A cohort study of the multipollutant effects of PM2.5, NO2, and O3 on C-reactive protein levels during pregnancy.

Background: PM2.5, NO2, and O3 contribute to the development of adverse pregnancy complications. While studies have investigated the independent effects of these exposures, literature on their combined effects is limited. Our objective was to study the multipollutant effects of PM2.5, NO2, and O3 on maternal systemic C-reactive protein (CRP) levels. Methods: We used data from 1170 pregnant women enrolled in the Maternal-Infant Research on Environmental Chemicals Study (MIREC) study in Canada. Air pollution exposures were assigned to each participant based on residential location. CRP was measured in third-trimester blood samples. We fit multipollutant linear regression models and evaluated the effects of air pollutant mixtures (14-day averages) using repeated-holdout Weighted Quantile Sum (WQS) regression and by calculating the Air Quality Health Index (AQHI). Results: In multipollutant models adjusting for NO2, O3, and green space, each interquartile range (IQR) increase in 14-day average PM2.5 (IQR: 6.9 µg/m3) was associated with 27.1% (95% confidence interval [CI] = 6.2, 50.7) higher CRP. In air pollution mixture models adjusting for green space, each IQR increase in AQHI was associated with 37.7% (95% CI = 13.9, 66.5) higher CRP; and an IQR increase in the WQS index was associated with 78.6% (95% CI = 29.7, 146.0) higher CRP. Conclusion: PM2.5 has the strongest relationship of the individual pollutants examined with maternal blood CRP concentrations. Mixtures incorporating all three pollutants, assessed using the AQHI and WQS index, showed stronger relationships with CRP compared with individual pollutants and illustrate the importance of conducting multipollutant analyses.

Ambient polycyclic aromatic hydrocarbon exposure and breast cancer risk in a population-based Canadian case-control study.

PURPOSE: Polycyclic aromatic hydrocarbons (PAHs) represent a class of ubiquitous pollutants recognized as established human carcinogens and endocrine-disrupting chemicals. PAHs have seldom been modeled at the population-level in epidemiological studies. Fluoranthene is a prevalent PAH in urban settings and correlates with the occurrence of other PAHs. The purpose of this study was to evaluate associations between long-term residential exposure to ambient PAHs and breast cancer risk, both pre- and post-menopausal, in Canada. METHODS: Using the National Enhanced Cancer Surveillance System (NECSS), a national-scale Canadian population-based case-control study, annual fluoranthene exposures were estimated using the GEM-MACH-PAH chemical transport model on the basis of geocoded residential histories throughout a 20-year exposure window. Odds ratios (ORs) and 95% confidence intervals (CIs) controlling for potential confounders were estimated using logistic regression. Separate analyses were conducted for Ontario and national samples given a finer-resolution exposure surface and additional risk factor information available for Ontario. RESULTS: Positive associations were observed between fluoranthene exposure and premenopausal breast cancer, with inconsistent findings for postmenopausal breast cancer. For premenopausal breast cancer, adjusted ORs of 2.48 (95% CI: 1.29, 4.77) and 1.59 (95% CI: 1.11, 2.29) were observed when comparing the second highest category of exposure to the lowest, among the Ontario and national samples, respectively. For postmenopausal breast cancer, adjusted ORs were 1.10 (95% CI: 0.67, 1.80) and 1.33 (95% CI: 1.02, 1.73). Associations for the highest level of exposure, across both samples and menopausal strata, were non-significant. CONCLUSION: This study provides support for the hypothesis that ambient PAH exposures increase the risk of premenopausal breast cancer.

Time spent in the sun and the risk of developing non-Hodgkin lymphoma: a Canadian cohort study.

