impact of covid 19 on society essay

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Societal Impacts of Pandemics: Comparing COVID-19 With History to Focus Our Response

Grace e patterson, k marie mcintyre, helen e clough, jonathan rushton.

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Edited by: Hideki Hashimoto, The University of Tokyo, Japan

Reviewed by: Tomoji Onozuka, The University of Tokyo, Japan; Natasa Djordjevic, University of Kragujevac, Serbia

*Correspondence: Jonathan Rushton [email protected]

This article was submitted to Health Economics, a section of the journal Frontiers in Public Health

Received 2020 Nov 17; Accepted 2021 Feb 19; Collection date 2021.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

COVID-19 has disrupted everyday life worldwide and is the first disease event since the 1918 H1N1 Spanish influenza (flu) pandemic to demand an urgent global healthcare response. There has been much debate on whether the damage of COVID-19 is due predominantly to the pathogen itself or our response to it. We compare SARS-CoV-2 against three other major pandemics (1347 Black Death, 1520's new world smallpox outbreaks, and 1918 Spanish Flu pandemic) over the course of 700 years to unearth similarities and differences in pathogen, social and medical context, human response and behavior, and long-term social and economic impact that should be used to shape COVID-19 decision-making. We conclude that <100 years ago, pandemic disease events were still largely uncontrolled and unexplained. The extensive damage wreaked by historical pandemics on health, economy, and society was a function of pathogen characteristics and lack of public health resources. Though there remain many similarities in patterns of disease spread and response from 1300 onwards, the major risks posed by COVID-19 arise not from the pathogen, but from indirect effects of control measures on health and core societal activities. Our understanding of the epidemiology and effective treatment of this virus has rapidly improved and attention is shifting toward the identification of long-term control strategies that balance consideration of health in at risk populations, societal behavior, and economic impact. Policymakers should use lessons from previous pandemics to develop appropriate risk assessments and control plans for now-endemic COVID-19, and for future pandemics.

Keywords: plague, smallpox, Spanish flu, economic impact, pandemic control, COVID-19

Introduction

COVID-19 has disrupted everyday life worldwide. It is the first disease event since the 1918–20 H1N1 Spanish influenza (flu) pandemic to demand an urgent global healthcare response, propagated by the speed and likelihood of potential transmission. An understanding of how much disruption is caused by the pathogen, and how much is caused by our reaction to its potential presence, is essential. We compare SARS-CoV-2 against three other pathogens known for the magnitude of their impact. Yersinia pestis , causative agent of the 1347 Black Death, is among the most destructive pathogens in human history. Variola major, cause of the 1520s smallpox outbreaks in the New World, exemplifies how disease impacts vary by population. Spanish flu is most similar to the current pathogen, yet major differences exist regarding scientific advancements and pre-existing immunity.

We compare across these four major disease events the rates of infection, likelihood of dying, and available diagnostics, therapeutics and vaccines ( Table 1 ). We examine the historical impact of these largely unchecked pathogens upon populations and economies. We discuss how culture and society's collective memory affect the response to pandemics and identify important lessons for decision-making as we adapt to a new normal.

Context and impacts of major pandemics.

Figures accurate as of 18 December, 2020 .

Epidemiology

SARS-CoV-2 differs from Y. pestis , V. major and Spanish flu in terms of disease transmission and pathophysiology. Of these four, it is the least deadly, and poses the lowest risk to otherwise healthy people; however increasing evidence suggests significant long-term sequelae for a proportion of individuals who have symptoms. The Black Death had exceedingly high case fatality rates (CFRs), approaching 100% for septicemic and pneumonic plague and 50–60% for the bubonic form of the disease ( 8 ). Over a third of the European population died during the 1347 outbreak, with some regions experiencing up to 75% mortality ( 22 ). CFRs for smallpox amongst immunologically naïve native Americans in the 1520s were estimated at 50% ( 9 ), and many survivors were left disfigured or blinded. Smallpox (and other European diseases) drove an estimated 90% decrease in indigenous populations in the Americas from 1500 to 1600 ( 2 ). Spanish flu had a CFR estimated at 2–3% ( 23 ) and few known long-term effects, other than occasional extended convalescence and limited instances of neuropsychiatric disorders ( 24 ). Current COVID-19 CFR estimations range from 0.3 to 3.0%, with lower estimates more likely to be accurate ( 10 ). There are growing reports of secondary and long-term impacts from COVID-19, typically among hospitalized patients but also among less severe cases. These include poor cardiovascular functioning ( 25 ), wide-ranging neurological symptoms ( 26 ), chronic fatigue ( 27 ), and others, with some patients needing long-term convalescence. While it is too early to fully understand the long-term impacts of COVID-19, similar post-viral syndromes have also been observed among those infected with SARS ( 28 ).

