The research, led by Andressa Pereira Cabral and Leandro Miranda-Alves at the Federal University of Rio de Janeiro with collaborators in Brazil and Portugal, is notable for its breadth. Rather than examining a single organ or a single biomarker, the team integrated thyroid histology, circulating hormone measurements, gene-expression profiling of the brain, thyroid and liver, and quantitative morphometry of renal tubules, all under identical exposure conditions. The concentrations tested, 1, 10 and 100 micrograms per liter, formed a logarithmic series deliberately centered on the WHO reference application concentration, with the lower and upper doses representing one order of magnitude on either side.

The zebrafish is a well-established model for endocrine toxicology because roughly 70 percent of its genes have human orthologs, including more than 80 percent of known disease-related genes, and its hypothalamic-pituitary-thyroid axis is functionally conserved with our own. In this axis, the hypothalamus releases thyrotropin-releasing hormone, which stimulates the pituitary to secrete thyroid-stimulating hormone, which in turn drives the thyroid follicular cells to synthesize and release thyroxine, or T4. Peripheral tissues, especially the liver, then convert T4 into the biologically active hormone T3 through enzymes called deiodinases. Disruption at any node of this loop can cascade through metabolism, development and stress responses.

What the researchers found was not a simple dose-response curve in which harm increases steadily with concentration. Instead, the pattern was non-monotonic, a hallmark increasingly recognized among endocrine-disrupting chemicals. The intermediate dose, 10 micrograms per liter, produced the strongest molecular signature of thyroid impairment: genes encoding the sodium-iodide symporter, thyroid peroxidase, the TSH receptor and the transcription factors nkx2.1 and pax2a were all significantly upregulated, while thyroglobulin, the iodinated protein precursor of thyroid hormone, was significantly repressed. This combination suggests a compensatory scramble: the gland appears to be pushing harder to import iodide and synthesize hormone even as a key component of that synthetic machinery is being suppressed.

The histology told a consistent story. In control fish, thyroid follicles were neatly organized, with a homogeneous colloid surrounded by a simple cuboidal epithelium. At 1 and 10 micrograms per liter, the follicular epithelium was significantly flattened and thinned, and follicle area shrank at the lowest dose, while the intermediate dose produced dilated follicles with enlarged colloid area. At 100 micrograms per liter, follicular profiles became irregular, although the standard morphometric measurements no longer differed significantly from controls. The authors caution that altered architecture alone does not prove impaired hormone secretion, particularly because plasma T4 levels remained unchanged at every dose tested, a dissociation they argue may make T4 alone an inadequate early-warning biomarker for pyriproxyfen-induced thyroid dysfunction.

The brain revealed the axis being actively rewired. At 1 microgram per liter, expression of the thyroid hormone receptor alpha, thyrotropin-releasing hormone and its receptor were all downregulated, indicating an initial suppression of central signaling. At 10 micrograms per liter, the hypothalamic genes rebounded and were significantly upregulated, an opposing response that reinforces the non-monotonic pattern. At the highest dose, expression of the pituitary beta subunit of TSH rose significantly, and plasma TSH concentrations were correspondingly elevated, even though T4 did not follow. The researchers interpret this as a compensatory stimulation of the thyroid axis under sustained stress, possibly reflecting primary thyroid dysfunction or altered peripheral sensitivity to thyroid hormone, and they emphasize that interference at this central level marks pyriproxyfen as a multi-tier endocrine disruptor whose effects extend well beyond the thyroid gland itself.

The liver added a metabolic dimension. Deiodinase type 1, which contributes to circulating hormone conversion, was significantly upregulated at 100 micrograms per liter, plausibly an adaptive attempt to fine-tune hormone availability under disrupted conditions, while deiodinase type 2 was unaffected. The antioxidant enzyme superoxide dismutase 3 was significantly increased at the intermediate dose, consistent with activation of defenses against redox disturbance, although the authors note this does not by itself demonstrate oxidative damage. Notably, the inflammatory marker tumor necrosis factor alpha was downregulated in thyroid tissue at the highest dose, and neither nrf2 nor tnfalpha shifted significantly in liver, suggesting that antioxidant defenses were mobilized without a strong pro-inflammatory trigger under these conditions.

