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Autism Spectrum Disorder (ASD) affects about 1 in 44 children and environmental exposures may contribute to disease onset. Air pollution has been associated with adverse neurobehavioral outcomes, yet little research has examined its association with autistic-like behaviors. Therefore, our objective was to examine the association between exposure to air pollution, including NO 2 and PM 2.5 , during pregnancy and the first year of life to ASD-like behaviors during childhood. Participants (n = 435) enrolled in the Cincinnati Childhood Allergy and Air Pollution Study and the Health Outcomes and Measures of the Environment Study were included in the analysis. Daily exposures to NO 2 and PM 2.5 at the residential addresses of participants were estimated using validated spatiotemporal models and averaged to obtain prenatal and first year exposure estimates. ASD-like behaviors were assessed via the Social Responsiveness Scale (SRS) questionnaire at age 12. Linear regression models adjusting for confounders were applied to estimate the association between pollutants and SRS scores. After adjusting for covariates, the association between NO 2 and PM 2.5 and SRS scores remained positive but were no longer statistically significant. Prenatal and first year exposure to NO 2 were associated with total SRS T-scores with an estimated 0.4 point increase (95% CI: -0.7, 1.6) per 5.2 ppb increase in NO 2 exposure and 0.7 point (95% CI: -0.3, 1.6) per 4.2 ppb increase in NO 2 exposure, respectively. For PM 2.5 , a 2.6 μg/m 3 increase in prenatal exposure was associated with a 0.1 point increase (95% CI: -1.1, 1.4) in SRS Total T-scores and a 1.3 μg/m 3 increase first year of life was associated with a 1 point increase (95% CI: -0.2, 2.3). In summary, exposure to NO 2 and PM 2.5 during pregnancy and the first year of life were not significantly associated with higher autistic-like behaviors measured with SRS scores after adjustment of covariates. Additional research is warranted given prior studies suggesting air pollution contributes to ASD., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Background: While air pollution has been associated with depression and anxiety in adults, its impact on childhood mental health is understudied., Objective: We examined lifetime exposure to traffic-related air pollution (TRAP) and symptoms of depression and anxiety at age 12 years in the Cincinnati Childhood Allergy and Air Pollution Study cohort., Methods: We estimated exposure to elemental carbon attributable to traffic (ECAT), a surrogate of diesel exhaust, at birth, age 12 years, and average exposure throughout childhood, using a validated land use regression model. We assessed depression and anxiety at age 12 years by parent report with the Behavior Assessment System for Children-2, and by child report with the Child Depression Inventory-2 (CDI-2) and the Spence Children's Anxiety Scale (SCAS). Associations between TRAP at birth, age 12 years, and childhood average and mental health outcomes were estimated using linear regression models adjusting for covariates including parent depression, secondhand smoke exposure, race, household income, and others., Results: Exposure to ECAT was not significantly associated with parent-reported depression or anxiety. However, exposure to ECAT at birth was associated with increased child-reported depression and anxiety. Each 0.25 µg/m 3 increase in ECAT was associated with a 3.5 point increase (95% CI 1.6-5.5) in CDI-2 scores and 2.3 point increase (95% CI 0.8-3.9) in SCAS total anxiety scores. We observed similar associations between average childhood ECAT exposures but not for concurrent exposures at age 12., Conclusions: TRAP exposure during early life and across childhood was significantly associated with self-reported depression and anxiety symptoms in children. The negative impact of air pollution on mental health previously reported among adults may also be present during childhood., (Copyright © 2019. Published by Elsevier Inc.)

