Neonicotinoids in global agriculture: evidence for a new pesticide treadmill?

Abstract

Overreliance on synthetic insecticides in global agriculture is the outcome of a "pesticide treadmill," in which insecticideinduced pest resistance development and the depletion of beneficial insect populations aggravate farmers' pesticide dependencies. Examples of the pesticide treadmill have been witnessed repeatedly over the past seven decades, prompting the question whether the rapid uptake and usage patterns of neonicotinoid insecticides and their associated environmental impact are in accordance with this recurrent phenomenon. We hypothesize a conceptual framework in which treadmills are enforced by enabling or disabling drivers within four domains: pest management decisions at the farm level, characteristics of farming landscapes, science and technology, and societal demands. These drivers then tend to create a self-enforcing pesticide "lock-in." We then analyze several post-1950s historical case studies with reference to this framework, e.g., those involving sprays of the highly hazardous DDT and methyl-parathion, in which the pesticide treadmill was initiated, sustained, and broken, and compare this with current patterns in neonicotinoid use. Historical case studies further illustrate how treadmills occur in three phases in which (i) a limited number of insecticides are routinely used, (ii) resistance development of pests results in the increased crop injury, prompting increased frequency of applications with a wider range of products, (iii) breaking out of the pesticide "lock-in" by policy change and adoption of alternative technologies that lowered chemical inputs and improved agro-ecosystem functioning. The analysis shows similarities as well as differences between neonicotinoid usage patterns and historic pesticide treadmills, and provides guidance on how to effectively avoid or dismantle pesticide treadmills in global agriculture.

Regenerative Agriculture: An agronomic perspective

“…Echoing the concerns about DDT raised by Carson, declines in populations of insectivorous birds were found to be associated with higher concentrations of neonicotinoids in the environment ( Hallmann et al, 2014 ). Further, neonicotinoids have been implicated in a new pesticide treadmill, where pesticide resistance and reduced populations of natural enemies lead to increased dependence on chemical control ( Bakker et al, 2020b ). With respect to weed control, the introduction of glyphosate was widely lauded as it was seen as environmentally benign compared with alternative herbicides.…”

What Socio-Economic and Political Factors Lead to Global Pesticide Dependence? A Critical Review from a Social Science Perspective

“…Pesticide resistance has been widely considered as one of the major causes of pesticide dependence [1,9,25,[29][30][31][32][33][53][54][55][56]. Pesticide resistance represents a genetic mechanism whereby pests (including weeds) develop evolutional abilities to adapt to pesticides, and then the same variety and dosage of pesticides do not work on the adapted pests.…”

“…The evolution of pesticide resistance by insect, pests and weeds has long been taken as the primary natural reason for pesticide dependence and various new varieties of pesticides have been constantly invented to combat the genetic evolutional process [25,[29][30][31][32][33]. However, overemphasizing the natural and technological processes, although important indeed, may conceal more deep-seated socio-economic and political factors in human society, as pesticide dependence 'is first and foremost a social question; technical fixes or regulatory changes will only acquire significance within the framework of serious social change' ( [34], p. 55).…”

When the Medicine Feeds the Problem; Do Nitrogen Fertilisers and Pesticides Enhance the Nutritional Quality of Crops for Their Pests and Pathogens?

“…In addition, and perhaps paradoxically, treatment of cropping systems with pesticides (e.g., insecticides, fungicides, acaricides, herbicides) may also reinforce subsequent P&P pressure; either by (i) suppressing the natural enemies (e.g., predators/parasitoids) of pest species, thereby creating ecological imbalances that allow pest populations to proliferate, (ii) promoting the evolution of pesticide resistance in some P&P species, and/or (iii) by inducing changes in the tissue biochemistry of crops that render them more susceptible. While the first two of these potential impacts are already welldescribed, and often cited as a causal mechanisms underlying occurrences of "pest resurgence" or "secondary pest outbreak" following pesticide use (e.g., Carson, 1962;Hardin et al, 1995;Bottrell and Schoenly, 2012;Bakker et al, 2020), the third impact has received little attention and is currently much less comprehensively understood.…”