Racial and Ethnic Identity and Vulnerability to Upper Respiratory Viral Infections Among US Children

Abstract

Background

It is unclear whether there are racial/ethnic disparities in the risk of upper respiratory viral infection acquisition and/or lower respiratory manifestations.

Methods

We studied all children and children with asthma aged 6 to 17 years in the National Health and Nutrition Examination Survey (2007–2012) to evaluate (1) the association between race/ethnicity and upper respiratory infection (URI) and (2) whether race/ethnicity is a risk factor for URI-associated pulmonary eosinophilic inflammation or decreased lung function.

Results

Children who identified as Black (adjusted odds ratio [aOR], 1.38; 95% CI, 1.10–1.75) and Mexican American (aOR, 1.50; 95% CI, 1.16–1.94) were more likely to report a URI than those who identified as White. Among those with asthma, Black children were more than twice as likely to report a URI than White children (aOR, 2.28; 95% CI, 1.31–3.95). Associations between URI and pulmonary eosinophilic inflammation or lung function did not differ by race/ethnicity.

Conclusions

Findings suggest that there may be racial and ethnic disparities in acquiring a URI but not in the severity of infection. Given that upper respiratory viral infection is tightly linked to asthma exacerbations in children, differences in the risk of infection among children with asthma may contribute to disparities in asthma exacerbations.

As compared with White children, Black and Mexican American children were more likely to have an upper respiratory infection, suggesting that there are racial and ethnic disparities in the risk of becoming infected.

Racial and ethnic disparities in rates of COVID-19 morbidity and mortality [1–4] have led to the question of whether there are similar disparities in other upper respiratory viral infections [5, 6]. Previous studies have demonstrated that Black and Hispanic/Latinx children have significantly higher rates of influenza-associated hospitalization and intensive care unit admission than White children [5, 7]. Similar findings were reported for respiratory syncytial virus (RSV)–associated hospitalization in Black children [7]. These observations suggest that Black and Hispanic children may be at greater risk for severe influenza and/or RSV infections. However, it is unclear from outpatient and hospital-based studies whether observed disparities are the result of an increased risk of becoming infected or the result of an increased risk of effects on the lower respiratory tract once infected.

Additionally, the focus of previous studies on influenza and RSV [5, 7] may reflect an excess risk specific to highly pathogenic viruses. What remains poorly understood is whether there are racial and ethnic disparities in upper respiratory viral infections more broadly, including those caused by common cold viruses that are less likely to result in emergent care. Having a better understanding of whether there are racial and ethnic disparities in upper respiratory infections (URIs) and whether they arise from differences in exposure to viruses, susceptibility to infection, or severity of illness is a critical first step toward targeting interventions to reduce them.

These questions are particularly important to address in children with asthma because upper respiratory viruses can affect lower airway physiology [8, 9] and are major drivers of asthma exacerbations [9–11]. Additionally, racial and ethnic disparities in asthma exacerbations are long-standing and well documented [12, 13]. Factors such as neighborhood poverty, socioeconomic status, access to health care, and asthma management do not fully explain why rates of emergency department visits and hospitalizations are higher in Black and Hispanic children than in White children with asthma [14, 15]. It is possible that a greater risk of upper respiratory viruses—in terms of infection and/or lower airway effects—among Black and/or Hispanic populations contributes to these disparities in asthma exacerbations [16].

A nationally representative survey sample was used to (1) determine the association between racial and ethnic identity and self-reported URI and (2) evaluate whether racial and/or ethnic identity is a risk factor for URI-associated pulmonary eosinophilic inflammation or decreased lung function, each of which is strongly tied to asthma exacerbations [17]. Analyses were conducted among all children and separately among children with asthma.

