Pollution's Impact: Trophic Levels And Their Vulnerability

The impact of pollution on different trophic levels is a pressing issue, particularly in aquatic ecosystems. Higher trophic levels, including apex predators such as birds, fish, and marine mammals, are often the most affected by pollution due to a process called biomagnification. This phenomenon occurs when toxins, such as heavy metals and toxic chemicals, accumulate in organisms and increase in concentration as they move up the food chain. As a result, higher-level predators experience greater exposure to dangerous levels of toxic materials, which can lead to various adverse effects, including disease, genetic mutations, and even death. Understanding the mechanisms of biomagnification is crucial for preserving the health of both marine life and humans, who also occupy a high trophic level in the food chain.

Bioaccumulation

Some examples of POPs include DDT (a post-WWII insecticide) and PCBs (flame retardants). Although their production was banned in the 1970s and 1980s, they can still be found in the oceans and in the tissues of marine animals due to their persistence in the environment, their ability to move within water, and their propensity to dissolve into the fatty tissues of living organisms.

Biomagnification can continue all the way up the food web, with toxins becoming more and more concentrated at each trophic level. This means that apex predators are at risk of gaining potentially fatal levels of POPs within their bodies. One example of this is the orca, in which researchers have found extremely high levels of PCBs within the blubber of Arctic orcas, leading to the label of “the most toxic animal in the Arctic”.

Additionally, mother orcas have been found to pass these contaminants to their young through their milk, and PCBs are known to cause reproductive problems.

Industrial, agricultural, and human waste

The trophic level of an organism is its position in a food web, which is determined by its feeding behaviour. The first trophic level consists of primary producers such as plants, which are consumed by herbivores at the second trophic level. Carnivores that eat these herbivores are at the third trophic level, and secondary carnivores that eat the primary carnivores are at the fourth trophic level.

Industrial waste, such as heavy metals, can contaminate aquatic ecosystems and be absorbed by fish gills and other sensitive organs of aquatic creatures. This can result in biomagnification, where toxins accumulate at higher concentrations in organisms at higher trophic levels. For example, arsenic has been found to biomagnify in marine ecosystems, particularly in tertiary consumers such as predatory fish. Similarly, mercury has the potential to biomagnify from lower trophic levels, such as particulate organic matter, to higher trophic levels, such as fish.

Agricultural waste, such as excess nutrients from fertilisers, can also impact trophic levels. For example, an increase in nutrient levels can cause algal blooms, which can lead to oxygen depletion in water bodies, affecting aquatic organisms at various trophic levels.

Human waste, such as untreated sewage, can introduce pollutants into ecosystems, affecting organisms at various trophic levels. For example, pharmaceuticals and personal care products can contaminate water bodies and have been found to impact the health of aquatic organisms, including fish and amphibians, which occupy different trophic levels.

Overall, while it is difficult to generalise due to the complex nature of food webs and the varying impacts of different types of pollution, it can be said that pollution from industrial, agricultural, and human waste can affect multiple trophic levels, particularly in aquatic ecosystems.

Toxins in marine animals

Marine toxins are poisons of biological origin that are produced by a wide array of organisms, ranging from small microbes to fish and snails. They are not infectious, but exposure to the toxins through envenomation, ingestion, or inhalation may lead to death through paralysis of cardiac or respiratory muscles.

Ciguatera Fish Poisoning

Ciguatera illness is caused by ciguatoxins, which are compounds that bioaccumulate in shallow, coastal water-dwelling fish. This amplification occurs as a consequence of the marine food web, where larger fish feed on smaller fish that utilize ciguatoxin-producing dinoflagellates as a food source. Ciguatoxins are heat-stable polyethers, so they cannot be 'cooked' away. Diagnosis for ciguatera poisoning is based on the patient’s clinical picture and an account of recent marine fish consumption that has been previously associated with ciguatera fish poisoning. Ciguatoxins act as potent activators of sodium channels and result in neurotoxicities. The complete clinical picture may include neurologic symptoms (parasthesia, dysesthesia, arthralgia, pruritus, asthenia, sensation of loose teeth), gastrointestinal symptoms (vomiting, diarrhea, stomach pain), and cardiovascular symptoms (arrhythmia, hypotension, bradycardia). Patients may take from days to weeks to recover, but there are case reports of symptoms lingering for years.

Paralytic Shellfish Poisoning

Paralytic shellfish poisoning (PSP) is a foodborne illness brought on by saxitoxin, a chemical compound produced by cyanobacteria of freshwater and by dinoflagellates of marine water. PSP is a potentially fatal syndrome resulting from the ingestion of one or more of a family of potent neurotoxins called saxitoxins. PSP is generally associated with the consumption of bivalve molluscs, although crabs and whelks have also been implicated. Saxitoxin interacts with sodium, potassium, and calcium channels, though its primary molecular target is voltage-gated sodium channels, where one molecule of toxin blocks one sodium channel. Symptoms are quick to onset and begin within one to two hours of toxin ingestion. Gastrointestinal symptoms are common and can be accompanied by neurologic manifestations that include paresthesias of the face, weakness, tingling, and paralysis.

