Asthma affects 8% to 13% of pregnancies and is associated with adverse maternal and fetal outcomes. The evidence consistently demonstrates that uncontrolled asthma in pregnancy is the primary driver of this pregnancy risk rather than the diagnosis alone. Compared with controlled disease, uncontrolled asthma has been associated with higher rates of preterm birth (adjusted odds ratio: 1.3 vs 1.6), hypertensive disorders of pregnancy (adjusted odds ratio: 1.2 vs 1.5), and impaired fetal growth or small-for-gestational-age neonates (adjusted odds ratio: 1.2 vs 1.4). This paper aimed to review the biologic pathways linking active asthma to adverse pregnancy outcomes, including airway inflammation, oxidative stress, placental dysfunction, and maternal hypoxemia. Building on modern understanding of asthma heterogeneity, this review integrates phenotype- and endotype-informed principles with pregnancy-specific immunologic shifts, highlighting how a Th2-predominant state may exacerbate disease activity and modify risk in susceptible patients. Multiple modifiable contributors, including viral infections, air pollution, indoor exposures, obesity, allergic rhinitis, gastroesophageal reflux disease, and obstructive sleep apnea, further influence disease activity and underscore the importance of active management. This study synthesizes updated, practical guidance aligned with international asthma guidelines emphasizing proactive monitoring, routine assessment of symptoms and objective measures, and continuation or escalation (“step-up”) of controller therapy to maintain control throughout pregnancy. In addition, this study reviewed contemporary strategies for asthma management, including anti-inflammatory reliever therapy and maintenance and reliever therapy, and highlighted nonpharmacologic interventions. Across this review, the emphasis lies on the importance of asthma control, with a goal of complete remission of symptoms, to optimize maternal-fetal outcomes. This study highlights areas of future research, including the implementation of precision-guided asthma care in pregnancy and the use of biologic therapies to prevent active disease.
Video
Introduction
Asthma is one of the most common chronic conditions in pregnancy, affecting between 8% and 12% of pregnant individuals. , Uncontrolled asthma is associated with higher risks of adverse pregnancy outcomes (APOs), including preeclampsia, fetal growth restriction (FGR), and preterm birth (PTB). ,,,, Despite these risks, both patients and clinicians often hesitate to initiate or continue therapy in pregnancy, and up to one-third of patients reduce inhaled corticosteroid (ICS) use, leading to loss of asthma control.
Asthma is classically defined as chronic airway inflammation (particularly of the small airways), airway hyperresponsiveness, and reversible obstruction. However, advances over the past 2 decades have reshaped the understanding of asthma as a heterogeneous disease with distinct inflammatory endotypes. This in turn has transformed therapy in the nonpregnant population: The Global Initiative for Asthma (GINA 2025) emphasizes anti-inflammatory reliever (AIR) strategies and precision-based management, yet obstetrical guidelines remain outdated. The 2008 American College of Obstetricians and Gynecologists (ACOG) guidelines predate major therapeutic advances, presenting an opportunity to update and reflect on current evidence.
As modern therapeutic approaches have improved asthma control, much of the pregnancy-associated morbidity associated with asthma in pregnancy can be prevented, underscoring the importance of updated and proactive management. Inflammation as a basis for asthma is well established. However, novel ways to both identify and manage asthma present a paradigm shift in pregnancy management. In this review, we synthesized the current evidence on the risks, mechanisms, and management of asthma in pregnancy and provided practical guidance for the obstetrical provider in line with modern asthma management.
Maternal-fetal outcomes
Asthma contributes to maternal morbidity during pregnancy, with 30% to 40% of pregnant patients diagnosed with asthma experiencing worsening control or exacerbation. , Asthma in pregnancy has been reported to be associated with the risk of multiple perinatal complications, including preeclampsia, gestational diabetes mellitus, preterm delivery, congenital malformations, spontaneous abortion, and low birthweight (LBW). The most consistent associations are with PTB, hypertensive disorders of pregnancy (HDPs)/preeclampsia, and impaired fetal growth. Other reported associations, including the risk of placenta previa, placental abruption, gestational diabetes mellitus, and miscarriage, are inconsistent across studies. There are differences in the presence and magnitude of these effects, which are related to differences in asthma severity, study design, and populations.
Uncontrolled asthma has been consistently associated with these adverse outcomes across multiple studies. Moreover, the increased risks seem to be driven by active disease and exacerbation rather than the diagnosis of asthma alone. This underscores the importance of rigorous management throughout pregnancy, with close monitoring and adjustment to maintain asthma control.
In addition, asthma exacerbates maternal health disparities. Asthma disproportionately affects populations already at a higher risk of APOs, including Black women and beneficiaries of public insurance, mediated by multiple factors, including environmental exposures, diet, genetics, social determinants of health, and greater prevalence of obesity. ,, In a large United States (US) cohort, poorly controlled asthma was more common among individuals with public insurance. These overlapping disparities highlight the need for more proactive and preventive approaches to optimize asthma and pregnancy health among vulnerable populations.
The following section summarizes the epidemiologic evidence for PTB, HDP, and FGR, followed by a review of the mechanistic pathways that may underlie these associations. Figure 1 presents a conceptual model illustrating the overlapping mechanisms linking asthma control with APOs. Figures 2 and 3 present a visual summary of the adjusted effect estimates across outcomes.
Pathways associated with maternal asthma, placental dysfunction, and adverse pregnancy outcomes
HIF-1α , hypoxia-inducible factor 1 alpha; IL-4 , interleukin 4; IL-5 , interleukin 5; IL-13 , interleukin 13.
Meislin. Asthma management in pregnancy. Am J Obstet Gynecol 2026 .
