How Pollution Impacts Pulmonary Hypertension Risk

Air pollution is a proven environmental risk factor for hypertension. Fine particulate matter (PM) in the air can have an independent effect on the body, or through potentially synergistic and antagonistic effects.

Several studies have demonstrated the relationship between PM2.5 levels, the concentration of pollutants associated with transport emissions, and BP elevation observed within hours to days. A study of 3,700 participants, aged 35–83, from a population cohort in Spain showed that a 10 μg/m3 increase in NO2 levels was associated with 1.34 mmHg higher systolic BP in those who did not receive treatment, after adjusting for traffic noise.

In a cohort of 35,303 non-hypertensive adults from Ontario, Canada, between 1996 and 2010, for each 10 μg/m3 increase in PM2.5, the hazard ratio of incident hypertension was 1.13. The results of a cohort prospective epidemiological study from urban Delhi, India, with 5,342 participants, demonstrate strong longitudinal associations using repeated measures between ambient PM2.5 exposure, BP, and incident hypertension. Both short- and long-term exposure contributed to higher BP and increased incident hypertension risk.

Some studies provide evidence toward a positive association between both short-term and long-term exposure to some air pollutants and BP among children and adolescents. In a meta-analysis of 14 articles, short-term exposure to PM10 and long-term exposure to NO2, PM10 and PM2.5 were significantly associated with elevated BP values. A 10 μg/m3 PM10 increase was significantly associated with a 0.276 mmHg systolic BP elevation. Long-term exposure to NO2, PM2.5, and PM10 was associated with systolic BP elevation and long-term exposure to PM2.5 and PM10 was associated with diastolic BP increase.

Pulmonary hypertension is high blood pressure in the pulmonary arteries, which carry oxygen-poor blood from the heart to the lungs. The earliest symptom is shortness of breath during your usual routine. The most common causes are heart disease, lung disease, and hypoxia.

Air pollution and the development of pulmonary hypertension

Air pollution is a proven environmental risk factor for the development of hypertension. It is one of the many environmental factors, alongside sedentary lifestyle, weight gain, increased sodium intake, an unhealthy diet, and the use of pro-hypertensive substances, that can contribute to the development of hypertension.

Particulate matter (PM) is a complex mixture of particles and gaseous components that can have an independent effect on the body or act synergistically with other components. The effects of air pollution on blood pressure have been observed in both short- and long-term exposures.

Several studies have demonstrated a relationship between PM2.5 levels and an increase in blood pressure. A controlled study of 3,700 participants from Spain showed that a 10 μg/m3 increase in NO2 levels was associated with a 1.34 mmHg higher systolic blood pressure in those who did not receive treatment. Another study of 35,303 non-hypertensive adults from Ontario, Canada, found that for each 10 μg/m3 increase in PM2.5, the hazard ratio of incident hypertension was 1.13.

Additionally, air pollution has been linked to an increased risk of stroke, with elevated concentrations of pollutants increasing hospital admissions and emergency visits for hypertensive disorders.

The development of hypertension is the result of the interaction between genetic predisposition and environmental factors. While individual measures can be proposed to reduce the impact of air pollution on cardiovascular health, reducing air pollution requires the involvement of governmental resources and public health systems.

The impact of air pollution on the right ventricle

Air pollution is a proven environmental risk factor for hypertension, and there is substantial evidence of the pathophysiological mechanisms linking air pollution and hypertension. Hypertension is a general diagnosis that means a person has high blood pressure in their pulmonary arteries. These are the blood vessels that carry oxygen-poor blood from the heart to the lungs.

Pulmonary hypertension is dangerous because it disrupts the flow of blood through the heart and lungs. High blood pressure in the pulmonary arteries causes these arteries to become narrow. As a result, the heart must work harder to pump oxygen-poor blood to the lungs. Over time, pulmonary hypertension damages the heart and causes problems throughout the body. It can be fatal without treatment.

The right ventricle (lower right chamber) is responsible for pumping oxygen-poor blood to the lungs. So, over time, pulmonary hypertension causes the right ventricle to get bigger due to the extra work. This condition (right ventricular hypertrophy) can lead to right-sided heart failure. Right-sided heart failure has a ripple effect throughout the body. It can disrupt the normal workings of many organs and systems.

