Abstract
Exposure to arsenic (As) is a global public health problem because of its association with various cancers and numerous other pathological effects, and millions of people worldwide are exposed to As on a regular basis. Increasing lines of evidence indicate that As may adversely affect the immune system, but its specific effects on immune function are poorly understood. Therefore, we conducted a literature search of non-cancer immune-related effects associated with As exposure and summarized the known immunotoxicological effects of As in humans, animals and in vitro models. Overall, the data show that chronic exposure to As has the potential to impair vital immune responses which could lead to increased risk of infections and chronic diseases, including various cancers. Although animal and in vitro models provide some insight into potential mechanisms of the As-related immunotoxicity observed in human populations, further investigation, particularly in humans, is needed to better understand the relationship between As exposure and the development of disease.
Highlights
Exposure to arsenic (As) is a global public health concern because As is widely distributed and associated with numerous adverse effects
Proposed mechanisms of toxicity include oxidative stress, inhibition of DNA repair, chromosomal aberrations, micronuclei formation, induction of apoptosis, modification of cellular signaling via altered activation, expression and DNA binding activity of transcription factors, epigenetic modifications resulting in aberrant gene expression, and altered phenotype of stem cell populations [12,13,14,15,16]
Human β-defensin-1 (HBD1) involvement Interestingly, we previously reported in two As-exposed populations from Nevada and Chile a significant inverse correlation in men between urinary levels of As and antimicrobial peptide human β-defensin-1 (HBD1) [50]
Summary
Exposure to arsenic (As) is a global public health concern because As is widely distributed and associated with numerous adverse effects. Lowdose As-mediated increased number of splenic nTreg lymphocytes inhibited generation of (auto-) immune responses, the beneficial effect of immunosuppression by low-dose As. two possible scenarios whereby As can interfere with self/non-self recognition exist: by i) preventing immune surveillance from recognizing “non-self” from “self”, leading to increased non-self antigen survival, as in allograft transplantation; or ii) inhibiting recognition of self antigens as “self”, which could arise from As-induced reduction of nTreg cell inhibitory activity, leading to “anti-self” antibody production indicative of autoimmune disease. Two possible scenarios whereby As can interfere with self/non-self recognition exist: by i) preventing immune surveillance from recognizing “non-self” from “self”, leading to increased non-self antigen survival, as in allograft transplantation; or ii) inhibiting recognition of self antigens as “self”, which could arise from As-induced reduction of nTreg cell inhibitory activity, leading to “anti-self” antibody production indicative of autoimmune disease Such effects would likely render the host immunocompromised and could have detrimental health consequences. The later study did not examine other immune functional parameters [109]; it stands to reason that As concentrations used were insufficient to achieve immunosuppressive effects
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