The Toxic Effects of Noise and What We’re Not Doing About It
Erica Walker had a studio in her Brookline, Mass. apartment where she worked as a bookbinder and furniture maker. That was until a family with two rowdy children moved in above her.
The kids ran amuck, disrupting her sleep and work. Ear plugs weren’t enough to blot out the commotion. Aside from anger and a sense of lost control, the noise increased her heart rate and made her stomach feel like it was dropping, she says.
That’s when Walker realized that noise is a public health problem, not merely an annoyance. She set up her own “mini study” on how the clamor was affecting her. She monitored sound levels in her apartment and sent saliva samples to a lab to measure her stress levels.
Walker ultimately sold her craft equipment and returned to school to study public health. Today she is assistant professor of epidemiology and director of the Community Noise Lab at the Brown University School of Public Health. “We treat noise like a first world problem—like a sacrifice we should have to make for modern conveniences. But it’s a serious environmental stressor,” she asserts.
Our daily soundscape is a cacophony of earsplitting jets, motorcycles, crying babies, construction sites or gunshots if you’re in the military. Noise exposure is the primary cause of preventable hearing loss. Researchers have identified links between excessive noise and a heightened risk of heart disease, metabolic disorders, anxiety, depression, sleep disorders, and impaired cognition. Even wildlife suffers. Blasting oil drills and loud shipping vessels impede the breeding, feeding and migration of whales and dolphins.
At one time, the federal government had our back… and our ears. Congress passed the Noise Control Act in 1972. The Environmental Protection Agency set up the Office of Noise Abatement and Control (ONAC) to launch research, explore solutions and establish noise emission standards. But ONAC was defunded in 1981 amidst a swirl of antiregulatory sentiment.
Impossibly Loud and Unhealthy
Daniel Fink. a physician, WHO consultant, and board chair of The Quiet Coalition, a program of the nonprofit Quiet Communities, likens the effect of noise to the invisible but cumulative harm of second-hand smoke. About 1 in 4 adults in the U.S. who report excellent to good hearing already have some hearing loss. The injury can happen after one loud concert or from years with a blaring TV. Some people are more genetically susceptible to noise-related hearing loss than others.
“People say noise isn’t a big deal but it bothers your body whether you realize it or not,” says Ted Rueter, director of Noise Free America: A Coalition to Promote Quiet. Noise can chip away at your ears or cardiovascular system even while you’re sleeping. Rueter became a “quiet advocate” while a professor at UCLA two decades ago. He was plagued by headaches, fatigue and sleep deprivation caused by the hubbub of Los Angeles, he says.
The louder a sound is, and the longer you are exposed to it, the more likely it will cause nerve damage and harmful fluid buildup in your inner ear. Normal speech is 50-60 decibels (dBs). The EPA recommends that 24-hour exposure to noise should be no higher than 70 weighted decibels over 24 hours (weighted to approximate how the human ear perceives the sound) to prevent hearing loss but a 55 dB limit is recommended to protect against other harms from noise, too.
The decibel scale is logarithmic. That means 80 dB is 10 times louder than 70 dB. Trucks and motorcycles run 90 dBs. A gas-powered leaf blower, jackhammer or snow blower will cost you 100 dBs. A rock concert is in the 110 dB range. Aircraft takeoffs or sirens? 120 dBs.
Walker, the Brown professor, says that sound measurements often use misleading metrics, though, because they don’t include low frequency sound that disturb the body. The high frequency of a screeching bus will register in decibels but the sound that makes your chest reverberate is not accounted for, she explains. ‘How loud?’ is a superficial take when it comes to noise, Walker says.
After realizing the impact of noise on her own health, Erica Walker was inspired to change careers and become director of the Community Noise Lab at the Brown University School of Public Health.
Fink adds that the extent to which noise impairs hearing is underestimated. People assume hearing loss is due to age but it’s not inevitable, he says. He cites studies of older people living in quiet, isolated areas who maintain excellent hearing. Just like you can prevent wrinkles by using sunscreen, you can preserve hearing by using ear plugs when attending fireworks or hockey games.
