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Biomedical subjects

J Mindell

Publications and source records attributed to J Mindell.

At least 19 recordsLinked to original sources
PubMed2004

Health impact assessment as an agent of policy change: improving the health impacts of the mayor of London's draft transport strategy.

OBJECTIVE: To increase the positive and mitigate the negative health impacts of the mayor's draft transport strategy for London. DESIGN: A rapid prospective health impact assessment (HIA) of the penultimate draft of the strategy, using a review commissioned by the regional director of public health; an appraisal of congestion charging; and a participatory workshop. Two audits of changes were performed to assess the impact on policy of the HIA process. SETTING: Regional government policy development. INTERVENTION: Recommendations from the rapid HIA were fed back into the drafting process. MAIN OUTCOME MEASURE: Changes (a) between the penultimate draft and the draft for public consultation and (b) between that and the final mayoral strategy. RESULTS: The draft transport strategy published for consultation differed in a number of respects from the previous version. Almost all the recommendations from the HIA were incorporated into the final strategy. Significant changes included promoting sustainable travel plans for workplaces and schools; giving priority to infrastructure and services that benefit London's deprived communities; increased emphasis on promoting walking and cycling and reducing reliance on private cars; and a commitment to track the health impacts of the final strategy and its implementation. Specific additions included re-allocating road space. CONCLUSION: HIA was successful in influencing the transport strategy for London, resulting in several improvements from a health viewpoint. HIA is an effective method both for bringing about significant change in policy proposals and in increasing policy makers' understanding of determinants of health and hence in changing attitudes of policy makers.

Environmental Health↗
PubMed2004

Enhancing the evidence base for health impact assessment.

Health impact assessment differs from other purposes for which evidence is collated in a number of ways, including:the focus on complex interventions or policy and their diverse effects on determinants of health;the need for evidence on the reversibility of adverse factors damaging to health;the diversity of the evidence in terms of relevant disciplines, study designs, quality criteria and sources of information;the broad range of stakeholders involved;the short timescale and limited resources generally available;the pragmatic need to inform decision makers regardless of the quality of the evidence. These have implications for commissioning and conducting reviews. Methods must be developed to: facilitate comprehensive searching across a broad range of disciplines and information sources; collate appropriate quality criteria to assess a range of study designs; synthesise different kinds of evidence; and facilitate timely stakeholder involvement. Good practice standards for reviews are needed to reduce the risk of poor quality recommendations. Advice to decision makers must make explicit limitations resulting from absent, conflicting, or poor quality evidence.

Decision Making↗
PubMed2004

Predicted health impacts of urban air quality management.

STUDY OBJECTIVE: The 1995 UK Environment Act required local authorities to review air quality and, where UK National Air Quality Strategy objectives (except ozone) are likely to be exceeded in 2005, to declare local air quality management areas and prepare action plans. This study modelled the impacts on health of reductions from current levels of PM(10) to these objectives. DESIGN: The framework for conducting quantified health impact assessment assessed causality, then, if appropriate, examined the shape and magnitude of the exposure-response relations. The study modelled declines in pollution to achieve the objectives, then modelled the numbers of deaths and admissions affected if air pollution declined from existing levels to meet the objectives, using routine data. SETTING: Westminster, central London. MAIN RESULTS: Attaining the 2004 PM(10) 24 hour objective in Westminster results in 1-21 lives no longer shortened in one year (annual deaths 1363). Reducing exceedences from 35 to seven almost doubles the estimates. The 2009 objective for the annual mean requires a substantial reduction in PM(10), which would delay 8-20 deaths. About 20 respiratory and 14-20 circulatory admissions would be affected and around 5% of emergency hospital attendances for asthma by attaining the lower annual mean target. The effects of long term exposure to particulates may be an order of magnitude higher: models predict about 24 deaths are delayed by reaching the 2004 annual target (40 microg/m(3)([gravimetric])) and a hundred deaths by reducing annual mean PM(10) to 20 microg/m(3)([gravimetric]). CONCLUSIONS: Modelling can be used to estimate the potential health impacts of air quality management programmes.