Perhaps the most sobering finding came from the kidney, an organ rarely at the center of endocrine-disruptor studies. The proximal tubule lumen area was markedly reduced at all three concentrations, the most consistently affected parameter in the study, while distal tubule area shrank at 10 and 100 micrograms per liter. Because the kidney participates in thyroid hormone clearance and metabolism, renal impairment could in principle feed back into endocrine dysfunction, compounding the systemic burden. The results extend earlier work by Gameiro and colleagues, who documented collecting-duct degeneration after acute 96-hour exposures to much higher concentrations of 0.5 to 1.5 milligrams per liter; the present study demonstrates quantitative tubular alterations at concentrations up to a hundredfold lower and over a longer, 14-day window.

Pyriproxyfen’s environmental footprint makes these findings consequential. Residues have been detected in soil, rivers, honey and other bee products, and the compound bioconcentrates in non-target aquatic organisms, with reported zebrafish bioconcentration factors of 1175 to 1246, just below the regulatory threshold of 2000 that defines a bioaccumulative substance. In several regions it is applied directly to household drinking-water tanks for mosquito control, meaning human exposure is not hypothetical. Previous studies had already shown that pyriproxyfen and its metabolite 4′-OH-PPF interfere with thyroid hormone signaling in neural stem cells and alter neurodevelopmental gene expression, and that adult zebrafish exposure disrupts reproductive endocrine homeostasis through the hypothalamic-pituitary-gonadal axis.

The authors are careful about the limits of extrapolation. Zebrafish share conserved thyroid regulatory machinery with humans, but the findings should not be directly transferred to human risk without validation in mammalian and human-relevant models. Still, their conclusion is pointed: the non-monotonic concentration-response centered on the WHO reference concentration should be factored into ecotoxicological risk assessment, thyroid and renal endpoints deserve systematic inclusion in future evaluations, and T4 measurements alone may miss early dysfunction. As vector-control programs worldwide intensify in the face of arbovirus outbreaks, the study adds weight to a growing argument that the tools we deploy against mosquitoes deserve the same rigorous, multi-organ scrutiny we demand of any other chemical entering our water.

Subject of Research: Endocrine and renal toxicity of the mosquito larvicide pyriproxyfen in adult female zebrafish

Article Title: Endocrine and systemic toxicity of pyriproxyfen in adult female zebrafish: disruption of the HPT axis and peripheral organ impairments

Article References: Cabral, A. P., dos Santos Maia, F. P., Azeredo, D. B. C., de Jesus Santana, A. S., de Brito Gitirana, L., de Paiva Coimbra, J. L., de Carvalho, D. P., Soares, P., Rios-Morris, E., & Miranda-Alves, L. (2026). Endocrine and systemic toxicity of pyriproxyfen in adult female zebrafish: disruption of the HPT axis and peripheral organ impairments. Environmental Science and Pollution Research. https://doi.org/10.1007/s11356-026-38319-1

Image Credits: AI Generated

DOI: 10.1007/s11356-026-38319-1

Keywords: pyriproxyfen, endocrine disruptor, thyroid, HPT axis, zebrafish, ecotoxicology, kidney toxicity, WHO drinking water, Aedes aegypti, non-monotonic dose-response, thyroid hormone, pesticide

Between 2022 and 2023, researchers collected 35 field populations of B. tabaci from 18 major agricultural regions spanning the country, from the tropical vegetable fields of Sanya on Hainan Island to the northern plains of Inner Mongolia. The sampling covered crops as varied as eggplant, tomato, cucumber, chili pepper, sweet potato, and winter melon. Each population was subjected to laboratory bioassays against nine widely used insecticides representing six chemical classes: the biological pesticide abamectin, the neonicotinoids thiamethoxam and imidacloprid, the chloronicotinyl compound thiacloprid, the pyrethroids bifenthrin and deltamethrin, the ketoenol spirotetramat, the diamide cyantraniliprole, and the insect growth regulator pyriproxyfen. Crucially, the team tested adults, eggs, and nymphs separately, recognizing that susceptibility can differ dramatically across the whitefly’s life stages.

The methodology was rigorous and standardized. For adult bioassays, treated cotton leaf discs were placed on agar in small tubes, each receiving 40 to 50 field-collected adults, with mortality scored after 48 hours. Egg assays involved dipping leaves bearing freshly laid eggs into serial insecticide dilutions and counting unhatched embryos seven days later, while nymph assays used root-dipped cotton seedlings infested with synchronized second-instar nymphs, evaluated after two weeks. All results were compared against a laboratory-susceptible reference strain, originally collected in 2008 and never exposed to pesticides, allowing the calculation of resistance factors, the ratio of the field population’s lethal concentration to that of the susceptible baseline. Resistance was classified on a five-tier scale ranging from susceptible to very high, with resistance factors above 100 marking the most alarming category.

