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SULFUR DIOXIDE

OSHA comments from the January 19, 1989 Final Rule on Air Contaminants Project extracted from 54FR2332 et. seq. This rule was remanded by the U.S. Circuit Court of Appeals and the limits are not currently in force.

CAS: 7446-09-5; Chemical formula: SO2

OSHA's former limit for sulfur dioxide (SO2) was 5 ppm as an 8-hour TWA. The Agency proposed to revise this limit to 2 ppm as an 8-hour TWA and to supplement this limit with a 15-minute STEL of 5 ppm. Although NIOSH recommends a limit of 0.5 ppm for sulfur dioxide, NIOSH did concur (Ex. 8-47, Table N1) with the proposed limits. The ACGIH has a TLV-TWA of 2 ppm and a TLV-STEL of 5 ppm. In the final rule, OSHA is establishing a 2-ppm 8-hour TWA and a 5-ppm 15-minute STEL for SO2. Sulfur dioxide is a colorless, nonflammable gas or liquid with a suffocating odor.

OSHA has studied the effects of occupational exposure to SO2 for several years. The Agency's 5-ppm limit for this substance was established in 1971 on the basis of the 1968 ACGIH TLV-TWA. In 1975, OSHA proposed to revise this limit downward to 2 ppm and held public hearings to gather information on industrial exposures to SO2. In response to shifting priorities within the Agency, OSHA did not promulgate a final standard at that time. The following discussion summarizes the record evidence relevant to SO2 both from the earlier (1975-1976) record and from the record of the present rulemaking.

Workplace exposure to sulfur dioxide causes both acute and chronic effects. The chronic effects of exposure include permanent pulmonary impairment, which is caused by repeated episodes of bronchoconstriction. A number of human and animal studies demonstrate this effect (Skalpe 1964/Ex. 1-438; Smith, Peters, Reading, and Castle 1977/Ex. 1-805; Archer and Gillam 1978/Ex. 1-711; Ministry of Health (Canada) 1976/Ex. 1-1208; Lewis, Campbell, and Vaughan 1969, as cited in ACGIH 1986/Ex. 1-3, p. 542).

Kehoe, Machle, Kitzmiller, and LeBlanc (1932/Ex. 1-339) studied two groups of male refrigeration workers with long-term (average of four years) exposures to average SO2 concentrations of 20 to 30 ppm, with a range of exposures from 10 to 70 ppm. These workers were believed to have been exposed prior to 1927 to SO2 levels considerably higher and averaging from 80 to 100 ppm. This study showed that SO2 exposure caused an increased incidence of nasopharyngitis, shortness of breath on exertion (dyspnea), and chronic fatigue (Kehoe, Machle, Kitzmiller, and LeBlanc 1932/Ex. 1-339).

In a study of Norwegian paperpulp mill workers, Skalpe (1964/Ex. 1-438) reported that average SO2 concentrations were believed to range from 2 to 36 ppm. Results showed a significantly higher frequency of respiratory disease symptoms, including coughing, expectoration, and dyspnea, among workers less than 50 years of age (i.e., those with the shortest exposure). Workers older than 50, however, did not display symptomatology different from that of controls.

More recently, Smith, Peters, Reading, and Castle (1977/Ex. 1-805) studied a group of smelter workers exposed, on average, to less than 2 ppm SO2 but concurrently exposed to respirable particulate at levels generally less than 2 mg/m3. These workers showed a decrement in forced vital capacity (FVC) and forced expiratory volume (FEV1) of 4.8 percent when compared with controls. These authors concluded that workers exposed to SO2 levels above 1 ppm had an accelerated loss of pulmonary function. This study has been criticized on the grounds that the control population itself may have been exposed to respiratory toxins and that other contaminants, such as iron sulfites, may have contributed to the pulmonary decrement seen in these smelter workers. On average, 60 percent more of the workers exposed to greater than 1 ppm SO2 reported symptoms of chronic cough than did workers who were exposed to SO2 at a concentration below 1 ppm. The prevalence of chronic sputum production was elevated for workers who had never smoked and who were exposed above 1 ppm.

