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The classic toxicology paradigm between exposure and response provides the justification for accurate measurement of exposure to underpin good epidemiological studies aimed at relating an environmental exposure to an adverse effect. The closer the exposure metric approaches the dose, the more accurate the response function. Toxicologists identify the true harmful entity in the dose as the biologically effective dose (BED)—the entity that drives the adverse effects. Measuring exposure is, however, notoriously difficult, and the relationship between a mass measure (the current convention for assessing environmental exposures) and the BED has not always been clear. In the past decade, the mass of particulate matter measured as PM10 or PM2.5 has proved useful in demonstrating associations between ambient particle levels and a wide range of health outcomes, including mortality and morbidity, among patients with cardiovascular and/or respiratory diseases.1,2 In the context of both toxicological and epidemiological research, it is well accepted that the PM10 mass is not ideal but represents a surrogate for the BED. This is self-evident from the fact that much of the PM10 mass consists of low-toxicity components such as ammonium sulphates and nitrates, sea salt (sodium chloride), crustal dust and road dust. By contrast, relatively tiny masses of transition metals and organic species may redox cycle and make a major contribution …
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