Four behaviours explain a majority of the socioeconomic disparities observed in the disease
Source: Wikimedia CC0
Lower socioeconomic status is associated with higher rates of death from coronary artery disease compared to higher socioeconomic status, and more than half of the disparities can be explained by four unhealthy behaviours. Dr Yachen Zhu of the Alcohol Research Group, US, and Dr Charlotte Probst of the Centre for Addiction and Mental Health, Canada, report these findings in a new study published September 17th in the open-access journal PLOS Medicine.
Coronary artery disease, also known as coronary heart disease or ischaemic heart disease, occurs when the arteries supplying the heart cannot deliver enough oxygen-rich blood due to plaque buildup, and is a major cause of death in the US. The condition poses a greater risk to people with lower socioeconomic status, but previous studies have reported conflicting results on whether certain unhealthy behaviours, like smoking, are primarily responsible for the observed disparities in deaths from the disease.
In the new study, researchers used data from 524 035 people aged 25 years and older whose mortality statuses were recorded in the National Death Index and who answered the National Health Interview Survey on demographics and health behaviours. The team used education as the primary indicator for socioeconomic status, and investigated four behavioural risk factors: smoking, alcohol use, physical inactivity and BMI. The four factors together explained 74% of the differences in mortality risk from coronary artery disease in men belonging to different socioeconomic levels and 61% in women.
The researchers conclude that their results highlight the need for effective public health policies and interventions that address each of these behaviours – both separately and together – because unhealthy behaviours often cluster among individuals from low socioeconomic backgrounds. They urge public health campaigns to raise awareness about heart health with messaging and outreach efforts customised for male and female audiences. The authors add, “These efforts are crucial to reducing the socioeconomic disparities in deaths from coronary artery disease in the US.”
Researchers at the University of Pittsburgh are pioneering a new approach to blood pressure monitoring, using the devices we carry with us every day. Ramakrishna Mukkamala, professor of bioengineering at Pitt’s Swanson School of Engineering, is passionate about developing accessible blood pressure (BP) detection tools. Instead of designing a new medical device to monitor BP, Mukkamala decided to take advantage of the sensors readily available in smartphones and figure out how to detect blood pressure with them.
“The most significant thing you can do to reduce your risk of cardiovascular disease is to lower high blood pressure through lifestyle changes, but in underserved populations, many people don’t have access to blood pressure cuffs, regular doctor’s appointments, or even know it’s a problem,” Mukkamala said. “But they do have smartphones.”
Mukkamala’s team harnessed tools already built into most smartphones, like motion-sensing accelerometers, front cameras, and touch sensors to build an Android smartphone application that can measure an individual’s pulse pressure.The user performs a hand-raising motion while holding the smartphone to make a measurement. The results of the project, published in Scientific Reports, demonstrate a promising new technology that could uniquely help reduce the burden of systolic hypertension globally, particularly in underserved populations.
Designing blood pressure technology for a touchscreen
Turning a smartphone into a monitoring device is no easy task, as Vishaal Dhamotharan, graduate student in the Cardiovascular Health Tech Laboratory, found out through multiple iterations of app development. Because smartphones don’t have force sensing tools, a crucial element of the project was figuring out how to replicate the effects of a traditional blood pressure exam using only a cell phone, which the team solved by using a familiar force – gravity.
“Because of gravity, there’s a hydrostatic pressure change in your thumb when you raise your hands up above your heart, and using the phone’s accelerometer, you’re able to convert that into the relative change in pressure.” Dhamotharan said.
By pairing this hand-raising motion with guided thumb maneuvers on the smartphone, the team was able to calculate each participant’s pulse pressure, the difference between systolic and diastolic numbers. For example, an individual with a BP measurement of 120/80 has a pulse pressure of 40. For Sanjeev Shroff, collaborator and bioengineering department chair, this publication is a promising advancement for blood pressure measurement devices.
