EPA-540/1-86-031
ce of Emergency and
Remedial Response
Washington DC 20460
Superfund
&EPA
Off'ce of Research and Development
Office of Health and Environmental
Assessment
Environmental Criteria and
Assessment Office
Cincinnati OH 45268
HEALTH EFFECTS ASSESSMENT
FOR SULFURIC ACID
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EPA/540/1-86-031
September 1984
HEALTH EFFECTS ASSESSMENT
FOR SULFURIC ACID
U.S. Environmental Protection Agency
Office of Research and Development
Office of Health and Environmental Assessment
Environmental Criteria and Assessment Office
Cincinnati, OH 45268
U.S. Environmental Protection Agency
Office of Emergency and Remedial Response
Office of Solid Waste and Emergency Response
Washington, OC 20460
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DISCLAIMER
This report has been funded wholly or In part by the United States
Environmental Protection Agency under Contract No. 68-03-3112 to Syracuse
Research Corporation. It has been subject to the Agency's peer and adminis-
trative review, and 1t has been approved for publication as an EPA document.
Mention of trade names or commercial products does not constitute endorse-
ment or recommendation for use.
11
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PREFACE
This report summarizes and evaluates information relevant to a prelimi-
nary interim assessment of adverse health effects associated with sulfuric
acid. All estimates of acceptable Intakes and carcinogenic potency present-
ed in this document should be considered as preliminary and reflect limited
resources allocated to this project. Pertinent toxicologic and environ-
mental data were located through on-Hne literature searches of the Chemical
Abstracts, TOXLINE, CANCERLINE and the CHEMFATE/DATALOG data bases. The
basic literature searched supporting this document is current up to
September, 1984. Secondary sources of Information have also been relied
upon in the preparation of this report and represent large-scale health
assessment efforts that entail extensive peer and Agency review. The
following Office of Health and Environmental Assessment (OHEA) source has
been extensively utilized:
U.S. EPA. 1982. Air Quality Criteria for Partlculate Matter and
Sulfur Oxides. Vol. II. Environmental Criteria and Assessment
Office, OHEA, Research Triangle Park, NC. EPA 600/8-82-029b. NTIS
PB 84-156793.
The intent In these assessments is to suggest acceptable exposure levels
whenever sufficient data were available. Values were not derived or larger
uncertainty factors were employed when the variable data were limited in
scope tending to generate conservative (I.e., protective) estimates. Never-
theless, the interim values presented reflect the relative degree of hazard
associated with exposure or risk to the chemlcal(s) addressed.
Whenever possible, two categories of values have been estimated for sys-
temic toxicants (toxicants for which cancer is not the endpoint of concern).
The first, the AIS or acceptable intake subchronic, Is an estimate of an
exposure level that would not be expected to cause adverse effects when
exposure occurs during a limited time Interval (I.e., for an Interval that
does not constitute a significant portion of the lifespan). This type of
exposure estimate has not been extensively used or rigorously defined, as
previous risk assessment efforts have been primarily directed towards
exposures from toxicants in ambient air or water where lifetime exposure is
assumed. Animal data used for AIS estimates generally include exposures
with durations of 30-90 days. Subchronic human data are rarely available.
Reported exposures are usually from chronic occupational exposure situations
or from reports of acute accidental exposure.
The AIC, acceptable intake chronic, is similar in concept to the ADI
(acceptable daily intake). It 1s an estimate of an exposure level that
would not be expected to cause adverse effects when exposure occurs for a
significant portion of the lifespan [see U.S. EPA (1980) for a discussion of
this concept]. The AIC is route specific and estimates acceptable exposure
for a given route with the implicit assumption that exposure by other routes
is insignificant.
111
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Composite scores (CSs) for noncarcinogens have also been calculated
where data permitted. These values are used for ranking reportable quanti-
ties; the methodology for their development is explained 1n U.S. EPA (1983).
For compounds for which there 1s sufficient evidence of cardnogenlclty,
AIS and AIC values are not derived. For a discussion of risk assessment
methodology for carcinogens refer to U.S. EPA (1980). Since cancer is a
process that 1s not characterized by a threshold, any exposure contributes
an Increment of risk. Consequently, derivation of AIS and AIC values would
be Inappropriate. For carcinogens, q-|*s have been computed based on oral
and inhalation data 1f available.
