Immunotoxicity of dibromoacetic acid administered via drinking water to female B₆C₃F₁ mice.
Dibromoacetic acid (DBA) is a disinfection by-product commonly found in drinking water as a result of chlorination/ ozonation processes. The Environmental Protection Agency estimates that more than 200 million people consume disinfected water in the United States. This study was conducted to evaluate the potential immunotoxicological effects of DBA exposure when administered for 28 days via drinking water to B₆C₃F₁ mice, at concentrations of 125, 500, and 1000 mg/L. Multiple endpoints were evaluated to assess innate, humoral, and cell-mediated immune components, as well as host resistance. Standard toxicological parameters were unaffected, with the exception of a dose-responsive increase in liver weight and a decrease in thymus weight at the two highest exposure levels. Splenocyte differentials were affected, although the effects were not dose-responsive. Exposure to DBA did not significantly affect humoral immunity (immunoglobulin M [IgM] plaque assay and serum IgM anti-sheep erythrocyte titers) or cell-mediated immunity (mixed-leukocyte response). No effects were observed on innate immune function in either interferon-γ-induced in vitro macrophage cytotoxic activity or basal natural killer (NK)-cell activity. Augmented NK-cell activity (following exposure to polyinosinic-polycytidylic acid) was decreased at the low dose, however the effect was not dose-responsive. Finally, DBA exposure had no effect on resistance to infection with either Streptococcus pneumoniae or Plasmodium yoelii, or challenge with B16F10 melanoma cells. With the exception of changes in thymus weight, these results indicate that DBA exposure resulted in no immunotoxic effects at concentrations much larger than those considered acceptable in human drinking water.
Department of Pharmacology and Toxicology, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA 23298, USA.
Matthew J
MJ
Smith
Dori R
DR
Germolec
Robert W
RW
Luebke
Christopher M
CM
Sheth
Wimolnut
W
Auttachoat
Tai L
TL
Guo
Kimber L
KL
White
D000085:Acetates / Q000008:administration & dosage*; D000818:Animals; D003602:Cytotoxicity, Immunologic / Q000187:drug effects; D004203:Disinfection; D005260:Female; D007110:Immunity, Active / Q000187:drug effects; D007111:Immunity, Cellular / Q000187:drug effects; D007113:Immunity, Innate / Q000187:drug effects; D008175:Lung Neoplasms / Q000188:drug therapy / Q000276:immunology* / Q000473:pathology; D008288:Malaria / Q000188:drug therapy / Q000276:immunology*; D008546:Melanoma, Experimental / Q000188:drug therapy / Q000276:immunology* / Q000473:pathology; D051379:Mice; D008815:Mice, Inbred Strains; D010967:Plasmodium yoelii / Q000276:immunology* / Q000472:pathogenicity; D011008:Pneumococcal Infections / Q000188:drug therapy / Q000276:immunology*; D013296:Streptococcus pneumoniae / Q000276:immunology* / Q000472:pathogenicity; D013950:Thymus Gland / Q000737:chemistry / Q000187:drug effects*; D014867:Water / Q000008:administration & dosage
D000085:Acetates; D014867:Water; C088674:dibromoacetic acid