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Fine particulate air pollution (PM2.5; particulate matter 2.5 μm or less in diameter) is thought to contribute to acute respiratory morbidity in part through oxidative stress. To examine the association between PM2.5 oxidative burden and emergency room visits for respiratory illnesses. We conducted a case-crossover study in Ontario, Canada between 2004 and 2011, including 127,836 cases of asthma, 298,751 cases of chronic obstructive pulmonary disease, and more than 1.1 million cases of all respiratory illnesses. Daily air pollution data were collected from ground monitors, and city-level PM2.5 oxidative potential was measured on the basis of a synthetic respiratory tract lining fluid containing the antioxidants glutathione and ascorbate. Conditional logistic regression was used to estimate associations between air pollution concentrations and emergency room visits, adjusting for time-varying covariates. Three-day mean PM2.5 concentrations were consistently associated with emergency room visits for all respiratory illnesses. Among children (<9 yr), each interquartile change (5.92 μg/m(3)) in 3-day mean PM2.5 was associated with a 7.2% (95% confidence interval, 4.2-10) increased risk of emergency room visits for asthma. Glutathione-related oxidative potential modified the impact of PM2.5 on emergency room visits for respiratory illnesses (P = 0.001) but only at low concentrations (≤10 μg/m(3)). Between-city differences in ascorbate-related oxidative potential did not modify the impact of PM2.5 on respiratory outcomes. Between-city differences in glutathione-related oxidative potential may modify the impact of PM2.5 on acute respiratory illnesses at low PM2.5 concentrations. This may explain in part how small changes in ambient PM2.5 mass concentrations can contribute to acute respiratory morbidity in low-pollution environments.

Objective: We reviewed epidemiologic evidence related to occupational pesticide exposures and cancer incidence in the Agricultural Health Study (AHS) cohort. Data sources: Studies were identified from the AHS publication list available at http://aghealth.nci.nih.gov as well as through a Medline/PubMed database search in March 2009. We also examined citation lists. Findings related to lifetime-days and/or intensity-weighted lifetime-days of pesticide use are the primary focus of this review, because these measures allow for the evaluation of potential exposure–response relationships. Data synthesis: We reviewed 28 studies; most of the 32 pesticides examined were not strongly associated with cancer incidence in pesticide applicators. Increased rate ratios (or odds ratios) and positive exposure–response patterns were reported for 12 pesticides currently registered in Canada and/or the United States (alachlor, aldicarb, carbaryl, chlorpyrifos, diazinon, dicamba, S-ethyl-N,N-dipropylthiocarbamate, imazethapyr, metolachlor, pendimethalin, permethrin, trifluralin). However, estimates of association for specific cancers were often imprecise because of small numbers of exposed cases, and clear monotonic exposure–response patterns were not always apparent. Exposure misclassification is also a concern in the AHS and may limit the analysis of exposure–response patterns. Epidemiologic evidence outside the AHS remains limited with respect to most of the observed associations, but animal toxicity data support the biological plausibility of relationships observed for alachlor, carbaryl, metolachlor, pendimethalin, permethrin, and trifluralin. Conclusions: Continued follow-up is needed to clarify associations reported to date. In particular, further evaluation of registered pesticides is warranted.

Persons of color have been exposed to a disproportionate burden of air pollution across the United States for decades. Yet, the inequality in exposure to known toxic elements of air pollution is unclear. Here, we find that populations living in racially segregated communities are exposed to a form of fine particulate matter with over three times higher mass proportions of known toxic and carcinogenic metals. While concentrations of total fine particulate matter are two times higher in racially segregated communities, concentrations of metals from anthropogenic sources are nearly ten times higher. Populations living in racially segregated communities have been disproportionately exposed to these environmental stressors throughout the past decade. We find evidence, however, that these disproportionate exposures may be abated though targeted regulatory action. For example, recent regulations on marine fuel oil not only reduced vanadium concentrations in coastal cities, but also sharply lessened differences in vanadium exposure by segregation. A new study assesses differences in exposure to particulate air pollution between racially segregated and racially integrated communities in the U.S, and finds that segregated communities are exposed to higher proportions of toxic and carcinogenic metals.

