Suicide among children and adolescents in Canada: trends and sex differences, 1980�C2008

Background:

Suicide is the second leading cause of death for young Canadians (10–19 years of age) — a disturbing trend that has shown little improvement in recent years. Our objective was to examine suicide trends among Canadian children and adolescents.

Methods:

We conducted a retrospective analysis of standardized suicide rates using Statistics Canada mortality data for the period spanning from 1980 to 2008. We analyzed the data by sex and by suicide method over time for two age groups: 10–14 year olds (children) and 15–19 year olds (adolescents). We quantified annual trends by calculating the average annual percent change (AAPC).

Results:

We found an average annual decrease of 1.0% (95% confidence interval [CI] −1.5 to −0.4) in the suicide rate for children and adolescents, but stratification by age and sex showed significant variation. We saw an increase in suicide by suffocation among female children (AAPC = 8.1%, 95% CI 6.0 to 10.4) and adolescents (AAPC = 8.0%, 95% CI 6.2 to 9.8). In addition, we noted a decrease in suicides involving poisoning and firearms during the study period.

Interpretation:

Our results show that suicide rates in Canada are increasing among female children and adolescents and decreasing among male children and adolescents. Limiting access to lethal means has some potential to mitigate risk. However, suffocation, which has become the predominant method for committing suicide for these age groups, is not amenable to this type of primary prevention.Suicide was ranked as the second leading cause of death among Canadians aged 10–34 years in 2008.¹ It is recognized that suicidal behaviour and ideation is an important public health issue among children and adolescents; disturbingly, suicide is a leading cause of Canadian childhood mortality (i.e., among youths aged 10–19 years).^2,3Between 1980 and 2008, there were substantial improvements in mortality attributable to unintentional injury among 10–19 year olds, with rates decreasing from 37.7 per 100 000 to 10.7 per 100 000; suicide rates, however, showed less improvement, with only a small reduction during the same period (from 6.2 per 100 000 in 1980 to 5.2 per 100 000 in 2008).¹Previous studies that looked at suicides among Canadian adolescents and young adults (i.e., people aged 15–25 years) have reported rates as being generally stable over time, but with a marked increase in suicides by suffocation and a decrease in those involving firearms.² There is limited literature on self-inflicted injuries among children 10–14 years of age in Canada and the United States, but there appears to be a trend toward younger children starting to self-harm.^3,4 Furthermore, the trend of suicide by suffocation moving to younger ages may be partly due to cases of the “choking game” (self-strangulation without intent to cause permanent harm) that have been misclassified as suicides.^5–7Risk factors for suicidal behaviour and ideation in young people include a psychiatric diagnosis (e.g., depression), substance abuse, past suicidal behaviour, family factors and other life stressors (e.g., relationships, bullying) that have complex interactions.⁸ A suicide attempt involves specific intent, plans and availability of lethal means, such as firearms,⁹ elevated structures¹⁰ or substances.¹¹ The existence of “pro-suicide” sites on the Internet and in social media¹² may further increase risk by providing details of various ways to commit suicide, as well as evaluations ranking these methods by effectiveness, amount of pain involved and length of time to produce death.^13–15Our primary objective was to present the patterns of suicide among children and adolescents (aged 10–19 years) in Canada.     

New Delhi metallo-��-lactamase-1: local acquisition in Ontario, Canada, and challenges in detection

New Delhi metallo-β-lactamase-1 (NDM-1) is a recently identified metallo-β-lactamase that confers resistance to carbapenems and all other β-lactam antibiotics, with the exception of aztreonam. NDM-1 is also associated with resistance to many other classes of antibiotics. The enzyme was first identified in organisms isolated from a patient in Sweden who had previously received medical treatment in India, but it is now recognized as endemic throughout India and Pakistan and has spread worldwide. The gene encoding NDM-1 has been found predominantly in Escherichia coli and Klebsiella pneumoniae. We describe the isolation NDM-1–producing organisms from two patients in Toronto, Ontario. To the best of our knowledge, this is the first report of an organism producing NDM-1 that was locally acquired in Canada. We also discuss the evidence that NDM-1 can affect bacterial species other than E. coli and K. pneumoniae, the limited options for treatment and the difficulty laboratories face in detecting organisms that produce NDM-1.New Delhi metallo-β-lactamase-1 (NDM-1) is a metallo-β-lactamase that confers resistance to carbapenems and all other β-lactam antibiotics, with the exception of aztreonam. It is predominantly found in the Enterobacteriaeceae. It was first identified in Escherichia coli and Klebsiella pneumoniae isolated from a patient in Sweden who had previously received medical treatment in India. It is now recognized as endemic throughout India and Pakistan and has spread worldwide due to travel, “medical tourism” and the ability of the genetic element encoding the enzyme to transfer between bacteria.^1–3 Three reports of organisms producing NDM-1 in Canada have been published to date. In each instance, the organisms were isolated from the urinary tracts of patients who had recently been admitted to hospitals in India. Two of the isolates were strains of K. pneumoniae and one was a strain of E. coli.^4–6 Additional reports of isolation of organisms producing NDM-1 from patients in Canada have been presented in the lay press.Organisms that produce NDM-1 have been associated with resistance to classes of antibiotics other than the β-lactams, thus severely limiting options for treatment.² Infection control guidance regarding the management of colonization by or infection with organisms that produce carbapenemases, such as NDM-1, have recently been published by Canadian and European authorities.^7–9 An essential component of these recommendations is the rapid and accurate identification of the organisms in a clinical microbiology laboratory. The Clinical Laboratory Standards Institute (CLSI) and the United States Centers for Disease Control and Prevention (CDC) recommend screening for the production of carbapenemase using the Modified Hodge Test.^10,11 If the result of that test is positive, then the presence and type of carbapenemase can be confirmed by polymerase chain reaction.⁴Herein, we summarize two additional instances in which organisms producing NDM-1 were isolated from patients in Canada and the first where the organism appears to have been acquired in Canada.     

Comparison of black–white disparities in preterm birth between Canada and the United States

Background:

A higher risk of preterm birth among black women than among white women is well established in the United States. We compared differences in preterm birth between non-Hispanic black and white women in Canada and the US, hypothesizing that disparities would be less extreme in Canada given the different historical experiences of black populations and Canada’s universal health care system.

Methods:

Using data on singleton live births in Canada and the US for 2004–2006, we estimated crude and adjusted risk ratios and risk differences in preterm birth (< 37 wk) and very preterm birth (< 32 wk) among non-Hispanic black versus non-Hispanic white women in each country. Adjusted models for the US were standardized to the covariate distribution of the Canadian cohort.

Results:

In Canada, 8.9% and 5.9% of infants born to black and white mothers, respectively, were preterm; the corresponding figures in the US were 12.7% and 8.0%. Crude risk ratios for preterm birth among black women relative to white women were 1.49 (95% confidence interval [CI] 1.32 to 1.66) in Canada and 1.57 (95% CI 1.56 to 1.58) in the US (p value for heterogeneity [p_H] = 0.3). The crude risk differences for preterm birth were 2.94 (95% CI 1.91 to 3.96) in Canada and 4.63 (95% CI 4.56 to 4.70) in the US (p_H = 0.003). Adjusted risk ratios for preterm birth (p_H = 0.1) were slightly higher in Canada than in the US, whereas adjusted risk differences were similar in both countries. Similar patterns were observed for racial disparities in very preterm birth.

