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Canadian Smog Science Assessment Highlights and Key Messages

Knowledge Gaps

The state of knowledge of smog science in Canada has greatly evolved over the last 10 years and is continuing to evolve. Knowledge gaps still remain, however, particularly with respect to the processing of emissions inventories, ambient monitoring, the understanding of some key smog formation processes, model sensitivity to all these factors, and the understanding of the dose-response relationships for ecosystem and human health impacts.

Sources and/or components--Ambient fine particulate matter (PM) concentrations continue to be largely characterized on a mass basis, even though it is known that the composition of PM varies between sources, regions and seasons. While to date there are indications that differential toxicity exists as a function of PM composition, nonetheless the evidence remains that PM of many types and from many sources exhibits toxicity, and at this point it is not possible to identify any component or source of PM as non-toxic.

Size fractions--Fine PM is currently the focus of regulatory programs, due to the preponderance of evidence and the depositional characteristics of this size fraction in the human lung. Evidence remains however that coarse particles 2.5–10 microns exert adverse effects. Although such effects of this larger size fraction are likely less than those seen in the 2.5 µm range, it is not clear if the risk management of PM2.5 accounts for PM10 related effects.

Of much greater potential importance are the health effects of ultra fine particles. Such particles are less than 0.1 µm in size, are highly reactive and, while accounting for relatively little mass, constitute a large number of particles and a large surface area (implying a corresponding potential for active chemistry). For these reasons, many in the health science community believe that a significant proportion of the health effects attributed to PM arise from ultra fine particles. However, this size range can be challenging to measure. Additionally, since they are not distributed uniformly over large areas, fixed ambient monitors are not useful in estimating population exposure, and cannot therefore be used in epidemiological investigations.

Exposure--While the ambient monitoring system has been shown to adequately represent population exposure for the purposes of conducting epidemiological studies, more precise understanding of exposure for individuals (especially within susceptible groups) is lacking. As well, as a better understanding of the toxicity of components and sources evolves, specific analysis will be needed to understand the dynamics of exposure to these sources/components.

Concentration-response relationship--The shape of the concentration-response function, including investigation of potential population threshold levels, has important implications for risk management and for estimates of risk from air pollution. Most of the available studies and analyses continue to report no clear threshold between ambient concentrations of PM2.5 or ozone (O3) and health endpoints such as premature mortality, hospital admissions and emergency department visits.

Role of co-pollutants--The extent to which other co-pollutants in ambient air may modify or contribute to the associations between ambient PM2.5 or O3 and morbidity or mortality continues to be important in the interpretation of the epidemiological findings.

Exposure durations of concern--Historically, most epidemiological research has investigated associations of health outcomes with ambient PM and O3 concentrations measured over 24 hours and several hours, respectively, with lags of up to 2 days. However, there are indications that some health outcomes are more strongly associated with shorter durations of exposure (e.g., one hour), and that risk estimates are often increased by using the average concentration over several days as the exposure metric rather than a single day lag, though the available data are limited.

At the other end of the temporal spectrum, there is only limited information on the effects of exposure to PM and O3 at longer time scales, including over entire seasons, years, or over multiple years.

Inflammation/oxidation and range of effects--While considerable knowledge has been developed concerning inflammation and oxidative stress caused by both PM and O3 the degree to which these mechanisms underlie the various observed effects, and the implications of these mechanisms for other health outcomes, is not entirely clear. Since these mechanisms play a role in most diseases, it is theoretically possible that these pollutants could be implicated in a much wider range of adverse effects than is currently accepted. Indeed, there are indications in the literature of effects of these pollutants beyond the respiratory and cardiac systems, with a number of reports of increases in risk of reproductive outcomes and specific diseases such as diabetes, and isolated reports of increases in more novel inflammatory diseases (e.g., appendicitis, inflammatory bowl disease).

Exacerbation versus disease development or progression--It is widely considered that ambient PM2.5 and O3 can exacerbate pre-existing diseases (e.g., asthma). However, the epidemiological associations with chronic exposure imply that these pollutants can also contribute to the development or progression of disease, and toxicological evidence demonstrates the mechanisms which could be involved. The relative impact of exacerbation of existing disease versus the development and progression of new disease has not been established, and could have enormous public health implications if these pollutants were linked to the development of prevalent diseases with serious health outcomes.

