What Hydrogen Peroxide Really Did to Trump's Reflecting Pool

When the National Park Service added hydrogen peroxide to the Lincoln Memorial Reflecting Pool, the internet immediately decided it had found the culprit behind the peeling coating.

But science doesn't work that way.

In this episode, Rudy Stankowitz takes a research-first approach to one of the most discussed pool stories of the year. Instead of asking whether hydrogen peroxide caused a coating failure, he asks a different question:

Why was hydrogen peroxide chosen in the first place?

Drawing from published scientific literature on cyanobacteria, harmful algal blooms, microbiology, biofilms, and water treatment, Rudy explores how hydrogen peroxide affects microorganisms, why mature biofilms are so difficult to eliminate, and why swimming pool professionals may need to rethink the way they've approached "black algae" for decades.

This isn't a product pitch.
It isn't a treatment recommendation.
And it certainly isn't clickbait.

It's an evidence-based discussion designed to separate what science has demonstrated from what still remains a hypothesis.

The episode also introduces the first part of Rudy's proposed research protocol—a hypothesis assembled from published mechanisms that has not been validated in controlled swimming pool research—and explains exactly where established science ends and new investigation begins.

If you're tired of opinions masquerading as facts, this episode is for you.

In This Episode

• Why the Lincoln Memorial Reflecting Pool was treated with hydrogen peroxide
• Why concentration matters more than percentage
• Correlation versus causation in coating failures
• What published research says about hydrogen peroxide and cyanobacterial blooms
• The difference between free-floating algae and mature cyanobacterial biofilms
• How extracellular polymeric substances (EPS) protect biofilms
• Why oxidants often struggle against established biofilms
• The biology behind oxidative stress
• Photosystem II, lipid peroxidation, and cellular damage explained
• Why mature biofilms deserve to be studied separately
• Why Rudy believes better questions lead to better science
• The first step in a proposed research protocol using aluminum sulfate
• Why coagulation and physical removal may reduce oxidant demand before disinfection
• Where the published literature ends—and where hypothesis generation begins

Key Takeaway

Science advances by asking better questions—not by rushing to conclusions.

This episode doesn't claim to have solved black algae. It challenges listeners to examine what the published research actually supports, recognize the limits of current knowledge, and think critically about where future swimming pool research should go.

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Special thanks to the companies that support education and the advancement of the swimming pool industry:

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Follow Talking Pools on your favorite podcast platform, and don't forget to subscribe so you don't miss Part 2, where the proposed research protocol continues with hydrogen peroxide, chlorine sequencing, and the remaining scientific questions surrounding mature cyanobacterial biofilms.

Test it. Dose it. Brush it. Brush it down.

Transcript

Rudy Stankowitz (00:00)
When we started this year's mentor award, I honestly had no idea where it would end up. We received over one hundred nominations. Every single nomination was read. Every story mattered. Then the finalists were blind, judged, names were removed, they were anonymized. Judges had no idea who they were scoring, just the stories. Now I am proud to introduce the top ten mentors.

For 2026. And before anybody starts trying to figure out who's first, who's tenth, relax. Don't. These are being announced in completely random order. Welcome to Friday. I am Rudy Stankowitz. This is the Talking Pools podcast. So happy that you could join us this weekend Eve. God bless you. You guys are the heroes of this industry. With that said.

Couple of weeks ago you saw something strange. You saw something odd. You saw members of the National Park Service pouring hydrogen peroxide into the reflecting pool at the Lincoln Memorial. Immediately afterwards, the dose of hydrogen peroxide was blamed for the peeling coating, which this episode is not gonna be about. But a lot of you asked me in emails and DMs, why hydrogen peroxide? Why would they add such a thing? So that's what I wanna talk about.

We got a monument at one end, we got a coating failure at the other, and seven million people on the internet pretending they majored in polymer science. The National Park Service had an algae problem, a highly visible algae problem, not some green spot behind a ladder at the Motel Six. This was the Lincoln Memorial Reflecting Pool. It's America's front yard. Thousands of feet of green water sitting between two of the most recognizable structures in the country.

