Abstract
Objectives
The effects of maternal coffee consumption during pregnancy on childhood allergic diseases (ADs) remain insufficiently established. This study aimed to investigate the association between maternal coffee consumption during pregnancy and the risk of ADs in offspring up to 36 months of age.
Methods
We analyzed data from 3,252 mother–child pairs enrolled in the Korean Children’s Environmental health Study (Ko-CHENS). Maternal coffee and caffeine intake were assessed using a food frequency questionnaire. Childhood ADs were identified based on caregiver reports of physician diagnoses. Cox proportional hazards models were applied to estimate hazard ratios (HRs) and 95% confidence intervals (CIs), with adjustment for potential confounding factors.
Results
Overall, two-thirds (67.5%) of children were reported to have at least one AD, with cumulative incidences at 36 months of age of 47.8% for atopic dermatitis, 23.9% for food allergy, 30.2% for allergic rhinitis, and 2.4% for asthma. Compared with no coffee intake, maternal coffee consumption of <1 serving/day was associated with a reduced risk of atopic dermatitis (HR = 0.89, 95% CI 0.81–0.99, p = 0.045) and food allergy (HR = 0.86, 95% CI 0.74–1.00, p = 0.061). Higher intake (≥1 serving/day) was significantly associated with a lower risk of food allergy (HR = 0.61, 95% CI 0.42–0.88, p = 0.009). No significant associations were observed for asthma or allergic rhinitis.
Conclusions
Mild maternal coffee intake during pregnancy may be associated with a reduced risk of specific ADs in early childhood.
Keywords: Atopic Dermatitis, Birth Cohort, Caffeine, Coffee, Food Hypersensitivity
I. Introduction
Allergic diseases (ADs) remain a major global public health challenge, with a steadily increasing prevalence among children over the past three decades [1]. In South Korea, nearly one in four children under six years of age has been diagnosed with an allergic condition, such as atopic dermatitis, asthma, or allergic rhinitis [2], and documented upward trends further underscore the need for evidence-based prevention strategies [3]. Prenatal genetic, epigenetic, and environmental factors, including maternal dietary patterns, play critical roles in the development of allergic disorders in offspring [4]. Among these multifactorial influences, maternal diet during pregnancy is increasingly recognized as a key modifiable determinant shaping offspring susceptibility to allergic conditions [5].
Coffee is one of the most frequently consumed beverages worldwide [6]. In addition to its well-documented health benefits related to metabolic disorders, coffee has been shown to attenuate allergic responses in adult populations [7]. However, extensive research has also demonstrated associations between high-dose caffeine exposure during pregnancy and adverse outcomes, including fetal growth restriction and low birth weight [8,9]. As a result, current guidelines recommend that pregnant women limit caffeine intake to no more than 200 mg per day [10]. With respect to offspring allergic outcomes, existing evidence remains inconsistent: one study reported an increased risk of food allergy with higher maternal caffeine intake [11], whereas another observed a decreased incidence of asthma following prenatal caffeine exposure [12]. These divergent findings, which often fail to distinguish whole-coffee consumption from isolated caffeine exposure, have complicated efforts to draw precise conclusions.
Several critical knowledge gaps remain to be addressed. Coffee consumption in South Korea has reached approximately 2.7 times the global average [6], yet contemporary data describing intake patterns among Korean pregnant women are limited. Moreover, coffee, as a complex mixture containing numerous bioactive compounds beyond caffeine, has not been sufficiently examined as a prenatal exposure relevant to the development of childhood ADs. Therefore, we investigated the association between maternal coffee consumption during pregnancy and the risk of ADs in children up to 36 months of age, using data from the Korean Children’s Environmental Health Study (Ko-CHENS).
II. Methods
1. Study Population and Design
We analyzed data from the Ko-CHENS, a nationwide prospective birth cohort that enrolled approximately 70,000 pregnant women to investigate environmental exposures and pediatric health outcomes. Detailed cohort methodology has been published previously [13]. Briefly, pregnant women were recruited between June 2015 and February 2019 from designated regional centers across South Korea. Eligibility criteria included a gestational age below 20 weeks, maternal age of 18 years or older, planned delivery at participating centers, and residence within designated study areas.
From the Core cohort of 5,431 mother–child dyads with completed baseline questionnaires, we excluded participants with multiple pregnancies (n = 248), preterm birth (n = 194), low birth weight (n = 37), congenital anomalies (n = 15), intrauterine growth restriction (n = 10), and stillbirth (n = 8), yielding 4,919 eligible pairs. We further excluded participants with missing coffee consumption data (n = 190) and those lacking allergic disease information at the 6-month follow-up (n = 1,477). The rationale for excluding participants with missing data at the first follow-up time point (6 months) was to ensure accurate baseline risk assessment and time-to-event calculations. Subsequent missing follow-up values at 12, 24, and 36 months were handled using the last observation carried forward method to maintain the longitudinal data structure while preserving sample size for survival analysis. Finally, data from 3,252 eligible participants were included in the analysis (Figure 1).
Figure 1.
Flowchart of study participants. Ko-CHENS: Korean Children’s Environmental health Study.
2. Exposure Assessment
Maternal dietary intake during pregnancy was assessed using a validated 139-item food frequency questionnaire. Participants reported consumption frequency of coffee and caffeinated beverages across ten categories ranging from “four or more times daily” to “rarely or never,” with portion sizes categorized as small (0.5), standard (1.0), or large (1.5). Daily coffee intake was calculated by multiplying frequency midpoints by portion size and converting values to servings per day. Coffee consumption was categorized into three groups: none, <1 serving/day, and ≥1 serving/day.
Total caffeine intake was estimated by summing contributions from coffee (75.2 mg/100 mL), coffee cream (63.2 mg/100 mL), soft drinks (24 mg/100 mL), and tea (12.4 mg/100 mL) [14]. Because soft drink items did not distinguish between caffeinated and non-caffeinated varieties, conservative estimates based on lower caffeine ranges were applied. Daily total caffeine intake was classified into two categories: ≤50 mg/day and >50 mg/day.
3. Outcome Assessment
ADs were ascertained through structured questionnaires administered to mothers or caregivers at 6, 12, 24, and 36 months postpartum. Children were classified as having an allergic disease if caregivers responded affirmatively to either of the following questions: “Has a doctor ever diagnosed your child with allergic disease?” or “Has your child ever visited the hospital for allergic disease treatment?” ADs were defined as the presence of at least one of the following conditions: asthma, allergic rhinitis, atopic dermatitis, or any food allergy.
