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In this course, the basic concepts, methods, and approaches in environmental toxicology will be introduced. Natural and synthetic chemicals commonly encountered in the air, water, and soil will be discussed regarding their occurrence, fate and transport, and toxicological effects on ecological species and humans. Case studies will be used to illustrate the complexity of environmental toxicology issues. New trends in chemical toxicity testing will be discussed. Contaminants of emerging concerns such as pharmaceutical and personal care products and engineered nanomaterials will also be introduced.
This module will introduce you to environmental toxicology. Specifically, the topics include the definition and scope of toxicology, brief history of toxicology, dose-response relationships, sources of toxic compounds, and the movement of toxicants in the environment.
In order for you to understand each technique, I have provided links at the Reference section which you can easily click to open.
At the end of this module, we will have a module quiz to assess your understanding and mastery of the topics/concepts discussed,.
After going through in this module, you should be able to:
➤ define important terms in environmental toxicology;
➤ explain the cascade of events leading from chemical exposure to toxicity;
➤ list the people and events who/which contributed in the development of environmental toxicology;
➤ describe the relationship between the dose of a chemical compound and the response elicited by an organism;
➤ identify the various sources of environmental toxicants; and ➤ briefly explain the processes involved in the absorption, distribution, metabolism, and elimination of environmental chemicals.
I want to know if you have any idea/ knowledge about Environmental Toxicology.
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I. DEFINITION AND SCOPE
A. DEFINITION OF TERMS
➤ the study of the detection, occurrence, properties, effects, and regulation of toxic substances; ➤ deals with natural or synthetic chemical substances in relation to the production of abnormal or undesirable results;
➤ focuses on the symptoms, methods, remedies, and detection of a poisoning.
➤ studies the interaction between chemicals and biological systems to determine the potential of chemicals to produce adverse effects in living organisms.
Adverse effects
➤ are detrimental to the survival or the normal functioning of the individual.
The variety of potential adverse effects and the diversity of chemicals present in our environment combine to make toxicology a very broad science.
Toxicology uses basic knowledge from clinical and theoretical medicine and natural sciences such as biology and chemistry (Figure 1).
Detection and quantitation of xenobiotics and their metabolites
Analytical chemistry
Physiology
Interference of toxic agents with physiological function
Figure 1. Scientific fields influencing the science of toxicology Source: Dekant & Vamvakas (2004)
Forensic medicine
Detection of intoxication
Treatment of Internal medicine Intensive care poisoning
Mutagenesis
Genetics
➤ studies the effects of chemicals on ecosystems and on humans after low-dose exposure from the environment
➤ studies the effects of chemicals released by man on wildlife and the ecosystem and thus indirectly on human health.
Forensic toxicology
➤ diagnoses poisoning by analytical procedures
➤ concerned with the legal aspects of the harmful effects of chemicals on humans.
➤ The expertise of the forensic toxicologist is invoked primarily to aid in establishing the cause of death and elucidating circumstances in a postmortem
Drug toxicology its investigation.
➤ studies potential effects of drugs after high doses, elucidates mechanisms of side effects
➤ plays a major role in the pre-clinical safety assessment of chemicals intended for use as drugs. ➤ elucidates the mechanisms of side effects observed during clinical application.
Clinical toxicology
➤ recognizes and treats poisoning, both chronic and acute.
➤ Efforts are directed at treating patients poisoned by chemicals and at the development of new techniques to treat these intoxications.
➤ studies the acute and chronic toxicity of chemicals encountered in the occupational environment. ➤ assesses potential adverse effects of chemicals used in the workplace
➤ helps in the development of safety procedures to prevent intoxications in the workplace and assists in the definition of exposure limit
➤ develops and interprets toxicity testing programs and is involved in controlling the use of chemicals
Pesticide toxicology
➤ involved in the development of new pesticides and the safety of pesticide formulations.
➤ characterizes potential health risks to the general population caused by pesticide residues in food and drinking water.
➤ the quantity to which a substance can have a negative or adverse effect;
➤ a cascade of events starting with exposure, proceeding through distribution and metabolism, and ending with interaction with cellular macromolecules (usually DNA or protein) and the expression of a toxic end point (Figure 2). This sequence may be mitigated by excretion and repair.
➤ The amount, the duration, and the type of exposure will determine the toxic outcome.
➤ Toxicity may be acute or chronic, and may vary from one organ to another as well as with age, genetics, gender, diet, physiological condition, or the health status of the organism.
