Mode of carcinogenic action of pesticides inducing thyroid follicular cell tumors in rodents.

Abstract

Of 240 pesticides screened for carcinogenicity by the U.S. Environmental Protection Agency Office of Pesticide Programs, at least 24 (10%) produce thyroid follicular cell tumors in rodents. Thirteen of the thyroid carcinogens also induce liver tumors, mainly in mice, and 9 chemicals produce tumors at other sites. Some mutagenic data are available on all 24 pesticides producing thyroid tumors. Mutagenicity does not seem to be a major determinant in thyroid carcinogenicity, except for possibly acetochlor; evidence is less convincing for ethylene thiourea and etridiazole. Studies on thyroid-pituitary functioning, including indications of thyroid cell growth and/or changes in thyroxine, triiodothyronine, or thyroid-stimulating hormone levels, are available on 19 pesticides. No such antithyroid information is available for etridiazole, N-octyl bicycloheptene dicarboximide, terbutryn, triadimefon, and trifluralin. Of the studied chemicals, only bromacil lacks antithyroid activity under study conditions. Intrathyroidal and extrathyroidal sites of action are found: amitrole, ethylene thiourea, and mancozeb are thyroid peroxidase inhibitors; and acetochlor, clofentezine, fenbuconazole, fipronil, pendimethalin, pentachloronitrobenzene, prodiamine, pyrimethanil, and thiazopyr seem to enhance the hepatic metabolism and excretion of thyroid hormone. Thus, with 12 pesticides that mode of action judgments can be made, 11 disrupt thyroid-pituitary homeostasis only; no chemical is mutagenic only; and acetochlor may have both antithyroid and some mutagenic activity. More information is needed to identify other potential antithyroid modes of thyroid carcinogenic action.

Assessing the efficacy of zinc oxide nanoparticles against Penicillium expansum by automated turbidimetric analysis

“…Compounds like benzimidazole, which effectively controlled blue mould for more than 20 years, are no longer effective due to the development of resistant populations of P. expansum (Sutton et al 2014), while applications of fludioxonil, pyrimethanil and pyraclostrobin-boscalidcan still provide good control of this disease (Sutton et al 2014). However, it has been shown that pyraclostrabin and fludioxonil are highly to very highly toxic to invertebrates, vertebrates and algae in freshwater and marine systems (Elskus 2012) while pyrimethanil is classified by the US Environmental Protection Agency as a possible human carcinogen since it produces thyroid tumours in rats (Hurley et al 1998; Elskus 2012). Postharvest disease management is thus currently suffering on one hand, as many control strategies are not anymore effective and, on the other hand, as most of the current effective compounds have shown to be toxic and harmful to humans or to aquatic communities.…”

Bioremediation of Acetochlor in Soil and Water Systems by Cyanobacterial Mat

“…Furthermore, several chloroacetanilides have been shown to cause health hazards, for instance, acetochlor can produce significant incidences of thyroid, bone, granular stomach and nasal cavity tumors in rats, and of liver and lung tumors in mouse [12]. It may also have induced glutathione-dependent cytotoxicity in cultured animal and human cells [13].…”

Metabolomic evaluation of rat liver and testis to characterize the toxicity of triazole fungicides

“…Triadimefon was hepatotoxic in chronic studies using Wistar Han rats, causing hepatomegaly at 25 mg/kg/day. At higher doses (90.0 mg/kg/day) triadimefon caused rat thyroid and pituitary adenomas (Hurley et al, 1998). In reproductive studies with rats, 90.0 mg/kg/day decreased male fertility and insemination, and increased plasma testosterone levels with no evidence of testicular histopathology (FAO/WHO, 1982, 1986.…”