Air Pollutants↗
PubMed2002

A framework for the evidence base to support Health Impact Assessment.

OBJECTIVE: To introduce a conceptual structure that can be used to organise the evidence base for Health Impact Assessment (HIA). BACKGROUND: HIA can be used to judge the potential health effects of a policy, programme or project on a population, and the distribution of those effects. Progress has been made in incorporating HIA into routine practice, especially (in the UK) at local level. However, these advances have mainly been restricted to process issues, including policy engagement and community involvement, while the evidence base has been relatively neglected. RELATING POLICIES TO THEIR IMPACT ON HEALTH: The key distinctive feature of HIA is that determinants of health are not taken as given, but rather as factors that themselves have determinants. Nine ways are distinguished in which evidence on health and its determinants can be related to policy, and examples are given from the literature. The most complete of these is an analysis of health effects in the context of a comparison of options. A simple model, the policy/risk assessment model (PRAM), is introduced as a framework that relates changes in levels of exposures or other risk factors to changes in health status. This approach allows a distinction to be made between the technical process of HIA and the political process of decision making, which involves lines of accountability. Extension of the PRAM model to complex policy areas and its adaptation to non-quantitative examples are discussed. ISSUES FOR THE FUTURE: A sound evidence base is essential to the long term reputation of HIA. Research gaps are discussed, especially the need for evidence connecting policy options with changes in determinants of health. It is proposed that policy options could be considered as "exposure" variables in research. The methodology needs to be developed in the course of work on specific issues, concentrated in policy areas that are relatively tractable. CONCLUSIONS: A system of coordination needs to be established, at national or supranational level, building on existing initiatives. The framework suggested in this paper can be used to collate and evaluate what is already known, both to identify gaps where research is required and to enable an informed judgement to be made about the potential health impacts of policy options. These judgements should be made widely available for policy makers and for those undertaking health impact assessment.

Evidence-Based Medicine↗
PubMed2001

Lessons from tobacco control for advocates of healthy transport.

Many parallels can be drawn between cigarettes and motor vehicles, smoking and car driving, and the tobacco and the auto/oil industries. Those promoting healthy and sustainable transport policies can learn lessons from tobacco control activities over the past 50 years. Evidence-based legislation is more effective than negotiated voluntary agreements between industry and government. Media advocacy is crucial to reframe the issues to allow changes in national policies that facilitate healthier choices. Worthwhile public health policies seen as a threat by multinational companies will be opposed by them but active national and international networks of healthcare professionals, voluntary organizations, charities and their supporters can match the political power of these industries.

Accidents, Traffic↗
PubMed2001

What do we need for robust, quantitative health impact assessment?

Health impact assessment (HIA) aims to make the health consequences of decisions explicit. Decision-makers need to know that the conclusions of HIA are robust. Quantified estimates of potential health impacts may be more influential but there are a number of concerns. First, not everything that can be quantified is important. Second, not everything that is being quantified at present should be, if this cannot be done robustly. Finally, not everything that is important can be quantified: rigorous qualitative HIA will still be needed for a thorough assessment. This paper presents the first published attempt to provide practical guidance on what is required to perform robust, quantitative HIA. Initial steps include profiling the affected populations, obtaining evidence for postulated impacts, and determining how differences in subgroups' exposures and susceptibilities affect impacts. Using epidemiological evidence for HIA is different from carrying out a new study. Key steps in quantifying impacts are mapping the causal pathway, selecting appropriate outcome measures and selecting or developing a statistical model. Evidence from different sources is needed. For many health impacts, evidence of an effect may be scarce and estimates of the size and nature of the relationship may be inadequate. Assumptions and uncertainties must therefore be explicit. Modelled data can sometimes be tested against empirical data but sensitivity analyses are crucial. When scientific problems occur, discontinuing the study is not an option, as HIA is usually intended to inform real decisions. Both qualitative and quantitative elements of HIA must be performed robustly to be of value.