It is unknown how many people were infected during the Black Death and 1520s smallpox outbreaks. An estimated 500 million people (1 in 3 worldwide) were infected with Spanish flu and 1–3% of the global population died from the disease ( 5 ). Thus far, 75.1 million people have been confirmed to have COVID-19 (~1 in 104), killing 0.02% of the global population ( 7 ).

Disease susceptibility and immunological naivety influence the outcome of pandemic disease events. Both plague and smallpox are highly infectious and affect people of all ages, though smallpox exhibits a significantly higher mortality rate amongst children compared to adults ( 9 ). Spanish flu had severe impacts amongst the otherwise healthy 15–40 age group while also affecting typically high-risk groups ( 23 ). COVID-19 is different; it has a low attack rate ( 29 ) and severe clinical disease occurs mainly in the old and those with pre-existing health conditions ( 11 ).

Y. pestis has evolved over centuries to evade and modulate innate and adaptive immune responses ( 30 ). In 1347, naïve Europeans would have had minimal immunological protection from the plague. Conversely, pre-existing herd immunity from years of smallpox circulation spared European colonizers the widespread mortality observed among naïve populations when smallpox was introduced to the New Word ( 9 ). While Spanish flu was likely a result of a novel variant, there is evidence of cross-protection in elderly populations who were exposed to historical flu outbreaks; this was also observed among survivors of later flu epidemics ( 23 ). It is unknown if exposure to commonly circulating coronaviruses provides protection against COVID-19, but reactivity against SARS-CoV-2 has been observed in T-cells from unexposed people ( 31 ).

While much of the modern world would be unrecognizable to our ancestors, certain dynamics of disease spread remain the same. Humans and domesticated animals historically lived at close quarters, and the risk of animal to human disease transmission was intuitively minimized thousands of years before a causal relationship was established ( 32 ). Communicable diseases spread more easily where there is poverty and/or high population density ( 33 , 34 ), as seen in Marseille where ~80% of the population perished in the Black Death ( 3 ). In India, Spanish flu mortality rates among members of the lowest social class were three times higher than that of other demographic groups ( 35 ). These risk factors remain relevant today: 73% of emerging infectious diseases in humans originate in animals ( 36 ), including COVID-19 ( 37 ). Large cities with international travel hubs, such as New York and London, were initially hit hard by COVID-19 and contributed to the unprecedented speed of global disease spread. Early understanding of the complex, multi-factorial role of socio-economic deprivation in COVID-19 spread, indicates that poverty remains a risk factor for poor outcome from infectious disease ( 38 ).

Mitigation and Economic Effects

Science and public health advances have accelerated over the last 100 years; we should be better equipped to respond to the current pandemic. The Black Death, New World smallpox outbreaks, and Spanish flu all occurred before the discovery of antibiotics and antivirals and the development of centralized public health surveillance; even the aetiological agent of each outbreak was unidentified at the time. Early forms of quarantine and isolation were employed during the Black Death, and sanitary cordons were enforced by armed guards ( 17 ). Outbreak spread was ultimately unmitigated for both the Black Death and New World smallpox, and no effective treatment protocols were available ( 9 , 39 ). The Native American custom of sleeping in close proximity to sick individuals would have spread smallpox even more efficiently ( 12 ). Mitigation tactics only slightly improved for Spanish flu, with sporadic use of non-pharmaceutical interventions such as track and trace, isolation, and social distancing ( 17 ). Late implementation, poor record-keeping, lack of a centralized global health body, and wartime priorities rendered these largely ineffectual. Public gathering spaces and schools were commonly shut down, but total lockdowns were not employed. Masks and disinfectants were used liberally, but ineffectively, and the only treatment was palliative care. Today, healthcare professionals can deploy antivirals, immune modulating drugs, antibiotics, oxygen, and ventilators to treat COVID-19 and related complications. At the time of writing (December 2020), the first doses of multiple vaccines for COVID-19 are being administered and surveillance systems have been established in many countries. Extensive lockdowns were enacted in most countries and travel restrictions, social distancing, and quarantine rules remain in place for the foreseeable future. Concern that healthcare capacity could be overwhelmed has stimulated rapid capacity building and shifting existing capacity away from day-to-day needs to help alleviate COVID-19. These modern tactics minimized harm from various infectious diseases but halted critical preventive activities, which may cause future chronic health burdens and global social and economic disruption surmounting that of COVID-19 alone ( 40 ). Countries such as Taiwan, which were able to locally eradicate the virus via swift but relatively short-lived enactment of nonpharmaceutical interventions, have suffered the least in terms of health, social and economic damage from COVID ( 41 ). Countries that have not been as successful in controlling spread of the virus (e.g., the United States - US) face long term health and economic damage from poorly coordinated and implemented control plans.