METHODS

Data Collection

The National Health and Nutrition Examination Survey employs a complex multistage design to collect health and nutritional data on a representative sample of the noninstitutionalized population in the United States. Individuals were sampled between 2007 and 2010 and again between 2011 and 2014. To improve the diversity of the sample and to limit the burden on any 1 primary sampling unit (usually a county), primary sampling units were selected in the latter sample to minimize the overlap between the samples [18]. Data were collected through interviews, physical examinations, and laboratory tests and released in 2-year survey cycles [18]. Parental consent was obtained for all children, and child assent was obtained from children aged 7 to 17 years [19]. Protocols were approved by the National Center for Health Statistics’ Research Ethics Review Board.

Surveys conducted between 2007 and 2012 included a respiratory health examination with 2 components: spirometry and measurement of fractional exhaled nitric oxide (FENO), a biomarker of eosinophilic inflammation of the airway that has been linked to rhinovirus infection [8]. Both components were applied to children aged 6 to 17 years. FENO was measured with the NIOX MINO (Aerocrine AB), which provides measurements of exhaled nitric oxide from 5 to 300 ppb. Two valid and reproducible measurements of FENO were averaged for analyses [20]. Lung function was measured through baseline spirometry—specifically, expiratory volume measured in the first second of a forceful exhalation (FEV₁; in liters) and the total volume of air exhaled in forced expiration (FVC; in liters). Participants aged 6 to 10 years were asked to exhale for at least 3 seconds and those aged 11 to 17 years for at least 6 seconds. The highest values of FEV₁ and FVC were taken from reproducible curves [21], and the quality of the results was evaluated according to whether they met American Thoracic Society (ATS) standards, which are based on 3 acceptable curves, 2 reproducible curves, and 2 observed values within 150 mL [22]. During the examination, a single question about URI was asked, which was framed as having a cough, cold, phlegm, runny nose, or other respiratory illness, excluding allergies or hay fever, in the past 7 days. Parents responded for children aged 6 to 11 years.

Data Analysis

We included children aged 6 to 17 years sampled from 2007 to 2012. Those selected for analysis had reproducible FENO measurements; FEV₁ and FVC results that met or exceeded ATS data collection standards; and nonmissing responses to questions about URI, asthma diagnosis, and current asthma. Asthma diagnosis and current asthma were self-reported in response to standardly used questions [23]: “Has a doctor or other health professional ever told you that you have asthma?” and “Do you still have asthma?” Two-year examination sampling weights were divided by 3, representing the number of survey cycles pooled for analysis. We evaluated the following outcomes: URI, FENO, percentage predicted FEV₁ and FVC, and raw FEV₁/FVC. Percentage predicted values were based on observed values in the numerator and predicted values in the denominator, as derived from the 2012 Global Lung Initiative reference equations [24] and the rspiro package in R (version 3.6.3) [25]. Reference equations accounted for age, sex, height, and ethnicity, which was specified as “other/mixed” for a race-agnostic prediction [26]. Values of percentage predicted FEV₁ <80% and decreased FEV₁/FVC may indicate pulmonary obstruction (difficulty exhaling air from the lungs), while values of percentage predicted FVC <80% and normal or increased FEV₁/FVC may indicate a restriction (difficulty filling the lungs with air) [27]. Analyses were conducted among all children and children with asthma.

To address the question about disparities in acquiring an infection, we calculated survey-weighted point-in-time prevalence of URI by race/ethnicity and compared prevalence estimates with survey-weighted chi-square tests using the survey package in R [28]. Survey-weighted logistic regression models were used to estimate odds ratio, adjusted odds ratio (aOR), and 95% CI for URI comparing children who identified as Black, Mexican American, other Hispanic, or other (includes non-Hispanic Asian) with those who identified as non-Hispanic White (henceforth, White). Multivariable models of URI were adjusted for confounders such as age and sex. To address the nonlinear association between age and URI—potentially induced by the self-report of URI among older children and the parents’ report of URI for younger children—age was categorized as 6 to 8, 9 to 11, and 12 to 17 years.

