Source: www.oma.org/phealth/ground.htm This paper was prepared by Judith MacPhail, project manager and researcher, with direction and support from Dr. Ted Boadway, executive director, Ms. Carol Jacobson, director, and Ms. Patricia North, project officer of the Ontario Medical Association (OMA) Health Policy Department.
The OMA wishes to express its gratitude to many individuals and representatives of groups for their contributions and valued comments during the development of this position paper, notably:
This paper may be reproduced for use as an advocacy document providing authorship is acknowledged.
|TABLE OF CONTENTS|
|Executive Summary||1. Introduction|
|2. Background||3. Air Pollutants:
Their Sources and Distribution
|4. Adverse Health Impacts of air pollution:
|5. Summary Of Research Related Health Effects Of Air Pollution|
|6. Summary of Research Related Health-Care System Effects of Air Pollution||7. Recommendations|
Glossary of Terms
This review of the evidence focuses on research conducted in Ontario. Seven key Ontario studies are cited. These findings are highly significant for people living in the Great Lakes Basin (and particularly the Windsor-Quebec Corridor), where high levels of certain air pollutants (e.g., ground-level ozone and ultra-fine particles) occur more frequently than in other parts of Canada.
These pollutants come from a variety of sources, blanketing large areas, both urban and rural. The primary source of sulphur dioxide and sulphate pollutants is coal when it is burned to generate electricity. Coal-burning power plants also produce nitrogen oxides and particles. These pollutants are emitted from tall power plant smokestacks and can travel long distances with prevailing winds. (see "Glossary of Terms"). As these gaseous pollutants move through the atmosphere, they are exposed to water vapor and sunlight, and undergo chemical change to form acid aerosols, which are known respiratory irritants. Emissions of nitrogen oxides are also produced by engines such as those in cars and heavy-duty diesel vehicles. Whatever the source, nitrogen oxides can lead to the production of ground-level ozone (a primary component of smog). This is different from 'stratospheric' ozone, which protects us from the sun's harmful ultraviolet rays. Suspended particles (TSP, PM10) are also emitted from cement plants, mining operations, residential wood combustion and dust emissions from fields and roads. Approximately half of the volatile organic compounds (VOCs) are from natural sources such as trees, whereas gasoline accounts for over 40 per cent of human-made VOC emissions in Canada. Pollutants are produced by local emission sources, but trans-boundary transport from midwestern U.S. states contributes in a major way to ozone, particulate matter and acid aerosol levels in southern Ontario.
This issue is a serious one, requiring an integrated and comprehensive approach by many stakeholders, including the active involvement of organized medicine. It is important that the health effects of these air pollutants are understood. Government must act to reduce emission levels through statute and/or regulation bolstered by non-compliance penalties.
The purpose of this paper is to outline the position of the Ontario Medical Association (OMA) with regard to the adverse health effects of these air pollutants. The negative effects are particularly significant for children because they are exposed as they play out-of-doors.
Air quality is of great concern to Ontarians. There is strong evidence from new research on people living in Ontario that increases in certain air pollutants such as ground-level ozone, acid aerosols and particulate matter are linked to increases in hospitalization for respiratory and cardiac disease. The health effects ascribed to exposure to air pollution are diverse, ranging from subclinical effects to increased hospitalizations and premature mortality. Some effects are shown in Table l of the appendix. The more sensitive subgroups include the elderly and those with cardiac and respiratory diseases such as asthma, emphysema and chronic bronchitis. Children's exposure and risk to ambient air pollution can be greater than adults because they breathe faster and in summer spend more time being active outdoors.
The physicians of Ontario have long been involved in the promotion of public health, and have been concerned about air pollution for more than three decades. In 1967, the OMA Council endorsed a program of air pollution control for the province, which included the establishment of monitoring stations and regulation of emissions from industry and vehicular traffic. Later in 1967, the government enacted the Air Pollution Control Act, which embodied most of the recommendations found in the OMA's program .
The recommendations included in this report will, if acted upon, lead to a significant reduction in the overall burden of illness from these air pollutants, especially in children and the elderly. These recommendations have been selected from a review of recommendations made by various authorities, and are those which the OMA feels a particular responsibility to support.
Ontario's air quality has a mixed record. Over the past 24 years, improvement has been shown for a number of pollutants as a result of abatement programs designed to reduce emissions, and enforcement of regulations by government. However, annual average ground-level ozone levels in the Great Lakes Basin (or southern Ontario, Windsor-Quebec Corridor) have been consistently higher than the National Ambient Air Quality Objective of 15 parts per billion (ppb) for the past several years. In general, levels of particulates and sulphates in the basin have not declined. Provincial average nitrogen oxide concentrations remained relatively constant throughout the latter half of the 1980s, followed by a slight decrease in the 1990s. However, a principal concern is the restructuring of the electricity generation sector, and the potential increase in the use of coal to generate low-cost electricity. In Ontario, fossil fuel generating stations are major emitters of pollutants such as nitrogen oxides and particulate matter.
3. Great Lakes Health Effects Program - GLHEP. Outdoor air and your health: A summary of research related to the health effects of outdoor air pollution in the Great Lakes Basin. Air Quality Health Effects Research Section, Environmental Health Directorate, Health Canada; March 1996.
4. Ministry of Environment, Ontario. Air Quality in Ontario 1995. Pibs 3596e, November 1997
5. Institute for Environmental Studies - University of Toronto in partnership with Pollution Probe. Emissions from coal-fired electric utilities: Environmental Health Effects and Reduction Options. January 19, 1998.
For Ontarians living in a province known for its open spaces and fresh air activities, air quality is a very important concern. The West Central Region of the Ministry of Environment and Energy, Ontario (MOEE) alone logs about 500 air quality complaints annually and the issue receives frequent media coverage .
7. Regional Municipality of Hamilton-Wentworth - RMHW. Hamilton-Wentworth Air Quality Initiative Summary Report. October 1997.
The scope of physician involvement with air pollution is broad, ranging from issues arising in the care of the individual patient to population health concerns. Although individual physicians manage the burden of disease in the form of patient illness and death, the causes of health effects by air pollution should be addressed collectively by physicians.
The purpose of this paper is to outline the OMA's position regarding the adverse health effects of ground-level ozone, particulates and acid aerosols. It provides an overview of the health effects of these pollutants from current research in the field, and recommends a set of key remedial strategies for the OMA, individual physicians, and the public.
During the 1970s, much rethinking of the concepts of health, the environment and their relationship took place. The Lalonde Report was a landmark document which recognized that health had multiple determinants, including human biology (genetic and physiological characteristics such as changes in the human body due to maturation and aging), the environment (both social and physical dimensions) and lifestyle (such as the proportion of the population who use tobacco products). 'Determinants' are factors which are not health problems per se, but are believed to be related to the development of disease. Air quality is a key environmental determinant of health.
9. Shah CP. Public Health and Preventive Medicine in Canada, 3rd edition. Toronto; Printed by University of Toronto Press, 1994.
Smog is the term given to the chemical 'soup' that is produced by photochemical reactions between nitrogen oxides and volatile organic compounds on hot, humid days. The main components of smog in eastern North America are elevated concentrations of ground-level ozone and particulates. Together, these contaminants combine to give southern Ontario, or more precisely the Windsor-Quebec corridor, the worst air quality problems in Canada. Other problem areas are the Lower Fraser Valley, B.C. and the South Atlantic provinces region .
11. Abelsohn A. Pamphlet for Primary Care Physicians: Smog and Human Health. Ontario College of Family Physicians, 1996.
It should also be noted that the pollutant mercury is now emerging as an important health problem. A brief description of mercury, its sources and health effects, is given in Appendix A. The OMA may turn its attention to this contaminant, and may take further action to study its health effects and advocate controls.
Ground-level ozone, as opposed to the natural stratospheric protective layer of ozone which screens out the sun’s harmful ultraviolet rays, is a gas that is formed when its air pollution precursors, oxides of nitrogen (NOx), oxygen and volatile organic compounds (VOCs), interact in the atmosphere in the presence of sunlight. Nitrogen oxide is emitted from the combustion of fuels, mainly from transportation vehicles such as heavy-duty diesel vehicles, but also from coal-burning power plants and natural gas processing. Human-made VOCs are also produced by motor vehicle exhaust, industrial processes and from the evaporation of solvents, oil-based paints and gasoline from gas pumps. Approximately half of the VOCs found in Canada are from natural sources, such as trees.
Particulate Matter and Acid Aerosols
Particulate matter and acid aerosols are fine solid or liquid particles produced by the combustion of fossil fuel, including emissions from diesel engines, coal-burning power plants, cement plants, mining operations, residential wood combustion, and dust emissions from fields and roads. Because of their small size, less than 10 micrometers (PM10) or less than 2.5 micrometers (PM2.5), particulates remain suspended in air and when inhaled penetrate deep into the airways. PM10 varies in chemical composition spatially and from day to day, but those with a large acidic fraction, called acid aerosols (mostly sulphates from burning fossil fuels), are likely to be the most harmful to the bronchioles and alveoli.
