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ATERNAL AND CHILD UNdernutrition is estimated to be the underlying cause of 3.5 million annual deaths and 35% of the total disease burden in children younger than 5 years. 1 The potential long-term consequences of nutritional imbalance or insult in fetal or early life also include cognitive impairment 2 and chronic diseases in adulthood. 3 Effective child nutrition interventions are available to reduce stunting, prevent consequences of micronutrient deficiencies, and improve survival. 4 The knowledge base is weaker regarding prenatal nutrition interventions of benefit for mother and offspring. Supplementation with balanced protein-energy supplements in low-income countries has resulted in increased birth weight, especially in periods of food insecurity. 5,6 A recent meta-analysis 7 of balanced proteinenergy supplementation to pregnant women estimated a mean effect on birth weight of 60 g (95% CI, 33-87 g). Recent meta-analyses of prenatal multiple micronutrient trials have demonstrated small increases in birth weight in comparison with iron-folic acid supplementation alone, 8,9 and a small reduction in the occurrence of smallfor-gestational-age outcomes, 10 but no reduction in risk of stillbirth, perina-For editorial comment see p 2094. Author Affiliations and the MINIMat Study Team are listed at the end of this article.

The authors evaluated the association of prenatal arsenic exposure with size at birth (birth weight, birth length, head and chest circumferences). This prospective cohort study, based on 1,578 mother-infant pairs, was conducted in Matlab, Bangladesh, in 2002-2003. Arsenic exposure was assessed by analysis of arsenic in urine collected at around gestational weeks 8 and 30. The association of arsenic exposure with size at birth was assessed by linear regression analyses. In analysis over the full range of exposure (6-978 microg/L), no dose-effect association was found with birth size. However, significant negative dose effects were found with birth weight and head and chest circumferences at a low level of arsenic exposure (<100 microg/L in urine). In this range of exposure, birth weight decreased by 1.68 (standard error (SE), 0.62) g for each 1-microg/L increase of arsenic in urine. For head and chest circumferences, the corresponding reductions were 0.05 (SE, 0.03) mm and 0.14 (SE, 0.03) mm per 1 microg/L, respectively. No further negative effects were shown at higher levels of arsenic exposure. The indicated negative effect on birth size at a low level of arsenic exposure warrants further investigation.

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BackgroundArsenic (As) exposure during pregnancy induces oxidative stress and increases the risk of fetal loss and low birth weight.ObjectivesIn this study we aimed to elucidate the effects of As exposure on immune markers in the placenta and cord blood, and the involvement of oxidative stress.MethodsPregnant women were enrolled around gestational week (GW) 8 in our longitudinal, population-based, mother–child cohort in Matlab, an area in rural Bangladesh with large variations in As concentrations in well water. Women (n = 130) delivering at local clinics were included in the present study. We collected maternal urine twice during pregnancy (GW8 and GW30) for measurements of As, and placenta and cord blood at delivery for assessment of immune and inflammatory markers. Placental markers were measured by immunohistochemistry, and cord blood cytokines by multiplex cytokine assay.ResultsIn multivariable adjusted models, maternal urinary As (U-As) exposure both at GW8 and at GW30 was significantly positively associated with placental markers of 8-oxoguanine (8-oxoG) and interleukin-1β (IL-1β); U-As at GW8, with tumor necrosis factor-α (TNFα) and interferon-γ (IFNγ); and U-As at GW30, with leptin; U-As at GW8 was inversely associated with CD3+ T cells in the placenta. Cord blood cytokines (IL-1β, IL-8, IFNγ, TNFα) showed a U-shaped association with U-As at GW30. Placental 8-oxoG was significantly positively associated with placental proinflammatory cytokines. Multivariable adjusted analyses suggested that enhanced placental cytokine expression (TNFα and IFNγ) was primarily influenced by oxidative stress, whereas leptin expression appeared to be mostly mediated by As, and IL-1β appeared to be influenced by both oxidative stress and As.ConclusionAs exposure during pregnancy appeared to enhance placental inflammatory responses (in part by increasing oxidative stress), reduce placental T cells, and alter cord blood cytokines. These findings suggest that effects of As on immune function may contribute to impaired fetal and infant health.