfish) 0.44 mg/l/96 hr, intermittent
chlorination at 15 deg C, toxic effect: distress. /Conditions of bioassay not
specified/ TL50 Pimephales promelas (fathead minnow) 0.1 mg/l/96 hr. /Conditions of
bioassay not specified/ LC50 Ictalurus punctatus (channel catfish) (fingerling) 0.07 mg/l/96 hr toxic
effect: gill sodium uptake drastically impaired. /Conditions of bioassay not
specified/ LC50 Emerald shiner (yearling) 0.23 mg/l/30 min test performed using Lake
Superior water at 25 deg C. /Conditions of bioassay not specified/
LC50 Emerald shiner (adult) 0.28 mg/l/30 min; test performed using Lake
Superior water at 25 deg C. /Conditions of bioassay not specified/
Lepomis cyanellus (green sunfish) 3.0 mg/l/24 hr; toxic effect: 28% killed.
/Conditions of bioassay not specified/ Carp 0.15 - 0.2 mg/l/12-16 days, toxic effect: 25% killed. /Conditions of
bioassay not specified/
Metabolism/Pharmacokinetics:
Metabolism/Metabolites: Chlorine persists as an element only
at a very low pH (less than 2), and at the higher pH found in living tissue it
is rapidly converted into hypochlorous acid. In this form, it apparently can
penetrate the cell and form N-chloro-derivatives that can damage cellular
integrity.
Absorption, Distribution & Excretion: Chlorine gas is found to accumulate
in the leaves of plants; entering via the stomata.
Mechanism of Action: Hypochlorous acid ... reacts with sulfhydryl groups in cysteine.
/Hypochlorous acid/ Hypochlorous acid ... inhibits ... aldolase enzyme essential for glucose
oxidation in Escherichia coli. /Hypochlorous acid/ Chlorine, as chlorine gas, chlorite ion, and hypochlorite,
is a strong oxidant that readily reacts with organic molecules to produce a
variety of chlorinated compounds. This reactivity in biological systems makes it
difficult to study the pharmacokinetics of chlorine and to separate the effects of chlorine from those of the chlorine compounds and metabolites.
... In microbial test systems, chlorine can ... disrupt cell wall
permeability, ... /causing/ edema and acute tissue injury.
The labile intermediates and stable end products formed by the reaction of
aqueous hypochlorous acid with thymine, uracil, and various uracil derivatives
were identified. ... The purine ring was more resistant to attack, but parabanic
acid resulted from the reaction of aqueous hypochlorite with guanine, adenine,
or xanthine for one week. ... /Hypochlorous acid/ Chlorine is a strong oxidizing agent
that forms both hypochlorous and hydrochloric acid on contact with moist mucous
membranes. The former cmpd decomposes into hypochloric acid and oxygen free
radicals (.O2-). Damage results from the disruption of cellular proteins. These
agents combine with sulfhydryl groups and disulfur bonds and form stable
hydrates of organic chlorine.
Interactions: An additive effect due to smoking in workers exposed to chlorine was observed by comparing maximal
mid-expiratory flow values in smokers and non-smokers. A significant decr of
mid-expiratory flow was established in exposed smokers in comparison with
non-smokers, and in both groups in comparison with workers without chlorine exposure.
Chlorine-nickel temperature
interactions were studied in rainbow trout (Salmo gairdneri). Mortality in chlorine-nickel test groups was significantly
greater than predicted by an additive interaction. Chlorine-nickel treatment groups with high
chlorine concentrations regardless of
the level of nickel showed greater percentage mortality than treatment groups
with either nickel or chlorine alone.
When chlorine and nickel were combined,
the chlorine concentration was the key
factor in determining mortality, even at sublethal levels of chlorine, for the concentrations tested.
Temperature did not influence toxicity as strongly as either chlorine or nickel concentrations. The
presence of 0.018 ppm total residual chlorine significantly increased nickel
accumulation in tissues from fish exposed to chlorine and nickel, when compared with tissue
samples from fish under similar exposure conditions in the absence of chlorine. The increased nickel concentration
may be attributed to an increase in the permeability of the gill to nickel
during chlorine exposures.
