BackgroundBlood 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).MethodsThe 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.ResultsResults 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.ConclusionsHigher 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.

BackgroundPrior experimental and epidemiologic data support a link between exposure to fine ambient particulate matter (<2.5 μm in aerodynamic diameter, PM2.5) and development of insulin resistance/Type II diabetes mellitus (Type II DM). We investigated the role of hypothalamic inflammation in PM2.5-mediated diabetes development.MethodsKKay mice, a genetically susceptible model of Type II DM, were assigned to either concentrated PM2.5 or filtered air (FA) for 4–8 weeks via a versatile aerosol concentrator and exposure system, or administered intra-cerebroventricular with either IKKβ inhibitor (IMD-0354) or TNFα antibody (infliximab) for 4–5 weeks simultaneously with PM2.5 exposure. Glucose tolerance, insulin sensitivity, oxygen consumption and heat production were evaluated. At euthanasia, blood, spleen, visceral adipose tissue and hypothalamus were collected to measure inflammatory cells using flow cytometry. Standard immunohistochemical methods and quantitative PCR were used to assess targets of interest.ResultsPM2.5 exposure led to hyperglycemia and insulin resistance, which was accompanied by increased hypothalamic IL-6, TNFα, and IKKβ mRNA expression and microglial/astrocyte reactivity. Targeting the NFκB pathway with intra-cerebroventricular administration of an IKKβ inhibitor [IMD-0354, n = 8 for each group)], but not TNFα blockade with infliximab [(n = 6 for each group], improved glucose tolerance, insulin sensitivity, rectified energy homeostasis (O2 consumption, CO2 production, respiratory exchange ratio and heat generation) and reduced peripheral inflammation in response to PM2.5.ConclusionsCentral inhibition of IKKβ prevents PM2.5 mediated peripheral inflammation and exaggeration of type II diabetes. These results provide novel insights into how air pollution may mediate susceptibility to insulin resistance and Type II DM.

We report on the research conducted by the Community Action Against Asthma (CAAA) in Detroit, Michigan, to evaluate personal and community-level exposures to particulate matter (PM) among children with asthma living in an urban environment. CAAA is a community-based participatory research collaboration among academia, health agencies, and community-based organizations. CAAA investigates the effects of environmental exposures on the residents of Detroit through a participatory process that engages participants from the affected communities in all aspects of the design and conduct of the research; disseminates the results to all parties involved; and uses the research results to design, in collaboration with all partners, interventions to reduce the identified environmental exposures. The CAAA PM exposure assessment includes four seasonal measurement campaigns each year that are conducted for a 2-week duration each season. In each seasonal measurement period, daily ambient measurements of PM 2.5 and PM 10 (particulate matter with a mass median aerodynamic diameter less than 2.5 µm and 10 µm, respectively) are collected at two elementary schools in the eastside and southwest communities of Detroit. Concurrently, indoor measurements of PM 2.5 and PM 10

Ambient levels of particulate matter have been linked to cardiovascular disease. The mechanisms mediating these associations are poorly understood. One candidate mechanism is inflammation. Using data from the Multi-Ethnic Study of Atherosclerosis (2000-2002), the authors investigated the relation between exposure to particulate matter of less than or equal to 2.5 microm in diameter (PM2.5) and C-reactive protein concentration in 5,634 persons aged 45-84 years who were free of cardiovascular disease. Data from US Environmental Protection Agency monitors were used to estimate PM2.5 exposures for the prior day, prior 2 days, prior week, prior 30 days, and prior 60 days. Only the 30-day and 60-day mean exposures showed a weak positive association with C-reactive protein, and confidence intervals were wide: relative increases in C-reactive protein per 10 microg/m3 of PM2.5 adjusted for person-level covariates were 3% (95% confidence interval (CI): -2, 10) for a 30-day mean and 4% (95% CI: -3, 11.0) for a 60-day mean. The means of 7-day, 30-day, and 60-day exposures were weakly, positively, and nonsignificantly associated with the odds of C-reactive protein of greater than or equal to 3 mg/liter: adjusted odds ratios were 1.05 (95% CI: 0.96, 1.15), 1.12 (95% CI: 0.98, 1.29), and 1.12 (95% CI: 0.96, 1.32), respectively. Slightly stronger associations were observed in persons without other risk factors for elevated C-reactive protein, but this heterogeneity was not statistically significant. The authors' results are not compatible with strong effects of particulate matter exposures on population levels of C-reactive protein.

The National Children’s Study is considering a wide spectrum of airborne pollutants that are hypothesized to potentially influence pregnancy outcomes, neurodevelopment, asthma, atopy, immune development, obesity, and pubertal development. In this article we summarize six applicable exposure assessment lessons learned from the Centers for Children’s Environmental Health and Disease Prevention Research that may enhance the National Children’s Study: a) Selecting individual study subjects with a wide range of pollution exposure profiles maximizes spatial-scale exposure contrasts for key pollutants of study interest. b) In studies with large sample sizes, long duration, and diverse outcomes and exposures, exposure assessment efforts should rely on modeling to provide estimates for the entire cohort, supported by subject-derived questionnaire data. c) Assessment of some exposures of interest requires individual measurements of exposures using snapshots of personal and microenvironmental exposures over short periods and/or in selected microenvironments. d) Understanding issues of spatial–temporal correlations of air pollutants, the surrogacy of specific pollutants for components of the complex mixture, and the exposure misclassification inherent in exposure estimates is critical in analysis and interpretation. e) “Usual” temporal, spatial, and physical patterns of activity can be used as modifiers of the exposure/outcome relationships. f) Biomarkers of exposure are useful for evaluation of specific exposures that have multiple routes of exposure. If these lessons are applied, the National Children’s Study offers a unique opportunity to assess the adverse effects of air pollution on interrelated health outcomes during the critical early life period.