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Atrazine is the most commonly detected pesticide contaminant of ground water, surface water, and precipitation. Atrazine is also an endocrine disruptor that, among other effects, alters male reproductive tissues when animals are exposed during development. Here, we apply the nine so-called “Hill criteria” (Strength, Consistency, Specificity, Temporality, Biological Gradient, Plausibility, Coherence, Experiment, and Analogy) for establishing cause–effect relationships to examine the evidence for atrazine as an endocrine disruptor that demasculinizes and feminizes the gonads of male vertebrates. We present experimental evidence that the effects of atrazine on male development are consistent across all vertebrate classes examined and we present a state of the art summary of the mechanisms by which atrazine acts as an endocrine disruptor to produce these effects. Atrazine demasculinizes male gonads producing testicular lesions associated with reduced germ cell numbers in teleost fish, amphibians, reptiles, and mammals, and induces partial and/or complete feminization in fish, amphibians, and reptiles. These effects are strong (statistically significant), consistent across vertebrate classes, and specific. Reductions in androgen levels and the induction of estrogen synthesis – demonstrated in fish, amphibians, reptiles, and mammals – represent plausible and coherent mechanisms that explain these effects. Biological gradients are observed in several of the cited studies, although threshold doses and patterns vary among species. Given that the effects on the male gonads described in all of these experimental studies occurred only after atrazine exposure, temporality is also met here. Thus the case for atrazine as an endocrine disruptor that demasculinizes and feminizes male vertebrates meets all nine of the “Hill criteria”.

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Due to their versatility, robustness, and low production costs, plastics are used in a wide variety of applications. Plasticizers are mixed with polymers to increase flexibility of plastics. However, plasticizers are not covalently bound to plastics, and thus leach from products into the environment. Several studies have reported that two common plasticizers, bisphenol A (BPA) and phthalates, induce adverse health effects in vertebrates; however few studies have addressed their toxicity to non-mammalian species. The aim of this review is to compare the effects of plasticizers in animals, with a focus on aquatic species. In summary, we identified three main chains of events that occur in animals exposed to BPA and phthalates. Firstly, plasticizers affect development by altering both the thyroid hormone and growth hormone axes. Secondly, these chemicals interfere with reproduction by decreasing cholesterol transport through the mitochondrial membrane, leading to reduced steroidogenesis. Lastly, exposure to plasticizers leads to the activation of peroxisome proliferator-activated receptors, the increase of fatty acid oxidation, and the reduction in the ability to cope with the augmented oxidative stress leading to reproductive organ malformations, reproductive defects, and decreased fertility.

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Recent research has suggested that con ants in the environment may influence sdifferentation and reproductive endocrine fimction in wildlie. Concentrations oforganochlorine contaminants (total polychlorinated biphenyls, pesticides) were higher in the blood plasma of snapping turtles from contaminated sites than in those from reference sites. The ratio of the precloacal length to the posterior lobe of the plastron (PPR) is sually dimorphic in snapp turdes. There were significant reductions in the PPR at three conm ted site versus two reference sites. The magnitude of the response was such that a sigificnty higher proportion of PPRs of males from a contaminated site (Cootes Paradise) overlapped with those of females than PPRs of males from a reference site (Lae Sasajewun). Observers can incorrety idenify the sex ofturtes at the contaminated site based on secondary sexual characteristics alone. Unlike the changs to the morphology, there were few changes in 17J-estradiol or testosterone levels, and where differences occurred, therewas more varnation among reference sites than between the reference and contaminated sites. Our results suggest that environmental CO minants may afiect sexually dimorphic morphology in snapping turles without affecting circulating testosterone or estrogen levls in the adults. &y words biomonitoring femintion, morphology, organochlorines, pesticides, snapping turtes, testosterone.