Rationale: The timing and duration of traffic-related air pollution (TRAP) exposure may be important for childhood wheezing and asthma development., Objectives: We examined the relationship between TRAP exposure and longitudinal wheezing phenotypes and asthma at age 7 years., Methods: Children completed clinical examinations annually from age 1 year through age 4 years and age 7 years. Parental-reported wheezing was assessed at each age, and longitudinal wheezing phenotypes (early-transient, late-onset, persistent) and asthma were defined at age 7 years. Participants' time-weighted exposure to TRAP, from birth through age 7 years, was estimated using a land-use regression model. The relationship between TRAP exposure and wheezing phenotypes and asthma was examined., Measurements and Main Results: High TRAP exposure at birth was significantly associated with both transient and persistent wheezing phenotypes (adjusted odds ratio [aOR] = 1.64; 95% confidence interval [CI], 1.04-2.57 and aOR = 2.31; 95% CI, 1.28-4.15, respectively); exposure from birth to age 1 year and age 1 to 2 years was also associated with persistent wheeze. Only children with high average TRAP exposure from birth through age 7 years were at significantly increased risk for asthma (aOR = 1.71; 95% CI, 1.01-2.88)., Conclusions: Early-life exposure to TRAP is associated with increased risk for persistent wheezing, but only long-term exposure to high levels of TRAP throughout childhood was associated with asthma development.

Background: Ultrafine particles (UFPs) have been associated with adverse health outcomes in children, but studies are often limited by surrogate estimates of exposure. Accurately characterizing children's personal exposure to UFP is difficult due to the high spatiotemporal variability of UFP and children's time-activity patterns., Objective: The objectives of this study were to conduct a field test of a personal sensor for UFP (PUFP) by measuring UFP exposure among children and assess the sensor's capabilities and limitations., Methods: Children wore the sensor at school, during transit periods between school and home, and in their home for 2-4h on 2 consecutive days and provided feedback regarding their experience with the sensor. The PUFP sensor recorded UFP number concentration at one second intervals and recorded GPS location allowing for comparisons of UFP exposure at homes, schools, and during transit. A mixed-effects linear model was used to compare the effect of microenvironment on personal UFP measurements., Results: The overall total median personal exposure to UFP was 12,900 particles/cm(3) (p/cm(3)). Median UFP exposure at homes, schools and during transit was 17,800, 11,900, and 13,600 p/cm(3), respectively. Results of the mixed-effects model found that riding in a car and walking were significantly associated with 1.36 (95% CI 1.33-1.39) and 2.51 (95% CI 2.44-2.57) times higher UFP concentrations compared to the home., Conclusions: The PUFP sensor can measure near real-time exposure to UFP with high spatiotemporal resolution. Children's exposure to UFP varies by location, with increased exposure during transit to and from school., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Though studies have investigated the association between air pollution and respiratory health outcomes in children, few have focused on night cough. The study objective was to simultaneously evaluate family factors (i.e., race, gender, maternal and paternal asthma, and breastfeeding), health (allergen sensitization and wheezing symptoms), home factors (dog, cat, mold, endotoxin, and dust mite), and other environmental exposures (traffic exhaust and second-hand tobacco smoke) for associations with recurrent dry night cough (RNC) during early childhood. A structural equation model with repeat measures was developed assessing RNC at ages one, two, and three. The prevalence of RNC was relatively large and similar at ages, one, two, and three at 21.6%, 17.3%, and 21.1%, respectively. Children exposed to the highest tertile of traffic exhaust had an estimated 45% increase in risk of RNC compared with children less exposed (adjusted OR 1.45, 95% CI: 1.09, 1.94). Also, wheezing was associated with a 76% higher risk of RNC (adjusted OR 1.76, 95% CI: 1.36, 2.26). A protective trend for breastfeeding was found with a 27% reduction in risk associated with breastfeeding (adjusted OR 0.73, 95% CI: 0.53, 1.01). No other factors were significant. These results suggest that traffic exhaust exposure may be a risk factor for night cough in young children.

