BACKGROUND Few cohort studies have evaluated the risk of mortality associated with long-term exposure to fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM(2.5))]. This is the first national-level cohort study to investigate these risks in Canada. OBJECTIVE We investigated the association between long-term exposure to ambient PM(2.5) and cardiovascular mortality in nonimmigrant Canadian adults. METHODS We assigned estimates of exposure to ambient PM(2.5) derived from satellite observations to a cohort of 2.1 million Canadian adults who in 1991 were among the 20% of the population mandated to provide detailed census data. We identified deaths occurring between 1991 and 2001 through record linkage. We calculated hazard ratios (HRs) and 95% confidence intervals (CIs) adjusted for available individual-level and contextual covariates using both standard Cox proportional survival models and nested, spatial random-effects survival models. RESULTS Using standard Cox models, we calculated HRs of 1.15 (95% CI: 1.13, 1.16) from nonaccidental causes and 1.31 (95% CI: 1.27, 1.35) from ischemic heart disease for each 10-μg/m(3) increase in concentrations of PM(2.5). Using spatial random-effects models controlling for the same variables, we calculated HRs of 1.10 (95% CI: 1.05, 1.15) and 1.30 (95% CI: 1.18, 1.43), respectively. We found similar associations between nonaccidental mortality and PM2.5 based on satellite-derived estimates and ground-based measurements in a subanalysis of subjects in 11 cities. CONCLUSIONS In this large national cohort of nonimmigrant Canadians, mortality was associated with long-term exposure to PM(2.5). Associations were observed with exposures to PM(2.5) at concentrations that were predominantly lower (mean, 8.7 μg/m(3); interquartile range, 6.2 μg/m(3)) than those reported previously.

BACKGROUND There is increasing evidence that specific ambient air pollutants are associated with coronary heart disease (CHD) morbidity and mortality. Because kidney transplant recipients have prevalent traditional and nontraditional risk factors, they may constitute a sensitive subgroup. STUDY DESIGN Retrospective cohort. SETTING & PARTICIPANTS This study includes 32,239 nonsmoking adult kidney transplant recipients who underwent transplant in 1997-2003, identified through the US Renal Data System and living in the United States within 50 km of an air pollution monitoring station. PREDICTOR Long-term ambient pollutant ozone and particulate matter ≤10 μm (PM(10)), assessed from monthly concentrations of ozone and PM(10) calculated from ambient monitoring data by the US Environmental Protection Agency Air Quality System and interpolated to zip code centroids according to patients' residence. OUTCOMES Outcomes of interest were death from CHD and natural-cause mortality. RESULTS For the entire transplant cohort, average pollutant levels for ozone and PM(10) were 25.5 ± 4.4 parts per billion (ppb) and 25.3 ± 6.4 μg/m(3), respectively. Correlation between ozone and PM(10) values was low, but statistically significant (P < 0.001). There were deaths from CHD (n = 267) and natural causes (n = 2,076) during the 7-year study period. For each 10-ppb increase in ozone, the risk of fatal CHD increased by 35%(RR, 1.35; 95% CI, 1.04-1.77) in the single-pollutant model and 34%(RR, 1.34; 95% CI, 1.03-1.76) in the 2-pollutant model. No independent association was found between CHD and PM(10). No significant association was identified for PM(10) or ozone level and natural-cause mortality (RR, 1.09; 95% CI, 0.99-1.21). LIMITATIONS Exposure assignment based on only residential location. CONCLUSIONS For kidney transplant recipients, ambient ozone levels potentially are associated with higher risk of fatal CHD. These findings may have implications for regulations governing air pollution and the development of individual CHD risk-reduction strategies.

RATIONALE Several studies have linked long-term exposure to particulate air pollution with increased cardiopulmonary mortality; only two have also examined incident circulatory disease. OBJECTIVES To examine associations of individualized long-term exposures to particulate and gaseous air pollution with incident myocardial infarction and stroke, as well as all-cause and cause specific mortality. METHODS We estimated long-term residential air pollution exposure for more than 100,000 participants in the California Teachers Study, a prospective cohort of female public school professionals.We linked geocoded residential addresses with inverse distance-weighted monthly pollutant surfaces for two measures of particulate matter and for several gaseous pollutants. We examined associations between exposure to these pollutants and risks of incident myocardial infarction and stroke, and of all-cause and cause-specific mortality, using Cox proportional hazards models. MEASUREMENTS AND MAIN RESULTS We found elevated hazard ratios linking long-term exposure to particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5), scaled to an increment of 10 μg/m3 with mortality from ischemic heart disease (IHD)(1.20; 95% confidence interval [CI], 1.02-1.41) and, particularly among postmenopausal women, incident stroke (1.19; 95% CI, 1.02-1.38). Long-term exposure to particulate matter less than 10 μm in aerodynamic diameter (PM10) was associated with elevated risks for IHD mortality (1.06; 95% CI, 0.99-1.14) and incident stroke (1.06; 95% CI, 1.00-1.13), while exposure to nitrogen oxides was associated with elevated risks for IHD and all cardiovascular mortality. CONCLUSIONS This study provides evidence linking long-term exposure to PM2.5 and PM10 with increased risks of incident stroke as well as IHD mortality; exposure to nitrogen oxides was also related to death from cardiovascular diseases.

