Covid-19 & its Relationship to Air Pollution
INTRODUCTION
The places where we inhabit, where we work, learn, and play, have a substantial impact on our health. They can and should be the setting for a good and healthy life. Unfortunately, as we are learning from this pandemic, they are making us sick. This is not to say that habitats are inherently sick. Industry, through its actions, including consumption, traffic, construction, and extraction, is filling our habitats with environmental pollutants. Pollution, such as noise, light, and air pollution, can have detrimental effects on our bodies, making us more susceptible to disease and depriving us of the resources we need to cope with and recover from disease. The Covid-19 pandemic is a brutal reminder that we must rehabilitate our cities to places that promote the health of people and the planet.
WHAT’S THE STORY?
In the context of Covid-19, air pollution presents a particularly insidious hazard given that the disease affects respiratory and cardio-vascular systems (source). These two systems are mechanically sensitive to air pollution meaning that air pollution directly damages the mechanics and as consequence the function of lungs, heart, and the circulatory system (source).
In addition, air pollution, indoors and outdoors, is one of the main environmental hazards identified that affects not only our lungs but, in fact, our whole body. With every breath we take, we breathe in oxygen, an element critical to our life. But we also breathe in harmful pollutants that enter our lungs and bloodstream to then travel through the whole of our system where they reach, virtually, all our cells (source). Pollutants directly damage our lungs and other organs, cause systemic inflammation (which can reduce the immune response), and initiate a stress response which, if chronic, can lead to subsequent damage to our bodies. Acute and chronic exposure to air pollution, therefore, weakens our whole system and depletes our body of resources that are essential to combat additional stressors, such as SARS-CoV-2, the virus that causes Covid-19.
There is another crucial factor to consider when it comes to the relationship between Covid-19 and air pollution, which is who will be affected by this relationship the most. This is crucial for recovery because those who already have experienced the worse effects of Covid-19 due to the places they live will be affected the most in the recovery process, i.e. it will take them longer to recover.
In considering who will be most affected, it is important to note the role of the lived experience in our exposure and biological response to air pollution. For example, a shift worker, who already has a dysregulation of their sleep/wake cycle will not only be more susceptible to air pollution, due to this dysregulation (source), but will also be more exposed to it through long transport times, living in environments with higher air pollution, or working in environments with high levels of AP. This illustrates that any research into this relationship and into solutions has to consider both a community living in a specific area and the lived experience of the individual.
This type of attention to variation and susceptibility to the relationship between Covid-19 and air pollution is part of an anti-racist and anti-classist approach, as it considers the habitat and the lived experience rather just the class or race a person belongs to. Notably it is structural classism and racism one should see as a risk factor, not a person’s race or class.
AIR POLLUTION & THE HPA-AXIS
To understand how air pollution affects us on a biological level, we must understand AP as a stress on the body, which will help frame the risk of AP on health. From there we can look at how in particular AP puts people at risk for Covid-19, makes the symptomology more acute, and affects recovery.
Our body is constantly responding and adapting to the external environment. External stressors, psychosocial and physical, lead our system to start a stress response which is mediated by the so-called Hypothalamic-Pituitary-Adrenal Axis (HPA-axis). In the urban environments of today, however, many of the external stressors, including air pollutants, are not acute but chronic and, therefore, cause a continuous stress response. This, in turn, can result in a dysregulation of the HPA-axis and a subsequent damage to the human body through a process known as ‘allostatic load’ which predisposes the individual to a range of physical and mental health problems.
When it comes to air pollution it is important to understand four things:
The first is that air pollution is a stressor to our system, meaning it engages our stress response. Studies show that exposure to gaseous and particulate pollutants can elicit neuroendocrine stress responses from the first point of contact with the pollutant.
There is now strong historical data supporting the view that particulate matter PM2.5 and PM10 are considered “the most important criteria pollutants with respect to disease and mortality”.