➤ The toxicity of a particular compound may vary with the portal of entry into the body, whether through the alimentary canal, the lungs, or the skin.
➤ Toxicity may vary as much as 10-fold with the route of administration.
➤ Following exposure, there are multiple possible routes of metabolism, both detoxifying and activating, and multiple possible toxic end points (Figure 1).
➤ Genetic variation is a most important factor in human toxicity since the human population is highly outbred and shows extensive genetic variation.
➤ Even the simplest measure of toxicity, the LD 50, is highly dependent on the extent to which the above variables are controlled. LD 50 values vary markedly from one laboratory to another.
Absorption into Bloodstream and Distribution to Body Tissues and Organs
Figure 2. Fate and effect of toxicants in the body
Source: Hodgson (2010)
➤ almost any substance being harmful at some doses but, at the same time, being without harmful effect at some lower dose.
➤ Between these two limits, there is a range of possible effects, from subtle long-term chronic toxicity to immediate lethality.
➤ vinyl chloride. A potent hepatotoxicant at high doses, a carcinogen with a long latent period at lower doses, and apparently without effect at very low doses.
➤ Aspirin. A relatively safe drug at recommended doses. Chronic use can cause deleterious effects on the gastric mucosa. Fatal at a dose of about 0.2-0.5 g/kg.
➤ iron, copper, magnesium, cobalt, manganese, zinc. These can be present in the diet at too low a level (deficiency), at an appropriate level (maintenance), or at too high a level (toxic).
Qualitative biological aspect:
➤ a compound, toxic to one species or genetic strain, may be relatively harmless to another.
➤ CCI 4. A potent hepatotoxicant in many species but relatively harmless to the chicken.
➤ Compounds may be toxic under some circumstances but not others or, perhaps, toxic in combination with another compound but nontoxic alone.
➤ methylenedioxyphenyl insecticide synergists, such as piperonyl butoxide. Of low toxicity to both insects and mammals when administered alone, but are, by virtue of their ability to inhibit xenobiotic-metabolizing enzymes, capable of causing dramatic increases in the toxicity of other compounds.
➤ the act of being in contact with something and its availability to be taken into the body.
➤ exposure of humans and other organisms to toxicants may result from many activities: intentional ingestion, occupational exposure, environmental exposure, accidental and intentional (suicidal or homicidal) poisoning.
➤ Potential environmental exposures include contaminated water, polluted air, household products, garden soil, and industrial waste.
➤ Category of the effects that result from the exposure to a toxic substance:
1. acute-short-term exposure and the effects occur quickly
2. chronic-long-term exposure and the effects take time to develop
➤ the reaction of an organism to a toxic substance and it is measured by the changes that occur.
➤ changes may range from minor (e.g. headaches) to severe (e.g. convulsions) to adverse effects (e.g. death)
Discussion
I. DEFINITION AND SCOPE
➤ the location in the body where a chemical causes adverse effects.
➤ This location can be an entire organ, a tissue, a cell, or genes (may cause mutation).
Inherent in the definition of toxicology are the following key issues:
1. Chemicals must come into close structural and/or functional contact with tissues or organs to cause injury.
2. All adverse effects depend on the amount of chemical in contact with the biological system (the dose) and the inherent toxicity of the chemical (hazard)
3. When possible, the observed toxic effect should be related to the degree of exposure. The influence of different exposure doses on the magnitude and incidence of the toxic effect should be quantitated (dose-response relationship).
I. DEFINITION AND SCOPE
B. SCOPE OF TOXICOLOGY
➤ describe an important molecular event in the cascade of events leading from exposure to toxicity.
a. Toxicity at the biochemical and molecular levels
➤ include enzymes that metabolize xenobiotics, generation of reactive intermediates, interaction of xenobiotics or their metabolites with macromolecules, gene expression and signaling pathways. b. Effects of toxicants on animal and human behavior
➤ involves both the peripheral and central nervous systems, as well as effects mediated by other organ systems, such as the endocrine glands.
d. Carcinogenesis c. Effects of diet on the expression of toxicity
➤ includes the chemical, biochemical, and molecular events that lead to the large number of effects on cell growth e. Teratogenesis
➤ includes the chemical, biochemical, and molecular events that lead to deleterious effects on development.
f. Mutagenesis
➤ toxic effects on the genetic material and the inheritance of these effects.
g. Organ toxicity
➤ effects at the level of organ function - neurotoxicity, hepatotoxicity, and nephrotoxicity.