You can enable push notifications on a Smart Watch to alert you at a bar exceeding healthy sound levels. Free apps like SoundPrint, iHEARu, or NoiseTube can do decibel checks, too, but you don’t need one, says Fink. “If you can’t carry a conversation at normal volume, it’s too loud and your auditory health is at risk,” he says.
About 40 million U.S. adults, ages 20-69, have noise-induced hearing loss. Fink is among them after experiencing tinnitus (ringing or buzzing in the ears) on leaving a raucous New Year’s Eve party in 2007. The condition is permanent and he wears earplugs now for protection.
Fewer are aware of the link between noise pollution and heart disease. Piercing noise is stressful, raising blood pressure and heart rate. If you live near a freeway or constantly barking dog, the chronic sound stress can trigger systemic inflammation and the vascular changes associated with heart attacks and stroke.
Researchers at Rutgers University’s Robert Wood Johnson Medical School, working with data from the state’s Bureau of Transportation, determined that 1 in 20 heart attacks in New Jersey during 2018 were due to noise from highways, trains and air traffic. That’s 800 heart attack hospitalizations in the state that year.
Another study showed that incidence of hypertension and hardening arteries decreased during the Covid-19 air lockdown among Poles in Krakow routinely exposed to aircraft noise. The authors, comparing their pre-pandemic 2015 results to 2020 data, concluded it was no coincidence.
Mental health takes a hit, too. Chronic noise can provoke anxiety, depression and violence. Cognitively, there is ample evidence that noise disturbance lowers student achievement and worker productivity, and hearing loss among older people can speed up cognitive decline.
Noise also contributes to health disparities. People in neighborhoods with low socioeconomic status and a higher percentage of minority residents bear the brunt of noise. Affluent people have the means to live far from airports, factories, and honking traffic.
Out, Out, Damn Noise
Europe is ahead of the U.S. in tackling noise pollution. The World Health Organization developed policy guidelines used by the European Environment Agency to establish noise regulations and standards, and progress reports are issued.
Americans are relying too much on personal protective equipment (PPE) instead of eliminating or controlling noise. The Centers of Disease Control and Prevention rank PPE as the least useful response. Earplugs and muffs are effective, says Walker, but these devices are “a band-aid on a waterfall.”
Editing out noise during product design is the goal. Engineers have an arsenal of techniques and know-how for that. The problem is that these solutions aren’t being applied.
A better way to lower the volume is by maintaining or substituting equipment intended for common use. Piercing building alarms can be replaced with visual signals that flash alerts. Clanking chain and gear drives can be swapped out with belt drives. Acoustical barriers can wall off highway noise. Hospitals can soften beeping monitors and limit loudspeaker blasts. Double paned windows preserve quiet.
Editing out noise during product design is the goal. Engineers have an arsenal of techniques and know-how for that. The problem is that these solutions aren’t being applied, says Jim Thompson, an engineer and editor of the Noise Control Engineering Journal, published by the Institute of Noise Control Engineering of the USA
Engineers have materials to insulate, absorb, reflect, block, seal or diffuse noise. Building walls can be padded. Metal gears and parts can be replaced with plastic. Clattering equipment wheels can be rubberized. In recent years, building certifications such as LEED have put more emphasis on designs that minimize harmful noise.
Walker faults urban planners, too. A city’s narrow streets and taller buildings create a canyon effect which intensifies noise. City planners could use bypasses, rerouting, and other infrastructure strategies to pump down traffic volume. Sound-absorbing asphalt pavement exists, too.
Some municipalities are taking innovative measures on their own. Noise cameras have been installed in Knoxville, Miami and New York City this year and six California cities will join suit next year. If your muffler or audio system registers 86 dB or higher, you may receive a warning, fine or citation, similar to how a red-light camera works. Rueter predicts these cameras will become commonplace.
