Science Friday - Office Air Pollution, Tetris Decisions, Alzheimer's Update. Oct 11, 2019, Part 2

Episode Date: October 11, 2019

If you live and work in an urban area, you might think about the air quality outside your home or workplace. But what about the air quality inside the office? It turns out that on average, indoor environments have higher concentrations of potentially harmful substances, such as aerosols and volatile organic compounds (VOCs). While past research has focused on chemical emissions from building materials, cleaning supplies, and even furniture, air pollution researchers are increasingly looking at another source of toxic air: us. New research from Purdue University to be presented at the American Association for Aerosol Research conference has found that the majority of indoor VOCs may be released by a seemingly innocuous source: human beings, their lunches and coffee breaks, and anything they may wear or bring to work. And many of these compounds, such as the terpenes released by peeling an orange, or the squalene released in human skin oil, react with ozone to form even more worrisome molecules. If you’ve ever played the classic puzzle-like computer game Tetris, you know that it starts out slowly. As the seven different pieces (called “zoids” by the initiated) descend from the top of the screen, a player has to shift the pieces horizontally and rotate them so that they fit into a gap in the stack of pieces at the bottom of the screen, or “well.” In early levels, the pieces might take 10-15 seconds to fall. The speed increases at each level. In world champion Tetris matches, players often start play at Level 18—in which pieces are on the screen for about a second. Wayne Gray, a professor of cognitive science at Rensselaer Polytechnic University, calls it a problem of “predictive processing and predictive action.” Champion-level expert players, he says, are able to take in the state of the gameboard and react almost immediately, without going through the mental steps of figuring out how to move the piece and rotate it that a novice player requires. “They can see the problem and reach a decision at the same time,” he said. Gray and colleagues have attended the Classic World Tetris Championship tournament for three years, collecting data from expert players using a modified version of the game that collects keystrokes and eye-tracking data. He joins Ira to discuss what the researchers are learning about expert decision-making, and what he hopes to study at this year’s upcoming Tetris tournament. The pharmaceutical industry has been on a 30 year mission to develop a drug to treat Alzheimer’s disease. The culprits behind the disease, they thought, were the amyloid plaques that build up in the brains of these patients. For many decades removing these plaques to treat Alzheimer’s was the goal. But then drug after drug targeting amyloid failed to improve the symptoms of Alzheimer’s—the so-called “amyloid hypothesis” wasn’t bearing out. But drug companies kept developing and testing drugs that attacked amyloid from every angle—perhaps at the expense of pursuing other avenues of treatment. This past summer, two more high profile clinical trials of drugs to treat Alzheimer’s failed. That brings the number of successful treatments for the disease, which affects 5.8 million Americans, to zero. George Perry, professor of biology at UT San Antonio and Derek Lower, a drug researcher and pharmaceutical industry expert join Ira to explain what led pharmaceutical companies to doggedly pursue the amyloid hypothesis for decades, and whether or not they are ready to start trying something else.   Subscribe to this podcast. Plus, to stay updated on all things science, sign up for Science Friday's newsletters.

This is Science Friday. I'm Ira Flato. A bit later in the hour and update on current Alzheimer's research. But first, if you've ever played the computer puzzle game, Tetris, you know how it is. It starts off slowly. The pieces drift down and you have maybe, what, 10, 15 seconds to think, position, position, position. Players have to take in the board. They have to assess the piece and play. You have to make a snap decision. But what happens? It gets faster. And at the top levels of play, pieces fall down the screen in a second or less. Can that teach us something about how the brain works in learning, cognition, or decision-making? Wayne Gray is a professor of cognitive science at Rensselaer Polytech in Troy, New York. And for the past three years, he's been bringing a team of cognitive science researchers to the classic Tetris World Championships. And this year's tournament starts next weekend, be there attending for the fourth year. Welcome back to the program.

Well, hello, thank you. Now, so you're going to the championship for the fourth year. Tell us what it's like there. Wow. Well, especially our first year, it was just chaos and confusion from our perspectives. The first day of the tournament, the first two days of the tournament, people were trying to qualify to get a slot on the championship playoff schedule, which they had 40. openings for. And people could play all day as many times as they'd like, but in their highest score would count on whether or not they made it. So there's a lot of sweat and nervousness going on.

