Substance use patterns in 9-10 year olds: Baseline findings from the adolescent brain cognitive development (ABCD) study.

BACKGROUND: The Adolescent Brain Cognitive Development ™ Study (ABCD Study®) is an open-science, multi-site, prospective, longitudinal study following over 11,800 9- and 10-year-old youth into early adulthood. The ABCD Study aims to prospectively examine the impact of substance use (SU) on neurocognitive and health outcomes. Although SU initiation typically occurs during teen years, relatively little is known about patterns of SU in children younger than 12. METHODS: This study aims to report the detailed ABCD Study® SU patterns at baseline (n = 11,875) in order to inform the greater scientific community about cohort's early SU. Along with a detailed description of SU, we ran mixed effects regression models to examine the association between early caffeine and alcohol sipping with demographic factors, externalizing symptoms and parental history of alcohol and substance use disorders (AUD/SUD). PRIMARY RESULTS: At baseline, the majority of youth had used caffeine (67.6 %) and 22.5 % reported sipping alcohol (22.5 %). There was little to no reported use of other drug categories (0.2 % full alcohol drink, 0.7 % used nicotine, <0.1 % used any other drug of abuse). Analyses revealed that total caffeine use and early alcohol sipping were associated with demographic variables (p's<.05), externalizing symptoms (caffeine p = 0002; sipping p = .0003), and parental history of AUD (sipping p = .03). CONCLUSIONS: ABCD Study participants aged 9-10 years old reported caffeine use and alcohol sipping experimentation, but very rare other SU. Variables linked with early childhood alcohol sipping and caffeine use should be examined as contributing factors in future longitudinal analyses examining escalating trajectories of SU in the ABCD Study cohort.

Effects of inhaled sympathomimetics on obstructive response to respiratory heat loss.

To investigate the influence of inhaled sympathomimetics on the obstructive response to airway cooling, we had six asymptomatic atopic asthmatics perform eucapnic hyperventilation with frigid air at various levels of ventilation after pretreatment with aerosols of metaproterenol or placebo in a random blind fashion. In control experiments, eucapnic hyperventilation produced a progressive decrease in 1-s forced expiratory volume in a stimulus-response fashion as the level of ventilation rose in successive challenges. Metaproterenol did not produce an all-or-none blockade, but rather a parallel shift in the stimulus-response curve so that its protective effects could be overcome by increasing the stimulus. There was no effect on respiratory heat loss. These results explain, in a quantitative fashion, why a treatment schedule that permits a person with asthma to perform a given exercise task without difficulty becomes ineffective as the thermal burden or severity of the task increases.

Reanalysis of the refractory period in exertional asthma.

In an effort to determine whether the refractory period in exercise-induced asthma derived from mediator consumption we had seven asthmatic subjects repeatedly perform both exercise and eucapnic hyperventilation at matched minute ventilations under precisely controlled inspired air conditions. We reasoned that, if airway cooling were causing an agent to be released whose depletion resulted in less responsiveness, we should be able to observe this phenomenon irrespective of how cooling was produced. Repetitive exercise at short intervals produced a diminution in the obstructive response that disappeared when the interval between challenges was extended to 2 h. However, the degree of obstruction that occurred after voluntary hyperventilation remained constant irrespective of when the provocations were performed and equaled that seen with the first and last exercise challenge. Because the thermal burdens were identical for each challenge and all time periods, these results are incompatible with mediator depletion and suggest that it may be the secondary sympathoadrenal consequences of repeated exercise that cause the airways to temporarily lose their responsivity.

The effects of cromolyn sodium on the airway response to hyperpnea and cold air in asthma.

In order to determine if cromolyn sodium provided protection against the marked bronchoconstriction that develops when the hyperpnea of exercise is combined with frigid air, we exposed a group of asymptomatic asthmatics to this stimulus, with and without pretreatment with this drug. Respiratory heat loss and retrotracheal and retrocardiac esophageal temperatures were measured during each challenge, and multiple aspects of pulmonary mechanics were recorded before commencement and after completion. The results demonstrated that, unlike anticholinergic agents, cromolyn sodium attenuates the obstructive response observed with these large thermal burdens, and does so without affecting airway cooling.

Effects of atropine on respiratory heat loss in asthma.

We have previously observed that although atropine does not alter the magnitude of the response to exercise while breathing cold air, it does cause the predominant site of obstruction to move into the lung periphery. To determine if this effect was due to changes in the conditioning of inspired air, we measured respiratory heat loss (RHL) and retrotracheal (Trt) and retrocardiac esophageal temperature in eight asthmatics while they performed eucapnic hyperventilation with cold air before and after the inhalation of atropine. Multiple aspects of pulmonary mechanics were also recorded. Significant and equivalent airway obstruction developed with and without atropine (control delta FEV1 = 1.0 +/- 0.2 (SE) liter; postatropine = 0.9 +/- 0.3 liter). Despite this, RHL was 17.1% greater and Trt fell 16% more after atropine. These data demonstrate that atropine can influence heat transfer within the lung and alter the sites of conditioning.

Airway responsiveness to cold air and hyperpnea in normal subjects and in those with hay fever and asthma.

Multiple aspects of pulmonary mechanics were measured before and after bronchial challenges consisting of hyperpnea with cold air inhalation in 20 normal control subjects, 16 subjects with hay fever, and 44 asymptomatic asthmatics. These challenges had no effect on the lung function of the normal subjects. In the hay fever group, however, postchallenge mechanics changed a small, but significant, amount, e.g., mean decrease in forced expiratory volume in one second (FEV1) was -5.1 +/- 1.7% (SEM). The asthmatics had a much more marked response (mean fall in FEV1, -32.7 +/- 2.6%). There was considerable overlap between the responses of the normal subjects and those with hay fever, but no overlap at all between asthmatic and normal subjects. The only subjects with hay fever whose responses overlapped the asthmatic response were those who had histories of occasional episodes of wheezing. This pattern of response suggests that the use of hyperpnea and subfreezing air is a very sensitive and highly specific means of detecting increased air reactivity.