Adverse pregnancy outcomes with, versus without, asthma (pooled adjusted odds ratios)
Dots represent pooled adjusted odds ratios (aORs) from published meta-analyses comparing pregnancies with and without asthma. Vertical lines indicate 95% confidence intervals. The dashed line at aOR = 1.0 denotes no difference in risk. Values >1 indicate increased risk in pregnancies complicated by asthma.
aOR , adjusted odds ratio.
Meislin. Asthma management in pregnancy. Am J Obstet Gynecol 2026 .
Adverse pregnancy outcomes by asthma severity (pooled adjusted odds ratios)
Dots represent pooled adjusted odds ratios (aORs) from published meta-analyses for preterm birth, low birth weight, and small for gestational age, stratified by asthma-related exposures, including exacerbations, asthma severity, and oral corticosteroid use. Colors correspond to specific comparisons as indicated in the figure. Vertical lines indicate 95% confidence intervals. The horizontal reference at aOR = 1.0 denotes no difference in risk. Values >1 indicate increased risk of the outcome.
aOR , adjusted odds ratio.
Meislin. Asthma management in pregnancy. Am J Obstet Gynecol 2026 .
Preterm birth
Asthma in pregnancy is consistently associated with an increased risk of PTB, especially when asthma is uncontrolled. Meta-analyses and large cohort studies have reported a significant increase in overall PTB risk from 17% to 60% above baseline (adjusted odds ratio [aOR], 1.17–1.60; adjusted relative risk [aRR], 1.15–1.39). ,,,,, These risks seem to be increased with active disease and exacerbation, with several studies finding a relationship between active disease and PTB. ,, Of note, 1 cohort study from Longo et al found that, when asthma is first diagnosed in pregnancy, there is an increased risk of PTB compared with the risk of asthma diagnosed before pregnancy.
The exact percentage of PTB associated with asthma during pregnancy that is spontaneous vs medically indicated is not well established, and available evidence suggests that both reasons for PTB contribute. For example, Mendola et al found higher odds of medically indicated PTB among women with asthma, whereas Gu et al found that pregnancy-associated asthma was an independent risk factor for spontaneous PTB (aOR, 7.71 [95% confidence interval (CI), 1.30–46.10]).
Multiple biologic pathways plausibly link uncontrolled asthma with APOs, such as PTB. Hypoxemia during exacerbations is more likely in pregnancy due to increased oxygen demand, airway edema, and reduced functional residual capacity. Hypoxia has been shown to activate fetal stress pathways involving hypoxia-inducible factors (HIFs), oxidative stress, and catecholamine release. These pathways potentially trigger preterm labor via uterine contractility and cervical ripening. Systemic and localized inflammations involving cytokines, such as interleukin 5 (IL-5) and interleukin 13 (IL-13), amplify circulating proinflammatory mediators, including tumor necrosis factor alpha and interleukin 6 (IL-6). , These mediators have been shown to promote myometrial activation and cervical remodeling. , Placental dysfunction due to asthma-related inflammation and oxidative stress may further impair spiral artery remodeling and angiogenesis, leading to fetal stress and preterm labor initiation. ,,, Previous studies reported that systemic allergic reactions and type 2 inflammation may contribute to uterine contractility, cervical remodeling, and preterm labor in a subset of pregnant patients with asthma through mast cell activation and release of mediators, such as histamine, leukotrienes, and prostaglandins. Available human data are limited primarily to case reports and experimental studies and provide biologic plausibility for an allergy-mediated PTB pathway. ,,, As we have reviewed above, the strongest predictor of PTB is not a diagnosis of asthma alone but the occurrence of exacerbations, especially those requiring systemic corticosteroids. This underscores the importance of asthma control during pregnancy to mitigate the risk of APOs.
Preeclampsia
Maternal asthma is consistently associated with an increased risk of preeclampsia. A large meta-analysis by Murphy et al reports a relative risk (RR) of 1.54 (95% CI, 1.32–1.81). Large US-based cohort studies have shown similar findings: Mendola et al reported an aOR of 1.14 (95% CI, 1.06–1.22), and Meislin et al reported an aOR of 1.21 (95% CI, 1.02–1.45). Importantly, similar to PTB, uncontrolled asthma is associated with a increase risk of preeclampsia, with several studies reporting more than 3 times increase (aORs: 3.55 [95% CI, 1.15–13.00] vs 3.58 [95% CI, 1.30–9.87]). , Conversely, multiple analyses support that the use of ICSs during pregnancy does not increase the risk of preeclampsia.
Possible mechanisms for the development of preeclampsia are multifactorial and include maternal hypoxia, oxidative stress, and systemic inflammation. Hypoxia is a shared feature of both uncontrolled asthma and preeclampsia. In preeclampsia, hypoxemic episodes may disrupt the processes of trophoblastic invasion and spiral artery remodeling, impairing angiogenic signaling. Hypoxia up-regulates the proinflammatory HIF mediators. HIFs in turn activate proinflammatory cytokines and promote differentiation of aberrant T-cell formation, driving inflammation in some subtypes of asthma. Moreover, human placental studies have shown elevated HIF-1α expression in placentas affected by preeclampsia, offering a plausible link between asthma-associated hypoxemia, immune dysregulation, and systemic inflammation relevant to placental dysfunction. These findings support that asthma-associated inflammation and hypoxia intersect with the same angiogenic and immune pathways implicated in preeclampsia pathogenesis.
Impaired fetal growth (fetal growth restriction and low birthweight)
Furthermore, uncontrolled asthma is associated with impaired fetal growth. A meta-analysis from 2013 of 138 publications found that both asthma exacerbations and the use of oral corticosteroids were associated with an increased risk of LBW or small-for-gestational-age (SGA) infants (pooled RR, 1.18–1.22). In contrast, the use of ICSs has not been shown to increase the risk of LBW/SGA offspring.