Crews treated the water with hydrogen peroxide. Available reporting confirms that the hydrogen peroxide was applied to combat the bloom along with nanobubble ozone technology. The material was reported as a 12% hydrogen peroxide solution. Although the total amount applied and the resulting concentration in the pool were not publicly documented in the material I could find.

That is missing information and it is not a minor detail. It's actually the whole damn calculation. Twelve percent tells us what was inside the container. It does not tell us what existed in the pool after the chemical was added. So there's a difference. It's a pretty important one. Twelve percent hydrogen peroxide percent.

poured from a container is a concentrated oxidizing solution. 12% hydrogen peroxide distributed through approximately 6.75 million gallons of water is no longer 12% hydrogen peroxide. It's been diluted. How much? Who knows? I can't tell and can anybody else that didn't slow down the internet because in no time at all, hydrogen peroxide was being accused of peeling the blue coating off the bottom of the reflecting pool. Case closed. Chemical convicted

No trial, no dosage, no exposure concentration, no contact time, no material testing, no examination of the bond line, no determination of whether the failure occurred between the concrete and the primer, between the primer and the membrane, between the layers of the coating system or inside the coating itself, just they poured peroxide in there, and then the coating started to peel. That is not forensic science. That is how my grandmother diagnosed car trouble.

It was running fine until you changed the radio station.

When we started this year's mentor award, I honestly had no idea where it would end up. We received over one hundred nominations. Every single nomination was read. Every story mattered. Then the finalists were blind, judged, names were removed, they were anonymized, judges had no idea who they were scoring, just the stories. Now I am proud to introduce the top

10 mentors for 2026. And before anybody starts trying to figure out who's first, who's tenth, relax, don't. These are being announced in completely random order. This is not the final ranking. So congratulations to Brandon Reed. Congratulations to Terry Tammanin. Congratulations to Chris Kavanaugh. Congratulations to Jeff.

Hampy. Congratulations to John Tikalis. Congratulations to Greg Beard. Congratulations to Tim McDowell. Congratulations to Jerry Wallace. Congratulations to Lacey Davis. Congratulations to

John Poma, ladies and gentlemen. Those are your top 10 mentors for 2026 in the Talking Pools mentor recognition. Because to be part of this 10 is to be part of an elite group. But top 10 mentors in the industry, I mean, think about that for a second. Out of more than 100 nominations, these 10 people rose to the top. Every one of them has changed lives.

Every one of them has invested in someone else's success. Every one of them has left the pool industry better than they found it.

One will be named the 2026 Talking Pools Mentor of the Year. We'll begin revealing the final rankings very soon. Until then, congratulations to the top 10. And thank you for proving that the greatest legacy you can leave this industry isn't the pools that you build, it's the people that you build. Greg Beard, John Poma, Jerry Wallace.

Jeff Hampi, Terry Tammanin, John Tikullis, Lacey Davis, Brandon Reed, Chris Kavanaugh, Tim McDowell.

Like to interrupt this broadcast talking about a scumbag, a total dirt bag. Someone in the pool industry, yes, one of our own, one of our pool service industry family preying on other pool service pros online. I'm talking about a crime that doesn't begin with a dark alley or a deserted road, begins with a keyboard. Recently, one of the hosts of the Talking Pools podcast became the target of an online harassment campaign that escalated into something far more.

Serious death threats directed not only at her but at her husband and their baby.

I know a lot of you might say, well that's what happens when you put yourself out there like that, and maybe that's true. Maybe that keeps a lot of people from putting themselves out there like that. The thought, the threat death threats. This isn't someone leaving a rude comment and going away. This isn't just the internet. Making a credible death threat is a crime. And

If it can happen to someone with a podcast, it can happen to anyone with a business, a social media account, or simply an opinion that someone else doesn't like. If you ever become the target of threats like these, here's what you should do. First, don't engage, don't reply, don't argue, don't try to outsmart them. Every response gives them exactly what they want, your attention. It can also complicate an investigation later. Second,

Preserve the evidence. Take screenshots that clearly show the threat, the username, the date, the time, and the web address if possible. Save emails, direct messages, text messages, and voicemails. Don't delete anything. If you think the post might disappear, photograph your screen with another device. Your goal isn't to win an argument, it's to preserve evidence. Third, report threat to the platform. Whether it's Facebook, Instagram, X, YouTube, or another service, use its reporting system. That

Creates an official record and may help preserve the information investigators can later request. Fourth, contact law enforcement. Death threats are criminal matters in many jurisdictions. Bring every screenshot, every piece of documentation that you have. If the threats involve your children, contain personal information, or appear to cross state lines, you should also file a report with the FBI's Internet Crime Complaints Center. Always ask for a case number and don't be afraid to follow up. Fifth, take every specific threat.

