How does ethnicity affect child health outcomes?

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Paediatricians have a moral obligation to promote health and wellbeing for all children. The Royal College of Paediatrics and Child Health (RCPCH) in the UK has stated: “The college is totally opposed to all forms of racism and it should have no place in our society. Everyone in society must take an active role in ending it and we are committed to doing our part”. (1) To achieve this for our patients, we must recognise when some individuals have a greater or unmet health need and in response, think carefully about how to adjust healthcare delivery to accommodate for it. 

In this, our second article of a blog series, we describe racial disparities across common paediatric conditions. There is indisputable and widespread evidence that child health outcomes vary between ethnic groups. By looking at the wider societal factors and care delivery, we will argue that at least some of this may be attributed to institutional or systemic racism and, more controversially, bias from healthcare professionals.

Death rates by ethnicity

The data from the UK are stark: worse healthcare outcomes in ethnic minority groups begin before birth. Between 2016-8 in England, maternal mortality was 4.35 times greater for a woman of Black ethnicity and 1.86 times greater for an Asian woman, as compared to a White woman. (2) Across the UK in 2018, babies of Black ethnicity had 2.2 times the stillbirth rate and a 45% increase in neonatal mortality rate compared to white babies. Both figures were also greater for Asian babies, with a 57% higher stillbirth rate and a 59% higher neonatal death rate in comparison to White babies. (3) Similarly, there are clear ethnic variations in newborn mortality in the USA. (4)

In 2019, across England and Wales, when compared to White children, the infant mortality rate was higher in Pakistani (2.23x), Indian (1.43x), Bangladeshi (1.73x), Black African (1.97x), Black Caribbean (2.6x), and mixed-race (1.17x) children (Figure 2). (5) Differences in infant mortality rate between ethnic groups are also evident in other high-income countries, such as Australia and Canada. (6, 7)

Infant mortality across England and Wales – 2019

A study looking at 11 Sub-Saharan African countries between 1990-5 showed significant variation in under-5 and under-1 mortality rates by ethnicity across all 11 Low and Middle-Income Countries (LMICs). (8) Another more recent study, looking at 415 ethnic groups in 36 AMICs over 25 countries had significant differences in under-5 mortality rates between ethnic groups. (9) Interestingly, the largest ethnic group did not have the lowest mortality in any of these countries. In fact, in some countries, like South Africa, the largest ethnic group had the highest mortality.

In many parts of the world, these disparities continue into adolescence and youth. In the USA between 2014-6, the death rate in those aged 1-24 years for Black children was 60.2 per 100 000, compared to 39 per 100 000 for Whites, and 21.1 per 100 000 for Asian/Pacific Islanders. (10) Data from the Netherlands (1979-93) showed the relative risk of death from children of Moroccan or Turkish origin aged 0-15 years was double that of native Dutch children. (11)

Disparities across common paediatric conditions

Chronic diseases tend to develop in childhood and affect around 13-27% of children in the UK alone. (12) In the USA, most chronic diseases are between 1.5 and 2 times as likely – and have increased mortality rates – in Black and other minority ethnic (BAME) children. (13) Common diseases of childhood – such as infections, asthma, head injuries – are not only often more prevalent in BAME children also have increased mortality rates reported. (14, 15) 

For asthma, one of the most common and important paediatric conditions, both the hospitalisation and mortality rates for Black children with asthma are worse than for White children. Research studies in the USA found that a Black child is twice as likely to develop asthma, three times more likely to be hospitalised with it and six to eight times more likely to die as a result. (15-17) 

Additionally, the prevalence of obesity varies between communities. In the USA, for example, black children and adolescents are 1.5 times more likely to be overweight or obese compared to their White counterparts. (18-21) Similarly, in the UK, 33% of White British primary school leavers are overweight or obese, and this figure rises to 45% in Bangladeshi children, 45% in Black Caribbean children, and 46% in Black African children. (22)

Other USA studies show variability in type 1 diabetes outcomes.  Black children tend to have poorer glycaemic control and up to a nine-fold higher mortality rate compared to their White counterparts. (23, 24) Furthermore, in the UK, a baby of Pakistani origin is 3.8 times as likely to be born with a fatal congenital anomaly than a White child. (5) One data set in the USA found that severe head injury was 7.24% more likely to lead to death in Black children compared to White children. (14) Further USA data reported that the odds ratio of dying with severe sepsis was 1.19 for Black children compared to White children, with disparity varying between geographical locations. (25) More research from the USA shows Black adolescent males have a significantly higher chance of premature death, as a result of suicide, in comparison to White adolescent males. (26) Ethnicity in the USA has also been shown to be associated with worse outcomes following paediatric surgery, or a cancer diagnosis. (27, 28) In the case of cancer, the disparity was much larger for conditions that had higher survival rates. Surgical complications were also more common in Black children in the USA, with 3.43 times the odds of dying within 30 days of surgery, and 18% greater odds of developing a postoperative complication than White children. (29)

