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Syst Biol Reprod Med. 2010 Apr;56(2):113-21. doi: 10.3109/19396360903244598.

Birth defects in wildlife: the role of environmental contaminants as inducers of reproductive and developmental dysfunction.

Author information

1
Department of Biology, University of Florida, Gainesville, FL 32611-8525, USA. hjhamlin@ufl.edu

Abstract

The etiology of adverse pregnancy outcomes is not well understood. Wildlife observations provide considerable evidence that environmental contaminants can play a critical role in reproductive and developmental dysfunction. Early evidence leading to a widespread awareness of the impact of environmental chemicals on surrounding wildlife was observed in the Laurentian Great Lakes. A suite of reproductive and congenital defects was identified in birds, reptiles, and mammals alike that were attributed to high concentrations of organochlorine pesticides and industrial chemicals. Due to the ubiquitous and persistent nature of many anthropogenic chemicals, these defects, including thyroid dysfunction, hatching success, egg shell thinning, and gross birth deformities, have since been identified in numerous wildlife populations across the world. Certain wildlife taxa such as amphibians are especially vulnerable to chemical perturbation and are suffering alarming population declines. Amphibian field studies have found severe hindlimb and other developmental abnormalities and it has been demonstrated that the greater the agricultural intensity, the greater the number and severity of defects in toad populations. Alligators living in contaminated lakes have shown a significant reduction in penis size and fish exposed to tributyltin have shown tail deformities and abnormal eye development. Physiological and molecular responses to chemical insult are often conserved across vertebrates, alerting scientists and medical professionals alike that greater attention needs to be paid to the roles environmental contaminants play in the etiology of congenital disorders in both humans and wildlife.

PMID:
20377310
DOI:
10.3109/19396360903244598
[Indexed for MEDLINE]

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