Seriously, someone mentioned your address, your family, your children's names, or claims they know where you live. Treat it as potentially credible until investigators determine otherwise. Contact your local police department immediately. If you believe you're in immediate danger, call nine one. Sixth, secure your digital life. Change your passwords.

Enable two-factor authentication on every important account. Search for your name and your family members online and remove personal information from data broker sites whenever possible. Avoid posting your location in real time and make sure your family understands not to engage with the person making the threats. Finally, tell the people closest to you, your spouse, your business partners, your employees, your moderators, anyone who could unknowingly share information or interact with the individual involved.

They need to know what's happening. And one more thing, threats like these don't just affect your sense of safety. They affect your peace of mind. If you're struggling after receiving threats, talk to someone you trust or seek professional support. You don't have to carry that burden alone. One final note, I am not the law. I am not a law enforcement officer.

I am not an attorney. This information is intended as general guidance, not legal advice. If you do believe you are in immediate danger, call 911 for legal remedies such as protective or restraining orders. Speak with a licensed attorney in your state. No one should have to fear for their life or the lives of their family, no matter what the fuck they say on Facebook, simply for speaking their mind. And no one making those threats should believe they'll remain anonymous forever.

Test it, dose it, brush it, brush it down.

Listen up, pool pros. I would like to give a nod to the sponsors of the mentor recognition, Title Sponsor Blu-ray XL, Title Sponsor United Chemical, Gold Sponsor Lamotte Company, Silver Sponsor, Revved Up Apparel, Supporting Sponsor Aqua Comfort Water Group. It makes perfect sense that these industry vendor badasses make celebrating the badasses who opted to help other individuals through a desire to lift the industry and expect nothing in return.

Well here I am saying expect the unexpected.

I've been getting Service Industry News since I first stepped into this business, and every time it landed, I did the same thing. Flip straight to the horror file. The weird installs, the absurd finds, the stuff only pool pros ever see. Then I'd go back and read the articles. Service Industry News is a twice-monthly trade publication for pool and spa service text, 24 issues a year, emailed free to over 10,000 texts and available on their app. Every issue covers nationwide industry news and

Real technical content you actually will use. Get your free subscription at serviceindustry news dot net. Again, that's serviceindustry news dot net. Do it now.

They poured peroxide in and then the coating started to peel. That is not forensic science. That is how my grandmother diagnosed car trouble. It was running fine until you changed the radio station. The timing of the two events does not establish that one caused the other. And in this case, even the timing creates problems for the accusation. Reporting the algae treatment confirms that the crews used hydrogen peroxide during the response to the to the bloom, but

Publicly available information does not establish that diluted peroxide initiated the coating separation. Rhino linings later described the reported condition as localized areas of finished coat separation. That wording matters. Finish coat separation is not automatically chemical destruction. Hydrogen peroxide was used against the algae bloom. That's it. The quantity no one knows. I mean, the NPS knows, but they haven't shared that information yet.

I think we will honestly get information about Area fifty one and UAPs before we find out what the chemical dose of hydrogen peroxide was. The final concentration achieved in the pool is unknown because we don't know how many gallons were added. The peroxide residual over time also unknown because I don't know were they testing it? I we weren't. The exact locations and application method are not fully documented in the material that I've reviewed either. And no publicly released laboratory analysis have I found that.

demonstrates hydrogen peroxide chemically degraded coatings and caused the observed separation. So that doesn't prove peroxide absolutely played a role. Science rarely gives you permission to say absolutely no role without testing. But it means the accusation has also outrun the evidence by several exits. Because while everybody else was asking whether hydrogen peroxide murdered the coating, I was thinking to myself that the NPS

beat me to the punch because as most of you know, I've developed something that I've been trying to prove wrong. So right now that's the stage that it's at. It's in the I don't know stage. Cause all I can say for sure is I don't know, but I am trying to prove something wrong. And I have put together a method of treating black algae, which we know now since 2018, my research there is a cyano bacteria biofilm. I've put together

something with several steps and hydrogen peroxide at a certain percentage at a certain dose is in those instructions or at least in those proposed instructions. Where does that information come from the fact that hydrogen peroxide is even something that we could use? Well if you look at lake management, drinking water reservoirs, harmful algae bloom research, microbiology, photosynthesis.

