Abstract
BackgroundArsenic and cadmium are environmental pollutants, and although the evidence for adverse immune effects after prenatal arsenic and cadmium exposures is increasing, little is known about the underlying immunological mechanisms.MethodsWe investigated the relationship between prenatal arsenic and cadmium exposures and a variety of T cell subpopulations measured in cord blood for 63 participants in the New Hampshire Birth Cohort Study. Post-partum toenail concentrations of arsenic and cadmium were used as an estimate of maternal exposure during pregnancy. The characteristics of cord blood proportions of T lymphocytes and subpopulations (expression of markers for Th1, Th2, Th17, Th1Th17, induced and natural regulatory T cells and NKTs) are presented.ResultsIn regression analyses, maternal arsenic exposure levels were inversely associated with cord blood T helper memory cells (-21%, 95% CI: -36%, -3%) and the association was found to be stronger in females. They were also inversely associated with activated T helper memory cells, particularly in males (-26%, 95% CI: -43%, -3%). Similarly, inverse associations were observed between cadmium exposure levels and activated T helper memory cells (-16%, 95% CI: -30%, -1%) and also for T helper memory cells in females (-20%, 95% CI: -35%, -3%).ConclusionThe results suggest that prenatal exposures to relatively low levels of arsenic and cadmium may contribute to altered distribution of T cell populations at birth. These changes in theory, could have contributed to the previously reported immunosuppressive effects observed later in infancy/childhood.
Highlights
Inorganic arsenic and cadmium are ranked at first and seventh, respectively, by the Agency of Toxic Substances and Disease Registry in the 2015 priority list of hazardous substances in the United States [1]
Maternal arsenic exposure levels were inversely associated with cord blood T helper memory cells (-21%, 95% CI: -36%, -3%) and the association was found to be stronger in females
The results suggest that prenatal exposures to relatively low levels of arsenic and cadmium may contribute to altered distribution of T cell populations at birth
Summary
Inorganic arsenic and cadmium are ranked at first and seventh, respectively, by the Agency of Toxic Substances and Disease Registry in the 2015 priority list of hazardous substances in the United States [1]. Millions are chronically exposed via drinking water to arsenic levels above the limit of 0.01 mg/L set by the World Health Organization [2]. The evidence for adverse immune effects after prenatal arsenic and cadmium exposures is increasing, data from human studies are limited and little is known about the underlying immunological mechanisms of these developmental contaminants. Increasing cadmium body burden in children has been reported to be associated with immunosuppressive effects [5]. Cadmium exposure in mothers was associated with altered DNA methylation profiles in leukocytes obtained from mothers and cord blood [7]. Arsenic and cadmium are environmental pollutants, and the evidence for adverse immune effects after prenatal arsenic and cadmium exposures is increasing, little is known about the underlying immunological mechanisms
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