How bad? We had our booths set up to collect some different sort of data from them. Okay. So let's talk about that. Let's first talk about how much better these people are than the regular person at Tetris. Wow. Well, we thought we knew Tetris before we went there because we had about 400 undergraduates play an hour of Tetris and a laboratory because everybody knows Tetris, right? That's why we picked this task to start with. None of those people got past the level, made at the end of level 16. In fact, only about eight got two, actually only about three got to level 15. They all died. And we said, well, of course. not because, you know, at level 15, it takes one in a third second for this piece to fall all 20 lines, and at level 16, it takes one second. So, of course, nobody can do that. And then we go to the Classic Tetris World Championship, and they start playing at level 18, where it takes

one second to fall from top to the bottom. That's amazing. So let's talk about the steps that are involved. You have to, what, you have to see the board, you see the piece coming, you have to rotate it, then you have to put into position. And the best players are better than anybody at doing these things. Yep. The best players are really, really good at that. Do they play it differently from us? Do they look at the board and just know or decide? They know where that piece is going quickly? Yes, yes. And this is all about what makes Tetris such an interesting thing for studying extreme expertise and these perceptual motor skills. All such skills are different, of course. racing car drivers or laparoscopic surgeons are very different than Tetris players.

But not different in the way they have to adapt, the way they have to learn to see things in advance before things happen. These people know when they see a zoid. They know exactly how far to rotate it, how fast to move it, and all that stuff. Whereas people like me will be spending a lot of time maybe moving the Tetris piece around the board looking for a good place with it as it's falling. But these guys and gals, they just C2Zoid, know where to put it and put it there by the shortest path, the minimum rotations, so that when it fits, it fits most tightly into the stack that they're building. That's amazing. And so how can you learn from them what you'd like to know about brain function?

Ah, very good question. Well, mechanically, we've been, this coming year, we're going back with different tasks than we had before. So one thing which we were always a little bit annoyed us is that when they play Tetris at our booth, and whenever we started at level zero, they'd be turning around in the chairs, talking to us as these pieces are flowing luxuriously and having a conversation up until the thing got about level 15, and then they start taking it seriously. This year, we're going to have them play their version of Speed Tetris, where the gold is not to get points, but to go from level zero to 19 as fast as possible. And the winner is the one who gets the most points, but again, gets there as fast as they can. And that's important because then we have good data at the lower, slower levels from the experts that we can use to compare it to our college students. When you say good data, what kind of data are you collecting? Oh, we collect everything.

We've written our own version of Tetris, not for sale, not for distribution. We hasten to add. Nuts. We could get in trouble for that. But every single keystroke is timestamped. to the nearest millisecond, every single zoid that's on the board, every Tetris piece on the board, every configuration, we know where the holes and gaps are. We know everything and have timed everything.

So we actually can play back our log files if we want to and watch a game be played. Do you create this special game? Yes, we did. One of my former doctoral students did, John Lidd said. And actually we now have a new version because it turned out that the old version didn't incorporate the right bugs. Believe it or not, well, I guess it's easy to believe

that the people who programmed Tetris the first time around actually hadn't played Tetris themselves. Yeah. The ones in the 80s who basically created the original software. So they left behind bugs because they weren't good enough

for the bugs to bother them. And it turns out that some of these bugs, apparently, Tetris lore has it, are what the extreme experts are exploiting to get to the higher level, places where, you know, the piece is falling from top to bottom in one second. How can you do that? That's too fast for most people to actually move a piece from the center to decide. But these people have all sorts of tricks for doing that.

Well, let me ask you about that. Do you find like in all sports there are naturals at the sport? Or can you be trained to be great at Tetris? You know, until last year, I thought there was an easy answer to this question because we get it a lot. But last year, the person who won the world championship was a fellow named Joseph, who's about 17 years old at the time. And apparently he'd been playing Tetris for about the last six months. And he basically trashed the European champion, the Japanese champion, and the former world champion. So it was quite an exciting Tetris tournament last year.

So you think it's natural talent then? Well, you know, at least not for most people. Joseph may have had something else going for him, and so we're very eager to get him back. We collected some data from him last year, and we'd like to get more data from him this year to see if we can pin it down. He played a lot of music and several musical instruments,

and he thinks that may have something to do with his uncannily ability to play Tetris so well. That is interesting. I understand that your research is funded by the Office of Naval Research, Why would the department, why would the Pentagon be interested in this? Believe it or not, I get asked this a lot. And your answer is? Well, my answer is, is that there's a lot of types of expertise out there which do involve

perception and action. And we are not very good at training those things. We don't really understand what do you have to do to train such things. And the first step on that is, well, how are these, what really are these skills? What makes people so fast? How are people able to do that? So we believe that learning how people get good at Tetris and what they do when they are good at Tetris

might lead us, for example, to design better laparoscopic trainers for Navy surgeons or perhaps better displays and controls for Navy pilots. People who, you know, Navy has a heavy investment in these real-time dynamic decision-making task where you just can't sit around doing nothing. You have to make a decision.

