Human Health Risk Assessment for Sulphur Dioxide: Executive Summary

The Air Quality Assessment Section of Health Canada undertook a health risk assessment of sulphur dioxide (SO2) in order to update the available information on adverse effects of SO2 to human health, determine recent Canadian SO2 exposure levels, and to inform the revision or development of Canadian ambient air quality objectives/standards.


The existing National Ambient Air Quality Objectives (NAAQOs) for SO2 were published in the Canada Gazette, Part I, in 1989.

Since that time a large number of publications relevant to potential human health effects of SO2 have become available.  Additionally, exposures have changed with total SO2 levels decreasing by 96% in Canada since 1970 (Environment Canada, 2011), largely as a result of the use of alternative (low-sulphur) fuels and pollution reduction programs that limited SO2 emissions (Chen et al., 2007).

Fine particles, including sulphate particles, were evaluated by Health Canada as part of the Canadian Smog Science Assessment document (Government of Canada, 2012). So, for the purposes of this current assessment, only gaseous SO2 was considered.

Environmental Concentrations of SO2 in Canada

National Air Pollution Surveillance (NAPS) data from the most recent year available (2011) were used to model Canadian exposures. NAPS data were analyzed on an all-monitor basis, as well as stratified by urban and rural designations.  Annual averages for SO2 ranged from below the detection limit to 8.6 ppb. The 24-h averages from urban residential sites ranged from below the detection limit to 56 ppb and the 1-h averages ranged from below the detection limit to 314 ppb.  The majority of NAPS monitors did not detect SO2 on a regular basis. Additional ambient monitoring during 2009–2011 by Airpointer monitors also indicated that SO2 levels are typically close to the limit of detection, but there are short-lived spikes in concentrations. Shorter-term averaging times were available from the Airpointer data (e.g. 30-min and 10-min) and reflect these spikes with a maximum 10-min value of 322 ppb for a site with a nearby industrial source.

Date published: 2016-02-12

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 PM2.5 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.


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