Acid aerosols are essentially particles which contain acid, and are not traditionally monitored on a routine basis to the same extent as other pollutants such as ozone. However, routine measurements have been made of sulphate levels, which correlate to some degree with actual acid measurements. Acid aerosols are acidic particulates (e.g. sulphates – often referred to as particulate sulphates). There is no known safe level for exposure to sulphate particles. Acid aerosols are the airborne precursors of acid rain. Sulphate compounds have been linked to respiratory irritation and disease, corrosion of materials, and reduction of visibility.
16. MOEE. Air quality in Ontario, 1992. Queen’s Printer, 1993.
18. The Acidifying Emissions Task Group. Towards a National Acid Rain Strategy. Ottawa: Environment Canada. October 1997.
Environment Canada issues smog advisories when ozone levels are expected to exceed a specified level - 82 ppb. The advisories include both environmental information (e.g. description of pollution sources), as well as health information to advise the public on the possible health risks associated with smog exposure. In 1993 and 1994, four advisories were issued - two in Saint John, N.B. and one each in southern Ontario and the Greater Vancouver Regional District, B.C. As Figure l shows, a significantly greater number of episodes of elevated ground-level ozone concentrations occurred in these areas in previous years.
There is a need to improve the quality of gasoline sold at the province's pumps. The sulphur levels in gasoline and diesel in Ontario are the highest in the country and among the highest in the developed world at 579 parts per million (ppm) in gasoline and diesel fuels of 2620 ppm off-road. By comparison, California, a state that has acted aggressively to reduce air pollution, limits sulphur in gasoline to 30 ppm. High-sulphur gasoline leads to increased amounts of nitrogen oxides - the chemicals that cause smog - and more sulphur dioxide, a key precursor of acid rain and acid aerosols. It also leads to the production of more sulphates, extremely small acidic particles that can become imbedded deep in lung tissue.
21. Health Canada. Health and Environmental Impact Assessment Panel Report: Joint Industry/Government Sulphur in Gasoline and Diesel Fuels. June 25, 1997.
22. Mittelstaedt M. Canadian gasoline fuels smog, federal study says. The Globe & Mail; March 7, 1998: A5.
In a review of available evidence for the Canadian Smog Advisory Program, two expert panels concluded that health and health-care system effects of ground-level ozone at levels that occur in Canada include lung inflammation, decreased lung function, airway hyper-reactivity, respiratory symptoms, possible increased medication use and physician/emergency room visits among individuals with heart or lung disease, reduced exercise capacity, increased hospital admissions and possible increased mortality. Similar effects were thought to occur in association with airborne particles, with the exception of inflammatory changes and with the additional effect of increased school absenteeism. At the time the review was conducted (prior to 1995), poor data on individual exposures were identified by the expert panels as a limitation of studies on hospital admissions and mortality.
More recent studies, however, show associations between increased hospital admissions and mortality and air pollutants. Several studies specific to the Utah Valley (known for the low smoking rates of its residents, low levels of ozone and acid aerosols and high levels of PM10, and the presence of an operating steel mill) have evaluated associations between various indicators of health and PM10 pollution. Taken together, they suggest a coherence of associations across various health end points for a specific location and population. Health effects found to be associated with elevated PM10 pollution included: increased respiratory hospital admissions and increased mortality, especially respiratory and cardiovascular mortality. It is improbable that these apparent air pollution-related health effects were due to methodological bias; in addition, confounding factors such as cigarette smoking and weather were ruled out by researchers.
There does not appear to be a "threshold level" for ground-level ozone or particulates below which no health effects are observed.
A critical analysis of recent key research studies that link ground-level ozone, acid aerosols and particulates to health effects, with an emphasis on Ontario, follows below. Expert panels of the American Thoracic Society describe the potential health effects of air pollution as occurring in a logical "pyramid" ranging from severe uncommon events (e.g., death) to mild common effects (e.g., eye, nose and throat irritation that may interfere with normal activity such as driving a car, if severe) and measurable changes of lung function which are asymptomatic, due to a naturally large lung reserve in healthy individuals. This "Health Effects Pyramid" illustrates the general correlation of the severity of documented health effects with the strength of the scientific evidence available[19, 24-25]. Thus, while individual severe health events would be less common, there is a large overall impact on health and well-being because of the large number of people involved .
25. Bates DV. Health indices of adverse effects of air pollution. The question of coherence. Environ Res 1992; 59: 336-49.
While it is commonly assumed that individual reactions to pollutants will be the same, research indicates that individual reactions vary widely. Once an individual begins to react to a pollutant, this reaction becomes established and recurs with further exposures. Health status is also important to individual reactions. Both healthy and ill individuals may be affected by certain air pollutants.
Sensitive subgroups are those with asthma, individuals addicted to tobacco products, the elderly, infants, persons with coronary heart disease, and persons with chronic obstructive pulmonary disease (COPD). Although healthy non-tobacco product users show a wide range of lung function changes in response to ozone exposure, nevertheless, any response shown by an individual is consistent with his or her responsiveness to ozone on subsequent re-exposure.
Individual reactions to air pollutants depend upon the type of pollutant, how much of the pollutant is present, the degree of exposure and the types and levels of individual activity (e.g., individuals working or exercising outdoors have greater exposure). Results of a study of berry pickers in the Fraser Valley of British Columbia indicate that even for individuals living and working in areas of relatively low ambient ozone concentrations (range: 13 to 84 ppb), ozone exposures were substantial enough to be associated with a decrease in lung function during the course of the day. This decrease persisted at least until the following day. Interestingly, the upper range of ozone concentration found in this study was only 2 ppb higher than the current standard in Canada.
These study results are of significance because individuals may be affected by air pollution without displaying symptoms. Hence, air pollutants affect everyone in the long run.
28. McDonnell WF, Horstman S, Abdul-Salaam S and House DE. Reproducibility of individual responses to ozone exposure. Am Rev Respir Dis 1985; 13l: 36-40.
29. Brauer M, Blair J, Vedal S. Effect of ambient ozone exposure on lung function in farm workers. Am J Respir Crit Care Med 1996; l54(4), pt. l: 98l-987.
31. EPA. Air quality criteria for oxides of nitrogen. Washington, DC, 1993.
32. Lebowitz MD. Epidemiological studies of the respiratory effects of air pollution. Eur Respir J 1996; 9(5): 1029-1054.
The literature on asthma epidemiology is very extensive. Patterns of medication and health-care practices (as shown by differences in mortality rates between countries) are believed to play a role in mortality effects. There have been indications that prevalence may have increased. In Canada, there has been a marked increase in hospital admission rates for asthma.
Asthma is a complex disease that is multifactorial: in many cases, a genetic predisposition followed by an environmental exposure is a common process sequence. There is good reason to be suspicious of the contemporary role of air pollutants, but proof about them causing increasing asthma prevalence is not available at the present time.
However, in a study by Thurston, et al. air pollution was found to be significantly and consistently correlated with acute asthma exacerbations, chest symptoms, and lung function decrements in asthmatic individuals. Most subjects had moderate to severe asthma. The pollutant most consistently associated with adverse health effects was ozone, although associations with sulfates and hydrogen ions suggest a possible role by fine particles as well.
Ozone, together with acid aerosols, may well be playing a combined role in the exacerbation (worsening) of asthma. Ozone in smog causes airway inflammation, and higher levels increase the frequency of symptomatic asthmatic attacks. It is not known whether any of these agents are affecting prevalence rates of the disease.
Strong evidence from North America has shown that the increased number of emergency visits for asthma and acute admissions for respiratory illness are related to ground-level ozone generated from oxides of nitrogen and hydrocarbons. This is hardly surprising, since ozone at very low concentrations induces lung inflammation and also potentiates the effect of any allergen encountered subsequently.
34. Mao Y, Semenciw R, Morrison H, MacWilliam L, Davies J, Wigle D. Increased rates of illness and death from asthma in Canada. Can Med Assoc J 1987; 137: 620-4.
35. Thurston GD, Lippmann M, Scott MB, Fine JM. Summertime haze air pollution and children with asthma. Am J Respir Crit Care Med 1997; 155(2): 654-660.
36. Bates DV. Ozone: A review of recent experimental, clinical and epidemiological evidence, with notes on causation Part l. Can Respir J 1995; 2(1): 25-3l.
37. Peden DB, Setzer RW Jr, Devlin RB. Ozone exposure has both a priming effect on allergen induced responses and an intrinsic inflammatory action in the nasal airways of perennially allergy asthmatics. Am J Respir Crit Care Med 1995; 151: 1336-45.
5.5 Chronic Effects
Long-term exposure to air pollutants is associated with decreased lung function and increased city-specific mortality rates.
The effects of long-term exposure to air pollutants were studied in eight different areas of Switzerland. The study's general conclusion was that air pollution from fossil fuel combustion, which is the main source of air pollution (producing sulphur dioxide, nitrogen dioxide and PM10 ) was associated with decreased lung function.
Studies from the U.S. show similar chronic effects. Survival analysis of mortality from a l4 to l6 year follow-up of 8,111 adults participating in the Harvard Six Cities Study showed increased city-specific mortality rates after adjusting for individual risk factors. Adjusted death rates appeared to increase most consistently with air concentrations of particles less than 2.5 micrometers in size. This association was not explained by tobacco use, occupational exposures, or history of chronic disease.