“Development of a cuffless blood pressure measurement device that does not require any external calibration is the holy grail – such a device currently does not exist,” Shroff said. “The research work reported in this publication is an important step in the right direction, and is also encouraging for additional work aimed at obtaining systolic, diastolic, and mean pressures.”
Although pulse pressure isn’t typically used in cardiovascular disease monitoring, the study revealed its significance as a metric for detecting hypertension, according to Céderick Landry, assistant professor at the University of Sherbrooke and former postdoctoral researcher in the lab.
“Guidelines typically require doctors to measure both systolic and diastolic blood pressure, and pulse pressure is just the difference between the two.” Landry said. “We showed that if you only have access to pulse pressure, it’s still very correlated with hypertension, so part of our challenge now is changing the mentality on how to best measure things.”
Hypertension management within reach
This app could bring blood pressure monitoring software to any smartphone owner, enabling consistent self-monitoring and easy sharing of results with healthcare providers. This innovation is especially promising for managing hypertension, which can often be lowered through lifestyle changes such as reducing salt intake, quitting smoking and exercising regularly.
“This app would be really useful in low-income settings where people may not even have existing access to blood pressure tools.” Dhamotharan said. “Being able to measure blood pressure more frequently would allow an individual to track any significant changes in blood pressure, monitor for hypertension, and be able to manage their conditions with that knowledge.”
“The research is here – we just need some help making the technology better.” Landry said. “This is the first method of its kind, and even better, it’s something that we can start implementing right now.”
Patients with throat problems were less able to regulate their blood pressure in a new study published in JAMA Otolaryngology. The baroreflex is a crucial part of the autonomic nervous system which detects changes in blood pressure, adjusting heart rate and blood vessel tone accordingly to maintain stable blood pressure. It is what prevents fainting when standing up.
Researchers from the University of Southampton and University Hospitals of Dorset Foundation Trust believe the findings could be explained by the Vagas nerve (which controls the autonomic nervous system) prioritising protection of the airways over less urgent functions, such as blood pressure regulation.
“Our immediate survival depends on the throat being able to separate air and food passages each time we swallow,” says the lead author of the study Reza Nouraei, Professor of Laryngology and Clinical Informatics at the University of Southampton.
“The throat does this using delicate reflexes, but when these reflexes are disturbed, for example, due to a viral infection like Covid or exposure to reflux affecting nerves in this region, the control of this critical junction becomes compromised, giving rise to symptoms like the feeling of a lump in the throat, throat clearing and coughing.
“To compensate for a faulty throat, the autonomic control system must expend significant amounts of energy to maintain a safe airway. We found that in patients with a faulty throat, the heart, specifically a function called baroreflex, is less well controlled. This is one of the Peters that has been robbed to pay Paul.
“The problem with robbing this Peter is that it likely impacts long-term survival, as patients with reduced baroreflex function are more likely to die of a heart attack or stroke in years to come.”
The researchers compared the heart rates, blood pressure and baroreflex sensitivity of 23 patients admitted to Ear, Nose and Throat (ENT) surgery with aerodigestive (laryngopharyngeal) symptoms and 30 patients admitted to Gastroenterology with digestive (oesophagogastric) symptoms at University Hospitals of Dorset NHS Foundation Trust.
Reflux was a common cause of symptoms in both groups – making up the majority of digestive group cases. Other causes like thinning of the vocal cord were present in the aerodigestive group.
The team found patients in the aerodigestive group had a higher resting heart rate, lower resting blood pressure, and lower baroreflex sensitivity, than those in the digestive group.
“Now, and especially since Covid which damages nerves, we are seeing more patients with throat symptoms,” says Professor Nouraei.
“Reduced baroreflex sensitivity impacts survival independent of other cardiovascular risks, so if the association we’ve discovered is confirmed by future studies, the need to make timely and accurate diagnoses and provide early and definitive treatments will become more pressing.”
The study adds to the increasing interest in the Vaus nerve and holistic health. As well as regulating blood pressure through the baroreflex, the Vagus nerve controls our heart rate, digestion, respiration, mood and a host of other bodily functions which affect our health and wellbeing.
