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Canada - United States Air Quality Agreement

2002 Progress Report

SECTION IV  Scientific Cooperation

HEALTH EFFECTS

In addition to the American Cancer Society cohort study, Canadian, American, and European researchers are collaborating on a joint analysis of the relationship between air pollution and mortality, with support from the Health Effects Institute and the European Union.¹¹

Research on the health effects of air pollution involves scientists from federal and provincial governments as well as university-based researchers. Health Canada maintains an in-house program of research in toxicology, epidemiology, and biostatistics, and also funds outside collaborators on a contractual basis. Until March 2002, Health Canada and Environment Canada also provided grants to external researchers through the Toxic Substances Research Initiative, one theme of which was the health effects of air pollution.¹²

Recent research in toxicology includes evidence linking exposure to particulate matter with the release of endothelin, which plays an important role in the pathophysiology of circulatory disease¹³. Controlled clinical studies of exposure to particulate matter and ozone have also identified modest effects on chemical mediators of thrombosis or blood clotting¹⁴. Related work in clinical studies produced evidence linking exposure to particulate matter with vascular reactivity or reversible constriction of blood vessels.¹⁵ A study of air pollution exposure and heart rate variability has also been completed and analysis is underway¹⁶.

In epidemiology and biostatistics research, a team of investigators including Health Canada researchers and scientists from Canadian and American universities recently reported results from extended follow-up of the American Cancer Society cohort study¹⁷. This significantly strengthened the evidence base linking long-term exposure to air pollution with cardiopulmonary mortality and provided persuasive evidence of a link with lung cancer. Canadian investigators have also reported evidence identifying circulatory conditions, including diabetes and congestive heart failure as factors that potentially increase the probability of adverse effects of air pollution.¹⁸ With respect to time-series studies, Health Canada scientists recently completed a meta-analysis of the more than 100 studies linking short-term air pollution exposure with mortality.¹⁹. A study in Hamilton, Ontario, also found that areas characterized by lower socioeconomic status experienced more pronounced adverse effects from air pollution exposure²⁰.

EPA continues to carry out a major PM research program that seeks to answer the following key questions about health effects:

• What characteristics of PM (e.g., size, chemical composition) cause harm?
• What are the physiologic mechanisms by which PM causes health problems?
• What is the role of PM, alone and in combination with other pollutants, in producing health problems?
• What groups of people (e.g., asthmatics, children, elderly) are most sensitive to PM and what are the critical levels of exposure for these groups?

This research program is consistent with the recommendations of the National Research Council's Committee on Research Priorities for Airborne Particulate Matter. Some of the research being conducted to answer the key questions is summarized below.

To better understand the health problems related to PM, EPA conducted a series of epidemiologic studies looking at the relationship between exposure to PM and physiologic responses in sensitive populations such as the elderly, children, and asthmatics. Several important findings emerged: the relationship between PM_2.5 and heart rate was consistent with findings from earlier studies; heart rate variability decreased at higher concentrations of PM_2.5; and respiratory function decreased with increasing PM_2.5 concentration. Decreased heart rate variability has been identified as a risk factor for death from cardiovascular disease.

To further characterize the effects of PM on humans, EPA scientists conducted clinical studies in which volunteers in a controlled exposure chamber were exposed to concentrated particles collected from outdoor air.²¹ Healthy young adult participants (18-35 years old) experienced no symptoms of illness, no reduction in lung function, and no change in heart rate variability after a total exposure of two hours, during which they exercised. However, when elderly participants (65-80 years old) were subjected to the same conditions, they immediately experienced decreased heart rate variability which persisted for many hours after exposure stopped. These findings are consistent with the studies conducted at retirement homes and suggest that PM exposure influences nervous system control of heart rate in older people.²²

EPA has a strong program in animal toxicology studies investigating PM and other air pollutant²³. The program encompasses studies of PM constituents, molecular mechanisms, and pathophysiologic outcomes in healthy and susceptible animal models. Recent findings include studies where rodents were exposed to PM and other pollutants collected from outdoor air²⁴. Exposure to PM was associated with reduced heart rate and an increased incidence of abnormal heart rhythms and death, especially among rodents with compromised heart or respiratory function.²⁵ EPA is exploring potential mechanisms responsible for these effects.

In a particularly interesting study, a labour strike that closed a steel mill in the Utah Valley for a year provided opportunities to evaluate the toxicity of ambient air particles. Previous epidemiologic studies found a reduction in hospital admissions for respiratory conditions when the mill was closed compared with when it was operating. EPA scientists, in collaboration with academic researchers, obtained particulate matter (PM₁₀) samples from a Utah Valley air monitoring station for the year before (year 1), the year during (year 2), and the year after (year 3) the steel mill closure. Year 2 dust had lowest concentrations of soluble iron, copper, and zinc and generated the lowest number of oxidants (reactive compounds believed to be a major cause of lung particulate matter) from each of the three years. Dust from years 1 and 3 caused significant lung injury and inflammation, whereas dust from year 2 caused minimal injury. This study, and additional laboratory research, suggests a potential mechanism for the health effects reported in the Utah Valley. EPA investigators demonstrated that cultured human lung cells exposed to particulate matter from years 1 and 3 produced significantly higher levels of inflammatory mediators than cells exposed to particulate matter from year 2. Researchers are currently using this in vitro system to investigate whether transition metals in Utah Valley particulate matter cause the inflammation.²⁶

In addition to in-house research, EPA has established five PM Research Centers to investigate the heath effects of PM (see http://www.epa.gov/ttn/amtic/pmcenter.html). University scientists are working with EPA to characterize the relationship between ambient PM levels and actual personal exposure, identify the toxic components of PM and their associated biological effects, investigate the amount and distribution of PM deposited in the respiratory tract, and identify groups of people that are particularly susceptible to the adverse effects of PM. Findings from the first two years of research include the following:

• Inhalation of PM at concentrations only slightly above peak ambient levels can cause airway inflammation which can lead to other physiological responses, such as thickening of the blood.
• Controlled exposure studies in humans and animals have shown associations between ultrafine particles and changes in heart rate, heart rate variability, abnormal heart rhythms, and other heart and blood characteristics.
• Asthmatics may be particularly sensitive to ultrafine particles because these particles tend to be deposited in central airways of the respiratory system.
• In a study of healthy senior citizens, outdoor PM_2.5 concentrations were significantly correlated with an individual's personal exposure to PM_2.5.
• An epidemiologic study found significant associations between mortality and exposure to PM from traffic and coal-combustion sources but not between mortality and exposure to PM from oil combustion or soil.

EPA is also conducting research related to health effects of pollutants such as air toxics and ozone. (For more information on PM research, see the international inventory of PM research activities at www.pmra.org)