Abstract
Background:
Epidemiologic studies have reported conflicting findings for cat or dog exposure and childhood asthma. No study has examined whether persistent pet exposure from early life to school age is associated with asthma or allergic sensitization in youth.
Objective:
To examine whether persistent ownership of a cat or a dog throughout childhood is associated with asthma in Puerto Rican youth, a group disproportionately affected with asthma.
Methods:
Prospective study of 384 youth who completed a baseline visit at ages 6 to 14 years and a second visit at ages 9 to 20 years. Persistent cat or dog ownership was defined as ownership of a cat or a dog in early life (during pregnancy or the first year of life) at either study visit (at school age). An allergen-specific IgE was considered positive if ≥0.35 IU/ml. Logistic regression was used for the multivariable analysis of asthma and allergic sensitization.
Results:
In an analysis adjusting for household income, family history of atopy, persistent overweight or obesity, a persistent unhealthy diet, the time interval between study visits, and other covariates, persistent cat ownership was significantly associated with 68% reduced odds of asthma (95% confidence interval for odds ratio= 0.11–0.92) but not with any allergic sensitization or sensitization to cat allergen. In contrast, persistent dog ownership was not significantly associated with asthma or allergic sensitization.
Conclusion:
Among school-aged Puerto Rican youth followed for an average of 5 years, persistent cat ownership from early life to school age was inversely associated with asthma.
Keywords: Persistent cat exposure, childhood asthma, Puerto Ricans
INTRODUCTION
Asthma, the most common chronic respiratory disease of childhood, affects over 260 million people and causes an estimated 455,000 deaths worldwide. In the United States, approximately 4.2 million individuals younger than 18 years have asthma1, with children living below the federal poverty level and non-Hispanic Black and Puerto Rican youth being disproportionately affected2.
From 2016 to 2018, estimates of the prevalence of current asthma in children were 6.6% in Mexicans, 6.8% in non-Hispanic whites, 14.2% in non-Hispanic Blacks, 13% in multiracial individuals, and 13.6% in Puerto Ricans3. During the same period, Puerto Rican children were nearly twice as likely to have had a visit to the emergency department (ED) or urgent care for asthma in the previous year as non-Hispanic white children (23.5% vs. 12.1%). The high burden of childhood asthma in Puerto Ricans is likely multifactorial and due to risk factors including indoor pollutants such as second-hand smoke, allergen exposure, an unhealthy diet, obesity, chronic stress, outdoor air pollutions, low parental literacy, and limited access to healthcare4,5.
The relationship between cat or dog exposure in early life and childhood asthma is unclear, given conflicting findings from multiple studies over the last three decades. In a recent meta-analysis of data from more than 77,000 children who participated in the European Union Child Cohort Network, exposure to cats or dogs in early life (from pregnancy to age 2 years) was not significantly associated with asthma or sensitization to cat or dog allergen later in childhood, and this was not modified by timing of exposure (prenatal vs. early postnatal life) or degree of ownership (the number of cats or dogs owned)6. Interestingly, however, there was suggestive evidence of an interaction between pet ownership in early life and subsequent pet allergen sensitization on asthma at school age. Compared to children who did not own a cat in early life and were not sensitized at school age, those who were sensitized to cat allergen at school age had higher risk of asthma at school age regardless of early-life pet ownership, with similar results for the comparison of groups stratified by dog ownership and dog allergen sensitization. On the other hand, children who owned a cat and did not become subsequently sensitized to cat allergen had lower odds of asthma at school age than those who did not own a cat in early life and were not sensitized to cat allergen (odds ratio [OR]=0.80, 95% confidence interval [CI]=0.64 to 1.0)6. Of note, that study did not account for persistent ownership of a cat or dog after age 2 years (i.e. at school age).
To date, there has been no prospective study of pet exposure and asthma or allergic sensitization in Puerto Rican youth. We hypothesized that children who owned a cat or a dog both in early life and at school age would have lower risk of allergic sensitization and asthma at school age than those who never owned a cat or a dog, We tested this hypothesis in a longitudinal study of Puerto Rican children and adolescents living in the island of Puerto Rico.
METHODS
Study population
Subject recruitment and the design of the PROspective study of Puerto Rican youth and Asthma (PROPRA) have been previously described7. All participants completed a first (baseline) visit at ages 6 to 14 years and a second (follow-up) visit at ages 9 to 20 years.
