Aquatic environments videos

1 09 2015

While developing and revising “ENVS 3450 – Aquatic Environments”, I’ve been discovering quite a few good aquatic environments videos, animated GIF files & interactive pages.  Inspired by Meghan Duffy’s Dynamic Ecology post on videos for teaching, I thought I’d compile a list of useful aquatic environments videos and share those here. Many thanks to Dr. Andrea Kirkwood who passed along great links!

The videos must illustrate an important scientific concept related to aquatic environments, and be useful for undergraduate and graduate classes. Beautiful photography and compelling storytelling also helps!

I’ve added another important criteria which is overlooked too often. The videos must be accessible through the use of subtitles and captions, published scripts or other visual cues within the video itself. This symbol (cc) indicates high quality captioning / subtitling already included in the video.

The list is far from complete. If you see missing videos or gaps below, please do let me know in the comments or send me a message via Twitter / email. I will continue updating this list. [New links will have a date next to them.]

Now, the videos and animated GIFs, loosely organized by category:

Water Science (physics, chemistry)

The Water Cycle


Limnology & oceanography (science & conservation)

Lakes & other aquatic habitats of the world

Plankton & microscopic organisms

Macroalgae (seaweed)


Macrophytes (aquatic plants)







How humans use & impact upon aquatic resources

Fisheries & overfishing:


Ecosystem impacts & manipulation

Series & Collections

Do you know of any other aquatic environment videos and animated GIFs which should be included in this list?


Great Lakes, Great Stakes! Part 2. Tilting at wind turbines.

11 05 2011

Lake Ontario is a beleaguered Great Lake. Millions of Americans and Canadians live around the lake and countless others depend on the Lake Ontario watershed for water, fish, transport and shipping. It is inevitable that harmful impacts will arise from all those people relying on the lake’s resources.  But, is it also possible to generate postive impacts?

TransAlta claims so.  They have built one of the largest wind farms in Ontario and are leading the forefront of the so-called, “green energy” industrial development in North America.  The wind farm is on the truly buccolic Wolfe Island, just a short ferry ride from the City of Kingston.

Wolfe Island wind turbines from air

Wolfe Island wind turbines from air

The area around Kingston is one of the windiest in Canada, making it a freshwater sailing mecca, and the host of many sailing  regattas and championships. As students at Queen’s University know, wind and kite surfers are a common sight along the shoreline. To take advantage of this energy bounty, TransAlta’s wind turbines, 86 of them, covers the entire island from head to foot, the description locals fondly use for the western and eastern tips. Every turbine, standing a gargantuan 80 meters tall (24 stories), is located on private land with TransAlta paying a generous fee to the land owner. Many farmers have found the turbines to be a significant boost, allowing them to expand their businesses and produce for local markets. However, many residents find the turbines to be ugly, noisy and harmful to the peace of their cherished island.

The IJNR fellows had happened to arrive on Wolfe Island on an important day.  Wednesday May 5 marked the beginning of  a tax-assessment hearing on the impact of wind turbines on property values.  As the Kingston Whig-Standard reported, Wolfe islanders were arguing that the wind turbines had lowered property values on the island.  Other opponents of wind farm developments elsewhere on Lake Ontario had come specifically to sit in the hearing.  As a result, the IJNR had to tread carefully and sensitively to avoid the impression of bias towards any group on the island.

An IJNR fellow photographing a wind turbine tower

An IJNR fellow photographing a wind turbine tower

We toured the island to see the wind turbines up close. They truly tower over the entire island which otherwise consists of farms and 2-story houses. The structures are so prominent in the landscape that local touring companies now have their boats go by the island specifically to view the turbines. Our lunch stop was  a church, which had been carefully selected because it represented neutral ground for all factions on the Island.  Farmers, TransAlta representatives and anti-wind community members then discussed issues with the journalists.  As a Queen’s professor and an observer, I did  not directly participate in those sessions but used this as an opportunity to listen and learn about the issues.

