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SCOEL concluded that primarily acute local effects on the respiratory tract should be prevented when establishing an occupational exposure limit. Therefore, the committee recommended adopting an occupational exposure limit for short-term exposure (STEL, 15 minutes). A STEL of 1.0 ppm (2.7 mg/m³) was proposed to limit peaks in exposure which could result in irritation.

Based on the weight of evidence from the large available database of findings in humans and animals it seems to be justified to use the STEL and the 8-hour TWA value for establishing acute/short-term and long-term DNEL values for local health effects, respectively, in healthy workers exposed to sulfur dioxide.

For asthmatics it is recommended to keep exposure at levels of 0.2 ppm sulfur dioxide (0.53 mg/m³) and below. This value will be established as a DNEL, local via inhalation for humans exposed via the environment, since this sub-population is considered more sensitive to the exposure towards sulfur dioxide, thus a higher level of protection is applicable.

 

TRGS 900 (2011):

The MAK Commission previously justified raising the maximum allowable concentration of sulfur dioxide and the derivation of the current DFG-MAC-value (0.5ppm) to 1 ppm as follows:

 

Considering the exposure situation in the Nowak study (1997), where hyperventilation was clearly accelerated to increase the penetration of SO2in the respiratory tract, and the low physical stress and thus less hyperventilation in two other studies (van Thriel et al. 2010 Raulf-Heimsoth et al. 2010) in healthy volunteers which documented exposure without adverse effect at 2 ppm, the AGW was provisionally set at 1 ppm. Since SO2is a locally acting irritant substance, it was assigned to the peak limit category I. The former exceedance factor of 1 was maintained due to the currently available limited data at moderate physical exertion.

 

Supplement 2013:

In the supplement of 2013, the MAC value was newly established at 2.7 mg/m³ (1 ppm) based on two studies with volunteers exposed to sulfur dioxide from 2010.

Additional information

Hazard identification - human data:

Sulfur dioxide irritates the eyes and the upper respiratory tract. Inhalation of high concentrations may cause rhinorrhae, coughing, shortness of breath, chest tightness, and choking sensation.

Epidemiological studies have associated chronic sulfur dioxide exposure with chronic coughing, bronchitis, increased susceptibility to airway infections, and increased susceptibility to allergy by airborne allergens. However, the evidence of these associations is weak, because a part of these studies showed limitations in study design and confounding factors were not sufficiently taken into account (lack of information on combined exposure with other toxic substances, smoking habits, and other personal lifestyle factors). Therefore, these studies are considered insufficient for quantitative risk assessment purposes.

A number of laboratory studies in healthy, non-smoking volunteers are available in which the toxic effects of sulfur dioxide on the upper and lower respiratory tract were investigated. The exposures ranged from 0.2 ppm to 25 ppm (0.53 to 67 mg/m³) sulfur dioxide and lasted from a few minutes up to a few hours, with or without physical evidence. The main adverse effects that have been observed were irritation of the upper respiratory tract and the eyes, and decreased lung function such as increased pulmonary airway resistance. These adverse effects were clearly present at exposure to concentrations of 1 ppm (2.7 mg/m³) or higher, but not at and below 0.75 ppm (2.0 mg/m³). Two studies showed no changes in lung function tests in volunteers exposed to 2.7 or 2.0 mg/m³ sulfur dioxide for 40 minutes or 4 hours, respectively, with moderate physical exercise. Three studies, which concern increased airway resistance or mild effects on the autonomic heart function near or below 2.0 mg/m³, are not considered suitable for risk assessment purposes because of limitations in study design or the little relevance of the findings. An inflammatory response in human lung was induced after exposure to concentrations of 4-5 ppm sulfur dioxide (10-13 mg/m³) and higher.

Based on these findings, a sulfur dioxide concentration of 0.75 ppm (2.0 mg/m³) can be derived as the NOAEC for short-term exposure of healthy subjects, whereas the sulfur dioxide concentration of 1.0 ppm (2.7 mg/m³) is considered as LOAEC.

Data obtained from epidemiological studies in the general population and from clinical studies indicate that people with asthma or with other diseases concerning the respiratory tract are more vulnerable to sulfur dioxide exposure than healthy people. For asthma, this finding is supported by animal data. The evidence from the studies indicates increased respiratory symptoms with peak (5-15 min) exposures to sulfur dioxide above 0.5 ppm (1.3 mg/m³) in asthmatic subjects.