PURPOSE: The objective was to explore the relationship of sun behavior patterns with the risk of developing non-Hodgkin lymphoma (NHL). METHODS: Sun behavior information from Alberta's Tomorrow Project, CARTaGENE, and Ontario Health Study were utilized. The relationship between time in the sun during summer months and risk of NHL was assessed using Cox proportional hazard models with age as the time scale and adjustment for confounders. Cohorts were analyzed separately and hazard ratios (HR) pooled with random effects meta-analysis. Joint effects of time in the sun and use of sun protection were examined. Patterns of exposure were explored via combinations of weekday and weekend time in the sun. RESULTS: During an average follow-up of 7.6 years, 205 NHL cases occurred among study participants (n = 79,803). Compared to < 30 min daily in the sun, we observed HRs of 0.84 (95% CI 0.55-1.28) for 30-59 min, 0.63 (95% CI 0.40-0.98) for 1-2 h, and 0.91 (95% CI 0.61-1.36) for > 2 h. There was suggestive evidence that > 2 h was protective against NHL with use of sun protection, but not without it. Compared to < 30 min daily, moderate exposure (30 min to 2 h on weekdays or weekend) was associated with a lower risk of NHL (HR 0.63, 95% CI 0.43-0.92), while intermittent (< 30 min on weekdays and > 2 h on weekends) and chronic (> 2 h daily) were not. CONCLUSION: This study provides evidence of a protective effect of moderate time spent in the sun on NHL risk.

An exposure-response meta-analysis of ambient PM2.5 during pregnancy and preeclampsia.

Relationships between PM2.5 exposure and preeclampsia have been the focus of four recent systematic reviews and meta-analyses. We expand on knowledge gaps in these reviews by characterizing the shape of the exposure-outcome relationship, and by assessing the heterogeneity in these associations by study characteristics. Studies of PM2.5 and preeclampsia were identified from reviews, and confounder-adjusted estimates were extracted. Estimates were derived using a random-effects model. Potential non-linearity was evaluated using a one-stage dose-response meta-analysis. Contrary to previous meta-analyses reporting stronger relationships, the overall adjusted relative risk (RR) for a 10 µg/m3 average increase in PM2.5 during pregnancy and preeclampsia was modest and not statistically significant (RR: 1.07, 95% CI: 0.99-1.15). This was mainly attributable to inclusion/exclusion decisions for studies made during this review. In addition, there was no evidence of non-linearity, and no important sub-group differences by characteristics such as region, exposure assessment, participant exclusions, and early versus late-onset preeclampsia. Overall, our analysis suggests a modest relationship between ambient PM2.5 and preeclampsia. We provide details on inclusion and exclusion decisions that were lacking in previous studies, and report novel investigations of non-linearity and heterogeneity.

Ambient air pollution and inflammatory effects in a Canadian pregnancy cohort.

BACKGROUND: Epidemiologic studies have consistently reported associations between air pollution and pregnancy outcomes including preeclampsia and gestational diabetes. However, the biologic mechanisms underlying these relationships remain unclear as few studies have collected relevant biomarker data. We examined relationships between ambient PM2.5 and NO2 with markers of inflammation during pregnancy in a prospective cohort of Canadian women. METHODS: We analyzed data from 1170 women enrolled in the Maternal-Infant Research on Environmental Chemicals study. Daily residential PM2.5 and NO2 exposures during pregnancy were estimated using satellite-based and land-use regression models and used to create 14-day and 30-day exposure windows before blood-draw. Inflammatory markers C-reactive protein, interleukin-6, interleukin-8, and tumor necrosis factor-α were measured in third trimester plasma samples. Multivariable linear regression was used to estimate associations for an interquartile range (IQR) increase in PM2.5 and NO2 and markers of inflammation, while adjusting for individual-level confounders. RESULTS: Fourteen-day (IQR: 6.85 µg/m3) and 30-day (IQR: 6.15 µg/m3) average PM2.5 exposures before blood-draw were positively associated with C-reactive protein after adjustment for covariates (24.6% [95% CI = 9.4, 41.9] and 17.4% [95% CI = 1.0, 35.0] increases, respectively). This association was found to be robust in several sensitivity analyses. Neither PM2.5 nor NO2 exposures were associated with interleukin-6, interleukin-8, or tumor necrosis factor-α. CONCLUSION: Exposure to ambient PM2.5 is positively associated with maternal inflammatory pathways in late pregnancy. This may contribute to positive associations between ambient PM2.5 and risk of adverse pregnancy outcomes.