Green energy initiatives are simply not as clean-cut as one would like, or the press would have us believe. Wind power does produce minimal pollution when generating energy, a big advantage in a province that relies on dirty coal-powered generating plants and controversial nuclear plants.  However, having such dominant structures planted throughout one’s community really changes one’s relationship to the land and landscape.  Wolfe Island is now an important case study for all communities and corporations considering wind power developments.

After Wolfe Island, we travelled to Picton where we had a lovely evening meal at one of the local restaurants. Frank Allen spoke in detail and gave some intriguing perspectives on environmental reporting and communicating complex ideas to the public.

Frank speaking on environmental journalism at IJNR dinner in Picton

Frank speaking on environmental journalism at IJNR dinner in Picton

The next day, they joined a fishing trip led by my colleague Tim Johnson, a scientist with the Ontario Ministry of Natural Resources fisheries research station in Glenora. I said my good byes that evening, but I’ll definitely be following the work of all the journalists I met during this trip.  It was a wonderful opportunity, not only for the journalists, but also for this scientist, to discuss Lake Ontario environmental issues.

My thanks go to the Institute of Journalism and Natural Resources for their invitation and hosting.

[Part 1 of this two-part post on the rising & declining fish populations in Lake Ontario is linked here.]

Great Lakes, Great Stakes! Part 1. The rise and fall of fish species.

10 05 2011

Are the Great Lakes important? Should people outside of the region care about our Great Lakes?  The Institutes for Journalism and Natural Resources (IJNR) think so.

Last week, a group of American and Canadian journalists travelled around Lake Ontario on an IJNR fellowship.  Travelling on a bus rented from a Montreal hockey team, they started their journey canoeing down the Don River in Toronto. After the canoe trip, they continued along their route, stopping at various sites to meet experts and learn about environmental issues affecting Lake Ontario.

Frank Allen of IJNR invited me to join them halfway through their trip.  I met the journalists in Sackets Harbor in New York and spent a lovely evening talking about science communication and the journalist perspective.  The next day, inspired and energized by the discussions from the night before, I joined several journalists on a charter fishing boat captained by “Megabite”.  The goal for the day was to land some trout, but the heavens opened early.

IJNR Fellows fishing in the rain

IJNR Fellows fishing in the rain

Despite the downpour, it was a good trip. We went to a deep trench in Lake Ontario by an island where trout and salmon congregate at their preferred cold temperatures and caught many fish.  And throughout the day we talked extensively about the science and economics of the introduced fish.

IJNR fellows interviewing Captain "Megabite"

IJNR fellows interviewing Captain "Megabite"

Most trout and all salmon in Lake Ontario are not native. They have been stocked by state and provincial governments for several decades.  They are the cornerstone of a thriving multi-million dollar sportfish and recreational fishing industry around the lake.

Just as I wrote about Lake Erie, Lake Ontario is not the same lake it was 50 years ago.  Invasive species, especially round goby, now make up a high proportion of the trout and salmon diets. After meeting with the charter boat captains and New York biologists we discussed native, introduced and invasive species. The Sackets Harbor captains mentioned that the round goby had very probably revived their fishing businesses in a big way!

Trout caught by IJNR fellows for lunch!

We then drove over the Canadian border to meet with a group of people working on the endangered American eel.  The rain simply would not abate, and we had to huddle under a bridge by small river for shelter. This particular river is an important site for young eels and we were to see a demonstration of electro-fishing. My colleague, John Casselman and his graduate students spoke about their work with American eel, which has an amazingly intricate marine-freshwater lifecycle that is threatened by dams along the St. Lawrence Seaway.

In addition, John Rorabeck, an expert commercial fisherman, spoke about the historical importance of American eel to fishing industries. Unfortunately the boat was not working so we could not collect American eel, but the journalists got to listen to top-notch stories by two leading experts.  It was wonderful to listen to John R, especially as he truly has close ties to Lake Ontario and he had worked with one of my graduate students on the Rideau Lakes catching fish for our food web analyses.

