BackgroundTraumatic brain injury (TBI) greatly contributes to morbidity and mortality in the pediatric population. We examined potential urban/rural disparities in mortality amongst Oregon pediatric patients with TBI treated in trauma hospitals.MethodsWe conducted a retrospective study of children ages 0–19 using the Oregon Trauma Registry for years 2009–2012. Geographic location of injury was classified using the National Center for Health Statistics Urban/Rural Classification Scheme. Incidence rates were calculated using Census data for denominators. Associations between urban/rural injury location and mortality were assessed using multivariable logistic regression, controlling for potential confounders. Generalized estimating equations were used to help account for clustering of data within hospitals.ResultsOf 2794 pediatric patients with TBI, 46.6 % were injured in large metropolitan locations, 24.8 % in medium/small metropolitan locations, and 28.6 % in non-metropolitan (rural) locations. Children with rural locations of injury had a greater annualized TBI incidence rate, at 107/100,000 children per year, than those from large metropolitan areas (71/100,000 per year). Compared to children injured in urban locations, those in rural locations had more than twice the crude odds of mortality (odds ratio [OR], 2.5; 95 % CI, 1.6–4.0). This association remained significant (OR, 1.8; 95 % CI, 1.04–3.3) while adjusting for age, gender, race, insurance status, injury severity, and type of TBI (blunt vs. penetrating).ConclusionWe observed higher rates of TBI and greater proportions of severe injury in rural compared to urban areas in Oregon. Rural children treated in the trauma system for TBI were more likely to die than urban children after controlling for demographic and injury factors associated with urban/rural residence. Further research is needed to examine treatment disparities by urban/rural location. Future work should also identify interventions that can reduce risk of TBI and TBI-related mortality among children, particularly those who live in rural areas.Electronic supplementary materialThe online version of this article (doi:10.1186/s40621-015-0063-2) contains supplementary material, which is available to authorized users.

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BackgroundAir ions are molecules of air that have become ionized—that is, they have either lost or gained an electrical charge. Past speculation has suggested that exposure to positive air ions may be harmful to one’s health, while exposure to negative air ions may be associated with beneficial health effects. Air ions arise from natural sources as well as direct-current transmission lines and commercial ionizers. Several recent clinical studies have suggested therapeutic effects of air ions on various types of depression at exposure levels 10- to 1000-fold higher than most previous human studies. The aim of this study was to assess the evidence from studies of laboratory animals for beneficial or adverse effects of air ions on health.MethodsSixty-two studies (1935–2015) in nine topics areas were evaluated for quality and potential systematic bias by ARRIVE guidelines. Standardized mean differences or proportional differences between exposed and control groups were computed for 44 studies to quantitatively assess the strength of the evidence for exposure-related effects.ResultsMany of the studies were conducted before 1990 and exhibited various reporting and methodological deficiencies, including small sample size, failure to control for the influence of potential confounding variables, lack of randomized assignment to treatment groups and blinded analyses, and statistical errors relating to treating group-exposed animals as individuals. The highest quality studies consistently reported no effects of exposure on any of the endpoints examined. There were no evident dose–response relationships within or across studies.ConclusionsExperimental studies of laboratory animals exposed to positive and negative air ions for minutes to years over a five-log unit range of intensities did not suggest any consistent or reliable effects on measures of behavior, learning and memory, neurotransmitters, tracheal function, respiratory infection, cardiovascular function, reproduction and growth, carcinogenesis, or other health endpoints. These data do not provide evidence of adverse or beneficial effects of air ion exposure on health, and did not suggest any biological mechanism of interaction, except perhaps for mechanosensory stimulation of body surfaces by static electric fields at high air ion concentrations.Electronic supplementary materialThe online version of this article (10.1186/s12938-018-0499-z) contains supplementary material, which is available to authorized users.

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Industry specific surveillance and interventions tailored to high-risk occupations are needed to further reduce severe injuries in this population. Am. J. Ind. Med. 59:948-958, 2016. © 2016 Wiley Periodicals, Inc.

Autism spectrum disorder (ASD) and attention deficit (hyperactivity) disorder (ADD/ADHD) are key focuses of current health research due to their increasing prevalence. The objective of this systematic literature search and critical review was to evaluate whether the human epidemiologic data indicate a pattern of association between ASD or ADD/ADHD and developmental exposure to particulate matter (PM), with a focus on exposures encountered before the age of three. A MEDLINE and EMBASE search was conducted; following preliminary and full-text screening, 14 relevant articles were identified for review. Three of the 14 studies were prospective cohort studies evaluating exposure to PM; 11 studies had a case-control design. There was no consistent association between developmental PM exposure and ASD across the three of the cohort studies. Seven of the case-control studies examined the relationship between PM and/or PM and ASD; four examined the relationship between developmental diesel PM exposure and ASD. Overall, there was low external consistency in results among studies of PM/PM and ASD, with some reporting high internal consistency without significant associations, others showing associations with high internal consistency for specific exposure windows only (e.g., third trimester), and still others showing high consistency for moderate to strong associations between PM and ASD. The majority of studies reporting significant results had low effect sizes in conjunction with small sample sizes. The four studies of diesel PM and ASD also had low external consistency of results. Only one study evaluated associations with ADD/ADHD, and it found no significant associations with PM. The inconsistent findings across studies of developmental exposure to PM and ASD may be attributed to differences in the study populations, exposure assessments, outcome assessments, or chance. Further research is needed to understand the underlying biological mechanisms that lead to ASD and ADD/ADHD and how PM might be involved in those mechanisms, if at all. High-quality epidemiologic studies are also needed to conclusively determine whether developmental PM exposure is a causal factor for ASD or ADD/ADHD, with focus on a well-developed exposure assessment.

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