Estimating the future cancer management costs attributable to modifiable risk factors in Canada.

OBJECTIVES: An estimated 33-37% of incident cancers in Canada are attributable to modifiable risk factors. Interventions targeting these risk factors would minimize the substantial health and economic burdens Canadians face due to cancer. We estimate the future health and economic burden of cancer in Canada by incorporating data from the Canadian Population Attributable Risk of Cancer (ComPARe) study into OncoSim, a web-based microsimulation tool. METHODS: Using the integrated OncoSim population attributable risk and population impact measures, we evaluated risk factor-targeted intervention scenarios implemented in 2020, assuming the targeted risk factor prevalence reduction would be achieved by 2032 with a 12-year latency period. RESULTS: We estimate that smoking will be the largest contributor to cancer-related costs, with a cost of CAD $44.4 billion between 2032 and 2044. An estimated CAD $3.3 billion of the cost could be avoided with a 30% reduction in smoking prevalence by 2022. Following smoking, the next highest cancer management costs are associated with inadequate physical activity and excess body weight, accounting for CAD $10.7 billion ($2.7 billion avoidable) and CAD $9.8 billion ($3.2 billion avoidable), respectively. Avoidable costs for other risk factors range from CAD $90 million to CAD $2.5 billion. CONCLUSION: Interventions targeting modifiable cancer risk factors could prevent a substantial number of incident cancer cases and billions of dollars in cancer management costs. With limited budgets and rising costs in cancer care in Canada, these simulation models and results are valuable for researchers and policymakers to inform decisions and prioritize and evaluate intervention programs.

RéSUMé: OBJECTIFS: Il est estimé que de 33 % à 37 % des cancers incidents au Canada sont imputables à des facteurs de risque modifiables. Des interventions ciblant ces facteurs de risque réduiraient le fardeau sanitaire et économique considérable du cancer dans la population canadienne. Nous avons estimé le futur fardeau sanitaire et économique du cancer au Canada en intégrant les données de l'étude ComPARe (Canadian Population Attributable Risk of Cancer) dans l'outil de microsimulation en ligne OncoSim. MéTHODE: À l'aide des indicateurs d'impact dans la population et du risque attribuable dans la population intégrés dans OncoSim, nous avons évalué des scénarios d'intervention mis en œuvre en 2020 axés sur les facteurs de risque, en partant de l'hypothèse que la réduction de la prévalence des facteurs de risque ciblés serait atteinte d'ici 2032 avec une période de latence de 12 ans. RéSULTATS: Nous estimons que le tabagisme sera le facteur qui contribuera le plus aux coûts du cancer, avec un coût de 44,4 milliards $ CA entre 2032 et 2044. Il est estimé qu'une part de 3,3 milliards $ CA de ce coût pourrait être évitée en réduisant de 30 % la prévalence du tabagisme d'ici 2022. Après le tabagisme, les coûts de prise en charge du cancer les plus élevés sont associés à l'inactivité physique et au surpoids, qui représentent respectivement 10,7 milliard $ CA (dont 2,7 milliards $ évitables) et 9,8 milliards $ CA (dont 3,2 milliards $ évitables). Les coûts évitables pour d'autres facteurs de risque vont de 90 millions $ CA à 2,5 milliards $ CA. CONCLUSION: Des interventions ciblant les facteurs de risque de cancer modifiables pourraient prévenir un nombre considérable de cas de cancers incidents et épargner des milliards de dollars en coûts de prise en charge du cancer. Avec les budgets serrés et la hausse des coûts des soins du cancer au Canada, ces modèles de simulation et leurs résultats permettent aux chercheurs et aux responsables des politiques d'éclairer les décisions et de hiérarchiser et d'évaluer les programmes d'intervention.

Estimates of future cancer mortality attributable to modifiable risk factors in Canada.