Guidelines as Topic↗
PubMed1997

Fuel pump promos.

Explore the source record for details and available documents.

Advertising↗
PubMed1994

Three-year follow-up of the Oxford Cholesterol Study: assessment of the efficacy and safety of simvastatin in preparation for a large mortality study.

We report the results of a randomized single-centre study designed to assess the effects of simvastatin on blood lipids, blood biochemistry, haematology and other measures of safety and tolerability in preparation for a large-scale multicentre mortality study. Six hundred and twenty-one individuals considered to be at increased risk of coronary heart disease were randomized, following a 2-month placebo 'run-in' period, to receive 40 mg daily simvastatin, 20 mg daily simvastatin or matching placebo. Their mean age was 63 years, 85% were male, 62% had a history of prior myocardial infarction (MI), and the mean baseline total cholesterol was 7.0 mmol.l-1. Median follow-up in the present report is 3.4 years. Eight weeks after randomization, 40 mg daily simvastatin had reduced non-fasting total cholesterol by 29.2% +/- 1.1 (2.03 +/- 0.08 mmol.l-1) and 20 mg daily simvastatin had reduced it by 26.8% +/- 1.0 (1.87 +/- 0.07 mmol.l-1). Almost all of the difference in total cholesterol at 8 weeks was due to the reduction in LDL cholesterol (40.8% +/- 1.6 and 38.2% +/- 1.4 among patients allocated 40 mg and 20 mg of simvastatin daily respectively), but simvastatin also reduced triglycerides substantially (19.0% and 17.3%) and produced a small increase in HDL cholesterol (6.4% and 4.8%). These effects were largely sustained over the next 3 years, with 40 mg daily simvastatin producing a slightly greater reduction in total cholesterol at 3 years (25.7% +/- 1.9 reduction) than did 20 mg daily simvastatin (22.2% +/- 1.8). There were no differences between the treatment groups in the numbers of reports of 'possible adverse effects' of treatment or of a range of different symptoms or conditions (including those related to sleep or mood) recorded at regular clinic follow-up. Mean levels of alanine aminotransferase, aspartate aminotransferase and creatine kinase were slightly increased by treatment, but there were no significant differences between the treatment groups in the numbers of patients with significantly elevated levels. A slightly lower platelet count in the simvastatin group was the only haematological difference from placebo, with no difference in the numbers of patients with low platelet counts. In summary, the simvastatin regimens studied produced large sustained reductions in total cholesterol, LDL cholesterol and triglyceride and small increases in HDL cholesterol. They were well tolerated, with no evidence of serious side-effects during the first 3 years of this study.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1993

Membrane translocation and channel-forming activities of diphtheria toxin are blocked by replacing isoleucine 364 with lysine.

A mutant of diphtheria toxin in which Ile-364 was replaced by Lys was at least 500-fold less toxic to Vero cells than the parental toxin. Its ability to undergo low-pH-triggered translocation across the plasma membrane was greatly diminished, as was its ability to form ion-conductive channels. In addition, the mutant toxin was inactive in the pH-dependent killing of Escherichia coli.

Animals↗
PubMed1992

Computer modelling of the transmembrane channel formed by a CNBr peptide of diphtheria toxin B fragment.

Diphtheria toxin (DT) forms transmembrane, voltage-dependent channels in a planar lipid bilayer. Channels with similar characteristics were obtained with CB1, a cyanogen bromide peptide of diphtheria toxin B fragment (DTB) (res 340-459). Tryptophan 398 is in interaction with the hydrophobic core of the lipid bilayer. Using the Eisenberg method in association with the Shiffer-Edmunson wheel representation, we have identified two amphipathic alpha-helices within CB1 (res 346-364 and 389-406) that could be involved in the interaction with lipids. Bearing this information in mind, we are providing a model for the structure of the CB1 channel.

Amino Acid Sequence↗