An equity and environmental justice assessment of anti-science actions during the Trump administration.

In the United States, science shapes federal health and safety protections, but political officials can and do politicize federal science and science-based safeguards. Many presidential administrations have politicized science, but under the administration of President Trump, these attacks on science-such as buried research, censored scientists, halted data collection-increased in number to unprecedented levels. Underserved communities bore the brunt of the harms. Such attacks disproportionately harm Black, Indigenous, low-income communities, and communities of color, all of whom have long been burdened by pollution exposure and other stressors. We analyze the effects on underserved communities of the Trump administration's anti-science environmental and public health policy actions and offer policy recommendations for current and future administrations. Our goal is to strengthen scientific integrity, prioritize health disparity research, and meaningfully engage affected communities in federal rulemaking.

The disinformation playbook: how industry manipulates the science-policy process-and how to restore scientific integrity.

For decades, corporate undermining of scientific consensus has eroded the scientific process worldwide. Guardrails for protecting science-informed processes, from peer review to regulatory decision making, have suffered sustained attacks, damaging public trust in the scientific enterprise and its aim to serve the public good. Government efforts to address corporate attacks have been inadequate. Researchers have cataloged corporate malfeasance that harms people's health across diverse industries. Well-known cases, like the tobacco industry's efforts to downplay the dangers of smoking, are representative of transnational industries, rather than unique. This contribution schematizes industry tactics to distort, delay, or distract the public from instituting measures that improve health-tactics that comprise the "disinformation playbook." Using a United States policy lens, we outline steps the scientific community should take to shield science from corporate interference, through individual actions (by scientists, peer reviewers, and editors) and collective initiatives (by research institutions, grant organizations, professional associations, and regulatory agencies).

Hazardous air pollutant emissions implications under 2018 guidance on U.S. Clean Air Act requirements for major sources.

On January 25, 2018, the United States Environmental Protection Agency withdrew a 1995 policy that mandates the use of maximum achievable control technology (MACT) to regulate emissions from major sources of hazardous air pollutants (HAPs), a category of toxic chemicals that may be carcinogenic, mutagenic, or cause other adverse health effects. To better understand the implications and scope of the change in regulatory guidance for HAP emissions of major sources that may reclassify as area sources, the increase in emissions that could legally occur under the new policy is assessed here. Based on facility-level data from a 2014 HAP national emissions inventory, it is estimated that 70% of major sources of HAPs qualify for reclassification as area sources, which could result in a maximum of 35,030 tons per year (tpy) of additional HAP emissions if all sources successfully reclassified. This amount would nearly triple the total volume of HAPs that qualifying major sources emitted in 2014. On average, qualifying sources could emit individually an additional 18.4 tpy. In the 21 states and territories that follow only federal guidelines for controlling HAPs, it is more likely that the estimates presented here could materialize compared to states that have additional guidelines for area sources of HAPs. The quantitative analysis of the potential emission changes resulting from regulatory change is instructive for industry, state and federal decisionmakers, and interested members of the public looking to understand and anticipate how relevant stakeholders will be affected by this policy change.Implications: Withdrawal of a U.S. Environmental Protection Agency policy that mandates the use of maximum achievable control technology (MACT) to regulate emissions from major sources of hazardous air pollutants (HAPs) could result in higher emissions of toxic chemicals that may be carcinogenic, mutagenic, or cause other adverse health effects. Analysis of potential emission changes resulting from regulatory change is instructive for industry, state, and federal decisionmakers, and interested members of the public looking to understand and anticipate how relevant stakeholders will be affected by this policy change.

The economic burden of stroke care in England, Wales and Northern Ireland: Using a national stroke register to estimate and report patient-level health economic outcomes in stroke.

INTRODUCTION: Stroke registries are used in many settings to measure stroke treatment and outcomes, but rarely include data on health economic outcomes. We aimed to extend the Sentinel Stroke National Audit Programme registry of England, Wales and Northern Ireland to derive and report patient-level estimates of the cost of stroke care. METHODS: An individual patient simulation model was built to estimate health and social care costs at one and five years after stroke, and the cost-benefits of thrombolysis and early supported discharge. Costs were stratified according to age, sex, stroke type (ischaemic or primary intracerebral haemorrhage) and stroke severity. The results were illustrated using data on all patients with stroke included in Sentinel Stroke National Audit Programme from April 2015 to March 2016 (n = 84,184). RESULTS: The total cost of health and social care for patients with acute stroke each year in England, Wales and Northern Ireland was £3.60 billion in the first five years after admission (mean per patient cost: £46,039). There was fivefold variation in the magnitude of costs between patients, ranging from £19,101 to £107,336. Costs increased with older age, increasing stroke severity and intracerebral hemorrhage stroke. Increasing the proportion of eligible patients receiving thrombolysis or early supported discharge was estimated to save health and social care costs by five years after stroke. DISCUSSION: The cost of stroke care is large and varies widely between patients. Increasing the proportion of eligible patients receiving thrombolysis or early supported discharge could contribute to reducing the financial burden of stroke. CONCLUSION: Extending stroke registers to report individualised data on costs may enhance their potential to support quality improvement and research.

