ToxSquad Outreach Blog
Issues in Environmental Health, Current events, and cutting edge research
Issues in Environmental Health, Current events, and cutting edge research
J Cucchiara and Dani Cucchiara
If the title grabbed your attention, you've most likely seen Game of Thrones. In season 6, episode 2 of Game of Thrones, we hear the character Tyrion Lannister (Peter Dinklage) state, “That’s what I do: I drink and I know things.” This is obviously not the character Jon Snow (Kit Harington) from the show, but there IS a real-life John Snow who deserves that kind of accolade.
In another time and place lived a hero named John Snow. This may sound like an introduction to a Game of Thrones, but it’s actually a chapter taken from our own past – in this case, London, England circa 1854. The story has been told numerous times by women and men of science and medicine.
A series of cholera outbreaks in 1832 and 1849 killed 14,137 people in London. In 1854, the third outbreak, part of a global pandemic reached the Soho district of the city of Westminster in London. This outbreak was responsible for the deaths of 616 people. As a local physician, Snow was concerned that his patients were dying and the ones who weren’t were fleeing the city.
At the time, germ theory, the idea that disease was caused by pathogenic microorganisms, didn’t exist. The best explanation for how people were getting this disease was “bad air,” or the established medical term “miasma.” The only way to change the air was to change where you lived, so people were trying to outrun the disease by moving somewhere else.
Snow didn’t subscribe to the miasma theory. Instead, he thought that cholera was being transmitted via water, but he couldn’t prove it, and the solution needed to be based in fact. Snow knew that he needed numbers, so he drew a map and began to collect data by going door-to-door. Snow interviewed people at each business and residence about those who had contracted and died from cholera.
The darkened lines on the map show the number of people who died at each location. Using this data, Snow was able to show how the number of people dying were distributed throughout Soho. In addition to this information, Snow also plotted the locations of water pumps located throughout the neighborhood. Careful examination of this map shows the Broad Street pump at nearly the exact center of the cholera outbreak. The further away from the pump, the less people dead from cholera.
Despite his diligence, Snow still needed more proof cholera was being spread from the Broad Street water pump. According to the working theory of miasma, bad air may have been centered around that area due to the deaths or the amount of open sewage. The proof Snow needed was also on the same map. Two locations within the Soho neighborhood, a workhouse and brewery, were close to the broad street pump but had significantly lower deaths than the surrounding homes and businesses. Both of these locations had their own water supply. It was enough proof for Snow to convince the local authorities to remove the pump handle from the Broad Street pump. This led to a significant reduction in people dying of cholera.
Later on, Snow found that infected body fluids were being dumped into cesspool located near the well and water pump. The pathogen that causes cholera, Vibrio cholerae, was able to gain access to the well water, infecting people who drank from the water pump. The disease had mostly run its course by the time they removed the pump handle, but what Snow accomplished was the prevention of subsequent outbreaks. By performing a simple statistical analysis of his cholera maps, he became the founding father of epidemiology.
It may be the story that makes John Snow famous today, but the Soho cholera mystery is not the only contribution he made to modern medicine. In fact, John Snow also pioneered the use of ether as an anesthetic. Prior to this there was no reliable anesthetic for people undergoing difficult procedures or surgery. He was able to calculate safe dosages and develop procedures for administering ether in a safe way. Ether allowed physicians to operate on people in an unconscious state so they would remain still and experience no pain until after the procedure was over.
Unlike his Westerosi counterpart, John Snow was a teetotaler. In one address given before he became an MD, he warned people of the evils of alcohol, saying, “I feel it my duty to endeavour to convince you of the physical evils sustained to your health by using intoxicating liquors even in the greatest moderation; and I leave to my colleagues the task of painting drunkenness in all its hideousness, of describing the manifold miseries and crimes it produces, and of proving to you that total abstinence is the only remedy for those evils.”
Apparently, he DIDN’T drink after all. He just knew things. Ironic that a brewery played a part in the events that put him in the history books. Ironic also that in Soho today there is a pub named after him. I wonder how he would have felt about that.
With the recent outbreaks of measles across the United States and an outbreak of mumps right here at the University of Florida back in May, it’s time we share a post on vaccines and how and why they work. Before you close this post and decide you aren’t interested in what can be a very controversial topic, let me make a disclaimer: this post will be based solely on the science of how vaccines work – we’ll be focusing exclusively on what happens in your body after receiving a vaccine, specifically what your immune system does in response to the vaccine and then future encounters with that pathogen. Though there is plenty of science to back up concepts like herd immunity and vaccine schedules, we will not address that here. Let’s get started!
