Epidemiologic Evidence of Cardiovascular Effects of Particulate Air Pollution

In the past decade researchers have developed a body of epidemiologic evidence showing increased daily cardiovascular mortality and morbidity associated with acute exposures to particulate air pollution. Associations have been found not only with cardiovascular deaths reported on death certificates but also with myocardial infarctions and ventricular fibrillation. Particulate air pollution exposure has been associated with indicators of autonomic function of the heart including increased heart rate, decreased heart rate variability, and increased cardiac arrhythmias. Several markers of increased risk for sudden cardiac death have also been associated with such exposures. These epidemiologic studies provide early guidance to possible pathways of particulate air pollution health effects, which can only be addressed fully in toxicologic and physiologic studies

Epidemiologic study design for investigating respiratory health effects of complex air pollution mixtures.

Epidemiologic studies of the respiratory health effects of air pollution are intrinsically difficult because exposure is common, expected effects at concentrations found in developed countries are weak, random misclassification of exposure is common, and the respiratory health indicators have multiple etiologies. Exposures to air pollutants also are multidimensional, generally consisting of a mixture of gases and particles. In this paper, epidemiologic study designs are described, and their potential for evaluating effects of complex pollutant mixtures are discussed. Power to detect the independent effects of individual pollutants in a complex pollutant mixture or to measure their interactions is in general very weak unless the study is specifically designed to test such hypotheses. However, with innovative and creative design, the independent and joint effects of multiple pollutants should be estimable in epidemiologic studies

An analytic study of the predictability of the flow in a dish-pan model of the atmosphere

Thesis (M.S.)--Massachusetts Institute of Technology, Dept. of Meteorology, September 1972."August, 1972."Includes bibliographical references (leaf 53).by Douglas William Dockery.M.S

Chronic Exposure to Fine Particles and Mortality: An Extended Follow-up of the Harvard Six Cities Study from 1974 to 2009

Background: Epidemiologic studies have reported associations between fine particles (aerodynamic diameter ≤ 2.5 µm; PM:2.5) and mortality. However, concerns have been raised regarding the sensitivity of the results to model specifications, lower exposures, and averaging time. Objective: We addressed these issues using 11 additional years of follow-up of the Harvard Six Cities study, incorporating recent lower exposures. Methods: We replicated the previously applied Cox regression, and examined different time lags, the shape of the concentration–response relationship using penalized splines, and changes in the slope of the relation over time. We then conducted Poisson survival analysis with time-varying effects for smoking, sex, and education. Results: Since 2001, average PM:2.5 levels, for all six cities, were < 18 µg/m3. Each increase in PM2.5 (10 µg/m3) was associated with an adjusted increased risk of all-cause mortality (PM2.5 average on previous year) of 14% [95% confidence interval (CI): 7, 22], and with 26% (95% CI: 14, 40) and 37% (95% CI: 7, 75) increases in cardiovascular and lung-cancer mortality (PM2.5 average of three previous years), respectively. The concentration–response relationship was linear down to PM2.5 concentrations of 8 µg/m3. Mortality rate ratios for PM2.5 fluctuated over time, but without clear trends despite a substantial drop in the sulfate fraction. Poisson models produced similar results. Conclusions: These results suggest that further public policy efforts that reduce fine particulate matter air pollution are likely to have continuing public health benefits

The effect of short-term changes in air pollution on respiratory and cardiovascular morbidity in Nicosia, Cyprus.

Presented at the 6th International Conference on Urban Air Quality, Limassol, March, 2007. Short-paper was submitted for peer-review and appears in proceedings of the conference.This study investigates the effect of daily changes in levels of PM10 on the daily volume of respiratory and cardiovascular admissions in Nicosia, Cyprus during 1995-2004. After controlling for long- (year and month) and short-term (day of the week) patterns as well as the effect of weather in Generalized Additive Poisson models, some positive associations were observed with all-cause and cause-specific admissions. Risk of hospitalization increased stepwise across quartiles of days with increasing levels of PM10 by 1.3% (-0.3, 2.8), 4.9% (3.3, 6.6), 5.6% (3.9, 7.3) as compared to days with the lowest concentrations. For every 10μg/m3 increase in daily average PM10 concentration, there was a 1.2% (-0.1%, 2.4%) increase in cardiovascular admissions. With respects to respiratory admissions, an effect was observed only in the warm season with a 1.8% (-0.22, 3.85) increase in admissions per 10μg/m3 increase in PM10. The effect on respiratory admissions seemed to be much stronger in women and, surprisingly, restricted to people of adult age

Within-Home versus Between-Home Variability of House Dust Endotoxin in a Birth Cohort