Oxidative stress biofilms. Researchers have investigated hydrogen peroxide as an emergency treatment for cyanobacterial blooms in lakes and reservoirs. Experimental work has shown that relatively low concentrations can suppress susceptible cyanobacteria, although effectiveness changes with the organism, biomass, light, temperature, nutrient conditions, surrounding microbial community, and rate at which

The peroxide is consumed. So just cliff notes, species, biomass, light, temperature, nutrients, microorganisms, peroxide demand. In other words, the chemical does not enter the water wearing a cape. It does not point at the cyanobacteria and yell, hey, I'm gonna kick your ass. It enters a complicated biological system and immediately starts reacting. Sometimes it works, sometimes it's consumed too quickly, sometimes surrounding organisms affect.

The result. Sometimes cyanobacteria recover. And mature biofilms are in an entirely different problem from cells floating freely in the water. That's where the original conversation fell apart. People kept calling everything algae. The green suspended bloom in the reflecting pool was algae or cyanobacterial material requiring identification. The black growth that pool professionals commonly call black algae is usually discussed as surface attached.

Cyanobacterial biofilm. Those are not automatically the same organism. I showed you in my research that black algae was always cyanobacteria as the primary constituent, but the species, the genre could differ in a distance as short as a mile, which is cool information. So we know we're not most likely not dealing with the same organism. We're certainly not dealing with the same physical target. Free-floating cells, they're exposed directly to the water around it.

A cell inside a mature biofilm embedded in a hydrated extracellular matrix, that matrix, commonly called EPS, extracellular polymeric substances, polysaccharides, proteins, lipids, extracellular DNA, pigments, trapped particles, bound metal, water. It's not just snot holding bacteria to a wall, although, scientifically speaking, it is some extremely sophisticated snot. The matrix anchors itself to the surface.

There's no roots. It just sticks to the surface. It helps organize the biofilm, traps the material from surrounding water, and changes how disinfectants and oxidizers move through that colony. What happens when hydrogen peroxide encounters cyanobacteria protected by EPS? Does it reach the cells? How quickly is it consumed?

Which cellular systems does it damage? How much of the dose is sacrificed reacting with the surrounding organic material? Does a mature biofilm respond the same way as a suspended biofilm? The published research gives us answers to some of those questions. Not all of them, and that's important, because I'm not about to stand here and tell you that hydrogen peroxide is a miracle cure for black algae. I don't know that. Nobody has shown me controlled pool research proving that.

What I can tell you is that hydrogen peroxide is more than the chemical sitting beside PHMB in the pool store. You know the product is Bakwashock. It is a concentrated aqueous hydrogen peroxide product. The 2018 safety data sheet identifies its hydrogen peroxide content as a range, only as a range, and they have it at 30 to 60% with a specific gravity of approximately 1.2.

Classifies the material as an oxidizer and corrosive substance, not as some mysterious proprietary black algae terminology. The pool industry has already handled concentrated peroxide. We have added it to pool water. We simply viewed it through one narrow application, oxidizing contaminants in a polyhexymethylene big guanide treated pool, PHMB for short.

Meanwhile, scientists outside our industry have been examining hydrogen peroxide as a tool against cyanobacteria. Same molecule, different question. Sometimes the breakthrough is not in finding a new chemical. Sometimes it's realizing the chemical you've been staring at for thirty years may have been doing a job you never bothered to study. That doesn't make it the answer. It does make it worth investigating. And before we talk about any proposed four step process, before anybody buys a drum, before

Some guy on YouTube dumps peroxide into a customer's pool while filming it vertically. We need to understand exactly what this chemical does to the EPS, to the cell membrane, to the pigments, to the photosystem too, to the enzymes that keep the cell alive. And to mature biofilm that has spent weeks or months building itself a microscopic bunker.

