In humans, immune development begins early in embryonic life and continues throughout the early postnatal period. Although a number of pesticides have been observed to induce developmental immunotoxicity in mice, few human studies have examined the long term effects of in utero pesticide exposure on childhood morbidity. Empirical evidence suggests that the vulnerable period for toxic insults to the developing immune system extends from early gestation to adolescence in humans and animals. Using data from the Ontario Farm Family Health Study, we examined the relationship between farm couple exposures to pesticides during pregnancy and subsequent health outcomes in their offspring, including: persistent cough or bronchitis, asthma, and allergies or hayfever. No strong associations between pesticide exposures during pregnancy and persistent cough or bronchitis, or asthma were found. There was suggestive evidence that allergies and hayfever appeared to be more common in offspring, especially male offspring, exposed to certain specific pesticides during the period of pregnancy. Nevertheless, given the indirect indicators of pesticide exposure used in this study, and the scarcity of human studies on in utero exposure to pesticides and the development of allergies and other child health outcomes, these findings serve primarily to generate hypotheses for future research.
Chlorination disinfection by-products (CDBPs) are produced during the treatment of water with chlorine to remove bacterial contamination. CDBPs have been associated with an increased risk of bladder cancer. There is also some evidence that they may increase the risk of pancreatic cancer. We report results from a population-based case-control study of 486 incident cases of pancreatic cancer and 3,596 age- and sex-matched controls. Exposure to chlorination by-products was estimated by linking lifetime residential histories to two different databases containing information on CDBP levels in municipal water supplies. Logistic regression analysis found no evidence of increased pancreatic cancer risk at higher CDBP concentrations (all odds ratios
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Erratum In: Environ Health Perspect. 2005 Aug;113(8):A511
A comprehensive analytical review of the risk assessment, risk management, and risk communication approaches currently being undertaken by key national, provincial/state, territorial, and international agencies was conducted. The information acquired for review was used to identify the differences, commonalities, strengths, and weaknesses among the various approaches, and to identify elements that should be included in an effective, current, and comprehensive approach applicable to environmental, human health and occupational health risks. More than 80 agencies, organizations, and advisory councils, encompassing more than 100 risk documents, were examined during the period from February 2000 until November 2002. An overview was made of the most important general frameworks for risk assessment, risk management, and risk communication for human health and ecological risk, and for occupational health risk. In addition, frameworks for specific applications were reviewed and summarized, including those for (1)contaminated sites; (2) northern contaminants; (3) priority substances; (4) standards development; (5) food safety; (6) medical devices; (7) prescription drug use; (8) emergency response; (9) transportation; (10) risk communication. Twelve frameworks were selected for more extensive review on the basis of representation of the areas of human health, ecological, and occupational health risk; relevance to Canadian risk management needs; representation of comprehensive and well-defined approaches; generalizability with their risk areas; representation of "state of the art" in Canada, the United States, and/or internationally; and extent of usage of potential usage within Canada. These 12 frameworks were: 1. Framework for Environmental Health Risk Management (US Presidential/Congressional Commission on Risk Assessment and Risk Management, 1997). 2. Health Risk Determination: The Challenge of Health Protection (Health and Welfare Canada, 1990). 3. Health Canada Decision-Making Framework for Identifying, Assessing and Managing Health Risks (Health Canada, 2000). 4. Canadian Environmental Protection Act: Human Health Risk Assessment of Priority Substances(Health Canada, 1994). 5. CSA-Q8550 Risk Management: Guidelines for Decision-Makers (Canada Standards Association, 1997). 6. Risk Assessment in the Federal Government: Managing the Process (US National Research Council, 1983). 7. Understanding Risk: Informing Decisions in a Democratic Society (US National Research Council, 1996). 8. Environmental Health Risk Assessment (enHealth Council of Australia, 2002). 9. A Framework for Ecological Risk Assessment (CCME, 1996). 10. Ecological Risk Assessments of Priority Substances Under the Canadian Environmental Protection Act (Environment Canada, 1996).11. Guidelines for Ecological Risk Assessment (US EPA, 1998b). 12. Proposed Model for Occupational Health Risk Assessment and Management (Rampal & Sadhra, 1999). Based on the extensive review of these frameworks, seven key elements that should be included in a comprehensive framework for human health, ecological, and occupational risk assessment and management were identified: 1. Problem formulation stage. 