The Hidden Crisis: Chronic Exposure to Neonicotinoids and the Decline of Pollinators

In the early 2000s, the use of neonicotinoid pesticides expanded dramatically across the United States.  According to research by Penn State in 2000, less than 5 percent of soybean acres and less than 30 percent of corn acres were treated with neonicotinoids, but by 2011, at least a third of all soybean acres and at least 79 percent of all corn acres were planted with neonicotinoid-coated seed.  The change in agricultural practices coincided with alarming changes in honey bee colonies. Beekeepers began reporting unusual colony behavior, increased mortality rates, and unexplained disappearances of adult worker bees.

The first report identifying Colony Collapse Disorder (CCD) was in mid-November 2006 and by 2007, CCD had officially emerged, devastating beekeeping operations nationwide with 30%-90% losses across the country. Beekeepers voiced growing concerns to the Environmental Protection Agency (EPA) and other regulatory bodies, urging them to investigate the connection between neonicotinoids and the escalating losses. For several years, regulatory agencies assured beekeepers that their concerns would be addressed in an upcoming conference, intended to bring together scientific experts and industry representatives to evaluate the risks of neonicotinoids and develop mitigation strategies.

When Policy Overruled Science: The 2011 Conference That Failed Bees 

The 2011 Pellston Workshop was intended to be a turning point in the EPA’s pollinator risk assessment, resulting in the 2014 publication of Pesticide Risk Assessment for Pollinators (Fisher & Moriarity, Eds.). The workshop aimed to address systemic pesticides like neonicotinoids, standardize and align risk assessment criteria across the U.S., Canada, and the EU which would allow pesticide manufacturers to submit a single data package for approval in all three regions, as well as allow for cooperative analyses and partnership among the regulatory agencies (EPA, PMRA and EFSA). However, despite these ambitious goals, the process exposed critical failures in pesticide regulation—failures that would have lasting consequences for pollinators.

Dr. Jim Frazier, a key participant in the workshop, reflected on its outcomes:

"As a member of the Steering Committee to design and organize the workshop, being a discussion leader of one of the workgroup sessions, and editor of the resulting chapter summarizing the workgroup discussions and conclusions, and participating in the editing of the book into its final published form, I was a part of the entire process from beginning to end, with the exception of the group who chose what portions of the workshop were accepted for the EPA improvements in risk assessment or the corresponding changes made at the PMRA in Canada or the EFSA in the EU. The overwhelming outcome of this process was the realization that this workshop was held more than 10 years after the first neonicotinoid systemic insecticide, imidacloprid was approved for use by the EPA, and subsequent additional neonicotinoids, thiamethoxam and chlorothalonil were given conditional registrations without mandated timelines for full data submissions, and allowed to be marketed without even the most basic aspects of risk assessments having been performed adequately. The second outcome was in knowing the large number of risk assessment improvements discussed at the workshop and included in the book that were never adopted for risk assessment improvements by the EPA. This included required chronic toxicity testing of larval and adult honey bees, inclusion of recommended non-apis bees in testing, added behavioral lab tests, and many others from other chapters. "

In understanding why large segments of the risk assessment improvements were not included in the final report, it is important to note that the conference was equally funded by the EPA and Bayer CropScience, the corporation responsible for developing and marketing neonicotinoids, including seed coatings. With final report writing and input also divided 50/50, the result was an inherently biased and incomplete assessment—one that failed to fully acknowledge the long-term risks of neonicotinoid exposure to pollinators. This imbalance in influence ultimately shaped regulatory decisions, allowing dangerous gaps in risk assessment to persist. The lack of mandated chronic exposure toxicity testing and the exclusion of non-Apis pollinators from risk assessments left glaring gaps in pesticide safety evaluations. The failure to act on well-documented scientific findings from the 2011 workshop fundamentally altered the course of pollinator protection, allowing prolonged, low-dose pesticide exposure to persist unchecked. 

This regulatory inaction reinforced a reactive, rather than preventative, approach to pesticide safety, with devastating consequences for pollinators and the ecosystems they support. As a result, the omission of chronic exposure data shaped regulatory decisions for years to come. Without accounting for sublethal effects, risk assessments failed to recognize the slow but deadly impact of prolonged exposure to neonicotinoids.

Cumulative Catastrophe: The Lethal Impact of Low-Dose Neonicotinoids 

The absence of chronic toxicity considerations in regulatory frameworks has been particularly damaging because sublethal, chronic exposure is far more prevalent than acute poisoning. With regard to exposure, honey bees seldom encounter a single, lethal dose of pesticide in the field. Instead, they are exposed to low concentrations over extended periods, leading to widespread physiological and behavioral impairments. Chronic exposure weakens immune function, disrupts navigation, and increases susceptibility to pathogens, all of which contribute to colony losses.

