Correspondence Comment on “Chronic Disease and Early Exposure to Air-Borne Mixtures. 2. Exposure Assessment” We are writing in response to several inaccuracies and inconsistencies in James Argo’s Chronic Disease and Early Exposure to Air-Borne Mixtures. 2. Exposure Assessment (1). The author reviews emissions reported from a number of industrial facilities in Canada between 1967 and 1970, improbably converts those complex emissions to units of potency compared to benzo[a]pyrene, asserts that doing so provides “an exact measure of dose” (p 7189), reviews the 1991 Canadian census data, and concludes that the “inverted” sex ratios (fewer males than expected) observed in communities near the industrial facilities in 1991 must be due to dioxin exposure. While there are a variety of issues worthy of comment here, we shall focus on the author’s assertions regarding dioxin and sex ratios. Decreases in sex ratio at birth (lower proportion of males) have inconsistently been reported in populations with highly elevated exposures to dioxins (reviewed in ref (2)). However, secular trends in North American dioxin exposure and sex ratio at birth do not support a finding of decreased sex ratio with increased dioxin exposures at environmental exposure levels. Dioxin levels in food, environmental media, and human tissues in North America and Western Europe have steadily declined since the 1960s (reviewed in ref (3)). The decline is particularly evident when serum data for 2,3,7,8-TCDD and for dioxin TEQs are compared. Young adults in the United States of reproductive age between 1971 and 1982 had serum lipid 2,3,7,8-TCDD and total TCDD toxic equivalency (TEQ) for chlorinated dibenzo-p-dioxins and dibenzofurans approximately 7-fold higher than do similarly aged people today (4–6). Similar trends have been reported in Western Europe (7). In the United States, the decline in dioxin exposure has been paralleled (perhaps coincidentally) by a slight decline in the sex ratio at birth from about 1,055 males per 1,000 females in the late 1960s to about 1,048 males per 1,000 females in 2002 (8). A similar slight decline has been reported in Canada (9). There are many factors that could account for the slight decline, including the increasing age at which women are becoming mothers (8). If the Argo conclusion that environmental dioxin exposure results in a reduced sex ratio were correct, the substantial decline in dioxin exposure in the general population would be associated with an increase in the relative number of males born, not a decrease as has been observed. Furthermore, Argo does not report whether the sex ratios in the areas supposedly affected by emissions differ from sex ratios in areas unaffected by emissions. In any case, it appears that Argo reviewed current census data for sex ratio, not sex ratio at birth. This ignores, among other potential biases, the impact of the well-known higher mortality rate among young males than among young females, an effect clearly shown in Canadian Life Tables (10). Even a slight survival difference would skew the observed sex ratio toward a lower proportion of males than the
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2008 American Chemical Society
proportion occurring at birth. Conclusions connecting 1991 population sex ratio data to alleged exposure to a single type of substance 24 years earlierswithout acknowledging the many other factors that could affect gender ratio in a community including mortality, migration, or other factors, and without actually demonstrating exposuresare wholly indefensible. The authors acknowledge that they have conducted research on topics related to dioxin exposure trends for the Chlorine Chemistry Division of the American Chemistry Council.
Literature Cited (1) Argo, J. Chronic disease and early exposure to air-borne mixtures. 2. Exposure assessment. Environ. Sci. Technol. 2007, 41, 7185–7191. (2) Rowlands, J. C.; Budinsky, R. A.; Aylward, L. L.; Faqi, A. S.; Carney, E. W. Sex ratio of the offspring of Sprague-Dawley rats exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in utero and lactationally in a three generation study. Toxicol. Appl. Pharmacol. 2006, 216, 29–33. (3) Hays, S. M.; Aylward, L. L. Dioxin risks in perspective: Past, present, and future. Regul. Toxicol. Pharmacol. 2003, 37, 202– 217. (4) Ferriby, L. L.; Knutsen, J. S.; Harris, M.; Nony, P.; Unice, K. M.; Paustenbach, D. J.; Haws, L. C.; Scott, P. Evaluation of PCDD/F and dioxin-like PCB serum concentration data from the 2001– 2002 National Health and Nutrition Examination Survey of United States citizens. J. Exp. Sci. Environ. Epidemiol. 2007, 17, 358–371. (5) U.S. Environmental Protection Agency. Dioxins and Dibenzofurans in Adipose Tissue of U.S. Vietnam Veterans and Controls; Report to U.S. Department of Veteran Affairs, EPA 560-5-89-002, NTIS PB-91-167585; U.S. EPA: Washington, DC, August 1990. (6) Patterson, D. G.; Canady, R.; Wong, L.-Y.; Lee, R.; Turner, W.; Caudill, S.; Needham, L.; Henderson, A. Age specific dioxin TEQ reference range. Organohalogen Compd. 2004, 66, 2878– 2883. (7) Wittsiepe, J.; Schrey, P.; Ewers, U.; Selenka, F.; Wilhelm, M. Decrease of PCDD/F levels in human blood from Germany over the past ten years (1989–1998). Chemosphere 2000, 40, 1103–1109. (8) Mathews, T. J.; Hamilton, B. E. Trend Analysis of the Sex Ratio at Birth in the United States;National Vital Statistics Reports Vol. 53, No. 20; National Center for Health Statistics: Hyattsville, MD, 2005. (9) Allan, B. B.; Brandt, R.; Seidel, J. E.; Jarrell, J. F. Declining sex ratios in Canada. Can. Med. Assoc. J. 1997, 156, 37–41. (10) University of Montreal, Department of Demography. Canadian Human Mortality Database; 2007; Accessed October 29, 2007 at http://www.bdlc.umontreal.ca/chmd/prov/can/ can.htm.
Lesa L. Aylward* Summit Toxicology, LLP, 6343 Carolyn Drive, Falls Church, Virginia 22044
Gail Charnley HealthRisk Strategies, Washington, DC
Julie Goodman and Lorenz Rhomberg Gradient Corp., Cambridge, MA ES702850Z
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