Professor Nouraei says: “This study helps us to think about patients more holistically. As a clinician, if you can fix a problem in the throat that is potentially taking away bandwidth from the Vagus, then it frees up the nerve to give to the rest of the body.
“If there is a chance that throat problems can affect functions like the baroreflex, or have a wider impact on overall wellbeing, then they need more consideration.”
The researchers will now look at the long-term impacts of throat conditions on autonomic health and the effects of treatment.
New research from Mayo Clinic suggests that artificial intelligence (AI) could improve the diagnosis of peripartum cardiomyopathy, a potentially life-threatening and treatable condition that weakens the heart muscle of women during pregnancy or in the months after giving birth. Researchers used an AI-enabled digital stethoscope that captures electrocardiogram (ECG) data and heart sounds to identify twice as many cases of peripartum cardiomyopathy as compared to regular care, according to a news release from the American Heart Association.
Identifying a weak heart pump caused by pregnancy is important because the symptoms, such as shortness of breath when lying down, swelling of hands and feet, weight gain, and rapid heartbeat, can be confused with normal symptoms of pregnancy.
Dr Demilade Adedinsewo, a cardiologist at Mayo Clinic, shared research insights during a late-breaking science presentation at the American Heart Association’s Scientific Sessions 2023.
Women in Nigeria have the highest reported incidence of peripartum cardiomyopathy. The randomised pragmatic clinical trial enrolled 1195 women receiving pregnancy care in Nigeria. Approximately half were evaluated with AI-guided screening using the digital stethoscope, and half received usual obstetric care in addition to a clinical ECG. An echocardiogram was used to confirm when the AI-enabled digital stethoscope predicted peripartum cardiomyopathy. Overall, 4% of the pregnant and postpartum women in the intervention arm of the clinical trial had cardiomyopathy compared to 2% in the control arm, suggesting that half are likely undetected with usual care.
Right side heart failure. Credit: Scientific Animations CC4.0
Finerenone reduced the composite of total first and recurrent heart failure (HF) events (hospitalisations for HF or urgent HF visits) and cardiovascular death in patients with HF and mildly reduced or preserved ejection fraction, according to an international clinical trial led by investigators from Brigham and Women’s Hospital.
Heart failure events and cardiovascular death were less common in the finerenone group than in the placebo group. Overall, the rate of serious adverse events was similar across the groups, but rates of hyperkalaemia were higher for the group taking finerenone. Results were presented at the European Society of Cardiology Congress 2024 and published simultaneously in the New England Journal of Medicine.
“We saw benefit regardless of the ejection fraction and even in patients who were on other approved therapies,” said trial principal investigator and corresponding author Scott Solomon, MD, the director of the Clinical Trials Outcomes Center at Mass General Brigham and the Edward D. Frohlich Distinguished Chair at Brigham and Women’s Hospital. “This drug represents a new drug class that may become a pillar of therapy for this disease.”
HF is the progressive decline in the heart’s ability to fill with and pump blood. It affects over 60 million people worldwide. Approximately half of all people living with HF have mildly reduced or preserved left ventricular ejection fraction, a condition with limited treatment options. These findings suggest that the non-steroidal mineralocorticoid receptor antagonist finerenone could represent a new therapeutic option for patients.
The FINEARTS-HF trial, funded by Bayer, assigned 6000 patients to receive either finerenone or placebo in addition to their existing therapies. The trial’s limitations include few Black patients, although the percentage of Black patients was proportional to their regional population. “Our group continues to study novel therapies for heart failure,” Solomon said. “There’s huge residual risk in these patients and so more room for new therapies.“
The demands of the working week, often influenced by school or work schedules, can lead to sleep disruption and deprivation. Fortunately, new research presented at ESC Congress 2024 shows that people that ‘catch up’ on their sleep by sleeping in at weekends may see their risk of heart disease fall by one-fifth.
