Global Climate Implications for Homelessness: A Scoping Review.

Homelessness is a persistent global challenge with significant health impacts on those affected. Homeless people are by definition the most exposed to weather conditions and the social and economic problems caused by extreme weather and climate change and variability. This systematic review was designed to synthesize the academic literature that addresses the health and social implications of global climate change for homelessness. The question examined in this systematic scoping review is the following: What is the current state of knowledge in the scientific literature on the health and social implications of global climate change for homelessness? A systematic scoping review method was used to identify and synthesize the peer-reviewed literature relevant to this question. The databases searched were PsycINFO, Medline, Scopus, and Google Scholar. Of the 26 papers identified in this review, 20 employed original data analyses with conclusions largely inferred from cross-sectional associations. Themes included the potential influence of climate change on homelessness prevalence, climate impacts that exacerbate specific vulnerabilities of homeless populations (e.g., chronic illness, exposure, stigmatization), and health and social outcomes. Service use and design implications were also addressed. Given the scale of the impacts of climate change on homelessness, the literature on this topic poses promising directions but is under-developed in its current state to adequately inform risk mitigation and response planning. A systems framework is proposed here to inform future research and service design.

An approach to estimating the environmental burden of cancer from known and probable carcinogens: application to Ontario, Canada.

BACKGROUND: Quantifying the potential cancer cases associated with environmental carcinogen exposure can help inform efforts to improve population health. This study developed an approach to estimate the environmental burden of cancer and applied it to Ontario, Canada. The purpose was to identify environmental carcinogens with the greatest impact on cancer burden to support evidence-based decision making. METHODS: We conducted a probabilistic assessment of the environmental burden of cancer in Ontario. We selected 23 carcinogens that we defined as "environmental" (e.g., pollutants) and were relevant to the province, based on select classifications provided by the International Agency for Research on Cancer. We evaluated population exposure to the carcinogens through inhalation of indoor/outdoor air; ingestion of food, water, and dust; and exposure to radiation. We obtained or calculated concentration-response functions relating carcinogen exposure and the risk of developing cancer. Using both human health risk assessment and population attributable fraction models in a Monte Carlo simulation, we estimated the annual cancer cases associated with each environmental carcinogen, reporting the simulation summary (e.g., mean and percentiles). RESULTS: We estimated between 3540 and 6510 annual cancer cases attributable to exposure to 23 environmental carcinogens in Ontario. Three carcinogens were responsible for over 90% of the environmental burden of cancer: solar ultraviolet (UV) radiation, radon in homes, and fine particulate matter (PM2.5) in outdoor air. Eight other carcinogens had an estimated mean burden of at least 10 annual cancer cases: acrylamide, arsenic, asbestos, chromium, diesel engine exhaust particulate matter, dioxins, formaldehyde, and second-hand smoke. The remaining 12 carcinogens had an estimated mean burden of less than 10 annual cancer cases in Ontario. CONCLUSIONS: We found the environmental burden of cancer in Ontario to fall between previously estimated burdens of alcohol and tobacco use. These results allow for a comparative assessment across carcinogens and offer insights into strategies to reduce the environmental burden of cancer. Our analysis could be adopted by other jurisdictions and repeated in the future for Ontario to track progress in reducing cancer burden, assess newly classified environmental carcinogens, and identify top burden contributors.

Estimates of healthcare utilisation and deaths from waterborne pathogen exposure in Ontario, Canada.

Burden of disease analyses can quantify the relative impact of different exposures on population health outcomes. Gastroenteritis where the causative pathogen was not determined and respiratory illness resulting from exposure to opportunistic pathogens transmitted by water aerosols have not always been considered in waterborne burden of disease estimates. We estimated the disease burden attributable to nine enteric pathogens, unspecified pathogens leading to gastroenteritis, and three opportunistic pathogens leading primarily to respiratory illness, in Ontario, Canada (population ~14 million). Employing a burden of disease framework, we attributed a fraction of annual (year 2016) emergency department (ED) visits, hospitalisations and deaths to waterborne transmission. Attributable fractions were developed from the literature and clinical input, and unattributed disease counts were obtained using administrative data. Our Monte Carlo simulation reflected uncertainty in the inputs. The estimated mean annual attributable rates for waterborne diseases were (per 100 000 population): 69 ED visits, 12 hospitalisations and 0.52 deaths. The corresponding 5th-95th percentile estimates were (per 100 000 population): 13-158 ED visits, 5-22 hospitalisations and 0.29-0.83 deaths. The burden of disease due to unspecified pathogens dominated these rates: 99% for ED visits, 63% for hospitalisations and 40% for deaths. However, when a causative pathogen was specified, the majority of hospitalisations (83%) and deaths (97%) resulted from exposure to the opportunistic pathogens Legionella spp., non-tuberculous mycobacteria and Pseudomonas spp. The waterborne disease burden in Ontario indicates the importance of gastroenteritis not traced back to a particular pathogen and of opportunistic pathogens transmitted primarily through contact with water aerosols.

