SULFUR DIOXIDE
CASRN: 7446-09-5
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~AAANVa4.e:1
Prior History of Accidents:
Meuse Valley, Belgium (1936). High sulfur
dioxide emissions from coal-burning plants combined with light winds to
produce several thousand cases of pulmonary irritation and 65 deaths (primary
cardiac failure in elderly pt).
Donora, Pennsylvania (1948). High concn of
particulate matter and sulfur dioxide emissions form
industrial smoke associated with poor environmental mixing of pollutants caused
a severe pollution episode. Twenty excess deaths were recorded, and almost half
of the city residents developed conjunctival and upper resp irritation along
with GI symptoms. These pt later had an incr prevalence of resp disease and incr
mortality rates.
London (1952). High particulate matter and sulfur
dioxide concn in the absence of air movement produced over 4000 excess
deaths.
Immediately Dangerous to Life or Health:
100 ppm
Skin, Eye and Respiratory Irritations:
VAPORS CAUSE SEVERE IRRITATION OF EYES &
THROAT ... .
... Strong irritant to eyes & mucous
membranes ... .
Irritating to ... resp system & skin.
HAZARD WARNING: Because of the high solubility
of sulfur dioxide, it is extremely irritating to the
eyes and upper respiratory tract.
Human Toxicity Excerpts:
SEVERE INJURIES OF HUMAN EYES BY SULFUR
DIOXIDE HAVE BEEN PRODUCED ONLY BY LIQUIFIED FORM. ... IMMEDIATELY AFTER
THE EYE HAS BEEN SPRAYED ... THE CORNEAL EPITHELIUM BECOMES GRAY &
IRREGULAR, BUT REMAINS ADHERENT TO STROMA ... SEVERAL HR LATER LIDS BECOME
SWOLLEN. CONJUNCTIVAL EPITHELIUM APPEARS WHITE & RATHER OPAQUE. VESSELS ...
MAY BE ... THROMBOSED.
A PERIOD OF ... EXPOSURE OF OVER 2 YR TO
VARIABLE CONCN ON THE ORDER OF 30 PPM WITH OCCASIONAL PEAKS OF UP TO 100 PPM ...
PRODUCED ... AN ALTERATION OF SENSES OF SMELL & TASTE, HIGH URINARY ACIDITY,
& INCREASED FATIGUE.
... DESTRUCTION OF PROTECTIVE CILIATED
EPITHELIUM, & INVASION OF LUNG BY BACTERIA ARE CONQUENCES OF ACUTE SULFUR
DIOXIDE POISONING.
INHALATION PRODUCES ALL GRADES OF RESPIRATORY
TRACT IRRITATION SOMETIMES WITH PULMONARY EDEMA. VAPOR CONCN PROBABLY DETERMINES
MODE OF DEATH: EG, SUFFOCATION FROM REFLEX RESP ARREST (VERY HIGH CONCN),
PULMONARY EDEMA (MODERATE CONCN), OR SYSTEMIC ACIDOSIS (LOW CONCN). THERE IS
SOME INDICATION OF SIGNIFICANT VARIATION IN INDIVIDUAL SUSCEPTIBILITY.
WITH ACUTE EXPOSURE, 5 PPM CAUSES DRYNESS OF
NOSE & THROAT AND A MEASUREABLE INCR IN RESISTANCE TO BRONCHIAL AIR FLOW; 6
TO 8 PPM CAUSES A DECR IN TIDAL RESP VOLUME. SNEEZING, COUGH & EYE
IRRITATION OCCUR AT 10 PPM; 20 PPM CAUSED BRONCHOSPASM; 50 PPM CAUSES EXTREME
DISCOMFORT BUT NO INJURY IN LESS THAN A 30-MIN EXPOSURE ... 1000 PPM CAUSES
DEATH IN FROM 10 MIN TO SEVERAL HR BY RESP DEPRESSION.
EXPOSURE TO HIGH CONCN CAUSE REFLEX CLOSURE OF
GLOTTIS FOR SEVERAL MINUTES. ... PERSONS SUBJECT TO ASTHMATIC ATTACKS WILL
EXPERIENCE ASTHMATIC PAROXYSM WHICH MAY PERSIST FOR SEVERAL DAYS FOLLOWING
EXPOSURE.
IN THE MORE ADVANCED STAGES, ... DILATION OF
BLOOD VESSELS IN CERTAIN REGIONS. ULCERATION OF NASAL SEPTUM, WHICH BLEEDS
READILY, MAY ... BE OBSERVED.
THERE MAY ALSO BE THORACIC PAIN &
STRICTION, DYSPNEA, LACRIMATION ... BURNING SENSATION & PAIN IN ESOPHAGUS
& STOMACH, NAUSEA & (ALTHOUGH RARELY) VOMITING.
INHIBITION OF THYROID FUNCTION & IN WOMEN,
MENSTRUAL DISORDERS ... .
PERSONS WHO HAVE A LONG HISTORY OF EXPOSURE TO
HIGH CONCN OF SULFUR DIOXIDE MAY SUFFER FROM CHRONIC
BRONCHITIS ACCOMPANIED BY EMPHYSEMA. ... NERVOUS SYSTEM DISORDERS ARE OF A
FUNCTIONAL NATURE-NEUROTIC & VEGETO-ASTHENIC-PROBABLY DUE TO THE GENERAL
TOXICITY OF SULFUR DIOXIDE ON THE BODY. STOMATOLOGICAL
EXAM MAY REVEAL DENTAL CARIES, & PERIDONTAL & GINGIVAL DISORDERS.
PATIENTS MAY COMPLAIN OF RAPID & PAINLESS DENTAL DESTRUCTION, LOSS OF
FILLINGS, & INCR TOOTH SENSITIVITY TO TEMP CHANGES.
DUE TO ITS HIGH SOLUBILITY, SULFUR
DIOXIDE IS RAPIDLY DISTRIBUTED THROUGHOUT THE BODY, PRODUCING METABOLIC
ACIDOSIS WITH A REDUCTION IN BLOOD ALKALI RESERVE & COMPENSATORY ELIMINATION
OF AMMONIA IN URINE & ALKALI IN SALIVA. THE GENERAL TOXIC ACTION IS
DEMONSTRATED BY PROTEIN & CARBOHYDRATE METABOLISM DISORDERS. IT IS PROBABLE
THAT THE ABSORPTION OF LARGE QUANTITIES ... HAS A PATHOLOGICAL EFFECT ON
HEMOPOIETIC SYSTEM AND MAY PRODUCE METHEMOGLOBIN.
Delayed particle clearance times have been
observed at low levels of sulfur dioxide exposure. This
indicates an impairment of the lung to function properly. This effect is more
prominent with prolonged exposure to low concentrations than for short exposures
to high concentrations.
Exposures of less than an hour to sulfur
dioxide at levels above 10 ppm in air are irritating to the nose and
throat, sometimes causing a choking sensation followed by nasal discharge,
sneezing, coughing, and increased mucous secretion.
Approx 10,000 workers in the British steel
industry were studied for chronic effects. At mean exposures to sulfur
dioxide of about 0.35 ppm (0.9 mg/cu m), no effects were found.
Twenty five healthy adults were tested and
found to have increased airway resistance (determined in a body plethysmograph)
at 5 ppm (13 mg/cu m) of sulfur dioxide and at higher
levels when breathing normally for 10 min, but not at lower levels. After 25
deep breaths, as might occur in laborers doing hard physical work, the subjects
had a statistically significant increase in airway resistance at 1 ppm and after
8 deep breaths at 3 ppm.
An ecological study examined the relationship
between ambient sulfur dioxide peaks and asthma attack
incidence in 2 inner-city areas of New York City (NYC). Statistical tests were
made for an association between days with sulfur dioxide peaks
above various levels (0.1 ppm, 0.3 ppm, 0.5 ppm), as identified from hourly
measurements obtained from the NYC Aerometric Network for the years 1969-1971,
and days with higher numbers of emergency room visits for asthma at 3 municipal
hospitals. No association was found.
... Sulfur dioxide together
with particulate matter and photochemical pollutants aggravate chronic pulmonary
disease and incr the risk of acute and chronic resp illness. These compounds
impair pulmonary mucociliary clearance, primarily in those pt with persisting
pulmonary disease, probably as a result of hydrogen ion deposition on the
bronchial lining.
