Based on a multiwave, two-year prospective design, this study is the first to examine the extent to which multilocus hypothalamic–pituitary–adrenal axis (HPA axis)-related genetic variants, childhood maltreatment, and recent stress jointly predicted prospective changes in adolescent depressive symptoms. A theory-driven multilocus genetic profile score (MGPS) was calculated to combine the effects of six common polymorphisms within HPA-axis related genes (CRHR1, NR3C1, NR3C2, FKBP5, COMT, and HTR1A) in a sample of Chinese Han adolescents (N = 827; 50.2% boys; Mage = 16.45 ± 1.36 years). The results showed that the three-way interaction of HPA-axis related MGPS, childhood maltreatment and recent interpersonal, but not noninterpersonal, stress significantly predicted prospective changes in adolescent depressive symptoms. For adolescents with high but not low HPA-axis related MGPS, exposure to severe childhood maltreatment predisposed individuals more vulnerable to recent interpersonal stress, exhibiting greater prospective changes in adolescent depressive symptoms. The findings provide preliminary evidence for the cumulative risk mechanism regarding gene-by-environment-by-environment (G × E1 × E2) interactions that underlie the longitudinal development of adolescent depressive symptoms and show effects specific to interpersonal stress.

Stressful experiences affect biological stress systems, such as the hypothalamic–pituitary–adrenal (HPA) axis. Life stress can potentially alter regulation of the HPA axis and has been associated with poorer physical and mental health. Little, however, is known about the relative influence of stressors that are encountered at different developmental periods on acute stress reactions in adulthood. In this study, we explored three models of the influence of stress exposure on cortisol reactivity to a modified version of the Trier Social Stress Test (TSST) by leveraging 37 years of longitudinal data in a high-risk birth cohort (N = 112). The cumulative stress model suggests that accumulated stress across the lifespan leads to dysregulated reactivity, whereas the biological embedding model implicates early childhood as a critical period. The sensitization model assumes that dysregulation should only occur when stress is high in both early childhood and concurrently. All of the models predicted altered reactivity, but do not anticipate its exact form. We found support for both cumulative and biological embedding effects. However, when pitted against each other, early life stress predicted more blunted cortisol responses at age 37 over and above cumulative life stress. Additional analyses revealed that stress exposure in middle childhood also predicted more blunted cortisol reactivity.

Eight field studies were conducted over a 3-yr period from 2008 to 2010 in Ridgetown, Ontario, Canada, to determine the cumulative stress caused by simulated glyphosate spray drift followed by an in-crop application of metribuzin in processing tomato. As the simulated glyphosate spray drift rate increased so did the degree of injury to the tomatoes. At a simulated spray drift rate of 22.5 g ae ha−1 (2.5% of the recommended glyphosate field rate), a 23% decrease in red tomato yield was observed. Yield reductions increased to 88% of the control when 180 g ae ha−1 glyphosate (20% of the recommended field rate) was applied. Similarly when simulated spray drift rates were followed 3 to 5 d later with an in-crop application of metribuzin at 250 g ai ha−1, tomato yields decreased by 22 to 85% depending on glyphosate rate applied. A transient synergistic interaction was observed only when 22.5 g ae ha−1 glyphosate was followed by metribuzin. The synergistic response was no longer evident by the 28-d injury rating. Herbicide interactions were additive for crop injury, dry weight, fruit counts, and yield when glyphosate spray drift rates of 45, 90, or 180 g ae ha−1 were followed by metribuzin.

Simulated drift rates of bromoxynil followed by an in-crop application of metribuzin were applied to processing tomato in eight field studies conducted from 2008 to 2010 in Ridgetown, Ontario, Canada, to determine if a synergistic interaction occurred due to the cumulative herbicide application. A transient synergistic response was observed 7 d after treatment (DAT) when bromoxynil drift rates of 8.5, 17, and 34 g ai ha−1 were followed 3 to 5 d later by metribuzin at 250 g ai ha−1. By 28 DAT, visible injury ratings were additive for 8.5, 17, and 34 g ha−1 bromoxynil followed by metribuzin treatments. However, when bromoxynil at 68 g ha−1 (20% of field rate) was followed by metribuzin, a synergistic interaction was evident and remained through harvest. Based on Colby's equation there was greater visible injury than expected at 7, 14, and 28 DAT when bromoxynil at 68 g ha−1 was followed by metribuzin. A corresponding synergistic reduction of plant dry weight and marketable tomato yield, compared with the nontreated control, was identified. Marketable yields were expected to be 65% of the control according to Colby's equation, but observed yield reductions were 49% when bromoxynil at 68 g ha−1 was followed by metribuzin. In general, tomato plants sprayed with metribuzin after bromoxynil drift had greater injury than treatments sprayed with bromoxynil alone.

The use of biological control insects is a promising option for suppressing spotted knapweed, a nonindigenous perennial forb that infests more than 3 million hectares of North American rangeland. Efficacy increases when spotted knapweed is attacked by more than one phytophagous insect; however, combined herbivory by biological control insects has not achieved widespread suppression of spotted knapweed in North America. Here we expand the concept of combined herbivory beyond two or more species of biological control insects to include a vertebrate herbivore, specifically targeted grazing by domestic sheep. Our experiment on foothill rangeland in northwestern Montana evaluated spotted knapweed response to three treatments: (1) biological control insects only, (2) biological control insects + targeted sheep grazing applied in late July (spotted knapweed in late bud–early flower stage), and (3) biological control insects + targeted sheep grazing applied in mid-August (spotted knapweed in full-flower stage). We combined targeted sheep grazing with herbivory by three species of biological control insects: knapweed flower weevil, knapweed root weevil, and sulfur knapweed root moth. Treatments were applied during four consecutive years (2009 to 2012). Spotted knapweed fitness was suppressed more where targeted sheep grazing and biological control insects were combined vs. areas treated with biological control insects alone. Combined herbivory was effective when targeted sheep grazing was applied during either late July or mid-August, but July grazing was more effective. Spotted knapweed produced 96 to 99% fewer viable seeds in sheep-grazed areas. After 4 yr of treatment, total spotted knapweed plant density (seedlings, juvenile, and adult plants) was 86% less in July-grazed areas and 61% less in August-grazed areas than in areas treated with biological control insects alone. Combined herbivory by targeted sheep grazing and biological control insects reduced adult plant density and prevented compensatory recruitment of spotted knapweed, but treatment with biological control insects alone did not.

Despite the widespread assumption that racial differences in stress exist and that stress is a key mediator linking racial status to poor health, relatively few studies have explicitly examined this premise. We examine the distribution of stress across racial groups and the role of stress vulnerability and exposure in explaining racial differences in health in a community sample of Black, Hispanic, and White adults, employing a modeling strategy that accounts for the correlation between types of stressors and the accumulation of stressors in the prediction of health outcomes. We find significant racial differences in overall and cumulative exposure to eight stress domains. Blacks exhibit a higher prevalence and greater clustering of high stress scores than Whites. American-born Hispanics show prevalence rates and patterns of accumulation of stressors comparable to Blacks, while foreign-born Hispanics have stress profiles similar to Whites. Multiple stressors correlate with poor physical and mental health, with financial and relationship stressors exhibiting the largest and most consistent effects. Though we find no support for the stress-vulnerability hypothesis, the stress-exposure hypothesis does account for some racial health disparities. We discuss implications for future research and policy.