The research, published in the journal Environmental Science and Technology, suggests that wildfire emissions even 10 days old can affect the properties of aerosols — suspended liquid or particles that are key to cloud formation.

Research in aerosols and particulate matter pollution related to wildfires has most often focused on the early hours of smoke plumes, not several days later after smoke has traveled to other areas.

Enhancing modeling

This research helps fill in a knowledge gap and can inform future predictions about the climate and atmospheric effects of wildfire over the lifetime of aerosols, particularly in rural or pristine areas with relatively clean air, said Qi Zhang, an environmental toxicology professor and lead author of the study.

“These parameters are really useful for atmospheric and chemical models,” she said. “It’s a really important component to solving the effects on climate. To capture those characteristics is super critical.”

Zhang, Ph.D. student Ryan Farley and others spent time in 2019 at the Mount Bachelor Observatory atop a volcanic mountain in Oregon. That year was relatively calm in terms of wildfire, but smoke plumes and aerosols were still observed. Some were at least 10 days old and came from as close as Northern California and as far as Siberia, Russia.

The properties and chemical composition of aerosols can do a number of things: scatter or absorb solar radiation affecting temperature, seed clouds to produce rain or snow, or change the reflectivity of clouds — all of which affect climate.

Aerosol properties change with age

Scientists found that particulate matter concentrations were low, but oxidized organic aerosols from burning biomass — such as trees, grasses and shrubs — were detected throughout the samples.

The aerosols, which have a life cycle of about two weeks, were larger in aged samples compared to those found shortly after a fire starts.

“The properties of the smoke determine the effects on the climate,” Zhang said. “The really aged aerosols can behave very differently than the fresh ones. You want to capture these aerosols over the lifetime to properly account for the effects.”

Aerosols in the background

Older aerosols produced by wildfires can be present but not obvious and still affect climate.

“It’s not something you just notice but it’s in the background,” she said.

Knowing that information becomes ever more important as “biomass burning has become more and more frequent,” Zhang said.

Shan Zhou and Sonya Collier from UC Davis also participated in the research as did scientists from University of Montana and University of Washington.

The National Science Foundation, the U.S. Department of Energy’s Atmospheric System Research Program, the California Agricultural Experiment Station and UC Davis funded the research.

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“Our results underscore the need to strengthen air pollutionregulations and prevention implementation in tribal territories and areas where AI populations live,” said Maggie Li, PhD candidate in the Department of Environmental Health Sciences at Columbia Mailman School, and first author.”Until now, insight into PM_2.5 exposure burdens in AI communities has been limited, in turn contributing to the lack of air pollution epidemiological studies which include this population in the contiguous U.S.”

The researchers compared ambient PM_2.5 average concentrations and trends in AI-populated vs. non-AI-populated counties in the contiguous U.S. from 2000 to 2018. They conducted their analysis at the county level, the most relevant unit to inform regulatory action. Population data and household income were obtained from the U.S. 2010 Census.

Average concentrations were 1.46 ?g/m³ lower for modeled PM_2.5 in AI-populated counties vs. non-AI-populated counties in 2000; however, towards the end of the study period, PM_2.5 concentrations in AI-populated counties became significantly higher compared to non-AI-populated counties. By 2018, concentrations were on average 0.66µg/m³higher in AI-populated counties than non-AI-populated counties. “Although we observed that average PM_2.5 concentrations were higher in non-AI-populated counties at baseline and across most of the study period, the gap between AI- and non-AI-populated counties decreased over time; after approximately 2015, average PM_2.5 concentrations were higher in AI-populated counties,” observed Li.

Short- and long-term exposure to particulate matter ? 2.5 µm (PM_2.5) increases the risk of cardiovascular and respiratory disease, among other health outcomes. In the U.S., socioeconomically disadvantaged communities are often exposed to higher PM_2.5 exposure levels. They bear a disproportionate burden of disease, even at levels well below air quality standards set by the U.S. Environmental Protection Agency.

