Environmental toxicants have different toxicities and effect the body differently. For this reason, it is important to study them individually to see how each will effect the body upon exposure. Deltamethrin, a synthetic insecticidal pyrethroid, is similar to the pyrethrins which are produced from the flowers of the genus Chrysanthemum. Deltamethrin is a class 2 pyrethroid which means that it is less susceptible to degradation by air and sunlight than those pyrethroids in class 1 and because of this, it is uniquely suited for agriculture. Unfortunately, class 2 pyrethroids are also more toxic to mammals than those in class 1. (1)
While more toxic than its counterparts in class 1, the pyrethroids like Deltamethrin are less toxic than organophosphates that are becoming more and more restricted for use. These restrictions have led to the increase of the use of this pyrethroids and ones like it for everyday use in the US and around the world. The lowered toxicity level is assumed to be because these chemicals are more easily detoxified by mammalian detoxification systems. However, mammalian detoxification systems are not fully developed in young animals and the effects of this chemical on the young was unknown before the conclusion of a study published in 2013. What had been observed before that time was that pyrethroid metabolites, including deltamethrin had been found in the urine of pregnant women and children.
During this 2013 study, pregnant mice were exposed to different levels, 0,1 and 3 mg/kg, of deltamethrin orally every 3 days during gestation and lactation. The purpose was to determine the effects of the pyrethroid on the development of the offspring. As the author describes, "adipose tissue is metabolically active and necessary for systemic energy balance. Adipogenesis requires a number of transcription factors which regulate their development. (2) Until recently, the Nrf2 pathway was thought only to activate antioxidant genes but it been determined that it has a number of other functions, including participating in adipogenesis. (3) Deltamethrin can be "detected in adipose tissue with a half-life of 5-6 days and is "persistent" in body fat of animal models." (2)
This study was the first to demonstrate that deltamethrin effects adipogenesis and lipid homeostasis at the transcription level in young mice and decrease the expression of some genes at low levels. Previous studies have shown that deltamethrin prevents weight gain with short-term exposure in a non-dose-dependent manner. These observations are consistent with this study's observations of decreased gene expression of adipogenesis. Also, there was a reduction in cytokines levels that may negatively influence the immune response and interaction with adipocytes. In addition, they found that gene expression of glucose transporters was reduced which consequently may alter glucose transport between tissues and result in an increased risk for obesity, diabetes and glucose intolerance. Thus, deltamethrin may affect normal responses to high fat diets or pharmacological interventions to promote adipogenesis to improve insulin resistance. Lastly, the researcher determined that many of the reductions in gene expression were due to the epigenetic downregulation by Nrf2 which could lead to alterations in responses to environmental toxicants like endocrine disruptors or obesogens or to changes in diet. (2)
As one can see that while effect of deltamethrin may not be as toxic as those by organophosphates, the impact of exposures to animals, including humans, during development or early in life may be life long. It is also important to be aware that the effects of exposures may not be overtly apparent at first but may be physiologically present through adulthood through epigenetic changes. Epigenetic changes may be permanent and lead to disease development or influence how a person reacts and detoxifies environmental toxicants later in life.
1. Wipedia.
2. Effects of developmental deltamethrin exposure on white adipose tissue gene expression. Journal of biochemical and molecular toxicology, Vol. 27, No. 2. (February 2013), pp. 165-171 by Laura E. Armstrong, Maureen V. Driscoll, Ajay C. Donepudi, et al.
3. Emerging role of Nrf2 in adipocytes and adipose biology. Advances in nutrition (Bethesda, Md.), Vol. 4, No. 1. (01 January 2013), pp. 62-66, doi:10.3945/an.112.003103 by Kevin S. Schneider, Jefferson Y. Chan
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