Archer and Gillam (1978/Ex. 1-711) studied workers at the same smelter facility and obtained results similar to those of Smith, Peters, Reading, and Castle (1977/Ex. 1-805). Significant reductions in FVC and FEV1 were found to be associated with chronic exposures to 0.4 to 3 ppm SO2 (TWA) with concomitant exposure to particulate. These authors also found a corresponding increase in some symptoms of respiratory disease (chronic bronchitis) that was not attributable to smoking. Tomono and coworkers (1961, as cited in ACGIH 1986/Ex. 1-3, p. 542) found that 1.6 ppm was the lowest concentration that produced bronchoconstriction in 46 healthy male subjects.

OSHA's June 7, 1988 proposal also discussed the basis for NIOSH's recommendation of a 0.5 ppm 8-hour TWA limit for SO2. In addition to the studies by Archer and Gillam (1977/Ex. 1-711) and Smith, Peters, Reading, and Castle (1977/Ex. 1-805) described above, NIOSH relied on a third study (Ministry of Health (Canada) 1976/Ex. 1-1208) of smelter workers exposed to SO2 levels of 2.5 ppm for 10 or more years, which showed an increased incidence of respiratory disease in these workers. A fourth study cited by NIOSH (NIOSH 1977m, as cited in ACGIH 1986/Ex. 1-3, p. 542) reported that 10,000 workers exposed to SO 2 at levels of 0.35 ppm showed no adverse exposure-related effects.

Alarie and co-workers (1970 and 1972, as cited in ACGIH 1986/Ex. 1-3, p. 542) found that guinea pigs exposed to SO2 by inhalation showed no decrement in pulmonary function at SO2 levels of 5 ppm; monkeys exposed to 1.3 ppm for 78 weeks also showed no deficit (Alarie, Ulrich, Busey et al. 1970 and 1972, both as cited in ACGIH 1986/Ex. 1-3, p. 542). However, in another study, dogs exposed continuously to 5 ppm for 225 days showed increased pulmonary flow resistance and a decrease in lung compliance (Lewis, Campbell, and Vaughan 1969, as cited in ACGIH 1986/Ex. 1-3, p. 542). In addition, rats exposed to 10 ppm SO2 daily for six weeks developed a thickening of the mucous layer that interfered with effective particle clearance (Dalhamn 1956, as cited in ACGIH 1986/Ex. 1-3, p. 542).

The acute effects of SO2 exposure have been recognized for years in industrial settings; symptoms of acute overexposure include upper respiratory tract irritation, rhinorrhea, choking, and coughing. These symptoms are so disagreeable that most persons will not tolerate exposure for longer than 15 minutes. Within 5 to 15 minutes of the onset of exposure, workers develop temporary reflex bronchoconstriction and increased airway resistance. Short-term exposure causes measurable bronchoconstriction (Frank, Amdur, Worcester, and Whittenburger 1962, as cited in ACGIH 1986/Ex. 1-3, p. 542; Weir, Stevens, and Bromberg 1972/Ex. 1-401); the ACGIH (1986/Ex. 1-3, p. 542) reports that this bronchoconstriction is dose-related and is manifested as an increase in pulmonary flow resistance.

Efforts have been made to quantify the acute no-adverse-effect level for SO2-induced increased airway resistance. Frank, Amdur, Worcester, and Whittenberger (1962, as cited in ACGIH 1986/Ex. 1-3, p. 542) reported that, at SO2 concentrations of 1 ppm, one in 11 healthy subjects developed pulmonary flow resistance; at concentrations of 5 or 13 ppm, there was a 39-and 72-percent increase, respectively, in such resistance. Weir, Stevens, and Bromberg (1972/Ex. 1-401) noted a statistically significant but reversible increase in small-airway resistance and a decrease in lung compliance at a concentration of 3 ppm; however, Burton et al. (1969) reported no effects, even among smokers, at a level of 2.1 ppm.

N.R. Frank, Professor of Medicine at the University of Washington State, commented during the 1977 hearing (NIOSH 1977m) that sulfur dioxide may not by itself be hazardous to the lungs but that an aerosol of sulfur dioxide and water or SO2 oxidized to sulfate particulate may increase the toxic potential of SO2 (Ex. 40, Docket H-039). Dr. Frank also presented evidence showing that a single short-term exposure to very high SO2 levels (200 to 1000 ppm) can produce lung damage (Ex. 40, Docket H-039).