Historically, severity of disease has correlated with severity of economic outcomes. The Black Death caused a major labor shortage, providing unprecedented market power to common people and sparking a European peasant revolt ( 18 ). While trade and industry were temporarily damaged, the socio-economic structure of society was permanently redressed as wages increased. Skilled workers were increasingly mobile and spread innovative technology faster and further than before ( 18 ). Smallpox had less dramatic effects on the evolution of economic systems, but its unequal impacts on native groups paved the way for European conquest of the New World, through which mining of natural resources funded European empire-building ( 4 ). Smallpox often preceded the conquistadors, decimating populations and leading to starvation among survivors as their societal structure collapsed ( 9 ). Spanish flu closely followed World War I (WWI); both were particularly deadly for young to middle-aged men, which led to labor shortages and stalling of industry ( 20 ). These shortages were not as economically transformative as for the Black Death, perhaps as industry was less dependent upon mass labor, a smaller proportion of the overall workforce died, and more women and minors went into work outside the home ( 42 ). There is little evidence that Spanish flu caused major GDP or consumption declines or stock market volatility; major fluctuations had already occurred due to WWI ( 43 , 44 ). These outbreaks contrast with COVID-19, which poses minimal physical risk to most of the labor force but major economic risk from the unprecedented lockdowns and non-pharmaceutical interventions employed to contain the virus. Early transient labor shortages were driven by shifts in demand and movement restrictions ( 45 ). Now, mitigation measures drive record unemployment. COVID-19 related stock market volatility is unprecedented ( 43 ) and national GDPs have plummeted ( 46 ). It remains to be seen what detrimental effects will persist in the global economy, though experts predict wage contraction and widespread poverty, with profound effects on emerging markets and developing economies ( 21 ).

Collective Social Memory and Human Behavior

The Black Death, smallpox, and Spanish flu no longer pose an imminent threat to the global population, but they changed global population structure and economies and prompted scientific advances in disease eradication, antibiotics, vaccines, and surveillance systems. It is too early to understand the long-term effects of SARS-CoV-2 or whether we will eradicate this pathogen, but we should seek inspiration from the past for how to move forward in control.

Bubonic plague, smallpox, and Spanish flu have been controlled by herd immunity and scientific advancements, though plague and flu still circulate. Localized hotspots of infection may be our COVID-19 future as this disease becomes endemic. Over the past 80 years, significant resources were spent developing surveillance systems, vaccines, and programs to monitor and manage flu ( 17 ). For COVID-19, it is unlikely we will develop curative treatments, and, as asymptomatic cases make up an estimated 17.9–30.8% of infections, disease eradication is unlikely ( 47 ). The best approach may be that birthed from the Spanish flu: develop vaccines, efficient monitoring systems, and an understanding the epidemiology of the virus, when endemic. The “end goal” would be high-level vaccine coverage coupled with notifiable disease status. This will potentially take a long time: until this is achieved, how can COVID-19 be managed with maximal public cooperation coupled with maximizing economic activity?

Public responses to pandemic disease are largely unchanged since the Black Death. Disbelief of disease presence, misinformation, unclear public communication, disregard for governmental proclamations, and poor personal risk assessment were and are still common. Despite the rapid onset of bubonic plague, it often took weeks for plague infection to be recognized in a population. In 1630s Italy, physicians were “insulted on the streets” for warning people about the arrival of the bubonic plague ( 48 ). Today, media touting COVID-19 conspiracy theories are amplified by prominent voices ( 49 ). Conflicting information about ongoing disease has long been spread (purposely or not) by news media, sometimes at the behest of governmental leadership. In an example of wartime censorship, the Italian government forced a Milan newspaper to stop printing daily death tolls during the Spanish flu because it was too demoralizing ( 17 ). In the US, public health officials hid the extent of disease spread and downplayed the danger it posed ( 20 ). In attempts to keep morale up, leaders inadvertently eroded trust in public institutions.