OBJECTIVES: Modifiable lifestyle, environmental, and infectious risk factors associated with cancer impact both cancer incidence and mortality at the population level. Most studies estimating this burden focus on cancer incidence. However, because these risk factors are associated with cancers of disparate mortality rates, the burden associated with cancer incidence could differ from cancer mortality. Therefore, estimating the cancer mortality attributable to these risk factors provides additional insight into cancer prevention. Here, we estimated future cancer deaths and the number of avoidable deaths in Canada due to modifiable risk factors. METHODS: The projected cancer mortality data came from OncoSim, a web-based microsimulation tool. These data were applied to the methodological framework that we previously used to estimate the population attributable risks and the potential impact fractions of modifiable risk factors on Canadian cancer incidence. RESULTS: We estimated that most cancer deaths will be attributed to tobacco smoking with an average of 27,900 deaths annually from 2024 to 2047. If Canada's current trends in excess body weight continue, cancer deaths attributable to excess body weight would double from 2786 deaths in 2024 to 5604 deaths in 2047, becoming the second leading modifiable cause of cancer death. Applying targets to reduce these risk factors, up to 34,600 cancer deaths could be prevented from 2024 to 2047. CONCLUSION: Our simulated results complement our previous findings on the cancer incidence burden since decreasing the overall burden of cancer will be accelerated through a combination of decreasing cancer incidence and improving survival outcomes through improved treatments.

RéSUMé: OBJECTIFS: Les facteurs de risque modifiables associés au cancer (liés au mode de vie, à l'environnement, aux maladies infectieuses) ont des effets à la fois sur l'incidence du cancer et sur la mortalité par cancer à l'échelle de la population. La plupart des études qui estiment ce fardeau portent sur l'incidence du cancer. Cependant, comme les facteurs de risque susmentionnés sont associés à des cancers dont les taux de mortalité sont disparates, le fardeau associé à l'incidence du cancer pourrait différer de la mortalité par cancer. En conséquence, l'estimation de la mortalité par cancer imputable à ces facteurs de risque pourrait éclairer la prévention du cancer. Nous estimons ici les décès futurs par cancer et le nombre de décès évitables au Canada dus à des facteurs de risque modifiables. MéTHODE: Les données projetées sur la mortalité par cancer proviennent d'OncoSim, un outil de microsimulation en ligne. Elles ont été appliquées au cadre méthodologique que nous avions déjà utilisé pour estimer les risques attribuables dans la population et les fractions de l'incidence potentielle des facteurs de risque modifiables sur l'incidence canadienne du cancer. RéSULTATS: Selon nos estimations, entre 2024 et 2047, la plupart des décès par cancer seront imputés au tabagisme, qui causera en moyenne 27 900 décès par année. Si les tendances actuelles au Canada en matière de surpoids se maintiennent, les décès par cancer attribuables au surpoids doubleraient, passant de 2 786 décès en 2024 à 5 604 en 2047, et le surpoids deviendrait la deuxième cause modifiable de décès par cancer. En appliquant des cibles de réduction de ces facteurs de risque, jusqu'à 34 600 décès par cancer pourraient être évités entre 2024 et 2047. CONCLUSION: Les résultats de notre simulation confirment nos constatations antérieures sur le fardeau de l'incidence du cancer, car la diminution du fardeau global du cancer sera accélérée par une combinaison de la diminution de l'incidence du cancer et de l'amélioration des résultats de survie grâce à l'amélioration des traitements.

The current burden of non-melanoma skin cancer attributable to ultraviolet radiation and related risk behaviours in Canada.

