Purpose The onset of adolescence is a time of dramatic changes, including changes in sleep, and a time of new health concerns related to increases in risk-taking, sensation-seeking, depression, substance use, and accidents. As part of a larger study examining puberty-specific changes in adolescents' reward-related brain function, the current paper focuses on the relationship between functional neuroimaging measures of reward and measures of sleep. Methods 58 healthy participants age 11-13 completed a functional magnetic resonance imaging scan using a guessing task with monetary rewards and four-days of at home actigraphy and self-reported sleep ratings. Sleep variables included actigraph measures of mean weekend minutes asleep, sleep onset time, and sleep offset time, as well as self-reported sleep quality. Results During reward anticipation, less activation in the caudate (part of the ventral striatum) was associated with fewer minutes asleep, later sleep onset time, and lower sleep quality. During reward outcome, less caudate activation was associated with later sleep onset time, earlier sleep offset time, and lower sleep quality. Conclusions It has been hypothesized that adolescents' low reactivity in reward-related brain areas could lead to compensatory increases in reward-driven behavior. This study's findings suggest that sleep could contribute to such behavior. Because decreased sleep has been associated with risky behavior and negative mood, these findings raise concerns about a negative spiral whereby the effects of puberty and sleep deprivation may have synergistic effects on reward processing, contributing to adolescent behavioral and emotional health problems.

Sleep timing shifts later during adolescence, thus conflicting with early school start times. This can lead to irregular weekday-weekend schedules and circadian misalignment, which have been linked to depression and substance abuse, consistent with disruptions in the processing of rewards. We tested associations between weekend-weekday shifts in sleep timing and the neural response to monetary reward in healthy adolescents, using actigraphy and a functional magnetic resonance imaging paradigm. Region-of-interest analyses focused on the medial prefrontal cortex (mPFC) and striatum, both of which are implicated in reward function. Analyses adjusted for pubertal stage, sex, and total sleep time. Greater weekend-weekday advances in midsleep were associated with decreased mPFC and striatal reactivity to reward, which could reflect reduced regulatory response and reward sensitivity. We speculate that circadian misalignment associated with weekend shifts in sleep timing may contribute to reward-related problems such as depression and substance abuse.

Wildfire smoke is an increasing environmental health threat to which children are particularly vulnerable, for both physiologic and behavioral reasons. To address the need for improved public health messaging this review summarizes current knowledge and knowledge gaps in the health effects of wildfire smoke in children, as well as tools for public health response aimed at children, including consideration of low-cost sensor data, respirators, and exposures in school environments. There is an established literature of health effects in children from components of ambient air pollution, which are also present in wildfire smoke, and an emerging literature on the effects of wildfire smoke, particularly for respiratory outcomes. Low-cost particulate sensors demonstrate the spatial variability of pollution, including wildfire smoke, where children live and play. Surgical masks and respirators can provide limited protection for children during wildfire events, with expected decreases of roughly 20% and 80% for surgical masks and N95 respirators, respectively. Schools should improve filtration to reduce exposure of our nation's children to smoke during wildfire events. The evidence base described may help clinical and public health authorities provide accurate information to families to improve their decision making.

Background Reward behavior in animals is influenced by circadian genes, including clock-pathway genes such as Period2 (PER2). Several forms of psychiatric illness are associated with both altered reward function and disturbances in circadian function. The PER2 single nucleotide polymorphism (SNP) rs2304672 has been associated with psychiatric illnesses involving reward dysfunction. Associations among circadian genes, function in neural reward circuits, and circadian-influenced behavior have not yet been studied in humans, however. Methods 90 healthy adolescents underwent functional magnetic resonance imaging during a guessing task with monetary reward, genotyping for two PER2 SNPs (rs2304672, rs2304674), and actigraphy to measure sleep in their home environments. Weekend sleep midpoint, a behavioral index of circadian function, was derived from actigraphy. Puberty was measured by physical exam. Results The rs2304672 SNP predicted blood oxygenation level-dependent response to monetary reward as constrained by sleep midpoint. Later sleep midpoint was associated with reduced activity in a key component of reward circuitry, medial prefrontal cortex (mPFC; Brodmann area 9/10/32), to reward outcome (pcorrected < .05). G allele carriers showed reduced activity in mPFC relative to CC homozygotes. Conclusions Our findings are the first to indicate that circadian genes have a significant impact upon circadian-relevant reward circuitry in humans. These findings have the potential to elucidate gene-brain-behavior relationships underlying reward processing and psychopathology.

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BACKGROUND: Ozone effects on lung function are particularly important to understand in the context of the air pollution-health outcomes epidemiologic literature, given the complex relationships between ozone and other air pollutants with known lung function effects.RESEARCH QUESTION: What has been learned about the association between ozone exposures and lung function from epidemiology studies published from 2013 through 2020?

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BackgroundAsthma is a common childhood disease that leads to many missed days of school and parents’ work. There are multiple environmental contributors to asthma symptoms and understanding the potential factors inside children’s homes is crucial.MethodsThis is a dual cohort study measuring household particulate matter (PM2.5), behaviors, and factors that influence air quality and asthma symptoms in the urban homes of children (ages 6–10) with asthma; one cohort had cigarette smoke exposure in the home (n = 13) and the other did not (n = 22). Exposure data included measurements every 5 minutes for a month.ResultsIn the entire study population, a large contributor to elevations in indoor PM2.5 above 35 μg/m3 was not using the stove hood when cooking (8.5% higher, CI 3.1–13.9%, p<0.005). Median PM values during cooking times were 0.88 μg/m3 higher than those during non-cooking times (95% CI 0.33–1.42). Mean monthly household PM2.5 level was significantly related to the presence of a cigarette smoker in the home (10.1 μg/m3 higher, 95% CI 5.2–15.1, p<0.001) when controlling for use of the stove hood and proximity to major roadway. There was a trend toward increased odds of persistent asthma with increases in average monthly PM2.5 (OR 1.1, 95% CI 0.97–1.3, p = 0.16).ConclusionsConsideration of only outdoor PM2.5 may obscure potentially modifiable risks for asthma symptoms. Specifically, this preliminary study suggests that cooking behaviors may contribute to the burden of PM2.5 in the homes of children with asthma and thus to asthma symptoms.