Interpretation:

Relative disparities in preterm birth and very preterm birth between non-Hispanic black and white women were similar in magnitude in Canada and the US. Absolute disparities were smaller in Canada, which reflects a lower overall risk of preterm birth in Canada than in the US in both black and white populations.In the United States, a higher risk of preterm birth among black women than among white women is well established.^1–3 This racial disparity is of great concern because preterm birth is a leading cause of perinatal mortality and is predictive of developmental problems and adverse health outcomes later in life.⁴ The underlying causes of the racial disparity in preterm birth in the US are not well understood, although research has suggested contributing roles for a wide range of factors, including socioeconomic disadvantage,⁵ poor neighbourhood conditions (e.g., poverty, crime),^5,6 lack of access to health care,⁷ psychosocial stress,⁸ racial discrimination⁹ and adverse health behaviours.¹⁰Rates of preterm birth have consistently been lower in Canada than in the US.^11,12 However, in contrast to the US, little is known about differences in rates by race or ethnicity in Canada. There is evidence that African-born and Caribbean-born women in the provinces of Quebec and Ontario have higher rates of preterm birth than Canadian-born women.^13–15 Although the magnitude of these differences is smaller than the disparity in preterm births between black and white women in the US,¹⁶ foreign-born black women in the US have been found to be at lower risk of preterm birth than US-born black women.^17,18In both Canada and the US, socioeconomic conditions at both individual and neighbourhood levels are important predictors of preterm birth.^19–21 Although the income gap between black and white people is markedly smaller in Canada than in the US,²² black populations in both countries have lower education levels, higher unemployment rates and a greater likelihood of living in low-quality neighbourhoods compared with white populations.²³ Canada and the US share similar social and economic influences, yet the historical experiences of black populations and the social welfare systems (e.g., universal health care) are quite different in the 2 countries. Black people constitute about 13% of the total US population, but only about 3% of the Canadian population.^24,25 The overwhelming majority of Canada’s black population are immigrants who entered the country after 1960 and their descendants, whereas more than 85% of black Americans can trace their ancestry 3 or more generations in the US, with most being descendants of slaves.²²The objectives of our study are twofold. First, using data from a new cohort linking birth registrations with information from the 2006 Canadian long-form census, we present Canada-wide estimates of differences in preterm birth rates between black and white populations. Second, we use comparable methodology to compare racial differences in preterm birth rates between Canada and the US. Given different historical experiences of black populations in the 2 countries, as well as Canada’s commitment to universal health care and its general perception as a more egalitarian society than the US,²² we hypothesized that we would observe smaller racial disparities in the rates in Canada than in the US.     

Incidence and mortality rates of keratinocyte carcinoma from 1998–2017: a population-based study of sex differences in Ontario,Canada

Background:Keratinocyte carcinoma is the most common malignant disease, but it is not captured in major registries. We aimed to describe differences by sex in the incidence and mortality rates of keratinocyte carcinoma in Ontario, Canada.Methods:We conducted a population-based retrospective study of adults residing in Ontario between Jan. 1, 1998, and Dec. 31, 2017, using linked health administrative databases. We identified the first diagnosis of keratinocyte carcinoma using a validated algorithm of health insurance claims, and deaths related to keratinocyte carcinoma from death certificates. We calculated the incidence and mortality rates of keratinocyte carcinoma, stratified by sex, age and income quintile. We evaluated trends using the average annual percentage change (AAPC) based on joinpoint regression.Results:After decreasing from 1998 to 2003, the incidence rate of keratinocyte carcinoma increased by 30% to 369 per 100 000 males and 345 per 100 000 females in 2017 (AAPC 1.9%, 95% confidence interval [CI] 1.7 to 2.1 from 2003 to 2017). The incidence rate was higher in females younger than 55 years, but higher in males aged 55 years or older. Between 2008 and 2017, the incidence rate rose faster in females than males aged 45–54 years (AAPC 1.2% v. 0.5%, p = 0.01) and 55–64 years (1.2% v. 0.1%, p < 0.01). The incidence was higher in males than females in the higher income quintiles. Between 1998 and 2017, the mortality rate of keratinocyte carcinoma was 1.8 times higher in males than females, on average, and rose 4.8-fold overall (AAPC 8.9%, 95% CI 6.4 to 11.4 in males; 8.0%, 95% CI 5.3–10.8 in females).Interpretation:The population burden of keratinocyte carcinoma is growing, and the incidence and mortality rates rose disproportionately among certain sex- and age-specific groups. This warrants further investigation into causal factors and renewed preventive public health measures.

Keratinocyte carcinoma comprises basal and squamous cell carcinomas, and is the most common malignant disease in Canada and the United States.^1–5 Although keratinocyte carcinoma has a low mortality rate, it is associated with substantial morbidity and impaired quality of life.^2,6,7 Among cancers, it also ranks fifth in health care costs in the US.⁸Epidemiological studies of keratinocyte carcinoma in North America are limited by its exclusion from most cancer registries. ⁹ Previous studies found that higher overall incidence of keratinocyte carcinoma is associated with male sex,^10–14 older age^15–17 and higher socioeconomic status.^18–21 However, differences in the incidence and mortality rates of keratinocyte carcinoma by sex in relation to age and socioeconomic status have not been well characterized.A better understanding of the epidemiology of keratinocyte carcinoma in Canada and differences by sex would inform public health initiatives, health services policy and patient education strategies. This is particularly relevant now, given the recent regulatory approval of systemic immunotherapies for locally advanced or metastatic squamous and basal cell carcinoma.^22–25 Our objective was to identify the population-based incidence and mortality trends of keratinocyte carcinoma in Ontario, Canada over 2 decades and to evaluate sex differences.     

Effect of a collaborative interdisciplinary maternity care program on perinatal outcomes

Background:

The number of physicians providing maternity care in Canada is decreasing, and the rate of cesarean delivery is increasing. We evaluated the effect on perinatal outcomes of an interdisciplinary program designed to promote physiologic birth and encourage active involvement of women and their families in maternity care.

Methods:

We conducted a retrospective cohort study involving 1238 women who attended the South Community Birth Program in Vancouver, Canada, from April 2004 to October 2010. The program offers comprehensive, collaborative, interdisciplinary care from family physicians, midwives, community health nurses and doulas to a multiethnic, low-income population. A comparison group, matched for neighbourhood of residence, maternal age, parity and gestational age at delivery, comprised 1238 women receiving standard care in community-based family physician, obstetrician and midwife practices. The primary outcome was the proportion of women who underwent cesarean delivery.

Results:

Compared with women receiving standard care, those in the birth program were more likely to be delivered by a midwife (41.9% v. 7.4%, p < 0.001) instead of an obstetrician (35.5% v. 69.6%, p < 0.001). The program participants were less likely than the matched controls to undergo cesarean delivery (relative risk [RR] 0.76, 95% confidence interval [CI] 0.68–0.84) and, among those with a previous cesarean delivery, more likely to plan a vaginal birth (RR 3.22, 95% CI 2.25–4.62). Length of stay in hospital was shorter in the program group for both the mothers (mean ± standard deviation 50.6 ± 47.1 v. 72.7 ± 66.7 h, p < 0.001) and the newborns (47.5 ± 92.6 v. 70.6 ± 126.7 h, p < 0.001). Women in the birth program were more likely than the matched controls to be breastfeeding exclusively at discharge (RR 2.10, 95% CI 1.85–2.39).