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Hydrogen peroxide is not magic, it's chemistry. So let's start right out the gate. It's not alive. It doesn't wake up in the morning, stretch, drink a cup of coffee, and say, hey, I'm gonna go out fuck up some cyanobacteria today. Chemicals don't make decisions, they react. That's it. Everything hydrogen peroxide does, it does because chemistry forces it to. There are no opinions, there are no politics, there are no Facebook groups, there are no YouTube comments from a guy wearing mirrored sunglasses.

Explaining water chemistry from the driver's seat of his pickup truck. Just chemistry. Hydrogen peroxide is relatively simple molecule. Two hydrogen atoms, two oxygen atoms. H2O2. It looks almost like water. One extra oxygen atom. That is the difference. One atom. One incredibly unstable atom, one atom nonetheless. That extra oxygen doesn't really want to stay there.

Sunlight speeds that up. Heat speeds that up. Transition metals like iron and copper, they speed that up. Organic contamination speeds it up. Even living organisms speed it up. Why? Because almost every aerobic organism has evolved ways to protect itself from hydrogen peroxide, including cyanobacteria. You'd think it just walks in and starts breaking things. Everybody dies, not exactly.

Cyanobacteria has defensive systems, catalyst, peroxidasis, superoxide dismutase. These enzymes continuously destroy reactive oxygen species before those molecules damage critical parts of the cell. So, in other words, cyanobacteria doesn't just sit there and take it, it fights back. And that's one reason concentration matters. So does dose exposure time. Species. One cyanobacterium can respond.

very differently than another. That's one reason environmental scientists don't just simply say use peroxide. They study dose, temperature, light, organic demand, species composition, and whether the bloom consists of free-floating cells or mature biofilms. Because those are completely different biological problems. Now let's take a look at what actually happens. Hydrogen peroxide reaches water. Immediately it starts reacting. Some of

Decomposes naturally into water and oxygen. Some reacts with dissolved organic matter. Some reacts with enzymes released by microorganisms. Some reacts with metals. Some eventually reaches cyanobacteria cells. If enough peroxide survives long enough, oxidative stress begins. Now, oxidative stress sounds like something your cardiologist says after looking at your blood work.

In microbiology, it just simply means the cell is accumulating more reactive oxygen species than it can safely neutralize. Think of it like sparks flying inside of an electrical panel. One spark, thousand sparks, eventually something's going to catch fire, except in this case nothing is literally burning. Electrons are moving where they shouldn't. Cellular components begin oxidizing. The first major target is photosynthesis. Cyanobacteria don't eat food, they manufacture it.

Just like plants, inside the cell are specialized membranes called thylakoid membranes. Those membranes contain the molecular machinery responsible for converting sunlight into usable chemical energy. One of the most important pieces of that machinery is called photosystem two. Photosystem two performs one of the most remarkable reactions in biology. It splits water molecules using sunlight. That process ultimately supplies electrons for photosynthesis.

And releases oxygen into the environment. It's also remarkably vulnerable to oxidative damage. Hydrogen peroxide and other reactive oxygen species can damage proteins associated with photosystem 2, particularly the D1 reaction center protein. Normally, the cell constantly repairs that protein. Damage, repair, damage, repair. It happens all day long. But if oxidative stress overwhelms the repair system,

The damage accumulates faster than the cell can fix it. Photosynthesis slows. Energy production declines. The cell becomes weaker. Now we're not finished because peroxide isn't only affecting photosynthesis. Reactive oxygen species also attack lipids. Lipids make up cellular membranes. When those membrane lipids oxidize, the membrane loses integrity. Think of a garden hose. Brand new, flexible, strong.

Keeps the water where it belongs. Leave it in the Florida sun for 15 years. It becomes brittle, it cracks, starts leaking. Cell membranes experience something similar under oxidative stress. Not because they're getting old, because they're being chemically damaged. Researchers refer to this process as lipid peroxidation. As membrane damage increases, the cell becomes less capable of maintaining normal ion gradients, transport systems begin to fail. Important molecules leak and

The cell spends more energy trying to survive while simultaneously producing less energy. Not exactly a winning strategy. Proteins become targets to enzymes, transport proteins, structural proteins, oxidation changes their three dimensional shape. Some stop functioning altogether, others function less efficiently. Still, others are destroyed.

