Exposure to ambient fine particulate matter (PM_2.5) is a major global health concern. Quantitative estimates of attributable mortality are based on disease-specific hazard ratio models that incorporate risk information from multiple PM_2.5sources (outdoor and indoor air pollution from use of solid fuels and secondhand and active smoking), requiring assumptions about equivalent exposure and toxicity. We relax these contentious assumptions by constructing a PM_2.5-mortality hazard ratio function based only on cohort studies of outdoor air pollution that covers the global exposure range. We modeled the shape of the association between PM_2.5and nonaccidental mortality using data from 41 cohorts from 16 countries—the Global Exposure Mortality Model (GEMM). We then constructed GEMMs for five specific causes of death examined by the global burden of disease (GBD). The GEMM predicts 8.9 million [95% confidence interval (CI): 7.5–10.3] deaths in 2015, a figure 30% larger than that predicted by the sum of deaths among the five specific causes (6.9; 95% CI: 4.9–8.5) and 120% larger than the risk function used in the GBD (4.0; 95% CI: 3.3–4.8). Differences between the GEMM and GBD risk functions are larger for a 20% reduction in concentrations, with the GEMM predicting 220% higher excess deaths. These results suggest that PM_2.5exposure may be related to additional causes of death than the five considered by the GBD and that incorporation of risk information from other, nonoutdoor, particle sources leads to underestimation of disease burden, especially at higher concentrations.

Relatively few studies have been conducted of the association between air pollution and emergency department (ED) visits, and most of these have been based on a small number of visits, for a limited number of health conditions and pollutants, and only daily measures of exposure and response. A time-series analysis was conducted on nearly 400,000 ED visits to 14 hospitals in seven Canadian cities during the 1990s and early 2000s. Associations were examined between carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), sulfur dioxide (SO2), and particulate matter (PM10 and PM2.5), and visits for angina/myocardial infarction, heart failure, dysrhythmia/conduction disturbance, asthma, chronic obstructive pulmonary disease (COPD), and respiratory infections. Daily and 3-hourly visit counts were modeled as quasi-Poisson and analyses controlled for effects of temporal cycles, weather, day of week and holidays. 24-hour average concentrations of CO and NO2 lag 0 days exhibited the most consistent associations with cardiac conditions (2.1% (95% CI, 0.0–4.2%) and 2.6% (95% CI, 0.2–5.0%) increase in visits for myocardial infarction/angina per 0.7 ppm CO and 18.4 ppb NO2 respectively; 3.8% (95% CI, 0.7–6.9%) and 4.7% (95% CI, 1.2–8.4%) increase in visits for heart failure). Ozone (lag 2 days) was most consistently associated with respiratory visits (3.2% (95% CI, 0.3–6.2%), and 3.7% (95% CI, -0.5–7.9%) increases in asthma and COPD visits respectively per 18.4 ppb). Associations tended to be of greater magnitude during the warm season (April – September). In particular, the associations of PM10 and PM2.5with asthma visits were respectively nearly three- and over fourfold larger vs. all year analyses (14.4% increase in visits, 95% CI, 0.2–30.7, per 20.6 μg/m3 PM10 and 7.6% increase in visits, 95% CI, 5.1–10.1, per 8.2 μg/m3 PM2.5). No consistent associations were observed between three hour average pollutant concentrations and same-day three hour averages of ED visits. In this large multicenter analysis, daily average concentrations of CO and NO2 exhibited the most consistent associations with ED visits for cardiac conditions, while ozone exhibited the most consistent associations with visits for respiratory conditions. PM10 and PM2.5 were strongly associated with asthma visits during the warm season.

Background: Comorbidity of depression, heart disease, and migraine has been observed in clinical practice, while ambient air pollution has been identified among different risk factors for these health conditions. Suicide attempts and ideations as the result of depression may be linked to air pollution exposure. Therefore the effects of ambient air pollution on emergency department (ED) visits for suicide attempts were investigated. Methods: Emergency visit data were collected in a hospital in Vancouver, Canada. The generalized linear mixed models technique was applied in the analysis of these data. A natural hierarchical structure of the data was used to define the clusters, with days nested in a 3-level structure (day of week, month, year). Poisson models were fitted to the clustered counts of ED visits with a single air pollutant, temperature and relative humidity. In addition, the case-crossover methodology was used with the same data for comparison. The analysis was performed by gender (all, males, females) and month (all: January-December, warm: April-September, cold: October-March). Results: Both hierarchical and case-crossover methods confirmed positive and statistically significant associations among carbon monoxide (CO), nitrogen dioxide (NO₂), sulphur dioxide (SO₂), and particulate matter (PM₁₀) for all suicide attempts in the cold period. The largest increase was observed for males in the cold period for a 1-day lagged exposure to NO₂, with an excess risk of 23.9% (95% CI: 7.8, 42.4) and odds ratio of 1.21 (95% CI: 1.03, 1.41). In warm months the associations were not statistically significant, and the highest positive value was obtained for ozone lagged by 1 day. Conclusion: The results indicate a potential association between air pollution and emergency department visits for suicide attempts.