The first visit was part of the Puerto Rico Genetics of Asthma and Lifestyle Study (PR-GOAL)8. In PR-GOAL, subjects were recruited from March 2009 through June 2010 using multistage probabilistic sampling, with randomly selected neighborhood clusters (based on the 2000 U.S. Census) as primary sampling units (PSUs), and randomly selected households within each PSU as secondary sampling units. A household was eligible if ≥1 resident was 6–14 years old. A total of 6,401 households selected for inclusion were contacted. Of these, 1,111 households had ≥1 child who met inclusion criteria other than age (four Puerto Rican grandparents and residence in the same household for ≥1 year). Of these 1,111 households, 438 (39.4%) had ≥1 eligible child with asthma (defined as physician-diagnosed asthma and wheeze in the prior year). From these 438 households, one child with asthma (a case) was selected (at random if there was more than one such child). Similarly, only one child without asthma (a control subject, having neither physician-diagnosed asthma nor wheeze in the prior year) was randomly selected from the remaining 673 households. To reach our target sample size (~700 children), we randomly selected and attempted to enroll 783 of the 1,111 eligible children. Parents of 105 (13.4%) of these 783 children refused to participate or could not be reached, leaving 678 study participants (351 children with asthma and 327 controls).
The second PROPRA visit was part of the Epigenetic Variation and Childhood Asthma in Puerto Ricans study (EVA-PR), which has been previously described in detail9. In EVA-PR, subjects were recruited between February 2014 and May 2017 and selected from the 1,111 households eligible for PR-GOAL. EVA-PR included 543 Puerto Rican youth ages 9 to 20 years with (n=269) and without (n=274) asthma. Of the 543 participants in EVA-PR, 406 had previously participated in PR-GOAL and were thus included in PROPRA. Of the 406 PROPRA participants, 384 (94.6%) had data on allergen-specific IgEs and were thus included in the current analysis. The average time interval between the two study visits was 5.3 ± 0.9 years.
The study was approved by the IRBs of the University of Puerto Rico and the University of Pittsburgh. Written parental consent and child assent were obtained for participants younger than 18 years, and written consent was obtained from participants 18 years and older.
Study procedures
All PROPRA participants completed a protocol that included administration of questionnaires to a child’s caretaker (the mother in ~93% of subjects), collection of blood samples, and spirometry at both study visits. The questionnaires were used to obtain information on demographics, general and respiratory health, family history of asthma and allergies, and household characteristics including pet ownership. A semiquantitative food frequency questionnaire (FFQ) developed for Hispanic populations was used to assess dietary patterns10,11.
Body mass index (BMI) z-score was calculated based on CDC growth charts, and persistent overweight or obesity was defined as a BMI z-score ≥ 85th percentile at both visits. Serum levels of total IgE and IgE specific to five common allergens in Puerto Rico (house dust mite [Der p 1], German cockroach [Bla g 2], cat dander [Fel d 1], dog dander [Can f 1], and mouse urinary protein [Mus m 1]) were measured using the UniCAP 100 system (Pharmacia & Upjohn, Kalamazoo, MI). For each allergen, an IgE level equal to or greater than 0.35 IU/ml was considered positive. At visit 1 (only), a global house dust sample was obtained by combining dust collected from three areas in the home: the one in which the child sleeps (where a mattress is located, usually the bedroom), the living room/television room, and the kitchen. The dust was sifted through a 50-mesh metal sieve. The fine dust was reweighed, extracted, and aliquoted for analysis of dog [Can f 1] and cat [Fel d 1] dander using monoclonal antibody Multiplex array assays that used the same reagents as in the established ELISA. Non-detectable allergen levels were assigned a constant (half the lowest detectable value) for data analysis.
In a prior study of Puerto Rican youth, four food groups were found to be associated with increased (dairy products and sweets) or decreased (vegetables and grains) odds of asthma12. A dietary score was then defined by the frequency of food group consumption, with study participants being assigned a score of +1 for high consumption of each “healthy” food group (associated with decreased odds of asthma) or −1 for the consumption of each “unhealthy” food group (associated with increased odds of asthma). An unhealthy diet was defined as a non-positive score (0, −1, or −2), and a healthy diet was defined as a positive score (+1 or +2). A persistently unhealthy diet was defined as having a non-positive dietary score at both study visits13.