Endotoxin exposure has been proposed as an environmental determinant of allergen responses in children. To better understand the implications of using a single measurement of house dust endotoxin to characterize exposure in the first year of life, we evaluated room-specific within-home and between-home variability in dust endotoxin obtained from 470 households in Boston, Massachusetts. Homes were sampled up to two times over 5–11 months. We analyzed 1,287 dust samples from the kitchen, family room, and baby’s bedroom for endotoxin. We fit a mixed-effects model to estimate mean levels and the variation of endotoxin between homes, between rooms, and between sampling times. Endotoxin ranged from 2 to 1,945 units per milligram of dust. Levels were highest during summer and lowest in the winter. Mean endotoxin levels varied significantly from room to room. Cross-sectionally, endotoxin was moderately correlated between family room and bedroom floor (r = 0.30), between family room and kitchen (r = 0.32), and between kitchen and bedroom (r = 0.42). Adjusting for season, the correlation of endotoxin levels within homes over time was 0.65 for both the bedroom and kitchen and 0.54 for the family room. The temporal within-home variance of endotoxin was lowest for bedroom floor samples and highest for kitchen samples. Between-home variance was lowest in the family room and highest for kitchen samples. Adjusting for season, within-home variation was less than between-home variation for all three rooms. These results suggest that room-to-room and home-to-home differences in endotoxin influence the total variability more than factors affecting endotoxin levels within a room over time

Workplace secondhand smoke exposure in the U.S. trucking industry.

BackgroundAlthough the smoking rate in the United States is declining because of an increase of smoke-free laws, among blue-collar workers it remains higher than that among many other occupational groups.ObjectivesWe evaluated the factors influencing workplace secondhand smoke (SHS) exposures in the U.S. unionized trucking industry.MethodsFrom 2003 through 2005, we measured workplace SHS exposure among 203 nonsmoking and 61 smoking workers in 25 trucking terminals. Workers in several job groups wore personal vapor-phase nicotine samplers on their lapels for two consecutive work shifts and completed a workplace SHS exposure questionnaire at the end of the personal sampling.ResultsMedian nicotine level was 0.87 microg/m3 for nonsmokers and 5.96 microg/m3 for smokers. As expected, smokers experienced higher SHS exposure duration and intensity than did nonsmokers. For nonsmokers, multiple regression analyses indicated that self-reported exposure duration combined with intensity, lack of a smoking policy as reported by workers, having a nondriver job, and lower educational level were independently associated with elevated personal nicotine levels (model R2 = 0.52). Nondriver job and amount of active smoking were associated with elevated personal nicotine level in smokers, but self-reported exposure, lack of a smoking policy, and lower educational level were not.ConclusionsDespite movements toward smoke-free laws, this population of blue-collar workers was still exposed to workplace SHS as recently as 2005. The perceived (reported by the workers), rather than the official (reported by the terminal managers), smoking policy was associated with measured SHS exposure levels among the nonsmokers. Job duties and educational level might also be important predictors of workplace SHS exposure

Secondhand smoke exposure and inflammatory markers in nonsmokers in the trucking industry.

BackgroundFew studies have directly assessed the association of secondhand smoke (SHS) with cardiovascular disease-related inflammatory markers, and the findings are inconsistent.ObjectivesWe assessed the association between SHS exposure and the inflammatory markers high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and soluble intercellular adhesion molecule-1 (sICAM-1) in 199 nonsmoking U.S. trucking industry workers.MethodsParticipants provided blood samples either by mail (blood drawn at local health care provider near home) or at the work site (blood drawn by research staff on-site) and completed a health and work history questionnaire at the time of blood draw. Exposure to SHS was measured by plasma cotinine concentrations. We used multivariate regression analyses to assess the associations between levels of cotinine and inflammatory markers.ResultsThe median cotinine level was 0.10 ng/mL (interquartile range, 0.04-0.23 ng/mL). The odds ratios of elevated hs-CRP (above highest CRP tertile, 1.5 mg/L) were 2.85 [95% confidence interval (CI), 1.03-7.89] for the high-cotinine group (&gt; 0.215 ng/mL) and 2.80 (95% CI, 1.11-7.10) for the moderate-cotinine group (0.05-0.215 ng/mL), compared with the low-cotinine group (&lt; 0.05 ng/mL), adjusting for age, sex, race, educational level, obesity, previous smoking history, job title, and medical history. Plasma cotinine levels were not associated with IL-6 or sICAM-1.ConclusionsSHS exposure, as assessed by plasma cotinine, was positively associated with hs-CRP in this group of blue-collar workers. The strength of the association with hs-CRP depended on the cut points selected for analysis