Format

Send to

Choose Destination
J Immunotoxicol. 2019 Dec;16(1):201-209. doi: 10.1080/1547691X.2019.1657993.

Exposure to low-dose arsenic in early life alters innate immune function in children.

Author information

1
Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, NY, USA.
2
Infectious Diseases Division, icddr,b, Dhaka, Bangladesh.
3
Columbia University and University of Chicago Research office in Bangladesh, Dhaka, Bangladesh.
4
Laboratory Sciences and Services Division, ICDDR,B, Dhaka, Bangladesh.
5
Department of Public Health Sciences, University of Chicago, Chicago, IL, USA.

Abstract

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 years-of-age, mothers and participating children (N = 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, ex vivo monocyte-derived-macrophage (MDM)-mediated killing of Streptococcus pneumoniae (Spn), and serum bactericidal antibody (SBA) responses against Haemophilus influenzae type b (Hib). Cyto-/chemokines produced by isolated peripheral blood mononuclear cells (PBMC) were assayed using a Multiplex system. Multivariable linear regression analyses revealed that maternal (p < 0.01) and child (p = 0.02) U-As were positively associated with plasma LL-37 levels. Decreased MDM-mediated Spn killing (p = 0.05) and SBA responses (p = 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-1α. 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.

KEYWORDS:

Arsenic; LL-37; macrophage function; respiratory pathogens; serum bactericidal antibody response

Supplemental Content

Full text links

Icon for Taylor & Francis
Loading ...
Support Center