Environmental pollution is a global problem. It is known that 93% of children under 15 years of age are breathing polluted air, which causes health problems such as lower respiratory tract infections, asthma, and impaired lung function [1]. Pollution with ozone (O₃), suspended particles called coarse with aerodynamic diameter <10 μm (PM10), fine with aerodynamic diameter <2.5 μm (PM_2.5) and nitrogen dioxide (NO²) have been associated with changes regarding decreased lung function in spirometry in both healthy and asthmatic children that could persist in the long term [2]. Even Ultrafine Particles (UFP) with aerodynamic diameter < 0.1 μm (PM_0.1) can penetrate the airway deeply and cause alterations in the respiratory and immune systems during childhood [3]. Household Air Pollution (HAP) from the use of wood, coal, kerosene and biomass combustion can affect lung function measured by spirometry in children [4]. On the other hand, a global study carried out in almost 200 countries showed that 40% of children are constantly exposed to second-hand tobacco [5]. Pre- or postnatal exposure to nicotine can cause premature birth, fetal mortality, birth defects, intrauterine growth restriction, sudden death, and alterations in the areas of: behavior, lung development, cardiovascular and immune systems [6]. Intrauterine smoking is associated with early impairment of lung function with decreases in forced respiratory volume in 1 second (FEV₁) and forced expiratory flow between 25-75% of forced vital capacity (FEF_25-75) that may persist even into early adulthood [7]. It has also been shown that children under 16 years of age who are persistently exposed to environmental tobacco follow trajectories with decreased FEV₁ into adulthood [8]. Most of the effects of pollution and tobacco on lung function in children and adolescents have been measured with spirometry, which has the disadvantage of only measuring alterations in the larger airways, lacking a proper sensitive to evaluate small airway alterations. Impulse Oscillometry (IOS) is a lung function test that has parameters that are more sensitive than spirometry for detecting alterations in the peripheral airways (less than 2 mm in diameter) in children [9]. In addition, the IOS has parameters that allow identifying whether the alteration is produced at the level of the total airway, such as the resistance at 5 Hertz (R5), of the proximal airway, such as the resistance at 20 Hertz (R20), or of the distal airway, such as the difference between 5 and 20 Hertz (R5-R20), the reactance at 5 Hertz (X5), the reactance area (AX), and the resonance frequency (Fres) [10,11]. The purpose of this review was to analyze whether there is evidence to support the use of the IOS as a follow-up examination of the effects of pollution and passive smoking in children and adolescents.

A search was conducted for the available scientific evidence on the usefulness of Impulse Oscillometry in monitoring the effect of pollution and tobacco on the respiratory health of children and adolescents. The search for articles was carried out in January 2025 in the databases Medline (PubMed), Web of Science (WOS), EBSCO Host, Science Direct, and SCOPUS. MeSH terms and free terms in their English version were used. The terms were grouped into four dimensions: i) Pollution ii) Prenatal or passive tobacco iii) Impulse oscillometry iv) Children and adolescents.

The articles found were grouped into five categories:

• Monitoring the effect on extra-domiciliary pollution
• Monitoring the effect on indoor pollution
• Monitoring the effect of pollution on asthma
• Monitoring the effect of prenatal smoking
• Monitoring the effect of passive smoking.

Monitoring the Effect of Extra-Household Pollution

A follow-up study looked at exposure to traffic pollutants and lung function measured by IOS in adolescence. The study showed that 16-year-old adolescents who had increases in nitrogen oxide (NO_x) concentrations above 10 mg/m3 in the first year of life had greater increases in R5-R20 and AX, reflecting greater small airway involvement [12]. In healthy children aged 6 to 12 years living in cities with different levels of pollution, it was shown that those living in less polluted cities had lower levels of airway resistance measured with IOS. Furthermore, this study demonstrated a high correlation between R5 and spirometry parameters reflecting proximal and distal airway involvement (FEV₁ and FEF_25-75, respectively) [13]. Some gender differences in the effect of pollution have been found. One study measured lung function in children and adolescents aged 9 to 16 years in two cities with different levels of PM_2.5, PM₁₀, NO₂, and Sulfur Dioxide (SO₂) pollution. In the most polluted city, boys were found to have significant changes in parameters reflecting the state of the small airways (decreased X5, increased R5-R19) when compared to boys in the less polluted city, differences that were not found in girls [14]. A cohort measured the effect of prolonged exposure (six weeks) to environmental pollution in children under two years of age during a coal mine fire in Australia, showing that three years later those exposed to higher levels of PM_2.5 had higher levels in AX [15]. Subsequently, the follow-up of these children was prolonged, showing that the IOS parameters that reflect peripheral airway alterations (X5, AX) improved moderately when patients reached 7 years of age [16]. A study conducted with schoolchildren aged 8 to 11 years showed that higher counts of the small size and large surface area of UFP derived from ambiental pollution (PM 0.1), were associated with lower values of X5 in the IOS, which would indicate that these children could have stiffer lungs [17].

