Hello and welcome everyone. My name is Dane Menke. I am the digital marketing manager here at Regenesis and LandScience. Before we get started with the webinar today, I have just a couple of administrative items to cover. Since we’re trying to keep this under an hour, today’s presentation will be conducted with the audience audio settings on mute. This will minimize unwanted background noise from the large number of participants joining us today. If the webinar or audio quality degrades, please try refreshing your browser. If that does not fix the issue, please disconnect and repeat the original login steps to rejoin the webcast.

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Today’s webinar will focus on the link to Parkinson’s disease resulting from chlorinated solvent exposure on a large U.S. Marine base. With that, I would like to introduce our presenters for today. We are pleased to have with us Dr. Samuel Goldman, professor in the Division of occupational, environmental, and climate medicine at the University of California, San Francisco. Dr. Goldman is also an investigator at the San Francisco VA healthcare system where he previously ran an environmental medicine clinic. He studied neuroscience at the University of Michigan, attended medical school at the University of Texas Houston, and trained in preventive medicine and environmental health science at UC Berkeley. He has published extensively on the epidemiology of Parkinson’s disease and other neurodegenerative disorders with a focus on environmental risk factors such as pesticides, solvents, and head injury and their interaction with genetic susceptibility factors.

We’re also pleased to have with us today, Ryan Miller, Director of Land Science. Ryan Miller oversees the overall operations and strategic direction of the division, ensuring the successful design, installation, and implementation of vapor mitigation systems including TerraShield, NitroSeal, MonoShield, and RetroCoat. He provides technical support, fosters collaboration, and drives advancements in vapor intrusion barrier technology. With extensive experience in the environmental consulting industry, he previously worked as a New Jersey licensed site remediation professional, focusing on Brownfield redevelopment projects and specializing in vapor intrusion mitigation. Ryan earned an MBA from Montclair State University Bachelor of Science degree in Environmental Science from Siena College. All right that concludes our introduction so now I will hand things over to Dr. Samuel Goldman to get us started.

Thanks very much. Thanks to Regenesis for inviting me to present some of our work relating to trichloroethylene and Parkinson’s disease. I have no disclosures relevant to today’s topic. A brief outline of what I’ll be presenting today. I’ll quickly go through a description of Parkinson’s disease, what it is, some of the descriptive epidemiology and the environmental epidemiology very succinctly. Then I’ll move into TCE and Parkinson’s disease, some of the earlier studies. Then I’ll talk about our work studying the relationship in Camp Lejeune and some animal studies and mechanisms of toxicity. And I’ll finish up with some background on TCE’s historical uses and ongoing exposures.

Here are some video examples of Parkinson’s disease, which is characterized by Parkinsonism, which is a clinical syndrome of bradykinesia, resting tremor, rigidity, and postural reflex impairment. In the upper right in this relatively low-quality video, sorry for that, you can see Gradykinesia, which is this extreme slowness of movement or paucity of movement, akinesia. In the bottom left, you can see the classic resting tremor. It’s a very characteristic frequency. It’s called a pill rolling tremor. And it’s typically asymmetric, at least at some point during the course of the disease. And here you can see this man is more severely affected on the right side. he also has a tremor of his jaw. On the bottom right is one of the more disabling features of the clinical syndrome. It’s the postural reflex impairment, and here it’ll go from examples of mild to severe. So this is the inability to adjust to perturbations in posture.

You can see increasingly severe examples. In this final example, this woman is extremely impaired. This very advanced disease, and she has no ability to keep herself upright with even the slightest perturbation. The neural substrate underlying Parkinsonism is disruption of dopaminergic transmission in the nigrostriatal system in the brain, and I’ll talk a little bit about that. Very briefly, the epidemiology of Parkinson’s. It’s the most common cause of Parkinsonism. There are other causes, I’ll talk a little bit about those, but we’re really interested in Parkinson’s disease here. We think it’s been around for a while. There are descriptions going back 800 years in Spain and in some ancient Indian texts that seem to reflect descriptions of Parkinson’s disease, but it wasn’t described fully until about 200 years ago by James Parkinson, and this is one of his monograph drawings in the upper right corner.

