On Jan. 7, two residents on opposite sides of Altadena — Francois Tissot, a Caltech professor who studies the geology of ancient Earth and our solar system, living in the east side of town; and Jane Potelle, an environmental advocate living in the west side — fled the intensifying red glow of the devastating Eaton fire.

The inferno devoured home after home, unleashing what experts estimate to be tons of dangerous metals and compounds, from lead to asbestos to the carcinogen benzene. Carried through the vicious winds, the toxins embedded deep into the soil, seeped into the blood of first responders, and leaked into structures in the area that hadn’t burned down.

Within weeks, Altadena residents whose homes had withstood the fire began to return — yet few were testing for contaminants both Tissot and Potelle knew were almost certainly sitting in their still-standing houses.

Working independently, they both decided to create a comprehensive picture of the contamination lurking within surviving homes, both in the burn area and miles outside it.

They came to similar results: In the houses inside the burn zone, there was lead — a metal capable of dealing irreversible damage to the brain and nervous system — at levels far exceeding 100 times the Environmental Protection Agency’s allowable limits. Tissot’s group also found lead levels exceeding the limit over five miles from the fire’s perimeter.

“Children exposed to lead will have diminished cognitive development,” said Tissot, referencing studies that found exposure to leaded gasoline in though the 1990s was correlated with a drop in children’s IQ (an imperfect but useful metric for reasoning ability) by up to seven points.

“To me, what’s at stake is the future of a generation of zero- to 3-year-olds,” Tissot said. “If nothing is done, then these children will be exposed. But it’s totally avoidable.”

Potelle, frustrated with the lack of government response to contamination concerns, started a grassroots organization with other Altadena residents with standing homes to collect and publish tests conducted by certified specialists.

The organization, Eaton Fire Residents United, or EFRU, found lead in every single one of the 90 homes for which they’ve collected test results. Of those, 76% were above the EPA limits.

EFRU and Tissot’s team were distressed by these data, particularly seeing debris-removal and remediation contractors work without masks in the burn area and some residents even begin to return home.

In early April, Anita Ghazarian, co-lead of EFRU’s political advocacy team, went back to her standing home within the burn zone to pick up mail. She watched as a grandmother pushed a toddler in a stroller down the street.

“She has no idea … this area is toxic,” Ghazarian recalled thinking. The gravity of the situation sunk in. “To me, it’s just — unfortunately — a calamity waiting to unfold.”

Evidence mounted in the 1950s that even small amounts of lead exposure could harm children’s brains. But by the time the U.S. banned lead in paint in 1978, roughly 96% of the homes in Altadena that burned in the Eaton fire were already built. In the Palisades, that number was 78% — smaller, but still significant.

Jared Franz looks at the state of his kitchen, which survived the Eaton Fire, but is inhabitable due to smoke damage.

(William Liang/For The Times)

Dust from the fire inside the Franz family’s home.

(William Liang/For The Times)

After the Eaton fire, Tissot did a quick back-of-the-envelope calculation to understand what his Altadena community might be dealing with: roughly 7,000 homes burnt with 100 liters of paint per house and 0.5% of that paint likely made of lead.

“That’s something like several tons of lead that have been released by the fire, and it’s been deposited where the fire plume went,” he said.

As the Eaton fire roared in the foothills of the Angeles National Forest the night of Jan. 7, Tissot fled with his two kids, along with the rest of east Altadena.

Meanwhile, Potelle sat awake in her living room on the west side of town, listening to the howling winds as the rest of her family slept.

When Potelle got the evacuation order on her phone around 3:30 a.m. Jan. 8, her family joined the exodus. As they raced to gather their belongings, Potelle grabbed protective goggles she had bought for her son’s upcoming Nerf-battle birthday party.

Even with them, the soot, smoke and ash made it impossible to see.

The family made it to a friend’s house in Glendale, but as the toxic smoke plume swelled, Potelle had to evacuate yet again, this time to a friend’s garage. Tissot, then in Eagle Rock, left for Santa Barbara the next day as the smoke’s incursion progressed southwest.

As Altadena turned into a ghost town on Jan. 9, some residents — including Potelle’s husband — crept back in to assess the damage. Potelle waited for her husband’s report and watched on social media from the safety of the garage.

“People are just videotaping themselves driving through Altadena, and it’s block after block after block of burnt-down homes. The reality of it started to strike me,” Potelle said. “This is not just carbon. This is like, refrigerators and dishwashers and laundry machines and dryers and cars.”