In addition, evidence suggests that the risk of growth restriction in pregnancies complicated by maternal asthma may differ according to fetal sex. Female fetuses are more likely to experience reduced growth even without asthma exacerbation, whereas male fetuses maintain normal growth until exacerbation occurs. Placental studies suggest a biologic basis: female placentas demonstrate increased inflammatory cytokine expression and impaired steroid metabolism, which are associated with greater vulnerability to FGR.
Additional proposed mechanisms include placental hypoperfusion resulting from vascular dysfunction, oxidative stress, and reduced angiogenic signaling—all pathways that compromise nutrient and oxygen delivery to the fetal-placental unit. ,,
Overall, these findings support that asthma control and not asthma diagnosis drives APOs. Physiological changes in pregnancy may further amplify these risks, as discussed in the next section.
Case 1
A 27-year-old gravida 1 para 0 at 22 weeks of gestation, with the last asthma exacerbation 2 months ago, presented to the hospital with increasing episodes of wheezing. The patient discontinued her combined ICS-formoterol inhaler in the first trimester of pregnancy when she discovered that she was pregnant and had been asymptomatic until recently. The patient is now using an albuterol inhaler about 4 times a week and has reported waking up at night with symptoms. The patient’s Asthma Control Test (ACT) score was 19, which is consistent with asthma that is not well controlled.
Findings
The patient had mild asthma with loss of control and self-discontinuation using a short-acting beta-agonist (SABA) alone.
Management
The management strategies are as follows:
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Counsel on pregnancy risks of uncontrolled asthma and medication safety.
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Start daily low-dose ICS-formoterol per GINA guidelines.
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Assess for barriers to obtaining medication.
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Assess environmental triggers and mitigation strategies.
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Review inhaler adherence and technique.
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Reassess symptoms at the next prenatal visit.
Key takeaway
A SABA alone is no longer recommended. AIR therapy decreases airway inflammation and exacerbations even in patients with mild asthma.
Immunologic adaptations and pathophysiology of asthma during pregnancy
Pregnancy is characterized by immune changes throughout pregnancy. Early pregnancy requires a proinflammatory state to support implantation and placental development. In the second trimester of pregnancy, there is a shift toward an anti-inflammatory profile that promotes maternal tolerance of the fetus, namely Th1. In addition, the Th17 cell response is decreased, whereas Th2 and Treg cells are activated. In the third trimester of pregnancy, the balance shifts back to a proinflammatory environment necessary for labor to begin. Overall, these changes favor Th2 cell predominance, with relative suppression of the Th1/Th17 pathways.
This Th2 predominance in pregnancy highlights how underlying asthma can be compounded by this physiological adaptation. Asthma is a heterogeneous disease composed of distinct endotypes—disease subtypes defined by pathogenic cellular and molecular pathways. These include Th2 high (eosinophilic, interleukin 4 [IL-4], interleukin 5 [IL-5], and interleukin 13 [IL-13] driven) and Th2 low (neutrophilic and obesity-associated types). Biomarkers from body fluids and/or affected tissues, including structural cells in the airway, can identify endotypes. Asthma phenotypes or clinical characteristics of the disease are based on asthma severity, respiratory symptoms, triggers, baseline lung function, response to therapies, and health care use. Th2-high asthma demonstrates increased responsiveness to corticosteroid treatment, whereas Th2-low asthma demonstrates neutrophilic airway inflammation and relatively less responsiveness. The identification of disease endotypes has informed the development and management of targeted therapy in asthma management. Universal asthma guidelines in the nonpregnant population incorporate biomarkers of asthma types, including eosinophils, fractional excretion of nitric oxide (FE NO ), and measurement of immunoglobulin E (IgE) into asthma management (GINA 2025). This illustrates the importance of phenotyping/endotyping, which is central to the management outside of pregnancy but not yet incorporated into obstetrical guidelines. A summary of key asthma endotypes, representative phenotypes, and treatment responsiveness is presented in Table 1 . These physiological, immunologic, and behavioral factors together explain the heterogeneity of asthma control in pregnancy and reinforce the need for monitoring discussed in the next section.
Table 1
Common phenotypes and endotypes of asthma
| Endotype | Phenotypes | Biomarkers | Treatment responsiveness |
|---|---|---|---|
| Type 2 high (Th2 high) | Allergic asthma; early-onset asthma | High eosinophils; high FE NO ; high IgE | Typically strong response to ICSs |
| Type 2 low (nontype 2) | Nonallergic asthma; neutrophilic asthma | Sputum neutrophils | Reduced response to ICSs |
| Obesity-related asthma; late-onset asthma | Systemic inflammation (elevated interleukin 6, leptin/adiponectin, and oxidative stress markers) | Variable; often reduced response to ICS | |
| Smoking-associated asthma | Sputum neutrophils | Reduced response to ICSs |
FE NO , fractional excretion of nitric oxide; ICS , inhaled corticosteroid; IgE , immunoglobulin E.
Meislin. Asthma management in pregnancy. Am J Obstet Gynecol 2026 .
Factors associated with loss of control
Asthma control during pregnancy may be unpredictable, with 20% to 30% of pregnant patients with asthma experiencing exacerbations. , Loss of asthma control during pregnancy may be attributed to many factors, including hormonal influences, environmental triggers, and physiological immunologic adaptations of pregnancy. , Furthermore, physiological changes, including higher tidal volume, minute ventilation, and an enlarged uterus resulting in decreased functional residual capacity, may increase dyspnea sensations, although not affecting asthma health per se. In addition, apart from these biologic mechanisms, provider and patient reluctance to use medications for asthma contributes to worse asthma control despite societal guidelines universally favoring the continuation of medications during pregnancy to maintain control.