The last 18 months of healthcare has been dominated by the COVID-19 pandemic, with outcomes varying by ethnicity. In the UK, compared with White children, Asian children were more likely to have COVID-19 hospital admissions (OR 1.62), including being admitted to intensive care (OR 2.11), and Black children had longer hospital admissions (≥36 hours) (OR 2.31). (30) In the USA, COVID-19 has 7.6 times more deaths in American Indian and Alaskan natives, 5.3 times more deaths in Black and 2.1 more deaths in Asian and Pacific Islander children. (31) Similarities are seen across the UK: across all age groups, there is a 1.9- and 1.8-times increased risk of death in Black and Asian (Bangladeshi, Pakistani and Indian) males respectively. (32)

It is shocking and distressing to read this list of disparities – and this was just a small sample of the emerging data around the links between ethnicity and poor health outcomes. As paediatricians, we might feel anger, outrage, or sadness – but we must ask ourselves, why is there such variation? Two common explanations are around genetic predisposition and confounding from adverse socio-economic factors.

Biological factors

Certain inherited diseases are more common within certain ethnic groups. For example, sickle cell disease (SCD) affects 1 in 365 Black Americans, whilst being extremely rare in White populations. (33) Other examples include Gaucher disease and Bloom syndrome in Ashkenazi Jewish populations and the Finnish genetic disease heritage. Cystic fibrosis (CF) is the most common autosomal recessive disorder in White northern European populations but does affect some individuals of other ethnicities. 

Monogenic conditions are rare. Most common, and important, paediatric conditions are multifactorial, with causation attributed to both polygenic inherited factors and environmental exposures. The genetic predisposition to asthma is becoming clearer, but environmental exposures (such as cigarette smoke, pollution, and respiratory tract infections) remain important to disease development. 

The heritable component of common multifactorial conditions may have ethnic variation. Within different populations, the risk alleles may exist at different frequencies. One of the best-known examples of this is that the HLA risk alleles for Coeliac disease are far more common in White British and Irish populations. (34) A recent landmark study into the genetic predisposition to youth-onset type 2 diabetes revealed several linked genetic changes, and each of these identified alleles will vary in frequency across populations. (35) The study found a novel association between youth-onset disease and a variant in PHF2, which had not previously been reported in any adult study. The risk allele shows huge ethnic variation, being present in >90% of African people, 82% of Asian people, but only 74% of those of White European ancestry. (35, 36) 

Polygenic variants which show ethnic variation certainly play a role in the disease prevalence and severity of many diseases. Is this enough to account for the disparity? It is highly unlikely to be completely due to genetic variation. Further, if we know that a disease is more likely in a particular group due to genetic risk, or that it is more likely to be severe in a particular group, do we have a duty to screen more effectively or treat more aggressively in those at highest risk? 

There may be an uncomfortable truth in that those conditions disproportionately affecting White northern European populations have had more research directed at them and have had better-targeted treatments. There is certainly an issue with a lack of ethnic minority participants in research trials. (37)

CF, a predominantly White disease, for example, used to be considered fatal in childhood. Now the expectation is that many children will live into adulthood with newer more expensive treatments, like Ivacaftor, emerging onto the market. It is, of course, right and a marker of progress that a devastating condition has had such rapid advancement. 

Let’s compare this to SCD. Both are inherited life-threatening diseases. One affects predominantly White individuals, whilst the other does not. In the USA, CF affects one third fewer people than SCD, but receives 7-11 times the research funding, resulting in a predictable disparity in treatment. (38) Be that as it may, there has been progress in SCD. In the UK, with newborn screening, early recognition, and penicillin V prophylaxis, childhood mortality has fallen from 10% in the 1980s to <1% today. (39) The first new therapy for SCD  in 20 years, crizanlizumab, was recently approved in the UK. (40) However, in the US, by the end of 2020, there had only been four medications approved for SCD compared to 11 for CF. (41)

Taking this further, as we will explore in the future, science has, in the past, been distorted to justify racist policies. (42) SCD, for example, historically portrayed as a Black disease, has been used to discourage inter-racial breeding, to discourage interracial blood transfusions, and even used to suggest sending Black people ‘back to Africa’ by misusing the science of malaria adaptation. (43-45) The same debate about inter-racial breeding has not been applied to White CF carriers, despite also being related to a devastating disease.