Air pollution can be considered a significant but potentially modifiable cardiovascular risk factor. Fine particulate matter (PM) and gaseous compounds such as ozone (O3), nitrogen dioxide (NO2), other nitrous oxides (NOx), and sulphur dioxide (SO2) are the main pollutants. PM2.5 is of particular interest, as these very small particles can reach the alveolar space and permeate the epithelium.

Several studies have shown that pollution and climate change may both have a direct impact on the pulmonary vasculature, as well as indirect effects by increasing the prevalence and severity of other diseases associated with pulmonary hypertension.

The direct impact of air pollution on the right ventricle

Air pollution causes local inflammation in the lungs. Gases and smaller PM can access the bloodstream, where they might directly affect nitric oxide (NO) production through increased scavenging of NO precursors by reactive oxygen species, or decreased bioavailability through reduced activity of endothelial NO synthetase. Since reduced NO activity is also a key mechanism in pulmonary hypertension, it is conceivable that pollution-caused endothelial dysfunction in the lungs may lead to vascular remodelling, and eventually to pulmonary hypertension.

Various animal models have shown that exposure to air contaminants such as PM and diesel exhaust alter the pulmonary vasculature. Air pollution causes airway hyperresponsiveness, inflammation, pulmonary artery vasoconstriction, vascular smooth muscle cell proliferation, endothelial cell apoptosis, and pulmonary vessel remodelling in animal models.

The indirect impact of air pollution on the right ventricle

The indirect effects of air pollution on the right ventricle are mediated through the increased prevalence and severity of other diseases associated with pulmonary hypertension. These include:

• Heart disease: The left side of the heart pumps blood out to the entire body. If there is a problem on this side of the heart, it affects the right side of the heart and the entire pulmonary circuit. Blood backs up in the heart, raising the pressure in the pulmonary arteries.
• Lung disease or hypoxia: Certain lung problems cause the arteries in the lungs to tighten. Less blood can flow through the lungs, raising the pressure in the pulmonary arteries.
• Blockages in the lungs: Blood clots or scars from blood clots prevent blood from flowing normally through the lungs. This puts more stress on the right side of the heart and raises pulmonary blood pressure.
• Other disorders: PH occurs along with other conditions like blood disorders and metabolic disorders. The exact mechanisms for how the condition triggers PH aren't always clear.

The impact of air pollution on the left ventricle

The left ventricle is responsible for pumping oxygen-rich blood to the body. Pulmonary hypertension is high blood pressure in the pulmonary arteries, which carry oxygen-poor blood from the heart to the lungs.

Air pollution is a proven environmental risk factor for hypertension incidence and prognosis. It can cause an increase in systolic and diastolic blood pressure, which can lead to an increased risk of stroke.

While there is evidence that air pollution affects the pulmonary circulation, there are no clinical studies focusing specifically on its effect on pulmonary hypertension associated with left-heart disease. However, some preclinical and clinical clues show a potential link between pollution, extreme temperatures, and left-heart-disease-associated pulmonary hypertension.

Air pollution can cause endothelial dysfunction, a marker of early cardiovascular disease. It can also cause systemic and pulmonary vasculopathy, which can lead to right-ventricular hypertrophy and eventually right-sided heart failure.

Overall, the evidence suggests that air pollution can impact the left ventricle, but more research is needed to fully understand the mechanisms involved.

The impact of air pollution on the lungs

Air pollution is a proven environmental risk factor for hypertension, which is high blood pressure in the pulmonary arteries. The earliest symptom of pulmonary hypertension is shortness of breath during your usual routine. The most common causes are heart disease, lung disease, and hypoxia.

Air pollution can cause serious problems in the body, including blood clots in the pulmonary arteries, and pericardial effusion. It can also be dangerous for pregnant people, causing complications for both the birthing parent and fetus. Without treatment, pulmonary hypertension can overtax the heart and even lead to death.

Air pollution, including fine particulate matter and gaseous compounds, can have an independent effect on the body or act synergistically with other pollutants. These pollutants can have both direct and indirect effects on the body. Direct effects include vasoconstriction, which is caused by particulate matter-induced autonomic nervous system imbalance. Indirect effects include increased sympathetic tone and potential arterial remodelling, which can lead to increased total peripheral resistance and a fixation of elevated blood pressure.

