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National Research Council (US) Committee on Toxicology. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2. Washington (DC): National Academies Press (US); 1984.

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2.

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Chemical formula:SO2
Molecular weight:64.07
CAS number:7446-09-5
Specific gravity (liquid):1.434
Specific gravity (gas):2.927
Solubility:Soluble in water, alcohols, acetic acid, and sulfuric acid
General characteristics:Colorless, nonflammable gas or liquid; strong suffocating odor
Conversion factors:1 ppm = 2.6 mg/m3
1 mg/m3 = 0.38 ppm


Sulfur dioxide is most noteworthy as an environmental pollutant. It is formed when materials containing sulfur are burned, and is thus an important air pollutant, especially in the vicinity of smelters and plants burning soft coal or high sulfur oil. Others are automobile exhaust, wood-burning stoves, pulp mills, and smelters. Note that, in addition to sulfur dioxide itself, many related compounds and decay products of sulfur dioxide--such as sulfurous and sulfuric acids, sulfates, sulfites, and bisulfites--are present in the ambient air. It is beyond the scope of this brief review to describe all the information on all these substances; only sulfur dioxide will be addressed.


Within the last 8 yr, three reviews of the toxic effects of sulfur dioxide in humans and animals have been published (Greenfield, Attaway and Tyler, 1976; International Electric Research Exchange, 1981; EPA, 1982). These reviews covered epidemiologic reports, health effects of acute and chronic low-dose exposures of humans, health effects of acute and chronic low- and high-dose exposures of animals, projected estimates of pollutant thresholds for adverse effects of short- and long-term exposures, and correlations of sulfur dioxide exposures with asthmatic attacks and effects on children.


Few recent reports have described accidental exposure to sulfur dioxide. Of historical interest is the report of a worker exposed directly to liquid sulfur dioxide who suffered effects of acute freezing of the skin and corneas (Kennon, 1927). A more recent report cited a case of an accidental exposure to sulfur dioxide at a high concentration for 15-20 min that led to the development of a severe, irreversible obstructive syndrome (Woodford et al., 1979). The pulmonary effects of accidental exposure to sulfur dioxide appear to be limited to gaseous sulfur dioxide.

An excellent review of studies involving controlled human exposure is available (Greenfield, Attaway and Tyler, 1976). Briefly, the major health effects of exposure to sulfur dioxide at less than 25 ppm (for various durations) are irritation of mucous membranes, throat, esophagus, and eyes; reflex cough; increase in respiratory rate associated with decrease in depth of respiration; decrease in nasal mucus flow; variable effects on tracheal and bronchial mucus flow; decrease in forced expiratory volume and flow; decrease in airway conductance; and increase in airway resistance.

An estimated 10-20% of the population will respond with hyperreactivity on exposure to sulfur dioxide. Koenig et al. (1980) have shown that asthmatic adolescents are more sensitive than healthy nonsmoking adults to sulfur dioxide at 1 ppm. As demonstrated by Lawther et al. (1975), the changes in airway resistance after exposure to sulfur dioxide at less than 30 ppm are short-lived. Greenfield, Attaway and Tyler, (1976) reviewed similar changes after short-term exposures to sulfur dioxide at concentrations greater than 25 ppm.

Another review (EPA, 1982) indicated that recovery to normal functional values can occur in as little as 5 min after acute exposure of normal resting subjects (Lawther et al., 1975), but may take 30-60 min after exposure during exercise (Bates and Hazucha, 1973), after exposure of exercising asthmatic subjects (Sheppard et al., 1981; Koenig et al., 1981), or after exposure of other sensitive subjects (Gokemeijer et al., 1973; Lawther et al., 1975). Weir and Bromberg (1975) suggested that persons with minimal airway disease are probably not more susceptible than normal persons to the effects of sulfur dioxide. However, this latter conclusion is questionable, in that the presence of pre-existing disease in the subjects interfered with attempts to define threshold concentrations of sulfur dioxide. Asthmatic subjects exposed to sulfur dioxide at 5 ppm for 5 min while exercising have had asthmatic attacks (Sheppard et al., 1980).

