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Wednesday, September 15, 2021

Particulates

From Wikipedia, the free encyclopedia

This diagram shows types, and size distribution in micrometres (μm), of atmospheric particulate matter.

Particulates – also known as atmospheric aerosol particles, atmospheric particulate matter, particulate matter (PM), or suspended particulate matter (SPM) – are microscopic particles of solid or liquid matter suspended in the air. The term aerosol commonly refers to the particulate/air mixture, as opposed to the particulate matter alone. Sources of particulate matter can be natural or anthropogenic. They have impacts on climate and precipitation that adversely affect human health, in ways additional to direct inhalation.

Types of atmospheric particles include suspended particulate matter; thoracic and respirable particles; inhalable coarse particles, designated PM10, which are coarse particles with a diameter of 10 micrometers (μm) or less; fine particles, designated PM2.5, with a diameter of 2.5 μm or less; ultrafine particles, with a diameter of 100 nm or less; and soot.

The IARC and WHO designate airborne particulates as a Group 1 carcinogen. Particulates are the most harmful form of air pollution due to their ability to penetrate deep into the lungs, blood streams and brain, causing health problems including heart attacks, respiratory disease, and premature death. In 2013, a study involving 312,944 people in nine European countries revealed that there was no safe level of particulates and that for every increase of 10 μg/m3 in PM10, the lung cancer rate rose 22% (95% CI [1.03–1.45]). The smaller PM2.5 were particularly deadly, with an 18% increase in lung cancer per 5 μg/m3 (95% CI [0.96–1.46]) as it can penetrate deeper into the lungs. Worldwide exposure to PM2.5 contributed to 4.1 million deaths from heart disease and stroke, lung cancer, chronic lung disease, and respiratory infections in 2016. Overall, ambient particulate matter ranks as the sixth leading risk factor for premature death globally.

Sources of atmospheric particulate matter

Some particulates occur naturally, originating from volcanoes, dust storms, forest and grassland fires, living vegetation and sea spray. Human activities, such as the burning of fossil fuels in vehicles, stubble burning, power plants, road dust, wet cooling towers in cooling systems and various industrial processes, also generate significant amounts of particulates. Coal combustion in developing countries is the primary method for heating homes and supplying energy. Because salt spray over the oceans is the overwhelmingly most common form of particulate in the atmosphere, anthropogenic aerosols—those made by human activities—currently account for about 10 percent of the total mass of aerosols in our atmosphere.

Composition

The composition and toxicity of aerosols, including particles, depends on their source and atmospheric chemistry and varies widely. Wind-blown mineral dust tends to be made of mineral oxides and other material blown from the Earth's crust; this particulate is light-absorbing. Sea salt is considered the second-largest contributor in the global aerosol budget, and consists mainly of sodium chloride originated from sea spray; other constituents of atmospheric sea salt reflect the composition of sea water, and thus include magnesium, sulfate, calcium, potassium, etc. In addition, sea spray aerosols may contain organic compounds, which influence their chemistry.

Some secondary particles derive from the oxidation of primary gases such as sulfur and nitrogen oxides into sulfuric acid (liquid) and nitric acid (gaseous) or from biogenic emissions. The precursors for these aerosols—i.e. the gases from which they originate—may have an anthropogenic origin (from any fossil fuel combustion) and a natural biogenic origin. In the presence of ammonia, secondary aerosols often take the form of ammonium salts; i.e. ammonium sulfate and ammonium nitrate (both can be dry or in aqueous solution); in the absence of ammonia, secondary compounds take an acidic form as sulfuric acid (liquid aerosol droplets) and nitric acid (atmospheric gas), all of which probably contribute to the health effects of particulates.

Secondary sulfate and nitrate aerosols are strong light-scatterers. This is mainly because the presence of sulfate and nitrate causes the aerosols to increase to a size that scatters light effectively.

Organic matter (OM) found in aerosols can be either primary or secondary, the latter part deriving from the oxidation of volatile organic compounds (VOCs); organic material in the atmosphere may either be biogenic or anthropogenic. Organic matter influences the atmospheric radiation field by both scattering and absorption. Some aerosols are predicted to include strongly light-absorbing material and are thought to yield large positive radiative forcing. Some secondary organic aerosols (SOAs) resulting from combustion products of internal combustion engines, have been identified as a danger to health. Particulate toxicity has been found to vary by region and source contribution which affects the particles chemical composition.

The chemical composition of the aerosol directly affects how it interacts with solar radiation. The chemical constituents within the aerosol change the overall refractive index. The refractive index will determine how much light is scattered and absorbed.

The composition of particulate matter that generally causes visual effects, haze, consists of sulfur dioxide, nitrogen oxides, carbon monoxide, mineral dust, and organic matter. The particles are hygroscopic due to the presence of sulfur, and SO2 is converted to sulfate when high humidity and low temperatures are present. This causes reduced visibility and yellow color.

Size distribution of particulates

A computer graphic showing how many PM10 particles can be wrapped around a human hair and how several PM2.5 particles can be wrapped around PM10
PM2.5 and PM10 compared with a human hair in a graphic from the Environmental Protection Agency
 

The false-color maps in the map of distribution of aerosol particles on this page show where there are natural aerosols, human pollution, or a mixture of both, monthly.

Among the most obvious patterns that the size distribution time series shows is that in the planet's most southerly latitudes, nearly all the aerosols are large, but in the high northern latitudes, smaller aerosols are very abundant. Most of the Southern Hemisphere is covered by the ocean, where the largest source of aerosols is natural sea salt from dried sea spray. Because the land is concentrated in the Northern Hemisphere, the amount of small aerosols from fires and human activities is greater there than in the Southern Hemisphere. Overland, patches of large-radius aerosols appear over deserts and arid regions, most prominently, the Sahara Desert in North Africa and the Arabian Peninsula, where dust storms are common. Places where human-triggered or natural fire activity is common (land-clearing fires in the Amazon from August–October, for example, or lightning-triggered fires in the forests of northern Canada in Northern Hemisphere summer) are dominated by smaller aerosols. Human-produced (fossil fuel) pollution is largely responsible for the areas of small aerosols overdeveloped areas such as the eastern United States and Europe, especially in their summer.

Satellite measurements of aerosols, called aerosol optical thickness, are based on the fact that the particles change the way the atmosphere reflects and absorbs visible and infrared light. As shown in the seventh image on this page, an optical thickness of less than 0.1 (palest yellow) indicates a crystal clear sky with maximum visibility, whereas a value of 1 (reddish-brown) indicates very hazy conditions.

Deposition processes

In general, the smaller and lighter a particle is, the longer it will stay in the air. Larger particles (greater than 10 micrometers in diameter) tend to settle to the ground by gravity in a matter of hours whereas the smallest particles (less than 1 micrometer) can stay in the atmosphere for weeks and are mostly removed by precipitation. Diesel particulate matter is highest near the source of emission. Any information regarding DPM and the atmosphere, flora, height, and distance from major sources is useful to determine health effects.

Controlling technologies

Fabric filters Hepa effect: without (outdoor) and with filter (indoor)
 

A complicated blend of solid and liquid particles result in particulate matter and these particulate matter emissions are highly regulated in most industrialized countries. Due to environmental concerns, most industries are required to operate some kind of dust collection system to control particulate emissions. These systems include inertial collectors (cyclonic separators), fabric filter collectors (baghouses), electrostatic filters used in facemasks, wet scrubbers, and electrostatic precipitators.

Cyclonic separators are useful for removing large, coarse particles and are often employed as a first step or "pre-cleaner" to other more efficient collectors. Well-designed cyclonic separators can be very efficient in removing even fine particulates, and may be operated continuously without requiring frequent shutdowns for maintenance.

Fabric filters or baghouses are the most commonly employed in general industry. They work by forcing dust-laden air through a bag-shaped fabric filter leaving the particulate to collect on the outer surface of the bag and allowing the now clean air to pass through to either be exhausted into the atmosphere or in some cases recirculated into the facility. Common fabrics include polyester and fiberglass and common fabric coatings include PTFE (commonly known as Teflon). The excess dust buildup is then cleaned from the bags and removed from the collector.

Wet scrubbers pass the dirty air through a scrubbing solution (usually a mixture of water and other compounds) allowing the particulate to attach to the liquid molecules. Electrostatic precipitators electrically charge the dirty air as it passes through. The now charged air then passes through large electrostatic plates which attract the charged particle in the airstream collecting them and leaving the now clean air to be exhausted or recirculated.

Besides removing particulates from the source of pollution, it can also be cleaned in the open air.

Climate effects

2005 radiative forcings and uncertainties as estimated by the IPCC.