Monitoring the Effect of Indoor Pollution

A study showed that at 4 years of age, pre-schoolers exposed to Carbon monoxide (CO) pollution prenatally and in early life had higher resistance values (R5, R20, R5-R20) and AX than unexposed children. Furthermore, the increase in total airway resistance (R5) was greater in children exposed to prenatal pollution than in those exposed only to pollution in early life [18]. In healthy schoolchildren aged 7 to 8 years, the association between Volatile Organic Compounds (VOC) measured in urine and lung function was analyzed. In this study, it was shown that elevated levels of benzene (Muconic acid) and xylene (o-methyl-hippuric acid) metabolites were significantly associated with increases in R5 in IOS [19]. Phthalates are contaminating particles found in polyvinyl chloride, medical devices, some solvents, and toys. They can be inhaled, swallowed, or absorbed through the skin, causing alterations in the endocrine, reproductive, and respiratory systems [20]. A study involving first graders in 11 schools investigated the association of metabolites of phthalates in urine with total airway dysfunction using acoustic rhinometry, IOS and spirometry. This study found that metabolites such as mono-2-ethyl-5-hydroxyhexyl phthalate (MEHHP) and Mono-isobutyl Phthalate (MiBP) were significantly associated with decreased nasal patency, increased R5 and AX in the lower airway, with no alterations found in spirometry. The authors conclude that these polluting metabolites simultaneously affect the upper and lower airways, which reinforces the concept of a united airway disease [21]. Another study showed that PM₁₀ levels > 40 μg/m³ measured in indoor home air in infants aged 4–6 months was associated with increased difference between end-expiratory and inspirational resistance in IOS performed when said children were 3 years old [22]. Home stoves are highly polluting during pregnancy and in children in their early stages of lung development. Some interventions have shown that early exposure to indoor pollution from stoves is associated with worse lung function in children [23]. It has been shown that even at two years of age, children exposed to high concentrations of PM_2.5 indoors generated from stoves (ethanol, firewood or kerosene), have more negative values of X5, which confirms that the smaller the size of the polluting particle, the greater the compromise of the small airway [24]. A follow-up study looked at the impact of household pollution from different types of stoves. This study looked at exposure to Liquefied Petroleum Gas (LPG) stoves, open-fire stoves, and improved biomass stoves from the prenatal period through their first birthday. The study showed that at age four, children who used LPG stoves had less negative X5 scores, less positive Fres scores, and R5-R20 scores than the open-fire stove group, indicating that they had less impact on the peripheral airway. On the other hand, children who used improved biomass stoves had worse results in some parameters of the IOS (X5, R20, and AX) than those who used open-fire stoves, indicating that this type of stove is the one that compromises the function of the central and peripheral airway, being the one of the three types that had the greatest impact on lung function measured by IOS [25].

Monitoring the Effect of Pollution on Asthma

Asthmatic children aged 5 to 13 years exposed to indoor and outdoor air pollution with PM 2.5 were shown to have higher levels of R5 and R5-R20 [26]. A double-blind, crossover study conducted in children with mild to moderate asthma showed that intervening with an unnamed device with a high-efficiency particulate air filtering system to eliminate PM2.5 pollution in their rooms decreased R5 by 24.4%, R5-R20 by 43.5%, Fres by 22.2% and increased X5 by 73.1% [27]. In preschool children with suspected or treated asthma, it has been shown that exercise-induced bronchoconstriction diagnosed with IOS after free running (R5 value after exercise ≥ to 40% of baseline) was more frequent in children exposed to PM 2.5 over 10 μg/m³ on the day of the examination [28].

Monitoring the Effect of Prenatal Smoking

A study evaluating the effect of intrauterine smoking on lung function showed that new-borns with elevated cotinine levels in the umbilical cord (over >2 ng/ml) had IOS at 4-5 years with higher AX levels than those who did not have these cotinine levels, differences that were not observed in spirometry by measuring Forced Expiratory Volume (FEV) at 0.5 seconds, demonstrating that IOS is more sensitive in monitoring changes in lung function [29]. A large long-term follow-up cohort demonstrated that maternal smoking history during pregnancy is associated with increased small airway resistance in adolescents when measured by the IOS parameter R5-R20 [30].