Epidemiologic data on sulfur dioxide are characteristically difficult to assess, because of the spectrum of pollutants and particles associated with ambient sulfur dioxide. A number of acute air-pollution episodes in this century have been associated with increased mortality. Incidents in the Meuse Valley, Donora (Pennsylvania), London, and New York City have provided evidence that increased pollution has observable effects on human health (Greenfield, Attaway and Tyler, 1976). Retrospective studies of these events have demonstrated that deaths most often occurred among persons over 45 who were already suffering from chronic heart or lung disease; the effects of sulfur dioxide alone were not assessed. Lung-function measurements made daily on four normal subjects and two with bronchitis in London showed that daily variations in lung function were small and were related to respiratory infections (EPA, 1982). Concentrations of sulfur dioxide correlated with variations in peak flow rates and airway resistance. Increased sulfur dioxide pollution has been related to decreases in lung function (FEV1) in children. Several long-term epidemiologic studies of chronic effects have found that populations living in areas characterized by high concentrations of particulate matter and sulfur dioxide tend to have a higher prevalence of respiratory illness and decreased lung function than groups in areas with lower pollution. However, the influence of particles and other factors associated with ambient sulfur dioxide confounds interpretation (EPA, 1982).

In one occupational study, the frequency of chromosomal aberrations was significantly increased among workers at a sulfite pulp factory in Sweden (Nordenson et al., 1980). This increase was found to be associated mainly with exposure to sulfur dioxide (boiling of sulfite pulp and handling of sulfuric acid) and not with chlorine and dust in other workplaces in the factory.


Alarie et al. (1972) reported an accidental exposure of cynomologus monkeys to sulfur dioxide at an estimated 200-1,000 ppm for 1 h. No animals died, but a deterioration in pulmonary function persisted for the following 48 wk of the study. Histopathologic lesions included thickening of alveolar walls, hyperplasia of bronchial epithelium, and bronchiolar plugging with proteinaceous material, macrophages, and leukocytes.

A comprehensive review (Greenfield, Attaway and Tyler, 1976) of published literature on controlled animal exposures to sulfur dioxide may be summarized as follows: Acute exposure of animals results in diminished pulmonary function similar to that seen in man, decreased tracheal mucus clearance, pneumonia, and lesions of the nasomaxillary turbinates. Acute effects generally are transient at lower sulfur dioxide concentrations (20 ppm). In various species, the effects of exposures at over 100 ppm appear to be time-dependent and range from transient physiologic manifestations to death.

Transient adverse effects on pulmonary function have been demonstrated in rabbits exposed to sulfur dioxide at 200 ppm for 3 h (Davies et al., 1978). Rats exposed at 400 ppm died after 22 h of exposure (Asmundsson et al., 1973). Rats exposed at 567 ppm 6 h/d died after 12 d (Laskin et al., 1970). Adaptation apparently occurs if recovery between exposure periods is sufficient.

Subchronic exposure (less than 90 d) of animals to sulfur dioxide has been reviewed (Greenfield, Attaway and Tyler, 1976). Studies in which animals were exposed at concentrations below 10 ppm have demonstrated functional abnormalities that are reversible. Studies with subacute exposures at higher concentrations are lacking.

Chronic exposures (over 90 d) of a variety of species to sulfur dioxide at both low and high concentrations have been reported. The notable effects of exposure of dogs at 500 ppm 2 h/d for 3-5 mo include hypersecretion of mucus, goblet-cell hyperplasia, bronchial-gland hypertrophy, increase in pulmonary resistance, decrease in airway responsiveness to inhaled mediators, and decrease in tracheal mucus clearance (Drazen et al., 1982; Chakrin and Saunders, 1974; Greene et al., 1982; and Islam et al., 1977). Early exposure effects, such as ocular and mucous-membrane irritation, diminished with repeated exposure; that indicates the existence of an adaptation mechanism.