Interpretation:

Women attending a collaborative program of interdisciplinary maternity care were less likely to have a cesarean delivery, had shorter hospital stays on average and were more likely to breastfeed exclusively than women receiving standard care.In the last 2 decades, Canada has seen a dramatic reduction in the number of physicians providing maternity care.^1,2 Reasons for this decline have included liability concerns, lifestyle issues and perceived competence.³ A large proportion of obstetricians and family physicians who practise maternity care will reach retirement age in the next 10 years.⁴ The reduction in maternity care providers has been linked with hospital closures in rural settings and increasing difficulty in accessing obstetric care for women in all settings.⁴ Although the introduction of regulated midwifery promises some relief, midwives currently attend less than 10% of births.⁵Recent times have also seen a dramatic increase in the rates of interventions during childbirth, particularly cesarean delivery, which has risen from 17% in the 1990s to 28% in 2009 in Canada.⁶ This increase has occurred despite a lack of evidence that maternal and neonatal outcomes are improved with cesarean delivery.^7–10 Increasing rates of surgical delivery have placed an added burden on care provider resources, because of the associated intrapartum and postpartum complications¹¹ and increased length of stay in hospital.¹²In addition, increasing diversity, especially in urban settings, has made the delivery of maternity care more challenging. In the province of British Columbia, 16% of the population speaks neither official language at home.¹³ This proportion is as high as 32% in Vancouver, the province’s largest city and the setting of our study. There is evidence that immigrant women are at increased risk of receiving obstetric interventions and less likely to breastfeed.^14,15In response to these issues, the South Community Birth Program was established to provide comprehensive, collaborative maternity care from family physicians, midwives, community health nurses and doulas to a multiethnic, low-income population. The program aims to promote physiologic birth while encouraging women and their families to assume an active role in their maternity care. In the current study, we evaluated the impact of the program on perinatal outcomes.     

Recent epidemiologic trends of diabetes mellitus among status Aboriginal adults

Background:

Little is known about longitudinal trends in diabetes mellitus among Aboriginal people in Canada. We compared the incidence and prevalence of diabetes, and its impact on mortality, among status Aboriginal adults and adults in the general population between 1995 and 2007.

Methods:

We examined de-identified data from Alberta Health and Wellness administrative databases for status Aboriginal people (First Nations and Inuit people with treaty status) and members of the general public aged 20 years and older who received a diagnosis of diabetes mellitus from Apr. 1, 1995, to Mar. 31, 2007. We calculated the incidence and prevalence of diabetes and mortality rate ratios by sex and ethnicity in 2007. We examined the average relative changes per year for longitudinal trends.

Results:

The average relative change per year in the prevalence of diabetes showed a smaller increase over time in the Aboriginal population than in the general population (2.39 v. 4.09, p < 0.001). A similar finding was observed for the incidence of diabetes. In the Aboriginal population, we found that the increase in the average relative change per year was greater among men than among women (3.13 v. 1.88 for prevalence, p < 0.001; 2.60 v. 0.02 for incidence, p = 0.001). Mortality among people with diabetes decreased over time to a similar extent in both populations. Among people without diabetes, mortality decreased in the general population but was unchanged in the Aboriginal population (−1.92 v. 0.11, p = 0.04). Overall, mortality was higher in the Aboriginal population than in the general population regardless of diabetes status.

Interpretation:

The increases in the incidence and prevalence of diabetes over the study period appeared to be slower in the status Aboriginal population than in the general population in Alberta, although the overall rates were higher in the Aboriginal population. Mortality decreased among people with diabetes in both populations but was higher overall in the Aboriginal population regardless of diabetes status.The health of Aboriginal people in Canada is generally poorer than their non-Aboriginal counterparts, and diabetes mellitus is a significant contributor.^1,2 Studies have shown that type 2 diabetes and its complications occur at rates two to five times higher in Canada’s Aboriginal population than in the general population.^3–7 In response, diverse diabetes programs have materialized, including various community-based prevention and screening projects.^8–10 The federally funded Aboriginal Diabetes Initiative was created to emphasize health promotion and diabetes prevention.¹¹ In addition, numerous Aboriginal communities have established their own diabetes and health programs.¹²Accurate diabetes surveillance data are essential for governments and health care organizations to plan health care delivery and translate knowledge into policy and funding decisions. However, research into the longitudinal trends of diabetes in Aboriginal populations is scarce. For the most part, data have come from small, community-based studies and self-reported surveys. Population-based studies of primary data are few and have been conducted only for limited periods. Even less is known about outcomes, mortality in particular, among Aboriginal individuals with diabetes.The use of administrative data is becoming more common for tracking diabetes in Canada.¹³ The National Diabetes Surveillance System uses administrative health data to document the burden of the disease, but it has little information on Aboriginal people. Dyck and colleagues recently used the methodology of the National Diabetes Surveillance System to examine the incidence and prevalence of diabetes among Aboriginal people in the province of Saskatchewan,¹⁴ and similar analyses were conducted in Manitoba and Ontario.^15,16As part of the Alberta Diabetes Surveillance System, we conducted this study to compare the incidence and prevalence of diabetes among people 20 years and older in the status Aboriginal population (First Nations and Inuit people with treaty status) and the general population in the province of Alberta between 1995 and 2007. We also compared trends in mortality in the two populations among people with and without diabetes.     

The Cedar Project: risk factors for transition to injection drug use among young, urban Aboriginal people

Background:

Studies suggest that Aboriginal people in Canada are over-represented among people using injection drugs. The factors associated with transitioning to the use of injection drugs among young Aboriginal people in Canada are not well understood.

Methods:

The Cedar Project is a prospective cohort study (2003–2007) involving young Aboriginal people in Vancouver and Prince George, British Columbia, who use illicit drugs. Participants’ venous blood samples were tested for antibodies to HIV and the hepatitis C virus, and drug use was confirmed using saliva screens. The primary outcomes were use of injection drugs at baseline and tranisition to injection drug use in the six months before each follow-up interview.

Results:

Of 605 participants, 335 (55.4%) reported using injection drugs at baseline. Young people who used injection drugs tended to be older than those who did not, female and in a relationship. Participants who injected drugs were also more likely than those who did not to have been denied shelter because of their drug use, to have been incarcerated, to have a mental illness and to have been involved in sex work. Transition to injection drug use occurred among 39 (14.4%) participants, yielding a crude incidence rate of 19.8% and an incidence density of 11.5 participants per 100 person-years. In unadjusted analysis, transition to injection drug use was associated with being female (odds ratio [OR] 1.98, 95% confidence interval (CI) 1.06–3.72), involved in sex work (OR 3.35, 95% CI 1.75–6.40), having a history of sexually transmitted infection (OR 2.01, 95% CI 1.07–3.78) and using drugs with sex-work clients (OR 2.51, 95% CI 1.19–5.32). In adjusted analysis, transition to injection drug use remained associated with involvement in sex work (adjusted OR 3.94, 95% CI 1.45–10.71).

Interpretation:

The initiation rate for injection drug use of 11.5 participants per 100 person-years among participants in the Cedar Project is distressing. Young Aboriginal women in our study were twice as likely to inject drugs as men, and participants who injected drugs at baseline were more than twice as likely as those who did not to be involved in sex work.Aboriginal leadership in Canada is deeply concerned about substance use, more specifically injection drug use and its association with the spread of HIV and the hepatitis C virus among Aboriginal young people.^1,2 Recent studies in Canada suggest that Aboriginal people are over-represented among people who use injection drugs.^3,4 For Aboriginal young people in Canada under the age of 24 years, injection drug use accounts for the majority of infections with the hepatitis C virus (70%–80%)^5,6 and over half (59%) of HIV infections.⁷Indigenous scholars have stated that research on substance use within Aboriginal communities must consider the context of colonization, including the intergenerational impacts of the residential school and child welfare systems.^8–11 It is now well documented that Aboriginal children experienced extensive psychological, sexual, physical and emotional abuses within those systems.^12,13 As former students of residential schools raise children and grandchildren, the intergenerational effects of abuse and familial fragmentation are evident in communities where interpersonal violence and drug dependence are pervasive.^14–16A priority for preventing infections with HIV and hepatitis C among young Aboriginal people is the development of programs and rights-based,^18,19 youth-informed¹⁷ policies aimed at preventing the use of injection drugs. However, research to date has not provided sufficient evidence to inform such development.^2,19 Concerns over this paucity of information led to the launch of a two-city cohort study in 2003 to address HIV-related vulnerabilities among young Aboriginal people in British Columbia — a unique study centred on at-risk youth and supported by and partnered with Aboriginal investigators and collaborators.We report here baseline and longitudinal data on the factors associated with injection drug use and the transition to injection drug use to inform the development of prevention programs and policies.     

