Books on the topic 'Hazard ratios'

This chapter explores survival analysis. It includes data censoring, functions of duration time (the survival function, and hazard function), Cox’s proportional hazards model, log-linearity, time varying predictors, and odds ratios.

Chapter 11 covers survival analysis, and includes Kaplan–Meier estimates, and the logrank test. Cox regression is used to do multifactorial analyses with results reported as adjusted hazard ratios. The chapter includes analyses using Stata, SAS, SPSS, and R.

This chapter gives the definition of confounding, a central issue in epidemiology and its dependence on two associations, with exposure and with outcome. It explains confounding in trials, cohort and case-control studies, and Simpson’s paradox. It explains the five methods of controlling confounding: restriction, randomisation, stratification, matching and multivariate methods. For randomised trials, the limits of randomisation, residual confounding, pre-stratification, intention-to-treat, management and explanatory trials, pragmatic trials are explained. It shows the Mantel–Haenszel risk ratio or odds ratio, direct and indirect standardisation, and effect modification. Frequency and individual matching, their value and limitations, over matching, confounding by indication, and calculation of matched odds ratio are shown. It explains multivariate methods, including linear, logistic, Poisson, and Cox’s proportionate hazards models, including the relationship between coefficients and odds ratios, dummy variables, conditional methods, and propensity scores.

Multivariate multilevel survival analysis is introduced for studying hazard rates of observed emotional behavior relevant for coercion theory. Finite time sampling reliability (FTSR) and short-term retest reliability (STRR) across two occasions (sessions) of observation during structured problem-solving tasks several weeks apart were determined for hazard rates of emotional behaviors for parent–child dyads. While FTSR was high (.80–.96), STRR was low (.16–.65), suggesting that emotional behaviors in the context of parent–child social interaction are not very stable over a period of several weeks. Using latent variable structural equation models that corrected for the low STRR, two hazard rates were predictive of change in child antisocial behavior over a 3-year period (kindergarten to third grade) net of initial child antisocial behavior. Low levels of parent positive emotion and increases from session 1 to 2 of child neutral behavior both accounted for unique variance in third grade antisocial behavior.

This chapter describes hazards for agricultural workers. This is a large and exceedingly diverse group, with work—often precarious work—being performed by very young and very old persons, workers who are often economically disadvantaged, and workers of many nationalities and languages. There is considerable variation in power between employers and workers who frequently lack authorization for legal employment in the United States. Emphasis is placed on the hazards faced by migrant workers and immigrant workers. A number of factors, including public policy and the hazards involved with agriculture, such as pesticides, impact worker health and safety. Agricultural workers do not have many of the regulatory protections provided to workers in most other industries in the United States. Mechanical, large-animal, environmental, and toxicologic challenges all contribute to the markedly elevated rates of fatal and nonfatal injuries in these workers. High rates of stress and suicide affect these young workers.

This chapter studies calculative risk-assessment practices in credit rating agencies. It identifies two fundamentally different methodological approaches for producing ratings, which in turn shape the respective conceptions of credit risk. The traditional approach sees ‘risk’ as an only partially calculable and predictable set of hazards that should be avoided or minimized. This approach is particularly evident in the production of country credit ratings and gives rise to ordinal rankings of risk. By contrast, structured finance rating practices conceive of ‘risk’ as both fully calculable and controllable; they construct cardinal measures of risk by assuming that ontological uncertainty does not exist and that models can capture all possible events in a probabilistic manner. This assumption—that uncertainty can be turned into measurable risk—is a necessary precondition for structured finance securities and has become an influential imaginary in financial markets.