The Druckrey-Küpfmüller equation demonstrates that the lower the exposure concentration, the longer the latent period before a lethal effect occurs, and the lower the lethal dose required. This toxicological principle demonstrates that even trace amounts of neonicotinoids can lead to devastating effects over time, as illustrated in the research of Dr. Henk Tennekes on the Lethal Effect of Imidacloprid on Honey Bees: Toxicity Reinforced by Exposure Time.

The data clearly demonstrate that as the exposure concentration of imidacloprid decreases, the time until lethal effect (latent period) increases, but the total lethal dose required drops significantly.

Looking at the changes in lethal dose across different concentrations:

• When the concentration drops from 57 to 37 μg/L, the lethal dose only decreases by about 2.6%.

• A further reduction from 37 to 10 μg/L results in a 35% drop in lethal dose.

• When the concentration is reduced from 10 to 1 μg/L, the lethal dose plummets by over 90%. A significant drop occurs between 1 to 0.1 μg/L, where the lethal dose falls by over 85%.

• There is a nearly 100% decrease in the lethal dose when the concentration drops from 57 μg/L to 0.1 μg/L, demonstrating that even extremely low doses become lethal over time.

This dramatic decline in lethal dose as concentration decreases aligns with the Druckrey-Küpfmüller equation, which states that toxicity accumulates over time. Even at extremely low concentrations, prolonged exposure leads to lethal effects. This means that regulatory risk assessments based on acute toxicity miss the true long-term danger of neonicotinoids, as bees exposed to minuscule amounts over days or weeks experience fatal effects.

Despite this well-documented reality, traditional toxicity testing still relies on fixed exposure durations that separate effects into arbitrary categories of "acute" or "chronic." This method is inherently flawed because it ignores the cumulative nature of pesticide exposure. A more accurate approach, such as Time-to-Event (TTE) analysis, was developed to track the long-term effects of pesticides by measuring the dose and duration needed to cause harm.

The Hidden Cost of Weak Detection:The Failure of Laboratory Testing Limits

Further compounding the issue is the inadequacy of current laboratory detection limits. Most pesticide testing detects neonicotinoids at concentrations of 1–10 parts per billion (ppB), but chronic exposure effects occur at levels as low as 10s to 100s of parts per trillion (ppT). Without sufficiently sensitive testing, critical toxicological effects go undetected, leading to a systematic underestimation of risk.

The long-term consequences of chronic neonicotinoid exposure resemble the dangers of lead or mercury poisoning. A single high dose of these heavy metals might be lethal within hours, but small amounts accumulated over time can cause severe, irreversible damage. In the case of neonicotinoids, prolonged exposure erodes colony health until the tipping point is reached, leading to mass die-offs.

Without laboratory equipment capable of detecting neonicotinoids at the ultra-low levels where chronic exposure occurs, the true scale of harm to pollinators remains invisible and unaccounted for. If we cannot measure these exposures, we cannot fully understand or prevent the slow poisoning of bee colonies, nor can we accurately assess the cumulative impact leading to their decline and collapse. All laboratories conducting pesticide exposure testing on bees must be equipped to detect neonicotinoids at levels as low as 10s to 100s of parts per trillion (ppT)—the range where chronic exposure causes harm. Without this capability, the true impact of prolonged, low-dose exposure remains invisible, underestimated, and unaddressed, allowing the silent decline of pollinators to continue unchecked. 

Regulatory agencies have failed to protect pollinators by ignoring the proven dangers of chronic exposure to neonicotinoids, focusing only on acute toxicity while dismissing the long-term, cumulative effects that weaken and kill colonies over time. Science has proven that even at trace levels, prolonged exposure disrupts immune function, impairs navigation, and leads to mass die-offs, yet risk assessments continue to rely on outdated models that fail to account for these delayed but devastating effects. Compounding this failure is the lack of proper laboratory testing standards—without equipment capable of detecting neonicotinoids at 10s to 100s of parts per trillion (ppT), the true scale of harm remains undetected and unaddressed. If we are serious about pollinator protection, we must demand regulatory reforms that recognize time-cumulative toxicity, set strict detection standards, and require the use of advanced lab equipment that can accurately measure the real-world impact of these pesticides. Anything less is a deliberate choice to turn a blind eye to an unfolding environmental catastrophe.