Commercial fisherman John R speaking about American eel

Commercial fisherman John R speaking about American eel

By the end of the day the complexity of the lake was becoming very apparent. We had considered introduced fish species which were benefiting from an invasive fish species, the trout and the round goby. We also discussed a native species fast declining in the Great Lakes.  Lake Ontario is changing very rapidly… what will it be like in the future? Even the most knowledgeable scientists and fishermen are not sure.

Tomorrow:  Tilting at wind turbines.

Agent Orange and the challenge of assessing toxicity – Part 3

17 03 2011

This is the third part of the Agent Orange series.  Part 1 discussed the make-up of the two herbicides that go into Agent Orange, and Part 2 covered the  chemistry that led the formation of toxic dioxins in Agent Orange during manufacture.  This part will cover the toxicity of the 2,3,7,8-TCDD in Agent Orange and why it is still of concern.

Before we get into the toxicity of 2,3,7,8-TCDD and Agent Orange, let’s go into the basics of risk assessment. Just because something is known to be toxic does not mean we need to worry.  Assessing the risk means we need to assess several key factors first.

For example,  as we all know, we depend on water for our health and functioning such that we cannot survive for long without water.  However, if drunk in sufficiently large amounts, water can be toxic because sodium in your body becomes diluted to the point where you cannot function.  Obviously, drinking such large quantities of water is not a concern for most of us, so we know that drinking water has low risk most of time, and is in fact highly recommended.

So when assessing risk of potentially toxic substances, scientists and medical workers tend to take into account three important and connected concepts:

  • Hazard – what are the hazards of this substance? For example, would it result in allergic reactions, illness or burns on exposure?
  • Exposure – What are the routes of exposure? Would it be inhaled, eaten, or absorbed through the skin? How much of this substance is being would be transferred through exposure?
  • Toxicity – what is the mechanism of toxicity after exposure?  How does the toxicity response show up?

So drinking freshwater water has low risk, due to its low hazard and toxicity only incurred to very high exposure through drinking.  Of course, water can be very risky in other settings, such as slipping on a puddle on a marble floor and breaking your hip, or drowning in the bathtub.

In terms of toxicity, 2,3,7,8-TCDD is quite the opposite of drinking water, and avoidance of this substance is highly recommended by all experts.  So how is it so toxic?

We’ll be delving into biochemistry in this posting this time! In brief, the toxicity of 2,3,7,8-TCDD is due to its ability to bind with a key receptor in our cells, which leads to a cascade of effects. As a part of our healthy cell functioning, there are thousands of receptors in our cells throughout our bodies which act as our messenger system.

The receptors bind to key chemical molecules. Usually, they are made of proteins with certain structures that enable chemical bonding on its surfaces in a manner often described as “a lock and a key”. Once a receptor is paired with its “chemical key”, it then can influence the DNA expression within a cell.  This helps to organize useful chemicals to enable healthy cell functioning.

In the case of 2,3,7,8-TCDD, scientists are the most concerned with Ahr, or the Aryl hydrocarbon receptor. It has been speculated that the Ah receptor may be a relic of from our long-past evolutionary history, with its “key” being a growth-regulating hormone which we no longer use. The Ah receptor is not only found in humans but also in numerous animal species. The Ah receptor in modern organisms now binds naturally occurring organic contaminants such as those produced by combustion of wood. In fact, dioxins are only toxic when the Ah receptor is involved!

The Ah receptor will bind with organic contaminants containing a 6-carbon hexagon ring. Once the Ah receptor binds with an organic contaminant, the Ahr-contaminant complex moves to the cell nucleus where DNA genes are activated. Enzymes are produced to break down the unwanted contaminant and remove it from the cell.   In this case, this involves a group of enzymes called the cytochrome P-450. If all goes well, those enzymes activate a reaction to break down the contaminant in the cell, and therefore helping to remove the toxic substances from the cell and the body.

In this case, 2,3,7,8-TCDD has been found to bind with the Ah receptor extremely well. In fact, 2,3,7,8-TCDD has the best binding constant with the Ah receptor among the various organic contaminants, explaining its extreme toxicity.  It has been hypothesized that the 2,3,7,8-TCDD may be very similar in structure to the original hormone partner of the Ah receptor before we lost this hormone a long time ago in our evolutionary history.

