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Background: The temporal and spatial scales of exposure assessment may influence observed associations between fine particulate air pollution (PM2.5) and mortality, but few studies have systematically examined this question.Methods: We followed 2.4 million adults in the 2001 Canadian Census Health and Environment Cohort for nonaccidental and cause-specific mortality between 2001 and 2011. We assigned PM2.5 exposures to residential locations using satellite-based estimates and compared three different temporal moving averages (1, 3, and 8 years) and three spatial scales (1, 5, and 10 km) of exposure assignment. In addition, we examined different spatial scales based on age, employment status, and urban/rural location, and adjustment for O3, NO2, or their combined oxidant capacity (Ox).Results: In general, longer moving averages resulted in stronger associations between PM2.5 and mortality. For nonaccidental mortality, we observed a hazard ratio of 1.11 (95% CI = 1.08, 1.13) for the 1-year moving average compared with 1.23 (95% CI = 1.20, 1.27) for the 8-year moving average. Respiratory and lung cancer mortality were most sensitive to the spatial scale of exposure assessment with stronger associations observed at smaller spatial scales. Adjustment for oxidant gases attenuated associations between PM2.5 and cardiovascular mortality and strengthened associations with lung cancer. Despite these variations, PM2.5 was associated with increased mortality in nearly all of the models examined.Conclusions: These findings support a relationship between outdoor PM2.5 and mortality at low concentrations and highlight the importance of longer-exposure windows, more spatially resolved exposure metrics, and adjustment for oxidant gases in characterizing this relationship. [ABSTRACT FROM AUTHOR]

We used a large national cohort in Canada to assess the incidence of acute myocardial infarction (AMI) and stroke hospitalizations in association with long-term exposure to fine particulate matter (PM 2.5), nitrogen dioxide (NO 2), and ozone (O 3). The study population comprised 2.7 million respondents from the 2006 Canadian Census Health and Environment Cohort (CanCHEC), followed for incident hospitalizations of AMI or stroke between 2006 and 2016. We estimated 10-year moving average estimates of PM 2.5 , NO 2 , and O 3 , annually. We used Cox proportional hazards models to examine the associations adjusting for various covariates. For AMI, each interquartile range (IQR) increase in exposure was found to be associated with a hazard ratio of 1.026 (95% CI: 1.007–1.046) for PM 2.5 , 1.025 (95% CI: 1.001–1.050) for NO 2 , and 1.062 (95% CI: 1.041–1.084) for O 3 , respectively. Similarly, for stroke, an IQR increase in exposure was associated with a hazard ratio of 1.078 (95% CI: 1.052–1.105) for PM 2.5 , 0.995 (95% CI: 0.965–1.030) for NO 2 , and 1.055 (95% CI: 1.028–1.082) for O 3 , respectively. We found consistent evidence of positive associations between long-term exposures to PM 2.5 , and O 3 , and to a lesser degree NO 2 , with incident AMI and stroke hospitalizations. [ABSTRACT FROM AUTHOR]

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., (© 2024. The Author(s).)

Emissions of fine particulate matter (PM 2.5 ) from human activities have been linked to substantial disease burdens, but evidence regarding how reducing PM 2.5 at its sources would improve public health is sparse. We followed a population-based cohort of 2.7 million adults across Canada from 2007 through 2016. For each participant, we estimated annual mean concentrations of PM 2.5 and the fractional contributions to PM 2.5 from the five leading anthropogenic sources at their residential address using satellite observations in combination with a global atmospheric chemistry transport model. For each source, we estimated the causal effects of six hypothetical interventions on 10-y nonaccidental mortality risk using the parametric g-formula, a structural causal model. We conducted stratified analyses by age, sex, and income. This cohort would have experienced tangible health gains had contributions to PM 2.5 from any of the five sources been reduced. Compared with no intervention, a 10% annual reduction in PM 2.5 contributions from transportation and power generation, Canada's largest and fifth-largest anthropogenic sources, would have prevented approximately 175 (95%CI: 123-226) and 90 (95%CI: 63-117) deaths per million by 2016, respectively. A more intensive 50% reduction per year in PM 2.5 contributions from the two sources would have averted 360 and 185 deaths per million, respectively, by 2016. The potential health benefits were greater among men, older adults, and low-income earners. In Canada, where PM 2.5 levels are among the lowest worldwide, reducing PM 2.5 contributions from anthropogenic sources by as little as 10% annually would yield meaningful health gains.