The best way to understand the human immune system is to imagine that your body is a country and your immune system is your army. This immune system army can be broken down into two divisions – innate immunity and adaptive immunity. Your innate immunity is always ready to fight anything foreign that enters your body. It isn’t specific – it can fight anything and everything, and it acts fast – within just a few hours or days. Your adaptive immunity, on the other hand, takes some time to mobilize. It waits for the message that something foreign has entered your body before it organizes and rises to fight, but once it starts fighting, it uses very specific tactics for each enemy (pathogen) that it faces, and this targeted approach makes it more effective against that pathogen. The adaptive immunity division can be further divided into humoral immunity and cell-mediated immunity. The main soldiers of cell-mediated immunity are T cells, while humoral immunity utilizes B cells and their weapons, antibodies. The coolest thing about the immune system is that all these different divisions and groups communicate and work together to protect you. Neither one works in isolation; in fact, their success is dependent on their ability to cooperate with one another.
When something foreign enters your body like the bacteria that causes strep throat or the influenza (flu) virus, the innate immune system recognizes the foreign invasion. Generally speaking, the part it recognizes is called an antigen, and this is the signal that tells your immune system army to fight and protect you. Antigens are specific to each pathogen; for example, the measles-causing rubeola virus has different antigens than flu viruses. After recognizing an invader, the innate immune system quickly organizes and begins the fight to keep the pathogen from spreading throughout your body and making you sick. Sometimes, it can do this all on its own, but other times it needs back up from the adaptive immune system. Therefore, it will carry the antigen to where your adaptive immune system lives (usually in your lymph nodes) and present it to the cell soldiers, encouraging them to rise up and fight too. It takes your adaptive immune system a few days to get organized, but once it does, it chooses a strategy based on the information learned from the antigen. If the foreign invader can get inside your host cells, like a virus, cancer, or some bacteria, your T cells will rise up to lead the fight. T cells fight infection by directly killing infected cells and releasing cytokines (chemicals that signal to other cells), which tell other cells to kill the infected ones. If the foreign invader does not need to enter your cells to cause infection, like some other bacteria, then your B cells and antibodies will lead the way. B cells fight by releasing antibodies, which block the ability of a pathogen to infect host cells, attach to pathogens as a way to tell other immune cells to destroy it, and communicate with and recruit other immune cells to help fight. All of this is really hard work for your body, which is why even when your immune system is doing a good job, you might still feel sick or run a fever. It’s because your immune system is fighting a hard, microscopic battle!
So why do we use vaccines? Wouldn’t exposing your body to something foreign start an unnecessary battle for your immune system? Well, kind of! But the vaccine battle is much easier for your immune system army, and the results will protect you for a long time. The battle is easier because vaccines do not contain the same pathogen that you would be exposed to normally – for example, after coming into contact with a sick person. The pathogen inside a vaccine is either dead or attenuated (meaning that it’s missing some pieces, so it won’t work the same way and wage the same big battle as its unattenuated counterpart). A vaccine pathogen still shows your immune system its antigen, encouraging your immune armies to rally, but the pathogen from the vaccine cannot actually wage a real battle against the immune system. It would be like if one country invaded another and only sent one or two weak and harmless soldiers to fight against a country with a full, well-equipped army. It’s pretty obvious who would win that battle, right? In the case of vaccines, it’s not just about winning but training the body for any future fights against a specific invader’s entire, fully-equipped army. The immune system learns from its easy little battle with the vaccine, and now knows which tricks will work best if an entire pathogen army ever showed up at the border. This is called immunologic memory, or the ability of the immune system to respond much more swiftly and with greater efficiency during a second, or later exposure to the same pathogen.
So, this is why vaccination works! Exposing someone to a tiny bit of weakened pathogen, that is unable to cause illness, trains the immune system army against that pathogen, so if/when they are re-exposed to the real thing in full force, their immune system can swiftly organize and attack the invader, preventing serious illness.
Reference: Owen, J. A., Punt, J., Stranford, S. A., Jones, P. P., & Kuby, J. (2013). Kuby immunology. New York: W.H. Freeman.
When in South Africa, do a wine tour!
That’s what I thought, anyway. This month, I was lucky enough to attend the Society of Environmental Toxicology and Chemistry Africa joint meeting with the Society for Risk Assessment in Cape Town South Africa. Prior to presenting my research, I took a little day trip to Franshhoek for wine tour, which got me wondering about the chemistry of wine and that infamous “red wine hangover” people talk about. Red wine headaches have been reported for centuries, and a 1988 blinded study found that 9 of 11 patients prone to migraines from red wine had a migraine following exposure, while 0 of 9 had a migraine from vodka (Littlewood et al. 1988).
What is it about wine that leaves some people so hungover? Sulfites? Histamines? Tannins? Let’s take a closer look!
Hangovers (in general)
First, let’s talk about what causes a hangover before moving on to why red wine hangovers are just so bad. Alcohol is readily absorbed into the blood through the gastrointestinal tract, where it travels throughout the body to the main site of metabolism, the liver. In the liver, alcohol dehydrogenases metabolize ethanol (the active component of alcoholic beverages) into acetaldehyde, and then aldehyde dehydrogenases convert acetaldehyde into acetate (Heit et al. 2015). Acetaldehyde is highly toxic and a carcinogen, while aldehyde is relatively harmless and is quickly converted to CO2 and H2O for excretion. Due to the importance of the liver in the metabolism of alcohol, this is why you should never take acetaminophen to cure a hangover, as that drug can cause liver damage when combined with alcohol!
