Pesticide Standards & The Precautionary Principle

The Environmental Protection Agency (EPA) classifies almost all pesticides based only on their acute toxicity levels, primarily focusing on the acute toxicity measure known as LD50 (Lethal Dose, 50%). That’s a dosage level that kills 50% of the test animals. EPA rarely tests for any other kind of pesticide toxicity during or after registration. This egregious failure to account for the wildly diverse Modes of Action of pesticides, which has cascaded throughout lazy and dangerous state Cannabis regulatory agencies, is exposing today’s generations of Cannabis users, and their children and grandchildren, to far-reaching multi-toxic effects of pesticide exposure that are not even hinted at by the pathetic and outdated EPA LD 50 standard.

The Precautionary Principle, which is widely applied in European law and regulations, has also been used, although not as widely, in the environmental decision-making process and in regulating drugs and other consumer products in the United States. Unfortunately it is completely ignored by EPA and by every state Cannabis regulatory agency.

The Precautionary Principle in its simplest form states: “When an activity raises threats of harm to human health or the environment, precautionary measures should be taken even if some cause-and-effect relationships are not fully established scientifically”. 

Nearly 100 diseases and degenerative conditions have a substantial body of published medical/scientific research linking them to chronic low-level pesticide exposure. None of these exposure scenarios remotely resemble the kind of multi-chemical inhalation exposure that cigarette and cannabis smokers experience, but nevertheless it’s well-established that all pesticide exposures carry risk, and there are several good reasons why chronic low-level exposure by inhalation almost certainly carries far more risk than any level of exposure by dietary ingestion. 

LD50 is a standard measure used in toxicology to assess the acute toxicity of a substance. It represents the dose required to kill 50% of a test population, typically laboratory animals, within a specified period. The LD50 value is usually expressed in milligrams of substance per kilogram of body weight (mg/kg). A lower LD50 value indicates higher toxicity, as it means a smaller amount of the substance is needed to cause death. This measure is used by regulatory agencies like the EPA to classify and compare the toxicity levels of different chemicals and substances.

This approach only scratches the surface of the complex and varied modes of action (MOA) by which pesticides exert their toxic effects. Understanding and regulating pesticide exposure with close reference to these diverse MOAs is crucial for a comprehensive approach to pesticide safety and to reducing or eliminating their potential long-term impacts on human health and the environment. 

Furthermore, EPA standards for pesticides on tobacco are for tobacco in the field, intended to protect tobacco workers – not on tobacco products, which are not tested or regulated for pesticide contamination. Using EPA standards as reference points for Cannabis is an ignorant, misinformed, and dangerous way for state regulators to behave, and fails to provide reasonable protection for Cannabis users from any MOA other than acute toxicity.

While pesticide regulation in Tobacco products seems to be a lost cause, it isn’t too late for the Cannabis industry to rise up and demand science- and medicine-based pesticide regulation. The Cannabis community is still in a position to demand that state regulators get real and make the changes that are absolutely needed to protect this and future generations of young Cannabis smokers and vapers.

Here’s an overview some of the wildly diverse MOAs of pesticide toxicity, highlighting the need for far more nuanced and thorough testing of these substances beyond the basic LD50 metric.

However, this approach only scratches the surface of the complex and varied modes of action (MOA) through which pesticides exert their toxic effects. Understanding these diverse MOAs is crucial to begin a comprehensive assessment of pesticide safety and their potential long-term impacts on human health and the environment. 

  1. ToxicityClassifications
    • Neurotoxicity: Affecting the human nervous system, leading to paralysis and death in insects (organophosphates, carbamates).
    • Acute Toxicity: Causing immediate or rapid organ system failure or death upon exposure (pyrethroids, neonicotinoids).
    • Chronic Toxicity: Long-term exposure leading to gradual body systems deterioration (organochlorines).
  2. Organ/System-Specific Toxicity
    • Respiratory Toxicity: Causing irritation and damage to the respiratory system (some fumigants, organophosphates).

3. Reproductive Toxicity: Affecting reproductive health, leading to infertility and birth defects (some organochlorines, certain herbicides).

4. Immunotoxicity: Weakens the immune system, making organisms more susceptible to diseases (some organophosphates, carbamates).

5. Developmental Toxicity: Affects the development of embryos and fetuses, leading to birth defects and developmental issues ( some organochlorines, certain herbicides).