When outdoor air pollution comes indoors it can have more acute effects due to being in smaller cubic space, change in toxicology, and low ventilation (the pollutants become trapped for longer). Soil vapours, which are excreted from soil, can travel indoors. Pathways include open windows, cracks in windows and walls, as well as from any doors that lead to the outdoors. A study on soil vapours done by Loughborough University concluded that soil vapours migrating into living spaces of houses may reach concentrations that could be harmful to human health. For example, it’s possible that the elevated levels of naphthalene found at the soil hospital of a brownfield development site in Southall, west London may have permeated into the indoor environments of proximal homes and accumulated, leading to the reported health effects.
The final point to understand is how air pollution leads to disease, this happens in two ways:
Direct effects of air pollution occur within the lungs. Here, inhaled particles containing threatening biological components, alongside resulting secondary reactive intermediates e.g. oxidised lipids, cause a local innate immune response resulting in immediate pulmonary inflammation and mucous secretion. Other elements of air pollution such as Volatile Organic Compounds (VOCs) and nitrogen oxides, will also aggravate lung function. In sum, these direct effects will cause irritation of the lungs, causing wheezing, coughing, fatigue and respiratory problems (e.g. acute bronchitis and aggravated asthma).
From a systems level, pulmonary inflammation in combination with a subsequent adaptive immune response, leaching of inorganic/organic pollutant elements into the circulatory system, and activation of the stress-response (HPA-axis) results in systemic inflammation. Long term, this chronic subclinical inflammation contributes to a range of diseases through a myriad of biological pathways (e.g. diabetes, cancers, allergic asthma, and depression).
// Note: Taken from Centric Lab’s Southall Study
KEY FRAMINGS
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This section will focus on how AP interacts with Covid-19 and why it plays such a key role in the development of the disease. The more we understand these mechanisms the more informed we will be for the recovery process as well as for future cases in the years to come.
Air pollution makes us ill, not only due to direct effects, for example, on the lungs, but by making us more susceptible to other diseases, such as cardiovascular diseases, cancers, and infections. There is evidence to suggest that air pollution may have played a crucial role in the Covid-19 pandemic that can explain in part why some regions have been hit harder by the pandemic than others, with higher levels of air pollution having been linked to higher infection rates, more severe courses of disease, and higher mortality (source).
One possible mechanism underlying the link between air pollution and Covid-19 is that air pollution may ease the transmission of the virus. SARS-CoV-2 is mainly transmitted through emissions of macro droplets (e.g. through coughing and sneezing). These are relatively heavy and, therefore, do not travel far. The virus may also be transmitted through aerosols (micro and nano droplets) which are lighter and, therefore, can travel further distances (though likely with fewer viable viruses). Transmission may further be facilitated by pollutants in the air. Particulate matter may function as a carrier of SARS-CoV-2, allowing the virus to travel further than it could on its own. High levels of pollutants in the air, therefore, may facilitate transmission and spread of Covid-19. Although this mechanism is certainly plausible, scientists emphasise that it needs further investigation (source / source).
A second mechanism is that direct exposure to air pollution results in the activation of the stress-response pathways, with resulting stress hormones (cortisol and adrenaline) shown to partly mediate the effects of air pollution in causing lung injury and inflammation (source). This, in turn, can lead to a worse Covid-19 outcome through increased susceptibility to viral infection (source / source).
Finally, chronic air pollution exposure also means a constant activation of the HPA-axis. Prolonged exposure to air pollution, similar to psychosocial stress, leads to allostatic load through dysregulation of interacting stress-response (HPA-axis), endocrine, immune, and metabolic systems (source). The effect of prolonged air pollution exposure on allostatic systems may increase Covid-19 susceptibility (morbidity and mortality) through a disrupted immune system response caused by a breakdown in the interplay between stress-hormones (cortisol) and immune-system cytokines (source).