➤ answer certain critically important questions: Is the substance likely to be toxic? What is its chemical identity? How much of it is present? How can we assay its toxic effect, and what is the minimum level at which this toxic effect can be detected?
➤ Toxicity testing involves the use of living systems to estimate toxic effects. It covers the range of tests (bioassays) from short-term tests for genotoxicity such as the Ames test and cell culture techniques to the use of intact animals for a variety of tests from acute toxicity to lifetime chronic toxicity.
I. DEFINITION AND SCOPE
B. SCOPE OF TOXICOLOGY
➤ Include synthetic chemicals and natural products (used for commercial and other purposes); ➤ Examples of such natural products include the insecticide, pyrethrin, the clinical drug, digitalis, and the drug of abuse, cocaine.
➤ Agricultural chemicals include insecticides, herbicides, fungicides, and rodenticides, in which toxicity to the target organism is a desired quality whereas toxicity to "nontarget species" is to be avoided.
➤ Drugs of abuse are chemicals taken for psychological or other effects and may cause dependence and toxicity.
➤ Food additives
➤ Naturally occurring substances include many phytotoxins, mycotoxins, minerals, and so on, all occurring in the environment. The recently expanded and now extensive use of herbal "remedies" and dietary supplements has become a cause of concern for toxicologists and regulators. Not only is their efficacy frequently dubious, but their potential toxicity is also largely unknown.
➤ Combustion products are generated primarily from fuels and other industrial chemicals.
➤ concerned with the formulation of laws and regulations authorized by laws, which are intended to minimize the effect of toxic chemicals on human health and the environment.
➤ Legal aspects - include formulation of laws and regulations and their enforcement.
➤ In the United States, enforcement falls under such government agencies as the Environmental Protection Agency (EPA), the Food and Drug Administration (FDA) and the Occupational Safety and Health Administration (OSHA).
➤ Similar government agencies exist in many other countries.
➤ Risk assessment - the definition of risks, potential risks, and the risk-benefit equations necessary for the regulation of toxic substances.
➤ In the Philippines, we have the following Environmental Laws:
REPUBLIC ACT 9003 ECOLOGICAL SOLID WASTE MANAGEMENT ACT OF 2000
➤ In partnership with stakeholders, the law aims to adopt a systematic, comprehensive and ecological solid waste management program that shall ensure the protection of public health and environment.
➤ The law ensures proper segregation, collection, storage, treatment and disposal of solid waste through the formulation and adaptation of best eco-waste products.
REPUBLIC ACT 9275 PHILIPPINE CLEAN WATER ACT OF 2004
➤ The law aims to protect the country's water bodies from pollution from land-based sources (industries and commercial establishments, agriculture and community/household activities).
➤ It provides for comprehensive and integrated strategy to prevent and minimize pollution through a multi-sectoral and participatory approach involving all the stakeholders.
REPUBLIC ACT 8749 PHILIPPINE CLEAN AIR ACT OF 1999
➤ The law aims to achieve and maintain clean air that meets the National Air Quality guideline values for criteria pollutants, throughout the Philippines, while minimizing the possible associated impacts to the economy.
REPUBLIC ACT 6969 TOXIC SUBSTANCES, HAZARDOUS AND NUCLEAR WASTE CONTROL ACT OF 1990
➤ The law aims to regulate restrict or prohibit the importation, manufacture, processing, sale, distribution, use and disposal of chemical substances and mixtures that present unreasonable risk to human health.
➤ It likewise prohibits the entry, even in transit, of hazardous and nuclear wastes and their disposal into the Philippine territorial limits for whatever purpose; and to provide advancement and facilitate research and studies on toxic chemicals.
PRESIDENTIAL DECREE 1586 ENVIRONMENTAL IMPACT STATEMENT (EIS) STATEMENT OF 1978
➤ The Environment Impact Assessment System was formally established in 1978 with the enactment of Presidential Decree no. 1586 to facilitate the attainment and maintenance of rational and orderly balance between socio-economic development and environmental protection.
➤ EIA is a planning and management tool that will help government, decision makers, the proponents and the affected community address the negative consequences or risks on the environment.
➤ The process assures implementation of environment-friendly projects.
➤ 1500 BC: The Ebers Papyrus is among the oldest written documentation of medicines in the ancient world. It is the oldest known ancient Egyptian medical scroll, dating back to a period between 1550 and 1500 BC.