BACKGROUND The association of all-cause mortality and cardiovascular outcomes with air pollution exposures has been well established in the literature. The number of studies examining chronic exposures in cohorts is growing, with more recent studies conducted among women finding risk estimates of greater magnitude. Questions remain regarding sex differences in the relationship of chronic particulate matter (PM) exposures with mortality and cardiovascular outcomes. OBJECTIVES In this study we explored these associations in the all-male Health Professionals Follow-Up Study prospective cohort. METHODS The same spatiotemporal exposure estimation models, similar outcomes, and biennially updated covariates were used as those previously applied in the female Nurses' Health Study cohort. RESULTS Among 17,545 men residing in the northeastern and midwestern United States, there were 2,813 deaths, including 746 cases of fatal coronary heart disease (CHD). An interquartile range change (4 µg/m3) in average exposure to PM ≤ 2.5 µm in diameter in the 12 previous months was not associated with all-cause mortality [hazard ratio (HR)= 0.94; 95% confidence interval (CI), 0.87-1.00] or fatal CHD (HR = 0.99; 95% CI, 0.87-1.13) in fully adjusted models. Findings were similar for separate models of exposure to PM ≤ 10 µm in diameter and PM between 2.5 and 10 µm in diameter and for copollutant models. CONCLUSIONS Among this cohort of men with high socioeconomic status living in the midwestern and northeastern United States, the results did not support an association of chronic PM exposures with all-cause mortality and cardiovascular outcomes in models with time-varying covariates. Whether these findings suggest sex differences in susceptibility or the protective impact of healthier lifestyles and higher socioeconomic status requires additional investigation.

BACKGROUND Evidence for a link between long-term exposure to air pollution and lung cancer is limited to Western populations. In this prospective cohort study, we examined this association in a Japanese population. METHODS The study comprised 63 520 participants living in 6 areas in 3 Japanese prefectures who were enrolled between 1983 and 1985. Exposure to particulate matter less than 2.5 µm in aerodynamic diameter (PM(2.5)), sulfur dioxide (SO(2)), and nitrogen dioxide (NO(2)) was assessed using data from monitoring stations located in or nearby each area. The Cox proportional hazards model was used to calculate the hazard ratios associated with the average concentrations of these air pollutants. RESULTS The 10-year average concentrations of PM(2.5), SO(2), and NO(2) before recruitment (1974-1983) were 16.8 to 41.9 µg/m(3), 2.4 to 19.0 ppb, and 1.2 to 33.7 ppb, respectively (inter-area range). During an average follow-up of 8.7 years, there were 6687 deaths, including 518 deaths from lung cancer. The hazard ratios for lung cancer mortality associated with a 10-unit increase in PM(2.5)(µg/m(3)), SO(2)(ppb), and NO(2)(ppb) were 1.24 (95% confidence interval: 1.12-1.37), 1.26 (1.07-1.48), and 1.17 (1.10-1.26), respectively, after adjustment for tobacco smoking and other confounding factors. In addition, a significant increase in risk was observed for male smokers and female never smokers. Respiratory diseases, particularly pneumonia, were also significantly associated with all the air pollutants. CONCLUSIONS Long-term exposure to air pollution is associated with lung cancer and respiratory diseases in Japan.

BACKGROUND Epidemiological, controlled human exposure, and toxicological studies have demonstrated a variety of health effects in response to particulate matter (PM) exposure with some of these studies indicating that populations with certain characteristics may be disproportionately affected. OBJECTIVE To identify populations potentially at greatest risk for PM-related health effects, we evaluated epidemiological studies that examined various characteristics that may influence susceptibility, while using results from controlled human exposure and toxicological studies as supporting evidence. Additionally, we formulated a definition of susceptibility, building from the varied and inconsistent definitions of susceptibility and vulnerability used throughout the literature. DATA SYNTHESIS We evaluated recent epidemiological studies to identify characteristics of populations potentially susceptible to PM-related health effects. Additionally, we evaluated controlled human exposure and toxicological studies to provide supporting evidence. We conducted a comprehensive review of epidemiological studies that presented stratified results (e.g.,< 65 vs. ≥ 65 years of age), controlled human exposure studies that examined individuals with underlying disease, and toxicological studies that used animal models of disease. We evaluated results for consistency across studies, coherence across disciplines, and biological plausibility to assess the potential for increased susceptibility to PM-related health effects in a specific population or life stage. CONCLUSIONS We identified a diverse group of characteristics that can lead to increased risk of PM-related health effects, including life stage (i.e., children and older adults), preexisting cardiovascular or respiratory diseases, genetic polymorphisms, and low-socioeconomic status. In addition, we crafted a comprehensive definition of susceptibility that can be used to encompass all populations potentially at increased risk of adverse health effects as a consequence of exposure to an air pollutant.