Entire books have been filled with pseudoscience on racial hierarchies. All of which have been thoroughly debunked. (42) Scientists are questioning the validity of genetic differences between races accounting for variability in physiology and disease outcomes. (46) As race becomes increasingly politicised, we need to be wary of race science being given excessive weight in the scientific discourse. 

Wider societal factors

Another possibility is that variation in clinical outcomes can be explained through confounding variables. Poverty and deprivation are common risk factors across multiple diseases and has a higher prevalence in minority groups. Over 83% of Black babies and 73% of Asian babies are born in the most deprived areas of England, using the Index of Multiple Deprivation (IMD) measure. (5) A model of biological “weathering” has been proposed to explain this, where social inequalities lead to an earlier and greater decline in health. (47) This includes a rise in risk for health conditions like hypertension and type 2 diabetes. These may have an adverse impact on pregnancy outcomes, particularly at younger maternal ages. (48)

Indeed, IMD correlates with stillbirth and infant mortality in Asian children in England. (5) It doesn’t, however, explain all variations. Stillbirth and infant mortality in Black children is consistently high regardless of IMD. (5) It is also important to note that minority communities are more likely to live in unhealthy conditions, in close proximity to sewage works, emitters of airborne particulate matter or busy roads. In the USA, even wealthy African Americans are more likely to be exposed to pollution than White Americans living in poverty, in both urban and rural settings. (49) Pollution is now getting more widely recognised in a wide range of disease aetiologies, with a recent UK court ruling that the Environment Agency needed to do more to ensure children were able to breathe healthy air to prevent childhood disease. (50)

In the LMIC study of 36 countries, 4 countries (Nigeria, Laos, India, and Guatemala), had a substantial reduction in ethnic mortality gaps after adjusting for wealth, education and place of residence. (9) However, the difference wasn’t fully eliminated and in other countries within the analysis, the ethnic gap wasn’t significantly affected. Other studies have reported that in some settings, socioeconomic factors may fully correct for any mortality differences between ethnic groups. (51) This highlights the importance of avoiding false generalisations from one environmental context to another.

Quality of care

It is clear that biological factors affect health risks and outcomes, and environmental factors also play a role. But is this sufficient to account for all the observed differences? We must consider whether all people are accessing and receiving the same quality of healthcare intervention. There are two aspects related to this: firstly, is there variability in recognition of healthcare needs, health-seeking behaviours and accessibility of services? And secondly, do some groups receive different healthcare treatment from others?

There are clear examples of disparities in access and utilisation of healthcare services amongst different ethnic groups, with socioeconomic factors partially, but not completely, accounting for it. One USA study noted that although minority children with special needs were more likely than White children to be hospitalised in the preceding year, they were generally less likely to have engaged with medical services. (52, 53) Healthcare professionals can do very little if children are not being brought forward for care when they need it. If we are to improve health outcomes for children in minority groups, we must investigate and address the barriers to accessing healthcare. This includes community education about available services, better communication (including translation services), flexibility in delivery methods and building trust, although it is unclear exactly we can achieve this.

What about the quality of care delivered when children utilise services? Asthma is arguably the most researched paediatric condition and – with the plethora of therapies available – many feel that asthma deaths should be a never event. However, in one USA study, Black children were seen less frequently by healthcare professionals and were less likely to be given a written asthma treatment plan, despite having a similar asthma severity to their White counterparts. (15, 54, 55) There is also evidence that important investigations for asthma control, like spirometry and pulse oximetry, are more accurate in White individuals. (56, 57) Furthermore, there is a lack of ethnic variation in clinical images. This may mean that cyanosis is diagnosed later in those with darker skin. This issue applies more widely to dermatology and assessment of dysmorphology, and can mean that a wider range of conditions is incorrectly or belatedly diagnosed.

For diabetes, medical care seems to be poorer in some ethnic groups. Despite having poorer glycaemic control, more frequent hospital admissions and a higher mortality rate, Black children in the USA were found to be less likely to be offered insulin pumps or a more intensive insulin regimen. (23, 24) Another USA study found that Hispanic children were 73% less likely to receive an attention deficit hyperactivity disorder (ADHD) diagnosis and were also 44% less likely to receive medication for their condition. (58) Whilst some differences in outcome might be explained by biological variation, the lack of clinic appointments, written treatment plans and trials of medication cannot be attributed to it. 

When it comes to more broad assessments, a recent USA study across 52 emergency departments highlighted that Black and Hispanic children were less likely to undergo any diagnostic imaging compared to White children. (59) CT scans have been looked at more specifically in the context of head injury: whilst there were no ethnic differences in requesting CT scans for the highest risk patients, in those who were at intermediate or low risk, Black or Hispanic children were less likely to receive one. (60)

In SCD, a condition almost exclusively affecting non-White people, patients may present with acutely painful crises. Instead of getting optimal analgesia, there is evidence that some might get labelled as drug seekers. All 40 participants in a UK-based focus group highlighted that patients with SCD had experienced stigmatisation as drug addicts. (61) Not only does this result in greater suffering, but because of perceived stigma (including racial stigma), it may result in disengagement with services and greater risk of life-threatening complications.