39. Dockery DW, Pope CA, Xu X, Spengler JD, Ware JH, Fay ME, Ferris BG, Speizer FA. An association between air pollution and mortality in six U.S. cities. N Eng J Med 1993; 329: l753-l759.
5.6 Excess Cardiorespiratory Mortality
Mortality is only the tip of a much larger morbidity problem. The air pollution disaster in London, England in December of 1952 established that very high levels of particulate-based smog can cause dramatic increases in daily mortality. The particles were derived from direct burning of coal for space heating. As the month began, stationary air resulted in a temperature inversion in the valley and an extremely rapid increase in particulate-based smog. The rapid increase in pollution was followed, with a lag of less than one day, by a rapid increase in the daily death rate in London, which peaked at 500 from a customary level of approximately 200 daily deaths. No other epidemics could account for this increase. In the Great Towns of England and Wales, the daily mortality also increased. The increase in pollution concentrations was much less outside London. Daily respiratory disease admissions to hospitals in greater London peaked at 460 cases, compared to an average of 175 cases per day immediately preceding the fog.
This event happened 46 years ago and outdoor air pollution is still a problem. Currently, there is a rapidly evolving area of research with provocative new epidemiologic information linking particle exposure, substantially lower than those seen in London in 1952, with mortality in older people who have pre-existing cardiorespiratory disease. Those concentrations of particulate air pollution are common occurrences in U.S. cities.
Numerous studies conducted worldwide show a significant acute health consequence of exposure to particles, and this pollutant may be responsible for from between one and 10 per cent of all non-accidental deaths.
Recent data, measured in six eastern U.S. cities, suggest that increased daily mortality is specifically associated with the concentration of fine particles in the air (less than 2.5 micrometers in aerodynamic diameter). The implication is that solutions should aim to reduce levels of fine particles in the air, by focusing on their sources. These include direct emissions and secondary reactions of combustion-related air pollutants.
Studies done locally demonstrate the same results. In Toronto, strong associations were observed between premature mortality due to respiratory disease and levels of airborne particles, ground-level ozone and nitrogen dioxide. In this study, a two to four per cent excess of respiratory deaths could be attributed to pollutant levels. Similar associations were observed for cardiovascular deaths. These data are also consistent with other studies in North America and Central America.
An association between inhalable particulates and increased mortality is found in metropolitan areas in North America, including Toronto and Detroit. Studies show that an increase of 10 micrograms per cubic meter could increase the total mortality rate by one per cent. The Ontario Smog Plan Workgroup has estimated that in Ontario, approximately 1,800 premature mortalities and l,400 hospital admissions per year are due to the effects of inhalable particles.
European studies show similar results. Evidence is accumulating that the presence of air pollution below the levels of national and international standards has adverse short-term health effects related to daily mortality. Data from l2 European cities showed that increases in sulphur dioxide and particulate matter were associated with increased total mortality. An increase of 50 micrograms per cubic metre in sulphur dioxide or black smoke was associated with a three per cent increase in daily mortality (both cardiovascular and respiratory) and the corresponding figure for PM10 was two per cent. The effects of the two pollutants seem to be independent. The authors of the study noted that the consistency of the results in western European cities with wide differences in climate and environmental conditions suggests that these associations may be causal. Although the reported relative risks are small, the short-term effects of air pollution are not a trivial public health problem if the omnipresence or “being everywhere” of air pollution exposure is taken into account. From a population health perspective, exposure of a large number of people to a small risk can result in more illness in the population than exposing a small number of people to a large risk factor. In short, researchers conclude that current low levels of sulphur dioxide and particles still have detectable short-term effects on health and further reductions are needed.
In the case of PM10 particles, an understanding of the biological mechanism is missing. Opinion is divided as to whether this should or should not prevent us from concluding that the relation between PM10 particles and mortality is causative - a not uncommon problem.
Conversely, Gamble and Lewis (who received partial funding by the Institute of Petroleum, London, England) reviewed recent epidemiological studies about health effects, including mortality and morbidity, to evaluate whether criteria for causality were met and concluded that they were not. Some of the methodological issues in studies of air pollution and daily counts of deaths or hospital admissions are noted in Appendix B.
The attacks and counterattacks in the scientific literature about the issue of causality demonstrate how hard it has been to prove unequivocally that air pollution can cause increases in daily mortality rates. There is discussion about exactly what pollutant produces health effects, and the severity of effects (e.g., acute or chronic exposure effects). In an attempt to resolve the controversy, Schwartz employed a technique called meta-analysis to examine 12 studies. He found that airborne particle concentration was a small but significant risk factor for elevated mortality. The relative risk was 1.06 (95 per cent CI = 1.05-1.07). Taken together, these studies present a coherent picture of associations with the full range of respiratory outcomes, including mortality. He concluded that the most reasonable interpretation of this pattern of results is that the association is causal.
The big issue of uncertainty concerning mortality effects of these pollutants is to measure the public health impact quantitatively. With the issue of premature mortality, questions arise, including: Who is affected? How much lifespan is being lost?, and What is their quality of life?
41. Thurston GD, Ito K, Hayes CG, Bates DV, Lippmann M. Respiratory hospital admissions and summertime haze air pollution in Toronto: Consideration of the role of acid aerosols. Environ Res 1994; 65(2): 27l-290.
42. Schwartz J, Dockery DW, Neas LM. Is daily mortality associated specifically with fine particles? J Air & Wast Manage Assoc 1996; 46 (10): 927-939.
43. Ozkaynak et al. Association between daily mortality and air pollution in Toronto, Canada. Proceedings of the International Society for Environmental Epidemiology. Noordwijkerhourt, The Netherlands. August 1995.
44. MOEE. Towards a smog plan for Ontario: A discussion paper. June 1996; PIBS 3434e.
45. IP/RP Workgroup, 1996. Bulletin on inhalable and respirable particulates (IP &RP), IP/RP Progress Note #l, prepared for Ontario Smog Plan, prepared by IP/RP Strategy Working Group, Chair: David Pengelly, November, 1996.
46. Katsouyanni et al. Short-term effects of ambient sulphur dioxide and particulate matter on mortality in 12 European cities: results from time series data from the APHEA project. BMJ 1997; 3l4: 1658-63.
47. Bates DV. Environmental health risks and public policy. Seattle: University of Washington Press 1994: 117.
48. Gamble JF, Lewis RJ. Health and respirable particulate (PM10) air pollution: A causal or statistical association? Environ Health Perspect 1996; 104(8): 838-850.
5.7 Effects of Air Pollutants on Children
Children are most at risk from exposure to ozone because they are active outside during the summertime, when ozone levels are at their highest. Increased morbidity from illnesses such as bronchitis and indirect health effect indicators such as school absences occur in both rural and urban Ontario communities.
Children represent the largest subgroup sensitive to adverse effects of air pollution due to: 1) differences in pulmonary anatomy and physiology (e.g., because of breathing patterns, small children are likely to inhale and retain greater quantities of particles per unit body weight than adults); 2) increased susceptibility to respiratory infections; and, 3) developmental susceptibility (e.g., animals, when exposed to high-level ozone, show permanent decreases in the number of respiratory bronchioles formed postnatally).
Children are most at risk from exposure to ozone because they are active outside during the summertime when ozone levels are at their highest. Data were obtained from six summer camp studies carried out by three separate investigative groups (including two studies in Ontario). Results confirm a measurable population-average mean decline in forced expiratory volume (FEV1) (a lung function test result) associated with ozone exposures that is qualitatively similar to that reported in laboratory studies. These results raise the concern that other effects observed in those studies (e.g., pulmonary inflammation) may also occur in young people exposed to ozone.
Ozone makes asthmatics more responsive to an allergen.
At present, only a limited number of studies have examined the effect of acute exposure to ozone or nitrogen dioxide on the response to inhaled allergen in human subjects. Molfino and colleagues found that the response to inhaled allergen after one hour exposure to air with ozone concentrations of 0.12 ppm was significantly greater than the response to an allergen after air without ozone in six of seven subjects.
Dr. Phillip Landrigan, chair of community medicine at Mount Sinai Hospital, New York, NY, has stressed that degradation of the environment results in disease, particularly in children. "Too frequently the environmental movement is seen as people worried about trees and the disappearance of species and is often seen as elitist upper middle class. But there are differential vulnerabilities. All kids are not equally affected. Minority inner-city children are the most heavily impacted by the exposure to (environmental) toxins, and when this is coupled with poor nutrition and housing, it's a prescription for disease," he concluded.
Income affects environmental health. Results of a southern California study indicate that ozone exposure is highest for children six to eleven years old, and demonstrates the importance of a socioeconomic perspective. While ozone exposure differences by race and ethnicity have diminished over time, on average, low-income areas may be experiencing a higher number of per capita hours of ozone exposure above the national standards than high-income areas, suggesting that environmental health risks (e.g., respiratory diseases) may be systematically higher for low-income groups. This observation may be true in the United States, but paradoxically it may not be so in Ontario. Because of the scavenging effect of NOx, ozone levels may well be higher in suburban or rural areas than they are in the downtown cores of Ontario's major cities.
There are indirect indicators of the effects of air pollution on children. Ransom and Pope showed convincingly that school absences in grades one to six were significantly associated with PM10 levels. The response was greater in those in grades one to three (six to nine years old) than in the older children. The authors concluded that weather variables were deemed unlikely to have been responsible for the findings.