Atmospheric aerosols affect the climate of the earth by changing the amount of incoming solar radiation and outgoing terrestrial longwave radiation retained in the earth's system. This occurs through several distinct mechanisms which are split into direct, indirect and semi-direct aerosol effects. The aerosol climate effects are the biggest source of uncertainty in future climate predictions. The Intergovernmental Panel on Climate Change, Third Assessment Report, says: While the radiative forcing due to greenhouse gases may be determined to a reasonably high degree of accuracy... the uncertainties relating to aerosol radiative forcings remain large, and rely to a large extent on the estimates from global modeling studies that are difficult to verify at the present time.

Aerosol radiative effects

Global aerosol optical thickness. The aerosol scale (yellow to dark reddish-brown) indicates the relative amount of particles that absorb sunlight.
 
File:MODAL2 M AER OD.ogv
These maps show average monthly aerosol amounts around the world based on observations from the Moderate Resolution Imaging Spectroradiometer (MODIS) on NASA's Terra satellite.

Direct effect

Particulates in the air causing shades of grey and pink in Mumbai during sunset
 
File:Display VSON WP6910 (air detector) -Location 45.44234 10.96862 Verona (Borgo Milano) Italy, strong burnt smell -pm2,5 OUTdoor particulate pollution, polveri sottili, smog (smoke heating systems???) -2020 04 02 (hour20 15).webm
Italian city polluted by particulates and optic air detector (laser)

The direct aerosol effect consists of any direct interaction of radiation with atmospheric aerosols, such as absorption or scattering. It affects both short and longwave radiation to produce a net negative radiative forcing. The magnitude of the resultant radiative forcing due to the direct effect of an aerosol is dependent on the albedo of the underlying surface, as this affects the net amount of radiation absorbed or scattered to space. e.g. if a highly scattering aerosol is above a surface of low albedo it has a greater radiative forcing than if it was above a surface of high albedo. The converse is true of absorbing aerosol, with the greatest radiative forcing arising from a highly absorbing aerosol over a surface of high albedo. The direct aerosol effect is a first-order effect and is therefore classified as a radiative forcing by the IPCC. The interaction of an aerosol with radiation is quantified by the single-scattering albedo (SSA), the ratio of scattering alone to scattering plus absorption (extinction) of radiation by a particle. The SSA tends to unity if scattering dominates, with relatively little absorption, and decreases as absorption increases, becoming zero for infinite absorption. For example, the sea-salt aerosol has an SSA of 1, as a sea-salt particle only scatters, whereas soot has an SSA of 0.23, showing that it is a major atmospheric aerosol absorber.

Indirect effect

The Indirect aerosol effect consists of any change to the earth's radiative budget due to the modification of clouds by atmospheric aerosols and consists of several distinct effects. Cloud droplets form onto pre-existing aerosol particles, known as cloud condensation nuclei (CCN). Droplets condensing around human-produced aerosols such as found in particulate pollution tend to be smaller and more numerous than those forming around aerosol particles of natural origin (such as windblown dust).

For any given meteorological conditions, an increase in CCN leads to an increase in the number of cloud droplets. This leads to more scattering of shortwave radiation i.e. an increase in the albedo of the cloud, known as the Cloud albedo effect, First indirect effect or Twomey effect. Evidence supporting the cloud albedo effect has been observed from the effects of ship exhaust plumes and biomass burning on cloud albedo compared to ambient clouds. The Cloud albedo aerosol effect is a first order effect and therefore classified as a radiative forcing by the IPCC.

An increase in cloud droplet number due to the introduction of aerosol acts to reduce the cloud droplet size, as the same amount of water is divided into more droplets. This has the effect of suppressing precipitation, increasing the cloud lifetime, known as the cloud lifetime aerosol effect, second indirect effect or Albrecht effect. This has been observed as the suppression of drizzle in ship exhaust plume compared to ambient clouds, and inhibited precipitation in biomass burning plumes. This cloud lifetime effect is classified as a climate feedback (rather than a radiative forcing) by the IPCC due to the interdependence between it and the hydrological cycle. However, it has previously been classified as a negative radiative forcing.

Semi-direct effect

The Semi-direct effect concerns any radiative effect caused by absorbing atmospheric aerosol such as soot, apart from direct scattering and absorption, which is classified as the direct effect. It encompasses many individual mechanisms, and in general is more poorly defined and understood than the direct and indirect aerosol effects. For instance, if absorbing aerosols are present in a layer aloft in the atmosphere, they can heat surrounding air which inhibits the condensation of water vapour, resulting in less cloud formation. Additionally, heating a layer of the atmosphere relative to the surface results in a more stable atmosphere due to the inhibition of atmospheric convection. This inhibits the convective uplift of moisture, which in turn reduces cloud formation. The heating of the atmosphere aloft also leads to a cooling of the surface, resulting in less evaporation of surface water. The effects described here all lead to a reduction in cloud cover i.e. an increase in planetary albedo. The semi-direct effect classified as a climate feedback) by the IPCC due to the interdependence between it and the hydrological cycle. However, it has previously been classified as a negative radiative forcing.

Roles of different aerosol species

Sulfate aerosol

Sulfate aerosol has two main effects, direct and indirect. The direct effect, via albedo, is a cooling effect that slows the overall rate of global warming: the IPCC's best estimate of the radiative forcing is −0.4 watts per square meter with a range of −0.2 to −0.8 W/m2. However there are substantial uncertainties. The effect varies strongly geographically, with most cooling believed to be at and downwind of major industrial centers. Modern climate models addressing the attribution of recent climate change take into account sulfate forcing, which appears to account (at least partly) for the slight drop in global temperature in the middle of the 20th century. The indirect effect via the aerosol acting as cloud condensation nuclei (CCN) and thereby modifying the cloud properties (albedo and lifetime) is more uncertain but is believed to be cooling.

Black carbon

Black carbon (BC), or carbon black, or elemental carbon (EC), often called soot, is composed of pure carbon clusters, skeleton balls and fullerenes, and is one of the most important absorbing aerosol species in the atmosphere. It should be distinguished from organic carbon (OC): clustered or aggregated organic molecules on their own or permeating an EC buckyball. Black carbon from fossil fuels is estimated by the IPCC in the Fourth Assessment Report of the IPCC, 4AR, to contribute a global mean radiative forcing of +0.2 W/m2 (was +0.1 W/m2 in the Second Assessment Report of the IPCC, SAR), with a range +0.1 to +0.4 W/m2. A study published in 2013 however, states that "the best estimate for the industrial-era (1750 to 2005) direct radiative forcing of atmospheric black carbon is +0.71 W/m2 with 90% uncertainty bounds of (+0.08, +1.27) W/m2" with "total direct forcing by all-black carbon sources, without subtracting the preindustrial background, is estimated as +0.88 (+0.17, +1.48) W/m2".

Instances of aerosol affecting climate

Solar radiation reduction due to volcanic eruptions

Volcanoes are a large natural source of aerosol and have been linked to changes in the earth's climate often with consequences for the human population. Eruptions linked to changes in climate include the 1600 eruption of Huaynaputina which was linked to the Russian famine of 1601 - 1603, leading to the deaths of two million, and the 1991 eruption of Mount Pinatubo which caused a global cooling of approximately 0.5 °C lasting several years. Research tracking the effect of light-scattering aerosols in the stratosphere during 2000 and 2010 and comparing its pattern to volcanic activity show a close correlation. Simulations of the effect of anthropogenic particles showed little influence at present levels.

Aerosols are also thought to affect weather and climate on a regional scale. The failure of the Indian monsoon has been linked to the suppression of evaporation of water from the Indian Ocean due to the semi-direct effect of anthropogenic aerosol.

Recent studies of the Sahel drought and major increases since 1967 in rainfall in Australia over the Northern Territory, Kimberley, Pilbara and around the Nullarbor Plain have led some scientists to conclude that the aerosol haze over South and East Asia has been steadily shifting tropical rainfall in both hemispheres southward.

The latest studies of severe rainfall decline over southern Australia since 1997 have led climatologists there to consider the possibility that these Asian aerosols have shifted not only tropical but also mid-latitude systems southward.

Health effects

Air pollution measurement station in Emden, Germany
 

Size, shape and solubility matter

The size of the particle is the main determinant of where in the respiratory tract the particle will come to rest when inhaled. Larger particles are generally filtered in the nose and throat via cilia and mucus, but particulate matter smaller than about 10 micrometers, can settle in the bronchi and lungs and cause health problems. The 10-micrometer size does not represent a strict boundary between respirable and non-respirable particles but has been agreed upon for monitoring of airborne particulate matter by most regulatory agencies. Because of their small size, particles on the order of 10 micrometers or less (coarse particulate matter, PM10) can penetrate the deepest part of the lungs such as the bronchioles or alveoli. When asthmatics are exposed to these conditions it can trigger bronchoconstriction.