Obesity
Obesity is a significant risk factor for asthma, complicating the management of pregnant patients with asthma and increasing the risk of asthma exacerbation during pregnancy. It is associated with heightened oxidative and nitrosative stress and systemic inflammation, which can result in more severe asthma symptoms and loss of asthma control. Furthermore, obesity can cause mechanical compression of the lungs, small airway disease, and reduced lung function, leading to worsening dyspnea during pregnancy by reducing lung volumes. In pregnant patients with asthma, obesity increases the risk of gestational diabetes mellitus, preeclampsia, and gestational hypertension.
Therefore, weight management and targeted gestational weight gain are important interventions. Stevens et al showed that higher adiposity and gestational weight gain are associated with increased asthma symptoms in pregnancy. Ali et al found that excessive gestational weight gain in the first trimester of pregnancy was a risk factor for asthma exacerbation, with a dose-dependent relationship between weight gain and exacerbation risk. In addition, the effectiveness of asthma medications, particularly corticosteroids, may be diminished in pregnant patients with asthma and comorbid obesity, compared with their lean counterparts. Patients with asthma with comorbid obesity report higher symptom burden, more frequent and severe exacerbations, reduced response to asthma medications, and a lower quality of life. ,,
Thus, obesity is a key, modifiable determinant of both maternal asthma health and pregnancy outcomes, warranting dedicated interventions. This is especially relevant for obesity-associated, Th2-low asthma in which pharmacologic control may be less effective.
Air pollution and environmental exposures
Both maternal tobacco smoking and secondhand smoke exposure are major modifiable risk factors for worsening asthma control during pregnancy, including more frequent and severe asthma exacerbations. , Tobacco exposure has transgenerational effects, such as increasing the risk of childhood wheezing and asthma in offspring. , Nicotine interferes with the fetal development of airways and alveoli and may contribute to achieving lower peak lung function later in life. , Consequently, pregnant individuals, particularly those with asthma, should be strongly encouraged to stop smoking and avoid secondhand smoke exposure to improve maternal-fetal outcomes. , In addition, the safety of vaping or electronic nicotine delivery systems in pregnancy has not been established and should not be considered as a safe alternative.
Ambient air pollution further contributes to asthma morbidity. Physiological pregnancy-associated alterations in cardiopulmonary physiology may increase maternal susceptibility to pollutants, such as PM 2.5 (fine particulate air pollution of <2.5 μm) and nitrate. , Ambient air pollution has been associated with APOs, including a greater risk of HDPs, LBW, PTB, and gestational diabetes mellitus and a higher infant mortality. ,,,, Prenatal PM 2.5 and nitrate exposures may increase the risk of childhood asthma and compromised lung function. ,,,, Indoor air pollution, including those generated from combustion activities (cooking fumes, cigarette smoke, etc.) and cleaning products, has been shown to worsen asthma control in other populations. In pregnancy, indoor PM 2.5 has been associated with PTB and LBW, possibly mediated by PM 2.5 -associated overproduction of reactive oxygen species, altered vasculature, and greater inflammation. , Moreover, household air pollution from cooking with solid fuels may increase the risk of APOs. A recent pilot study demonstrated that high indoor levels of PM 2.5 measured longitudinally across pregnancy in a US population were associated with increased maternal respiratory symptoms, worsening asthma control, and decreased maternal lung function, suggesting a potential direct effect of indoor air pollution on maternal asthma morbidity. Given that indoor air quality is modifiable, these data support the counseling of pregnant patients to avoid activities that contribute to indoor air pollution and highlight the importance of designing future public health interventions to mitigate indoor exposures.
Coexisting conditions affecting asthma control
Comorbid conditions, such as allergic disease, gastroesophageal reflux disease (GERD), obstructive sleep apnea (OSA), and infection, can adversely influence asthma control.
Allergic disease and atopy
In Th-2-high asthma phenotypes, in addition to upper airway disease, environmental allergens, food allergy, and medication allergy may contribute to poor asthma symptom control. , Similar to asthma, allergic rhinitis is associated with Th-2-predominant inflammation and increased airway reactivity. In the general population, approximately 30% of patients with allergic rhinitis have asthma. ,,, Allergen exposure may more readily activate inflammatory cells, particularly mast cells and eosinophils, amplifying systemic inflammatory signaling. Obtaining a comprehensive allergy history, including environmental triggers, food allergies, previous anaphylaxis, and medication sensitivity, is important for identifying possible modifiable factors associated with poor asthma control. Therefore, the management of asthma should include the recognition and management of allergic rhinitis, including the avoidance of triggers and the use of intranasal corticosteroids and oral antihistamines.
GERD is commonly seen in pregnant patients secondary to physiological changes, including progesterone-mediated changes in the smooth muscle of the gastrointestinal tract, and mechanical factors whereby the enlarging uterus causes abdominal pressure. In the nonpregnant population, GERD is an independent risk factor for asthma exacerbation, although the exact causal mechanism is uncertain but may include airway irritation from microaspiration and vagus nerve–mediated bronchoconstriction. , In patients with symptomatic GERD, including frequent reflux symptoms of heartburn and cough, the management of GERD may help diminish reflux-related asthma triggers. There is no randomized controlled trial (RCT) investigating GERD management for asthma control in pregnancy.
