Cognitive Development and Prenatal Air Pollution Exposure in the CHAMACOS Cohort.

BACKGROUND: Because fine particulate matter [PM, with aerodynamic diameter ≤2.5µm (PM2.5)] is a ubiquitous environmental exposure, small changes in cognition associated with PM2.5 exposure could have great societal costs. Prior studies have demonstrated a relationship between in utero PM2.5 exposure and cognitive development in urban populations, but it is not known whether these effects are similar in rural populations and whether they persist into late childhood. OBJECTIVES: In this study, we tested for associations between prenatal PM2.5 exposure and both full-scale and subscale measures of IQ among a longitudinal cohort at age 10.5 y. METHODS: This analysis used data from 568 children enrolled in the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS), a birth cohort study in California's agricultural Salinas Valley. Exposures were estimated at residential addresses during pregnancy using state of the art, modeled PM2.5 surfaces. IQ testing was performed by bilingual psychometricians in the dominant language of the child. RESULTS: A 3-µg/m3 higher average PM2.5 over pregnancy was associated with -1.79 full-scale IQ points [95% confidence interval (CI): -2.98, -0.58], with decrements specifically in Working Memory IQ (WMIQ) and Processing Speed IQ (PSIQ) subscales [WMIQ -1.72 (95% CI: -2.98, -0.45) and PSIQ -1.19 (95% CI: -2.54, 0.16)]. Flexible modeling over the course of pregnancy illustrated mid-to-late pregnancy (months 5-7) as particularly susceptible times, with sex differences in the timing of susceptible windows and in which subscales were most affected [Verbal Comprehension IQ (VCIQ) and WMIQ in males; and PSIQ in females]. DISCUSSION: We found that small increases in outdoor PM2.5 exposure in utero were associated with slightly lower IQ in late childhood, robust to many sensitivity analyses. In this cohort there was a larger effect of PM2.5 on childhood IQ than has previously been observed, perhaps due to differences in PM composition or because developmental disruption could alter the cognitive trajectory and thus appear more pronounced as children get older. https://doi.org/10.1289/EHP10812.

Associations between prenatal and early-life air pollution exposure and lung function in young children: Exploring influential windows of exposure on lung development.

BACKGROUND: Evidence in the literature suggests that air pollution exposures experienced prenatally and early in life can be detrimental to normal lung development, however the specific timing of critical windows during development is not fully understood. OBJECTIVES: We evaluated air pollution exposures during the prenatal and early-life period in association with lung function at ages 6-9, in an effort to identify potentially influential windows of exposure for lung development. METHODS: Our study population consisted of 222 children aged 6-9 from the Fresno-Clovis metro area in California with spirometry data collected between May 2015 and May 2017. We used distributed-lag non-linear models to flexibly model the exposure-lag-response for monthly average exposure to fine particulate matter (PM2.5) and ozone (O3) during the prenatal months and first three years of life in association with forced vital capacity (FVC), and forced expiratory volume in the first second (FEV1), adjusted for covariates. RESULTS: PM2.5 exposure during the prenatal period and the first 3-years of life was associated with lower FVC and FEV1 assessed at ages 6-9. Specifically, an increase from the 5th percentile of the observed monthly average exposure (7.55 µg/m3) to the median observed exposure (12.69 µg/m3) for the duration of the window was associated with 0.42 L lower FVC (95% confidence interval (CI): -0.82, -0.03) and 0.38 L lower FEV1 (95% CI: -0.75, -0.02). The shape of the lag-response indicated that the second half of pregnancy may be a particularly influential window of exposure. Associations for ozone were not as strong and typically CIs included the null. CONCLUSIONS: Our findings indicate that prenatal and early-life exposures to PM2.5 are associated with decreased lung function later in childhood. Exposures during the latter months of pregnancy may be especially influential.

The Association between Ambient PM2.5 and Low Birth Weight in California.

Previous studies have shown associations between air pollutants and low birth weight. However, few studies assess whether poverty and race/ethnicity are effect modifiers for this relationship. We used publicly available data on 7785 California census tracts from the California Communities Environmental Health Screening Tool (CalEnviroScreen). Multivariable linear regression was used to examine the association between outdoor PM2.5 and low birth weight (LBW), including stratification by poverty and race/ethnicity (as a proxy for experienced racism). A 1 µg m-3 increase in PM2.5 was associated with a 0.03% (95% CI: 0.01, 0.04) increase in the percentage of LBW infants in a census tract. The association between PM2.5 and LBW was stronger in census tracts with the majority living in poverty (0.06% increase; 95% CI: 0.03, 0.08) compared to those with fewer people living in poverty (0.02% increase; 95% CI: 0.00, 0.03). Our results show that exposure to outdoor PM2.5 is associated with a small increase in the percentage of LBW infants in a census tract, with a further increase in tracts with high poverty. The results for effect modification by race/ethnicity were less conclusive.