In a study of respiratory health effects of exposure to acidic air pollution among 13,369 white children, aged eight to twelve years old, from 24 communities in the U.S. and Canada (including children from rural Ontario²), between 1988 and 199l children living in the community with the highest levels of airborne acids were significantly more likely to report at least one episode of bronchitis in the past year compared to children living in the least-polluted community. Reported bronchitis was associated with elevated levels of airborne acids for those children living in a non-urban environment. Potential confounding factors such as history of allergies and current smoking in the home were adjusted. These data indicate that chronic exposure to acid aerosol pollution may have observable negative consequences on the health of children. Although the long-term consequences of bronchitis in these children remain unclear, respiratory illnesses in childhood may be a risk factor for development of chronic obstructive pulmonary disease (COPD), which can be fatal. These children also may be at a higher risk from other environmental or respiratory pollutants (e.g., personal exposure to second-hand smoke) and occupational exposures later in life.
This snapshot of the available evidence on the impact of air pollution on children shows that, when all the data are taken together, there is no doubt that relatively low levels of pollution are responsible for increased morbidity in children. This is particularly true of the pollution that follows uncontrolled coal burning.
50. Kinney PL, Thurston GD, Raizenne M. The effects of ambient ozone on lung function in children: A reanalysis of six summer camp studies. Environ Health Perspect 1996; 104(2): 170-174.
51. Gordon T, Fine J. The contribution of ambient air pollution to allergic asthma. TEN 1997; 4(1): 20-24.
52. Molfino NA, Wright SC, Katz I, Tarlo S, Silverman F, McClean PA, Szalai JP, Raizenne M, Slutsky AS and Zamel N. Effect of low concentrations of ozone on inhaled allergen responses in asthmatic subjects. Lancet, July 1991; 338(8761): 199-203.
53. Marwick C. New focus on children's environmental health JAMA 1997; 277(11): 87l-872.
54. Korc ME. A socioeconomic assessment of human exposure to ozone in the South Coast Air Basin of California. Journal of the Air & Waste Management Association 1996; 46 (6): 547-557.
55. Pengelly LD. PhD, McMaster University, Hamilton, ON. Correspondance to OMA Health Policy Dept. February, 1998.
56. Ransom MR, Pope CA lll. Elementary school absences and PM10 pollution in Utah Valley. Environ Res 1992; 58: 204-219.
57. Dockery DW, Cunningham J, Damokosh AI, Neas LM, Spengler JD, Koutrakis P, Ware JH, Raizenne M, Speizer FE. Health effects of acid aerosols on North American children: Respiratory symptoms. Environ Health Perspect 1996; 104(5): 500-505.
58. Raizenne M et al. Health effects of acid aerosols on North American children: Pulmonary function. Environ Health Perspect 1996; 104(5): 506-514.
59. Bates DV. The effects of air pollution on children. Environ Health Perspect 1995; l03 (suppl 6) : 49-53.
5.8 Effects of Air Pollutants on the Elderly
The elderly and those with cardiac or respiratory diseases, such as asthma, emphysema and chronic bronchitis, are especially sensitive to these air pollutants.
The elderly population, already large, will continue to grow dramatically over the next decade. This demographic trend will result in an increasingly large population prone to the health effects of air pollution. By the year 2030, today's baby boomers will comprise nearly one-quarter of the population, eight million Canadians over 65 years of age, and they may be particularly affected by air pollution. People aged 75 and over are much more likely than other adults to have health problems (e.g., cardiorespiratory disease) and use health-care services. Some of these problems and increased usage will be attributable to air pollution.
Age and health status are important predictors of an individual's reaction to air pollutants. In general, the more susceptible populations include the elderly and those with cardiac or respiratory diseases such as asthma, emphysema and chronic bronchitis. In 1993, ground-level ozone, particulate matter (PM10, PM2.5), and the sulfate fraction of PM2.5 were all positively associated with respiratory emergency room visits for patients over age 64 in Montreal, Quebec. Studying the physiological effects of air pollutants on older individuals is therefore important, not only for biological reasons, but also because of the significant health-care resources which will be utilized by this group, given their growing proportion in the Ontario population.
61. Rosenberg MW, Moore EG. The health of Canada's elderly population: current status and future implications. Can Med Assoc J, 1997; 157 (8): 1025-1032.
62. Delfino RJ, Murphy-Mouton AM, Burnett RT, Brook JR, Becklake MR. Effects of air pollution on emergency room visits for respiratory illnesses in Montreal, Quebec. Am J Respir Crit Care Med 1997; 155(2): 568-576.
Health Effects and Air Pollution: Conclusions
Ground-level ozone, acid aerosols and particulates have created a serious health problem in both Canada and the United States.
6. Summary of Research-Related Health-Care System Effects of Air Pollution
Individuals, including physicians, nurses and other health-care professionals are most concerned with how air pollutants affect the health of patients. A complete analysis must take into account, however, the impact of these air pollutants on the health sector. Our institutional health-care system, as well as our economy are being stressed. The main concerns fall into three groups: 1) increased emergency room visits; 2) increased hospital admissions; and 3) negative economic impacts.
It is important to note that the vast majority of asthma is treated in the community by primary care physicians or self-medication in the home under the direction of a physician. Currently, in the community setting, there is no method to quantify the frequency and severity of asthma exacerbations because data are not available. Hence, this burden of illness may be definitely greater than data revealed by hospital admission and emergency room visit rates.
6.1 Increased Emergency Room Visits
Health effects of these pollutants result in increased visits to a doctor or an emergency room, and increases in medication use.
Increased utilization of health-care is an important issue, particularly in an era of cost-containment. An association was found between acute respiratory admissions to 79 acute care hospitals in southern Ontario and ozone levels. A later and more detailed analysis confirmed the association between summer ozone levels and hospital admissions for acute respiratory disease and showed that the association was observed for both sulphates and for ozone. It was shown that asthma admissions for children for a period of 24 hours after ozone had exceeded the Canadian objective of 0.08 ppm for one hour were consistently elevated compared with admissions on all summer days. In this and similar studies, it has proved difficult to separate the effects of these pollutants (i.e. sulphate particles and ozone) since, in this region, they commonly rise and fall together. The association of hospital admissions with sulphate levels in southern Ontario was confirmed by Plagiannakos and Parker. These two analyses in southern Ontario, though planned and conducted independently, reinforce each other in terms of the relationship they established between morbidity indices and sulphates.
Similar findings have been reported on emergency or urgent daily respiratory admissions to all l68 acute care hospitals in Ontario below the 47th parallel (representing the majority of Ontario hospitals), over a six-year period from January 1983 to December 1988. Summer respiratory admissions were closely associated with ozone levels, and among infants, l5 per cent of summer admissions were pollutant-associated, whereas among the elderly only four per cent were.
Additional support for the above findings is offered from another jurisdiction. Elevated concentrations of ground-level ozone in the Saint John, N.B. area have been shown to be associated with increases in emergency department visits. Asthma visits increased by 33 per cent two days after the daily ozone maximum exceeded 75 ppb. This finding is especially significant since the majority of ozone levels recorded in this study were below the one-hour national standard for ozone of 82 ppb.
Study results also suggest an effect on quality of life and economic burden in relation to episodes of cardiorespiratory disease. Outcomes commonly reported in a study to examine the relationship between air pollution and the frequency of cardiorespiratory emergency department visits include: increases in medication use, reduced activity days, increased days spent in bed, increased physician office visits, and increased out-of-pocket expenses such as medication, parking fees, workdays lost and child care for siblings.
64. Bates DV, Sizto R. Hospital admissions and air pollutants in southern Ontario: the acid summer haze effect. Environ Res 1987; 43: 3l7-33l.
65. Bates DV. The strength of the evidence relating air pollutants to adverse health effects. Carolina Environmental Essay Series. Chapel Hill: Institute for Environmental Studies, University of North Carolina, 1985.
66. Keeber et al. Transported acid aerosols measured in southern Ontario Atmospher Environ 1990; 2AA: 2935-50.
67. Plagiannakos T, Parker J. An assessment of air pollution effects on human health in Ontario Energy Economics Section, Economic and Forecasters Division, Ontario Hydro, File No 706.0l (#260) March 1988.
68. Bates DV. Ozone: A review of recent experimental, clinical and epidemiological evidence, with notes on causation Part 2. Can Respir J 1995; 2(3): 161-17l.
69. Burnett RT et al. Effects of low ambient levels of ozone and sulfates on frequency of respiratory admissions to Ontario hospitals. Environ Res 1994; 65(2): 172-194.
70. Stieb D, Burnett RT, Beveridge RC, Brook JR. Association between ozone and asthma emergency department visits in Saint John New Brunswick, Canada. Environ Health Perspect 1996; 104 (l2): l354-l360.
71. Stieb D, Beveridge RC, Brook JR, Burnett RT, Anis AH and Dales RE. The Saint John Particle Health Effects Study. Measuring Health Effects, Health Costs and Quality of Life Impacts using Enhanced Administrative Data: Design and Preliminary Results. In Particulate Matter: Health and Regulatory Issues, Proceedings of an International Speciality Conference, Pittsburgh, Pennsylvania, April 4-6, 1995. Pittsburgh: Air and Waste Management Association, pp. l3l-l42.