Diagnosed hypertension in Canada: incidence, prevalence and associated mortality

Background:

Hypertension is a leading risk factor for cardiovascular diseases. Our objectives were to examine the prevalence and incidence of diagnosed hypertension in Canada and compare mortality among people with and without diagnosed hypertension.

Methods:

We obtained data from linked health administrative databases from each province and territory for adults aged 20 years and older. We used a validated case definition to identify people with hypertension diagnosed between 1998/99 and 2007/08. We excluded pregnant women from the analysis.

Results:

This retrospective population-based study included more than 26 million people. In 2007/08, about 6 million adults (23.0%) were living with diagnosed hypertension and about 418 000 had a new diagnosis. The age-standardized prevalence increased significantly from 12.5% in 1998/99 to 19.6% in 2007/08, and the incidence decreased from 2.7 to 2.4 per 100. Among people aged 60 years and older, the prevalence was higher among women than among men, as was the incidence among people aged 75 years and older. The prevalence and incidence were highest in the Atlantic region. For all age groups, all-cause mortality was higher among adults with diagnosed hypertension than among those without diagnosed hypertension.

Interpretation:

The overall prevalence of diagnosed hypertension in Canada from 1998 to 2008 was high and increasing, whereas the incidence declined during the same period. These findings highlight the need to continue monitoring the effectiveness of efforts for managing hypertension and to enhance public health programs aimed at preventing hypertension.Globally, raised blood pressure is the leading risk factor for death, accounting for about 13% of all deaths,^1,2 and it is the strongest risk factor for lost years of healthy life.¹ Left untreated, hypertension can increase the risk of stroke, coronary artery disease, dementia, heart and kidney failure, and other chronic diseases.^3–6 Managing hypertension through lifestyle modification or the use of antihypertensive medications, or both, can help mitigate these outcomes.⁷ Over the past decades in Canada, mortality associated with cardiovascular diseases has decreased,⁸ partly because of increased awareness and diagnosis of hypertension and better control of blood pressure.^9,10 However, the prevalence of hypertension remains high, and currently there are no mechanisms to track new cases at the national level.To date, information about hypertension in Canada has been mainly obtained by health surveys conducted at the provincial or national levels. Such surveys typically provide prevalence (not incidence) data and include limited data about trends over time.^11–15 National health surveys in Canada are resource intensive, do not include information about people who live in remote areas or institutions, and may underestimate hypertension prevalence because of recall bias and non-response.¹⁶ The use of administrative data that is population-based and routinely collected, such as physician claims and hospital discharge data, allows for a more comprehensive picture of this condition. Other important advantages of using administrative data include the readiness of the data to be analyzed, cost-efficiency, wide geographic coverage and the relatively complete capture of patient contact with the health care system (i.e., less prone to selection bias).Several recent studies in Canada and the United States have established valid methods for using administrative data to identify cases of hypertension.^16–23 In a study conducted in Ontario involving women and men aged 20 years and older, Tu and colleagues found that the prevalence and incidence of diagnosed hypertension were 24.5% in 2005 and 3.2% in 2004, respectively.²⁴ We used the same validated case definition to examine the prevalence and incidence of diagnosed hypertension in Canada from 1998/99 to 2007/08 by age and by province and territory. We also compared all-cause mortality by age and sex among those with and without diagnosed hypertension.     

Association between different growth curve definitions of overweight and obesity and cardiometabolic risk in children

Background:

Overweight and obesity in young people are assessed by comparing body mass index (BMI) with a reference population. However, two widely used reference standards, the Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO) growth curves, have different definitions of overweight and obesity, thus affecting estimates of prevalence. We compared the associations between overweight and obesity as defined by each of these curves and the presence of cardiometabolic risk factors.

Methods:

We obtained data from a population-representative study involving 2466 boys and girls aged 9, 13 and 16 years in Quebec, Canada. We calculated BMI percentiles using the CDC and WHO growth curves and compared their abilities to detect unfavourable levels of fasting lipids, glucose and insulin, and systolic and diastolic blood pressure using receiver operating characteristic curves, sensitivity, specificity and kappa coefficients.

Results:

The z scores for BMI using the WHO growth curves were higher than those using the CDC growth curves (0.35–0.43 v. 0.12–0.28, p < 0.001 for all comparisons). The WHO and CDC growth curves generated virtually identical receiver operating characteristic curves for individual or combined cardiometabolic risk factors. The definitions of overweight and obesity had low sensitivities but adequate specificities for cardiometabolic risk. Obesity as defined by the WHO or CDC growth curves discriminated cardiometabolic risk similarly, but overweight as defined by the WHO curves had marginally higher sensitivities (by 0.6%–8.6%) and lower specificities (by 2.6%–4.2%) than the CDC curves.

Interpretation:

The WHO growth curves show no significant discriminatory advantage over the CDC growth curves in detecting cardiometabolic abnormalities in children aged 9–16 years.Pediatric obesity is associated with dyslipidemia, insulin resistance and elevated blood pressure.^1–6 Thus, accurately identifying children with obesity is crucial for clinical management and public health surveillance.Lipid screening is recommended for young people who are overweight,^7,8 but studies show that estimates of the prevalence of overweight and obesity are 1%–7% lower using the growth curves of the Centers for Disease Control and Prevention (CDC) versus those of the World Health Organization (WHO).^9–11 Although the CDC and WHO definitions of overweight and obesity both use approximations of overweight and obese values of body mass index (BMI) when children reach 19 years of age, the CDC growth curves use data from more recent samples of young people.^12,13 Given the recent rise in the prevalence of obesity among young people, using a heavier reference population may lead to fewer children being identified as overweight and obese, and an identical BMI value may not trigger a clinical investigation.⁷ The Canadian Paediatric Society, in collaboration with the College of Family Physicians of Canada, Dietitians of Canada and Community Health Nurses of Canada, recently recommended that physicians switch from the CDC to the WHO growth curves for monitoring growth for Canadian children aged 5–19 years.¹⁴ This is a major change for health providers caring for the estimated 8 million children in Canada.¹⁵Understanding how using the different growth curves affects the identification of adverse cardiometabolic risk profiles is essential for the appropriate management of overweight and obesity among young people. Thus, our objectives were to assess whether the association between BMI percentiles and cardiometabolic risk differs between the definitions of overweight and obesity based on the WHO and CDC growth curves, and to compare the sensitivity and specificity of these definitions in detecting cardiometabolic risk.     

Income-related differences in mortality among people with diabetes mellitus

Background

Mortality has declined substantially among people with diabetes mellitus over the last decade. Whether all income groups have benefited equally, however, is unclear. We examined the impact of income on mortality trends among people with diabetes.

Methods

In this population-based, retrospective cohort study, we compared changes in mortality from Apr. 1, 1994, to Mar. 31, 2005, by neighbourhood income strata among people with diabetes aged 30 years or more in the province of Ontario, Canada.