And, you know, they have to do that everywhere in the military. Maybe their training is being applied to operating drones and making quick decisions like that or, you know, remote battlefield. Exactly. And we do have some colleagues at other parts of the country who are studying drone pilots, probably not from the level of expertise that we are. But perhaps after we get to talk to them more about our Tetris findings, they will want to bring in more expert-level drone pilots. So you don't have any idea how there is a transfer of skills here. If you're good at Tetris, you're good at something else and can be carried over. Well, think about it this way, though.

You know, if you're good at playing chess or you're good at playing go, if you're good at typing on a curtie keyboard or you're also good at writing script, the nature of expertise is that you become very, very good at something, which most people are just sort of okay at. You know, if you're good at four Olympic sports, are you also the best person for the broad jump? Probably not. The specialization seems to be the key here to getting really, really good. I mean, most people could get good at any one or two things they put their minds to.

But, you know, we just don't have the time. We don't care enough about being, you know, the world's fastest touch typist or the world's best Tetris player. Okay. Well, can you teach artificial intelligence to learn? from what these people are doing. Ah, ah. Well, as a matter of fact, my doctoral student, Catherine Seiber, has models of Tetris plane, which she has been building to try to figure out what do these models tell

us about decision-making in Tetris. Obviously, the models can move pieces at the blink of an eye, so we can't look at that component of it, but she's trying to isolate the decision-making component. itself and how much this is influenced by things like time. It turns out that when we take one of her models, which can play over a million lines of Tetris, and we say, okay, let's see how what are you doing after 500 lines of Tetris? Well, 500 is the number we picked because that's sort of the, about the highest number that we ever had a human being play in our laboratory. So for Rinsler students, surviving 500 lines would be very good. Well, it turns out that

The models that are good in human skills start looking at like humans. So the models that play forever, they do this by playing one piece at a time, only clearing one line at a time. The ones who stop at 500 lines, they're more likely to get four line clears at once, which is what's called a Tetris, and you get 7.5 times as many points as you do clearing one line four times. So it's very interesting. The constraints of the task environment, the constraints of the situation seem to force both the models and perhaps the humans to adopt similar strategies if they're only going to be playing for 500 lines. Well, Dr. Gray, I want to thank you for taking time to be with us. We're all more knowledgeable about Tetris, Wayne Gray, Professor of Cognitive Science at Rensselaer Polytech in Troy, New York. Thanks again for taking time to be with us today.

Well, thank you very much for having us. You're welcome. And when we come back, we're going to update on the state of Alzheimer's. treatments? Are we ready to let go of the amyloid hypothesis, which really hasn't led to any drugs that really, really work? We'll talk about why that is after the break, so stay with us. This is Science Friday. I'm Ira Flato. Drug companies have been on a 30-year mission to develop a treatment for Alzheimer's disease. The usual suspects behind the disease are the amyloid plaques that build up in the brains of these patients. Remove the plaques, treat the disease. Well, from any

decades, that has been the goal, and, well, it certainly hasn't worked out that way. Drug after drug targeting amyloid has failed to improve the symptoms of Alzheimer's. The so-called amyloid hypothesis was not bearing out. But drug companies, they didn't give up. They kept developing and testing drugs that attacked amyloid from every angle, even perhaps at the expense of pursuing other avenues of treatment. This past summer, two more high-profile clinical trials of drug. drugs to treat Alzheimer's to more failed. That brings the number of successful treatments for the

disease, which affects 5.8 million Americans. The number is zero. So are drug makers finally ready to move on from the amyloid hypothesis and what led pharma companies to doggedly pursue it for decades in the first place? Here to try and help us answer those questions and to give us a sense of where the field goes from here are my next two guests. Dr. George Perry, Professor of Biology at the U.T. San Antonio, an editor-in-chief of the journal Alzheimer's Disease. Welcome to Science Friday. Thank you for having me. You're welcome.

And Derek Lowe, a drug researcher and author of Science Magazines in the pipeline blog covering the pharmaceutical industry. Thank you for joining us, Dr. Lowe. Glad to be here. Dr. Perry, let me begin with you. It has been 30 years since the amyloid hypothesis was proposed. and there have really been zero successful treatments developed, you know, based on it. So how did we get there? Well, when it was first proposed, the cascade hypothesis made a lot of sense based on the genetics of the disease.