6.2 Increased Hospitalizations:
Exacerbations of Chronic Respiratory Diseases
Increases in certain air pollutants are linked to increases in hospitalization for respiratory and cardiac disease.
Increased hospitalizations represent an outcome measure (health indicator) of air pollution. Burnett, et al. found an association between low levels of ozone and respiratory diseases severe enough to require hospitalization in l6 Canadian cities3 representing 12.6 million people. The association between ozone and respiratory hospitalizations varied among cities. Particulate matter and carbon monoxide were also positively associated with respiratory hospitalizations. These results suggest that ambient air pollution, at relatively low concentrations of pollutants, is associated with excess admissions to hospital for respiratory diseases in populations experiencing diverse climates and air pollution profiles.
A study in one large urban area found similar results. An analysis of 22 acute-care hospitals in Toronto indicated that exacerbations of pre-existing respiratory disease, including asthma, were associated with community exposures to elevated levels of summertime haze, ground-level ozone, and acid air pollution. On average, summertime haze air pollution was associated with 24 per cent of all respiratory admissions (2l per cent with ground-level ozone, three per cent with acid air pollution). On peak pollution days, however, aerosol acidity yielded the highest relative risk estimates (e.g., RR=1.5 Ī 0.25 at 391 nmole/m3 H+), and summertime haze was associated with roughly half of all respiratory admissions. Results of this paper must be viewed in light of the conclusions of its companion paper concerning the nature and origins of acid summer haze air pollution. Together, these two studies suggest that, not only are acidic summertime haze air pollutants being transported in the atmosphere to Toronto from upwind regions of the United States, but also that this transported pollution has measurable adverse health consequences in that city. Thus, to ameliorate this environmental health problem in Toronto and its vicinity, co-operation between the United States and Canada will clearly be required.
Of particular relevance to this issue is the fact that the Great Lakes Basin has consistently high levels of certain air pollutants because of wind patterns, geographic location and sources of pollution. Annual average ozone levels in the basin have been consistently above the national objective of 15 ppb for the past several years. In general, levels of particulates and sulphates have not declined over the same period.
73. Thurston et al. The nature and origins of acid summer haze air pollution in metropolitan Toronto, Ontario. Environ Res 1994; 65: 254-270.
6.3 Economic Impacts
The health effects of air pollution exact a large and avoidable economic toll.
Economics describes the utilization of society's resources. Resources utilized for one purpose are unavailable for another, a concept known as opportunity cost. The economic burden of ill health is measured in terms of direct costs (e.g., hospitalizations) and indirect costs (e.g., loss of workdays, restricted activity days or school days).
Assessing the economic impact of air pollution is a complex task. Once the simpler measures have been taken to limit the emissions of pollutants from single sources, further control measures are more costly and more difficult to implement. Specifically, reducing nitrogen dioxide emissions from cars and trucks is not simple, and reducing PM10 may prove to be even more difficult. In this situation, there should be an expectation that calculations will be made of the current economic impact of air pollution before costly and difficult control measures are instituted. For example, is PM10 likely to be the same everywhere? How should the cost of a premature death be evaluated in relation to age? Is death accelerated by only a few days in the majority of instances? These and other questions have to be answered before any estimate can be produced.
Increased daily mortality rates, however, should not be the only measure of the negative health effects of air pollution. For example, averted asthma should be portrayed as a longer-term state of susceptibility, with effects on emotional well-being and social interaction involving not only the patient, but often also a caregiver. Depicting asthma merely as discrete episodes of shortness of breath may lead to an undervaluation.
Industrial interests, capable of exerting substantial economic pressure, will attempt to minimize the importance of effects such as the increased risk of lower respiratory infections among children. For this reason, economic calculations may prove useful in reminding legislators that there is further work to be done. Some believe there is a conflict between pollution control and economic development. It was formerly taken for granted that the costs of better air pollution control were a burden on industry and interfered with prosperity and full employment. But few countries take into proper account the long-term costs and inefficiencies that follow human disease, in adults and children, related to air pollution (e.g., higher taxes to subsidize increased health-care costs).
Clean air is common property, yet zero man-made ozone concentrations are unlikely to be a viable option, because of other public and private priorities. A full economic appraisal for setting an optimal air quality goal for any substance is therefore required to determine the value of the health and other benefits (e.g., enhanced commercial crop yields) expected from varying levels of abatement (e.g., minor or moderate emissions reductions). These would be compared with the expected costs of achieving each level of abatement (e.g., monitoring and enforcement).
It should be noted that these economic valuation exercises are quite controversial, but in the spirit of public disclosure, the numbers are presented here. To calculate the health, environmental and economic benefits of reducing the precursors of ozone (one component of smog), the Ontario Ministry of Environment and Energy (since renamed), started from a baseline which assumes that no reduction activities will have taken place between 1990 and 20l5. If that were the case, then it is projected that by year 20l5, emission levels would reach 933 kilotonnes per year of nitrogen oxide (NOx) and l,2l5 kilotonnes per year of volatile organic compounds (VOCs). From this baseline, the projected benefits of reducing emissions of these ozone precursors was calculated using two scenarios: Scenario l – existing and readily available reductions, and Scenario 2 – 45 per cent reductions from 1990 levels of NOx and VOC emissions in Ontario. Table 2 in the Appendix shows that with committed and readily available efforts to reduce NOx and VOC emissions as indicated in Scenario l, there could be as many as 63 fewer deaths a year by 20l5 due to decreases in ozone and inhalable particulate exposures. Table 3 in the Appendix summarizes the range of total estimated annual monetary values associated with reduced mortality and morbidity for Ontario if reduction goals are achieved by 20l5. By 20l5, in Ontario, total monetary values that may be attributed to reduced mortality and morbidity range from $398 million to as much as $l.2 billion.
Reductions in human health effects associated with sulphur dioxide (SO2) emission reduction scenarios are listed in Table 4. This Table illustrates what is possible with emission reduction and the cost involved with each scenario. For example, a 75 per cent sulphur dioxide reduction in both Canada and the U.S. will achieve a benefit of $890 million to $8 billion.
In summary, the physicians of Ontario consider this health problem to be costly. Although economic analysis is not the venue of physicians, we believe that this issue deserves study by experts in the field.
75. Guest CS, Morgan P, Moss JF, Woodward AJ, McMichael AJ. Abatement of tropospheric ozone: effects of strategies to improve air quality on public health and other sectors. Australian and New Zealand Journal of Public Health 1996; 20(3): 30l-308.
The Health-Care System and Air Pollution:
The impact of ground-level ozone, acid aerosols and particulates on the health-care system is also negative. It has been demonstrated that increases in these air pollutants are linked to:
It is clear that there is a broad range of adverse health effects from ground-level ozone, acid aerosols and particles. These health damages range from mild chronic illness to death. The sources of the pollutants which cause these effects are numerous and well-known, including electric power generation, industrial, transportation and small individual sources.
Medical evidence reviewed in this paper clearly establishes the need for more stringent and mandatory emission reduction strategies. As part of our analysis, we have consulted with experts and authors in this field and have determined that there are several levels of recommendations to be made: items actionable by government, by the OMA as a group, by individual physicians, and by the public.
The OMA believes that public policies in this area must address both how much pollutant people are being exposed to and for how long, as well as the quantity of emissions from industrial and other sources. Tonne for tonne, emissions of ozone-smog pollutants have heavier health impacts on people in the area where they are released. But emissions from distant upwind regions can add to the harm from more local emission sources. For this reason, the only effective way to reduce ozone-smog and fine particulate matter is to reduce nitrogen oxide and sulfur dioxide emissions throughout eastern North America, and to achieve strong controls on hydrocarbon emissions in the immediate vicinity of areas experiencing high ozone levels.
It is now well-established that more than half of southeastern Canada's acid rain and related air pollution problems originate in the United States. Research has also demonstrated that point sources in Ontario (and possibly elsewhere in Eastern Canada) contribute to pollution loadings both in the province itself and in the U.S. northeast. Therefore, any recommended solutions to the air pollution problem in this province and elsewhere in Canada must include actions which need to be taken both in Canada and the United States.
It is also important to note that the U.S. system for determining standards differs significantly from the Canadian system. The American approach depends on a combination of command-and-control regulatory strategies and market-based mechanisms, under which tonnage reductions and target dates are established, with associated legislation, regulations, timetables, emission credit trading mechanisms and non-compliance penalties. In contrast, the Canadian system tends frequently to be voluntary, with criteria or guidelines established for which there are no mandatory compliance dates or non-compliance penalties. Notable exceptions in the latter case include Ontario's countdown acid rain program regulations established in 1985.
While approaches to controlling air pollution in the U.S. include both ambient air quality standards and emission reduction strategies, Canadian jurisdictions do not generally set the same type of air quality standards as those found in, for example, the new U.S. national ambient air quality standards approved last year. The OMA believes that mandatory air quality standards must be developed in Canada, at least for parts of the country like the Windsor-Quebec corridor which suffer from significantly elevated levels of exposure to ozone and other air pollutants.