4. Covariates
Maternal variables obtained from baseline questionnaires included age at delivery, pre-pregnancy body mass index (BMI), BMI change at delivery, maternal education level, household income, smoking status, alcohol consumption during pregnancy, parity, and parental history of allergic disease. Child variables included sex, birth weight obtained from medical records, and breastfeeding history collected through follow-up questionnaires. These covariates were selected based on existing evidence supporting their potential influence on the development of allergic diseases in offspring [15].
5. Statistical Analysis
Baseline characteristics were summarized across coffee consumption categories using Kruskal–Wallis tests for continuous variables and chi-square or Fisher exact tests for categorical variables, as appropriate, following assessment of normality using the Shapiro–Wilk test. Missing follow-up data for ADs at 12 months (5.6%, n = 182), 24 months (13.6%, n = 443), and 36 months (19.9%, n = 649) were handled using the last observation carried forward method. Sensitivity analyses using complete case analysis, multiple imputation, and right censoring at the last contact were conducted to evaluate the robustness of the missing data handling approach. Cox proportional hazards regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between maternal coffee and caffeine intake and the risk of childhood ADs. Time-to-event was calculated as the number of months from birth until the first diagnosis of allergic disease, with administrative censoring at 36 months for children without an event.
Analyses were performed using univariate and multivariate models: model 1 (unadjusted), model 2 (adjusted for maternal age and child sex), and model 3 (adjusted for model 2 covariates plus maternal allergy, paternal allergy, maternal BMI change during pregnancy, household income, maternal education level, child birth weight, parity, and breastfeeding status). Pre-specified exploratory subgroup analyses were conducted to assess the consistency of associations across maternal characteristics, with stratification by maternal age (<30, 30–34, ≥35 years) and maternal pre-pregnancy BMI (<18.5, 18.5–24.9, ≥25 kg/m2). The proportional hazards assumption was evaluated using Schoenfeld residuals; violations identified for atopic dermatitis and allergic rhinitis were addressed through covariate stratification. The primary exposure variables satisfied the proportional hazards assumption across all models (p > 0.05).
All reported p-values were two-sided, and the threshold for statistical significance was set at <0.05. Statistical analyses were performed using R version 4.1.2 (R Foundation for Statistical Computing, Vienna, Austria).
6. Ethics
The Ko-CHENS protocol was approved by the Institutional Review Board of the National Institute of Environmental Research (NIER-2015-BR-005-01). The present analysis received approval from the Institutional Review Board of Ewha Womans University Hospital (SEUMC IRB 2024-12-012). All participants provided written informed consent for themselves and their children. All procedures were conducted in accordance with the principles of the Declaration of Helsinki.
III. Results
1. Characteristics of the Study Participants
Demographic and clinical characteristics of the 3,252 mother–child pairs, stratified by maternal consumption of coffee, tea, and soft drinks, are summarized in Table 1. Regular coffee consumers (≥1 serving/day) exhibited higher concurrent intake of tea (0.1 vs. 0.0 servings/day) and soft drinks (0.3 vs. 0.2 servings/day) compared with non-consumers (p < 0.001 for both comparisons). Maternal age differed across coffee consumption categories (p = 0.002), with higher consumers being older (33.3 ± 3.4 years) than non-consumers (32.6 ± 3.9 years). Multiparous women consumed coffee more frequently than primiparous women. Smoking during pregnancy was rare across all groups; however, alcohol consumption during pregnancy increased progressively with coffee intake, from 0.9% among non-consumers to 3.2% among women consuming ≥1 serving/day. Breastfeeding rates were significantly higher among coffee consumers, increasing from 32% in non-consumers to 60% in the highest consumption group (p < 0.001). Neither parental allergy history nor infant birth weight differed significantly across coffee consumption categories.
Table 1.
General characteristics of the study participants stratified by coffee, tea, and soft drink consumption category
