Basic Toxicology

  • basic toxicology_photo credit: ocw.jhsph.eduToxicology is defined as the study of adverse effects of chemicals on living organisms. Toxicology literally translates into the science of poisons. The basic assumption of toxicology is that all substances are poisons and there is none that is not a poison. The right dose (whether it be a medication or pesticides being applied) is what differentiates a poison from a remedy. On this page we will focus on ecological measurements of hazard and exposure.


  • Haber's law helps us better understand the essential principle behind all toxicology. Haber's law explains that increased adverse effects are based on both time(t) of exposure and (d) dose. If one is not exposed to a toxic compound, then one cannot manifest adverse effects.

Habers Law: E= D x T, Where E= Effect, D= Dose, & T=Time

  • Environmental Toxicology examines how environmental exposures to chemical pollutants may present risks to biological organisms - particularly terrestrial and aquatic invertebrates, plants (vascular and non-vascular), birds, fish as well as mammals.

For ecological toxicity and exposure testing for a pesticide, the EPA uses several measures (on several different organisms - see value/ranking section) to determine how toxic a substance can be to the physical, chemical, and biological environment on both an acute (short-term) and chronic (long-term) basis. In some cases safety factors are applied in an attempt to provide extra protection (if needed) for acute toxicity values during risk characterization. Generally, the LD50 or LC50 derived from bioassays are used for acute measurements and the NOAEL or NOAEC values are used for chronic measurements of toxicity.

Measures of Toxicity

product development in the pesticide industryIn order to generate all data required for registration of a new pesticide, it generally takes manufacturers over a decade and approximately $150 million before all aspects of the new pesticide have been analyzed.

Ecological Data

The generated data are submitted to the EPA to determine the pesticide's effect on ecological health; these data are coupled with environmental chemistry data to determine environmental fate of compounds as well. Each assay performed and considered has an assigned Office of Chemical Safety and Pollution Prevention (OCSPP) guideline number associated with it so that testing regimes are standardized for all pesticides (EPA 2013). The EPA requires the registrant to submit hazard data (toxicological data) for both terrestrial and aquatic species. Values of toxicity are usually generated in dose-response curves. This helps decision-makers determine a range of safe doses. At this point various computer models are run with pesticide values to determine safe application rates, frequency, and methods as well as fate and transport of the pesticide. Additionally, for acute toxicity, a safety factor (3X) may be tacked on if there are federally listed threatened or endangered species where pesticide application is occurring. The EPA ensures a pesticide is safe (if applied according to label standards), and therefore requires multiple assays to make this judgement call - making best efforts to minimize adverse effects to organisms by setting conservative Levels of Concern (LOCs) with set environment concentrations not to be exceeded. (Above figure generously provided by Dave Volz, Ph.D., University of South Carolina)

dose response curve

The EPA testing guidlines for hazard are outlined in detail concerning the requirements of the bioassay and can be accessed from:

Reference site for toxicity guidelines

Some of the EPA OCSPP assays used in the cumulative ranking of residential compounds include:

  • Acute Toxicity: Acute Oral Rat Toxicity – updated in 1996; GLN #: 870.1100
  • Chronic Toxicity: Chronic Feeding Study – updated in 1998; GLN #: 870.4100
  • Acute Toxicity: Avian Acute Oral Toxicity Test – updated 2012; GLN #: 850.2100
  • Chronic Toxicity: Avian Dietary Toxicity Test – updated 2012; GLN #: 850.2200
  • Acute Toxicity: Honeybee Acute Contact Toxicity – updated 2012; GLN #: 850.3020
  • Acute Toxicity: Aquatic Invertebrate Acute Toxicity Test – updated 1996; GLN #: 850.1010
  • Chronic Toxicity: Daphnid Chronic Toxicity Test – updated 1996; GLN #: 850.1300
  • Acute Toxicity: Fish Acute Toxicity Test – updated 1996; GLN #: 850.1075
  • Chronic Toxicity: Fish Early Life-stage Toxicity Test – updated 1996; GLN #: 850.1400
  • Acute Toxicity: Algae Toxicity Test –updated 1996; GLN #: 850.5400


ADE_color_codedWhile exposure experiments are being conducted, for each organism being exposed, the following are considered and are commonly referred to by the acronym ADME: absorption, distribution through the body, metabolism, and excretion of a compound. In some cases, there is not always data on every aspect of this process for each organism and some values are estimated; the above figure depicts possible pathways once human exposure occurs and the different target organs based on route of exposure. For example, ingestion may be more or less toxic to the organism depending on the compound. The majority of the time ADME data and models are generated for human health scenarios. However, ADME processes occur in other organisms and if exposure occurs to an active ingredient (AI), enzymatic activity results in metabolites possibly more toxic then the AI itself. The internal anatomy of both vertebrates and invertebrates - as well as the target and critical organs - are vital to know concerning the Mode of Action (MOA) and ultimately how a pesticide will effect various organisms, and whether it is more target-specific or a broad-spectrum pesticide.

Internal Anatomy of Some Vertebrate and Invertebrate Speciesanatomy of ecological important species

Move on and learn more about Pesticide Movement in the Environment