Serum Bisphenol A Level in Boys with Cryptorchidism: A Step to Male Infertility?

Komarowska, Marta; Hermanowicz, Adam; Czyżewska, Urszula; Milewski, Robert; Matuszczak, Ewa; Miltyk, Wojciech; Dębek, Wojciech

doi:10.1155/2015/973154

Cited by 44 publications

(34 citation statements)

References 54 publications

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“…)21Fenichel et al . (2012)Southern FranceFrench studies on cryptorchidism in Nice and GrasseCase-referent46/106CryptochidismCord bloodBisphenol AMean unconjugated Bisphenol A marginally higher in cases but not significant ( P = 0.38)61Komarowska et al . (2015)PolandChildren 0–4 years admitted to paediatric departmentCase-referent98/57CryptochidismSerumBisphenol AFree serum BPA level in cryptorchid boys and in the control group was not statistically significant but the conjugated and total serumBPA level was elevated in cryptorchid boys31

a CR: completeness of reporting on a scale from 0 (low completeness) to 11 (high completeness).

b Bias and confounding: 1 = higher risk of bias, 0 = lower risk of bias.

…”

Section: Methodsmentioning

confidence: 98%

“…Studies reporting alternative measures of association such as difference in mean values of exposure levels in cases and controls were also included, and the authors were contacted to get risk estimates (Hosie et al ., 2000; Damgaard et al ., 2006; Main et al ., 2007; Choi et al ., 2012; Fenichel et al ., 2012; Komarowska et al ., 2015; Virtanen et al ., 2012). Several authors responded positively but reanalysis of the original data could not be accomplished within the given time-frame and the studies were therefore not included in the present review.…”

Section: Methodsmentioning

confidence: 99%

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The epidemiologic evidence linking prenatal and postnatal exposure to endocrine disrupting chemicals with male reproductive disorders: a systematic review and meta-analysis

Bonde

Flachs

Rimborg

et al. 2016

Hum. Reprod. Update

253

128

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BACKGROUNDMore than 20 years ago, it was hypothesized that exposure to prenatal and early postnatal environmental xenobiotics with the potential to disrupt endogenous hormone signaling might be on the causal path to cryptorchidism, hypospadias, low sperm count and testicular cancer. Several consensus statements and narrative reviews in recent years have divided the scientific community and have elicited a call for systematic transparent reviews. We aimed to fill this gap in knowledge in the field of male reproductive disorders.OBJECTIVE AND RATIONALEThe aim of this study was to systematically synthesize published data on the risk of cryptorchidism, hypospadias, low sperm counts and testicular cancer following in utero or infant exposure to chemicals that have been included on the European Commission's list of Category 1 endocrine disrupting chemicals defined as having documented adverse effects due to endocrine disruption in at least one intact organism.SEARCH METHODSA systematic literature search for original peer reviewed papers was performed in the databases PubMed and Embase to identify epidemiological studies reporting associations between the outcomes of interest and exposures documented by biochemical analyses of biospecimens including maternal blood or urine, placenta or fat tissue as well as amnion fluid, cord blood or breast milk; this was followed by meta-analysis of quantitative data.OUTCOMESThe literature search resulted in 1314 references among which we identified 33 papers(28 study populations) fulfilling the eligibility criteria. These provided 85 risk estimates of links between persistent organic pollutants and rapidly metabolized compounds (phthalates and Bisphenol A) and male reproductive disorders. The overall odds ratio (OR) across all exposures and outcomes was 1.11 (95% CI 0.91–1.35). When assessing four specific chemical subgroups with sufficient data for meta-analysis for all outcomes, we found that exposure to one of the four compounds, p,p′-DDE, was related to an elevated risk: OR 1.35 (95% CI 1.04–1.74). The data did not indicate that this increased risk was driven by any specific disorder.WIDER IMPLICATIONSThe current epidemiological evidence is compatible with a small increased risk of male reproductive disorders following prenatal and postnatal exposure to some persistent environmental chemicals classified as endocrine disruptors but the evidence is limited. Future epidemiological studies may change the weight of the evidence in either direction. No evidence of distortion due to publication bias was found, but exposure–response relationships are not evident. There are insufficient data on rapidly metabolized endocrine disruptors and on specific exposure–outcome relations. A particular data gap is evident with respect to delayed effects on semen quality and testicular cancer. Although high quality epidemiological studies are still sparse, future systematic and transparent reviews may provide pieces of evidence contributing to the narrative and weight of the evidence assessments in th...

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a CR: completeness of reporting on a scale from 0 (low completeness) to 11 (high completeness).

b Bias and confounding: 1 = higher risk of bias, 0 = lower risk of bias.