1v
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ABSTRACT
In order to place the risk assessment evaluation in proper context,
refer to the preface of this document. The preface outlines limitations
applicable to all documents of this series as well as the appropriate Inter-
pretation and use of the quantitative estimates presented.
Although considerable data are available concerning the effects of
sulfurlc add, reported effects Include only localized Irritant effects at
the point of entry following Inhalation {respiratory tree and lungs). Data
regarding systemic toxic effects are lacking. Therefore, an estimate of AIS
or AIC, which by definition estimate absorbed dose In mg/day 1n relation to
systemic toxldty, would be Inappropriate. Available data, however, do
allow estimation of an acceptable air exposure concentration of 0.07
mg/m3. A CS of 26.8 was calculated for the effects of dental etching and
erosions that occur rapidly at relatively low atmospheric concentrations.
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ACKNOWLEDGEMENTS
The Initial draft of this report was prepared by Syracuse Research
Corporation under Contract No. 68-03-3112 for EPA's Environmental Criteria
and Assessment Office, Cincinnati, OH. Dr. Christopher DeRosa and Karen
Blackburn were the Technical Project Monitors and Helen Ball was*the Project
Officer. The final documents 1n this series were prepared for the Office of
Emergency and Remedial Response, Washington, DC.
Scientists from the following U.S. EPA offices provided review comments
for this document series:
Environmental Criteria and Assessment Office, Cincinnati, OH
Carcinogen Assessment Group
Office of A1r Quality Planning and Standards
Office of Solid Waste
Office of Toxic Substances
Office of Drinking Water
Editorial review for the document series was provided by:
Judith Olsen and Erma Ourden
Environmental Criteria and Assessment Office
Cincinnati, OH
Technical support services for the document series was provided by:
Bette Zwayer, Pat Daunt, Karen Mann and Jacky Bohanon
Environmental Criteria and Assessment Office
Cincinnati, OH
v1
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TABLE OF CONTENTS
1.
2.
3.
ENVIRONMENTAL CHEMISTRY AND FATE
ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS . . .
2.1.
2.2.
ORAL
INHALATION
TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
3.1.
3.2.
SUBCHRONIC
3.1.1. Oral
3.1.2. Inhalation
CHRONIC
3.2.1. Oral
3.2.2. Inhalation
Page
1
3
. . . 3
3
4
4
. . . 4
4
6
. . . 6
. . . 6
3.3. TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS.
3.4.
3.3.1. Oral
3.3.2. Inhalation
TOXICANT INTERACTIONS
4. CARCINOGENICITY
4.1.
4.2.
4.3.
4.4.
5. REGULl
HUMAN DATA
4.1.1. Oral
4.1.2. Inhalation
BIOASSAYS
4.2.1. Oral
4.2.2. Inhalation ,
OTHER RELEVANT DATA
WEIGHT OF EVIDENCE
VTORY STANDARDS AND CRITERIA
8
8
, 8
10
10
10
10
10
10
10
10
10
11
V11
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TABLE OF CONTENTS (cont.)
Page
6. RISK ASSESSMENT 12
6.1. ACCEPTABLE INTAKE SUBCHRONIC (AIS) 12
6.1.1. Oral 12
6.1.2. Inhalation 12
6.2. ACCEPTABLE INTAKE CHRONIC (AICJ 12
6.2.1. Oral 12
6.2.2. Inhalation 12
6.3. CARCINOGENIC POTENCY (q-j*) 14
6.3.1. Oral 14
6.3.2. Inhalation 14
7. REFERENCES 15
APPENDIX: Summary Table for SulfuMc Acid 22
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LIST OF ABBREVIATIONS
ADI Acceptable dally intake
AIC Acceptable intake chronic
AIS Acceptable intake subchronlc
CAS Chemical Abstract Service
CS Composite score
NOEL No-observed-effect level
TLV Threshold limit value
TWA Time-weighted average
ix
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1. ENVIRONMENTAL CHEMISTRY AND FATE
Sulfuric acid (CAS No. 7664-93-9), H2S04, is a colorless, viscous
liquid with a molecular weight of 98.08 and a specific gravity of 1.8357
(Donovan and Salamone, 1983). SulfuMc acid 1s soluble 1n water in all
proportions with evolution of heat and 1t has a vapor pressure of 1 mm Hg at
145.8°C (Weast, 1980).