PURPOSE: Ultraviolet radiation (UVR) is an established cause of non-melanoma skin cancer (NMSC)-basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). The aim of this study was to estimate the current burden of BCC and SCC associated with UVR and modifiable UVR behaviours (sunburn, sunbathing, and indoor tanning) in Canada in 2015. METHODS: The current burden of BCC and SCC associated with UVR was estimated by comparing 2015 incidence rates with rates of less exposed body sites (trunk and lower limbs) after adjusting for estimated surface areas. The burden associated with modifiable UVR behaviours was estimated by using prevalence estimates among Caucasians from the Second National Sun Survey, and relative risks that are generalizable to Canadians from conducting meta-analyses of relevant studies. RESULTS: We estimated that 80.5% of BCCs and 83.0% of SCCs were attributable to UVR. Adult sunburn was associated with relative risks of 1.85 (95% CI 1.15-3.00) for BCC and 1.41 (95% CI 0.91-2.18) for SCC, while adult sunbathing was associated with relative risks of 1.82 (95% CI 1.52-2.17) for BCC and 1.14 (95% CI 0.53-2.46) for SCC. We estimated that 18.6% of BCCs and 9.9% of SCCs were attributable to adult sunburn, while 28.1% of BCCs were attributable to adult sunbathing. We estimated that 46.2% of BCCs and 17.3% of SCCs were attributable to modifiable UVR behaviours combined. CONCLUSION: Our results provide quantifiable estimates of the potentially avoidable burden of NMSCs among Canadians. These estimates can be used to motivate prevention efforts in Canada.

The effect of acute outdoor air pollution on peak expiratory flow in individuals with asthma: A systematic review and meta-analysis.

OBJECTIVES: Acute exposures to outdoor air pollution have been shown to reduce lung function in children with asthma, but the effect on adults with asthma has not been established in a meta-analysis. The objective of this study was to conduct a systematic literature review and meta-analysis of studies that assessed the relationship of outdoor air pollution and peak expiratory flow (PEF) in adults with asthma. METHODS: Studies that contained data on outdoor air pollution levels (PM10, PM2.5, or NO2) and PEF in adults with asthma were eligible for inclusion. Effect estimates were quantified for each air pollution measure using random effects models. Heterogeneity was investigated with the Q-test and I2 statistics. Meta-regression and subgroup analyses were conducted to determine differences in effect by air pollution measures and the inclusion of smokers. RESULTS: A total of 22 effect estimates from 15 studies were included in this review. A 10 µg/m3 increase in acute PM10 exposure was associated with a -0.19 L/min (95% CI: 0.30, -0.09) change in PEF. For both PM10 and PM2.5, the inclusion of current smokers was a significant source of heterogeneity among studies (meta-regression: p = 0.04 and p = 0.03). Among studies that only included non-smokers, a 10 µg/m3 increase in acute exposure to PM10 and PM2.5 was associated with changes in PEF of -0.25 L/min (95% CI: 0.38, -0.13) and -1.02 L/min (95% CI: 1.79, -0.24), respectively. CONCLUSIONS: This study provides evidence that acute increases in PM10 and PM2.5 levels are associated with decreases in PEF in adults with asthma, particularly among non-smokers.

Mortality due to cancer treatment delay: systematic review and meta-analysis.

OBJECTIVE: To quantify the association of cancer treatment delay and mortality for each four week increase in delay to inform cancer treatment pathways. DESIGN: Systematic review and meta-analysis. DATA SOURCES: Published studies in Medline from 1 January 2000 to 10 April 2020. ELIGIBILITY CRITERIA FOR SELECTING STUDIES: Curative, neoadjuvant, and adjuvant indications for surgery, systemic treatment, or radiotherapy for cancers of the bladder, breast, colon, rectum, lung, cervix, and head and neck were included. The main outcome measure was the hazard ratio for overall survival for each four week delay for each indication. Delay was measured from diagnosis to first treatment, or from the completion of one treatment to the start of the next. The primary analysis only included high validity studies controlling for major prognostic factors. Hazard ratios were assumed to be log linear in relation to overall survival and were converted to an effect for each four week delay. Pooled effects were estimated using DerSimonian and Laird random effect models. RESULTS: The review included 34 studies for 17 indications (n=1 272 681 patients). No high validity data were found for five of the radiotherapy indications or for cervical cancer surgery. The association between delay and increased mortality was significant (P<0.05) for 13 of 17 indications. Surgery findings were consistent, with a mortality risk for each four week delay of 1.06-1.08 (eg, colectomy 1.06, 95% confidence interval 1.01 to 1.12; breast surgery 1.08, 1.03 to 1.13). Estimates for systemic treatment varied (hazard ratio range 1.01-1.28). Radiotherapy estimates were for radical radiotherapy for head and neck cancer (hazard ratio 1.09, 95% confidence interval 1.05 to 1.14), adjuvant radiotherapy after breast conserving surgery (0.98, 0.88 to 1.09), and cervix cancer adjuvant radiotherapy (1.23, 1.00 to 1.50). A sensitivity analysis of studies that had been excluded because of lack of information on comorbidities or functional status did not change the findings. CONCLUSIONS: Cancer treatment delay is a problem in health systems worldwide. The impact of delay on mortality can now be quantified for prioritisation and modelling. Even a four week delay of cancer treatment is associated with increased mortality across surgical, systemic treatment, and radiotherapy indications for seven cancers. Policies focused on minimising system level delays to cancer treatment initiation could improve population level survival outcomes.