➤ 400-250 BC: the surviving medical works of Hippocrates, Aristotle, and Theophrastus, all include some mention of poisons;
➤ 3 BC: Nicander of Colophon (Greek poet) - author of two treatises on poison: Theriaca ( deals with the bites of venomous snakes, spiders, and scorpions, and how to remedy them) and Alexipharmica (enumerates additional animal, vegetable, and mineral poisons, including aconite, white lead, hemlock, and opium, together with their symptoms and specific remedies). The cures are almost always herbal and often include olive oil as an emetic to induce vomiting. ➤ 50 AD: Dioscorides, a Greek employed by the Roman emperor Nero, wrote the earliest surviving attempt to classify plants according to their toxic and therapeutic effects. His classification of poisons into plant, animal, and mineral groups provided a framework for future toxicologists to build upon;
➤ 131-200: Galen. He was the first physician to use the pulse as a sign of illness;
➤ 1493-1541: Paracelsus laid the groundwork for the later development of modern toxicology by recognizing the importance of the dose-response relationship. His famous statement "All substances are poisons; there is none that is not a poison. The right dose differentiates a poison and a remedy.. His belief in the value of experimentation was also a break with earlier tradition. ➤ 1700: Bernardino Ramazzini (Italian) published Diseases of Workers which led to his recognition as the father of occupational medicine. Hei focused on workers' health problems; ➤ 1775: Sir Percival Pott recognized that the high rate of scrotal cancer among chimney sweeps in England was linked to their exposure to soot;
➤ 1761: John Hill reported the correlation of nasal cancer and snuff use (nasal snuff causing cancer of the nose);
➤ 1787-1853: Mateu Joseph Bonaventura Orfila i Rotger, a Spanish chemist, is generally regarded as the father of modern toxicology. He clearly identified toxicology as a separate science and, in 1815, published the first book devoted exclusively to toxicology. An English translation in 1817 was entitled A General System of Toxicology or, A Treatise on Poisons, Found in the Mineral, Vegetable and Animal Kingdoms, Considered in Their Relations with Physiology, Pathology and Medical Jurisprudence. He established basic principles of modern medicine and pharmacology;
➤ 1833: Alfred Nobel: Swedish chemist, engineer, innovator, armaments manufacturer and the inventor of dynamite.
➤ 1840: James Marsh: Chemist developed and perfected the Marsh test for arsenic. The improved Marsh test used forensically for the first during the trial of Marie Lafarge.
➤ 1847: Ascansio Sobrer: Italian chemist, discovered nitroglycerine in 1847, a powerful explosive and vasodilator. Alfred Nobel was his student.
➤ 1939: DDT: Recognized as insecticide by the Swiss scientist Paul Hermann Müller, who was awarded the 1948 Nobel Prize in Physiology and Medicine. Banned in 1972.
➤ 1944: Thomas Midgley Jr: American chemist who developed both the tetra- ethyl lead (TEL), additive to gasoline, and chlorofluorocarbons (CFCs).
➤ 1950 Minamata (1950s): Minamata Bay contaminated with mercury by chemical industry. Thousands adults and children were poisoned from eating fish contaminated with methyl mercury.
➤ 1952: London Great Smog: London was overwhelmed by The Great Smog, also referred to as the Big Smoke, starting on December 5, 1952, and lasted until December 9, 1952. This catastrophic event caused or advanced the death of as many as 12 000 people
➤ 1959: Thalidomide (1959-1960s): Drug prescribed to pregnant women for morning sickness induced birth defects. Frances Oldham Kelsey of the Food and Drug Administration (FDA) blocked approval in U.S.
➤ 1962: Rachel Carson: Scientist who led the crusade against the use of DDT. Published Silent Spring in 1962. Her book is often credited as the catalyst leading to the establishment of the U.S. EPA and she is regarded by many as the mother of the environmental movement.
➤ 1960s: toxicology has entered a phase of rapid development and has changed from a science that was largely descriptive to one in which the importance of mechanisms of toxic action is generally recognized.
➤ 1970s: with increased emphasis on the use of the techniques of molecular biology, the pace of change has increased even further, and significant advances have been made in many areas, including chemical carcinogenesis and xenobiotic metabolism.
➤ 1970s: studies indicated that the pesticide dibromochloropropane can cause infertility in male production workers and pesticide applicators.
➤ 1970: Earth Day held for the first time on April 22nd.
➤ 1970: Occupational Safety and Health Act passed to ensure workers have a safe workplace. ➤ 1970: Environmental Protection Agency (EPA) established.