6-12 ppm: May cause nasal and throat
irritation. 10 ppm: Upper resp irritation, some nosebleeds. 20 ppm: Definitely
irritating to eyes. Chronic resp symptoms develop at this level.
Acute effects: Direct resp tract irritation,
cough, burning, lacrimation, conjunctival injection, difficulty in swallowing,
and oropharyngeal erythema occur after substantial exposures. Vomiting,
diarrhea, abdominal pain, fever, headache, vertigo, agitation, tremor,
convulsions, and peripheral neuritis also have been noted. Acute high-dose
exposures may produce immediate bronchospasm and pulmonary edema with subsequent
resp failure. Clinical severity usually is readily apparent. Acute high-dose sulfur
dioxide exposures have resulted in severe obstructive and restrictive
defects 3 months postexposure, which failed to respond to bronchodilators.
Rarely, such exposures have been associated with long-term, moderately severe,
obstructive defects and persistent, productive cough.
High concentrations of sulfur
dioxide may cause respiratory paralysis and pulmonary edema. In addition,
about 10 to 20% of the adult population is estimated to be hypersensitive to the
adverse respiratory effects of sulfur dioxide; however,
workers regularly exposed to compound show an adaptation effect. Even though
olfactory fatigue is a reported effect of exposure, the compound is so
irritating that it is considered to have good warning properties.
Symptomology: Inhalation: Irritation of the
eyes, nose, throat, and skin; cough; sneezing and lacrimation; rhinorrhea;
anosmia; reflex bronchoconstriction; increased pulmonary resistance to air flow;
bronchial asthma; high pitched rales; thoracic pain and struction;
nasopharyingitis; tracheitis, laryngeal edema; chemical bronchopneumonia;
pulmonary edema; cyanosis; systemic acidosis; asphyxia; death. Ingestion:
Irritation, lacrimation, iritis, burns, corneal damage, blindness. Skin contact:
Irritation, Urticaria, lesions, burns.
... 15 healthy subjects remained in an
exposure chamber for 7-8 hours; control values were obtained, sulfur
dioxide was gradually introduced, and the concentration was maintained at
1, 5, or 25 ppm for up to 6 hours. In seven subjects, the concentration of Sulfur
dioxide was measured in pharyngeal gas samples obtained after exposure to
the gas; in no subject was the concentration greater than 0.25 ppm, the smallest
amount detectable by the methods used. ... Significant changes in nasal
mucociliary flow rate at 5 and 25 ppm, and in nasal airway resistance and forced
expiratory flow at 1, 5, and 25 ppm. No change in closing volume was found;
changes in forced expiratory volume were significant only for the highest level
of exposure.
12 healthy male adults were exposed to three
concentrations of sulfur dioxide with and without the
addition of sodium chloride aerosol. Pulmonary flow resistance did not increase
significantly over control values at 1-2 ppm, but did at higher concentrations:
an average increase of 39% over control values occurred 10 minutes after
exposure to 4-6 ppm of sulfur dioxide. The addition of
sodium chloride particles at concentrations of up to 24 mg/cu m did not increase
the effects of sulfur dioxide observed at any
concentration.
Men working in a refrigerator company in the
USA where sulfur dioxide was the refrigerant /were
studied/. Exposures averaged 60-90 mg/cu m (20-32 ppm) with peaks as high as 200
mg/cu m (70 ppm). These peaks had probably been higher in the past ranging up to
290 mg/cu m (100 ppm) or more. The exposed group had significantly more
respiratory symptoms and colds. They also complained more of fatigue and
shortness of breath on exertion. Chest X-rays of the exposed and unexposed
groups showed the same distribution of abnormalities. /It was concluded that/
there was no injury to the tracheobronchial tree or alveoli.
In a study in Norway, pulp mill workers were
compared with paper mill workers using a standard questionnaire on respiration
and simple tests of pulmonary function. The smoking histories of the subjects
were also studied. Levels of sulfur dioxide ranged from
6-100 mg/cu m (2-36 ppm) with peaks of 290 mg/cu m (100 ppm) when the digester
was blowing. The exposed group had more cough, sputum, and dyspnea than the
unexposed group but the vital capacities were simliar in both groups. The
expiratory peak flows, however, of the exposed men under 50 years of age were
lower than those in comparable unexposed group.
In a study, comprising a series of experiments
over a period of 4 yr, a small increase in specific airway flow resistance (flow
resistance corrected for lung volume) was seen in response to sulfur
dioxide at 1 ppm, but only if the subjects took 25 maximal breaths of the
gas starting from residual volume. The procedure was designed to increase dosage
to the laryngotracheobronchial airways. In one subject, there was a threefold
increase in specific airway flow resistance with this procedure. As expected, sulfur
dioxide at 3 ppm elicited greater changes in function than did 1 ppm. The
magnitudes of these changes were proportional to the numbers of deep breaths
taken.
The effects of sulfur
dioxide and ozone alone and in combinations /were studied/, on young
normal subjects under conditions of light exercise. When breathed alone, 0.37
ppm of sulfur dioxide had no effect on any measurement
of lung function; 0.37 ppm of ozone produced a just significant decline of
ventilatory function at the end of a 2 hour exposure. However, when the two
gases were present together in eight normal young subjects who were non-smokers,
the maximal mid-expiratory flow rate dropped to 67% of its initial value at the
end of 2 hours; the forced expiratory volume was 78% of its initial value, and
the mid-expiratory flow rate (50% vital capacity) was only 54% of the initial
value. A 2 hour exposure to 0.75 ppm of Sulfur dioxide alone
dropped the maximal mid-expiratory flow rate to 90% of its control value. /It
was/ concluded that sulfur dioxide and ozone are
exceedingly corrosive when present together, that "standard" must
specify the presence or absence of the other, and that there is a growing
incidence of the joint presence of the two pollutants in urban environments.
The 0.75 second forced expiratory volume of
school children in Cincinnati, Chattanooga, and New York City, was studied, and
examined differences by race, sex, socioeconomic levels, and exposure to total
particulates, suspended sulfates, and sulfur dioxide. These
authors were able to demonstrate differences in forced expiratory volume to
support a relationship between suspended sulfates, other particulates and
impaired function; the diference was apparent only after matching for age, sex,
race, and socioeconomic status and when no overt clinical manifestations were
present. The most dramatic difference occurred in Cincinnati, where children in
"clean" neighborhoods had similar levels of sulfur
dioxide but different levels of total particulates (61-85 ug/cu m in the
clean area vs 96-133 ug/cu m polluted areas) and in suspended sulfates (7.7-9.1
ug/cu m vs. 8.9-10.1 ug/cu m).
Two recent studies have involved persons with
underlying lung disease, as well as healthy persons. Nonsmoking health subjects
and smokers who demonstrated functional defects associated with early
obstructive pulmonary disease /were exposed/ to sulfur dioxide
at 0, 0.3, 1.0, and 3.0 ppm. The subjects resided in an environmental
chamber maintained at 22 + or - 1 deg C and 50 + or - 5% relative humidity. The
exposures were administered in random sequence for 120 hr continuously to the
healthy subjects, and for 96 hr to the smokers. Testing was done at 24 hr
intervals. Sulfur dioxide at 0.3 ppm elicited no
functional changes. Sulfur dioxide at 1.0 ppm caused a
significant reduction in dynamic compliance measured at 120 breaths/min after 24
and 48 hr of exposure; results of other tests of ventilation and respiratory
mechanics were unaffected. The reduction in dynamic compliance was greater and
more prolonged with sulfur dioxide at 3.0 ppm. A
notable finding was the absence of clear cut evidence of functional changes
among the subjects with underlying lung disease. Their intersubject and
intrasubject variability far exceeded the variation associated with exposure to
all concentrations of sulfur dioxide. A variety of
symptoms were noted in both groups: headache, nasal congestion, throat soreness,
cough, nosebleed, gastrointestinal discomfort, and rash.
40 healthy nonsmokers and 40 subjects with
mild asthma /were exposed/ to air and to sulfur dioxide at
0.5 ppm for periods of 3 hr. Forced expiratory performance, closing volume,
airway flow resistance, and lung volumes were measured. As a group, the healthy
subjects showed no functional changes that could be judged adverse; indeed,
vital capacity, maximal volume of gas that can be forcefully exhaled in 1 second
after full inspiration, and maximal mid-expiratory flow rate tended to rise with
time, whether clean air or sulfur dioxide was
administered. The response of the group with asthma to sulfur
dioxide was interpreted as showing slight functional impairment; ie,
maximal mid-expiratory flow rate was said to increase less to sulfur
dioxide than during the sham exposure. The other functional tests were
unaffected. Among the healthy subjects, a 13 yr old boy experienced shortness of
breath and had functional evidence of bronchoconstriction. On the evening after
exposure to sulfur dioxide, two of the asthmatic
subjects experienced shortness of breath, which required medication.
