22
Jan
Review Finds Reproductive Toxicity from Neonicotinoid Insecticides, Highlighting Widespread Hazard
(Beyond Pesticides, January 22, 2026) Published in Environmental Research, a review of experimental studies by George Mason University researchers regarding reproductive toxicity of neonicotinoid pesticides (neonics) in rodents finds that all studies “demonstrated negative impacts on male reproductive endpoints in association with neonic exposure, including reduced sperm count, reduced sperm motility, and altered sperm morphology.†These studies highlight how neonics, designed to target insect nervous systems, can affect mammalian systems, representing risks to human health.
Criteria for inclusion in the review was restricted to endocrine and/or reproductive outcomes in male rats and mice, leading the authors to analyze 21 studies published between 2005 and 2025. “This narrative review employed a systematic approach and determined that neonics exhibit reproductive toxicity in male rats and mice, particularly impairing testicular function and sperm quality at high exposure levels,†the researchers report. They continue, “Despite species-specific differences, the conserved nature [core mechanism] of reproductive processes across mammals supports the relevance of these findings to human health.â€
Study Background
Neonicotinoids are a class of insecticides that share a common mode of action that affects the central nervous system of insects, resulting in paralysis and death. There is a wide body of science on the effects of neonicotinoids on nontarget organisms, particularly pollinators, as documented by Beyond Pesticides in Daily News and on the What the Science Shows on Biodiversity page. (See Beyond Pesticides’ resource page here for more information.)
More recent research links a range of adverse effects on mammals, including humans, with exposure to neonics regarding neurological harm, reproductive dysfunction, endocrine disruption, and cancer risks. (See additional health effects and related studies in the Pesticide-Induced Diseases Database.) Research demonstrates that neonics activate “chemical pathways similar to nicotine in the mammalian brain, raising concerns about their safety in humans and other vertebrates.†(See here and here.)
As the review states: “10.00%–23.20% of couples worldwide [are] dealing with the challenges of infertility, with male reproductive issues playing a role in 30.00% of all cases. The World Health Organization (WHO) estimates that in the Americas, lifetime infertility prevalence is 20.00%, a drastic increase from the 1960s where infertility rates were between 7.00% and 8.00 %.†Over the last 50 years, there has also been a 50% decline in sperm health as well. (See research here and here.) This review analyzes the role of environmental contaminants, specifically neonics, in these adverse male reproductive impacts.
Neonics can disperse throughout the entire plant after being sprayed onto the surrounding soil or from the coating on seeds. “Because neonics are systemic pesticides and are absorbed by plants and distributed throughout all their tissues, they cannot be washed off, leading to dietary exposures in human populations,†the authors note. The most widely used neonics in the U.S., as highlighted in the review, include imidacloprid (IMI), thiamethoxam (THX), clothianidin (CLO), acetamiprid (ACE), and dinotefuran (DINO).
The authors state: “[D]espite evidence of endocrine-disrupting properties of neonics, there are limited studies concerning male reproductive toxicity… [T]his topical review systematically examined the current literature on the reproductive health impacts of neonics, focusing specifically on experimental rodent models.â€
Review Methodology and Results
Twenty-one peer-reviewed studies that met the inclusion criteria, published from January 1, 2005, through August 31, 2025, were identified and included in the review. Within the studies, four neonics are investigated. “IMI was the most studied neonic, with eleven studies, followed by ACE, with four studies,†the authors report. “CLO was examined in four studies and thiacloprid (THIA) was studied in two.â€
Of note, all four studies investigating ACE as a reproductive toxicant reveal statistically significant results, demonstrating a negative association between exposure and reproductive parameters. When incorporating all four neonics within the research, fifteen of the twenty-one studies find damage to sperm motility, decreased sperm count, and abnormal sperm morphology (shape/form).
Noteworthy results include:
- One study reports significant reproductive toxicity in male and female mice exposed to higher doses of ACE for 180 days. Adverse impacts include “reduced body weight, impaired seminiferous epithelium, decreased spermatogenesis markers (Ki67, Top2a), and downregulation of steroidogenic genes (LHR, Star, Cyp11a1, Hsd17b1), with elevated ACE levels and decreased nicotinic acetylcholine receptor expression.â€
- Male rats exposed to ACE also show “dose-dependent reductions in sperm count and testosterone, increased gonadotropins (GnRH, FSH, LH) [reproductive hormones] at low and medium doses, oxidative stress, and apoptosis [cell death] at higher doses.†(See studies here and here.)
- IMI exposure leads to reduced sperm concentration, motility, and viability; increased abnormal sperm morphology; DNA fragmentation; decreased testosterone; and histopathological (diseased tissue) damage. (See here.)
- Additional studies of IMI exposure show reduced testis size, Leydig cell hypertrophy (condition affecting testis), and lower serum testosterone in male rats, as well as impaired sperm motility, reduced epididymal sperm concentration, germ cell apoptosis, and DNA fragmentation. (See research here, here, and here.)