“Sufficient compensatory sleep is linked to a lower risk of heart disease,” said study co-author Mr Yanjun Song of the State Key Laboratory of Infectious Disease, Fuwai Hospital, National Centre for Cardiovascular Disease, Beijing, China. “The association becomes even more pronounced among individuals who regularly experience inadequate sleep on weekdays.”
It is well known that people who suffer sleep deprivation ‘sleep in’ on days off to mitigate the effects of sleep deprivation. However, there is a lack of research on whether this compensatory sleep helps heart health.
The authors used data from 90 903 subjects involved in the UK Biobank project, and to evaluate the relationship between compensated weekend sleep and heart disease, sleep data was recorded using accelerometers and grouped by quartiles (divided into four approximately equal groups from most compensated sleep to least). Q1 (n = 22 475 was the least compensated, having -16.05 hours to -0.26 hours (ie, having even less sleep); Q2 (n = 22 901) had -0.26 to +0.45 hours; Q3 (n=22 692) had +0.45 to +1.28 hours, and Q4 (n=22 695) had the most compensatory sleep (1.28 to 16.06 hours).
Sleep deprivation was self-reported, with those self-reporting less than 7 hours sleep per night defined as having sleep deprivation. A total of 19 816 (21.8%) of participants were defined as sleep deprived. The rest of the cohort may have experienced occasional inadequate sleep, but on average, their daily hours of sleep did not meet the criteria for sleep deprivation – the authors recognise this a limitation to their data.
Hospitalisation records and cause of death registry information were used to diagnose various cardiac diseases including ischaemic heart disease (IHD), heart failure (HF), atrial fibrillation (AF), and stroke.
With a median follow-up of almost 14 years, participants in the group with the most compensatory sleep (quartile 4) were 19% less likely to develop heart disease than those with the least (quartile 1). In the subgroup of patients with daily sleep deprivation those with the most compensatory sleep had a 20% lower risk of developing heart disease than those with the least. The analysis did not show any differences between men and women.
Co-author Mr Zechen Liu, also of State Key Laboratory of Infectious Disease, Fuwai Hospital, National Centre for Cardiovascular Disease, Beijing, China, added: “Our results show that for the significant proportion of the population in modern society that suffers from sleep deprivation, those who have the most ‘catch-up’ sleep at weekends have significantly lower rates of heart disease than those with the least.”
For patients with a history of myocardial infarction (MI), cardiovascular safety of interrupting beta-blocker could not be shown in comparison to continuation and there was no benefit to the patients’ quality of life, according to late-breaking research presented in a Hot Line session today at ESC Congress 2024.1
“Improvements in MI management and data from observational studies have led physicians to question whether continuing beta-blockers after one year post-MI is needed since unnecessary treatment may result in side effects.2-5 We conducted the ABYSS trial to provide conclusive randomised data on the effects of beta-blocker interruption vs. continuation on cardiovascular events and quality of life, but we were unable to show safety preservation in terms of clinical events nor any benefit on quality of life with beta-blocker interruption,” said Principal Investigator, Professor Johanne Silvain of the Sorbonne University, Paris, France.
The open-label, non-inferiority, randomised ABYSS trial, conducted by the ACTION Group, included patients with a prior MI taking long-term beta-blockers, with a left ventricular ejection fraction of at least 40% and no cardiovascular events in the previous six months. Participants were randomised (1:1) to interrupting or continuing their β-blocker medication.
The primary endpoint was a composite of death, non-fatal MI, non-fatal stroke or hospitalisation for cardiovascular reasons at the longest follow-up (minimum, one year), according to an analysis of non-inferiority (defined as a between-group absolute difference of < 3 percentage points for the upper boundary of the two-sided 95% confidence interval [CI]). The main secondary endpoint was the change in quality of life as measured by the European Quality of Life–5 Dimensions questionnaire.
In total 3698 patients were randomised from 49 sites in France. The mean age was 64 years and 17% were female. The median time between last MI and randomisation was 2.9 years (interquartile range 1.2–6.4 years).