Estimated burden of disease from arsenic in drinking water supplied by domestic wells in the United States.

Well water around the world can be contaminated with arsenic, a naturally occurring geological element that has been associated with myriad adverse health effects. Persons obtaining their drinking water from private wells are often responsible for well testing and water treatment. High levels of arsenic have been reported in well water-supplied areas of the United States. We quantified - in cases and dollars - the potential burden of disease associated with the ingestion of arsenic through private well drinking water supplies in the United States. To estimate cancer and cardiovascular disease burden, we developed a Monte Carlo model integrating three input streams: (1) regional concentrations of arsenic in drinking water wells across the United States; (2) dose-response relationships in the form of cancer slope factors and hazard ratios; and (3) economic cost estimates developed for morbidity endpoints using 'cost-of-illness' methods and for mortality using 'value per statistical life' estimates. Exposure to arsenic in drinking water from U.S. domestic wells is modeled to contribute 500 annual premature deaths from ischemic heart disease and 1,000 annual cancer cases (half of them fatal), monetized at $10.9 billion (2017 USD) annually. These considerable public health burden estimates can be compared with the burdens of other priority public health issues to assist in decision-making.

Estimated Annual Deaths, Hospitalizations, and Emergency Department and Physician Office Visits from Foodborne Illness in Ontario.

Public Health Ontario is working to estimate the burden of disease from environmental hazards in Ontario, Canada. As part of this effort, we estimated deaths and health care utilization resulting from exposure to pathogens and toxic substances in food. We applied fractions for the proportion of illness attributable to foodborne transmission to the annual (2008-2012) counts of deaths, hospitalizations, emergency department (ED) visits, and physician office visits for 15 diseases (13 pathogen-specific diseases and 2 nonspecific syndromes) captured by administrative health data. Nonspecific gastroenteritis (causative agent unknown) was the dominant disease, accounting for 98% of ED visits, 94% of hospitalizations, and 88% of deaths annually attributed to the 15 diseases. We estimated that foodborne nonspecific gastroenteritis results in ∼137,000 physician office visits (1000/100,000 population), 40,000 ED visits (310/100,000), 6200 hospitalizations (47/100,000), and 59 deaths (0.45/100,000) in Ontario per year (mean estimates). Our results indicate that pathogen-specific approaches to foodborne disease surveillance can substantially underestimate the deaths and illness resulting from exposure to foodborne pathogens and other causes of foodborne illness.

Benefits of Decreased Mortality Risk from Reductions in Primary Mobile Source Fine Particulate Matter: A Limited Data Approach for Urban Areas Worldwide.

We developed an approach to estimate the public health benefits resulting from transportation projects or environmental actions that reduce mobile source fine particulate matter (PM2.5 ) in select urban areas worldwide when input data are limited or when a rapid order-of-magnitude assessment is needed. For a given reduction in direct PM2.5 emissions, we can use this approach to quantify (1) the subsequent reduction in ambient primary PM2.5 concentration in the urban area; (2) the public health benefits associated with mortality risk reductions, measured in terms of avoided premature deaths; and (3) the economic value of the reduced mortality risk. To illustrate our approach, we estimated the impact of a 100-metric-ton reduction in primary PM2.5 mobile source emissions in the year 2010 for 42 large, global cities. Our estimates of public health benefits and their economic value varied by city, as did the sensitivity to key assumptions and inputs. The estimated number of premature deaths avoided per 100-metric-ton reduction in PM2.5 emissions ranged from 12 to 202. City-level variability in these estimates was driven by the magnitude of the reduction in ambient PM2.5 concentration, the size of the urban population, and the baseline PM2.5 concentration. The economic value of mortality risk reductions per 100-metric-ton reduction in PM2.5 emissions ranged from $2 million to $328 million in 2010 U.S. dollars. Income per capita was the most important driver of the variability in the economic values across countries.

A method to screen U.S. environmental biomonitoring data for race/ethnicity and income-related disparity.