Parkinson’s currently is thought to affect around a million people in the U.S. It has approximately a 2% prevalence over age 65, and you can see here in this chart of incidents that is quite rare before age 50 and then increases exponentially after that. At all ages, men are more frequently affected than women, and probably whites are more frequently affected than so that’s not entirely certain. As I mentioned, the Parkinsonism is due to a loss of dopaminergic neurons in the brain. So on the left is a healthy neuron with lots of vesicles full of dopamine. In Parkinson’s disease, in this cartoon here, you can see the loss of neuron cell bodies in the substantia nigra pars compactus, sliced through the midbrain. These are pigmented neurons. It’s called the substantia nigra because it’s the black substance that’s pigmented with neuromelanin, which is a metabolic byproduct of dopamine breakdown. And with Parkinson’s disease, there are fewer and fewer of these neurons, less and less dopamine. And there’s also accumulation of aggregates of alpha-synuclein protein that clump up to form Lewy bodies in the affected dying neurons. And I’ll talk more about that in a minute.

This is a gross anatomy section of what we just saw in a cartoon form. This is a normal brain stem here. You can see quite a bit of black substance in the substantia nigra. In a patient with Parkinson’s disease, you can see nearly complete loss of that pigmentation. And this is what a Lewy body looks like. This is an inclusion in a dopaminergic neuron cell body, and it’s comprised predominantly of alpha-synuclein protein. Here you can see little granules of neuromelanin that tells us that this is indeed a dopaminergic neuron. But even though this sort of pathology affects the substantia nigra, we know now that Parkinson’s is a systemic disease. They’re sustaining for alpha-synuclein pathology in the gut, in the myenteric plexus, and they’re sustaining for alpha-synuclein pathology in the olfactory bulb. And the symptoms of Parkinson’s disease are also systemic and not just related to movement.

This is really key in Parkinson’s disease epidemiology is that it’s got a very long evolutionary period. So we know that this is the point when the diagnosis occurs based on the symptoms that I talked about, bradykinesia, rigidity and tremor. But five to 30 or even longer years before the diagnosis, we know there was an ongoing disease process and there are symptoms that manifest prior to the motor symptoms, including things like REM sleep behavior disorder, which is a sleep disturbance, constipation, depression, loss of sense of smell as we get closer to the diagnostic period. Parkinson’s disease is the world’s fastest growing in number brain disorder.

Diagram on the left shows the growth in the largest countries from 2005 to 2030, so it’s more than doubled in Brazil, China, and India, and Indonesia here and increased substantially in most other developed countries. We think that by 2040, there will be around 17 million cases of Parkinson’s disease in the world. That is up about sevenfold from 1990. So very briefly, I’m going to talk about what we know about the causes of Parkinson’s disease. The debate as to whether Parkinson’s is predominantly genetic or environmental has been going on for well over a hundred years. Sarico thought that it’s not a familial disease, Gowers thought that perhaps it is a familial disease, and in fact a large Italian-American family called the Cantorzi kindred was identified during the 1990s that had autosomal dominantly inherited Parkinson’s disease, so a large number of affected individuals, and by studying this or investigators were able to identify that they had a mutation in the alpha-synuclein gene.

Turns out this mutation is extremely rare, but what we learned from this study is that alpha-synuclein is indeed the protein that accumulates in all forms of Parkinson’s disease. Later, over the past couple of decades, several other so-called Mendelian mutations have been identified, meaning these are mutations where there’s a clearly identifiable pattern inheritance, they’re highly penetrant. But the most common of these is only about 1% of Parkinson’s disease. And since then, there’s been a lot of focus on what are called genome-wide association studies, which look for single nucleotide polymorphisms, so a common variance in about 90 genes that very slightly increase Parkinson’s disease risk. But we don’t think Parkinson’s disease is largely a genetic disorder, and I’ll show you several lines of evidence to support that environment is the predominant determinant of disease risk.