➤ 1978: Love Canal, August 7, 1978: U.S. President Jimmy Carter declared Love Canal a federal emergency. 42 million pounds of over 200 chemicals contaminated Love Canal, disrupting many lives.
➤ 1984: Bhopal Disaster: Release of 40 tons of methyl isocyanate from a Union Carbide plant in India killed thousands and injured hundreds of people.
➤ 1986: Chernobyl accident at the nuclear power plant meltdown released radioactive waste into the atmosphere poisoning hundreds of thousands of people.
➤ 1995: Tokyo subway sarin gas attack: Members of religious group Aum Shinrikyo released sarin gas in five places in Tokyo subway, killing 12 and injuring 6000.
➤ 2001: Anthrax terrorists send poisoned letters that cripple the U.S. postal service and poisoned many..
II. BRIEF HISTORY OF TOXICOLOGY
Did you know?
The Minamata disease was identified 50 years ago in Minamata city, Kumamoto, Japan. It was caused by release of methyl mercury in industrial wastewater from Chisso Corporation's chemical factory which continued from 1932-1968. It resulted in poisoning from fish contaminated by mercury discharges to the surrounding sea. But even today, unfortunately, thousands of victims are still fighting for compensation from the company.
Malformations due to matemal ingestion of thalidomide (Schardein 1982 and Moore 1993)..
About 22,000 tons of over 200 different chemicals were dumped in the ditch from 1942 to 1953...
The first recognition of the relationship between the dose of a compound and the response elicited has been attributed to Paracelsus. His statement includes not only that all substances can be toxic at some dose, but that “the right dose differentiates a poison from a remedy," a concept that is the basis for pharmaceutical therapy.
"All things are poison and nothing without poison; only the dose determines that a thing is not poison."
Philippus Theophrastus Aureolus Bombastus von Hohenheim (Paracelsus, 1493-1541)
- alchemist, physician and astrologer
The toxic effects that manifest from the chemical depend on the way it got into the body. As well, the amount (dose) that is actually absorbed into the body (Table 1).
All toxic effects are products of the amount of chemical to which the organism is exposed and the inherent toxicity of the chemical; they also depend on the sensitivity of the biological system.
Substance
Alcohol
Table 1. Toxic doses of some chemicals
An adult weighing 100 pounds who quickly consumes 9 or 10 standard drinks in less than one hour.
Salt
An adult man weighing 220 pounds would need to consume 300 grams of salt.
A cat weighting 5 kilogram would need to eat 60,000 cockroaches with DDT residue in one day.
An adult weighing 150 pounds would need to ingest .07 milligrams.
An adult weighing 154 pound would need 3,000 units (Botox® injections of 20- 70 units per treatment are generally used for cosmetic purposes).
Dose
Discussion
➤ used to characterize the total amount of material to which an organism is exposed;
➤ defines the amount of chemical given in relation to body weight.
➤ usually implies the exposure dose, the total amount of chemical administered to an organism or incorporated into a test system.
➤ may not be directly proportional to the toxic effects since toxicity depends on the amount of chemical absorbed.
correctly describes only the actual amount of chemical absorbed when the chemical is administered orally or by injection.
➤ Under these circumstances, the administered dose is identical to the absorbed dose; other routes of application such as dermal application or inhalation do not define the amount of agent absorbed.
Different chemicals have a wide spectrum of doses needed to induce toxic effects or death.
➤ To characterize the acute toxicity of different chemicals, LD 50 values are frequently used as a basis for comparisons.
➤ Certain chemicals are very toxic and produce death after administration of microgram doses, while others are tolerated without serious toxicity in gram doses.
Table 2. LD 50 values (rats) for some chemicals
A typical dose-response curve is shown in Figure 3, which plots the relationship between the toxicant dose and the health effects.
In addition, a chemical can produce harmful effects to one living organism while not harming another (selective toxicology). For example, an antibiotic may kill strep throat bacteria, but it will not kill you.
People can also respond to chemical substances in different ways. Some may be exposed and may not develop a negative effect, while others may be more sensitive to a chemical and can develop negative effects from an exposure.
No two individuals are the same; therefore the response to a dose varies considering age, lifestyle, and genetics (biological variation). Yet, if there is no exposure to a chemical, there will not be an effect.
When an organism is exposed to a toxic substance, it follows toxicity phases.
1st phase: Exposure phase - a toxicant is taken up by the organism's system via the mouth (oral), lungs (inhalation), or skin (dermal).
