Objective: The Hotel Study was initiated in Vancouver's Downtown East Side (DTES) neighborhood to investigate multimorbidity in homeless or marginally housed people. We evaluated the clinical effectiveness of existing, illness-specific treatment strategies and assessed the effectiveness of health care delivery for multimorbid illnesses. Method: For context, we mapped the housing locations of patients presenting for 552,062 visits to the catchment hospital emergency department (2005)(2006)(2007)(2008)(2009)(2010)(2011)(2012)(2013). Aggregate data on 22,519 apprehensions of mentally ill people were provided by the Vancouver Police Department (2009)(2010)(2011)(2012)(2013)(2014)(2015). The primary strategy was a longitudinal cohort study of 375 people living in the DTES (2008)(2009)(2010)(2011)(2012)(2013)(2014)(2015). We analysed mortality and evaluated the clinical and health service delivery effectiveness for infection with human immunodeficiency virus or hepatitis C virus, opioid dependence, and psychosis.Results: Mapping confirmed the association between poverty and greater number of emergency visits related to substance use and mental illness. The annual change in police apprehensions did not differ between the DTES and other policing districts. During 1581 person-years of cohort observation, the standardized mortality ratio was 8.43 (95% confidence interval, 6.19 to 11.50). Physician visits were common (84.3% of participants over 6 months). Clinical treatment effectiveness was highest for HIV/AIDS, intermediate for opioid dependence, and lowest for psychosis. Health service delivery mechanisms provided examples of poor access, poor treatment adherence, and little effect on multimorbid illnesses.Conclusions: Clinical effectiveness was variable, and illness-specific service delivery appeared to have little effect on multimorbidity. New models of care may need to be implemented.

BackgroundTools for estimating population exposures to environmental carcinogens are required to support evidence-based policies to reduce chronic exposures and associated cancers. Our objective was to develop indicators of population exposure to selected environmental carcinogens that can be easily updated over time, and allow comparisons and prioritization between different carcinogens and exposure pathways.MethodsWe employed a risk assessment-based approach to produce screening-level estimates of lifetime excess cancer risk for selected substances listed as known carcinogens by the International Agency for Research on Cancer. Estimates of lifetime average daily intake were calculated using population characteristics combined with concentrations (circa 2006) in outdoor air, indoor air, dust, drinking water, and food and beverages from existing monitoring databases or comprehensive literature reviews. Intake estimates were then multiplied by cancer potency factors from Health Canada, the United States Environmental Protection Agency, and the California Office of Environmental Health Hazard Assessment to estimate lifetime excess cancer risks associated with each substance and exposure pathway. Lifetime excess cancer risks in excess of 1 per million people are identified as potential priorities for further attention.ResultsBased on data representing average conditions circa 2006, a total of 18 carcinogen-exposure pathways had potential lifetime excess cancer risks greater than 1 per million, based on varying data quality. Carcinogens with moderate to high data quality and lifetime excess cancer risk greater than 1 per million included benzene, 1,3-butadiene and radon in outdoor air; benzene and radon in indoor air; and arsenic and hexavalent chromium in drinking water. Important data gaps were identified for asbestos, hexavalent chromium and diesel exhaust in outdoor and indoor air, while little data were available to assess risk for substances in dust, food and beverages.ConclusionsThe ability to track changes in potential population exposures to environmental carcinogens over time, as well as to compare between different substances and exposure pathways, is necessary to support comprehensive, evidence-based prevention policy. We used estimates of lifetime excess cancer risk as indicators that, although based on a number of simplifying assumptions, help to identify important data gaps and prioritize more detailed data collection and exposure assessment needs.

R adon is a colourless, odourless, naturally occurring gas released from the breakdown of uranium in soils. Exposure to radon occurs primarily indoors, where levels can accumulate to high concentrations. The majority of lung cancers are due to tobacco smoke; however, radon increases the risk of lung cancer for smokers as well as for individuals who have never smoked. 1-4 In Canada, approximately 16% of lung cancers (3,261 cases annually) are estimated to be attributable to residential radon exposure. 5 While radon is recognized as being causally associated with lung cancer, national-level studies are important to estimate attributable disease burden, increase awareness and develop population health policy. To date, only one residential radon epidemiological study has been conducted in Canada. This study was in Winnipeg and reported no associations between residential radon concentrations and lung cancer. 6 Similar to most epidemiological studies of residential radon, exposure was assessed using indoor residential measurements. While this method is the gold standard for characterizing radon exposure, studies using this method typically have limited statistical power due to the difficulty in measuring residential radon for large populations. Alternatively to using individual residential measurements, two epidemiological studies conducted in the United States and Denmark used maps and spatial prediction models to estimate long-term ecological residential radon concentrations in larger population samples, the approach we follow in this analysis. For the Cancer Prevention Study II cohort in the United States, average county-level radon measurements were linked to study participants' zip codes to estimate ecological radon exposure, and a 100 Bq/m 3 increase in radon was associated with a 15% (95% CI: 1-31%) increase in lung cancer mortality. 7 In the Danish Diet, Cancer and Health cohort, information on geology and housing characteristics were used to predict radon concentrations at residential locations for 57,053 subjects (589 lung cancer cases) and a 4% (95% CI:-31-56%) increase in lung cancer risk was observed per 100 Bq/m 3 increase in predicted radon concentrations. 8 Here we present two national radon risk maps for Canada and estimate the associated lung cancer risks by applying these maps to 20 years of residential histories using a population-based casecontrol study of 2,390 histological confirmed lung cancer incidence cases and 3,507 population controls. Based on the existing evidence for radon as a risk factor for lung cancer, we expect that lung cancer incidence in this population-based case-control study will be increased in individuals living in high radon risk areas. METHODS Radon mapping Two distinct approaches were used to create radon risk maps for Canada. The first (Figure 1a) and a priori best estimate of radon exposure used a recently completed residential radon survey of three-month radon measurements collected from approximately 14,000 households across Canada. 9 The sampling frame for this sur

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