So first of all, genetic diseases, incidence does not increase dramatically over time unless there’s some huge competitive advantage to having that mutation, and with late-life diseases that’s not going to be the case. This is a study from Olmstead County, the Mayo Clinic in Minnesota, showing that there’s been about a 20% increase in Parkinson’s disease age-adjusted incidents per decade over the past 30 to 40 years. So this is not due to aging of the population. Another line of evidence comes from twin studies. Our group conducted two studies in about 32 ,000 twins. This is a really interesting cohort that was put together by Michael DeBakey, the heart surgeon back in the 1950s. The idea here is that identical twins, monozygotic twins, share 100% of their genes. Fraternal or dizygotic twins share about 50%. So if a disease is primarily genetic, then concordance, that is both twins having the disease, should be much more frequent in identical twins than in fraternal twins. And what we observed is that for disease onset under age 50, which I showed you before, is quite rare. There is indeed a high genetic heritability.

But for typical disease onset over age 50, heritability was only around 20%. So the conclusion from this is that environment is the major contributor to typical Parkinson’s disease. And an interesting observation here is that there was relatively high concordance in the dizygotic twins, so around 13%, and they’re actually no more genetically related than typical siblings, and in typical siblings we see about 4% concordance. So this implicates shared early environmental factors.

The final line of evidence I’m going to show you to support that environment is the key determinant is this little video, again I apologize for the poor quality, this is back from the mid-80s. And this is a group of individuals who began showing up to emergency rooms in Silicon Valley in the mid-80s. You can see bradykinesia. You can see this is cogwheeling rigidity. And if you’ll think back to the videos I showed you earlier, here we have an asymmetric resting tremor. Looks very much like Parkinson’s disease. And it responds to levodopa, which is the primary treatment for Parkinson’s disease, as you can see here. This is the gentleman for levodopa treatment, and the next, this is shortly after levodopa treatment, and his movements are fluid and rapid, and he’s able to smoke, which people did in hospitals back in the 80s, as some of us will recall.

So what is that? Well, that is not Parkinson’s disease. That is intoxication with methyl phenol tetrahydropyridine, the molecule shown above. This was identified by Bill Langston back in the 80s. So challenges in studying neurodegenerative diseases is that there are few or no diagnostic tests, currently at least, although this is changing, we hope. The misdiagnosis rate in Parkinson’s is really, really high, which complicates epidemiologic studies. It’s clinically variable, it’s pathologically variable, we think it’s etiologically heterogeneous, and one of the biggest impediments is that exposures may occur decades before symptoms manifest. So this is an incredibly brief overview here of what we know about Parkinson’s disease environmental associations. These are some factors that with some degree of consistency have been shown to increase risk for PD. Those that are bolded have stronger and more consistent evidence and factors that are associated with reduced risk.

So increased risk associated with certain pesticides, particularly paraquat rotenone and several others, solvents, which I’ll be talking about shortly, several other factors, and then reduced risk, which is associated with cigarette smoking, unfortunately, and coffee and tea drinking and their clear dose response relationships with those in reducing risk.

So let’s get to the meat of our topic today, TCE and Parkinson’s disease. Solvents and Parkinson’s disease have been studied for a while and we’ve known that acute solvent intoxications can cause Parkinsonism, but these are not Parkinson’s disease. They are generally there’s much more diffuse damage to the central nervous system and Parkinsonism is just one of many characteristic features of these acute intoxications. Associations with PD per se are not consistent, but there are real problems with most of the studies of solvents that have been done to date and specific compounds have rarely been studied. Oftentimes, the study will ask a question such as, have you ever been exposed to solvents? And as you can imagine, that’s not particularly useful. People don’t know what they’ve been exposed to, and there’s a lot of misclassification.

So this is, I’m not going to spend any time on this, but this just shows that there’s quite a lot of variability in studies to date that have looked at solvents, but as I mentioned, these very rarely have specific agents been looked at. This changed back in 2008 when a PD cluster was identified by Gash et al. in a small Kentucky plant with about 30 employees and he was an astute clinician and noticed that several of his patients worked at this plant. There were three co-workers with Parkinson’s disease and he went out to the plant to examine co-workers and noted that 14 others had some mild Parkinsonian signs, and the work environment was in close proximity to a vapor degreasing tank that was filled with trichloroethylene.