Sleep-disordered breathing, such as OSA, is associated with airway inflammation and worse asthma control. OSA and asthma are closely related: Individuals with asthma, especially those with suboptimal control, have a higher risk of developing OSA, which can worsen asthma control. , OSA is associated with APOs, including preeclampsia and gestational diabetes mellitus. Physiological changes associated with pregnancy, such as weight gain, airway edema, and reduced functional residual capacity, can exacerbate OSA. Pregnancy-related changes may add an additional layer to the bidirectional relationship between OSA and asthma, as pregnancy is a risk factor for both OSA and asthma exacerbation. A recent 2025 study assessing this possible synergy between OSA and asthma in pregnancy found higher central airways resistance in pregnant patients with both OSA and asthma than in those with either condition alone. This points to the role of inflammation and hypoxemia contributing to worse asthma control and increasing the risk of exacerbations.
Infection
Pregnancy is a time of heightened vulnerability to viral infections, such as influenza and rhinovirus, which increase the risk of asthma flare. , The same immunologic mechanisms that enable tolerance to the developing fetus may contribute to a heightened inflammatory response to upper and lower respiratory tract infections, increasing vulnerability to asthma exacerbation secondary to infectious triggers and explaining why prevention of infection is an important component of asthma care in pregnancy. , Specifically, as part of a mechanism to promote fetal tolerance in pregnancy, there is a decrease in the innate antiviral interferon response, including interferon alpha and interferon gamma, making patients more susceptible to viruses. Studies have shown that this is higher in patients with asthma in pregnancy. , The immune profile of pregnancy further amplifies inflammation once infection occurs.
Case 2
A 30-year-old para 0 at 26 weeks of gestation with asthma, well-maintained on ICS-formoterol twice daily in pregnancy, presented with increased wheezing, which responds to additional doses of ICS-formoterol taken per maintenance and reliever therapy (MART). The patient reported that her husband had been deep cleaning their apartment nightly to avoid dust and allergen exposure. The patient’s husband used bleach and aerosol sprays in a poorly ventilated, small space.
Findings
Common cleaning activities can create indoor pollutants that can lead to the acute worsening of asthma control.
Management
The management strategies are as follows:
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Improve indoor environment, minimize exposure, and increase ventilation with open windows or a high-efficiency particulate air (HEPA) purifier during cleaning.
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Continue the use of ICS-formoterol as prescribed and reassess control after environmental mitigation.
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Review inhaler adherence and technique.
Key takeaway
Environmental triggers can lead to loss of asthma control even when patients are on the appropriate therapy, and identifying and mitigating exposure are part of management.
Clinical management of asthma in pregnancy: monitoring and treatment approaches
Because active asthma is associated with APOs, the overarching objective of asthma management during pregnancy is to achieve optimal control of asthma symptoms for both maternal and fetal well-being. This involves the frequent monitoring of both symptoms and objective measures and a stepwise approach to pharmacologic treatment. Figure 4 demonstrates an overview of the management of asthma.
A clinical framework for asthma management across pregnancy
ACQ , Asthma Control Questionnaire; ACT , Asthma Control Test; GERD , gastroesophageal reflux disease; GINA , Global Initiative for Asthma; OSA , obstructive sleep apnea.
Meislin. Asthma management in pregnancy. Am J Obstet Gynecol 2026 .
Asthma management in pregnancy should align with established national and international guidelines. Although ACOG recommendations (2008) predate major shifts in asthma management, the Global Initiative for Asthma (GINA 2025) and the National Asthma Education and Prevention Program (NAEPP 2020) both emphasize that asthma treatment should be guided by the level of control rather than static severity of disease classification alone ( Figure 5 ). ,, Both GINA and NAEPP recommend a step-up/step-down approach, adjusting therapy to the degree of control. The goals of management include achieving symptom control and disease remission and preventing exacerbations in a dynamic model. Control is classified by GINA as well controlled, partly controlled, or uncontrolled based on symptom frequency, nighttime awakening, activity limitation, and need for a reliever inhaler in the past 4 weeks. In contrast, asthma severity refers to the level of treatment required to achieve and maintain control and is classified as mild, moderate, or severe.
Initial asthma treatment in adults and adolescents (reprinted guidelines)
Reprinted with permission from the Global Initiative for Asthma.
ICS , inhaled corticosteroid; LABA , long-acting beta-agonist; MART , maintenance and reliever therapy; OCS , oral corticosteroids; SABA , short-acting beta-agonist.
Meislin. Asthma management in pregnancy. Am J Obstet Gynecol 2026 .
In the past decade, there have been substantial changes and updates to asthma management involving a shift away from using SABA-only reliever therapy to using an ICS and formoterol (long-acting beta-agonist [ICS-formoterol]) combination therapy for both controller and reliever due to its anti-inflammatory effects and exacerbation reduction not found with SABA. The following sections summarize asthma monitoring and management relevant to pregnancy. Understanding this framework is crucial for the obstetrical clinician to know when to continue or escalate therapy with the goal of optimizing asthma control. The following subsections outline monitoring, pharmacologic therapy, and emerging biologic therapies that are increasingly used in pregnancy. Table 2 presents the medication strategies for asthma management, which are aligned with GINA recommendations, pregnancy-specific considerations, and a review of medication safety.
