Visual representation of low-frequency environmental noise coming from climate control systems.
Photo Credit: Sumeet Kulkarni, Nagoya University.
Scientific Frontline: Extended "At a Glance" Summary: Low-Frequency Environmental Noise and Kidney Health
The Core Concept: Exposure to ubiquitous, low-frequency environmental noise below 100 hertz can induce kidney dysfunction by damaging the microscopic blood vessels responsible for filtration.
Key Distinction/Mechanism: Unlike higher-frequency sounds, low-frequency acoustic vibrations trigger an overproduction of endothelin-1, a signaling molecule that excessively constricts renal blood vessels and thickens the delicate membranes of the glomeruli.
Major Frameworks/Components:
- Frequency Specificity: Kidney damage is triggered exclusively by sound frequencies at or below 100 hertz, occurring even when the acoustic waves are entirely below the subject's audible range.
- Glomerular Injury: The low-frequency acoustic exposure causes swelling and membrane thickening in the glomeruli, which act as the primary filtration networks of the kidney.
- Endothelin Signaling Pathway: The acoustic stress induces elevated production of endothelin-1, leading to severe vasoconstriction and elevated markers of kidney failure, such as serum creatinine and blood urea nitrogen.
- Pharmacological Intervention: The administration of ambrisentan, a hypertension medication that blocks endothelin receptors, successfully mitigates the acoustic-induced kidney damage.
Branch of Science: Environmental Health, Public Health, Nephrology, Acoustics, and Molecular Physiology.
Future Application: These findings could inform new occupational safety standards, drive the engineering of vibration-dampened machinery, and direct future human epidemiological studies to assess the systemic health impacts of chronic noise exposure.
Why It Matters: Because low-frequency vibrations are inescapable in modern environments—emanating from air conditioners, heat pumps, and distant traffic—understanding their physiological impact is vital for identifying and preventing hidden environmental health hazards.
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| The effect of environmental noise and its division into low- and high-frequency components on serum creatine (sCRE) and blood urea nitrogen (BUN), two markers of kidney health. The low-frequency noise shows elevated sCRE and BUN levels compared to control just like the whole spectrum of noise, while its high-frequency component shows no effect. Image Credit: Kagawa et al., Environ. Sci. Technol. 2026. |
Researchers at Nagoya University have identified ways in which low-frequency environmental noise from sources such as air conditioners and water pumps can trigger blood vessel damage in the kidneys of mice.
Close your eyes and listen for a few seconds. No matter where you are, countless low, deep rumblings feed into your ears from air-conditioning units, elevator motors, distant traffic, and ventilation ducts.
These rumbles constitute low-frequency noise below 100 hertz (Hz), which is about the same pitch as a kick drum. Almost all of these sources are human-made, making them a relatively new environmental factor. Living things were not meant to be immersed in this kind of noise.
Previous studies have suggested that people surrounded by more environmental noise tend to have poorer kidney function. However, these studies could not identify which component of the noise was to blame or the specific mechanisms by which it affected the kidneys.
Now, a team led by Takumi Kagawa and Masashi Kato at the Department of Occupational and Environmental Health at the Nagoya University Graduate School of Medicine has provided the first direct experimental evidence that the low-frequency component of environmental noise is the culprit behind adverse kidney health in mice. Their findings were published in the journal Environmental Science & Technology.
Pitch Matters More Than Volume
Kagawa and Kato began by recording actual noise from two ordinary household machines: the outdoor unit of an air conditioner and a heat-pump water heater. Using audio software, they split each recording into two tracks: a low-frequency version containing only sounds at or below 100 Hz, and a high-frequency version containing everything above that threshold.
Mice were exposed to these sounds for twelve hours a day over five days during the nighttime, when they are naturally active. The researchers then measured two standard markers of kidney health in the animals’ blood: creatinine and urea nitrogen, which accumulate when the kidneys stop filtering waste efficiently.
The researchers analyzed the effects of environmental noise and its division into low- and high-frequency components on serum creatinine (sCRE) and blood urea nitrogen (BUN). Much like the full spectrum of noise, the low-frequency noise caused elevated sCRE and BUN levels compared to a control group, while the high-frequency component showed no such effect.
Playing the unedited environmental noise, which contained all frequencies, increased both markers, signifying kidney damage. However, when only the high-frequency noise was played, no changes occurred. This indicated that the lower frequencies were responsible for elevating the creatinine and urea nitrogen levels, a finding the researchers soon verified.
“The biggest surprise to me was that the low-frequency component caused kidney dysfunction even though it was below the hearing range of mice,” Kagawa said. “In contrast, the higher-frequency component did not cause kidney dysfunction, even when both had the same physical sound pressure level,” he added, implying that the frequency of the noise mattered more than its loudness.
Squeezed Blood Vessels
To determine the mechanism of action, the researchers examined the mice's kidneys. Kidneys filter the blood using a vast network of glomeruli—tiny knots of blood vessels that act as the organ’s filters. In the exposed mice, these filters were swollen, and their delicate filtering membranes had thickened.
Additionally, the damaged kidneys produced more endothelin-1, a peptide that binds to receptors to constrict blood vessels. Under normal conditions, endothelin-1 helps regulate blood flow, but the researchers suspected that low-frequency noise pushed it into overdrive, causing constricted renal blood vessels.
To test this hypothesis, the researchers administered ambrisentan—a drug already prescribed to human patients to treat hypertension that blocks the effects of endothelin—to a second group of mice. The treated animals maintained kidney markers closer to normal levels and exhibited significantly less damage to their glomeruli, confirming endothelin signaling as a key pathway.
Because this study was conducted in mice, its relevance to humans remains unknown. However, “our findings highlight the importance of considering low-frequency noise, which has often been overlooked, in future human studies on environmental noise,” Kato said.
A Double-Edged Sword
The results are also intriguing because the same researchers previously found some beneficial effects of low-frequency sound, such as reducing motion sickness and altering blood flow in skin blood vessels.
This suggests that “the biological effects of low-frequency sound depend on its frequency, sound level, and duration of exposure,” Kato said. “Moving forward, we hope to investigate both the beneficial and adverse effects of low-frequency sound and scientifically clarify which exposure conditions are harmful and which promote health.”
Funding: This work was supported in part by Grants-in-Aid for Scientific Research (B) (22K11731, 23H03147, 25K02875, and 23K27837), Challenging Research (Exploratory) (25K22731, 25K22732, and 25K22741), Young Research (24K19748 and 26K20515), and the Fund for the Promotion of Joint International Research (22KK0145) from the Ministry of Education, Culture, Sports, Science and Technology (MEXT); a Grant-in-Aid for JSPS Research Fellows (22J22680 and 22KJ1602) from the Japan Society for the Promotion of Science; the Frontier Next-Generation Researcher Program of the Tokai Higher Education and Research System (JPMJSP2125) from JST SPRING; and JKA and its promotion funds from KEIRIN RACE (2023M-407).
Disclaimer: The funders had no role in the study design, data collection and analysis, decision to publish, or manuscript preparation.
Published in journal: Environmental Science & Technology
Authors: Takumi Kagawa, Dijie Chen, Nobutaka Ohgami, Keming Tong, Yanjun Gao, Naruhito Iwasaki, Akihito Harusato, Toyonori Tsuzuki, Takumi Hayashi, Yuuki Shimizu, Toyoaki Murohara, and Masashi Kato
Source/Credit: Nagoya University
Edited by: Scientific Frontline
Reference Number: ph081026_01