- One study “observed significantly altered gene expression in steroidogenesis and DNA repair pathways in both IMI-exposed mature and IMI-exposed immature rats.â€
- Studies of CLO find that adult male rats “exposed to moderate to high CLO doses for 60–90 days exhibited decreased body weight, abnormal sperm morphology, reduced epididymal sperm concentration, lower testosterone, and increased testicular fatty acids.†(See studies here and here.)
- THIA exposure results in “reduced body weight gain, sexual behavior, and spermatogenic cell content at 50–100 mg/kg THIA in male mice over 4 weeks, with increased abnormal sperm and decreased expression of STAR and CYP11A1 [proteins involved in steroidogenesis].†(See here.)
- Another study finds impairment of male fertility in rats with THIA exposure, including “reduced body and testicular weights, decreased sperm count, motility, viability, abnormal morphology, lowered testosterone and steroidogenic enzyme levels, increased LH and FSH [gonadotropins], greater oxidative stress, testicular degeneration, and DNA fragmentation.â€
In comparing the male reproductive toxicity for the studied neonics, the researchers conclude that THIA is the most potent of the four. In summary, the authors conclude that: “[T]he collective evidence demonstrates that neonicotinoids consistently impair testicular function, disrupt spermatogenesis, and compromise sperm parameters such as count, motility, viability, and morphology. Mechanistic investigations further indicate that oxidative stress, DNA damage, mitochondrial dysfunction, and disruption of steroidogenic pathways are central mediators of toxicity. In vitro and transgenerational studies add weight to these findings by showing that neonicotinoid exposure can alter gene expression, compromise early embryonic development, and produce heritable [passed down through genetics] reproductive effects.â€
Previous Research
As demonstrated in this review, with data originating from 21 studies conducted between 2005-2025, exposure to neonics consistently degrades male reproductive function. Aside from the experimental studies incorporating the four neonics IMI, ACE, CLO, and THIA, additional research is cited that links exposure to neonics to impacts on reproductive health. This includes in vitro studies (performed in test tubes or cell culture dishes) that “provide valuable mechanistic insights into how neonic pesticides may impair male reproductive health by directly targeting sperm, embryonic cells, and testicular cell function,†the authors state. They continue, “These experiments highlight cellular pathways of toxicity, such as impaired fertilization, altered embryonic development, and disruption of DNA replication and cell cycle regulation.â€
One study reports that “high IMI, ACE, and nicotine exposure levels impaired mouse sperm function and early embryonic development in vitro, primarily affecting fertilization, zygote formation, and the first embryo cleavage.†Embryos exposed to IMI show morphological effects, including increased fragmentation, as well as developmental delays. Another in vitro study finds ACE can induce apoptosis (cell death) and affect gene expression, particularly in those associated with DNA replication/repair and cell cycle regulation. While there are limited studies that directly examine the impact on male reproductive health from neonic exposure, the existing “in vitro research suggests that neonics can impair sperm function, early embryonic development, and testicular cell viability, providing mechanistic insight into potential pathways of toxicity,†the researchers say.
These studies are crucial, as neonicotinoids are ubiquitous in the environment. The chemicals contaminate soils, water, and food, resulting in exposure to wildlife and humans as a result of their persistent and systemic nature. Research finds neonicotinoids and their metabolites (breakdown products) within human biomonitoring samples, such as in a study on Thai farmworkers where urine samples were collected and N-dm-ACE (a metabolite of ACE), IMI, and THIA were identified. (See here.)
Another biomonitoring study, sampling over 3,000 representative individuals in the U.S., concludes that approximately half of the U.S. general population three years of age and older are exposed to neonics. A study of 314 patients, conducted at a hospital in China, detects neonics and their metabolites in the cerebrospinal fluid of 99% of individuals, with a metabolite of ACE as the most highly detected in 85.4% of samples. A cross-sectional study of human seminal plasma finds concentrations of neonic metabolites that are also associated with decreased sperm motility, further supporting the results of the current review.
The Path Forward
To protect reproductive health, in both men and women, the transition to organic agriculture and land management is imperative. Systemic pesticides like neonicotinoids are particularly threatening to humans and wildlife, such as pollinators, with their ability to be absorbed by crop plants and translocate throughout the plant’s vascular system and move into pollen, nectar, and guttation droplets. Contamination of neonics in food and water can be avoided with the adoption of the holistic solution of organic practices.
Critically, the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) and the Environmental Protection Agency’s (EPA) pesticide program allow toxic chemicals to be dispersed, resulting in widespread negative impacts, without regard for the availability of cost-effective and profitable alternatives that are eco-sensitive and health protective. Consideration of the essentiality of synthetic substance use in agriculture is addressed in the Organic Foods Production Act (OFPA), along with stringent restrictions on their approval in certified organic production. The success of organic food production and land management practices demonstrates how pointless this dispersal of toxic chemicals is. Take action and Tell Congress to hold oversight hearings to determine how EPA can eliminate the use of toxic pesticides that are no longer needed to grow food or manage landscapes cost-effectively.
All unattributed positions and opinions in this piece are those of Beyond Pesticides.
Source:
Irfan, S. et al. (2025) Reproductive Risk of Neonicotinoids: A Review of Male Rodent Studies, Environmental Research. Available at: https://www.sciencedirect.com/science/article/pii/S0013935125021553.