“Our findings build upon existing studies showing that socioeconomically disadvantaged communities experience disproportionate burdens of environmental hazards, such as ambient air pollution. Native Americans may be particularly susceptible to the adverse health effects of PM_2.5 and air pollution, but research quantifying air pollution exposures and impacts on health among this population is lacking,” said Marianthi-Anna Kioumourtzoglou, ScD, assistant professor of environmental health sciences at Columbia Mailman School, and senior author. “These communities already face a large disease burden attributable to environmental pollution due, for instance, to extensive mining and water contamination on Tribal Lands.”

Cardiovascular disease, one of the outcomes associated with exposure to PM_2.5, and the leading cause of death in AI populations, occurs at significantly higher rates than in white populations. “There is a critical need for future investigations of health impacts associated with air pollution exposure in AI populations, as well as of interventions to ensure the observed inequalities can be eliminated,” noted Ana Navas-Acien, MD, PhD, professor of environmental health sciences at Columbia Mailman School, and a senior co-author.

Co-authors are Markus Hilpert, Jenni A. Shearston, and Jeff Goldsmith, Columbia University Mailman School of Public Health; Jada Brooks, the University of North Carolina School of Nursing at Chapel Hill; Steven Chillrud, Lamont-Doherty Earth Observatory, Columbia University; Tauqeer Ali, University of Oklahoma Health Sciences Center; Jason Umans, Georgetown-Howard Universities Center for Clinical and Translational Sciences; Lyle Best and Joseph Yracheta, Missouri Breaks Industries Research, Inc.; Aaron van Donkelaar and Randall Martin, Department of Energy, Environmental & Chemical Engineering, Washington University at St. Louis.

Support for the study was provided by the National Institute of Environmental Health Sciences, grants T32 ES007322, P30 ES09089, R01 ES030616, and P42ES010349.

“Our results suggest people using statins may have a lower risk of parkinsonism and that may be partly caused by the protective effect statins may have on arteries in the brain,” said study author Shahram Oveisgharan, MD, of Rush University Medical Center in Chicago. “Our results are exciting, because movement problems in older adults that come under the umbrella of parkinsonism are common, often debilitating and generally untreatable.”

The study looked 2,841 people with an average age of 76 who did not have parkinsonism at the start of the study. Of those, 936 people, or 33%, were taking statins.

Researchers followed up with participants annually for an average of six years to check the statins they were taking and to test for signs of parkinsonism.

People were considered to have parkinsonism if they met the requirement for mild impairment for two or more of the following symptoms: tremor, stiffness, parkinsonian gait, which is marked by small shuffling steps and a general slowness of movement, and bradykinesia, a hallmark of parkinsonism which is difficulty moving the body quickly on command.

By the end of the study, 1,432 people, or 50%, developed signs of parkinsonism. Out of 936 people taking statins, 418 people, or 45%, developed parkinsonism six years later, compared to 1,014 out of 1,905 people, or 53%, of those who had not been taking statins.

After controlling for age, sex and vascular risks like smoking and diabetes that could affect risk of parkinsonism, researchers found that people who had been taking statins, on average, had 16% lower risk of developing parkinsonism six years later compared to those who had not been taking statins. About 79% of people on statin therapy were taking moderate or high intensity statins. Researchers found that people taking higher intensity statins had a 7% lower risk of developing parkinsonism compared to those on low intensity statins.

Researchers also examined the brains of 1,044 people who died during the study. They found those who had been using statins had, on average, 37% lower odds of having atherosclerosis compared to those who had not been using statins.

“More research is needed, but statins could be a therapeutic option in the future to help reduce the effects of parkinsonism in the general population of older adults, not just people with high cholesterol or who are at risk for stroke,” Oveisgharan said. “At a minimum, our study suggests brain scans or vascular testing may be beneficial for older adults who show signs of parkinsonism but don’t have classic signs of Parkinson’s disease or do not respond to Parkinson’s disease medications.”

A limitation of the study is that parkinsonism evaluations were not performed by movement disorder specialists, so cases of Parkinson’s disease may have been misclassified.

The study was supported by the National Institutes of Health.

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“Heart failure with preserved ejection fraction affects millions of people around the globe, but we currently have little to offer these patients because the mechanisms behind it have been unknown. It’s been called the single greatest unmet need in cardiovascular medicine,” said the article’s senior author Joseph Hill, M.D., Ph.D., Professor of Internal Medicine and Molecular Biology and Chief of Cardiology at UT Southwestern. “We now have insight into this condition that we didn’t have even five years ago, observations that could lead to viable clinical targets.”