A combination of 0.37 ppm sulfur
dioxide with 0.037 ppm ozone decr the human midexpiratory flow rate to
almost half ... .
The effects of sulfur
dioxide on 190 workers employed in a broom manufacturing factory where sulfur
dioxide was used for bleaching broom corn were studied. Concentrations of
sulfur dioxide in the air, sulfates in the urine,
methemoglobin and sulfhemoglobin in the blood, and irritant effects on the
workers were analyzed. Measurements were made in summer when open windows
provided natural ventilation and in winter when the building was closed. Sulfur
dioxide in air averaged 45.7 mg/cu m in winter and 0.2 mg/cu m in summer.
When compared to control groups not exposed to sulfur dioxide in
the workplace (43 workers checked for methemoglobin and 39 for sulfates),
differences in all parameters were statistically significant. In winter the mean
values were: total urinary sulfates 21.2 umol/l (p< 0.01), organic urinary
sulfates 4.1 umol/l (p< 0.01) methemoglobin 1.6% (p< 0.01), and
sulfhemoglobin 0.7% (p< 0.05). In summer the mean values were: total urinary
sulfates 19.3 umol/l (p< 0.05), organic urinary sulfates 3.7 umol/l (p<
0.01), methemoglobin 0.7% (p< 0.05), and sulfhemoglobin 0.5% (p< 0.05).
Corresponding values for controls were 16.7 umol/l, 1.8 umol/l, 0.5%, and
<0.5%, respectively. Interviews with 190 workers revealed the following
discomforts: coughing (94.2%), difficulty in breathing (91.0%), burning
sensation in throat (83.7%), burning sensation in eyes (80.0%), sub-sternal pain
(75.3%), burning sensation in throat (74.7%), sore throat (65.8%), tearing
(64.7%), hoarseness (56.3%), pain in nose (49.5%), pain in eyes (39.5%), red
eyelids (35.5%), red eyes (16.3%), nose bleeding (3.7%), and sneezing (3.2%).
Exposures of two miners to sulfur
dioxide concentrations of at least 40 ppm resulted in severe airway
obstruction, hypoxemia, markedly reduced exercise tolerance, ventilation
perfusion mismatch, and evidence of active inflammation as documented by a
positive gallium lung scan. Serial ventilation-perfusion scans over the first 12
months showed progressive improvement without returning to normal. This status
has remained for 2 years.
A basic physiological response to inhalation
of sulfur dioxide is a mild degree of bronchial
constriction that is dependent on intact parasympathetic innervation. When
exposed to 5 ppm of sulfur dioxide for 10 minutes, most
human subjects show increased resistance to the flow of air. Asthmatics have an
increased sensitivity to sulfur dioxide; bronchoconstriction
may occur at concentrations as low as 0.25 ppm.
... /Authors/ conducted controlled studies in
15 nose-breathing volunteers who inhaled 1, 5, or 25 ppm sulfur
dioxide for 6 hr. A significant reduction in nasal mucous flow rate
occurred after exposure at 5 and 25 ppm and reduced forced expiratory volume and
forced expiratory flow were seen at all exposure concentrations. Irritation and
complaints of discomfort were said to be proportional to the sulfur
dioxide concentration but were judged never to be excessive. Based on
these data, ... /the authors/ expressed the opinion that the TLV for sulfur
dioxide should be reduced to 1 ppm or less, given that exposure at 1 ppm
from 1 to 6 hours caused constriction of the upper airways in young, healthy
(20-28 years of age) adult males. It is important to note that the ... protocol
allowed the subjects to become acclimated slowly to the higher concentrations,
whereas subjects who had to enter the chamber abruptly found a distinct sulfur
dioxide smell at 1 ppm, strong discomfort and cough at 5 ppm, and 25 ppm
was intolerable on first contact. These individuals, however, adapted rapidly,
and coughing and rhinorrhea resolved within a few minutes.
... /Authors/ found that exposure at 1 ppm sulfur
dioxide produced increased flow resistance in 1 of 11 human subjects. A
concentration of 5 ppm produced an average increase of 39% compared to the
control; the value for 13 ppm was 72% above the control. The response was
related to concentration, not to total dose; extending exposure time from 10
minutes to 30 minutes failed to increase the response. Repeated exposure
following a 15 minute interval of clean air produced a lesser response than did
the initial exposure.
In humans, survivors of massive sulfur
dioxide exposure have shown a chronic, obstructive defect in serial
pulmonary function studies, along with bronchial hyperreactivity. The extent to
which recurrent occupational or environmental exposures to sulfur
dioxide produce adverse effects in humans is not clear, however, in part
because in both contexts there are usually confounding exposures to particulates
or other irritants. Although some investigations suggest that occupational sulfur
dioxide exposure (even at levels below the current TLV) is associated
with increased upper and lower respiratory symptoms and decrements in various
spirometric indices, others have not.
Bronchoalveolar lavage of 12 healthy,
nonsmoking subjects 24 hours after exposure for 20 minutes to 4 or 8 ppm (10.5
or 21 mg/cu m) sulfur dioxide showed increased alveolar
macrophage lysosomal activity; at the higher level, the numbers of macrophages
and lymphocytes in the lavage fluid were increased. No effect on lung function
was observed.
The prevalence of chronic bronchitis was
significantly increased over that in controls in workers exposed to sulfur
dioxide while working in a sulfite pulp factory in Sweden. During the
three years before the study was performed, more than 50% of the daily mean
values for sulfur dioxide in the sulfite pulp mill were
above 14 mg/cu m (5 ppm), with occasional peak exposures up to 140 mg/cu m. The
mean annual concentration of sulfur dioxide in the
surrounding community was 6.5-40 ug/cu m.
The frequency of chromosomal aberrations in
cultured lymphocytes from seven workers exposed to sulfur
dioxide in a sulfite pulp mill in Sweden was compared with that of 15
controls. The exposed subjects had been employed for > 15 years at the mill,
and one was a smoker. The controls were healthy men from Umea, Sweden, five of
whom were smokers. The mean numbers of breaks/100 cells were 3.72 + or - 0.31
(standard deviations) for the sulfur dioxide exposed
workers and 0.66 + or - 0.81 for the controls, analyzed on the basis of
individual values (t = 5.79; p < 0.001). The frequency of gaps was also
increased in the exposed workers (p < 0.01).
Skin, Eye and Respiratory Irritations:
VAPORS CAUSE SEVERE IRRITATION OF EYES &
THROAT ... .
... Strong irritant to eyes & mucous
membranes ... .
Irritating to ... resp system & skin.
HAZARD WARNING: Because of the high solubility
of sulfur dioxide, it is extremely irritating to the
eyes and upper respiratory tract.
Medical Surveillance:
Preplacement and annual medical examinations
should be done whenever TWA exposures exceed 0.25 ppm (0.65 mg/cu m). These
examinations should be directed toward complaints of mucous membrane irritation,
cough and shortness of breath. They should ascertain that nasal passages are
open. Persons with a history of asthma or with subnormal pulmonary function
should be watched closely. Simple expiratory function tests should be a part of
the examination. They are useful for several purposes: (a) determining whether
or not a person is a suitable candidate for using respirators; (b) identifying
"reactors", ie, persons who may be most susceptible to the effects of
SO2. This can be done by comparing preshift and postshift tests; (c) when done
periodically, they can be used to determine whether or not a person's expiratory
functions are declining at a faster than normal rate. Such determinations are
much more sensitive when pooled data from a number of individuals are used. The
forced expiratory volume at 1 second and the maximum mid-expiratory flow rate
appear to be the most useful of the simple pulmonary function tests.
PERSONS TO BE EMPLOYED ON WORK WHERE THERE MAY
BE EXPOSURE TO SULFUR DIOXIDE SHOULD RECEIVE
PREEMPLOYMENT MEDICAL EXAMINATION: PERSONS SUFFERING FROM CHRONIC CONJUNCTIVITIS
OR LARYNGITIS, BRONCHITIS, EMPHYSEMA, BRONCHIAL ASTHMA, ANY DISORDER INHIBITING
NASAL RESP, OR ANY CARDIOVASCULAR DISEASE MUST BE ADEQUATELY EXPOSED TO THIS
SUBSTANCE.