| Characteristic | Total (n = 3,252) | Coffee consumption | Tea consumption | Soft drinks consumption | |||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
|
|
|
|||||||||||
| None (n = 1,809) | <1 serving/day (n = 1,255) | ≥1 servings/day (n = 188) | p-value | None (n = 2,856) | <1 serving/day (n = 383) | ≥1 servings/day (n = 13) | p-value | None (n = 839) | <1 serving/day (n = 2,348) | ≥1 servings/day (n = 65) | p-value | ||
| Continuous variables | |||||||||||||
|
| |||||||||||||
| Daily caffeine consumption (mg/day) | 17.1 ± 26.0 | 4.6 ± 8.5 | 24.3 ± 16.4 | 88.2 ± 48.1 | <0.001a | 16.3 ± 25.3 | 21.3 ± 27.6 | 66.7 ± 56.1 | <0.001a | 9.1 ± 26.0 | 18.7 ± 24.0 | 58.6 ± 40.5 | <0.001a |
|
| |||||||||||||
| Daily coffee consumption (serving/day) | 0.2 ± 0.3 | 0 ± 0 | 0.2 ± 0.2 | 1.2 ± 0.6 | <0.001a | 0.2 ± 0.3 | 0.2 ± 0.4 | 0.6 ± 0.9 | <0.001a | 0.1 ± 0.3 | 0.2 ± 0.3 | 0.4 ± 0.6 | <0.001a |
|
| |||||||||||||
| Daily tea consumption (serving/day) | 0.0 ± 0.1 | 0.0 ± 0.1 | 0.0 ± 0.5 | 0.1 ± 0.2 | <0.001a | 0 ± 0 | 0.1 ± 0.2 | 1.5 ± 0.9 | <0.001a | 0.0 ± 0.1 | 0.0 ± 0.1 | 0.1 ± 0.3 | <0.001a |
|
| |||||||||||||
| Daily soft-drinks consumption (serving/day) | 0.2 ± 0.3 | 0.2 ± 0.3 | 0.2 ± 0.3 | 0.3 ± 0.4 | <0.001a | 0.2 ± 0.3 | 0.2 ± 0.2 | 0.4 ± 0.3 | <0.001a | 0 ± 0 | 0.2 ± 0.2 | 1.6 ± 0.9 | <0.001a |
|
| |||||||||||||
| Maternal age (yr) | 32.8 ± 3.8 | 32.6 ± 3.9 | 32.9 ± 3.7 | 33.3 ± 3.4 | 0.002a | 32.8 ± 3.8 | 32.4 ± 3.9 | 32.5 ± 4.1 | 0.115a | 33.5 ± 3.9 | 32.5 ± 3.7 | 31.8 ± 4.2 | <0.001a |
|
| |||||||||||||
| Pre-pregnancy BMI (kg/m2) | 22.1 ± 3.5 | 22.0 ± 3.5 | 22.2 ± 3.5 | 22.3 ± 3.2 | 0.061a | 22.1 ± 3.5 | 22.0 ± 3.3 | 20.0 ± 1.8 | 0.043a | 21.9 ± 3.2 | 22.1 ± 3.5 | 23.6 ± 4.3 | <0.005a |
|
| |||||||||||||
| BMI change at delivery (kg/m2) | 4.8 ± 1.9 | 4.7 ± 1.9 | 4.8 ± 1.9 | 4.9 ± 1.8 | 0.672a | 4.8 ± 1.9 | 4.8 ± 1.9 | 3.9 ± 1.4 | 0.158a | 4.7 ± 1.9 | 4.8 ± 1.9 | 4.7 ± 1.8 | 0.319a |
|
| |||||||||||||
| Birth weight (g) | 3,268 ± 385 | 3,258 ± 396 | 3,283 ± 371 | 3,272 ± 366 | 0.184a | 3,267 ± 387 | 3,280 ± 369 | 3,184 ± 325 | 0.592a | 3,234 ± 394 | 3,277 ± 377 | 3,380 ± 484 | 0.017a |
|
| |||||||||||||
| Categorical variables | |||||||||||||
|
| |||||||||||||
| Maternal age group (yr) | 0.004b | 0.156c | <0.001b | ||||||||||
| <30 | 616 (18.9) | 382 (62.0) | 210 (34.1) | 24 (3.9) | 525 (85.2) | 89 (14.5) | 2 (0.3) | 129 (21.0) | 469 (76.1) | 18 (2.9) | |||
| 30–34 | 1,570 (48.3) | 862 (54.9) | 608 (38.7) | 100 (6.4) | 1,379 (87.8) | 184 (11.7) | 7 (0.5) | 360 (22.9) | 1,178 (75.0) | 32 (2.1) | |||
| ≥35 | 1,066 (32.8) | 565 (53.0) | 437 (41.0) | 64 (6.0) | 952 (89.3) | 110 (10.3) | 4 (0.4) | 350 (32.8) | 701 (65.8) | 15 (1.4) | |||
|
| |||||||||||||
| Maternal pre-pregnancy BMI group (kg/m2) | 0.077b | 0.181c | 0.021c | ||||||||||
| <18.5 | 335 (10) | 205 (61.2) | 120 (35.8) | 10 (3.0) | 287 (85.7) | 45 (13.4) | 3 (0.9) | 85 (25.4) | 248 (74.0) | 2 (0.6) | |||
| 18.5–24.9 | 2,361 (72.6) | 1,301 (55.1) | 913 (38.7) | 147 (6.2) | 2,073 (87.8) | 278 (11.8) | 10 (0.4) | 622 (26.4) | 1,696 (71.8) | 43 (1.8) | |||
| ≥25 | 556 (17.1) | 303 (54.5) | 222 (39.9) | 31 (5.6) | 496 (89.2) | 60 (10.8) | 0 (0.0) | 132 (23.7) | 404 (72.7) | 20 (3.6) | |||
|
| |||||||||||||
| Maternal education | 0.012b | 0.002c | 0.061b | ||||||||||
| <University | 1,385 (42.6) | 735 (53.1) | 575 (41.5) | 75 (5.4) | 1,248 (90.1) | 134 (9.7) | 3 (0.2) | 332 (24.0) | 1,020 (73.6) | 33 (2.4) | |||
| ≥University | 1,867 (57.4) | 1,074 (57.5) | 680 (36.4) | 113 (6.1) | 1,608 (86.1) | 249 (13.3) | 10 (0.6) | 507 (27.2) | 1,328 (71.1) | 32 (1.7) | |||
|
| |||||||||||||
| Household income (million won/mo) | 0.124b | 0.659c | 0.002b | ||||||||||
| <4 | 1,876 (57.7) | 1,036(55.2) | 743(39.6) | 97(5.2) | 1,655 (88.2) | 213 (11.4) | 8 (0.4) | 455 (24.3) | 1,372 (73.1) | 49 (2.6) | |||
| ≥4 | 1,376 (42.3) | 773(56.2) | 512(37.2) | 91(6.6) | 1,201 (87.3) | 170 (12.3) | 5 (0.4) | 384 (27.9) | 976 (70.9) | 16 (1.2) | |||
|
| |||||||||||||
| Residence | 0.306b | 0.919c | 0.004b | ||||||||||
| Rural | 313 (9.6) | 168 (53.7) | 121 (38.7) | 24 (7.7) | 277 (88.5) | 35 (11.2) | 1 (0.3) | 81 (25.9) | 218 (69.6) | 14 (4.5) | |||
| Urban | 2,939 (90.4) | 1,641 (55.8) | 1,134 (38.6) | 164 (5.6) | 2,579 (87.8) | 348 (11.8) | 12 (0.4) | 758 (25.8) | 2,130 (72.5) | 51 (1.7) | |||
|
| |||||||||||||
| Parity | <0.001b | 0.024c | <0.001b | ||||||||||
| Primiparous | 2,136 (65.7) | 1,321 (61.8) | 724 (33.9) | 91 (4.3) | 1,872 (87.6) | 260 (12.2) | 4 (0.2) | 597 (27.9) | 1,505 (70.5) | 34 (1.6) | |||
| Multiparous | 1,116 (34.3) | 488 (43.7) | 531 (47.6) | 97 (8.7) | 984 (88.2) | 123 (11.0) | 9 (0.8) | 242 (21.7) | 843 (75.5) | 31 (2.8) | |||