BACKGROUND Several studies have reported associations between long-term exposure to ambient fine particulate matter (PM) and cardiovascular mortality. However, the health impacts of long-term exposure to specific constituents of PM(2.5)(PM with aerodynamic diameter < or = 2.5 microm) have not been explored. METHODS We used data from the California Teachers Study, a prospective cohort of active and former female public school professionals. We developed estimates of long-term exposures to PM(2.5) and several of its constituents, including elemental carbon, organic carbon (OC), sulfates, nitrates, iron, potassium, silicon, and zinc. Monthly averages of exposure were created using pollution data from June 2002 through July 2007. We included participants whose residential addresses were within 8 and 30 km of a monitor collecting PM(2.5) constituent data. Hazard ratios (HRs) were estimated for long-term exposure for mortality from all nontraumatic causes, cardiopulmonary disease, ischemic heart disease (IHD), and pulmonary disease. RESULTS Approximately 45,000 women with 2,600 deaths lived within 30 km of a monitor. We observed associations of all-cause, cardiopulmonary, and IHD mortality with PM(2.5) mass and each of its measured constituents, and between pulmonary mortality and several constituents. For example, for cardiopulmonary mortality, HRs for interquartile ranges of PM(2.5), OC, and sulfates were 1.55 [95% confidence interval (CI), 1.431.69], 1.80 (95% CI, 1.681.93), and 1.79 (95% CI, 1.582.03), respectively. Subsequent analyses indicated that, of the constituents analyzed, OC and sulfates had the strongest associations with all four outcomes. CONCLUSIONS Long-term exposures to PM(2.5) and several of its constituents were associated with increased risks of all-cause and cardiopulmonary mortality in this cohort. Constituents derived from combustion of fossil fuel (including diesel), as well as those of crustal origin, were associated with some of the greatest risks. These results provide additional evidence that reduction of ambient PM(2.5) may provide significant public health benefits.

BACKGROUND There is increasing evidence that specific ambient air pollutants are associated with coronary heart disease (CHD) morbidity and mortality. Because kidney transplant recipients have prevalent traditional and nontraditional risk factors, they may constitute a sensitive subgroup. STUDY DESIGN Retrospective cohort. SETTING & PARTICIPANTS This study includes 32,239 nonsmoking adult kidney transplant recipients who underwent transplant in 1997-2003, identified through the US Renal Data System and living in the United States within 50 km of an air pollution monitoring station. PREDICTOR Long-term ambient pollutant ozone and particulate matter ≤10 μm (PM(10)), assessed from monthly concentrations of ozone and PM(10) calculated from ambient monitoring data by the US Environmental Protection Agency Air Quality System and interpolated to zip code centroids according to patients' residence. OUTCOMES Outcomes of interest were death from CHD and natural-cause mortality. RESULTS For the entire transplant cohort, average pollutant levels for ozone and PM(10) were 25.5 ± 4.4 parts per billion (ppb) and 25.3 ± 6.4 μg/m(3), respectively. Correlation between ozone and PM(10) values was low, but statistically significant (P < 0.001). There were deaths from CHD (n = 267) and natural causes (n = 2,076) during the 7-year study period. For each 10-ppb increase in ozone, the risk of fatal CHD increased by 35%(RR, 1.35; 95% CI, 1.04-1.77) in the single-pollutant model and 34%(RR, 1.34; 95% CI, 1.03-1.76) in the 2-pollutant model. No independent association was found between CHD and PM(10). No significant association was identified for PM(10) or ozone level and natural-cause mortality (RR, 1.09; 95% CI, 0.99-1.21). LIMITATIONS Exposure assignment based on only residential location. CONCLUSIONS For kidney transplant recipients, ambient ozone levels potentially are associated with higher risk of fatal CHD. These findings may have implications for regulations governing air pollution and the development of individual CHD risk-reduction strategies.

Soy milk has become a popular substitute for dairy milk with important health claims. We hypothesized that soy milk, based on its nutrient composition, is comparable to dairy products and, therefore, beneficial for bone health. To test this hypothesis, we examined the benefit of soy milk and dairy products intake on bone health using broadband ultrasound attenuation of the calcaneus. Postmenopausal white women (n = 337) who had completed a lifestyle and dietary questionnaire at enrollment into the Adventist Health Study-2 had their calcaneal broadband ultrasound attenuation measured 2 years later. The association between osteoporosis (defined as a T-score <-1.8) and some dietary factors (soy milk, dairy) and selected lifestyle factors was assessed using logistic regression. In a multivariable model adjusted for demographics, hormone use, and other dietary factors, osteoporosis was positively associated with age (odds ratio [OR]= 1.08; 95% confidence interval [CI], 1.06-1.12) and inversely associated with body mass index (OR = 0.91; 95% CI, 0.86-0.97) and current estrogen use (OR = 0.27; 95% CI, 0.13-0.56). Compared with women who did not drink soy milk, women drinking soy milk once a day or more had 56% lower odds of osteoporosis (OR = 0.44; 95% CI, 0.20-0.98; P(trend)=.04). Women whose dairy intake was once a day or more had a 62% reduction in the likelihood of having osteoporosis (OR = 0.38; 95% CI, 0.17-0.86; P(trend)=.02) compared with women whose dairy intake was less than twice a week. Among individual dairy products, only cheese showed an independent and significant protection (OR = 0.28; 95% CI, 0.12-0.66; P(trend)=.004) for women eating cheese more than once per week vs those who ate cheese less than once a week. We concluded that osteoporosis is inversely associated with soy milk intake to a similar degree as dairy intake after accounting for age, body mass index, and estrogen use.

