DEADLY, DANGEROUS AND JUST PLAIN BAD H2S GAS
(HYDROGEN SULFIDE GAS)
DEADLY, DANGEROUS AND JUST PLAIN BAD H2S GAS
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Exposure to Reduced Sulfur Gases Impairs Neurobehavioral Function KAYE H. KILBURN, MD, Los Angeles, Calif Abstract Background. In the 19th century, deaths
from acute exposure to hydrogen sulfide (H2S) portended permanent brain
injury from nonlethal doses. The neurobehavioral effects of H2S exposures
lasting from moments to years were compared in 16 subjects, 2 years to
22 years afterward. Methods. Neurophysiologic and psychologic
tests were used to appraise mood status and frequencies of 35 symptoms.
Functions and frequencies, described as percent predicted adjusted for
age, sex, educational achievement, and other factors, were compared with
those in an unexposed population. Results. Frequencies were elevated for
31 of 33 symptoms. Balance was impaired (246% predicted with eyes closed,
159% predicted with eyes open), and simple and choice reaction times were
prolonged (151% and 130% predicted, respectively). Visual fields performance
was decreased to 72% predicted (right) and 55% predicted (left), color
discrimination was abnormal, and hearing was decreased. Psychologic domains
showed cognitive disability, reduced perceptual motor speed, impaired verbal
recall and remote memory, and abnormal mood status. Conclusions. Exposure to H2S must be avoided. CONCENTRATED hydrogen sulfide H2S (>1,000
parts per million [ppm]) produces immediate death either in coma or by
convulsions. Lethargy, sickness, colic, and poorly defined chest pains
were described 150 years ago from exposures to H2S ìtoo slight to
cause serious mischief.î1 The concept that permanent neurobehavioral
impairment may follow nonfatal exposures has evolved slowly from reports
measuring a few patientsí impairment after massive exposures to
H2S and finding that patients admitted to the hospital in a coma entered
a chronic vegetative state and then died. In one such patient, computed
tomography (CT) of the brain showed symmetrical lucent lesions representing
necrotic zones in the lenticular nucleus and other parts of the basal ganglia.2
In a child who survived long-term low-dose environmental H2S exposure,
CT showed similar low-density areas in both basal ganglia.3 Six patients
who had unconsciousness from H2S poisoning had severe neurologic and neuropsychologic
dysfunction 5 years later.4 In another study, three patients had persistent
neurocognitive dysfunction, personality and affective impairment, and abnormal
event-related potentials (P-300 latency) at intervals after H2S exposure,
without unconsciousness.5 An oil field worker studied 3 years after H2S-induced
unconsciousness had slowing of blink reflex latency and abnormalities of
balance, cognitive function, perceptual motor speed, and recall.6 That
case initiated this study of H2S-related impairment of neuropsychologic
function. It is not possible to discern which of the unconscious patients
had been apneic and thus candidates for brain damage from hypoxia. The
fates of people who were not unconscious or who had a chronic low-level
H2S poisoning need to be elucidated.7 The key questions are (1) does acute
exposure cause neurobehavioral impairment, and (2) do years of downwind
exposure to H2S, presumably at low doses, cause permanent impairment? In
this study, 16 patients were examined, by a battery of neurobehavioral
tests, from 2 years to 22 years after beginning H2S exposure. Five of them
had been unconscious after H2S exposure while working at refineries, and
four had environmental (downwind) exposures. METHODS The 16 subjects had been referred for evaluation
of effects of exposure to reduced sulfur gas, including H2S and other gases,
especially reduced sulfur (oil-refinery) gases (subsequently referred to
as H2S). Five acutely exposed men (minutes group) in Texas and Louisiana
worked in oil fields (crude oil). Of 6 exposed for hours but less than
a day (hours group), 2 worked in oil refinery laboratories, 2 worked in
asphalt shipping in Louisiana, 1 made deliveries near an oil refinery,
and 1 was exposed to H2S generated inside a tank truck. Of the 5 patients
with chronic exposure (years group), 3 were exposed downwind from oil fields
in Kentucky and Texas, 1 was exposed to H2S from sewage treatment, and
1 was exposed to H2S evolved in a chemical laboratory. For comparison and analysis, 353 referents
were studied as the match for an environmentally chemically exposed group.7,8
The national referents were from Wickenburg, Ariz; Springhill and Waverly,
Tenn; and Smithfield, La, and had been recruited as control subjects matched
for sex, age, and years of education (highest school grade attained) with
the 16 patients in the three exposed groups. There was no evidence of chemical
contamination of air or water in the four sites. Referent subjects were
picked at random from voter registration rolls and were contacted by telephone
to ascertain whether they met the matching criteria and were willing to
be tested. Tested subjects were reimbursed for their time and mileage.