Pharmacology:
Interactions: An additive effect due to smoking in workers exposed to chlorine was observed by comparing maximal
mid-expiratory flow values in smokers and non-smokers. A significant decr of
mid-expiratory flow was established in exposed smokers in comparison with
non-smokers, and in both groups in comparison with workers without chlorine exposure.
Chlorine-nickel temperature
interactions were studied in rainbow trout (Salmo gairdneri). Mortality in chlorine-nickel test groups was significantly
greater than predicted by an additive interaction. Chlorine-nickel treatment groups with high
chlorine concentrations regardless of
the level of nickel showed greater percentage mortality than treatment groups
with either nickel or chlorine alone.
When chlorine and nickel were combined,
the chlorine concentration was the key
factor in determining mortality, even at sublethal levels of chlorine, for the concentrations tested.
Temperature did not influence toxicity as strongly as either chlorine or nickel concentrations. The
presence of 0.018 ppm total residual chlorine significantly increased nickel
accumulation in tissues from fish exposed to chlorine and nickel, when compared with tissue
samples from fish under similar exposure conditions in the absence of chlorine. The increased nickel concentration
may be attributed to an increase in the permeability of the gill to nickel
during chlorine exposures.
Environmental Fate & Exposure:
Probable Routes of Human Exposure: Dermal contact from handling chlorine
or its products in home and industry; inhalation from ambient air and workspace
exposure and ingestion of food and water treated with chlorine. Exposures most commonly result from either storage or transportation
accidents involving the pressurized liquid form. Other poisonings occur in
industrial accidents, school chemistry experiments, accidental release of chlorine from swimming pool operations, and
mixing of cleaning agents (adding acidic cleaning agents to hypochlorite bleach
releases chlorine gases).
Artificial Pollution Sources: The most important manmade emissions of chlorine are from processes involving the
production, transportation, and use of chlorine ...
Environmental Fate: Aquatic Fate: The stability of free chlorine in natural water is very low because
it is a strong oxidizing agent and rapidly oxidizes inorganic compounds. It also
oxidizes organic compounds, but more slowly than inorganic compounds.
AQUATIC FATE: ... CHLORINE REACTS
WITH ORGANIC PRECURSORS THAT ARE FOUND IN MANY SOURCE WATERS TO PRODUCE A
POTENTIAL CARCINOGEN, /SUCH AS/ CHLOROFORM (CHCL3).
Environmental Abiotic Degradation: Chlorination studies conducted on natural and artificial seawater, have shown
two phases of chlorine losses in
seawater: a rapid initial loss followed by a continuous loss at a sharply
reduced rate. The initial loss reaches a saturation level that varies widely
between natural seawater samples and appears to be related to a true organic
demand. Losses continue over 10 day periods and are pronounced in seawater
containing bromine. Other studies have indicated that the loss of chlorine is associated with the bromide
chemical system in seawater. The fate of the lost chlorine was not determined.
Environmental Bioconcentration: Chlorine is highly toxic to all forms
of aquatic life, there is no potential for bioaccumulation or bioconcentration.
Environmental Water Concentrations: Finished water from different USA cities chlorine levels: Cincinnati, 2.7 mg/l; Miami,
2.3 mg/l; Ottumwa, 1.4 mg/l; Philadelphia, 2.0 mg/l and Seattle, 0.0 mg/l.