…”

Section: Methodsmentioning

confidence: 98%

Section: Methodsmentioning

confidence: 99%

The epidemiologic evidence linking prenatal and postnatal exposure to endocrine disrupting chemicals with male reproductive disorders: a systematic review and meta-analysis

Bonde

Flachs

Rimborg

et al. 2016

Hum. Reprod. Update

253

128

View full text Add to dashboard Cite

show abstract

“…Some authors have observed higher levels of the compounds bisphenol A , 176 dibutylin 169 dioxin , 164,173 heptachloroepoxide , 174 hexachlorobenzene , 174 polychlorinated biphenyls 164,173,177 and polybrominateddiphenyl ethers 159,164 among boys (and/or their mothers) who developed cryptorchidism compared to those who did not; however a substantial number of studies (at least some of which were adequately powered to detect an association) have directly evaluated these and other biologically-plausible compounds and found no such association. 56,60,152–157,160,163,168,172,178 In some cases, studies have found substantial regional heterogeneity, including conflicting results between countries within the same study.…”

Section: Endocrine-disrupting Chemicalsmentioning

confidence: 99%

“…Those studies investigating early-life environmental exposure to endocrine-disrupting chemicals as a risk factor for cryptorchidism have generally drawn blood from the children themselves. 175,176 …”

Section: Endocrine-disrupting Chemicalsmentioning

confidence: 99%

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Risk factors for cryptorchidism

et al. 2017

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The condition known as cryptorchidism – undescended testis – is one of the most common congenital abnormalities found among males, and is one of the few known risk factors for testicular cancer (TC). Like testicular cancer, the key exposures in the occurrence of cryptorchidism remain elusive. Testicular descent is thought to occur during two hormonally-controlled phases – between 8–15 weeks and 25–35 weeks gestation – and while it is clear that a failure of testes to descend permanently is likely due to disruptions to one or both of these phases, the cause(s) and mechanism(s) of such disruption are still unclear. In this manuscript, we review the broad range of putative risk factors that have been evaluated in relation to the development of cryptorchidism to date, discuss their plausibility, and make suggestions regarding further approaches to understand aetiology. There are few exposures for which there is consistent evidence of an association with cryptorchidism; and in those cases where evidence appears unequivocal – for example, the relationship between cryptorchidism and gestational measures such as low birth weight – the measured exposure is likely to be a surrogate for the true causal exposure. The relative importance of each risk factor may vary considerably between mother/son pairs depending on an array of genetic, maternal, placental and foetal factors – all of which could vary between regions.

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The effects of perinatal bisphenol A exposure on thyroid hormone homeostasis and glucose metabolism in the prefrontal cortex and hippocampus of rats

et al. 2019

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Introduction Bisphenol A (BPA) is an endocrine disruptor widely used to manufacture consumer goods. Although the thyroid hormone (TH) disrupting potential of BPA has been thought to be responsible for the neuropsychiatric deficits in the animals that experienced perinatal BPA exposure, the TH availability change at the level of specific brain structures has not been subject to systematic investigation. Methods In the present study the impacts of perinatal BPA exposure (0.1 mg/L in drinking water) spanning gestation and lactation on TH homeostasis in the prefrontal cortex (PFC) and hippocampus were assessed in male Sprague–Dawley rats at postnatal day 21 (PND21) and PND90. As TH regulates brain glucose metabolism at multiple levels，the effects of BPA treatment on glucose metabolism in the brain tissues were also assessed in adult rats. Results The results showed heterogeneous changes in TH concentration induced by BPA between serum and brain tissues, additionally, in the BPA–treated pups, up–regulated expression of the TH transporter monocarboxylate 8 mRNA at PND21 and increased type 3 iodothyronine deiodinase mRNA expressions at PND21 and PND90 were observed. Meanwhile, decreased glucose metabolism was seen in the PFC and hippocampus, while deficits in locomotor activity, spatial memory and social behaviors occurred in BPA‐treated groups. Conclusion These data support the concept that the developing brain possesses potent mechanisms to compensate for a small reduction in serum TH, such as serum hypothyrodism induced by BPA exposure, however, the long‐term negative effect of BPA treatment on TH homeostasis and glucose metabolism may be attributable to neuropsychiatric deficits after mature.

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Serum Bisphenol A Level in Boys with Cryptorchidism: A Step to Male Infertility?

Cited by 44 publications

References 54 publications

The epidemiologic evidence linking prenatal and postnatal exposure to endocrine disrupting chemicals with male reproductive disorders: a systematic review and meta-analysis

The epidemiologic evidence linking prenatal and postnatal exposure to endocrine disrupting chemicals with male reproductive disorders: a systematic review and meta-analysis

Risk factors for cryptorchidism

The effects of perinatal bisphenol A exposure on thyroid hormone homeostasis and glucose metabolism in the prefrontal cortex and hippocampus of rats

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