Outdoor air pollution as a possible modifiable risk factor to reduce mortality in post-stroke population.

Outdoor air pollution is a known risk factor for mortality and morbidity. The type of air pollutant most reliably associated with disease is particulate matter (PM), especially finer particulate matter that can reach deeper into the lungs like PM2.5 (particulate matter diameter < 2.5 µm). Some subpopulations may be particularly vulnerable to PM pollution. This review focuses on one subgroup, long-term stroke survivors, and the emerging evidence suggesting that survivors of a stroke may be at a higher risk from the deleterious effects of PM pollution. While the mechanisms for mortality are still under debate, long-term stroke survivors may be vulnerable to similar mechanisms that underlie the well-established association between PM pollution and cardiovascular disease. The fact that long-term stroke survivors of ischemic, but not hemorrhagic, strokes appear to be more vulnerable to the risk of death from higher PM pollution may also bolster the connection to ischemic heart disease. Survivors of an ischemic stroke may be more vulnerable to dying from higher concentrations of PM pollution than the general population. The clinical implications of this association suggest that reduced exposure to PM pollution may result in fewer deaths amongst stroke survivors.

Effect of Exhaust- and Nonexhaust-Related Components of Particulate Matter on Long-Term Survival After Stroke.

BACKGROUND AND PURPOSE: Outdoor air pollution represents a potentially modifiable risk factor for stroke. We examined the link between ambient pollution and mortality up to 5 years poststroke, especially for pollutants associated with vehicle exhaust. METHODS: Data from the South London Stroke Register, a population-based register covering an urban, multiethnic population, were used. Hazard ratios (HR) for a 1 interquartile range increase in particulate matter <2.5 µm diameter (PM2.5) and PM <10 µm (PM10) were estimated poststroke using Cox regression, overall and broken down into exhaust and nonexhaust components. Analysis was stratified for ischemic and hemorrhagic strokes and was further broken down by Oxford Community Stroke Project classification. RESULTS: The hazard of death associated with PM2.5 up to 5 years after stroke was significantly elevated (P=0.006) for all strokes (HR=1.28; 95% confidence interval [CI], 1.08-1.53) and ischemic strokes (HR, 1.32; 95% CI, 1.08-1.62). Within ischemic subtypes, PM2.5 pollution increased mortality risk for total anterior circulation infarcts by 2-fold (HR, 2.01; 95% CI, 1.17-3.48; P=0.012) and by 78% for lacunar infarcts (HR, 1.78; 95% CI, 1.18-2.66; P=0.006). PM10 pollution was associated with 45% increased mortality risk for lacunar infarct strokes (HR, 1.45; 95% CI, 1.06-2.00; P=0.022). Separating PM2.5 and PM10 into exhaust and nonexhaust components did not show increased mortality. CONCLUSIONS: Exposure to certain outdoor PM pollution, particularly PM2.5, increased mortality risk poststroke up to 5 years after the initial stroke.

Decreases in energy and increases in phase locking of event-related oscillations to auditory stimuli occur during adolescence in human and rodent brain.

Synchrony of phase (phase locking) of event-related oscillations (EROs) within and between different brain areas has been suggested to reflect communication exchange between neural networks and as such may be a sensitive and translational measure of changes in brain remodeling that occur during adolescence. This study sought to investigate developmental changes in EROs using a similar auditory event-related potential (ERP) paradigm in both rats and humans. Energy and phase variability of EROs collected from 38 young adult men (aged 18-25 years), 33 periadolescent boys (aged 10-14 years), 15 male periadolescent rats [at postnatal day (PD) 36] and 19 male adult rats (at PD103) were investigated. Three channels of ERP data (frontal cortex, central cortex and parietal cortex) were collected from the humans using an 'oddball plus noise' paradigm that was presented under passive (no behavioral response required) conditions in the periadolescents and under active conditions (where each subject was instructed to depress a counter each time he detected an infrequent target tone) in adults and adolescents. ERPs were recorded in rats using only the passive paradigm. In order to compare the tasks used in rats to those used in humans, we first studied whether three ERO measures [energy, phase locking index (PLI) within an electrode site and phase difference locking index (PDLI) between different electrode sites] differentiated the 'active' from 'passive' ERP tasks. Secondly, we explored our main question of whether the three ERO measures differentiated adults from periadolescents in a similar manner in both humans and rats. No significant changes were found in measures of ERO energy between the active and passive tasks in the periadolescent human participants. There was a smaller but significant increase in PLI but not PDLI as a function of active task requirements. Developmental differences were found in energy, PLI and PDLI values between the periadolescents and adults in both the rats and the human participants. Neuronal synchrony as indexed by PLI and PDLI was significantly higher to the infrequent (target) tone compared to the frequent (nontarget) tone in all brain sites in all of the regions of interest time-frequency intervals. Significantly higher ERO energy and significantly lower synchrony was seen in the periadolescent humans and rats compared to their adult counterparts. Taken together these findings are consistent with the hypothesis that adolescent remodeling of the brain includes decreases in energy and increases in synchrony over a wide frequency range both within and between neuronal networks and that these effects are conserved over evolution.