Combinations of modifiable lifestyle behaviours in relation to colorectal cancer risk in Alberta's Tomorrow Project.

The objective of this study was to identify distinct clusters of individuals that exhibit unique patterns of modifiable lifestyle-related behaviours and to determine how these patterns are associated with the risk of developing colorectal cancer (CRC). The study consisted of 26,460 participants and 267 CRC cases from Alberta's Tomorrow Project. Exploratory latent class analysis of risk behaviours (obesity, physical inactivity, meat consumption, smoking, alcohol consumption, and fruit and vegetable consumption) and Cox proportional hazard models were utilized. Seven unique behavioural groups were identified, where the risk of CRC was 2.34 to 2.87 times greater for high risk groups compared to the low risk group. Sex-specific models identified higher risk groups among men (Hazard Ratios [HRs]: 3.15 to 3.89) than among women (HRs: 1.99 to 2.19). Targeting groups defined by clustering of behaviours could potentially lead to more effective prevention of CRC on a population level.

The relationship between colorectal cancer risk factors and LINE-1 DNA methylation in healthy colon tissue.

Aim: LINE-1 DNA methylation is a modifiable epigenetic process linked to colorectal cancer (CRC). However, studies of methylation in the tissue of interest are limited. This research examines associations between CRC risk factors and LINE-1 DNA methylation in healthy colon tissue. Materials & methods: LINE-1 methylation was measured in colon tissue samples from 317 patients undergoing a screening colonoscopy. Associations were examined with established CRC risk factors including alcohol consumption, smoking, BMI, NSAIDs, physical activity and fruit and vegetable consumption. Results: All studied risk factors were not related to LINE-1 DNA methylation in this population. Conclusion: The observed results may reflect that the effect of this set of established risk factors is not mediated through LINE-1 DNA methylation in the healthy colon.

Solar Ultraviolet Radiation and Breast Cancer Risk: A Systematic Review and Meta-Analysis.

BACKGROUND: A protective relationship has been hypothesized between exposure to solar ultraviolet radiation (UVR) and the development of breast cancer. OBJECTIVE: The objective of this study was to conduct a systematic literature review and meta-analysis of studies examining the association of exposure to solar UVR and breast cancer risk. METHODS: We searched Medline, EMBASE, and Web of Science for all studies investigating exposure to solar UVR and breast cancer risk. Separate analyses were performed using estimates of time spent in the sun, and ambient UVR. Associations were estimated using DerSimonian and Laird random-effect models. Heterogeneity was investigated through subgroup analyses and I2 statistics. RESULTS: Fourteen studies were included in the review and 13 in the meta-analysis, with the majority (n=8) conducted in North America. We observed a decreased risk of breast cancer for individuals spending ≥1h/d in the sun during summer months over a lifetime or usual adulthood compared with <1h/d [pooled relative risk (RR)=0.84; 95% CI: 0.77, 0.91]. Spending ≥2h/d in the sun had a similar protective effect as 1 to <2h/d when compared with <1h/d (RR=0.83; 95% CI: 0.75, 0.93 vs. 0.83; 95% CI: 0.78, 0.89). Exposure during adolescence was suggestive of a lower risk of breast cancer than exposure later in life (≥45 years of age) (RR=0.83; 95% CI: 0.71, 0.98 vs. 0.97; 95% CI: 0.85, 1.11). Ambient UVR was not associated with the risk of breast cancer (RR=1.00; 95% CI: 0.93, 1.09). DISCUSSION: To our knowledge, this was the first meta-analysis to estimate the risk of developing breast cancer associated with time spent in the sun. The results suggest that obtaining greater than an hour a day in the sun during the summer months could decrease the risk of developing breast cancer. https://doi.org/10.1289/EHP4861.

