Particulate Matter Exposure Assessment

Zeger et al. (1) did an excellent job of presenting some of the possible effects of errors in particulate matter (PM) exposure assessment in time--series mortality analyses. However, they (1) state,

   our assessment of bias assumed that the health effects of personal
   exposures to particles originating indoors and outdoors are the same.

This assumption seems to ignore the vast toxicology literature, such as the work of Amdur et al. (2), which establishes that different particles do have different toxicity. There are no traffic and industrial PM emissions originating in a home. House dust and cigarette smoke greatly affect indoor PM concentrations, but barely affect ambient PM measurements. Furthermore, ambient PM may photochemically react with hydroxide radicals, ozone, and nitrogen dioxide and so may contain partially oxidized and nitrated species not present in indoor-generated PM. Inhalation of grams per cubic meter of soil particles during the 1935 dust bowl days (3) and milligrams per cubic meter of tars in tobacco smoke by smokers may produce delayed and chronic mortality effects from pneumonia and cancer, respectively, but no report in the literature states that such PM exposures produce a next-day increase in mortality, which is the basis for the PM time-series mortality model of Zeger et al. (1).

It has been shown (4), with the same PTEAM data used by Zeger et al. (1), that I, the exposure to indoor generated PM, I = (x - [Alpha]z), is uncorrelated with the magnitude of z, where z is the outdoor PM concentration at the subject's home, x is the subject's measured total personal PM exposure, and [Alpha] is the time-weighted average fraction of the outdoor PM to which the subject was exposed. That is, the exposure to PM, from personal and indoor sources of PM, was independent of z, which is expected given the fact that z was unknown; thus the people in the subjects' homes could not consciously influence their decisions to smoke, dust, or cook more or less in relation to the changing value of z. This supports Wilson and Suh (5), who argued that the personal exposure measure desired is [Alpha]z, the total personal exposure to particles from outdoor sources, not total personal exposure. If the above analysis is valid, Zeger et al. (1) agree that "the two types of particles are more appropriately treated as separate pollutants." I therefore encourage the authors to continue their fine work with that alternative premise because their conclusion of a negative bias, by treating indoor and ambient PM as a single pollutant, may be incorrect.

REFERENCES AND NOTES

(1.) Zeger SL, Thomas, D, Dominici F, Samet JM, Schwartz J, Dockery D, Cohen A. Exposure measurement error in time--series studies of air pollution: concepts and consequences. Environ Health Perspect 108:419-426 (2000).

(2.) Amdur MO, Bayles J, Ugro V, Underhill DW. Comparative irritant potency of sulfate salts. Environ Res 16 (1-3):1-8 (1978).

(3.) Mage DT. Coarse particles and dust storm mortality [Letter]. Environ Health Perspect 108:A12 (2000).

(4.) Mage D, Wilson W, Hasselblad V, Grant L. Assessment of human exposure to ambient particulate matter. J Air Waste Manage Assoc 49:1280-1291 (1999).

(5.) Wilson W, Suh H. Fine particles and coarse particles: concentration relationships relevant to epidemiologic studies. J Air Waste Manage Assoc 47:1238-1249 (1997).

David T. Mage Institute for Survey Research Temple University Philadelphia, Pennsylvania E-mail: davidm@temss2.isr.temple.edu

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