The National Organics Reconnaissance Survey (NORS) tested 80 water supplies
throughout the United States, of which 20% were ground water, 33% were lakes
& reservoirs, and 47% were rivers. 99% of the utilities used chlorination
somewhere in their treatment system. Sixty facilities practiced raw water
chlorination; of these sites, 86% applied chlorine at a range of 1-6 mg/l with 34% at
0-2 mg/l, 26% at 2-4 mg/l and 26% at 4-6 mg/l. Free residual levels were 0-0.4
mg/l for 41%; 0.4-0.8 mg/l for 19%, 0.2-0.8 mg/l for 4% and 1.2-1.6 mg/l for 20%
of the 80 locations. Combined residual levels of 0-0.4 mg/l accounted for 60% of
the locations, 0.4-0.8 mg/l accounted for 20% of the sites and remaining sites
had levels from 0.8-2.8 mg/l. Chlorine application in water
treatment facilities serving 19 Massachusetts communities ranged from a minimum
of 4.3 mg/l to a maximum of 29.7 mg/l with a mean of 15.2 + or - 7.44 mg/l.
These treatment levels produced finished water with a free residual chlorine levels at a mean of 1.3 mg/l; the
minimum was 0.3 mg/l and the maximum was 4.0 mg/l. Maximum total residual chlorine amounted to 6.0 mg/l, with a minimum
of 0.4 mg/l and a mean of 1.5 mg/l. Levels in the distribution system ranged
from 0.0-2.0 mg/l for free residual chlorine and from 0.0-2.5 mg/l for total
residual chlorine.
Atmospheric Concentrations: Mean ambient air levels /have been reported/ between 1 and 3.7 mg/cu m (0.344
and 1.27 ppm). Atmospheric levels of approximately 0.001 ppm (2.9 ug/cu m) have been
measured from coastal areas, and ambient levels in metropolitan areas such as
Cincinnati or Baltimore average 0.02 ppm (58.0 ug/cu m).
Environmental Standards & Regulations:
CERCLA Reportable Quantities: Persons in charge of vessels or facilities are required to notify the
National Response Center (NRC) immediately, when there is a release of this
designated hazardous substance, in an amount equal to or greater than its
reportable quantity of 10 lb or 4.54 kg. The toll free number of the NRC is
(800) 424-8802; In the Washington D.C. metropolitan area (202) 426-2675. The
rule for determining when notification is required is stated in 40 CFR 302.4
(section IV. D.3.b). Releases of CERCLA hazardous substances are subject to the release reporting
requirement of CERCLA section 103, codified at 40 CFR part 302, in addition to
the requirements of 40 CFR part 355. Chlorine is an extremely hazardous substance
(EHS) subject to reporting requirements when stored in amounts in excess of its
threshold planning quantity (TPQ) of 100 lbs.
Atmospheric Standards: Listed as a hazardous air pollutant (HAP) generally known or suspected to
cause serious health problems. The Clean Air Act, as amended in 1990, directs
EPA to set standards requiring major sources to sharply reduce routine emissions
of toxic pollutants. EPA is required to establish and phase in specific
performance based standards for all air emission sources that emit one or more
of the listed pollutants. Chlorine is
included on this list.
Clean Water Act Requirements: Designated as a hazardous substance under section 311(b)(2)(A) of the Federal
Water Pollution Control Act and further regulated by the Clean Water Act
Amendments of 1977 and 1978. These regulations apply to discharges of this
substance. The ambient water quality criterion for chlorine based on a daily water consumption of
2 l to protect human health is recommended to be 10.0
mg/l. Freshwater aquatic organisms and their uses should not be affected
unacceptably if the 4 day average concn of total residual chlorine does not exceed 11 ug/l more than
once every 3 years on the average concn does not exceed 19 ug/l more than once
every 3 years on the average. Saltwater aquatic organisms and their uses should not be affected
unacceptably if the 4 day average concn of chlorine produced oxidants does not exceed 7.5
ug/l more than once every 3 years on the average and if the 1 hr average concn
does not exceed 13 ug/l more than once every 3 years on the
average.
Federal Drinking Water Standards: EPA 4000 ug/l
Federal Drinking Water Guidelines: EPA 4000 ug/l
Allowable Tolerances: Chlorine gas is exempted from the
requirement of a tolerance when used preharvest or postharvest in solution on
all raw agricultural commodities.
Chemical/Physical Properties:
Molecular Formula: Cl2
Molecular Weight: 70.906
Color/Form: GREENISH-YELLOW, DIATOMIC GAS Greenish-yellow gas ... (Note: Shipped as a liquefied compressed gas).
