Explore the vast range of titles available.

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.

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: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.

OBJECTIVE:The aim of this study was to assess cardiorespiratory effects of air pollution in older adults exercising outdoors in winter. METHODS:Adults 55 years of age and older completed daily measurements of blood pressure, peak expiratory flow and oximetry, and weekly measurements of heart rate variability, endothelial function, spirometry, fraction of exhaled nitric oxide and urinary oxidative stress markers, before and after outdoor exercise, for 10 weeks. Data were analyzed using linear mixed effect models. RESULTS:Pooled estimates combining 2014 (n = 36 participants) and 2015 (n = 34) indicated that an interquartile increase in the Air Quality Health Index was associated with a significant (P < 0.05) increase in heart rate (0.33%) and significant decreases in forced expiratory volume (0.30%), and systolic (0.28%) and diastolic blood pressure (0.39%). CONCLUSION:Acute subclinical effects of air pollution were observed in older adults exercising outdoors in winter.

To examine cardio-respiratory effects of air pollution in rural older adults exercising outdoors. Adults 55 and over completed measurements of blood pressure, peak expiratory flow and oximetry daily, and of heart rate variability, endothelial function, spirometry, fraction of exhaled nitric oxide and urinary oxidative stress markers weekly, before and after outdoor exercise, for 10 weeks. Data were analyzed using linear mixed effect models. Pooled estimates combining 2013 (n = 36 participants) and 2014 (n = 41) indicated that an interquartile increase in the air quality health index (AQHI) was associated with a significant (P < 0.05) increase in heart rate (2.1%) and significant decreases in high frequency power (-19.1%), root mean square of successive differences (-9.5%), and reactive hyperemia index (-6.5%). We observed acute subclinical adverse effects of air pollution in rural older adults exercising outdoors.

Airborne fine particle mass concentrations (PM sub(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 sub(2.5)-induced cardiorespiratory outcomes in an effort to summarize existing evidence related to oxidative stress defence and the health effects of PM sub(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 sub(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 sub(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 sub(2.5)-induced health effects is required, particularly for chronic outcomes. Similarly, while an exposure metric that captures the ability of PM sub(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.

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: 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.

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.