DNA can also be damaged under severe oxidative conditions. Hydroxyl radicals, which may be generated under certain conditions involving catalytic metals, are among the most reactive molecules known in biology. They can damage nucleic acids almost immediately after they form. Fortunately, they also react so quickly that they rarely travel very far. They're less like bullets, more like

Tiny grenades exploding exactly where they're created. So if hydrogen peroxide can damage photosynthesis, membranes, protein, and DNA, why doesn't it just simply wipe out every cyanobacterial colony cyanobacterial colony that it encounters? Because nature cheats. Not really. Sometimes it feels like it. The answer is biofilms. More specifically, EPS. Extracellular polymeric substances. If you've listened to this podcast before, you've heard me describe EPS as slime. That's not wrong.

It's just incomplete. EPS is an organized extracellular matrix, mostly water, but also polysaccharides, proteins, lipids, extracellular DNA, pigments, absorbed materials, and all kinds of organic material trapped inside the matrix. Imagine pouring concrete. Imagine pouring concrete. The cement is not the whole sidewalk. You need gravel, sand, water, reinforcement, everything working together.

EPS is the same way. It's a composite material, and that material changes everything. Inside of every cyanobacteria cell sitting naked in the water, the colony builds itself a neighborhood. Actually, again, more like a bunker. The outer layers become the first thing oxidants encounter. Not the cells, the matrix. Hydrogen peroxide can react with components of that matrix.

Proteins, pigments, various organic molecules. Some peroxide may never reach the deeper layers because it's consumed before it actually gets there. Researchers studying mature cyanobacterial biofilms have shown that peroxide treatment does not necessarily eradicate the colony. Some biofilms recover. Some respond differently depending on species. That finding is super important because not

Because perox not because peroxide failed, because it tells us mature biofilms behave differently than free floating cyanobacteria. And that's exactly what experienced pool professionals have been observing for decades. You brush black algae, shock it. Think you've won three weeks later, there it is again.

Because that's where the published research leaves us. Hydrogen peroxide clearly damages cyanobacteria. That is well established. Hydrogen peroxide clearly induces oxidative stress. Also well established. Hydrogen peroxide has been investigated extensively harmful cyanobacterial blooms. Also well established. Hydrogen peroxide alone consistently eliminates mature cyanobacterial biofilms under all conditions. That is not what the literature says. In fact

The literature says mature biofilms deserve their own conversation. We've spent decades asking what kills black algae? Maybe the better question is what makes mature cyanobacterial biofilms so difficult to kill in the first place? Cause once you understand the battlefield, you stop expecting every chemical to fight the same war.

So now we arrive at the part where I make everybody nervous because I'm gonna lay out a process and somebody will immediately hear the word process, ignore every disclaimer, dive into a chemical supplier and begin conducting unauthorized microbiology experiments in somebody else's backyard. Please don't. This is not a treatment recommendation.

This is not an instruction sheet. This is not me announcing that I have cured black algae. I have not. This is a research question built from separate pieces of published science.

Rudy Stankovich (30:53)
Trying to determine whether this hypothesis is supported or refuted by the published evidence. Everything from this point forward is gonna be hypothesis generation. Each individual mechanism I discuss has support somewhere in the published scientific literature, what has not been demonstrated is that combining these mechanisms into a single treatment sequence produces the desired outcome in a controlled swimming pool environment. That

Is precisely the question I'm trying to answer.

Rudy Stankowitz (31:26)
does this idea survives contact with evidence. And the first step in the process is not peroxide, it's not chlorine, not copper, it's aluminum sulfate. Alum. The same chemical I've used and discussed for cyanuric acid reduction. The proposed dose eight point three three pounds of aluminum sulfate per ten thousand gallons of water converted into metric units. That's a

100 milligrams of alum per liter of water. So we get 100 parts per million. Before adding it, I would bring the pH to seven point zero and the total alkalinity into a controlled range. I have previously worked with alkalinity in the range of eighty to a hundred parts per million for the alum based cyanuric acid reduction procedure, but let's slow it down there because alum does not enter water politely. It changes the chemistry. When aluminum sulfate dissolves,

Aluminum undergoes a series of hydrolysis reactions. Under suitable pH conditions, those reactions form aluminum hydroxide precipitates. That precipitate appears as a soft reviews of cyanobacterial control strategies distinguish this physical removal and nutrient sequestering and nutrient sequesteration and nutrient sequestration role from the direct killing of from the direct killing action of algacides.

