Characteristics and magnitude of acute pesticide-related illnesses and injuries associated with pyrethrin and pyrethroid exposures--11 states, 2000-2008.

BACKGROUND: Excluding disinfectants, pyrethrins and pyrethroids are the pesticides used most commonly in and around homes. Respiratory effects and paresthesia are among the concerns about pyrethrin/pyrethroid exposures. METHODS: Acute pesticide-related illness/injury cases were identified from the Sentinel Event Notification System for Occupational Risks-Pesticides Program and the California Department of Pesticide Regulation from 2000-2008. Characteristics and incidence rates were determined for acute pyrethrin/pyrethroid-related illness/injury cases. Logistic regression analyses were performed to determine odds of respiratory and dermal symptoms in persons with illness/injury following pyrethrin/pyrethroid exposure compared to persons with illness/injury following exposure to other pesticides. RESULTS: A total of 4,974 cases of acute pyrethrin/pyrethroid-related illness were identified. Incidence rates increased over time, reaching 8 cases/million population in 2008. The majority of cases were low severity (85%) and 34% were work-related. Respiratory effects were the most common symptoms reported (48%). Risk of acute respiratory effects were significantly elevated among persons exposed only to pyrethrins (adjusted odds ratio [aOR] 1.79; 95% confidence interval [95% CI]: 1.49-2.16), only to pyrethroids (aOR 1.99 95% CI: 1.77-2.24), to a mixture of pyrethroids (aOR 2.36; 95% CI: 1.99-2.81) or to a mixture containing both pyrethrins and pyrethroids (aOR 2.99; 95% CI: 2.33-3.84) compared to those with illness arising from exposure to other pesticides. The most common factors contributing to pyrethrin/pyrethroid-related illness included exposure from spills/splashes, improper storage, and failure to evacuate during pesticide application. CONCLUSIONS: The magnitude of acute pyrethrin/pyrethroid-related illness/injury is relatively low but is increasing. As such, additional measures to prevent them are needed.

slo K(+) channel gene regulation mediates rapid drug tolerance.

Changes in neural activity caused by exposure to drugs may trigger homeostatic mechanisms that attempt to restore normal neural excitability. In Drosophila, a single sedation with the anesthetic benzyl alcohol changes the expression of the slo K(+) channel gene and induces rapid drug tolerance. We demonstrate linkage between these two phenomena by using a mutation and a transgene. A mutation that eliminates slo expression prevents tolerance, whereas expression from an inducible slo transgene mimics tolerance in naive animals. The behavioral response to benzyl alcohol can be separated into an initial phase of hyperkinesis and a subsequent phase of sedation. The hyperkinetic phase causes a drop in slo gene expression and makes animals more sensitive to benzyl alcohol. It is the sedative phase that stimulates slo gene expression and induces tolerance. We demonstrate that the expression level of slo is a predictor of drug sensitivity.