Dr. Hill explained that heart failure — the heart’s inability to effectively pump blood — comes in two broad types: heart failure with reduced ejection fraction (HFrEF), in which the amount of blood that leaves the heart with each beat declines, and heart failure with preserved ejection fraction (HFpEF), in which the heart is unable to fill with blood to capacity. While HFrEF has long been the most common form, HFpEF — which is associated with obesity, diabetes, and other components of metabolic syndrome — has grown in prevalence over the last several decades and overtaken HFrEF as the most common form.

Numerous treatments exist for various types of HFrEF, but these interventions have no discernible effect on HFpEF. This is because the two conditions are caused by different underlying mechanisms, said Dr. Hill, a topic that his lab has studied for years. Although HFpEF can be improved through weight loss, losing weight is something that many individuals struggle with, he added, prompting the need for treatments.

In the review article, Hill and his colleagues outline findings made over the past several years that point to joint metabolic and immune dysfunction as the root cause of HFpEF. For example, fat tissue secretes inflammatory molecules that migrate to the heart, recruiting immune cells evident in heart biopsy samples from individuals with HFpEF. At the same time, heart toxicity caused by overuse of fatty acids as fuel in individuals with metabolic syndrome appears to stimulate an immune response, leading to a vicious cycle.

Crosstalk between fat tissue, the immune system, and the heart appears to amplify both immune and metabolic stress, ultimately causing the heart to fail over time. But how this crosstalk occurs, the effects it produces, and how to block them remain unclear, Dr. Hill said. Research into this new field of immunometabolism is shedding some light on these questions, but more research will be necessary to produce effective interventions for HFpEF patients, he added.

“Research from our lab and others is raising possibilities of therapeutic targets that need to be investigated,” Dr. Hill said. “There’s a reasonable chance that we could have therapies available for this intractable condition within the next decade.”

U.S. News and World Report ranks UT Southwestern as the No.1 hospital in Texas for Cardiology and Heart Surgery and No.11 in the nation.

Dr. Hill holds the James T. Willerson, M.D., Distinguished Chair in Cardiovascular Diseases and the Frank M. Ryburn Jr. Chair in Heart Research.

Thomas G. Gillette, Ph.D., Associate Professor of Internal Medicine at UT Southwestern, contributed to the review article.

This work was supported by grants from the DZHK (German Centre for Cardiovascular Research); the Deutsche Forschungsgemeinschaft (German Research Foundation, SFB-1470-A02), IMI2-CARDIATEAM (no. 821508); the Netherlands Cardiovascular Research Initiative, Dutch Cardiovascular Alliance CVON2016-Early HFPEF, 2015-10, CVON She-PREDICTS, no. 2017-21; National Institutes of Health (HL144477, HL122309, HL126012, HL128215, HL120732, HL147933 and HL155765), and the American Heart Association (19TPA34910006).

In 2015, researchers from Penn’s School of Veterinary Medicine learned that dogs could develop a form of inherited night blindness with strong similarities to the condition in people. In 2019, the team identified the gene responsible.

Today, in the journal Proceedings of the National Academy of Sciences, they’ve reported a major advance: a gene therapy that returns night vision to dogs born with CSNB. The success of this approach, which targets a group of cells deep in the retina called ON bipolar cells, charts a significant step toward a goal of developing a treatment for both dogs and people with this condition, as well as other vision problems that involve ON bipolar cell function.

Dogs with CSNB that received a single injection of the gene therapy began to express the healthy LRIT3 protein in their retinas and were able to ably navigate a maze in dim light. The treatment also appears lasting, with a sustained therapeutic effect lasting a year or longer.

“The results of this pilot study are very promising,” says Keiko Miyadera, lead author on the study and an assistant professor at Penn Vet. “In people and dogs with congenital stationary night blindness, the severity of disease is consistent and unchanged throughout their lives. And we were able to treat these dogs as adults, between 1 and 3 years of age. That makes these findings promising and relevant to the human patient population, as we could theoretically intervene even in adulthood and see an improvement in night vision.”