Results from human clinical studies demonstrated decreases in lung function (e. g. decreased forced expiratory volume in 1 sec [FEV1] and increased specific airway resistance [sRaw]) following peak exposures to sulfur dioxide. These effects have clearly and consistently been shown among individuals with asthma. Asthmatics exhibited significant decrements in lung function following 5- to 15-min exposures to sulfur dioxide concentrations of as low as 0.5 ppm (1.3 mg/m³) while performing moderate levels of exercise. However, some sensitive asthmatics showed such significant decrements in lung function already at sulfur dioxide exposures of as low as 0.25 ppm (0.67 mg/m³) during moderate exercise. The effect of peak sulfur dioxide exposure on lung function has been shown to increase in magnitude with increasing concentrations above 0.5 ppm sulfur dioxide (1.3 mg/m³).

Numerous studies with asthmatics showed that the level of susceptibility is strongly influenced by a variety of non-exposure factors, such as by the presence of heart diseases or other lung diseases, (forced) physical activity, and atmospheric conditions (dry, cold air). All these factors may aggravate asthma. However, it is concerned that asthmatics are at higher risk when exposed to sulfur dioxide in combination with these non-specific asthma-aggravating factors.

 

In TRGS 900, the original justification for raising the maximum allowable concentration of sulfur dioxide and the derivation of the current DFG-MAC-value (0.5ppm) to 1 ppm was given as follows: Considering the exposure situation in the Nowak study (1997), where hyperventilation was clearly accelerated to increase the penetration of SO2in the respiratory tract, and the low physical stress and thus less hyperventilation in two other studies (van Thriel et al. 2010 Raulf-Heimsoth et al. 2010) in healthy volunteers documented exposure without adverse effect at 2 ppm of AGW is provisionally set at 1 ppm. Since SO2is a locally acting irritant substance, it is assigned to the peak limit category I. The former exceeding factor of 1 is maintained due to the currently available limited data at moderate physical exertion.

In a supplement from 2013, the MAK value was newly established at 2.7 mg/m³ (1 ppm) based on two studies with volunteers exposed to sulfur dioxide from 2010.

 

Conclusion - human data:

The Scientific Committee on Occupational Exposure Limits (SCOEL) updated its scientific evaluation of the data on the toxicity of sulfur dioxide, as published in December 2008 (SCOEL/SUM/27).

SCOEL recommended an occupational exposure limit of 0.5 ppm (1.3 mg/m³) sulfur dioxide (8-hour TWA). It was based on a LOAEC of 1.0 ppm (2.7 mg/m³) sulfur dioxide, at which functional changes were found in healthy adult volunteers. A short-term exposure limit (STEL, 15 minutes) of 1.0 ppm (2.7 mg/m³) was proposed to limit peaks in exposure which could result in irritation. It should be noted that the proposed values should afford protection to most individuals, but not for all those suffering from bronchial asthma or chronic bronchitis. For asthmatics it is recommended to keep exposure at levels of 0.2 ppm sulfur dioxide (0.53 mg/m³) and below.

An update on this assessment was published in 2011 (TRGS 900 and MAC Supplement) which proposed to raise the 8-hour TWA to 1 ppm considering the exposure situation in the Nowak study (1997), where hyperventilation was clearly accelerated to increase the penetration of SO2in the respiratory tract, and the low physical stress and thus less hyperventilation in two other studies (van Thriel et al. 2010 Raulf-Heimsoth et al. 2010) in healthy volunteers whichdocumented exposure without adverse effect at 2 ppm of AGW.

Based on the weight of evidence from the large available database of findings in humans and animals it seems to be justified to use the STEL (1.0ppm) and the 8 -hour TWA (1ppm) value for establishing acute/short-term and long-term DNEL values for local health effects, respectively, in healthy workers exposed to sulfur dioxide.

The proposed value of 0.2 ppm for asthmatics will be established as a DNEL, local via inhalation for humans exposed via the environment, since this sub-population is considered more sensitive to the exposure towards sulfur dioxide, thus a higher level of protection is applicable.