After exposure and uptake, the 2,3,7,8-TCDD-Ahr complex will then proceed to the DNA in the cell nucleus, where activated genes will result in (1) production of the P450 enzymes; and (2) regulatory chemicals important for growth and division of cells.  In some ways, the dioxin mimics the behaviour of hormones regulating important cell functions. Also , it is thought that by binding with the Ah receptor for too long, it could result in the wrong signals being sent out during development, resulting in birth defects and developmental delays after birth.

Those two actions will lead to a cascade of effects throughout the cell and the affected organ.  First, due to the high affinity of 2,3,7,8-TCDD for the Ah receptor, sometimes the dioxin is not broken down. Therefore, P-450 enzymes are produced in the cell for an extra long time.   All those extra enzymes does not break down the dioxin immediately, but it can lead to the breakdown of other hormones.   The breakdown of regulatory hormones can lead to dysfunctional cells and promote cancer.  Down below is a figure that illustrates the pathways within a cell:


Dioxin and Ah receptor cascade in cell

Dioxin and Ah receptor cascade from Mandal (2005)

Second, the Ah receptor has other functions beyond enzyme induction. It can control certain genes and cell functions particularly those governing rowth and differentation. As an example, 2,3,7,8-TCDD is somewhat similar to an important thryoid hormone, the thryoxine, as shown below:

2,3,7,8-TCDD and Throxine

As a result, 2,3,7,8-TCDD may mimic certain hormones after binding with the Ah receptor.  Since hormones to not act alone, this interaction of dioxin hormone mimics with hormones can result in a cascade of effects throughout the body.

There has been many studies showing that certain cancers and diseases respond with increasing exposure to dioxins. But it has been difficult to precisely pin down the association due to the complex biochemistry and the cascading domino effect whenever hormonal systems in cells are affected.

So what?  The discovery of dioxins in Agent Orange and the subsequent explosion of biochemical and environmental research into dioxins world-wide has led to our much improved understanding of organic contaminants, their toxicity and the need to better regulate and monitor those contaminants.

Should we be worried?  Yes.  2,3,7,8-TCDD is one of the most toxic compounds people have ever produced due to its ability to bind so strongly to the Ar receptor found in numerous organisms.  But there are good news.

Over past 50 years, as our awareness of environmental contaminants and management of sources improved, the release of dioxins to the environment and the accumulation of dioxins in wildlife has been steadily decreasing.  As a population, our overall environmental exposure is decreasing on average.

However, dioxins are persistent in the environment, often present for decades. Scientists can still measure dioxins in lake sediments from the 1950’s!  Dioxins also can accumulate in fatty tissues and in soil, where they can be transferred up the food chain.  As a result, exposure to dioxins can include both immediate exposure to the chemicals such as Agent Orange, and long-term exposure through food and skin contact from accumulated dioxins in the environment.  This further adds to the complexity of understanding dioxin toxicity and relating heath concerns with environmental exposure over a long period.

However, remember that risk assessment of a chemical depends on three things, hazard, toxicity and exposure. The extent of toxicity and health impacts depends on the length of exposure and how people were exposed. As a result, the occasional driver who drove by Ontario’s highways during spraying have far less to worry about compared to the highway workers who sprayed Agent Orange on unwanted foliage.  However, showing causation and relationship between current heath issues to past dioxin exposure is exceedingly difficult even for exposed workers.  We are exposed to so many organic contaminants which also trigger the Ah receptor cascade, and each of us respond differently depending on our genetic make-up.   Despite over 50 years of research, there is still much that needs to be unravelled.