Based on understanding how metabolic processes affect noise-induced hearing loss in animal models, scientists are exploring whether pharmacological interventions might work to inhibit cellular damage or improve cellular defenses against noise.
Washington, DC, and the University of Southern California have banned gas-powered leaf blowers in lieu of quieter battery-powered models to reduce both noise and air pollution. California will be the first state to ban the sale of gas-powered lawn equipment starting 2024.
New York state legislators enacted the SLEEP (Stop Loud and Excessive Exhaust Pollution) Act in 2021. This measure increases enforcement and fines against motorists and repair shops that illegally modify mufflers and exhaust systems for effect.
“A lot more basic science and application research is needed [to control noise],” says Thompson, noting that funding for this largely dried up after the 1970s. Based on understanding how metabolic processes affect noise-induced hearing loss in animal models, scientists are exploring whether pharmacological interventions might work to inhibit cellular damage or improve cellular defenses against noise.
Studying biochemical or known genetic markers for noise risk could lead to other methods for preventing hearing loss. This would offer an opportunity to identify people with significant risk so those more susceptible to hearing loss could start taking precautions to avoid noise or protect their ears in childhood.
These efforts could become more pressing in the near future, with the anticipated onslaught of drones, rising needs for air conditioners, and urban sprawl boding poorly for the soundscape. This, as deforestation destroys natural carbon absorption reservoirs and removes sound-buffering trees.
“Local and state governments don’t have a plan to deal with [noise] now or in the future,” says Walker. “We need to think about this with intentionality.”
Swiss researchers have discovered a third type of brain cell that appears to be a hybrid of the two other primary types — and it could lead to new treatments for many brain disorders.
The challenge: Most of the cells in the brain are either neurons or glial cells. While neurons use electrical and chemical signals to send messages to one another across small gaps called synapses, glial cells exist to support and protect neurons.
Astrocytes are a type of glial cell found near synapses. This close proximity to the place where brain signals are sent and received has led researchers to suspect that astrocytes might play an active role in the transmission of information inside the brain — a.k.a. “neurotransmission” — but no one has been able to prove the theory.
A new brain cell: Researchers at the Wyss Center for Bio and Neuroengineering and the University of Lausanne believe they’ve definitively proven that some astrocytes do actively participate in neurotransmission, making them a sort of hybrid of neurons and glial cells.
According to the researchers, this third type of brain cell, which they call a “glutamatergic astrocyte,” could offer a way to treat Alzheimer’s, Parkinson’s, and other disorders of the nervous system.
“Its discovery opens up immense research prospects,” said study co-director Andrea Volterra.
The study: Neurotransmission starts with a neuron releasing a chemical called a neurotransmitter, so the first thing the researchers did in their study was look at whether astrocytes can release the main neurotransmitter used by neurons: glutamate.
By analyzing astrocytes taken from the brains of mice, they discovered that certain astrocytes in the brain’s hippocampus did include the “molecular machinery” needed to excrete glutamate. They found evidence of the same machinery when they looked at datasets of human glial cells.
Finally, to demonstrate that these hybrid cells are actually playing a role in brain signaling, the researchers suppressed their ability to secrete glutamate in the brains of mice. This caused the rodents to experience memory problems.
“Our next studies will explore the potential protective role of this type of cell against memory impairment in Alzheimer’s disease, as well as its role in other regions and pathologies than those explored here,” said Andrea Volterra, University of Lausanne.
But why? The researchers aren’t sure why the brain needs glutamatergic astrocytes when it already has neurons, but Volterra suspects the hybrid brain cells may help with the distribution of signals — a single astrocyte can be in contact with thousands of synapses.
“Often, we have neuronal information that needs to spread to larger ensembles, and neurons are not very good for the coordination of this,” researcher Ludovic Telley told New Scientist.