Populations at Special Risk:
Persons with a history of asthma or with
subnormal pulmonary function should be watched closely ... .
Clear cut evidence has ... been obtained that
asthmatic individuals are especially sensitive to sulfur
dioxide. ... The degree of sensitivity to Sulfur
dioxide appears to depend on the magnitude of preexisting airway
hypersensitivity.
Persons suffering from ... any ...
cardiovascular disease should be adequately protected to this substance.
In high-exposure communities (community mean
specific sulfur dioxide level of 45 ug/cu m over 5 yr),
smokers and nonsmokers had a higher incidence or persistent cough and sputum
production compared with controls in low-exposure communities. Smoking remained
the most important variable of the prevalence of persistent cough and sputum
production.
PERSONS SUFFERING FROM CHRONIC CONJUNCTIVITIS
OR LARYNGITIS, BRONCHITIS, EMPHYSEMA, BRONCHIAL ASTHMA, ANY DISORDER INHIBITING
NASAL RESP, OR ANY CARDIOVASCULAR DISEASE SHOULD NOT BE EXPOSED TO THIS
SUBSTANCE.
Probable Routes of Human Exposure:
Inhalation ... /or/ direct contact of gas or
liquid phase on ... mucous membranes.
It has been estimated by the Department of
Labor that approx 600,000 American workers may be occupationally exposed to sulphur
dioxide. Some of the highest exposures occur when it is a by product, as
in the metal smelting industry, and in the processing or combustion of high
sulfur coal or oil. Other exposures occur in manufacture of sulfuric acid,
fumigating, food preservation, wine making, and bleaching of many substances.
Antidote and Emergency Treatment:
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. Anticipate
seizures 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.
Administer activated charcoal. Cover skin burns with sterile dressings after
decontamination.
For advanced treatment: Consider orotracheal
or nasotracheal intubation for airway control in the patient who is unconscious.
Early intubation at the first sign of upper airway obstruction may be necessary.
Monitor cardiac rhythm and treat arrhythmias if necessary. Start an IV with D5W
TKO. Use lactated Ringer's if signs of hypovolemia are present. Watch for signs
of fluid overload. Consider drug therapy for pulmonary edema. Treat seizures
with diazepam (Valium). For hypotension with signs of hypovolemia, administer
fluid cautiously. Consider vasopressors for hypotension with a normal fluid
volume. Watch for signs of fluid overload. Use proparacaine hydrochloride to
assist eye irrigation.
Animal Toxicity Studies:
Evidence for Carcinogenicity:
Evaluation: There is inadequate evidence for
the carcinogenicity in humans of sulfur dioxide, sulfites,
bisulfites and metabisulfites. There is limited evidence for the carcinogenicity
in experimental animals of sulfur dioxide. There is
inadequate evidence for the carcinogenicity in experimental animals of sulfites,
bisulfites and metabisulfites. Overall evaluation: Sulfur
dioxide, sulfites, bisulfites and metabisulfites are not classifiable as
to their carcinogenicity to humans (Group 3).
Non-Human Toxicity Excerpts:
POISONING IN CATTLE ... /AT/ A DAILY DOSE OF
80-160 G OF ... SULFUR DIOXIDE GAS CAUSED ANOREXIA:
MASSIVE DOSES ADMIN THROUGH RUMEN FISTULAE WERE FATAL. ... MORE SEVERE TISSUE
CHANGES WERE CONFINED TO THE FIRST PART OF THE DIGESTIVE TRACT: MOST CONSISTENT
LESIONS WERE IN THE LARYNX & IN THE MUCOSA OF THE VENTRAL WALL OF THE
TRACHEA.
... SULFUR DIOXIDE POISONING
IN A HORSE FOLLOWING BRIEF PERIOD OF EXPOSURE TO THE GAS ... /PRODUCED/ SEVERE
RESPIRATORY & CIRCULATORY DISTURBANCES ... SEVERE IRRITATION OF NASAL &
PLEURAL MUCOUS MEMBRANES WAS OBSERVED POST MORTEM. ... PIGS EXPOSED TO CONCN OF
5 TO 40 PPM FOR 8 HR SHOWED CLINICAL EVIDENCE OF EYE & RESPIRATORY TRACT
IRRITATION, & PULMONARY HEMORRHAGE & EMPHYSEMA ... .
... 200 PPM ARE REQUIRED TO SLOW CILIA OF
RABBIT TRACHEA IN VIVO; ONLY 7 PPM ARE REQUIRED FOR ISOLATED RABBIT TRACHEA.
... SLIGHT INCREASE IN PULMONARY FLOW
RESISTANCE IN GUINEA PIGS @ 0.16 PPM; THE INCR WAS DOUBLED @ 2.6 PPM, BUT ONLY
SLIGHTLY MORE @ 19 PPM.
... MOST ANIMALS SURVIVE EXPOSURES OF 1 TO 5
HR @ 400 PPM, BUT DEATHS RESULTED FROM 600 TO 800 PPM IN SOME SPECIES.
... INFLUENZA-INFECTED MICE EXPOSED TO SULFUR
DIOXIDE DEVELOPED MORE PNEUMONIA THAN VIRUS CONTROLLED MICE. ... INCR IN
PNEUMONIA WAS DUE TO ... INDUCED LOW-GRADE INFLAMMATORY CHANGES IN LUNGS.
... RATS /WERE GIVEN/ SULFUR
DIOXIDE AT ... 750 PPM IN DRINKING WATER EXPERIMENTS THAT LASTED NEARLY 3
YR WITH 3 GENERATIONS OF ANIMALS. ... /IT WAS/ REPORTED /THAT/ NO EFFECTS ON
GROWTH, INTAKE OF FOOD & FLUID, OUTPUT OF FECES, FERTILITY, WEIGHT OF
NEWBORN OR FREQUENCY OF TUMOR DEVELOPMENT.
Eye irritation occurs at 6 ppm/4 hr in the
rabbit.
WHEN WHOLE ANIMAL HAS BEEN EXPOSED, KERATITIS
& CORNEAL CLOUDING IN RABBITS & GUINEA PIGS HAVE OCCURRED ONLY UNDER
CONDITIONS OF TIME & CONCN WHICH HAVE ULTIMATELY BEEN LETHAL (460 TO 490 PPM
FOR 30 HR OR 800 TO 1000 PPM FOR 24 HR).
Dogs exposed to 500-600 ppm (1300-1560 mg/cu
m) for 2 hr periods twice weekly for 4 to 5 mo showed an incr in goblet cells
near the ends of bronchi and bronchioles, and hyperplasia of bronchial glands,
with an excess of mucopurulent exudate. ... /It was/ concluded that sulfur
dioxide produces chronic bronchitis in dogs.
... Green plants are extremely sensitive to
atmospheric sulfur dioxide. Alfalfa, barley, cotton,
and wheat can be injured at levels between 0.15 and 0.20 ppm, while potatoes,
onions, and corn are far more resistant.
Exposure of Euglena cells to 5.0 ppm of sulfur
dioxide increased the concentration of chlorophyll but reduced the rate
of photosynthesis.
Cynomolgus monkeys exposed continuously for 78
weeks to sulfur dioxide levels up to 3.7 mg/cu m (1.3
ppm) did not show any significant pathological changes.
Cynomolgus monkeys and guinea pigs were
exposed to mixtures of sulfur dioxide, fly ash, and
sulfuric acid mist, were studied for 18 months after an 8 week baseline period.
Exposure concentrations varied from ... 0.1 to 5.0 ppm for sulfur
dioxide and from 0.1 to 1 mg/cu m for sulfuric acid mist; the
concentration of fly ash was approximately 0.5 mg/cu m. Particle size (MMD)
varied from 0.53 to 3.11 um in the acid mist and from 4.1 to 5.8 um in the fly
ash. Pulmonary function tests and serumbiochemcial and hematological analyses
were conducted prior to, and periodically during, the exposure. Lungs were
examined microscopically at the end of the experiment. Sulfuric acid mist
appeared to be responsible for the effects observed. These were largly
histopathological changes in the lungs. No synergistic action was noted between
the pollutants.
Rats were exposed for 96 days to sulfur
dioxide at concentrations of 0.1, 0.5, and 1.5 mg/cu m (0.04, 0.18 &
0.53 ppm). Histological examination showed interstitial pneumonia, bronchitis,
tracheitis, and peribronchitis after exposures to the two higher levels.