2. Stakeholder involvement. 3. Communication. 4. Quantitative risk assessment components. 5. Iteration and evaluation. 6. Informed decision making. 7. Flexibility. On the basis of this overarching approach to risk management, the following "checklist" to ensure a good risk management decision is proposed: - Make sure you're solving the right problem. - Consider the problem and the risk within the full context of the situation, using a broad perspective. - Acknowledge, incorporate, and balance the multiple dimensions of risk. - Ensure the highest degree of reliability for all components of the risk management process. - Involve interested and effected parties from the outset of the process. - Commit to honest and open communication between all parties. - Employ continuous evaluation throughout the process (formative, process, and outcome evaluation), and be prepared to change the decision if new information becomes available. Comprehensive and sound principles are critical to providing structure and integrity to risk management frameworks. Guiding principles are intended to provide an ethical grounding for considering the many factors involved in risk management decision making. Ten principles are proposed to guide risk management decision making. The first four principles were adapted and modified from Hattis (1996) along with the addition of two more principles by Hrudey (2000). These have been supplemented by another four principles to make the 10 presented. The principles are based in fundamental ethical principles and values. These principles are intended to be aspirational rather than prescriptive--their application requires flexibility and practical judgement. Risk management is inherently a process in search of balance among competing interests and concerns. Each risk management decision will be "balancing act" of competing priorities, and trade-offs may sometimes have to be made between seemingly conflicting principles. The 10 decision-making principles, with the corresponding ethical principle in italics are: 1. Do more good than harm (beneficence, nonmalificence).- The ultimate goal of good risk management is to prevent or minimize risk, or to "do good" as much as possible. 2. Fair process of decision making (fairness, natural justice). - Risk management must be just, equitable, impartial, unbiased, dispassionate, and objective as far as possible given the circumstances of each situation. 3. Ensure an equitable distribution of risk (equity). - An equitable process of risk management would ensure fair outcomes and equal treatment of all concerned through an equal distribution of benefits and burdens (includes the concept of distributive justice, i.e., equal opportunities for all individuals). 4. Seek optimal use of limited risk management resources (utility). - Optimal risk management demands using limited resources where they will achieve the most risk reduction of overall benefit. 5. Promise no more risk management that can be delivered (honesty).- Unrealistic expectations of risk management can be avoided with honest and candid public accounting of what we know and don't know, and what we can and can't do using risk assessment and risk management. 6. Impose no more risk that you would tolerate yourself (the Golden Rule). - The Golden Rule is important in risk management because it forces decision makers to abandon complete detachment from their decisions so they may understand the perspectives of those affected. 7. Be cautious in the face of uncertainty ("better safe than sorry"). - Risk management must adopt a cautious approach when faced with a potentially serous risk, even if the evidence is uncertain. 8. Foster informed risk decision making for all stakeholders (autonomy). - Fostering autonomous decision making involves both providing people with the opportunity to participate, and full and honest disclosure of all the information required for informed decisions. 9. Risk management processes must be flexible and evolutionary to be open to new knowledge and understanding (evolution, evaluation, iterative process). - The incorporation of new evidence requires that risk management be a flexible, evolutionary, and iterative process, and that evaluation is employed at the beginning and througthout the process. 10. the complete elimination fo risk is not possible (life is not risk free).- Risk is pervasive in our society, and cannot be totally eliminated despite an oft-expressed public desire for "zero risk". However, the level of risk that may ve tolerable by any individual is dependent on values of beliefs, as well as scientific information. Each agency must continue to employ a process that meets the needs of their specific application of risk management. A single approach cannot satisfy the diverse areas to which risk decisions are being applied. However, with increasing experience in the application of the approaches, we are evolving to a common understanding of the essential elements and principles required for successful risk assessment, risk management, and risk communication. Risk management will continue to be a balancing act of competing priorities and needs. Flexibility and good judgement are ultimately the key to successfully making appropriate risk decisions.