To address the question about URI-associated lower respiratory tract effects, we used survey-weighted linear regression models of FENO (modeled on a base 2 [log₂] scale), percentage predicted FEV₁ and FVC, and raw FEV₁/FVC. Results for FENO were back-transformed and presented on the antilog scale, and estimates of main effects are interpreted as relative mean differences in FENO. Multivariable models of FENO and FEV₁/FVC were adjusted for URI, race/ethnicity, age (continuous), sex, and current asthma (among all children only). Multivariable models of percentage predicted FEV₁ and FVC were adjusted for URI, race/ethnicity, and current asthma (among all children only). Age and sex were excluded from these models given that predicted estimates of FEV₁ and FVC were dependent on age and sex. While comorbidities such as obesity, socioeconomic status, health care access, and household environmental exposures may be associated with the outcomes of interest, these factors were hypothesized to be in the causal pathway between race/ethnicity and our outcomes. Although we describe these factors in the study population, they were excluded from our regression models to ensure that we did not underestimate the associations between race/ethnicity and our outcomes. Multivariable models were fitted with main effects and separately with terms for interactions between race/ethnicity and URI. By using the latter model form, linear combinations of model coefficients and their 95% CIs were derived to describe associations between URI and FENO and between URI and lung function measures by race/ethnicity group. A 4-df Wald test was used to test the joint hypothesis that all interaction effects in a single model were null.

Sensitivity analyses of main findings were performed (1) in a subset of children without current asthma and (2) with multiply imputed data. Associations were estimated in children without asthma to better understand whether findings in the general population of children were driven by associations in children with asthma. Missing data on asthma diagnosis, URI, FENO, and lung function measures were imputed for all children aged 6 to 17 years via the mice package in R [29]. Variables used to inform the imputation included those already in the analysis as well as markers of household socioeconomic status. Survey-weighted logistic and linear regression models were employed as previously described and multiple imputation estimates pooled across 100 data sets.

RESULTS

Of the 6791 children aged 6 to 17 years surveyed between 2007 and 2012, our analysis comprised 4411 children (65%) with reproducible FENO measurements, high or acceptable quality spirometry measurements, and complete information about a cold and current asthma. Demographics among children excluded from the analysis were similar to those who were included, with the exception of race: children in the main analysis were more likely to identify as White (Supplementary Table 1). Accounting for survey weights, the population was 60% White, 13% Black, 14% Mexican American, and 6% other Hispanic (Table 1). This distribution resembled that of the 2010 US census population in the same age range, which was 54% White, 14% Black, and 23% Hispanic [30]. In our study population, 19.6% (95% CI, 17.7%–21.6%) reported a URI in the past 7 days: 11.3% (95% CI, 9.6%–13.2%) among children aged 6 to 11 years and 26.1% (95% CI, 23.4%–28.9%) among children aged 12 to 17 years. The prevalence of a URI was higher in Black children (23.4%; 95% CI, 20.2%–26.9%) and Mexican American children (23.6%; 95% CI, 20.2%–27.3%) than in White children (17.9%; 95% CI, 15.4%–20.8%; P = .02; Supplementary Table 2). In the subset of children with asthma (n = 521), 21.8% (95% CI, 17.3%–27.1%) had a URI: 15.0% (95% CI, 10.2%–21.7%) among those aged 6 to 11 years and 25.7% (95% CI, 20.1%–32.4%) among those aged 12 to 17 years. The prevalence in Black, Mexican American, and White children with asthma was 32.0% (95% CI, 26.1%–38.6%), 27.9% (95% CI, 18.6%–39.7%), and 18.3% (95% CI, 11.6%–27.6%), respectively.

Table 1.

Characteristics of the Study Population: National Health and Nutrition Examination Survey, 2007–2012

	% or Median (IQR), Survey Weighted
All children (N = 4411)
Race/ethnicity
White	59.6
Black	12.9
Mexican American	13.7
Other Hispanic	6.3
Other	7.5
Age, y	12 (9–15)
Male	49.8
FENO, ppb	11.0 (7.0–18.0)
Percentage predicted, L
FEV1	108 (98.2–117)
FVC	110 (102–120)
FEV1/FVC, %	86.5 (82.4–90.3)
Reported a URI	19.6
Children with current asthma (n = 521)
Race/ethnicity
White	58.0
Black	18.9
Mexican American	8.4
Other Hispanic	6.9
Other	7.9
Age, y	13 (10–15)
Male	51.3
FENO, ppb	14.5 (8.0–34.5)
Percentage predicted, L
FEV1	106 (93.4–114)
FVC	110 (101–120)
FEV1/FVC, %	84.1 (79.2–88.2)
Reported a URI	21.8