6. Nephrotoxicity: Pesticides that specifically harm the kidneys, leading to long-term renal issues (certain fungicides, herbicides).

7. Hepatotoxicity: Pesticides that specifically cause liver damage or liver disease (some insecticides, fungicides).

8. Dermal Toxicity: Pesticides that specifically cause skin irritation or dermatitis upon contact (some insecticides, herbicides).

9. Ocular Toxicity: Pesticides that specifically cause irritation or damage to the eyes (certain fumigants, herbicides).

10. Alimentary Toxicity: Pesticides that specifically cause harm to the digestive system, leading to gastrointestinal issues (certain insecticides, rodenticides).

11. Carcinogenicity: Pesticides that have been strongly associated with or proven to cause (Groups 1, 2 A & 2B) one or more of 100+ cancers (some organochlorines, certain herbicides).

12. Oxidative Stress: Cell Death: Causes damage to cells through oxidative stress, leading to cell death and tissue damage (glyphosate-based herbicides, Organophosphorus).

13. Mutagenicity: Genotoxicity: Causes specific genetic mutations that lead to cancer and other genetic disorders (some organochlorines, certain herbicides).

14. Endocrine Disruption:

  • Hormone Mimicry: Pesticides that mimic natural hormones, disrupting normal hormonal functions (some organochlorines, pyrethroids).
  • Hormone Blockers: Pesticides that prevent natural hormones from binding to their receptors, leading to hormonal imbalances (certain herbicides, fungicides).
  • Certain endocrine disrupting pesticides exhibit estrogenic properties and have anti-androgenic effects. 
  • In males, exposure to endocrine-disrupting pesticides can lead to obesity, infertility, risk of testicular and prostate cancers, atypical sexual development, changes in the functions of the pituitary and thyroid glands, weakened immune responses, and potential neurobehavioral consequences. 
  • Meanwhile, in women, endocrine-disrupting pesticide exposure can lead to obesity and abnormal reproductive outcomes including reduced fertility, miscarriages, stillbirths, preterm deliveries, underweight newborns, birth defects, ovarian irregularities, and disturbances in hormonal function.”
  • Disturbances in hormonal function include:
  1. Interference With Hormone Synthesis
  2. Interference With Hormone Storage and Release
  3. Interference With Hormone Transport and Clearance
  4. Binding and Activating the Estrogen Receptor
  5. Binding Other Receptors
  6. Interference With Hormone Post-Receptor Activation
  7. Interference With the Thyroid Function
  8. Behavioral Changes: Behavioral Disruption: Pesticides that alter the behavior of organisms, affecting their ability to survive and reproduce (some neonicotinoids, pyrethroids).

15. Epigenetic Changes:

  1. Gene Expression Alteration: Pesticides can cause changes in gene expression without altering the DNA sequence, potentially leading to long-term health effects across generations (some herbicides, organochlorines)
  2. Organochlorines like DDT (dichlorodiphenyltrichloroethane) which is a pesticide well-known to have transgenerational effects. Studies have shown that exposure to DDT can lead to epigenetic changes that are passed down through multiple generations, even if those generations are not directly exposed to the pesticide. While banned worldwide, DDT is still in widespread clandestine use and appears regularly in tobacco products.

16. Bioaccumulative toxicity: Tissue Accumulation: Pesticides that accumulate in the tissues of organisms over time, leading to long-term and transgenerational health effects (organochlorines).

17. Mitochondrial Dysfunction: Energy Production Disruption: Pesticides that interfere with mitochondrial function, disrupting energy production in cells (glyphosate-based herbicides, Organochlorines, Organophosphorus).

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panaceachronicles

When I was a child I moved around the world with my military family, always traveling by ship in the days before aircraft could cross oceans. I would spend hours on deck writing messages, sealing them with candle wax in bottles I snagged from somewhere on board, and then consigning them to the sea knowing in my heart that they were on their way to someone, somewhere who would read them. Sometime replies arrived at my grandparents’ house years later, and they would forward them to me wherever I was living. From these contacts I developed pen-pals who I stayed in touch with for many years. I was fortunate to develop, very early in my life, a sense of the network that invisibly but seamlessly connects us all. Thank you for picking up this message in a bottle, dear reader. We are all here together.

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