Looking ahead: More research is needed to see how the new brain cell functions in people, but the discovery that it plays a role in memory in mice suggests it might be a worthwhile target for Alzheimer’s disease treatments.
The researchers also found evidence during their study that the cell might play a role in brain circuits linked to seizures and voluntary movements, meaning it’s also a new lead in the hunt for better epilepsy and Parkinson’s treatments.
“Our next studies will explore the potential protective role of this type of cell against memory impairment in Alzheimer’s disease, as well as its role in other regions and pathologies than those explored here,” said Volterra.
Martin Taylor was only 32 when he was diagnosed with Parkinson's, a disease that causes tremors, stiff muscles and slow physical movement - symptoms that steadily get worse as time goes on.
“It's horrible having Parkinson's,” says Taylor, a data analyst, now 41. “It limits my ability to be the dad and husband that I want to be in many cruel and debilitating ways.”
Today, more than 10 million people worldwide live with Parkinson's. Most are diagnosed when they're considerably older than Taylor, after age 60. Although recent research has called into question certain aspects of the disease’s origins, Parkinson’s eventually kills the nerve cells in the brain that produce dopamine, a signaling chemical that carries messages around the body to control movement. Many patients have lost 60 to 80 percent of these cells by the time they are diagnosed.
For years, there's been little improvement in the standard treatment. Patients are typically given the drug levodopa, a chemical that's absorbed by the brain’s nerve cells, or neurons, and converted into dopamine. This drug addresses the symptoms but has no impact on the course of the disease as patients continue to lose dopamine producing neurons. Eventually, the treatment stops working effectively.
BlueRock Therapeutics, a cell therapy company based in Massachusetts, is taking a different approach by focusing on the use of stem cells, which can divide into and generate new specialized cells. The company makes the dopamine-producing cells that patients have lost and inserts these cells into patients' brains. “We have a disease with a high unmet need,” says Ahmed Enayetallah, the senior vice president and head of development at BlueRock. “We know [which] cells…are lost to the disease, and we can make them. So it really came together to use stem cells in Parkinson's.”
In a phase 1 research trial announced late last month, patients reported that their symptoms had improved after a year of treatment. Brain scans also showed an increased number of neurons generating dopamine in patients’ brains.
Increases in dopamine signals
The recent phase 1 trial focused on deploying BlueRock’s cell therapy, called bemdaneprocel, to treat 12 patients suffering from Parkinson’s. The team developed the new nerve cells and implanted them into specific locations on each side of the patient's brain through two small holes in the skull made by a neurosurgeon. “We implant cells into the places in the brain where we think they have the potential to reform the neural networks that are lost to Parkinson's disease,” Enayetallah says. The goal is to restore motor function to patients over the long-term.
Five patients were given a relatively low dose of cells while seven got higher doses. Specialized brain scans showed evidence that the transplanted cells had survived, increasing the overall number of dopamine producing cells. The team compared the baseline number of these cells before surgery to the levels one year later. “The scans tell us there is evidence of increased dopamine signals in the part of the brain affected by Parkinson's,” Enayetallah says. “Normally you’d expect the signal to go down in untreated Parkinson’s patients.”
"I think it has a real chance to reverse motor symptoms, essentially replacing a missing part," says Tilo Kunath, a professor of regenerative neurobiology at the University of Edinburgh.
The team also asked patients to use a specific type of home diary to log the times when symptoms were well controlled and when they prevented normal activity. After a year of treatment, patients taking the higher dose reported symptoms were under control for an average of 2.16 hours per day above their baselines. At the smaller dose, these improvements were significantly lower, 0.72 hours per day. The higher-dose patients reported a corresponding decrease in the amount of time when symptoms were uncontrolled, by an average of 1.91 hours, compared to 0.75 hours for the lower dose. The trial was safe, and patients tolerated the year of immunosuppression needed to make sure their bodies could handle the foreign cells.