Estimates of the current and future burden of lung cancer attributable to residential radon exposure in Canada.

Radon is widely recognized as a human carcinogen and findings from epidemiologic studies support a causal association between residential radon exposure and lung cancer risk. Our aim was to derive population attributable risks (PAR) to estimate the numbers of incident lung cancer due to residential radon exposure in Canada in 2015. Potential impact fractions for 2042 were estimated based on a series of counterfactuals. A meta-analysis was conducted to estimate the relative risk of lung cancer per 100 Becquerels (Bq)/m3 increase in residential radon exposure, with a pooled estimate of 1.16 (95% CI: 1.07-1.24). The population distribution of annual residential radon exposure was estimated based on a national survey with adjustment for changes in the population distribution over time, the proportion of Canadians living in high-rise buildings, and to reflect annual rather than winter levels. An estimated 6.9% of lung cancer cases in 2015 were attributable to exposure to residential radon, accounting for 1741 attributable cases. If mitigation efforts were to reduce all residential radon exposures that are above current Canadian policy guidelines of 200 Bq/m3 (3% of Canadians) to 50 Bq/m3, 293 cases could be prevented in 2042, and 2322 cumulative cases could be prevented between 2016 and 2042. Our results show that mitigation that exclusively targets Canadian homes with radon exposures above current Canadian guidelines may not greatly alleviate the future projected lung cancer burden. Mitigation of residential radon levels below current guidelines may be required to substantially reduce the overall lung cancer burden in the Canadian population.

The current and future burden of cancer attributable to modifiable risk factors in Canada: Summary of results.

Nearly one in two Canadians are expected to be diagnosed with cancer in their lifetime. However, there are opportunities to reduce the impact of modifiable cancer risk factors through well-informed interventions and policies. Since no comprehensive Canadian estimates have been available previously, we estimated the proportion of cancer diagnosed in 2015 and the future burden in 2042 attributable to lifestyle and environmental factors, and infections. Population-based historical estimates of exposure prevalence and their associated risks for each exposure-cancer site pair were obtained to estimate population attributable risks, assuming the exposures were distributed independently and that the risk estimates were multiplicative. We estimated that between 33 and 37% (up to 70,000 cases) of incident cancer cases among adults aged 30 years and over in 2015 were attributable to preventable risk factors. Similar proportions of cancer cases in males (34%) and females (33%) were attributable to these risk factors. Tobacco smoking and a lack of physical activity were associated with the highest proportions of cancer cases. Cancers with the highest number of preventable cases were lung (20,100), colorectal (9800) and female breast (5300) cancer. If current trends in the prevalence of preventable risk factors continue into the future, we project that by 2042 approximately 102,000 incident cancer cases are expected to be attributable to these risk factors per year, which would account for roughly one-third of all incident cancers. Through various risk reduction interventions, policies and public health campaigns, an estimated 10,600 to 39,700 cancer cases per year could be prevented by 2042.

The burden of cancer attributable to modifiable risk factors in Canada: Methods overview.