Results

Overall, the annual age- and sex-adjusted mortality declined, from 4.05% in 1994/95 (95% confidence interval [CI] 3.98%–4.11%) to 2.69% in 2005/06 (95% CI 2.66%–2.73%). The decrease was significantly greater in the highest income group (by 36%) than in the lowest income group (by 31%; p < 0.001). This trend was most pronounced in the younger group (age 30–64 years): the mortality rate ratio widened by more than 40% between the lowest and highest income groups, from 1.12 to 1.59 among women and from 1.14 to 1.60 among men. Income had a much smaller effect on mortality trends in the older group, whose drug costs are subsidized: the income-related difference rose by only 0.9% over the study period.

Interpretation

Mortality declined overall among people with diabetes from 1994 to 2005; however, the decrease was substantially greater in the highest income group than in the lowest, particularly among those aged 30–64 years. These findings illustrate the increasing impact of income on the health of people with diabetes even in a publicly funded health care setting. Further studies are needed to explore factors responsible for these income-related differences in mortality.The number of people with diabetes mellitus has increased dramatically over the last 20 years^1,2 and is estimated to double to about 366 million by 2030.³ Diabetes is associated with a 2-fold increase in mortality, with the majority of deaths attributed to cardiovascular causes.⁴ However, survival among people with diabetes has improved substantially over the last decade,^1,5,6 in part because of better diabetes care and a reduction in cardiovascular events.⁶Income is a well-known predictor of survival.^7,8 Even in Canada, where much of health care is universally funded, income-based inequities in health and access to care remain.^9–12 Although income-related differences in all-cause mortality have decreased since the advent of provincially subsidized health care in Canada,^8,9 the income gap may be increasing for certain causes of death, including those related to diabetes.⁸ The shift to more complex medical care involving a greater number of drug therapies has resulted in improved diabetes-related outcomes overall.¹³ However, patients in lower-income groups may not have benefited from advances in diabetes care as much as more affluent patients have because of the financial burden of out-of-pocket expenses for such medications and diabetes supplies.We conducted a population-based study to examine income-related differences in mortality from 1994 to 2005 among people with diabetes.     

Scientific dissent and public policy

The temptation to silence dissenters whose non-mainstream views negatively affect public policies is powerful. However, silencing dissent, no matter how scientifically unsound it might be, can cause the public to mistrust science in general.Dissent is crucial for the advancement of science. Disagreement is at the heart of peer review and is important for uncovering unjustified assumptions, flawed methodologies and problematic reasoning. Enabling and encouraging dissent also helps to generate alternative hypotheses, models and explanations. Yet, despite the importance of dissent in science, there is growing concern that dissenting voices have a negative effect on the public perception of science, on policy-making and public health. In some cases, dissenting views are deliberately used to derail certain policies. For example, dissenting positions on climate change, environmental toxins or the hazards of tobacco smoke [1,2] seem to laypeople as equally valid conflicting opinions and thereby create or increase uncertainty. Critics often use legitimate scientific disagreements about narrow claims to reinforce the impression of uncertainty about general and widely accepted truths; for instance, that a given substance is harmful [3,4]. This impression of uncertainty about the evidence is then used to question particular policies [1,2,5,6].The negative effects of dissent on establishing public polices are present in cases in which the disagreements are scientifically well-grounded, but the significance of the dissent is misunderstood or blown out of proportion. A study showing that many factors affect the size of reef islands, to the effect that they will not necessarily be reduced in size as sea levels rise [7], was simplistically interpreted by the media as evidence that climate change will not have a negative impact on reef islands [8].In other instances, dissenting voices affect the public perception of and motivation to follow public-health policies or recommendations. For example, the publication of a now debunked link between the measles, mumps and rubella vaccine and autism [9], as well as the claim that the mercury preservative thimerosal, which was used in childhood vaccines, was a possible risk factor for autism [10,11], created public doubts about the safety of vaccinating children. Although later studies showed no evidence for these claims, doubts led many parents to reject vaccinations for their children, risking the herd immunity for diseases that had been largely eradicated from the industrialized world [12,13,14,15]. Many scientists have therefore come to regard dissent as problematic if it has the potential to affect public behaviour and policy-making. However, we argue that such concerns about dissent as an obstacle to public policy are both dangerous and misguided.Whether dissent is based on genuine scientific evidence or is unfounded, interested parties can use it to sow doubt, thwart public policies, promote problematic alternatives and lead the public to ignore sound advice. In response, scientists have adopted several strategies to limit these negative effects of dissent—masking dissent, silencing dissent and discrediting dissenters. The first strategy aims to present a united front to the public. Scientists mask existing disagreements among themselves by presenting only those claims or pieces of evidence about which they agree [16]. Although there is nearly universal agreement among scientists that average global temperatures are increasing, there are also legitimate disagreements about how much warming will occur, how quickly it will occur and the impact it might have [7,17,18,19]. As presenting these disagreements to the public probably creates more doubt and uncertainty than is warranted, scientists react by presenting only general claims [20].A second strategy is to silence dissenting views that might have negative consequences. This can take the form of self-censorship when scientists are reluctant to publish or publicly discuss research that might—incorrectly—be used to question existing scientific knowledge. For example, there are genuine disagreements about how best to model cloud formation, water vapour feedback and aerosols in general circulation paradigms, all of which have significant effects on the magnitude of global climate change predictions [17,19]. Yet, some scientists are hesitant to make these disagreements public, for fear that they will be accused of being denialists, faulted for confusing the public and policy-makers, censured for abating climate-change deniers, or criticized for undermining public policy [21,22,23,24].…there is growing concern that dissenting voices can have a negative effect on the public perception of science, on policy-making and public healthAnother strategy is to discredit dissenters, especially in cases in which the dissent seems to be ideologically motivated. This could involve publicizing the financial or political ties of the dissenters [2,6,25], which would call attention to their probable bias. In other cases, scientists might discredit the expertise of the dissenter. One such example concerns a 2007 study published in the Proceedings of the National Academy of Sciences USA, which claimed that cadis fly larvae consuming Bt maize pollen die at twice the rate of flies feeding on non-Bt maize pollen [26]. Immediately after publication, both the authors and the study itself became the target of relentless and sometimes scathing attacks from a group of scientists who were concerned that anti-GMO (genetically modified organism) interest groups would seize on the study to advance their agenda [27]. The article was criticized for its methodology and its conclusions, the Proceedings of the National Academy of Sciences USA was criticized for publishing the article and the US National Science Foundation was criticized for funding the study in the first place.Public policies, health advice and regulatory decisions should be based on the best available evidence and knowledge. As the public often lack the expertise to assess the quality of dissenting views, disagreements have the potential to cast doubt over the reliability of scientific knowledge and lead the public to question relevant policies. Strategies to block dissent therefore seem reasonable as a means to protect much needed or effective health policies, advice and regulations. However, even if the public were unable to evaluate the science appropriately, targeting dissent is not the most appropriate strategy to prevent negative side effects for several reasons. Chiefly, it contributes to the problems that the critics of dissent seek to address, namely increasing the cacophony of dissenting voices that only aim to create doubt. Focusing on dissent as a problematic activity sends the message to policy-makers and the public that any dissent undermines scientific knowledge. Reinforcing this false assumption further incentivizes those who seek merely to create doubt to thwart particular policies. Not surprisingly, think-tanks, industry and other organizations are willing to manufacture dissent simply to derail policies that they find economically or ideologically undesirable.Another danger of targeting dissent is that it probably stifles legitimate crucial voices that are needed for both advancing science and informing sound policy decisions. Attacking dissent makes scientists reluctant to voice genuine doubts, especially if they believe that doing so might harm their reputations, damage their careers and undermine prevailing theories or policies needed. For instance, a panel of scientists for the US National Academy of Sciences, when presenting a risk assessment of radiation in 1956, omitted wildly different predictions about the potential genetic harm of radiation [16]. They did not include this wide range of predictions in their final report precisely because they thought the differences would undermine confidence in their recommendations. Yet, this information could have been relevant to policy-makers. As such, targeting dissent as an obstacle to public policy might simply reinforce self-censorship and stifle legitimate and scientifically informed debate. If this happens, scientific progress is hindered.Second, even if the public has mistaken beliefs about science or the state of the knowledge of the science in question, focusing on dissent is not an effective way to protect public policy from false claims. It fails to address the presumed cause of the problem—the apparent lack of understanding of the science by the public. A better alternative would be to promote the public''s scientific literacy. If the public were educated to better assess the quality of the dissent and thus disregard instances of ideological, unsupported or unsound dissent, dissenting voices would not have such a negative effect. Of course, one might argue that educating the public would be costly and difficult, and that therefore, the public should simply listen to scientists about which dissent to ignore and which to consider. This is, however, a paternalistic attitude that requires the public to remain ignorant ‘for their own good''; a position that seems unjustified on many levels as there are better alternatives for addressing the problem.Moreover, silencing dissent, rather than promoting scientific literacy, risks undermining public trust in science even if the dissent is invalid. This was exemplified by the 2009 case of hacked e-mails from a computer server at the University of East Anglia''s Climate Research Unit (CRU). After the selective leaking of the e-mails, climate scientists at the CRU came under fire because some of the quotes, which were taken out of context, seemed to suggest that they were fudging data or suppressing dissenting views [28,29,30,31]. The stolen e-mails gave further ammunition to those opposing policies to reduce greenhouse emissions as they could use accusations of data ‘cover up'' as proof that climate scientists were not being honest with the public [29,30,31]. It also allowed critics to present climate scientists as conspirators who were trying to push a political agenda [32]. As a result, although there was nothing scientifically inappropriate revealed in the ‘climategate'' e-mails, it had the consequence of undermining the public''s trust in climate science [33,34,35,36].A significant amount of evidence shows that the ‘deficit model'' of public understanding of science, as described above, is too simplistic to account correctly for the public''s reluctance to accept particular policy decisions [37,38,39,40]. It ignores other important factors such as people''s attitudes towards science and technology, their social, political and ethical values, their past experiences and the public''s trust in governmental institutions [41,42,43,44]. The development of sound public policy depends not only on good science, but also on value judgements. One can agree with the scientific evidence for the safety of GMOs, for instance, but still disagree with the widespread use of GMOs because of social justice concerns about the developing world''s dependence on the interests of the global market. Similarly, one need not reject the scientific evidence about the harmful health effects of sugar to reject regulations on sugary drinks. One could rationally challenge such regulations on the grounds that informed citizens ought to be able to make free decisions about what they consume. Whether or not these value judgements are justified is an open question, but the focus on dissent hinders our ability to have that debate.Focusing on dissent as a problematic activity sends the message to policy-makers and the public that any dissent undermines scientific knowledgeAs such, targeting dissent completely fails to address the real issues. The focus on dissent, and the threat that it seems to pose to public policy, misdiagnoses the problem as one of the public misunderstanding science, its quality and its authority. It assumes that scientific or technological knowledge is the only relevant factor in the development of policy and it ignores the role of other factors, such as value judgements about social benefits and harms, and institutional trust and reliability [45,46]. The emphasis on dissent, and thus on scientific knowledge, as the only or main factor in public policy decisions does not give due attention to these legitimate considerations.Furthermore, by misdiagnosing the problem, targeting dissent also impedes more effective solutions and prevents an informed debate about the values that should guide public policy. By framing policy debates solely as debates over scientific facts, the normative aspects of public policy are hidden and neglected. Relevant ethical, social and political values fail to be publicly acknowledged and openly discussed.Controversies over GMOs and climate policies have called attention to the negative effects of dissent in the scientific community. Based on the assumption that the public''s reluctance to support particular policies is the result of their inability to properly understand scientific evidence, scientists have tried to limit dissenting views that create doubt. However, as outlined above, targeting dissent as an obstacle to public policy probably does more harm than good. It fails to focus on the real problem at stake—that science is not the only relevant factor in sound policy-making. Of course, we do not deny that scientific evidence is important to the develop.ment of public policy and behavioural decisions. Rather, our claim is that this role is misunderstood and often oversimplified in ways that actually contribute to problems in developing sound science-based policies.? Open in a separate windowInmaculada de Melo-MartínOpen in a separate windowKristen Intemann     