Beagle dogs exposed to a sulfur
dioxide concentration of 13.4 mg/cu m (4.7 ppm) for 21 hr per day, for
620 days did not develop any specific histopathological changes.
... 16 to 19 ppm of sulfur
dioxide killed sunfish in 1 hour. ... Concentrations of 10 ppm of sulfur
dioxide in tap water caused trout to float within 10 minutes and also
reports that 5 ppm of sulfur dioxide killed trout in 1
hour.
When rabbits inhaled 300 ppm of sulfur
dioxide, ciliary action in the upper airways was inhibited, and at 400
ppm, mucosal irritation, mucous gland hypertrophy, and proliferation of
pulmonary goblet cells occurred.
Studies in intact rodents have failed
consistently to induce genotoxicity.
Prolonged exposure of dogs to high
concentrations of sulfur dioxide (200 ppm) causes a
syndrome similar to human chronic bronchitis, involving chronic airway
obstruction, airway inflammation, and symptoms of cough and mucus hypersecretion.
However, unlike human disease, in this animal model there is decreased airway
responsiveness to inhaled bronchoconstrictor agents, which appears to be
associated with chronic airway inflammation. When exposed to 15 ppm using the
same experimental protocol, none of these effects is evident. With few
exceptions, chronic exposure of animals to sulfur dioxide does
not produce observable adverse effects at concentrations lower than 20 ppm.
Groups of 10 female albino rats (weighing
165-185 g) were exposed for 12 hours per day for three months to 0, 0.159 or
4.97 mg/ cu m sulfur dioxide. An additional group was
exposed to 2.52 mg/cu m sulfur dioxide in combination
with 1.20 mg/cu nitrogen dioxide. Oestrus cyclicity was determined for 24 days
prior to exposure, during exposure and during a recovery period. Females with a
normal oestrus cycle were tested for fertility. The ovaries, uterus and
pituitary, thyroid and adrenal glands from four rats per group were examined by
histopathology at the end of exposure. It was reported that the higher exposure
level prolonged the interestrual period (dioestrus) and the oestrus and that
these females had fewer monthly oestrus cycles. Cycle length returned to normal
within seven months after exposure. Circulatory changes were found in the
ovaries and uteri of females in the high exposure group. In a second experiment,
decreased litter sizes were found in similarly exposed groups of seven females.
Body weights of the offspring were reduced at least through postnatal day 12 in
these groups.
An experimental group of 35 male and 30 female
LX mice and a control group of 41 males and 39 females, three months old, were
exposed to 0 or 500 ppm (1310 mg/cu m) sulfur dioxide (purity
unspecified) for 5 min per day on five days a week for life. Only mice that
survived for 300 days or more were considered in the results (average survival
time not shown), since lung tumors were not seen before that time. Female mice
exposed to sulfur dioxide had an increased incidence of
lung tumors: 13/30 adenomas and carcinomas versus 5/30 in controls, (p= 0.02;
Peto@@s incidental test); 4/30 lung carcinomas versus none in the controls. The
incidence of lung neoplasias was higher in treated males (15/28 versus 11/35 in
controls), but the difference was not significant; lung carcinomas occurred with
equal frequency in treated and control males (2/28 and 2/35).
Groups of 40 or 32 CF-1 mice were exposed for
7 hours per day to filtered air or to sulfur dioxide (purity,
99.98%) at 25 ppm (66 mg/cu m) on days 6-15 of gestation, and groups of 20 New
Zealand white rabbits were exposed to filtered air or sulfur
dioxide at 70 ppm (183 mg/cu m) on days 6-18 of gestation. In both
species, less food was consumed during the first few days of exposure to sulfur
dioxide; no other significant effect was seen in the dams. In mice, fetal
weight was reduced by 5% by exposure to sulfur dioxide; ossification
of the sternebrae and occipital was retarded (data not shown), but the incidence
of malformations was not significantly increased. In rabbits, the incidence of a
few minor skeletal variants was significantly increased (data not shown) in
group exposed to sulfur dioxide.
Non-Human Toxicity Values:
LC50 Mice inhalation 150 ppm/847 hr
LC50 Guinea pig inhalation 1000 ppm/20 hr
LC50 Mouse inhalation 1000 ppm/4 hr
LC50 Guinea pig inhalation 130 ppm/154 hr
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
Once absorbed, sulfur
dioxide appears to be metabolized rapidly to sulfate by the widely
distributed enzyme sulfite oxidase. After it has been oxidized to sulfate, it
becomes part of the large sulfate pool within the body. /It was reported/
relatively large differences in sulfite oxidase activity among five species:
rats had the highest levels and rabbits the lowest. An inverse correlation was
shown between enzyme activity and sensitivity to bisulfite toxicity. These
results reflect species differences in rate of S-sulfonate formation.
Absorption, Distribution & Excretion:
BLOOD (35)SULFUR LEVELS ROSE WHILE DOGS WERE
EXPOSED TO (35)SULFUR DIOXIDE ... PROTEIN BOUND
(35)SULFUR, ACCOUNTING FOR LESS THAN 50% OF PLASMA (35)SULFUR, WAS ASSOCIATED
MORE WITH ALPHA-GLOBULINS THAN WITH OTHER PROTEINS. URINARY (35)SULFUR WAS
MAINLY (35)SULFATE ION.
INHALED SULFUR DIOXIDE IS
ONLY SLOWLY REMOVED FROM THE RESP TRACT. RADIOACTIVITY CAN BE DETECTED IN THE
RESP SYSTEM FOR WK OR MORE FOLLOWING EXPOSURE. SOME OF THE (35)SULFUR APPEARS TO
BE ATTACHED TO PROTEIN.
IT MAY ENTER THE BODY VIA RESP TRACT OR,
FOLLOWING DILUTION IN SALIVA, IT MAY BE SWALLOWED & ENTER GASTROINTESTINAL
TRACT IN FORM OF SULFUROUS ACID. ... /SOME STUDIES INDICATE THAT/ IT CAN ENTER
THE BODY VIA SKIN. DUE TO ITS HIGH SOLUBILITY, SULFUR DIOXIDE IS
RAPIDLY DISTRIBUTED THROUGHOUT THE BODY ... IN THE BLOOD, SULFURIC ACID IS
METABOLIZED TO SULFATES WHICH ARE EXCRETED IN THE URINE.
By the use of (35)sulfur
dioxide ... the absorption /of sulfur dioxide/ by
the upper respiratory tract of rabbits over a concn range of 0.05 to 700 ppm
/was examined/. At higher concn removal was 90.0% or greater; this is in
agreement with the findings of other workers on dogs and human subjects. At
concn below 1 ppm, however, only 5.0% or less was removed by the upper resp
tract. ... The penetration of sulfur dioxide to the
lungs is greater during mouth breathing than during nose breathing. In dogs
breathing orally, 99.0% of 1 ppm was removed orally at a flow rate of 3.5 l/min.
Increasing the flow rate tenfold decreased the removal efficiency to 33.0%. ...
Studies using (35)sulfur dioxide have shown that
inhaled sulfur dioxide is readily distributed
throughout the body.
Most studies on both man and animals have
indicated that 40 to 90% or more of inhaled sulfur dioxide is
absorbed in the upper respiratory tract. Taken into the blood stream, it appears
to be widely distributed throughout the body, metabolized, and excreted via the
urinary tract.
Sulfur dioxide is
highly soluble in aqueous media. Absorption after inhalation has been studied in
rabbits and man. In rabbits, about 40% of the inhaled sulfur
dioxide is absorbed in the nose and pharynx when concentrations of about
290 ug/cu m (0.1 ppm) are inhaled. At higher concentrations (29-290 mg/cu m,
10-100 ppm), the fraction absorbed is much higher (about 95%). The reasons for
these different rates of absorption are not clear. In dogs, more than 99% of the
inhaled sulfur dioxide is absorbed by the nose at
exposure levels of 2.9-140 mg/cum (1-50 ppm).