2nd phase: Processing phase - the toxicant is transported and stored inside the body. The rate at how it is processed varies from person to person.
3rd phase: Expression phase - describes the resulting effects that appear in the organism (e.g. lesion or headache).
Increasing effect no effect range range of increasing effect with increasing dose
Figure 3. A dose-response curve showing as the dose increases, so does the response Source: Dose-response curve - Labster/2025 Toxicology Education Foundation.
Discussion
➤ For many chemicals and effects, there will be a dose below where no effect or response is observed. This is known as the threshold dose.
➤ This concept implies that a no observed adverse effect level (NOAEL) can be determined and that this value can be used to determine the safe intake for food additives and contaminants such as pesticides.
➤ Noncarcinogenic substances are characterized by a threshold below which the body is able to cope with or recover from the exposure. A brief or low exposure leaves no consequence until the next exposure.
➤ Carcinogenic substances are different as they have no such threshold. All repeated exposures to a carcinogenic substance add up, and the risk is never zero. At low doses, the risk is proportional to the exposure.
e Figure 3. Dose response curves. LOAEL; lowest- observed-adverse-effect level, ED 50; median effective dose, LD 50 ; median lethal dose. Source:
Dose-response curves for carcinogens are assumed to have no threshold; that is, any exposure produces some chance of causing cancer.
Everything in the environment is made out of chemicals. These chemicals can either be naturally occurring or synthetic. Both types can be toxic to living organisms; thus natural chemicals can also cause negative effects. Just because they are "natural," does not mean that they are safe.
People often have a misconception about chemicals. Frequently, they only think about synthetic, toxic compounds. It is important to highlight that we use chemicals in our everyday lives, from the time we wakeup until the time we fall asleep.
For example, toothpaste contains fluoride, sodium lauryl sulfate, calcium phosphate, strontium chloride, and hydrogen peroxide, etc. And so, we come into contact with these chemicals while brushing our teeth.
Given the enormous number of toxicants, it is difficult to classify them, either chemically, by function, or by mode of action since many of them would fall into several classes. Some are natural products, many are synthetic organic chemicals of use to society, while some are byproducts of industrial processes and waste disposal.
It is useful to categorize toxicants according to the expected routes of exposure or according to their uses.
➤ include toxicants in food, air, water, and soil as well as toxicants characteristic of domestic and occupational settings.
➤ include drugs of abuse, therapeutic drugs, agricultural chemicals, food additives and contaminants, metals, solvents, combustion products, cosmetics, and toxins.
➤ Some of these, such as combustion products, are the products of use processes rather than being use classes.
Chemicals released into the environment rarely remain in the form, or at the location, of release.
For example, agricultural chemicals used as sprays may drift from the point of application as air contaminants or enter run-off water as water contaminants.
Many of these chemicals are susceptible to fungal or bacterial degradation and are rapidly detoxified, frequently being broken down to products that can enter the carbon, nitrogen, and oxygen cycles.
Other agricultural chemicals, particularly halogenated organic compounds, are recalcitrant to a greater or lesser degree to metabolism by microorganisms and persist in soil and water as contaminants; they may enter biologic food chains and move to higher trophic levels or persist in processed crops as food contaminants. This same scenario is applicable to any toxicant released into the environment either for a specific use or as a result of industrial processes, combustion, and so on.
Chemicals released into the environment are also susceptible to chemical degradation, a process often stimulated by ultraviolet light.
SO₂ acid rain and acid deposition coal-fired power plant
NO logging drilling rig photochemical smog erosion mine
NO oil woll farmland cars and highways toxic runoff sediment loading algal bloom nitrogen (N) and lake toxic runoff wastewater plastics phosphorus (P) surface runoff algal bloom ocean effluent
N and P runoff toxic seepage (from surface)
toxic runoff oil spills petroleum seepage (from surface)
oxygen depletion plastic pollution ocean acidification groundwater contamination seepage petroleum seepage fracking
(associated with drill pipe)
Figure 4 Fate and transport of chemical contaminants in the environment
Source: https://rupiperlab.engr.ucr.edu/enve-135-fate-and-transport-contaminants-environment
V. MOVEMENT OF TOXICANT IN THE ENVIRONMENT
➤ Although most transport between inanimate phases of the environment results in wider dissemination, but, at the same time, dilution of the toxicant in question, transfer between living creatures may result in increased concentration or bioaccumulation.