And that matters, alum does not need to kill cyanobacteria to be useful in this proposed process. In this proposed process. It may be useful simply because it removes material from the water before the peroxide is introduced. And that's what I'm intending to do here. Remove as much as I can from the water before.

Once hydrogen peroxide enters the water, anything capable of reacting with it becomes competition. Suspended cells, detached pieces of biofilm, dead organisms, proteins, pigments, dissolved organic matter, leaves, pollen, fine debris, whatever organic carnival is already happening in the pool. Every reaction consumes part of the peroxide dose. So why would I start by adding peroxide into water loaded with material?

That I could physically remove first. I'm gonna get it out of there. If I can get it out first, and I know it'll use up my peroxide, I'm gonna wanna get it out first, I'm gonna do it. And alum is the way to get it out. So I mean, if I just added the peroxide first, that would be like trying to disinfect a restaurant kitchen without taking the garbage outside. I mean, sure, you can spray bleach over the trash bags, but I'm not convinced that qualifies as sanitation. The research supportive role for alum in this sequence is therefore pretty straightforward.

Remove suspended biomass, remove colloidal material, capture some cell associated and electric and extracellular organic matter, settle detached cyanobacterial colonies or fragments, reduce turbidity, bind some soluble reactive phosphorus under favorable conditions, and bind some soluble reactive phosphorus. And according to the alum process I have previously researched, potentially remove a portion of cyanuric acid and

under prescribed conditions. But we have to be careful with language. Alum has been studied extensively for removing suspended cyanobacteria from water. That does not mean alum has been proven to strip a mature cyanobacterial colony off of a swimming pool wall. Those are different targets. A suspended colony is surrounded by treated water. A firmly attached colony is anchored to a surface by extracellular polymeric substances. Coagulation

Can capture material after it's suspended. It may capture fragments removed by brushing or natural detachment. It may interact with exposed extracellular material. But I have not found research proving that a 100 part per million alum dose penetrates an intact, mature, surface-attached cyanobacterial biofilm and dismantles it in place. So I'm not going to tell you that it does. That would be a wild claim. Wild claims are what happens when somebody reads the abstract.

Skips the methods, ignores the limitations, and immersely starts designing a product label. So what does the research tell us about EPS and coagulation? It tells us that EPS matters a lot. Cyanobacterial EPS can consist of diverse polysaccharides, proteins, uronic acids, extracellular DNA, lipids, pigments, and associated ions. Its composition varies by organism and environmental conditions. The matrix helps colonies form.

Holds cells together, binds material from the surrounding water, and influences interactions between the cells and treated chemicals. EPS can either help or interfere with coagulation. I know that sounds annoyingly vague. Welcome to biology. Some extracellular polymers can act as bridges between cells and particles, promoting aggregation. Other EPS components can stabilize suspensions, increase coagulant demand, shield.

Cell surfaces or interfere with the formation of strong settylable flocks. The result depends on amount, composition, molecular weight, charge, and distribution of the extracellular material. A study specifically examining the influence of EPS on cyanobacterial coagulation found that the matrix surrounding cells materially affected coagulation behavior. So the important takeaway is not that EPS always helps coagulation or defeats it.

The takeaway is that the organism's protective material changes the treatment process. There is no honest one sentence rule that applies to every species in every body of water, which means the 100 part per million alum dose cannot be presented as universally optimal for cyanobacteria. The dose comes from my existing alum procedure. It gives us a defined experimental c condition. It does not eliminate the need for jar testing.

Jar testing is where you take multiple water samples, apply different coagulant doses, control mixing, watch flock development, measure settling, and determine which conditions actually work in that particular water. In other words, what it you ask the water what dose it wants. Instead of screaming a number at it because it worked in somebody else's pool, temperature matters, pH matters, alkalinity matters, phosphate matters, organic carbon matters.

