{"id":41351,"date":"2026-04-07T00:01:09","date_gmt":"2026-04-07T04:01:09","guid":{"rendered":"https:\/\/beyondpesticides.org\/dailynewsblog\/?p=41351"},"modified":"2026-04-03T17:52:20","modified_gmt":"2026-04-03T21:52:20","slug":"multigenerational-abnormalities-linked-to-prostate-cancer-associated-with-neonicotinoid-insecticide","status":"publish","type":"post","link":"https:\/\/beyondpesticides.org\/dailynewsblog\/2026\/04\/multigenerational-abnormalities-linked-to-prostate-cancer-associated-with-neonicotinoid-insecticide\/","title":{"rendered":"Multigenerational Abnormalities Linked to Prostate Cancer Associated with Neonicotinoid Insecticide"},"content":{"rendered":"

(Beyond Pesticides<\/em>, April 7, 2026) In the International Journal of Molecular Sciences<\/em><\/a>, a study of gestational (during pregnancy) exposure to the neonicotinoid insecticide thiacloprid<\/a> shows epigenetic<\/a> effects (alterations in genes without altering underlying DNA) within prostate tissues. To analyze the role of gene expression in subsequent generations after initial thiacloprid exposure, the authors exposed pregnant outbred Swiss mice to the insecticide in order to assess the offspring for multiple generations. As a result, the researchers from the Universit\u00e9 de Rennes<\/a> in France state, \u201cOur study revealed that exposure to thiacloprid induces [cell] proliferation<\/a> and is associated with epigenetic alterations in the sperm of genes important for prostate development.\u201d Increased cell proliferation in the prostate can cause the development of conditions such as benign prostatic hyperplasia<\/a> (BPH) and prostatic intraepithelial neoplasia<\/a> (PIN), and lead to prostate cancer<\/a>.<\/p>\n

The study also finds elevated levels of specific biomarkers within the prostates of both the first and third generations, including phosphorylated histone H3, a marker crucial for cell division. Hox<\/em> gene expression in both generations was also impacted, which plays a role in prostate development, based on the altered DNA methylation (abnormal changes) in the sperm of the analyzed mice.<\/p>\n

\u201cIn this study, we aimed to reveal the effects of thiacloprid on prostate morphology and to gain insight into the epigenetic mechanisms involved in the regulation of genes important for prostate functioning and development using a mouse model,\u201d the authors say. They continue, \u201cAlthough the mouse prostate is anatomically and histologically different from the human prostate, there is extensive evidence<\/a> that the genetic lesions in human prostate cancer can lead to neoplasia in the murine prostate, suggesting that there is a common conserved mechanism of prostate pathology development.\u201d<\/p>\n

Study Importance<\/strong><\/p>\n

A wide body of science, that continues to grow, connects the intensive use of neonicotinoids to adverse health effects in a multitude of organisms. Most notably, dramatic declines in bees and other pollinators are linked to neonicotinoids<\/a> and neonicotinoid-treated seeds<\/a>. (See What the Science Shows on Biodiversity<\/a> for more information on the effect of pesticides on pollinators and other beneficial organisms.)<\/p>\n

As the current study authors point out, neonicotinoids in Europe were banned in 2018 but continue to be detected in the environment and contaminate organisms. For instance, studies find that thiacloprid is detected in aquatic invertebrates in the Danube River, as well as in honey samples, years after the ban. (See research here<\/a>, here<\/a>, and here<\/a>.) Birds in Europe, such as the house sparrow Passer domesticus<\/em>, have detectable neonicotinoid residues<\/a> in their feathers. Residues in farmland birds<\/a>, including gray partridges and Montagu\u2019s harrier<\/a> chicks, also show the persistence of neonicotinoids in nature.<\/p>\n

Additional studies find thiacloprid in mammals. One study<\/a> finds levels of thiacloprid in the urine of domesticated dogs and cats, while another shows residues in the hair<\/a> of small mammals. A human biomonitoring study<\/a> finds urinary neonicotinoids and their metabolites correlated with oxidative stress<\/a> biomarkers. This widespread and persistent presence of neonicotinoids in organisms, particularly where their use has been banned, shows the long-lasting effects that need to be taken into consideration prior to permitting the release of hazardous or potentially harmful chemicals into the environment.<\/p>\n

Methodology and Results<\/strong><\/p>\n

In this study, multiple generations of Swiss mice are assessed for potential changes in gene expression within the prostate with exposure to thiacloprid. The control mice and the pregnant mice with neonicotinoid exposure represent the F0 generation, while their immediate offspring are F1. The researchers further describe, \u201cBoth control and exposed F1 generation males were crossed with non-related, untreated females to obtain the F2 generation. Both control and exposed male progeny of F2 were crossed with non-related, untreated females to obtain the F3 generation.\u201d<\/p>\n

For the F0 mice that were exposed to thiacloprid, this occurred over 10 days during the embryonic period based on the lowest-observed-adverse-effect level<\/a> (LOAEL), the lowest concentration of a substance in which adverse alterations of morphology or function occur. As the authors point out, \u201cThe chosen dose was approximately four times lower than the LOAEL established by the EPA [Environmental Protection Agency] for thiacloprid for mice\u201d and \u201c~5 times lower than the human equivalent LOAEL dose established by the EPA.\u201d The entire experiment, from the F0 generation to the F3 generation, was performed twice.<\/p>\n

The results of the study show some epigenetic effects in both the F1 and F3 generations, while other effects are only noted in the F1 generation despite the persistence of epigenetic markers. The researchers explain, saying: \u201c[I]t is likely that gestational exposure to thiacloprid induces some alterations in the F1 generation, causing an increase in proliferation, based on analysis of markers. However, the effects were not detected in F3, suggesting that most of the effects induced in F1 were not transgenerational but intergenerational.\u201d<\/p>\n

Other effects show variation between the generations. \u201cWe also noted that alterations in our studies in F1 and F3 epigenetic marks had opposite effects,\u201d the authors state. They continue: \u201cWe cannot simply explain this phenomenon; we suggest that some unknown mechanisms compensate for the previously induced epigenetic alterations in F3 males. Similar opposite effects were observed in our previous study<\/a> in prostates exposed to chlordecone<\/a>. We suggest that compensatory effects could be promoted during fertilization.\u201d This variation requires further research to elucidate the mechanisms at play, but continues to expand the current knowledge regarding the effects of neonicotinoids through solely laboratory-based transgenerational exposure and without any direct exposure as would be encountered in the environment.<\/p>\n

Gestational exposure to thiacloprid increases epithelial hyperplasia in the anterior prostate in the F1 generation, as well as elevates the expression of mitosis. As the researchers share, additional study results include:<\/p>\n