Similarly, so called fine particulate matter (PM2.5), tends to penetrate into the gas exchange regions of the lung (alveolus), and very small particles (ultrafine particulate matter, PM0.1) may pass through the lungs to affect other organs. Penetration of particles is not wholly dependent on their size; shape and chemical composition also play a part. To avoid this complication, simple nomenclature is used to indicate the different degrees of relative penetration of a PM particle into the cardiovascular system. Inhalable particles penetrate no further than the bronchi as they are filtered out by the cilia. Thoracic particles can penetrate right into terminal bronchioles whereas PM0.1, which can penetrate to alveoli, the gas exchange area, and hence the circulatory system are termed respirable particles. In analogy, the inhalable dust fraction is the fraction of dust entering the nose and mouth which may be deposited anywhere in the respiratory tract. The thoracic fraction is the fraction that enters the thorax and is deposited within the lung's airways. The respirable fraction is what is deposited in the gas exchange regions (alveoli).

The smallest particles, less than 100 nanometers (nanoparticles), may be even more damaging to the cardiovascular system. Nanoparticles can pass through cell membranes and migrate into other organs, including the brain. Particles emitted from modern diesel engines (commonly referred to as Diesel Particulate Matter, or DPM) are typically in the size range of 100 nanometers (0.1 micrometers). These soot particles also carry carcinogens like benzopyrenes adsorbed on their surface. Particulate mass is not a proper measure of the health hazard, because one particle of 10 μm diameter has approximately the same mass as 1 million particles of 100  nm diameter, but is much less hazardous, as it is unlikely to enter the alveoli. Legislative limits for engine emissions based on mass are therefore not protective. Proposals for new regulations exist in some countries, with suggestions to limit the particle surface area or the particle count (numerical quantity) instead.

The site and extent of absorption of inhaled gases and vapors are determined by their solubility in water. Absorption is also dependent upon air flow rates and the partial pressure of the gases in the inspired air. The fate of a specific contaminant is dependent upon the form in which it exists (aerosol or particulate). Inhalation also depends upon the breathing rate of the subject.

Another complexity not entirely documented is how the shape of PM can affect health, except for the needle-like shape of asbestos which can lodge itself in the lungs. Geometrically angular shapes have more surface area than rounder shapes, which in turn affects the binding capacity of the particle to other, possibly more dangerous substances.

Health problems

Air quality information on PM10 displayed in Katowice, Poland

The effects of inhaling particulate matter that have been widely studied in humans and animals include asthma, lung cancer, respiratory diseases, cardiovascular disease, premature delivery, birth defects, low birth weight, and premature death. Outdoor fine particulates with diameter less than 2.5 microns accounts for 4.2 million annual deaths worldwide, and more than 103 million disability-adjusted life-years lost, making it the fifth leading risk factor for death. Particulates may cause tissue damage by entering organs directly, or indirectly by systemic inflammation. Adverse impacts may obtain even at exposure levels lower than published air quality standards deemed safe.

Anthropogenic fine particulates as main hazard

Increased levels of fine particles in the air as a result of anthropogenic particulate air pollution "is consistently and independently related to the most serious effects, including lung cancer and other cardiopulmonary mortality." The association between a large number of deaths and other health problems and particulate pollution was first demonstrated in the early 1970s and has been reproduced many times since. PM pollution is estimated to cause 22,000–52,000 deaths per year in the United States (from 2000) contributed to ~370,000 premature deaths in Europe during 2005. and 3.22 million deaths globally in 2010 per the global burden of disease collaboration.

A study in 2000 conducted in the U.S. explored how fine particulate matter may be more harmful than coarse particulate matter. The study was based on six different cities. They found that deaths and hospital visits that were caused by particulate matter in the air were primarily due fine particulate matter. Similarly, a 1987 study of American air pollution data found that fine particles and sulfates, as opposed to coarser particles, most consistently and significantly correlated to total annual mortality rates in standard metropolitan statistical areas.

Pregnancy, fetuses and birth effects

Higher rates of infertility have been correlated with exposure to particulates.

In addition, inhalation of PM2.5 – PM10 is associated with elevated risk of adverse pregnancy outcomes, such as low birth weight. Maternal PM2.5 exposure during pregnancy is also associated with high blood pressure in children. Exposure to PM2.5 has been associated with greater reductions in birth weight than exposure to PM10. PM exposure can cause inflammation, oxidative stress, endocrine disruption, and impaired oxygen transport access to the placenta, all of which are mechanisms for heightening the risk of low birth weight. Overall epidemiologic and toxicological evidence suggests that a causal relationship exists between long-term exposures to PM2.5 and developmental outcomes (i.e. low birth weight). However, studies investigating the significance of trimester-specific exposure have proven to be inconclusive, and results of international studies have been inconsistent in drawing associations of prenatal particulate matter exposure and low birth weight.  As perinatal outcomes have been associated with lifelong health and exposure to particulate matter is widespread, this issue is of critical public health importance and additional research will be essential to inform public policy on the matter.

Cardiovascular and respiratory disease

A 2002 study indicated that PM2.5 leads to high plaque deposits in arteries, causing vascular inflammation and atherosclerosis – a hardening of the arteries that reduces elasticity, which can lead to heart attacks and other cardiovascular problems. A 2014 meta analysis reported that long term exposure to particulate matter is linked to coronary events. The study included 11 cohorts participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE) with 100,166 participants, followed for an average of 11.5 years. An increase in estimated annual exposure to PM 2.5 of just 5 μg/m3 was linked with a 13% increased risk of heart attacks. In 2017 a study revealed that PM not only affects human cells and tissues, but also impacts bacteria which cause disease in humans. This study concluded that biofilm formation, antibiotic tolerance, and colonisation of both Staphylococcus aureus and Streptococcus pneumoniae was altered by black carbon exposure.

The largest US study on acute health effects of coarse particle pollution between 2.5 and 10 micrometers in diameter was published 2008 and found an association with hospital admissions for cardiovascular diseases but no evidence of an association with the number of hospital admissions for respiratory diseases. After taking into account fine particle levels (PM2.5 and less), the association with coarse particles remained but was no longer statistically significant, which means the effect is due to the subsection of fine particles.

The Mongolian government agency recorded a 45% increase in the rate of respiratory illness in the past five years (reported in September 2014). Bronchial asthma, chronic obstructive pulmonary disease, and interstitial pneumonia were the most common ailments treated by area hospitals. Levels of premature death, chronic bronchitis, and cardiovascular disease are increasing at a rapid rate.

Cognitive hazards

The effects of air pollution and particulate matter on cognitive performance has become an active area of research. A recent longitudinal study in China comparing air pollution and particulate exposure with verbal and mathematics test scores found that accumulative exposure impeded verbal test scores of men and women significantly more than the math scores. The negative impact in verbal reasoning as a result of particulate exposure was more pronounced as people aged and affected men more than women. The level of cognitive decline in verbal reasoning scores was more pronounced in less educated (middle school diploma or lower) subjects. Short term exposure to particulate matter has been linked to short term cognitive decline in otherwise healthy adults.

Particulates also appear to have a role in the pathogenesis of Alzheimer's disease and premature brain aging

Increased death

The World Health Organization (WHO) estimated in 2005 that "... fine particulate air pollution (PM(2.5)), causes about 3% of mortality from cardiopulmonary disease, about 5% of mortality from cancer of the trachea, bronchus, and lung, and about 1% of mortality from acute respiratory infections in children under 5 years, worldwide." A 2011 study concluded that traffic exhaust is the single most serious preventable cause of heart attack in the general public, the cause of 7.4% of all attacks.

Particulate matter studies in Bangkok, Thailand from 2008 indicated a 1.9% increased risk of dying from cardiovascular disease, and 1.0% risk of all disease for every 10 micrograms per cubic meter. Levels averaged 65 in 1996, 68 in 2002, and 52 in 2004. Decreasing levels may be attributed to conversions of diesel to natural gas combustion as well as improved regulations.

