Noise, defined as any unwanted or excessively intense sound, is measured in decibels (dB). A quiet daytime environment is typically around 30–40 dB, while sounds above 85 dB already represent a health risk if prolonged over time. In extreme cases (over 140 dB), acoustic energy can cause immediate ear damage and, in explosion scenarios, systemic injuries severe enough to be potentially fatal.

Acute Damage: Acoustic Trauma and Blast Injuries

Acoustic Trauma
Acoustic trauma is a direct injury to the inner ear caused by impulsive sounds of very high intensity and extremely short duration, typical of explosions, gunfire, or sudden blasts.

  • At intensities above 132 dB SPL, sound energy can induce necrosis of cochlear hair cells, leading to permanent sensorineural hearing loss and persistent tinnitus.
  • At extreme intensities, above 184 dB, tympanic membrane rupture may occur, with potential involvement of the ossicles in the middle ear and transmission of the damaging wave to the central nervous system. In such conditions, trauma is not limited to the auditory system: excessive pressure can cause severe systemic complications, including pulmonary air embolism due to overpressure (Primary Blast Lung Injury), resulting in acute respiratory failure.

Systemic Blast Injuries
Explosions generate shock waves that propagate at supersonic speeds, releasing enormous amounts of mechanical energy within milliseconds. Victims located near the epicenter are subjected to physical forces capable of producing multisystem injuries, not limited to the auditory apparatus:

  • Respiratory system: alveolar rupture, pneumothorax, pulmonary hemorrhage, and diffuse contusions, potentially progressing to acute respiratory failure.
  • Digestive system: intestinal perforations, intra-abdominal hemorrhage, and visceral damage from overdistension.
  • Cardiovascular system: arrhythmias, myocardial contusions, and internal hemorrhage due to abrupt pressure changes.
  • Central nervous system: concussion, intracranial hemorrhage, and post-concussive syndromes caused by the transmission of the blast wave through cranial structures.

Clinical Implications
Blast trauma thus represents a complex clinical condition combining permanent auditory damage with potentially fatal systemic injuries. The severity depends on the intensity of the shock wave, the distance from the explosion, and the presence of protective structures or barriers. Diagnosis and management require a multidisciplinary approach, involving otolaryngology, pulmonology, surgery, and emergency medicine.

Chronic Health Effects

Hearing Loss and Quality of Life
Continuous exposure to sound levels above 85 dB for more than eight hours per day represents a significant risk to auditory health. This condition causes progressive noise-induced hearing loss, resulting from the accumulation of micro-injuries to cochlear hair cells, which cannot regenerate once damaged. Hearing deterioration is not immediate but develops gradually through an irreversible loss of sensitivity, initially affecting high frequencies.

According to data from the Centers for Disease Control and Prevention (CDC), the occupational impact of this condition in the United States is substantial: each year, an average loss of about 2.5 healthy life years per 1,000 exposed workers is estimated, due not only to diminished hearing capacity but also to secondary disabilities, including communication difficulties, social isolation, and reduced quality of professional and personal life.

Sleep Disorders and Stress
Prolonged exposure to environmental noise above 55 dB is considered by the World Health Organization (WHO) as a critical threshold beyond which adverse health effects occur. The most immediate consequences include sleep disturbances, difficulty falling asleep, and frequent nighttime awakenings, which in the long term compromise sleep quality and promote chronic fatigue and reduced daytime concentration.

Persistent noise also increases irritability and psychological stress, directly affecting psycho-emotional well-being. Physiologically, the body reacts to noise as an alerting stimulus: chronic stimulation of the hypothalamic-pituitary-adrenal (HPA) axis leads to increased secretion of cortisol and catecholamines (adrenaline and noradrenaline). When sustained over time, this neuroendocrine activation contributes to chronic stress.

These biological mechanisms promote the onset and progression of cardiovascular diseases (hypertension, ischemic heart disease, stroke), metabolic disorders (metabolic syndrome, type 2 diabetes), and more generally chronic conditions characterized by systemic inflammation and reduced physiological resilience. Thus, the impact of environmental noise is not limited to subjective discomfort but represents a significant public health risk, with both clinical and socio-economic consequences.

Epidemiological Impact of Environmental Noise on Cardiovascular Diseases

In Europe, environmental noise is a major determinant of public health. According to estimates from the European Environment Agency (EEA), chronic exposure to excessive noise contributes annually to about 48,000 new cases of ischemic heart disease and more than 12,000 premature deaths in the European Union. These data highlight that noise is not merely a nuisance or discomfort, but a true environmental risk factor with clinically significant consequences.