Uncertainty and desperation can drive people to use of dubious modes of protection during disease outbreaks. Physicians in the 1300s recommended bloodletting and drinking wine to ward off the plague ( 15 ). During the Spanish flu people wore camphor bags and gargled saltwater, while early in the COVID-19 pandemic, many sought protection from zinc lozenges and off-label medications ( 50 ). In a parallel to modern times, official Anti-Mask Leagues were formed in the US during the Spanish flu, citing insufficient scientific evidence for mask use and violation of constitutional rights. These examples demonstrate that public response to pandemics is driven by personal assessment of risks as shaped by individual circumstances and belief systems, not necessarily government mandates. In an attempt to save their economy during COVID-19, the Swedish government did not impose lockdown. However, Sweden still experienced economic losses similar to their neighbors, as people spontaneously reduced mobility and economic activity ( 51 ), being unconvinced by the herd immunity strategy ( 52 ), and presumably having made a decision based their individual assessment of risk.

COVID-19 poses a more targeted threat to health than previous pandemics however we have more understanding of its etiology and epidemiology than would have been possible in previous centuries. Why then has our global response been so profound? Our collective understanding of pandemics, as shaped by literature and culture, may play some role. The historical fascination with plagues is evidenced by some of the earliest surviving English literature and is observed across art and entertainment. Geoffrey Chaucer's 1386 “Canterbury Tales” describes the effects of total social upheaval that arose from the Black Death and provides insight into a world shaped by the threat of plague. Albert Camus's 1947 “The Plague” accurately captures the now familiar atmosphere of lockdown, obsession with case counts, and feelings of powerlessness. More recent movies such as Outbreak and Contagion may be a modern individual's reference point for predicting the possibilities of horrific disease outbreaks (and indeed, sales of these increased markedly at the pandemic's outset) ( 53 ). All explore the effects of pandemics on fear as well as fear on pandemics ( 54 ). A specific challenge for the modern era comes via the immediacy of social media, where genuine and “fake” information are frequently presented with apparently equal credibility. The myriad collective experiences and cognitive biases innate to humanity are further challenges that scientists, policymakers, figureheads and communicators should be aware of in themselves and their audiences when formulating and communicating response plans ( 55 ).

In the era of COVID-19, scientific and medical advances have enabled us to identify and treat disease in a way that would have been unimaginable to previous generations. Therefore, the biggest danger we face are reactions that are disproportionate to the nature of risks from COVID-19, leading to challenges in core social activities of food production, provision of education, healthcare, and basic health needs. Indeed, one legacy of COVID-19 may be the corollary deaths that stem from disease control strategies ( 40 ). Major economic downturns are correlated with chronic disease and mental disorder-associated mortalities; already in 2020 we have observed short-term excess deaths not attributed to COVID-19 and reduced healthcare uptake. To minimize long-term harm to global health targets, decision-makers must balance the direct health risks from the virus against those from the socioeconomic effects of control strategies. The underpinning evidence and reasoning must be unified across government, medicine, and media, and presented to a mistrustful public with transparency. As seen in the past, illogical decision-making and poor leadership have the potential to multiply harm caused by disease. We must minimize the impact of this pandemic by accurately assessing and proportionately responding to the true threats of COVID-19 and its legacy.

Data Availability Statement

The original contributions presented in the study are included in the article/supplementary material, further inquiries can be directed to the corresponding author/s.

Author Contributions

The idea for this paper was initiated by JR and developed by GP, with input from KM and HC. GP wrote the first draft, with edits by JR, KM, and HC. All authors contributed to the article and approved the submitted version.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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• Volume 74, Issue 11
• The COVID-19 pandemic and health inequalities
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• http://orcid.org/0000-0002-1294-6851 Clare Bambra 1 ,
• Ryan Riordan 2 ,
• John Ford 2 ,
• Fiona Matthews 1
• 1 Population Health Sciences Institute, Newcastle University Institute for Health and Society , Newcastle upon Tyne , UK
• 2 School of Clinical Medicine, Cambridge University , Cambridge , UK
• Correspondence to Clare Bambra, Population Health Sciences Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne NE1 4LP, UK; clare.bambra{at}newcastle.ac.uk

This essay examines the implications of the COVID-19 pandemic for health inequalities. It outlines historical and contemporary evidence of inequalities in pandemics—drawing on international research into the Spanish influenza pandemic of 1918, the H1N1 outbreak of 2009 and the emerging international estimates of socio-economic, ethnic and geographical inequalities in COVID-19 infection and mortality rates. It then examines how these inequalities in COVID-19 are related to existing inequalities in chronic diseases and the social determinants of health, arguing that we are experiencing a syndemic pandemic . It then explores the potential consequences for health inequalities of the lockdown measures implemented internationally as a response to the COVID-19 pandemic, focusing on the likely unequal impacts of the economic crisis. The essay concludes by reflecting on the longer-term public health policy responses needed to ensure that the COVID-19 pandemic does not increase health inequalities for future generations.

