Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide

Abstract

Reproduction impairments in metal-polluted environments and parental hormones: no evidence for a causal association in an experimental study in breeding feral pigeons exposed to lead and zinc.

Abstract

Humans are responsible for land-cover changes resulting in the emission of hazardous chemical elements including metallic trace elements i.e. MTEs. As a consequence, urban wildlife is exposed to high concentrations of MTEs, which exposure is linked to reproductive impairments. MTE effects on reproduction outputs might result from MTE exposure disrupting the endocrine pathways involved in reproductive behaviours. In birds, there is strong evidence that prolactin, corticosterone and testosterone are all involved in the regulation of parental effort during incubation and chick rearing. Endocrine-disrupting chemicals might stimulate or inhibit the production of those hormones and consequently alter parental investment and reproductive success outcomes. We measured baseline corticosterone, prolactin and testosterone plasma levels, and the corticosterone stress response of breeding feral pigeons (Columba livia) experimentally exposed to ecologically relevant lead and/or zinc concentrations. Independently of lead and/or zinc exposure, male and female plasma levels of corticosterone and prolactin (but not testosterone) showed temporal variations along the reproduction stages (i.e. incubation, early rearing and late rearing). In addition, both hatching and fledging success were slightly correlated with corticosterone, prolactin and testosterone levels. However, our study did not find any influence of lead or zinc exposure on hormone levels, suggesting that MTE effects on reproductive outputs might not be explained by MTE-induced modifications of corticosterone, prolactin and testosterone-linked behaviours during incubation and rearing. Alternatively, MTE-induced reproductive impairments might result from MTE exposure having direct effects on offspring phenotypes or prenatal indirect effects on the embryo (e.g. maternal transfer of MTEs, hormones or immune compounds).