Endocrine disrupting chemicals: a new and emerging public health problem?

Acerini, Carlo L.; Hughes, Ieuan A.

doi:10.1136/adc.2005.088500

Cited by 66 publications

(30 citation statements)

References 37 publications

(29 reference statements)

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“…Humans are exposed to more than 80 000 chemicals some of which have properties that have estrogenic effects or can interfere with androgen synthesis and action. These include pesticides, phthalates and bisphenol A (47). Studies in rodents can replicate the effects of androgen insufficiency by administering such compounds to pregnant dams anddemonstrating undescended testes, hypospadias and reduced anogenital distance in male offspring (48).…”

Section: Environmental Factorsmentioning

confidence: 99%

Factors controlling testis descent

Hughes¹,

Acerini²

2008

European Journal of Endocrinology

139

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Descent of the testis from an intra-abdominal site in foetal life to an extracorporeal location after birth is a mandatory developmental process to ensure that the mature testis promotes normal spermatogenesis. The two phases of transabdominal and inguinoscrotal descent occur approximately during the first and last thirds of gestation respectively. Key anatomical events to release the testis from its urogenital ridge location and to guide the free gonad into the scrotum are the degeneration of the cranio-suspensory ligament and a thickening of the gubernaculum. Androgens play a role in both these processes, particularly with respect to enabling the testis to traverse the inguinal canal in the final phase of descent. Experiments in animals suggest that androgens mediate this effect via the release of calcitonin gene-related peptide by the genitofemoral nerve, but direct evidence for such a mechanism is lacking in humans. The transabdominal phase of descent is under the control of insulinlike 3 (INSL3), a product of the Leydig cells. Definitive evidence of its role in rodent testis descent is illustrated by the phenotype of bilateral cryptorchidism in Insl3K/K null mice. Circulating levels of INSL3 are higher in boys at puberty, are undetectable in girls and are lower in boys with undescended testes. A minority also have a mutation either in the INSL3 gene or affecting its receptor gene, relaxin/insulin-like family peptide receptor 2 (LGRF8). Other factors that may play a role in testis descent include the anti-Mullerian hormone and members of the HOX gene family. Evidence that the prevalence of undescended testis may be increasing provides a phenotypic readout for the effects of postulated chemicals in the environment interfering in some way with the action of factors that control testis descent. Epidemiological studies point to profound geographical variations in prevalence in countries such as Denmark and Finland. Associations have been found with levels of chemicals labelled as endocrine disruptors being higher in breast milk samples from mothers with cryptorchid boys when compared with controls. The adverse effects of these compounds (e.g. bisphenol A) can be replicated in the offspring of dams exposed during pregnancy. A sensitive marker of an anti-androgen effect of a compound is a reduction in the anogenital distance, an anthropometric measurement that is significantly greater in males compared with females. The observation of an association between the anogenital distance in infant boys and the level of pesticides in the urine of their mothers in late gestation indicates that this has the potential to be a useful surrogate marker of the effects of environmental chemicals on testis descent in human population studies. The rightful place for the testis at birth is in the scrotum in order to provide the temperature differential essential for normal spermatogenesis. Appropriate screening programmes and early surgical intervention are the prerequisites to ensure optimal fertility in adulthood and a con...

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Section: Environmental Factorsmentioning

confidence: 99%

Factors controlling testis descent

Hughes¹,

Acerini²

2008

European Journal of Endocrinology

139

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“…More than 100,000 man-made chemicals are available on the market including approximately 1,500 new molecules released yearly [20,21] for manufacturing products whose primary use is for human well-being and socioeconomic development. Since the 1990s, EDs have been one of the most controversial issues, attracting the attention of the scientific community, international agencies and organizations, governments and the general public.…”