Cardiovascular disease after Escherichia coli O157:H7 gastroenteritis

Background:

Escherichia coli O157:H7 is one cause of acute bacterial gastroenteritis, which can be devastating in outbreak situations. We studied the risk of cardiovascular disease following such an outbreak in Walkerton, Ontario, in May 2000.

Methods:

In this community-based cohort study, we linked data from the Walkerton Health Study (2002–2008) to Ontario’s large healthcare databases. We included 4 groups of adults: 3 groups of Walkerton participants (153 with severe gastroenteritis, 414 with mild gastroenteritis, 331 with no gastroenteritis) and a group of 11 263 residents from the surrounding communities that were unaffected by the outbreak. The primary outcome was a composite of death or first major cardiovascular event (admission to hospital for acute myocardial infarction, stroke or congestive heart failure, or evidence of associated procedures). The secondary outcome was first major cardiovascular event censored for death. Adults were followed for an average of 7.4 years.

Results:

During the study period, 1174 adults (9.7%) died or experienced a major cardiovascular event. Compared with residents of the surrounding communities, the risk of death or cardiovascular event was not elevated among Walkerton participants with severe or mild gastroenteritis (hazard ratio [HR] for severe gastroenteritis 0.74, 95% confidence interval [CI] 0.38–1.43, mild gastroenteritis HR 0.64, 95% CI 0.42–0.98). Compared with Walkerton participants who had no gastroenteritis, risk of death or cardiovascular event was not elevated among participants with severe or mild gastroenteritis.

Interpretation:

There was no increase in the risk of cardiovascular disease in the decade following acute infection during a major E. coli O157:H7 outbreak.Escherichia coli O157:H7 is one cause of acute bacterial gastroenteritis, causing 63 000 infections each year and 12 major outbreaks since 2006 in the United States alone.^1,2 This strain was most recently implicated in the outbreak involving beef from XL Foods (September 2012), with 17 confirmed cases across Canada.³ A similar enterohemorrhagic strain E. coli O104:H4 was responsible for an outbreak in Germany in May 2011, causing 3792 cases of gastroenteritis and 43 deaths.^4,5Most patients fully recover from acute gastroenteritis caused by E. coli. However, such an illness may predispose patients to long-term disease. Shiga toxin is produced by E. coli O157:H7; this toxin damages the microvasculature of the kidneys leading to hypertension^6–13 and directly damages the systemic vasculature.^14–16 Infected people may progress from a state of acute inflammation of the vasculature to subclinical chronic inflammation, which could promote atherosclerosis.^17–20In Walkerton, Ontario, in May 2000, heavy rains transported bovine fecal matter into the town’s well, contaminating the inadequately chlorinated municipal water supply with E. coli O157:H7.²¹ Over 2300 people developed acute gastroenteritis, and 7 people died.²² The unique circumstances of this outbreak provided a rare opportunity to study the natural history following exposure to this pathogen in a single cohort.²³ Other outbreaks have been geographically dispersed, making it difficult to track cases.^24,25In Walkerton, affected individuals were followed annually in a clinic to assess their long-term outcomes (Walkerton Health Study, 2002–2008). We previously reported that adults who experienced acute gastroenteritis during the outbreak had a higher than expected incidence of hypertension, chronic kidney disease and self-reported cardiovascular disease in follow-up.²³ However, 46% of participants were lost to follow-up by the end of the study, and there were limitations associated with the assessment of cardiovascular disease by participant recall. Thus, we conducted an expanded and extended follow-up study, linking the Walkerton study data to Ontario’s health care databases. Our objective was to more accurately determine the 10-year risk of major cardiovascular events after exposure to E. coli O157:H7.     