The way these work, they’re very common. There’s TCE down here at the bottom in liquid form. There’s a heating coil here, heats up the TCE into a vapor form. You lower down whatever you want to de-grease into this area, and the grease strips off. They come out nice and clean, and then up here at the top of the tank, there’s a cooling coil, and the TCE condenses out drops back in to solution. But a lot of it escapes into the room. So we thought this was an incredibly interesting observation and we had the opportunity to investigate the TCE association in our twin study. So we had conducted very detailed occupational history in twins with Parkinson’s disease and their co-twins without. So we looked at 99 discordant pairs and we assigned exposure to six solvents in a blinded fashion by an industrial hygienist who was unaware of case status, and this is the results of that study. So we found a six-fold increased risk of Parkinson’s disease in the twin who had worked with TCE or with PCE, tetrachloroethylene.

Other solvents imparted mild increased risks, but those were not statistically significant. And so some work has been done in animals back around that time, and it was observed that TCE administered orally to rats caused a dose-related degeneration of dopaminergic neurons in the substantia nigra. On the left, this is a stain for dopaminergic neurons. It’s a tyrosine hydroxylase, and you can see this is a control animal, and this is the TCE-treated animal, and you can see the profound loss of dopaminergic neurons. And this is very specific, so unlike those and solvent intoxications. And we think that a possible proximate toxicant is a compound called Taeclo that forms from TCE and PCE in neurons that have CYP2E1. And it’s been shown that Taeclo forms spontaneously in rat brain after TCE dosing. And I’ll talk more about that later, but you can see structurally Taeclo is rather similar to the toxin MPTP that I showed you earlier.

So let’s get to Camp Lejeune. Camp Lejeune had a water supply that was contaminated with TCE, PCE, vinyl chloride and benzene and several other compounds from 1953 until the late 1980s. The contaminants were discovered in the 80s and the wells were closed in 1987 and subsequently became an EPA Superfund site. Camp Lejeune is one of the largest Marine Corps bases in the country, about a third of all Marines rotate through here at some point during their training. And the levels of toxicants in the water were extremely high. From 1975 to 85, the TCE level was more than 70-fold, and this is median, levels at some areas on the base were more than 70-fold, the EPA maximum contaminant level. And PCE was about 17-fold higher. Those were the primary contaminants. and over a million were exposed during this period. Could have been oral exposure or inhalational or even dermal.

In 2017, the VA determined that Parkinson’s disease was a presumptive service-connected condition for vets who had been stationed at Lejeune for at least 30 days, and vets are entitled to benefits and families to healthcare coverage. But at the when this determination was made back in 2017, the total human epidemiology amounted to around 16 reported cases. So we tried for a while to get funding to conduct this study and finally did thanks to the VA, and this work was recently published in JAMA Neurology in May of 2023. So our specific aims were to determine if PD risk was higher in Marines who served at Camp Lejeune compared with those who served at a presumably uncontaminated base at Camp Pendleton, another large Marine Corps base. And we also wanted to study whether risk of some of the PD prodromal features, I showed you that very long developmental phase before PD is diagnosed. So we wanted to study if those might be more common in Camp Lejeune as well.

The cohort was established by the Agency for Toxic Substances and Disease Registry, or ATSDR, And they had identified about 170 ,000 individuals at Lejeune as well as at Pendleton, who had lived at those bases between 1975 and 1985. And they also did some exposure modeling and reconstruction of exposures so that they could construct residence-specific and time-specific estimates of peak and cumulative exposures to TCE in individuals who resided at Lejeune. So we took advantage of all the work that they had done before us. We ascertained our cases by doing a search of the VA electronic medical record databases and also Medicare. We searched for ICD-9 and 10 codes for PD and other forms of neurodegenerative Parkinsonism. We also searched for PD-related medications and exclusionary codes such as secondary Parkinsonism caused by various medications. And then we validated the diagnoses by reviewing all the medical records for these individuals.