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In thinking of recovery, we must also consider the role AP plays in the comorbidities that made certain communities more at risk for Covid-19. However, some clarity and specificity needs to be addressed. Whilst the identification of the comorbidities is correct, the full reasons behind their disease pathology have not been communicated. Environmental pollutants play a crucial role in developing diseases like diabetes and obesity, and in some cases these stressors have more weight than a person’s dietary habits. It is not to say that diet does not matter; it does, however, it is only one factor in a very complex disease pathology.
Chronic air pollution exposure increases the risk of developing cardiovascular and metabolic diseases through increased allostatic load (source). Specifically, chronic stress exposure results in increased amygdala sensitivity, raised inflammation and cortisol levels, and metabolic changes. In turn, this increases the risk of developing atherosclerosis and type-2 diabetes (source). Such comorbidities have been shown to increase the risk of Covid-19 contraction (source).
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The research overwhelmingly highlights how the habitats we live in affect our health (source). This changes the framing of health from the individual to the ecological level, moving away from the current inaccuracies in the research, which have put an onus on race, ethnicity, and behaviours (source). Given that the places we live play such a crucial role in our health, we must consider the distribution of environmental stressors and who lives in the worst hit areas.
Exposure to air pollution is not randomly distributed in the population. There are structural determinants that put particular groups, minority populations and people living in deprivation, at disproportionately high risk of being exposed to high levels of air pollution (source / source / source). The reason for this is systemic racism and classism, forcing Black, Asian, and Minority Ethnic (BAME) populations and people living in deprivation to disproportionately live in unhealthy environments, for example, in neighbourhoods with high levels of traffic, low levels of green-space, and poor housing conditions, all of which are associated with increased exposure to air pollution (source).
The general trend of AP as shown in Figure 1 is ‘the more central the more AP’. However, when we look at the data by ward we can begin to see the differences, for example, Peckham (a predominantly Black and deprived area) is within a dark red ward, which means high levels of AP. In contrast East Dulwich (a predominantly affluent and white area) is in light pink, indicating lower levels of AP. When a pattern emerges, driven by purposeful factors, resulting in unequal distribution, it is called inequity.
This inequity, which often results in Black, Indigenous, People of Colour living in disproportionately polluted environments can be identified as structural racism. It is important to note and understand that structural racism has nothing to do with how you personally feel about people, it is concerned with the outputs of actions. In the case of the built environment, they are the policies, which influence zoning, traffic distribution, construction rates, where waste sites are located, how well green spaces are distributed, who has access to clean water, the standards for social housing, etc.
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One of the key misunderstandings in the data of AP is the levels of variation: Why will some people be affected while others may not? Research is highlighting that exposure to chronic air pollution levels alone does not necessarily confer a greater risk to Covid-19 contraction or poorer outcomes (morbidity and mortality). Rather, it is the interplay between exposure to air pollution and psychosocial stressors that determines how susceptible an individual is to the stress-damaging effects of air pollution (source). Take the example of air pollution and asthma etiology. Geographic Information System (GIS) analysis has shown that a significant relationship between NO2 exposure and asthma development could only be observed in children who were exposed to high levels of violence (psychosocial stress) (source).
The mechanisms underpinning the complex, possible synergistic relationship between physical and psychosocial stressors exposure on disease risk is only beginning to be understood (source).
A similar interaction may be occurring with Covid-19 risk, where increased exposure to psychosocial and physical stressors is associated with increased Covid-19 mortality (source). To understand how certain subpopulations may experience differing levels of Covid-19 risk, the concept of susceptibility must first be understood. Susceptibility is the idea that individuals are at a heightened risk of disease contraction and suffering more acute symptomology due to their unique stressor exposure profile (source).
Understanding Covid-19 risk as being partly brought about by the dysregulation of allostatic systems, due to cumulative exposure to interacting physical (air pollution) and psychosocial stressors, allows us to understand the pandemic from a more ecological perspective. In turn, this allows us to identify the most vulnerable populations, i.e. individuals experiencing disproportionate levels of psychosocial and air pollution exposure, and to begin to develop new interventions to lessen Covid-19 risk.