Some alcohol makes it into the brain, where it is metabolized by catalase or cytochrome P450 2E1 (CYP2E1). While alcohol can cause long term effects through its carcinogenic metabolite, the immediate hangover is mainly a result of dehydration. Ethanol decreases your body’s production of antidiuretic hormone (vasopressin), which decreases the kidney’s ability to re-uptake water and can cause you to expel up to 4 times more liquid than you take in (Swift and Davidson 1998). This dehydration and subsequent imbalance in electrolytes is the main reason you feel so bad after a night of heavy drinking.
So, what makes a red wine hangover different?
Red Wine Hangovers
Let’s start with sulfites. Sulfites are used to preserve food products and help prevent wine from becoming vinegar (which happens to wine that’s been open for too long). In the United States, wine can contain up to 350 parts per million (ppm) of sulfites, and any wine containing more than 10 ppm must be appropriately labeled. While most consumers believe that sulfites are the cause of wine headaches, the Federal Drug Administration (FDA) has found that only 1% of the US population is actually “sulfite sensitive” and sulfites are likely not the reason for most red wine hangovers, as many other foods contain levels of sulfites in excess of those in wines. Additionally, red wines actually contain less sulfites than white wines. For more information about public perception of headaches from sulfites and the willingness to pay extra for “sulfite-free” wine, see this article.
Histamines are proteins released by the body during allergic reactions and can lead to adverse effects, such as headaches (Maintz and Novak 2007). Histamines can also be ingested from food products. These histamines are degraded by diamine oxidase (DAO), so if levels of DAO are low or the level of histamines is high, one may experience symptoms of allergic reaction (Maintz and Novak 2007). So, what does this have to do with wine and headaches? Well, red wines have 20 to 200 times more histamines in them than white wine, which suggests that this may be a reason that red wine triggers these hangover headaches, though Krymchantowski and Jevoux (2014) found a lack of literature supporting this mechanism. That being said, for the small percentage who are histamine intolerant (those with no DAO or reduced DAO activity), this is likely to contribute to red wine headaches (Panconesi 2008).
Tannins & Flavonoids
So, sulfites and histamines are likely not the culprits (at least for most people), but what about congeners? Darker colored alcohols have more congeners, or impurities, than lighter colored alcohols. One famous group of congeners is tannins, which are bitter compounds that come from grapes. Red wines generally have a higher tannin content than white wines, as they are in contact with the tannin-containing grape skins for a longer period of time, and this contributes to their unique astringency. While red wines have a higher level of tannins and are associated with migraines, mechanistic evidence for this relationship are lacking and further studies are needed (Krymchantowski and Jevoux 2014).
Tannins themselves belong to a larger class of congeners called flavonoids, which are naturally occurring phenols and polyphenols that can form radicals (compounds containing an unpaired electron that are highly reactive and therefore toxic) (Figure 1). Phenols can inhibit phenosulphotransferase (PST) enzymes, leading to the accumulation of free radicals and their subsequent toxicity, which can manifest in headaches. Red wines contain up to 50x more flavonoids than white wines, and it has been shown that even heavily diluted red wine can inhibit PSTs by up to 50%. Around 30% of the flavonoids in red white are thought to contribute to its color, which is why they are in lower levels in white wines (Krymchantowski and Jevoux 2014; Panconesi 2008).
Furthermore, certain flavonoids found in red wines can cause platelets to release 5-hydroxytryptamine (serotonin), and this release is unique to red wine compare to white wine and beer. Once released following red wine consumption, reuptake and binding of serotonin is inhibited. Though the inhibition of serotonin binding to its receptors is unclear, this may be the cause of red wine headaches (Krymchantowski and Jevoux 2014; Panconesi 2008).
Lastly, methanol is a common congener that occurs in red wines more often than white wines (Swift and Davidson 1998). Methanol is a type of alcohol with one fewer carbon and two fewer hydrogens than ethanol. Though methanol is metabolized by the same enzymes as ethanol, its metabolites, formaldehyde and formic acid, are more toxic. Interestingly, ethanol is metabolized faster than methanol, which may be why hangover symptoms take so long to kick in.
In the end, what’s causing your red wine headaches? Probably a combination of things. But congeners such as flavonoids and methanol seem the most likely culprits for most people. I think I’ll stick to my white wine, thank you very much.