Expert opinion from Canada, the United States and European Union countries was solicited to examine the regulatory and non-regulatory approaches used to protect children's environmental health. Thirty-five experts were interviewed by telephone from June 2004 to March 2005 using an open-ended survey questionnaire. Experts were asked to name legislative and non-legislative tools used to protect children's environmental health in their jurisdiction as well as the effectiveness of approaches taken, barriers, facilitators, methods of evaluation, and recommendations for improving children's health protection. A number of common themes were revealed by experts in different countries as well as novel approaches that could be used to improve children's environmental health. Determining what types of governance and non-governance instruments are most effective based on experience from other jurisdictions, allows for the determination of common, effective, policy choice from shared children's health environmental risks. It also provides a broad classification of different approaches that have been used for children's environmental health. Three main areas suggested for strengthening children's environmental health protection included: research and surveillance, institutional organization, and regulatory capacity.
This report provides the methodology and findings from the project: Air Pollution and Health: a European and North American Approach (APHENA). The principal purpose of the project was to provide an understanding of the degree of consistency among findings of multicity time-series studies on the effects of air pollution on mortality and hospitalization in several North American and European cities. The project included parallel and combined analyses of existing data. The investigators sought to understand how methodological differences might contribute to variation in effect estimates from different studies, to characterize the extent of heterogeneity in effect estimates, and to evaluate determinants of heterogeneity. The APHENA project was based on data collected by three groups of investigators for three earlier studies: (1) Air Pollution and Health: A European Approach (APHEA), which comprised two multicity projects in Europe. (Phase 1 [APHEA1] involving 15 cities, and Phase 2 [APHEA2] involving 32 cities); (2) the National Morbidity, Mortality, and Air Pollution Study (NMMAPS), conducted in the 90 largest U.S. cities; and (3) multicity research on the health effects of air pollution in 12 Canadian cities.
The project involved the initial development of analytic approaches for first-stage and second-stage analyses of the time-series data and the subsequent application of the resulting methods to the time-series data. With regard to the first-stage analysis, the various investigative groups had used conceptually similar approaches to the key issues of controlling for temporal confounding and temperature; however, specific methods differed. Consequently, the investigators needed to establish a standard protocol, but one that would be linked to prior approaches. Based on exploratory analyses and simulation studies, a first-stage analysis protocol was developed that used generalized linear models (GLM) with either penalized splines (PS) or natural splines (NS) to adjust for seasonality, with 3, 8, or 12 degrees of freedom (df) per year and also the number of degrees of freedom chosen by minimizing the partial autocorrelation function (PACF) of the model's residuals. For hospitalization data, the approach for model specification followed that used for mortality, accounting for seasonal patterns, but also, for weekend and vacation effects, and for epidemics of respiratory disease. The data were also analyzed to detect potential thresholds in the concentration-response relationships. The second-stage analysis used pooling approaches and assessed potential effect modification by sociodemographic characteristics and indicators of the pollution mixture across study regions. Specific quality control exercises were also undertaken. Risks were estimated for two pollutants: particulate matter - 10 pm in aerodynamic diameter (PM10) and ozone (O3).