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• Health inequalities

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https://doi.org/10.1136/jech-2020-214401

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INTRODUCTION

In 1931, Edgar Sydenstricker outlined inequalities by socio-economic class in the 1918 Spanish influenza epidemic in America, reporting a significantly higher incidence among the working classes. 1 This challenged the widely held popular and scientific consensus of the time which held that ‘the flu hit the rich and the poor alike’. 2 In the COVID-19 pandemic, there have been similar claims made by politicians and the media - that we are ‘all in it together’ and that the COVID-19 virus ‘does not discriminate’. 3 This essay aims to dispel this myth of COVID-19 as a socially neutral disease, by discussing how, just as 100 years ago, there are inequalities in COVID-19 morbidity and mortality rates—reflecting existing unequal experiences of chronic diseases and the social determinants of health. The essay is structured in three main parts. Part 1 examines historical and contemporary evidence of inequalities in pandemics—drawing on international research into the Spanish influenza pandemic of 1918, the H1N1 outbreak of 2009 and the emerging international estimates of socio-economic, ethnic and geographical inequalities in COVID-19 infection and mortality rates. Part 2 examines how these inequalities in COVID-19 are related to existing inequalities in chronic diseases and the social determinants of health, arguing that we are experiencing a syndemic pandemic . In Part 3, we explore the potential consequences for health inequalities of the lockdown measures implemented internationally as a response to the COVID-19 pandemic, focusing on the likely unequal impacts of the economic crisis. The essay concludes by reflecting on the longer-term public health policy responses needed to ensure that the COVID-19 pandemic does not increase health inequalities for future generations.

PART 1. HISTORICAL AND CONTEMPORARY EVIDENCE OF INEQUALITIES IN PANDEMICS

More recent studies have confirmed Sydenstricker’s early findings: there were significant inequalities in the 1918 Spanish influenza pandemic. The international literature demonstrates that there were inequalities in prevalence and mortality rates: between high-income and low-income countries, more and less affluent neighbourhoods, higher and lower socio-economic groups, and urban and rural areas. For example, India had a mortality rate 40 times higher than Denmark and the mortality rate was 20 times higher in some South American countries than in Europe. 4 In Norway, mortality rates were highest among the working-class districts of Oslo 5 ; in the USA, they were highest among the unemployed and the urban poor in Chicago, 6 and across Sweden, there were inequalities in mortality between the highest and lowest occupational classes—particularly among men. 7 In contrast, countries with smaller pre-existing social and economic inequalities, such as New Zealand, did not experience any socio-economic inequalities in mortality. 8 9 An urban–rural effect was also observed in the 1918 influenza pandemic whereby, for example, in England and Wales, the mortality was 30%–40% higher in urban areas. 10 There is also some evidence from the USA that the pandemic had long-term impacts on inequalities in child health and development. 11

Several studies have also demonstrated inequalities in the 2009 H1N1 influenza pandemic. For example, globally, Mexico experienced a higher mortality rate than that in higher-income countries. 12 In terms of socio-economic inequalities, themortality rate from H1N1 in the most deprived neighbourhoods of England was three times higher than in the least deprived. 13 It was also higher in urban compared to rural areas. 13 Similarly, a Canadian study in Ontario found that hospitalisation rates for H1N1 were associated with lower educational attainment and living in a high deprivation neighbourhood. 14 Another study found positive associations between people with financial issues (eg, financial barriers to healthcare access) and influenza-like illnesses during the 2009 H1N1 pandemic in the USA. 15 Various studies on cyclical winter influenza in North America have also found associations between mortality, morbidity and symptom severity and socio-economic status among adults and children. 16 17

Just as in 1918 and 2009, evidence of social inequalities is already emerging in relation to COVID-19 from Spain, the USA and the UK. Intermediate data published by the Catalonian government in Spain suggest that the rate of COVID-19 infection is six or seven times higher in the most deprived areas of the region compared to the least deprived. 18 Similarly, in preliminary USA analysis, Chen and Krieger (2020) found area-level socio-spatial gradients in confirmed cases in Illinois and positive test results in New York City, with dramatically increased risk of death observed among residents of the most disadvantaged counties. 19 With regard to ethnic inequalities in COVID-19, data from England and Wales have found that people who are black, Asian and minority ethnic (BAME) accounted for 34.5% of 4873 critically ill COVID-19 patients (in the period ending April 16, 2020) and much higher than the 11.5% seen for viral pneumonia between 2017 and 2019. 20 Only 14% of the population of England and Wales are from BAME backgrounds. Even more stark is the data on racial inequalities in COVID-19 infections and deaths that are being released by various states and municipalities in the USA. For example, in Chicago (in the period ending April 17, 2020), 59.2% of COVID-19 deaths were among black residents and the COVID-19 mortality rate for black Chicagoans was 34.8 per 100 000 population compared to 8.2 per 100 000 population among white residents. 21 There will likely be an interaction of race and socio-economic inequalities, demonstrating the intersectionality of multiple aspects of disadvantage coalescing to further compound illness and increase the risk of mortality. 22