The primary sources of sulfuric acid in the atmosphere are vehicular
emissions, combustion sources, explosive manufacture, furnace soot, sulfuric
acid manufacture, steel manufacture and volcanic emissions (Graedel, 1978).
Sulfuric add is present in the atmosphere in the form of aerosols. The
size fractionation of sulfur-containing aerosols [which primarily consists
of H SO and (NH4)2 S04] show that in dry weather the aerosol is
found in sub-0.65 ym particle size fractions, while under humid condi-
tions, the aerosol is found in the 0.65-3.6 vm particle size range (U.S.
EPA, 1982). Size fraction analysis of sulfate aerosol in the atmosphere
also showed that the predominant amount (70%) of sulfate ions are present in
the submicron particle range (U.S. EPA, 1982).
The fate of sulfuric add aerosols in the environment has been studied
by a limited number of Investigators (U.S. EPA, 1982) and significant data
gaps exist in this area. It is likely that sulfuric add aerosol will react
chemically with other species in the atmosphere. The source of Inorganic
sulfates 1n the atmosphere, particularly ammonium sulfate, has been demon-
strated to be due primarily to chemical reactions In the atmosphere (U.S.
EPA, 1982). Similarly, depending upon the amount of dilution by the
moisture in the atmosphere, sulfuric acid aerosols may react with organics
in the atmosphere to form sulfonates.
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Besides chemical transformation, sulfurlc acid aerosols in the atmo-
sphere are likely to be removed through wet and dry deposition; however, no
estimate of the half-life of atmospheric sulfurlc acid due to Us chemical
transformation and physical removal processes was located in the available
literature.
In aquatic media of pH >7, sulfurlc add reacts with carbonate,
bicarbonate or hydroxides 1n the sediment or suspended particles, with the
formation of sulfates. Since the majority of sulfates, with the exception
of lead and calcium, are soluble in water, this reaction may remobilize the
precipitated metals from the aquatic phase and decrease the pH of the
solution. In aquatic media of pH <7, at least a part of the sulfuric acid
may remain Ionized in solution and may be mobile.
The majority of sulfurlc acid 1n soils is expected to be removed by
reaction with Inorganic minerals or organic matter in soils. The extent of
this chemical reaction may depend on the strength of the sulfurlc acid In
the soil. As the concentration of the add decreases through reactions or
dilution through water, the reactivity should also decrease. In highly
sandy soil, sulfurlc acid probably leaches Into groundwater.
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2. ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS
2.1. ORAL
Pertinent data regarding the absorption of sulfurlc add from the
gastrointestinal tract could not be located 1n the available literature.
Since the major toxic effect of sulfurlc add 1s local Irritation, and
because of the buffering capacity of the blood, 1t Is unlikely that signifi-
cant systemic exposures occur.
2.2. INHALATION
Pertinent data regarding the absorption of Inhaled sulfurlc add could
not be located 1n the available literature. Since the major toxic effect of
sulfurlc add Is local Irritation and since inhaled sulfurlc add 1s largely
neutralized by NH in the expired air, it is unlikely that significant
O
systemic exposure to sulfurlc add occurs.
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3. TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
Carson et al. (1981) reviewed more than 400 studies on the effects of
sulfurlc add on humans and experimental animals. A thorough analysis of
these data Is not possible within the constraints of the current project.
Therefore, the following review will concentrate on those studies that
provide data on the effects of near threshold doses of sulfurlc add
(Table 3-1).
3.1. SUBCHRONIC
3.1.1. Oral. Pertinent data regarding the subchronlc oral toxidty of
sulfurlc add could not be located in the available literature.