Sulfur dioxide is
soluble in water and thus tends to be efficiently absorbed in the upper
respiratory tract. Two factors affecting the efficiency of absorption are the
mode of breathing (oral versus oronasal) and ventilation rate. The nose filters
out most inhaled sulfur dioxide, preventing its passage
to sensitive irritant receptors at and below the larynx. At rest, most people
(about 85%) breathe through the nose, providing protection against sulfur
dioxide toxicity. Mouth breathing, particularly at higher airflow rates,
substantially increases the fraction of sulfur dioxide reaching
the lung. Thus, voluntary hyperventilation or exercise at a level of exertion
requiring oronasal breathing lowers the threshold for sulfur
dioxide-induced respiratory symptoms and bronchomotor responsiveness.
Deep lung penetration and toxicity are enhanced by oxidation and adsorption to
submicron acidic particles.
Radiolabeled sulfur dioxide is
absorbed from the respiratory tract of experimental animals in the blood and is
distributed throughout the body, concentrating in the liver, spleen, esophagus,
and kidneys. It is metabolized to a variety of sulfur-containing compounds and
is excreted principally via the urine as sulfate. Significant quantities of sulfur
dioxide may be retained for a week or more in the lungs and trachea of
experimental animals.
Mechanism of Action:
On contact with moist mucous membranes, sulfur
dioxide produces sulfurous acid, which is a direct irritant and inhibits
mucociliary transport. ... Most of the inhaled sulfur dioxide is
detoxified by the liver through the molybdenum-dependent, sulfite oxidase
pathway to sulfates. The irritant induced stimulation of airway sensory end
organs causes vagal stimulation and airway smooth muscle contraction.
Interactions:
AEROSOLS THAT HAVE PRODUCED ... POTENTIATION
OF RESPONSE TO SULFUR DIOXIDE ARE SOLUBLE SALTS OF SUCH
METALS AS MANGANESE, FERROUS IRON, & VANADIUM. ... THESE AEROSOLS POTENTIATE
RESPONSE ABOUT THREE FOLD WHEN PRESENT AT CONCN OF 1 MG/CU M @ 50% RELATIVE
HUMIDITY.
Sulfur dioxide increases
the carcinogenicity of benzopyrene by promoting its metabolism.
... Mortality among arsenic exposed smelter
workers was greater when exposures had been to high arsenic combined with
moderate or high sulfur dioxide exposures.
The effects of sulfur
dioxide and ozone alone and in combinations /were studied/, on young
normal subjects under conditions of light exercise. ... When the two gases were
present together in eight normal young subjects who were non-smokers, the
maximal mid-expiratory flow rate dropped to 67% of its initial value at the end
of 2 hours; the forced expiratory volume was 78% of its initial value, and the
mid-expiratory flow rate (50% vital capacity) was only 54% of the initial value.
... /It was/ concluded that sulfur dioxide and ozone
are exceedingly corrosive when present together, that "standard" must
specify the presence or absence of the other, and that there is a growing
incidence of the joint presence of the two pollutants in urban environments.
Pharmacology:
Therapeutic Uses:
MEDICATION (VET): AS FUMIGANT AGAINST LICE
& MITES IN BUILDINGS (MINIMUM EFFECTIVE AEROSOL CONCN FOR LICE IS 1%; FOR
MANGE CAUSING MITES IS 4% ACCOMPLISHED BY COMPLETELY BURNING 2-8 LB SULFUR
RESPECTIVELY/1000 CU FT OF SPACE).
Interactions:
AEROSOLS THAT HAVE PRODUCED ... POTENTIATION
OF RESPONSE TO SULFUR DIOXIDE ARE SOLUBLE SALTS OF SUCH
METALS AS MANGANESE, FERROUS IRON, & VANADIUM. ... THESE AEROSOLS POTENTIATE
RESPONSE ABOUT THREE FOLD WHEN PRESENT AT CONCN OF 1 MG/CU M @ 50% RELATIVE
HUMIDITY.
Sulfur dioxide increases
the carcinogenicity of benzopyrene by promoting its metabolism.
... Mortality among arsenic exposed smelter
workers was greater when exposures had been to high arsenic combined with
moderate or high sulfur dioxide exposures.
The effects of sulfur
dioxide and ozone alone and in combinations /were studied/, on young
normal subjects under conditions of light exercise. ... When the two gases were
present together in eight normal young subjects who were non-smokers, the
maximal mid-expiratory flow rate dropped to 67% of its initial value at the end
of 2 hours; the forced expiratory volume was 78% of its initial value, and the
mid-expiratory flow rate (50% vital capacity) was only 54% of the initial value.
... /It was/ concluded that sulfur dioxide and ozone
are exceedingly corrosive when present together, that "standard" must
specify the presence or absence of the other, and that there is a growing
incidence of the joint presence of the two pollutants in urban environments.
Environmental Fate & Exposure:
Probable Routes of Human Exposure:
Inhalation ... /or/ direct contact of gas or
liquid phase on ... mucous membranes.
It has been estimated by the Department of
Labor that approx 600,000 American workers may be occupationally exposed to sulphur
dioxide. Some of the highest exposures occur when it is a by product, as
in the metal smelting industry, and in the processing or combustion of high
sulfur coal or oil. Other exposures occur in manufacture of sulfuric acid,
fumigating, food preservation, wine making, and bleaching of many substances.
Natural Pollution Sources:
Hydrogen sulfide, from the natural decay of
vegetation on land, marsh lands and in the oceans, is probably oxidized to sulfur
dioxide within hours.
Volcanoes are a sporadic, yet possibly
significant, natural emissions source of sulfur dioxide.
Artificial Pollution Sources:
... POTENTIAL HAZARD HAS ARISEN FROM
INTRODUCTION OF SODIUM BISULFITE AS PRESERVATIVE FOR SILAGE; SULFUR
DIOXIDE IS EVOLVED FROM BISULFITE DURING FERMENTATION PROCESS.
On a global basis, fossil fuel combustion
accounts for 75 to 85% of man-made sulfur dioxide emissions,
and industrial processes such as refining and smelting account for the
remainder.
It is estimated that 93.5% of sulfur
dioxide pollution is produced in the Northern Hemisphere, and the
remaining 6.5% in the Southern Hemisphere.
North-western Europe, an area about 1% of the
Earth's surface, accounts for an estimated 13x10+12 or approximately 20% of the
global total.
... In several industrial countries, emission
of sulfur dioxide from coal burning power plants by
tall stacks ... /has produced/ widespread dispersion of low levels of sulfur
dioxide, sulfuric acid, sulfate, and nitric oxide that combine to
measurable incr of local sulfur air concn and precipitation ... .
The global sulfur cycle involves an
atmospheric flux of about (140-350)X10+6 tons/annum, with (40-60)X10+6 tons as
anthropogenic sulfur, in the form of sulfur dioxide, sulfuric
acid, and sulfate.
Most emissions of sulfur into the air are in
the form of sulfur dioxide resulting from the
combustion of fossil fuel for heating and energy production. Various industrial
activities such as petroleum processing, smelter operations, wood, pulping, etc
also produce significant emissions of sulfur dioxide and
other sulfur compounds.
Emissions of sulfur dioxide from
base metal smelting operations, such as nickel, copper, lead, and zinc, or
sintering of iron sulfides, constitute strong local sources.
Environmental Fate:
Atmospheric Fate: Direct surface uptake of sulfur
dioxide is the most important dry removal process for atmospheric sulfur;
... good sinks /include/ oceans (pH= 8), other non acidic moist surfaces, and
some crops and forest species at certain growth stages; where as dry, snow
covered surfaces and soils, for example, are less efficient.
Atmospheric Fate: Deposition by precipitation
(wet deposition) is the result of both in cloud and below cloud capture of sulfur
dioxide and particulate sulfate. In cloud processes include sulfate
particles serving as condensation nuclei, coagulation, and diffusional uptake of
sulfur dioxide. Below cloud processes include
interception of particles by falling drops and diffusional uptake of sulfur
dioxide. In cloud scavenging processes are more important in clean air,
ie where sulfur dioxide levels below the clouds are
low.
Atmospheric Fate: Wet deposition is, in
general, much more easily measured than is dry deposition. ... Routine
measurement of wet deposition ... is determined from ... sulfate concn in
precipitation samples and precipitation amount. Typically, the removal rate for
particulate sulfate is of the order of 40% per hr, and for sulfur
dioxide, an order of magnitude less. The overall efficiency of wet
removal depends on many factors: precipitation type, intensity, duration,
frequency, the relative amounts of sulfur dioxide and
sulfate present, and the size distribution of particulate sulfate.