The hazards of anaesthesia should be considered in the context of the hazard of surgery and of the pathology for which the surgery is being undertaken. Anaesthesia has become progressively safer since the successful demonstration of ether anaesthesia in Boston, Massachusetts, United States in 1846 and the first reported death under anaesthesia in 1847. The best estimation of the rate of anaesthesia-related mortality comes from the anaesthesia mortality review committees in Australia and New Zealand, where data have been collected under essentially consistent definitions since 1960, and reports are amalgamated under the auspices of the Australian and New Zealand College of Surgeons. An internationally accepted definition of anaesthetic mortality is overdue. Extending the time for inclusion of deaths from 24 h to 30 days or longer substantially increases estimated rates of mortality. Attribution of cause of death may be problematic. Even quite small degrees of myocardial injury in patients undergoing non-cardiac surgery increase the risk of subsequent mortality, and in older patients, 30-day all-cause mortality following inpatient surgery may be surprisingly high. Patients should be given a single estimate of the combined risk of surgery and anaesthesia, rather than placing undue emphasis on the risk from anaesthesia alone. Hazards may arise from equipment or from drugs either directly or through error. Error often underlies harmful events in anaesthesia and may be made more likely by fatigue or circadian factors, but violations are also important. Training in expert skills and knowledge, and in human factors, teamwork, and communication is key to improving safety.

“Can’t intubate, can’t oxygenate” crises and aspiration of gastric contents are important hazards in anaesthesia, and may result in the death of relatively young and healthy patients. Airway difficulties may manifest at the end of anaesthesia as well as at induction and are commoner in emergency departments and intensive care settings than during anaesthesia in operating rooms. Elements of poor management characterize the majority of airway complications. Emergency cricothyroidotomy performed by anaesthetists is associated with a high rate of failure. Other important hazards associated with anaesthesia may involve excessive or inadequate levels of oxygen or carbon dioxide in the blood, hypertension or hypotension, hypothermia or hyperthermia (including malignant hyperpyrexia), hypovolaemia, embolism of gas or thrombus, awareness, infection, and injury to the peripheral or central nervous system, or the eyes. Stroke and postoperative cognitive dysfunction may be particularly devastating for patients. These hazards are typically increased in low- and middle-income countries. The World Federation of Societies of Anaesthesiologists and the World Health Organization have endorsed international standards for a safe practice of anaesthesia, which are structured to reflect different levels of resource. The Lifebox Foundation seeks to improve the safety of surgery and anaesthesia in resource-constrained areas, notably by closing the substantial global gap in pulse oximetry. Several hazards are integral to the occupation of anaesthesia, including certain infections, increased rates of suicide, and medico-legal risks. In the end, the best way to mitigate these risks is through focusing on the safety of our patients.

How does being discriminated against affect one’s health, and through what mechanisms? Most research has focused on two causal pathways, highlighting how discrimination increases psychological stress and exposure to neighborhood hazards. This chapter advances an alternative, complementary set of mechanisms through which stigma and discrimination may shape health. Grounded in evolutionary biology’s life history theory, the framework holds that discrimination alters aspects of the physical and social ecologies in which people live (e.g., sex ratio, unpredictable extrinsic causes of mortality). These discriminating ecologies pull for specific behaviors and physiological responses (e.g., risk-taking, sexual activity, offspring care, fat storage) that are active, strategic, and rational given the threats and opportunities afforded by these ecologies but that also have downstream implications for health. This framework generates a wide range of nuanced insights and unique hypotheses about the discrimination-health relationship, and suggests specific approaches to intervention while pointing to complex ethical issues.