As in prior work, residential distance to a major road was used as a marker of traffic-related air pollution (TRAP). The home address of each participant was first geocoded, and centroids were created by obtaining X, Y coordinates for the center of individual census blocks based on a 2000 US Census map for Puerto Rico, using the program ArcMAP10.1 (Arc-GIS 10.1, Esri, Redlands, California). The distance from the residential block centroid of a participant to the nearest major road (defined by Esri 2012 Data and Maps major road layer) was then calculated. Residential distance to a major road was classified as within 441 meters vs greater than 441 meters (corresponding to the first to third quartiles vs. the upper quartile)14.
Statistical analysis
Our exposure of interest was self-reported pet ownership. For each pet (cat or dog), ownership was considered separately and categorized into four groups, as follows: never owned (reference group), ownership in early life (during pregnancy or in the first year of life) but not at school age (i.e. at neither study visit), ownership in at least one study visit but not in early life (i.e. ownership at school age), and ownership in early life and at least one study visit (i.e. persistent pet ownership). Our main outcomes of interest were asthma (defined as physician-diagnosed asthma and ≥1 episode of wheeze in the year prior to the second visit) and sensitization (a positive IgE) to: cat allergen, dog allergen, or ≥1 allergen at the second visit.
Wald chi-square or Fisher’s exact test and t-tests or Wilcoxon rank-sum test were used for bivariate analyses, as appropriate. Logistic or linear regression was used for the multivariable analysis of cat or dog ownership and the outcomes of interest. All models were adjusted for covariates known to be potential confounders or associated with asthma or atopy in our prior studies. All models for asthma and atopy were adjusted for age, sex, annual household income (≥ vs. <$15,000 per year), parental education (at least one parent had completed high school vs. none), family history of atopy (history of asthma, allergic rhinitis, or eczema in the participant’s parents or siblings), early-life exposure to second-hand smoke (SHS), persistent (i.e. at both study visits) overweight or obesity, a persistently unhealthy diet, and the time interval between visits. Given results of bivariate analyses, sighting mold or mildew in the child’s house in the prior year was considered for inclusion but ultimately excluded from the final models as it was not significantly associated with or changed the effect estimates for any outcome. All analyses were performed using SAS version 9.4 (SAS Institute, Cary, NC).
RESULTS
A comparison of the main baseline characteristics of the 384 individuals included in the current analysis (as they were PROPRA participants with allergen-specific IgE measurements) versus those of the 294 individuals excluded from this analysis (either because they completed the first but not the second PROPRA study visit (n=272) or lack IgE measurements (n=22)) is shown in E-Table 1 in the Online Supplement. Compared with individuals included in the current analysis, those excluded were more likely to be exposed to current SHS and to live in an apartment at the baseline study visit. There were no significant differences in cat or dog ownership, Fel d 1 or Can f 1 levels in house dust, or having a positive IgE to cat or dog allergen at the baseline study visit between subjects who were and were not included in this analysis.
Table 1 shows a comparison of the main baseline characteristics of the 384 study participants included in the current analysis. Compared with 173 children without asthma (control subjects), those with asthma (cases, n=211) were significantly more likely to be male and to have: a parental report of mold or mildew in the house in the prior year, a family history of atopy, ≥1 positive allergen-specific IgE, an unhealthy diet, and a higher BMI z-score. There were no significant differences in indicators of socioeconomic status (SES), cat or dog ownership, levels of cat or dog allergen in house dust, a positive IgE to cat or dog allergen, sights of pests (cockroaches or rodents) in the prior year, or any other characteristic between cases and control subjects.
Table 1.
