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 ------- 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 ------- 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 ------- 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 ------- 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 ------- 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. ------- 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 ------- 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 ------- 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 ------- 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 ------- 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. -1- ------- 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. -2- ------- 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. -3- ------- 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, -4- ------- 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 ------- 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 -6- ------- 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 -7- ------- 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 -8- ------- 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. -9- ------- 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. -10- ------- 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). -11- ------- 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. -12- ------- 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 -13- ------- 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. -14- ------- 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) Alarle, Y.C., A.A. Krumm, W.M. Busey, C.E. Ulrich and R.J. Kantz. 1975. Long-term exposure to sulfur dioxide, sulfurlc add mist, fly ash, and their mixtures. Results of studies 1n monkeys and guinea pigs. Arch. Environ. Health. 30: 254-262. (Cited in Carson et al., 1981) Anfleld, B.D., and C.G. Warner. 1968. A study of Industrial mists contain- ing sufluric add. Ann. Occup. Hyg. 11: 185-194. (Cited in Gamble et al., 1984) Barrow, C.S. and W.H. Stelnhagen. 1980. Ammonia concentrations in the expired air of the rat: Importance to inhalation toxicology. Toxicol. Appl. Pharmacol. 53(1): 116-121. (Cited In Carson et al., 1981) Bloch, W.N., Jr., T.R. Lewis, K.A. Busch, J.G. Orthoefer and J.F. Stara. 1972. Cardiovascular status of female beagles exposed to air pollutants. Arch. Environ Health. 24: 343-353. (Cited in Carson et al., 1981) -15- ------- Bloch, W.N., Jr., S. LassHer, O.F. Stara and T.R. Lewis. 1973. Blood rheology of dogs chronically exposed to air pollutants. Toxlcol. Appl. Pharmacol. 25: 576-581. (Cited 1n Carson et al., 1981) Bushtueva, K.A. 1957. The determination of the limit of allowable concen- tration of sulfuric acid In atmospheric air [Materialy k Ustanovleniyu Predel'no Dopustlmoi Kontsentratsil Aerozolya Sernoi Klsloty Atmosfer nom Vozdukhe]. 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(Cited in Carson et al., 1981) -21- ------- 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 ------- |