The first-stage analysis yielded estimates that were relatively robust to the underlying smoothing approach and to the number of degrees of freedom. The first-stage APHENA results generally replicated the previous independent analyses performed by the three groups of investigators. PM10 effects on mortality risk estimates from the APHEA2 and NMMAPS databases were quite close, while estimates from the Canadian studies were substantially higher. For hospitalization, results were more variable without discernable patterns of variation among the three data sets. PM10 effect-modification patterns, explored only for cities with daily pollution data (i.e., 22 in Europe and 15 in the U.S.), were not entirely consistent across centers. Thus, the levels of pollutants modified the effects differently in Europe than in the United States. Climatic variables were important only in Europe. In both Europe and the United States, a higher proportion of older persons in the study population was associated with increased PM10 risk estimates, as was a higher rate of unemployment - the sole indicator of socioeconomic status uniformly available across the data sets. APHENA study results on the effects of O3 on mortality were less comprehensive than for PM10 because the studies from the three regions varied in whether they analyzed data for the full year or only for the summer months. The effects tended to be larger for summer in Europe and the United States. In the United States they were lower when controlled for PM10. The estimated effect of O3 varied by degrees of freedom and across the three geographic regions. The effects of O3 on mortality were larger in Canada, and there was little consistent indication of effect modification in any location.
APHENA has shown that mortality findings obtained with the new standardized analysis were generally comparable to those obtained in the earlier studies, and that they were relatively robust to the data analysis method used. For PM10, the effect-modification patterns observed were not entirely consistent between Europe and the United States. For O3, there was no indication of strong effect modification in any of the three data sets.
Epidemiologic studies of uranium miners and other underground miners have consistently shown miners exposed to high levels of radon to be at increased risk of lung cancer. More recently, concern has arisen about lung cancer risks among people exposed to lower levels of radon in homes. The current Canadian guideline for residential radon exposure was set in 1988 at 800 Bq/m(3). Because of the accumulation of a considerable body of new scientific evidence on radon lung cancer risks since that time, Health Canada sponsored a workshop to review the current state-of-the-science on radon health risks. The specific objectives of the workshop were (1) to collect and assess scientific information relevant to setting national radon policy in Canada, and (2) to gather information on social, political, and operational considerations in setting national policy. The workshop, held on 3-4 March 2004, was attended by 38 invited scientists, regulators, and other stakeholders from Canada and the United States. The presentations on the first day dealt primarily with scientific issues. The combined analysis of North American residential radon and lung cancer studies was reviewed. The analysis confirmed a small but detectable increase in lung cancer risk at residential exposure levels. Current estimates suggest that radon in homes is responsible for approximately 10% of all lung cancer deaths in Canada, making radon the second leading cause of lung cancer after tobacco smoking. This was followed by a perspective from an UNSCEAR (United Nations Scientific Committee on the Effects of Atomic Radiation) working group on radon. There were two presentations on occupational exposures to radon and two presentations considered the possibility of radon as a causative factor for cardiovascular disease and for cancer in other organs besides the lung. The possible contribution of environmental tobacco smoke to lung cancers in nonsmokers was also considered. Areas for future research were identified. The second day was devoted to policy and operational issues. The presentations began with a perspective from the U.S. Environmental Protection Agency, followed by a history of radon policy development in Canada. Subsequent presentations dealt with the cost-effectiveness of radon mitigation, Canadian building codes and radon, and a summary of radon standards from around the world. Provincial representatives and a private consultant were given opportunities to present their viewpoints. A number of strategies for reducing residential radon exposure in Canada were recognized, including testing and mitigation of existing homes (on either a widespread or targeted basis) and changing the building code to require that radon mitigation devices be installed at the time a new home is constructed. The various elements of a comprehensive national radon policy were set forth.