OBJECTIVE: To assess race-specific validity of food and food group intakes measured using an FFQ. DESIGN: Calibration study participants were randomly selected from the Adventist Health Study-2 (AHS-2) cohort by church, and then by subject-within-church. Intakes of forty-seven foods and food groups were assessed using an FFQ and then compared with intake estimates measured using six 24 h dietary recalls (24HDR). We used two approaches to assess the validity of the questionnaire:(i) cross-classification by quartile and (ii) de-attenuated correlation coefficients. SETTING: Seventh-day Adventist church members geographically spread throughout the USA and Canada. SUBJECTS: Members of the AHS-2 calibration study (550 whites and 461 blacks). RESULTS: The proportion of participants with exact quartile agreement in the FFQ and 24HDR averaged 46 %(range: 29-87 %) in whites and 44 %(range: 25-88 %) in blacks. The proportion of quartile gross misclassification ranged from 1 % to 11 % in whites and from 1 % to 15 % in blacks. De-attenuated validity correlations averaged 0·59 in whites and 0·48 in blacks. Of the forty-seven foods and food groups, forty-three in whites and thirty-three in blacks had validity correlations >0·4. CONCLUSIONS: The AHS-2 questionnaire has good validity for most foods in both races; however, validity correlations tend to be higher in whites than in blacks.

Colorectal cancer (CRC) is a leading cause of cancer death in the United States. The majority of CRC arise in adenomatous polyps and 25-35% of colon adenoma risk could be avoidable by modifying diet and lifestyle habits. We assessed the association between diet and the risk of self-reported physician-diagnosed colorectal polyps among 2,818 subjects who had undergone colonoscopy. Subjects participated in 2 cohort studies: the AHS-1 in 1976 and the AHS-2 from 2002-2005. Multivariate logistic regression analysis was used to estimate the period risk of incident cases of polyps; 441 cases of colorectal polyps were identified. Multivariate analysis adjusted by age, sex, body mass index, and education showed a protective association with higher frequency of consumption of cooked green vegetables (OR 1 time/d vs.<5/wk = 0.76, 95% CI = 0.59-0.97) and dried fruit (OR 3+ times/wk vs.<1 time/wk = 0.76, 95%CI = 0.58-0.99). Consumption of legumes at least 3 times/wk reduced the risk by 33% after adjusting for meat intake. Consumption of brown rice at least 1 time/wk reduced the risk by 40%. These associations showed a dose-response effect. High frequency of consumption of cooked green vegetables, dried fruit, legumes, and brown rice was associated with a decreased risk of colorectal polyps.

OBJECTIVE: To validate a 204-item quantitative FFQ for measurement of nutrient intake in the Adventist Health Study-2 (AHS-2). DESIGN: Calibration study participants were randomly selected from the AHS-2 cohort by church, and then subject-within-church. Each participant provided two sets of three weighted 24 h dietary recalls and a 204-item FFQ. Race-specific correlation coefficients (r), corrected for attenuation from within-person variation in the recalls, were calculated for selected energy-adjusted macro- and micronutrients. SETTING: Adult members of the AHS-2 cohort geographically spread throughout the USA and Canada. SUBJECTS: Calibration study participants included 461 blacks of American and Caribbean origin and 550 whites. RESULTS: Calibration study subjects represented the total cohort very well with respect to demographic variables. Approximately 33 % were males. Whites were older, had higher education and lower BMI compared with blacks. Across fifty-one variables, average deattenuated energy-adjusted validity correlations were 0.60 in whites and 0.52 in blacks. Individual components of protein had validity ranging from 0.40 to 0.68 in blacks and from 0.63 to 0.85 in whites; for total fat and fatty acids, validity ranged from 0.43 to 0.75 in blacks and from 0.46 to 0.77 in whites. Of the eighteen micronutrients assessed, sixteen in blacks and sixteen in whites had deattenuated energy-adjusted correlations >/=0.4, averaging 0.60 and 0.53 in whites and blacks, respectively. CONCLUSIONS: With few exceptions validity coefficients were moderate to high for macronutrients, fatty acids, vitamins, minerals and fibre. We expect to successfully use these data for measurement error correction in analyses of diet and disease risk.

BACKGROUND Evidence suggesting that a diet high in fruits and vegetables may be beneficial to bone health has sparked interest in the potential benefit of a vegetarian diet. However, other studies have raised a question regarding the adequacy of protein in such a diet. OBJECTIVE The aim of the present study was to take a whole foods approach in examining the effects of foods high in protein on the risk of wrist fracture (WF) in a cohort with a significant proportion consuming a meat-free diet. DESIGN A cohort study of women who completed two lifestyle surveys 25 years apart. SUBJECTS One thousand eight hundred and sixty-five peri- and postmenopausal women at the time of the first survey. RESULTS There was a significant interaction between meat consumption and foods high in vegetable protein. Among vegetarians, those who consumed the least vegetable protein intake were at highest risk for fracture. However, increasing levels of plant-based high-protein foods decreased WF risk, with a 68% reduction in risk (hazard ratio (HR)= 0.32, 95% confidence interval (CI) 0.13-0.79) in the highest intake group. Among those with lowest vegetable protein consumption, increasing meat intake decreased the risk of WF, with the highest consumption decreasing risk by 80%(HR = 0.20, 95% CI 0.06-0.66). CONCLUSIONS The finding that higher consumption frequencies of foods rich in protein were associated with reduced WF supports the importance of adequate protein for bone health. The similarity in risk reduction by vegetable protein foods compared with meat intake suggests that adequate protein intake is attainable in a vegetarian diet.