Black children are less likely to receive optimal treatment across a wide range of clinical settings, including receiving adequate pain relief, antibiotics, insulin pumps, and even renal transplants. (23, 62-64) The systemic processes underlying these outcomes need to be urgently examined and addressed, in order to provide the best quality care to all patient groups.

Controversially, some studies have suggested that such differences may be a manifestation of racial discordance between physicians and patients. One USA study examining 1.8 million births found that when cared for by Black doctors, Black babies had improved mortality outcomes compared to White doctor-led care, with 257 fewer deaths per 100 000 babies. (65) No significant difference existed for White babies. This alone, at least within the regions in which the study was conducted, should signal alarm bells as to whether doctors are delivering appropriate care to those outside their own ethnic group. The underlying causes of this need to be looked at urgently.

Conclusion 

We don’t need any more data to prove that healthcare inequalities exist between ethnic groups around the world. We need immediate, unequivocal recognition that childhood mortality and morbidity are related to ethnicity. Your ethnicity predicts the likelihood of both suffering from childhood disease and dying before adulthood across many parts of the world. The causes of this disparity are massively complex and multifactorial. Some of this variation is caused by biological factors, but socioeconomic differences, cultural health behaviours and medical responses are also all likely to be partly responsible. 

Our knee-jerk reaction might be that “biological factors can’t be racist”. Whilst this is true, our response (or rather lack of response) to these differences can be a form of systemic racism. Similarly, we must recognise that because the NHS was founded in 1948, it was designed and set up for an ethnically White, British ‘market’; however, our nation is now hugely multi-cultural. Cultural and ethnic differences in health-seeking behaviours and engagement with medical services are not racist – but if we identify a barrier to access within a particular community, and do not adapt our services appropriately, we are propagating an institutionally racist health system.  

We would argue that our services need to be improved, in a way that better meets the diversity of needs within our population. In many cases, it seems to be that children from non-White backgrounds have poorer outcomes than White children. We have explored how this might be due to differing attitudes to seeking medical attention, differences in imaging or investigations, or different rates of therapeutic intervention. Controversially, there might even be an element of bias from doctors themselves – where in some hospitals, having a racially concordant doctor may lead to better healthcare outcomes. In each scenario, it is almost certainly a mixture of many different factors, and it will take time and effort to understand these differences, and even longer to implement effective change to alleviate the damage. 

We would strongly urge all hospitals to review their local data on both disease outcomes and medical interventions by ethnicity and act accordingly on the results. In this way, we can empower healthcare professionals to provide an anti-racist service which supports children from all ethnic backgrounds to obtain the highest standard of health.

Acknowledgments 

The authors would like to thank Dr Helen Oram for providing feedback on an initial draft of the manuscript.

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About the authors

  • Dr Zeshan Qureshi is a Paediatric Registrar based in London. He edits the Unofficial Guide to Medicine textbook series and speaks passionately about race and wellbeing issues in medicine. Having just had twins, he is currently taking time out to study issues around race and medicine at Cambridge University.

  • Alexandra Richards is a final year medical student at Cardiff University and the current Vice President for the UK Aspiring Paediatrics Society.

  • Professor Ian Sinha is a consultant respiratory paediatrician with a particular interest in childhood asthma, neonatal lung disease, and the impact of poverty on child health.

  • Dr Oluwakemi Lokulo-Sodipe is a Paediatric Registrar in Diabetes and Endocrinology in the Thames Valley and Wessex deaneries.  She is particularly interested in growth disorders and involved in research in Silver-Russell syndrome.  

  • Dr Anna M. Rose is an NIHR Clinical Lecturer in Paediatrics at the University of Oxford. Her clinical interest is children's cancer, and in her research, she is developing novel, targeted treatments for paediatric solid tumours. Anna loves teaching and is regularly involved in undergraduate MedEd - in her formal role on the University of Oxford Medicine course, but also with other Universities and through online platforms. Outside of work, she likes dogs and boats.

KEEP READING

High flow therapy – when and how?

Chest compressions in traumatic cardiac arrest

Searching for sepsis

The missing link? Children and transmission of SARS-CoV-2

Don’t Forget the Brain Busters – Round 2

An evidence summary of Paediatric COVID-19 literature

Urticaria

The fidget spinner craze – the good, the bad and the ugly

Parenteral Nutrition

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