BACKGROUND: A number of studies have shown associations between chronic exposure to particulate air pollution and increased mortality, particularly from cardiovascular disease, but fewer studies have examined the association between long term exposure to fine particulate air pollution and specific cardiovascular events, such as acute myocardial infarction (AMI). OBJECTIVE: To understand how long-term exposure to area particulate matter impacts onset of AMI, and to distinguish between area and local pollutants. METHODS: Building on the Worcester Heart Attack Study, an ongoing community wide investigation examining changes over time in MI incidence in greater Worcester, Massachusetts, we conducted a case-control study of 4,467 confirmed cases of AMI diagnosed between 1995 and 2003 and 9,072 matched controls selected from Massachusetts resident lists. We used a prediction model based on satellite aerosol optical depth (AOD) measurements to generate both exposure to particulate matter less than 2.5 microns in diameter (PM2.5) at the area level (10 x 10 km) and the local level (100 m) based on local land use variables. We then examined the association between area and local particulate pollution and occurrence of AMI. RESULTS: An interquartile range (IQR) increase in area PM2.5 (0.59 μg/m3) was associated with a 16% increase in the odds of AMI (95% CI: 1.04, 1.29). An IQR increase in total PM2.5 (area + local, 1.05 μg/m3) was weakly associated with a 4% increase in the odds of AMI (95% CI: 0.96, 1.11). CONCLUSIONS: Residential exposure to PM2.5 may best be represented by a combination of area and local PM2.5 and it is important to consider spatial gradients within a single metropolitan area when examining the relationship between particulate matter exposure and cardiovascular events.

BACKGROUND: Most heat-related deaths occur in cities and future trends in global climate change and urbanization may amplify this trend. Understanding how neighborhoods affect heat mortality fills an important gap between studies of individual susceptibility to heat and broadly comparative studies of temperature-mortality relationships in cities. OBJECTIVES: We estimated neighborhood effects of population characteristics and the built and natural environments on deaths due to heat exposure in Maricopa County, Arizona (2000-2008). METHODS: We used U.S. Census data and remotely sensed vegetation and land surface temperature to construct indicators of neighborhood vulnerability and a Geographic Information System to map vulnerability and residential addresses of people who died from heat exposure in 2,081 census block groups. Binary logistic regression and spatial analysis were used to associate deaths with neighborhoods. RESULTS: Neighborhood scores on three factors - Socioeconomic Vulnerability, Elderly/Isolation, and Unvegetated Area - varied widely throughout the study area. The preferred model (based on fit and parsimony) for predicting the odds of one or more deaths from heat exposure within a census block group included the first two factors and surface temperature in residential neighborhoods, holding constant population size. Spatial analysis identified clusters of neighborhoods with the highest heat vulnerability scores. A large proportion of deaths occurred among people, including homeless persons, who lived in the inner cores of the largest cities and an industrial corridor. CONCLUSIONS: Place-based indicators of vulnerability complement analyses of person-level heat risk factors. Surface temperature might be used in Maricopa County to identify the most heat-vulnerable neighborhoods but more attention to the socio-ecological complexities of climate adaptation is needed.

BACKGROUND: Evidence suggesting that persistent environmental pollutants may be reproductive toxicants underscores the need for prospective studies of couples for whom exposures are measured. OBJECTIVES: To determine the relation between selected persistent pollutants and couple fecundity as measured by time-to-pregnancy. METHODS: A cohort comprising 501 couples discontinuing contraception to become pregnant was prospectively followed for 12 months of trying to conceive or until a human chorionic gonadotrophin test confirmed pregnancy. Couples completed daily journals on lifestyle and provided biospecimens for the quantification of 9 organochlorine pesticides, 1 polybrominated biphenyl, 10 polybrominated diphenyl ethers, 36 polychlorinated biphenyls (PCBs), and 7 perfluorochemicals (PFCs) in serum. Using Cox models for discrete time, fecundability odds ratios (FORs) and 95% confidence intervals (CIs) were estimated separately for each partner's concentrations adjusting for age, body mass index, serum cotinine, serum lipids (except for PFCs), and study site (Michigan or Texas); sensitivity models further adjusted for left truncation or time off contraception (≤2 months) before enrollment. RESULTS: The adjusted reduction in fecundability associated with standard deviation increases in log-transformed serum concentrations ranged between 18%-21% for PCB congeners 118, 167, 209, and perfluorooctane sulfonamide in females, and 17%-29% for p,p'-DDE and PCB congeners 138, 156, 157, 167, 170, 172, and 209 in males. The strongest associations were observed for PCB 167 (FOR 0.79; 95% CI 0.64, 0.97) in females and PCB 138 (FOR=0.71; 95% CI 0.52, 0.98) in males. CONCLUSIONS: In a couple-based prospective cohort study with preconception enrollment and quantification of exposures in both female and male partners, a subset of persistent environmental chemicals were associated with reduced fecundity.