Monitoring the Effect of Passive Smoking

Preschool children with multiple trigger wheezing who are exposed to environmental tobacco smoke by their parents have significantly higher levels of R5 in the IOS compared to unexposed children [31]. In pre-schoolers aged 3 to 7 years with late prematurity (34 to 36 weeks gestational age) and exposure to passive smoking, significantly higher averages were found in R5, R20, resistance at 10, 15 hertz (R10, R15), and lower in reactance at 10 hertz (X10) compared to non-exposed children [32]. In healthy children and adolescents aged 6 to 14 years, it was shown that those exposed to passive smoking at home had higher averages in R20%, Fres% and AX% than those not exposed, demonstrating that passive smoking is associated with alterations in the central and peripheral airways that can be detected with IOS [33].

Extra-household pollution produced by urban vehicular traffic or coal mine fires has been shown to be associated with small airway alterations in IOS in the follow-up of healthy children and adolescents. Intra-domiciliary contamination from stoves, toys, plastics or solvents has been linked to alterations in the IOS of both the central and peripheral airways in the follow-up of healthy children. Children with asthma are a group particularly affected by environmental pollution (especially PM_2.5) which can be demonstrated by increases in airway resistance measured with alterations in baseline parameters or in a bronchial provocation test after a free run with IOS. Prenatal exposure to passive smoking has been associated with small airway abnormalities in IOS in children followed from 4 to 16 years of age. Parent-reported passive smoking has also been linked to alterations in the IOS of children and adolescents. There is a lack of follow up studies that demonstrate an appropriate way to measure the effects of preventive strategies and interventions to mitigate the impact of pollution and smoking from the fetal stage and infant stage and into adulthood.

Declaration of Competing Interests

The author declares no conflict of interest

Information on the Financing

The author declares that he has no funding for this review.