Susceptible populations--Improving our understanding of subpopulations that are more susceptible to the adverse effects of ambient PM and O3 is important to inform risk management to reduce public health risks from these pollutants. While persons with pre-existing cardiac and respiratory disease are recognized as susceptible populations, additional health conditions that may confer susceptibility to these pollutants continue to be identified. There are also important uncertainties with respect to the key windows of development during which PM and O3 may cause respiratory-related effects in children, another susceptible group of the population. Finally, animal and human studies continue to reveal the presence of specific genotypes that are more affected by these pollutants than the general population, and thereby provide additional information on susceptibility and on pathways and mechanisms of action.

While emissions inventories are constantly being refined, they generally do not adequately represent the actual emissions at any given time, particularly as levels of uncertainty can be high depending on sources and methods used for estimating emissions. In turn, there are often discrepancies between concentrations estimated from emissions inventory and ambient observations. In particular, there is room for improvement in the quantification of non-point sources such as dust emissions, PM2.5 and volatile organic compounds (VOC) species, ammonia (NH3) and spatially-allocated mobile emissions in major urban areas. The contribution of expanding emissions sectors (e.g., offshore oil and gas, marine transportation) is uncertain, as is the magnitude of impact of emissions from local industries and/or residential wood combustion on smaller communities and rural areas.

Although there are considerable observations available from monitoring and special field studies across Canada, there are areas where more measurements are needed. One of the pressing needs is for more measurement sites required to draw conclusions about the chemical composition and temporal trends of PM across the country, such as during winter smog events in Alberta and changes in visibility in high interest areas such as national parks. In addition, it is currently difficult to assess the baseline PM2.5 temporal trend due to insufficient long-term PM2.5 measurements at regionally representative sites.

While the spatial coverage of O3 monitoring sites is more extensive than other pollutants, there are still limitations particularly where spatial patterns are complex (i.e., over and near the Great Lakes, over the southern Atlantic region, and above the layer of air adjacent to the ground). There are insufficient O3 measurements in rural and remote areas that are potentially impacted by human activities such as downwind of Edmonton and Calgary and in the eastern parts of the Lower Fraser Valley. There are even greater limitations on the ability to characterize ambient levels of individual VOC species and NO2 due to gaps in the existing measurement network.

There is a lack of in-depth understanding of many PM and O3 processes and mechanisms as reductions in precursor emissions do not always translate into the anticipated reductions in ambient concentrations of PM2.5 and O3 (referred to as non-linearity in the processes). For example, reducing sulphur dioxide (SO2) emissions may in certain circumstances (e.g., in the presence of high concentrations of NH3) result in an increase in PM2.5 and as precursor emissions continue to decline in North America, the role of NH3 in PM2.5 formation may increasingly become more important. It is also often very difficult to predict ambient O3 concentrations due to the complexities of O3 formation associated with ambient VOC/NOX concentration ratios and varying reactivity of dominant VOC in an airshed.

Air quality model performance is greatly influenced by uncertainties in emissions inventories and the state of understanding of atmospheric physical and chemical processes. In general, there is less confidence in modelling secondary pollutants and predictions at finer spatial and temporal scales. Some of the key model inputs that need clarification include the understanding in the sources, characteristics and processes of various organic components of PM2.5. A major gap is also the effect of climate change on the formation of PM2.5 and O3 since climate change has the potential to affect conclusions from modelling analyses of the efficacy of proposed emissions regulations.

Finally, there are also important knowledge gaps in the understanding of the effects of PM and O3 on human and ecosystem health and how these affect the socio-economic welfare of Canadians. There is a lack of understanding in linking multi-pollutant concentrations (i.e., pollutants beyond PM2.5 and O3) and potential changes in toxicity to population exposure. Vegetation exposure-response functions, of the greatest use to regulators, are still in short supply in the published literature. There is a clear paucity of research available on the effects of PM and O3 on an ecosystem level, especially with the direct effects of exposure on wildlife species.