Background: The pathogenesis of appendicitis is unclear. We evaluated whether exposure to air pollution was associated with an increased incidence of appendicitis. Methods: We identified 5191 adults who had been admitted to hospital with appendicitis between Apr. 1, 1999, and Dec. 31, 2006. The air pollutants studied were ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide, and suspended particulate matter of less than 10 μ and less than 2.5 μ in diameter. We estimated the odds of appendicitis relative to short-term increases in concentrations of selected pollutants, alone and in combination, after controlling for temperature and relative humidity as well as the effects of age, sex and season. Results: An increase in the interquartile range of the 5-day average of ozone was associated with appendicitis (odds ratio [OR] 1.14, 95% confidence interval [CI] 1.03–1.25). In summer (July–August), the effects were most pronounced for ozone (OR 1.32, 95% CI 1.10–1.57), sulfur dioxide (OR 1.30, 95% CI 1.03–1.63), nitrogen dioxide (OR 1.76, 95% CI 1.20–2.58), carbon monoxide (OR 1.35, 95% CI 1.01–1.80) and particulate matter less than 10 μ in diameter (OR 1.20, 95% CI 1.05–1.38). We observed a significant effect of the air pollutants in the summer months among men but not among women (e.g., OR for increase in the 5-day average of nitrogen dioxide 2.05, 95% CI 1.21–3.47, among men and 1.48, 95% CI 0.85–2.59, among women). The double-pollutant model of exposure to ozone and nitrogen dioxide in the summer months was associated with attenuation of the effects of ozone (OR 1.22, 95% CI 1.01–1.48) and nitrogen dioxide (OR 1.48, 95% CI 0.97–2.24). Interpretation: Our findings suggest that some cases of appendicitis may be triggered by short-term exposure to air pollution. If these findings are confirmed, measures to improve air quality may help to decrease rates of appendicitis.

The effectiveness of regulatory actions designed to improve air quality is often assessed by predicting changes in public health resulting from their implementation. Risk of premature mortality from long-term exposure to ambient air pollution is the single most important contributor to such assessments and is estimated from observational studies generally assuming a log-linear, no-threshold association between ambient concentrations and death. There has been only limited assessment of this assumption in part because of a lack of methods to estimate the shape of the exposure-response function in very large study populations. In this paper, we propose a new class of variable coefficient risk functions capable of capturing a variety of potentially non-linear associations which are suitable for health impact assessment. We construct the class by defining transformations of concentration as the product of either a linear or log-linear function of concentration multiplied by a logistic weighting function. These risk functions can be estimated using hazard regression survival models with currently available computer software and can accommodate large population-based cohorts which are increasingly being used for this purpose. We illustrate our modeling approach with two large cohort studies of long-term concentrations of ambient air pollution and mortality: the American Cancer Society Cancer Prevention Study II (CPS II) cohort and the Canadian Census Health and Environment Cohort (CanCHEC). We then estimate the number of deaths attributable to changes in fine particulate matter concentrations over the 2000 to 2010 time period in both Canada and the USA using both linear and non-linear hazard function models.

Background: The aim of this study was to investigate the associations between ambient air pollution and emergency department (ED) visits for depression. Methods: Health data were retrieved from the National Ambulatory Care Reporting System. ED visits for depression were retrieved from the National Ambulatory Care Reporting System using the International Classification of Diseases (ICD-10), Tenth revision codes; ICD-10: F32 (mild depressive episode) and ICD-10: F33 (recurrent depressive disorder). A case-crossover design was employed for this study. Conditional logistic regression models were used to estimate odds ratios. Results: For females, exposure to ozone was associated with increased risk of an ED visit for depression between 1 and 7 days after exposure, for males, between 1 and 5, and 8 days after exposure, with odds ratios ranging between 1.02 and 1.03. Conclusions: These findings suggest that, as hypothesized, there is a positive association between exposure to air pollution and ED visits for depression.