Updating and formulating new Canadian air quality standards may be a time-consuming process. The medical (and terrestrial and aquatic) evidence indicates that we do not have time to wait for the conclusion of an extended exposure standard formulation process. At the same time, it is clear from many authorities that good information exists concerning levels of emission reductions which must be implemented in the near term, if we are to avoid continuing adverse health effects from the air pollutants studied in this paper. During the OMA's review of various air pollution-control strategies and scenarios, it quickly became clear that the coal-fired power plant produces most of the pollutants at issue. Key strategies must therefore concentrate on power plants and motor vehicles situated in both the U.S. Midwest and in Ontario.
There are several pollutants for which emission reductions are necessary: sulphur dioxide (SO2), oxides of nitrogen (NOx) from power plants, and NOx and hydrocarbons from transportation sector emissions.
When making recommendations, the OMA is particularly concerned to reduce the impacts of air pollutants on children. There is considerable concern that the increase in rates of childhood asthma are in part related to air pollution levels. We also know that children's lungs can be particularly susceptible to impacts from air pollution and other irritants like second-hand smoke. Children's lungs are smaller, they breathe faster, and their risks of negative effects can be proportionately greater than for adults.
The balance of these recommendations focuses on pollutants within two major sectors: the electricity generation sector (specifically coal-fired power plants) and the transportation sector. They have been selected from a review of recommendations made by the various agencies, and are those which the Ontario Medical Association feels a particular responsibility to support.
CONTROLLING SULPHUR AND NITROGEN EMISSIONS FROM THE ELECTRICITY GENERATION SECTOR
Coal-fired power plants produce two types of emissions which the research reviewed in this paper identifies as major causes of the health effects under consideration: sulphur dioxide (SO2) and oxides of nitrogen (NOx). SO2 is a precursor both of acid rain (deposition of weak sulphuric acid in rainfall or snowfall) and fine particles which have been identified in this paper as a major contributor to negative respiratory health effects. NOx is a precursor of both acid rain and ground-level ozone (and fine particles).
Action was taken in the mid-1980s to significantly reduce SO2 from Ontario power plants and non-ferrous metal smelters, and the 1990 U.S. Clean Air Act mandated significant SO2 reductions from the electricity generation sector. A recent review by the Canadian Acidifying Emissions Task Group, however, clearly demonstrated that existing reductions have not been sufficient to alleviate either health or environmental damage from acid rain-causing emissions.
In light of the medical evidence cited in this paper, it is incomprehensible that the Ontario Ministry of the Environment apparently intends to allow a significant increase in emissions from Ontario Hydro and will not require emission controls comparable to those being proposed by the U.S. Environmental Protection Agency.
While the emission rates of Ontario power plants are lower than many older (and higher-polluting) U.S. midwestern power plants, emission increases resulting from the nuclear shutdown will worsen local air quality. As noted earlier, impacts of provincial power plants on local air quality are, tonne for tonne, more significant than pollution from more distant sources.
It should also be noted that Ontario Hydro's power plants make a contribution to acid aerosol loadings and ground-level ozone in the northeast U.S. states.
As in the past, interested Canadian individuals and groups from the health, environment and other sectors need to be active at the USEPA and at other federal and state government agencies in order to make the case for further U.S. emission reductions. This activity cannot be credible if the Ontario government allows SO2 and NOx emissions from Ontario Hydro's plants to increase without any additional investment by the corporation in SO2 and NOx controls, especially when these control costs are modest. Current estimates indicate that controls could be implemented for perhaps one to two per cent of the capital costs associated with Hydro's nuclear recovery plans. Effective emission controls would establish a strong and credible foundation for the Canadian case in support of U.S. emission reductions. Canadian credibility with U.S. decision-makers in this area will be strong as long as there is steady, proactive progress in controlling Canadian emissions. A record of backsliding or inaction in Ontario will not only destroy that credibility, but could provide additional support for some industries and governments south of the border which are resisting the implementation of emission control standards.
7.1 Recommendations Concerning
Restructuring Of The Electricity Generation Sector
The electricity generation sector is being restructured in both Canada and the United States. Legislation will be considered by the Ontario government, the U.S. Congress and probably other governments in the near future.
The transportation sector is a major producer of both NOx and other ozone precursors, as well as fine particles. Part of the approach in dealing with the transportation sector involves engine and fuel modifications. Part of the approach involves appropriate and effective vehicle emission inspection and maintenance (I/M) programs.
7.5 Using Section 115 Of The U.S. Clean Air Act
Depending on the outcome of current rulemakings underway at the USEPA, transboundary flows of air pollution from the U.S. into Canada may continue to cause negative health and environmental effects. There is another remedy available to Canadians which should be considered. Section 115 of the U.S. Clean Air Act allows for a petition by a foreign country (with Canada clearly in mind) to the USEPA administrator for relief from U.S. pollution which is affecting that country. Action under Section 115 may be taken once a duly constituted international authority has determined that such damage is occurring, and also requires that Canada have reciprocal legislation permitting a similar U.S. intervention. Recent reports by, among others, the Commission for Environmental Co-operation established under the North American Free Trade Agreement have concluded that U.S. air pollution is damaging Canada. Reciprocity has been in place in Canadian legislation since the 1980s.
The OMA should assist individual physicians in developing prescriptive advice for patients about health risks associated with air pollution exposure and environmental messages to advise the public on actions to take to reduce the emission of pollutants. It is recommended that health message content include: an emphasis on "diagnostic" versus "prescriptive" messages (those that identify expected health effects versus those that recommend protective actions); identification of target groups; accurate reflection of the scientific evidence without unduly raising public concern; and selection of an appropriate threshold for the ground-level ozone advisory. Prescriptive advice should be obtained from local public health authorities and/or personal health-care providers familiar with an individual's clinical history.
The OMA should form partnerships for education and health promotion. Working with stakeholders such as the Registered Nurses Association of Ontario, Public Health Units, the Lung Association, Ontario College of Family Physicians, and Pollution Probe will help to ensure that the public is informed of these air pollution health effects.
Continued co-operative participation is required for the "Physician Education Project in Workplace Health (PEWPH), an initiative begun in 1995 by the OMA Section on Occupational and Environmental Medicine, supported by the OMA, and operating under the aegis of Educating Future Physicians of Ontario (EFPO). EFPO is supported by the five faculties of medicine of Ontario, the Ministry of Health, and a consortium of associated medical services. Its goal is to make medical education more responsive to the evolving needs of Ontario society.
Research is needed to define how fine particles affect cardiorespiratory disease, and how important air toxics (known or suspected to cause cancer or developmental abnormalities) are to overall cancer risk. Inhalable particulates, especially their sulphate component, had the greatest impact on air pollution premature mortality and hospital admissions in the Hamilton area study. Improved access to data associated with health effects of these pollutants is required (particularly emergency room visits, and visits to physicians’ offices or walk-in clinics).
For example, better co-ordination of activities of the various committees, task forces and other government groups dealing with sulphate particles is needed in order to organize and rationalize the various initiatives (especially at the federal level). Also, the OMA should insist that health issues are built into the activities of air-quality initiatives. Personnel should be assigned to provide health advice to the Ministry of Environment.
On the health effects of the particulate matter, for example, a forum of eminent scientists might be drawn together to establish uniform terms and definitions so that future research does not suffer from inexactness. This expert panel could be composed of members from the Royal Society of Canada and the U.S. National Academy of Sciences.
Physicians have been identified as important players in raising public awareness, the communication of risk, and the communication and promotion of strategies of how to avoid harmful exposure, and of how to change behavior in order to reduce smog levels[19, 77].
In Ontario, the MOE reports daily on the air quality index (AQI), which is an aggregate of the six most common urban air pollutants: carbon monoxide, nitrogen dioxide, sulphur dioxide, suspended particles, total reduced sulphur, and ozone. Since 1993, smog advisories have been issued when ozone levels are forecast to be significantly elevated (average regional levels greater than 80 ppb). About five such episodes are likely to occur over a summer. These smog advisories (much like the UV Index) are reported by the media with health and environmental messages. Table 5 shows the health impacts of the AQI pollutants at various levels. It is recommended that implementation strategies, such as education programmes, be directed towards individuals at risk, as well as parents, teachers, athletes, coaches, health professionals and public health officials.
There are health risks associated with smog exposure.
"During the episode, you may experience eye irritation. Heavy outdoor exercise during the episode may cause respiratory symptoms. People with heart or lung disease (including asthma) may experience worsening of their condition. Outdoor activity should be reduced, and, if necessary, consult your physician."
Environmental messages advise the public on actions to take to reduce the emission of pollutants. Short-term behavior change will not produce immediate environmental improvement, and it is not wise to walk or cycle, thereby increasing personal exposure, in order to help reduce smog during smog episodes. During a smog advisory, reduce car use by using transit or car pooling, and delay using other engines, such as lawn mowers, etc.
In the long term, primary prevention includes empowering patients to become part of the solution, by reducing emissions as follows:
There can be little doubt that ground-level ozone, particulates and acid aerosols are linked to increases in hospitalization for respiratory and cardiac disease, and to increased premature mortality. Socioeconomic effects include an unfair burden on children, and it is estimated that approximately l,400 hospital admissions per year in all of Ontario are due to the effects of inhalable particulates alone. Most importantly, there does not appear to be a “threshold level” for ground-level ozone or particulates below which no effects are observed; even low levels of ground-level ozone and particulates are damaging to the cardiorespiratory system.