PART 2. THE SYNDEMIC OF COVID-19, CHRONIC DISEASE AND THE SOCIAL DETERMINANTS OF HEALTH

The COVID-19 pandemic is occurring against a backdrop of social and economic inequalities in existing non-communicable diseases (NCDs) as well as inequalities in the social determinants of health. Inequalities in COVID-19 infection and mortality rates are therefore arising as a result of a syndemic of COVID-19, inequalities in chronic diseases and the social determinants of health. The prevalence and severity of the COVID-19 pandemic is magnified because of the pre-existing epidemics of chronic disease—which are themselves socially patterned and associated with the social determinants of health. The concept of a syndemic was originally developed by Merrill Singer to help understand the relationships between HIV/AIDS, substance use and violence in the USA in the 1990s. 23 A syndemic exists when risk factors or comorbidities are intertwined, interactive and cumulative—adversely exacerbating the disease burden and additively increasing its negative effects: ‘A syndemic is a set of closely intertwined and mutual enhancing health problems that significantly affect the overall health status of a population within the context of a perpetuating configuration of noxious social conditions’ [24 p13]. We argue that for the most disadvantaged communities, COVID-19 is experienced as a syndemic—a co-occurring, synergistic pandemic that interacts with and exacerbates their existing NCDs and social conditions ( figure 1 ).

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The syndemic of COVID-19, non-communicable diseases (NCDs) and the social determinants of health (adapted from Singer 23 and Dahlgren and Whitehead 25 ).

Minority ethnic groups, people living in areas of higher socio-economic deprivation, those in poverty and other marginalised groups (such as homeless people, prisoners and street-based sex workers) generally have a greater number of coexisting NCDs, which are more severe and experienced at at a younger age. For example, people living in more socio-economically disadvantaged neighbourhoods and minority ethnic groups have higher rates of almost all of the known underlying clinical risk factors that increase the severity and mortality of COVID-19, including hypertension, diabetes, asthma, chronic obstructive pulmonary disease (COPD), heart disease, liver disease, renal disease, cancer, cardiovascular disease, obesity and smoking. 26–29 Likewise, minority ethnic groups in Europe, the USA and other high-income countries experience higher rates of the key COVID-19 risk factors, including coronary heart disease and diabetes. 28 Similarly, the Gypsy/Roma community—one of the most marginalised minority groups in Europe—has a smoking rate that is two to three times the European average and increased rates of respiratory diseases (such as COPD) and other COVID-19 risk factors. 29

These inequalities in chronic conditions arise as a result of inequalities in exposure to the social determinants of health: the conditions in which people ‘live, work, grow and age’ including working conditions, unemployment, access to essential goods and services (eg, water, sanitation and food), housing and access to healthcare. 25 30 By way of example, there are considerable occupational inequalities in exposure to adverse working conditions (eg, ergonomic hazards, repetitive work, long hours, shift work, low wages, job insecurity)—they are concentrated in lower-skill jobs. These working conditions are associated with increased risks of respiratory diseases, certain cancers, musculoskeletal disease, hypertension, stress and anxiety. 31 In addition to these long-term exposures, inequalities in working conditions may well be impacting the unequal distribution of the COVID-19 disease burden. For example, lower-paid workers (where BAME groups are disproportionately represented)—particularly in the service sector (eg, food, cleaning or delivery services)—are much more likely to be designated as key workers and thereby are still required to go to work and rely on public transport for doing so. All these increase their exposure to the virus.

Similarly, access to healthcare is lower in disadvantaged and marginalised communities—even in universal healthcare systems. 32 In England, the number of patients per general practitioner is 15% higher in the most deprived areas than that in the least deprived areas. 33 Medical care is even more unequally distributed in countries such as the USA where around 33 million Americans—from the most disadvantaged and marginalised groups—have insufficient or no healthcare insurance. 27 This reduced access to healthcare—before and during the outbreak—contributes to inequalities in chronic disease and is also likely to lead to worse outcomes from COVID-19 in more disadvantaged areas and marginalised communities. People with existing chronic conditions (eg, cancer or cardiovascular disease (CVD)) are less likely to receive treatment and diagnosis as health services are overwhelmed by dealing with the pandemic.