3.1.2. Inhalation. Schleslnger et al. (1978, 1979) reported that
exposure of donkeys to -0.1 mg HpS04/m3 (0.102-0.106 mg/m3) for 1
hour/day, 5 days/week, for 6 months resulted in erratic bronchial clearance
1n the last week of exposure. Respiratory rates were reduced in all four
animals, and two of the four donkeys sustained Impairment of clearance with
erratic improvement during a 3-month follow-up period. Concentrations as
low as 0.071 mg/m3 administered as "repeated doses" were reported to
decrease the rate of bronchial mucodliary clearance, but the duration of
these exposures was not reported.
Loscutoff et al. (1978) exposed dogs to atmospheres containing 1.0 mg
H-SO./m3 for "repeated doses." The number of animals, sex, duration
and number of exposures were not reported. No effects were reported and all
exhaled sulfate was in the form of an ammonium salt.
Rats appear to be relatively insensitive to the effects of sulfuric add
aerosols. Lawkowski et al. (1979) exposed groups of 10 male Sprague-Dawley
rats to ambient atmospheres or atmospheres containing 2.37 mg H_SO./m3,
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TABLE 3-1
Threshold Doses for Sulfurlc Acid Toxlclty*
Species rag HpSO^m3
(particle size)
Nonkey -0.1 plus fly ash and/or
S02 (NR)
Donkey 0.102 or 0.106 (0.5 urn)
Donkey 0.071-1.364 (0.3-0.6 tun)
Dog 1.0 (NR)
\
in
1 Dog -0.09 In auto exhausts
(NR)
\ "™ /
Guinea pig 0.08 (0.84*0.60 ym)
Rat 2.37 (0.5*1.0 ,nn)
Rat 0.61 SOf (presumably most
H2S04) In auto exhausts
Exposure
Conditions
22-24 hours/day
1 hour/day;
5 days/week
1 hour by nasal
catheter
"repeated doses*
16 hours/day
22-23 hours/day
continuous
24 hours/day
Length of Length of Comments
Exposure Study
18 months 18 months NOEL for some combina-
tions of pollutants
6 months 6 months Sustained Impairment In
bronchial mucoclllary
clearance In two of four
donkeys. Some Improve-
ment within 3-month
recovery period.
NR NR Bronchial mucoclllary
clearance slowed.
NR NR NOEL (at 3.5 mg/m>).
Increased pulmonary
resistance.
68 months 104 months Emphysema tous and other
microscopic lung changes
3 years after 68-month
exposure.
12 months 12 months Lowered growth rate In
females. NOEL In other
studies.
14 weeks 14 weeks NOEL (lung function,
blood chemistry,
behavior).
7 days 7 days Lower body weight.
Reference
Alarle et al., 1975
Schleslnger et al.,
1979
Schleslnger et al.,
1978
Loscutoff et al.,
1978
Lewis el al., 1974;
Bloch et al., 1972,
1973; Orthoefer et
al.. 1976; Hyde et
al., 1978; Vaughan
et al., 1969
Alarle et al.,
1973. 1975
Lawkowsk! et al.,
1979
Lee et al., 1976
*Source: Carson et al.. 1981
NR = Not reported
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24 hours/day, 7 days/week, for 14 weeks. There were no significant effects
on behavior, as measured by spontaneous motor activity, lung function or
blood acid-base chemistry. Lee et al. (1976) reported decreased body weight
gain 1n female Sprague-Oawley rats (10/group) exposed to 0.6 mg SO^/m3 In
auto exhausts 24 hours/day for 7 days. The S0]j was, presumably, mostly
In the form of H2S04-
3.2. CHRONIC
3.2.1. Oral. Pertinent data regarding the chronic oral toxldty of
sulfuMc add could not be located 1n the available literature.
3.2.2. Inhalation. Alarle et al. (1975) exposed groups of nine
Cynomolgus monkeys of both sexes to atmospheres containing 0.09-0.99 mg
H_SO /m3 1n combination with varying amounts of fly ash and/or SO,,.
At concentrations of 0.1-0.11 mg HpSO./m3, significant time-related
Increases 1n pulmonary resistance were reported for some combinations. No
treatment-related effects were reported for any combination of exposures
with a sulfurlc add concentration of 0.09 mg/m3.