|
| |||||||||||||
| Smoking during pregnancy | 0.379c | 0.713c | 0.259c | ||||||||||
| Non-smoker | 3,237 (99.5) | 1,802 (55.7) | 1,247 (38.5) | 188 (5.8) | 2,843 (87.8) | 381 (11.8) | 13 (0.4) | 838 (25.9) | 2,334 (72.1) | 65 (2.0) | |||
| Smoker | 15 (0.5) | 7 (46.7) | 8 (53.3) | 0 (0.0) | 13 (86.7) | 2 (13.3) | 0 (0.0) | 1 (6.7) | 14 (93.3) | 0 (0.0) | |||
|
| |||||||||||||
| Drinking during pregnancy | <0.001b | 0.183c | 0.015c | ||||||||||
| No | 3,197 (98.3) | 1,793 (56.1) | 1,222 (38.2) | 182 (5.7) | 2,812 (88.0) | 372 (11.6) | 13 (0.4) | 833 (26.1) | 2,301 (71.9) | 63 (2.0) | |||
| Yes | 55 (1.7) | 16 (29.1) | 33 (60.0) | 6 (10.9) | 44 (80.0) | 11 (20.0) | 0 (0.0) | 6 (10.9) | 47 (85.5) | 2 (3.6) | |||
|
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| Maternal allergy history | 0.142b | 0.800c | 0.241b | ||||||||||
| No | 2,172 (66.8) | 1,230 (56.6) | 826 (38.0) | 116 (5.3) | 1,907 (87.8) | 255 (11.7) | 10 (0.5) | 580 (26.7) | 1,550 (71.4) | 42 (1.9) | |||
| Yes | 1,080 (33.2) | 579 (53.6) | 429 (39.7) | 72 (6.7) | 949 (87.9) | 128 (11.9) | 3 (0.2) | 259 (24.0) | 798 (73.9) | 23 (2.1) | |||
|
| |||||||||||||
| Paternal allergy history | 0.527b | 0.388c | 0.652b | ||||||||||
| No | 2,405 (74.0) | 1,326 (55.1) | 935 (38.9) | 144 (6.0) | 2,123 (88.3) | 272 (11.3) | 10 (0.4) | 624 (26.0) | 1,730 (71.9) | 51 (2.1) | |||
| Yes | 847 (26.0) | 483 (57.0) | 320 (37.8) | 44 (5.2) | 733 (86.5) | 111 (13.1) | 3 (0.4) | 215 (25.4) | 618 (73.0) | 14 (1.6) | |||
|
| |||||||||||||
| Sex of child | 0.079b | 0.773b | 0.838b | ||||||||||
| Male | 1,715 (52.7) | 962 (56.1) | 641 (37.4) | 112 (6.5) | 1,502 (87.6) | 207 (12.1) | 6 (0.3) | 449 (26.2) | 1,233 (71.9) | 33 (1.9) | |||
| Female | 1,537 (47.3) | 847 (55.1) | 614 (39.9) | 76 (4.9) | 1,354 (88.1) | 176 (11.4) | 7 (0.5) | 390 (25.4) | 1,115 (72.5) | 32 (2.1) | |||
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| Breastfeeding | <0.001b | 0.071c | <0.001b | ||||||||||
| No | 1,965 (60.4) | 1,239 (63.1) | 651 (33.1) | 75 (3.8) | 1,722 (87.6) | 239 (12.2) | 4 (0.2) | 566 (28.8) | 1,369 (69.7) | 30 (1.5) | |||
| Yes | 1,287 (39.6) | 570 (44.3) | 604 (46.9) | 113 (8.8) | 1,134 (88.1) | 144 (11.2) | 9 (0.7) | 273 (21.2) | 979 (76.1) | 35 (2.7) | |||
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| Child’s allergic disease | |||||||||||||
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| Any allergic disease | 0.027b | 0.879c | 0.759b | ||||||||||
| No | 1,058 (32.5) | 553 (52.3) | 438 (41.4) | 67 (6.3) | 930 (87.9) | 123 (11.6) | 5 (0.5) | 279 (26.4) | 760 (71.8) | 19 (1.8) | |||
| Yes | 2,194 (67.5) | 1,256 (57.3) | 817 (37.2) | 121 (5.5) | 1,926 (87.8) | 260 (11.9) | 8 (0.3) | 560 (25.5) | 1,588 (72.4) | 46 (2.1) | |||
|
| |||||||||||||
| Atopic dermatitis | 0.013b | 0.642c | 0.642b | ||||||||||
| No | 1,698 (52.2) | 903 (53.2) | 691 (40.7) | 104 (6.1) | 1,479 (87.1) | 211 (12.4) | 8 (0.5) | 427 (25.2) | 1,238 (72.9) | 33 (1.9) | |||
| Yes | 1,554 (47.8) | 906 (58.3) | 564 (36.3) | 84 (5.4) | 1,377 (88.6) | 172 (11.1) | 5 (0.3) | 412 (26.5) | 1,110 (71.4) | 32 (2.1) | |||
|
| |||||||||||||
| Food allergy | <0.001b | 0.035c | 0.187b | ||||||||||
| No | 2,475 (76.1) | 1,332 (53.8) | 984 (39.8) | 159 (6.4) | 2,189 (88.4) | 274 (11.1) | 12 (0.5) | 624 (25.2) | 1,797 (72.6) | 54 (2.2) | |||
| Yes | 777 (23.9) | 477 (61.4) | 271 (34.9) | 29 (3.7) | 667 (85.9) | 109 (14.0) | 1 (0.1) | 215 (27.7) | 551 (70.9) | 11 (1.4) | |||
|
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| Allergic rhinitis | 0.313b | 0.278c | 0.004b | ||||||||||
| No | 2,270 (69.8) | 1,279 (56.3) | 867 (38.2) | 124 (5.5) | 2,007 (88.4) | 254 (11.2) | 9 (0.4) | 621 (27.3) | 1,609 (70.9) | 40 (1.8) | |||
| Yes | 982 (30.2) | 530 (54.0) | 388 (39.5) | 64 (6.5) | 849 (86.5) | 129 (13.1) | 4 (0.4) | 218 (22.2) | 739 (75.3) | 25 (2.5) | |||
|
| |||||||||||||
| Asthma | 0.893c | 0.067c | 0.931c | ||||||||||
| No | 3,175 (97.6) | 1,768 (55.7) | 1,223 (38.5) | 184 (5.8) | 2,784 (87.7) | 379 (11.9) | 12 (0.4) | 818 (25.8) | 2,293 (72.2) | 64 (2.0) | |||
| Yes | 77 (2.4) | 41 (53.2) | 32 (41.6) | 4 (5.2) | 72 (93.5) | 4 (5.2) | 1 (1.3) | 21 (27.3) | 55 (71.4) | 1 (1.3) | |||
Values are presented as mean ± standard deviation or number (%).
BMI: body mass index.
Kruskal-Wallis rank sum test,
Pearson chi-squared test,
Fisher exact test.
During the 36-month follow-up period, 2,194 children (67.5%) developed at least one AD. The cumulative incidence was 47.8% for atopic dermatitis, 30.2% for allergic rhinitis, 23.9% for food allergy, and 2.4% for asthma.
