Joel D. Kaufman

Particulate Matter Air Pollution and Cardiovascular Disease An Update to the Scientific Statement From the American Heart Association

In 2004, the first American Heart Association scientific statement on “Air Pollution and Cardiovascular Disease” concluded that exposure to particulate matter (PM) air pollution contributes to cardiovascular morbidity and mortality. In the interim, numerous studies have expanded our understanding of this association and further elucidated the physiological and molecular mechanisms involved. The main objective of this updated American Heart Association scientific statement is to provide a comprehensive review of the new evidence linking PM exposure with cardiovascular disease, with a specific focus on highlighting the clinical implications for researchers and healthcare providers. The writing group also sought to provide expert consensus opinions on many aspects of the current state of science and updated suggestions for areas of future research. On the basis of the findings of this review, several new conclusions were reached, including the following: Exposure to PM <2.5 &mgr;m in diameter (PM2.5) over a few hours to weeks can trigger cardiovascular disease–related mortality and nonfatal events; longer-term exposure (eg, a few years) increases the risk for cardiovascular mortality to an even greater extent than exposures over a few days and reduces life expectancy within more highly exposed segments of the population by several months to a few years; reductions in PM levels are associated with decreases in cardiovascular mortality within a time frame as short as a few years; and many credible pathological mechanisms have been elucidated that lend biological plausibility to these findings. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM2.5 exposure and cardiovascular morbidity and mortality. This body of evidence has grown and been strengthened substantially since the first American Heart Association scientific statement was published. Finally, PM2.5 exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality.

Referent selection in case-crossover analyses of acute health effects of air pollution.

The case-crossover design was proposed for the study of a transient effect of an intermittent exposure on the subsequent occurrence of a rare acute-onset disease. This design can be an alternative to Poisson time series regression for studying the health effects of fine particulate matter air pollution. Characteristics of time-series of particulate matter, including long-term time trends, seasonal trends, and short-term autocorrelations, require that referent selection in the case-crossover design be considered carefully and adapted to minimize bias. We performed simulations to evaluate the bias associated with various referent selection strategies for a proposed case-crossover study of associations between particulate matter and primary cardiac arrest. Some a priori reasonable strategies were associated with a relative bias as large as 10%, but for most strategies the relative bias was less than 2% with confidence interval coverage within 1% of the nominal level. We show that referent selection for case–crossover designs raises the same issues as selection of smoothing method for time series analyses. In addition, conditional logistic regression analysis is not strictly valid for some case–crossover designs, introducing further bias.

Comparison of self-report, video observation and direct measurement methods for upper extremity musculoskeletal disorder physical risk factors

The prevention of work-related musculoskeletal disorders has become a national priority in many countries. Increasingly, attempts are made to quantify those exposures that increase risk in order to set exposure limit values. This study used commonly employed field measurement methods and tools in order to perform an inter-method comparison between three primary methods of risk factor exposure assessment: self-report questionnaires, observational video analysis and direct measurement. Extreme posture duration, repetition, hand force (estimated from electromyography) and movement velocity were assessed for 18 subjects while performing each of three jobs processing tree seedlings. Results indicated that self-reports were the least precise assessment method, which consistently overestimated exposures for each of the measured risk factors. However, adjustment of the reports as psychophysical scales may increase agreement on a group level. Wrist flexion/extension duration and repetition were best measured by electrogoniometer. Electrogoniometric measures of wrist deviation duration and frequency were less precise than video analysis. Forearm rotation duration and repetition, grip force and velocity appeared to be best quantified by direct measurement as measured by electrogoniometer and electromyography (EMG) (as root-mean-square amplitude). The results highlight the fact that it is as important to consider and report estimated measurement error in order to reduce potential exposure misclassification in epidemiologic studies.

