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Objectives: The aim of this study was to update a cohort of Vermont talc workers to include 37 additional years of follow-up time., Methods: Standardized mortality ratios (SMR) and 95% confidence intervals (CIs) were calculated for 70+ causes of death. US population mortality rates were used as reference., Results: All-cause mortality was 30% higher than the US population (SMR 133.4, 95% CI, 119.7 to 148.3). Significant elevations occurred in nonmalignant respiratory disease (NMRD) (SMR 273.0, 95% CI, 210.2 to 348.6) and other nonmalignant respiratory disease (ONMRD) (SMR 413.1, 95% CI, 287.7 to 574.5). ONMRD was elevated across all length of employment categories and a test for linear trend was significant (P = 0.007)., Conclusions: This study provides further evidence that excess deaths among Vermont talc workers are due largely to excess mortality from NMRD; there is no evidence of increased risk of respiratory cancer.

Background: Neurotoxic effects of high-level occupational exposure to manganese (Mn) are well established; however, whether lower-level environmental exposure to Mn in early life causes neurodevelopmental toxicity in children is unclear., Methods: A systematic literature review was conducted to identify and evaluate epidemiologic studies of specific Mn biomarkers assessed during gestation, childhood, or adolescence in association with neurodevelopmental outcomes, focusing on quantitative exposure-response estimates with specific endpoints that were assessed in multiple independent study populations. Study quality was evaluated using the revised RTI item bank and the Cochrane Risk of Bias tool, and the overall weight of epidemiologic evidence for causality was evaluated according to the Bradford Hill considerations., Results: Twenty-two epidemiologic studies were identified that estimated associations between early-life Mn biomarkers and neurodevelopmental outcomes. Seven of these studies provided adjusted estimates for the association with child intelligence assessed using versions of the Wechsler Intelligence Scales for Children; no other specific neurodevelopmental endpoints were assessed in more than three independent study populations each. Among the studies of child intelligence, five studies in four independent populations measured blood Mn, three studies measured hair Mn, and one measured dentin Mn. Overall, cross-sectional associations between Mn biomarkers and measures of child intelligence were mostly statistically nonsignificant but in a negative direction; however, the lone prospective cohort study found mostly null results, with some positive (favorable) associations between dentin Mn and child intelligence. Studies were methodologically limited by their cross-sectional design and potential for confounding and selection bias, as well as unaddressed questions on exposure assessment validity and biological plausibility., Conclusions: The statistical associations reported in the few studies of specific Mn biomarkers and specific neurodevelopmental endpoints do not establish causal effects based on the Bradford Hill considerations. Additional prospective cohort studies of Mn biomarkers and validated neurodevelopmental outcomes, and a better understanding of the etiologic relevance of Mn biomarkers, are needed to shed light on whether environmental exposure to Mn causes adverse neurodevelopmental effects in children., (Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: Advanced heart failure (HF) can be treated conservatively or aggressively, with left ventricular assist devices (LVADs) and heart transplant (HT) being the most aggressive strategies., Objective: The goal of this review was to identify, describe, critique and summarize published cost-effectiveness analyses on LVADs for adults with HF., Methods: We conducted a literature search using PubMed and ProQuest DIALOG databases to identify English-language publications from 2006 to 2017 describing cost-effectiveness analyses of LVADs and reviewed them against inclusion criteria. Those that met criteria were obtained for full-text review and abstracted if they continued to meet study requirements., Results: A total of 12 cost-effectiveness studies (13 articles) were identified, all of which described models; they were almost evenly split between those examining LVADs as destination therapy (DT) or as bridge to transplant (BTT). Studies were Markov or semi-Markov models with one- or three-month cycles that followed patients until death. Inputs came from a variety of sources, with the REMATCH trial and INTERMACS registry common clinical data sources, although some publications also used data from studies at their own institutions. Costs were derived from standard sources in many studies but from individual hospital data in some. Inputs for health utilities, which were used in 11 of 12 studies, were generally derived from two studies. None of the studies reported a societal perspective, that is, included non-medical costs such as caregiving., Conclusions: No study found LVADs to be cost effective for DT or BTT with base case assumptions, although incremental cost-effectiveness ratios met thresholds for cost effectiveness in some probabilistic analyses. With constant improvements in LVADs and expanding indications, understanding and re-evaluating the cost effectiveness of their use will be critical to making treatment decisions.

Aims: We assessed the animal and epidemiological data to determine if chloroform exposure causes developmental and/or reproductive toxicity., Results and Discussion: Initial scoping identified developmental toxicity as the primary area of concern. At levels producing maternal toxicity in rats and mice, chloroform caused decrements in fetal weights and associated delays in ossification. In a single mouse inhalation study, exposure to a high concentration of chloroform was associated with small fetuses and increased cleft palate. However, oral exposure of mice to chloroform at a dose 4 times higher was negative for cleft palate; multiple inhalation studies in rats were also negative. Epidemiologic data on low birth weight and small for gestational age were generally equivocal, preventing conclusions from being drawn for humans. The animal data also show evidence of very early (peri-implantation) total litter losses at very high exposure levels. This effect is likely maternally mediated rather than a direct effect on the offspring. Finally, the epidemiologic data indicate a possible association of higher chloroform exposure with lower risk of preterm birth (<37 weeks gestation)., Conclusions: The available animal data suggest that exposures lower than those causing maternal toxicity should be without developmental effects in the offspring. Also, most studies in humans rely on group-level geographic exposure data, providing only weak epidemiologic evidence for an association with development outcomes and fail to establish a causal role for chloroform in the induction of adverse developmental outcomes at environmentally relevant concentrations., (© 2018 Wiley Periodicals, Inc.)

Background: Air 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., Methods: Sixty-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., Results: Many 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., Conclusions: Experimental 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.

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 10 ; 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 2.5 and/or PM 10 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 2.5 /PM 10 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 10 . 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.

Background: The electric power industry represents a unique subset of the U.S. workforce. We aimed to evaluate the relationships between occupational category, nature of injury, and injury severity among electric power industry workers., Methods: The Occupational Health and Safety Database (1995-2013) was used to calculate injury rates, assess patterns of injury severity, and identify at-risk occupations in this population., Results: Over the surveillance period, a total of 63,193 injuries were reported. Overall, and severe injury rates were 3.20 and 0.52 per 100 employee-years, respectively. The fatal injury rate was 3.29 per 100,000 employee-years. Line workers experienced the highest risk for fatal injuries and second highest for non-fatal severe injuries, following meter readers. The most severe non-fatal injuries were hernia and rupture; multiple injuries; and CTD/RSI. Fatal injuries were most commonly associated with vehicle collisions and contact with electric current., Conclusions: 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., (© 2016 Wiley Periodicals, Inc.)

Background: Traumatic 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., Methods: We 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., Results: Of 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)., Conclusion: We 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.