Fires like these, with smoke made of car batteries, paints, insulation and appliances — and not trees and shrubs — are becoming increasingly common in California. These fuels can contain a litany of toxic substances like lead and arsenic that are not present in vegetation, waiting to be unlocked by flame.

Potelle’s home sustained visible smoke damage. So, she made two trips to a disaster support center set up temporarily at Pasadena City College, hoping to get support from her insurance company and the government for soil and in-home contamination testing.

Officials directed Potelle back and forth between her insurance company, FEMA, the L.A. County Department of Public Health, and the California Department of Insurance. Potelle — who, at this point, had already started to develop a cough and chest pain, which she suspects came from her visits to the burn area — left with without clear answers, feeling dejected.

“I’m driving, going back to my friend’s garage … and I’m just realizing there’s no one looking out for us,” she said.

Potelle set out to find the answers herself.

“Here’s the thing, if you don’t know what’s in your home when you remediate, you could just be pushing those contaminants deeper into your walls, deeper into your personal items,” Potelle said.

Tissot, meanwhile, visited his home a week after the fires to find the windows exploded, melted or warped; the walls cracked; and ash and soot everywhere. He too decided that he ought to do his own testing for contamination.

In his day job, Tissot runs a lab with sophisticated machinery able to discern what metals are present in samples of material, usually comprised of rock and dirt, based on their atomic mass: Only lead has an atomic mass of 0.34 trillion billionths of a gram. He normally uses the machine to study rare elements and isotopes from space and eons ago.

He gathered his lab team together on the Caltech campus to use the equipment to test samples from their own backyard.

The team took 100 samples from windowsills, desks and stairwells in the Caltech geology and planetary science buildings. Some surfaces were untouched since the fire; others had been cleaned by Caltech’s trained custodians.

The team found multiple uncleaned surfaces with lead levels above the EPA’s limits. And while the cleaned surfaces had about 90% less lead, some still exceeded the limits.

Tissot quickly set up a webinar to announce the findings. The chat exploded with requests from homeowners in Altadena asking Tissot to test their houses.

Around the same time, Potelle noticed some folks on Facebook sharing the results of in-home contamination testing — which in many cases, they had paid for out of pocket.

Inspired, she advertised a Zoom meeting to discuss a strategy for mapping the test results. Sixty residents showed up; Potelle coordinated the group so that residents could submit results to EFRU’s Data Unification team for analysis.

Meanwhile, Tissot connected with residents who messaged him to set up a testing campaign. The researchers donned full hazmat suits in early February and entered the burn area to test homes and meet with homeowners.

ERFU posted its first dataset of 53 homes on March 24. Tissot’s group announced their results, which included data from 52 homes, just a week later, confirming what many had feared: There was lead everywhere.

“What was surprising to me is how far it went,” said Tissot. “We got very high levels of lead even miles away from the fire, and what’s difficult is that we still can’t really answer a simple question: How far is far enough to be safe?”

The two groups hope their data can help homeowners make better-informed decisions about their remediation and health — and apply pressure on leaders to take more action.

Tissot wants to see the government update its guidebooks and policy on fire recovery to reflect the contamination risks for intense urban fires, and to require testing companies to report their results to a public database.

Nicole Maccalla, a core member of EFRU’s Data Unification team, hopes to see officials enforce a common standard for insurance claims for testing and remediation so every resident doesn’t have to go through the same exact fight.

“You’ve got people stepping up to fill the void,” she said. “There should be an organized, systematic approach to this stuff, but it’s not happening.”

Times data journalist Sandhya Kambhampati contributed to this report.

Health officials in Hood River County, Ore., are investigating three cases of a rare and fatal brain disease known as Creutzfeldt-Jakob disease.

Two people have died and a third person is showing symptoms consistent with the disease. The disease has been confirmed in one of the deceased through an autopsy; the other two cases are considered probable, according to a statement from the Hood River County Health Department.

All three cases were diagnosed in the last eight months. County health officials declined to provide particulars about the individuals, such as their age, gender or town of residence.

“At this time, there is no identifiable link between these three cases,” a Hood River County statement said. The county has a population of about 24,000.

Creutzfeldt-Jakob disease is a neurodegenerative disorder caused by misfolded proteins known as prions. These prions lead to rapid brain deterioration, resulting in severe neurological symptoms and death. Although the disease is known for its sporadic occurrence, clusters raise concerns among public health officials about potential environmental or dietary exposure.