Sulfur dioxide is not generally considered to be carcinogenic. One study (Laskin et al., 1970) has demonstrated a higher incidence of squamous-cell carcinomas of the lung in rats that inhaled benzo[a]pyrene in combination with sulfur dioxide at 10 ppm than in rats that inhaled only benzo[a]pyrene. This does not show that sulfur dioxide is carcinogenic, but it does suggest that it may increase the carcinogenic activity of known carcinogens.

The embryotoxic and teratogenic potentials of sulfur dioxide have been evaluated in mice and rabbits (Murray et al., 1979). Exposure of mice at 25 ppm and of rabbits at 70 ppm for days 6-15 and days 6-18 of gestation, respectively, yielded no evidence of a teratogenic effect related to sulfur dioxide exposure; however, significant increases in the incidence of minor skeletal variants were observed in both species.


The penetration of sulfur dioxide to the lungs is greater during mouth breathing than during nose breathing. Sulfur dioxide is readily removed during passage through the upper respiratory tract. At concentrations higher than 1 ppm, removal is over 90% (Strandberg, 1964). Sulfur dioxide is converted to bisulfite ion (HSO3 ) on mixing with water. It has been shown that inhaled sulfuric acid mists with droplets of 0.4-1.1 μm in mass median aerodynamic diameter have deposition patterns similar to those of dry aerosols and that the effect of hygroscopicity is not dominant in determining the site of deposition (Dahl et al., 1983). Studies using [35S] sulfur dioxide have shown that inhaled sulfur dioxide is readily distributed throughout the body. Inhaled sulfur dioxide is only slowly removed from the lower respiratory tract. Radioactivity from inhaled labeled sulfur dioxide can be detected a week or more after inhalation and may be due to 35S binding with protein. Recent work has shown that [35S] sulfuric acid is cleared faster from smaller-diameter than from larger-diameter airways of dogs (A.R. Dahl et al., unpublished manuscript). In addition, species differences have been noted: clearance is slower in guinea pigs than in dogs and slower in dogs than in rats.


Much information is available on ambient sulfur dioxide concentrations, and the assay system is well standardized and reasonably accurate. Among the procedures used are acidimetry, colorimetry, electrochemistry, fluorimetry, flame photometry, and emission and absorption spectroscopy (Cheremisinoff and Morresi, 1981; Perry and Young, 1977). It is important to remember that sulfur dioxide is dynamically related to SO4 2− (sulfate). The rates of oxidation of sulfur dioxide to sulfuric acid and conversion to sulfate are greatly increased in polluted air (Rall, 1974). The atmospheric chemistry of these reactions is complex and not completely understood.


OSHA (1983) recommended a TWA limit of 2 ppm. ACGIH (1980, 1983) recommended a TLV-TWA of 2 ppm for an 8-h period and a STEL of 5 ppm for 15 min. The reduction of the TLV from 5 to 2 ppm was based on available data and, in the opinion of the ACGIH committee, effects reported below 2 ppm were not serious enough to justify a lower limit.


The Committee on Toxicology previously recommended EELs and CEL in 1966. After reviewing the current literature, the Committee recommended no changes in the EELs and CEL.

The present Committee's recommended EELs and CEL for sulfur dioxide and the limits proposed in 1966 are shown below.

10-min EEL30 ppm30 ppm
30-min EEL20 ppm20 ppm
60-min EEL10 ppm10 ppm
24-h EEL5 ppm5 ppm
90-d CEL1 ppm1 ppm