Recent studies have suggested that a high level of recent physical activity increases the risk of a wrist fracture in postmenopausal women. The relationship of more distant past physical activity to wrist fracture is less clear, and most studies have relied on recall of physical activity much earlier in life. The aim of this study was to assess the risk of wrist fracture in a subset of women who had completed a recent questionnaire and also had participated in a cohort study 25 years earlier, 1865 women who were perimenopausal and postmenopausal in 1976 and had completed the 1976 and 2002 Adventist Health Study lifestyle questionnaires. Data on risk factors including physical activity were collected from the 1976 survey. Subjects reported wrist fractures occurring since baseline, and the approximate time of fracture, in the 2002 questionnaire. Incidence of wrist fracture was 3.7/1000 person-years of follow up. There was a dose-response inverse relationship between level of physical activity and wrist fracture with a 37% reduction of risk for the highest level of physical activity with respect to the lowest level (HR, 0.63; 95% CI, 0.45, 0.89). The effect of physical activity changed little in the final multivariable model (HR, 0.61; 95% CI, 0.43, 0.87). In this cohort of women with a relatively low incidence of wrist fracture, higher levels of physical activity at baseline were protective against risk of fracture during 25 years of follow-up.

We tested the hypothesis that walnut consumption can exert effects on markers of inflammation and endothelial activation similar to those produced by fish consumption. In a crossover dietary intervention trial, 25 normal to mildly hyperlipidemic men and women were randomly assigned to one of three isoenergetic diets: a walnut diet incorporating 42.5g of walnuts per 10.1mJ 6 times per week (1.8% of energy n-3 fat); a fish diet providing 113g of fatty fish per 10.1mJ 2 times per week (0.8% of energy n-3 fat), or a control diet (no nuts or fish, 0.4% of energy n-3 fat) for 4 weeks on each diet. Both the walnut and fish diets inhibited circulating concentrations of prostaglandin E metabolite (PGEM) and 11-dehydro thromboxane B2, but demonstrated no effect on blood interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α¯ (TNF-α¯), and C-reactive protein (CRP) or the number of circulating lymphocyte subsets. On the walnut diet the proportion of plasma phospholipid α¯-linolenic acid (ALA) increased 140% and arachidonic acid (AA) decreased 7% compared to both the control and fish diets. The proportion of plasma phospholipid eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) increased about 200% and 900% respectively on the fish diet relative to either the control or walnut diet. The walnut diet inhibited E-selectin by 12.7% relative to the fish diet, and the fish diet inhibited secretory intercellular adhesion molecule-1 (s-ICAM-1) by 4.5% relative to the control diet. Both walnuts and fish in commonly consumed amounts may have modest albeit distinct effects on circulating adhesion molecules.

Background/Aims Cigarette smoking is an important risk factor for multiple serious health outcomes and has significant consequences for health care management and research. However, the completeness and accuracy of the smoking information in the electronic medical record (EMR) system remain unknown. We assessed the accuracy of diagnosis coding for cigarette smoking in the EMR using self-reported smoking status collected from Kaiser Permanente Southern California (KPSC) male members who participated in the California Men's Health study (CMHS). Methods Ever smokers in the CMHS were identified based on their self-reported smoking status in the initial (2002-2003) and/or follow-up (2006) study surveys. Smoking diagnosis coding (SDC) was ascertained based on tobacco-related ICD-9 diagnosis codes, CPT procedure codes, and smoking history from KPSC's integrated EMR system after the initial CMHS survey date. Sensitivity and positive predictive value (PPV) of the SDC were calculated. Logistic regression was used to study the association between SDC and demographics and clinical characteristics among self-reported ever- smokers. Results A total of 13,539 (65.9%) of 20,554 self-reported ever smokers from the CMHS had SDC in the EMR. The overall sensitivities were 19%, 58%, and 65% during the time periods of 2003-2005, 2006-2008, and 2009-2010, respectively. The sensitivities were higher among those with higher co-morbidity scores and smoking-related chronic diseases, especially chronic obstructive pulmonary disease [78%(95% CI: 74-82%) in 2009-2010]. The overall sensitivity increased to 92% among self-reported current smokers from the CMHS in 2009-2010. The PPV ranged from 76% to 94% during the study period. In multivariable Logistic regression, increased health service utilization and smoking duration were associated with a higher likelihood of having SDC among self-reported ever-smokers. On the other hand, Asian race and Spanish language preference was linked to a lower likelihood of having SDC. Discussion We found that completeness of SDC in the EMR increased significantly over time. Of note, Asian men and men with Spanish language preference may be at risk of being under coded for smoking history. Although considerable progress has been made, results highlight the need for greater efforts by the health plan to screen for and code patients' tobacco use.