In our analysis, we did a logistic regression adjusting for age, sex, race, ethnicity, rank, smoking, and head injury. And we did a number of sensitivity analyses to try to ensure that our results were valid and not due to various sorts of statistical and epidemiologic biases. So here demographic characteristics of the population, we had healthcare data available for 160 ,000 or so. You can see that demographically, those at Lejeune and Pendleton were quite similar. Their attained age was around 60, so still relatively young for the PD incidence curve that I showed you, mostly male. And just note that the average time living on the base was just slightly more than two years. We reviewed over 1 ,500 medical records and of note, only 46% of individuals who had a PD diagnostic code actually ended up having PD after further review.

So highlighting the difficulties conducting these studies. We found a total of 430 individuals at both bases with Parkinson’s disease. And we found that those who had resided at Camp Lejeune had about a 70% higher risk of having Parkinson’s disease than those who had resided at Camp Pendleton. And importantly, the latency, the time between exposure and disease diagnosis was nearly 34 years. Similarly, we found increased risk of prodromal PD-related diagnoses at Lejeune. So there was a higher risk of tremor, there was a higher risk of olfactory impairment, erectile dysfunction, anxiety, and seborrheic dermatitis, and these are all characteristics and diagnoses that we see during the prodromal period of Parkinson’s disease. So, and overall, individuals at Lejeune had about a 20% higher risk of having a likely prodromal PD diagnosis. So, emphasizes the need to continue studying this cohort that is at risk for Parkinson’s disease.

In recent subsequent work, We also studied whether individuals who had higher levels of exposure to TCE and other volatile organic compounds in water at Lejeune might have a more rapid course or a more aggressive phenotype to their Parkinson’s disease. So the hypothesis is that individuals exposed to these environmental agents might have a more severe form of Parkinson’s disease. We did time to event analyses, looking at individuals who, based on the ATSDR estimates, were ever exposed or never exposed to these compounds in residential water. And we looked at outcomes that we could relatively easily ascertain from the medical record. So time until psychosis, which is a common long-term outcome in Parkinson’s disease, time to falling, time to fracturing, and time to death. And this is a survival curve. If you’re not used to looking at these, basically this is how many individuals developed psychosis over time. Time is down here. So this is a thousand days, 2 ,000 days, 3 ,000 days.

And in this, we’re looking at time to psychosis in exposed individuals, but in the red curve and unexposed in the blue curve. And you can see clearly that those who had been exposed two residential contaminants had a faster progression to psychosis. They had a faster progression to time until first fracture and time until first fall. And this is time from the Parkinson’s disease diagnosis. So ultimately, we also identified an apparent dose response. So, individuals who had with a comparison to no exposure, low exposure, and high exposure, we found a increasing risk of psychosis with greater exposure, an increasing risk of fall, and an increasing risk of fracture. So, this very strongly supports a true biological mechanism underlying these observations.

The strengths and limitations of the studied strength It’s very large and the PD diagnosis was validated by chart review, which is really important in these types of EMR-based studies. And we had unbiased exposure determination, so the individuals at Lejeune who in the progression sub-study had no idea what their exposures were, so it was unlikely to bias that. Possible limitations relate to ascertainment bias because the people at Lejeune are aware that PD is a presumptive connected diagnosis and that they may be at greater risk. So we tried to deal with that by truncating observations and sensitivity analyses where we only looked at individuals whose PD onset was before that determination was made by the VA. We don’t think that that ascertainment bias is likely to explain the associations with prodromal PD because those individuals don’t have Parkinson’s diagnosis yet. And the progression sub-study, I think, is very convincing that bias is not underlying these observations. Then finally, the exposure estimates were very imprecise.

So we had estimates for residential water exposure, but clearly people would be exposed anywhere on the base where they worked or where they exercised. And though TCE was the highest concentration organic compound, other compounds or mixtures may be important. So in conclusion, we found that there was a 70% higher risk of Parkinson’s in individuals who had resided at Camp Lejeune when these levels of TCE were very high in the drinking water. It’s important to realize that this was relatively brief exposure. So only 25 months, there was a very long latency, which is typical for Parkinson’s disease environmental risk factor associations. And we think that TCE exposure may cause a more severe form of Parkinson’s disease. And this adds to a growing body of human epidemiology, animal modeling, and mechanistic data that implicate TCE in Parkinson’s etiology.