The cyanobacterial species matters. The concentration of suspended solids matters. And the amount and type of EPS matter. This is why real water treatment plans do not dose chemicals by vibes. Now let's talk about pH. Alum hydrolysis consumes alkalinity and can lower pH. That is not optional chemistry. It happens. The aluminum species present in water change as pH changes. Flock formation and residual dissolved aluminum areas.

are both affected by that pH. If the water does not have enough buffering capacity, a substantial alum dose can drive the pH much lower than intended. So starting at 7.0 and an alkalinity between 80 and 100 parts per million is not the end of the calculation. It's the beginning of monitoring. That water must be tested after the alum is added, not next week, not after lunch, during the process because if pH crashes, the treatment conditions change.

the form of aluminum in water changes. And the whole experiment starts wandering away from the one that you thought you were conducting. This one of the reasons I do not want somebody hearing eight point three three pounds and treating it like a sacred number carved into a stone tablet. It is not a defined research dose. The actual behavior

must be measured af after the alum is introduced and properly mixed, after the flock is allowed to develop and settle. And then comes one of the least glamorous but most important steps. You gotta vacuum it out to waste slowly, thoroughly, painfully slowly. The entire point of coagulation is removal. If you form a beautiful aluminum hydroxide flock, trapped cells and organic matter in inside of it,

then blast the vacuum across the bottom of the floor like you're trying to qualify for NASCAR, you have accomplished nothing except giving the particles another tour of the pool. You want the material out, not broken apart, not sent into the filter unless the system and procedure were specifically designed for that. You don't want it stirred back into suspension. No, you want it out. That physical removal matters for another reason. Cyanobacterial cells can contain intracellular compounds, including toxins in

Toxinogenic strains. Some control methods that lys cells may release intracellular material into the surrounding water. Coagulation and settling can remove intact cells without necessarily requiring immediate cell destruction. Although treatment conditions can still affect cell integrity, toxin behavior, and toxin behavior. Published reviews emphasize that bloom controlled methods must consider not only cell removal but also toxin release.

Treatment residuals rebound and effects on non-target organisms. Now, does that mean the black cyanobacterial growth in every swimming pool is producing dangerous cyanotoxins? No. Do we do we don't have enough evidence to support that blanket claim? Different cyanobacteria have different genetic capabilities. Even within toxin-associated genre, not every strain produces the same compounds. So identification matters.

Testing matters. So we don't use the word toxin as a horror movie sound effect, but if this process is ever formally studied, the patient the org the organism should be identified and intracellular and extracellular toxins should be considered when relevant. Otherwise we might celebrate because the visible colony disappeared while ignoring what entered the water while the cells were damaged. That would be the scientific equivalent of cleaning your garage by throwing everything into the living room. Garage looks great. You're

Spouse is gonna have some concerns. So after the alum step, what can we responsibly say we accomplished? Well, if the coagulation works as intended, we should have removed a portion of the suspended cells and fine material. We should have removed some detached EPS and organic debris. We should have reduced the oxidant demand presented by that removable material. We may have bound and removed some phosphorus, we may have reduced cyanuric acid according to the separate alum based.

a loop alum based process being followed. And we should now have a cleaner body of water in which to study the next chemical. That is the supported claim. Not alum killed biofilm, not alum dissolved EPS, not alum cured black algae. It prepared the water. It removed what could be coagulated, settled, and vacuumed away. And that's an important job. It is simply not the same job as disinfection. Do not

Ask peroxide to oxidize material you can remove first. Do not ask chlorine to fight through debris. You could have vacuumed out yesterday. Do not confuse killing with removal. And do not confuse removing suspended biomass with eradicating an attached biofilm. Keep hypotheses from turning into bullshit. Once the flock has been removed, the chlorine must be brought to zero before the peroxide step. And I think we're only about halfway through this conversation. So

That's where we're going end it today. We will pick up next week with part two. And I hope everybody looks at hydrogen peroxide at this point a little bit differently than we have in the past. And I hope it gives us a little bit better of an understanding of where the National Park Service was trying to head with the dose of H2O2 that they were dumping into that reflecting pool. So until next week.

You good? Be safe.