Odor: SUFFOCATING Pungent, irritating
Boiling Point: -34.04 DEG C
Melting Point: -105.5 DEG C
Corrosivity: CHLORINE WILL ATTACK SOME FORMS OF
PLASTICS, RUBBER, AND COATINGS.
Critical Temperature & Pressure: CRITICAL TEMP: 144 DEG C; CRITICAL PRESSURE: 76.1 ATM
Density/Specific Gravity: (LIQUID) 1.5649 @ -35 DEG C, 0.9949 ATM; 1.4085 @ 20 DEG C, 6.864 ATM
Solubilities: 310 CC/100 CC WATER @ 10 DEG C 1.46 G/100 CC WATER @ 0 DEG C 177 CC/100 CC WATER @ 30 DEG C 0.57 G/100 CC WATER @ 30 DEG C SOL IN ALKALI Sol in chlorides and alcohols /Liquid/ Soluble in water at 25 deg C, more soluble in alkalies
Spectral Properties: INDEX OF REFRACTION: 1.0008 (GAS); 1.367 (LIQ)
Surface Tension: 18.4 dynes/cm @ 20 deg C in contact with vapor
Vapor Density: 2.5 (air= 1 at boiling point of chlorine)
Vapor Pressure: 5.83X10+3 mm Hg @ 25 deg C /from experimentally derived coefficients/
Other Chemical/Physical Properties: DISSOCIATION ENERGY (25 DEG C)= 57.978 KCAL; NATURAL ISOTOPES: 35 (75.53%);
37 (24.47%); HEAT CAPACITY (GAS, 25 DEG C) 8.11 CAL/MOLE/DEG C; ACTS AS
ELECTRON-ACCEPTOR IN FORMING COMPLEXES WITH MANY DONOR SPECIES; COMBINES READILY
WITH ALL ELEMENTS EXCEPT THE RARE GASES (XENON EXCLUDED) & NITROGEN
Heat of fusion: 1531 cal/gmole; 22.8 cal/g Heat of formation: 121.3 kJ/mole at 25 deg C Liquefaction pressure: 7.86 atm @ 25 deg C & 1 atm at -35 deg C; Critical
vol: 1.763 l/kg; strongly electronegative; 1 l of liq= 456.8 l of gas @ 0 deg C
and 1 atm Ratio of Specific Heats of Vapor (Gas): 1.325 Chlorine weighs 13 lb/gal
Diffusivity: 1.44x10-5 sq cm/s in water at 25 deg C (calculated).
Saturation concentration: 882.3 g/cu m at -7 deg C.
Heat capacity: constant pressure (cp): 0.473 kj/kg deg C; constant volume
(cv): 0.348 kj/kg deg C. Dielectric constant (gas): 1.0005480 at 101.325 kPa @ 20 deg C; dielectric
constant (liquid): 1.454 @ 70.15 K Critical volume: 3.216 cu dm/kg Critical density: 0.311 kg/cu m One l of liquid chlorine produces 434
l of chlorine gas at 25 deg C
Saturated vapor pressure: 74.040 lb/sq inch at 50 deg F
Saturated vapor density: 0.95960 lb/cu ft at 50 deg F
Ideal gas heat capacity: 0.114 btu/lb-deg F at 75 deg F
Diffusion coefficient: 0.033 sq m/hr (calculated)
Ionization potential: 11.48 eV RHOMBIC CRYSTALS /TEMPERATURE AND PRESSURE CONDITIONS NOT GIVEN/
Amber liquid /Temperature and pressure conditions not given/
Viscosity: 0.385 cp at 0 deg C /Chlorine, liquid/ 5 atm @ 10.3 deg C Acts as electron-acceptor in forming complexes with many donor species: Bent,
Chem Rev 68, 587 (1968); forms explosive mixtures with hydrogen; many finely
divided metals will burn in an atmosphere of chlorine; oxides are strong oxidizing agents
and explosive; monatomic chlorine is
unstable under ordinary conditions, however, it can be formed as a result of
thermal or optical dissociation, by an electrical discharge, or as an
intermediate during chemical reactions Chlorine persists as an element only
at a very low pH (less than 2), and at the higher pH found in living tissue it
is rapidly converted into hypochlorous acid. In this form, it apparently can
penetrate the cell and form N-chloro-derivatives that can damage cellular
integrity.