In the current generic rulemaking, participants such as the American Iron and Steel Institute (AISI) (Exs. 3-1123 and 188) and the Corn Refiners Association (Exs. 8-65 and 177) raised issues similar to those raised during OSHA's 1977 rulemaking on SO2. These included:

- Lack of evidence that long-term exposure to SO2 causes chronic respiratory disease; and

- The potentiation of SO2's adverse effects by the formation of sulfates or higher sulfur oxides from interactions between SO2 and water or SO2 and particulate matter.

Regarding the first point, the Corn Refiners Association (CRA) referred OSHA to studies and testimony on the effects of SO2 exposure on employees in corn wet-milling from the earlier rulemaking (Ex. 66, Docket H-039). The CRA reported that the chronic respiratory disease and pulmonary impairment seen in SO2-exposed smelter workers did not occur in corn milling plant employees (Ex. 66-1, Docket H-039). The CRA sponsored a study performed by Drs. Ferris and Essex from the Harvard School of Public Health (Ex. 66-3, Docket H-039). Fifty corn wet-milling workers involved in the early, SO2-using stage of the wet-milling process were studied. Exposures (8-hour TWAs) in this group ranged from 0.5 to more than 5 ppm SO2, particulates ranged from 0.0 to 0.17 mg/m3, and water-soluble sulfates ranged from 0.0 to 40.0 mg/m3. Results of this study showed that, at levels of about 3 ppm SO2, acute symptoms such as coughing developed, but chronic, irreversible symptoms were not seen at exposure levels below 5 ppm (Ex. 66-1, Docket H-039). These authors concluded:

Taken as a whole, the results suggest that no significant chronic
respiratory impairments occurred at exposure levels under 5 ppm. The
lack of association between the most serious symptoms of respiratory
disease and exposure levels below 5 ppm also suggests that the
atmosphere in question is quite distinct from that found in the copper
smelter studies (Ex. 66-3, Docket H-039).

In addition, the studies by Smith, Peters, Reading, and Castle (1977/Ex. 1-373) and Archer and Gillam (1978/Ex. 1-711) were criticized in OSHA's earlier rulemaking for not taking into consideration the impact on the studied workers' health of the higher SO2 levels to which these employees had been exposed in prior years. Arthur D. Little, Inc. (Ex. 95, Docket H-044) also criticized these studies, noting that their observation periods were too short to derive reliable data on chronic effects.

These criticisms and the lack of chronic effects observed in animals at levels below 5 ppm (Alarie, Ulrich, Busey et al. 1970 and 1972, as cited in ACGIH 1986/Ex. 1-3, p. 542) caused commenters to question whether chronic lung disease results from long-term exposure to SO2 below the current 5-ppm PEL. Dr. Alarie appeared at the 1977 hearing and testified on animal studies conducted by him and others on sulfur dioxide (NIOSH 1977m, as cited in ACGIH 1986/Ex. 1-3, p. 542). He testified that, in his opinion, the long-term studies in animals support the establishment of a ceiling value for SO2 but do not indicate that benefits would be gained by reducing the time-weighted average from 5 to 2 ppm. OSHA agrees with Dr. Alarie that a STEL is necessary to minimize high short-term exposures to SO2; however, OSHA does not agree that no effects have been seen in animals at levels at or below 5 ppm. For example, Lewis, Campbell, and Vaughan (1969, as cited in ACGIH 1986/Ex. 1-3, p. 542) showed that beagles exposed to 5 ppm SO2 exhibited decreased dynamic compliance and increased flow resistance. In addition, NIOSH (1974b/Ex. 1-235) has reported:

[M]an is considered to be more sensitive than other mammals to the
effects of sulfur dioxide in ranges commonly employed
experimentally...(Ex. 1-235).

It is therefore not surprising that humans have also been shown to develop respiratory effects, including bronchoconstriction, coughing, and sputum production, at levels below 5 ppm (Smith, Peters, Reading, and Castle 1977/Ex. 1-805; Archer and Gillam 1978/Ex. 1-711; Frank, Amdur, Worcester, and Whittenburger 1962, as cited in ACGIH 1986/Ex. 1-3, p. 542; Weir, Stevens, and Bromburg 1972/Ex. 1-401).