Rationale: Murine models demonstrate a synergistic production of reactive oxygen species on coexposure to diesel exhaust particles and endotoxin., Objectives: It was hypothesized that coexposure to traffic-related particles and endotoxin would have an additive effect on persistent wheezing during early childhood., Methods: Persistent wheezing at age 36 months was assessed in the Cincinnati Childhood Allergy and Air Pollution Study, a high-risk birth cohort. A time-weighted average exposure to traffic-related particles was determined by applying a land-use regression model to the homes, day cares, and other locations where children spent time from birth through age 36 months. Indoor levels of endotoxin were measured from dust samples collected before age 12 months. The relationship between dichotomized (or=75th percentile) traffic-related particle and endotoxin exposure and persistent wheezing, controlling for potential covariates, was examined., Measurements and Main Results: Persistent wheezing at age 36 months was significantly associated with exposure to increased levels of traffic-related particles before age 12 months (OR = 1.75; 95% confidence interval, 1.07-2.87). Coexposure to endotoxin had a synergistic effect with traffic exposure on persistent wheeze (OR = 5.85; 95% confidence interval, 1.89-18.13) after adjustment for significant covariates., Conclusions: The association between traffic-related particle exposure and persistent wheezing at age 36 months is modified by exposure to endotoxin. This finding supports prior toxicological studies demonstrating a synergistic production of reactive oxygen species after coexposure to diesel exhaust particles and endotoxin. The effect of early versus later exposure to traffic-related particles, however, remains to be studied because of the high correlation between exposure throughout the first 3 years of life.

The objective of our study was to investigate the association between daily pediatric asthma hospital visits and daily concentrations of aeroallergens and their specific species. Records of daily asthma visits in Cincinnati area were retrieved from Cincinnati Children's Hospital Medical Center and aeroallergen sampling was performed by the Button Inhalable Sampler. The Poisson generalized linear model was carried out in which the log of the number of asthma hospital visits was related to aeroallergen level, treated as a continuous variable with adjustment for seasonal time trend, day of the week, ozone and PM(2.5) concentrations, temperature and humidity. The aeroallergens having a significant impact on asthma hospital visits were ragweed, oak/maple and Pinaceae pollen. Their relative risks on asthma hospital visits with respect to a 100 counts/m(3) increase in concentration were in the range of 1.23 to 1.54. The effects in causing the asthma exacerbation were delayed by 3 or 5 days.

In this study, we have examined the relationships between the concentrations of ambient inhalable airborne fungi and pollen with PM10, PM2.5, ozone, organic carbon, selected trace metals (cadmium, copper, lead, and zinc), temperature, and relative humidity. The database was collected in Cincinnati, Ohio, USA, during two consecutive years. Measurements of all environmental variables were performed at the same site continuously 5 days a week except during winter months. The airborne concentrations of biological and non-biological pollutants ranged as follows: total fungi: 184-16 979 spores m(-3); total pollen: 0-6692 pollen m(-3); PM10: 6.70-65.38 microg m(-3); PM2.5: 5.04-45.02 microg m(-3); and ozone: 2.54-64.17 ppb. Higher levels of total inhalable fungi and particulate matter were found during fall and summer months. In contrast, total pollen concentration showed elevated levels in spring. Peak concentrations of ozone were observed during summer and beginning of fall. Our study concluded that several types of inhalable airborne fungi and pollen, particulate matter, and ozone could be positively correlated as a result of the atmospheric temperature influence.

The objective of this study was to determine if there is an exposure gradient in particulate matter concentrations for people living near interstate highways, and to determine how far from the highway the gradient extends. Air samples were collected in a residential area of Greater Cincinnati in the vicinity of two major highways. The measurements were conducted at different distances from the highways by using ultrafine particle counters (measurement range: 0.02-1 microm), optical particle counters (0.3-20 microm), and PM2.5 Harvard Impactors (0.02-2.5 microm). The collected PM2.5 samples were analyzed for mass concentration, for elemental and organic carbon, and for elemental concentrations. The results show that the aerosol concentration gradient was most clearly seen in the particle number concentration measured by the ultrafine particle counters. The concentration of ultrafine particles decreased to half between the sampling points located at 50 m and 150 m downwind from the highway. Additionally, elemental analysis revealed a gradient in sulfur concentrations up to 400 m from the highway in a residential area that does not have major nearby industrial sources. This gradient was qualitatively attributed to the sulfate particle emissions from diesel engine exhausts, and was supported by the concentration data on several key elements indicative of traffic sources (road dust and diesel exhaust). As different particulate components gave different profiles of the diesel exposure gradient, these results indicate that no single element or component of diesel exhaust can be used as a surrogate for diesel exposure, but more comprehensive signature analysis is needed. This characterization is crucial especially when the exposure data are to be used in epidemiological studies.