➤ Lipid-soluble toxicants are readily taken up by organisms following exposure in air, water, or soil. ➤ Unless rapidly metabolized, they persist in the tissues long enough to be transferred to the next trophic level.
➤ At each level, the lipophilic toxicant tends to be retained while the bulk of the food is digested, utilized, and excreted, thus increasing the toxicant concentration (biomagnification).
➤ At some point in the chain, the toxicant can become deleterious, particularly if the organism at that level is more susceptible than those at the level preceding it.
➤ For example, the eggshell thinning in certain raptorial birds was almost certainly due to the uptake of DDT (1,1,1-trichloro-2,2-bis(4-chlorophenyl) ethane) and DDE (1,1-dichloro-2,2-bis(4- chlorophenyl) ethane) and their particular susceptibility to this type of toxicity.
(A) Chemical structures of DDT (dichloro-diphenyl-trichloroethane) and its metabolic by-product, DDE. DDT is an estrogenic compound, while DDE is an androgen inhibitor.
(B) One notable effect of environmental bioaccumulation of these chemicals was the prevalence of thin, nonviable eggshells found among many bird species (particularly birds of prey), with subsequent severe population declines. This brown pelican egg cracked open long before the embryo inside was ready to hatch.
Figure 5. The effects of pesticide bioaccumulation and biomagnification Sources: https://cup.gr/wp-content/uploads/Files/files/11e.devbio.com/wt2404.html & https://www.geeksforgeeks.org/biology/biomagnification
The transport of chemical toxicants can occur through both aquatic and terrestrial food chains, although in the former, higher members of the chains, such as fish, can accumulate large amounts of toxicants directly from the medium.
This accumulation occurs because of the large area of gill filaments, their intimate contact with the water, and the high flow rate of water over them.
Given these characteristics and a toxicant with a high partition coefficient between lipid membranes and water, considerable uptake is inevitable.
Toxic chemicals accumulate at the top of the food chain
Figure 6. Aquatic food chains are vulnerable to contamination by POPs and their "dioxinlike" components as a result of the lipophilic characteristics of these chemicals and their resistance to breakdown. Organisms occupying high trophic levels are often exposed to high concentrations of such chemicals as a result of biomagnification.
Source:
https://www.researchgate.net/publication/248944648_Integrated_Human_and_Ecological_Risk_Assessm ent_A_Case Study_of_Persistent_Organic_Pollutants_POPs_in_Humans_and_Wildlife/figures?lo=1
In order for a chemical substance to have any effect, it must first enter the body. Living organisms can ingest them, inhale them, or absorb them through their skin (Figure 7). They may also travel inside the body via mucous in the nose, eye, or ear canals. These pathways are termed routes of exposure.
Absorption is the mechanism by which a substance passes through and enters the body. Yet, before it is absorbed, the substance must be available to be transported and processed by the body.
Bioavailability describes the extent to which a chemical can be absorbed by the organism's system. For example, in order for salt to increase blood pressure in the body, it must be ingested orally in large quantities. If a large quantity of salt is poured onto the skin, it cannot readily travel inside to cause an increase in blood pressure.
After the chemical substance is absorbed, it is distributed throughout the body. Typically, it is distributed from the bloodstream to cells or a particular storage site(s). A storage site might or might not be where the toxicity occurs. Sometimes, it may be used as a protective barrier since the substance is not freely moving.
The absorbed substance can also undergo metabolic changes (biotransformation) at the site.
Finally, the substance is passed outside of the body (excretion) via such means as sweat, tears, saliva, milk, bile, and feces.
Inhalation
Do we breathe it in? This is the most common route of entry.
Does it pass through the skin, eyes or other membranes?
Injection
Does it enter through a puncture or cut?
Source: https://www.oshacademy.com/courses/training/705-hazard-communication-program/705-2-4.php
V. MOVEMENT OF TOXICANTS IN THE ENVIRONMENT
Figure 8. The toxicological process. Absorption, distribution, metabolism, and excretion processes and their relationships with effects and responses within living organisms, leading to toxicity or efficacy depending on the chemical substance they are exposed to. Sources:
https://www.researchgate.net/publication/309656865_Evidencebased_absorption_distribution_metabolism_excretion_ADME_and_its_interplay_with_alternative
_toxicity_methods/figures?lo=1 https://www.researchgate.net/publication/363981997_Generic_Solving_of_Physiologicallybased_Kinetic_Models_in_Support_of_Next_Generation_Risk Assessment_Due_to_Chemicals/f igures?lo=1
V. MOVEMENT OF TOXICANTS IN THE ENVIRONMENT
b. general locus of action (local, systemic, organ specific)
c. basic mechanisms of toxicity (reversible vs irreversible)
➤ those that occur after brief exposure to a chemical;
➤ usually develop rapidly after single or multiple administrations of a chemical; however, acute exposure may also produce delayed toxicity.
