Effects of Conventional and Organic Insecticides on the Lacewing Chrysoperla rufilabris (Neuroptera: Chrysopidae), 2015

Laboratory experiments were conducted to assess the toxicity and residual effects of 14 selected insecticides (conventional and organic) on the green lacewing Chrysoperla rufilabris (Burmeister) (Neuroptera: Chrysopidae). The insecticides tested were: the carbamates carbaryl (Sevin 80WSP at 2.3 lbs/acre) and methomyl (Lannate LV at 1.9 pts/acre); the organophosphates malathion (Malathion 8 Aquamul at 1.3 pts/acre) and phosmet (Imidan 70WP at 2.7 lbs/acre); the pyrethroids bifenthrin (Bifenture 10DF at 10.7 oz/acre) and fenpropathrin (Danitol 2.4EC at 13.3 fl oz/acre); the neonicotinoids acetamiprid (Assail 30SG at 3.9 oz/acre) and imidacloprid (Admire Pro at 1.9 fl oz/acre); the insect growth regulators (IGRs) novaluron (Rimon 0.83EC at 21 fl oz/acre) and methoxyfenozide (Intrepid 2F at 10 fl oz/acre); the diamines chlorantraniliprole (Altacor 35WG at 3.8 oz/acre) and cyantraniliprole (Exirel 10SE at 15.3 fl oz/acre); and the organic insecticides Bacillus thuringiensis Berliner (Bt) (Dipel DF at 1.3 lbs/acre) and azadirachtin (Aza-Direct at 1.5 fl oz/acre). These insecticides were selected because they are recommended in berry crops, i.e., highbush blueberry (Vaccinium corymbosum L.) and cranberry (Vaccinium macrocarpon Aiton), to control insect pests in the United States. Adult males and females of C. rufilabris were exposed to two rates of each insecticide: (1) a recommended label rate for berry crops such as blueberries and cranberries (i.e., the rates indicated above), and (2) a rate equivalent to half of the recommended label rate (i.e., a ‘residual’ rate). In addition, an untreated control (deionized water) was included; for a total of 15 treatments.

All experiments were conducted at the Rutgers P.E. Marucci Center for Blueberry and Cranberry Research and Extension in Chatsworth, New Jersey (United States). Treatments were applied to the inner surfaces of (47-mm diameter) plastic Petri dish bottoms (Fisher, Pittsburgh, PA) using a Potter precision spray tower (Burkard Scientific, Uxbridge, United Kingdom), with an output equivalent to 284 liters per ha (30 gal/acre) spray volume. The tops of the Petri dishes were covered with a white mesh (0.1 mm pore size) to provide ventilation. One C. rufilabris male or female was placed in each Petri dish, and insects and Petri dishes were maintained in a laboratory at 20 ± 5°C and a photoperiod of 16:8 (L:D) h. Adults of C. rufilabris (mixed sexes, unknown age) were obtained in a single container from Rincon-Vitova Insectaries, Inc. (Ventura, CA), used within 4 d after arrival, and thus assumed mated. In addition, a mix of honey and yeast (as food source) and a piece of wet cotton (as water source) were added to each Petri dish. A total of 16 and 18 replicates (individual Petri dishes = a replicate) per treatment and sex combination were used for the recommended and residual rates, respectively. Adult mortality and the number of eggs laid were recorded at 2, 24, 48, and 72 h after insecticide exposure. Insects that were not moving or did not move when touched with a probe were considered dead. Percent mortality (at each time point) and total number of eggs laid (sum of all eggs laid per female for all four time points) were analyzed using analysis of variance (ANOVA) (Minitab, State College, PA). Percent data were arcsin(sqrt(x/100)) transformed before ANOVA. Means were compared at P ≤ 0.05 significance level using Tukey Pairwise Comparisons tests. We also used Pearson correlation (Minitab) to correlate female final (72 h) mortality with the total number of eggs laid.