Traffic-related air pollution, biomarkers of metabolic dysfunction, oxidative stress, and CC16 in children.

BACKGROUND: Previous research has revealed links between air pollution exposure and metabolic syndrome in adults; however, these associations are less explored in children. OBJECTIVE: This study aims to investigate the association between traffic-related air pollutants (TRAP) and biomarkers of metabolic dysregulation, oxidative stress, and lung epithelial damage in children. METHODS: We conducted cross-sectional analyses in a sample of predominantly Latinx, low-income children (n = 218) to examine associations between air pollutants (nitrogen dioxide (NO2), nitrogen oxides (NOx), elemental carbon, polycyclic aromatic hydrocarbons, carbon monoxide (CO), fine particulates (PM2.5)) and biomarkers of metabolic function (high-density lipoprotein (HDL), hemoglobin A1c (HbA1c), oxidative stress (8-isoprostane), and lung epithelial damage (club cell protein 16 (CC16)). RESULTS: HDL cholesterol showed an inverse association with NO2 and NOx, with the strongest relationship between HDL and 3-month exposure to NO2 (-15.4 mg/dL per IQR increase in 3-month NO2, 95% CI = -27.4, -3.4). 8-isoprostane showed a consistent pattern of increasing values with 1-day and 1-week exposure across all pollutants. Non-significant increases in % HbA1c were found during 1-month time frames and decreasing CC16 in 3-month exposure time frames. CONCLUSION: Our results suggest that TRAP is significantly associated with decreased HDL cholesterol in longer-term time frames and elevated 8-isoprostane in shorter-term time frames. TRAP could have the potential to influence lifelong metabolic patterns, through metabolic effects in childhood.

Systematic Review of Ozone Effects on Human Lung Function, 2013 Through 2020.

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? STUDY DESIGN AND METHODS: On March 18, 2018, and September 8, 2020, PubMed was searched using the terms health AND ozone, filtering to articles in English and about humans, from 2013 or later. An additional focused review searching for ozone AND (lung function OR FEV1OR FVC) was performed June 26, 2021. Articles were selected for this review if they reported a specific relationship between a lung function outcome and ozone exposure. RESULTS: Of 3,271 articles screened, 53 ultimately met criteria for inclusion. A systematic review with assessment of potential for bias was conducted, but a meta-analysis was not carried out because of differences in exposure duration and outcome quantification. Consistent evidence exists of small decreases in children's lung function, even associated with very low levels of short-term ozone exposure. The effects on adult lung function from exposure to low-level, short-term ozone are less clear, although ozone-associated decrements may occur in the elderly. Finally, long-term ozone exposure decreases both lung function and lung function growth in children, although few new studies have examined long-term ozone and lung function in adults. INTERPRETATION: Much of this literature involves concentrations below the current US Environmental Protection Agency's National Ambient Air Quality Standard of 70 parts per billion over an 8-h averaging time, suggesting that this current standard may not protect children adequately from ozone-related decrements in lung function.

No fire without smoke (particles).

Pollution from landscape fires, which are increasing with climate change, leads to babies being born with lower birthweights in low- and middle-income countries.

Traffic-related air pollution is associated with glucose dysregulation, blood pressure, and oxidative stress in children.

BACKGROUND: Metabolic syndrome increases the risk of cardiovascular disease in adults. Antecedents likely begin in childhood and whether childhood exposure to air pollution plays a contributory role is not well understood. OBJECTIVES: To assess whether children's exposure to air pollution is associated with markers of risk for metabolic syndrome and oxidative stress, a hypothesized mediator of air pollution-related health effects. METHODS: We studied 299 children (ages 6-8) living in the Fresno, CA area. At a study center visit, questionnaire and biomarker data were collected. Outcomes included hemoglobin A1c (HbA1c), urinary 8-isoprostane, systolic blood pressure (SBP), and BMI. Individual-level exposure estimates for a set of four pollutants that are constituents of traffic-related air pollution (TRAP) - the sum of 4-, 5-, and 6-ring polycyclic aromatic hydrocarbon compounds (PAH456), NO2, elemental carbon, and fine particulate matter (PM2.5) - were modeled at the primary residential location for 1-day lag, and 1-week, 1-month, 3-month, 6-month, and 1-year averages prior to each participant's visit date. Generalized additive models were used to estimate associations between each air pollutant exposure and outcome. RESULTS: The study population was 53% male, 80% Latinx, 11% Black and largely low-income (6% were White and 3% were Asian/Pacific Islander). HbA1c percentage was associated with longer-term increases in TRAP; for example a 4.42 ng/m3 increase in 6-month average PAH456 was associated with a 0.07% increase (95% CI: 0.01, 0.14) and a 3.62 µg/m3 increase in 6-month average PM2.5 was associated with a 0.06% increase (95% CI: 0.01, 0.10). The influence of air pollutants on blood pressure was strongest at 3 months; for example, a 6.2 ppb increase in 3-month average NO2 was associated with a 9.4 mmHg increase in SBP (95% CI: 2.8, 15.9). TRAP concentrations were not significantly associated with anthropometric or adipokine measures. Short-term TRAP exposure averages were significantly associated with creatinine-adjusted urinary 8-isoprostane. DISCUSSION: Our results suggest that both short- and longer-term estimated individual-level outdoor residential exposures to several traffic-related air pollutants, including ambient PAHs, are associated with biomarkers of risk for metabolic syndrome and oxidative stress in children.