Devrah Arndt, PhD
I have only lived in Florida for three years, but I have had the privilege of witnessing the landfall of four major hurricanes since living here. Hurricane Matthew formed on October 1st, 2016 and skirted the entire east coast of Florida (Fig. 1). Hurricane Irma formed September 5th, 2017 and sent the entire state of Florida into a panic. Irma was HUGE and it wasn’t clear which coastline would be impacted, resulting in the evacuation of more than a third of the state’s population with just two days before landfall. Hurricane Maria formed just weeks later on September 18th, 2017 and tore through regions that were already battered from Hurricane Irma (most notably Puerto Rico). Hurricane Michael formed October 7th, 2018 and made making Category 5 status (157 mph+). Three of these four hurricanes had their names retired by the World Meteorological Organization (Matthew, Irma, and Maria), and Hurricane Michael is also currently being considered for retirement at the time of this writing.
I reside in Gainesville, FL – a city that is a two hour drive from the Atlantic coast and from the Gulf coast. My central location in Florida has buffered me from direct exposure to category 4 and 5 force hurricane winds, but I have experienced the hysteria that goes along with these devastating natural disasters. I have seen grocery stores run out of water and produce. I have sat in line at a gas station to get gas, and I have seen gas stations run out of gas completely (Fig. 2). I have lost power for over 24 hours when it was 100 °F outside. I remember listening to the radio shortly before Irma made landfall and hearing an older woman beg a radio host for help after she was abandoned in an evacuated county. Shortly after Hurricane Michael hit, I drove through the Florida panhandle to get to a volleyball tournament in Destin – the 25 miles where Michael’s eye made landfall looked like a tree lawnmower had come through and leveled all the trees (Fig. 3). After thinking I’d driven through the worst of it, I stopped in Marianna to get McDonalds; however, the restaurant was damaged and the whole city was under a 6 pm curfew. Everyone in the town looked like a zombie…and not superficially, but like real zombies. I didn’t belong there, I was too clean and well-rested. The atmosphere was somber, the sounds and colors were muted – I was a natural disaster tourist and I couldn’t wait to get out of there.
I’m huge fan of Stephen King, and I couldn’t help but feel like I was living in one of his apocalyptic novels when these major hurricanes hit. I am originally from the Midwest – specifically Wisconsin – and I had never experienced anything like this before, let alone multiple times. I have to ask the question if this is normal?
Public documents on Atlantic hurricane history are available from the National Hurricane Center (NHC), the National Weather Service (NWS), and the American Meteorological Society. For the purposes of this blog post, I pulled summarized data from tables in Wikipedia on hurricanes in the Atlantic Basin, but if I was going to publish this data in a peer reviewed journal I would be using the data from official sources.
Reliable tropical cyclone record keeping started in 1851, satellite tracking started in 1962, hurricanes were given names in 1953, and the Saffir-Simpson scale was developed in 1971. A total of 925 hurricanes developed in the Atlantic basin since record keeping began in 1851. When these hurricanes are graphed by decade (Fig. 4a), there are no clear changes in the number of hurricane occurrences over time. Peak decades for the development of hurricanes appear at 50-70 year intervals and include 1880-1889, 1950-1959, and 2000-2009.
Of the 925 hurricanes that have occurred since 1851, 153 of them had wind speeds greater than 130 mph (category 4 and 5 on the Saffir-Simpson scale). When these 153 storms are graphed by decade, there is a clear trend for more strong storms to occur in more recent decades (Fig. 4b), and the first category 5 hurricane (sustained winds of 157+ mph) wasn’t recorded until the 1920’s (Fig. 4c).
The 2019 hurricane season hasn’t happened yet, but if you graph the nine years that have been recorded so far in this decade (Figure 5, uncolored bars), this past decade is going to match or exceed previous decades in the number of hurricane occurrences and the number of strong hurricane occurrences. So to answer my question… Is this normal? If I only consider the last 20 years, then yes I would say that my exposure to strong hurricanes over the last three years in Florida is normal. However, if I compared my hurricane exposure to anyone who lived in the Atlantic basin before 1930, I would say that my exposure to strong hurricanes is abnormal.
I feel lucky that I live in an era with the infrastructure (building codes) and technology (warning systems) that can significantly improve my chances of survival in one of these storms. However, I can also see the irony in the relationship between today’s improved infrastructure and technology with the Industrial Revolution of the 1800’s, and the absence of pre-industrial era strong Atlantic hurricanes coupled with the presence post-industrial era strong Atlantic hurricanes. Between 1800 and 2019 the world’s population grew from 1 billion to 7.7 billion. Industrialization and urbanization in the late 1800’s expanded agricultural markets, and the number of farms in the U. S. quadrupled from 1.4 million in 1850 to 6.4 million in 1910. The world also witnessed the advent of the automotive industry in the 1890’s. It would be irresponsible to not at least mention the correlation (and likely causation) between the events of the industrial revolution (1760-1900) and the onset of strong hurricanes in the Atlantic basin. Though it is outside the scope of this blog post, there is a wealth of data and evidence linking climate change to the onset of stronger and more destructive hurricanes [1-7].