The good news first: abamectin remains a rare bright spot. Across 27 tested populations, adults were either fully susceptible or showed only low resistance, and several regions, including Sanya, Jinan, Hangzhou, Beijing, and Yuncheng, actually became more sensitive to the compound in 2023 than in 2022. This suggests that, when used appropriately, abamectin continues to deliver effective field control in China, a finding consistent with earlier nationwide monitoring from 2015 to 2021. In an era when many once-reliable insecticides are failing, the durability of this biological pesticide stands out.

The neonicotinoids tell a very different story. Resistance to imidacloprid ranged from a modest 1.79-fold to a staggering 255-fold in a Sanya population, with very high resistance also recorded in Yuncheng. Thiamethoxam resistance reached high levels in three populations, peaking at 71-fold, and thiacloprid resistance climbed to 140-fold in Sanya. Year-over-year comparisons revealed troubling upward trends in several regions, particularly in central and southern China, where median resistance factors for neonicotinoids exceeded 50. The authors attribute this escalation to prolonged and intensive use of these compounds, and note that cross-resistance mediated by metabolic detoxification enzymes, particularly cytochrome P450s and esterases, likely accelerates the problem. Continued reliance on neonicotinoids, they warn, risks eroding their long-term efficacy entirely.

Pyrethroid resistance presented a more mixed picture. Bifenthrin resistance remained low to moderate nationwide, peaking at around 16-fold, but deltamethrin resistance spanned an extraordinary range, from 2-fold to nearly 105-fold, with the highest value recorded in Yunnan’s Yuanmou region. Southwest China emerged as a pyrethroid hotspot, with median resistance factors exceeding 40. The researchers also compared molecular genotyping data with the bioassay phenotypes and found a crucial nuance: resistance-associated mutations alone do not fully determine phenotypic resistance. Some mutations appeared even in susceptible reference insects, indicating that genetic background, mutation frequency, and metabolic mechanisms all interact to shape real-world resistance. Molecular diagnostics, the authors conclude, must always be interpreted alongside bioassay data.

The newer chemistries, often promoted as solutions to resistance problems, showed their own warning signs. Egg-stage bioassays revealed consistently high resistance to spirotetramat, with resistance factors exceeding 300 in multiple populations and peaking at 357-fold in Suzhou, Anhui. Cyantraniliprole resistance was generally moderate, but a few populations displayed extreme values, with Hangzhou eggs showing a resistance factor above 4,000, and Tianjin above 2,000. Among nymphs, spirotetramat resistance reached 204-fold in Yueyang, while cyantraniliprole resistance peaked at 721-fold in Beijing in 2022, though it declined sharply the following year. Pyriproxyfen, an insect growth regulator used against whitefly nymphs since 1989, showed consistently high resistance across most monitored regions, with values up to 195-fold. The authors suggest that in some areas pyriproxyfen may no longer be suitable for whitefly control at all, a striking verdict for a compound with decades of market history.

Beneath the chemical story lies an evolutionary one. Genotyping of the ace1 acetylcholinesterase gene and the voltage-gated sodium channel gene revealed that resistance-associated alleles are already widespread. At the F331W locus, 15 of 18 populations were homozygous resistant, a legacy of more than 60 years of organophosphate exposure. The pyrethroid-linked mutations L925I and T929V were also common, often appearing as heterozygotes or mixed genotypes that signal ongoing selection and gene flow among populations. Equally significant was the species composition: of the 35 populations sampled, 31 were exclusively the Mediterranean (MED) cryptic species, with only four mixed MEAM1-MED populations, all from Sanya. MED, known for its superior insecticide tolerance and more efficient virus transmission, has essentially completed its displacement of MEAM1 across China, likely because it survives better under intensive neonicotinoid and pyriproxyfen spraying.

The virus dimension amplifies the concern. TYLCV, transmitted exclusively by B. tabaci, was detected in 10 of 11 tomato-derived populations, with infection rates exceeding 95 percent in nearly all of them. The virus also appeared in chili, cucumber, watermelon, and hami melon samples, though at more variable rates. Previous research has shown that TYLCV infection actually enhances MED survival and reproduction while shortening development time, creating a feedback loop in which the most insecticide-resistant vector is also the most efficient virus spreader. This dual threat, resistant insects and rampant virus, is precisely the scenario that integrated pest management programs are designed to prevent, and the study’s authors argue it demands coordinated action.