Abbreviations: FENO, fractional exhaled nitric oxide; FEV₁, volume of air measured in the first second of a forceful exhalation; FVC, total volume of air exhaled in forced expiration; URI, upper respiratory infection.

By adjusting for age and sex in the general population, the odds of reporting a URI was significantly higher among Black and Mexican American children when compared with White children (aOR, 1.38 [95% CI, 1.10–1.75] and 1.50 [95% CI, 1.16–1.94], respectively; Figure 1 and Supplementary Table 3). Children who identified as “other Hispanic” also had a higher odds of reporting a URI than White children, although this result was not statistically significant (aOR, 1.19; 95% CI, .88–1.60). Disparities were even more striking among children with asthma: the odds of reporting a URI in Black children were approximately double that of White children (aOR, 2.28; 95% CI, 1.31–3.95). The odds of reporting a URI among Mexican American children were nearly double those of White children, although the 95% CI of the estimate did include the null value (aOR, 1.88; 95% CI, .81–4.34). A sensitivity analysis excluding children with asthma from the general population produced similar results: Black, Mexican American, and other Hispanic children had increased odds of a URI vs White children, although this was statistically significant only for Mexican American children (aOR, 1.22 [95% CI, .94–1.60], 1.56 [95% CI, 1.22–2.00], and 1.23 [95% CI, .92–1.65], respectively). Results were consistent when missing data were imputed (Supplementary Table 4).

Figure 1.

Adjusted odds ratios associated with report of an upper respiratory infection in the past 7 days by racial and ethnic identity (reference, White) among all children (top) and children with asthma (bottom). Odds ratios are adjusted for age and sex. Error bars indicate 95% CI. URI, upper respiratory infection.

Median FENO was 13.0 ppb (IQR, 8.0–23.0) and 10.5 ppb (IQR, 7.0–17.0) in the general population of children with and without a URI, respectively, suggesting that median FENO is 24% higher in those with a URI. This is larger than the clinically important difference of 20% following inhaled corticosteroids cited by ATS [17]. In a model adjusted for race/ethnicity, age, sex, and current asthma among the general population of children, URI was associated with a 16% mean difference in FENO (95% CI, 7%–26%; Table 2, Supplementary Table 5). By adjusting for race/ethnicity, age, and sex among children with asthma, URI was associated with a 27% mean difference in FENO (95% CI, 3%–57%; Table 3). Associations between URI and FENO did not significantly differ by race/ethnicity: URI-associated differences in FENO were similar among Black, Mexican American, and White children (Tables 2 and 3). Results were comparable in a sensitivity analysis including the general population but excluding those with asthma and in sensitivity analyses using imputed data (Supplementary Table 6).

Table 2.

Associations of Pulmonary Eosinophilic Inflammation and Measures of Lung Function to Self-reported URI, by Racial and Ethnic Identity Among All Children

Association to URI	β (95% CI)	P Valuea
FENOb		.78
White	1.12 (.99 to 1.28)
Black	1.21 (1.06 to 1.38)
Mexican American	1.18 (1.07 to 1.30)
Other Hispanic	1.11 (.90 to 1.37)
Other	1.32 (1.03 to 1.70)
All	1.16 (1.07 to 1.26)
Percentage predicted FEV1		.87
White	−0.53 (−2.53 to 1.48)
Black	1.01 (−1.04 to 3.06)
Mexican American	0.21 (−1.71 to 2.14)
Other Hispanic	−0.24 (−3.10 to 2.62)
Other	1.04 (−3.68 to 5.75)
All	−0.06 (−1.39 to 1.27)
Percentage predicted FVC		.80
White	0.84 (−1.76 to 3.44)
Black	0.63 (−1.22 to 2.48)
Mexican American	0.81 (−.68 to 2.30)
Other Hispanic	−0.60 (−3.29 to 2.09)
Other	2.45 (−1.85 to 6.75)
All	0.83 (−.72 to 2.38)
FEV1/FVC		.14
White	−1.09 (−1.98 to −.21)
Black	0.29 (−.70 to 1.28)
Mexican American	−0.53 (−1.71 to .64)
Other Hispanic	0.21 (−1.22 to 1.63)
Other	−1.44 (−2.98 to .11)
All	−0.74 (−1.22 to −.26)