Gut microbiota of healthy Canadian infants: profiles by mode of delivery and infant diet at 4 months

Background:

The gut microbiota is essential to human health throughout life, yet the acquisition and development of this microbial community during infancy remains poorly understood. Meanwhile, there is increasing concern over rising rates of cesarean delivery and insufficient exclusive breastfeeding of infants in developed countries. In this article, we characterize the gut microbiota of healthy Canadian infants and describe the influence of cesarean delivery and formula feeding.

Methods:

We included a subset of 24 term infants from the Canadian Healthy Infant Longitudinal Development (CHILD) birth cohort. Mode of delivery was obtained from medical records, and mothers were asked to report on infant diet and medication use. Fecal samples were collected at 4 months of age, and we characterized the microbiota composition using high-throughput DNA sequencing.

Results:

We observed high variability in the profiles of fecal microbiota among the infants. The profiles were generally dominated by Actinobacteria (mainly the genus Bifidobacterium) and Firmicutes (with diverse representation from numerous genera). Compared with breastfed infants, formula-fed infants had increased richness of species, with overrepresentation of Clostridium difficile. Escherichia–Shigella and Bacteroides species were underrepresented in infants born by cesarean delivery. Infants born by elective cesarean delivery had particularly low bacterial richness and diversity.

Interpretation:

These findings advance our understanding of the gut microbiota in healthy infants. They also provide new evidence for the effects of delivery mode and infant diet as determinants of this essential microbial community in early life.The human body harbours trillions of microbes, known collectively as the “human microbiome.” By far the highest density of commensal bacteria is found in the digestive tract, where resident microbes outnumber host cells by at least 10 to 1. Gut bacteria play a fundamental role in human health by promoting intestinal homeostasis, stimulating development of the immune system, providing protection against pathogens, and contributing to the processing of nutrients and harvesting of energy.^1,2 The disruption of the gut microbiota has been linked to an increasing number of diseases, including inflammatory bowel disease, necrotizing enterocolitis, diabetes, obesity, cancer, allergies and asthma.¹ Despite this evidence and a growing appreciation for the integral role of the gut microbiota in lifelong health, relatively little is known about the acquisition and development of this complex microbial community during infancy.³Two of the best-studied determinants of the gut microbiota during infancy are mode of delivery and exposure to breast milk.^4,5 Cesarean delivery perturbs normal colonization of the infant gut by preventing exposure to maternal microbes, whereas breastfeeding promotes a “healthy” gut microbiota by providing selective metabolic substrates for beneficial bacteria.^3,5 Despite recommendations from the World Health Organization,⁶ the rate of cesarean delivery has continued to rise in developed countries and rates of breastfeeding decrease substantially within the first few months of life.^7,8 In Canada, more than 1 in 4 newborns are born by cesarean delivery, and less than 15% of infants are exclusively breastfed for the recommended duration of 6 months.^9,10 In some parts of the world, elective cesarean deliveries are performed by maternal request, often because of apprehension about pain during childbirth, and sometimes for patient–physician convenience.¹¹The potential long-term consequences of decisions regarding mode of delivery and infant diet are not to be underestimated. Infants born by cesarean delivery are at increased risk of asthma, obesity and type 1 diabetes,¹² whereas breastfeeding is variably protective against these and other disorders.¹³ These long-term health consequences may be partially attributable to disruption of the gut microbiota.^12,14Historically, the gut microbiota has been studied with the use of culture-based methodologies to examine individual organisms. However, up to 80% of intestinal microbes cannot be grown in culture.^3,15 New technology using culture-independent DNA sequencing enables comprehensive detection of intestinal microbes and permits simultaneous characterization of entire microbial communities. Multinational consortia have been established to characterize the “normal” adult microbiome using these exciting new methods;¹⁶ however, these methods have been underused in infant studies. Because early colonization may have long-lasting effects on health, infant studies are vital.^3,4 Among the few studies of infant gut microbiota using DNA sequencing, most were conducted in restricted populations, such as infants delivered vaginally,¹⁷ infants born by cesarean delivery who were formula-fed¹⁸ or preterm infants with necrotizing enterocolitis.¹⁹Thus, the gut microbiota is essential to human health, yet the acquisition and development of this microbial community during infancy remains poorly understood.³ In the current study, we address this gap in knowledge using new sequencing technology and detailed exposure assessments²⁰ of healthy Canadian infants selected from a national birth cohort to provide representative, comprehensive profiles of gut microbiota according to mode of delivery and infant diet.     

A qualitative investigation of smoke-free policies on hospital property

Background:

Many hospitals have adopted smoke-free policies on their property. We examined the consequences of such polices at two Canadian tertiary acute-care hospitals.

Methods:

We conducted a qualitative study using ethnographic techniques over a six-month period. Participants (n = 186) shared their perspectives on and experiences with tobacco dependence and managing the use of tobacco, as well as their impressions of the smoke-free policy. We interviewed inpatients individually from eight wards (n = 82), key policy-makers (n = 9) and support staff (n = 14) and held 16 focus groups with health care providers and ward staff (n = 81). We also reviewed ward documents relating to tobacco dependence and looked at smoking-related activities on hospital property.

Results:

Noncompliance with the policy and exposure to secondhand smoke were ongoing concerns. Peoples’ impressions of the use of tobacco varied, including divergent opinions as to whether such use was a bad habit or an addiction. Treatment for tobacco dependence and the management of symptoms of withdrawal were offered inconsistently. Participants voiced concerns over patient safety and leaving the ward to smoke.

Interpretation:

Policies mandating smoke-free hospital property have important consequences beyond noncompliance, including concerns over patient safety and disruptions to care. Without adequately available and accessible support for withdrawal from tobacco, patients will continue to face personal risk when they leave hospital property to smoke.Canadian cities and provinces have passed smoking bans with the goal of reducing people’s exposure to secondhand smoke in workplaces, public spaces and on the property adjacent to public buildings.^1,2 In response, Canadian health authorities and hospitals began implementing policies mandating smoke-free hospital property, with the goals of reducing the exposure of workers, patients and visitors to tobacco smoke while delivering a public health message about the dangers of smoking.^2–5 An additional anticipated outcome was the reduced use of tobacco among patients and staff. The impetuses for adopting smoke-free policies include public support for such legislation and the potential for litigation for exposure to second-hand smoke.^2,4Tobacco use is a modifiable risk factor associated with a variety of cancers, cardiovascular diseases and respiratory conditions.^6–11 Patients in hospital who use tobacco tend to have more surgical complications and exacerbations of acute and chronic health conditions than patients who do not use tobacco.^6–11 Any policy aimed at reducing exposure to tobacco in hospitals is well supported by evidence, as is the integration of interventions targetting tobacco dependence.¹² Unfortunately, most of the nearly five million Canadians who smoke will receive suboptimal treatment,¹³ as the routine provision of interventions for tobacco dependence in hospital settings is not a practice norm.^14–16 In smoke-free hospitals, two studies suggest minimal support is offered for withdrawal, ^17,18 and one reports an increased use of nicotine-replacement therapy after the implementation of the smoke-free policy.¹⁹Assessments of the effectiveness of smoke-free policies for hospital property tend to focus on noncompliance and related issues of enforcement.^17,20,21 Although evidence of noncompliance and litter on hospital property^2,17,20 implies ongoing exposure to tobacco smoke, half of the participating hospital sites in one study reported less exposure to tobacco smoke within hospital buildings and on the property.¹⁸ In addition, there is evidence to suggest some decline in smoking among staff.^18,19,21,22We sought to determine the consequences of policies mandating smoke-free hospital property in two Canadian acute-care hospitals by eliciting lived experiences of the people faced with enacting the policies: patients and health care providers. In addition, we elicited stories from hospital support staff and administrators regarding the policies.     