It is clear that air pollution and health effects are of great concern to Ontarians. Not only are people concerned about air pollution, but investigations show people are prepared to pay for improvements to air quality as well.
The research that was reviewed by the OMA shows a number of gaps in knowledge and areas for further research (particularly concerning asthma). More details about the health and environmental effects of the pollutants, the sources of pollutants and projections of future trends in emissions are needed to create an effective strategy to improve air quality in Ontario.
Public policy should be based upon the best available evidence so as to give priority to those strategies that are clearly effective. The public deserves a role in the process of determining rational risk choices. It is the public which bears the burden of illness and injury, as well as the economic impacts of air pollution. The people of Ontario must have meaningful representation of their views, no matter how much of a challenge this process may be to implement.
Actions must be taken on the findings and recommendations in this paper. Ground-level ozone, acid aerosols and particulate matter pose a serious health risk to the people of Ontario. An integrated and comprehensive approach by many stakeholders, including the active involvement of organized medicine, is required to address this important issue. While cognizant of the barriers to implementation of these recommendations, the OMA believes that the end benefits far outweigh the obstacles. The result would be a healthier society, and in particular, healthier children. The challenge we face is to determine the best method to reduce these environmental emissions in a manner that is accepted and understood by industry and government. There are a great number of groups in our community who have an intense interest in and responsibility for this health problem, including health-care providers, educators, parents, environmental agencies and groups, and legislators. The OMA urges every community to address the issue of health effects of ground-level ozone, acid aerosols and particulate matter in an aggressive and timely fashion.
Glossary of Terms
Acid aerosols are essentially particles which contain acid, and are not traditionally monitored on a routine basis to the same extent as other air pollutants. However, routine measurements have been made of sulfate levels, which correlate to some degree with actual acid measurements. Acid aerosols are acidic particulates (e.g., sulphates - often referred to as particulate sulphates).
Acid rain is a phenomenon commonly associated with the emission of acidic substances and subsequent acidification of rainfall.
Airborne particulates are very small solids or liquids that vary in size and chemical composition. The finer particles are of most concern because only these are small enough to travel deeply into the lungs. Airborne particulates also carry attached chemicals into the lung (e.g., metals).
Air quality index (AQI) is an indicator of the pollutant which is highest relative to the criteria of the six most common urban air pollutants in Ontario: carbon monoxide, nitrogen dioxide, sulphur dioxide, suspended particles, total reduced sulphur, and ozone. The AQI measures and reports on these air pollutants.
Ambient air refers to the open air, external to buildings.
Confounding factor is a cause of disease that is not under investigation, but that distorts the cause-effect relationship under study (e.g., weather and seasonality).
Emission refers to any pollutant which makes its way into the air as a result of human activity.
Epidemiology is the science that studies statistical relationships between patterns of disease and the occurrence of possible causing or contributing factors.
Environmental health refers to conditions in the natural and built environment which can influence human health and well-being.
Inhalable particulate (IP) refers to particulate matter equal to or less than 10 micrometers in aerodynamic diameter, which are particles that are easily inhaled.*
MOE is an acronym for Ontario Ministry of Environment.
Morbidity means various adverse health effects, other than mortality; for example, asthma.
Mortality means premature death.
NO2: Nitrogen dioxide is one of a group of gases called nitrogen oxides, which are composed of nitrogen and oxygen. Like sulphur dioxide, nitrogen oxides can react with other chemicals in the atmosphere in the presence of sunlight to form acidic pollutants, including nitric acid.
NOx: Nitrogen Oxides is the sum of nitric oxide (NO) and nitrogen dioxide (NO2). Nitrogen oxides react with volatile organic compounds in the presence of sunlight to form ground-level ozone.*
O3: Ground-level ozone is a gas that is formed when nitrogen oxides react with oxygen and volatile organic compounds (VOCs) in the presence of sunlight. Ground-level ozone is the primary component of smog and is different from the blanket of ozone high above the earth ("stratospheric" ozone or "the ozone layer"), which protects us from the sun's harmful UV rays.
ppb: Pollutant concentration in units of parts per billion, volume/volume.
Particulate matter (PM) is a general term for airborne particles including dust, smoke ash and pollen.
PM10: Particles equal to or less than l0 micrometers in an average aerodynamic diameter, also referred to as inhalable particulates or coarse particles (i.e. larger than 2.5 micrometers). PM10 by definition also includes PM2.5. Coarse particles equal the difference between PM10 and PM2.5 (i.e. PM10 minus PM2.5).*
PM2.5: Particles equal to or less than 2.5 micrometers in an average aerodynamic diameter, also referred to as respirable particulates or fine particles. These fine particles are so small that several thousand of them could fit on the period at the end of this sentence. They originate from fuel combustion, power plants, and diesel buses and trucks. They are a health concern because they easily reach the deepest recesses of the lungs. *
Photochemical reaction is a chemical reaction influenced or initiated by light, particularly ultraviolet light.
Respirable particulates are particles equal to or less than 2.5 micrometers in aerodynamic diameter, that can easily penetrate into the lung.
Smog is a term that comes from the words "smoke" and "fog" and is a harmful mixture of gaseous and inhalable pollutants. It is sometimes associated with the brown-yellowish haze we often see blanketing the horizon in urban centres during summer and fall months. Important components of smog in the summer are ground-level ozone and inhalable particulates. In winter, it is primarily airborne inhalable particulates.
Southern Ontario Corridor is approximately the area in Ontario south of a line on the map joining Grand Bend on Lake Huron and Arnprior on the Ottawa River.
SO2: Sulphur dioxide is a colorless gaseous pollutant (with a strong pungent odor at air concentrations over five parts per million) that can be chemically transformed in the atmosphere in the presence of other chemicals and sunlight to form acidic pollutants such as sulfuric acid and sulphate aerosols. These compounds are major components of acid rain.*
Standard is a legally enforceable limit for a pollutant.
TSP: Total suspended particulates are particles that are generally smaller than or equal to 100 micrometers in aerodynamic diameter.
Toxicology is a science that studies the effects of poisons on humans, animals, or other organisms.
Ķm: Micrometre or micron, one-one millionth of a meter in length, which is a commonly used measure of the effective diameter of small particles.
Ķg/m3: Micrograms per cubic metre, a commonly used concentration unit for air pollution.
VOC: Volatile organic compounds are a class of compounds containing at least one carbon atom and are volatile. Nitrogen oxides react with volatile organic compounds in the presence of sunlight to form ground-level ozone.*
Windsor-Quebec Corridor consists of an Ontario and a Quebec portion, and extends from Windsor, Ontario, to Quebec City, Quebec. The Ontario portion is referred to as the Southern Ontario Corridor (see Southern Ontario Corridor).
* Further details on these compounds can be found in The Lung Association Hamilton-Wentworth's, 502 Concession St. Hamilton, Ont. L9A 1C4, phone: (905)383-1615, series of six fact sheets (1996)
Suggested further readings:
Abelsohn A. Pamphlet for Primary Care Physicians: Smog and Human Health. 1996. Environmental Health Committee, Ontario College of Family Physicians, 357 Bay St, Ste 800 Toronto M5H 2T7.
American Lung Association (ALA) National Washington Office. A summary of recent studies of the health effects of air pollution: Ozone Air Pollution. Available from ALA, 1726 M St. NW, Suite 902, Washington, D.C. 20036-4502 - phone (202) 785-3355.
Federal-Provincial Working Group on Air Quality Objectives and Guidelines. Protocol for the Development of National Ambient Air Quality Objectives, Part 1: Science Assessment Document and Derivation of the Reference Level(s). Environment Canada, Health Canada. November 1996, Catalogue En42-17/5-1-1997E. Request for copies to Director, Science Assessment & Policy Integration Division, Atmospheric Environment Service, Environment Canada, 1905 Dufferin St. Toronto, Ontario M3H 5T4.
Health and Environment: A Handbook for Health Professionals. March 1995. Prepared by The Great Lakes Health Effects Program Health Protection Branch, Health Canada, and The Environmental Health and Toxicology Unit Public Health Branch, Ontario Ministry of Health. For further information about this Handbook, please contact (613) 957-1876
Liu L (ed). 1997 Canadian Acid Rain Assessment, Volume 5, The Effects on Human Health. Issued by the Authority of the Minister of Environment. Copyright Minister of Supply and Services Canada, 1997. Catalogue number EN56-123/5-1997E. For copies, please call Environment Canada’s enquiry centre at 1-800-668-6767.
Pope AM, Rall DP, Editors. (1995). Environmental Medicine: Integrating a Missing Element into Medical Education. Washington DC, Institute of Medicine, National Academy Press.
U.S. Environmental Protection Agency (EPA). Health and Environmental Effects of Particulate Matter: Fact Sheet. July 17, 1997; and U.S. EPA. EPA’s Revised Ozone Standard. July 17, 1997. Anyone with a computer and a modem can download the new standards and these fact sheets from the Clean Air Act Amendments bulletin board of EPA's electronic Technology Transfer Network (TTN) by calling (919) 541-5742 (look under "Recently Signed Rules").
