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.

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.

Salivary Alpha-Amylase Reactivity in Breast Cancer Survivors.

The two main components of the stress system are the hypothalamic-pituitary-adrenal (HPA) and sympathetic-adrenal-medullary (SAM) axes. While cortisol has been commonly used as a biomarker of HPA functioning, much less attention has been paid to the role of the SAM in this context. Studies have shown that long-term breast cancer survivors display abnormal reactive cortisol patterns, suggesting a dysregulation of their HPA axis. To fully understand the integrity of the stress response in this population, this paper explored the diurnal and acute alpha-amylase profiles of 22 breast cancer survivors and 26 women with no history of cancer. Results revealed that breast cancer survivors displayed identical but elevated patterns of alpha-amylase concentrations in both diurnal and acute profiles relative to that of healthy women, F (1, 39) = 17.95, p < 0.001 and F (1, 37) = 7.29, p = 0.010, respectively. The average area under the curve for the diurnal and reactive profiles was 631.54 ± 66.94 SEM and 1238.78 ± 111.84 SEM, respectively. This is in sharp contrast to their cortisol results, which showed normal diurnal and blunted acute patterns. The complexity of the stress system necessitates further investigation to understand the synergistic relationship of the HPA and SAM axes.