Bromide is a surprisingly potent larvicide for Anopheles gambiae in the laboratory

below 10 µM for its sodium potassium salt. This sensitivity is more than 10-fold greater than that observed for the sodium salts of fluoride, chloride and iodide. Bromide toxicity is stage-specific with An. gambiae larvae displaying 300-fold greater sensitivity than adults while eggs and pupae remain unaffected by 5 mM sodium bromide. Anopheles stephensi larvae exhibit similar sensitivity, whereas Aedes aegypti and Culex quinquefasciatus larvae are approximately 10-fold more tolerant of sodium bromide. Mechanistically, bromide toxicity operates independently of pathways targeted by conventional insecticides. Co-administration of diflubenzuron or spinosad neither suppressed nor enhanced bromide's effects. Bromide exposure induced overexpression of GluCl and CCC-2 ion channels without affecting Rdl, Best, or KCC expression. Chloride also protected against bromide toxicity, suggesting these halides share a common receptor. Thoracic swelling in dying larvae indicates that bromide disrupts osmotic or hydration balance. These findings are unexpected given that bromide is generally considered non-toxic to aquatic and terrestrial organisms, revealing a previously unknown vulnerability specific to Anopheles mosquitoes. The selective toxicity of bromide toward Anopheles larvae, combined with its independence from existing insecticide resistance mechanisms, may serve as a new lead for controlling malaria vectors. Targeting this bromide-sensitive pathway may complement current larvicidal approaches and provide an alternative for populations resistant to standard insecticides. The use of bromide itself will still require significant environmental and field-based studies prior to its possible application.