Racial disparities

There have been many studies linking race to increased proximity to particulate matter, and thus susceptibility to adverse health effects that go in tandem with long term exposure.  In a study analyzing the effects of air pollution on racially segregated neighborhoods in the United States, results show that “the proportions of Black residents in a tract was linked to higher asthma rates”.  Many scholars link this disproportionality to racial housing segregation and their respective inequalities in “toxic exposures”.  This reality is made worse by the finding that “health care occurs in the context of broader historic and contemporary social and economic inequality and persistent racial and ethnic discrimination in many sectors of American life”.  Residential proximity to particulate emitting facilities increases exposure to PM 2.5 which is linked to increased morbidity and mortality rates.  Multiple studies confirm the burden of PM emissions is higher among non-White and poverty ridden populations, though some say that income does not drive these differences.  This correlation between race and housing related health repercussions stems from a longstanding environmental justice problem linked to the practice of historic redlining.  An example of these factors contextualized is an area of Southeastern Louisiana, colloquially dubbed ‘Cancer Alley’ for its high concentration of cancer related deaths due to neighboring chemical plants.  Cancer Alley being a majority African American community, with the neighborhood nearest to the plant being 90% Black, perpetuates the scientific narrative that Black populations are located disproportionately closer to areas of high PM output than White populations.  A 2020 article relates the long term health effects of living in high PM concentrations to increased risk, spread, and mortality rates from the SARS-CoV-2 or COVID-19, and faults a history of racism for this outcome. 

Wildfire smoke risk

There is an increased risk of particulate exposure in regions where wildfires are persistent. Smoke from wildfires may impact sensitive groups such as the elderly, children, pregnant women, and people with lung, and cardiovascular disease. A study found that in the 2008 wildfire season in California, the particulate matter was much more toxic to human lungs, as increased neutrophil infiltrate, cell influx and edema was observed versus particulate matter from ambient air. Furthermore, particulate matter from wildfires have been linked to be a triggering factor of acute coronary events such as ischemic heart disease. Wildfires also have been associated with increased emergency department visits due to particulate matter exposure, as well as an increased risk of asthma related events. Furthermore, a link between PM2.5 from wildfires and increased risk of hospitalizations for cardiopulmonary diseases has been discovered.

Energy industry knowledge and response to adverse health effects

Major energy companies understood at least since the 1960s that use of their products causes widespread adverse health effects and death but continued aggressive political lobbying in the United States and elsewhere against clean air regulation and launched major corporate propaganda campaigns to sow doubt regarding the causative link between the burning of fossil fuels and major risks to human life. Internal company memoranda reveal that energy industry scientists and executives knew that air pollutants created by fossil fuels lodge deep in human lung tissue, and cause birth defects in children of oil industry workers. The industry memos acknowledge that automobiles “are by far the greatest sources of air pollution” and also that air pollution causes adverse health effects and lodges toxins, including carcinogens, “deep into the lungs which would otherwise be removed in the throat.”

In response to mounting public concern, the industry eventually created the Global Climate Coalition, an industry lobby group, to derail governments' attempts to regulate air pollution and to create confusion in the public mind about the necessity of such regulation. Similar lobbying and corporate public relations efforts were undertaken by the American Petroleum Institute, a trade association of the oil and gas industry, and the climate change denier private think tank, The Heartland Institute. “The response from fossil-fuel interests has been from the same playbook – first they know, then they scheme, then they deny and then they delay. They’ve fallen back on delay, subtle forms of propaganda and the undermining of regulation,” said Geoffrey Supran, a Harvard University researcher of the history of fossil-fuel companies and climate change. These efforts have been compared, by policy analysts such as Carroll Muffett of the Center for International Environmental Law, to the tobacco industry strategy of lobbying and corporate propaganda campaigns to create doubt regarding the causal connection between cigarette smoking and cancer and to forestall its regulation. In addition, industry-funded advocates, when appointed to senior government positions in the United States, have revised scientific findings showing the deadly effects of air pollution and have rolled back its regulation.

Effects on vegetation

Particulate matter can clog stomatal openings of plants and interfere with photosynthesis functions. In this manner, high particulate matter concentrations in the atmosphere can lead to growth stunting or mortality in some plant species.

Regulation

Due to the highly toxic health effects of particulate matter, most governments have created regulations both for the emissions allowed from certain types of pollution sources (motor vehicles, industrial emissions etc.) and for the ambient concentration of particulates. The IARC and WHO designate particulates a Group 1 carcinogen. Particulates are the deadliest form of air pollution due to their ability to penetrate deep into the lungs and blood streams unfiltered, causing respiratory diseases, heart attacks, and premature death. In 2013, the ESCAPE study involving 312,944 people in nine European countries revealed that there was no safe level of particulates and that for every increase of 10 μg/m3 in PM10, the lung cancer rate rose 22%. For PM2.5 there was a 36% increase in lung cancer per 10 μg/m3. In a 2014 meta-analysis of 18 studies globally including the ESCAPE data, for every increase of 10 μg/m3 in PM2.5, the lung cancer rate rose 9%.

Australia


PM10 PM2.5
Yearly average 25 μg/m3 8 μg/m3
Daily average (24-hour)

Allowed number of exceedences per year

50 μg/m3

None

25 μg/m3

None

Australia has set limits for particulates in the air:

Canada

In Canada the standard for particulate matter is set nationally by the federal-provincial Canadian Council of Ministers of the Environment (CCME). Jurisdictions (provinces and territories) may set more stringent standards. The CCME standard for particulate matter 2.5 (PM2.5) as of 2015 is 28 μg/m3 (calculated using the 3-year average of the annual 98th percentile of the daily 24-hr average concentrations) and 10 μg/m3 (3-year average of annual mean). PM2.5 standards will increase in stringency in 2020.

China


PM10 PM2.5
Yearly average 70 μg/m3 35 μg/m3
Daily average (24-hour)

Allowed number of exceedences per year

150 μg/m3

None

75 μg/m3

None

China has set limits for particulates in the air:

European Union


PM10 PM2.5
Yearly average 40 μg/m3 25 μg/m3
Daily average (24-hour)

Allowed number of exceedences per year

50 μg/m3

35

None

None

The European Union has established the European emission standards, which include limits for particulates in the air:

European Air Quality Index Good Fair Moderate Poor Very poor Extremely poor
Particles less than 2.5μm (PM2,5) 0-10 μg/m3 10-20 μg/m3 20-25 μg/m3 25-50 μg/m3 50-75 μg/m3 75-800 μg/m3
Particles less than 10μm (PM10) 0-20 μg/m3 20-40 μg/m3 40-50 μg/m3 50-100 μg/m3 100-150 μg/m3 150-1200 μg/m3

Hong Kong


PM10 PM2.5
Yearly average 50 μg/m3 35 μg/m3
Daily average (24-hour)

Allowed number of exceedences per year

100 μg/m3

9

75 μg/m3

9

Hong Kong has set limits for particulates in the air:

Japan


PM10 PM2.5
Yearly average None 15 μg/m3
Daily average (24-hour)

Allowed number of exceedences per year

100 μg/m3

None

35 μg/m3

None

Japan has set limits for particulates in the air:

South Korea


PM10 PM2.5
Yearly average 50 μg/m3 15 μg/m3
Daily average (24-hour)

Allowed number of exceedences per year

100 μg/m3

None

35 μg/m3

None

South Korea has set limits for particulates in the air:

Taiwan


PM10 PM2.5
Yearly average 65 μg/m3 15 μg/m3
Daily average (24-hour)

Allowed number of exceedences per year

125 μg/m3

None

35 μg/m3

None

Taiwan has set limits for particulates in the air:

United States


PM10 PM2.5
Yearly average None 12 μg/m3
Daily average (24-hour)

Allowed number of exceedences per year

150 μg/m3

1

35 μg/m3

Not applicable 

The United States Environmental Protection Agency (EPA) has set standards for PM10 and PM2.5 concentrations.

Air quality trends in the United States

California

Air quality trends in the western United States

In October 2008, the Department of Toxic Substances Control (DTSC), within the California Environmental Protection Agency, announced its intent to request information regarding analytical test methods, fate and transport in the environment, and other relevant information from manufacturers of carbon nanotubes. DTSC is exercising its authority under the California Health and Safety Code, Chapter 699, sections 57018-57020. These sections were added as a result of the adoption of Assembly Bill AB 289 (2006). They are intended to make information on the fate and transport, detection and analysis, and other information on chemicals more available. The law places the responsibility to provide this information to the Department on those who manufacture or import the chemicals.

On 22 January 2009, a formal information request letter was sent to manufacturers who produce or import carbon nanotubes in California, or who may export carbon nanotubes into the State. This letter constitutes the first formal implementation of the authorities placed into statute by AB 289 and is directed to manufacturers of carbon nanotubes, both industry, and academia within the State, and to manufacturers outside California who export carbon nanotubes to California. This request for information must be met by the manufacturers within one year. DTSC is waiting for the upcoming 22 January 2010 deadline for responses to the data call-in.

The California Nano Industry Network and DTSC hosted a full-day symposium on 16 November 2009 in Sacramento, CA. This symposium provided an opportunity to hear from nanotechnology industry experts and discuss future regulatory considerations in California.