➤ For example, inhalation of a lethal dose of HCN causes death in less than a minute, whereas lethal doses of 2,3,7,8-tetra-chlorodibenzodioxin will result in the death of experimental animals after more than two weeks.
Chronic toxic effects
➤ those that appear after repetitive exposure to a substance;
➤ many compounds require several months of continuous exposure to produce adverse effects.
➤ Often, the chronic effects of chemicals are different from those seen after acute exposure (Table 2).
➤ For example, inhalation of chloroform for a short period of time may cause anesthesia; long- term inhalation of much lower chloroform concentrations causes liver damage.
➤ Carcinogenic effects of chemicals usually have a long latency period; tumors may be observed years (in rodents) or even decades (in humans) after exposure.
Table 2. Toxic effects of different chemicals categorized by time scale and general locus of action
Effect lung edema liver damage narcosis sensitization neurotoxicity bronchitis nasal carcinoma bladder carcinoma kidney damage
Chemical chlorine gas carbon tetrachloride halothane toluene diisocyanate hexane sulfur dioxide formaldehyde 4-amino-biphenyl cadmium
V. MOVEMENT OF TOXICANTS IN THE ENVIRONMENT
Categories of Toxic effects
➤ When reversible interactions are responsible for toxic effects, the concentration of the chemical present at the site of action is the only determinant of toxic outcome.
➤ When the concentration of the xenobiotic is decreased by excretion or biotransformation, a parallel decrease of toxic effects is observed.
After complete excretion of the toxic agent, toxic effects are reduced to zero.
➤ For example, carbon monoxide binds to hemoglobin and, due to the formation of the stable hemoglobin-carbon monoxide complex, binding of oxygen is blocked. As a result of the impaired oxygen transport in blood from the lung, tissue oxygen concentrations are reduced and cells sensitive to oxygen deprivation will die. The toxic effects of carbon monoxide are directly correlated with the extent of carboxyhemoglobin in blood, the concentration of which is dependent on the inhaled concentration of carbon monoxide. After exhalation of carbon monoxide and survival of the acute intoxication, no toxic effect remains.
Irreversible toxic effects
➤ often caused by the covalent binding of toxic chemicals to biological macromolecules.
➤ Under extreme conditions, the modified macromolecule is not repaired; after excretion of the toxic agent, the effect persists.
➤ Further exposure to the toxic agent will produce additive effects.
➤ many chemicals carcinogens are believed to act through irreversible changes.
Table 3. Reversible and irreversible interactions of chemicals with cellular macromolecules as a basis for toxic response
Toxic response neurotoxicity cancer oxygen deprivation in tissues neurotoxicity
Example tri-o-cresylphosphate dimethylnitrosamine carbon monoxide carbamate pesticides
V. MOVEMENT OF TOXICANTS IN THE ENVIRONMENT
Categories of Toxic effects
➤ occurs at the site of first contact between the biological system and the toxic agent.
➤ Local effects to the skin, the respiratory tract, or the alimentary tract may be produced by skin contact with a corrosive agent, by inhalation of irritant gases, or by ingestion of tissue-damaging materials.
usually restricted to the tissues with direct contact to the agent.
➤ life-threatening intoxications may occur if vital organs like the lung are damaged.
➤ For example, inhaled phosgene damages the alveoli of the lung and causes lung edema. The massive damage to the lung results in the substantial mortality observed after phosgene intoxication.
➤ characterized by the absorption of the chemical and distribution from the port of entry to a distant site where toxic effects are produced.
➤ Except for highly reactive xenobiotics, which mainly act locally, most chemicals act systemically. ➤ Many chemicals that produce systemic toxicity only cause damage to certain organs, tissues, or cell types within organs.
➤ Selective damage to certain organs or tissues by systemically distributed chemicals is termed organ- or tissue-specific toxicity; the organs damaged are referred to as target organs.
Table 4. Organ-specific toxic effects induced by chemicals that are distributed systemically in the organism
Target organ bone marrow humans rodents damage to proximal tubules of the kidney lung rodents, humans humans nervous system humans kidney humans, testes rodents rodents, nervous system humans humans heart
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