Table 2
Stepwise pharmacologic management of asthma in pregnancy
| GINA step | Medication strategy | Example medication and dosing | Efficacy | Safety |
|---|---|---|---|---|
| 1 | Minimal symptom burden (1–2 d/wk or less, preserved lung function). | |||
| 1 (track 1) | ICS-formoterol as needed (AIR) | Budesonide-formoterol 160/4.5 μg 1–2 inhalations every 4 h as needed. Maximum dose is 12 inhalations/d. ,,, | ICS reduces risk of exacerbations (evidence A) (GINA); ICS use in pregnancy lowers risk of preterm delivery, LBW, perinatal mortality, ,,,, and reduces asthma risk in offspring (GINA). As-needed ICS-formoterol reduces severe exacerbations by 65% vs SABA alone and 37% vs daily ICS + SABA (GINA). | ICS and beta-agonists are not associated with increased risk of congenital malformations, preterm delivery, or LBW. |
| 1 (track 2) | ICS + SABA as needed | Low-dose budesonide 200–400 μg inhaled per day, taken whenever SABA (albuterol 90 μg/actuation 1–2 puffs inhaled every 4–6 h as needed) is taken. Alternatively, budesonide 80 μg + albuterol 90 μg combination inhaler 2 puffs inhaled every 4 h as needed (max 12 inhalations/d). | ICS + SABA as needed significantly reduces exacerbations compared with SABA alone (GINA). , | |
| 2 | Symptoms <3 to 5 d per week, with normal or mildly reduced lung function. | |||
| 2 (track 1) | ICS-formoterol as needed (AIR) | Budesonide-formoterol 160/4.5 μg 1–2 inhalations every 4 h as needed. Maximum dose is 12 inhalations/d. | ||
| 2 (track 2) | Daily ICS + SABA as needed | Daily budesonide (180 μg/actuation) 2 puffs inhaled twice a day + SABA (albuterol 90 μg/actuation 1–2 puffs inhaled every 4–6 h as needed). | Reduces risk of exacerbations, hospitalizations, and mortality and improves symptoms (evidence A) (GINA). | |
| 3 | Moderate symptom burden (symptoms most days, waking due to asthma once a week or more, or impaired lung function). | |||
| 3 (track 1) | Low dose ICS-formoterol MART | Budesonide-formoterol 160/4.5 μg 1 inhalation twice a day + as needed. Maximum dose is 12 inhalations/d. | MART reduces severe exacerbations and offers similar asthma control vs high-dose ICS + SABA as needed and vs ICS-LABA + SABA as needed (evidence A) (GINA). ,, | |
| 3 (track 2) | Daily ICS-LABA + SABA as needed | Daily budesonide-formoterol 80/4.5 or 160/4.5 μg 2 puffs inhaled twice a day + SABA (albuterol 90 μg/actuation 1–2 puffs inhaled every 4–6 h) as needed. | GINA track 1 (MART) is preferred because it reduces exacerbations compared with the same or higher dose of ICS-LABA maintenance plus as-needed SABA reliever (GINA). | |
| 4 | Daily asthma symptoms, awakening at night once a week or more, with impaired lung function. | |||
| 4 (track 1) | ICS-formoterol MART | Budesonide-formoterol 160/4.5 μg 2 inhalations twice a day + as needed. Maximum dose is 12 inhalations/d. | MART reduces severe exacerbations and offers similar asthma control vs high-dose ICS + SABA as needed and vs ICS-LABA + SABA as needed (evidence A) (GINA). , | |
| 4 (track 2) | Daily ICS-LABA + SABA as needed | Daily budesonide-formoterol 160/4.5 μg 2 puffs inhaled twice a day + SABA (albuterol 90 μg/actuation 1–2 puffs inhaled every 4–6 h) as needed. | GINA track 1 (MART) is preferred because it reduces exacerbations compared with the same or higher dose of ICS-LABA maintenance plus as-needed SABA reliever (GINA). | |
| 5 | Uncontrolled asthma despite high-dose maintenance, these medications should be added on (continue above therapy). | |||
| 5 | LAMA | Tiotropium (soft mist inhaler) 1.25 μg/actuation 2 inhalations once daily. | Modestly improves lung function (evidence A) (GINA), but without significant improvement in symptoms. In meta-analyses, reduces severe exacerbations by ∼17% (evidence A) (GINA). Case series in pregnancy: asthma control often remains poor, but no major APO or congenital malformation observed. , | No data in pregnancy for tiotropium; case series and observational data of other LAMAs show no major APO or congenital malformation. |
| 5 | Azithromycin | Add-on azithromycin 250–500 mg oral 3 times a week. | ECG should be obtained before initiation to assess for prolonged QTc. Of note, 2 clinical trials showed reduced exacerbations with add-on azithromycin. , | Gastrointestinal upset, particularly diarrhea, is relatively common. Azithromycin is not associated with specific pregnancy-related risks. |
| 5 | Leukotriene receptor antagonist | Montelukast 10 mg oral daily. | Offers modest improvements in symptoms and lung function but limited effect on exacerbation rates compared with ICS-based regimens. ICS remains the preferred controller because of superior efficacy across all major outcomes, including exacerbation reduction. | No increased risk of major birth defects. Should counsel patients on small but significant risk of potential neuropsychiatric adverse events (GINA). , |
| Biologics | ||||
| 5 | Omalizumab (anti-IgE) | 150–375 mg SC every 2–4 wk (dosing dependent on serum IgE and body weight). | Meta-analyses of RCTs found that add-on omalizumab leads to a 44% reduction in severe exacerbations and improved quality of life in patients with elevated serum IgE. Also small improvements in symptom control and lung function. | No increase in congenital anomalies, preterm birth, or stillbirth compared with background rates (EXPECT registry). , |
| 5 | Dupilumab (anti-IL-4, anti-IL-13) | 400–600 mg load, followed by 200–300 mg SC every 2 wk. | Add-on for Th-2-high asthma associated with significant reduction in severe exacerbation rates, better lung function, and improved asthma control. Indicated for patients with serum eosinophilia on oral corticosteroids or nasal polyposis. ,, | Safety data for pregnancy are limited to case reports and case series. No risk of congenital anomalies, miscarriage, or adverse maternal or fetal outcomes. Animal studies in pregnant monkeys exposed to doses up to 10 times the maximum human dose showed no adverse effects on embryo-fetal toxicity, malformations, or postnatal development through 6 mo of age. , |
| 5 | Reslizumab, mepolizumab, benralizumab (anti–IL-5) | 3 mg/kg, 100 mg, 30 mg every 4, 4, 4–8 wk, respectively. | Add-on for severe eosinophilic asthma with meta-analyses showing reduced severe asthma exacerbations by 47%–54% compared with placebo (GINA). | No evidence of teratogenicity or major fetal harm in animal studies for reslizumab, mepolizumab, or benralizumab. Human data are limited but reassuring; no clear increase in major congenital anomalies or miscarriage. ,, |
| 5 | Tezepelumab (antithymic stromal lymphopoietin) | 210 mg SC every 4 wk. | Add-on for severe asthma in RCTs resulted in significantly lower exacerbation rates (independent of serum eosinophil count), better lung function, asthma control, and quality of life compared with placebo. | No safety data in pregnant women. Animal studies showed no evidence of fetal harm, APOs, embryo-fetal development, or neonatal growth and development up to 6.5 mo of age. |
AIR , anti-inflammatory reliever; APO , adverse pregnancy outcome; ECG , electrocardiogram; EXPECT , The Observational Study of the Use and Safety of Xolair (omalizumab) during Pregnancy; GINA , Global Initiative for Asthma; ICS , inhaled corticosteroid; IgE , immunoglobulin E; IL-4 , interleukin 4; IL-5 , interleukin 5; IL-13 , interleukin 13; LABA , long-acting beta-agonist; LAMA , long-acting muscarinic antagonist; LBW , low birthweight; MART , maintenance and reliever therapy; OCS , oral corticosteroids; RCT , randomized controlled trial; SABA , short-acting beta-agonist; SC , subcutaneous.