Neurotoxic Shellfish Poisoning

Neurotoxic shellfish poisoning (NSP) is thought of as a 'milder' case of the paralytic shellfish poisoning. Its cause is brevetoxin, a group of more than 10 lipid-soluble polyether compounds. These bind to voltage-gated sodium channels and have the ability to cross the blood-brain barrier and lead to severe numbness, ataxia, and even require respiratory support. Though mainly produced by the dinoflagellate Karenia brevis, brevetoxin has also been found in a bloom of Chattonella cf. verruculosa. As with the other marine toxins, brevetoxin has no antidote for human use. However, Karenia brevis does produce a natural antagonist named brevenal. This compound is currently studied in animals for inhaled brevetoxin poisoning, as aerosolized toxin can find its way from the algal blooms to mammalian airways. Similar to the management of the other toxins, treatment for NSP is largely supportive.

Tetrodotoxin

Tetrodotoxin (TTX) is perhaps the most well-known of the marine toxins. Its notoriety arises from the popularity of pufferfish. This Japanese delicacy, among other terrestrial and marine organisms, harbors the toxin in its organs and can be deadly if improperly prepared. TTX is an extremely potent sodium channel blocker; even small amounts ingested can have powerful effects on nerve conduction. This results in 'intoxication' symptoms that are scored from grade 1 to 4. These can range from mild isolated facial paresthesias and abdominal pain to severe respiratory paralysis and cardiac arrhythmias.

Scombroid Syndrome

A red herring in the recognition of fish food poisoning is scombroid syndrome. This illness is commonly mistaken for fish allergy, but instead results from improper storage and transportation of fish belonging to the Scombroidiae family. Scombroid syndrome is caused by histamine, which is not eradicated through cooking. Sometimes the compound may alter the taste of the fish, though this is not always true. Thus, prevention of this syndrome is reliant on appropriate cooling and transportation.

Food chain length

In aquatic ecosystems, for example, heavy metals and toxic chemicals from industrial, agricultural, and human waste runoff can contaminate rivers and oceans. These pollutants are then absorbed by organisms at the base of the food chain, such as phytoplankton, through processes like bioaccumulation. As longer food chains progress, the concentration of these pollutants magnifies at each trophic level, affecting secondary consumers, tertiary consumers, and apex predators the most.

For instance, in a marine food chain, contaminants such as Persistent Organic Pollutants (POPs) like DDT and PCBs can accumulate in phytoplankton, which are then consumed by zooplankton. The concentration of these toxins increases as larger organisms feed on contaminated zooplankton, and the process continues up the food chain. Seabirds, fish, and marine mammals at the top of the food chain can accumulate fatal levels of toxic materials due to the length of the food chain and the resulting biomagnification.

The impact of pollution on different trophic levels is not limited to marine ecosystems. In terrestrial food chains, pollutants from agricultural practices, industrial activities, and human sources can contaminate plants, which are then consumed by herbivores, and the toxins biomagnify as they progress up the food chain to carnivores and top predators. The length of these food chains plays a crucial role in determining the severity of pollution impacts on different trophic levels.

Understanding the dynamics of food chain length and its influence on pollution effects is essential for mitigating ecological risks. By studying these relationships, scientists can develop strategies to reduce pollution inputs, promote ecological balance, and protect vulnerable species, especially those occupying higher trophic levels in lengthy food chains.

Environmental degradation

The process responsible for this concentration of pollutants at higher trophic levels is known as biomagnification. It occurs when toxins are passed from one trophic level to the next, resulting in an increase in their concentration within a food web. This phenomenon is particularly pronounced in aquatic ecosystems, where contaminants like heavy metals and synthetic chemicals are introduced. These pollutants are not easily broken down and have a tendency to accumulate in the fatty tissues of organisms.

An example of a pollutant that undergoes biomagnification is mercury, which is released into the environment through industrial waste and other anthropogenic sources. As it contaminates marine environments, mercury is consumed by organisms living or feeding on bottom sediments, such as clams. These clams are then eaten by fish, and the mercury stored in their tissues is passed on to the fish. Birds that feed on these contaminated fish accumulate even higher levels of mercury, which can reach fatal concentrations. Thus, the impact of pollution is felt most strongly by predators and birds at the top of the food chain.

Another example of a synthetic chemical that undergoes biomagnification is DDT, an insecticide that was extensively used after World War II. Despite its production being banned in the 1970s, DDT can still be found in the oceans and the tissues of marine animals. This persistence in the environment, along with its ability to dissolve into fatty tissues, makes DDT a potent bioaccumulator and biomagnifier. As a result, apex predators like orcas are at risk of accumulating potentially fatal levels of DDT and other similar pollutants.

The environmental degradation caused by these pollutants has not gone unnoticed, and governments are taking steps to address the issue. For instance, the Stockholm Convention on Persistent Organic Pollutants, which came into effect in 2004, internationally bans the production of chemicals like PCBs and DDT. These efforts are showing results, with environmental levels of some toxins beginning to decrease. However, more stringent measures and a shift towards sustainable practices are necessary to mitigate the harmful effects of pollution on higher trophic levels and preserve the delicate balance of our ecosystems.

Frequently asked questions