Whether referentsí unexposed status was known or unknown to the
testers made no difference in test results. All subjects gave informed
consent, and the protocol was approved by the Human Studies Research Committee
of the University of Southern California School of Medicine. Comparison
of these tests showed that the means of three referent groups were not
statistically different, so they were combined to calculate prediction
equations. These adjusted for age, sex, educational level, and height when
they were factors in each test. The prediction equations permitted results
for each exposed subject to be considered as percent predicted. The H2S
exposure status of the 16 subjects was known to the author-tester. Twelve
were plaintiffs in lawsuits. Exposure Minutes Group. The first oil field worker
carried an H2S meter, which read to full scale at 10,000 ppm during an
exposure that rendered him semiconscious.6 The other four were overcome
in an 8-foot deep excavation of a pipeline in which H2S was later measured
at 328 ppm. Hours Group. All 6 of these subjects smelled
ìrotten eggsî (H2S), so exposures were estimated between 1
ppm and 10 ppm (that is, beneath the threshold for olfactory fatigue).
However, exposure of the two bargemen who were pumping oil refinery asphalt
was probably 25 ppm to 50 ppm since they had headache, chest and back pain,
and inability to smell H2S after 1 hour of exposure. The 2 process technicians
were in an adjoining chemical plant and smelled H2S, so exposure was below
50 ppm. One man delivering chicken feed was exposed for 1 or 2 hours to
downwind H2S released after the flame on an oil well vent pipe flared out.
The tank cleaner was exposed to H2S generated from mixing sodium hyposulfite
and acid within a tanker truck. Years Group. The man and woman living downwind
from wells pumping to a crude oil collection tank in Kentucky associated
memory loss and difficulty concentrating with a strong H2S odor when a
vent flare was unlit. The presence of a flame produced a sharp pungent
odor associated with chest pain and tightness and asthma, typical effects
of sulfur dioxide. The sewage treatment worker smelled H2S (which varied
with wind direction) for 11 years. The woman exposed in an analytical laboratory
also noticed the odor. The minister was exposed to H2S in Odessa, Texas,
in his church and rectory, which were immediately downwind from two H2S-emitting
oil refineries. He reported that when the wind shifted toward the church
during services, numerous members of his congregation rushed outside to
vomit. A self-administered questionnaire was given
to each subject and checked for completion by computer-guided card reading.
The questionnaire included the American Rheumatism Associationís
criteria for lupus erythematosus9; standard queries regarding respiratory
symptoms10; occupational history, including exposure to chemicals, pesticides,
and herbicides; tobacco, alcohol, and drug use (prescription and illicit);
neurologic disorders, including unconsciousness, anesthesia, and head trauma;
and medical history. The frequencies of 35 complaints were estimated by
each subject on an 11-point scale.11 All patients had complete physical
and clinical screening neurologic examinations, including the cranial nerves,
deep tendon reflexes, and response to peripheral pain, touch, and vibration.