Chemical Safety & Handling:
DOT Emergency Guidelines: Health: TOXIC; may be fatal if inhaled or absorbed through skin. Fire will
produce irritating, corrosive and/or toxic gases. Contact with gas or liquefied
gas may cause burns, severe injury and/or frostbite. Runoff from fire control
may cause pollution. Fire or explosion: Substance does not burn but will support combustion.
Vapors from liquefied gas are initially heavier than air and spread along
ground. These are strong oxidizers and will react vigorously or explosively with
many materials including fuels. May ignite combustibles (wood, paper, oil,
clothing, etc.). Some will react violently with air, moist air and/or water.
Containers may explode when heated. Ruptured cylinders may rocket.
Public safety: CALL Emergency Response Telephone Number. ... Isolate spill or
leak area immediately for at least 100 to 200 meters (330 to 660 feet) in all
directions. Keep unauthorized personnel away. Stay upwind. Many gases are
heavier than air and will spread along ground and collect in low or confined
areas (sewers, basements, tanks). Keep out of low areas. Ventilate closed spaces
before entering. Protective clothing: Wear positive pressure self-contained breathing
apparatus (SCBA). Wear chemical protective clothing which is specifically
recommended by the manufacturer. It may provide little or no thermal protection.
Structural firefighters' protective clothing provides limited protection in fire
situations ONLY; it is not effective in spill situations.
Evacuation: ... Fire: If tank, rail car or tank truck is involved in a fire,
ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial
evacuation for 800 meters (1/2 mile) in all directions. Fire: Small Fires: Water only; no dry chemical, CO2 or Halon. Contain fire
and let burn. If fire must be fought, water spray or fog is recommended. Do not
get water inside containers. Move containers from fire area if you can do it
without risk. Damaged cylinders should be handled only by specialists. Fire
involving Tanks: Fight fire from maximum distance or use unmanned hose holders
or monitor nozzles. Cool containers with flooding quantities of water until well
after fire is out. Do not direct water at source of leak or safety devices;
icing may occur. Withdraw immediately in case of rising sound from venting
safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in
fire. For massive fire, use unmanned hose holders or monitor nozzles; if this is
impossible withdraw from area and let fire burn. Spill or leak: Fully encapsulating, vapor protective clothing should be worn
for spills and leaks with no fire. Do not touch or walk through spilled
material. Keep combustibles (wood, paper, oil, etc.) away from spilled material.
Stop leak if you can do it without risk. Use water spray to reduce vapors or
divert vapor cloud drift. Avoid allowing water runoff to contact spilled
material. Do not direct water at spill or source of leak. If possible, turn
leaking containers so that gas escapes rather than liquid. Prevent entry into
waterways, sewers, basements or confined areas. Isolate area until gas has
dispersed. Ventilate the area. First aid: Move victim to fresh air. Call 911 or emergency medical service.
Apply artificial respiration if victim is not breathing. Do not use
mouth-to-mouth method if victim ingested or inhaled the substance; induce
artificial respiration with the aid of a pocket mask equipped with a one-way
valve or other proper respiratory medical device. Administer oxygen if breathing
is difficult. Clothing frozen to the skin should be thawed before being removed.
Remove and isolate contaminated clothing and shoes. In case of contact with
substance, immediately flush skin or eyes with running water for at least 20
minutes. Keep victim warm and quiet. Keep victim under observation. Effects of
contact or inhalation may be delayed. Ensure that medical personnel are aware of
the material(s) involved, and take precautions to protect themselves.
