Male Reproductive Toxicology

Editor's Choice
Main Category: Fertility
Also Included In: Urology / Nephrology;  Men's health
Article Date: 24 Nov 2008 - 0:00 PDT

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SAN FRANCISCO, CA, USA (UroToday.com) - This symposium discussed the topic of male reproduction and toxicology against the back drop of the reports of decreasing sperm counts over the last 50 years1, and the increasing incidence of testicular cancer, cryptorchidism and hypospadias2.

These effects may be mediated via endocrine disruptors which are defined as exogenous agents that interfere with the synthesis, secretion, transport, binding, action or elimination of natural hormones in the body and that are responsible for the maintenance of homeostasis, reproduction, development and/or behavior. Of the top 10 toxins being monitored by the government, three are metals (cadmium, lead, mercury). There are several examples of endocrine disruptors in nature affecting wild life phenotypes. Dichlorobromopropane, an insecticide, has been implicated in male infertility3. The purported effects of Cadmium, lead, phthalates were presented. Dr. Benoff then reviewed the possible mechanisms by which toxicants can exert their adverse effects:

a. Endocrine disruption,
b. Ionic mimicry,
c. Oxidative stress.

Genetics alterations that can occur are:

a. Genetic (DNA sequence) mutations, or
b. epigentic (chromatin remodeling) via acetylation, methylation,
phosporylation, ubiquitination and ADP ribosylation.

Dr. Benoff discussed the current suspected reproductive toxicants:

* Current-use pesticides
* Phthalates
* Bisphenol A
* Polybrominated flame retardants (PBDEs)
* Perfluorinated compounds (PFCs)
* Octyl/nonylphenols
* Metals

As well as potential routes of exposure:

* Food
* Bottled and tap water
* Prescription drugs
* IV tubing
* Neutraceutical supplements
* Personal care products

Exposures can also be occupational (DCBP, see above) and geographic (Smog, Los Angeles). The difficulties inherent in assessing the impact of these factors on fertility are complex and include the fact that,

1. Single contaminants may affect multiple endpoints,
2. multiple contaminants may effect the same end point,
3. there is genetic variability that may affect the susceptibility to a contaminant,
4. the timing duration and magnitude of exposure may impact on expression.

Clearly more investigation of this critical area is required.

References:
1. Carlsen et al 1992 BMJ 305:609; Swan et al 2000 Environ Health Persp 108:961.
2. Matsuda et al. Jap J Clin Onc: 2008 8:578 Paulozzi. Environ Health Perspect. 1999 107: 297;
Travison et al Clin Endo Metab 2007 92:196.
3. Slutsky et al Int J Occup Environ Health 1999 5:116.

Presented by Susan Benoff and Mark Sigman at the 64th Annual Meeting of the American Society for Reproductive Medicine - November 8 - 12, 2008 - San Francisco, California

Reported by UroToday.com Contributing Editor Harris M. Nagler, MD

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