Associations between Recent Exposure to Ambient Fine Particulate Matter and Blood Pressure in the Multi-Ethnic Study of Atherosclerosis (MESA)

Background Blood pressure (BP) may be implicated in associations observed between ambient particulate matter and cardiovascular morbidity and mortality. This study examined cross-sectional associations between short-term ambient fine particles (particulate matter ≤ 2.5 μm in aerodynamic diameter; PM2.5) and BP: systolic (SBP), diastolic (DBP), mean arterial (MAP), and pulse pressure (PP). Methods The study sample included 5,112 persons 45–84 years of age, free of cardiovascular disease at the Multi-Ethnic Study of Atherosclerosis baseline examination (2000–2002). Data from U.S. Environmental Protection Agency monitors were used to estimate ambient PM2.5 exposures for the preceding 1, 2, 7, 30, and 60 days. Roadway data were used to estimate local exposures to traffic-related particles. Results Results from linear regression found PP and SBP positively associated with PM2.5. For example, a 10-μg/m3 increase in PM2.5 30-day mean was associated with 1.12 mmHg higher pulse pressure [95% confidence interval (CI), 0.28–1.97] and 0.99 mmHg higher systolic BP (95% CI, –0.15 to 2.13), adjusted for age, sex, race/ethnicity, income, education, body mass index, diabetes, cigarette smoking and environmental tobacco smoke, alcohol use, physical activity, medications, atmospheric pressure, and temperature. Results were much weaker and not statistically significant for MAP and DBP. Although traffic-related variables were not themselves associated with BP, the association between PM2.5 and BP was stronger in the presence of higher traffic exposure. Conclusions Higher SBP and PP were associated with ambient levels of PM2.5 and the association was stronger in the presence of roadway traffic, suggesting that impairment of blood pressure regulation may play a role in response to air pollution.

The outdoor air pollution and brain health workshop

Accumulating evidence suggests that outdoor air pollution may have a significant impact on central nervous system (CNS) health and disease. To address this issue, the National Institute of Environmental Health Sciences/National Institute of Health convened a panel of research scientists that was assigned the task of identifying research gaps and priority goals essential for advancing this growing field and addressing an emerging human health concern. Here, we review recent findings that have established the effects of inhaled air pollutants in the brain, explore the potential mechanisms driving these phenomena, and discuss the recommended research priorities/approaches that were identified by the panel.

Diesel Exhaust Inhalation Elicits Acute Vasoconstriction in Vivo

Background Traffic-related air pollution is consistently associated with cardiovascular morbidity and mortality. Recent human and animal studies suggest that exposure to air pollutants affects vascular function. Diesel exhaust (DE) is a major source of traffic-related air pollution. Objectives Our goal was to study the effects of short-term exposure to DE on vascular reactivity and on mediators of vascular tone. Methods In a double-blind, crossover, controlled exposure study, 27 adult volunteers (10 healthy and 17 with metabolic syndrome) were exposed in randomized order to filtered air (FA) and each of two levels of diluted DE (100 or 200 μg/m3 of fine particulate matter) in 2-hr sessions. Before and after each exposure, we assessed the brachial artery diameter (BAd) by B-mode ultrasound and collected blood samples for endothelin-1 (ET-1) and catecholamines. Postexposure we also assessed endothelium-dependent flow-mediated dilation (FMD). Results Compared with FA, DE at 200 μg/m3 elicited a decrease in BAd (0.11 mm; 95% confidence interval, 0.02–0.18), and the effect appeared linearly dose related with a smaller effect at 100 μg/m3. Plasma levels of ET-1 increased after 200 μg/m3 DE but not after FA (p = 0.01). There was no consistent impact of DE on plasma catecholamines or FMD. Conclusions These results demonstrate that short-term exposure to DE is associated with acute endothelial response and vasoconstriction of a conductance artery. Elucidation of the signaling pathways controlling vascular tone that underlie this observation requires further study.

Semen quality of men employed at a lead smelter.