Housing is also an important factor in driving health inequalities. 34 For example, exposure to poor quality housing is associated with certain health outcomes, for example, damp housing can lead to respiratory diseases such as asthma while overcrowding can result in higher infection rates and increased risk of injury from household accidents. 34 Housing also impacts health inequalities materially through costs (eg, as a result of high rents) and psychosocially through insecurity (eg, short-term leases). 34 Lower socio-economic groups have a higher exposure to poor quality or unaffordable, insecure housing and therefore have a higher rate of negative health consequences. 35 These inequalities in housing conditions may also be contributing to inequalities in COVID-19. For example, deprived neighbourhoods are more likely to contain houses of multiple occupation and smaller houses with a lack of outside space, as well as have higher population densities (particularly in deprived urban areas) and lower access to communal green space. 27 These will likely increase COVID-19 transmission rates—as was the case with H1N1 where strong associations were found with urbanity. 13

The social determinants of health also work to make people from marginalised communities more vulnerable to infection from COVID-19—even when they have no underlying health conditions. Decades of research into the psychosocial determinants of health have found that the chronic stress of material and psychological deprivation is associated with immunosuppression. 36 Psychosocial feelings of subordination or inferiority as a result of occupying a low position on the social hierarchy stimulate physiological stress responses (eg, raised cortisol levels), which, when prolonged (chronic), can have long-term adverse consequences for physical and mental health. 37 By way of example, studies have found consistent associations between low job status (eg, low control and high demands), stress-related morbidity and various chronic conditions including coronary heart disease, hypertension, obesity, musculoskeletal conditions, and psychological ill health. 38 Likewise, there is increasing evidence that living in disadvantaged environments may produce a sense of powerlessness and collective threat among residents, leading to chronic stressors that, in time, damage health. 39 Studies have also confirmed that adverse psychosocial circumstances increase susceptibility—influencing the onset, course and outcome of infectious diseases—including respiratory diseases like COVID-19. 40

PART 3. THE GREAT LOCKDOWN: THE COVID-19 ECONOMIC CRISIS AND HEALTH INEQUALITIES

The impact of COVID-19 on health inequalities will not just be in terms of virus-related infection and mortality, but also in terms of the health consequences of the policy responses undertaken in most countries. While traditional public health surveillance measures of contact tracing and individual quarantine were successfully pursued by some countries (most notably by South Korea and Germany) as a way of tackling the virus in the early stages, most other countries failed to do so, and governments worldwide were eventually forced to implement mass quarantine measures—in the form of lockdowns. These state-imposed restrictions—usually requiring the government to take on emergency powers—have been implemented to varying levels of severity, but all have in common a significant increase in social isolation and confinement within the home and immediate neighbourhood. The aims of these unprecedented measures are to increase social and physical distancing and thereby reduce the effective reproduction number (eR0) of the virus to less than 1. For example, in the UK, individuals were only allowed to leave the home for one of four reasons (shopping for basic necessities, exercise, medical needs, travelling for work purposes). Following Wuhan province in China, most of the lockdowns have been implemented for 8 to 12 weeks.

The immediate pathways through which the COVID-19 emergency lockdowns are likely to have unequal health impacts are multiple—ranging from unequal experiences of lockdown (eg, due to job and income loss, overcrowding, urbanity, access to green space, key worker roles), how the lockdown itself is shaping the social determinants of health (eg, reduced access to healthcare services for non-COVID-19 reasons as the system is overwhelmed by the pandemic) and inequalities in the immediate health impacts of the lockdown (eg, in mental health and gender-based violence). However, arguably, the longer-term and largest consequences of the ‘great lockdown’ for health inequalities will be through political and economic pathways ( figure 1 ). The world economy has been severely impacted by COVID-19—with almost daily record stock market falls, oil prices have crashed and there are record levels of unemployment (eg, 5.2 million people filed for unemployment benefit in just 1 week in April 2020 in the USA), despite the unprecedented interventionist measures undertaken by some governments and central banks—such as the £300 billion injection by the UK government to support workers and businesses. The pandemic has slowed China’s economy with a predicted loss of $65 billion as a minimum in the first quarter of 2020. Economists fear that the economic impact will be far greater than the financial crisis of 2007/2008, and they say that it is likely to be worse in depth than the Great Depression of the 1930s. Just like the 1918 influenza pandemic (which had severe impacts on economic performance and increased poverty rates), the COVID-19 crisis will have huge economic, social and—ultimately—health consequences.