Previous studies have explored the association between air pollution levels and adverse birth outcomes such as lower birth weight. Existing literature suggests an association, although results across studies are not consistent. Additional research is needed to confirm the effect, investigate the exposure window of importance, and distinguish which pollutants cause harm. We assessed the association between ambient pollutant concentrations and term birth weight for 1,548,904 births in TX from 1998 to 2004. Assignment of prenatal exposure to air pollutants was based on maternal county of residence at the time of delivery. Pollutants examined included particulate matter with aerodynamic diameter < or = 10 and < or = 2.5 microm (PM10 and PM2.5), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3). We applied a linear model with birth weight as a continuous variable. The model was adjusted for known risk factors and region. We assessed pollutant effects by trimester to identify biological exposure window of concern, and explored interaction due to race/ethnicity. An interquartile increase in ambient pollutant concentrations of SO2 and O3 was associated with a 4.99-g (95% confidence interval [CI], 1.87-8.11) and 2. 72-g (95% CI, 1.11-4.33) decrease in birth weight, respectively. Lower birth weight was associated with exposure to O3 in the first and second trimester; whereas results were not significant for other pollutants by trimester A positive association was exhibited for PM2.5 in the first trimester. Effects estimates for PM10 and PM2.5 were inconsistent across race/ethnic groups. Current ambient air pollution levels may be increasing the risk of lower birth weight for some pollutants. These risks may be increased for certain racial/ethnic groups. Additional research including consideration of improved methodology is needed to investigate these findings. Future studies should examine the influence of residual confounding.

ABSTRACT: BACKGROUND: While several studies have investigated the effects of short-term air pollution on cardiovascular disease, less is known about its effects on cerebrovascular disease, including stroke and transient ischaemic attack (TIA). The aim of the study was to assess the effects of short-term variation in air pollutants on the onset of TIA and minor stroke. METHODS: We performed secondary analyses of data collected prospectively in the North West of England in a multi-centre study (NORTHSTAR) of patients with recent TIA or minor stroke. A case - crossover study was conducted to determine the association between occurrence of TIA and the concentration of ambient PM10 or gaseous pollutants. RESULTS: A total of 709 cases were recruited from the Manchester (n = 335) and Liverpool (n = 374) areas. Data for the Manchester cohort showed an association between ambient nitric oxide (NO) and risk of occurrence of TIA and minor stroke with a lag of 3 days (odds ratio 1.06, 95% CI: 1.01 -- 1.11), whereas negative association was found for the patients from Liverpool. Effects of similar magnitude, although not statistically significant, were generally observed with other pollutants. In a two pollutant model the effect of NO remained stronger and statistically significant when analysed in combination with CO or SO2, but was marginal in combination with NO2 or ozone and non-significant with PM10. There was evidence of effect modification by age, gender and season. CONCLUSIONS: Our data suggest an association between NO and occurrence of TIA and minor stroke in Greater Manchester.

Objectives Epidemiological studies of air pollution on cardiovascular health show associations of cardiac mortality and admissions with exposure to nitrogen dioxide (NO(2)) at low concentrations. These associations could be causal or NO(2) could be acting as a surrogate measure for another air pollutant, most likely ultrafine particles. No studies of cardiac susceptibility to acute exposure to NO(2) have been undertaken. Methods Randomised controlled exposures to NO(2)(400 ppb for 1 h) and air in subjects with coronary heart disease and impaired left ventricular systolic function not taking β adrenoceptor blocking drugs. Results There were no significant changes in heart rate, blood pressure, leucocyte coping capacity or any heart rate variability measure following NO(2) exposure compared with air. Conclusion These findings suggest that NO(2) does not affect heart rate variability at these concentrations (which are high for urban background levels) and in the absence of other pollutants. While a synergistic effect has not been ruled out, these data lend support to the idea that the epidemiological data associating cardiac outcomes with NO(2) are more likely due to an associated pollutant rather than NO(2) itself.

Short-term exposure to ambient air pollution is associated with increased cardiovascular mortality and morbidity. This adverse health effect is suggested to be mediated by inflammatory processes. The purpose of this study was to determine if low levels of particulate matter, typical for smaller cities, are associated with acute systemic inflammation. Fifty-two elderly individuals with ischemic heart disease were followed for six months with biweekly clinical visits in the city of Kotka, Finland. Blood samples were collected for the determination of inflammatory markers interleukin (IL)-1β, IL-6, IL-8, IL-12, interferon (IFN)γ, C-reactive protein (CRP), fibrinogen, myeloperoxidase and white blood cell count. Particle number concentration and fine particle (particles with aerodynamic diameters <2.5 μm (PM(2.5))) as well as thoracic particle (particles with aerodynamic diameters <10 μm (PM(10))) mass concentration were measured daily at a fixed outdoor measurement site. Light-absorbance of PM(2.5) filter samples, an indicator of combustion derived particles, was measured with a smoke-stain reflectometer. In addition, personal exposure to PM(2.5) was measured with portable photometers. During the study period, wildfires in Eastern Europe led to a 12-day air pollution episode, which was excluded from the main analyses. Average ambient PM(2.5) concentration was 8.7 μg/m(3). Of the studied pollutants, PM(2.5) and absorbance were most strongly associated with increased levels of inflammatory markers; most notably with C-reactive protein and IL-12 within a few days of exposure. There was also some evidence of an effect of particulate air pollution on fibrinogen and myeloperoxidase. The concentration of IL-12 was considerably (227%) higher during than before the forest fire episode. These findings show that even low levels of particulate air pollution from urban sources are associated with acute systemic inflammation. Also particles from wildfires may exhibit pro-inflammatory effects.