Over median follow-up of 3 years, interruption of long-term beta-blocker treatment was not shown to be non-inferior to beta-blocker continuation. A primary-outcome event occurred in 23.8% of patients in the interruption group and in 21.1% in the continuation group (risk difference 2.8 percentage points; 95% CI <0.1–5.5), with a hazard ratio of 1.16 (95% CI 1.01–1.33; p = 0.44 for non-inferiority).
Death occurred in 4.1% in the interruption group and 4.0% in the continuation group, while MI occurred in 2.5% and 2.4%, respectively. Of note, hospitalisation for cardiovascular causes occurred in 18.9% in the interruption group and 16.6% in the continuation group. Beta-blocker interruption was also associated with increases in systolic and diastolic blood pressure and heart rate at 6 months (all p<0.001 vs. beta-blocker continuation) and during the study follow up. Beta-blocker interruption did not improve the patients’ quality of life.
Summing up the evidence from the ABYSS trial, Professor Silvain concluded: “Differences between the groups with respect to hospitalisation for cardiovascular reasons and the negative effect on blood pressure levels, together with the absence of quality-of-life improvement do not support interruption of a chronic beta-blocker treatment in post-MI patients. These results must be put into context with recent findings from the open-label REDUCE-MI6 trial and ongoing trials to provide additional evidence on the optimal use of beta-blockers after MI.”
References
‘Beta blocker interruption in patients with prior myocardial infarction: results of the ABYSS trial and effect on blood pressure and heart rate control’ will be discussed during Hot Line 1 on Friday 30 August in room London.
Holt A, Blanche P, Zareini B, et al. Effect of long-term beta-blocker treatment following myocardial infarction among stable, optimally treated patients without heart failure in the reperfusion era: a Danish, nationwide cohort study. Eur Heart J. 2021;42:907–914.
Park CS, Yang H-M, Ki Y-J, et al. Left ventricular ejection fraction 1 year after acute myocardial infarction identifies the benefits of the long-term use of beta-blockers: analysis of data from the KAMIR-NIH Registry. Circ Cardiovasc Interv. 2021;14:e010159.
Puymirat E, Riant E, Aissaoui N, et al. β Blockers and mortality after myocardial infarction in patients without heart failure: multicentre prospective cohort study. BMJ. 2016;354:i4801.
Kim J, Kang D, Park H, et al. Long-term β-blocker therapy and clinical outcomes after acute myocardial infarction in patients without heart failure: nationwide cohort study. Eur Heart J. 2020;41:3521–3529.
Yndigegn T, Lindahl B, Mars K, et al. Beta-blockers after myocardial infarction and preserved ejection fraction. N Engl J Med. 2024;390:1372–1381.
Enhancing prefrontal cortex (PFC) cognitive functions requires identifying suitable exercises that increase cerebral blood flow. A recent study using functional near-infrared spectroscopy found that short-duration, low-intensity physical exercises, except static stretching with monotonous movements, increased oxygenated haemoglobin (oxy-Hb) levels, thereby activating the PFC and enhancing blood flow in children. This study marks a significant step toward improving both the physical and mental health of children.
Cognitive functions, also known as intellectual functions, encompass thinking, understanding, memory, language, computation, and judgment, and are performed in the cerebrum. The prefrontal cortex (PFC), located in the frontal lobe of the cerebral cortex, handles these functions. Studies have shown that exercise improves cognitive function through mechanisms such as enhanced cerebral blood flow, structural changes in the brain, and promotion of neurogenesis. However, 81% of children globally do not engage in enough physical activity, leading to high levels of sedentary behavior and insufficient exercise. This lack of physical activity raises concerns about its negative impact on children’s healthy brain development and cognitive function.