Baseline characteristics of participants in PROPRA, by asthma status (n=384)
| Characteristics | Asthma | |
|---|---|---|
| No (n=173) | Yes (n=211) | |
| Age, years | 9.9 ± 2.8 | 10.0 ± 2.5 |
| Male sex | 81 (46.8) | 123 (58.3)† |
| Neither parent completed high school | 39 (22.5) | 35 (16.6) |
| Annual household income < $15,000 | 106 (64.6) | 128 (62.4) |
| No private or employer-based health insurance | 112 (64.7) | 134 (63.5) |
| Family history of atopy | 100 (58.8) | 187 (89.1)† |
| Current exposure to second-hand smoke | 62 (35.8) | 77 (36.7) |
| Early life exposure to second-hand smoke | 66 (40.2) | 101 (49.3)† |
| Prematurity | 9 (5.2) | 14 (6.7) |
| Breastfeeding | ||
| Never | 77 (45.3) | 92 (44.0) |
| ≤ 6 months | 71 (41.8) | 83 (39.7) |
| > 6 months | 22 (12.9) | 34 (16.3) |
| Unhealthy diet* | 50 (28.9) | 94 (44.6)† |
| Body mass index, z-score | 0.58 ± 1.10 | 0.87 ± 1.15† |
| ≥1 allergen-specific IgE ≥0.35 IU/ml | 87 (53.4) | 125 (67.6)† |
| IgE to Can f 1 ≥0.35 IU/ml | 28 (17.2) | 35 (18.9) |
| IgE to Fel d 1 ≥0.35 IU/ml | 15 (9.3) | 16 (8.7) |
| Time interval between study visits (years) | 5.4 ± 0.8 | 5.3 ± 0.9 |
| Home environment characteristics | ||
| Dog ownership | ||
| Never | 38 (22.0) | 31 (14.7) |
| Only in early life | 1 (0.6) | 4 (1.9) |
| Only at school age | 85 (49.1) | 103 (48.8) |
| Both in early life and at school age | 49 (28.3) | 73 (34.6) |
| Cat ownership | ||
| Never | 126 (72.8) | 149 (70.6) |
| Only in early life | 9 (5.2) | 11 (5.2) |
| Only at school age | 28 (16.2) | 38 (18.0) |
| Both in early life and at school age | 10 (5.8) | 13 (6.2) |
| Can f 1 level in house dust (mcg/gram)§ | 0.11 (0.03, 0.72) | 0.16 (0.04, 1.44) |
| Fel d 1 level in house dust (mcg/gram)§ | 0.02 (0.01, 0.18) | 0.02 (0.01, 0.05) |
| Living in a house (vs. apartment/condo) | 100 (57.8) | 129 (61.1) |
| Ever gave away animals due to asthma | -- | 20 (9.6) |
| Mold or mildew in the house, prior year | 59 (34.3) | 95 (45.0)† |
| Sights of cockroaches, prior year | 133 (76.9) | 167 (79.2) |
| Sights of mice or rats, prior year | 47 (27.2) | 69 (32.7) |
| Residential proximity (<441 m) to a major road | 130 (75.1) | 161 (76.7) |
PROPRA= Prospective Study of Puerto Rican Youth and Asthma study. Data shown as number (%) for categorical variables and as mean ± standard deviation (SD) or median (interquartile range) for continuous variables. Numbers may differ due to missingness
Unhealthy diet: a dietary score <= 0.
House dust samples were missing for 37 participants.
P<0.05 for comparison between the two groups.
Table 2 shows the results of the multivariable analysis of cat or dog ownership and asthma. In an analysis adjusting for age, sex, household income, parental education, family history of atopic diseases, early-life exposure to SHS, persistent overweight or obesity, a persistently unhealthy diet, and the time interval between study visits, children who owned a cat in early life and at school age had 68% lower odds of asthma than those who never owned a cat (95% confidence interval [CI] for odds ratio [OR]=0.11 to 0.92). In this analysis, cat ownership in early life only or at school age only was not significantly associated with asthma. In a multivariable analysis adjusting for the same covariates as in the analysis of cat ownership, dog ownership (whether in early life only, at school age only, or at both early life and school age) was not significantly associated with asthma (Model 2). Similar results for both cat and dog ownership were obtained when both were included in the same multivariable model (Model 3).
Table 2.
Multivariable analysis of cat or dog ownership and asthma in PROPRA
| Model 1 | Model 2 | Model 3 | |
|---|---|---|---|
| Variables | OR (95% confidence interval) | ||
| Cat ownership | |||
| Never | 1.0 | 1.0 | |
| Only in early life | 0.84 (0.31, 2.26) | 0.70 (0.25, 1.97) | |
| Only at school age | 1.10 (0.57, 2.13) | 1.10 (0.57, 2.15) | |
| In early life and at school age | 0.32 (0.11, 0.92) * | 0.31 (0.10, 0.90) * | |
| Dog ownership | |||
| Never | 1.0 | 1.0 | |
| Only in early life | 4.78 (0.28, 82.15) | 4.91 (0.27, 87.83) | |
| Only at school age | 1.26 (0.65, 2.45) | 1.38 (0.71, 2.70) | |
| In early life and at school age | 1.38 (0.67, 2.84) | 1.49 (0.71, 3.11) | |
PROPRA= Prospective Study of Puerto Rican Youth and Asthma study.
