Relationship between agrochemical compounds and mammary gland development and breast cancer
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Authors: Kass, Laura; Gomez, Ayelen L.; Altamirano, Gabriela A.
Abstract
The exposure to agrochemical pesticides has been associated with several chronic diseases, including different types of cancer and reproductive disorders. In addition, because agrochemical pesticides may act as endocrine disrupting chemicals (EDCs) during different windows of susceptibility, they can increase the risk of impairing the normal development of the mammary gland and/or of developing mammary lesions. Therefore, the aim of this review is to summarize how exposure to different agrochemical pesticides suspected of being EDCs can interfere with the normal development of the mammary gland and the possible association with breast cancer. It has been shown that the mammary glands of male and female rats and mice are susceptible to exposure to non-organochlorine (vinclozolin, atrazine, glyphosate, chlorpyrifos) and organochlorine (endosulfan, methoxychlor, hexachlorobenzene) pesticides. Some of the effects of these compounds in experimental models include increased or decreased mammary development, impaired cell proliferation and steroid receptor expression and signaling, increased malignant cellular transformation and tumor development and angiogenesis. Contradictory findings have been found as to whether there is a causal link between the exposure or the pesticide body burden and breast cancer in humans. However, an association has been observed between pesticides (especially organochlorine compounds) and specific subtypes of breast cancer. Further studies are needed in both humans and experimental models to understand how agrochemical pesticides can induce or promote changes in the development, differentiation and/or malignant transformation of the mammary gland.
Mobility, Degradation, and Uptake of Indaziflam under Greenhouse Conditions
HORTSCIENCE
Authors: Gonzalez-Delgado, Amir M.; Shukla, Manoj K.
Abstract
The objectives of this study were to evaluate the leaching, degradation, uptake, and mass balance of indaziflam, as well as its potential to produce phytotoxicity effects on young pecan trees. Pecan trees were planted in pots with homogeneous porous media (sandy loam soil), preferential flow channels open to the soil surface, and shallow tillage at the soil surface. Pots were treated with indaziflam at two application rates of 25 and 50 g a.i./ha in 2014 and 2015. Each pecan tree was irrigated with 7 L of water every 2 weeks during the growing season. An irrigation volume of 2 L was used to maximize indaziflam retention time in the soil from Dec. 2015 until the end of the trees' dormant stage. In 2014, leachate samples were collected after each irrigation for quantifying indaziflam mobility. Soil samples were collected at depths of 0 to 12 and 12 to 24 cm after 45, 90, and 135 days of indaziflam application, and leaf samples were collected at the end of the growing season to quantify mobility and uptake. Indaziflam was detected in leachate samples, and the leaf indaziflam content increased with increasing application rate. Indaziflam and its breakdown products were detected at both sampling depths. Mass recovery and half-life values for indaziflam in the soil ranged from 38% to 68% and 63 to 99 days, respectively. No phytotoxicity effects were observed from increasing application rate and retention time of indaziflam in the soil. Most of the applied indaziflam was retained in the soil at shallow depth.