Background Regional differences in the oxidative potential of fine particulate air pollution (PM 2.5 ) may modify its impact on the risk of myocardial infarction. Methods A case-crossover study was conducted in 16 cities in Ontario, Canada to evaluate the impact of regional PM 2.5 oxidative potential on the relationship between PM 2.5 and emergency room visits for myocardial infarction. Daily air pollution and meteorological data were collected between 2004 and 2011 from provincial monitoring sites and regional estimates of glutathione (OP GSH ) and ascorbate-related (OP AA ) oxidative potential were determined using an acellular assay based on a synthetic respiratory tract lining fluid. Exposure variables for the combined oxidant capacity of NO 2 and O 3 were also examined using their sum (O x ) and a weighted average (O x wt ) based on their redox potentials. Results In total, 30,101 cases of myocardial infarction were included in the analysis. For regions above the 90 th percentile of OP GSH each 5 μg/m 3 increase in same-day PM 2.5 was associated with a 7.9 % (95 % CI: 4.1, 12) increased risk of myocardial infarction whereas a 4.1 % (95 % CI: 0.26, 8.0) increase was observed in regions above the 75 th percentile and no association was observed below the 50 th percentile ( p -interaction = 0.026). A significant 3-way interaction was detected with the strongest associations between PM 2.5 and myocardial infarction occurring in areas with high regional OP GSH and high O x wt ( p -interaction < 0.001). Conclusions Regional PM 2.5 oxidative potential may modify the impact of PM 2.5 on the risk of myocardial infarction. The combined oxidant capacity of NO 2 and O 3 may magnify this effect.

Wildfires release a range of known human carcinogens and tend to occur in the same regions each year. As a result, long-term exposures to wildfire pollutants are a concern and will probably increase cancer risk in exposed populations. Actionable solutions are available to reduce exposures and mitigate these risks. Wildfires emit carcinogenic pollutants, raising long-term cancer risks in affected populations. In this Comment, Weichenthal highlights these concerns and outlines actionable solutions to reduce exposure and mitigate risks.

Background Approximately 2.9 million deaths are attributed to ambient fine particle air pollution around the world each year (PM 2.5 ). In general, cohort studies of mortality and outdoor PM 2.5 concentrations have limited information on individuals exposed to low levels of PM 2.5 as well as covariates such as smoking behaviours, alcohol consumption, and diet which may confound relationships with mortality. This study provides an updated and extended analysis of the Canadian Community Health Survey-Mortality cohort: a population-based cohort with detailed PM 2.5 exposure data and information on a number of important individual-level behavioural risk factors. We also used this rich dataset to provide insight into the shape of the concentration-response curve for mortality at low levels of PM 2.5 . Methods Respondents to the Canadian Community Health Survey from 2000 to 2012 were linked by postal code history from 1981 to 2016 to high resolution PM 2.5 exposure estimates, and mortality incidence to 2016. Cox proportional hazard models were used to estimate the relationship between non-accidental mortality and ambient PM 2.5 concentrations (measured as a three-year average with a one-year lag) adjusted for socio-economic, behavioural, and time-varying contextual covariates. Results In total, 50,700 deaths from non-accidental causes occurred in the cohort over the follow-up period. Annual average ambient PM 2.5 concentrations were low (i.e. 5.9 μg/m 3 , s.d. 2.0) and each 10 μg/m 3 increase in exposure was associated with an increase in non-accidental mortality (HR = 1.11; 95% CI 1.04–1.18). Adjustment for behavioural covariates did not materially change this relationship. We estimated a supra-linear concentration-response curve extending to concentrations below 2 μg/m 3 using a shape constrained health impact function. Mortality risks associated with exposure to PM 2.5 were increased for males, those under age 65, and non-immigrants. Hazard ratios for PM 2.5 and mortality were attenuated when gaseous pollutants were included in models. Conclusions Outdoor PM 2.5 concentrations were associated with non-accidental mortality and adjusting for individual-level behavioural covariates did not materially change this relationship. The concentration-response curve was supra-linear with increased mortality risks extending to low outdoor PM 2.5 concentrations.

Background: Few studies have examined the acute health effects of air pollution exposures experienced while cycling in traffic. Objectives: We conducted a crossover study to examine the relationship between traffic pollution and acute changes in heart rate variability. We also collected spirometry and exhaled nitric oxide measures. Methods: Forty-two healthy adults cycled for 1 hr on high-and low-traffic routes as well as indoors. Health measures were collected before cycling and 1-4 hr after the start of cycling. Ultrafine particles (UFPs; ≤ 0.1 μm in aerodynamic diameter), paniculate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5), black carbon, and volatile organic compounds were measured along each cycling route, and ambient nitrogen dioxide (NO₂) and ozone (O₃) levels were recorded from a fixed-site monitor. Mixed-effects models were used to estimate associations between air pollutants and changes in health outcome measures relative to precycling baseline values. Results: An interquartile range increase in UFP levels (18,200/cm³) was associated with a significant decrease in high-frequency power 4 hr after the start of cycling [β = -224 msec²; 95% confidence interval (CI), -386 to -63 msec²]. Ambient NO₂ levels were inversely associated with the standard deviation of normal-to-normal (NN) intervals (β = -10 msec; 95% CI, -20 to -0.34 msec) and positively associated with the ratio of low-frequency to high-frequency power (β = 1.4; 95% CI, 0.35 to 2.5) 2 hr after the start of cycling. We also observed significant inverse associations between ambient O₃ levels and the root mean square of successive differences in adjacent NN intervals 3 hr after the start of cycling. Conclusions: Short-term exposures to traffic pollution may contribute to altered autonomie modulation of the heart in the hours immediately after cycling.

