A pesticide can stop a caterpillar from eating, yet the more important warning may appear inside its cells. This study compares both effects instead of treating pest control as a single yes-or-no question. The cotton leafworm is a destructive pest that damages many plant species across tropical and subtropical regions.

It threatens agriculture because it reproduces quickly and can develop resistance to conventional chemical groups. That is why pest-management programs need non-conventional or low-risk insecticides. The larvae are especially damaging because they aggressively infest plant leaves and other economically important plant parts.

The study compares five insecticides with different ways of acting on the insect. It looks at what happens to the larvae’s feeding and growth, rather than only asking whether the insects die. It also evaluates DNA damage.

Together, feeding, growth, and DNA damage show how these treatments can weaken the insect’s overall fitness. The researchers tested how treated leaves changed the insect’s feeding activity. Each insecticide was examined at two levels, one lower and one higher, so the effects could be compared across treatments.

A range of concentrations was prepared for each insecticide by repeatedly diluting it with water. All the insecticides increased feeding deterrence, meaning they made the larvae less willing to eat. The bacterial treatment produced the strongest deterrence, while the chemical treatment thiacloprid followed behind.

But eating less was only part of the story. Treated larvae generally converted less food into body mass, and growth was generally suppressed across the treatments. The strongest feeding disruption came from thiacloprid at the higher LC fifty level, which produced the largest recorded decrease in consumption.

At that same higher level, thiacloprid also produced the lowest recorded growth rate among the treatments for the larvae. Even after digesting food, many treated larvae still failed to grow, as shown by the negative ECD values recorded for most insecticides. The researchers then examined DNA inside the insects’ cells.

The highest amount of broken DNA appeared after thiacloprid treatment, while the bacterial treatment produced the lowest amount and shorter fragments. The bacterial treatment caused only slight, statistically significant DNA strand breakage, classified as type one, or one to twenty-five percent tail DNA.

All the other insecticides produced the more moderate damage category, with comets classified as type two, representing twenty-five to forty-five percent tail DNA. Thiacloprid also created a longer trail than the bacterial treatment, as DNA strand fragments moved farther through the comet assay.

Overall, the cell-damage measure showed no significant difference between the bacterial treatment and untreated insects, while the other treatments differed significantly. Thiacloprid produced the strongest effect among them. The three measures rise in parallel across treatments, while the letter groupings make the separation between slight and moderate damage especially clear.

A computer-based safety analysis gave emamectin benzoate a mixed profile. The strongest predicted concerns involved effects on the immune system and breathing. The model classified several other possible harms as inactive, but some of those predictions were uncertain.

These included effects on the nervous system and the wider environment. These are predicted hazards, not experimentally confirmed toxic effects. The results therefore need to be checked with laboratory studies of cell damage, body chemistry, and effects on organisms that are not pests.

The study identifies thiacloprid as the strongest cause of DNA damage because it produced the highest DNA damage measure and a one-and-a-half-fold increase in the overall damage measure. The longer DNA trail indicates many breaks in the genetic material. One possible explanation is oxidative stress, which can happen when protective enzymes are reduced and reactive chemicals affect DNA.

The results show why insecticide performance cannot be judged by feeding deterrence alone. The bacterial treatment had a more positive overall profile, while thiacloprid and Coragen strongly deterred feeding but also disrupted food use and growth.

For someone choosing pest control, the practical lesson is to weigh how well a treatment stops feeding against what else it may do inside the insect, including food conversion and growth. The strongest deterrent was not automatically the safest choice: the bacterial treatment sharply discouraged feeding with less cell damage, while some chemical treatments disrupted growth and damaged DNA.

That distinction matters when choosing controls that protect crops without adding wider risks.