Libri sul tema "Household exposures"

A wide variety of manmade and naturally occurring air pollutants are known to cause cancer. Diverse exposures such as tobacco smoke, radionuclides (radon), chemicals (benzene, mustard gas, and volatile organic compounds), fibers (asbestos), and metals and metalloids (chromium, nickel, and arsenic) have long been classified as carcinogenic to humans. Historically, these classifications were based predominantly on high levels of exposure in occupational settings. Over the last thirty to forty years, scientific attention has focused on quantifying the adverse health effects of indoor and outdoor air pollutants at exposure levels several orders of magnitude lower than were studied initially. These include secondhand smoke, household exposure to radon, residential and environmental exposure to asbestos, soot from diesel-powered engines, ambient exposures to small particles (PM2.5), and indoor air pollution from the combustion of biomass and coal. This chapter provides an overview of recent epidemiologic studies of air pollutants and cancer.

Human activities associated with environmental degradation are threatening urban and rural water supplies throughout the world. Although water quality in the United States surpasses that in most of the world, increasing challenges from an aging infrastructure, poorly controlled disposal of pharmaceuticals, household chemical products, and biologically active industrial chemicals are causing widespread degradation. Toxicology studies have highlighted the role of chronic, low-level chemical exposures of children in the development of disease later in life and demonstrated the chemicals’ epigenetic effects. Despite billions of dollars spent annually to purify diminishing water resources, most purified water is used for waste disposal a for agricultural and industrial processes that do not necessarily require good-quality water. Chapter 5 addresses some of the current threats to water supplies and proposes approaches to increase awareness and provide solutions for the protection of human and environmental health.

The chapter describes the Greco-Roman and Jewish household, including its members, customs, domestic rituals, and gender roles, along with their intersections with New Testament and other early Christian writings. It presents nomenclature used to describe what we today call “family” and its differences from modern usage. The architectural forms of ancient households (domus, oikos, insula, taberna) are described. The chapter discusses the respective domestic roles of males and females as husbands, wives, and slaves. Children, the practices of infant exposure and adoption as slaves, domestic obligations, education, household economic contribution, laws of inheritance, and rituals associated with birth and maturity are considered. The discussion also contrasts laws of slavery and manumission in the western and eastern Mediterranean. It considers the economic power of slaves and freedpersons, the typical costs of slaves, and freedperson-master obligations. It presents rituals and beliefs surrounding the deceased. Finally, it treats the role of fictive kinship language and how it patterned relationships of Christians with God and one another.

Explains the neurological, emotional, and behavioral impacts of violence and trauma experienced by newborns, infants, children, and teenagers. Traumatic events known as adverse childhood experiences (ACEs) can affect children physically, mentally, and emotionally, sometimes with long-term health and behavioral effects. Abuse, neglect, exposure to community and domestic violence, and household dysfunction all have the potential to alter brain development and behavior, but few people are able to recognize or respond to trauma in children. Given the prevalence of childhood exposure to violence—with one in four children ages 5 to 15 living in households with only moderate levels of safety and nurturance and infants and children ages 0 to 3 comprising the highest percentage of those maltreated—it is imperative that students and professionals alike be able to identify types and consequences of violence and trauma. This book provides readers with the information they need in order to know how to detect and prevent ACEs and to help children who have lived through them.

Explains the neurological, emotional, and behavioral impacts of violence and trauma experienced by newborns, infants, children, and teenagers. Traumatic events known as adverse childhood experiences (ACEs) can affect children physically, mentally, and emotionally, sometimes with long-term health and behavioral effects. Abuse, neglect, exposure to community and domestic violence, and household dysfunction all have the potential to alter brain development and behavior, but few people are able to recognize or respond to trauma in children. Given the prevalence of childhood exposure to violence—with one in four children ages 5 to 15 living in households with only moderate levels of safety and nurturance and infants and children ages 0 to 3 comprising the highest percentage of those maltreated—it is imperative that students and professionals alike be able to identify types and consequences of violence and trauma. This book provides readers with the information they need in order to know how to detect and prevent ACEs and to help children who have lived through them.

Use of personal care products and household and commercial cleaners with antibacterial capabilities has increased human exposure to an array of chemicals. Because these products are washed down the drain, they are discharged with wastewater into fields, lakes, streams, oceans, and municipal water systems. This chapter focuses on the uses, persistence, routes of human exposure, and potential health effects of four common environmental chemicals or chemical classes—parabens, triclosan, triclocarban, and quaternary ammonium compounds—because exposure to them is ubiquitous, environmental contamination is significant, and evidence of harm has emerged. These man-made environmental contaminants illustrate how the rapid introduction of new chemicals into consumer products must be weighed against the unavoidable environmental contamination and potential biologic effects that may ensue.

Remote control tuning encourages a form of interactive television using a technology already available in 80 percent of American households. Editors Walker and Bellamy have compiled the first book of state-of-the-art research on a topic of growing interest to media researchers, practitioners, and students. Chapter authors combine survey measurements with recorded observations of viewing behavior, an analysis of the program sources accessed during grazing, experimental studies of remote control use, and historical and critical analyses. Specific topics include: the history of the remote control device, gender differences in its use, family communication and parental control of the device, remote controls and selective exposure to media messages, the impact of remote controls on programming and promotion, remote controls and critical perspective on television, and future technologies. This volume is rooted in social scientific research, but theoretically and methodologically broad in scope.

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.