Socioeconomic status and incidence of sudden cardiac arrest

Background:

Low socioeconomic status is associated with poor cardiovascular health. We evaluated the association between socioeconomic status and the incidence of sudden cardiac arrest, a condition that accounts for a substantial proportion of cardiovascular-related deaths, in seven large North American urban populations.

Methods:

Using a population-based registry, we collected data on out-of-hospital sudden cardiac arrests occurring at home or at a residential institution from Apr. 1, 2006, to Mar. 31, 2007. We limited the analysis to cardiac arrests in seven metropolitan areas in the United States (Dallas, Texas; Pittsburgh, Pennsylvania; Portland, Oregon; and Seattle–King County, Washington) and Canada (Ottawa and Toronto, Ontario; and Vancouver, British Columbia). Each incident was linked to a census tract; tracts were classified into quartiles of median household income.

Results:

A total of 9235 sudden cardiac arrests were included in the analysis. For all sites combined, the incidence of sudden cardiac arrestin the lowest socioeconomic quartile was nearly double that in the highest quartile (incidence rate ratio [IRR] 1.9, 95% confidence interval [CI] 1.8–2.0). This disparity was greater among people less than 65 years old (IRR 2.7, 95% CI 2.5–3.0) than among those 65 or older (IRR 1.3, 95% CI 1.2–1.4). After adjustment for study site and for population age structure of each census tract, the disparity across socioeconomic quartiles for all ages combined was greater in the United States (IRR 2.0, 95% CI 1.9–2.2) than in Canada (IRR 1.8, 95% CI 1.6–2.0) (p < 0.001 for interaction).

Interpretation:

The incidence of sudden cardiac arrest at home or at a residential institution was higher in poorer neighbourhoods of the US and Canadian sites studied, although the association was attenuated in Canada. The disparity across socioeconomic quartiles was greatest among people younger than 65. The association between socioeconomic status and incidence of sudden cardiac arrest merits consideration in the development of strategies to improve survival from sudden cardiac arrest, and possibly to identify opportunities for prevention.An estimated 250 000–300 000 sudden cardiac arrests occur each year in the United States,¹ accounting for up to 63% of cardiac-related deaths annually.² Despite advances in resuscitation, more than 95% of people who experience sudden cardiac arrest die,³ and up to 50% of sudden cardiac arrests occur in people who do not have a history of coronary artery disease.⁴Socioeconomic status has been shown to predict many health outcomes, including all-cause mortality,⁵ prevalence of risk factors for cardiovascular disease⁶ and incidence of cardiovascular disease.^7–9 Despite this substantial literature, we found only three studies that examined the potential association between socioeconomic status and sudden cardiac arrest. Although the studies were small and conducted in single communities, each showed that the incidence of sudden cardiac arrest was significantly higher in lower socioeconomic areas.^10–12 The Oregon Sudden Unexplained Death Study (Ore-SUDS) reported a 30%–80% higher incidence of sudden cardiac arrest in poorer neighbourhoods. A stronger association was observed among people less than 65 years old, a group for whom basic health care funding is not guaranteed in the United States.¹¹Low socioeconomic status may be linked to an increased risk of sudden cardiac arrest by a variety of mechanisms related to individual risk factors or health-promoting behaviours or neighbourhood characteristics. Individuals of lower socioeconomic status have been found to have a greater burden of risk factors for cardiovascular disease,¹³ poorer control of established cardiovascular risk factors¹⁴ and longer delays in seeking hospital care for acute myocardial infarction.¹⁵ Numerous studies have also shown that disparities in health outcomes are apparent across the spectrum of socioeconomic status.¹⁶A better understanding of community-level patterns in the distribution of sudden cardiac arrest may identify opportunities for improving survival, such as effective targeting of community training for cardiopulmonary resuscitation and placement of automated external defibrillators in lower-income communities. We tested the hypothesis that disparities in the incidence of sudden cardiac arrest by level of socioeconomic status would be evident in a variety of urban communities in the United States and Canada, and that this association would be most prominent among people less than 65 years old residing in US communities.     

Association of macrosomia with perinatal and postneonatal mortality among First Nations people in Quebec

Background

High prevalence of infant macrosomia (up to 36%, the highest in the world) has been reported in some First Nations communities in the Canadian province of Quebec and the eastern area of the province of Ontario. We aimed to assess whether infant macrosomia was associated with elevated risks of perinatal and postneonatal mortality among First Nations people in Quebec.

Methods

We calculated risk ratios (RRs) of perinatal and postneonatal mortality by birthweight for gestational age, comparing births to First Nations women (n = 5193) versus women whose mother tongue is French (n = 653 424, the majority reference group) in Quebec 1991–2000.

Results

The prevalence of infant macrosomia (birthweight for gestational age > 90th percentile) was 27.5% among births to First Nations women, which was 3.3 times (confidence interval [CI] 3.2–3.5) higher than the prevalence (8.3%) among births to women whose mother tongue is French. Risk ratios for perinatal mortality among births to First Nations women were 1.8 (95% CI 1.3–2.5) for births with weight appropriate for gestational age, 4.1 (95% CI 2.4–7.0) for small-for-gestational-age (< 10th percentile) births and < 1 (not significant) for macrosomic births compared to births among women whose mother tongue is French. The RRs for postneonatal mortality were 4.3 (95% CI 2.7–6.7) for infants with appropriate-for-gestational-age birthweight and 8.3 (95% CI 4.0–17.0) for infants with macrosomia.

Interpretation

Macrosomia was associated with a generally protective effect against perinatal death, but substantially greater risks of postneonatal death among births to First Nations women in Quebec versus women whose mother tongue is French.A trend toward higher birthweights has emerged in recent decades.^1–3 Reflected in this trend is a rise in the prevalence of infant macrosomia, commonly defined as either a birthweight greater than 4000 g or a birthweight for gestational age greater than the 90th percentile relative to a fetal growth standard.^4–8 Maternal obesity, impaired glucose tolerance and gestational diabetes mellitus are important risk factors for infant macrosomia^9,10 and are known to afflict a much higher proportion of people in Aboriginal populations than in the general population.^11–14 This is true especially for Aboriginal populations in which a traditional lifestyle has changed to a less physically active, modern lifestyle in recent decades. A high prevalence of infant macrosomia (up to 36%, which, to the best of our knowledge, is the highest in the world) has been reported in some First Nations communities of Quebec and eastern Ontario in Canada.^15–17 However, little is known about the implications of this high prevalence for perinatal and infant health of First Nations people in these regions. We examined whether infant macrosomia was associated with increased risk for perinatal and postneonatal death among First Nations infants in Quebec.