A Review of the Immunotoxicity of the Pesticide 3,4-Dichloropropionanalide

Abstract

The pesticide 3,4-dichloropropionanilide (propanil or, alternatively, DCPA) is a member of the acetanilide chemical family and is predominantly used for the control of weeds on commercial rice crops worldwide. This article was written to provide a brief review of the general toxicity of propanil followed by a detailed summary of the immunotoxicity studies that were performed to date in mammalian in vivo and in vitro models. Propanil affects the immune system at organ, cellular, and molecular levels. Studies demonstrated that it produces thymic atrophy and splenomegaly and decreases developing T- and B-cell populations in the thymus and bone marrow. Natural killer (NK) cells and macrophages are critical components of the innate immune system. NK cell cytotoxicity and the ability of macrophages to phagocytose, kill pathogenic bacteria, and produce inflammatory cytokines are suppressed by propanil. Propanil also affects the respiratory burst of macrophages, inhibiting reactive oxygen and nitrogen species production. Molecular mechanisms responsible for propanil's effects have begun to be elucidated and include alterations in nuclear factor (NF)-κB transcription factor activity and intracellular Ca²⁺ signaling. Propanil exposure alters a number of functions of mature T lymphocytes and B lymphocytes that impacts the adaptive immune response. T-cell cytotoxic activity and cytokine production are major T-cell functions inhibited by propanil. The humoral antibody response to model antigens and intact bacteria is differentially affected after propanil exposure. How these changes in innate and adaptive immune responses impact the host response to bacterial challenge or vaccination has begun to be examined.

K. D. Salazar and I. V. Ustyugova contributed equally to this work.

This work was supported by the National Institutes of Health, grants ES007512 (J.B.B.), ES011311 (J.B.B.), ES010953 (J.B.B.), and ES07460 (R.S.). The Flow Cytometric Core Facility is supported by the National Institutes of Health, grant RR16440. The authors also acknowledge all of the present and past members of the Barnett and Schafer laboratories for their contributions to the research cited here.

Present address for Keith Salazar, Phd, is Department of Molecular Biomedical Sciences, CVM Research Building, Box 8401, NCSU Campus, Raleigh, NC 27695, USA. [email protected]

Notes

∗Xie et al. (1997a) and Xie et al. (1997b) were originally published with incorrect doses for the in vitro studies. The doses cited here are the correct doses

∗Zhao et al. (1998) and Zhao et al. (1999) were originally published with incorrect doses for the in vitro studies. The doses cited here are the correct doses.