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We now understand that living in an area with high levels of air pollution puts the individual at higher risk of contracting SARS-CoV-2 and of experiencing severe symptoms. Already alarming enough, this, unfortunately, is only one side of the story. In addition to momentary and short-term effects (cases, severity, and mortality), we must acknowledge the long-term effects of Covid-19. In their report ‘Secondary Effects of COVID’, Centric Lab describes thoroughly the long-term effects that different demographic groups will face. Here, we want to point out two conditions that have been identified and are of particular concern: Long-Haul Covid-19 and multisystem inflammatory syndrome in children. These conditions will make those people who are already suffering from these conditions also more susceptible to the negative health consequences caused by air pollution. In other words, we are facing a reinforcing feedback loop: people living in areas with higher air pollution are more likely to contract the virus and to get the disease which, in turn, makes them more susceptible to the negative health effects of air pollution they are continuously exposed to. The ultimate consequence is further health inequities.
One in ten people with Covid-19 will suffer from Long-Haul Covid-19. They will have symptoms for more than three months, often for much longer, that will impact negatively on their health, well-being, and quality of life. Another highly worrying condition that has been associated with a Covid-19 infection is multisystem inflammatory syndrome in children (MIS-C). This is a condition in that many different parts of the body can become inflamed, including the heart, the lungs, and the brain, and that is associated with various symptoms, such as abdominal pain, skin rash, and feeling especially tired. While observed mainly in children, a similar condition has also been reported in adults, i.e. multi-system inflammatory syndrome in adults (MIS-A).
Long-Haul Covid-19 and MIS-C are associated with a Covid-19 infection from which the body does not fully recover, leaving those with these conditions much more vulnerable and susceptible to other diseases and to the negative health consequences of air pollution.
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Covid-19 has tragically cemented what epidemiologists have been saying for over 100 years (the first study on linking habitat to health was in the early 1900’s), namely that city infrastructure shapes health outcomes. Therefore, it is important that those working in the built environment recognise that they are working in public health. Ensuring that people live in homes and neighbourhoods that support their sleep, their cardio-vascular system, and their microbial gut health, and that provide dignity must be a standard. A cornerstone of this is providing people with cleaner air.
Research must now turn its attention to studying in more detail how clean air plays a role in sustaining health (source). We should be creating policy around how well an area supports health rather than just reducing risk.
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Centric recognises that the use of BAME is not the best descriptor for the variances in communities. Therefore, we do not use it as a determinant or risk factor but rather as a variable of oppression within the data. What this means is that we acknowledge that a person’s race or ethnicity is a made-up construction of colonialism and white supremacy rather than a biological or natural construct. Furthermore, these categories were constructed for oppression, and that is why they matter from a data perspective. It is this oppression that leads to environmental racism and, thus, the poor health outcomes.
Some principles, policies, and framings for cleaner air.
Clean air is a human right.
There is no safe level of air pollution; the body begins its ‘damage control’ from first contact.
Air pollution should be framed as a HAZARD not a risk. This would be in line with the framing of, for example, asbestos or smoking. Additionally, this should be used for policy frameworks.
Research on the effects of AP should not focus on data alone but need to include people’s lived experience.
Racism and classism are the risk factors not a person’s race or ethnicity.
Environmental racism and injustice should be part of the policy lexicon moving forward.
Those who build cities and infrastructure should be held accountable for their contributions to poor health outcomes.
Built environment experts should be framed as public health practitioners, given the strong evidence linking AP to poor health outcomes.
We need to start moving from research to practice. There is now more than enough evidence on the hazardous effects AP has on the human body and on biodiversity. Therefore, it is time that policies and laws reflect science.
Research must now turn its attention to studying in more detail how clean air plays a role in sustaining health (source). We should be creating policy around how well an area supports health rather than just reducing risk.
RELATED WORK