Ethical Statement

Not applicable/No human participants included

1. Aithal SS, Sachdeva I, Kurmi OP. Air quality and respiratory health in children. Breathe (Sheffield, England). 2023; 19: 230040.
2. Garcia E, Rice MB, Gold DR. Air pollution and lung function in children. The J allergy and clinical immunology. 2021; 148: 1-14.
3. E Oliveira JRC, Base LH, de Abreu LC, Filho CF, Ferreira C, Morawska, L. Ultrafine particles and children's health: Literature review. Paediatric respiratory reviews. 2019; 32: 73-81.
4. Aithal SS, Gill S, Satia I, Tyagi SK, Bolton CE, Kurmi OP. The Effects of Household Air Pollution (HAP) on Lung Function in Children: A Systematic Review. Int J environmental research and public health. 2021; 18: 11973.
5. Oberg M, Jaakkola MS, Woodward A, Peruga A, Pruss-Ustun A. Worldwide burden of disease from exposure to second-hand smoke: a retrospective analysis of data from 192 countries. Lancet. 2011; 377: 139-146.
6. McGrath-Morrow SA, Gorzkowski J, Groner JA, Rule AM, Wilson K, Tanski SE, et al. The Effects of Nicotine on Development. Pediatrics. 2020; 145: e20191346.
7. McEvoy CT, Spindel ER. Pulmonary Effects of Maternal Smoking on the Fetus and Child: Effects on Lung Development, Respiratory Morbidities, and Life Long Lung Health. Paediatric respiratory reviews. 2017; 21: 27-33.
8. Belgrave DCM, Granell R, Turner SW, Curtin JA, Buchan IE, Le Souef PN, et al. Lung function trajectories from pre-school age to adulthood and their associations with early life factors: a retrospective analysis of three population-based birth cohort studies. The Lancet. Respiratory medicine. 2018; 6: 526-534.
9. Komarow HD, Myles IA, Uzzaman A, Metcalfe DD. Impulse oscillometry in the evaluation of diseases of the airways in children. Annals of allergy, asthma and immunology. 2011; 106: 191-199.
10. Bickel S, Popler J, Lesnick B, Eid N. Impulse oscillometry: interpretation and practical applications. Chest. 2014; 146: 841-847.
11. Bednarek M, Grabicki M, Piorunek T, Batura-Gabryel H. Current place of impulse oscillometry in the assessment of pulmonary diseases. Respiratory medicine. 2020; 170: 105952.
12. Schultz ES, Hallberg J, Gustafsson PM, Bottai M, Bellander T, Bergstrom A, et al. Early life exposure to traffic-related air pollution and lung function in adolescence assessed with impulse oscillometry. J allergy and clinical immunology. 2016; 138: 930-932.
13. De S. Long-term ambient air pollution exposure and respiratory impedance in children: A cross-sectional study. Respiratory medicine. 2020; 170: 105795.
14. Linares-Segovia B, Bermudez-Perez R, Jimenez-Garza O, Moreira-Meyer A, Monroy-torres R. Correlation between spirometry and impulse ocillometry in children without asthma exposed to air pollutants. E-Poster Viewing Abstract. Chest. 2022; 161: A582.
15. Shao J, Zosky GR, Hall GL, Wheeler AJ, Dharmage S, Melody SD, et al. Early life exposure to coal mine fire smoke emissions and altered lung function in young children. Respirology. 2020; 25: 198-205.
16. Hemstock EJ, Foong RE, Hall GL, Wheeler AJ, Dharmage SC, Dalton M, et al. Lung function changes in children exposed to mine fire smoke in infancy. Respirology. 2024; 29: 295-303.
17. Robinson PD, Salimi F, Cowie CT, Clifford S, King GG, Thamrin C, et al. Ultrafine particle exposure and biomarkers of effect on small airways in children. Environmental research. 2022; 214: 113860.
18. Lee A, Kaali S, Jack D, Dwomoh R, Mujtaba M, Tawiah T, et al. Prenatal and Early Childhood Household Air Pollution Exposure Alters Lung Function at Age Four Years: Evidence from GRAPHS. Am J Respir Crit Care Med. 2020; 201: A4616.
19. Park D, Ha EK, Jung H, Kim JH, Shin J, Kim MA, et al. Associations of personal urinary volatile organic compounds and lung function in children. J asthma. 2024; 61: 801-807.
20. Wang Y, Zhu H, Kannan K. A Review of Biomonitoring of Phthalate Exposures. Toxics. 2019; 7: 21.
21. Kim MA, Yon DK, Jee HM, Kim JH, Park J, Lee SW, et al. Association of phthalates with nasal patency and small airway dysfunction in first-grade elementary school children. Allergy. 2020; 75: 2967-2969.
22. Chaya S, Vanker A, Brittain K, MacGinty R, Jacobs C, Hantos Z, et al. The impact of antenatal and postnatal indoor air pollution or tobacco smoke exposure on lung function at 3 years in an African birth cohort. Respirology. 2023; 28: 1154-1165.
23. Heinzerling AP, Guarnieri MJ, Mann JK, Diaz JV, Thompson LM, Diaz A, et al. Lung function in woodsmoke-exposed Guatemalan children following a chimney stove intervention. Thorax. 2016; 71: 421-428.
24. Dutta A, Alaka M, Ibigbami T, Adepoju D, Adekunle S, Olamijulo J, et al. Impact of prenatal and postnatal household air pollution exposure on lung function of 2-year old Nigerian children by oscillometry. The Science of the total environment. 2021; 755: 143419.
25. Agyapong PD, Jack D, Kaali S, Colicino E, Mujtaba MN, Chillrud SN, et al. Household Air Pollution and Child Lung Function: The Ghana Randomized Air Pollution and Health Study. American j respiratory and critical care medicine. 2024; 209: 716-726.
26. He L, Li Z, Teng Y, Cui X, Barkjohn KK, Norris C, et al. Associations of personal exposure to air pollutants with airway mechanics in children with asthma. Environment int. 2020; 138; 105647.
27. Cui X, Li Z, Teng Y, Barkjohn KK, Norris CL, Fang L, et al. Association between Bedroom Particulate Matter Filtration and Changes in Airway Pathophysiology in Children with Asthma. JAMA pediatrics. 2020; 174: 533-542.
28. Tikkakoski AP, Tikkakoski A, Sipila K, Kivisto JE, Huhtala H, Kahonen M, et al. Exercise-induced bronchoconstriction is associated with air humidity and particulate matter concentration in preschool children. Pediatric pulmonology. 2023; 58: 996-1003.
29. Kattan M, Bacharier LB, O'Connor GT, Cohen R, Sorkness RL, Morgan W, et al. Spirometry and Impulse Oscillometry in Preschool Children: Acceptability and Relationship to Maternal Smoking in Pregnancy. The j allergy and clinical immunology. In practice. 2018; 6: 1596-1603.
30. Thacher JD, Schultz ES, Hallberg J, Hellberg U, Kull I, Thunqvist P, et al. Tobacco smoke exposure in early life and adolescence in relation to lung function. The European respiratory j. 2018; 51: 1702111.
31. Kalliola S, Pelkonen AS, Malmberg LP, Sarna S, Hamalainen M, Mononen I, et al. Maternal smoking affects lung function and airway inflammation in young children with multiple-trigger wheeze. The J allergy and clinical immunology. 2013; 131: 730-735.
32. Gunlemez A, Er I, Baydemir C, Arisoy A. Effects of passive smoking on lung function tests in preschool children born late-preterm: a preventable health priority. J maternal-fetal and neonatal medicine. 2019; 32: 2412-2417.
33. Schivinski CIS, de Assumpcao MS, de Figueiredo FCXS, Wamosy RMG, Ferreira LG, Ribeiro JD. Impulse oscillometry, spirometry, and passive smoking in healthy children and adolescents. Revista portuguesa de pneumologia. 2017; 23: 311-316.