The path forward, the researchers emphasize, is resistance-informed and region-specific management. Because resistance profiles differ sharply across China’s cropping systems and climates, a one-size-fits-all spraying schedule is doomed to fail. Instead, they recommend rotating insecticides with distinct modes of action, selecting compounds according to the susceptibility of specific life stages, using molecular monitoring as an early-warning system for emerging resistance alleles, and pairing chemical control with virus suppression tactics such as removing infected plants, managing weed hosts, and reducing vector populations early in the crop cycle. Although the survey focused on China, the patterns it documents, rapid susceptibility shifts, strong regional selection pressures, immature-stage resistance, MED dominance, and widespread virus transmission, mirror challenges reported from Spain and Israel to Australia and Pakistan. Continuous surveillance, cross-regional data sharing, and adaptive management, the authors conclude, will be essential to curb further resistance escalation and protect agricultural productivity far beyond China’s borders.

Subject of Research: Nationwide monitoring of insecticide resistance, cryptic species composition, and TYLCV prevalence in Bemisia tabaci across China

Article Title: Nationwide spatiotemporal monitoring of insecticide resistance in Bemisia tabaci in China (2022–2023)

Article References: Yang, J., Li, Q., Zhang, Y., Ji, Y., Du, H., Guo, Z., Xie, W., Wang, S., Wu, Q., Zhang, Y., & Yang, X. (2026). Nationwide spatiotemporal monitoring of insecticide resistance in Bemisia tabaci in China (2022–2023). Journal of Agriculture and Food Research, 31, Article 103339. https://doi.org/10.1016/j.jafr.2026.103339

Image Credits: AI Generated

DOI: 10.1016/j.jafr.2026.103339

Keywords: Bemisia tabaci, insecticide resistance, whitefly, neonicotinoids, TYLCV, MED cryptic species, pyriproxyfen, spirotetramat, cyantraniliprole, resistance monitoring, integrated pest management, China

The research team collected Aedes aegypti mosquitoes from two contrasting environments: the densely urbanized metropolitan area of Kingston and the parish of St Andrew, referred to in the study as KSA, and the rural community of Lances Bay in the parish of Hanover. They also collected Aedes albopictus, the Asian tiger mosquito, from the urban KSA area to assess whether a second potential vector species shared the same vulnerability profile. Field-derived mosquitoes were then subjected to Centers for Disease Control and Prevention bottle bioassays, a standardized technique in which mosquitoes are exposed to a diagnostic dose of insecticide inside coated glass bottles and mortality is recorded over time. The CDC threshold for declaring a population susceptible requires mortality at or above 98 percent at the diagnostic time point, and by that measure every population tested failed, often spectacularly.

The numbers reveal the depth of the problem. At the 30-minute diagnostic time point, urban Aedes aegypti from KSA showed zero percent mortality to permethrin, meaning not a single mosquito was killed by the pyrethroid. Mortality to deltamethrin, another pyrethroid, stood at just 22.0 percent with a standard deviation of 2.7 percent, while malathion, an organophosphate, fared somewhat better at 70.5 percent with a standard deviation of 9.8 percent, still far below the susceptibility threshold. The rural Hanover population was, if anything, in worse condition: zero percent mortality to both permethrin and malathion, and only 8.1 percent mortality to deltamethrin. Aedes albopictus from KSA also demonstrated resistance to deltamethrin, with mortality below the CDC threshold, confirming that resistance is not confined to a single species.

What makes these results particularly concerning for public health officials is the multi-class nature of the resistance. Pyrethroids and organophosphates act through fundamentally different mechanisms: pyrethroids target voltage-gated sodium channels in insect neurons, while malathion inhibits acetylcholinesterase, an enzyme essential for nerve impulse termination. When a mosquito population simultaneously withstands compounds from both classes, control programs lose their two most important chemical tools at once. In Jamaica, where dengue outbreaks recur and ultra-low-volume spraying with pyrethroids is a mainstay of emergency response, the practical implications are immediate. Spraying campaigns that would have knocked down susceptible populations may now leave the majority of vector mosquitoes unharmed, while giving communities a false sense of protection.

To understand the molecular machinery behind this resistance, the researchers turned to transcriptomics, the study of gene expression patterns across the entire genome. They exposed Aedes aegypti collected from KSA to two compounds: malathion, the organophosphate already in use, and pyriproxyfen, an insect growth regulator belonging to a class of chemicals used to disrupt mosquito development. Using RNA sequencing, the team compared gene expression in exposed mosquitoes against untreated field mosquitoes and against the Rockefeller strain, a long-established insecticide-susceptible laboratory reference line. Principal component analysis and hierarchical clustering of the sequencing samples confirmed that the biological replicates grouped consistently by treatment, lending statistical confidence to the downstream comparisons.