Meislin. Asthma management in pregnancy. Am J Obstet Gynecol 2026 .
Monitoring
Asthma control should be consistently assessed, beginning at the initial prenatal visit and repeatedly throughout pregnancy in 4- to 6-week intervals. This is consistent with the GINA and NAEPP guidelines. Patients should be asked about their respiratory symptoms, including cough, wheezing, chest tightness, and shortness of breath that disrupt activities or cause nighttime awakenings, use of and adherence to controller medication, frequency of needing rescue inhaler therapy, and frequency of exacerbations. Commonly, inhaler technique and adherence limit drug delivery to the airways.
Questionnaires for patients, such as the ACT or Asthma Control Questionnaire (ACQ), are validated tools used to objectively assess symptoms and medication use. ,,, The ACT has been validated in 1 study with a modified version for pregnancy, The Pregnancy Asthma Control Test. The ACQ incorporates objective lung function with forced expiratory volume in 1 s (FEV 1 ) and has been used in clinical studies on asthma in pregnancy. ,
Objective measures of asthma control include spirometry, peak expiratory flow (PEF) measurement, FE NO , and blood serum markers. Spirometry remains the gold standard for assessing airway obstruction, defined as the ratio of the FEV 1 to forced vital capacity below the lower limit of normal. Performed by a pulmonologist, and increasingly in real-time office settings, spirometry is well studied, and minimally affected by pregnancy, as airway mechanics do not substantially change. The interpretation of spirometry and flow-volume loops should follow the established guidance from the American Thoracic Society and European Respiratory Society. Evaluating spirometry during pregnancy may provide objective insight into asthma severity, control, and treatment response throughout pregnancy. To overcome barriers where spirometry may not be readily accessible, low-touch efforts to conduct spirometry remotely have been investigated and found to be feasible in a recent pilot study of pregnant patients with asthma. Devices that measure PEF are an alternative, offering an inexpensive, portable option. Pregnant patients with asthma may monitor their PEF daily and can demonstrate it at a prenatal visit. A significant decline (>20%) from personal best PEF suggests worsening airflow obstruction and the need for reassessment and medication adjustment.
The FE NO , a biomarker of type 2 airway inflammation, has been proposed as a noninvasive method to guide asthma care in pregnancy. , Patients exhale into a handheld device, which captures the amount of nitric oxide, a signaling molecule indicating higher levels of airways inflammation in certain asthma phenotypes. FE NO is measured in parts per billion, with elevated levels of >40 to 50 indicating the presence of inflammation. At the time of asthma diagnosis, FE NO is useful for classifying asthma endotype, and FE NO levels are not altered by pregnancy. Elevated FE NO levels are associated with an increased risk of future exacerbation. , In addition, blood eosinophil counts and total serum IgE levels may be obtained to support characterizing asthma by endotype, with higher levels associated with an allergic phenotype.
RCTs have demonstrated the effectiveness of a symptom control algorithm using FE NO in reducing asthma exacerbations during pregnancy while also minimizing medication exposure. In the Managing Asthma in Pregnancy (MAP) study, FE NO was used to guide medication management in pregnant women with asthma, resulting in a 50% reduction in exacerbation rates and improved quality of life, even among patients with noneosinophilic asthma, compared with standard of care. Thus, FE NO may offer a useful and noninvasive way to monitor prenatal asthma control. However, although FE NO may improve asthma control in the mother, The Breathing for Life Trial, a multicenter, parallel-group, RCT, found that it did not improve perinatal outcomes compared with usual care. The primary composite perinatal outcome, which included PTB, SGA, perinatal mortality, or neonatal hospitalization, showed no significant difference between the FE NO -guided group and the control group (odds ratio [OR], 1.21 [95% CI, 0.94–1.56]; P =.15). A secondary analysis of the MAP trial further demonstrated that FE NO -guided management can help avoid overtreatment while maintaining asthma control. These findings support the use of FE NO as a biomarker for individualized therapy in pregnancy.