Several Investigators (Lewis et al., 1974; Bloch et al., 1972, 1973;
Orthoefer et al., 1976; Vaughan et al., 1969; Hyde et al., 1978) exposed
purebred female dogs (12/group, 20 controls) to atmospheres containing
0.09-0.11 mg HpSO./m3 and varying concentrations of S02 and auto
exhaust 16 hours/day, 7 days/week, for up to 68 months, followed by observa-
tion for an additional 32-36 months. At the end of the 3-year observation
period, there was significant ciliary loss, squamous metaplasia, air-space
enlargement and nondllated bronchlolar cell hyperplasla (Hyde et al., 1978).
Alarle et al. (1973, 1975) Investigated the effects of chronic exposure
of guinea pigs to sulfurlc add, with or without simultaneous exposure to
0.45 mg fly ash/m3. Groups of 50 male and 50 female Hartley guinea pigs
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were exposed to atmospheres containing 0, 0.08, 0.10 or 0.30 mg HpSO./m3,
22-23 hours/day for 12 months. No effects were observed on survival,
hematology or histology at any dose level. Exposure to sulfurlc acid alone
resulted In decreased growth rates 1n the females exposed to 0.08 or 0.10,
but not 0.30 mg/m3. No effects were reported 1n guinea pigs exposed to
0.08 mg H SO /m3 and 0.45 mg fly ash/m3.
Flnklea et al. (1975a,b) estimated the threshold for Increase In ambient
air sulfate with Increasing air pollution In terms of adverse effects 1n
humans, based on ep1dem1olog1cal studies (Table 3-2). They estimated that
exposure to as little as 0.01 mg H?SO./m3 for up to 10 years can
result 1n an Increased risk of chronic bronchitis In smokers. Total sulfate
was determined 1n the atmosphere, but sulfurlc add 1s usually considered to
be a major fraction of the measured sulfate. It 1s also often Impossible to
separate the effects of sulfurlc add from those of other pollutants
(particularly 0„, NO , S00, HC1).
j X c
Occupational exposures have been associated with Increased dental
erosion, eye Irritation and effects on the respiratory system (Tadzhlbaeva
and GoVeva, 1976; El-Sad1k et al., 1972; Williams, 1970; Malcolm and Paul,
1961; ten Bruggen Gate, 1958; Jones and Gamble, 1984; Gamble et al., 1984).
The toxldty of sulfurlc add vapors to the human respiratory tract Is well
recognized. Williams (1970) observed a slight Increase 1n bronchitis among
workers exposed to sulfurlc acid 1n a battery manufacturing plant compared
with nonexposed workers at the same plant. Exposure levels had previously
been estimated at 1.4 mg/m3, which 1s sufficient to cause dental erosion
1n the exposed workers (Anfleld and Warner, 1968). A higher Incidence (36%)
of bronchitis of apparently greater severity was noted by El-Sad1k et al.
(1972) In a group of 33 workers 1n two battery factories. The Incidence of
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bronchitis was 21% 1n unexposed controls (what size not reported). Some of
the increased incidence of bronchitis in the exposed workers and the high
incidence in controls appeared to be related to smoking habits. Dental
Infections and tooth discolorations were also observed in exposed workers
and the incidence and severity appeared to correlate positively with
duration of exposure.
Malcolm and Paul (1961) also reported severe tooth erosion among 160
acid-battery factory workers. The incidence and severity were more severe
at concentrations of 3-16 mg/m3 than at 0.8-2.5 mg/m3. In some workers
exposed to the higher levels the height of their incisors was decreased by
as much as 50%. In a more recent investigation of the effects of sulfuric
acid on the teeth, erosions were observed in workers exposed to atmospheres
of 0-1.7 mg/m3 (average 0.18 mg/m3) (Jones and Gamble, 1984; Gamble et
al., 1984). Exposure to 0.23 mg/m3 for 4 months was sufficient to
initiate erosion.
3.3. TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS
3.3.1. Oral. Pertinent data regarding the teratogenicity or other repro-
ductive effects of orally administered sulfuric add could not be located In
the available literature.
3.3.2. Inhalation. Pertinent data regarding the teratogenicity or other
reproductive effects of inhaled sulfuric acid could not be located in the
available literature.
