Evaluation of the public health impacts of traffic congestion: a health risk assessment

Background: Traffic congestion is a significant issue in urban areas in the United States and around the world. Previous analyses have estimated the economic costs of congestion, related to fuel and time wasted, but few have quantified the public health impacts or determined how these impacts compare in magnitude to the economic costs. Moreover, the relative magnitudes of economic and public health impacts of congestion would be expected to vary significantly across urban areas, as a function of road infrastructure, population density, and atmospheric conditions influencing pollutant formation, but this variability has not been explored. Methods: In this study, we evaluate the public health impacts of ambient exposures to fine particulate matter (PM2.5) concentrations associated with a business-as-usual scenario of predicted traffic congestion. We evaluate 83 individual urban areas using traffic demand models to estimate the degree of congestion in each area from 2000 to 2030. We link traffic volume and speed data with the MOBILE6 model to characterize emissions of PM2.5 and particle precursors attributable to congestion, and we use a source-receptor matrix to evaluate the impact of these emissions on ambient PM2.5 concentrations. Marginal concentration changes are related to a concentration-response function for mortality, with a value of statistical life approach used to monetize the impacts. Results: We estimate that the monetized value of PM2.5-related mortality attributable to congestion in these 83 cities in 2000 was approximately $31 billion (2007 dollars), as compared with a value of time and fuel wasted of$60 billion. In future years, the economic impacts grow (to over $100 billion in 2030) while the public health impacts decrease to$13 billion in 2020 before increasing to $17 billion in 2030, given increasing population and congestion but lower emissions per vehicle. Across cities and years, the public health impacts range from more than an order of magnitude less to in excess of the economic impacts. Conclusions: Our analyses indicate that the public health impacts of congestion may be significant enough in magnitude, at least in some urban areas, to be considered in future evaluations of the benefits of policies to mitigate congestion

Role of Mutagenicity in Asbestos Fiber-Induced Carcinogenicity and Other Diseases

The cellular and molecular mechanisms of how asbestos fibers induce cancers and other diseases are not well understood. Both serpentine and amphibole asbestos fibers have been shown to induce oxidative stress, inflammatory responses, cellular toxicity and tissue injuries, genetic changes, and epigenetic alterations in target cells in vitro and tissues in vivo. Most of these mechanisms are believe to be shared by both fiber-induced cancers and noncancerous diseases. This article summarizes the findings from existing literature with a focus on genetic changes, specifically, mutagenicity of asbestos fibers. Thus far, experimental evidence suggesting the involvement of mutagenesis in asbestos carcinogenicity is more convincing than asbestos-induced fibrotic diseases. The potential contributions of mutagenicity to asbestos-induced diseases, with an emphasis on carcinogenicity, are reviewed from five aspects: (1) whether there is a mutagenic mode of action (MOA) in fiber-induced carcinogenesis; (2) mutagenicity/carcinogenicity at low dose; (3) biological activities that contribute to mutagenicity and impact of target tissue/cell type; (4) health endpoints with or without mutagenicity as a key event; and finally, (5) determinant factors of toxicity in mutagenicity. At the end of this review, a consensus statement of what is known, what is believed to be factual but requires confirmation, and existing data gaps, as well as future research needs and directions, is provided

Pulmonary Endpoints (Lung Carcinomas and Asbestosis) Following Inhalation Exposure to Asbestos

Lung carcinomas and pulmonary fibrosis (asbestosis) occur in asbestos workers. Understanding the pathogenesis of these diseases is complicated because of potential confounding factors, such as smoking, which is not a risk factor in mesothelioma. The modes of action (MOA) of various types of asbestos in the development of lung cancers, asbestosis, and mesotheliomas appear to be different. Moreover, asbestos fibers may act differentially at various stages of these diseases, and have different potencies as compared to other naturally occurring and synthetic fibers. This literature review describes patterns of deposition and retention of various types of asbestos and other fibers after inhalation, methods of translocation within the lung, and dissolution of various fiber types in lung compartments and cells in vitro. Comprehensive dose-response studies at fiber concentrations inhaled by humans as well as bivariate size distributions (lengths and widths), types, and sources of fibers are rarely defined in published studies and are needed. Species-specific responses may occur. Mechanistic studies have some of these limitations, but have suggested that changes in gene expression (either fiber-catalyzed directly or by cell elaboration of oxidants), epigenetic changes, and receptor-mediated or other intracellular signaling cascades may play roles in various stages of the development of lung cancers or asbestosis

Characteristics and health implications of fine and coarse particulates at roadside, urban background and rural sites in UK

Recent studies have pointed to evidence that fine particles in the air could be significant contributors to respiratory and cardiovascular diseases and mortality. Epidemiologists looking at the health effects of particulate pollution need more information from various receptor locations to improve the understanding of this problem. Detailed information on temporal, spatial and size distributions of particulate pollution in urban areas also is important for air quality modellers as well as being an aid to decision and policy makers of local authorities. This paper presents a detailed analysis of temporal and seasonal variation of PM10 and PM2.5 levels at one urban roadside, one urban background and one rural monitoring location. Levels of PM10, PM2.5 and coarse fraction of particulates are compared. In addition, particulate levels are compared with NO2 and CO concentrations. The study concludes that PM10 and PM2.5 are closely related at urban locations. Diurnal variation in PM2.5/PM10 ratio shows the influence of vehicular emission and movement on size distribution. This ratio is higher in winter than in summer indicating a build-up or longer residence time of finer particulates or washout due to wet weather in winter. In the second part of this study, a disease burden analysis is carried out based on the dose-response relationships recommended by the UK Committee on the Medical Effects of Air Pollution. The disease burden analysis indicates that if Marylebone Road levels of PM10 were prevalent all over London, it will result in around 2.5% increase in death rates due to all causes. Whereas, if Bloomsbury levels were prevalent in London, which is more likely to occur as this is more representative of the urban background environment to which people in London are likely to be exposed, the corresponding increase would be around 1.7%. Considering this, in London, at Bloomsbury levels 973 deaths and 1515 Respiratory Hospital Admissions (RHA) are attributable to PM10 while 2140 RHA are attributable to NO2. After deducting the disease burden due to background levels at Rochester, PM10 emission caused by anthropogenic activities in London equate to 273 additional deaths and 410 additional RHA while NO2 account for additional 1205 incidences of RHA