Previous research has found that sudden economic shocks (like the collapse of communism in the early 1990s and the global financial crisis (GFC) of 2008 41 ) lead to increases in morbidity, mental ill health, suicide and death from alcohol and substance use. For example, following the GFC, worldwide an excess of suicides were observed in the USA, England, Spain and Ireland. 42 There is also evidence of other increases in poor mental health after the GFC including self-harm and psychiatric morbidity. 41 42 These health impacts were not shared equally though—areas of the UK with higher unemployment rates had greater increases in suicide rates and inequalities in mental health increased with people living in the most deprived areas experiencing the largest increases in psychiatric morbidity and self-harm. 43 Further, unemployment (and its well-established negative health impacts in terms of morbidity and mortality 38 ) is disproportionately experienced by those with lower skills or who live in less buoyant local labour markets. 27 So, the health consequences of the COVID-19 economic crisis are likely to be similarly unequally distributed—exacerbating heath inequalities.

However, the effects of recessions on health inequalities also vary by public policy response with countries such as the UK, Greece, Italy and Spain who imposed austerity (significant cuts in health and social protection budgets) after the GFC experiencing worse population health effects than those countries such as Germany, Iceland and Sweden who opted to maintain public spending and social safety nets. 41 Indeed, research has found that countries with higher rates of social protection (such as Sweden) did not experience increases in health inequalities during the 1990s economic recession. 44 Similarly, old-age pensions in the UK were protected from austerity cuts after the GFC and research has suggested that this prevented health inequalities increasing amongst the older population. 45 These findings are in keeping with previous studies of the effects of public sector and welfare state contractions and expansions on trends in health inequalities in the UK, USA and New Zealand. 27 46–49 For example, inequalities in premature mortality and infant mortality by income and ethnicity in the USA decreased during the period of welfare expansion in the USA (‘war on poverty’ era 1966 to 1980), but they increased again during the Reagan–Bush period (1980–2002) when welfare services and healthcare coverage were cut. 46 Similarly, in England, inequalities in infant mortality rates reduced as child poverty decreased in a period of public sector and welfare state expansion (from 2000 to 2010), 47 but increased again when austerity was implemented and child poverty rates increased (from 2010 to 2017). 48

So this essay makes for grim reading for researchers, practitioners and policymakers concerned with health inequalities. Historically, pandemics have been experienced unequally with higher rates of infection and mortality among the most disadvantaged communities—particularly in more socially unequal countries. 8 9 Emerging evidence from a variety of countries suggests that these inequalities are being mirrored today in the COVID-19 pandemic. Both then and now, these inequalities have emerged through the syndemic nature of COVID-19—as it interacts with and exacerbates existing social inequalities in chronic disease and the social determinants of health. COVID-19 has laid bare our longstanding social, economic and political inequalities - even before the COVID-19 pandemic, life expectancy amongst the poorest groups was already declining in the UK and the USA and health inequalities in some European countries have been increasing over the last decade. 50 It seems likely that there will be a post-COVID-19 global economic slump—which could make the health equity situation even worse, particularly if health-damaging policies of austerity are implemented again. It is vital that this time, the right public policy responses (such as expanding social protection and public services and pursuing green inclusive growth strategies) are undertaken so that the COVID-19 pandemic does not increase health inequalities for future generations. Public health must ‘win the peace’ as well as the ‘war’.

Acknowledgments

We would like to thank Chris Orton from the Cartographic Unit, Department of Geography, Durham University, for his assistance with the graphics for figure 1 .

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Twitter Clare Bambra @ProfBambra.

Funding CB is a senior investigator in the National Institute for Health Research (NIHR) ARC North East and North Cumbria, NIHR Policy Research Unit in Behavioural Science, NIHR School of Public Health Research, the UK Prevention Research Partnership SIPHER: Systems science in Public Health and Health Economics Research consortium, and the Norwegian Research Council Centre for Global Health Inequalities Research. JF is a senior investigator in the NIHR ARC East of England. FM is a senior investigator in the NIHR Policy Research Unit in Ageing and Frailty. The views expressed in this publication are those of the authors and not necessarily those of the funders.

Competing interests We have read and understood the BMJ Group policy on declaration of interests and declare the following interests: none.

Patient consent for publication Not required.

Data sharing statement Data sharing not applicable as no datasets generated and/or analysed for this study.

Provenance and peer review Not commissioned; internally peer reviewed.

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