Carta Acesso aberto Revisado por pares

Anogenital Distance: Defining “Normal”

2006; National Institute of Environmental Health Sciences; Volume: 114; Issue: 7 Linguagem: Inglês

10.1289/ehp.114-a399a

ISSN

1552-9924

Autores

Bernard Weiss,

Tópico(s)

Effects and risks of endocrine disrupting chemicals

Resumo

Vol. 114, No. 7 PerspectivesOpen AccessAnogenital Distance: Defining "Normal"is companion ofAnogenital Distance: Bailey and Renner Respond Bernard Weiss Bernard Weiss Published:1 July 2006https://doi.org/10.1289/ehp.114-a399aCited by:7AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit In their letter to EHP, McEwen and Renner (2006) dismissed the findings of Swan et al. (2005), who reported a significant relationship between a measure of anogenital distance (AGD) in boys and levels of phthalate metabolites in their mothers' urine during pregnancy. AGD is a sexually dimorphic index that, on average, is twice as great in males as in females, so it serves as a marker of proper male development. McEwen and Renner based their argument on an idiosyncratic form of logic. They asserted thatAll male infants evaluated in the study appeared normal … there is no evidence for potential adverse effect in the test population. … no conclusion can be drawn whether the reported values are normal or abnormal. The range of AGD values … likely represents typical biologic variation that would be expected to occur among normal study subjects.McEwen and Renner seem to be wholly unfamiliar with the meaning of a modest or even a slight shift in the mean of an index that reflects the distribution of susceptibility in a population. I have pointed out (Weiss 1988) that even a 5-point (5%) reduction in mean intelligence quotient in a population of 100 million increases the number of individuals classified as retarded from 6 million to 9.4 million. It is this kind of relationship that eventually prompted the Centers for Disease Control and Prevention (CDC) to lower its definition of elevated lead risk levels in blood, set at 40 μg/dL in 1970, to 10 μg/dL in 1991 (CDC 1991). Bellinger (2006) put it this way:A small change in the mean signals predictable accompanying changes in the proportions of individuals in the source population who fall into the tails of the distribution, where individuals who meet diagnostic criteria are found. Thus, the importance of a shift in group mean lies not in what it indicates about the average change among members of the study sample, but what it implies about the changes in the tails of the distribution in the population from which the study sample was drawn.He noted, based on Rose (1981), that in a population with a prevalence of clinically defined hypertension of 15%, a 5-mm reduction in mean systolic blood pressure would result in a 33% decrease in prevalence (Bellinger 2006). Epidemiologists recognize that a slight decrease in mean blood pressure in a population is translated into a major decrease in the incidence of serious cardiovascular events such as heart attacks.We already know that shortened AGD at birth is one element, the leading edge, as it were, of the "phthalate syndrome" in rats, which is marked by testicular pathology, reduced spermatogenesis, hypospadias, and cryptorchidism, a compilation of signs indicating disordered male development that Sharpe (2001) and others have noted to be on the increase in industrialized nations. An almost imperceptible shift to a lower mean AGD in the human male would foreshadow a heightened prevalence of reproductive system dysfunction. Is that the connection now emerging in the clinic?If McEwen and Renner's (2006) criteria for "normal" were to govern the way in which we define the health risks of lead exposure, we would be basing our criteria on the number of children brought into hospital emergency rooms with lead poisoning rather than on the threats it poses to their neurobehavioral development. No parent, and no community, would tolerate such a definition these days.ReferenceBellinger DC 2006. Neurobehavioral assessment in studies of exposures to neurotoxicants. In: Neurotoxicity and Developmental Disorders (Davidson PW, Myers CJ, Weiss B, eds). San Diego, CA:Elsevier Academic Press, 263–300. Google ScholarCDC 1991. Preventing Lead Poisoning in Young Children. Atlanta, GA:Centers for Disease Control and Prevention. Google ScholarMcEwen GN, Renner G. 2006. Validity of anogenital distance as a marker of in utero phthalate exposure. Environ Health Perspect 114:A19-2016393642. Link, Google ScholarRose G. 1981. Strategy of prevention: lessons from cardiovascular disease. BMJ 282:1847-18516786649. Crossref, Medline, Google ScholarSharpe RM. 2001. Hormones and testis development and the possible adverse effects of environmental chemicals. Toxicol Lett 120:221-32211323180. Crossref, Medline, Google ScholarSwan SH, Main KM, Liu F, Stewart SL, Kruse RL, Calafat AMet al.. 2005. Decrease in anogenital distance among male infants with prenatal phthalate exposure. Environ Health Perspect 113:1056-106116079079. Link, Google ScholarWeiss B. 1988. Neurobehavioral toxicity as a basis for risk assessment. Trends Pharmacol Sci 9:59-623072731. Crossref, Medline, Google ScholarFiguresReferencesRelatedDetailsCited by Vandenberg L, Luthi D and Quinerly D (2017) Plastic bodies in a plastic world: multi-disciplinary approaches to study endocrine disrupting chemicals, Journal of Cleaner Production, 10.1016/j.jclepro.2015.01.071, 140, (373-385), Online publication date: 1-Jan-2017. Trasande L, Vandenberg L, Bourguignon J, Myers J, Slama R, vom Saal F and Zoeller R (2016) Peer-reviewed and unbiased research, rather than 'sound science', should be used to evaluate endocrine-disrupting chemicals, Journal of Epidemiology and Community Health, 10.1136/jech-2016-207841, 70:11, (1051-1056), Online publication date: 1-Nov-2016. Kay V, Bloom M and Foster W (2014) Reproductive and developmental effects of phthalate diesters in males, Critical Reviews in Toxicology, 10.3109/10408444.2013.875983, 44:6, (467-498), Online publication date: 1-Jul-2014. Vandenberg L, Colborn T, Hayes T, Heindel J, Jacobs D, Lee D, Myers J, Shioda T, Soto A, vom Saal F, Welshons W and Zoeller R (2013) Regulatory decisions on endocrine disrupting chemicals should be based on the principles of endocrinology, Reproductive Toxicology, 10.1016/j.reprotox.2013.02.002, 38, (1-15), Online publication date: 1-Jul-2013. Malone P, Hall-Craggs M, Mouriquand P and Caldamone A (2012) The anatomical assessment of disorders of sex development (DSD), Journal of Pediatric Urology, 10.1016/j.jpurol.2012.08.009, 8:6, (585-591), Online publication date: 1-Dec-2012. Rekiel A, Więcek J, Wojtasik M, Ptak J, Blicharski T and Mroczko L Effect of Sex Ratio in the Litter in Which Polish Large White and Polish Landrace Sows were Born on the Number of Piglets Born and Reared, Annals of Animal Science, 10.2478/v10220-012-0015-5, 12:2, (179-185) Vandenberg L, Colborn T, Hayes T, Heindel J, Jacobs D, Lee D, Shioda T, Soto A, vom Saal F, Welshons W, Zoeller R and Myers J (2012) Hormones and Endocrine-Disrupting Chemicals: Low-Dose Effects and Nonmonotonic Dose Responses, Endocrine Reviews, 10.1210/er.2011-1050, 33:3, (378-455), Online publication date: 1-Jun-2012. Related articlesAnogenital Distance: Bailey and Renner Respond1 July 2006Environmental Health Perspectives Vol. 114, No. 7 July 2006Metrics About Article Metrics Publication History Originally published1 July 2006Published in print1 July 2006 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.

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