Section: Endocrine Disruptors In Drinking Water: Public Health Relevancementioning

confidence: 99%

“…The nature and origin of EDs is diverse and includes groups of compounds such as: active ingredients in medicines with collateral hormonal effect, pesticides and adjuvants for their application, products to increase growth and weight gain in livestock, personal care and hygiene products, flame retardants, chemicals for use in the plastic industry and other frequently used industrial chemicals, natural and synthetic hormones, as well as products for manufacturing consumer goods and degradation by products [20,[22][23][24][25][26].…”

Section: Origin and Occurrence Of Eds In Drinking Watermentioning

confidence: 99%

Endocrine Disruptors in Water Sources: Human Health Risks and EDs Removal from Water Through Nanofiltration

Muñoz¹,

Mólgora²,

Domínguez³

et al. 2013

International Perspectives on Water Quality Management and Pollutant Control

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“…Assessment of the role of EDCs on pubertal onset, however, is complicated by the significant contributions of genetics, nutrition, somatic growth, and overall health on pubertal timing. Nevertheless, a geographically based increase in the incidence of hypospadias, cryptorchidism, and testicular germ cell cancers has been observed, and sperm counts and fertility rates have declined worldwide raising concerns about environmental influences on male reproductive health (Sharpe & Skakkebaek 1993, Acerini & Hughes 2006. To explain these observations, the testicular dysgenesis syndrome has been proposed to hypothesize that fetal exposure to estrogenic chemicals during testicular development leads to long-term effects on male reproductive health (Sharpe & Skakkebaek 1993).…”

Section: Figurementioning

confidence: 99%

“…An important contributor to the secular trend in female pubertal timing is the significant improvement in overall public health over the past century. Multiple reports, however, also emphasize the potential role of environmental chemicals, specifically endocrine-disrupting compounds (EDCs; Acerini & Hughes 2006, Euling et al 2008b, Mouritsen et al 2010, Toppari & Juul 2010. EDCs are hormonally active compounds that are speculated to have a causative role in the recent decline in sperm counts and impaired fertility worldwide, as well as the regionspecific changes in the prevalence of hypospadias and cryptorchidism, and reproductive tract cancers (Sharpe & Skakkebaek 1993).…”

Section: Introductionmentioning

confidence: 99%

Male pubertal development: are endocrine-disrupting compounds shifting the norms?

Zawatski¹,

Lee²

2013

Journal of Endocrinology

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Endocrine-disrupting compounds (EDCs) are synthetic or natural compounds that interfere with endogenous endocrine action. The frequent use of chemicals with endocrine active properties in household products and contamination of soil, water, and food sources by persistent chemical pollutants result in ubiquitous exposures. Wildlife observations and animal toxicological studies reveal adverse effects of EDCs on reproductive health. In humans, a growing number of epidemiological studies report an association with altered pubertal timing and progression. While these data are primarily reported in females, this review will focus on the small number of studies performed in males that report an association of polychlorinated biphenyls with earlier sexual maturity rating and confirm subtle effects of lead, dioxins, and endosulfan on delaying pubertal onset and progression in boys. Recent studies have also demonstrated that EDC exposure may affect pubertal testosterone production without having a noticeable effect on sexual maturity rating. A limitation to understand the effects of EDCs in humans is the potential for confounding due to the long temporal lag from early-life exposures to adult outcomes. The complex interplay of multiple environmental exposures over time also complicates the interpretation of human studies. These studies have identified critical windows of vulnerability during development when exposures to EDCs alter critical pathways and affect postnatal reproductive health. Contemporaneous exposures can also disrupt the hypothalamic-pituitary-gonadal axis. This paper will review the normal process of puberty in males and summarize human data that suggest potential perturbations in pubertal onset and tempo with early-life exposures to EDCs.

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Endocrine disrupting chemicals: a new and emerging public health problem?

Cited by 66 publications

References 37 publications

Factors controlling testis descent

Factors controlling testis descent

Endocrine Disruptors in Water Sources: Human Health Risks and EDs Removal from Water Through Nanofiltration

Male pubertal development: are endocrine-disrupting compounds shifting the norms?

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