3.4. TOXICANT INTERACTIONS
The toxidty of inhaled sulfuric acid is heavily influenced by, among
other factors, the presence of other particulates in the air (Carson et al.,
1981). Due to the hygroscopic nature of sulfuric acid, there is a tendency
for sulfuric acid droplets to absorb water from the breath, creating larger
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droplets that Impact high 1n the upper respiratory tract where they cause
less damage. When the sulfurlc add 1s absorbed to other partlculates, 1t
may be carried deeper Into the respiratory tract.
Inhaled sulfurlc acid mists are rapidly neutralized by NH3 1n the
expired air (Barrow and Stelnhagen, 1980). This neutralization 1s reduced
when the sulfurlc add 1s absorbed to airborne partlculates (Lawther, 1980).
Synerglsm has also been demonstrated between sulfurlc add and the
pollutants normally found 1n auto exhausts (SO^, ozone, metallic aerosols)
(Carson et al., 1981). The specific Interactions Involved have not been
fully elucidated and studies In humans have not consistently demonstrated
the synerglstlc effects observed 1n experimental animals.
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4. CARCINOGENICITY
4.1. HUMAN DATA
4.1.1. Oral. Pertinent data regarding the cardnogenldty of orally
administered sulfurlc add could not be located 1n the available literature.
4.1.2. Inhalation. Pertinent data regarding the cardnogenldty of
Inhaled sulfurlc add could not be located 1n the available literature.
4.2. BIOASSAY
4.2.1. Oral. Pertinent data regarding the cardnogenldty of orally
administered sulfurlc add could not be located 1n the available literature.
4.2.2. Inhalation. Pertinent data regarding the cardnogenldty of
Inhaled sulfurlc add could not be located 1n the available literature.
4.3. OTHER RELEVANT DATA
One study was located 1n which Escherlchla coll (strain unspecified)
were treated with 0.002-0.005% sulfurlc acid solutions for 3 hours (Oemerec
et al., 1950, 1951). No Increase In mutation frequency was observed.
4.4. WEIGHT OF EVIDENCE
IARC has not evaluated the risk to humans associated with oral or
Inhalation exposure to sulfurlc add. Data were not available regarding the
cardnogenldty of sulfurlc add 1n humans or animals. Applying the
criteria for evaluating the overall weight of evidence of cardnogenldty to
humans proposed by the Carcinogen Assessment Group of the U.S. EPA (Federal
Register, 1984), sulfurlc add 1s most appropriately designated a Group D -
Not Classified chemical.
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5. REGULATORY STANDARDS AND CRITERIA
The ACGIH (1980) has recommended a TLV of 1 mg/m3. This value 1s
recommended to "prevent pulmonary Irritation and Injury to the teeth." The
USSR has established an average maximum allowable concentration for the
ambient air of populated places of 0.1 mg H2S04/m3 with an allowable
peak value of 0.3 mg/m3 (USSR State Committee of the Ministers for Con-
struction, 1972). The ACGIH (1980) reports that both the USSR and Czecho-
slovakia have recommended a limit of 1 mg H SO /m3 for Industrial
exposures. The U.S. Occupational Safety and Health Administration has
established an 8-hour TWA of 1 mg H2S04/m3 (Code of Federal Regula-
tions, 1981).
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6. RISK ASSESSMENT
6.1. ACCEPTABLE INTAKE SUBCHRONIC (AIS)
6.1.1. Oral. Pertinent data regarding the subchronlc oral toxldty of
sulfuMc add could not be located 1n the available literature.
6.1.2. Inhalation. The only reported effects of exposure to Inhaled
sulfuMc add were localized effects at the point of entry. Since an
Interim AIS 1s based on the absorbed dose, It 1s Inappropriate to derive
these numbers from local irritant effects. Based on studies with donkeys,
which have respiratory systems anatomically similar to humans, subchronlc
exposure to atmospheric concentrations as low as 71 yg H_SO./m3 may
produce a measurable decrease in the rate of bronchial mucodliary clearance
(Schlesinger et a!., 1978, 1979).
6.2. ACCEPTABLE INTAKE CHRONIC (AIC)
6.2.1. Oral. Pertinent data regarding the chronic oral toxicity of
sulfuMc acid could not be located in the available literature.