DTSC is expanding the Specific Chemical Information Call-in to members of the nanometal oxides, the latest information can be found on their website.

Colorado

Air quality trends in the southwestern United States

Key points in the Colorado Plan include reducing emission levels and solutions by sector. Agriculture, transportation, green electricity, and renewable energy research are the main concepts and goals in this plan. Political programs such as mandatory vehicle emissions testing and the prohibition of smoking indoors are actions taken by local government to create public awareness and participation in cleaner air. The location of Denver next to the Rocky Mountains and wide expanse of plains makes the metro area of Colorado's capital city a likely place for smog and visible air pollution.

Affected areas

U.S. counties violating national PM2.5 standards
 
U.S. counties violating national PM10 standards
 
Concentration of PM10 in Europe
 
Concentration of PM2,5 (European Air Quality Index) during time slot in a city in Italy 2019-2020

The most concentrated particulate matter pollution resulting from the burning of fossil fuels by transportation and industrial sources tends to be in densely populated metropolitan areas in developing countries, such as Delhi and Beijing.

Australia

PM10 pollution in coal mining areas in Australia such as the Latrobe Valley in Victoria and the Hunter Region in New South Wales significantly increased during 2004 to 2014. Although the increase did not significantly add to non-attainment statistics the rate of increase has risen each year during 2010 to 2014.[122]

China

Some cities in Northern China and South Asia have had concentrations above 200 μg/m3 up to a few years ago[when?].[citation needed] The PM levels in Chinese cities have been extreme in recent years[when?], reaching an all-time high in Beijing on 12 January 2013, of 993 μg/m3.[19]

To monitor the air quality of south China, the U.S. Consulate Guangzhou set a PM 2.5 monitor on Shamian Island in Guangzhou and displays readings on its official website and social platforms.[123]

Ulaanbaatar

Mongolia's capital city Ulaanbaatar has an annual average mean temperature of about 0 °C, making it the world's coldest capital city. About 40% of the population lives in apartments, 80% of which are supplied with central heating systems from 3 combined heat and power plants. In 2007, the power plants consumed almost 3.4 million tons of coal. The pollution control technology is in poor condition.[citation needed]

The other 60% of the population reside in shantytowns (Ger districts), which have developed due to the country's new market economy and the very cold winter seasons. The poor in these districts cook and heat their wood houses with indoor stoves fueled by wood or coal. The resulting air pollution is characterized by raised sulfur dioxide and nitrogen oxide levels and very high concentrations of airborne particles and particulate matter (PM).[19] Annual seasonal average particulate matter concentrations have been recorded as high as 279 μg/m3 (micrograms per cubic meter).[citation needed] The World Health Organization's recommended annual mean PM10 level is 20 μg/m3,[124] which means that Ulaanbaatar's PM10 annual mean levels are 14 times higher than recommended.[citation needed]

During the winter months, in particular, the air pollution obscures the air, affecting the visibility in the city to such an extent that airplanes on some occasions are prevented from landing at the airport.[125]

In addition to stack emissions, another source unaccounted for in the emission inventory is fly ash from ash ponds, the final disposal place for fly ash that has been collected in settling tanks. Ash ponds are continually eroded by wind during the dry season.[126]

See also

Cardiovascular disease

From Wikipedia, the free encyclopedia
 
Cardiovascular disease
Cardiac amyloidosis very high mag movat.jpg
Micrograph of a heart with fibrosis (yellow) and amyloidosis (brown). Movat's stain.
SpecialtyCardiology
SymptomsChest pain, shortness of breath
ComplicationsCardiac arrest
Usual onsetOlder adults
TypesCoronary artery diseases, stroke, heart failure, hypertensive heart disease, rheumatic heart disease, cardiomyopathy
PreventionHealthy eating, exercise, avoiding tobacco smoke, limited alcohol intake
TreatmentTreating high blood pressure, high blood lipids, diabetes
Deaths17.9 million / 32% (2015)

Cardiovascular disease (CVD) is a class of diseases that involve the heart or blood vessels. CVD includes coronary artery diseases (CAD) such as angina and myocardial infarction (commonly known as a heart attack). Other CVDs include stroke, heart failure, hypertensive heart disease, rheumatic heart disease, cardiomyopathy, abnormal heart rhythms, congenital heart disease, valvular heart disease, carditis, aortic aneurysms, peripheral artery disease, thromboembolic disease, and venous thrombosis.

The underlying mechanisms vary depending on the disease. Coronary artery disease, stroke, and peripheral artery disease involve atherosclerosis. This may be caused by high blood pressure, smoking, diabetes mellitus, lack of exercise, obesity, high blood cholesterol, poor diet, excessive alcohol consumption, and poor sleep, among others. High blood pressure is estimated to account for approximately 13% of CVD deaths, while tobacco accounts for 9%, diabetes 6%, lack of exercise 6% and obesity 5%. Rheumatic heart disease may follow untreated strep throat.

It is estimated that up to 90% of CVD may be preventable. Prevention of CVD involves improving risk factors through: healthy eating, exercise, avoidance of tobacco smoke and limiting alcohol intake. Treating risk factors, such as high blood pressure, blood lipids and diabetes is also beneficial. Treating people who have strep throat with antibiotics can decrease the risk of rheumatic heart disease. The use of aspirin in people, who are otherwise healthy, is of unclear benefit.

Cardiovascular diseases are the leading cause of death worldwide except Africa. Together CVD resulted in 17.9 million deaths (32.1%) in 2015, up from 12.3 million (25.8%) in 1990. Deaths, at a given age, from CVD are more common and have been increasing in much of the developing world, while rates have declined in most of the developed world since the 1970s. Coronary artery disease and stroke account for 80% of CVD deaths in males and 75% of CVD deaths in females. Most cardiovascular disease affects older adults. In the United States 11% of people between 20 and 40 have CVD, while 37% between 40 and 60, 71% of people between 60 and 80, and 85% of people over 80 have CVD. The average age of death from coronary artery disease in the developed world is around 80 while it is around 68 in the developing world. Diagnosis of disease typically occurs seven to ten years earlier in men as compared to women.

Types

Disability-adjusted life year for inflammatory heart diseases per 100,000 inhabitants in 2004
  No data
  Less than 70
  70–140
  140–210
  210–280
  280–350
  350–420
  420–490
  490–560
  560–630
  630–700
  700–770
  More than 770

There are many cardiovascular diseases involving the blood vessels. They are known as vascular diseases.

There are also many cardiovascular diseases that involve the heart.

Risk factors

There are many risk factors for heart diseases: age, sex, tobacco use, physical inactivity, excessive alcohol consumption, unhealthy diet, obesity, genetic predisposition and family history of cardiovascular disease, raised blood pressure (hypertension), raised blood sugar (diabetes mellitus), raised blood cholesterol (hyperlipidemia), undiagnosed celiac disease, psychosocial factors, poverty and low educational status, air pollution and poor sleep. While the individual contribution of each risk factor varies between different communities or ethnic groups the overall contribution of these risk factors is very consistent. Some of these risk factors, such as age, sex or family history/genetic predisposition, are immutable; however, many important cardiovascular risk factors are modifiable by lifestyle change, social change, drug treatment (for example prevention of hypertension, hyperlipidemia, and diabetes). People with obesity are at increased risk of atherosclerosis of the coronary arteries.

Genetics

Genetic factors influence the development of cardiovascular disease in men who are less than 55 years old and in women who are less than 65 years old. Cardiovascular disease in a person's parents increases their risk by 3 fold. Multiple single nucleotide polymorphisms (SNP) have been found to be associated with cardiovascular disease in genetic association studies, but usually, their individual influence is small, and genetic contributions to cardiovascular disease are poorly understood.

Age

Calcified heart of an older woman with cardiomegaly

Age is the most important risk factor in developing cardiovascular or heart diseases, with approximately a tripling of risk with each decade of life. Coronary fatty streaks can begin to form in adolescence. It is estimated that 82 percent of people who die of coronary heart disease are 65 and older. Simultaneously, the risk of stroke doubles every decade after age 55.

Multiple explanations are proposed to explain why age increases the risk of cardiovascular/heart diseases. One of them relates to serum cholesterol level. In most populations, the serum total cholesterol level increases as age increases. In men, this increase levels off around age 45 to 50 years. In women, the increase continues sharply until age 60 to 65 years.

Aging is also associated with changes in the mechanical and structural properties of the vascular wall, which leads to the loss of arterial elasticity and reduced arterial compliance and may subsequently lead to coronary artery disease.