2. Maternal Coffee, Tea and Soft Drink Intake and Childhood ADs
Multivariable Cox proportional hazards regression analyses were conducted using a single fully adjusted model to examine associations between maternal consumption of coffee, tea, and soft drinks and the risk of childhood ADs; results are presented in Table 2. Covariates included maternal age, child sex, parental allergy history, maternal BMI change during pregnancy, household income, maternal education level, birth weight, parity, and breastfeeding status. Maternal coffee intake was inversely associated with the risk of atopic dermatitis (HR = 0.90, 95% CI 0.81–0.99, p = 0.041) and food allergy (HR = 0.83, 95% CI 0.72–0.96, p = 0.014). Tea consumption showed no significant associations with any allergic outcomes examined. In contrast, soft drink intake was positively associated with the risk of allergic rhinitis (HR = 1.22, 95% CI 1.05–1.42, p = 0.010).
Table 2.
Multivariate Cox regression analysis for the associations between maternal coffee, tea, and soft drink intake and the risk of allergic diseases in children
| Variable | Any allergic disease | Allergic dermatitis | Food allergy | Allergic rhinitis | Asthma | |||||
|---|---|---|---|---|---|---|---|---|---|---|
|
|
|
|
|
|
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| HR (95% CI)a | p-value | HR (95% CI)a | p-value | HR (95% CI)a | p-value | HR (95% CI)a | p-value | HR (95% CI)a | p-value | |
| Coffee intake | ||||||||||
| No | Reference | Reference | Reference | Reference | Reference | |||||
| Yes | 0.92 (0.85–1.00) | 0.061 | 0.90 (0.81–0.99) | 0.041 | 0.83 (0.72–0.96) | 0.014 | 1.10 (0.96–1.25) | 0.165 | 1.11 (0.70–1.75) | 0.665 |
|
| ||||||||||
| Tea intake | ||||||||||
| No | Reference | Reference | Reference | Reference | Reference | |||||
| Yes | 0.96 (0.84–1.09) | 0.532 | 0.87(0.74–1.02) | 0.081 | 1.20 (0.98–1.47) | 0.076 | 1.14 (0.95–1.37) | 0.150 | 0.48 (0.19–1.19) | 0.111 |
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| Soft drinks intakeb | ||||||||||
| No | Reference | Reference | Reference | Reference | Reference | |||||
| Yes | 1.02 (0.92–1.12) | 0.696 | 0.97 (0.86–1.08) | 0.549 | 0.92 (0.78–1.08) | 0.299 | 1.22 (1.05–1.42) | 0.010 | 0.88 (0.53–1.46) | 0.618 |
HR: hazard ratio, CI: confidence interval.
Adjusted for mother’s age, child’s sex, presence of maternal allergy, presence of paternal allergy, body mass index (BMI) change of mother during pregnancy, household income, mothers’ education level, birth weight of child, parity and breast-feeding status
Soft drinks included both caffeinated and non-caffeinated beverages.
Significant values (p < 0.05) are in bold.
3. Maternal Coffee Consumption Categories and ADs in Children
Table 3 presents HRs for allergic outcomes according to maternal coffee consumption categories. In unadjusted analyses, children whose mothers consumed <1 serving/day had a lower overall risk of allergic disease (HR = 0.87, 95% CI 0.79–0.95, p = 0.002) compared with non-consumers. After full covariate adjustment, this association was attenuated and no longer statistically significant (HR = 0.92, 95% CI 0.84–1.01, p = 0.078).
Table 3.
Multivariable Cox regression analysis for categorical maternal coffee consumption during pregnancy and the risk of allergic diseases in children
| Allergic disease | Daily coffee consumption | Cases/total (%) | Model 1 | Model 2 | Model 3 | |||
|---|---|---|---|---|---|---|---|---|
|
|
|
|
||||||
| HR (95% CI) | p-value | HR (95% CI) | p-value | HR (95% CI) | p-value | |||
| Any allergic disease | Total | 2,194/3,252 (67.5) | ||||||
| None | 1,256/1,809 (69.4) | Reference | Reference | Reference | ||||
| <1 servinga | 817/1,255 (65.1) | 0.87 (0.79–0.95) | 0.002 | 0.88 (0.81–0.96) | 0.005 | 0.92 (0.84–1.01) | 0.078 | |
| ≥1 serving | 121/188 (64.4) | 0.85 (0.71–1.03) | 0.103 | 0.86 (0.71–1.04) | 0.126 | 0.91 (0.75–1.10) | 0.329 | |
|
| ||||||||
| Atopic dermatitis | Total | 1,554/3,252 (47.8) | ||||||
| None | 906/1,809 (50.1) | Reference | Reference | Reference | ||||
| <1 servinga | 564/1,255 (44.9) | 0.85 (0.76–0.94) | 0.002 | 0.86 (0.77–0.95) | 0.004 | 0.89 (0.81–0.99) | 0.045 | |
| ≥1 serving | 84/188 (44.7) | 0.85 (0.68–1.06) | 0.151 | 0.85 (0.68–1.07) | 0.165 | 0.92 (0.73–1.15) | 0.429 | |
|
| ||||||||
| Food allergy | Total | 777/3,252 (23.9) | ||||||
| None | 477/1,809 (26.4) | Reference | Reference | Reference | ||||
| <1 servinga | 271/1,255 (21.6) | 0.80 (0.67–0.93) | 0.002 | 0.81 (0.70–0.94) | 0.005 | 0.86 (0.74–1.01) | 0.061 | |
| ≥1 serving | 29/188 (15.4) | 0.55 (0.38–0.80) | 0.001 | 0.55 (0.38–0.80) | 0.002 | 0.61 (0.42–0.88) | 0.009 | |
|
| ||||||||
| Allergic rhinitis | Total | 982/3,252 (30.2) | ||||||
| None | 530/1,809 (29.3) | Reference | Reference | Reference | ||||
| <1 servinga | 388/1,255 (30.9) | 1.06 (0.94–1.22) | 0.321 | 1.08 (0.95–1.23) | 0.247 | 1.08 (0.94–1.23) | 0.254 | |
| ≥1 serving | 64/188 (34.0) | 1.23 (0.95–1.59) | 0.119 | 1.23 (0.95–1.59) | 0.120 | 1.21 (0.93–1.58) | 0.157 | |
|
| ||||||||
| Asthma | Total | 77/3,252 (2.4) | ||||||
| None | 41/1,809 (2.3) | Reference | Reference | Reference | ||||
| <1 servinga | 32/1,255 (2.5) | 1.13 (0.71–1.79) | 0.614 | 1.15 (0.73–1.84) | 0.532 | 1.14 (0.71–1.82) | 0.593 | |
| ≥1 serving | 4/188 (2.1) | 0.94 (0.34–2.62) | 0.903 | 0.94 (0.34–2.62) | 0.904 | 0.90 (0.32–2.57) | 0.845 | |
HR: hazard ratio, CI: confidence interval.