BACKGROUND:Long-term exposure to fine particulate matter (PM2.5) has been associated with increased mortality, especially from cardiovascular disease. There are, however, uncertainties about the nature of the exposure–response relation at lower concentrations. In Canada, where ambient air pollution levels are substantially lower than in most other countries, there have been few attempts to study associations between long-term exposure to PM2.5 and mortality. METHODS:We present a prospective cohort analysis of 89,248 women who enrolled in the Canadian National Breast Screening Study between 1980 and 1985, and for whom residential measures of PM2.5 could be assigned. We derived individual-level estimates of long-term exposure to PM2.5 from satellite observations. We linked cohort records to national mortality data to ascertain mortality between 1980 and 2005. We used Cox proportional hazards models to characterize associations between PM2.5 and several causes of death. The hazard ratios (HRs) and 95% confidence intervals (CIs) computed from these models were adjusted for several individual and neighborhood-level characteristics. RESULTS:The cohort was composed predominantly of Canadian-born (82%) and married (80%) women. The median residential concentration of PM2.5 was 9.1 μg/m (standard deviation = 3.4). In fully adjusted models, a 10 μg/m increase in PM2.5 exposure was associated with elevated risks of nonaccidental (HR1.12; 95% CI = 1.04, 1.19), and ischemic heart disease mortality (HR1.34; 95% CI = 1.09, 1.66). CONCLUSIONS:The findings from this study provide additional support for the hypothesis that exposure to very low levels of ambient PM2.5 increases the risk of cardiovascular mortality.

Airborne fine particle mass concentrations (PM 2.5 ) are used for ambient air quality management worldwide based in part on known cardiorespiratory health effects. While oxidative stress is generally thought to be an important mechanism in determining these effects, relatively few studies have specifically examined how oxidant defence may impact susceptibility to particulate air pollution. Here we review studies that explore the impact of polymorphisms in anti-oxidant related genes or anti-oxidant supplementation on PM 2.5 -induced cardiorespiratory outcomes in an effort to summarize existing evidence related to oxidative stress defence and the health effects of PM 2.5 . Recent studies of PM-oxidative burden were also examined. In total, nine studies were identified and reviewed and existing evidence generally suggests that oxidant defence may modify the impact of PM 2.5 exposure on various health outcomes, particularly heart rate variability (a measure of autonomic function) which was the most common outcome examined in the studies reviewed. Few studies examined interactions between PM 2.5 and oxidant defence for respiratory outcomes, and in general studies focused primarily on acute health effects. Therefore, further evaluation of the potential modifying role of oxidant defence in PM 2.5 -induced health effects is required, particularly for chronic outcomes. Similarly, while an exposure metric that captures the ability of PM 2.5 to cause oxidative stress may offer advantages over traditional mass concentration measurements, little epidemiological evidence is currently available to evaluate the potential benefits of such an approach. Therefore, further evaluation is required to determine how this metric may be incorporated in ambient air quality management.

Magnetite nanoparticles are small, strongly magnetic iron oxide particles which are produced during high-temperature combustion and friction processes and form part of the outdoor air pollution mixture. These particles can translocate to the brain and have been found in human brain tissue. In this study, we estimated associations between within-city spatial variations in concentrations of magnetite nanoparticles in outdoor fine particulate matter (PM 2.5 ) and brain cancer incidence. We performed a cohort study of 1.29 million participants in four cycles of the Canadian Census Health and Environment Cohort in Montreal and Toronto, Canada who were followed for malignant brain tumour (glioma) incidence. As a proxy for magnetite nanoparticle content, we measured the susceptibility of anhysteretic remanent magnetization (χ ARM ) in PM 2.5 samples (N = 124 in Montreal, N = 110 in Toronto), and values were assigned to residential locations. Stratified Cox proportional hazards models were used to estimate hazard ratios (per IQR change in volume-normalized χ ARM ). ARM was not associated with brain tumour incidence (HR = 0.998, 95% CI 0.988, 1.009) after adjusting for relevant potential confounders. Although we found no evidence of an important relationship between within-city spatial variations in airborne magnetite nanoparticles and brain tumour incidence, further research is needed to evaluate this understudied exposure, and other measures of exposure to magnetite nanoparticles should be considered.