Human Health Risk Assessment for Sulphur Dioxide: Executive Summary

Human Health Assessment

Based upon the US EPA Integrated Science Assessment for Sulfur Oxides – Health Criteria (US EPA, 2008) and an evaluation of the toxicology, controlled human exposure, epidemiology and mode of action/mechanistic literature since 2007, as well as the guidance on causal determinations, it has been concluded that the evidence supports a causal relationship between short-term exposure to ambient levels of SO₂ and respiratory morbidity in adults, particularly in the asthmatic subpopulation. Similarly, the literature is suggestive of a causal relationship between short-term exposure to ambient levels of SO₂ and respiratory morbidity in children. The epidemiology papers on respiratory morbidity support effects on lung function after short-term exposures to concentrations below the short-term maximum concentration identified in the NAPS data, suggesting a potential risk to the Canadian population. The effects of co-pollutants and confounding factors cannot be fully ruled out in epidemiology studies; therefore, the lowest observed adverse effect concentration (LOAEC) for lung function decrements, from controlled human exposure studies of asthmatics exposed to SO₂ for 5–10 min at increased ventilation, was used to derive a reference concentration (RfC). Individuals in the controlled human exposure studies were found to react at a level that was below the maximum measured ambient concentration for the 10-min averaging time, which suggests that there is a potential risk to the Canadian population at current exposure levels.

The available information is suggestive of a causal relationship between short-term SO₂ exposures and all-cause and cardiopulmonary mortality at current ambient exposure concentrations, particularly in people over 40 years of age (most strongly associated with the over 65 age group). However, some inconsistency in this database and confounding of the signal in these studies is possibly indicative of SO₂ acting as a surrogate for certain sources (e.g. coal fired power plants) or reflecting effects after conversion to a particulate form.

The literature is weakly suggestive of a causal relationship with preterm birth and congenital heart malformation in babies exposed to SO₂ in utero. The epidemiology data on reproductive and developmental endpoints identified risks of congenital malformations and preterm delivery after SO₂ exposures during gestation at concentrations below the ambient annual maximum concentration identified in the NAPS data, suggesting a potential risk to the Canadian population at current exposure levels. However, even moreso than the case above, SO₂ may be acting in these studies as a surrogate for source or other pollutant(s) with which it is correlated.

The databases were found to be inadequate to infer a causal relationship for other endpoints, including mortality and respiratory morbidity with long-term exposures, cardiovascular morbidity with short- or long-term exposures, carcinogenicity and low birth weights.

It should be noted that there are a number of issues related to interpretation of the epidemiology literature. Most importantly, it remains difficult to determine the role of confounding co-pollutants such as PM_2.5 and PM₁₀ on the effects being reported. Therefore, it is important to consider data from controlled human exposure studies, which are available for respiratory morbidity, in conjunction with the epidemiology literature. Additional lines of evidence are also considered to support the epidemiology findings, including evidence for potential mechanisms or modes of action and personal exposure analyses for systemic effects.

A 10-min RfC of 67 ppb was derived from the controlled human exposure studies for respiratory morbidity and uncertainties, including intraspecies variability.

Public Health Impacts

Although the magnitudes of the risks of health effects associated in the epidemiology, with respect to SO₂ exposures, are relatively small, they represent important impacts on public health due to the number of people potentially affected. The subpopulations that appear to have increased susceptibility to adverse effects from SO₂ exposure represent a considerable proportion of the population, with asthmatics and the elderly alone accounting for 8.9% and 14.8% of Canadians, respectively (Statistics Canada, 2011; Asthma Society of Canada, 2012).

Similarly, with respect to the amount of SO₂-related mortality, Judek et al. (2004) estimated that 8% of total non-accidental mortality in Canadian urban census divisions between 1998 and 2000 was due to air pollution (described by a multi-pollutant model of PM, ozone, nitrogen dioxide, SO₂ and carbon monoxide), and that most of this was due to long-term exposure to ambient fine PM, which has a strong signal correlation to SO₂.

While there is currently insufficient information to relate SO₂ to specific reproductive effects, the lifelong implications of pre-term birth and various congenital issues indicates that this is an area in need of more attention.

Conclusions and Recommendations

In conclusion, the human health assessment has identified potential health risks to the Canadian population from exposures to ambient concentrations of SO₂, which are below the current National Ambient Air Quality Objectives. It is therefore recommended that the current National Ambient Air Quality Objectives be revised or new Ambient Air Quality Objectives or Standards be introduced with consideration of the following:

• The strongest evidence of causality was between short-term SO₂ exposures and respiratory morbidity, based largely on the 5-10 minute controlled human exposure studies.  A 10-min human health RfC of 67 ppb has been identified in the assessment.
• The more recent literature also adds to the weight of evidence for a "suggestive of causal" relationship between non-accidental and cardiopulmonary mortality risks and short-term exposures to SO₂.
• Additional endpoints (reproductive/developmental) have been identified based on the more recent literature. Although these endpoints have also been designated as having a weakly "suggestive of causal" relationship with SO₂ exposures, the database is limited.
• Intermittent spikes in exposures are linked to respiratory morbidity and are suspected for most other endpoints, including reproductive/developmental. Current Canadian monitoring data support that Canadians are likely to be exposed to intermittent spikes in concentrations. Mechanistic and personal exposure modeling also support intermittent spikes in exposure as being relevant to the health effects observed.
• There is "inadequate evidence to infer a causal relationship" between long-term exposures of SO₂ and health effects.

References

• Asthma Society of Canada. 2012. About Asthma.
• Chen TM, Shofer S, Gokhale J, and Kuschner WG. 2007. Outdoor air pollution: overview and historical perspective. Am J Med Sci 333:230–34.
• Environment Canada. 2011. National Air Pollution Surveillance Program (NAPS)
• Government of Canada. 2012. Canadian smog science assessment. Highlights and key messages.
• Judek S, Jessiman B, and Stieb D. 2004. Estimated number of excess deaths in Canada due to air pollution. Unpublished document dated August 30, 2004, from Air Health Effects Assessment Division, Health Canada.
• Statistics Canada. 2011. Canadian Census Data. 2011.
• US EPA. 2008. Integrated Science Assessment for Sulphur Oxides – Health Criteria.