Model 1: unadjusted, Model 2: adjusted for mother’s age and child’s sex, Model 3: adjusted for model 2 covariates, in addition to the presence of maternal allergy, presence of paternal allergy, body mass index (BMI) change of mother during pregnancy, household income, mothers’ education level, birth weight of child, parity and breast-feeding status.
”<1 serving/day” coffee consumption refers to individuals who do not consume coffee daily, rather drink it occasionally with an average intake of less than one serving per day (e.g., a few times per week).
Significant values (p < 0.05) are in bold.
Food allergy demonstrated the strongest inverse associations with maternal coffee consumption. In fully adjusted models, maternal intake of ≥1 serving/day was associated with a 39% lower risk of food allergy (HR = 0.61, 95% CI 0.42–0.88, p = 0.009), while consumption of <1 serving/day showed a borderline reduction in risk (HR = 0.86, 95% CI 0.74–1.01, p = 0.061). For atopic dermatitis, consumption of <1 serving/day retained marginal statistical significance after full adjustment (HR = 0.89, 95% CI 0.81–0.99, p = 0.045), whereas higher consumption yielded similar but non-significant estimates (HR = 0.92, 95% CI 0.73–1.15, p = 0.429). No associations were observed between maternal coffee intake and the risk of allergic rhinitis or asthma across any model.
4. Maternal Total Caffeine Consumption and ADs in Children
Table 4 summarizes associations between total daily caffeine intake from the specified sources and the risk of childhood ADs. Compared with intake ≤50 mg/day, consumption >50 mg/day was associated with a reduced risk of food allergy across all models, with fully adjusted estimates indicating a 30% risk reduction (HR = 0.70, 95% CI 0.53–0.93, p = 0.015). No significant associations were observed between total caffeine intake and other allergic outcomes.
Table 4.
Multivariable Cox regression analysis for categorical maternal total caffeine intake during pregnancy and the risk of allergic diseases in children
| Allergic disease | Daily total caffeine consumption | Cases/total (%) | Model 1 | Model 2 | Model 3 | |||
|---|---|---|---|---|---|---|---|---|
|
|
|
|
||||||
| HR (95% CI) | p-value) | HR (95% CI | p-value | HR (95% CI) | p-value | |||
| Any allergic disease | Total | 2,194/3,252 (67.5) | ||||||
| ≤50 mg | 2,003/2,952 (67.9) | Reference | Reference | Reference | ||||
| >50 mg | 191/300 (63.7) | 0.89(0.77–1.04) | 0.141 | 0.91(0.78–1.05) | 0.188 | 0.93(0.80–1.08) | 0.321 | |
|
| ||||||||
| Atopic dermatitis | Total | 1,554/3,252 (47.8) | ||||||
| ≤50 mg | 1,415/2,952 (47.9) | Reference | Reference | Reference | ||||
| >50 mg | 139/300 (46.3) | 0.94(0.80–1.13) | 0.556 | 0.96(0.80–1.14) | 0.627 | 0.99(0.84–1.19) | 0.991 | |
|
| ||||||||
| Food allergy | Total | 777/3,252 (23.9) | ||||||
| ≤50 mg | 726/2,952 (24.6) | Reference | Reference | Reference | ||||
| >50 mg | 51/300 (17.0) | 0.66 (0.50–0.88) | 0.004 | 0.66 (0.50–0.88) | 0.005 | 0.70 (0.53–0.93) | 0.015 | |
|
| ||||||||
| Allergic rhinitis | Total | 982/3,252 (30.2) | ||||||
| ≤50 mg | 886/2,952 (30.0) | Reference | Reference | Reference | ||||
| >50 mg | 96/300 (32.0) | 1.10(0.89–1.35) | 0.399 | 1.10(0.89–1.35) | 0.395 | 1.05(0.85–1.31) | 0.626 | |
|
| ||||||||
| Asthma | Total | 77/3,252 (2.4) | ||||||
| ≤50 mg | 73/2,952 (2.5) | Reference | Reference | Reference | ||||
| >50 mg | 4/300 (1.3) | 0.54(0.20–1.47) | 0.225 | 0.53(0.20–1.46) | 0.223 | 0.51(0.18–1.40) | 0.191 | |
HR: hazard ratio, CI: confidence interval.
Model 1: unadjusted, Model 2: adjusted for mother’s age and child’s sex, Model 3: adjusted for model 2 covariates, in addition to the presence of maternal allergy, presence of paternal allergy, body mass index (BMI) change of mother during pregnancy, household income, mothers’ education level, birth weight of child, parity and breastfeeding status.
Significant values (p < 0.05) are in bold.
Dose–response relationships evaluated using penalized spline models (Supplementary Figure S1) showed no statistically significant departures from linearity for any outcome (likelihood ratio test p > 0.05 for all comparisons).
5. Subgroup and Sensitivity Analyses
Pre-specified exploratory subgroup analyses stratified by maternal age and pre-pregnancy BMI, presented in Figure 2, revealed no statistically significant interactions (all interaction p-values > 0.05; Supplementary Tables S1–S5). Inverse associations with food allergy and atopic dermatitis were generally consistent across maternal characteristics, whereas estimates for allergic rhinitis and asthma were less precise, with wider confidence intervals and no discernible patterns.
Figure 2.
Subgroup analysis according to maternal age groups and pre-pregnancy body mass index (BMI) groups. Summary of hazard ratios and 95% confidence intervals (x-axis) of coffee intake as serving per day for (A) any allergic disease, (B) atopic dermatitis, (C) food allergy, (D) allergic rhinitis, and (E) asthma. Adjusted by mother’s age, child’s sex, presence of maternal allergy, presence of paternal allergy, mother’s BMI change during pregnancy, household income, mothers’ education level, birth weight of child, and breastfeeding status. The dashed vertical line indicates the null reference value of 1.
Sensitivity analyses were conducted to evaluate robustness to assumptions regarding missing data using three approaches: (1) complete case analysis (n = 2,484), (2) multiple imputation with 30 imputations using chained equations (Supplementary Table S6), and (3) right-censoring at the last contact (Supplementary Table S7). All approaches yielded results consistent with the primary last observation carried forward analysis (n = 3,252), with minimal differences in hazard ratios (maximum difference = 0.05), overlapping confidence intervals, and no changes in statistical significance across outcomes. This consistency supports the robustness of the study findings.