1. Bender, M.A., et al., Modeled impact of anthropogenic warming on the frequency of intense Atlantic hurricanes. Science, 2010. 327: p. 454-458.
2. Elsner, J.B., Evidence in support of the climate change–Atlantic hurricane hypothesis. Geophysical Research Letters, 2006. 33(16).
3. Holland, G. and C.L. Bruyère, Recent intense hurricane response to global climate change. Climate Dynamics, 2013. 42(3-4): p. 617-627.
4. Mousavi, M.E., et al., Global warming and hurricanes: the potential impact of hurricane intensification and sea level rise on coastal flooding. Climatic Change, 2010. 104(3-4): p. 575-597.
5. Murakami, H., et al., Simulation and Prediction of Category 4 and 5 Hurricanes in the High-Resolution GFDL HiFLOR Coupled Climate Model*. Journal of Climate, 2015. 28(23): p. 9058-9079.
6. Trenberth, K.E., et al., Hurricane Harvey Links to Ocean Heat Content and Climate Change Adaptation. Earth's Future, 2018. 6(5): p. 730-744.
7. Wuebbles, D.J., et al., Severe weather in the United States under a changing climate. EOS, 2014. 95(18): p. 149-150.
J. Cucchiara, MA
Saint Patrick's day. It's practically synonymous with Ireland, and in turn with all things green. Green has also been the operative buzz word (color?) for all things environmental. Sure, Saint Patrick is not the patron saint of the environment; however, Ireland and environment health are more closely related than one may immediately imagine.
Allow me to introduce Richard Bruton TD, Irish Minister for Communications, Climate Action and Environment. Since October of 2018, Bruton has applied his extensive political career and current ambitions toward the environment of Ireland. According to Bruton’s website, he has made it his priority to 1) Address climate disruption by implementing rapid and far-reaching changes to decouple progress from carbon and meet commitments, 2) Harness the communications revolution so that every citizen has equal opportunity to enjoy its benefits and is protected from its risks, 3) Use resources with care and responsibility: minimizing the generation of waste; achieving a leadership position in renewable energy and enhancing our environment, 4) Ensure public policy and sectoral regulation is alert and effective, is exercised without fear or favor in the interest of all citizens; and is based on best international practice and research on future needs, and 5) Position Ireland to develop thriving enterprise opportunities in a de-carbonizing world supporting an ambitious transition program.
In short, Richard Bruton is a man in the unique position of attempting to make Ireland more green. What’s more is that he’s not stopping there! This past Wednesday, March 13th, Bruton announced a partnership between Northeastern University, Boston and AMBER, the SFI (Science Foundation Ireland) Research Centre for Advanced Materials and BioEngineering, at Trinity College Dublin. The goal is “to address scientific, societal and clinical challenges in the context of the UN Sustainable Development Goals and to advance resilience in the face of 21st century risks.”
The more I read about Burton, the more impressed I became with the announcements, recognition, and awards he has been a part of in the past week alone. Then, in a moment of clarity it occurred to me that the remarkable thing in all of this was not just one person - in fact, Richard Bruton is only doing his job. The Irish Department of Communications, Climate Action, and Environment is the source of a greener, more science-focused Ireland. They are a bridge between those who live in the environment (i.e. everyone) and those who have power to change the environment (not everyone...hint: it’s politicians and people with money).
My mind works in reverse sometimes, and as a result, I found myself asking a question that I should have had when I started writing this article: What do communications, climate action, and the environment have to do with one another? The latter two are obviously connected. To me, the connection between communications and environmental health seemed as obvious as the connection between nutrition and fast food. It was there, but it was pretty loose... until it wasn’t.
The answer is something that I haven’t seen very much of here in the United States: personal responsibility towards the environment. The reason that communications, climate action, and the environment are all connected is that someone realized that all research is worth something only if it is accessible, so Ireland chooses to educate its people in these matters by explaining the issues, what is being done about these issues, and what everyone needs to do to be more sustainable in the future… If more world leaders followed this example, maybe it would make a difference in the coming decades.
I didn’t start out writing this as a political editorial - I wanted to make a connection between St. Patrick's day and environmental health. I know it can be dangerous to mix religion and science - just like I know that it’s highly improbable for someone to have driven all of the snakes off of an island that never had snakes to begin with. Instead, I like to believe that St. Patrick made people care so much about keeping Ireland green, that they took responsibility upon themselves. If that’s the case, I’ll exchange the former miracle for the latter.
J. Cucchiara received his MA in Cultural Anthropology from the University of Central Florida. He has instructed Anthropology courses at the University of Central Florida and Valencia College. He has traveled to many European countries in search of the perfect pint of beer. His master's thesis is entitled, Pubs, Punters, and Pints: Anthropological Reflections on Pub Life in Ireland.” Yes, really.
With the hazards of plastics as such a hot topic in the news today, more companies are trying different methods to reduce the overall usage of single-use plastics. According to an article from the New York Times, 300 million tons of plastic is produced globally each year with only 10% of the waste recycled. Many groups are working together to cut down the plastic waste – including one mega coffee franchise.