So what we know about mechanisms, we know that MPTP is a mitochondrial poison. It is a very potent inhibitor of mitochondrial complex 1. Rotenone similarly affects complex 1, one of the pesticides that’s associated. Paraquat is toxic to mitochondria, and we think now that TCE and PCE, perhaps through this takelo, intermediate are toxic to mitochondria, and takelo is a very potent complex 1 inhibitor, just like MPTP and rotenone. So why is this important? TCE is in the environment. It has been used for over 100 years now. It’s largely now used predominantly for degreasing metal parts, but it’s been used for lots of other applications. It was the primary dry cleaning solvent during the 1950s. It was used as a surgical anesthetic until the late 70s and even later in Great Britain, and particularly as an obstetrical anesthetic. It was used to decaffeinate coffee through the 1970s, and lots and lots of household products contained it.

Perhaps most importantly, it was and is one of the most frequently reported organic contaminants in groundwater supplies in the US and subsurface so-called plumes are very common with potential vapor intrusion into homes. So here’s a plume in Tucson, here’s a plume in Dayton, Ohio, a plume in Brooklyn, a plume in Minneapolis, a plume in Mountain View, California. So these plumes are all over the place. Basically, if you look, you find, and they travel in subsurface soils and persist for a very long time. And this here, I just pulled down from the EWG Environmental Working Group website, and it’s a compendium of TCE and public water supplies from 2019. You can see here in the legend, the larger the circle, the larger the population that is affected, and the darker the color, the higher the concentration of TCE in the public water supply.

This is back in just in 2019. So this is not just a problem for people who work with TCE. This is not just a problem for people at Camp Lejeune. This is a problem that is very, very widespread. The final thoughts on this data and on our studies, there’s converging evidence that strongly implicates TCE as a cause of Parkinson’s disease. The Lejeune cohort is still relatively young and continued follow-up is extremely important, particularly given the observations of higher risk for prodromal PD features. There’s a pending EPA ban on TCE that we certainly hope will not be derailed by the new administration. It’s a major step forward, but millions have been exposed, and you saw the 30-year latency is key, and millions will continue to be exposed through prior contaminations of air, water, and food.

I want to take a moment to acknowledge our funder on this project, which is the VA CSR &D and co-investigators at UCSF, the Heinz VA, and I particularly want to call out Frank Bovee at the ATSDR, who was a huge help in us getting this study underway. And now I’ll hand things over to Ryan Miller, and I’ll be happy to address any questions after he speaks.

All right. Thank you, Dr. Goldman.

So I’ll take this time to with the discussion to something you know we at Regenesis are very proud of and that is developing advanced remediation and mitigation technologies which are specifically designed to protect communities and the environment. So for many of us in the environmental field you know we face projects with these types of contaminants on a daily basis but I think the conversation that we just heard brings it into sharper focus the importance of the work that we do every day. At Regenesis, we understand the critical need to address chlorinated solvents in groundwater and to mitigate risks associated with the exposure to some of these chemicals like TCE.

So to that end, we’ve developed a suite of innovative technology specifically designed to target chlorinated solvent contamination in soil, groundwater, soil vapor. These technologies include colloidal amendments engineered to overcome subsurface challenges. really, with the goal of enhancing distribution, reactivity, persistence, which allows us to effectively address contamination at key points along the plume. In addition to that, Land Science, a division of Regenesis focused on vapor intrusion mitigation, has developed a suite of technologies designed to mitigate vapor intrusion for all building types, including new construction and existing structures. And I think this graph helps illustrate the comprehensive range of solutions available from Regenesis and land science. And the reason why we have such a comprehensive range of technologies is because our work has been built on 30 years of continuous innovation.