Many rulemaking participants (Exs. 3-1123, 8-57, 86, 86A, 117, 177, and 188) were of the opinion that the lack of chronic effects demonstrated that exposure to SO2 did not cause material impairment of health at levels below 5 ppm. For example, the Edison Electric Institute (EEI) (Ex. 133) criticized the Ferris et al. (1967/Ex. 1-316) study as being too old to be relevant. According to the EEI, the finding that the control group in the Ferris et al. (1967/Ex. 1-316) study also had an elevated incidence of disease and that there was no statistically significant difference in the extent of the respiratory disease incidence between the controls and the SO2-exposed group invalidates this study's finding of a serious pulmonary effect in the SO2-exposed workers. OSHA does not agree with this interpretation of the Ferris et al. (1967/Ex. 1-316) study. OSHA believes that a more accurate interpretation of the results of this study would be that both groups of workers were occupationally exposed to respiratory toxins; this is a very likely occupational scenario because the SO2-exposed workers in this study were pulpmill workers, while those in the control group worked in a papermill, an occupational environment also recognized as hazardous.

Taken together, the evidence from all of the studies described in this subsection clearly shows that exposure to SO2 below 5 ppm does cause respiratory symptoms, including repeated episodes of bronchoconstriction. The studies by Smith, Peters, Reading, and Castle (1977/Ex. 1-373), Archer and Gillam (1978/Ex. 1-711), and Frank, Amdur, Worcester, and Whittenberger (1962, as cited in ACGIH 1986/Ex. 1-3, p. 542) consistently demonstrate that persons exposed to concentrations of SO2 below 5 ppm have an accelerated loss of pulmonary function and exhibit adverse pulmonary symptoms.

OSHA believes that these effects constitute material impairments of health and are significant. In addition, OSHA does not agree that these studies demonstrate the absence of chronic effects at low SO2 exposure levels; long-term exposure to SO2 has produced pulmonary function changes in dogs, and daily exposures of rats to 10 ppm (only twice the former PEL) for six weeks produced a thickened mucous layer and reduced the effectiveness of particle clearance from the trachea (Dalhamn 1956, as cited in ACGIH 1986/Ex. 1-3, p. 542).

The second point raised by commenters concerned the formation of other toxic and irritating products from the interaction between SO2 and water or between SO2 and particles. Some of the participants in the earlier rulemaking, such as Dr. Colucci of the Corn Refiners Association, testified that it would be more protective to identify and limit exposure to each of these by-products, rather than to regulate SO2 alone. OSHA disagrees with this approach; since these products are all formed from sulfur dioxide, limiting exposure to SO2 will concurrently limit exposure to these SO2 by-products. This approach is more straightforward and easier to implement than attempting to identify the myriad decay products that may be formed in different industrial settings. Furthermore, the studies discussed above clearly establish a relationship between airborne SO2 levels and adverse effects; no quantitative relationship on which to base a PEL has been established for the decay products of SO2 reactions. Therefore, to reduce the significant risk of respiratory symptoms among exposed workers, OSHA finds that limiting exposure to SO2 will be effective.

After considering all of the relevant evidence from both the 1977 and the present dockets, OSHA concludes that a TWA of 2 ppm and a STEL of 5 ppm are necessary to reduce the significant risk of adverse respiratory effects that have been demonstrated to occur in workers exposed to SO2 above these levels. Accordingly, OSHA is establishing these limits in the final rule. The Agency finds that the coughing, increase in sputum production, and bronchoconstriction observed in workers exposed to SO2 at the levels permitted by the former limit constitute material impairments of health and functional capacity, and must be protected against. This discussion is also a final statement of reasons for the 1977 rulemaking.

Some evidence has been submitted by the steel and nonferrous metal industries that the STEL cannot be regularly achieved with engineering and work-practice controls in specific operations in SIC 33. These involve furnace areas in nonferrous metal smelters, blast furnace operations, and the sulfur plant. There is no evidence to the contrary in the record. See the further discussion in the Feasibility section.

OSHA will, therefore, permit more flexibility in the use of respirators for these operations. The burden of proof will not be on employers to demonstrate that compliance with engineering and work-practice controls are infeasible in a compliance action for these operations in SIC 33 as related to meeting the requirements of the STEL.

There may be a few other operations in this category, and for the TWA, where the record is unclear for SIC 33. Based on an appropriate showing pursuant to the OSH Act, OSHA would favorably consider requests for variances for specific operations in Sector 33 on methods of compliance for the STEL and for the TWA. Of course, all requests for variances or any matters will be considered based on their merits.

 

 
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