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Long-term exposure to PM2.5 and incidence of acute myocardial infarction.

Madrigano J, Kloog I, Goldberg R, Coull BA, Mittleman MA, Schwartz J - Environ. Health Perspect. (2012)

Bottom Line: We then examined the association between area and local particulate pollution and occurrence of AMI.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).

View Article: PubMed Central - PubMed

Affiliation: The Earth Institute, Columbia University, New York, New York 10032, USA. jm3731@columbia.edu

ABSTRACT

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: We examined how long-term exposure to area particulate matter affects the onset of AMI, and we distinguished between area and local pollutants.

Methods: Building on the Worcester Heart Attack Study, an ongoing community-wide investigation examining changes over time in myocardial infarction 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 ≤ 2.5 μm in diameter (PM2.5) at the area level (10 × 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.

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Related in: MedlinePlus

Map of the study area (Worcester, MA) showing the residential location of subjects (cases and controls) with a sample mean PM2.5 (µg/m3) 10 × 10 km pollution grid for the year 2000.
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f1: Map of the study area (Worcester, MA) showing the residential location of subjects (cases and controls) with a sample mean PM2.5 (µg/m3) 10 × 10 km pollution grid for the year 2000.

Mentions: Exposure and covariate information by study area section for cases and controls is presented in Table 1. Figure 1 shows the residential location for our study subjects according to their 10 × 10 km pollution grid cell. Exposure was divided into two parts: a) area PM2.5 predicted for the 10 × 10 km grid cell that each case or control lived in, and b) local PM2.5 from the local land use prediction model. In the year 2000, the interquartile range (IQR) for area PM2.5 was 0.6 μg/m3, and the IQR for local PM2.5 was 1.1 μg/m3. Area PM2.5 was highest in section 2 of our study area, but there was more variability in this exposure metric in sections 1 and 3 (Table 1). Local PM2.5 (and the variability of local PM2.5 estimates) was highest in section 1. We also examined the degree to which exposure was correlated with area-based measures of SES in control subjects. There was moderate correlation between area PM2.5 and percent poverty within a census block group (ρ = 0.35), but a small inverse correlation with local PM2.5 (ρ = –0.07), resulting in a weak correction with total PM2.5 (ρ = 0.1).


Long-term exposure to PM2.5 and incidence of acute myocardial infarction.

Madrigano J, Kloog I, Goldberg R, Coull BA, Mittleman MA, Schwartz J - Environ. Health Perspect. (2012)

Map of the study area (Worcester, MA) showing the residential location of subjects (cases and controls) with a sample mean PM2.5 (µg/m3) 10 × 10 km pollution grid for the year 2000.
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3569684&req=5

f1: Map of the study area (Worcester, MA) showing the residential location of subjects (cases and controls) with a sample mean PM2.5 (µg/m3) 10 × 10 km pollution grid for the year 2000.
Mentions: Exposure and covariate information by study area section for cases and controls is presented in Table 1. Figure 1 shows the residential location for our study subjects according to their 10 × 10 km pollution grid cell. Exposure was divided into two parts: a) area PM2.5 predicted for the 10 × 10 km grid cell that each case or control lived in, and b) local PM2.5 from the local land use prediction model. In the year 2000, the interquartile range (IQR) for area PM2.5 was 0.6 μg/m3, and the IQR for local PM2.5 was 1.1 μg/m3. Area PM2.5 was highest in section 2 of our study area, but there was more variability in this exposure metric in sections 1 and 3 (Table 1). Local PM2.5 (and the variability of local PM2.5 estimates) was highest in section 1. We also examined the degree to which exposure was correlated with area-based measures of SES in control subjects. There was moderate correlation between area PM2.5 and percent poverty within a census block group (ρ = 0.35), but a small inverse correlation with local PM2.5 (ρ = –0.07), resulting in a weak correction with total PM2.5 (ρ = 0.1).

Bottom Line: We then examined the association between area and local particulate pollution and occurrence of AMI.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).

View Article: PubMed Central - PubMed

Affiliation: The Earth Institute, Columbia University, New York, New York 10032, USA. jm3731@columbia.edu

ABSTRACT

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: We examined how long-term exposure to area particulate matter affects the onset of AMI, and we distinguished between area and local pollutants.

Methods: Building on the Worcester Heart Attack Study, an ongoing community-wide investigation examining changes over time in myocardial infarction 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 ≤ 2.5 μm in diameter (PM2.5) at the area level (10 × 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.

Show MeSH
Related in: MedlinePlus