Particulate Matter Research:
Progress and Next Steps
Over the last 15 years an increasing number of epidemiological studies have reported associations between particulate matter (PM) and adverse respiratory and cardiovascular health effects – particularly in sensitive people, such as the elderly and asthmatics. In addition, clinical and toxicological research has been emerging to evaluate PM’s effects and to better understand the underlying biological mechanisms for how PM causes various adverse effects.
Recent human exposure studies provide suggestive evidence that components of PM (e.g., metals, sulfates) induce inflammatory responses in the lung airways. Experiments in vitro and in vivo also suggest that metal and organic components of PM induce cell mediated responses (e.g., cytokine and chemokine formation) as a result of oxidative stress in cells. These effects may cause damage to epithelial tissues and immune cells, such as macrophages, resulting in decreases in respiratory function, particularly in people whose airways are already compromised by asthma, emphysema, and bronchitis.
Research also suggests that fine and ultrafine PM can precipitate acute cardiac events, such as cardiac arrhythmias and myocardial infarction. While the mechanisms for cardiovascular effects have not been established, several plausible mechanisms are being studied. Some studies have shown PM dependent increases in fibrinogen, plasma viscosity, C-reactive proteins, and associations between PM and other cardiovascular disease factors, such as increases in hypertension and decreases in heart rate variability.
Research also suggests that not all components of PM are equally toxic (for a list of potentially toxic components, see Chemical Components of PM and Their Biologic Effects). Studies are underway to better understand the mechanisms by which these components cause adverse health effects. In addition, air monitoring data are being collected to better understand the composition of PM in Minnesota.
While substantial progress has been made in recent years, several scientific questions remain about the relationship between PM and disease. These include:
- What specific attribute(s) or component(s) of PM are responsible for the observed increases in morbidity and mortality? Do some sources of PM pose relatively more risk to public health than others?
- What are the biological mechanisms of action (i.e., How might PM cause the adverse health effects)?
- To what extent are other pollutants, which occur along with PM, responsible for the observed increases in morbidity and mortality? Are there synergistic or antagonistic effects with other co-pollutants (i.e., greater than or lesser than additive effects due to cumulative exposures to multiple chemicals)?
- To what extent are the associations observed in epidemiological studies influenced by confounding factors (e.g., differences in socioeconomic status or health care)?
- Do studies which rely on exposures estimated from central air pollution monitors accurately characterize the PM exposure in people who, in general, spend most of their time indoors?
- To what extent, and for what reason, are various population subgroups particularly sensitive to PM air pollution? (e.g., people with respiratory or cardiovascular conditions, children, the elderly, etc.)
- What is the quantitative relationship between exposures to current levels of ambient PM in Minnesota and various health effects?
In summary, an increasing body of research suggests that PM is associated with cardiovascular and respiratory effects in people, especially sensitive individuals, such as the elderly and people with asthma. Research is underway to determine how PM causes adverse effects, and to evaluate the role of specific risk factors (e.g., age, gender, pre-existing disease) and effect modifiers (e.g., co-pollutant concentrations). Also, air monitoring data are being collected to better understand the composition of PM in Minnesota, and to evaluate health risks.
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