BACKGROUND: Environmental biomonitoring data provide one way to examine race/ethnicity and income-related exposure disparity and identify potential environmental justice concerns. METHODS: We screened U.S. National Health and Nutrition Examination Survey (NHANES) 2001-2008 biomonitoring data for 228 chemicals for race/ethnicity and income-related disparity. We defined six subgroups by race/ethnicity-Mexican American, non-Hispanic black, non-Hispanic white-and income-Low Income: poverty income ratio (PIR) <2, High Income: PIR ≥ 2. We assessed disparity by comparing the central tendency (geometric mean [GM]) of the biomonitoring concentrations of each subgroup to that of the reference subgroup (non-Hispanic white/High Income), adjusting for multiple comparisons using the Holm-Bonferroni procedure. RESULTS: There were sufficient data to estimate at least one geometric mean ratio (GMR) for 108 chemicals; 37 had at least one GMR statistically different from one. There was evidence of potential environmental justice concern (GMR significantly >1) for 12 chemicals: cotinine; antimony; lead; thallium; 2,4- and 2,5-dichlorophenol; p,p'-dichlorodiphenyldichloroethylene; methyl and propyl paraben; and mono-ethyl, mono-isobutyl, and mono-n-butyl phthalate. There was also evidence of GMR significantly <1 for 25 chemicals (of which 17 were polychlorinated biphenyls). CONCLUSIONS: Although many of our results were consistent with the U.S. literature, findings relevant to environmental justice were novel for dichlorophenols and some metals.

Evaluating efficiency-equality tradeoffs for mobile source control strategies in an urban area.

In environmental risk management, there are often interests in maximizing public health benefits (efficiency) and addressing inequality in the distribution of health outcomes. However, both dimensions are not generally considered within a single analytical framework. In this study, we estimate both total population health benefits and changes in quantitative indicators of health inequality for a number of alternative spatial distributions of diesel particulate filter retrofits across half of an urban bus fleet in Boston, Massachusetts. We focus on the impact of emissions controls on primary fine particulate matter (PM(2.5)) emissions, modeling the effect on PM(2.5) concentrations and premature mortality. Given spatial heterogeneity in baseline mortality rates, we apply the Atkinson index and other inequality indicators to quantify changes in the distribution of mortality risk. Across the different spatial distributions of control strategies, the public health benefits varied by more than a factor of two, related to factors such as mileage driven per day, population density near roadways, and baseline mortality rates in exposed populations. Changes in health inequality indicators varied across control strategies, with the subset of optimal strategies considering both efficiency and equality generally robust across different parametric assumptions and inequality indicators. Our analysis demonstrates the viability of formal analytical approaches to jointly address both efficiency and equality in risk assessment, providing a tool for decisionmakers who wish to consider both issues.

Factors influencing mobile source particulate matter emissions-to-exposure relationships in the Boston urban area.

Benefit-cost and regulatory impact analyses often use atmospheric dispersion models with coarse resolution to estimate the benefits of proposed mobile source emission control regulations. This approach may bias health estimates or miss important intra-urban variability for primary air pollutants. In this study, we estimate primary fine particulate matter (PM2.5) intake fractions (iF; the fraction of a pollutant emitted from a source that is inhaled by the population) for each of 23 398 road segments in the Boston Metro Core area to evaluate the potential for intra-urban variability in the emissions-to-exposure relationship. We estimate iFs using the CAL3QHCR line source model combined with residential populations within 5000 m of each road segment. The annual average values for the road segments range from 0.8 to 53 per million, with a mean of 12 per million. On average, 46% of the total exposure is realized within 200 m of the road segment, though this varies from 0 to 93% largely due to variable population patterns. Our findings indicate the likelihood of substantial intra-urban variability in mobile source primary PM2.5 iF that accounting for population movement with time, localized meteorological conditions, and street-canyon configurations would likely increase.

Ragaglitazar improves glycemic control and lipid profile in type 2 diabetic subjects: a 12-week, double-blind, placebo-controlled dose-ranging study with an open pioglitazone arm.