IV. Discussion
We analyzed data from a nationwide prospective birth cohort comprising 3,252 mother–child pairs enrolled between 2015 and 2019, with follow-up from pregnancy through the child’s third year of life. Our findings indicate that mild maternal coffee consumption during pregnancy was not associated with an increased risk of asthma or allergic rhinitis, but was instead associated with a reduced risk of atopic dermatitis and food allergy in children up to 36 months of age, compared with no coffee consumption. For atopic dermatitis, maternal coffee consumption of <1 serving/day was associated with a statistically significant 11% risk reduction by 36 months in the fully adjusted model, an effect that was not observed with caffeine intake alone. This discordance raises the hypothesis that non-caffeine bioactive compounds in coffee may contribute to the observed protective association, although this interpretation should be considered preliminary given the relatively small number of mothers with higher levels of coffee consumption in our cohort. Food allergy exhibited a distinct pattern, with both higher coffee consumption (≥1 serving/day) and higher caffeine intake showing significant risk reductions in fully adjusted models. Collectively, these findings suggest that the relationship between maternal coffee consumption and childhood allergic disease risk may be complex and potentially dependent on both consumption level and the specific allergic outcome. We hypothesize that both caffeine and non-caffeine bioactive components of coffee may contribute to these associations; however, such mechanistic interpretations warrant confirmation in larger studies with sufficient statistical power to evaluate dose–response relationships.
Our study population demonstrated relatively low coffee and caffeine consumption during pregnancy, with 44.4% of mothers reporting any coffee intake. Among coffee consumers, the majority (86.9%) consumed less than one serving per day, whereas only 13.0% consumed one or more servings daily, and just 0.002% were high consumers reporting four or more servings per day. This pattern was mirrored in overall caffeine intake, with a median daily intake of 6.68 mg and a mean intake of 17 mg/day. Notably, 98.6% of pregnant women consumed ≤100 mg of caffeine per day, corresponding to approximately half of the recommended upper limit of 200 mg/day during pregnancy [10]. Even among women consuming >100 mg/day, who comprised only 1.4% of the cohort, the average intake was 143 mg/day, which remained below the recommended threshold.
These findings are broadly consistent with data from European populations demonstrating conservative caffeine consumption during pregnancy. A Polish mother–child cohort reported that 79% of mothers consumed less than 100 mg of caffeine daily, with no adverse neonatal outcomes observed [16]. Similarly, a Portuguese prospective birth cohort with comparable caffeine intake levels (median 8.62 mg/day) reported that pregnancy caffeine consumption was associated with a reduced risk of childhood asthma up to 10 years of age at intake levels below 93 mg/day [12]. In contrast, studies conducted in Japanese cohorts reported substantially higher caffeine consumption (>200 mg/day), with one study demonstrating that maternal caffeine intake (median 232.3 mg/day) was associated with increased odds of food allergy in children [11]. Taken together, these divergent findings suggest that the association between maternal caffeine consumption and childhood allergic outcomes may follow a non-linear dose–response pattern, whereby moderate intake may be protective, whereas higher levels of consumption could be detrimental.
Several biological mechanisms may plausibly underlie the observed associations between maternal coffee or caffeine intake and reduced childhood allergic disease risk, including anti-inflammatory, antioxidant, metabolic, and gutmodulating effects. Experimental and observational studies have demonstrated that coffee exerts predominantly anti-inflammatory actions, whereas caffeine appears to have more complex immunomodulatory effects, exhibiting both pro-inflammatory and anti-inflammatory responses depending on context [17–19]. Coffee-derived dietary fiber and polyphenols, particularly chlorogenic acid, can modulate the gut microbiota by promoting the growth of short-chain fatty acid (SCFA)–producing bacteria, thereby increasing levels of primary SCFAs such as acetate, propionate, and butyrate [20–22]. These SCFAs can enter the maternal circulation and cross the placenta to reach the fetus, a process that has been linked to fetal immune programming, including induction of regulatory T cells that are critical for immune tolerance and reduced allergy risk [23]. Supporting this mechanism, in vivo experimental studies have shown that maternal high-fiber or acetate supplementation during pregnancy confers protection against allergic airway disease in adult offspring, with exposed progeny demonstrating significantly attenuated allergic responses compared with controls [24]. In addition, several studies have suggested that moderate coffee intake (up to four cups per day) is associated with increased abundance of SCFA-producing gut microbiota belonging to the Firmicutes, Bacteroidetes, and Actinobacteria phyla, including Bifidobacterium spp. (Actinobacteria), Lawsonibacter asaccharolyticus (Firmicutes), and Prevotella spp. (Bacteroidetes) [21,25]. A nested case–control study within a prebirth cohort further demonstrated that maternal carriage of Prevotella, an SCFA-producing gut commensal, during pregnancy strongly predicted the absence of food allergy in offspring during infancy [26]. Another study reported lower Prevotella abundance among mothers of infants and toddlers with atopic dermatitis compared with control mothers, although this difference was not statistically significant in subsequent analyses [27].
To our knowledge, this is the first Korean birth cohort study to investigate associations between maternal coffee and caffeine consumption during pregnancy and the development of allergic diseases in children during the first 36 months of life. The prospective design and comprehensive adjustment for multiple potential confounders in multivariable models represent key methodological strengths. Nevertheless, several limitations should be considered. Maternal coffee and caffeinated beverage consumption was assessed using a food frequency questionnaire and may therefore be subject to measurement error and recall bias inherent in self-reported dietary assessments. Such misclassification is likely non-differential, as maternal dietary reporting would not be influenced by subsequent childhood allergic disease development, and would therefore tend to bias associations toward the null; consequently, the observed protective associations may represent conservative estimates. In addition, estimation of caffeine intake was limited to beverages, including coffee, tea, and soft drinks, and did not account for caffeine-containing foods such as chocolate-based products or cocoa powder, nor for decaffeinated coffee or tea. Although we observed a significant positive association between prenatal soft drink consumption and childhood allergic rhinitis risk, we were unable to further explore the relative contributions of caffeine and non-caffeine components of soft drinks, as the food frequency questionnaire did not distinguish between caffeinated and non-caffeinated soft drinks. Maslova et al. [28] reported that consumption of artificially sweetened carbonated soft drinks during pregnancy was associated with higher risks of asthma and allergic rhinitis in children (odds ratio [OR] = 1.30, 95% CI 1.01–1.66 and OR = 1.31, 95% CI 0.98–1.74, respectively). A separate meta-analysis similarly reported that prenatal soft drink consumption was associated with a marginally increased risk of childhood asthma (OR = 1.11, 95% CI 1.00–1.23) [29]. Accordingly, our findings highlight the need for future studies to investigate prenatal soft drink intake, differentiated by caffeinated and non-caffeinated categories, in relation to childhood allergic disease risk.