Recurrent events such as repeated hospital admissions for the same health outcome occur frequently in environmental health studies. Dewanji and Moolgavkar proposed a flexible parametric model and a conditional likelihood analysis for recurrent events based on a Poisson process formulation. In this paper, we examine the statistical properties of the Dewanji-Moolgavkar (DM) estimator of the risk of an adverse health outcome associated with environmental exposures based on recurrent event data using computer simulation. We also compare the DM approach with both case-crossover analysis for multiple observations and time series analysis when there are no subject-specific covariates. When using a correctly specified model, the DM method produced better estimates with respect to relative mean square error when each subject had constant or curved baseline intensity functions than it did when baseline intensities were increasing or decreasing in a linear fashion. For under-specified models, the DM method outperformed case-crossover analysis for decreasing straight line intensity functions, was outperformed by case-crossover analysis for increasing straight line intensity functions, and was roughly equivalent to case-crossover analysis for constant and curved intensity functions. Case-crossover analysis produced superior risk estimates more frequently than the other two methods in the cases considered here, especially for linear representations of the baseline intensities.
Following a comprehensive evaluation of the health risks of radon, the U.S. National Research Council (US-NRC) concluded that the radon inside the homes of U.S. residents is an important cause of lung cancer. To assess lung cancer risks associated with radon exposure in Canadian homes, we apply the new (US-NRC) techniques, tailoring assumptions to the Canadian context. A two-dimensional uncertainty analysis is used to provide both population-based (population attributable risk, PAR; excess lifetime risk ratio, ELRR; and life-years lost, LYL) and individual-based (ELRR and LYL) estimates. Our primary results obtained for the Canadian population reveal mean estimates for ELRR, PAR, and LYL are 0.08, 8%, and 0.10 years, respectively. Results are also available and stratified by smoking status (ever versus never). Conveniently, the three indices (ELRR, PAR, and LYL) reveal similar output uncertainty (geometric standard deviation, GSD approximately 1.3), and in the case of ELRR and LYL, comparable variability and uncertainty combined (GSD approximately 4.2). Simplifying relationships are identified between ELRR, LYL, PAR, and the age-specific excess rate ratio (ERR), which suggest a way to scale results from one population to another. This insight is applied in scaling our baseline results to obtain gender-specific estimates, as well as in simplifying and illuminating sensitivity analysis.
Occupational exposure is an important potential confounder in air pollution studies because it is plausible that individuals who live in highly polluted areas also work in more polluted environments. While the original investigators made some efforts to control for possible confounding by occupational variables, it was felt that these could be improved upon. The reanalysis team attempted to control for occupational confounding by supplementing the original data sets with two new variables, an indicator of the "dirtiness" of a subject's job and an indicator of possible exposure to occupational lung carcinogens. The attribution of these variables was based on the job title recorded by the original investigators and on the judgment of our experts concerning typical exposure patterns in different occupations. We fitted Cox proportional-hazards models identical to those that had been used by the original investigators while also including one or both of the new occupational covariates in the models. In none of the analyses did the inclusion of the occupational variables materially change the results. It would therefore appear that, in general, the results reported by the original investigators were not distorted by inadequate control of occupational variables. We also carried out some analyses using the dirtiness index as a stratification variable to assess effect modification. There was some indication, albeit inconsistent, that the effect of air pollution on mortality was greater among subjects with dirty jobs than among those with clean jobs.
In this study, the authors assessed the impact of particulate air pollution on first respiratory hospitalization. Study subjects were children less than 3 years of age living in Vancouver, British Columbia, who had their first hospitalization as a result of any respiratory disease (ICD-9 codes 460-519) during the period from June 1, 1995, to March 31, 1999. The authors used logistic regression to estimate the associations between ambient concentrations of particulate matter (PM) and first hospitalization. The adjusted odds ratios for first respiratory hospitalization associated with mean and maximal PM10-2.5 with a lag of 3 days were 1.12 (95% confidence interval: 0.98, 1.28) and 1.13 (1.00, 1.27). After adjustment for gaseous pollutants, the corresponding odds ratios were 1.22 (1.02, 1.48) and 1.14 (0.99, 1.32). The data indicated the possibility of harmful effects from coarse PM on first hospitalization for respiratory disease in early childhood.