OBJECTIVE: Ragaglitazar is a novel insulin sensitizer with dual peroxisome proliferator-activated receptor (PPAR)-gamma and PPAR-alpha stimulating activities that improve plasma glucose and lipid profiles. The aim of the present dose-ranging study was to assess the efficacy and safety of ragaglitazar in patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: This study included 177 hypertriglyceridemic type 2 diabetic subjects who participated in a 12-week, double-blind, parallel, randomized, placebo-controlled dose-ranging study (open pioglitazone arm). Subjects received ragaglitazar (0.1, 1, 4, or 10 mg), placebo, or pioglitazone (45 mg). Efficacy parameters included fasting plasma levels of triglycerides and glucose (FPG) along with other lipid levels, A1C, and insulin. RESULTS: Ragaglitazar in doses of 1, 4, and 10 mg resulted in a significant decrease from baseline as compared with placebo in FPG (-48, -74, -77 mg/dl) and triglycerides (-40, -62, -51%), free fatty acids (-36, -54, -62%), apolipoprotein B (-13, -29, -25%), LDL cholesterol (-14 and -19% for 4- and 10-mg groups), and total cholesterol (-16 and -15% for 4 and 10 mg) and a significant increase in HDL cholesterol (20 and 31% for 1- and 4-mg groups, respectively). Changes in triglycerides and FPG for pioglitazone treatment were similar to 1 mg ragaglitazar. Mean A1C values of the 1-, 4-, and 10-mg ragaglitazar and pioglitazone groups were significantly reduced compared with placebo (-0.5, -1.3, -1.1, and -0.3%, respectively). Common adverse events were edema, weight increase, leukopenia, and anemia. CONCLUSIONS: Ragaglitazar provided glycemic control that was comparable with that of pioglitazone and, compared with placebo, provided significant improvement in the lipid profile.

Treatment of type 2 diabetes with a combination regimen of repaglinide plus pioglitazone.

The efficacy and safety of combination therapy (repaglinide plus pioglitazone) was compared to repaglinide or pioglitazone in 24-week treatment of type 2 diabetes. This randomized, multicenter, open-label, parallel-group study enrolled 246 adults (age 24-85) who had shown inadequate response in previous sulfonylurea or metformin monotherapy (HbA(1c) > 7%). Prior therapy was withdrawn for 2 weeks, followed by randomization to repaglinide, pioglitazone, or repaglinide/pioglitazone. In the first 12 weeks of treatment, repaglinide doses were optimized, followed by 12 weeks of maintenance therapy. Pioglitazone dosage was fixed at 30 mg per day. Baseline HbA(1c) values were comparable (9.0% for repaglinide, 9.1% for pioglitazone, 9.3% for combination). Mean changes in HbA(1c) values at the end of treatment were -1.76% for repaglinide/pioglitazone, -0.18% for repaglinide, +0.32% for pioglitazone. Fasting plasma glucose reductions were -82 mg/dl for combination therapy, -34 mg/dl for repaglinide, -18 mg/dl for pioglitazone. Minor hypoglycemia occurred in 5% of patients for the combination, 8% for repaglinide, and 3% for pioglitazone. Weight gains for combination therapy were correlated to individual HbA(1c) reductions. In summary, for patients who had previously failed oral antidiabetic monotherapy, the combination repaglinide/pioglitazone had acceptable safety, with greater reductions of glycemic parameters than therapy using either agent alone.

The importance of population susceptibility for air pollution risk assessment: a case study of power plants near Washington, DC.

In evaluating risks from air pollution, health impact assessments often focus on the magnitude of the impacts without explicitly considering the distribution of impacts across subpopulations. In this study, we constructed a model to estimate the magnitude and distribution of health benefits associated with emission controls at five older power plants in the Washington, DC, area. We used the CALPUFF atmospheric dispersion model to determine the primary and secondary fine-particulate-matter (< 2.5 micro m in aerodynamic diameter) concentration reductions associated with the hypothetical application of "Best Available Control Technology" to the selected power plants. We combined these concentration reductions with concentration-response functions for mortality and selected morbidity outcomes, using a conventional approach as well as considering susceptible subpopulations. Incorporating susceptibility had a minimal effect on total benefits, with central estimates of approximately 240 fewer premature deaths, 60 fewer cardiovascular hospital admissions (CHA), and 160 fewer pediatric asthma emergency room visits (ERV) per year. However, because individuals with lower education appear to have both higher background mortality rates and higher relative risks for air-pollution-related mortality, stratifying by educational attainment implies that 51% of the mortality benefits accrue among the 25% of the population with less than high school education. Similarly, diabetics and African Americans bear disproportionate shares of the CHA and ERV benefits, respectively. Although our ability to characterize subpopulations is constrained by the available information, our analysis demonstrates that incorporation of susceptibility information significantly affects demographic and geographic patterns of health benefits and enhances our understanding of individuals likely to benefit from emission controls.