Executive Summary

Introduction

Ground-level Ozone

Particulate Matter in Air

Conclusions

References

National Ambient Air Quality Standards : proposed decisions on particulate matter and ozone

Ground-level Ozone

• Current Canadian Ground-Level Ozone Objectives
• Current Canadian Air Quality
• Ground-Level Ozone: The Science

Current Canadian Ground-Level Ozone Objectives

The current air quality objective for ozone was established in 1976 under Canada's Clean Air Act of 1973 and confirmed in 1989 under the 1988 Canadian Environmental Protection Act (CEPA). Based on the scientific information available at the time, the Canadian national objective for ozone was set at 82 ppb 1-hour. This objective is 50% more stringent than the existing U.S. standard of 120 ppb 1-hour and about 25% more stringent than the proposal being made by the EPA for a 80 ppb 8-hour standard. Only the level of 70 ppb 8-hour being considered by the EPA is close to the existing Canadian objective for ozone.

Current Canadian ambient air quality objective and standards for ground-level ozone are illustrated in TABLE 1 and compared with the U.S. NAAQS proposal.

TABLE 1: Ambient Ozone Standards and Objectives in Canada and United States

Current Canadian Air Quality

Three regions in Canada regularly experience ground-level ozone levels in excess of Canada's 1 hour ambient air quality objective of 82 ppb: the Lower Fraser Valley in British Columbia, the Windsor-Québec City Corridor in Ontario and Québec and the Southern Atlantic Region which includes New Brunswick and Nova Scotia.

Contributions to Canadian ozone formation by U.S. sources is an important factor in the Windsor-Québec City Corridor and the Southern Atlantic Region.

The following map showing the distribution of ozone exceedences in Canadian cities from 1987 to 1992 demonstrates clearly the nature of the ground-level ozone problem in Canada.

Follow this link to obtain a larger image. Use your browser's "back" button to return to this page.

In 1991, the Canadian Council of Ministers of the Environment (CCME) agreed to a three phase N0x/VOC Management Plan to put control strategies in place to enable all parts of the country to meet the 82 ppb objective. The second phase of the Plan is being developed by federal and provincial governments for presentation to Canadian Governments in the Fall, 1997.

A comprehensive science assessment to support the development of the second phase management program is nearing completion. The science assessment is comprised of seven scientific reports and a summary for policy makers that delivers key science results to the policy community.

The science reports include a review of the current ozone objectives based on health and vegetation effects, analysis of ambient ground-level ozone and its precursors, monitoring guidelines and implementation, emissions inventories, modelling of ground-level ozone in the Windsor-Québec City Corridor and in the Southern Atlantic Region, and modelling of ground-level ozone in the Lower Fraser Valley of the British Columbia.

The NOx/VOC Science Assessment reports will be published by May, 1997.

Ground-Level Ozone: The Science

The NOx/VOC Science Assessment Health Objectives report reviews the current ozone objectives in Canada based on health and vegetation effects. The scientific evidence has led to the following clear conclusions regarding the health impact of ozone.

1. There is clear evidence of associations between daily variations in ozone at ambient concentrations commonly encountered in Canada and acute adverse health effects. These effects range from small lung function changes, increases in symptoms of respiratory discomfort, increases in medication use, increased doctor's and hospital Emergency Department visits, through to increased hospitalizations. The evidence is less clear that there is an association between ozone and increases in mortality.
2. In terms of human health, a "safe" level on which to base an objective cannot be distinguished. The concentration-response relationship observed in the epidemiological studies provided no evidence of a threshold, monotonically increasing from an ozone concentration as low as 20 ppb up to 95 ppb.
3. The vast majority (>95%) of the Canadian population was exposed at least once during 1988 - the year studied, to 1-h daily maximum ozone levels above 50 ppb in a range associated with adverse health effects in the epidemiological studies. It is clear that these ozone-associated increases in adverse effects are occurring below the current 1-hour Canadian National Ambient Air Quality Objective of 82 ppb (roughly equivalent to 70 ppb 8-hour which is 10 ppb lower than the NAAQS proposals). The mean and 95th percentile of the 1-hr daily maximum, averaged over an 11 year period from April to September in the 16-city Canadian study, were 39 and 70 ppb, respectively. Summertime 1-hr maximum ozone levels have been recorded in Canada up to 213 ppb.
4. The controlled human chamber/clinical studies provide a plausible link between exposure to ozone at known concentrations and the adverse health effects on the respiratory system observed in the epidemiological studies. The dose-response was similar, with both the frequency and intensity of response increasing monotonically as both ozone concentration and ventilation rate increased, thus increasing the delivered dose.
5. In considering the question of "who is at risk", the clinical studies do provide evidence that normal individuals who are very actively exercising outdoors in summer constitute a susceptible group, due to increased ventilation rates, and thus to increased doses of ozone to the target tissues of the respiratory tract. Children are expected to be more susceptible by reason of their high activity levels during play, and greater outdoor exposure at times during the day when ozone concentrations are at the peak.
6. There is some evidence that asthmatics and "hyper-responder" (atopic and non-atopic), when under stress of exercise constitute another group more susceptible than the normal population, though this has been difficult to establish because of the lack of available studies on moderate or severe cases. This group has been shown in a few studies to have lower baseline lung function, and possibly to react somewhat more strongly to ozone than normal, the net effect being to reduce lung function considerably below normal values.
7. The clinical results for asthmatics, combined with the epidemiological evidence of hospitalizations, emergency room visits and reduced activity days, suggest the likelihood that the population which is compromised by pre-existing respiratory and lower baseline respiratory function is the one most susceptible to exacerbation of effects by ozone. This helps to explain the findings from the population-based epidemiology studies of a quasi-linear concentration response curve and supports this circumstantial evidence that ozone is acting on a subpopulation within the whole.
8. A principal question for consideration is whether the associations observed between adverse respiratory effects and environmental ozone is causal. Associations were consistently observed in studies which carefully controlled for underlying cyclic variation in health endpoints and in pollutant variables. The coherence of effects seen in all the studies including the epidemiological studies on hospitalizations, field study results, and even mortality, and the controlled chamber/clinical studies, also lend support to an assumption of causality.
9. Strong evidence for the biological plausibility of the hypothesis of a causal relationship between ozone and adverse respiratory health effects is obtained from the findings from the animal toxicology studies, supported by clinical studies, of a strong inflammatory response mechanism resulting from ozone exposure. This is also known to occur in asthmatic individuals, who have been shown to be at increased risk of hospitalizations and other adverse health effects due to exposure to ozone.