Fine particulate air pollution (PM 2.5 ) is a leading contributor to the overall global burden of disease. Traditionally, outdoor PM 2.5 has been characterized using mass concentrations which treat all particles as equally harmful. Oxidative potential (OP) (per μg) and oxidative burden (OB) (per m 3 ) are complementary metrics that estimate the ability of PM 2.5 to cause oxidative stress, which is an important mechanism in air pollution health effects. Here, we provide the first national estimates of spatial variations in multiple measures (glutathione, ascorbate, and dithiothreitol depletion) of annual median outdoor PM 2.5 OB across Canada. To do this, we combined a large database of ground-level OB measurements collected monthly prospectively across Canada for 2 years (2016-2018) with PM 2.5 components estimated using a chemical transport model (GEOS-Chem) and satellite aerosol observations. Our predicted ground-level OB values of all three methods were consistent with ground-level observations (cross-validation R 2 = 0.63-0.74). We found that forested regions and urban areas had the highest OB, predicted primarily by black carbon and organic carbon from wildfires and transportation sources. Importantly, the dominant components associated with OB were different than those contributing to PM 2.5 mass concentrations (secondary inorganic aerosol); thus, OB metrics may better indicate harmful components and sources on health than the bulk PM 2.5 mass, reinforcing that OB estimates can complement the existing PM 2.5 data in future national-level epidemiological studies.

Background: Immigrants make up 20% of the Canadian population; however, little is known about the mortality impacts of fine particulate matter (PM 2.5 ) air pollution on immigrants compared with non-immigrants, or about how impacts may change with duration in Canada., Data and Methods: This study used the 2001 Canadian Census Health and Environment Cohort, a longitudinal cohort of 3.5 million individuals, of which 764,000 were classified as immigrants (foreign-born). Postal codes from annual income tax files were used to account for mobility among respondents and to assign annual PM 2.5 concentrations from 1998 to 2016. Exposures were estimated as a three-year moving average prior to the follow-up year. Cox survival models were used to determine hazard ratios (HRs) for cause-specific mortality, comparing the Canadian and foreign-born populations, with further stratification by year of immigration grouped into 10-year cohorts., Results: Differences in urban-rural settlement patterns resulted in greater exposure to PM 2.5 for immigrants compared with non-immigrants (mean = 9.3 vs. 7.5 μg/m 3 ), with higher exposures among more recent immigrants. In fully adjusted models, immigrants had higher HRs per 10 μg/m 3 increase in PM 2.5 concentration compared with Canadian-born individuals for cardiovascular mortality (HR [95% confidence interval] = 1.22 [1.12 to 1.34] vs. 1.12 [1.07 to 1.18]) and cerebrovascular mortality (HR = 1.25 [1.03 to 1.52] vs. 1.03 [0.93 to 1.15]), respectively. However, tests for differences between the two groups were not significant when Cochran's Q test was used. No significant associations were found for respiratory outcomes, except for lung cancer in non-immigrants (HR = 1.10 [1.02 to 1.18]). When stratified by year of immigration, differences in HRs across varied by cause of death., Discussion: In Canada, PM 2.5 is an equal-opportunity risk factor, with immigrants experiencing similar if not higher mortality risks compared with non-immigrants for cardiovascular-related causes of death. Some notable differences also existed with cerebrovascular and lung cancer deaths. Continued reductions in air pollution, particularly in urban areas, will improve the health of the Canadian population as a whole.

Background: Ambient fine particulate air pollution with aerodynamic diameter ≤ 2.5   μ m ( PM 2.5 ) is an important contributor to the global burden of disease. Information on the shape of the concentration-response relationship at low concentrations is critical for estimating this burden, setting air quality standards, and in benefits assessments., Objectives: We examined the concentration-response relationship between PM 2.5 and nonaccidental mortality in three Canadian Census Health and Environment Cohorts (CanCHECs) based on the 1991, 1996, and 2001 census cycles linked to mobility and mortality data., Methods: Census respondents were linked with death records through 2016, resulting in 8.5 million adults, 150 million years of follow-up, and 1.5 million deaths. Using annual mailing address, we assigned time-varying contextual variables and 3-y moving-average ambient PM 2.5 at a 1 × 1   km spatial resolution from 1988 to 2015. We ran Cox proportional hazards models for PM 2.5 adjusted for eight subject-level indicators of socioeconomic status, seven contextual covariates, ozone, nitrogen dioxide, and combined oxidative potential. We used three statistical methods to examine the shape of the concentration-response relationship between PM 2.5 and nonaccidental mortality., Results: The mean 3-y annual average estimate of PM 2.5 exposure ranged from 6.7 to 8.0   μ g / m 3 over the three cohorts. We estimated a hazard ratio (HR) of 1.053 [95% confidence interval (CI): 1.041, 1.065] per 10 - μ g / m 3 change in PM 2.5 after pooling the three cohort-specific hazard ratios, with some variation between cohorts (1.041 for the 1991 and 1996 cohorts and 1.084 for the 2001 cohort). We observed a supralinear association in all three cohorts. The lower bound of the 95% CIs exceeded unity for all concentrations in the 1991 cohort, for concentrations above 2   μ g / m 3 in the 1996 cohort, and above 5   μ g / m 3 in the 2001 cohort., Discussion: In a very large population-based cohort with up to 25 y of follow-up, PM 2.5 was associated with nonaccidental mortality at concentrations as low as 5   μ g / m 3 . https://doi.org/10.1289/EHP5204.

