Epidemiology and Cost of Nosocomial Gastroenteritis, Avon, England, 2002–2003

Implementing control measures rapidly may be effective in controlling gastroenteritis outbreaks

Current Antibiotic Treatment and Outcome for Lower Respiratory Tract Infections

A number of national guidelines have been published to aid the antimicrobial management of community-acquired pneumonia. However, data on prescriptions for lower respiratory tract infection (LRTI) indicate considerable variation in the choice of first-line and subsequent therapy at national and local levels. Outcomes research in LRTI, whether based on clinical, economic or patient-focused criteria, is still evolving. Clinical outcomes are best studied for both pneumonia and exacerbation of chronic obstructive pulmonary disease. Economic evaluations often do not encompass all of the costs, for example, time off from work or the economic impact of antibacterial resistance. Duration of hospital stay is a good marker of costs for hospital providers and may be affected by age. marital status and comorbidities. Antibiotic choice may have an impact on the duration of hospital stay by increasing side effects, predisposing patients to hospitalacquired infection or reduced clinical efficacy. Patient expectation is largely unstudied in pulmonary infection

A Systematic Review and Meta-Analysis of Multiple Airborne Pollutants and Autism Spectrum Disorder.

BackgroundExposure to ambient air pollution is widespread and may be detrimental to human brain development and a potential risk factor for Autism Spectrum Disorder (ASD). We conducted a systematic review of the human evidence on the relationship between ASD and exposure to all airborne pollutants, including particulate matter air pollutants and others (e.g. pesticides and metals).ObjectiveTo answer the question: "is developmental exposure to air pollution associated with ASD?"MethodsWe conducted a comprehensive search of the literature, identified relevant studies using inclusion/exclusion criteria pre-specified in our protocol (registered in PROSPERO, CRD # 42015017890), evaluated the potential risk of bias for each included study and identified an appropriate subset of studies to combine in a meta-analysis. We then rated the overall quality and strength of the evidence collectively across all air pollutants.ResultsOf 1,158 total references identified, 23 human studies met our inclusion criteria (17 case-control, 4 ecological, 2 cohort). Risk of bias was generally low across studies for most domains; study limitations were related to potential confounding and accuracy of exposure assessment methods. We rated the quality of the body of evidence across all air pollutants as "moderate." From our meta-analysis, we found statistically significant summary odds ratios (ORs) of 1.07 (95% CI: 1.06, 1.08) per 10-μg/m3 increase in PM10 exposure (n = 6 studies) and 2.32 (95% CI: 2.15, 2.51) per 10-μg/m3 increase in PM2.5 exposure (n = 3 studies). For pollutants not included in a meta-analysis, we collectively evaluated evidence from each study in rating the strength and quality of overall evidence considering factors such as inconsistency, imprecision, and evidence of dose-response. All included studies generally showed increased risk of ASD with increasing exposure to air pollution, although not consistently across all chemical components.ConclusionAfter considering strengths and limitations of the body of research, we concluded that there is "limited evidence of toxicity" for the association between early life exposure to air pollution as a whole and diagnosis of ASD. The strongest evidence was between prenatal exposure to particulate matter and ASD. However, the small number of studies in the meta-analysis and unexplained statistical heterogeneity across the individual study estimates means that the effect could be larger or smaller (including not significant) than these studies estimate. Our research supports the need for health protective public policy to reduce exposures to harmful airborne contaminants among pregnant women and children and suggests opportunities for optimizing future research

A Systematic Review and Meta-Analysis of Multiple Airborne Pollutants and Autism Spectrum Disorder

<div><p>Background</p><p>Exposure to ambient air pollution is widespread and may be detrimental to human brain development and a potential risk factor for Autism Spectrum Disorder (ASD). We conducted a systematic review of the human evidence on the relationship between ASD and exposure to all airborne pollutants, including particulate matter air pollutants and others (e.g. pesticides and metals).</p><p>Objective</p><p>To answer the question: “is developmental exposure to air pollution associated with ASD?”</p><p>Methods</p><p>We conducted a comprehensive search of the literature, identified relevant studies using inclusion/exclusion criteria pre-specified in our protocol (registered in PROSPERO, CRD # 42015017890), evaluated the potential risk of bias for each included study and identified an appropriate subset of studies to combine in a meta-analysis. We then rated the overall quality and strength of the evidence collectively across all air pollutants.</p><p>Results</p><p>Of 1,158 total references identified, 23 human studies met our inclusion criteria (17 case-control, 4 ecological, 2 cohort). Risk of bias was generally low across studies for most domains; study limitations were related to potential confounding and accuracy of exposure assessment methods. We rated the quality of the body of evidence across all air pollutants as “moderate.” From our meta-analysis, we found statistically significant summary odds ratios (ORs) of 1.07 (95% CI: 1.06, 1.08) per 10-μg/m³ increase in PM₁₀ exposure (n = 6 studies) and 2.32 (95% CI: 2.15, 2.51) per 10-μg/m³ increase in PM_2.5 exposure (n = 3 studies). For pollutants not included in a meta-analysis, we collectively evaluated evidence from each study in rating the strength and quality of overall evidence considering factors such as inconsistency, imprecision, and evidence of dose-response. All included studies generally showed increased risk of ASD with increasing exposure to air pollution, although not consistently across all chemical components.</p><p>Conclusion</p><p>After considering strengths and limitations of the body of research, we concluded that there is “limited evidence of toxicity” for the association between early life exposure to air pollution as a whole and diagnosis of ASD. The strongest evidence was between prenatal exposure to particulate matter and ASD. However, the small number of studies in the meta-analysis and unexplained statistical heterogeneity across the individual study estimates means that the effect could be larger or smaller (including not significant) than these studies estimate. Our research supports the need for health protective public policy to reduce exposures to harmful airborne contaminants among pregnant women and children and suggests opportunities for optimizing future research.</p></div

Strength of evidence definitions.

<p>Strength of evidence definitions.</p

Search results for studies relevant to air pollution exposure and ASD outcome.

<p>Search results for studies relevant to air pollution exposure and ASD outcome.</p

Summary of rating quality and strength of the human evidence.

<p>Summary of rating quality and strength of the human evidence.</p

Risk of bias ratings for included human studies relevant to air pollution exposure and ASD outcome.

<p>A, All criteria except exposure assessment criteria. B, Exposure assessment criteria.</p

Characteristics of included human studies on air pollution and ASD, by publication date and study design.

<p>Characteristics of included human studies on air pollution and ASD, by publication date and study design.</p

Meta-analysis of human studies; reported effect estimates [95% confidence interval] from individual studies (inverse-variance weighted, represented by size of rectangle) and overall pooled estimate from random effects (RE) model for PM_2.5 exposure and ASD.

<p>Meta-analysis of human studies; reported effect estimates [95% confidence interval] from individual studies (inverse-variance weighted, represented by size of rectangle) and overall pooled estimate from random effects (RE) model for PM_2.5 exposure and ASD.</p