Sex

Men are at greater risk of heart disease than pre-menopausal women. Once past menopause, it has been argued that a woman's risk is similar to a man's although more recent data from the WHO and UN disputes this. If a female has diabetes, she is more likely to develop heart disease than a male with diabetes.

Coronary heart diseases are 2 to 5 times more common among middle-aged men than women. In a study done by the World Health Organization, sex contributes to approximately 40% of the variation in sex ratios of coronary heart disease mortality. Another study reports similar results finding that sex differences explains nearly half the risk associated with cardiovascular diseases One of the proposed explanations for sex differences in cardiovascular diseases is hormonal difference. Among women, estrogen is the predominant sex hormone. Estrogen may have protective effects on glucose metabolism and hemostatic system, and may have direct effect in improving endothelial cell function. The production of estrogen decreases after menopause, and this may change the female lipid metabolism toward a more atherogenic form by decreasing the HDL cholesterol level while increasing LDL and total cholesterol levels.

Among men and women, there are differences in body weight, height, body fat distribution, heart rate, stroke volume, and arterial compliance. In the very elderly, age-related large artery pulsatility and stiffness is more pronounced among women than men. This may be caused by the women's smaller body size and arterial dimensions which are independent of menopause.

Tobacco

Cigarettes are the major form of smoked tobacco. Risks to health from tobacco use result not only from direct consumption of tobacco, but also from exposure to second-hand smoke. Approximately 10% of cardiovascular disease is attributed to smoking; however, people who quit smoking by age 30 have almost as low a risk of death as never smokers.

Physical inactivity

Insufficient physical activity (defined as less than 5 x 30 minutes of moderate activity per week, or less than 3 x 20 minutes of vigorous activity per week) is currently the fourth leading risk factor for mortality worldwide. In 2008, 31.3% of adults aged 15 or older (28.2% men and 34.4% women) were insufficiently physically active. The risk of ischemic heart disease and diabetes mellitus is reduced by almost a third in adults who participate in 150 minutes of moderate physical activity each week (or equivalent). In addition, physical activity assists weight loss and improves blood glucose control, blood pressure, lipid profile and insulin sensitivity. These effects may, at least in part, explain its cardiovascular benefits.

Diet

High dietary intakes of saturated fat, trans-fats and salt, and low intake of fruits, vegetables and fish are linked to cardiovascular risk, although whether all these associations indicate causes is disputed. The World Health Organization attributes approximately 1.7 million deaths worldwide to low fruit and vegetable consumption. Frequent consumption of high-energy foods, such as processed foods that are high in fats and sugars, promotes obesity and may increase cardiovascular risk. The amount of dietary salt consumed may also be an important determinant of blood pressure levels and overall cardiovascular risk. There is moderate quality evidence that reducing saturated fat intake for at least two years reduces the risk of cardiovascular disease. High trans-fat intake has adverse effects on blood lipids and circulating inflammatory markers, and elimination of trans-fat from diets has been widely advocated. In 2018 the World Health Organization estimated that trans fats were the cause of more than half a million deaths per year. There is evidence that higher consumption of sugar is associated with higher blood pressure and unfavorable blood lipids, and sugar intake also increases the risk of diabetes mellitus. High consumption of processed meats is associated with an increased risk of cardiovascular disease, possibly in part due to increased dietary salt intake.

Alcohol

The relationship between alcohol consumption and cardiovascular disease is complex, and may depend on the amount of alcohol consumed. There is a direct relationship between high levels of drinking alcohol and cardiovascular disease. Drinking at low levels without episodes of heavy drinking may be associated with a reduced risk of cardiovascular disease, but there is evidence that associations between moderate alcohol consumption and protection from stroke are non-causal. At the population level, the health risks of drinking alcohol exceed any potential benefits.

Celiac disease

Untreated celiac disease can cause the development of many types of cardiovascular diseases, most of which improve or resolve with a gluten-free diet and intestinal healing. However, delays in recognition and diagnosis of celiac disease can cause irreversible heart damage.

Sleep

Not getting good sleep, in amount or quality, is documented as increasing cardiovascular risk in both adults and teens. Recommendations suggest that Infants typically need 12 or more hours of sleep per day, adolescent at least eight or nine hours, and adults seven or eight. About one-third of adult Americans get less than the recommended seven hours of sleep per night, and in a study of teenagers, just 2.2 percent of those studied got enough sleep, many of whom did not get good quality sleep. Studies have shown that short sleepers getting less than seven hours sleep per night have a 10 percent to 30 percent higher risk of cardiovascular disease.

Sleep disorders such as sleep disordered breathing and insomnia, are also associated with a higher cardiometabolic risk. An estimated 50 to 70 million Americans suffer from insomnia, sleep apnea or other chronic sleep disorders.

In addition, sleep research displays differences in race and class. Short sleep and poor sleep tend to be more frequently reported in ethnic minorities than in whites. African-Americans report experiencing short durations of sleep five times more often than whites, possibly as a result of social and environmental factors. Black children and children in disadvantaged neighborhoods have much higher rates of sleep apnea than white children,

Socioeconomic disadvantage

Cardiovascular disease affects low- and middle-income countries even more than high-income countries. There is relatively little information regarding social patterns of cardiovascular disease within low- and middle-income countries, but within high-income countries low income and low educational status are consistently associated with greater risk of cardiovascular disease.

Policies that have resulted in increased socio-economic inequalities have been associated with greater subsequent socio-economic differences in cardiovascular disease implying a cause and effect relationship. Psychosocial factors, environmental exposures, health behaviours, and health-care access and quality contribute to socio-economic differentials in cardiovascular disease. The Commission on Social Determinants of Health recommended that more equal distributions of power, wealth, education, housing, environmental factors, nutrition, and health care were needed to address inequalities in cardiovascular disease and non-communicable diseases.

Air pollution

Particulate matter has been studied for its short- and long-term exposure effects on cardiovascular disease. Currently, airborne particles under 2.5 micrometers in diameter (PM2.5) are the major focus, in which gradients are used to determine CVD risk. Overall, long-term PM exposure increased rate of atherosclerosis and inflammation. In regards to short-term exposure (2 hours), every 25 μg/m3 of PM2.5 resulted in a 48% increase of CVD mortality risk. In addition, after only 5 days of exposure, a rise in systolic (2.8 mmHg) and diastolic (2.7 mmHg) blood pressure occurred for every 10.5 μg/m3 of PM2.5. Other research has implicated PM2.5 in irregular heart rhythm, reduced heart rate variability (decreased vagal tone), and most notably heart failure. PM2.5 is also linked to carotid artery thickening and increased risk of acute myocardial infarction.

Cardiovascular risk assessment

Existing cardiovascular disease or a previous cardiovascular event, such as a heart attack or stroke, is the strongest predictor of a future cardiovascular event. Age, sex, smoking, blood pressure, blood lipids and diabetes are important predictors of future cardiovascular disease in people who are not known to have cardiovascular disease. These measures, and sometimes others, may be combined into composite risk scores to estimate an individual's future risk of cardiovascular disease. Numerous risk scores exist although their respective merits are debated. Other diagnostic tests and biomarkers remain under evaluation but currently these lack clear-cut evidence to support their routine use. They include family history, coronary artery calcification score, high sensitivity C-reactive protein (hs-CRP), ankle–brachial pressure index, lipoprotein subclasses and particle concentration, lipoprotein(a), apolipoproteins A-I and B, fibrinogen, white blood cell count, homocysteine, N-terminal pro B-type natriuretic peptide (NT-proBNP), and markers of kidney function. High blood phosphorus is also linked to an increased risk.

Depression and traumatic stress

There is evidence that mental health problems, in particular depression and traumatic stress, is linked to cardiovascular diseases. Whereas mental health problems are known to be associated with risk factors for cardiovascular diseases such as smoking, poor diet, and a sedentary lifestyle, these factors alone do not explain the increased risk of cardiovascular diseases seen in depression, stress, and anxiety. Moreover, posttraumatic stress disorder is independently associated with increased risk for incident coronary heart disease, even after adjusting for depression and other covariates.

Occupational exposure

Little is known about the relationship between work and cardiovascular disease, but links have been established between certain toxins, extreme heat and cold, exposure to tobacco smoke, and mental health concerns such as stress and depression.

Non-chemical risk factors

A 2015 SBU-report looking at non-chemical factors found an association for those:

  • with mentally stressful work with a lack of control over their working situation — with an effort-reward imbalance
  • who experience low social support at work; who experience injustice or experience insufficient opportunities for personal development; or those who experience job insecurity
  • those who work night schedules; or have long working weeks
  • those who are exposed to noise

Specifically the risk of stroke was also increased by exposure to ionizing radiation. Hypertension develops more often in those who experience job strain and who have shift-work. Differences between women and men in risk are small, however men risk suffering and dying of heart attacks or stroke twice as often as women during working life.

