CORRESPONDENCE/REBUTTAL pubs.acs.org/est
Comment on “ Are Oral Contraceptives a Significant Contributor to the Estrogenicity of Drinking Water?”. n their publication Wise et al.1 address public’s concerns about contribution of oral contraceptives to environmental pollution. The authors review literature on the subject and discuss importance of 17-R-ethynylestradiol (EE2) used in contraceptive pills. I disagree with the authors’ opinion that oral contraceptives do not pose a serious threat to public health and wildlife. I will try to prove my point by showing weaknesses of the paper. To begin with, Figure 2 was not “adapted from ref 51” but copied from a PhD thesis by Titia de Mes “Fate of estrogens in biological treatment of concentrated black water”.2 In my opinion, the original figure caption “Contribution of different groups of the Dutch population to the amount of total excreted natural estrogens and 17- R-ethynylestradiol” is better than that given by the paper’s authors “Estimated contribution of total natural estrogens (E1+E2+E3) and EE2 excretion to total estrogen excretion in the Dutch population”. Notwithstanding, the figure is not informative. The first impression is that it shows percentage of synthetic estrogen plus percentage of population subgroups. What is more, the presented subgroups seem to overlap. Generally, “women” should consist of female “children 14 19 yrs”. If they had been accounted for separately, natural estrogens would have been overestimated. Anyway, the reference supporting Figure 2 “(51) Central Bureau of Statistics Statline. http:// www.cbs.nl” is not precise enough. Table 1, contrary to the author’s description, does not show “total estrogens” since the authors did not include EE2. The daily dose of 10.5 μg, taken from ref 3 may be misleading regarding environmental impact of EE2. In my opinion, EE2-sulfate conjugates should not be regarded as “inactive EE2”. The only difference between glucoronide and sulfate conjugate is that the latter becomes active later. In addition, percentage of EE2 oxidation seems to be too high in the light of research on in vitro metabolism of EE2.4,5 The authors are right that potency of the estrogens should be taken into account. The problem is that their estimates of estrogen potency are not correct. Quote: “The potency of these estrogens are typically measured in relation to E2 (having a value of 1) and are estimated to have the following relative potencies: EE2: 2.0; E2: 1; E1: 0.2 0.4; E3: 0.024 0.026”. This statement is supposedly supported by refs 6, 12, 48, 49. I have checked these references and the results are as follows: • Ref 6 contains no original data on the potency of estrogens; quote: “The relative efficiency of the estrogens to induce vitellogenesis is EE2 > E2 > E1, but the exact relationship is difficult to estimate”. • Ref 12 contains no data on the potency of estrogens. • Ref 48 quote: “Ethynylestradiol-17alfa was consistently the most potent steroid tested, with an estrogenic potency between 11 and 27 times greater than that of E2 and between 33 and 66 times greater than that of E1”. • Ref 49 quote: “it is clear that EE2 is a very potent inducer of VTG with a relative potency of about 30 times higher than E2”. One can estimate contribution of EE2 to total estrogenicity using Dutch population statistics6 and data on estrogens excretion
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presented in the paper. Assuming that the relative potency of EE2 is 20, its share in the total estrogenicity exceeds 50%. I finish my comment attempting to answer the title question “Are Oral Contraceptives a Significant Contributor to the Estrogenicity of Drinking Water?”. To do so, I used Table 5 medians and assumed that relative potency of EE2 is 20. The calculation suggests that oral contraceptives are responsible for 93% of estrogenicity in German drinking water. Thus, I question the authors’ conclusion that “EE2 is a relatively small contributor to the overall estrogenicity of drinking water”. Waldemar Grzybowski Institute of Oceanography, University of Gdansk, Poland
’ AUTHOR INFORMATION Corresponding Author
Phone: +48 58 523 68 27; fax: +48 58 523 66 78; e-mail:
[email protected].
’ REFERENCES (1) Wise, A.; O’Brien, K.; Woodruff, T. Are oral contraceptives a significant contributor to the estrogenicity of drinking water? Environ. Sci. Technol. 2011, 45, 51–60. (2) De Mes, T. Z. D. Fate of Estrogens in Biological Treatment of Concentrated Black Water, PhD Thesis. Wageningen University, Wageningen, The Netherlands 2007; http://edepot.wur.nl/2488. (3) Johnson, A. C.; Williams, R. J. A model to estimate influent and effluent concentrations of estradiol, estrone, and ethinylestradiol at sewage treatment works. Environ. Sci. Technol. 2004, 38, 3649–3658. (4) Rogers, S. M.; Back, D. J.; Orme, M. L. Intestinal metabolism of ethinyloestradiol and paracetamol in vitro: studies using Ussing chambers. Br. J. Clin. Pharmacol. 1987, 23, 727–734. (5) Li, P; Hartman, N. R.; Lu, C.; Collins, J. M.; Strong, J. M. Effects of cytochrome P450 inducers on 17-R-ethinyloestradiol (EE2) conjugation by primary human hepatocytes. Br. J. Clin. Pharmacol. 1999, 48, 733–742. (6) Central Bureau of Statistics Statline. http://www.cbs.nl/enGB/menu/themas/bevolking/cijfers/extra/piramide-fx.htm (accessed June 10, 2011).
Published: August 12, 2011 7605
dx.doi.org/10.1021/es201802r | Environ. Sci. Technol. 2011, 45, 7605–7605