Initial Isolation and Protective Action Distances: Small Spills (from a small
package or small leak from a large package): First, ISOLATE in all Directions 30
meters (100 feet); then, PROTECT persons Downwind during DAY 0.3 kilometers (0.2
miles) and NIGHT 1.1 kilometers (0.7 miles). LARGE SPILLS (from a large package
or from many small packages): First, ISOLATE in all Directions 275 meters (900
feet); then, PROTECT persons Downwind during DAY 2.7 kilometers (1.7 miles) and
NIGHT 6.8 kilometers (4.2 miles).
Odor Threshold: Water odor threshold: 0.0020 mg/l. Air odor threshold: 0.31 ppm. Odor Safety
Class: C. C= Odor safety factor from 1-26. Less than 50% of distracted persons
perceive warning of threshold limit value. Low odor threshold= 0.0300 mg/cu m. High odor threshold= 15.0000 mg/cu m.
Irritating concn= 9.00 mg/cu m.
Skin, Eye and Respiratory Irritations: ... Irritating to nose & throat at 5 ppm or above ...
... Highly irritating especially to the mucous membranes of the eyes and
respiratory tract. Caution: Potential symptoms of overexposure are burning of eyes, nose and
mouth; lacrimation, rhinorrhea; coughing, choking and substernal pain; nausea,
vomiting; headache, dizziness; syncope; pulmonary edema; pneumonia; hypoxemia;
dermatitis; eye and skin burns.
Fire Potential: MOST COMBUSTIBLES WILL BURN IN CHLORINE, FORMING IRRITATING AND TOXIC GASES.
CYLINDERS MAY VENT RAPIDLY OR EXPLODE WHEN HEATED. FLAME IMPINGEMENT UPON STEEL
CHLORINE CONTAINER WILL RESULT IN
IRON/CHLORINE FIRE CAUSING RUPTURE OF
THE CONTAINER. Nonflammable ...
NFPA Hazard Classification: Health: 4. 4= Materials that, on very short exposure, could cause death or
major residual injury, including those that are too dangerous to be approached
without specialized protective equipment. A few whiffs of the vapor or gas can
cause death, or contact with the vapor or liquid may be fatal, if it penetrates
the fire fighter's normal protective gear. The normal full protective clothing
and breathing apparatus available to the typical fire fighter will not provide
adequate protection against inhalation or skin contact with these materials.
Flammability: 0. 0= Any material that will not burn. Reactivity: 0. 0= Includes materials that are normally stable, even under
fire exposure conditions, and that do not react with water. Normal fire fighting
procedures may be used.
Fire Fighting Procedures: USE WATER SPRAY TO KEEP FIRE EXPOSED CONTAINERS COOL. EXTINGUISH FIRE USING
AGENT SUITABLE FOR SURROUNDING FIRE. If material involved in fire: Extinguish fire using agent suitable for type
of surrounding fire. (Material itself does not burn or burns with difficulty.)
Cool all affected containers with flooding quantities of water. Apply water from
as far a distance as possible. Use water spray to knock down vapors.
Respiratory protection for chlorine
... /during/ fire fighting: self contained breathing apparatus with a full
facepiece operated in pressure demand or other positive pressure mode.
Not flammable. May cause fire on contact with combustibles. Poisonous gases
are produced in fires. Stop flow of gas if possible. Cool exposed containers and
protect men effecting shutoff with water. Wear Goggles, self-contained breathing
apparatus, and rubber overclothing (including gloves).
Toxic Combustion Products: ... WHEN HEATED, IT EMITS HIGHLY TOXIC FUMES.
Firefighting Hazards: May combine with water or steam to produce toxic and corrosive fumes of
hydrochloric acid.
Hazardous Reactivities & Incompatibilities: Antimony burns spontaneously in gaseous chlorine; with liquid chlorine, antimony ignites at 33 deg C.
Arsenic burns spontaneously in gaseous chlorine; with liquid chlorine, arsenic ignites at 33 deg C.
Arsenic disulfide ignites (in a rapid stream) in chlorine. When chlorine is bubbled into arsine,
each bubble produces a flame. Powdered bismuth burns spontaneously in gaseous chlorine; with liquid chlorine, bismuth ignites at 80 deg C.