Up-to-date estimates of current and projected future cancer burden attributable to various exposures are essential for planning and implementing cancer prevention initiatives. The Canadian Population Attributable Risk of Cancer (ComPARe) study was conducted to: i) estimate the number and proportion of cancers diagnosed among adults in Canada in 2015 that are attributable to modifiable risk factors and ii) project the future avoidable cancers by 2042 under various intervention targets. We estimated the population attributable risk (with 95% confidence intervals) and the potential impact fraction of cancers associated with selected lifestyle, environmental, and infectious factors. Exposure-specific sensitivity analyses were also completed where appropriate. Several exposures of interest included active and passive smoking, obesity and abdominal adiposity, leisure-time physical inactivity, sedentary behaviour, alcohol consumption, insufficient fruit and vegetable intake, red and processed meat consumption, air pollution (PM2.5, NO2), indoor radon gas, ultraviolet radiation (UVR), hepatitis B and C virus, Helicobacter pylori, Epstein-Barr virus, human papillomavirus, human herpesvirus type 8 and human T-cell lymphotropic virus type 1. We used the 2015 cancer incidence data for 35 cancer sites from the Canadian Cancer Registry and projected cancer incidence to 2042 using historical data from 1983 to 2012. Here, we provide an overview of the data sources and methods used in estimating the current and future cancer burden in Canada. Specific methodologic details for each exposure are included in the individual articles included as part of this special issue.

Estimates of the current and future burden of melanoma attributable to ultraviolet radiation in Canada.

Exposure to ultraviolet radiation (UVR) is an established cause of cutaneous melanoma. The purpose of this study was to estimate the current attributable and future avoidable burden of melanoma related to exposure to UVR and modifiable UVR risk behaviors (sunburn, sunbathing, and indoor tanning). The population attributable risk (PAR) associated with UVR in 2015 was estimated by comparing Canadian melanoma incidence rates in 2015 to estimated incidence rates of a 1920 birth cohort. Rates were adjusted for changes in reporting and ethnicity. We estimated PARs for modifiable UVR risk behaviors using Caucasian prevalence data from the Second National Sun Survey and relative risks that are generalizable to Canada from meta-analyses of relevant studies. Attributable cases apply to 98.9% of melanomas in Canada that occur in Caucasians. We also estimated the future burden of UVR risk behaviors using the potential impact fraction framework and potential reductions in prevalence of 10% to 50% from 2018 to 2042. Adult sunburn and sunbathing were associated with increased risks of melanoma of 1.28 (95% CI: 1.15, 1.43) and 1.44 (95% CI: 1.18, 1.76), respectively. In 2015, we estimate that 62.3% of melanomas in Canada were attributable to exposure to UVR and that 29.7% were attributable to the combination of sunburn (7.4%), sunbathing (17.8%), and indoor tanning (7.0%). A 50% reduction in modifiable UVR behaviors could avoid an estimated 11,980 melanoma cases by 2042. Prevention strategies aimed at modifiable UVR behaviors are crucial to reduce the growing burden of melanoma in Canada.

Estimates of the current and future burden of lung cancer attributable to PM2.5 in Canada.

The International Agency for Research on Cancer has classified PM2.5 (fine particulate matter, PM2.5) as a lung cancer carcinogen in humans. We estimated the proportion of lung cancer cases attributable to PM2.5 exposure in Canada in 2015, and future avoidable cancers over the period 2016-2042 under different future exposure scenarios. A meta-analysis was conducted to estimate the relative risk of lung cancer associated with PM2.5 that was generalizable to Canada. A population-weighted Canadian distribution of residential PM2.5 exposure was estimated annually using ecological-level, satellite-derived PM2.5 data for the period 1990 to 2009. Population attributable risks (PAR) were estimated for PM2.5 and applied to lung cancer incidence from the Canadian Cancer Registry. Potential impact fractions based on counterfactual scenarios for the year 2042 were estimated, along with cumulative preventable cases from 2016 to 2042. The relative risk of lung cancer associated with PM2.5 was 1.09 (95% CI: 1.06-1.12) per an increase of 10 µg/m3. The average population-weighted exposure to PM2.5 corresponding to a 20-year exposure window from 1990 to 2009 was 8.3 µg/m3. The PAR for PM2.5 was estimated at 6.9%, accounting for 1739 attributable lung cancer cases in 2015. If patterns of decline in PM2.5 continue, over 3000 lung cancer cases could be prevented between 2016 and 2042. Exposure to PM2.5 contributes to a considerable burden of lung cancer in Canada and policies aimed at sustaining outdoor PM2.5 declines are important for lung cancer prevention in Canada.