There are a small number of patients that have mutations that change the metabolism of amyloid and are associated with the chance of developing Alzheimer's disease. These are mutations in the amyloid precursor protein, pre-Cinilin-1, pre-sinillin-2. Also, the fact that Alzheimer's disease is defined by plaques and neurofibrillary tangles, which are made of another protein studied extensively called tau protein. And so the hypothesis was put forward that they were driving the disease. and also under some circumstances, amyloid can be toxic in some culture systems. We've actually, with these most recent trials, really tested the hypothesis at the most rigorous degree

because we've actually removed the amyloid from the brain of some of the patients, and they haven't improved at all. Wow. Dr. Lowe, how did the drug companies get hooked on the amyloid hypothesis in the first place? Well, it's true that it really has. has been the best-looking hypothesis for many, many years. And you have to be very careful when you're going into the field developing a drug because Alzheimer's is such a tough disease. You have to have a huge number of patients and dose them for years and years because it's so slow developing. So you have to be ready to spend at least $500 million and probably quite a bit more if you're

going to go after it. So you have to go with the most solid-looking hypothesis you can possibly find. And that's pretty much been amyloid. There are a lot of other ideas, but nothing had that foundation. That said, I think we have pretty much beaten the amyloid hypothesis as far down as it can go. So, Dr. Perry, Dr. Lowe, where do we go? What is the next best, or is there not a next best hypothesis of where to go? I would like to add that we haven't ruled out that amyloid is important in the disease. The genetics, the fact that amyloid, is both there and genetically linked to it, shows that it's an important element in the disease, but it may not be an important element for targeting drugs.

That's absolutely true, yeah. I think when we get to the final explanation of Alzheimer's, it's going to have a lot about amyloid in it, but there's something more. So we don't really understand the beginnings of Alzheimer's yet. You've got it exactly right, Ira. We don't understand the initial phase, and that initial phase doesn't just mean amyloid. It probably means something that is more linked to metabolism, more linked to the similarities with other chronic conditions. Exactly. And that's the area that we're going to have to be

able to target with a drug. Because once the damage is done in an Alzheimer's patient's brain, I don't think you're ever really going to be able to reverse that. You have to know what the initial cause is and we just don't. Yeah, I'm less certain about that about the eye. idea that the brain couldn't repair itself to some extent if you remove the driving force. Oh, that would be good. What we know about the brain is there's a tremendous amount of plasticity and reconnections that happen in drastic conditions, like in small strokes. Patients recover, and parts of the brain is dead. So I would imagine if we could remove the driver, maybe people wouldn't recover to normalcy, but they would have increased function.

Let me go to the phones because, of course, you can imagine how many people want to talk about that. Let me go to Savannah, Georgia. Hi, Rick. Welcome to Science Friday. Go ahead. When it comes to dealing with the non-familiar form of outlook any further than in nutritional, the evidence is clear that people who are EEs that form look at people who live like AD about that. Dr. Perry?

Yeah, I think this is one of the most exciting elements of Alzheimer's disease that's emerged in the last five to ten years. that similarities to conditions like heart disease, which is that diet, exercise, stress reduction, all make a tremendous differences in this. And, of course, I like your mention about the AGEs, the advanced aging medication products, because this is one of the things we identified in Alzheimer's disease almost 30 years ago. Please tell us what that is. AGEEs are products of sugars reacting with proteins. They're increased during diabetes.

They're part of the aging process, but when you have poor sugar control, such as diabetics have, that sugars react with proteins and change their characteristics so they become non-functional. It plays an important role in cataract formation. It plays an important role in skin elasticity changes. and connective tissue, like when you were talking earlier about the cartilage, those type of tissues that don't renew themselves get modified by sugars. There certainly is a connection between Alzheimer's and cholesterol because one of the only genes that we can really tie definitively to Alzheimer's risk is called APOE4,

and it is a lipoprotein handling gene makes a lipoprotein. So there's some connection there, but at the same time, All the clinical trials and real-world experience with cardiovascular therapies and cholesterol-lowering drugs haven't shown that much of a connection with reducing Alzheimer's risk. So it's complex. I'm sorry, Dr. Perry, did you want to jump in there? Well, I wanted to jump in when the person was talking about the blue zones. Those are areas in which people are much healthier than average. is also intervention studies such as a finger study, which was done in Finland.

It showed that if you change diet, you can lower your risk of Alzheimer's disease tremendously. So lifestyle plays a tremendous role in things that you can do, especially as mentioned earlier about cholesterol during middle age, obesity, etc. During middle age has a tremendous effect and your chance of having Alzheimer's disease. and studies that show that certain ethnic groups, African Americans and Hispanic Americans, are at higher risk of having the disease. All of his points to lifestyle being an important element. What about inflammation?

Doctors talk about inflammation as being important in many diseases. I would imagine you'd have to look at that for Alzheimer's also. And inflammation is tied to things like obesity and diet, et cetera. stress causes inflammation. But its direct linkage is still less clear, just like the cholesterol linkage is there, but it's not straightforward. Exactly.