Long-term exposure to air pollution has been linked to increased blood pressure and hypertension in both rural and urban populations. Studies have shown a positive association between exposure to air pollutants and elevated blood pressure values, with stronger effects observed in males, smokers, drinkers, individuals with a high-fat diet, and those with high-level physical activity.

Air pollution has also been associated with an increased risk of stroke and other cardiovascular diseases. Certain lung problems caused by air pollution, such as chronic obstructive pulmonary disease and interstitial lung disease, can lead to the tightening of arteries in the lungs, reducing blood flow and increasing blood pressure.

Additionally, air pollution can affect the development and prognosis of pulmonary hypertension, a general diagnosis for high blood pressure in the pulmonary arteries. Pulmonary hypertension has many different causes, including heart disease, lung disease, and exposure to toxins and drugs. It disrupts the flow of blood through the heart and lungs, forcing the heart to work harder to pump oxygen-poor blood. Over time, pulmonary hypertension can damage the heart and cause problems throughout the body.

Preventive measures and solutions

To reduce the impact of air pollution on the pulmonary circulation and the incidence of pulmonary hypertension, it is essential to implement preventive measures and solutions. These include:

• Reducing personal impact by using portable air purifiers and personal respirators for air purification.
• Modifying behavioural habits by avoiding areas and times of high pollution and limiting outdoor physical activity during periods of higher pollution.
• Implementing community-level policies, such as using nature landscaping in urban areas to reduce heat and build temperature shelters, and regulating waste disposal and new building plans.
• Addressing the health sector's impact on emissions through industrial production, waste, and energy consumption.

The impact of air pollution on the pulmonary circulation

Air pollution is a proven environmental risk factor for the incidence and prognosis of hypertension. Fine particulate matter (PM) is a key contributor to air pollution, and substantial evidence indicates the pathophysiological mechanisms linking air pollution and hypertension.

The development of hypertension

The development of hypertension is the result of the interaction between genetic predisposition to elevated blood pressure and environmental factors. Environmental factors of a larger geographical scale, such as air pollution, are less frequently assessed. However, reducing air pollution requires the involvement of governmental resources and public health systems.

Air pollution and the incidence of hypertension

Analysis of hypertension worldwide from 1975 to 2015 suggests that mean systolic blood pressure (SBP) in men and women has decreased in rich industrialised countries in Europe, Central Asia, the Middle East, the Caribbean and Latin America. However, there has been an increase in mean SBP and diastolic blood pressure (DBP) in sub-Saharan Africa, South Asia and Southeast Asia. It is assumed that this is a consequence of industrial activity and related environmental pollution.

Air pollution and hypertension prognosis

A meta-analysis of 6.2 million events in 28 countries demonstrated a significant association between stroke hospitalisation and/or mortality and exposure to elevated concentrations of PM2.5 and PM10.

The main pathophysiological mechanisms

In recent decades, numerous studies have been conducted to elucidate the pathophysiological mechanisms of BP elevation and increased cardiovascular risk due to pollution. These potential mechanisms include:

• Disorders of the autonomic nervous system (ANS) and/or sympathoadrenal overactivity
• Release of pro-inflammatory mediators, modified lipids or phospholipids and activation of leukocyte populations
• Endothelial dysfunction caused by oxidative stress
• Activation of prothrombotic pathways

Direct and indirect effects of pollution on systemic vasculature

An indirect effect of particulate matter exposure, mediated through systemic proinflammatory and oxidative responses, may lead to increased sympathetic tone and potentially cause arterial remodelling. Experimental and clinical data show that PM-induced oxidative stress and reduced nitric oxide bioavailability are likely to be key factors in systemic vascular dysfunction.

A direct effect of particulate matter exposure is vasoconstriction, which is a result of PM2.5-induced ANS imbalance.

Acute and chronic responses after exposure to pollution

Acute responses may occur within seconds, minutes or hours after PM inhalation, and are probably associated with an imbalance in the ANS and/or sympathetic overactivity, endothelial dysfunction, and the release of procoagulant proteins.

Individual strategies

Individual strategies to mitigate the effects of environmental pollution include:

• Reducing personal impact
• Behavioural habits modification
• Pharmacological approaches

Preventive, mitigating and adaptive measures

A change in life habits (e.g. active transportation and lifestyle, a plant-based diet, smoke cessation), besides helping to reduce carbon emissions, is a useful preventive measure to reduce the incidence of heart and lung diseases commonly associated with pulmonary hypertension.

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