Pyrethroid Pesticides as Endocrine Disruptors: Molecular Mechanisms in Vertebrates with a Focus on Fishes

Abstract

Pyrethroids are now the fourth most used group of insecticides worldwide. Employed in agriculture and in urban areas, they are detected in waterways at concentrations that are lethally and sublethally toxic to aquatic organisms. Highly lipophilic, pyrethroids accumulate in sediments and bioaccumulate in fishes. Additionally, these compounds are demonstrated to act as endocrine disrupting compounds (or EDCs) in mammals and fishes, and therefore interfere with endocrine signaling by blocking, mimicking, or synergizing endogenous hormones through direct receptor interactions, and indirectly via upstream signaling pathways. Pyrethroid metabolites have greater endocrine activity than their parent structures, and this activity is dependent on the enantiomer present, as some pyrethroids are chiral. Many EDCs studied thus far in fish have known estrogenic or antiestrogenic effects, and as such cause the inappropriate or altered expression of genes or proteins (i.e., Vtg-vitellogenin, Chg-choriogenin), often leading to physiological or reproductive effects. Additionally, these compounds can also interfere with other endocrine pathways and immune response. This review highlights studies that focus on the mechanisms of pyrethroid biotransformation and endocrine toxicity to fishes across a broad range of different pyrethroid types, and integrates literature on the in vitro and mammalian responses that inform these mechanisms.

The effects of bifenthrin and temperature on the endocrinology of juvenile Chinook salmon

“…Although bifenthrin is not acutely toxic to humans and other mammals, many studies have demonstrated that bifenthrin has adverse sublethal effects in fish (Brander et al 2016). Thus, juvenile fish may experience increased seasonal temperatures during bifenthrin runoff events.…”

Endocrine disruption in aquatic systems: up‐scaling research to address ecological consequences

“…The requirement for information on population effects of EDC exposure to inform ecological risk assessments has led to the extrapolation of individual-based experimental bioassays (e.g. Jobling et al, 2002b;Miller & Ankley, 2004;Gutjahr-Gobell et al, 2006;Lange et al, 2008;Brander et al, 2016). Such extrapolations assume, however, that the effects of EDC exposure within individual-based bioassays generally show simple, direct and invariant relationships with impacts on populations and communities, even if safety factors are used to account for uncertainties associated with these extrapolations.…”

Multiple exposures to environmental pollutants and oxidative stress: Is there a sex specific risk of developmental complications for fetuses?

“…The intensive use of pesticides causes long-term environmental contamination, resulting in human exposure. Pregnant women are particularly vulnerable to pesticide exposure because many of these human-made agricultural chemicals in use today (Brander et al, 2016;Monteagudo et al, 2016;Ventura et al, 2016) are endocrine disruptors with potentially adverse effects on embryonic and fetal development, and offspring health outcomes (Rauh et al, 2012;Dewan et al, 2013). The toxic and teratogenicity effects of pesticides could be also explained by ROS-induced oxidative stress (Al-Gubory, 2014), Animal studies show that pesticides have adverse effects on the function of the reproductive tract and the early embryonic development and survival.…”