6.2.2. Inhalation. The only reported effects of chronic exposure to
Inhaled sulfuric add are localized effects at the point of entry. Since an
Interim AIC 1s based on the absorbed dose, it is Inappropriate to derive
these values from the available data. There are some Indications that
tolerance to the Irritant effects of sulfuric add develops with repeated
exposures (Hackney, 1978; Bushtueva, 1957). Thus, individuals may be able
to tolerate chronic exposure to concentrations of sulfuric add which would
produce significant irritation during the initial exposure. Carson et al.
(1981) estimated that "a lower exposure level that appears to be safe for
man 1s 1n the range of 0.066-0.098 mg/m3." They point out that this value
may be influenced by a number of factors, including particle size, frequency
and duration of exposure and synerglstic effects.
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This estimate correlates with the monkey data of Alarle et al. (1975)
which showed a NOAEL of 0.09 mg/m3 even when sulfuMc add was combined
with various combinations of fly ash and/or S0? which would be expected to
exacerbate pulmonary Irritation. In addition, the TLV has been set at 1
mg/m3; therefore, this suggested range Incorporates a minimum of a 10-fold
uncertainty factor for protection of more sensitive segments of the general
population. Still troubling are the donkey data (Schlesinger et al., 1978,
1979), which show decreases in bronchial mucociliary clearance at 0.071
mg/m3. It is uncertain whether the donkey Is unusually susceptible to
sulfuric acid irritation or whether this study evaluated more sensitive
endpoints than the other reports. The decrease In clearance could represent
a metaplastic response of the bronchial epithelium to Irritation, and this
would not be detected as a deficit in pulmonary function. This deficit In
clearance capacity, however, could compromise the ability to clear other
resplrable pollutants.
For these reasons, the range suggested by Carson et al. (1981) of
0.066-0.098 mg/m3 should be protective for exposures to sulfuric acid
alone. As more data become available revision of this estimate may be
required.
A CS was calculated for the respiratory tract effects observed in humans
and animals and for the tooth erosion and etching that occurred in battery
manufacturing workers exposed for as little as 4 months to sulfuric acid at
0.23 mg/m3. In the latter case, the exposure was expanded to continuous,
assuming workers inhale 10 m3 of air during working hours on 5 days/week.
An uncertainty factor of 10 was applied to convert from short-term to
chronic exposure since 1t seems certain that prolonged exposure would result
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1n increased severity of the effect. A human MED of 0.16 mg/day resulted,
corresponding to an RV. of 6.7. Tooth erosion and etching were assigned
an RV of 4. A CS of 26.8, the product of RV. and RV , resulted.
e u e
6.3. CARCINOGENIC POTENCY (q^)
6.3.1. Oral. Pertinent data regarding the cardnogenicity of orally
administered sulfuric add could not be located in the available literature.
6.3.2. Inhalation. Pertinent data regarding the cardnogenlcHy of
inhaled sulfuric add could not be located in the available literature.
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7. REFERENCES
ACGIH (American Conference of Governmental Industrial Hyg1en1sts). 1980.
Documentation of the Threshold Limit Values, 4th ed. Cincinnati, OH.
p. 377-378.
AlaMe, Y., W.M. Busey, A.A. Krumm and C.E. Ulrich. 1973. Long-term
continuous exposure to sulfuMc add mist 1n cynomolgus monkeys and guinea
pigs. Arch. Environ. Health. 27: 16-24. (Cited 1n Carson et al., 1981)
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APPENDIX
Summary Table for Sulfurlc Acid
Inhalation
AIS
AIC
Maximum
composite
score
Species Experimental
Dose/Exposure
human 0.23 mg/m3
occupational
(0.16 mg/kg/day)b
Effect Acceptable Intake Reference
(AIS or AIC)
NDa
N0a
tooth etching and 26.8 Jones and
erosion (RVe = 4) Gamble, 1984;
Gamble
I\J
I
(RVd = 6.7)
et al., 1984
Oral
AIS
AIC
ND
ND
aSee text for suggested maximum air concentration and rationale for not estimating acceptable Intakes.
uncertainty factor of 10 was applied to convert from subchronlc to chronic exposure; assumed:
worker breathes 10 m3 of air during working hours for 5 days/week.
ND - Not derived
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