Developmental Neurotoxicity of Pyrethroid Insecticides: Critical Review and Future Research Needs
TL;DR: To better understand the potential for developmental exposure to pyrethroids to cause neurotoxicity, additional, well-designed and well-executed developmental neurotoxicity studies are needed.
read more
Abstract: Pyrethroid insecticides have been used for more than 40 years and account for 25% of the worldwide insecticide market. Although their acute neurotoxicity to adults has been well characterized, information regarding the potential developmental neurotoxicity of this class of compounds is limited. There is a large age dependence to the acute toxicity of pyrethroids in which neonatal rats are at least an order of magnitude more sensitive than adults to two pyrethroids. There is no information on age-dependent toxicity for most pyrethroids. In the present review we examine the scientific data related to potential for age-dependent and developmental neurotoxicity of pyrethroids. As a basis for understanding this neurotoxicity, we discuss the heterogeneity and ontogeny of voltage-sensitive sodium channels, a primary neuronal target of pyrethroids. We also summarize 22 studies of the developmental neurotoxicity of pyrethroids and review the strengths and limitations of these studies. These studies examined numerous end points, with changes in motor activity and muscarinic acetylcholine receptor density the most common. Many of the developmental neurotoxicity studies suffer from inadequate study design, problematic statistical analyses, use of formulated products, and/or inadequate controls. These factors confound interpretation of results. To better understand the potential for developmental exposure to pyrethroids to cause neurotoxicity, additional, well-designed and well-executed developmental neurotoxicity studies are needed. These studies should employ state-of-the-science methods to promote a greater understanding of the mode of action of pyrethroids in the developing nervous system.
read more
Chat with Paper
AI Agents for this Paper
Find similar papers on Google Scholar, PubMed and Arxiv
Write a critical review of this paper
Analyze citations of this paper to find unaddressed research gaps
Citations
An Innovative Nanobody-Based Electrochemical Immunosensor Using Decorated Nylon Nanofibers for Point-of-Care Monitoring of Human Exposure to Pyrethroid Insecticides
TL;DR: The established immunosensor proved to be a viable alternative to the conventional methods for 3-PBA detection in human urine even without sample cleanup and showed excellent properties and stability over time.
57
Low dose extended exposure to saxitoxin and its potential neurodevelopmental effects: A review.
TL;DR: The neurodevelopmental toxicity of STX, the risk of extended or repeated exposure to doses with neuro developmental effects, the potential implications of this exposure and briefly, the steps taken and difficulties faced in preventing exposure are examined.
57
Prallethrin induced biochemical changes in erythrocyte membrane and red cell osmotic haemolysis in human volunteers.
TL;DR: Increases in generation and availability of nitric oxide might have rendered tolerance to erythrocyte membrane by protecting the cells from haemolysis and a significant decrease in membrane lipid peroxidation suggested that PS is a sensitive phospholipid species to the pyrethroid action.
56
Effects of pyrethroids on brain development and behavior: Deltamethrin.
TL;DR: The most consistent neurochemical findings are reductions in the dopamine transporter and the dopamine D1 receptor in mice and rats after early exposure to Deltamethrin this article, which is a Type II pyrethroid pesticide widely used in agriculture, homes, public spaces and medicine.
56
Inflammatory and oxidative mechanisms potentiate bifenthrin-induced neurological alterations and anxiety-like behavior in adult rats.
Brahim Gargouri,Brahim Gargouri,Harsharan S. Bhatia,Harsharan S. Bhatia,Michèle Bouchard,Bernd L. Fiebich,Hamadi Fetoui +6 more
TL;DR: It is suggested that BF induced neurological alterations in the frontal cortex and striatum of rats, and that this may be associated with neuroinflammation and oxidative stress via the activation of Nrf2/NF-kBp65 pathways, which might promote anxiety-like behavior.
56
References
Nomenclature of voltage-gated sodium channels.
Alan L. Goldin,Robert L. Barchi,John H. Caldwell,Franz Hofmann,James R. Howe,John C. Hunter,Roland G. Kallen,Gail Mandel,Miriam H. Meisler,Yoheved Berwald Netter,Masahara Noda,Michael M. Tamkun,Steven G. Waxman,John N. Wood,William A. Catterall +14 more
TL;DR: The present alphabetical nomenclature does not reveal the structural relationships among the α1 subunits of Ca2+ channels, but it is apparent that these two alphabeticals will overlap at α1L, which may not mediate an L-type Ca2- current and therefore may create confusion.
1.5K
De novo mutations in the sodium-channel gene SCN1A cause severe myoclonic epilepsy of infancy.
L Claes,Jurgen Del-Favero,Berten Ceulemans,Lieven Lagae,Christine Van Broeckhoven,Peter De Jonghe +5 more
TL;DR: Missense mutations in the gene that codes for a neuronal voltage-gated sodium-channel alpha-subunit (SCN1A) were identified in families with generalized epilepsy with febrile seizures plus (GEFS+) and seven unrelated patients with SMEI were screened for mutations.
1.3K
Mechanisms of pyrethroid neurotoxicity: Implications for cumulative risk assessment
David M. Soderlund,John M. Clark,Larry P. Sheets,Linda S. Mullin,Vincent J Piccirillo,Dana Sargent,James T Stevens,Myra L. Weiner +7 more
TL;DR: The diverse toxic actions and pharmacological effects of pyrethroids suggest that simple additivity models based on combined actions at a single target are not appropriate to assess the risks of cumulative exposure to multiple pyre Throids.
875
The tetrodotoxin-resistant sodium channel SNS has a specialized function in pain pathways
Armen N. Akopian,Veronika Souslova,Steven England,Steven England,Kenji Okuse,Nobukuni Ogata,Jan Ure,Andrew J.H. Smith,Bradley J. Kerr,Steven B. McMahon,Sue Boyce,Raymond G. Hill,Louise C. Stanfa,Anthony H. Dickenson,John N. Wood +14 more
TL;DR: Data show that SNS is involved in pain pathways and suggest that blockade of SNS expression or function may produce analgesia without side effects, and show that TTX-resistant sodium channel α subunit is encoded by the sns gene.
837
Structure/activity relationships
TL;DR: Structural studies on diphenylethanes, such as dichlorodiphenyltrichloroethane (DDT), demonstrate the significance of the substituents present on both the aryl rings and the side-chain.
741