Inflammation is such a common process, and it's associated with so many disease states, and indeed sometimes with aging itself, that's really hard to disentangle that. Let me go to the phones again, to let's go to Fort Dodge, Iowa. Greg, hi, welcome to Science Friday. Hi, thanks for having me.

I was a couple of months ago at the Alzheimer's Association's International Research Conference out in L.A. And they were talking about some of the different types of related dementias. One of the newest ones was limbic predominant, age-related Tdb-43 encephalopathy or late. And how much that's kind of changing our paradigm of what Alzheimer's disease is. So as we learn more about what some of these related systems are, how does that change where the research is heading and does that kind of account for, why some of the research in the past maybe wasn't as successful or maybe didn't reach the end point

is a better way to say it than what we anticipated. Dr. Perry, Dr. Lowe, how related are all of the other neural? You know that? Oh. No, go ahead. I'll let you feel that one. Okay. Well, when you have age-related dementia, there's many different diseases.

When I started in this field in the early 80s, there was sort of Alzheimer's disease and PIC disease, and that was pretty much it. Since then, we've determined a number of different diseases that are all related. And this limbic condition has just been described as a condition of older individuals, meaning over 85 years old or so. Could that be important in the clinical trials is heterogeneity? Of course it is. But even in subgroup analysis, and I think Dr. Lowe is in a better position to be able to comment

on this. It isn't, there wasn't a miraculous cure for any of the groups that have been analyzed. Well, that's absolutely true. People have gone over the clinical data looking for some sort of group that looked more likely to have benefited from any of the treatments. It has been futile. Eli Lilly spent a really inordinate amount of money going back with one of their Alzheimer's amyloid antibodies and doing the whole trial again in what they thought was a more likely group and nothing nothing worked. Let me then, in the few minutes we have remaining, let's talk about how we create a new roadmap then. What could be a new roadmap if we're not going to use the amyloid hypothesis? How do we handle this?

Hmm. That's not an easy one to answer. Yeah, that's not an easy one to answer at all. I mean, yeah. I mean, from a drug discovery and drug development standpoint, I'm going to be a little contrarian and say right now you might, if you're a drug company, you might not want to work on Alzheimer's for a bit. You might want to take that money and plow it into basic research or go off and work in other therapeutic areas where you could have a bigger impact on human health. Right now it is such a tough feel that you run a very high risk of spending a lot of money for no return. Let me just jump in and say, I'm Ira Flato. This is Science Friday from WNYC Studios. That would be an unfortunate situation that we'd have to have a hiatus on trials.

Oh, certainly. Well, if you're a drug company and you're not making any money after all this research. I mean, after all, you're in the business of making money, right? I know. I know they're in the business of making money and helping people. I think that the key thing as the field, we need to be looking at new theories for studying Alzheimer's disease. All right. Give me a couple of two or three new theory.

So, well, our own work, we focused on the issue of whether there's a metabolic element to the disease, whether it deals with mitochondrial problems and others. But one thing that we're doing together with Jim Chersard, a donor, is sponsoring a prize for new ideas in Alzheimer's disease, at which the top price will be $2 million. Excellent. There are some ideas out there, and I really am curious to see how they come out. And I think that a lot of funding should go into non-ameloid ideas. It may just be a little bit longer before someone's willing to commit the time and effort to it on drug discovery.

And as a drug discovery chemist myself, we need something to work on. We need a hypothesis that we can screen and test against. Give me one of those ideas that you have not mentioned. Well, there's one kicking around that amyloid might be a response of the brain to other stress, such as even infectious disease. I don't think there's a single infectious cause for Alzheimer's, but it might be that amyloid is sort of a side show to something else. And this needs a lot more work put into it,

but it's at least something different than the classic. There are several companies doing trials on this related to periodontal disease. Yes. Our own work, when I was mentioning in study mitochondria metabolism, we think that the amyloid is a protective response to the disease. We suggested this beginning about 20 years ago that amyloid removal will have a detrimental effect for patients because it's playing an antioxidant role. It's true. It may be that amyloid doesn't give you Alzheimer's, but Alzheimer's gives you amyloid.