Boron burns spontaneously in gaseous chlorine. Boron ignites in chlorine at 410 deg C.
Boron trisulfide ignites in chlorine,
even if cold. Finely divided calcium burns spontaneously in chlorine. Solid calcium burns spontaneously in
chlorine at elevated temperatures.
When moist chlorine was passed over
calcium carbide and potassium hydroxide, a solution of 58% dichloroacetylene was
/produced and/ collected in ether. The solution burned spontaneously and filled
the laboratory with phosgene. Calcium nitride reacts in the cold with chlorine, with incandescence.
Mixtures of chlorine and calcium
phosphide react readily at about 100 deg C. The mixture of /carbon and chlorine/
spontaneously ignites in the dry state. Cesium acetylene carbide burns in cold chlorine ... Unless precautions are taken, the reaction of chlorine with alkylphosphines or
dialkylphosphines is a vigorous decomposing reaction. Diethyl zinc is spontaneously flammable in ... chlorine. Hydrazine ignites in contact with chlorine. Hydroxylamine is spontaneously flammable in chlorine. The reaction between liquid chlorine
and iodine is violent. Iron carbide burns in chlorine below
100 deg C with incandescence ... Magnesium phosphide burns brilliantly when heated in chlorine ... vapors. Manganese ... /ditritaphosphide/ ignites when gently heated in chlorine. Chlorine reacts rapidly at room
temperature with both mercuric oxide and silver oxide. Mercuric sulfide burns in chlorine
with incandescence. The polymer of oxomonosilane ignites in ... chlorine. The reaction of phosphorus isocyanate and chlorine is vigorous, forming a yellow oil.
When phosphorus oxide is thrown into a jar of chlorine vapor, it ignites instantly.
Liquid chlorine reacts exothermically
with polychlorinated biphenyl heat transfer liquid. Potassium acetylene carbide ignites spontaneously in cold chlorine, forming hydrogen chloride plus
carbon. Potassium hydride burns in fluorine or chlorine spontaneously.
Silicon hydride ignites in a chlorine
atmosphere. Sodium carbide burns in chlorine gas.
Sodium hydride is spontaneously flammable in ... chlorine when moisture is present.
The reaction of chlorine and stannous
fluoride occurs with flaming. Mixtures of ... /strontium phosphide and chlorine/ ignite at about 30 deg C.
Warm chlorine attacks with tellurium
with incandescence. Tetramethyl diarsine is spontaneously flammable in chlorine. When tungsten dioxide is heated in chlorine, the reaction occurs with
incandescence. Zinc burns in moist chlorine.
REACTS WITH ORGANIC MATERIALS, ACTIVE METALS, REDUCING AGENTS, AND AMMONIA.
REACTS WITH WATER TO FORM CORROSIVE, ACIDIC SOLUTIONS. ... ISOLATE FROM
ACETYLENE, AMMONIA, HYDROCARBONS, HYDROGEN, ETHER, TURPENTINE, AND FINELY
DIVIDED METALS. When ether is poured into chlorine
gas, an explosion results. Reaction of fluorine and chlorine is
accompanied by flames. In the presence of a spark, a violent explosion occurs.
A mixture of hydrogen and chlorine is
exploded by almost any form of energy (heat, sunlight, sparks etc). Explosive
range: 5-95%. Powdered vanadium explodes with chlorine even at 0 deg C.
Liquid chlorine reacts explosively
with polypropylene, drawing wax, polydimethylsiloxane, dibutyl phthalate,
glycerol, and linseed oil. Diborane explodes in contact with chlorine at ordinary temperatures.
The reaction of chlorine and methane
is explosive at room temperature over yellow mercuric oxide.
Ethylene reacts explosively with chlorine in sunlight or ultraviolet light. The
reaction of chlorine and ethylene is
explosive at room temperature over yellow mercuric oxide, mercurous oxide, or
silver oxide. A mixture of ethylphosphine and chlorine explodes. When liquid chlorine was added to
carbon disulfide in an iron cylinder, the iron catalyzed an explosive reaction.