Chemical risk factors

A 2017 SBU report found evidence that workplace exposure to silica dust, engine exhaust or welding fumes is associated with heart disease. Associations also exist for exposure to arsenic, benzopyrenes, lead, dynamite, carbon disulphide, carbon monoxide, metalworking fluids and occupational exposure to tobacco smoke. Working with the electrolytic production of aluminium or the production of paper when the sulphate pulping process is used is associated with heart disease. An association was also found between heart disease and exposure to compounds which are no longer permitted in certain work environments, such as phenoxy acids containing TCDD(dioxin) or asbestos.

Workplace exposure to silica dust or asbestos is also associated with pulmonary heart disease. There is evidence that workplace exposure to lead, carbon disulphide, phenoxyacids containing TCDD, as well as working in an environment where aluminum is being electrolytically produced, is associated with stroke.

Somatic mutations

As of 2017, evidence suggests that certain leukemia-associated mutations in blood cells may also lead to increased risk of cardiovascular disease. Several large-scale research projects looking at human genetic data have found a robust link between the presence of these mutations, a condition known as clonal hematopoiesis, and cardiovascular disease-related incidents and mortality.

Radiation therapy

Radiation treatments for cancer can increase the risk of heart disease and death, as observed in breast cancer therapy. Therapeutic radiation increases the risk of a subsequent heart attack or stroke by 1.5 to 4 times the normal rate. The increase is dose-dependent, depending on the dose strength, volume, and location.

Side-effects from radiation therapy for cardiovascular diseases have been termed radiation-induced heart disease or radiation-induced vascular disease. Symptoms are dose-dependent and include cardiomyopathy, myocardial fibrosis, valvular heart disease, coronary artery disease, heart arrhythmia and peripheral artery disease. Radiation-induced fibrosis, vascular cell damage and oxidative stress can lead to these and other late side-effect symptoms.

Pathophysiology

Density-Dependent Colour Scanning Electron Micrograph SEM (DDC-SEM) of cardiovascular calcification, showing in orange calcium phosphate spherical particles (denser material) and, in green, the extracellular matrix (less dense material)

Population-based studies show that atherosclerosis, the major precursor of cardiovascular disease, begins in childhood. The Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study demonstrated that intimal lesions appear in all the aortas and more than half of the right coronary arteries of youths aged 7–9 years.

This is extremely important considering that 1 in 3 people die from complications attributable to atherosclerosis. In order to stem the tide, education and awareness that cardiovascular disease poses the greatest threat, and measures to prevent or reverse this disease must be taken.

Obesity and diabetes mellitus are often linked to cardiovascular disease, as are a history of chronic kidney disease and hypercholesterolaemia. In fact, cardiovascular disease is the most life-threatening of the diabetic complications and diabetics are two- to four-fold more likely to die of cardiovascular-related causes than nondiabetics.

Screening

Screening ECGs (either at rest or with exercise) are not recommended in those without symptoms who are at low risk. This includes those who are young without risk factors. In those at higher risk the evidence for screening with ECGs is inconclusive. Additionally echocardiography, myocardial perfusion imaging, and cardiac stress testing is not recommended in those at low risk who do not have symptoms. Some biomarkers may add to conventional cardiovascular risk factors in predicting the risk of future cardiovascular disease; however, the value of some biomarkers is questionable. Ankle-brachial index (ABI), high-sensitivity C-reactive protein (hsCRP), and coronary artery calcium, are also of unclear benefit in those without symptoms as of 2018.

The NIH recommends lipid testing in children beginning at the age of 2 if there is a family history of heart disease or lipid problems. It is hoped that early testing will improve lifestyle factors in those at risk such as diet and exercise.

Screening and selection for primary prevention interventions has traditionally been done through absolute risk using a variety of scores (ex. Framingham or Reynolds risk scores). This stratification has separated people who receive the lifestyle interventions (generally lower and intermediate risk) from the medication (higher risk). The number and variety of risk scores available for use has multiplied, but their efficacy according to a 2016 review was unclear due to lack of external validation or impact analysis. Risk stratification models often lack sensitivity for population groups and do not account for the large number of negative events among the intermediate and low risk groups. As a result, future preventative screening appears to shift toward applying prevention according to randomized trial results of each intervention rather than large-scale risk assessment.

Prevention

Up to 90% of cardiovascular disease may be preventable if established risk factors are avoided. Currently practiced measures to prevent cardiovascular disease include:

  • Reduction in consumption of saturated fat: there is moderate quality evidence that reducing the proportion of saturated fat in the diet, and replacing it with unsaturated fats or carbohydrates over a period of at least two years, leads to a reduction in the risk of cardiovascular disease.
  • Stopping smoking and avoidance of second-hand smoke. Stopping smoking reduces risk by about 35%.
  • Maintain a healthy diet, such as the Mediterranean diet. Dietary interventions are effective in reducing cardiovascular risk factors over a year, but the longer term effects of such interventions and their impact on cardiovascular disease events is uncertain.
  • At least 150 minutes (2 hours and 30 minutes) of moderate exercise per week.
  • Limit alcohol consumption to the recommended daily limits; People who moderately consume alcoholic drinks have a 25–30% lower risk of cardiovascular disease. However, people who are genetically predisposed to consume less alcohol have lower rates of cardiovascular disease suggesting that alcohol itself may not be protective. Excessive alcohol intake increases the risk of cardiovascular disease and consumption of alcohol is associated with increased risk of a cardiovascular event in the day following consumption.
  • Lower blood pressure, if elevated. A 10 mmHg reduction in blood pressure reduces risk by about 20%. Lowering blood pressure appears to be effective even at normal blood pressure ranges.
  • Decrease non-HDL cholesterol. Statin treatment reduces cardiovascular mortality by about 31%.
  • Decrease body fat if overweight or obese. The effect of weight loss is often difficult to distinguish from dietary change, and evidence on weight reducing diets is limited. In observational studies of people with severe obesity, weight loss following bariatric surgery is associated with a 46% reduction in cardiovascular risk.
  • Decrease psychosocial stress. This measure may be complicated by imprecise definitions of what constitute psychosocial interventions. Mental stress–induced myocardial ischemia is associated with an increased risk of heart problems in those with previous heart disease. Severe emotional and physical stress leads to a form of heart dysfunction known as Takotsubo syndrome in some people. Stress, however, plays a relatively minor role in hypertension. Specific relaxation therapies are of unclear benefit.
  • There have been studies that show that garlic and soy may help with lowering cholesterol, However, the effects of holistic dietary supplements are relatively insignificant when compared to medicines prescribed for lowering cholesterol.
  • Stress relieving techniques such as practices like yoga, meditation, and tai chi have been shown to provide some positive effects on managing blood pressure.
  • Ethylene diamine tetra-acetic acid is a new therapy that has shown some promising evidence for reducing the risks of coronary disease in people with diabetes However, the therapy is still being studied and because there has only been a single clinical trial the results are not sufficient enough for clinical use at this time.
  • Not enough sleep also raises the risk of high blood pressure. Adults need about 7-9 hours of sleep. Sleep apnea is also a major risk as it causes one to stop breathing which can put stress on your body which can raise your risk of heart disease.

Most guidelines recommend combining preventive strategies. There is some evidence that interventions aiming to reduce more than one cardiovascular risk factor may have beneficial effects on blood pressure, body mass index and waist circumference; however, evidence was limited and the authors were unable to draw firm conclusions on the effects on cardiovascular events and mortality. For adults without a known diagnosis of hypertension, diabetes, hyperlipidemia, or cardiovascular disease, routine counseling to advise them to improve their diet and increase their physical activity has not been found to significantly alter behavior, and thus is not recommended. There is additional evidence to suggest that simply providing people with a cardiovascular disease risk score may reduce cardiovascular disease risk factors by a small amount compared to usual care. However, there was some uncertainty as to whether providing these scores had any effect on cardiovascular disease events. It is unclear whether or not dental care in those with periodontitis affects their risk of cardiovascular disease.

Diet

A diet high in fruits and vegetables decreases the risk of cardiovascular disease and death. Evidence suggests that the Mediterranean diet may improve cardiovascular outcomes. There is also evidence that a Mediterranean diet may be more effective than a low-fat diet in bringing about long-term changes to cardiovascular risk factors (e.g., lower cholesterol level and blood pressure). The DASH diet (high in nuts, fish, fruits and vegetables, and low in sweets, red meat and fat) has been shown to reduce blood pressure, lower total and low density lipoprotein cholesterol and improve metabolic syndrome; but the long-term benefits have been questioned. A high fiber diet is associated with lower risks of cardiovascular disease.

