ABSTRACT Nutritional additives and environmental pollution are linked with Helicobacter pylori infection (HPI), but the combined effects in early life on childhood HPI during and after the COVID‐19 epidemic are unclear. To explore the associations between early‐life intake of nutritional additives, household environmental factors (HEFs), and outdoor air pollutant (OAP) exposure and their interactions on childhood HPI during and after the COVID‐19 epidemic. We collected 20,730 questionnaires through a mother‐child retrospective cohort study from five Chinese cities, covering data on individual characteristics, nutritional additives, health outcomes, and HEFs. Individual OAP exposure was calculated through data from environmental monitoring reports and the inverse distance weighting (IDW) method. Multilevel logistic regression models were conducted to establish the impacts of early‐life nutritional additives, HEFs, and OAP exposures on childhood HPI during and after the COVID‐19 epidemic. Childhood HPI was negatively associated with maternal intake of nutritional additives in utero, with OR (95% CI) = 0.79 (0.62–1.00), and childhood intake of zinc, vitamins B and C, and cod‐liver oil, with ORs (95% CIs) = 0.69 (0.54–0.89) and 0.78 (0.63–0.98). Furthermore, HPI was negatively associated with the use of ceramic tile/stone/cement flooring, mosquito coil/repellents, and incense, with ORs (95% CIs) = 0.72 (0.56–0.92), 0.79 (0.63–0.97), and 0.61 (0.44–0.84), whereas it was positively associated with laminate/PVC/chemical fiber carpet flooring and wool/hemp carpet flooring, water/latex/lime/cement/seaweed mud, and plastic toys, with ORs (95% CIs) = 1.24 (1.01–1.53) and 4.71 (1.94–11.42). Additionally, outdoor PM 2.5‐10 and SO 2 exposure before and during pregnancy increased HPI risk, with ORs (95% CIs) = 1.08 (1.01–1.16) and 1.17 (1.01–1.34). Nutritional additive intake during pregnancy and after birth mitigated the adverse effects of HEFs and OAPs on HPI risk. During and after the COVID‐19 epidemic, early‐life nutritional additives, HEFs, and OAP exposures independently and interactively affect children's HPI, supporting the “(Pre‐)Fetal origins of childhood HPI” hypothesis through the “gut–uterine axis” and “nutrition–environment interaction.”
Lu et al. (Sat,) studied this question.