Another limitation is that parental self-reporting of allergic diseases may introduce diagnostic misclassification, recall bias, and potential overestimation of disease prevalence. Although we adjusted for a broad range of known confounders influencing allergic disease development, the absence of data on certain factors, such as delivery mode, pet exposure, and antibiotic use, may have resulted in residual confounding. In our cohort, mothers who consumed higher amounts of coffee tended to be older, have higher educational attainment, be more frequently multiparous, and report higher postpartum breastfeeding rates, all of which are independently associated with lower allergic disease risk in offspring. Importantly, even after adjustment for these characteristics, protective associations between maternal coffee consumption and both food allergy and atopic dermatitis persisted, outcomes that had sufficient case numbers and prevalence to allow robust analysis. Nevertheless, the possibility of unmeasured confounding cannot be excluded and warrants further investigation. Additionally, coffee and caffeine consumption among Korean pregnant women was generally low, with very few participants exceeding the European Food Safety Authority–recommended threshold of <200 mg/day [10], limiting our ability to assess effects of very high intake levels or to fully characterize dose–response relationships. Despite this limitation, an important strength of the study is the demonstration that coffee consumption within recommended caffeine limits was not associated with an increased risk of childhood allergic diseases, providing reassuring evidence regarding safety within this exposure range.
In conclusion, our findings suggest an inverse association between prenatal coffee consumption and childhood allergic diseases, with statistically significant risk reductions observed for atopic dermatitis and food allergy by 36 months of age. Further in-depth studies are needed to elucidate the contributions of specific coffee constituents during the prenatal period and to better understand their potential roles in the development of allergic diseases in children.
Footnotes
Conflict of Interest
No potential conflict of interest relevant to this article was reported.
Acknowledgments
This work is part of a doctoral dissertation by Sharmin Afroz for the degree of Doctor of Philosophy at Ewha Womans University.
This work supported by a grant (NIER-2019-03-01-001) from the National Institute of Environmental Research (NIER), funded by the Ministry of Environment (MOE), Republic of Korea.
This study was prepared on behalf of the Ko-CHENS Study Group—Suejin Kim, Choonghee Park, Sanghwan Song, Jueun Lee, Huibyeol Park, JungHeum Jo, A-Ra Jung, Seung Do Yu, Hyun Jeong Kim, Soon-Won Jung, Sooyeon Hong (National Institute of Environmental Research, Ministry of Environment); Heung Won Seo, Namkyoung Hwang, Tack Shin Kang, Dong Jin Jeong, Seungjune Lee (Office of Environmental Health, Ministry of Environment); Eunhee Ha, Yi-Jun Kim, Surabhi Shah, Jongmin Oh (Ewha Womans University School of Medicine); Hwan-Cheol Kim (Inha University School of Medicine); Kyoung Sook Jeong (Wonju Severance Christian Hospital); Byungmi Kim (National Cancer Center); Seulbi Lee (National Health Insurance Service); Hyesook Kim (Wonkwang University); Hoon Kook, Hee Jo Baek, Jai Dong Moon, Won Ju Park, Myung-Geun Shin (Chonnam National University Hwasun Hospital); Mina Ha, Ki-Chung Paik, Ho-Jang Kwon (Dankook University College of Medicine); Myung-Ho Lim, Seung Jin Yoo (Dankook University Medical Center); Sanghyuk Bae (College of Medicine, The Catholic University of Korea); Jin Kyung Kim, Jisuk Bae (Daegu Catholic University School of Medicine); Young-Seoub Hong, Hyunjin Son (Dong-A University College of Medicine), Yu-Mi Kim (Hanyang University College of Medicine); Mi-Hye Park (Ewha Womans University College of Medicine); Dae Hyun Lim, Jeong Hee Kim (Inha University School of Medicine); Sung-Chul Hong, Keun Hwa Lee, Su-Young Kim (Jeju National University College of Medicine); Woo Jin Kim, Myoung-Nam Lim (Kangwon National University), Sunghun Na (Kangwon National University Hospital); Young Yoo, Dae Jin Song, Jue Seong Lee, Wonsuck Yoon, Seung-Ah Choe, Seunghyun Kim, Ji Tae Choung (Korea University Medical College); Sukyung Kim, Jihyun Kim, Kangmo Ahn (Samsung Medical Center); Yun-Chul Hong, Baek-Yong Choi, Seung-Woo Ryoo, Seok-Yoon Son, Ji-Hyeon Lee, Dong-Wook Lee (Seoul National University College of Medicine); KuckHyeun Woo, Seong Yong Yoon (Soonchunhyang University Gumi Hospital); Jongil Hur, Seung-Hwa Lee, Yeonhee Chu, Jung-Ah Kim (Taean Environmental Health Center); Kyung-Hwa Choi (Dankook University College of Medicine); Myung-Sook Park (Seoul National University College of Medicine); Yangho Kim, Jiho Lee, Chang Sun Sim, A Ram Kim, Inbo Oh (University of Ulsan College of Medicine).
Data Availability Statement
The data used in this study were obtained from the Korean CHildren’s ENvironmental health Study (Ko-CHENS), a nationwide prospective birth cohort managed by the Ministry of Environment and the National Institute of Environmental Research, Republic of Korea. Due to privacy and ethical regulations, these data are not publicly accessible. However, detailed datasets supporting the findings are available from the corresponding authors upon reasonable request, subject to approval from the Ko-CHENS data access committee and relevant Institutional Review Boards.
Supplementary Materials
Supplementary materials can be found via https://doi.org/10.4258/hir.2026.32.1.77.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
The data used in this study were obtained from the Korean CHildren’s ENvironmental health Study (Ko-CHENS), a nationwide prospective birth cohort managed by the Ministry of Environment and the National Institute of Environmental Research, Republic of Korea. Due to privacy and ethical regulations, these data are not publicly accessible. However, detailed datasets supporting the findings are available from the corresponding authors upon reasonable request, subject to approval from the Ko-CHENS data access committee and relevant Institutional Review Boards.