Mold

Pregnancy

MotherToBaby says pregnancy exposure to household mold has not been well studied. Its page reports that miscarriage risk is unknown, that no human risk from airborne mold has been established, and that it is not known whether mold causes other pregnancy problems. These statements describe an evidence gap, not proof that exposure has no effect. The strongest directly relevant study is Oh et al. (2026), an ECHO cohort of 11,483 mother-infant dyads at 31 U.S. sites. Reported household mold/mildew and water damage were not associated with gestational duration or fetal growth overall. Mold/mildew was a combined self-report item; stillbirths were excluded, and miscarriage and congenital anomalies were not study outcomes. An exploratory subgroup showed higher odds of preterm birth among mothers with higher educational attainment (OR 1.44, 95% CI 1.01-2.06); the authors call for replication. Lee et al. studied 1,446 participants in the Korean COCOA birth cohort and reported an association between questionnaire-reported prenatal mold and atopic dermatitis at age one (aOR 1.36, 95% CI 1.01-1.83). This is one observational infant-allergy finding, not evidence of birth defects or pregnancy loss. Grant et al. (2026) retrospectively described eight women from seven highly contaminated homes and 21 pregnancies; the article reports eight miscarriages and 13 infants, but its anomaly count is inconsistent between the abstract, table, and results text. The series had no comparison group, referral-based selection, nonstandard exposure timing, and an assay that screened for macrocyclic trichothecenes as a group. The authors state that direct epidemiological evidence linking the measured exposures with obstetrical or neonatal complications is absent. These selected case reports cannot estimate risk or establish cause. Warden et al. (2026) included dampness/fungi among several questionnaire-based prenatal exposures in 617 Isle of Wight cohort children; its abstract reports no prenatal environmental exposure association with diagnosed asthma, allergic rhinitis, or eczema but provides no mold-specific estimate. Mycotoxin studies and the Kyei et al. (2020) review primarily concern food-related exposures and cannot be used as estimates for household airborne mold. No study provided trimester-specific pregnancy risk estimates.

Breastfeeding

MotherToBaby states that mold passes into breast milk in small amounts and that breastfeeding can help protect infants from asthma and allergies, including those related to mold exposure at home. The source statement is not independently confirmed by the published evidence below. Güneş et al. (2023) followed 19 lactating women and measured zearalenone and deoxynivalenol, two individual mycotoxins, in milk at three visits during the first five months. The authors discuss foods as a source of these compounds. The study did not measure airborne mold in the home or infant clinical effects, and detection of separate fungal chemicals does not show that mold itself passes into milk. Grant et al. (2026) described lactation and infant problems in its retrospective case series and concluded that breastfeeding with indoor exposure appears hazardous, but there was no comparison group, other exposures could not be excluded, and its milk assay screened for a group of compounds. The case series does not establish that household mold enters milk or causes infant effects through breastfeeding. No direct human outcome study of household airborne mold exposure during breastfeeding is described in these sources.

What was tested

Studies used different exposure measures and outcomes. The ECHO cohort (Oh et al., 2026; 11,483 dyads) used questionnaires about mold/mildew and water damage and examined gestational duration and fetal growth. The Korean COCOA cohort (Lee et al.; 1,446 participants) used parent questionnaires about visible home mold and assessed atopic dermatitis at age one. The Grant et al. (2026) series reviewed medical records for eight referred women, seven homes, and 21 pregnancies; it included environmental inspection and urine/milk testing, but had no comparison group and used an assay that screened for macrocyclic trichothecenes as a group. The Warden et al. cohort (2026; 617 children) included early-pregnancy dampness/fungi among several questionnaire exposures, with no mold-specific estimate in the abstract. The Espoo cohort (Maaranen et al., 2025; 2,568 participants) used questionnaire-reported water damage, moisture, visible mold, and mold odor and assessed respiratory infections through age 27, not pregnancy complications. The Güneş et al. milk study (2023; 19 women) measured two dietary-associated mycotoxins in milk and did not assess household mold or infant clinical outcomes.