On July 9, 2018, Starbucks debuted their strawless lids in response to the company pledge to remove all straw use by 2020 (That’s right, our pumpkin spice lattes are about to get even cooler). Though a very innovative idea, critics have complained that the lids use more plastic to make than a straw would normally use. And it’s true, the lids are made of plastic, but unlike straws, they are much more easily recycled. Although eliminating plastic straws will not do much address plastic pollution (since plastic straws make up less than 1 percent of the total plastic waste in the world), supporters of this move see it as a small step to gain more momentum in solving the plastic problem.
The debate will continue on whether these lids will be beneficial or not to the waste problem. The strawless lids could be a small step to a better solution, or a quick fix to an eventual bigger problem. No matter the outcome, more solutions should be innovated to tackle the waste dilemma – maybe the biggest impact of these strawless lids will to provide inspiration for tackling the problems of tomorrow.
Plastics have been around since the early 20th century, but only recently has the problem of plastic pollution started to attract attention. We’ve all seen the unnerving images of marine animals in distress from plastic exposure (just check out this video of a turtle getting a straw removed from its nostril or this article about a dead whale with a stomach full of plastic bags). National Geographic recognized plastic pollution as one of mankind’s most pressing issues to date, and the U. S. and United Kingdom have recently passed laws banning the use of microplastics in certain commercial products. The ubiquitous nature of plastics in our society begs the question: Just what is all the hype about? And if there really is a problem, can we do anything to fix it?
As it turns out, plastic pollution does pose a real threat to humans and the environment, but the problem is much more complex than a whale with a stomach full of plastic bags.
What is all the hype about?
Gut obstruction and animal confinement. The most well-known problem associated with plastic pollution is gut obstruction in marine animals and birds and the incidental confinement of marine animals by plastic debris. Both can result in death or injury for the animal
Sorption of secondary contaminants. Although plastics are biologically inert, they can grab onto secondary contaminants like a toxic ocean flypaper. These contaminants usually include organic pollutants like pesticides and industrial chemicals. Such organic pollutants are often resistant to environmental degradation, tend to hang out in fatty tissues, and love to accumulate on the surface of plastics. In fact, the concentrations of contaminants stuck on a plastic surface can greatly exceed ambient concentrations in the surrounding waters.
Now the real question is.....What can we do about this?
Reduce. Reuse. Recycle. The most effective way to address plastic pollution on a personal level is to replace single-use plastic items with reusable items. Grocery shop with a reusable bag. Avoid using plastic straws at restaurants. Carry a reusable water bottle instead of a crinkly plastic one. These small lifestyle changes will help us turn the tides on the plastic pollution problem, and you might even find that the reusable items work better than the single-use plastic items! When you must use plastic materials, make sure to choose plastic materials that can be recycled - and actually recycle them!
Make your voice heard. The use of plastic microbeads in personal care products was banned in the United States in 2015, but the use of microplastics in other products (cosmetics, sunscreen, glitter, toothpaste, nail polish, abrasives in dish detergent pods) has not been addressed. And although some companies are taking action to reduce single-use plastics in their business design, the problem of single-use plastics has not been formally addressed by state or federal regulations. Be vocal and let your legislature know how you feel about these problems!
There is often a historical truth behind fictional characters, no matter how absurd it may seem. I was 22 years old, in my first class as a PhD student, when I learned that there was something more to an iconic character from my childhood than I realized. Alice in Wonderland’s Mad Hatter may not have been just this fun, crazy, unpredictable character - he was possibly inspired by real-life hat makers suffering from chronic mercury poisoning.
Often cited as a classic example in occupational toxicology, Mad Hatter Disease (also known as Erethism) is a neurological condition resulting from daily exposure to mercury fumes. Mercury was used to help hatters manipulate felt into hats. However prolonged (chronic) inhalation exposure to mercury often led to hatters experiencing tremors and various psychological symptoms, including depression, irritability, and even hallucinations. Various reports of this disease and its relationship to hat-making emerged as early as the 1800s; in fact, a cohort of New Jersey hat makers were experiencing these symptoms in 1860, just 5 years prior to the publication of Alice in Wonderland by Lewis Carroll.
Long after the hazards of occupational mercury exposure were first observed, the United States outlawed the use of mercury in the felt industry in 1941. This was not the only time the United States government has acted to protect workers from occupational hazards; for instance, in 1989 the Environmental Protection Agency banned the use of asbestos in building materials after evidence emerged that asbestos exposure results in chronic respiratory problems. As technology continues to advance, we must work to proactively protect workers before they become ill. While the Mad Hatter is an iconic and beloved character, the reality behind his origin is heartbreaking, and is a powerful reminder of the importance of occupational safety procedures and regulations.