Atmospheric Fate: Wet and dry deposition
appear to be of comparable importance, on an annual basis, over those large
areas where measurments and calculations have been made. Dry deposition is more
important closer to source regions where concn are higher, and, in principle, it
goes on all the time. /Conversely/, wet deposition occurs only periodically.
Terrestial Fate: Although snow covered
surfaces are inefficient receptors of gaseous and particulate sulfur cmpd, the
spring melt of the accumulated winter snowpack can result in rapid, short term
inputs of high sulfate, low pH water to freshwater systems with resulting
disastrous effects on fish.
Atmospheric Fate: A photochemically generated
aerosol, with sulfates as a major component, accumulates within summertime high
pressure systems which affect the northeastern United States. As the high
pressure system moves eastward with the accumulating aerosol, total suspended
particles and sulfate concn in the New York metropolitan area significantly
increase.
Atmospheric Fate: The avg residence time of
pollution sulfur is usually between one and five days, depending on the climate
of a region. /Sulfur cmpd/
Environmental Abiotic Degradation:
Suggested values of reaction rates for gas
phase oxidation of sulfur dioxide to sulfate for the
western European summer range from 0.5 to 5%/hr in sunlight, depending on the
degree of pollution of the atmosphere, with the lower figure relating to clean
air. This oxidation involves other short lived pollutants which have been
photochemically generated, therefore, the direct photo-oxidation of sulfur
dioxide is not important. Because these reactions are dependent on solar
radiation, their importance decreases significantly in winter time and at night.
Catalyzed, liquid phase, oxidation in the
presence of metals (eg iron, manganese) is important in urban plumes and perhaps
urban fogs where their concentrations are sufficiently high, but probably not in
cleaner, rural air.
Liquid phase oxidation involving the strong
oxidizing agents ozone and hydrogen peroxide may also be very important (eg
hydrogen sulfide and other organic sulfides oxidized to sulfur
dioxide); however, reaction rates and atmospheric concentrations,
respectively, for these two substances are not sufficiently well known.
The relative importance of chemical versus
dispersion processes in the oxidation of sulfur dioxide in
atmospheric plumes is governed by atmospheric conditions (eg after long plume
travel times, chemical reactions, rather than the rate of mixing of ambient air,
are likely to become the dominant rate limiting factor; and vice versa).
Sulfur dioxide reduces
visibility by taking part in reactions between organic cmpd and nitrogen oxides
to form particulates. Oxidation to sulfur trioxide, which then combines with
water to form small droplets of sulfuric acid, also reduces visibility.
IN MOIST AIR OR FOGS, IT COMBINES WITH WATER
TO FORM SULFUROUS ACID, BUT IT IS ONLY VERY SLOWLY OXIDIZED TO SULFURIC ACID.
The oxidation of sulfur
dioxide to sulfuric acid and sulfates in the atmosphere is important with
regard to air pollution studies. Radicals, eg hydrogen monoxide, water, and
carboxcylic acid, appear to be the principal species responsible for the
homogeneous oxidation of sulfur dioxide in the
atmosphere, which occurs at rates as high as 4.0%/hr.
Soil Adsorption/Mobility:
Sulfur dioxide uptake
is dependent upon soil pH and moisture content.
Effluent Concentrations:
Sulfur dioxide was
emitted from man made sources in the United States at an estimated rate of 30
teragram/yr in 1973. The fuel combustion exclusive of transportation accounted
for 78%, industrial processes (primary metal industry, petroleum industry,
chemical manufacturing, etc) for 20%, and tansportation for 2%. Of the fuels
used by utilities and industry, about 65% of the national anthropogenic emission
of sulfur dioxide came from coal combustion and 13%
from oil combustion.
Annually, the equivalent of about 1X10+8 tons
sulfur is emitted into the atmosphere as an atmospheric pollutant from smelters,
ore roasting, and coal-fired electric power plant emission. /Sulfur/
Atmospheric Concentrations:
Representative concn of sulfur
dioxide and sulfate in air and precipitation are as follows: 1) rural
North America 3 to 5 ug sulfur per cu m for sulfur dioxide, 1
to 3 ug sulfur per cu m for particulate sulfate, and 1 to 2 mg sulfur per l for
excess precipitation-sulfate; 2) clean global background (land) up to 1.7 ug
sulfur per cu m for sulfur dioxide, 0.1 to 0.5 ug
sulfur per cu m for particulate sulfate, and 0.1 mg sulfur per l for excess
precipitation sulfate.
The national max annual avg for sulfur
dioxide in community air is 0.03 ppm, and the max 24 hr avg is 0.14 ppm.
Sulfur dioxide exists
in remote areas of the earth at 50-120 parts per trillion, and in urban
atmosphere at levels between 1 ppb and 1 ppm.
Atmospheric sulfur dioxide concentrations
display an enormous range, depending upon the intensity of industrial and urban
activities. Values vary from about 1-5 ug/cu m for very remote clean areas,
through 28.6-286 ug/cu m for very remote clean areas, to at least 6000 ug/cu m
in industrial areas.
Other Environmental Concentrations:
It was found that sulfur
dioxide was taken up from atmosphere by sulfate treated plants ... .
Environmental Standards & Regulations:
FIFRA Requirements:
Residues from the use of sulfur
dioxide in liquid grain-fumigant formulations for marker or
fire-retardant purposes at levels not exceeding 5% by wt of such formulations
are exempted from the requirement of a tolerance in or on barley, buckwheat,
corn, oats, popcorn, rice, rye, grain sorghum (milo), wheat.
Residues of sulfur dioxide resulting
from post harvest fungical use are exempted from the requirement of tolerances
in or on corn for feed use only.
As the federal pesticide law FIFRA directs,
EPA is conducting a comprehensive review of older pesticides to consider their
health and environmental effects and make decisions about their future use.
Under this pesticide reregistration program, EPA examines health and safety data
for pesticide active ingredients initially registered before November 1, 1984,
and determines whether they are eligible for reregistration. In addition, all
pesticides must meet the new safety standard of the Food Quality Protection Act
of 1996. Pesticides for which EPA had not issued Registration Standards prior to
the effective date of FIFRA, as amended in 1988, were divided into three lists
based upon their potential for human exposure and other factors, with List B
containing pesticides of greater concern and List D pesticides of less concern. Sulfur
dioxide is found on List D. Case No: 4056; Pesticide type: fungicide;
Case Status: OPP is reviewing data from the pesticide's producers regarding its
human health and/or environmental effects, or OPP is determining the pesticide's
eligibility for reregistration and developing the Reregistration Eligibility
Decision (RED) document.; Active ingredient (AI): Sulfur
dioxide; Data Call-in (DCI) Date(s): 09/30/93, 10/13/95; AI Status: The
producers of the pesticide has made commitments to conduct the studies and pay
the fees required for reregistration, and are meeting those commitments in a
timely manner.
Allowable Tolerances:
Residues from the use of sulfur
dioxide in liquid grain-fumigant formulations for marker or
fire-retardant purposes at levels not exceeding 5% by wt of such formulations
are exempted from the requirement of a tolerance in or on barley, buckwheat,
corn, oats, popcorn, rice, rye, grain sorghum (milo), wheat.
Residues of sulfur dioxide resulting
from post harvest fungical use are exempted from the requirement of tolerances
in or on corn for feed use only.
Chemical/Physical Properties:
Molecular Formula:
SO2
Molecular Weight:
64.065
Color/Form:
COLORLESS NON-FLAMMABLE GAS
Colorless gas ... [Note: A liquid below 14
degrees F. Shipped as a liquefied compressed gas].
Odor:
STRONG SUFFOCATING ODOR
Irritating odor
... Characteristic, irritating, pungent odor
...
Taste:
Acid taste
Boiling Point:
-10.05 DEG C
Melting Point:
-75.5 DEG C
Corrosivity:
Corrodes aluminum
Iron, steel, nickel, copper-nickel alloys,
& inconel nickel-chromium-iron are satisfactory for dry or hot sulfur
dioxide, but they are readily corroded below the dew point or by wet sulfur
dioxide gas. Liquid sulfur dioxide produces
serious corrosion of iron, brass, copper at about 0.2 wt% or higher moisture
content.
