This study looked at Bangladeshi children who were exposed to low levels of arsenic early in life and measured how their innate immune system worked. It found that higher arsenic levels were linked to higher blood levels of the natural antimicrobial peptide LL‑37, but also to weaker ability of immune cells to kill bacteria and altered cytokine patterns. The research suggests that early arsenic exposure can mess up the body’s first line of defense, which might affect health later on.

Early-life exposure to arsenic (As) increases risks of respiratory diseases/infections in children. However, data on the ability of the innate immune system to combat bacterial infections in the respiratory tracts of As-exposed children are scarce. To evaluate whether persistent low-dose As exposure alters innate immune function among children younger than 5&#x2009;years-of-age, mothers and participating children (<i>N</i>&#x2009;=&#x2009;51) that were members of the Health Effects of Arsenic Longitudinal Study (HEALS) cohort in rural Bangladesh were recruited. Household water As, past and concurrent maternal urinary As (U-As) as well as child U-As were all measured at enrollment. In addition, U-As metabolites were evaluated. Innate immune function was examined via measures of cathelicidin LL-37 in plasma, <i>ex vivo</i> monocyte-derived-macrophage (MDM)-mediated killing of <i>Streptococcus pneumoniae</i> (<i>Spn</i>), and serum bactericidal antibody (SBA) responses against <i>Haemophilus influenzae</i> type b (<i>Hib</i>). Cyto-/chemokines produced by isolated peripheral blood mononuclear cells (PBMC) were assayed using a Multiplex system. Multivariable linear regression analyses revealed that maternal (<i>p</i>&#x2009;&lt;&#x2009;0.01) and child (<i>p</i>&#x2009;=&#x2009;0.02) U-As were positively associated with plasma LL-37 levels. Decreased MDM-mediated <i>Spn</i> killing (<i>p</i>&#x2009;=&#x2009;0.05) and SBA responses (<i>p</i>&#x2009;=&#x2009;0.02) were seen to be each associated with fractions of mono-methylarsonic acid (MMA; a U-As metabolite) in the children. In addition, U-As levels were seen to be negatively associated with PBMC formation of fractalkine and IL-7, and positively associated with that for IL-13, IL-17 and MIP-1&#x3b1;. These findings suggested that early-life As exposure may disrupt the innate host defense pathway in these children. It is possible that such disruptions may have health consequences later in life.