All models were adjusted for age, sex, annual household income, parental education, family history of atopic diseases (asthma, allergic rhinitis, or eczema), early-life exposure to second-hand smoke, persistent overweight or obesity, a persistently unhealthy diet, the time interval between study visits, and the variables shown for each model.
P<0.05
To further assess the observed inverse association between persistent cat ownership and asthma, we compared the main characteristics of children who owned a cat in early life and at school age (n=23) with those who never owned a cat (n=275)(E-Table 2). Parents of children with persistent cat ownership were more likely to have given away an animal due to asthma and to have higher Fel d 1 levels in house dust than those who never owned a cat. There were no significant differences in indicators of SES, a positive IgE (to ≥1 allergen, to cat allergen, or to dog allergen), or any other characteristic between the two groups.
Table 3 shows the results of the multivariable analysis of cat or dog ownership and having a positive IgE to cat or dog allergen, or to ≥1 allergen. In this analysis, cat ownership was not significantly associated with a positive IgE to cat allergen or to ≥1 allergen. In this analysis, dog ownership at school age only (but not in early life only or persistently) was significantly associated with a positive IgE to dog allergen. However, no category of dog ownership was significantly associated with a positive IgE to ≥1 allergen.
Table 3.
Multivariable analysis of cat or dog ownership and allergic sensitization
| Allergic sensitization at the second visit | ||
|---|---|---|
| Variables | OR (95% confidence interval), P-value | |
| Cat ownership | Positive IgE* to Fel d 1 | ≥1 positive IgE to allergens † |
| Never | 1.0 | 1.0 |
| Only in early life | 1.33 (0.26, 6.74) | 2.15 (0.64, 7.23) |
| Only at school age | 1.71 (0.71, 4.11) | 0.75 (0.40, 1.42) |
| In early life and at school age | 2.53 (0.61, 10.44) | 0.67 (0.22, 1.99) |
| Dog ownership | Positive IgE* to Can f 1 | ≥1 positive IgE to allergens † |
| Never | 1.0 | 1.0 |
| Only in early life | 0.85 (0.08, 8.66) | 0.98 (0.13, 6.91) |
| Only at school age | 2.11 (1.05, 4.24)‡ | 1.31 (0.67, 2.53) |
| In early life and at school age | 1.77 (0.84, 3.77) | 1.20 (0.58, 2.45) |
An allergen-specific IgE ≥0.35 IU/ml.
Der p 1 (dust mite), Bla g 1 (German cockroach), Fel d 1 (cat dander), Can f 1 (dog dander), and Mus m 1 (mouse urinary protein).
All models were adjusted for asthma status, age, sex, annual household income, parental education, family history of atopic diseases (asthma, allergic rhinitis, or eczema), early life exposure to second-hand smoke, persistent overweight or obesity, a persistently unhealthy diet, and the time interval between study visits
P<0.05
We conducted two sensitivity analyses to further assess our findings. In the first such analysis (Table 4), we examined the relation between persistent cat or dog ownership and asthma in 294 children whose families never gave away any animals, obtaining similar results for persistent cat ownership and asthma despite smaller sample size (aOR=0.21, 95% CI=0.06–0.81). In another sensitivity analysis, we excluded 24 participants with cat ownership at visit 2 only (i.e. neither in early life nor at visit 1), as this could represent cross-sectional exposure. This analysis yielded similar results despite smaller sample size (see E-Table 3 in the Online Supplement).
Table 4.
Multivariable analysis of cat or dog ownership and asthma among 294 children whose families never gave away animals
| Cat ownership | Dog ownership | |
|---|---|---|
| OR (95% confidence interval), P-value | ||
| Never | 1.0 | 1.0 |
| Only in early life | 0.97 (0.33, 2.84) | 4.11 (0.21, 81.72) |
| Only at school age | 1.00 (0.49, 2.03) | 1.14 (0.57, 2.27) |
| In early life and at school age | 0.21 (0.06, 0.81) * | 1.26 (0.59, 2.69) |
All models adjusting for age, sex, annual household income, parental education, family history of atopy, early life exposure to second-hand smoking, persistent overweight, persistent unhealthy diet, and the time interval between study visits
P<0.05
DISCUSSION
In a prospective study of 384 Puerto Rican youth followed for ~5 years on average, persistent ownership of a cat from early life to school age was associated with lower odds of asthma at school age, and this association was not explained by a link between persistent cat ownership and sensitization to cat allergen or to ≥1 allergen. In this study, persistent dog ownership was not associated with asthma or allergic sensitization.