Linear combination of regression coefficients with 95% CIs from multivariable linear regression models of FENO, percentage predicted FEV₁ and FVC, and raw FEV₁/FVC. Each row represents associations to URI. Models of FENO and FEV₁/FVC were adjusted for age, sex, and current asthma. Models of percentage predicted FEV₁ and FVC were adjusted for current asthma. Race/ethnicity-specific estimates were derived from models with interaction terms between race/ethnicity and URI.

Abbreviations: FENO, fractional exhaled nitric oxide (in parts per billion); FEV₁, volume of air measured in the first second of a forceful exhalation (in liters); FVC, total volume of air exhaled in forced expiration (in liters); URI, upper respiratory infection.

^aWald test with 4 df to test the joint hypothesis that the 4 interaction effects are null.

^bFENO was modeled on a log₂ scale. The antilogarithm of the β estimates is shown in the table.

Table 3.

Associations of Pulmonary Eosinophilic Inflammation and Measures of Lung Function to Self-reported URI, by Racial and Ethnic Identity Among Children With Asthma

Association to URI	β (95% CI)	P Valuea
FENOb		.14
White	1.18 (.82 to 1.70)
Black	1.21 (.93 to 1.58)
Mexican American	1.37 (.96 to 1.95)
Other Hispanic	0.95 (.42 to 2.12)
Other	3.36 (1.61 to 7.04)
All	1.27 (1.03 to 1.57)
Percentage predicted FEV1		.59
White	0.79 (−7.44 to 9.01)
Black	2.23 (−2.02 to 6.49)
Mexican American	−1.74 (−9.60 to 6.13)
Other Hispanic	1.43 (−10.07 to 12.94)
Other	−5.27 (−14.64 to 4.11)
All	0.55 (−4.05 to 5.15)
Percentage predicted FVC		.81
White	0.78 (−6.47 to 8.03)
Black	1.75 (−2.38 to 5.89)
Mexican American	0.68 (−6.88 to 8.25)
Other Hispanic	0.92 (−10.29 to 12.13)
Other	−2.95 (−8.95 to 3.05)
All	0.79 (−3.07 to 4.64)
FEV1/FVC		.72
White	−0.24 (−3.57 to 3.08)
Black	0.86 (−2.05 to 3.76)
Mexican American	−2.18 (−5.87 to 1.50)
Other Hispanic	0.34 (−3.15 to 3.83)
Other	−2.01 (−8.60 to 4.58)
All	−0.24 (−2.27 to 1.79)

Linear combination of regression coefficients with 95% CIs from multivariable linear regression models of FENO, percentage predicted FEV₁ and FVC, and raw FEV₁/FVC. Each row represents associations to URI. Models of FENO and FEV₁/FVC were adjusted for age and sex. Race/ethnicity-specific estimates were derived from models with interaction terms between race/ethnicity and URI.

Abbreviations: FENO, fractional exhaled nitric oxide (in parts per billion); FEV₁, volume of air measured in the first second of a forceful exhalation (in liters); FVC, total volume of air exhaled in forced expiration (in liters); URI, upper respiratory infection.

^aWald test with 4 df to test the joint hypothesis that the 4 interaction effects are null.

^bFENO was modeled on a log₂ scale. The antilogarithm of the β estimates is shown in the table.