In recent years, a number of studies have applied generalized additive models to time series data to estimate associations between exposure to air pollution and cardiorespiratory morbidity and mortality. If concurvity, the nonparametric analogue of multicollinearity, is present in the data, statistical software such as S-plus can seriously underestimate the variance of fitted model parameters, leading to significance tests with inflated type 1 error. This paper uses computer simulation and analyses of actual epidemiologic data to explore this underestimation of standard errors. We provide a method for assessing concurvity in data and an alternate class of models that is unaffected by concurvity. We argue that some degree of concurvity is likely to be present in all epidemiologic time series datasets and we explore through the use of meta-analysis the possible impact of concurvity on the existing body of work relating ambient levels of sulfate particles to mortality.
The use of pesticides has enhanced the health and economies of nations around the world by improving crop production. However, pesticides may pose health risks, particularly to the fetus and young children. In a secondary analysis of the Ontario Farm Family Health Study, we explored the relationship between birth defects and parental pesticide exposure during the 3 months prior to conception and the first trimester of pregnancy. A total of 3412 pregnancies were included in the study. Logistic regression fit by maximum likelihood was used in the analysis. The results showed that pre-conception exposure to both cyanazine (odds ratio=4.99, 95% confidence interval: 1.63-15.27) and dicamba (OR=2.42, 95% CI: 1.06-5.53) were associated with increased risk of birth defects in male offspring. Nevertheless, given the self-reported nature of the exposure and outcomes in this study, the present findings should be considered primarily as hypothesis generating, requiring verification in subsequent investigations.
Managing risks to human health and the environment produced by endocrine-active chemicals (EAC) is dependent on sound principles of risk assessment and risk management, which need to be adapted to address the uncertainties in the state of the science of EAC. Quantifying EAC hazard identification, mechanisms of action, and dose-response curves is complicated by a range of chemical structure/toxicology classes, receptors and receptor subtypes, and nonlinear dose-response curves with low-dose effects. Advances in risk science including toxicogenomics and quantitative structure-activity relationships (QSAR) along with a return to the biological process of hormesis are proposed to complement existing risk assessment strategies, including that of the Endocrine Disruptor Screening and Testing Advisory Committee (EDSTAC 1998). EAC represents a policy issue that has captured the public's fears and concerns about environmental health. This overview describes the process of EAC risk assessment and risk management in the context of traditional risk management frameworks, with emphasis on the National Research Council Framework (1983), taking into consideration the strategies for EAC management in Canada, the United States, and the European Union.
Breast cancer is the most frequently diagnosed cancer among Canadian women, accounting for about 30% of all new cancer cases each year. Although the incidence of breast cancer has increased over the past 50 years, the cause of this rise is unknown. Risk factors for breast cancer may be classified into four broad categories: (1) genetic/familial, (2) reproductive/hormonal, (3) lifestyle, and (4) environmental. Established risk factors for breast cancer include older age, later age at first full-term pregnancy, no full-term pregnancies, postmenopausal obesity, and genetic factors. However, these known risk factors cannot account for the majority of cases. In the early 1990s, it was suggested that exposure to some environmental chemicals such as organochlorine compounds may play a causal role in the etiology of breast cancer through estrogen-related pathways. The relationship between organochlorines and breast cancer risk has been studied extensively in the past decade and more, and at this point there is no clear evidence to support a causal role of most organochlorine pesticides in the etiology of human breast cancer, but more evidence is needed to assess risk associated with polychlorinated biphenyls (PCBs). Future studies need to consider the combined effects of exposures, concentrate on vulnerable groups such as those with higher levels of exposure, only consider exposures occurring during the most etiologically relevant time periods, and more thoroughly consider gene-environment interactions.