Rachel Louise Carson was born on May 27, 1907 (she would celebrate her 101st birthday today!) in Springdale, Pennsylvania, a small town along the Allegheny River just east of Pittsburgh. She grew up in a poor family, but was awarded a scholarship to attend the Pennsylvania College of Women - today known as Chatham University in Pittsburgh. She originally planned to study English and writing, but realized that years exploring the wilderness around her childhood home had fostered a love for biology and the environment. After receiving a bachelor’s degree in biology, she continued her studies at the oceanographic institute at Woods Hole, Massachusetts and at Johns Hopkins University, where she earned a master’s degree in zoology. Carson then went on to work for the U.S. Bureau of Fisheries where she wrote radio segments about marine life. In her spare time, she wrote freelance pieces for newspapers and magazines on the topics of conservation and nature. She was eventually promoted to Editor-in-Chief of all Fish and Wildlife Service publications. During this time, she also published three acclaimed books about aquatic life, Under the Sea-Wind (1941), The Sea Around Us (1951), and The Edge of the Sea (1955).
However, it is her fourth book, called Silent Spring, which makes her a renowned figure in the fields of ecology, toxicology, and environmental health. Published in 1962, Silent Spring outlines the negative impact of pesticide use on the environment, ecosystems, and human health. She wrote specifically about the insecticide DDT (dichlorodiphenyltrichloroethane), which at that time was sprayed aerially throughout the United States to control insect populations. DDT had been linked to the thinning of eagle eggshells, causing them to crack during incubation and ultimately leading to a decline in the eagle population. The book was a bestseller, and launched the environmental justice movement in the United States. Silent Spring and Carson faced substantial backlash from chemical companies, but also made Americans more aware of the fragility of our environment and the need to protect it from irresponsible chemical use. Her book and subsequent appearance before the Senate subcommittee in 1963 would plant the seeds for the founding of the Environmental Protection Agency in 1970, the passage of the Clean Air and Water Acts, the establishment of Earth Day, and the eventual banning of DDT in the United States in 1972. Unfortunately, Carson did not live to see the full impacts of her work, and lost her battle to breast cancer on April 14, 1964. Posthumously awarded the Presidential Medal of Freedom, she left behind a legacy of appreciating and protecting the environment, best illustrated by her quote:
“The more clearly we can focus our attention on the wonders and realities of the universe about us, the less taste we shall have for destruction.”
This month, the University of Toronto’s Green Chemistry Initiative and the Gainesville ToxSquad teamed up to co-author a post about the Indian Vulture Crisis…
Shira Joudan (Green Chemistry Initiative) and Alexis Wormington (ToxSquad)
Pharmaceuticals have drastically changed our society, quality of life, and life expectancy. Advances in chemistry are the driving forces behind the optimization of pharmaceuticals and other synthetic chemicals which have shaped the way we live our lives. Sometimes, a chemical used has undesired side effects, such as non-target toxicity to animals in the environment. A historic example of the consequences of chemical use is the toxicity of the pesticide dichlorodiphenyltrichloroethane (DDT) to eagles, which was profiled in Rachel Carson’s famous book Silent Spring. Although current regulations require extensive toxicity testing for new chemicals, those with a high production volume can still elicit unforeseen environmental effects on the environment.
More recently, there have been unforeseen environmental implications of chemical use in another essential bird population in India, a phenomenon now known as the Indian Vulture Crisis. Between 1993 and 2000, Indian vultures (Gyps bengalensis, Figure 1) began to mysteriously disappear, with the population declining by over 97% in less than 10 years (Figure 2). Researchers worked frantically to identify the cause, and came up with several theories ranging from infectious disease to food shortage to chemical exposure. Scientists began noticing visceral gout on a majority of the dead vultures, which is a sign of kidney failure in birds, and from there it didn’t take long to determine the culprit was a chemical contaminant. In 2004, a paper reported startling amounts of diclofenac (Figure 3) in the tissues of the dead vultures, providing compelling evidence that the non-steroidal anti-inflammatory drug (NSAID) was the cause of the population collapse.3 To figure out how to restore the vulture population, or at least slow down its decline, researchers needed to figure out how the vultures were being exposed to diclofenac, why it was killing them, and if there was a chemical alternative to the deadly pharmaceutical.
So, What Happened?
The problem began when diclofenac was approved for veterinary use in India in the early 1990s, where it was widely utilized to treat inflammation in cattle due to its efficacy and affordable cost. As a result, many livestock carcasses in India were contaminated with diclofenac, which brought catastrophic consequences to any vulture that consumed the carcasses. Vultures within the Gyps genus cannot metabolize diclofenac, and are extremely sensitive to the drug, with toxic doses ranging from just 0.1-0.8 mg/kg depending on the species.1 A vulture would receive a lethal dose of diclofenac after consuming a small amount of contaminated tissue, and die of renal failure within 48 hours. Just one contaminated carcass affected several vultures at once due to their group feeding behaviour, and because of this, diclofenac contamination in as little as 1 of every 200 carcasses would have been enough to cause the decline in the vulture population.