Given the increased risk of impaired fetal growth associated with active asthma, fetal growth assessment may be considered for patients with moderate to severe disease. Although evidence is limited, we have demonstrated the biologically plausible rationale for placental dysfunction with maternal inflammation.
A multidisciplinary approach
Patients with moderate to severe asthma, frequent exacerbations, and candidates for biologics would benefit from multidisciplinary care, including expertise from a pulmonologist. In general, multidisciplinary care teams are frequently used to care for pregnant patients with complex medical comorbidities. For example, the ACOG guidelines recommend a multidisciplinary “Pregnancy Heart Team” to manage pregnant patients with moderate- and high-risk cardiovascular disease. Multidisciplinary care models have been shown to improve outcomes in pregnant patients with asthma. The Multidisciplinary Approach to Management of Maternal Asthma trial demonstrated that coordinated care among a team of obstetricians, pharmacists, nurses, and respiratory specialists significantly improved asthma control with fewer exacerbations compared with usual care. In a second, prospective cohort study of high-risk, urban-dwelling pregnant patients with asthma, patients who were seen in a pulmonary clinic integrated into usual prenatal care had increasing rates of step-up therapy and improved asthma control, supporting improvements in the care of pregnant individuals with asthma through a collaborative care team.
In addition, telehealth is a care model well suited for asthma during pregnancy. The management of asthma with supportive telehealth of respiratory function in pregnancy (MASTERY) trial found that a mobile phone application for self-monitoring of asthma symptoms and medication usage during pregnancy resulted in improved asthma control compared with usual care. Future studies incorporating interdisciplinary collaborations, telehealth, remote spirometry, and other novel technologies into the care for the pregnant individual with asthma are warranted.
Pharmacologic treatment and biologic therapy
As reviewed above in the Monitoring section, frequent reassessment of symptoms should guide pharmacologic management with a goal toward control and absence of exacerbation, aligning with GINA 2025 and NAEPP 2020 guidelines. The GINA 2025 guidelines highlight pregnancy as a condition where maintaining control is paramount, given the morbidity associated with uncontrolled disease. We agree with their approach. For individuals with minimal symptom burden, such as symptoms <3 to 5 days per week and preserved lung function, GINA recommends the AIR approach, with as-needed-only low-dose ICS-formoterol. The AIR approach has been demonstrated to be superior to traditional SABA reliever therapy in reducing exacerbations based on evidence from multiple randomized clinical trials. A network meta-analysis of 27 RCTs demonstrated that the use of ICS-SABA and ICS-formoterol is associated with a 4.7% reduction and 10.3% reduction, respectively, in the risk of severe exacerbation, compared with SABA alone. Alternatively, a low-dose ICS with as-needed SABA or a combined ICS-SABA may be used. This approach is safe in pregnancy and has been endorsed by GINA for reducing exacerbations.
Asthma treatment in pregnancy should follow the same stepwise approach as in the nonpregnant population, emphasizing control of disease, with attention to maternal and fetal safety. Outside of pregnancy, there is a move to treatment beyond symptoms to “complete remission,” defined as the absence of symptoms with stable lung function. , Including targeted biologic therapies and AIR has made remission achievable for some patients. Although remission has not been specifically studied in pregnancy, the goal of expecting perfection, with as few symptoms and exacerbations as possible, should also guide management during pregnancy. As reviewed, early and sustained control of airway inflammation can prevent exacerbation and reduce adverse maternal and fetal outcomes. Further research is needed to determine how this goal of remission can be most effectively applied to a pregnant population.
Case 3
A 32-year-old para 1 at 14 weeks of gestation, maintained on low-dose ICS-formoterol reliever as needed, reported daily wheezing and chest tightness. The patient was using this inhaler daily. The patient’s ACT score was 14, which was consistent with poor control. The patient had no infectious symptoms and no new environmental exposures. The patient’s peak flow meter was 25% below her personal best.
Findings
The patient had persistent loss of control of asthma, and step-up therapy was indicated to achieve control.
Management
The management strategies are as follows:
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Step up to MART and start low-dose ICS-formoterol twice a day.
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Continue the same inhaler for as-needed relief.
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Review inhaler adherence and technique.
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Reassess symptoms, ACT score, and peak flow in 4 weeks.
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Consider referral to pulmonology for classification of asthma endotype and lung function testing.
Key takeaway
Step-up therapy to MART is indicated for persistent asthma symptoms on AIR alone. For patients with a greater symptom burden, specifically symptoms most of the day or waking at night once a week or more, or with objectively impaired lung function, a maintenance inhaler is required. The MART approach uses an ICS-formoterol as both the preferred maintenance and reliever therapy of choice for patients with persistent asthma symptoms. Compared with previous strategies using SABA as the reliever, the MART approach has been shown to be more effective at reducing the risk of severe exacerbations, with similar symptom control and lung function, in nonpregnant populations. The use of ICS-formoterol is further supported by multiple RCTs and meta-analyses that demonstrate reduced asthma exacerbations and improved asthma control and lung function. , This is supported by GINA 2025 and NAEPP 2020 guidelines. This is in contrast to older ACOG (2008) guidelines that still advise former recommendations of using a SABA for “intermittent” asthma. For those with uncontrolled asthma despite high-dose maintenance ICS-formoterol and a reliever, next steps include consideration of adding on a long-acting muscarinic antagonist (LAMA), a leukotriene receptor antagonist, azithromycin, a low-dose oral corticosteroid, and/or a biologic agent.
Admittedly, the AIR and MART approaches have not been directly studied in pregnant populations. However, the established risks of uncontrolled asthma, along with the safety of both ICS and formoterol, support the application of GINA recommendations to pregnancy. Importantly, this highlights a crucial gap in evidence supporting pregnancy-specific asthma management and underscores the importance of including pregnant populations in future asthma trials.
