Early Life Exposure to Air Pollution and Autism Spectrum Disorder: Findings from a Multisite Case-Control Study

BACKGROUND: Epidemiologic studies have reported associations between prenatal and early postnatal air pollution exposure and autism spectrum disorder (ASD); however, findings differ by pollutant and developmental window. OBJECTIVES: We examined associations between early life exposure to particulate matter ≤2.5 µm in diameter (PM2.5) and ozone in association with ASD across multiple US regions. METHODS: Our study participants included 674 children with confirmed ASD and 855 population controls from the Study to Explore Early Development, a multi-site case-control study of children born from 2003 to 2006 in the United States. We used a satellite-based model to assign air pollutant exposure averages during several critical periods of neurodevelopment: 3 months before pregnancy; each trimester of pregnancy; the entire pregnancy; and the first year of life. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs), adjusting for study site, maternal age, maternal education, maternal race/ethnicity, maternal smoking, and month and year of birth. RESULTS: The air pollution-ASD associations appeared to vary by exposure time period. Ozone exposure during the third trimester was associated with ASD, with an OR of 1.2 (95% CI: 1.1, 1.4) per 6.6 ppb increase in ozone. We additionally observed a positive association with PM2.5 exposure during the first year of life (OR = 1.3 [95% CI: 1.0, 1.6] per 1.6 µg/m increase in PM2.5). CONCLUSIONS: Our study corroborates previous findings of a positive association between early life air pollution exposure and ASD, and identifies a potential critical window of exposure during the late prenatal and early postnatal periods

Cardiometabolic Pregnancy Complications in Association With Autism-Related Traits as Measured by the Social Responsiveness Scale in ECHO

Prior work has examined associations between cardiometabolic pregnancy complications and autism spectrum disorder (ASD) but not how these complications may relate to social communication traits more broadly. We addressed this question within the Environmental Inf luences on Child Health Outcomes program, with 6,778 participants from 40 cohorts conducted from 1998–2021 with information on ASD-related traits via the Social Responsiveness Scale. Four metabolic pregnancy complications were examined individually, and combined, in association with Social Responsiveness Scale scores, using crude and adjusted linear regression as well as quantile regression analyses. We also examined associations stratified by ASD diagnosis, and potential mediation by preterm birth and low birth weight, and modification by child sex and enriched risk of ASD. Increases in ASD-related traits were associated with obesity (β = 4.64, 95% confidence interval: 3.27, 6.01) and gestational diabetes (β = 5.21, 95% confidence interval: 2.41, 8.02), specifically, but not with hypertension or preeclampsia. Results among children without ASD were similar to main analyses, but weaker among ASD cases. There was not strong evidence for mediation or modification. Results suggest that common cardiometabolic pregnancy complications may inf luence child ASD-related traits, not only above a diagnostic threshold relevant to ASD but also across the population

Maternal tobacco smoking and offspring autism spectrum disorder or traits in ECHO cohorts

Given inconsistent evidence on preconception or prenatal tobacco use and offspring autism spectrum disorder (ASD), this study assessed associations of maternal smoking with ASD and ASD-related traits. Among 72 cohorts in the Environmental Influences on Child Health Outcomes consortium, 11 had ASD diagnosis and prenatal tobaccosmoking (n = 8648). and 7 had Social Responsiveness Scale (SRS) scores of ASD traits (n = 2399). Cohorts had diagnoses alone (6), traits alone (2), or both (5). Diagnoses drew from parent/caregiver report, review of records, or standardized instruments. Regression models estimated smoking-related odds ratios (ORs) for diagnoses and standardized mean differences for SRS scores. Cohort-specific ORs were meta-analyzed. Overall, maternal smoking was unassociated with child ASD (adjusted OR, 1.08; 95% confidence interval [CI], 0.72–1.61). However, heterogeneity across studies was strong: preterm cohorts showed reduced ASD risk for exposed children. After excluding preterm cohorts (biased by restrictions on causal intermediate and exposure opportunity) and small cohorts (very few ASD cases in either smoking category), the adjusted OR for ASD from maternal smoking was 1.44 (95% CI, 1.02–2.03). Children of smoking (versus non-smoking) mothers had more ASD traits (SRS T-score + 2.37 points, 95% CI, 0.73–4.01 points), with results homogeneous across cohorts. Maternal preconception/prenatal smoking was consistently associated with quantitative ASD traits and modestly associated with ASD diagnosis among sufficiently powered United States cohorts of non-preterm children. Limitations resulting from self-reported smoking and unmeasured confounders preclude definitive conclusions. Nevertheless, counseling on potential and known risks to the child from maternal smoking is warranted for pregnant women and pregnancy planners. Lay Summary: Evidence on the association between maternal prenatal smoking and the child's risk for autism spectrum disorder has been conflicting, with some studies reporting harmful effects, and others finding reduced risks. Our analysis of children in the ECHO consortium found that maternal prenatal tobacco smoking is consistently associated with an increase in autism-related symptoms in the general population and modestly associated with elevated risk for a diagnosis of autism spectrum disorder when looking at a combined analysis from multiple studies that each included both pre- and full-term births. However, this study is not proof of a causal connection. Future studies to clarify the role of smoking in autism-like behaviors or autism diagnoses should collect more reliable data on smoking and measure other exposures or lifestyle factors that might have confounded our results

