A comprehensive scientific review has concluded that neonicotinoid pesticides—the most widely used class of insecticides globally—consistently harm male reproductive health in laboratory rodents. The findings, published in Environmental Research, draw on two decades of data and raise concerns about potential fertility risks for humans routinely exposed to these chemicals.

The analysis examined 21 studies conducted between 2005 and 2025, covering multiple rodent species and a range of neonicotinoid compounds and dosing regimens. Despite variations in study design, more than two-thirds of the experiments reported clear signs of testicular toxicity, impaired sperm quality, altered hormone levels, or structural damage to reproductive tissues. The effects were stronger at higher doses or with long-term exposure, often resulting in more severe or irreversible injury.

According to the review, neonics reduced sperm counts, slowed sperm movement, and increased abnormalities in sperm shape. Multiple studies showed disruptions to testicular function, including degeneration of the cells responsible for producing sperm and hormones. Researchers also observed oxidative stress, mitochondrial dysfunction, and disruptions in gene activity that are essential for healthy reproductive development. Some experiments found evidence that damage caused by these pesticides could be passed on to subsequent generations.

Neonicotinoids—commonly referred to as neonics—are banned in the European Union but remain widely used in the United States, particularly as seed coatings. Unlike conventional pesticide sprays, neonics are systemic: once applied to seeds or soil, they circulate throughout the entire plant, including its pollen, nectar, and fruit. Because they become embedded within plant tissues, they cannot be removed by washing. This characteristic has contributed to their pervasive presence across agricultural landscapes and ecosystems.

Testing in recent years has detected neonics in numerous environmental and biological samples, including food, crops, waterways, wildlife, and human tissues such as blood, urine, breast milk, cerebrospinal fluid, and umbilical-cord blood. One national survey reported that nearly half of individuals aged three and older had measurable levels of these pesticide residues.

The review’s findings add urgency to ongoing questions about the real-world health implications of chronic pesticide exposure. Scientists note that although rodents are not perfect stand-ins for humans, the basic structure and function of the reproductive system are conserved across mammals. Because only three human studies to date have directly examined the connection between neonic exposure and male fertility, researchers argue that the consistent animal evidence warrants expanded human investigation.

Early human data offer concerning signals. One study linked higher neonic exposure to delayed puberty in boys. Another reported that a tenfold increase in total neonic levels corresponded to a 38 percent reduction in testosterone. A third found pesticide metabolites in semen, associated with reduced sperm motility.

The review highlights that different neonicotinoid compounds carry different risks. The most studied chemical, imidacloprid, was repeatedly shown to cause widespread testicular damage, lower sperm counts, reduced hormone levels, and abnormalities in sperm shape and movement. Several studies documented DNA damage and degeneration of sperm-producing cells.

Acetamiprid exposure was associated with hormone disruption and impaired gene activity required for testosterone production. Clothianidin reduced sperm quality, caused smaller reproductive organs, induced abnormal sperm development, and increased testicular cell death at higher doses. Stress conditions amplified these effects. A lesser-studied compound, thiacloprid—already restricted or phased out in many regions—caused decreases in sperm count and hormone levels even at modest doses, along with pronounced declines in sperm viability and substantial tissue damage when exposure increased.

The review also underscores the growing importance of examining pesticide mixtures rather than single chemicals. Some fungicides, for example, inhibit the enzymes that break down neonics, making them far more potent. This interaction can dramatically increase toxicity, yet regulatory agencies generally do not evaluate the combined impacts of multiple pesticides, despite their widespread co-occurrence in farm environments.

These findings coincide with increasing scrutiny of neonic-coated seeds, their economic value, and their ecological risks. Several U.S. states have taken steps to restrict their use, citing environmental concerns and uncertainty surrounding long-term human health outcomes.

With global male fertility declining and environmental exposures recognized as one contributing factor, the review calls for comprehensive research that better reflects real-world conditions. Recommended priorities include studies tracking individuals from early development through adulthood, investigations of common pesticide mixtures, and assessments of prolonged, low-dose exposures more typical of agricultural communities.

The authors of the review emphasize that current evidence points to a substantial gap in safety assessments and regulatory oversight. As millions of people encounter these chemicals daily through food, water, and the environment, understanding their potential reproductive impacts is increasingly urgent.