In the earlier work, the Penn Vet team, working in collaboration with groups from Japan, Germany, and the United States, discovered a population of dogs with CSNB and determined that mutations in the LRIT3 gene were responsible for the dogs’ night vision impairment. The same gene has been implicated in certain cases of human CSNB as well.

This mutation affects the ON bipolar cells’ function, but, unlike in some blinding diseases, the overall structure of the retina as a whole remained intact. That gave the research team hope that supplying a normal copy of the LRIT3 gene could restore night vision to affected dogs.

Yet while Penn Vet researchers from the Division of Experimental Retinal Therapies have developed effective gene therapies for a variety of other blinding disorders, none of these earlier treatments has targeted the ON bipolar cells, located deep within the middle layer of the retina.

“We’ve stepped into the no-man’s land of the retina with this gene therapy,” says William A. Beltran, a coauthor and professor at Penn Vet. “This opens the door to treating other diseases that impact the ON bipolar cells.”

The researchers overcame the hurdle of targeting these relatively inaccessible cells with two key findings. First, through a rigorous screening process conducted in collaboration with colleagues at the University of California, Berkeley, led by John Flannery and at the University of Pittsburgh led by Leah Byrne, they identified a vector for the healthy LRIT3 gene that would enable the treatment to reach the intended cells. And, second, they paired the healthy gene with a promoter — the genetic sequence that helps initiate the “reading” of the therapeutic gene — that would act in a cell-specific fashion.

“Prior therapies we’ve worked on have targeted photoreceptors or retinal pigment epithelium cells,” says coauthor Gustavo D. Aguirre, a Penn Vet professor. “But the promoter we use here is very specific in targeting the ON bipolar cells, which helps avoid potential off-target effects and toxicity.”

The researchers suspect that restoring the functional LRIT3 gene enables signals to cross from the photoreceptor cells to the ON bipolar cells. “LRIT3 is expressed at the ‘finger’ tips of these cells,” says Beltran. “Introducing this transgene is essentially allowing the two cells to shake hands and communicate again.”

An open question is whether targeting both photoreceptor cells and ON bipolar cells together could lead to even greater improvements in night vision. Other research groups studying these conditions in mice have targeted the therapy to photoreceptor cells and found some vision to be restored, suggesting a possible path to enhance the effects of gene therapy.

And while the therapy enabled functional recovery — dogs were able to navigate a maze when their treated eye was uncovered but not when it was covered — the healthy copy of the gene was only expressed as much as 30% of ON bipolar cells. In follow-up work, the researchers hope to augment this uptake.

“We had great success in this study, but we saw some dogs get better recovery than others,” says Miyadera. “We’d like to continue working to maximize the therapeutic benefit while still ensuring safety. And we’ve seen that this treatment is durable, but is it lifelong after one injection? That’s something we’d like to find out.”

The team also plans to amend the therapy to use the human version of the LRIT3 gene, a necessary step toward translating the treatment to people with CSNB with an eventual clinical trial.

Miyadera, Beltran, and Aguirre coauthored the study with Penn Vet’s Evelyn Santana, Karolina Roszak, Sommer Iffrig, Yu Sato, Alexa Gray, Ana Ripolles Garcia, and Valerie Dufour; Charles River Laboratories’ Simone Iwabe, Ryan F. Boyd, and, Joshua T. Bartoe; and the University of California, Berkeley’s Meike Visel, John G. Flannery, and Leah C. Byrne (now at the University of Pittsburgh).

Keiko Miyadera is an assistant professor of ophthalmology in Penn Vet’s Department of Clinical Sciences & Advanced Medicine.

William Beltran is a professor of ophthalmology in Penn Vet’s Department of Clinical Sciences & Advanced Medicine and director of the Division of Experimental Retinal Therapies.

Gustavo D. Aguirre is a professor of medical genetics and ophthalmology in Penn Vet’s Department of Clinical Sciences & Advanced Medicine.

The study was supported by the Margaret Q. Landenberger Research Foundation, National Eye Institute/National Institute of Health (Grant EY-006855), Foundation Fighting Blindness, Van Sloun Foundation for Canine Genetic Research, and Sanford and Susan Greenberg End Blindness Outstanding Achievement Prize.