Symptoms include issues with memory, walking, coordination, speech and behavior changes, according to experts. It does not spread through the air, water, touch or social contact, according to Hood River County health officials.

The disease is considered incurable and is always fatal. Roughly 350 cases are diagnosed in the United States every year, according to the National Institutes of Health.

The disease is rare in people, affecting roughly 1.4 people per million. However, because the disease takes years to develop, any person’s chance of developing the disease is closer to 1 in 5,000 or 6,000, said Michael Geschwind, a professor of neurology at UC San Francisco in the Memory and Aging Center.

The disease is similar to chronic wasting disease, or CWD, which is also a prion-fueled disease, and was detected for the first time in wild deer in California and Washington last year.

CWD was first reported in 1967, in a captive Colorado deer. It has since spread to deer in 36 states. There are no known cases of the disease in Oregon wildlife.

For decades there has been concern that CWD could move into human populations through the ingestion of contaminated meat.

That’s because in the 1980s, a prion disease in sheep, known as scrapies — which humans do not seem to get — moved into cows, and soon people throughout the United Kingdom, France and elsewhere were becoming infected with mad cow disease, or bovine spongiform encephalopathy.

Since then, public health officials from the Centers for Disease Control and Prevention and several states have been paying close attention to clusters of Creutzfeldt-Jakob disease — investigating outbreaks to determine whether infected deer, elk or moose meat was involved.

They — and researchers from other agencies, such as the U.S. Geological Survey’s National Wildlife Health Center — also have been monitoring wild deer populations and keeping tabs on hunters who may have been exposed.

Although widespread geographically throughout the United States and Canada, the disease is considered relatively rare in wild populations of deer, elk and moose, said Brian Richardson, the emerging-disease coordinator at the USGS wildlife center.

“It may well be [in Oregon], but it’s hard to find rare events,” he said.

To date, there are no known incidents of people acquiring a prion disease by consuming deer, elk or moose meat, said Geschwind, the UCSF professor.

He said roughly 85% to 90% of Creutzfeldt-Jakob cases are considered sporadic, with no identified cause or source of infection. In 10% to 15% of the cases, the disease appears to be genetically inherited — with some people acquiring mutations associated with the disease.

However, there have been a few cases in which sources of infection or contamination have been identified, and almost all of them were from a medical mishap.

Prions are notoriously difficult to inactivate or destroy — withstanding standard sterilization techniques — and can remain intact for months and years on a surface, Geschwind said.

In a small number of cases, he said, people acquired the disease as a result of contaminated and improperly cleaned surgical equipment. In a few other cases, it was acquired by people who used products — such as growth hormone, or who received corneal transplants — derived, inadvertently, from infected cadavers.

It’s these proteins’ durability and longevity that have many researchers worried. Studies have shown that deer that harbor the disease can pass the infectious prions to other deer through saliva, blood, urine and feces.

“So, if the animal is licking a plant or licking a salt lick, for example, and another animal comes along and licks that plant or salt lick, then that might be a way of spreading the disease,” Geschwind said.

In addition, the decomposing body of a deer that died of the disease can infect the surrounding environment where the animal expired — potentially contaminating plants, seeds, fungi and soil, Richardson said.

He said not only is there the issue of surface contamination, but also research has shown that the proteins can “be taken up via rootlets and deposited in aerial plant tissues. Whether these plants contribute to chronic wasting disease transmission and what type of risk these plants pose to humans remain open questions.”

Geschwind noted that the work done by federal researchers to better understand the disease, provide diagnostic autopsies on presumptive cases, monitor wildlife and investigate clusters has provided a level of protection for the American public, which could be destabilized by proposed cuts to federal agencies.

“The idea of cutting government funding of rare disease is very short-sighted, because even though CJD is a rare disease, what we have learned from prion diseases has implications for all neurodegenerative diseases,” he said, noting Alzheimer’s disease, frontotemporal dementia, Parkinson’s disease and multiple system atrophy.

“All these diseases act in a prion-like manner in which normal proteins misfold, and those misfolded proteins cause the cells to not work partly and lead to disease,” he said. “But the basic mechanism that we’ve learned from this very rare disease applies to diseases that are thousands of times more common. To get rid of the research? It’d be a very grave mistake.”