Pesticides and Genetic Engineering

Multiple choice

Q1 — C: SIT works through reproductive failure — wild females that mate with sterile males produce no offspring. Over successive generations, the number of fertile matings declines, each generation produces fewer individuals, and the population collapses. Competition for food (A) is not the mechanism. Pheromone repulsion (B) is not how SIT works. Sterile males do not carry pathogens (D).

Q2 — A: SIT is species-specific (sterile males only compete for mates within their own species) and resistance cannot develop because there is no selectable trait — wild females cannot detect which males are sterile, so there is no fitness advantage to avoiding them. (B) is wrong — SIT requires expensive mass-rearing facilities and is generally more costly than pesticide use. (C) is wrong — SIT requires multiple generations to reduce population. (D) is wrong — each species requires its own rearing and release program.

Q3 — D: Resistance develops through natural selection — pre-existing mutations conferring resistance survive pyrethroid exposure and reproduce. Mosquitoes do not deliberately evolve (A). Pyrethroids do not mutate mosquito genes (B). Behavioural avoidance of bed nets is a separate phenomenon from biochemical resistance (C), and it is not "conditioning" in the classical sense.

Q4 — B: The self-limiting gene requires tetracycline to suppress — in the wild environment without tetracycline, offspring die before reproducing. The gene cannot spread or accumulate in the wild population. Releases must be continued to maintain population suppression. (A) is wrong — the gene eliminates itself. (C) describes gene drive — not OX513A. (D) is wrong — genes cannot transfer horizontally between animals as described.

Q5 — C: DDT use was restricted primarily because of resistance development in mosquito populations and environmental persistence causing bioaccumulation through food chains — particularly affecting birds of prey (peregrine falcon, bald eagle) through thinning of eggshells. (A) is wrong — cost was not the primary reason. (B) is partially supported (some carcinogenic evidence) but was not the primary driver of the ban. (D) is biologically incorrect.

Short Answer Model Answers

SA1: The sterile insect technique (SIT) works by overwhelming the wild insect population with sterile males. Large numbers of the target insect are reared in a controlled facility, males are sterilised (typically using low-dose radiation that disrupts sperm without affecting mating behaviour or competitiveness), and then released into the wild in numbers that greatly exceed the wild male population. Wild females encounter and mate predominantly with sterile males. Since the mating is biologically normal but produces no viable offspring, each generation produces fewer individuals than the last. If the release ratio (sterile males to wild males) remains sufficiently high and is sustained, the wild population declines with each generation and can be eradicated from the target area. Resistance to SIT is very unlikely to develop because there is no selectable trait available to select for. In pesticide resistance, resistant individuals survive lethal exposure and reproduce — their resistance gene provides a direct survival advantage that natural selection can act upon. In SIT, females cannot distinguish sterile from fertile males by any physical, chemical, or behavioural cue. There is therefore no variation in fitness between females that "avoid" sterile males (who cannot detect them) and those that do not — no resistance trait can be selected. A female that somehow "preferred" fertile males would need to be able to identify them, which is biologically not possible in species where SIT succeeds.

SA2: Chemical pesticides — example: pyrethroids in insecticide-treated bed nets (ITNs) for malaria prevention. Pyrethroids are highly effective at killing Anopheles mosquitoes on contact with treated nets, immediately reducing the number of infective bites received by people sleeping inside. Effectiveness is high in the short term but is being progressively undermined by widespread pyrethroid resistance in Anopheles populations across sub-Saharan Africa — the primary malaria burden region. Resistance develops through natural selection: mosquitoes with sodium channel mutations survive pyrethroid exposure and reproduce. Ecologically, pyrethroids can affect non-target insects including aquatic invertebrates and pollinators when used as spray applications, though bed net applications are more contained. Genetic engineering — example: OX513A self-limiting GM Aedes aegypti for dengue control. OX513A males carry a self-limiting gene — offspring die before adulthood unless tetracycline is present. Field trials in Brazil and Florida showed 70–90% population reductions. Resistance risk is very low: the self-limiting gene eliminates itself with each generation and cannot accumulate. Ecological impact is minimal — the approach targets only Aedes aegypti (its own species) and introduces no chemical residues. However, OX513A requires continuous releases (the gene does not persist without maintenance), faces regulatory hurdles in many countries, and public acceptance is variable. Comparing the two: both are effective, but pyrethroids are cheaper and provide immediate effect while GM approaches are more targeted, produce no chemical residues, and carry lower resistance risk. Pyrethroids face a serious and worsening resistance problem; GM approaches face regulatory and social acceptance barriers. Neither approach alone is sufficient — integrated vector management combining multiple strategies is most effective.

SA3: The screwworm eradication program provides compelling evidence of SIT effectiveness. The New World screwworm was causing hundreds of millions of dollars in annual livestock losses in the United States in the 1950s. Beginning with a successful island trial on Curaçao in 1958 (eradication within months), the program was scaled to the continental United States. At peak operation, the rearing facility in Mission, Texas produced and released approximately 2 billion sterile flies per week. The screwworm was eradicated from the continental United States by 1966 and subsequently from Mexico and Central America by 1991. A sterile fly barrier is now maintained at the Panama-Colombia border to prevent re-invasion from South America where the species persists. This represents complete eradication of a major livestock pest from an entire continent without chemical pesticide use — an extraordinary outcome that has never been matched by pesticide-based approaches for a vertebrate livestock pest. Despite this success, SIT has significant limitations. It is expensive: mass-rearing, sterilisation, and release logistics require sustained investment. It does not prevent re-invasion — the Panama barrier requires continuous maintenance. It is most effective against species where females mate only once in their lifetime (as screwworm females do) — if females can re-mate after encountering a sterile male, the effectiveness of each sterile mating is reduced. The required release ratio (sterile males must substantially outnumber wild males) means that in large, dense wild populations, the logistical scale becomes challenging. SIT is most likely to succeed when: (1) the target species has single-mating females, maximising the impact of each sterile mating; (2) the target area has geographic barriers that limit re-invasion (islands, isthmuses, mountain ranges); (3) the species can be mass-reared in large numbers under controlled conditions; and (4) sufficient funding and political will sustain releases for multiple generations. Overall, SIT is a highly effective, ecologically clean, and resistance-proof approach to vector control in appropriate conditions. Its limitations are logistical and economic rather than biological — which distinguishes it favourably from the escalating resistance challenges facing chemical pesticide programs.