Claire Bale, the associate director of research at Parkinson's U.K., sees the promise of BlueRock's approach, while noting the need for more research on a possible placebo effect. The trial participants knew they were getting the active treatment, and placebo effects are known to be a potential factor in Parkinson’s research. Even so, “The results indicate that this therapy produces improvements in symptoms for Parkinson's, which is very encouraging,” Bale says.
Tilo Kunath, a professor of regenerative neurobiology at the University of Edinburgh, also finds the results intriguing. “I think it's excellent,” he says. “I think it has a real chance to reverse motor symptoms, essentially replacing a missing part.” However, it could take time for this therapy to become widely available, Kunath says, and patients in the late stages of the disease may not benefit as much. “Data from cell transplantation with fetal tissue in the 1980s and 90s show that cells did not survive well and release dopamine in these [late-stage] patients.”
Searching for the right approach
There's a long history of using cell therapy as a treatment for Parkinson's. About four decades ago, scientists at the University of Lund in Sweden developed a method in which they transferred parts of fetal brain tissue to patients with Parkinson's so that their nerve cells would produce dopamine. Many benefited, and some were able to stop their medication. However, the use of fetal tissue was highly controversial at that time, and the tissues were difficult to obtain. Later trials in the U.S. showed that people benefited only if a significant amount of the tissue was used, and several patients experienced side effects. Eventually, the work lost momentum.
“Like many in the community, I'm aware of the long history of cell therapy,” says Taylor, the patient living with Parkinson's. “They've long had that cure over the horizon.”
In 2000, Lorenz Studer led a team at the Memorial Sloan Kettering Centre, in New York, to find the chemical signals needed to get stem cells to differentiate into cells that release dopamine. Back then, the team managed to make cells that produced some dopamine, but they led to only limited improvements in animals. About a decade later, in 2011, Studer and his team found the specific signals needed to guide embryonic cells to become the right kind of dopamine producing cells. Their experiments in mice, rats and monkeys showed that their implanted cells had a significant impact, restoring lost movement.
Studer then co-founded BlueRock Therapeutics in 2016. Forming the most effective stem cells has been one of the biggest challenges, says Enayetallah, the BlueRock VP. “It's taken a lot of effort and investment to manufacture and make the cells at the right scale under the right conditions.” The team is now using cells that were first isolated in 1998 at the University of Wisconsin, a major advantage because they’re available in a virtually unlimited supply.
Other efforts underway
In the past several years, University of Lund researchers have begun to collaborate with the University of Cambridge on a project to use embryonic stem cells, similar to BlueRock’s approach. They began clinical trials this year.
A company in Japan called Sumitomo is using a different strategy; instead of stem cells from embryos, they’re reprogramming adults' blood or skin cells into induced pluripotent stem cells - meaning they can turn into any cell type - and then directing them into dopamine producing neurons. Although Sumitomo started clinical trials earlier than BlueRock, they haven’t yet revealed any results.
“It's a rapidly evolving field,” says Emma Lane, a pharmacologist at the University of Cardiff who researches clinical interventions for Parkinson’s. “But BlueRock’s trial is the first full phase 1 trial to report such positive findings with stem cell based therapies.” The company’s upcoming phase 2 research will be critical to show how effectively the therapy can improve disease symptoms, she added.
The cure over the horizon
BlueRock will continue to look at data from patients in the phase 1 trial to monitor the treatment’s effects over a two-year period. Meanwhile, the team is planning the phase 2 trial with more participants, including a placebo group.
For patients with Parkinson’s like Martin Taylor, the therapy offers some hope, though Taylor recognizes that more research is needed.
“Like many in the community, I'm aware of the long history of cell therapy,” he says. “They've long had that cure over the horizon.” His expectations are somewhat guarded, he says, but, “it's certainly positive to see…movement in the field again.”
"If we can demonstrate what we’re seeing today in a more robust study, that would be great,” Enayetallah says. “At the end of the day, we want to address that unmet need in a field that's been waiting for a long time.”