URI was not associated with percentage predicted FEV₁ or FVC (Supplementary Table 7). In the general population of children, URI was associated with a 1–percentage point mean lower level of raw FEV₁/FVC (95% CI, −1.2% to −.3%), which is a magnitude observed in studies of air pollution and lung function, suggesting that it is likely meaningful on a population level [31, 32]. In the general population of children and among children with asthma, associations between URI and lung function measures did not significantly differ by race or ethnicity. Conclusions were the same in the general population of children without asthma and in the general population and among children with asthma using imputed data (Supplementary Tables 8 and 9).

DISCUSSION

In this nationally representative sample of children in the United States, 1 in 5 reported a recent URI. Black and Mexican American children were 30% to 50% more likely to report a recent URI than White children. Among children with asthma, the racial and ethnic disparities associated with reporting a URI were even larger, with Black children approximately twice as likely to do so. Among all children and among children with asthma, URI was associated with higher FENO. Among all children, URI was associated with lower FEV₁/FVC. Associations between URI and FENO and between URI and lung function did not vary by racial and ethnic identity. Together, these results suggest that children who identify as Black and Mexican American may be more likely to get infected but not more likely to have lower respiratory tract effects once infected. The increased risk of URI among children who identify as Black and Mexican American could translate into more frequently missed school and work, which may have socioeconomic consequences. Additionally, because URIs are triggers for asthma exacerbations, these differences may contribute to racial and ethnic disparities in asthma exacerbations [12, 13].

The prevalence of symptomatic URI observed in the general population of children is higher than that indicated by Berendes et al [33], who found that 13% of children aged 5 to 17 years reported a cold in the National Health Interview Survey, but it is consistent with that from Ginde et al [34], who cited a prevalence of 22% among adolescents aged 12 to 19 years in National Health and Nutrition Examination Survey III. Our findings also align with Byington et al [35], who conducted a prospective study and found that children aged 5 to 17 years had respiratory or gastrointestinal symptoms in 22% of 1597 person-weeks. Children in this age range may have between 4 and 6 URIs per year [35–37]. Because of their high frequency, URIs in children can lead to a substantial loss of learning for children and income for parents owing to staying home with sick children and/or paying for health care. Fendrick et al [38] estimated that across the United States, URI results in >189 million missed school days, 126 million missed workdays among caregivers, and an additional 70 million missed workdays among adults who are infected themselves. Others have found that adults who work while ill do so with decreased productivity [39]. Our finding that children who identify as Black and Mexican American are more likely to report a URI indicates that a disproportionate share of the social and economic burden of URI falls on racial and ethnic minority populations.

This disproportionate burden of URI may be amplified in children with asthma. A doubling in the risk of URI among Black children with asthma may contribute to the racial and ethnic disparities in asthma exacerbations. Specifically, these findings suggest that the disparity in asthma exacerbations may be explained, at least in part, by an increase in the risk of getting infected and not in the risk of lower respiratory effects once infected. Longitudinal studies conducted in Black, Hispanic, and White children with asthma are needed to test this hypothesis. Still, our results do align with those by Zelner et al [40] and Holden et al [41], who compared observed vs counterfactual COVID-19 mortality rates. Counterfactual mortality rates were obtained by swapping Black- or Hispanic- with White-specific incidence and case fatality rates. By accounting for age, higher rates of COVID-19–related mortality among Black and Hispanic individuals were primarily driven by higher rates of infection and not case fatality [40, 41]. Whether these disparities in SARS-CoV-2 and URI in general are caused by differential exposure to respiratory viruses or differences in the risk of infection once exposed remains unclear.

Race, a social construct, is not independent of contextual factors stemming from structural racism. A history of racist policies and oppression in the United States have led to neighborhood segregation, poverty, and limited social mobility, which have in turn led to contextual factors that are more prevalent among Black and Hispanic communities [42–45]. These contextual factors may be risk factors for URI. For example, among racial and ethnic minority populations, overcrowding and poor ventilation at home and in schools may increase exposure to respiratory viruses [46–48]. At the neighborhood or community level, limited paid sick leave could disincentivize keeping sick children at home or staying home from work while sick, potentially increasing risk of exposure at school and in workplaces [33, 49, 50]. Additionally, psychosocial stress, indoor allergens, and air pollution may increase susceptibility to viral infection once exposed [51–53]. Further research is needed to better understand the contribution of these contextual factors to the observed disparities in URI and URI-associated exacerbations in children with asthma.