Recommended Label Rate

For C. rufilabris males, there were significant differences in adult mortality among treatments at 2 h (F = 11.81, df = 14, 225, P < 0.001), 24 h (F = 21.62, df = 14, 225, P < 0.001), 48 h (F = 18.96, df = 14, 225, P < 0.001), and 72 h (F = 20.37, df = 14, 225, P < 0.001) after insecticide exposure. Similarly, for C. rufilabris females, there were significant differences in adult mortality among treatments at 2 h (F = 3.23, df = 14, 225, P < 0.001), 24 h (F = 20.97, df = 14, 225, P < 0.001), 48 h (F = 27.73, df = 14, 225, P < 0.001), and 72 h (F = 18.74, df = 14, 225, P < 0.001) after insecticide exposure. For both males and females, the carbamates (carbaryl and methomyl), the organophosphates (malathion and phosmet), the pyrethroids (bifenthrin and fenpropathrin), and the neonicotinoids (acetamiprid and imidacloprid) caused the highest mortality, particularly after 24 h of exposure (Table 1). The diamides chlorantraniliprole and cyantraniliprole and the organic insecticide azadirachtin had moderate-to-high toxicity after 24 h of exposure (Table 1). The least toxic insecticides to C. rufilabris males were the IGRs novaluron and methoxyfenozide and the organic insecticide Bt, which were not different than the control (Table 1).

There were also significant differences among treatments on the number of eggs laid (F = 24.5, df = 14, 225, P < 0.001). The highest numbers of eggs were laid on the control and IGR (novaluron and methoxyfenozyde) treatments (Table 1). This was followed by the organic insecticides (Bt and azadirachtin) and then by the two diamides (chlorantraniliprole and cyantraniliprole). A significantly lower number of eggs were laid when females were exposed to the carbamate methomyl and the neonicotinoids acetamiprid and imidacloprid; although the lowest egg numbers were laid by females exposed to the broad-spectrum insecticides carbaryl, malathion, phosmet, bifenthrin, and fenpropathrin (Table 1). As expected, there was a significant negative correlation (Pearson correlation = −0.960, P < 0.001) between fecundity and female mortality, showing that C. rufilabris fecundity decreases as insecticide toxicity increases.

Half of Recommended Label (‘Residual’) Rate

For C. rufilabris males, there were significant differences in adult mortality among treatments at 2 h (F = 2.02, df = 14, 255, P = 0.017), 24 h (F = 24.66, df = 14, 255, P < 0.001), 48 h (F = 17.09, df = 14, 255, P < 0.001), and 72 h (F = 15.87, df = 14, 255, P < 0.001) after insecticide exposure. Similarly, for C. rufilabris females, there were significant differences in adult mortality among treatments at 2 h (F = 5.16, df = 14, 255, P < 0.001), 24 h (F = 11.47, df = 14, 255, P < 0.001), 48 h (F = 12.75, df = 14, 255, P < 0.001), and 72 h (F = 9.5, df = 14, 255, P < 0.001) after insecticide exposure. For both males and females, the carbamate carbaryl, the organophosphates (malathion and phosmet), and the pyrethroids (bifenthrin and fenpropathrin) were highly toxic, particularly after 24 h of exposure (Table 2). Although toxicity was still high, the carbamate methomyl and the neonicotinoids (acetamiprid and imidacloprid) had lower toxicities than carbaryl and the two organophosphates and two pyrethroids. Residual toxicity of all other insecticides including the diamides chlorantraniliprole and cyantraniliprole, the IGRs novaluron and methoxyfenozyde, and the organic insecticides azadirachtin and Bt were lower than 50% and not significantly different than the control (Table 2).

There were also significant differences among treatments on the number of eggs laid (F = 11.35, df = 14, 255, P < 0.001). The highest numbers of eggs were laid on the control followed closely by the organic insecticides (Bt and azadirachtin) and then by the IGRs (novaluron and methoxyfenozyde) (Table 2). Residual exposure to the two diamides (chlorantraniliprole and cyantraniliprole) resulted in half the number of eggs laid compared to the control. A significantly lower number of eggs was laid when females were exposed to the carbamate methomyl and the neonicotinoids acetamiprid and imidacloprid. However, the lowest egg numbers were laid by females exposed to the broad-spectrum insecticides phosmet, malathion, fenpropathrin, bifenthrin, and carbaryl (Table 2). We also found a negative correlation between C. rufilabris fecundity and female mortality (Pearson correlation = −0.929, P < 0.001).¹

Footnotes