Correct, and it follows the disease really well, and it was too simplistic. And why we developed this idea, we've initially pursued the amyloid hypothesis, and then as we did further experiments, we found that the amyloid was playing always a protective role to keep neurons alive. Wow. Did doctors get together and just, you know, throw out ideas about research, where we should head, they have meetings? I mean, it sounds like you could go anywhere with this. That's the good part and the bad part. Yes, but, you know, there's been a tremendous amount of orthodoxy pushing the amy amyloid idea. There was a recent article in stat talking about the amyloid cabal and dealing with

how many negative repercussions there were for people to question the amyloid hypothesis. Yeah, it's true. I mean, drug companies put a lot of money down on these ideas, but in academia, people put their careers down on them too, and it can be very hard to change course. It's very hard to come up for a new idea to break through after we've worked on something for so long, I can understand that. We come across that all the time when we talk about stuff here. But I want to thank both of you for opening our eyes to different ways of thinking that to George Perry, Professor Biology, U.T. San Antonio, an editor-in-chief of the Journal of Alzheimer's Disease,

Dr. Derek Lowe, Drug Researcher, and author of In the Pipeline Blog for Science Magazine. Thank you, gentlemen, for taking time to be with us today. Oh, thank you. Thank you. And check back with us if you come up with a great idea, okay? We'll do. Thank you. We're going to take a break.

And after the break, if you worry about air pollution in your office, you may think first about cleaning supplies, but more research is pointing to another culprit that might be you. We'll talk about why you may be the source of the air pollution after this break. Stay with us. We'll be right back. That's a Science Friday. I'm Ira Flato.

If you work in an office, you know, especially one of those big open plan ones, You might have some gripes about your coworkers. Maybe they're too loud on the phone or they leave their coffee cup in the sink instead of washing it. But new research to be presented next week to the American Association of Aerosol Research has another thing you can blame on your colleagues. Or they might blame on you. Indoor air pollution. Yep, it looks like we, just by showing up to work, are bringing with us high concentrations of volatile organic compounds. and other kinds of air pollution, from the oils in our skin to our deodorant

to the seemingly harmless act of peeling in orange. And unlike that tune as someone just put through the microwave, you're not likely to smell these. Here to explain more is Dr. Brandon Boar, assistant professor of civil engineering at Purdue University and co-author on that research. Welcome to Science Friday. Thanks, Ira. It's great to be here.

Nice to have you. Explain first what's the big deal with volatile organic compounds. What are they? Why should we be concerned? So volatile organic compounds are a class of chemicals that want to exist as a gas or vapor. And they come from many different sources in the indoor environment. We know that many furniture items and building materials and consumer products can off-gas VOCs to the air. This is fairly well established. We're also looking now at how people release VOCs into the air in an office environment. And we found that basically the human body is a big source of different types of VOCs. We call it, or we refer to it as the volatileome. So we know that there's about 2,000 VOCs associated with the human body.

We know that exhale breath contains many different types of VOCs, about 1,000. And these molecules are produced in our bodies as a result of metabolism. through bacteria in our gut, food or medicine that we may consume, as well as smoking or vaping. I'm just shocked to hear about all the things our bodies are giving off. Were you surprised at that number? You said a thousand VOCs from our breath alone? Yes, so research on exhale breath has shown that there can be about 1,000 different VOCs in our breath, which is quite fascinating if you think about it.

And I think from my perspective, I never really thought of as people as a significant source of VOCs. Most of the attention has always been on what's off gassing from the floor or paint on the walls, mattresses and sofas and things like that. But, you know, recent research has shown that really people are a pretty important source of many different types of VOCs. And that's through our breath, our skin, and our sweat, and the personal care products that we apply to our body. essentially to make us smell nice. Let's get into some of those. But let me first remind our audience,

if you want to talk about you and your skin and your air pollution in your office, our number is 844-724-8255. 844-724-8255, or you can tweet us at SciFRI. Let's get into some of those. Let's get into first what you just mentioned, some of the skincare products. What VOCs are being given off there?

So an important class of VOCs, that are released from personal care products like deodorant or lotions or hairspray are called psloxanes. And we found levels of many psiloxanes, including one called deca-methyclopentosyloxane, or D5, to peak in the morning after people walked into the office with freshly applied deodorant. And our findings are similar to a recent study at the University of California, Berkeley, where they also found these sloxanes to be in great abundance in a classroom, and to actually be the most abundant VOC released from students in that classroom. And along with psaloxanes we see VOCs referred to as monoturpians,

and these are added to these products to give them a pleasant scent, like citrus fruit, pine trees, and lavender. If enough people enter an office, a closed space with enough of this on them, could they be violating some sort of standard for VOCs? That's a good question. I'm not exactly sure about that. I don't know if there's any standards for emissions from people, but I think the concern really would be in environments

where there is a high density of people. And this would include an open plan office, a classroom. I just taught a class. We have 90 students, so you have a lot of people in a small volume of air, movie theaters, and so forth. So you have a lot of people present. We're all emitting these different VOCs. and if that particular space is not well-ventilated, concentrations can build up quite rapidly.

