Decrease in anogenital distance among male infants with prenatal phthalate exposure
Open accessAbstract
Prenatal phthalate exposure impairs testicular function and shortens anogenital distance (AGD) in male rodents. We present data from the first study to examine AGD and other genital measurements in relation to prenatal phthalate exposure in humans. A standardized measure of AGD was obtained in 134 boys 2-36 months of age. AGD was significantly correlated with penile volume (R = 0.27, p = 0.001) and the proportion of boys with incomplete testicular descent (R = 0.20, p = 0.02). We defined the anogenital index (AGI) as AGD divided by weight at examination [AGI = AGD/weight (mm/kg)] and calculated the age-adjusted AGI by regression analysis. We examined nine phthalate monoester metabolites, measured in prenatal urine samples, as predictors of age-adjusted AGI in regression and categorical analyses that included all participants with prenatal urine samples (n = 85). Urinary concentrations of four phthalate metabolites [monoethyl phthalate (MEP), mono-n-butyl phthalate (MBP), monobenzyl phthalate (MBzP), and monoisobutyl phthalate (MiBP)] were inversely related to AGI. After adjusting for age at examination, p-values for regression coefficients ranged from 0.007 to 0.097. Comparing boys with prenatal MBP concentration in the highest quartile with those in the lowest quartile, the odds ratio for a shorter than expected AGI was 10.2 (95% confidence interval, 2.5 to 42.2). The corresponding odds ratios for MEP, MBzP, and MiBP were 4.7, 3.8, and 9.1, respectively (all p-values < 0.05). We defined a summary phthalate score to quantify joint exposure to these four phthalate metabolites. The age-adjusted AGI decreased significantly with increasing phthalate score (p-value for slope = 0.009). The associations between male genital development and phthalate exposure seen here are consistent with the phthalate-related syndrome of incomplete virilization that has been reported in prenatally exposed rodents. The median concentrations of phthalate metabolites that are associated with short AGI and incomplete testicular descent are below those found in one-quarter of the female population of the United States, based on a nationwide sample. These data support the hypothesis that prenatal phthalate exposure at environmental levels can adversely affect male reproductive development in humans.
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Perinatal exposure to phthalates can impair sexual differentiation in humans, as evidenced by shortened anogenital distance in male newborns.
“Perinatal exposure can impair sexual differentiation in humans, as evidenced by, among other things, a shortened anogenital distance in male newborns (Swan et al., 2005).”
From Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction (2026) · cites this paper as Swan et al., 2005
The Discussion reports shortened anogenital distance in boys whose mothers had elevated prenatal phthalate exposure and suggests that phthalates may undervirilize humans. However, the Abstract says the boys were examined at 2–36 months of age, not as newborns, and frames an adverse effect as a hypothesis supported by the data rather than an established causal finding. (LLM, conf=0.89)
Experimental — accuracy not yet measuredAnimal studies have shown that phthalates inhibit testosterone production in the testicles.
“Animal studies have shown that phthalates inhibit testosterone production in the testicles (Howdeshell et al., 2008; Swan et al., 2005).”
From Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction (2026) · cites this paper as Swan et al., 2005
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- Authors
- Swan, S. H., Main, K. M., Liu, F., Stewart, S. L., Kruse, R. L., Calafat, A. M., Mao, C. S., Redmon, J. B., Ternand, C. L., Sullivan, S., Teague, J. L., & the Study for Future Families Research Team
- Affiliations
- University of Rochester Medicine (US)
- University of Copenhagen (DK)
- Department of Family and Community Medicine, University of Missouri-Columbia, Columbia, Missouri, USA
- University of Missouri (US)
- Centers for Disease Control and Prevention (US)
- University of California, Los Angeles (US)
- Departments of Pediatrics and
- University of Minnesota (US)
- University of Iowa (US)
- Venue
- Environmental Health Perspectives
- Publisher
- American Chemical Society (ACS)
- Published
- 2005-05-27
- Volume
- 113
- Issue
- 8
- Pages
- 1056-1061
- ISSN
- 0091-6765 (ISSN-L)
- 1552-9924
- PMC
- PMC1280349
- OpenAlex
- W2058759573
- Cited by
- 1,586
- References
- 1
- Citations by year
- 2026: 24 · 2025: 27 · 2024: 30 · 2023: 60 · 2022: 41 · 2021: 65 · 2020: 64 · 2019: 78 · 2018: 84 · 2017: 83 · 2016: 60 · 2015: 99 · 2014: 114 · 2013: 104 · 2012: 112
- FWCI
- 64.49
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Environmental Health Perspectives (publishedVersion, cc-by)
- PubMed Central (publishedVersion, other-oa)
- PubMed (publishedVersion)
- MOspace Institutional Repository (University of Missouri) (submittedVersion)
- Funders
- U.S. Environmental Protection Agency
- University of Missouri (R01-ES09916)
- University of Minnesota (MO1-RR00400)
- National Institutes of Health (MO1‐RR00400, RR00400)
- National Institute of Environmental Health Sciences (R01 ES09916, R01ES009916)
- National Center for Research Resources (M01RR000400, M01-RR00400, M01RR0425, M01RR000425)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sexual Differentiation and Disorders
- Health Sciences › Medicine › Urology › Urological Disorders and Treatments
- Keywords
- prenatal phthalate exposure, anogenital distance, male infants, endocrine disruptors, urinary biomarkers, male genital development, mono-n-butyl phthalate, monoethyl phthalate, monobenzyl phthalate
- MeSH terms
- Child, Preschool, Environmental Pollutants, Female, Genitalia, Male, Humans, Infant, Male, Phthalic Acids, Pregnancy, Prenatal Exposure Delayed Effects, Maternal Exposure
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