Error in DEHP background concentration.

resins using HPLC with the fluorescence detector [abstract; in Japanese]. Jpn J Dent Mater 17(special issue 321:119 (1998). 4. Schmalz G, Preiss A, Arenholt-Bindslev D. Bisphenol A content of resin monomers and degradation products[abstract]. J Dent Res 77(special issue B):823 (1998). 5. Nathanson D, Lertpitayakun P, Lamkin MS, Mahnaz EB, Lee-Chou L. In vitro elution of leachable components from dental sealants. J Am Dent Assoc 128:1517-1523 (1997). 6. Steinmetz R, Brown NG, Allen DL, Bigsby RM, BenJonathan N. The environmental estrogen bisphenol A stimulates prolactin release in vitro and in vivo. Endocrinology 138:1780-1786 (1997). 7. Colerangle JB, Deodutta R. Profound effects of the weak environmental estrogen-like chemical bisphenol A on the growth of the mammary gland of Noble rats. J Steroid Biochem Mol Biol 60:153-160 (1997). 8. Pfeiffer E, Rosenberg B, Deuschel S, Metzler M. Interference with microtubules and induction of micronuclei in vitro by various bisphenols. Mutat Res 390:21-31 (1997). 9. Dodge JA, Glasebrook AL, Magee DE, Phillips DL, Sato M, Short LL, Bryant HU. Enviromental estrogens: effects on cholesterol lowering and bone in the ovariectomized rat. J Steroid Biochem Mol Biol 59:155-161 (1996). 10. Ratnasabapathy R, Tom M, Post C. Modulation of the hepatic expression of the estrogen-regulated messenger-RNA stabilizing factor by estrogenic and antiestrogenic nonsteroidal xenobiotics. Biochem Pharmacol 53 :1425-1434 (1997). 11. Nagel SC, vom Saal FS, Thayer KA, Dhar MG, Boechler M, Welshons WV. Relative binding affinityserum modified access (RBA-SMA( assay predicts the relative in vivo bioactivity of the xenoestrogens bisphenol A and octylphenol. Environ Health Perspect 105:70-76 (1997). 12. Perez P, Pulgar R, Olea-Serrano F, Villalobos M, Rivas A, Metzler M, Pedraza V, Olea N. The estrogenicity of bisphenol A-related diphenylalkanes with various substituents at the central carbon and the hydroxy groups. Environ Health Perspect 106:167-174 (1998). 13. Soderholm KJ, Mariotti A. BIS-GMA-based resins in dentistry: are they safe? J Am Dent Assoc 130:201-209 (1999).

." Their Table  2 (1) shows that the background concentration used for DEHP was 1.6 pg/m3. That value was taken from Howard (2) who reported "mean remote ocean air concentrations" for DEHP of 0.07-0.17 ppb, citing Atlas and Giam (3). However, Atlas and Giam (3) actually reported remote DEHP air concentrations to be 0.32-2.68 ng/m3, with a mean of 1.4 ng/m3 a value more than 1,000 times less than the background value used for the CEP analysis. The panel has alerted the EPA to this error, and the EPA accordingly has corrected the CEP modeling report (4). TIable 2 of Woodruff et al. (1) shows that if the erroneous background value of 1.6 pg/m3 is disregarded, the CEP model predicts DEHP air concentrations to exceed the health benchmark of 0.25 pg/m3 in only 18 census tracts. Even this estimate probably exaggerates the potential health hazard for two reasons. First, to the panel's knowledge, the highest measured ambient DEHP air concentration in the United States that has been reported in the literature is 28 ng/m3 (5)-an order of magnitude below the EPA's cancer health benchmark. Second, the EPA's health benchmark of 0.25 pg/m3 was derived using an upper-bound unit risk methodology to extrapolate tumor data in rats and mice to human risk (6,7). However, numerous investigators now conclude that peroxisome proliferators such as DEHP pose little if any human cancer risk and that the quantitative risk assessment for such compounds should be based on a margin of exposure approach (8)(9)(10). This would significantly increase the health benchmark for DEHP and decrease (probably to zero) the number of census tracts in which modeled air concentrations would exceed the health benchmark.

DEHP Correction
We thank Courtney Price for pointing out an error in the background concentration for bis(2-ethylhexyl)phthalate (DEHP) in our paper "Public Health Implications of 1990 Air Toxics Concentrations across the United States" (1). In this paper, emissions data from stationary and mobile sources are used in an atmospheric dispersion model to estimate outdoor concentrations of 148 toxic air contaminants for each of the 60,803 census tracts in the contiguous United States.
Outdoor concentrations of air toxics were compared to previously defined benchmark concentrations for cancer and noncancer health effects. Benchmark concentrations are based on standard toxicological references and represent air toxic levels above which health risks may occur.
The results reported for DEHP are incorrect due to an error in the estimated background concentration for DEHP. We had originally used a value of 1.6 pg/m3 for DEHP, which was reported by Howard (2). As pointed out by Price, Howard (2) had incorrectly reported the value from another source, Atlas and Giam (3). Consequently, we have revised the background concentration for DEHP to 0.0014 pg/m3, consistent with the mean value reported by Atlas and Giam.
We had reported that the background concentration for DEHP was greater than the cancer benchmark for DEHP. However, the revised background concentration is much lower than the cancer benchmark.
Thus, DEHP should not be included in the list of pollutants in Table 2 for which background concentrations alone exceeded cancer benchmark concentrations (1). The A292 Volume107 Number6,June1999 Environmental Health Perspectives