Understanding the sectoral contribution of emissions to fine particulate matter (PM 2.5 ) offers information for air quality management, and for investigation of association with health outcomes. This study evaluates the contribution of different emission sectors to PM 2.5 in 2013 for Canada using the GEOS-Chem chemical transport model, downscaled with satellite-based PM 2.5 . Despite the low population-weighted PM 2.5 concentrations of 5.5 μg m -3 across Canada, we find that over 70% of population-weighted PM 2.5 originates from Canadian sources followed by 30% from the contiguous United States. The three leading sectoral contributors to population-weighted PM 2.5 over Canada are wildfires with 1.0 μg m -3 (17%), transportation with 0.96 μg m -3 (16%), and residential combustion with 0.91 μg m -3 (15%). The relative contribution to population-weighted PM 2.5 of different sectors varies regionally with residential combustion as the leading contributor in Central Canada (19%), while wildfires dominate over Northern Canada (59%), Atlantic Canada (34%), and Western Canada (18%). The contribution from U.S. sources is larger over Central Canada (33%) than over Western Canada (17%), Atlantic Canada (17%), and Northern Canada (<2%). Sectoral trend analysis showed that the contribution from anthropogenic sources to population-weighted PM 2.5 decreased from 7.1 μg m -3 to 3.4 μg m -3 over the past two decades.

Gray mold is a devastating disease on strawberry, and may be caused by several species of Botrytis. The goal of this study was to better understand and characterize the species of Botrytis with reduced sensitivity to the fungicide Polyoxin D, particularly Botrytis fragariae. In total, 78 Botrytis isolates of unknown species that were sensitive (28 isolates; S), moderately sensitive (22 isolates; MS), or reduced sensitive (28 isolates; RS) to Polyoxin-D were collected from commercial strawberry fields of five states in the United States, identified to the species level, and characterized. The majority (75%) of S isolates were Botrytis cinerea and the majority (79%) of RS isolates were the recently described species B. fragariae, indicating an innate ability of B. fragariae to tolerate Polyoxin-D. B. fragariae produced fluffy, white mycelium and was less likely to sporulate on potato dextrose agar than B. cinerea. Isolates from a commercial field recovered from blossoms in early spring were all B. fragariae, those from leaves of the same plants in late spring were a mixture of B. fragariae and B. cinerea, and those from fruit in early summer were all B. cinerea, indicating that B. fragariae may preferentially colonize blossom tissue. A polymerase chain reaction-based assay was developed based on NEP2 sequence variability to distinguish B. fragariae from other Botrytis spp. that have been reported on strawberry, including B. cinerea, B. mali, B. caroliniana, and B. ricini. None of the isolates collected from Canada, California, or North Carolina nurseries were B. fragariae, indicating that the newly described species may not exist or not be widely distributed in planting stock.

Deep-sea hydrothermal vents are one of the most unique and fascinating ecosystems on Earth. Although phylogenetic diversity of vent communities has been extensively examined, their physiological diversity is poorly understood. In this study, a GeoChip-based, high-throughput metagenomics technology revealed dramatic differences in microbial metabolic functions in a newly grown protochimney (inner section, Proto-I; outer section, Proto-O) and the outer section of a mature chimney (4143-1) at the Juan de Fuca Ridge. Very limited numbers of functional genes were detected in Proto-I (113 genes), whereas much higher numbers of genes were detected in Proto-O (504 genes) and 4143-1 (5,414 genes). Microbial functional genes/populations in Proto-O and Proto-I were substantially different (around 1% common genes), suggesting a rapid change in the microbial community composition during the growth of the chimney. Previously retrieved cbbL and cbbM genes involved in the Calvin Benson Bassham (CBB) cycle from deep-sea hydrothermal vents were predominant in Proto-O and 4143-1, whereas photosynthetic green-like cbbL genes were the major components in Proto-I. In addition, genes involved in methanogenesis, aerobic and anaerobic methane oxidation (e.g., ANME1 and ANME2), nitrification, denitrification, sulfate reduction, degradation of complex carbon substrates, and metal resistance were also detected. Clone libraries supported the GeoChip results but were less effective than the microarray in delineating microbial populations of low biomass. Overall, these results suggest that the hydrothermal microbial communities are metabolically and physiologically highly diverse, and the communities appear to be undergoing rapid dynamic succession and adaptation in response to the steep temperature and chemical gradients across the chimney.