A recent study from Waseda University published in Scientific Reports, by doctoral student Takashi Naito from the Graduate School of Sport Sciences, along with Professors Kaori Ishii and Koichiro Oka from the Faculty of Sport Sciences, offers insights into potential solutions. The study investigated the effects of short-duration and light-intensity exercise on increasing cerebral blood flow in children. “Our goal is to develop a light-intensity exercise program that is accessible to everyone, aiming to enhance brain function and reduce children’s sedentary behaviour. We hope to promote and implement this program in schools through collaborative efforts,” says Naito.
To enhance cognitive performance, it is essential to develop exercise programs that increase cerebral blood flow. While previous studies have established the benefits of moderate-to-vigorous exercise on cognitive functions, changes in cerebral blood flow during light-intensity exercise, particularly in children, is yet to be investigated. To address this gap, the team conducted an experimental study to examine the effects of short-term, light-intensity exercises on prefrontal cortex (PFC) hemodynamics. They focused on exercises that can be easily performed on the spot without special equipment, such as stretching. Functional near-infrared spectroscopy (fNIRS), an imaging technique that measures changes in cerebral blood flow through oxy-Hb concentrations, was used for this purpose.
The study enrolled 41 healthy children ranging from fifth-grade elementary to third-year junior high school students. The children were taught seven different types of low-intensity exercises along with associated safety measures. These exercises included Upward Stretch, Shoulder Stretch, Elbow Circles, Trunk Twist, Washing Hands, Thumb and Pinky, and Single-leg Balance. The exercises were performed while seated except Single-leg Balance, with movement patterns lasting for 10 and 20 seconds. Researchers recorded and compared oxy-Hb levels at rest and during exercise.
The study’s results were highly promising, showing a significant increase in oxy-Hb levels in multiple regions of the PFC during all forms of exercise compared to the resting state. However, no significant change in oxy-Hb levels was observed during static stretching with movement in one direction. “By combining the types of exercise that easily increase blood flow in the PFC identified in this study, it is possible to develop an exercise program that everyone can easily engage in to improve children’s executive functions. It may also be used in the future to prevent cognitive decline in adults and the elderly,” explains Naito optimistically.
In conclusion, this groundbreaking study represents a significant step forward in combating sedentary lifestyles and activating brain functions in children, thereby supporting their physical and mental growth. Although this study demonstrated that even short-duration, low-intensity exercise can increase cerebral blood flow in the prefrontal cortex, future research is needed to confirm whether such exercises actually lead to improved cognitive function.
A new study from researchers with UCLA Health and collaborating organisations has found that asporin, a protein encoded by the ASPN gene, plays a protective role in pulmonary arterial hypertension (PAH).
Their findings, out now in the peer-reviewed journal Circulation, offer new insights into this incurable, often-fatal disease and suggest potential new ways to treat it. The ASPN gene is part of a group of genes associated with the cartilage matrix.
“We were surprised to find that asporin, which previously had not been linked to PAH, gets upregulated to increased levels as a response to counteract this disease process,” said Dr Jason Hong, a pulmonary and critical care physician at UCLA Health and the study’s corresponding author. “This novel finding opens up new avenues for understanding PAH pathobiology and developing potential therapies.”
Pulmonary hypertension is a serious medical condition characterised by high blood pressure in the arteries that supply the lungs. It causes these arteries to narrow or become blocked, which, in turn, slows blood flow to the heart, requiring it to work harder to pump blood through the lungs. Eventually, the heart muscle becomes weak and begins to fail.
Need for New Therapies
According to recent estimates, PAH affects about 1% of the global population, but that number climbs to 10% in people who are 65 or older.
There’s no cure for the disease, but medications and lifestyle changes can help slow progression, manage symptoms and prolong life.
The urgent need for new therapies, combined with the potential of multiomics – an integrated approach to drive discovery across multiple levels of biology – inspired Hong and research colleagues, including co-first author Lejla Medzikovic and senior author Mansoureh Eghbali to take a deep dive into the disease. Both work at UCLA’s Eghbali Laboratory.
