Limits...
Long-Term Air Pollution Exposure and Blood Pressure in the Sister Study.

Chan SH, Van Hee VC, Bergen S, Szpiro AA, DeRoo LA, London SJ, Marshall JD, Kaufman JD, Sandler DP - Environ. Health Perspect. (2015)

Bottom Line: Generalized additive models were used to examine the relationship between pollutants and measured BP at study entry, adjusting for cardiovascular disease risk factors and including thin plate splines for potential spatial confounding.A 10-μg/m(3) increase in PM2.5 was associated with 1.4-mmHg higher systolic BP (95% CI: 0.6, 2.3; p < 0.001), 1.0-mmHg higher pulse pressure (95% CI: 0.4, 1.7; p = 0.001), 0.8-mmHg higher mean arterial pressure (95% CI: 0.2, 1.4; p = 0.01), and no significant association with diastolic BP.A 10-ppb increase in NO2 was associated with a 0.4-mmHg (95% CI: 0.2, 0.6; p < 0.001) higher pulse pressure.

View Article: PubMed Central - PubMed

Affiliation: Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, Washington, USA.

ABSTRACT

Background: Exposure to air pollution has been consistently associated with cardiovascular morbidity and mortality, but mechanisms remain uncertain. Associations with blood pressure (BP) may help to explain the cardiovascular effects of air pollution.

Objective: We examined the cross-sectional relationship between long-term (annual average) residential air pollution exposure and BP in the National Institute of Environmental Health Sciences' Sister Study, a large U.S. cohort study investigating risk factors for breast cancer and other outcomes.

Methods: This analysis included 43,629 women 35-76 years of age, enrolled 2003-2009, who had a sister with breast cancer. Geographic information systems contributed to satellite-based nitrogen dioxide (NO2) and fine particulate matter (≤ 2.5 μm; PM2.5) predictions at participant residences at study entry. Generalized additive models were used to examine the relationship between pollutants and measured BP at study entry, adjusting for cardiovascular disease risk factors and including thin plate splines for potential spatial confounding.

Results: A 10-μg/m(3) increase in PM2.5 was associated with 1.4-mmHg higher systolic BP (95% CI: 0.6, 2.3; p < 0.001), 1.0-mmHg higher pulse pressure (95% CI: 0.4, 1.7; p = 0.001), 0.8-mmHg higher mean arterial pressure (95% CI: 0.2, 1.4; p = 0.01), and no significant association with diastolic BP. A 10-ppb increase in NO2 was associated with a 0.4-mmHg (95% CI: 0.2, 0.6; p < 0.001) higher pulse pressure.

Conclusions: Long-term PM2.5 and NO2 exposures were associated with higher blood pressure. On a population scale, such air pollution-related increases in blood pressure could, in part, account for the increases in cardiovascular disease morbidity and mortality seen in prior studies.

No MeSH data available.


Related in: MedlinePlus

United States map of participant residential locations, with number of participants per state. Each participant is represented by an open blue circle.
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4590742&req=5

f1: United States map of participant residential locations, with number of participants per state. Each participant is represented by an open blue circle.

Mentions: Residential pollutant exposures. Figure 1 shows the distribution of participants’ geocoded residential locations, with numbers representing the number of participants per state. The distribution of participants generally corresponds to the distribution of population across the United States. Figure 2 presents boxplots of the distribution of exposure predictions for PM2.5 and NO2, by U.S. census division. See Supplemental Material, Figures S1 and S2, for maps of mean pollutant levels of participants by U.S. census tract. PM2.5 shows large-scale spatial structure across the United States. NO2 exhibits a different spatial pattern, with high levels in highly urbanized areas, reflecting the traffic-related nature of NO2. Thus, PM2.5 exhibits greater between-city variability, whereas NO2 exhibits more within-city variability.


Long-Term Air Pollution Exposure and Blood Pressure in the Sister Study.

Chan SH, Van Hee VC, Bergen S, Szpiro AA, DeRoo LA, London SJ, Marshall JD, Kaufman JD, Sandler DP - Environ. Health Perspect. (2015)

United States map of participant residential locations, with number of participants per state. Each participant is represented by an open blue circle.
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4590742&req=5

f1: United States map of participant residential locations, with number of participants per state. Each participant is represented by an open blue circle.
Mentions: Residential pollutant exposures. Figure 1 shows the distribution of participants’ geocoded residential locations, with numbers representing the number of participants per state. The distribution of participants generally corresponds to the distribution of population across the United States. Figure 2 presents boxplots of the distribution of exposure predictions for PM2.5 and NO2, by U.S. census division. See Supplemental Material, Figures S1 and S2, for maps of mean pollutant levels of participants by U.S. census tract. PM2.5 shows large-scale spatial structure across the United States. NO2 exhibits a different spatial pattern, with high levels in highly urbanized areas, reflecting the traffic-related nature of NO2. Thus, PM2.5 exhibits greater between-city variability, whereas NO2 exhibits more within-city variability.

Bottom Line: Generalized additive models were used to examine the relationship between pollutants and measured BP at study entry, adjusting for cardiovascular disease risk factors and including thin plate splines for potential spatial confounding.A 10-μg/m(3) increase in PM2.5 was associated with 1.4-mmHg higher systolic BP (95% CI: 0.6, 2.3; p < 0.001), 1.0-mmHg higher pulse pressure (95% CI: 0.4, 1.7; p = 0.001), 0.8-mmHg higher mean arterial pressure (95% CI: 0.2, 1.4; p = 0.01), and no significant association with diastolic BP.A 10-ppb increase in NO2 was associated with a 0.4-mmHg (95% CI: 0.2, 0.6; p < 0.001) higher pulse pressure.

View Article: PubMed Central - PubMed

Affiliation: Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, Washington, USA.

ABSTRACT

Background: Exposure to air pollution has been consistently associated with cardiovascular morbidity and mortality, but mechanisms remain uncertain. Associations with blood pressure (BP) may help to explain the cardiovascular effects of air pollution.

Objective: We examined the cross-sectional relationship between long-term (annual average) residential air pollution exposure and BP in the National Institute of Environmental Health Sciences' Sister Study, a large U.S. cohort study investigating risk factors for breast cancer and other outcomes.

Methods: This analysis included 43,629 women 35-76 years of age, enrolled 2003-2009, who had a sister with breast cancer. Geographic information systems contributed to satellite-based nitrogen dioxide (NO2) and fine particulate matter (≤ 2.5 μm; PM2.5) predictions at participant residences at study entry. Generalized additive models were used to examine the relationship between pollutants and measured BP at study entry, adjusting for cardiovascular disease risk factors and including thin plate splines for potential spatial confounding.

Results: A 10-μg/m(3) increase in PM2.5 was associated with 1.4-mmHg higher systolic BP (95% CI: 0.6, 2.3; p < 0.001), 1.0-mmHg higher pulse pressure (95% CI: 0.4, 1.7; p = 0.001), 0.8-mmHg higher mean arterial pressure (95% CI: 0.2, 1.4; p = 0.01), and no significant association with diastolic BP. A 10-ppb increase in NO2 was associated with a 0.4-mmHg (95% CI: 0.2, 0.6; p < 0.001) higher pulse pressure.

Conclusions: Long-term PM2.5 and NO2 exposures were associated with higher blood pressure. On a population scale, such air pollution-related increases in blood pressure could, in part, account for the increases in cardiovascular disease morbidity and mortality seen in prior studies.

No MeSH data available.


Related in: MedlinePlus