Increasing evidence links air pollution to the risk of cardiovascular disease. This study investigated the association between ischemic heart disease (IHD) prevalence and exposure to traffic-related air pollution (nitrogen dioxide [NO₂], fine particulate matter [PM₂.₅], and ozone [O₃]) in a population of susceptible subjects in Toronto. Local (NO₂) exposures were modeled using land use regression based on extensive field monitoring. Regional exposures (PM₂.₅, O₃) were modeled as confounders using inverse distance weighted interpolation based on government monitoring data. The study sample consisted of 2360 patients referred during 1992 to 1999 to a pulmonary clinic at the Toronto Western Hospital in Toronto, Ontario, Canada, to diagnose or manage a respiratory complaint. IHD status was determined by clinical database linkages (ICD-9-CM 412-414). The association between IHD and air pollutants was assessed with a modified Poisson regression resulting in relative risk estimates. Confounding was controlled with individual and neighborhood-level covariates. After adjusting for multiple covariates, NO₂ was significantly associated with increased IHD risk, relative risk (RR)= 1.33 (95% confidence interval [CI]: 1.2, 1.47). Subjects living near major roads and highways had a trend toward an elevated risk of IHD, RR = 1.08 (95% CI: 0.99, 1.18). Regional PM₂.₅ and O₃ were not associated with risk of IHD.

In metropolitan areas, road traffic is a major contributor to ambient air pollution and the dominant source of community noise. The authors investigated the independent and joint influences of community noise and traffic-related air pollution on risk of coronary heart disease (CHD) mortality in a population-based cohort study with a 5-year exposure period (January 1994-December 1998) and a 4-year follow-up period (January 1999-December 2002). Individuals who were 45-85 years of age and resided in metropolitan Vancouver, Canada, during the exposure period and did not have known CHD at baseline were included (n = 445,868). Individual exposures to community noise and traffic-related air pollutants, including black carbon, particulate matter less than or equal to 2.5 μm in aerodynamic diameter, nitrogen dioxide, and nitric oxide, were estimated at each person's residence using a noise prediction model and land-use regression models, respectively. CHD deaths were identified from the provincial death registration database. After adjustment for potential confounders, including traffic-related air pollutants or noise, elevations in noise and black carbon equal to the interquartile ranges were associated with 6%(95% confidence interval: 1, 11) and 4%(95% confidence interval: 1, 8) increases, respectively, in CHD mortality. Subjects in the highest noise decile had a 22%(95% confidence interval: 4, 43) increase in CHD mortality compared with persons in the lowest decile. These findings suggest that there are independent effects of traffic-related noise and air pollution on CHD mortality.

The biologic mechanisms involved in airway inflammatory response to air pollution are not clearly understood. The authors conducted a longitudinal study to investigate whether exposure to ambient air pollutants affected inflammatory cells and mediators from nasal lavage in schoolchildren. Study participants were 100 elementary and middle-school students in New Taipei City, Taiwan. A structured respiratory health questionnaire was administered in September 2007, followed by monthly measurement of nasal inflammation from October 2007 to November 2009. During the study period, daily concentrations of air pollutants were obtained from the Environmental Protection Administration monitoring station and the Aerosol Supersite. Mixed-effects models were applied to examine the association between air pollution and nasal inflammatory cells and mediators, including percentages of neutrophils, eosinophils, and monocytes in lavaged cells and interleukin-8. A total of 824 measurements were obtained from 100 participants over a period of 10 months. The level of particulate matter with an aerodynamic diameter of 2.5 μm or less (PM(2.5)) was found to be associated with percentage of neutrophils (β = 3.45%, 95% confidence interval: 0.89, 6.01) and interleukin-8 level (β = 29.98 pg/mL, 95% confidence interval: 3.26, 56.69) in the nasal lavage on the day of exposure. In this longitudinal cohort study of schoolchildren, results indicated that exposure to PM(2.5) might induce nasal inflammation.