The Lung Association, Hamilton-Wentworth & Hamilton-Wentworth Air Quality Initiative, 1996, "The Air Pollution Picture", Fact Sheets 1-6. 502 Concession St. Hamilton L9A 1C4, Phone: (905) 383-1616.
Mercury (Hg) is a highly toxic, bioaccumulative, persistent substance<5>. A study reports cognitive deficits (especially involving language) in seven-year-old children with prenatal exposure to mercury. The effects on brain function were detectable at exposure levels currently considered safe.
Sources and Distribution While not all the pollutants of concern to human health are emitted from smokestacks, a key pollutant that is, but that has not received much public attention, is mercury. Governments across North America and Europe have targeted the phasing-out of the exposure to mercury as a priority. While the element mercury has previously had many applications in industry and consumer products, its presence as a pollutant in the environment is of significant concern.
Almost all mercury contamination in the Great Lakes Basin is a result of air pollution. Three-quarters of this contamination is a result of human activity. Coal-fired power plants are the single largest source of mercury in the atmosphere. In 1995, coal-fired plants were responsible for 10 per cent of all mercury emissions in Ontario and 21 per cent in the U.S.. Mercury emitted to the atmosphere deposits in lakes, where it bioaccumulates in fish to the point where fish consumption can be hazardous to human health. Mercury is also a global pollutant since it can remain suspended in the atmosphere for more than 30 days and travel hundreds of kilometres. The most toxic form of mercury to humans and wildlife is methylmercury.
Two other air pollution-related factors in the Northeast which are thought to promote the deposition of mercury in aquatic ecosystems where it can be transformed into an organic form – methylmercury – include: 1) the acidified condition of many lakes, ponds, and streams (which is associated with high levels of methylmercury); and 2) elevated summertime levels of tropospheric ozone (which facilitates the conversion of inorganic forms of mercury in the atmosphere to chemical forms that are more susceptible to deposition).
83. Pollution Probe. Mercury Elimination and Reduction Symposium: Toward National Partnerships. May 5-6, 1997.
84. Northeast States for Coordinated Air Use Management, Northeast Waste Management Officials' Association, New England Interstate Water Pollution Control Commission, Canadian Ecological Monitoring and Assessment Network. Northeast States and Eastern Canadian Provinces Mercury Study: A Framework for Action. February 1998.
Health Effects Mercury is a potent neurotoxin. Exposure to high levels of mercury is of particular concern to developing fetuses (through their mother) and children. One study reports cognitive deficits in seven-year-old children with prenatal exposure to methylmercury. Mercury-related neuropsychological damage was most pronounced in the domains of language, attention, and memory, and to a lesser extent in visuospatial and motor functions. These associations remained after adjustment for other factors such as alcohol or smoking during pregnancy, and after exclusion of children with high mercury concentrations in the maternal scalp. It has been estimated that the risk of fetal brain damage increases when the mercury concentration in maternal scalp hair exceeds a certain level.
In a living organism, mercury disrupts the neurological, immunological, hormonal and enzymatic functions of cells. Methylmercury can bioaccumulate through the food chain in aquatic systems to reach levels in large predatory fish millions of times greater than those levels found in the water. This can be particularly harmful to populations that rely on fish, such as aboriginal communities. One study found that mercury was a toxin in Quebec Inuit blood samples, a population living far from many possible point sources of mercury emissions. Although levels found among the Inuit were too low to endanger adults, the neurotoxic effects of mercury could be of concern for fetal development and breast-fed infants.
The fact that exposure to methylmercury can impair the human nervous system and kidney function is well-established, as are the approximate dose levels that lead to overt adverse effects (e.g., incidents of large-scale poisoning in Iraq). While inhalation or bodily contact with inorganic forms of mercury can produce serious health effects, these types of exposures tend to occur under unique circumstances (e.g., in cases of accidental spills). The methylated forms of mercury are nearly 99 per cent absorbed by humans when ingested and are excreted only very slowly. In other words, methylmercury is more toxic at lower doses relative to inorganic mercury.
Table 111-1 lists specific health effects associated with exposure to methylmercury and, for comparison, health effects associated with inorganic mercury. Although the absorption and distribution of these forms of mercury in the body are different, it is possible that the toxic actions at the cellular level may be similar.
Ingested methylmercury is distributed throughout the body and has been found in all regions of the brain in exposed adults. The highest levels are found in the kidney, liver, and brain a few days after exposure. In the adult brain, methylmercury appears to concentrate in the motor and visual regions, where it can produce focal lesions that are associated with paresthesia, or numbness and loss of feeling in the legs and arms. The onset of paresthesia is delayed for several days or weeks after exposure. Excretion of methylmercury from the body is slow, often taking several weeks to months. Lactation speeds the removal of methylmercury from the body, decreasing the half-life of elimination in lactating women but providing a pathway of exposure to the nursing child.
The effects of methylmercury exposure appear to differ depending on age at the time of exposure. In the embryo/fetus or young child, methylmercury can inhibit the normal development of the nervous system and produce generalized lesions throughout the brain[91-92]. Studies suggest that damage can occur at low exposure levels and that it frequently may not be apparent until later in the development process when the child’s motor and verbal skills are found to be delayed or abnormal. Developmental effects have been found in children who were exposed in utero, even though their mothers did not experience any of the symptoms of adult toxicity.
86. Stern AH. Reevaluation of the Reference Dose for Methylmercury and assessment of current exposure levels. Risk Anal. 1993; 13(3): 355-364.
87. World Health Organization (WHO). Methyl Mercury. Volume 101. World Health Organization International Programme on Chemical Safety. Geneva, Switzerland, 1990.
88. USEPA (U.S. Environmental Protection Agency). 1996b. Mercury Study: Report To Congress. Science Advisory Board Draft. US EPA-452/R-96-001d. Volume 1V: Health Effects of Mercury and Mercury Compounds. Office of Air Quality Planning and Standards and Office of Research and Development. Washington, D.C. June.
89. Institute of Medicine. 1991. Seafood Safety. National Academy Press. Wash.D.C.
90. Rice DC. Sensory and Cognitive Effects of Developmental Methyl Mercury Exposure in Monkeys and Comparison to effects in Rodents. Neurotoxicology 1995; 17: 139-154.
91. Clarkson TW. 1987. Metal Toxicity in the Central Nervous System. Environmental Health Perspectives. 75: 539-564.
92. Marsh DO, Clarkson TW, Cox C, Amin-Zaki L, Al-Tikriti S. Fetal Methylmercury poisoning: Relationship between concentration in single strands of maternal hair and child effect. Arch. Neurol. 1987; 44:1017-1022.
93. Marsh DO et al. 1995. The Seychelles Study of Fetal Methy Hg Exposure and Child Development: Introduction. Neurotoxicology. 16(4): 583-596.
Summary The available science indicates a potential health risk, especially to the embryo/fetus and child, from methylmercury exposure. At low levels of exposure, subtle but significant effects may occur that would be difficult to detect. The difficulty of demonstrating a link between mercury exposure and neurological damage is compounded by the fact that researchers have not yet determined which stage, or stages, of brain development are most sensitive to methylmercury effects, and by the existence of a considerable latency period between exposure and the appearance of symptoms. In light of these uncertainties, a conservative approach to the management of the relevant health risks is warranted.
The available science also indicates that adverse health effects associated with exposure to mercury may not be reversible, increasing the significance of the potential health risk. The slow removal of mercury from the body suggests that this toxin will accumulate as exposures continue or recur, thereby increasing the probability that adverse health effects will result from periodic consumption of contaminated fish.
Methodological issues in studies of air pollution and daily counts of deaths or hospital admissions.
Some researchers have questioned the validity of using ecological studies to perform hypothesis testing is questioned. A review of the evidence suggests that associations from these studies are statistical rather than cause-effect (e.g., strength of association is weak and confounding by other pollutants is likely and it is not possible to separate individual pollutant effects).
The central methodological issue in studies of air pollution and daily counts of deaths or hospital admissions is control for seasonality. Both over and under control are possible, and the use of diagnostics, including plots, is necessary. Weather dependence is probably non-linear, and adequate methods are necessary to adjust for this. However, several adequate methods exist to control for weather and seasonality while examining the associations between air pollution and daily counts of mortality and morbidity. In each case, care and judgment are required.
It has been argued that hospital records are too unreliable to be used in epidemiologic studies of admission rates and air pollution. However, a study indicates that such records are reliable enough. Delfino, et al. in Quebec showed that there was 95 per cent congruence between the diagnosis of asthma among inpatients, and subsequent confirmation of their diagnosis after a detailed investigation by the hospital. The diagnoses are communicated to a computerized database. This high confidence level is possible because of the high quality of Canada's health information system.
In recent years, there has been a dramatic increase in the use of numerical simulation models in the earth sciences as a means of evaluating large-scale or complex physical processes. In some cases, the predictions generated by these models are considered as a basis for public policy decisions such as air pollution and daily deaths. Oreskes, Shrader-Frechette and Belitz argue that verification and validation of numerical models of natural systems is impossible. This is because natural systems are never closed and because model results are always non-unique. Models can only be evaluated in relative terms and their predictive value is always open to question. The primary value of models is heuristic: models are representations, useful for guiding further study but not susceptible to proof.