While there have been numerous studies of pet ownership in early life and asthma and allergies, to our knowledge this the first prospective study to examine persistent cat or dog ownership from early life (in utero or in the first year of life) to school age (comprising ages 6 to 14 years at the first study visit and 9 to 20 years at the second study visit). We note that a previous cross-sectional study examined pet ownership in the first year of life and/or “currently” (at the time of a survey administered once between birth and age 8 years) and parental report of asthma, asthma symptoms, allergic rhinitis, and eczema (at any age, between birth and age 8 years) in 7,366 Chinese children15. Bivariate analyses were shown for early-life, current, and persistent (“all the time”) exposure to any pet (including cats, dogs, birds, fish, and rodents) and asthma and other outcomes, but there were no bivariate or multivariable analyses of persistent cat or dog exposure and asthma or any other outcome. In that study, models adjusting for age, sex, income, house dampness, home location, and family history of atopy showed that cat ownership in the first year of life and (separately) current cat ownership were associated with higher odds of asthma, and that current cat or dog ownership was associated with higher odds of eczema. In contrast to that cross-sectional study, ours excluded children younger than six years (in whom asthma cannot be confidently diagnosed), measured allergen-specific IgEs, and examined persistent cat or dog exposure and asthma or allergen-specific IgEs in a prospective analysis accounting for potential confounders.
Studies examining associations between early-life cat exposure and later risk of childhood asthma have produced conflicting results, with reports of no, positive, or inverse associations6,16,17. Such discrepant results could be explained by variability in exposure or outcome assessment, or by genetic or environmental modifiers of potential effects of cat allergen on asthma. Alternatively, persistently high levels of cat allergen exposure from early life to school age could induce immune tolerance through induction of Treg cells, coupled with a reduction in Th2 responses and increased allergen-specific IgG1, IgG4, and IgA levels18.
We acknowledge several study limitations. First, selection bias is possible in any observational study. However, this is unlikely to explain our findings, as there was no significant difference in cat ownership, a positive IgE to cat allergen, home dust level of cat dander, or SES indicators between children who were and were not included in the current analysis (eTable 1). Moreover, our results were unchanged after restricting the analysis to youth whose families had not given away any animals (Table 4). Second, we lack data on cat allergen level outside of the home. Although recall bias of cat ownership in early life or school age is unlikely, exposure to lower levels of cat allergen can occur at school or by contact with friends or relatives living in households with a cat, and such exposure may be relevant to the risk of asthma or allergic sensitization. Third, consistent with prior reports, cat allergen levels in the homes of study participants were lower than those reported for households of predominantly non-Hispanic white children or Puerto Rican children living in cities in the U.S. Northeast, a finding that may be partly explained by relatively low rates of cat ownership in San Juan (PR)19,20. Fourth, we cannot assess whether genetic variants21 or early-life environmental exposures (e.g., outdoor air pollutants) confound or modify the estimated effects of cat ownership on asthma, because of lack of such environmental data or statistical power to detect gene-by-cat ownership interactions. Similarly, we lacked statistical power to detect modest associations between cat or dog ownership and a positive IgE to cat or dog allergen, though neither cat nor dog ownership was associated with sensitization to ≥1 allergen (Table 3). Fifth, we measured IgE levels to five common allergens in Puerto Rico but not to certain allergens such as mold or pollens. However, we previously showed that most atopic children in Puerto Rico are both identified by a positive IgE to dust mite and sensitized to multiple allergens22. Finally, our results must be cautiously interpreted pending replication, due to small sample size for two categories of cat ownership.
In summary, our findings suggest that persistent exposure to a cat throughout childhood may be inversely associated with reduced risk of asthma in Puerto Rican youth, a high-risk group for asthma morbidity. Future studies with larger sample size should examine whether and how long-term exposure to high levels of cat allergen may ameliorate asthma risk in this and other marginalized populations.
Supplementary Material
Conflicts of interest:
Dr. Celedón has received research materials from Merck (inhaled steroids) to provide medications free of cost to participants in an NIH-funded study unrelated to this work. The other authors have no conflicts of interest to declare.
Funding:
This work was supported by grants HL079966, HL117191, and HL168539 from the U.S. National Institutes of Health (NIH). The sponsor had no role in the design or implementation of the study, or the drafting and submission of the manuscript.
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