References & Resources:

Birnbaum (1994). The Mechanism of dioxin toxicity: relationship to risk assessment Environmental Health Perspectives, 102, 157-167 [Subscription required]

Mandal, P. (2005). Dioxin: a review of its environmental effects and its aryl hydrocarbon receptor biology Journal of Comparative Physiology B, 175 (4), 221-230 DOI: 10.1007/s00360-005-0483-3 [Subscription required]

Schecter, A., Birnbaum, L., Ryan, J., & Constable, J. (2006). Dioxins: An overview Environmental Research, 101 (3), 419-428 DOI: 10.1016/j.envres.2005.12.003 [Subscription required; another link to the PDF here.]

Health Canada. 2005. Dioxins and Furans – It’s Your Health. Healthy Living Series. [website] (Last accessed March 14, 2011).  [Free access]

Images of 2,3,7,8-TCDD and thryoxine are from the  Wikipedia Commons image library.

Thank you to Nathan Ackyrod, Rob Thacker and anonymous reviewers for their comments.

ResearchBlogging.orgThis post was chosen as an Editor's Selection for

How Agent Orange became toxic: dioxin formation – Part 2

16 03 2011

Note: This is Part 2 of a 3-part blog posting.  Part 1 discussed the primary components of the Agent Orange herbicide, while here we’ll discuss how even more toxic compounds were formed during the manufacture of Agent Orange.  The third part will cover the toxicity of dioxins to to humans and other organisms.


Dioxins and furans are are persistent contaminants that can remain in the environment for decades. Typically, dioxins and furans are not created for specific purposes, but are accidental byproducts of the combustion of organic materials at high temperatures. No one ever wants the presence of those toxic compounds during manufacture or release to the environment due to their high health and environmental costs. Here we’ll focus on one dioxin that is an highly toxic compound found in certain batches of Agent Orange.

Making chemical compounds is a bit like baking bread.  There are many steps which have to be done in the right order, and the bread has to be allowed to rise and then baked at just the right temperature.  If any of those steps are missed, or if there is a mistake with the recipe, the bread just won’t turn out right.

So let’s look at the recipe for 2,3,5-T, and how a simple mistake in temperatures meant that a very toxic dioxin contaminant was introduced to Agent Orange by accident.

In Part 1, the structure of chlorophenoxyacetic acids formulated for Agent Orange and its ‘rainbow’ herbicide cousins was outlined. Here is the structure for 2,4,5-T, one of the two compounds in Agent Orange:


Chemical structure for 2,4,5-trichlorophenoxyacetic acid


2,4,5-trichlorophenoxyacetic acid

Take a look at the forked acetic acid structure connected to the 6-carbon hexagon ring by an oxygen atom.  This is an important clue in how dioxins had formed in Agent Orange and other rainbow herbicides.

Remember the “O” in the diagram above?  The first step in this recipe is to create this “oxy-” part of the 2,3,5-T.  To do this, two ingredients are needed.  Those are benzene (6-carbon hexagon ring) with four chlorides, and the other is sodium hydroxide (NaOH).  Increasing the temperature and adding NaOH means that an “OH” molecule is included on the benzene ring. The chemical equation looks like this:

2,3,4,5 benzene with NaOH and heat results in 2,3,4 phenol

2,3,4,5 benzene + NaOH + heat results in 2,3,5 chlorophenol (From Hites, 2011)

So, after combining the top two ingredients,  we now have what is called 2,3,5-chlorophenol.

We need to add the acetic acid fork to the structure to make the 2,3,5-T herbicide.  How do we do that?  This second step is done by adding chloro-acetic acid to the mixture, which replaces the “H” on the 2,3,5-chlorophenol like this:

2,3,5-chlorophenol plus acetic acid to form 2,3,5-trichlorooxyacetic acid

2,3,5-chlorophenol plus acetic acid to form 2,3,5-trichlorooxyacetic acid

The procedure is actually fairly easy. However, maintaining the correct temperature is absolutely vital.  Somewhat like  baking bread, which has to be done exactly at the right temperature if you don’t want to end up with burnt hard pastry or a soggy mess, monitoring the temperature during the first and second steps of making 2,4,5-T is necessary to making sure the reaction happens at the right speed.