Ontogeny and adolescent alcohol exposure in Wistar rats: open field conflict, light/dark box and forced swim test.

Epidemiological studies have demonstrated that heavy drinking and alcohol abuse and dependence peak during the transition between late adolescence and early adulthood. Studies in animal models have demonstrated that alcohol exposure during adolescence can cause a modification in some aspects of behavioral development, causing the "adolescent phenotype" to be retained into adulthood. However, the "adolescent phenotype" has not been studied for a number of behavioral tests. The objective of the present study was to investigate the ontogeny of behaviors over adolescence/young adulthood in the light/dark box, open field conflict and forced swim test in male Wistar rats. These data were compared to previously published data from rats that received intermittent alcohol vapor exposure during adolescence (AIE) to test whether they retained the "adolescent phenotype" in these behavioral tests. Three age groups of rats were tested (post-natal day (PD) 34-42; PD55-63; PD69-77). In the light/dark box test, younger rats escaped the light box faster than older adults, whereas AIE rats returned to the light box faster and exhibited more rears in the light than controls. In the open field conflict test, both younger and AIE rats had shorter times to first enter the center, spent more time in the center of the field, were closer to the food, and consumed more food than controls. In the forced swim test no clear developmental pattern emerged. The results of the light/dark box and the forced swim test do not support the hypothesis that adolescent ethanol vapor exposure can "lock-in" all adolescent phenotypes. However, data from the open field conflict test suggest that the adolescent and the AIE rats both engaged in more "disinhibited" and food motivated behaviors. These data suggest that, in some behavioral tests, AIE may result in a similar form of behavioral disinhibition to what is seen in adolescence.

Event-related potential responses to the acute and chronic effects of alcohol in adolescent and adult Wistar rats.

BACKGROUND: This study explored the hypothesis that adolescent ethanol (EtOH) exposure may cause long-lasting changes in EtOH sensitivity by exploring the age-related effects of acute alcohol on intoxication and on event-related potential (ERP) responses to acoustic stimuli in EtOH-naïve adolescent and adult male Wistar rats and in adult rats that were exposed to chronic EtOH/control conditions during adolescence. METHODS: EtOH-naïve adolescent (postnatal day 32 [PD32]) and adult male rats (PD99) were included in the first study. In a second study, rats were exposed to 5 weeks of EtOH vapor (blood EtOH concentrations at 175 mg%) or air from PD24 to 59 and allowed to mature until PD90. In both studies, rats were implanted with cortical recording electrodes, and the effects of acute EtOH (0.0, 1.5, and 3.0 g/kg) on behavioral and ERP responses were assessed. RESULTS: Adolescents were found to have higher amplitude and longer latency P3a and P3b components at baseline as compared to adult rats, and EtOH was found to produce a robust dose-dependent increase in the latency of the P3a and P3b components of the auditory ERP recorded in cortical sites in both adolescents and adults. However, EtOH produced significantly larger delays in P3a and P3b latencies in adults as compared to adolescents. Acute EtOH administration was also found to produce a robust dose-dependent increase in the latency of the P3a and P3b components in adult animals exposed to EtOH vapor as adolescents and air exposed controls; however, larger acute EtOH-induced increases in P3a and P3b latencies were seen in controls as compared to adolescent vapor exposed rats. CONCLUSIONS: Adolescent rats have a less intense P3 latency response to acute EtOH administration when compared to adult rats. Exposure to chronic EtOH during adolescence can cause "retention" of the adolescent phenotype of reduced P3 latency sensitivity to EtOH.

Developmental differences in EEG and sleep responses to acute ethanol administration and its withdrawal (hangover) in adolescent and adult Wistar rats.

Age-related differences in sensitivity to the acute effects of alcohol may play an important role in the increased risk for the development of alcoholism seen in teens that begin drinking at an early age. The present study evaluated the acute and protracted (hangover) effects of ethanol in adolescent (P33-P40) and adult (P100-P107) Wistar rats, using the cortical electroencephalogram (EEG). Six minutes of EEG was recorded during waking, 15 min after administration of 0, 1.5, or 3.0 g/kg ethanol, and for 3 h at 20 h post ethanol, during the rats' next sleep cycle. Significantly higher overall frontal and parietal cortical power was seen in a wide range of EEG frequencies in adolescent rats as compared to adult rats in their waking EEG. Acute administration of ethanol did not produce differences between adolescents and adults on behavioral measures of acute intoxication. However, it did produce a significantly less intense acute EEG response to ethanol in the theta frequencies in parietal cortex in the adolescents as compared to the adults. At 20 h following acute ethanol administration, during the rats' next sleep cycle, a decrease in slow-wave frequencies (1-4 Hz) was seen and the adolescent rats were found to display more reduction in the slow-wave frequencies than the adults did. The present study found that adolescent rats, as compared to adults, demonstrate low sensitivity to acute ethanol administration in the theta frequencies and more susceptibility to disruption of slow-wave sleep during hangover. These studies may lend support to the idea that these traits may contribute to increased risk for alcohol use disorders seen in adults who begin drinking in their early teenage years.