Worldwide, dietary guidelines recommend a reduction in saturated fat, and although the role of dietary fat in cardiovascular disease is complex and controversial there is a long-standing consensus that replacing saturated fat with unsaturated fat in the diet is sound medical advice. Total fat intake has not been found to be associated with cardiovascular risk. A 2020 systematic review found moderate quality evidence that reducing saturated fat intake for at least 2 years caused a reduction in cardiovascular events. A 2015 meta-analysis of observational studies however did not find a convincing association between saturated fat intake and cardiovascular disease. Variation in what is used as a substitute for saturated fat may explain some differences in findings. The benefit from replacement with polyunsaturated fats appears greatest, while replacement of saturated fats with carbohydrates does not appear to have a beneficial effect. A diet high in trans fatty acids is associated with higher rates of cardiovascular disease, and in 2015 the Food and Drug Administration (FDA) determined that there was 'no longer a consensus among qualified experts that partially hydrogenated oils (PHOs), which are the primary dietary source of industrially produced trans fatty acids (IP-TFA), are generally recognized as safe (GRAS) for any use in human food'. There is conflicting evidence concerning dietary supplements of omega-3 fatty acids (a type of polysaturated fat in oily fish) added to diet improve cardiovascular risk. The benefits of recommending a low-salt diet in people with high or normal blood pressure are not clear. In those with heart failure, after one study was left out, the rest of the trials show a trend to benefit. Another review of dietary salt concluded that there is strong evidence that high dietary salt intake increases blood pressure and worsens hypertension, and that it increases the number of cardiovascular disease events; both as a result of the increased blood pressure and, quite likely, through other mechanisms. Moderate evidence was found that high salt intake increases cardiovascular mortality; and some evidence was found for an increase in overall mortality, strokes, and left ventricular hypertrophy.

Intermittent fasting

Overall, the current body of scientific evidence is uncertain on whether intermittent fasting could prevent cardiovascular disease. Intermittent fasting may help people lose more weight than regular eating patterns, but was not different than energy restriction diets.

Medication

Blood pressure medication reduces cardiovascular disease in people at risk, irrespective of age, the baseline level of cardiovascular risk, or baseline blood pressure. The commonly-used drug regimens have similar efficacy in reducing the risk of all major cardiovascular events, although there may be differences between drugs in their ability to prevent specific outcomes. Larger reductions in blood pressure produce larger reductions in risk, and most people with high blood pressure require more than one drug to achieve adequate reduction in blood pressure. Adherence to medications is often poor and while mobile phone text messaging has been tried to improve adherence, there is insufficient evidence that it alters secondary prevention of cardiovascular disease.

Statins are effective in preventing further cardiovascular disease in people with a history of cardiovascular disease. As the event rate is higher in men than in women, the decrease in events is more easily seen in men than women. In those at risk, but without a history of cardiovascular disease (primary prevention), statins decrease the risk of death and combined fatal and non-fatal cardiovascular disease. The benefit, however, is small. A United States guideline recommends statins in those who have a 12% or greater risk of cardiovascular disease over the next ten years. Niacin, fibrates and CETP Inhibitors, while they may increase HDL cholesterol do not affect the risk of cardiovascular disease in those who are already on statins. Fibrates lower the risk of cardiovascular and coronary events, but there is no evidence to suggest that they reduce all-cause mortality.

Anti-diabetic medication may reduce cardiovascular risk in people with Type 2 Diabetes, although evidence is not conclusive. A meta-analysis in 2009 including 27,049 participants and 2,370 major vascular events showed a 15% relative risk reduction in cardiovascular disease with more-intensive glucose lowering over an average follow-up period of 4.4 years, but an increased risk of major hypoglycemia.

Aspirin has been found to be of only modest benefit in those at low risk of heart disease as the risk of serious bleeding is almost equal to the benefit with respect to cardiovascular problems. In those at very low risk, including those over the age of 70, it is not recommended. The United States Preventive Services Task Force recommends against use of aspirin for prevention in women less than 55 and men less than 45 years old; however, in those who are older it is recommends in some individuals.

The use of vasoactive agents for people with pulmonary hypertension with left heart disease or hypoxemic lung diseases may cause harm and unnecessary expense.

Antibiotics for secondary prevention of coronary heart disease

Antibiotics may help patients with coronary disease to reduce the risk of heart attacks and strokes. However, the latest evidence suggests that antibiotics for secondary prevention of coronary heart disease are harmful with increased mortality and occurrence of stroke. So, the use of antibiotics is not currently supported for preventing secondary coronary heart disease.

Physical activity

Exercise-based cardiac rehabilitation following a heart attack reduces the risk of death from cardiovascular disease and leads to less hospitalizations. There have been few high quality studies of the benefits of exercise training in people with increased cardiovascular risk but no history of cardiovascular disease.

A systematic review estimated that inactivity is responsible for 6% of the burden of disease from coronary heart disease worldwide. The authors estimated that 121,000 deaths from coronary heart disease could have been averted in Europe in 2008, if physical inactivity had been removed. Low quality evidence from a limited number of studies suggest that yoga has beneficial effects on blood pressure and cholesterol. Tentative evidence suggests that home-based exercise programs may be more efficient at improving exercise adherence.

Dietary supplements

While a healthy diet is beneficial, the effect of antioxidant supplementation (vitamin E, vitamin C, etc.) or vitamins has not been shown to protect against cardiovascular disease and in some cases may possibly result in harm. Mineral supplements have also not been found to be useful. Niacin, a type of vitamin B3, may be an exception with a modest decrease in the risk of cardiovascular events in those at high risk. Magnesium supplementation lowers high blood pressure in a dose dependent manner. Magnesium therapy is recommended for people with ventricular arrhythmia associated with torsades de pointes who present with long QT syndrome as well as for the treatment of people with digoxin intoxication-induced arrhythmias. There is no evidence to support omega-3 fatty acid supplementation.

Management

Cardiovascular disease is treatable with initial treatment primarily focused on diet and lifestyle interventions. Influenza may make heart attacks and strokes more likely and therefore influenza vaccination may decrease the chance of cardiovascular events and death in people with heart disease.

Proper CVD management necessitates a focus on MI and stroke cases due to their combined high mortality rate, keeping in mind the cost-effectiveness of any intervention, especially in developing countries with low or middle-income levels. Regarding MI, strategies using aspirin, atenolol, streptokinase or tissue plasminogen activator have been compared for quality-adjusted life-year (QALY) in regions of low and middle income. The costs for a single QALY for aspirin and atenolol were less than $25, streptokinase was about $680, and t-PA was $16,000. Aspirin, ACE inhibitors, beta-blockers, and statins used together for secondary CVD prevention in the same regions showed single QALY costs of $350.

There is probably no additional benefit in terms of mortality and serious adverse events when blood pressure targets were lowered to ≤ 135/85 mmHg from ≤ 140 to 160/90 to 100 mmHg.

Epidemiology

Cardiovascular diseases deaths per million persons in 2012
  318–925
  926–1,148
  1,149–1,294
  1,295–1,449
  1,450–1,802
  1,803–2,098
  2,099–2,624
  2,625–3,203
  3,204–5,271
  5,272–10233
Disability-adjusted life year for cardiovascular diseases per 100,000 inhabitants in 2004
  no data
  <900
  900–1650
  1650–2300
  2300–3000
  3000–3700
  3700–4400
  4400–5100
  5100–5800
  5800–6500
  6500–7200
  7200–7900
  >7900

Cardiovascular diseases are the leading cause of death worldwide and in all regions except Africa. In 2008, 30% of all global death was attributed to cardiovascular diseases. Death caused by cardiovascular diseases are also higher in low- and middle-income countries as over 80% of all global deaths caused by cardiovascular diseases occurred in those countries. It is also estimated that by 2030, over 23 million people will die from cardiovascular diseases each year.

It is estimated that 60% of the world's cardiovascular disease burden will occur in the South Asian subcontinent despite only accounting for 20% of the world's population. This may be secondary to a combination of genetic predisposition and environmental factors. Organizations such as the Indian Heart Association are working with the World Heart Federation to raise awareness about this issue.

Research

There is evidence that cardiovascular disease existed in pre-history, and research into cardiovascular disease dates from at least the 18th century. The causes, prevention, and/or treatment of all forms of cardiovascular disease remain active fields of biomedical research, with hundreds of scientific studies being published on a weekly basis.

Recent areas of research include the link between inflammation and atherosclerosis the potential for novel therapeutic interventions, and the genetics of coronary heart disease.

Radio propagation

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