And as in our office, we see that concentrations of many of these BOCs can be factor 5 to factor 10, greater indoors than in the surrounding outdoor environment. I don't know how to ask this next question, gingerly, but I'm going to ask it anyhow. Are we talking about something different than body odor here? Or is this body odor basically, in essence, those smells you're talking about? Yes, certainly some of these VOCs are associated with body odor and sweat. In sweat particularly, we have a number of organic acids, acetic acid, lactic acid. But then there's others that would not necessarily detect the odor.

Their concentrations are too low. But they're still important. You know, I was surprised to see there's some interesting chemistry that happens just from peeling an orange. Yeah, so this is very exciting. So an orange, you know, in the skin contains a lot of oils. And when you peel the orange or a mandarin, you release feoces into the air. And these are called monotropines. In an orange, the prominent monoturpine is called limanine.

and limanine is very reactive of ozone. So we know ground level ozone is a big player outdoors in atmospheric chemistry, but in an office environment, it's delivered indoors through the ventilation system. And this is because we often have some amount of outdoor air that we must provide to meet office ventilation standards. So we had this ozone that's entering the office space. You peel the orange, release these terpians. The two react together, and what ends up happening is that you produce very small,

airborne particles, which we also refer to as aerosols. And this process is called new particle formation. And we know that this is very important in influencing outdoor air quality, as well as the formation of clouds. But now that we see that it can happen in an occupied office environment. So every time that we peeled an orange in the office, and my doctoral students did this quite many times, we generate a substantial number of particles on the order of tens, thousands of particles in each cubic centimeter of indoor air.

So we're essentially seeing that the VOC is coming out of the orange are reacting at the ozone, and we're creating new particles, and these particles are as small as a single nanometer, which is one billionth of a meter. Wow, let's go to the phones because they have lit up after the oranges came out. The phone's lit up. Let's go to Casey in Kansas City. Hi, Casey.

Hi, thanks for taking my call. question about possible solutions to VOCs. We know that air purifiers, you know, the machinery works, but I'd like to know both of your thoughts on moths, M-O-S, as in the stuff that grows on the ground, both real and preserved moss. I'd like to know your thoughts on the effectiveness of moths in absorbing VOCs. Good question.

Thanks, Casey. So there's a good amount of research on what we refer to as biofiltration using plants to effectively filter the air. And in biofiltration, you draw air through the soil of the plant. And it can be a complex array of plants that are growing through some sort of wall configuration. And there's a number of large-scale biofiltration systems out there. And those have shown to be somewhat effective at removing VOCs. Just having potted plants in the office space itself or any indoor environment are not going to clean the air.

So you have to draw air through the soil. When that happens, the bacteria in the soil can help break down some of those VOCs. Yeah, you talked about the problem happening when it interacts with the ozone. Ozone is everywhere in a city, right, from cars and things like that? Yep. Is there any way to filter out the ozone? So there are some... Just going to be there.

Yeah, it is challenging. And we do want to provide outdoor air to an office environment. and really any indoor environment to help dilute concentrations of VOCs and other pollutants that are generated indoors. But when we do that, we do deliver ozone, nitrogen oxides, and ambient particulate matter indoors. With particles, there's great filtration strategies

to remove them from the air. You can buy a very high-efficiency filter to capture those particles. With ozone and VOCs, it can be a little bit more challenging. There's some advanced air cleaning strategies that you can deploy in a ventilation system to help scrub out those contaminants. Let's go to the phone so everybody would like to talk about it. Joe in Palo Alto. Hi, Joe.

Hi, quick question. I keep hearing a lot about VOCs these days, and I'm curious, what are the actual demonstrated health impacts of VOCs? Good question. Yeah, that's a great question. And so we know that indoors are exposed to a complex mixture of pollutants. And this certainly includes VOCs, and there's many hundreds of VOCs, but we also have a diverse spectrum of particles, ozone, and nitrogen oxide.

So when we talk about the health effects of indoor air pollution, I always want to emphasize that we're exposed to a complex mixture of contaminants. And we need to look at how that complex mixture affects our health and well-being. With VOCs, we know there's a lot of research out there, that fragrance consumer products that we use inside, such as deodorant, perfume, air fresheners, cleaning products. They can cause headaches, chest tightness, irritation of our airways and eyes, reduce pulmonary function, and worsened asthma symptoms. These psaloxanes that I mentioned that are found in personal care products, we know that they can bioaccumulate and they're persistent in the environment. Are the emissions that people give off in a group setting?