  • Alarie, Y., Ulrich, C.E., Busey, W.M., Krumm, A.A., and MacFarland, H.N. 1972. Long-term continuous exposure to sulfur dioxide in cynomolgus monkeys. Arch. Environ. Health 24:115-128. [PubMed: 4621425]
  • American Conference of Governmental Industrial Hygienists. 1980. Documentation of the Threshold Limit Values. 4th ed. Cincinnati, Ohio: American Conference of Governmental Industrial Hygienists. p.375-376.
  • American Conference of Governmental Industrial Hygienists. 1983. TLVs(R): Threshold Limit Values for Chemical Substances an Physical Agents in the Work Environment with Intended Changes for 1983-1984. Cincinnati, Ohio: American Conference of Governmental Hygienists. p. 93.
  • Asmundsson, T., Kilburn, K.H., and McKenzie, W.N. 1973. Injury and metaplasia of airway cells due to SO2. Lab. Invest. 29:41-53. [PubMed: 4728356]
  • Bates, D.V., and Hazucha, M. 1973. The short-term effects of ozone on the human lung. Proceedings of the Conference on Health Effects of Air Pollutants. National Academy of Sciences-National Research Council. Assembly of Life Sciences, October 3-5, 1973. Prepared for the Committee on Public Works, United States Senate. Serial No. 93-15. Washington, D.C. p.507-540.
  • Chakrin, L.W., and Saunders, L.Z. 1974. Experimental chronic bronchitis: Pathology in the dog. Lab. Invest. 30:145-154. [PubMed: 4817817]
  • Cheremisinoff, P.N., and Morresi, A.C. 1981. Air Pollution Sampling and Analysis Deskbook. Ann Arbor, MI: Ann Arbor Science Publishers, Inc. 490 p.
  • Dahl, A.R., Felicetti, S.A., and Muggenburg, B.A. 1983. Clearance of sulfuric acid-introduced 35S from the respiratory tracts of rats, guinea pigs and dogs following inhalation or instillation. Fundam. Appl. Toxicol. 3:293-297. [PubMed: 6628891]
  • Dahl, A.R., Snipes, M.B., Muggenburg, B.A., and Young, T.C. 1983. Deposition of sulfuric acid mists in the respiratory tract of beagle dogs. J. Toxicol. Environ. Health 11:141-149. [PubMed: 6827621]
  • Davies, A., Dixon, M., Penman, R., Widdicombe, J.G., and Wise, J.C.M. 1978. Effect of repeated exposures to high concentrations of sulphur dioxide on respiratory reflexes in rabbits. Bull. Eur. Physiopathol. Respir. 14:41-52. [PubMed: 752394]
  • Drazen, J.M., O'Cain, C.F., and Ingram, R.H., Jr. 1982. Experimental induction of chronic bronchitis in dogs: Effects on airway obstruction and responsiveness. Am. Rev. Respir. Dis. 126:75-79. [PubMed: 6953777]
  • Environmental Protection Agency. 1982. Review of the National Ambient Air Quality Standards for Sulfur Oxides: Assessment of Scientific and Technical Information. Report No. EPA-450/5-82-007. Research Triangle Park, NC: U.S. Environmental Protection Agency, Office of Air Quality and Program Standards. 225 p. [Available from National Technical Information Service, Springfield, Va., as PB84-102920.]
  • Gökemeijer, J.D., DeVries, K., and Orie, N.G. 1973. Response of the bronchial tree to chemical stimuli. Rev. Inst. Hyg. Mines 28:195-197. [PubMed: 4155121]
  • Greene, S.A., Wolff, R.K., Hahn, F.F., Mauderly, J.L., and Lundgren, D.L. 1982. Chronic bronchitis in dogs exposed to SO2 . In Inhalation Toxicology Research Institute Annual Report 1981-1982, Report no. LMF-102. Albuquerque, N.M.: Lovelace Biomedical and Environmental Research Institute. p.439-444.
  • Greenfield, Attaway and Tyler. 1976. Sulfur oxides: Current Status of Knowledge. FINAL REPORT. EPRI EA-316. Palo Alto, Calif.: Electric Power Research Institute. 155 p.