The neurophysiologic and neuropsychologic test battery was modified slightly
from that used in studies of histology technicians,12 of firemen exposed
to thermolysis products of polychlorinated biphenyls (PCBs),13 and of a
population exposed to solvents.11 Alcohol was measured in air expired after
a 20-second breath-hold, using a fuel cell analyzer. Neurophysiologic Tests Simple reaction time and visual two-choice
reaction time were measured with a computerized instrument.14 Body balance
with the subject standing erect with feet together was measured by head
tracking as mean speed of sway in centimeters per second.15 The blink reflex
was measured with surface electromyographic (EMG) electrodes from lateral
orbicularis oculi muscles bilaterally16 after tapping of the right and
left supraorbital notches with a light hammer, which triggered a recording
computer.17 Color discrimination was measured with the desaturated Lanthony
15 hue test under constant illumination18 and was scored by the method
of Bowman.19 Visual fields were threshold tested using automated perimetry
(Allergan-Humphrey) and scored by comparison with our referents. Vibration
was tested to extinction with a 128 Hertz tuning fork by comparison with
the investigator. Neuropsychologic Tests Immediate memory or recall was measured
by verbal and visual recall and digits forward and backward from Wechslerís
Memory Scale.20 The Culture Fair battery 2A tested nonverbal nonarithmetical
intelligence21,22 patterned on Ravenís progressive matrices.23 Block
designs and digit symbol from the Wechsler Adult Intelligence Scale (WAIS)24
tested constructional, interpretative attention, and integrative capacity.
Slotted pegboard, trail-making A and B, and fingertip number writing tests,
which measure dexterity, coordination, decision making, and peripheral
sensation and discrimination, were given from the Halstead-Reitan battery.25,26
The vocabulary test was from the Multidimensional Aptitude Battery.27 In
the Profile of Mood States (POMS),28 subjects self-judged their emotional
reaction to 65 inquiries applied to the preceding week. All scores and computed data for sway,
blink, and reaction time were entered into a Tri-Star 486 EISA bus computer
and descriptive and analytical computations, including t tests and analysis
of variance, were done with Stata Statistical Software (Stata Corp, College
Station, Tex). Data are first shown as prevalence of abnormality (% 1.5
standard deviations) by comparison, as percent predicted, with 202 national
referents. The exposed groupsí test scores were expressed as percentage
of predicted, thereby adjusting for effects of independent factors that
affected them including age, sex, educational attainment, and height. Then,
the percent predicted values were compared with those of a national unexposed
group by analysis of variance (ANOVA). The subjects in the three exposure
duration groupsóminutes (n = 5), hours (n = 6), and years (n = 5)ówere
also compared with those in the referent group individually. Statistical
significance was defined as P < .05. RESULTS Exposed subjects ranged in age from 21
years to 68 years (mean age, 44.7 years) and had educational levels ranging
from 0 years to 18 years (mean, 10.0 years), which was significantly below
that of the referents because three men had no formal education (Table
1). Durations of H2S exposures were minutes in patients 1 to 5, 1 hour
to 24 hours in patients 6 to 11, and 11 years to 22 years in patients 12
to 16. Intervals from onset of exposure to evaluation varied considerably
but were longer in those with years of duration. Smoking status was not
a significant factor (8 had never smoked and 8 were ex-smokers). Clinical
physical and neurologic examinations were unremarkable except for diminished
vibration sense. Symptom frequencies as group means in eight
categories of mucous irritation, chest symptoms, sleep, memory, balance,
mood, gastrointestinal symptoms, and limbic functions were elevated significantly
above those in the unexposed group (Table 2). These frequencies were similar
to those found in other exposed groups.7,8,11 One woman had cough and asthma
that were attributed to intermittent sulfur dioxide exposure when the flare
was burning upwind. Neurobehavioral testing showed that balance
with eyes closed was impaired in 75% of subjects. Mean sway speed in the
group was 2.95 cm/sec (246% predicted) compared with 1.18 cm/sec (100%
predicted) in referents Because neuropsychologic tests must be
adjusted for educational level, they are considered by percent predicted
comparison (Table 4). Scores on cognitive domain tests (Culture Fair, block
design, digit symbol, and vocabulary) were all significantly below expected.