The ideal temperature for this reaction is at 180 ºC (356 ºF) and best industrial practices ensure that this temperature is maintained. Unfortunately, if not monitored and adjusted properly, the excess heat from the chemical reactions and other sources  will mean that the solution goes above this temperature.

If the temperatures are not monitored and adjusted correctly and exceed 180 ºC, then what happens is that the 2,3,5 chlorophenol molecules become very reactive and start reacting with each other.  This creates the toxic compound, “2,3,7,8-tetrachorodibenzo-p-dioxin” like this:

two 2,3,5 chlorophenols reacting to form 2,3,7,8-TCDD

2,3,5 chlorophenols reacting together to form 2,3,7,8-TCDD + hydrochloride (From Hites, 2011)

Saying “2,3,7,8-tetrachorodibenzo-p-dioxin” is not easy! It also takes too long to pronounce, so many scientists will just say “dioxins” or to be more specific, “2,3,7,8-TCDD”.  Like 2,4,5-T, this long chemical name can be broken down to little units, although it takes some effort:

  • 2.3.7,8-tetrachloro = this chemical has 4 chloride molecules attached at specific locations on each of the hexagon rings.
  • dibenzo = two benzene (hexagon) rings with three double bonds between carbon atoms, with an oxygen molecule attached
  • p- = the type of bond between the benzene rings. It means that there is one oxygen molecule on the opposite side, and the oxygen molecules are not bound to each other.
  • dioxin = the name of this chemical class.

By a very unfortunate coincidence, 2,3,7,8-TCDD is also one of the most toxic human-made substances ever made! Laboratory tests revealed that  extremely small amounts would kill mammals.

It is not known how much 2,3,7,8-TCDD was in each batch of Agent Orange produced because at that time, people were only starting to realize the issues.   After measuring concentrations in the environment in Vietnam and other places in North America it  is now estimated that approximately 3 parts per million of Agent Orange consisted of this toxic contaminant, which is a very small amount.  This is about one drop of water in a bathtub!

So the creation of this dangerous chemical all came down to incorrect temperatures. Yet how can such a small amount of contaminant in a herbicide designed to break down quickly still be considered a serious health risk?

Tomorrow: Toxicity and risk of 2,3,7,8-TCDD in Agent Orange.


References & Resources:

Hites, R. (2011). Dioxins: An Overview and History. Environmental Science & Technology, 45 (1), 16-20 DOI: 10.1021/es1013664 [Subscription required]

Alvin Young. 2009. Agent Orange and Dioxin Contamination. Chapter 5. in The History, Use, Disposition and Environmental Fate of Agent Orange. pages 1-30. [book] DOI: 10.1007/978-0-387-87486-9_5 [Subscription required]

Arseen Seys. Chapter 9. Dioxins and Furans in the Chemical Industry. United Nations Environmental Programme Chemicals: Persistent Organic Pollutants. [website] (UNEP POP home page: (Accessed March 14, 2011) [Free access]

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The re-emergence of Agent Orange: why are we still so worried? Part 1.

14 03 2011

“Agent Orange”, “Agent White” and “Agent Purple”.  They may sound like characters from Quentin Tarantino’s film, ‘Reservoir Dogs’,  but they’re actually chemical herbicides used to remove tree leaves and plants on a massive scale.

Agent Orange recently reemerged in the Canadian news when it was revealed that the Ontario government had permitted the use of this defoliant in northern forests, along the highway system and the power line corridors throughout the province until 1981.

But just what is Agent Orange, and why are people so worried about it?

NOTE: This posting will come in three parts.

  • The first part: The basic chemical structure of two herbicides in Agent Orange.
  • The second part: How did Agent Orange get contaminated with dioxins?
  • The third part: Why dioxins are so toxic?

(Cosmoboy says that the first post was a bit difficult to read, but it provided the necessary background.  He found the second post much easier!)

Agent Orange belongs to a family of so-called “rainbow herbicides”, designated by a colour-coded stripe on barrels containing each chemical. The herbicides were formulated by Monsanto, Dow and other international multinational chemical manufacturers.