Background: Air pollution exposure increases cardiovascular morbidity and mortality and is a major global public health concern.Objectives: We investigated the benefits of reducing personal exposure to urban air pollution in patients with coronary heart disease.Methods: In an open randomized crossover trial, 98 patients with coronary heart disease walked on a predefined route in central Beijing, China, under different conditions: once while using a highly efficient face mask, and once while not using the mask. Symptoms, exercise, personal air pollution exposure, blood pressure, heart rate, and 12-lead electrocardiography were monitored throughout the 24-hr study period.Results: Ambient air pollutants were dominated by fine and ultrafine particulate matter (PM) that was present at high levels [74 μg/m3 for PM2.5 (PM with aerodynamic diamater <2.5 µm)]. Consistent with traffic-derived sources, this PM contained organic carbon and polycyclic aromatic hydrocarbons and was highly oxidizing, generating large amounts of free radicals. The face mask was well tolerated, and its use was associated with decreased self-reported symptoms and reduced maximal ST segment depression (-142 vs.-156 μV, p = 0.046) over the 24-hr period. When the face mask was used during the prescribed walk, mean arterial pressure was lower (93 ± 10 vs. 96 ± 10 mmHg, p = 0.025) and heart rate variability increased (high-frequency power: 54 vs. 40 msec2, p = 0.005; high-frequency normalized power: 23.5 vs. 20.5 msec, p = 0.001; root mean square successive differences: 16.7 vs. 14.8 msec, p = 0.007). However, mask use did not appear to influence heart rate or energy expenditure.Conclusions: Reducing personal exposure to air pollution using a highly efficient face mask appeared to reduce symptoms and improve a range of cardiovascular health measures in patients with coronary heart disease. Such interventions to reduce personal exposure to PM air pollution have the potential to reduce the incidence of cardiovascular events in this highly susceptible population.

CONTEXT Short-term exposure to high levels of air pollution may trigger myocardial infarction (MI), but this association remains unclear. OBJECTIVE To assess and quantify the association between short-term exposure to major air pollutants (ozone, carbon monoxide, nitrogen dioxide, sulfur dioxide, and particulate matter ≤10 μm [PM(10)] and ≤2.5 μm [PM(2.5)] in diameter) on MI risk. DATA SOURCES EMBASE, Ovid MEDLINE in-process and other nonindexed citations, and Ovid MEDLINE (between 1948 and November 28, 2011), and EBM Reviews-Cochrane Central Register of Controlled Trials and EBM Reviews-Cochrane Database of Systematic Reviews (between 2005 and November 28, 2011) were searched for a combination of keywords related to the type of exposure (air pollution, ozone, carbon monoxide, nitrogen dioxide, sulfur dioxide, PM(10), and PM(2.5)) and to the type of outcome (MI, heart attack, acute coronary syndrome). STUDY SELECTION Two independent reviewers selected studies of any study design and in any language, using original data and investigating the association between short-term exposure (for up to 7 days) to 1 or more air pollutants and subsequent MI risk. Selection was performed from abstracts and titles and pursued by reviewing the full text of potentially eligible studies. DATA EXTRACTION Descriptive and quantitative information was extracted from each selected study. Using a random effects model, relative risks (RRs) and 95% CIs were calculated for each increment of 10 μg/m(3) in pollutant concentration, with the exception of carbon monoxide, for which an increase of 1 mg/m(3) was considered. DATA SYNTHESIS After a detailed screening of 117 studies, 34 studies were identified. All the main air pollutants, with the exception of ozone, were significantly associated with an increase in MI risk (carbon monoxide: 1.048; 95% CI, 1.026-1.070; nitrogen dioxide: 1.011; 95% CI, 1.006-1.016; sulfur dioxide: 1.010; 95% CI, 1.003-1.017; PM(10): 1.006; 95% CI, 1.002-1.009; and PM(2.5): 1.025; 95% CI, 1.015-1.036). For ozone, the RR was 1.003 (95% CI, 0.997-1.010; P =.36). Subgroup analyses provided results comparable with those of the overall analyses. Population attributable fractions ranged between 0.6% and 4.5%, depending on the air pollutant. CONCLUSION All the main air pollutants, with the exception of ozone, were significantly associated with a near-term increase in MI risk.

BACKGROUND: Some observational and experimental studies have suggested a short-term relationship between air pollutants and ischaemic stroke; however, the results conflict. AIMS: The objective of this study was to investigate the association between particulate matter less than 2·5 and 10 microns in aerodynamic diameter, nitrogen dioxide, sulphur dioxide and ozone, and short-term risk of ischaemic stroke in Lyon, France. METHODS: The AVC69 study was a multicenter cohort study in which all consecutive adult patients admitted to one of the emergency or neurological departments of the Rhône area for suspicion of stroke were included during a seven-month period. Only patients with ischaemic stroke living within the study area, composed of Lyon and 18 neighbouring communities with homogenous air pollutants exposure, formed the basis of our study. We adopted a time-stratified case-crossover design to analyse the short-term effect (up to two-days) of air pollutants on ischaemic stroke incidence. Models were adjusted for temperature, variation of atmospheric pressure, minimal relative humidity, influenza epidemics, pollen count, and holidays. Stratified analyses by gender and class age were performed. Different lag times were analysed. RESULTS:  376 patients were included. Mean age was 76·6 years (±13·7). 53·7% were women. No association was observed between air pollutants and short-term risk of ischaemic stroke after adjustment for main confounding factors. Results remained unchanged whatever the gender or age. CONCLUSIONS: These results suggest a lack of association between air pollutant exposure and short-term risk of ischaemic stroke in a French urban area.