The dose-response relationship between noise and cardiovascular risk has been investigated in a meta-analysis by Babisch (2014), which showed that for every 10 dB increase in the average day-night level (L_den), there is an 8% increase in relative risk of coronary heart disease (RR 1.08; 95% CI 1.04–1.13). This confirms a strong and statistically significant association, with important implications for defining safe exposure thresholds.

More recent evidence extends the field of observation beyond ischemic heart disease. A systematic review found that road traffic noise exposure is associated with an increased risk of stroke (RR 1.06; 95% CI 1.02–1.11) per 10 dB increase. Likewise, other studies documented a 4% higher risk of heart failure per 10 dB increase in environmental noise.

Taken together, these data confirm that noise acts as a chronic stressor, influencing neuroendocrine regulation and promoting pathophysiological processes underlying major cardiovascular diseases, thereby contributing to a significant burden of preventable morbidity and mortality.

Biological Mechanisms of Noise Impact on Cardiovascular Health

The harmful effect of environmental noise on the cardiovascular system is not mediated solely by perceived annoyance but occurs through complex biological mechanisms involving neuroendocrine, immune, and metabolic regulation.

  1. Non-specific Stress Activation
    Intense noise, particularly if sudden or persistent, activates the sympathetic nervous system and the HPA axis. This leads to catecholamine release (adrenaline and noradrenaline), peripheral vasoconstriction, and increased blood pressure. These effects may also occur during sleep, preventing the normal nighttime blood pressure decline (“nocturnal dipping”) and predisposing to chronic hypertension and endothelial dysfunction.
  2. Systemic Inflammation and Oxidative Stress
    Chronic noise exposure is linked to elevated levels of pro-inflammatory cytokines (such as IL-6 and TNF-α) and C-reactive protein (CRP), predictive markers of cardiovascular risk. Simultaneously, there is increased production of reactive oxygen species (ROS), reducing nitric oxide (NO) bioavailability and impairing endothelial function. These processes accelerate atherosclerosis and favor the progression of coronary and cerebrovascular disease.
  3. Circadian Rhythm and Metabolic Dysregulation
    Nighttime noise causes sleep fragmentation and reduction of deep, restorative phases, resulting in circadian dysregulation. This alters glucose and lipid metabolism, promoting insulin resistance, dyslipidemia, and visceral obesity. These factors further amplify the risk of cardiovascular disease and metabolic syndrome.

In summary, the impact of environmental noise on health is not limited to psychological discomfort but triggers a cascade of neuroendocrine, inflammatory, and metabolic mechanisms that synergistically contribute to hypertension, atherosclerosis, coronary heart disease, stroke, and heart failure.

Guidelines and Prevention

The management of environmental noise is a public health priority, since its effects are widespread, cumulative, and largely preventable.

International Guidelines
The WHO Environmental Noise Guidelines for the European Region (2018) recommend exposure thresholds to reduce health risks:

  • Daytime noise (L_den): maximum 53 dB, above which the likelihood of cardiovascular disease, particularly ischemic heart disease, increases.
  • Nighttime noise (L_night): maximum 45 dB, above which the risk of sleep disturbances significantly increases, with repercussions on metabolism and the cardiovascular system.

These values serve as essential benchmarks for health protection policies and urban planning.

Collective Noise Reduction Measures
Primary prevention is achieved mainly through structural and urban interventions aimed at reducing population exposure:

  • installation of noise barriers along road and rail infrastructures;
  • maintenance of road surfaces to reduce tire–asphalt friction noise;
  • urban planning that considers residential and sensitive areas (hospitals, schools, nursing homes), avoiding their proximity to major noise sources;
  • use of sound-absorbing materials and construction techniques to improve building insulation.

Individual Protection
In contexts where noise exposure is high and difficult to eliminate (industrial settings, construction sites, concerts, recreational events), the use of personal protective equipment (PPE) such as earplugs or noise-canceling earmuffs is recommended, tailored to the required level of attenuation. Preventive effectiveness depends on correct selection, fitting, and consistent use.

Integrated Approach
Ultimately, preventing noise-induced health damage requires a multilevel approach, combining policy, environmental, and individual strategies, with the goal of reducing not only sound intensity but also the associated burden of disease.

What Is the Loudest Noise Ever Recorded?

The loudest noise ever recorded was produced by the paroxysmal eruption of the Krakatoa volcano on August 27, 1883. The third and most violent detonation is considered the loudest sound in human history, with an estimated acoustic level near 310 dB at the source and still 180 dB at 160 km away. It was powerful enough to rupture eardrums and destroy surrounding structures, and it was heard up to 4,800 km away, where witnesses described it as sounding like a “cannon shot next to the ship.”

This explosion not only generated blast waves lethal to the human ear but also triggered deadly tsunamis and projected volcanic ash up to 27 km into the atmosphere, standing as an extreme example of how a geophysical phenomenon can produce the most powerful noise ever experienced by humanity.