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Disparities in cardiovascular risk from organophosphate‐based pesticide exposure in susceptible populations
Author(s) -
Smith Edward G,
Mack Cina M,
Gordon Christopher J
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a313
Subject(s) - blood pressure , medicine , genetic predisposition , organophosphate , contractility , population , physiology , cardiology , pesticide , environmental health , disease , biology , agronomy
High blood pressure (hypertension), the most common of all cardiovascular (CVD) diseases, is a major cause of morbidity and mortality in the United States, and a large percentage of the population manifests a genetic predisposition. Hypertension is polygenetically inherited, environmentally influenced, and involves numerous regulatory pathways. Organophosphate (OP)‐based pesticide exposure has been implicated in derangements in blood pressure regulation. In North Carolina, migrant workers of Mexican descent and rural African Americans work extensively in tobacco fields and farmlands where there is broad OP use. These populations have a higher incidence of hypertension and metabolic syndrome and therefore might be at greater risk for CVD from pesticide exposure. The purpose of this translational research is to study the effects of chlorpyrifos (CHP), an OP, on blood pressure regulation in the Spontaneously Hypertensive Rat (SHR). Four month old male SHR and WKY rats were implanted with radiotransmitters and dosed orally with CHP (25 mg/kg) or corn oil. In the SHRs CHP induced a transient increase in cardiac contractility, prolonged tachycardia and an exacerbated hypertensive responsive. Using the SHR strain as a model to study susceptible populations, our data suggest that individuals with a predisposition to hypertension may exhibit a differential sensitivity and increased vulnerability in terms of regulation of blood pressure, heart rate, cardiac contractility, and the development of CVD. This abstract does not necessarily reflect US EPA policy.