Recurrent events, such as repeated hospital admissions for the same health outcome, occur frequently in environmental health studies. In this study, we conducted an analysis of data on repeated respiratory hospitalizations among the elderly in Vancouver, Canada, for the period of June 1, 1995, to March 31, 1999, using a new method proposed by (Dewanji and Moolgavkar 2000, 2002) for recurrent events, and compared it with some traditional methods. In particular, we assessed the impact of ambient gaseous (SO2, NO2, CO, and O3) and particulate pollutants (PM10, PM2.5, and PM10-2.5) as well as the coefficient of haze (CoH) on recurrent respiratory hospital admissions. Using the new procedure, significant associations were found between admissions and 3-day, 5-day, and 7-day moving averages of the ambient SO2 concentrations, with the strongest association observed at the 7-day lag (RR = 1.044, 95% CI: 1.018-1.070). We also found PM10-2.5 for 3-day and 5-day lag to be significant, with the strongest association at 5-day lag (RR = 1.020, 95% CI: 1.001-1.039). No significant associations with admission were found with current day exposure.
Epidemiological and toxicological studies established positive associations between environmental hazards and adverse child health outcomes, including cancer, learning disabilities, behavioral problems, developmental effects, low birth weight, and birth defects. The economic and societal costs associated with children's environmental health disorders were estimated to be substantial. The existence of knowledge gaps, lack of capacity, and the jurisdictional overlap of children's environmental health issues are some of the barriers that impede effective policy decision making. To improve children's environmental health and reduce economic and societal costs, current legislative frameworks could implement a series of amendments. The main federal, provincial, and municipal legislation used to protect children in Canada, either explicitly or implicitly, is reviewed. Recommendations for improving the existing framework for protecting and strengthening children's environmental health are proposed.
In this study, we used both case-crossover and time-series analyses to assess the associations between size-fractionated particulate matter and asthma hospitalization among children 6-12 years old living in Toronto between 1981 and 1993. Specifically, we used exposures averaged over periods varying from 1 to 7 days to assess the effects of particulate matter on asthma hospitalization. We calculated estimates of the relative risk of asthma hospitalization adjusted for daily weather conditions (maximum and minimum temperatures, and average relative humidity) for an incremental exposure corresponding to the interquartile range in particulate matter. Both bidirectional case-crossover and time-series analyses revealed that coarse particulate matter (PM10-2.5) averaged over 5-6 days was significantly associated with asthma hospitalization in both males and females. The magnitude of this effect appeared to increase with increasing number of days of exposure averaging for most models, with the relative risk estimates stabilizing at about 6 days. Using a bidirectional case-crossover analysis, the estimated relative risks were 1.14 [95% confidence interval (CI), 1.02, 1.28] for males and 1.18 (95% CI, 1.02, 1.36) for females, for an increment of 8.4 microg/m(3) in 6-day averages of PM10-2.5. The corresponding relative risk estimates were 1.10 and 1.18, respectively, when we used time-series analysis. The effect of PM10-2.5 remained positive after adjustment for the effects of the gaseous pollutants carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and ozone (O3). We did not find significant effects of fine particulate matter (PM2.5) or of thoracic particulate matter (PM10) on asthma hospitalizations using either of these two analytic approaches. For the most part, relative risk estimates from the unidirectional case-crossover analysis were more pronounced compared with both bidirectional case-crossover and time-series analyses.
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The objective of this investigation was to determine the effectiveness of Canada's residential radon exposure guideline in influencing individuals' health protection decisions.
Homeowners with known exposure levels in a high residential radon area (Winnipeg, Manitoba) were surveyed to document what they had done and spent to reduce their exposure to radon. The 507 respondents were then re-surveyed to elucidate their response to hypothetical scenarios. Logistic regression was used to model risk reduction decisions as a function of exposure and other explanatory variables.
Homeowners were only likely to have taken action to reduce exposure at levels exceeding 1,100 Bq/m3, well above Canada's guideline of 800 Bq/m3. However, when informed of the guideline, respondents indicated they would act at exposures of 702 Bq/m3.
The Canadian residential radon exposure guideline, as it has been implemented, has not effectively prompted homeowner actions to reduce exposures to radon.