Use of Agent Orange peaked during the Vietnam War. US forces in jungle regions were constantly under fire from well-camoflaged guerilla fighters. To reduce this threat, the US military requested herbicides, in particular Agent Orange, be used to help their soldiers better see the guerillas.  Furthermore, the Canadian government collaborated with the US military to test the effectiveness of those herbicides at the Gagetown Canadian Forces Base in New Brunswick. After the Vietnam,  Agent Orange and its chemical cousins also were used to keep many North American highways free of plant growth to improve visibility and safety.

The effectiveness of Agent Orange led to  many,  many people around the world being exposed to this herbicide. Its toxicity, and that of the other rainbow herbicides, became better understood when exposed people showed obvious and serious health impacts during the 1960’s.  All of this has inevitably led to years of controversy and public debate that still rages over half a century later.

Much of the public information available relates to the use of Agent Orange and its herbicide cousins in Vietnam War, Gagetown, New Brunswick and elsewhere. Articles tend to focus on the association of Agent Orange with recorded birth defects, certain types of cancers and other diseases.  For example, Wikipedia has several entries which list a reasonably accurate history and also issues associated with Agent Orange in the Vietnam War.

Usually, substances in the herbicide such as “2,4,5-T” and “2,4-D” are mentioned in those discussions.   But what exactly is “2,4,5-T” and “2,4-D”?  What are dioxins? This type of information can be difficult to find.

Apart from the highly-technical peer-review scientific literature, there seems to be very little easy access information about the actual substances in Agent Orange,  why it is so toxic, and also how it is toxic.

This is probably because detailed chemistry is involved, and is often presented in an inaccessible way.  However, understanding the conceptual basics behind the toxicity of Agent Orange is essential for public decision-making and public understanding, so here, I’ll try to tackle some key aspects of those chemical concepts.  Wish me luck!

The primary active constituents of Agent Orange are made of two types of “chlorophenoxyacetic acids” . That long scientific name is a way to summarize the basic chemical structure. If you break down this long word into its 4 parts: chloro, phen, oxy, and acetic-acid, this name actually tells you what the chemical look like.  For example:

  • Chloro-” tells us that it has chlorine, which is written like this : Cl.
  • Phen-” tells us that it has a a ring of 6 carbons (C) linked together, which is a extremely stable chemical structure. It is often drawn as a hexagon, with each joint representing a carbon atom.  This is the backbone for the entire chemical.
  • Oxy-” tells us that it has one or more oxygen (O) in the molecule.
  • Acetic acid” is the same as as vinegar.  It has one carbon linked to a hydrogen (H) and an oxygen-hydrogen (O-H) molecule. Drawn on paper, it looks like a forked tail.

Ok, if we string those components together, we get this chemical structure:

2-chlorophenoxyacetic acid

2-chlorophenoxyacetic acid

Do bear with me… all will become clear!

In the diagram above, you can see the 6-carbon hexagon ring.  The acetic acid’s “forked tail” is linked to the oxygen which is then attached to one of the carbons in the hexagon ring. The chlorine is attached to the second carbon link.

Why is understanding the chemical structure so important? Because the hexagon ring and its attachments holds the clue to the toxicity of many pesticides and herbicides.

The hexagon ring is the basis of many organic compounds. It is stable and does not break apart easily. This is one of the key carbon “backbones” important to all life. Our own biology and the biology of every living creature on the planet uses compounds based on the hexagon ring. In fact, many of our hormones and hormone receptors are actually based on the hexagon ring structure!  I will discuss this in the third part oft the blog.

Now, do you see the single “Cl” on the hexagon ring?  Precisely how it is attached to the hexagon ring will give the substance its chemical name.  What you see above is called “2-chlorophenoxyacetic acid”.  If you number the carbons in the hexagon ring, starting with the oxy-acetic acid attachment, the chlorine  atom is on the second site.

The hexagon ring can hold many chlorine atoms. In fact, all five remaining sites on the hexagon ring can have chlorine atoms.