In the perceptual motor domain, skills in peg placement and trail-making
A and B were decreased. Verbal recall was reduced to 69% predicted. Scores
on two of three long-term memory tests were decreased significantly.
The 5 men exposed to H2S for a few minutes
showed abnormalities on the physiologic tests and most of the psychologic
tests; only long-term memory was unaffected (Table 5). The 6 subjects with
hours of exposure did not show abnormalities on Culture Fair, block design,
and vocabulary in the cognitive domain, and verbal recall tests and remote
memory were intact. The 5 subjects exposed to H2S for years showed the
least effect as percent predicted in controls, but scores on the most sensitive
tests were still significantly different from those of unexposed subjects.
Thus, balance with eyes closed and with eyes open was abnormal, simple
reaction time was slowed, visual performance for the left eye was decreased,
and verbal recall was diminished. The only incon- sistency, for a greater
effect from chronic to ultra acute exposure, was for verbal recall. As
Table 3 shows, above-average scores for verbal recall by subjects 7 and
9 skewed the mean. The POMS score was elevated in 63% of patients,
and the mean was significantly elevated (Table 3). Depression after H2S
exposures (reactive or chemically induced) was frequent and often led to
treatment. Frequencies of 35 symptoms were elevated significantly above
referent levels (Table 2). Extensive questionnaire inquiry for medical,
neurologic, and psychiatric diseases showed no causative factors at home
and no occupational exposures to chemical or other neurotoxins. Nor did
these patientsí impairment patterns resemble those of posttraumatic
stress syndrome, minimal head injury, or chronic fatigue syndrome.29-31
DISCUSSION Permanent Impairment Permanent neurobehavioral impairment was
apparent in all 16 subjects who were tested months to years after momentary
to long-term exposure to reduced sulfur gases. Among those who had chronic
low-dose exposure, the most sensitive tests were those showing impaired
balance, simple reaction time, left visual field, and verbal recall. The
group exposed to H2S for hours had abnormal choice reaction, impairment
of both visual fields, and abnormal Culture Fair and block design scores,
as well as abnormal results of neuropsychologic tests of vocabulary, cognitive
function, peg placement, and trail-making A, though remote memory was intact.
The 5 men with momentary (knock-down) exposure had a complete blanket of
deficits. Thus, brief high doses were devastating, whereas protracted low
doses showed effects on the more sensitive tests. Limitations Consistent sensitive observations of ìnatural
experimentsî as in this study focus attention on the danger of H2S
exposure, but they are rarely considered definite proof. The doubts aroused
should stimulate epidemiologic studies. It is unlikely that the symptoms
found in this study could be attributed to other causes, since extensive
questionnaire data showed that head injury or other causes of unconsciousness
and neurologic and psychiatric disease were rare in exposed subjects. Clearly,
cerebral hypoxia may have contributed to the impairment in the 5 momentarily
exposed men who were unconscious, but it could not have affected the 11
other subjects. Although 12 were plaintiffs in lawsuits, these objective
physiologic function tests are not susceptible to ìcompensation
bias.î Symptom frequencies were higher in the group with only minutes
of exposure but then differed inconsistently between the groups. Furthermore,
evidence of malingering was absent in psychologic testing and questionnaire
responses. Finally, with the exception of patients 12 and 15, these individuals
lacked the educational background to understand manipulating test results.