We’ve been at the forefront of developing technologies that address complex contamination challenges, particularly chlorinate solvents like TCE. And I think what sets us apart is our commitment to research and innovation. So PlumeStop as an example, a liquid activated carbon. This technology has been critical in treating thousands of chlorinated solvent impacted sites with proven results since its inception. And the reason we’ve been so successful in remediating CVOC sites is due to our focus on colloidal amendments, which have been specifically engineered to overcome challenges by Improving distribution, so remember, this is a contact sport, reactivity, quicker cleanups, longevity to ensure long-term effectiveness, and compatibility.

I mean, really, at the end of the day, our goal is to maximize distribution, increase reactivity and persistence, and ensure compatibility at diverse site conditions with the goal of a single application to achieve the cleanup goals and achieve those cleanup goals sooner and ultimately reduce the total project cost. So from a strategic perspective, these technologies can be applied at critical locations along the plume, whether that’s source zones, hot spots, plume boundaries. This allows us to efficiently achieve stringent cleanup goals, protect things like drinking water resources, which we just heard about, and really helping to eliminate the exposure to these harmful chemicals.

So with advancements in colloidal amendments, we not only achieve successful remediation, but also prevent exposure pathways that could harm people and their communities. So doing this by effectively targeting plumes from source to plume boundaries with single batch treatments, we could achieve concentration reduction within days, get reliable performance over decades, addressing rebound concerns, and stack colloidal technologies to ensure low regulatory standards are met.

And this brings us to vapor intrusion mitigation. While groundwater contamination serves as really the primary driver for site remediation, vapor intrusion poses an equally significant risk. Through cracks in foundations, utility penetrations, TCE and other contaminants can enter indoor air, creating direct exposure risks for building occupants. So at LandScience, we’re proud to maintain our position as an industry leader in providing innovative and reliable vapor barrier technologies. We offer mitigation options for new construction and existing buildings, complete with QAQC programs to ensure the barrier is installed properly and is functioning as designed. Our systems are proven to mitigate against CVOCs like TCE and other harmful contaminants like methane and radon.

So whether that’s new construction, as seen here, utilizing a spray applied vapor barrier system, or applying a concrete coating vapor barrier, such as retro coat, as you can see in this photo, land science has technologies that will fit almost all scenarios. And when looking at the evaluation of vapor barriers, we at land science often talk about two main areas. chemical resistance, how well the vapor barrier will block the vapors, and constructability, how easily is it installed. And the need for a vapor barrier to be chemically resistant may seem obvious, right? And this is often the first criteria that design engineers and regulators look to when beginning the vapor barrier selection process. And rightfully so.

A vapor barrier that is specified for a project should have testing showing the barrier’s ability to limit diffusion of contaminants. Contaminants like petroleum hydrocarbons, methane, or TCE, as we’ve been discussing today. So how do we know the vapor barrier technologies will work and perform as needed? Well, we test them. This is an example of the equipment we use to simulate a saturated contaminant vapor condition. You’re looking at a two chamber active diffusion testing platform, which is designed to set up and test the relative performance of really any barrier or material that we can put into that small black compartment between the bottom and top chamber.

So like I said, this setup is designed to simulate a real-world VOC condition. So in that bottom chamber, we would introduce a challenge concentration, TCE, into the water and allow it to reach equilibrium with the air in the bottom chamber. So, vapor conditions in both top and bottom chambers are sampled over a period of time to measure the mass flux of contaminants across that membrane. And once we know the mass of contaminants that have migrated across that membrane, we can then calculate a diffusion coefficient to observe its relative performance. And from that point, we have a critical tool for advancing our understanding and evaluating the performance of our vapor barrier and mitigation systems.

So again, just to reiterate, it’s really important that the vapor barrier system that you’re using or that you may propose has the appropriate testing behind it. So all of land science vapor barrier options do have TCE-specific diffusion coefficients. And so I’ll wrap on that note, but in closing, I think we all understand the importance of protecting human health and the environment. And there are remediation options and vapor mitigation tools that make this a reality. We can address contamination and prevent exposure to harmful chemicals like TCE, which we’ve discussed today.

So thank you all for joining. And I am also happy to stick around for questions.