So, when chemists originally formulated Agent Orange, they were looking for certain properties associated with number and location of chlorines.  They decided on 2,4,5-trichlorophenoxyacetic acid and 2,4-dichlorophenoxyacetic acid.

Even chemists don’t have time to pronounce long chemical names every day, so those two chemical compounds are shortened to “2,4,5-T” and “2,4-D“.  Those names tell you that the first molecule has three chlorine atoms on the hexagon ring, while the second molecule only has two. This is what their chemical structures look like:

Chemical structure for 2,4-dichlorophenoxyacetic acid
Chemical structure for 2,4,5-trichlorophenoxyacetic acid

Take a look at the “Cl” symbols and count their locations around their hexagon ring. You can see how the number of Cl and their location corresponds with the name for each molecule.

This actually affects the chemistry of each molecule so the properties of 2,4-D and 2,4,5-T are slightly different.  In combination, they make an effective defoliant because the molecules directly act upon plants as growth inhibitors and cause them to lose their leaves.

Both 2,4-D and 2,4,5-T are also known to be toxic to humans and wildlife, but have short half-life in the environment; i.e., the compounds rapidly break down in the environment to non-detectable concentrations.  Long-term toxicity and associated issues are usually not a concern if exposure to those compounds are minimized.

In fact, 2,4-D is still used in some parts of North America as a a broad-leaf weedkiller used for household gardens, agriculture and landscaping. Even so, many regions and municipalities have recently banned this substance.

So why is understanding the chemical structures of chlorophenols in Agent Orange important?  I will discuss this in my next post on the formation of dioxin contaminants in Agent Orange tomorrow.  For now, take a careful look at the oxygen holding together the acetic acid “forked tail” and the hexagon ring…. this is an important clue in how Agent Orange became even more toxic.

Tomorrow- Part 2: formation of dioxin contaminants in Agent Orange.


References & Resources:

Alvin Young. 2009. The History, Use, Disposition and Environmental Fate of Agent Orange. [book] DOI: [Subscription required]

Roland Weber, Mats Tysklind and Caroline Gaus.  2008. Dioxin – Contemporary and Future Challenges of Historical Legacies. Environmental  Science Pollution Research. 15(2):96-100. [article] DOI: [Subscription required]

Anonymous. Agent Orange.  Wikipedia entry. (accessed March 14, 2011). [Free access]

Note: Chemical structure images from Wikipedia Creative Commons image collection.

This post was chosen as an Editor's Selection for

Project 52 No 18. Fishing for fun? Then take care of the fish!

15 02 2011

¡Hola de Bariloche! While I doubt very much we’d get the opportunity to sample Nahuelito, the local monster, we did get a pretty good representation of key species from the entire food web in each of the 3 sites in Lake Nahuel Huapi over the past two weeks. Last Thursday and Friday, we sampled the third and final site, the southernmost bay near Dina Huapi and the Rio Limay, a famous trout river.   Nahuel Huapi National Park is renowned internationally for its trout fishing, with all of its trout species introduced since early 1900’s until about 1950-60’s.  Now, all trout species are self-sustaining and provide very important economic revenue for the region.

While we were searching for a place on the Dina Huapi beach to put the boat in, I came across this dead trout, likely a rainbow trout (Oncorhynchus mykiss), although I couldn’t confirm the identification.  Within the Park boundaries, anglers are not permitted to keep the fish they catch, but must release all fish.  The cause of death for this trout is likely exhaustion and poor handling after capture.

This image reveals the other side of trophy and sport fishing – fish do suffer and do not always recover rapidly from being caught especially if there is a long fight on the line and a tricky hook to take out.   I liked this image as it contrasted textures and colours of the pale decaying trout against the beautiful  cobblestones under the water in the very harsh morning light.  As such, the presence of death  in such hard surroundings sends a powerful message. 

Exhausted trout near Limay River

I am not against recreational fishing.  However, it is good to be reminded that all actions we undertake will have consequences, and it is always wise to minimize the negative impacts of those acts when we can.

Here is a shot of the nearby river and the Park signage:

Fly fishing in Nahual Huapi