Unquestionably, refineries leak carbon monoxide and reduced sulfur gases
such as carbon bisulfide3 and mercaptans, which accompany H2S and have
the same toxic mechanism and are therefore operationally inseparable. Others
gases such as toluene, xylene, and benzene are distinctive by odor and
mechanism but are liquids and lack the leakage profile of H2S. Therefore,
to tentatively attribute human impairment to the effects of reduced sulfur
gases seems plausible. There are four possible conclusions. First,
sensitive testing in subjects who had a broad spectrum of H2S exposureófrom
acute, with unconsciousness, to prolonged exposure to ìnuisance
levelsî at or above the olfactory threshold (approximately 1 ppm
to 50 ppm)óshowed chronic neurobehavioral impairment months to years
after H2S exposure. Second, such impairment occurred from downwind environmental
exposures as well as in the workplace. Third, chronic exposure at or above
the olfactory threshold for H2S caused permanent ill effects. Fourth, a
few hours of occupational H2S exposure without unconsciousness or respiratory
distress permanently impaired neurobehavioral function. Permanent Impairment From Sublethal Exposure
The most surprising finding was that even
moderate occupational exposure and insidious downwind environmental exposure
to H2S can cause permanent impairment. Although alternative explanations
(eg, exposures to other chemicals, including drugs and ethanol, and neurologic/psychiatric
diseases) were considered in each individual, the composite experience
makes neurobehavioral toxicity from H2S most probable. To strengthen this
conclusion, epidemiologic studies with sensitive human measurements and
monitoring of H2S levels should be done on subjects environmentally32 or
occupationally exposed to H2S.33 These observations contribute to recent
reports,4-6 including a pilot study of downwind neighbors of a refinery,7
that neurobehavioral impairment occurs after insidious H2S exposure. Even
in the absence of unconsciousness and resultant hypoxia, it appears that
H2S exposure produces chronic impairment, and this answers the question
raised by the Norwegian patients4 and those from northern California.5
In the present study, CNS hypoxia due to respiratory failure was not present
in 11 of the 16 patients and thus could not explain the findings. Beyond
hypoxia, the considerable knowledge about cellular mechanisms is applicable
to H2S-induced neurotoxicity. Hydrogen sulfide inhibits cytochrome-c
oxidase to cause cell death and also blocks sodium channels33 as well as
combining with hemoglobin.34 Certain areas of the brain attract sulfides
and sulfites, and the kinetics of their metabolism vary among individual
subjects. Thus, there are a number of suggested mechanisms for chronic
functional impairment of the brain and the retina. Defects in visual fields
and color vision impairment have been attributed to carbon bisulfide or
carboxyl sulfide products of circulating H2S.35 The toxicity of H2S has
been reviewed recently,33 and experimental exposure to H2S has been studied.34
Fatal human poisoning produced greenish discoloration of the cerebral cortex,
basal ganglia, caudate nucleus, putamen, and globus pallidus,36 and subsequently,
CT showed abnormally low density of the basal ganglia and surrounding white
matter after a fatal exposure2 and in a survivor.3 The downwind neurotoxicity in these 5 tested
patients extends the observations made in survivors of the 1952 Ponza Rica,
Mexico, refinery leak of H2S in which 22 neighboring people were killed
and 47 were hospitalized for respiratory and central nervous system symptoms.32
The unstated question from this disaster and from reviewing almost 500
reports of H2S poisoning from before 198931,32,36-39 is why chronic CNS
impairment was neglected after Ahlborg described persistent balance and
gait disturbances and extreme fatigue in several shale oil workers exposed
to H2S.37 Most likely, impairment was not looked for with sensitive measurements
of balance, mapping of the visual fields, and choice reaction time, and
such changes are not usually detected by clinical neurologic examination.
Well beyond calling for epidemiologic studies,
these findings imply that neighborhoods near refineries and other industrial
sites where H2S is released deliberately or inadvertently are unsafe. Because
hydrogen sulfide is heavier than air,33 it should never be vented into
the atmosphere so it can descend downwind to repeat the tragedy of Ponza
Rica32 and the impairments at Nipoma, Calif.7 People living near oil wells
and refineries should have sensitive studies to detect neurologic ill effects,
coupled with simultaneous air monitoring for low levels of H2S to establish
the range of exposures that impair neurobehavioral function. These dose-response
ranges would guide ameliorative steps, including removal of persons from
exposure, or if effects are widespread, moving oil refineries to unpopulated
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