Response to Briggs

association between [chronic PM] air pollution exposure and health [mortality]." In applying these criteria, I have included experimental studies in animals and epi-demiologic studies in humans (6). Rodents exposed to high concentrations of diesel exhaust for life did not show early or increased mortality (6). The available epi-demiologic studies (3-5) showed only weak associations across a narrow exposure range. The possible role of PM and lung function in the Six Cities Study suggested that there were differences in lung function between cities, but no measurable effect attributable to PM2 5' In the Seventh Day Adventist Study (5), there appeared to be a coherent relationship between PM and self-reported symptoms, but not between PM and mortality. However, the analyses required to evaluate fully this PM-symptoms association were not reported. Furthermore, short-term exposures and hospital admissions may have little to no relevance for mortality from chronic exposure (6,11). Finally, individual-level measurements of an analogous/surrogate PM2,5 exposure from the same populations and same cities provided a test of the internal consistency and biological coherence of the ambient PM25 associations. I know of no other experimental or clinical human studies that can be used as a more appropriate test. I did not say or mean to imply that all of Hill's (1) criteria must be obeyed before accepting cause and effect. The only criterion that must be met is that exposure must precede the effect (6,12). I agree with Loomis et al. that Hill's (1) guidelines can be "helpful at the margins of epidemiologic interpretations" (as with PM), but also provide a good framework for assessing causali-ty in general. I do not believe that evidence was excluded, as alleged by Loomis et al., although further tests of the plausibility and coherence of these associations with PM may be possible. Regarding the use of Hertz-Picciotto's criteria (2), my point was to assess whether the EPA was justified in developing quantitative concentration-response information useful in developing an annual PM2.5 standard from these studies. Table 5 in my paper (6) was an attempt to do this; because both studies were of the same design, the criteria were applied to both the design and the two individual studies. I conduded (6) that none of the Hertz-Picciotto criteria for quantifi-cation of risk and setting air quality standards using [these] epidemiology studies are met. I believe these are useful guidelines and that they do "contribute to a firmer scientific foundation …