OBJECTIVE: To evaluate the effects of recent and long term occupational lead exposure on indicators of male reproductive health. METHODS: In a cross sectional study of male employees of a lead smelter (n = 2469), blood samples were obtained from 152 workers including 119 who also provided semen samples. Semen analysis and serum concentrations of testosterone, follicle stimulating hormone, and luteinising hormone were used as indicators of reproductive health. Semen and hormone variables were examined in relation to measures of current and long term body lead burden estimated from current blood lead concentrations and historical blood lead monitoring data. RESULTS: For current blood lead concentration groups of < 15, 15-24, 25-39, > 40 micrograms/dl, the geometric mean sperm concentrations were, respectively, 79.1, 56.5, 62.7, and 44.4 million cells/ml and geometric mean total sperm counts were 186, 153, 137, and 89 million cells (P for trend 0.04). Compared with workers with blood lead concentrations less than 15 micrograms/dl, workers with current blood lead concentrations of 40 micrograms/dl or more had an increased risk of below normal sperm concentration (odds ratio (OR) 8.2, 95% confidence interval (95% CI) 1.2-57.9) and total sperm count (OR 2.6, 95% CI 0.4-15.7), based on World Health Organisation standards. Independent of current lead exposure, sperm concentration, total sperm count, and total motile sperm count were inversely related to measures of long term lead exposure. No association was found between lead exposure and measures of sperm motility, sperm morphology, or serum concentrations of reproductive hormones. CONCLUSIONS: Blood lead concentrations below the currently accepted worker protection criteria seem to adversely affect spermatogenesis.

A Case-crossover Analysis of Particulate Matter Air Pollution and Out-of-hospital Primary Cardiac Arrest

Numerous epidemiologic studies have reported increases in the daily incidence of cardiovascular mortality and morbidity associated with increases in daily levels of particulate matter air pollution. We studied the association between the incidence of primary cardiac arrest and two daily measures of particulate matter using a case-crossover study of 362 cases of out-of-hospital cardiac arrest. All cases were attended by paramedics and had no history of clinically recognized heart disease or life-threatening comorbidities. We compared particulate matter levels at index times with particulate matter levels from referent days matched on day of week within strata defined by month and year. The estimated relative risk at a lag of 1 day for an interquartile range (IQR) change in nephelometry (0.51 × 10-1 km-1) was 0.893 (95% CI = 0.779–1.024). The estimated relative risk at a lag of 1 day for an IQR change in PM10 (19.3 &mgr;gm-3) was 0.868 (95% CI = 0.744–1.012). Other lag periods gave similar results. We did not find evidence of confounding by carbon monoxide or sulfur dioxide. Analysis of effect modification by individual-level variables did not reveal any susceptible subgroups. These findings do no support an association between particulate matter and increased risk of primary cardiac arrest among persons without clinically recognized heart disease. The null results of this study may result from several factors, including the highly selected nature of this case series and the relatively low particulate matter levels in the Seattle metropolitan area.

Fine Particulate Air Pollution and the Progression of Carotid Intima-Medial Thickness: A Prospective Cohort Study from the Multi-Ethnic Study of Atherosclerosis and Air Pollution

In a prospective cohort study, Sara Adar and colleagues find that decreasing levels of fine particulate matter in multiple US urban areas are associated with slowed progression of intima-medial thickness, a surrogate measure of atherosclerosis.

Long-term Exposure to Ambient Particulate Matter and Prevalence of Subclinical Atherosclerosis in the Multi-Ethnic Study of Atherosclerosis

Exposure to airborne particulate matter has been linked to cardiovascular events. Whether this finding reflects an effect of particulate matter exposure on the triggering of events or development of atherosclerosis remains unknown. Using data from the Multi-Ethnic Study of Atherosclerosis collected at baseline (2000-2002), the authors investigated associations of 20-year exposures to particulate matter with measures of subclinical disease (coronary calcium, common carotid intimal-medial thickness, and ankle-brachial index) in 5,172 US adults without clinical cardiovascular disease. Particulate matter exposures for the 20 years prior to assessment of subclinical disease were obtained from a space-time model of Environmental Protection Agency monitor data linked to residential history data for each participant. Intimal-medial thickness was weakly, positively associated with exposures to particulate matter <10 microm in aerodynamic diameter and <2.5 microm in aerodynamic diameter after controlling for age, sex, race/ethnicity, socioeconomic factors, diet, smoking, physical activity, blood lipids, diabetes, hypertension, and body mass index (1-4% increase per 21-microg/m(3) increase in particulate matter <10 microm in aerodynamic diameter or a 12.5-microg/m(3) increase in particulate matter <2.5 microm in aerodynamic diameter). No consistent associations with other measures of atherosclerosis were observed. There was no evidence of effect modification by sociodemographic factors, lipid status, smoking, diabetes, body mass index, or site. Results are compatible with some effect of particulate matter exposures on development of carotid atherosclerosis.