Methodology
For the study, the researchers applied novel computational methods, including transcriptomic profiling and deep phenotyping, to lung samples of 96 PAH patients and 52 control subjects without the condition from the largest multicenter PAH lung biobank available to-date. They integrated this data with clinical information, genome-wide association studies, graphic models of probabilities and multiomics analysis.
“Our detailed analysis found higher levels of asporin in the lungs and plasma of PAH patients, which were linked to less severe disease,” Hong said.
Additionally, Medzikovic noted that their cell and living-organism experiments found that asporin inhibited pulmonary artery smooth muscle cell proliferation and a key signaling pathway that occurs with PAH.
“We also demonstrated that recombinant asporin treatment reduced PAH severity in preclinical models,” said Medzikovic.
Next Steps
Hong and colleagues plan to further investigate the mechanisms by which asporin exerts its protective effects in PAH and explore potential therapeutic applications, focusing on how to translate their findings into clinical trials.
“Asporin represents a promising new target for therapeutic intervention in pulmonary arterial hypertension,” he explained. “Enhancing asporin levels in PAH patients could potentially lead to improved clinical outcomes and reduced disease progression.”
Noise exposure is a known occupational hazard in some jobs, particularly for hearing loss, physical and psychological stress, and reduced concentration. A new study presented at the ACC Asia 2024 conference found in adult power loom weavers, chronic noise exposure not only increased their blood pressure overall, but also each year of exposure increased their odds of having high blood pressure by 10%.
“While the mechanism is still not well-explored, it is thought that the stress response by the body to chronic sound exposure causes hormonal imbalances that gradually leads to a permanent elevation of blood pressure,” said Golam Dastageer Prince, MBBS, MPH, medical officer at DGHS Bangladesh and the study’s lead author. “High blood pressure impacts more than a billion people worldwide and just 1 in 5 have it under control, yet it is a major cause of premature death. In addition to treating the high blood pressure through appropriate means, we must find ways to mitigate the exposure to the noise if we want to reduce the cardiovascular risk of these patients.”
Researchers at the Directorate of General Health Services in Bangladesh looked at 289 adult workers in selected weaving factories in the Araihazar sub-district of Narayanganj, Bangladesh, from January to December 2023. Participants took a face-to-face interview to complete a questionnaire covering sociodemographic variables, behaviour, dietary habits and family medical history. Blood pressure, height, weight and noise intensity were measured following standard procedures by the researchers.
The study cohort was predominantly male and married and were about 34 years of age on average. According to the researchers, a notable proportion of the cohort was illiterate. Workplace exposure duration averaged nearly 16 years, with noise intensity ranging from 96–111 decibels. In the United States the National Institute for Occupational Safety and Health has established the recommended exposure limits for occupational noise exposures to be 85 decibels on average over an eight-hour workday. Sounds at or below 70 decibels are generally considered safe.
According to Prince, none of the study population was found to be wearing ear protection personal protective equipment.
“Hopefully we can raise awareness of not only noise-induced hearing loss, but the impact of noise on blood pressure and workers’ behaviors and attitudes towards using personal protective equipment,” Prince said. “Pushing for structural improvements to industries may also help us improve the health safety of these workers.”
The study population had a 31.5% rate of high blood pressure with an additional 53.3% being prehypertensive. The study also found a positive correlation between blood pressure and noise exposure duration. Each year of exposure was found to increase high blood pressure odds by 10%, even after adjusting for age, body mass index and smoking status.
“As the study focused on workers exposed to more than 85 decibels noise for long periods of time, any profession causing workers to experience similar exposure might experience similar blood pressure impacts,” Prince said. “We definitely need more exploratory studies to reveal more information about the potential mechanisms and long-term health outcomes.”
Recent studies have shown that living near noise pollution, including highways, trains and air traffic, can have an impact on cardiovascular health. However, the current study may not apply to noise experienced during daily life. Noise pollution experienced near home typically ebbs and flows, while the industrial exposures in the study are typically continuous in pattern due to the machinery and remain at a constant sound level, according to Prince.