Local oedema and general excitation of cutaneous sensory receptors produced by electrical stimulation of the saphenous nerve in the rat

Recordings were made from multifibre strands of the saphenous nerve of rats anaesthetized with urethane and given Evan's blue intravenously. Stimulation of A plus C fibres of the saphenous nerve, but not A fibres alone, at 10 Hz for 5 min produced dye leakage in the skin of the hind limb. Stimulation of the nerve at A plus C fibre voltages with the stimulating electrodes placed distal to the recording electrodes produced reversible block of nerve impulses at the stimulating electrodes. However, when the stimulating electrodes were placed proximal to the recording electrodes, stimulation of the nerve at A plus C fibre voltages, but not at A fibre voltages, produced an increase in activity in nerve strands. An increase in activity was also observed in experiments where the contralateral saphenous nerve was stimulated. These effects were not abolished by pretreatment of rats with reserpine. The early phase of the local oedema response appeared to be reduced by local pretreatment with compound 48 80 but the excitatory action on nerve terminals was not. The effects of nerve stimulation were not mimicked by intravenous injection of 5HT, ATP or adenosine into the contralateral saphenous vein. It is suggested that several substances might be released on antidromic stimulation of C fibres and that the resulting general excitation of sensory nerve terminals might play a role in modifying the central nervous system response to nociceptive information

THE EFFECTS OF PROSTAGLANDINS E1, E2 AND F2α ON THE CUTANEOUS VASCULATURE OF THE RAT

The responses of the rat cutaneous vasculature to prostaglandins E, E and F have been investigated by a photomicrographic technique. Prostaglandin E produced transient arterial constriction which was blocked by local pretreatment of preparations with compound 48/80 or methysergide. It was concluded that prostaglandin E produced vasoconstriction by release of 5‐hydroxytryptamine (5‐HT) from mast cells. The magnitude of the vasoconstrictor response appeared to be subject to seasonal variation. Prostaglandin F produced arterial constriction of longer duration which was not blocked by compound 48/80, methysergide or phenoxybenzamine. Preparations pretreated with prostaglandin F were found to be more sensitive to the venous constrictor effect, and less sensitive to the arterial constrictor effect, of noradrenaline. Prostaglandin E produced arterial constriction which was usually partially blocked by compound 48/80 and methysergide and it was concluded that a major component of the vasoconstrictor response to prostaglandin E was of the E type but some component was of the F type. 1976 British Pharmacological Societ

Ion implanted and laser processed solar cells made from EFG ribbon

The use of ion implantation and laser processing has a number of conceptual advantages which could result in a low-cost process for manufacturing high performance solar cells from EFG ribbon. Samples were phosphorus ion implanted, laser processed using either a pulse large area ruby laser or a scanned YAG laser with a second harmonic generator, and then processed into solar cells. Many of the samples had high reverse leakage and it was determined that this was due to too high a laser processing power. This effect was determined to be more severe for the scanned YAG laser, and is thought to be due to point defects. Cells were made from EFG ribbon with a low laser energy density which had efficiencies of up to 10% at AMI demonstrating the feasibility of this approach. High efficiencies should be attainable by optimizing the laser processing parameters