  • International Electric Research Exchange. 1981. Effects of SO2 and its Derivatives on Health and Ecology. Vols. 1 and 2. Palo Alto, CA: Electric Power Research Institute.
  • Islam, M.S., Oellig, W.-P., and Weller, W. 1977. Respiratory damage casued by long-term inhalation of high concentration of sulphur-dioxide in dogs. Res. Exp. Med. 171:211-218. [PubMed: 594496]
  • Kennon, B.R. 1927. Report of a case of injury to the skin and eyes by liquid sulphur dioxide. J. Ind. Hyg. 9:486-487.
  • Koenig, J.Q., Pierson, W.E., and Frank, R. 1980. Acute effects of inhaled SO2 plus NaCl droplet aerosol on pulmonary function in asthmatic adolescents. Environ. Res. 22:145-153. [PubMed: 7418673]
  • Koenig, J.Q., Pierson, W.E., Horike, M., and Frank, R. 1981. Effects of SO2 plus NaCl aerosol combined with moderate exercise on pulmonary function in asthmatic adolescents. Environ. Res. 25:340-348. [PubMed: 7274197]
  • Laskin, S., Kuschner, M., and Drew, R.T. 1970. Studies in pulmonary carcinogenesis. Pp. 321-350 in Hanna, M.G., Jr., editor; , Nettesheim, P., editor; , and Gilbert, J.R., editor. , eds. Inhalation Carcinogenesis. AEC Symposium Series 18. Oak Ridge: U.S. Atomic Energy Commission. Division of Technical Information.
  • Lawther, P.J., Macfarlane, A.J., Waller, R.E., and Brooks, A.G.F. 1975. Pulmonary function and sulphur dioxide, some preliminary findings. Environ. Res. 10:355-367. [PubMed: 1213017]
  • Murray, F.J., Schwetz, B.A., Crawford, A.A., Henck, J.W., Quast, J.F., and Staples, R.E. 1979. Embryotoxicity of inhaled sulfur dioxide and carbon monoxide in mice and rabbits. J. Environ. Sci. Health C13:233-250. [PubMed: 555466]
  • Nordenson, I., Beckman, G., Beckman, L., Rosenhall, L. and Stjernberg, N. 1980. Is exposure to sulphur dioxide clastogenic? Chromosomal aberrations among workers at a sulphite pulp factory. Hereditas 93:161-164. [PubMed: 7440236]
  • Occupational Safety and Health Administration. 1983. Toxic and Hazardous Substances. Air Contaminants. 29 CFR 1910.1000.
  • Perry, R., and Young, R.J. 1977. Handbook of Air Pollution Analysis. New York: John Wiley & Sons. Distributed in the U.S.A. by Halsted Press. 506 p.
  • Rall, D.P. 1974. Review of the health effects of sulfur oxides. Environ. Health Perspect. 8:97-121. [PMC free article: PMC1474939] [PubMed: 4470921]
  • Sheppard, D., Wong, W.S., Uehara, C.F., Nadel, J.A., and Boushey, H.A. 1980. Lower threshold and greater bronchomotor responsiveness of asthmatic subjects to sulfur dioxide. Am. Rev. Respir. Dis. 122:873-878. [PubMed: 7458061]
  • Sheppard, D., Saisho, A., Nadel, J.A., and Boushey, H.A. 1981. Exercise increases sulfur dioxide-induced bronchoconstriction in asthmatic subjects. Am. Rev. Respir. Dis. 123:486-491. [PubMed: 7235370]
  • Strandberg, L.G. 1964. SO2 absorption in the respiratory tract. Studies on the absorption in rabbit, its dependence on concentration and breathing phase. Arch. Environ. Health 9:160-166. [PubMed: 14155049]
  • Weir, F.W., and Bromberg, P.A. 1975. Effects of sulfur dioxide on healthy and peripheral airway impaired subjects. Recent Advances in the Assessment of the Health Effects of Environmental Pollution. Vol. IV: 1989-2000. EUR 5360. Luxembourg: Commission of the European Communities.
  • Woodford, D.M., Coutu, R.E., and Gaensler, E.A. 1979. Obstructive lung disease from acute sulfur dioxide exposure. Respiration 38:238-245. [PubMed: 523832]
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