Mixtures of chlorine and bromine
pentafluoride explode on heating. The reaction of chlorine and a dilute
solution of calcium chlorite evolves explosive chlorine dioxide. Ethyleneimine plus chlorine forms an
explosive compound, 1-chloroethyleneimine. Combines with moisture to form HCl. An explosion occurred during the chlorination of S-ethylisothiourea sulfate
and formamidine thiolacetic acid-hydrochloric acid. Formation of spontaneously
explosive nitrogen trichloride was the suggested cause. Reacts explosively or forms explosive compounds with many common substances
such as acetylene, ether, turpentine, ammonia, fuel gas, hydrogen & finely
divided metals. With cobalt (II) chloride and methanol: During the preparation of
cis-dichlorobis(2,2'-bipyridyl)cobalt(III) chloride ... passage of chlorine into an ice cold solution of cobalt
chloride, bipyridyl and lithium chloride in methanol soon caused an explosion
followed by the ignition of the methanol inside the reaction vessel.
With aluminum: Corrosive failure of a vaporizer used in manufacture of
aluminum chloride caused liquid chlorine
to contact molten aluminum. A series of explosions occurred.
With amidosulfuric acid: Chlorination of aq sulfamic acid led to an explosion
from formation of nitrogen trichloride. With butyl rubber and naphtha: Chlorination of butyl rubber in naphtha with
chlorine-nitrogen mixtures may lead to
explosion if nitrogen contents below 77% or chlorine contents above 16% are used.
With chlorinated pyridine and iron powder: An explosion occurred during the
preparation of iron(III) chloride from iron powder and chlorine gas in a chlorinated pyridine
solvent. This was attributed to formation of iron(II) chloride, its interaction
with the solvent to give iron(III) chloride, then reduction of the latter by
iron to iron(II) chloride. The exotherm and incr evolution of hydrogen chloride
caused the reactor to fail. With dimethyl phosphoramidate: In a 1.5 g mol preparation of dimethyl
N,N-dichlorophosphoramidate by chlorination of the ester, a violent explosion
occurred during the period of stirring after the reaction.
With non-metals: Liquid chlorine at
-34 deg C explodes with white phosphorus, and a solution in heptane at 0 deg C
ignites red phosphorus. Boron, active carbon, silicon and phosphorus all ignite
in contact with gaseous chlorine at
ambient temp. Arsenic incandesces on contact with liquid chlorine at -34 deg C, and the powder ignited
when sprinkled into the gas at ambient temp. Tellurium must be warmed slightly
before incandescence occurs. With silicones: Silicone process oils mixed with liquid chlorine confined in a stainless steel bomb
reacted explosively on heating; polydimethylsiloxane at 88-118 deg C, and
polymethyltrifluoropropylsiloxane at 68-114 deg C. Previously, leakage of a
silicone pump oil into a liq chlorine
feed system had caused rupture of a stainless steel ball valve under a pressure
surge of about 2 kbar. With sodium hydroxide: Attempted disposal of a small amt of liq chlorine by pouring it into 20% sodium
hydroxide soln caused a violent reaction leading to personal contamination.
With tert-butanol: Rate of admission of chlorine into the alcohol during the
preparation of tert-butyl hypochlorite must be regulated to keep temperature
below 20 deg C to prevent explosion. With 3-chloropropyne: A vigorous explosion during chlorination of
3-chloropropyne in benzene at 0 deg C over 4 hours was attributed to the
presence of excess chlorine arising from
the slow rate of reaction at low temperature. With phosphorus compounds: Boronidiiodophosphide, phosphine, phosphorus
trioxide and trimercury tetraphosphide all ignite in contact with chlorine at ambient temp. Trimagnesium
diphosphide and trimanganese diphosphide ignite in warm phosphide incandesces in
chlorine.
Copper foil burns spontaneously in gaseous chlorine. Copper reacts vigorously with chl |