The malathion results were striking. Exposure to the organophosphate triggered strong overexpression of genes associated with detoxification and with cuticle structure. Detoxification genes in mosquitoes typically include the three great enzyme families of insecticide metabolism: cytochrome P450 monooxygenases, glutathione S-transferases, and carboxylesterases, all of which can chemically modify or sequester toxic compounds before they reach their molecular targets. Cuticle-associated genes matter because the insect exoskeleton is the first barrier an insecticide must cross; a thicker or chemically altered cuticle can slow penetration and give internal detoxification systems time to neutralize the incoming dose. The coordinated upregulation of both gene categories suggests that Jamaican mosquitoes are mounting a layered defense, combining reduced uptake with enhanced metabolic breakdown.

Pyriproxyfen produced a different and more nuanced transcriptional signature. Rather than a concentrated detoxification response, the insect growth regulator elicited a moderate but broad response spanning metabolic and endocrine pathways. This pattern is biologically coherent: pyriproxyfen mimics juvenile hormone, a master regulator of insect metamorphosis, so exposure would be expected to perturb the expression of genes involved in hormone signaling and development alongside general metabolic machinery. The authors interpret these findings as evidence that transcriptional responses to insecticide exposure occur across multiple gene families rather than within a single pathway, a realization with important consequences for how resistance is monitored and predicted.

The transcriptomic dataset also included a comparison between the Rockefeller susceptible strain and untreated field-derived mosquitoes, capturing the baseline genetic differences that distinguish resistant Jamaican populations from their susceptible counterparts even before any laboratory exposure. Supplementary tables accompanying the paper document the significantly differentially expressed genes in each comparison, complete with log2 fold-change values, adjusted P-values, and normalized expression levels, providing a public resource for other researchers studying Caribbean vector populations. The study was supported by a Research and Publication Grant from the University of the West Indies, and the team included entomologists from the CDC’s Entomology Branch within the Division of Parasitic Diseases and Malaria, underscoring the international collaboration behind the work.

For the Caribbean region, the study arrives at a critical moment. Aedes aegypti is the principal urban vector of dengue virus, which causes periodic explosive outbreaks across the islands, as well as chikungunya and Zika, both of which swept through the Americas in the last decade. Resistance in Aedes aegypti has previously been documented in Jamaican urban and rural settings, but the susceptibility of other potential vector species and the transcriptional responses to insecticide exposure had remained poorly characterized. By showing that Aedes albopictus shares deltamethrin resistance with its more famous cousin, and by mapping the gene families involved, the study fills two significant gaps in regional surveillance knowledge. It also demonstrates that resistance profiles can differ dramatically between locations separated by only a few hundred kilometers, with the rural Hanover population showing even lower mortality than the urban KSA population for two of the three insecticides tested.

The authors conclude that insecticide resistance in Jamaican Aedes populations is widespread, heterogeneous, and dynamic, and they argue that these findings support locally informed resistance surveillance and integrated vector management strategies that go beyond reliance on pyrethroids. Integrated vector management, endorsed by the World Health Organization, combines chemical, biological, and environmental approaches, including source reduction through the elimination of standing water, larval control with agents less prone to resistance, and community engagement, reserving insecticides for targeted use where susceptibility still exists. The alternative, continuing to spray compounds to which local mosquitoes no longer respond, wastes scarce public health resources and accelerates the selection of even hardier mosquito populations. As dengue risk grows across a warming Caribbean, the Jamaican data serve as a warning that the chemical arsenal against Aedes mosquitoes is eroding, and that molecular surveillance of the kind performed in this study will be essential to staying ahead of the next outbreak.

Subject of Research: Insecticide resistance and resistance-associated gene expression in Jamaican Aedes mosquito populations

Article Title: Phenotypic insecticide resistance in Jamaican Aedes spp. and resistance-associated transcripts in Aedes aegypti

Article References: Tai, D., Irvine, W., Francis, F., Mackenzie-Impoinvil, L., Buchanan, L., Reimer, L., Lenhart, A., Roye, M., & Francis, S. (2026). Phenotypic insecticide resistance in Jamaican Aedes spp. and resistance-associated transcripts in Aedes aegypti. Parasites & Vectors. https://doi.org/10.1186/s13071-026-07666-w

Image Credits: AI Generated

DOI: 10.1186/s13071-026-07666-w

Keywords: Aedes aegypti, Aedes albopictus, insecticide resistance, Jamaica, pyrethroids, malathion, pyriproxyfen, transcriptomics, CDC bottle bioassay, dengue, vector control, Caribbean