Poorer renal function is associated with increasing morbidity and mortality. In the wider population this is mainly as a consequence of cardiovascular disease. Renal patients are more likely to progress to end-stage renal disease, but also have high cardiovascular risk. Aiming to reduce both progression of renal impairment and cardiovascular disease are not contradictory. Focusing on the management of high-risk patients with proteinuria and reduced glomerular filtration rates, it is recommended that blood pressure should be kept below 140/90, or 130/80 if proteinuria is > 1 g/24 h (protein:creatinine ratio (PCR) >100 mg/mmol or 0.9 g/g). These targets may be modified according to age and other factors. Angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor antagonists should form part of the therapy for patients with proteinuria > 0.5 g/24 h (PCR > 50 mg/mmol or 0.45 g/g). Use of ACEIs or angiotensin receptor blockers in patients with lower levels of proteinuria may be indicated in some patient groups even in the absence of hypertension, notably in diabetic nephropathy. Evidence that other agents that reduce proteinuria bring additional benefits is weak at present. The best studies of ‘dual-blockade’ with various combinations of ACEIs, ARBs, and renin inhibitors have shown additional hazard with little evidence of additional benefit. Hyperlipidaemia—regardless of lipid levels, statin therapy is indicated in secondary cardiovascular prevention, and in primary prevention where cardiovascular risk is high, noting that current risk estimation tools do not adequately account for the increased risk of patients with CKD. There is not substantial evidence that lipid lowering therapy impacts on average rates of loss of GFR in progressive CKD. Non-drug lifestyle interventions to reduce cardiovascular risk, including stopping smoking, are important for all. Acidosis—in more advanced CKD it is justified to treat acidosis with oral sodium bicarbonate. Diet—sodium restriction to < 100 mmol/day (6 g/day) and avoidance of excessive dietary protein are justified in early to moderate CKD. Recommendations to limit levels of protein to 0.8 g/kg body weight are suggested by some, but additional protective effects of this are likely to be slight in patients who are otherwise well managed. Low-protein diets may carry some risk. Lower-protein diets may however be used to prevent symptoms in advanced CKD not treated by dialysis.

Nineteenth-century male death rates were more influenced by occupation than by social class. This was because major variations in exposure, depending on where someone lived and the hazards which he faced at work, were more important than income or status. Over time the risk rankings of many occupations changed markedly. By the mid-twentieth century class gradients in mortality were clear, especially at the top and bottom of the hierarchy. However, it remains the case that even after controlling for social class, significant differences in mortality remain. Research since the 1980s has shown that including controls for area deprivation still does not wholly account for what is observed. In particular, a ‘Glasgow effect’ of enhanced mortality remains unexplained. A range of possible reasons have been offered for Glasgow’s enhanced mortality, including recent research on epigenetic effects.

Guidelines for Mine Waste Dump and Stockpile Design is a comprehensive, practical guide to the investigation, design, operation and monitoring of mine waste dumps, dragline spoils and major stockpiles associated with large open pit mines. These facilities are some of the largest man-made structures on Earth, and while most have performed very well, there are cases where instabilities have occurred with severe consequences, including loss of life and extensive environmental and economic damage. Developed and written by industry experts with extensive knowledge and experience, this book is an initiative of the Large Open Pit (LOP) Project. It comprises 16 chapters that follow the life cycle of a mine waste dump, dragline spoil or stockpile from site selection to closure and reclamation. It describes the investigation and design process, introduces a comprehensive stability rating and hazard classification system, provides guidance on acceptability criteria, and sets out the key elements of stability and runout analysis. Chapters on site and material characterisation, surface water and groundwater characterisation and management, risk assessment, operations and monitoring, management of ARD, emerging technologies and closure are included. A chapter is also dedicated to the analysis and design of dragline spoils. Guidelines for Mine Waste Dump and Stockpile Design summarises the current state of practice and provides insight and guidance to mine operators, geotechnical engineers, mining engineers, hydrogeologists, geologists and other individuals that are responsible at the mine site level for ensuring the stability and performance of these structures. Readership includes mining engineers, geotechnical engineers, civil engineers, engineering geologists, hydrogeologists, environmental scientists, and other professionals involved in the site selection, investigation, design, permitting, construction, operation, monitoring, closure and reclamation of mine waste dumps and stockpiles.