Findings should be interpreted considering study limitations. Self-report of upper respiratory symptoms (excluding allergies and hay fever) in the past 7 days was used as a proxy for upper respiratory viral infection. Given the exclusion of asymptomatic infection by the nature of the question, our analysis may not have accurately reflected differences by race/ethnicity in infection overall. Additionally, cold-like symptoms could have had other nonviral causes and may have been confused with environmental allergies. For example, prior studies have shown that rates of infection with common cold viruses are similar among children with and without asthma [54, 55]; yet, among Black, Mexican American, and other Hispanic (but not White) children, we observed a higher prevalence of URI in those with asthma vs those without. It is possible that children with asthma are more prone to symptomatic illness (upper or lower respiratory tract symptoms) or they have more allergic symptoms that may have been misinterpreted, leading to increased reports of a URI in children with asthma. However, previous studies cited the detection of upper respiratory viruses in 60% to 66% of children reporting cold-like symptoms [34, 56], and our finding that URI was associated with higher FENO and lower FEV₁/FVC is expected [57], lending some face validity to the use of self-reported symptoms. It is also possible that there were differences in self-report of symptoms by season (which was not available in the data set), race, or ethnicity. Other limitations include the potential for selection bias by race or ethnicity—for example, if Black and Hispanic children were more likely to be too sick to undergo a respiratory examination—and the smaller sample of children with asthma, which may have limited our power to detect statistically significant associations in this subpopulation. Nonetheless, these limitations are balanced by the novelty of the research question, which has not yet been studied and merits further research through prospective study designs. Furthermore, our use of nationally representative data lends itself to results that are generalizable to the US population. Multiple years of data were selected for analysis, and in these years, Black and Mexican American individuals were oversampled [18], creating the opportunity to calculate estimates for these subgroups.

URI may disproportionately affect Black and Mexican American children, which could lead to a disproportionate socioeconomic burden resulting from missed school and work. These results also suggest that an increased vulnerability to URI could contribute to racial and ethnic disparities in asthma exacerbations, which are largely driven by respiratory viruses. Interestingly, there was no evidence that Black or Mexican American children, with or without asthma, were at greater risk for lower respiratory tract effects of URI, suggesting that increased severity of URI is not a contributor to disparities in asthma exacerbation. Studies of racial and ethnic disparities in URI following the COVID-19 pandemic and altered patterns of RSV [58] would help to highlight how these associations may have changed in recent years. The mechanisms underlying this increased risk of URI are unclear, although a number of contextual factors could increase exposure or susceptibility to infection when exposed. These contextual factors are modifiable, and examination of their contribution to the disproportionate burden of URI could help to inform public health interventions to reduce these disparities.

Supplementary Data

Supplementary materials are available at The Journal of Infectious Diseases online (http://jid.oxfordjournals.org/). Supplementary materials consist of data provided by the author that are published to benefit the reader. The posted materials are not copyedited. The contents of all supplementary data are the sole responsibility of the authors. Questions or messages regarding errors should be addressed to the author.

Notes

Disclaimer. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Financial support. This work was supported by the National Center for Advancing Translational Sciences, National Institutes of Health (KL2 TR002646 to D. B.); the Dell Medical School's Health Transformation Research Institute Pilot Project Award (2022; D. B.); core funds of the Dell Medical School at the University of Texas at Austin (P. J. R., D. B.); the National Institutes of Health (K24AI114769, R01ES023447, R01ES026170 to E. C. M.; T32HL140290-02 to E. A. C.); and the National Eczema Association and Pediatric Dermatology Research Alliance (E. A. C.).