Health effects of wildfire smoke in children and public health tools: a narrative review.

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.

Differences in the Estimation of Wildfire-Associated Air Pollution by Satellite Mapping of Smoke Plumes and Ground-Level Monitoring.

Wildfires, which are becoming more frequent and intense in many countries, pose serious threats to human health. To determine health impacts and provide public health messaging, satellite-based smoke plume data are sometimes used as a proxy for directly measured particulate matter levels. We collected data on particulate matter <2.5 µm in diameter (PM2.5) concentration from 16 ground-level monitoring stations in the San Francisco Bay Area and smoke plume density from satellite imagery for the 2017-2018 California wildfire seasons. We tested for trends and calculated bootstrapped differences in the median PM2.5 concentrations by plume density category on a 0-3 scale. The median PM2.5 concentrations for categories 0, 1, 2, and 3 were 16, 22, 25, and 63 µg/m3, respectively, and there was much variability in PM2.5 concentrations within each category. A case study of the Camp Fire illustrates that in San Francisco, PM2.5 concentrations reached their maximum many days after the peak for plume density scores. We found that air pollution characterization by satellite imagery did not precisely align with ground-level PM2.5 concentrations. Public health practitioners should recognize the need to combine multiple sources of data regarding smoke patterns when developing public guidance to limit the health effects of wildfire smoke.

Do we know how best to disinfect child care sites in the United States? A review of available disinfectant efficacy data and health risks of the major disinfectant classes.

BACKGROUND: Children in child care settings have a high infectious burden. They are frequently exposed to sanitizing and disinfecting agents, whose toxicities have not been studied in these settings. Current guidance on the preferred disinfection agents for child care is vague. METHODS: This article combines 2 different sources of information: the Environmental Protection Agency registration data on the efficacy of hospital-grade disinfectants and a review of the research on the toxicities of the most common of these disinfectants to summarize information that could be used for more evidence-based early care and education disinfection regulations and guidelines. RESULTS: Coverage of these organisms varied both between disinfectant classes (defined by active ingredient), as well as within classes. The 3 most common active ingredients in the database-quaternary ammonias, bleaches, and hydrogen peroxides-had 251, 63, and 31 products, respectively. Quaternary ammonias and bleaches are both known asthmagens, with the potential for toxic gas release when mixed. Quaternary ammonias may also cause reproductive toxicity. Disinfectant-grade peroxides have relatively low inhalational toxicity. CONCLUSIONS: A clear rationale is needed to establish policies for determining preferable disinfection products for use in child care settings, based on efficacy against relevant pathogens, toxicity, ease of use, and cost. When other factors are equal, the use of peroxide-based disinfectant products is recommended to minimize inhalational toxicity.

Cooking behaviors are related to household particulate matter exposure in children with asthma in the urban East Bay Area of Northern California.

BACKGROUND: Asthma 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. METHODS: This 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. RESULTS: In 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). CONCLUSIONS: Consideration 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.

Weekend-weekday advances in sleep timing are associated with altered reward-related brain function in healthy adolescents.

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.

PER2 rs2304672 polymorphism moderates circadian-relevant reward circuitry activity in adolescents.

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 (p(corrected) < .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.

Reward-related brain function and sleep in pre/early pubertal and mid/late pubertal adolescents.

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 article focuses on the relationship between functional neuroimaging measures of reward and measures of sleep. METHODS: A total of 58 healthy participants 11-13 years of age completed a functional magnetic resonance imaging scan using a guessing task with monetary rewards and 4 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.