Rearing young stock for replacement heifers is probably one of the least well understood and practised aspects of herd and feeding management on dairy farms throughout the world, particularly on small holder dairy farms in the tropics. This book addresses all the major concerns of the small holder dairy farmer in Asia. It shows how to attain optimal growth in young stock, so that as cows, they can calve at an appropriate early age at the lowest cost and promptly substitute for any cows culled from the milking herd. This provides continuing returns on the investments of feed, labour and other farm resources. Low reproductive rates and high calf mortality are the major causes of reproductive wastage. This has a direct bearing on culling and replacement strategies and on genetic improvement. In many tropical countries, calf mortality can be as high as 50%. In some areas this can be due to climatic stress on temperate or crossbred stock. While climatic stress compounds the other hazards of calf life, high calf mortality is usually due to diseases and poor feeding management. Rearing Young Stock on Tropical Dairy Farms in Asia encourages the small holder dairy farmer to maintain their investment in replacement heifers and gives them the tools necessary to achieve realistic targets for mortalities, live weight gain, mating age, and age and live weight at first calving. It is a companion volume to three previous manuals written by John Moran: Tropical Dairy Farming, Business Management for Tropical Dairy Farmers and Managing High Grade Dairy Cows in the Tropics.

Stories of long-lived animal species—from thousand-year-old tubeworms to 400-year-old sharks—and what they might teach us about human health and longevity. Opossums in the wild don't make it to the age of three; our pet cats can live for a decade and a half; cicadas live for seventeen years (spending most of them underground). Whales, however, can live for two centuries and tubeworms for several millennia. Meanwhile, human life expectancy tops out around the mid-eighties, with some outliers living past 100 or even 110. Is there anything humans can learn from the exceptional longevity of some animals in the wild? In Methuselah's Zoo, Steven Austad tells the stories of some extraordinary animals, considering why, for example, animal species that fly live longer than earthbound species and why animals found in the ocean live longest of all. Austad—the leading authority on longevity in animals—argues that the best way we will learn from these long-lived animals is by studying them in the wild. Accordingly, he proceeds habitat by habitat, examining animals that spend most of their lives in the air, comparing insects, birds, and bats; animals that live on, and under, the ground—from mole rats to elephants; and animals that live in the sea, including quahogs, carp, and dolphins. Humans have dramatically increased their lifespan with only a limited increase in healthspan; we're more and more prone to diseases as we grow older. By contrast, these species have successfully avoided both environmental hazards and the depredations of aging. Can we be more like them?

Infection with Marburg and Ebola viruses cause haemorrhagic fevers that are characterized by organ malfunction, bleeding complications, and high mortality. The viruses are members of the family Filoviridae, a group of membrane-enveloped filamentous RNA viruses. Five distinct species of the genus Ebolavirus have been reported; the genus Marburgvirus contains only one species. Both Marburg and Ebola virus diseases are zoonotic infections whose primary hosts are thought to be bats. The initial human infection is acquired from wildlife and subsequent person-to-person spread propagates the outbreak until it is brought under control. Ebola and Marburg viruses are classified as hazard or risk group 4 pathogens because of the very high case fatality rates observed for Ebola and Marburg virus diseases, the frequency of person-to-person transmission and community spread, and the lack of an approved vaccine or antiviral therapy. This mandates that infectious materials are handled and studied in maximum containment laboratory facilities. Epidemics have occurred sporadically since the discovery of Marburg in 1967 and Ebola virus in 1976. While some of these outbreaks have been relatively large, infecting a few hundreds of individuals, they have generally occurred in rural settings and have been controlled relatively easily. However, the 2013–2016 epidemic of Ebola virus disease in West Africa was different, representing the first emergence of the Zaire species of Ebola in a high-density urban location. Consequently, this has been the largest recorded filovirus outbreak in both the number of people infected and the range of geographical spread. Many of the reported and confirmed cases were among people living in high-density and impoverished urban environments. The chapter summarizes the most up-to-date taxonomic status of the family Filoviridae. It focuses on Marburg and Ebola viruses in a historical context, culminating in the 2013–2016 outbreak of Ebola virus in West Africa. Virus biology of the most well-studied member is described, with details of the viral genome and the protein machinery necessary to propagate viruses at the molecular and cellular level. This information is used to build a wider-scale virus–host perspective with detail on the pathology and pathogenesis of Ebola virus disease. The consequences of cell infection are examined, together with our current understanding of the immune response to Ebola virus, leading to a broader description of the clinical features of disease. The chapter closes by drawing information together in a section on diagnosis, ecology, prevention, and control.

Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.