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| EDITORIAL |
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| Year : 2022 | Volume
: 2
| Issue : 1 | Page : 2-4 |
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Epidemiology and risk factors for allergic rhinitis
PA Mahesh
Department of Respiratory Medicine, JSS Medical College, JSSAHER, Mysore, Karnataka, India
| Date of Submission | 06-Nov-2021 |
| Date of Acceptance | 06-Nov-2021 |
| Date of Web Publication | 17-Jan-2022 |
Correspondence Address:
Dr. P A Mahesh
Department of Respiratory Medicine, JSS Medical College, JSSAHER, Mysore, Karnataka
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/jalh.jalh_24_21
How to cite this article:
Mahesh P A. Epidemiology and risk factors for allergic rhinitis. J Adv Lung Health 2022;2:2-4 |
| Epidemiology | |  |
The prevalence of allergic rhinitis worldwide according to the ISAAC Phase III study varies from 1.4% to 39.7% in children aged 13–14 years.[1] In Asian countries, the prevalence ranged from 27% to 32% among children in the same age group.[2] Allergic rhinitis is no longer considered an innocuous disease due to its overall global impact on a person's life.[1],[3] It is the most important risk factor for asthma and increases the risk for hospitalization in children by 19 times.[2] Although the predisposition to allergic rhinitis is predominantly genetic, environmental influences play a major role in the onset and persistence of allergic rhinitis.[3] Since genetic factors cannot be modified, a detailed evaluation of environmental influences is necessary to identify the most relevant modifiable risk factors. The list of risk factors as well as protective factors for allergic rhinitis identified from Asia is presented in [Table 1].[2] When there were several studies evaluating a risk factor, the highest odds ratios and 95% confidence intervals were enumerated. | Table 1: Individual and environmental risk factors associated with allergic rhinitis
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| Risk Factors for Allergy and the Exposomes | | |
Allergic rhinitis is a result of a complex gene–environment interaction that is best studied with an exposome analysis. Exposome analysis aims to include a global exposure of all the factors over an individual's lifetime.[3] The exposome analysis includes multiple domains such as the internal and external. The internal domain includes various factors that are host related. These include genetics, epigenetics, metabolome, proteomics, race, gender, and current age.
The external domain includes social, cultural, dietary, economic, geographic, environmental, and psychological factors. The environmental factors include cigarette smoking and exposure to air pollution in outdoor, indoor, and occupational environments.[3]
Gender studies have confirmed that both asthma and allergic rhinitis are more common in boys than girls in early childhood and reach equivalence in both genders in adolescence.[4] A systematic review of nearly 4000 adolescents observed a male:female sex ratio for the prevalence of allergic rhinitis of 0.8 (0.71–0.90), indicating that it was higher in females.[4] In children <10 years of age, among more than 56,000 children, the sex ratio was 1.25 (1.19–1.32), indicating that it was more common among male children.[4] A sex switch was clearly observed in the prevalence of allergic rhinitis from childhood to adolescence. Estrogen and progesterone enhance type 2 inflammation and are likely the main reason behind this observation.[4],[5] Testosterone, on the other hand, suppresses type 2 inflammation. Estrogen enhances mast cell activation, while progesterone increases IgE production.[4],[6]
Longitudinal studies are ideally placed to evaluate the role of various factors influencing the development of allergic rhinitis. The Canadian Healthy Infant Longitudinal Development is a birth cohort study including 3500 pregnant women, evaluating the various factors associated with the onset of allergies, and has studied environmental exposures in the antenatal and postnatal life of these children.[7] Another important cohort is the Kingston Allergy Birth Cohort which studies similar antenatal and postnatal factors.[8] Both the studies observed that higher socioeconomic status, including housing type, urban residence, delivery by cesarean section, higher gestational age, prenatal tobacco smoke exposure, mold, and air freshner usage were associated with higher risk of allergic rhinitis. A detailed systematic review by Chong and Chew in Asia observed other relevant factors influencing allergic rhinitis including reduced sleep and increased stress, higher parental education and household income, smaller family size of <3, higher computer usage, especially above 4 h per day, lower duration of exclusive breastfeeding, earlier introduction of other foods, maternal depression and parasitic infestations, home renovation, and use of carpets as risk factors for the development of allergic rhinitis.[2]
Sensitization to house dust mites, pollens, fungi, and insects is an important intermediate step in the development of clinical allergies, including allergic rhinitis. While indoor allergens such as house dust mites are more relevant for persistent rhinitis throughout the year, outdoor allergens such as pollens are likely to be relevant for seasonal symptoms of allergic rhinitis.[9],[10] House dust mites are the most common clinically relevant allergen for nearly 60% of patients. Fungi are ubiquitous in both the indoor and outdoor environment and are associated with more severe allergic rhinitis, chronic rhinosinusitis with polyposis as well as severe asthma.[9]
Air pollution, exposure to fumes, and occupational exposure – Air pollution includes gaseous, liquid, and solid particulate matter (SPM) emissions from a variety of sources such as traffic, industries, and power generators are common sources of outdoor pollution and fossil fuels (biomass) burning for cooking and heating for indoor pollution. Studies have confirmed that air pollution constituents (NO2, NO, SO2, SPM, and diesel exhaust particles) have been associated with new onset of allergies as well as exacerbations of existing allergies.[3] One of the most important modifiable risk factors for allergies includes active as well as passive smoking. Smoking induces airway inflammation and increases the risk of sensitization to various allergens and subsequent allergic diseases.