Let's say you have a number of people together. Would it be greater than the VOCs that gets outgassed from the furniture or the carpeting? Yes, that's what we found in our particular office environment, which is in a relatively new building, that it's really the people that are driving the emissions of VOCs. And we see this because we're tracking occupancy. So we're looking at how many people are in the office throughout the day, and we're doing that by embedding, embedding temperature sensors in each chair.

So when people sit down, the temperature goes up, and we can see that they're there. So if that information, we can compare the levels of many different VOCs when there's a lot of people in the office, and then in the evening when there's nobody in there. And for many different VOCs, we see that the levels are much greater during these occupied periods. So they're coming from people from our breath, skin, sweat,

and the personal care products. And I would imagine in the morning would be the best because they're fresh, right, with all these things on their skin? Yeah, that's an interesting time because we often apply deodorant when we leave our house and go to work. And what we see in our office is that there's a spike in the concentration of these psaloxanes in the early morning. So all the students come in, in this case, we have graduate students working there with freshly applied deodorant or other personal care products, the emission spike in the morning, and then they drop off over time. And this, you know, could present a concern if you're trying to work at that point in time.

No concern that this is Science Friday from WNYC Studios. We have a submission from Phil and Auburn through our Science Friday Voxpop app, and he's more worried about the cleaning products that might enter the space after hours. For many offices, ventilation stops after hours. Then when janitors or cleaning people work, the air becomes. more polluted without fresh air entering the office. Brandon, did you do research at that, look at that possible problem? Yeah, that's a great point.

And I think Castodial staff is, you know, perhaps people that we may not think about and it's certainly very important because they are in the buildings in the late evening. And, you know, at that time, the ventilation rate often does or is reduced for energy saving purposes. So if they're using products like Pine Soll, we know that emits a lot of different. VOCs, including monotropians. And we did some measurements this past summer of researchers at Indiana University, and we tested different cleaning products, including Pinesaw,

and we see, you know, very elevated levels of VOCs. But what's also interesting is not just the VOCs, but when you have some ozone coming in to the office, the two will react, as I just mentioned, like with the orange, and you could end up forming these small particles. So sometimes with cleaning products and other VOCs, sources, you have to be concerned both about that VOC and then the reaction products that form, which may be more toxic than the VOC that was originally emitted.

Is there any metering or something I can buy and stick in my office to know if the levels are getting too high? Yes, there's a lot of focus now on low-cost air quality sensors. For VOCs, there's nothing that's really going to speciate and tell you that different types of VOCs that are present. We have sensors that can give you a rough indicator about the total mass of VOC in the office space or any indoor environment. But I would say that those are not terribly reliable. In our particular study, we used a very expensive instrument that, you know, is for research purposes, that tells us all the different VOCs that are in the air and, you know, separates them very

nicely. One last question. Quick question from Sunny in Pittsburgh. Sunny. Sunny, are you there? I think the lights went out on that call. Sunny wanted to know, what are the top three things we can do? Oh, that's a great question. So I would say that the best strategies for maintaining good indoor air quality in your home or your office, the first is to minimize the sources of indoor pollutants, to minimize the emissions. In an office environment, that's challenging if people are producing a lot of the VOCs. But if you're looking at personal care products or scented products, you could try to find products that emit less quantities of VOCs.

The second thing we can do, and I think this is often very effective, is to improve the ventilation of the building, basically allowing the indoor space to breathe better. And we can do this by providing greater quantities of outdoor air, and this air should be filtered. and then, you know, an environment like an office or classroom, the amount of ventilation that you provide should be scaled with occupancy. So if people are a source of EOCs and there's more people in the room, we should provide more outdoor air. And the last thing?

The last thing would be filtration and air cleaning. So you can go to your home improvement store and buy a high efficiency filter to capture particles. You can use a portable air purifier in your home or office. and then perhaps some other air cleaning technologies in the ventilation system. Dr. Bore, you've been very helpful. Brandon Bore is Assistant Professor of Civil Engineering at Purdue in West Lafayette, Indiana. Thank you very much for taking time to be with us today. Thanks, Ira. It's great to talk to you today.

Nice to have you. You're welcome. One last thing we want to hear your voice on Science Friday with the Science Friday Vox Pop app. We've been asking you if you thought about relocating due to flooding, fire or other climate change-related hardships. Now we want to know from those of you who have relocated, how did you manage it? Was it easy or hard when you relocated? Let us know on the Science Friday Vox Pop app wherever you get your apps.

We want to know from those of you who have relocated, how did you manage it? Was it easy or hard on our Science Friday Voxpop app wherever you get your apps? Have a great weekend. We'll see you next week. I'm Ira Flato in New York.