Liquid sulfur dioxide will
attack some forms of plastic, rubber, & coatings
Critical Temperature & Pressure:
Critical temp: 315 deg F= 157 deg C= 430 K;
Critical pressure: 1142 psia= 77.69 atm= 7.870 mn/sq m
Density/Specific Gravity:
2.811 g/l
Heat of Vaporization:
171 BTU/LB= 94.8 CAL/G= 3.97X10+5 J/KG
Solubilities:
17.7% in water @ 0 deg C
11.9% in water @ 15 deg C
8.5% in water @ 25 deg C
6.4% in water @ 35 deg C
25% in alc
32% in methanol
SOL IN CHLOROFORM
SOL IN ETHER
SOL IN ACETIC ACID, SULFURIC ACID
Water solubliity in mol fractions: .0345 at
288.15 K; .029 at 293.15 K; .0246 at 298.15 K; .021 at 303.15 K; .018 at 308.15
K
0.58 g/100 CC water @ 90 deg C
11.3 g/100 CC water @ 20 deg C
Moderately soluble in benzene, acetone and
carbon tetrachloride
water solubility = 1.07X10+5 mg/l @ 21 deg C
Spectral Properties:
INDEX OF REFRACTION (LIQ): 1.410 @ 24 DEG C
Surface Tension:
28.59 mN/m (liquid @ 10 deg C)
Vapor Density:
2.263 at 0 deg C (air = 1)
Vapor Pressure:
vapor pressure = 3X10+3 mm Hg @ 25 deg C/ from
experimentally derived coefficients
Relative Evaporation Rate:
Greater than 1 (Butyl acetate = 1)
Viscosity:
Gas: 0.0124 mPa.s @ 18 deg C. Liquid: 0.368
mPa.s @ 0 deg C.
Other Chemical/Physical Properties:
MIXED WITH OXYGEN & PASSED OVER RED-HOT
PLATINUM, IT IS CONVERTED INTO SULFUR TRIOXIDE
WITH WATER FORMS SULFUROUS ACID (H2SO3);
BLEACHES VEGETABLE COLORS
1 PPM IS EQUIV TO 2.62 MG/CU M & 1 MG/CU M
IS EQUIV TO 0.38 PPM @ 25 DEG C, 760 MM HG
RATIO OF SPECIFIC HEATS OF VAPOR (GAS): 1.265
HEAT OF SOLN: -94.1 BTU/LB= -52.3 CAL/G=
-2.19X10+5 J/KG
SULFUR DIOXIDE IS
VOLATILE & TENDS TO DISAPPEAR FROM OPEN SYSTEMS & MUCH MAY BE
INACTIVATED BY COMBINATION WITH FOOD COMPONENTS. DESTROYING THIAMINE, IT IS
SOMEWHAT CORROSIVE
Condensation point: -10 deg C
Ionization potential 12.3 eV
Extremely stable to heat, even up to 2000 deg
C
An oxidizing and reducing agent
Ideal gas heat capacity= 0.149 BTU/lb-deg F @
75 deg F
Saturated vapor density= 0.47050 lb/cu ft @ 60
deg F
Latent heat of fusion: 7.4 KJ/mole @ -75.5 deg
C
Latent heat of sublimation: 30.6 KJ/mole (est)
Latent heat of vaporization: -296.8 KJ/mole @
25 deg C
Entropy: 248.1 J/(mole deg C)(25 deg C)
pH of aqueous solution: produces a slightly
acidic aqueous solution when combined with the water in the atmosphere or on
hand.
VAPOR PRESSURE: 3.2 ATM @ 20 DEG C
The oxidation of sulfur
dioxide leads to sulfurous acid and sulfur trioxide, which is rapidly
converted to sulfuric acid; a major constituent of acid rain.
Chemical Safety & Handling:
Hazards Summary:
The major hazards encountered in the use and
handling of sulfur dioxide stem from its toxicologic
properties. Exposure to this strong-smelling, colorless gas or liquid
(compressed gas) may occur from its use as a fumigant, as an intermediate in the
manufacture of sulfuric acid and other sulfur compounds, in oil, mineral, food
and paper processing, and in water treatment. Effects from exposure may include
contact burns to the eyes, skin, and mucous membranes, frostbite,
bronchoconstriction, and pulmonary edema. OSHA has established a time weighted
average (TWA) limit of 2 ppm and a short term exposure limit (STEL) of 5 ppm, to
become effective December 31, 1992. Engineering controls, including local
exhaust ventilation, should be used to maintain sulfur dioxide
at or below the permissible limit. In activities and situations where
over-exposure may occur, wear chemical protective clothing and a self-contained
breathing apparatus. If contact should occur, immediately remove contaminated
clothing (to be left at worksite for cleaning), irrigate exposed eyes with
copiousamounts of tepid water for at least 15 minutes, flush exposed skin with
water, and treat for possible frostbite. Emergency eyewash facilities should be
available in sulfur dioxide work areas. While sulfur
dioxide does not ignite easily, it may burn, and cylinders of the
compressed material can explode in the heat of a fire. For fires involving sulfur
dioxide, extinguish with dry chemical, CO2, Halon, water spray, fog, or
standard foam. If water is used, apply from as far a distance as possible
because material will react with water to form toxic and corrosive fumes. Sulfur
dioxide may be shipped domestically via air (cargo only), rail (cargo
only), road, and water, in containers bearing the label, "Nonflammable
gas." Sulfur dioxide should be stored in tightly
closed containers, in cool, well-ventilated areas, and away from sources of
physical damage. For spills of liquid sulfur dioxide, first
evacuate area for 50 feet in all directions, use water spray to reduce vapor,
and neutralize spilled material with limestone, soda ash, or lime. Keep material
from entering water sources and sewers. Before implementing land disposal of sulfur
dioxide waste, consult with environmental regulatory agencies for
guidance.
DOT Emergency Guidelines:
Health: TOXIC; may be fatal if inhaled. Vapors
are extremely irritating and corrosive. Contact with gas or liquefied gas may
cause burns, severe injury and/or frostbite. Fire will produce irritating,
corrosive and/or toxic gases. Runoff from fire control may cause pollution. /Sulfur
dioxide; Sulfur dioxide, liquefied/
Fire or explosion: Some may burn, but none
ignite readily. Vapors from liquefied gas are initially heavier than air and
spread along ground. Some of these materials may react violently with water.
Containers may explode when heated. Ruptured cylinders may rocket. /Sulfur
dioxide; Sulfur dioxide, liquefied/
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. /Sulfur
dioxide; Sulfur dioxide, liquefied/
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 is
recommended for fire situations ONLY; it is not effective in spill situations. /Sulfur
dioxide; Sulfur dioxide, liquefied/
Evacuation: ... Fire: If tank, rail car or
tank truck is involved in a fire, ISOLATE for 1600 meters (1 mile) in all
directions; also, consider initial evacuation for 1600 meters (1 mile) in all
directions. /Sulfur dioxide; Sulfur dioxide, liquefied/
Fire: Small fires: Dry chemical or CO2. Large
fires: Water spray, fog or regular foam. Move containers from fire area if you
can do it without risk. Do not get water inside containers. 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 the ends of tanks.
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. Stop leak if you can do it without risk.
If possible, turn leaking containers so that gas escapes rather than liquid.
Prevent entry into waterways, sewers, basements or confined areas. Do not direct
water at spill or source of leak. Use water spray to reduce vapors or divert
vapor cloud drift. Isolate area until gas has dispersed. /Sulfur
dioxide; Sulfur dioxide, liquefied/
First aid: Move victim to fresh air. Call
emergency medical care. 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. Remove and isolate contaminated clothing and shoes. In
case of contact with liquefied gas, thaw frosted parts with lukewarm water. 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. /Sulfur dioxide; Sulfur dioxide, liquefied/
Initial Isolation and Protective Action
Distances: Small Spills (from a small package or small leak from a large
package): First, ISOLATE in all Directions 125 meters (400 feet); then, PROTECT
persons Downwind during DAY 0.8 kilometers (0.5 miles) and NIGHT 3.4 kilometers
(2.1 miles). LARGE SPILLS (from a large package or from many small packages):
First, ISOLATE in all Directions 365 meters (1200 feet); then, PROTECT persons
Downwind during DAY 2.7 kilometers (1.7 miles) and NIGHT 11.0+ kilometers (7.0+
miles). /Sulfur dioxide; Sulfur dioxide, liquefied/
Odor Threshold:
4.70X10-1 ppm (recognition in air, chemically
pure)
Odor threshold: 0.1 ppm (low); 3.0 ppm (high)
Odor threshold: 1.1750 mg/cu m (low); 12.5000
mg/cu m (high); Irritating odor concn: 5.0 mg/cu m.
Fire Potential:
NONCOMBUSTIBLE