India’s cotton fields are confronting a pest that is becoming harder to stop, as pink bollworm populations show reduced sensitivity to several widely used insecticides and unusually high activity of enzymes that can neutralize toxic compounds. A study published in Ecotoxicology has found that resistance is unevenly distributed across the country, with some populations requiring many times more insecticide to achieve the same level of control as a laboratory strain known to be susceptible. The findings raise concerns about a possible widening gap between the chemicals available to farmers and the biological defenses evolving inside one of cotton’s most destructive enemies, Pectinophora gossypiella.
Pink bollworm is a small moth whose larvae invade cotton bolls, the plant structures that contain the valuable fiber and seeds. Once inside a boll, the caterpillars are shielded from many sprays, making early control especially important. The pest can damage developing fibers, reduce yield and quality, and promote boll rot. In India, the challenge intensified after the widespread adoption of genetically engineered Bt cotton, which produces insecticidal proteins derived from the soil bacterium Bacillus thuringiensis. Cotton varieties expressing Cry1Ac, followed by varieties combining Cry1Ac and Cry2Ab, initially delivered powerful protection. Over time, however, field-evolved resistance to these toxins allowed pink bollworm to survive and reproduce in crops designed to kill it.
The new research examines a second layer of the problem: resistance to chemical insecticides used when Bt cotton no longer provides reliable control. The investigators compared pink bollworm collected from major cotton-growing regions with a laboratory-susceptible population. They exposed the insects to profenofos, chlorantraniliprole, emamectin benzoate, lambda-cyhalothrin, indoxacarb and spinetoram, representing several insecticide classes and modes of action. Rather than asking only whether a dose killed an insect, the researchers estimated the LC50—the concentration expected to kill 50 percent of a test population. Comparing field and laboratory LC50 values produces a resistance ratio, a standard measure of how far a population has shifted from baseline susceptibility.
The strongest warning signs appeared in different places for different chemicals, suggesting that resistance is not a single nationwide trait but a patchwork shaped by local spraying histories, crop practices, pest movement and selection pressure. The Nagpur population had the highest reported resistance to profenofos, with a resistance ratio of fourfold. Adilabad showed a 6.81-fold ratio for chlorantraniliprole and an 8.09-fold ratio for lambda-cyhalothrin. Sriganganagar stood out for emamectin benzoate, reaching 24.86-fold resistance, and also showed a 2.53-fold ratio for indoxacarb. Bathinda recorded a 15.45-fold ratio for spinetoram. By contrast, populations from Coimbatore and Surat exhibited the lowest resistance across the insecticides tested, demonstrating how strongly susceptibility can vary between regions.
A resistance ratio does not mean that a chemical has become completely useless, nor does it directly predict performance under every field condition. Weather, application quality, insect age, spray coverage and the location of larvae inside cotton bolls can all influence control. But a high ratio is a biological alarm: the population has shifted substantially relative to a susceptible reference, and standard recommendations may deliver less reliable results. The particularly high values recorded for emamectin benzoate in Sriganganagar and spinetoram in Bathinda are significant because these compounds are often regarded as newer or more targeted tools than older broad-spectrum insecticides. Resistance emerging against multiple chemistries narrows the options for rotating modes of action and increases the risk that repeated treatments will accelerate the problem.
The biochemical results offer clues about how some of these insects survive exposure. Field populations showed esterase activity ranging from 2.83 to 5.29 micromoles per minute per microgram of protein, compared with 2.49 in the susceptible strain. Their glutathione S-transferase, or GST, activity ranged from 11.29 to 21.43 micromoles per minute per microgram of protein, whereas the susceptible insects recorded 2.78. These enzymes belong to detoxification systems that help insects process foreign molecules. Esterases can hydrolyze or bind certain insecticides, reducing the amount that reaches its intended target. GSTs attach the small antioxidant molecule glutathione to reactive chemical groups, making compounds easier to transform and excrete. Increased activity can therefore lower the effective dose inside the insect’s tissues.
This mechanism is known as metabolic resistance, and it is one of several ways insects can evade pesticides. Other mechanisms include mutations that alter an insecticide’s molecular target, changes in the insect’s outer cuticle that slow chemical penetration, and behavioral avoidance. In the case of Bt toxins, resistance can involve changes in the larval midgut, where Cry proteins are activated, bind to receptors and disrupt the intestinal lining. The elevated esterases and GSTs reported in this study do not prove that these enzymes alone caused resistance to every insecticide tested; resistance is often genetically complex and chemical-specific. Nevertheless, the enzyme patterns are consistent with a greater capacity to detoxify toxic compounds and provide a useful biological marker for monitoring populations before control failures become widespread.
The study’s geographic variation also carries a practical message for pest management. Treating India’s cotton belt as a single resistance zone could lead to excessive spraying in areas where susceptibility remains relatively high and inadequate protection where resistance is already severe. Regional surveillance can identify which compounds are losing effectiveness and where alternative measures should be prioritized. Regular bioassays, in which field populations are exposed to diagnostic concentrations, can reveal shifts in susceptibility over time. Enzyme assays can complement those tests by showing whether detoxification activity is rising. Together, these approaches can help distinguish a local outbreak from a broader evolutionary trend and allow recommendations to be adjusted before farmers invest heavily in ineffective applications.
The researchers argue that the results make integrated resistance management urgent. Such management is not simply a matter of switching from one insecticide to another. It involves rotating compounds with different biochemical targets, avoiding repeated applications of the same mode of action, using treatments only when monitoring indicates that intervention is needed, and following label rates and timing closely. Nonchemical measures are equally important, including synchronized planting and crop destruction after harvest to reduce surviving larvae, pheromone-based monitoring, biological control and agronomic practices that interrupt the pest’s life cycle. Bt resistance management also depends on strategies such as maintaining effective refuge systems where appropriate and deploying toxin combinations carefully, because a stacked crop is not automatically protected against all evolutionary pathways.
For cotton growers, the immediate implication is neither that every insecticide has failed nor that chemical control should be abandoned. It is that decisions must become more precise, locally informed and biologically disciplined. The lowest-resistance populations identified in Coimbatore and Surat show that susceptibility can persist, while the sharply elevated ratios elsewhere reveal how quickly intensive selection can reshape pest populations. The authors’ conclusion is ultimately a warning about sustainability: without coordinated resistance monitoring and integrated control, pink bollworm could continue accumulating defenses against both engineered toxins and chemical insecticides. Preserving India’s cotton production will depend on treating resistance not as a sudden emergency after sprays stop working, but as an evolutionary process that must be tracked and managed continuously.
