Document 9J6EnDpO5MmeqDQeep5B4njBL

OR-6828-D REV. 5-84 ($T49U5.HCD 1802 E. I. d u Po n t d e Ne mo u r s & Co mp a n y 9 INCORPORATED Pe t r o l e u m La b o r a t o r y WILMINGTON, DELAWARE 19896 Te l e p h o n e Ar e a Co d e 609-299-5000 July 18, 1983 Editor The New England Journal of Medicine 10 Shattuck Street Boston, MA 02115 Dear Sir: We wish to submit the attached comments for publication in the Correspondence section of the New England Journal of Medicine. Yours very truly, JMP/er Enc. 'John M. Pierrard Engineering Fellow Environmental Activities N33819 BETTER THINGS FOR BETTER LIVING . . . THROUGH CHEMISTRY TEH 0532459 To the Editor: In their recent article1 on chronological trends in blood lead levels Annest et al state that "the most likely ex planation for the fall in blood lead levels is a reduction in the lead content of gasoline". Based on analyses we did using the same NHANE5II data, and employing a number of different models and assumptions, we see no evidence that gasoline lead exposure is the most likely cause of the decrease in U.S. blood lead levels. Our analysis indicates that site-specific gasoline lead exposure accounts for only 0.5 to 1 ug/dl of the observed 5 ug/dl decrease, which is consistent with the observed national average air lead decrease (0.3 ug/m3)^, and the we11-documented blood lead response to air lead change (range 1 to 2 ug/dl per ug/m3)3. Changing demo graphics of the sampled sites can account for most of the four year decrease, about 3 ug/dl. The remaining unexplained portion of the decrease may be due to improved sample handling during the course of the study, effectiveness of numerous government programs to reduce lead intake, or other unquantified causes. Our initial methodology^ and subsequent modifications utilizing a split plot analysis of covariance raodel^ first ad justed blood lead levels for "within" and "between" sampling site demographic descriptors, and also for a site-specific gasoline lead exposure variable. We then regressed the residuals of the adjusted blood lead levels on time to evaluate the time trend contributions. Our results consistently showed that over 50$ of the apparent trend was accounted for by changing site demographics and less than 20$ was attributable to gasoline lead exposure. TEH 0532460 DUP050033725 -2Our site-specific measure of gasoline lead exposure density (tonnes/mi2/quarter) was computed from data on lead and gasoline use and site county population and land area, based on the correlation between population and gasoline use^. Annest et al used the total national gasoline lead use which reflects the overall trend, but does not account for the widely different ex posures observed at the 64 sites in the study. The apparent explanatory power of total national gasoline lead use as employed by Annest et al seems to be an artifact arising from confounding among the true exposure to gasoline lead, differential site demographics, and other unquantified time-related effects on blood lead. E. I. du Pont de Nemours & Co. Inc, Wilmington, DE John M. Pierrard, Ph. D, Ronald D. Snee, Ph. D. Charles G. Pfeifer, Ph. D. 1. Annest JL, Pirkle JL, Makuc D, et al. Chronological trend in blood lead levels between 1976 and 1980. N Engl J Med 1983; 308, 1373-7. 2. EPA Office Of Air Quality Standards. National air quality and emissions trends report, 1981. 3- Snee RD. Evaluation of studies of the relationship between blood lead and air lead. Int Arch Occup Environ Health 1981; 48:219-42. 4. Pierrard JM, Pfeifer CG, Snee RD. Assessment of blood lead levels in the USA from NHANESII data. Proe Inti Conf Heavy Metals in the Environ 1983, in press. TEH 0532461 DUP050033726  w -35. Kempthorne, 0. Design and analysis of experiments, John Wiley & 9 Sons, New York 1952, 6. Pierrard JM, Willis RL, Cantwell EN. Vehicle emissions controls and ambient air quality. Soc Auto Eng-Australasia Jubilee Year Conf, Melbourne Australia, 1977- TEH 0532462 DUP050033727