The exact relationship between respiratory infections and the onset of allergic rhinitis is not clear. Allergic subjects have higher levels of Intercellular adhesion molecule-1 (ICAM-1) in their airway epithelia which predispose them to recurrent infections since many viruses enter the cells through binding to ICAM-1.[9] Several viruses such as the rhinoviruses and respiratory syncytial virus infection have been shown to predispose to the development of allergic rhinitis and asthma.[9] Further longitudinal studies are needed to understand the relevance of respiratory infections, especially viruses and allergic rhinitis in the community.
There is a need for longitudinal studies, especially in low-middle-income countries (LMIC), to study the exposomes related to allergic rhinitis. Even in developed countries, there is a paucity of information among adolescents. There are many birth cohorts that have evaluated the role of influencing factors in the development of childhood allergies, and studies such as ECRHS in Europe have detailed information on allergies in adults. The study on the prevalence of allergic rhinitis among adolescents in Mangalore, South India,[11] in this issue is a step in the right direction for further multicenter studies in India with additional inclusion of various exposomes in future studies to unravel the gene–environment interactions related to the development of allergic rhinitis in LMIC countries.
| References | | |
| 1. | Fernandes SS, Andrade CR, Alvim CG, Camargos PA, Ibiapina CD. Epidemiological trends of allergic diseases in adolescents. J Bras Pneumol 2017;43:368-72.  |
| 2. | Chong SN, Chew FT. Epidemiology of allergic rhinitis and associated risk factors in Asia. World Allergy Organ J 2018;11:17. |
| 3. | Li CH, Sayeau K, Ellis AK. Air pollution and allergic rhinitis: Role in symptom exacerbation and strategies for management. J Asthma Allergy 2020;13:285-92. |
| 4. | Fröhlich M, Pinart M, Keller T, Reich A, Cabieses B, Hohmann C, et al. Is there a sex-shift in prevalence of allergic rhinitis and comorbid asthma from childhood to adulthood? A meta-analysis. Clin Transl Allergy 2017;7:44. |
| 5. | Chen W, Mempel M, Schober W, Behrendt H, Ring J. Gender difference, sex hormones, and immediate type hypersensitivity reactions. Allergy 2008;63:1418-27. |
| 6. | Roved J, Westerdahl H, Hasselquist D. Sex differences in immune responses: Hormonal effects, antagonistic selection, and evolutionary consequences. Horm Behav 2017;88:95-105. |
| 7. | Subbarao P, Anand SS, Becker AB, Befus AD, Brauer M, Brook JR, et al. The Canadian Healthy Infant Longitudinal Development (CHILD) study: Examining developmental origins of allergy and asthma. Thorax 2015;70:998-1000. |
| 8. | North ML, Brook JR, Lee EY, Omana V, Daniel NM, Steacy LM, et al. The Kingston allergy birth cohort: Exploring parentally reported respiratory outcomes through the lens of the exposome. Ann Allergy Asthma Immunol 2017;118:465-73. |
| 9. | Passali D, Cingi C, Staffa P, Passali F, Muluk NB, Bellussi ML. The international study of the allergic rhinitis survey: Outcomes from 4 geographical regions. Asia Pac Allergy 2018;8:e7. |
| 10. | Schuler Iv CF, Montejo JM. Allergic rhinitis in children and adolescents. Pediatr Clin North Am 2019;66:981-93. |
| 11. | Sheik IA, Moleyar VS. Prevalence of allergic rhinitis among students in the age group of 16-20 years in a south Indian city. J Adv Lung Health 2022;2:13-21. [Full text] |
[Table 1]
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