Although diclofenac is either banned or not used for veterinary purposes in most countries, it is still legally utilized throughout Europe, which has drawn controversy in those countries where it is approved for use in food animals.
Human Health Impact of the Vulture Crisis
India is a developing country and relies more on natural processes for the removal of dead animals, where scavengers like vultures play a huge role. With the loss of the vultures, less efficient scavengers such as rats and dogs have moved in to replace them, leading to major problems with disease in the affected areas. Unlike vultures, which are terminal hosts for pathogens due to their strong stomach acid, dogs and rats are reservoirs for diseases – and now these animals are the primary scavengers in India. A rise in feral dogs has caused an increase in the number of rabies cases in humans, which has cost India approximately 998-1095 billion Rupees in healthcare costs between 1992 and 2006 (15-16.5 billion USD).
In addition to the economic and health costs associated with a rise in infectious diseases, the disappearance of the vultures has also lead to issues with the prolonged decomposition of carcasses. Vultures play a major role in the decomposition process – a group of them can skeletonize a body within a few hours. But in their absence, bodies take days or months to decompose, which can lead to issues with water or food contamination. This ‘carcass crisis’ has had cultural implications as well, threatening the ancient Parsi burial tradition where bodies are not buried, but disposed of through natural means (i.e. vultures). Without the vultures, the Parsis struggle to continue the two-thousand-year-long practice and are forced to seek alternative methods of body disposal, causing a deep divide within the community.
Diclofenac and Green Chemistry: Could This Have Been Prevented?
The short answer: probably not. For a drug to be approved for human or animal use, toxicity research must be conducted (although these requirements vary by country, read more about how drugs are approved in Canada10 and how drugs are approved in the USA11). Unfortunately, potential ecosystem toxicity (ecotoxicity) is not often at the forefront of the drug-approval process. Even if ecotoxicity studies were performed with diclofenac, it is unlikely that the toxicity to vultures would have been discovered before drug approval, as vultures are not a common test animal used in these types of studies. Only a full chemical assessment with ecosystem modelling and subsequent toxicity tests could have predicted the toxicity to the vultures; but these tests are expensive, time consuming, and not the norm during the current drug-approval process.
In India, farmers cannot afford to lose animals, and rely on affordable NSAIDs such as diclofenac to improve the health and quality of life of their livestock. Since NSAID use cannot be prevented, it is up to green chemists to find a suitable replacement for diclofenac that is efficient, affordable, and less toxic to vultures.
To predict the potential toxicity of a pharmaceutical or chemical to humans and the environment, it is important to consider all interactions that occur once the compound enters the body. Every pharmaceutical has a “therapeutic index” (the difference between an effective and toxic dose), which can vary between different species or susceptible populations (e.g. infants, elderly). If the concentration of a drug exceeds the toxic level, toxic endpoints such as renal failure or death could be observed. The toxic level of a drug depends on two major processes: drug excretion and metabolism. The sum of these two processes determines how quickly a pharmaceutical is broken down and eliminated from the body. In the case of diclofenac, vultures could not metabolize or eliminate the drug, so it was free to wreak havoc on susceptible organ systems. For an NSAID to be a suitable replacement for diclofenac, vultures should be able to break it down and excrete it safely.
Currently, meloxicam has replaced diclofenac as an NSAID for livestock in India. Both drugs have a similar mechanism of action in the treatment of inflammation; however, unlike diclofenac, meloxicam is rapidly metabolized and excreted by vultures. In a study where different vulture species were administered meloxicam, researchers observed the production of three metabolites identical to those observed in humans during clinical trials. Vultures have the enzymes required for the metabolism of meloxicam (specifically cytochrome P450s and glucuronide transferase). The formation of metabolites alters the biological activity of meloxicam, increasing its water solubility and allowing for faster renal excretion.
Understanding the biological interactions of a drug can also help us eliminate potential replacements for diclofenac. An example of a poor replacement for diclofenac in cattle would be aceclofenac, because it is metabolized to form diclofenac via hydrolysis. This particular pharmaceutical would not do anything to improve the vulture population, and should not be selected as a replacement for diclofenac.
Current Status and Remaining Challenges
In 2016, the Indian minister of the environment launched the Gyps Vulture Reintroduction Programme with the hope of restoring the vulture population to 40 million individuals within the next decade through breeding programs. Although this effort to restore the Indian vultures is a step in the right direction, there are still many challenges in way of their recovery. Despite the fact that meloxicam is a safer NSAID for use in livestock, diclofenac is still obtained and used illegally among farmers in India due to its affordability. Since the ban of diclofenac for veterinary use in 2006, the decline rate of Gyps has decreased, but vultures are still likely to decline by 18% per year despite the ban. Until the drug is completely removed from the equation, the reintroduction and recovery of the vultures remains a challenge.