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Chronic residential exposure to particulate matter air pollution and systemic inflammatory markers.

Hoffmann B, Moebus S, Dragano N, Stang A, Möhlenkamp S, Schmermund A, Memmesheimer M, Bröcker-Preuss M, Mann K, Erbel R, Jöckel KH - Environ. Health Perspect. (2009)

Bottom Line: The induction of a low-grade systemic inflammatory state is a plausible mechanistic pathway.In the adjusted analysis, a cross-sectional exposure difference of 3.91 microg/m(3) in PM(2.5) (interdecile range) was associated with increases in hs-CRP of 23.9% [95% confidence interval (CI), 4.1 to 47.4%] and fibrinogen of 3.9% (95% CI, 0.3 to 7.7%) in men, whereas we found no association in women.This might provide a link between air pollution and coronary atherosclerosis.

View Article: PubMed Central - PubMed

Affiliation: Institute for Medical Informatics, Biometry, and Epidemiology, University of Duisburg-Essen, Essen, Germany. barbara.hoffmann@uk-essen.de

ABSTRACT

Background: Long-term exposure to urban air pollution may accelerate atherogenesis, but mechanisms are still unclear. The induction of a low-grade systemic inflammatory state is a plausible mechanistic pathway.

Objectives: We analyzed the association of residential long-term exposure to particulate matter (PM) and high traffic with systemic inflammatory markers.

Methods: We used baseline data from the German Heinz Nixdorf Recall Study, a population-based, prospective cohort study of 4,814 participants that started in 2000. Fine PM [aerodynamic diameter

Results: In the adjusted analysis, a cross-sectional exposure difference of 3.91 microg/m(3) in PM(2.5) (interdecile range) was associated with increases in hs-CRP of 23.9% [95% confidence interval (CI), 4.1 to 47.4%] and fibrinogen of 3.9% (95% CI, 0.3 to 7.7%) in men, whereas we found no association in women. Chronic traffic exposure was not associated with inflammatory markers. Short-term exposures to air pollutants and temperature did not influence the results markedly.

Conclusions: Our study indicates that long-term residential exposure to high levels of PM(2.5) is associated with systemic inflammatory markers in men. This might provide a link between air pollution and coronary atherosclerosis.

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Causal diagram for the investigation of the relationship of residential air pollution exposure with inflammatory markers.
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f1-ehp-117-1302: Causal diagram for the investigation of the relationship of residential air pollution exposure with inflammatory markers.

Mentions: Although we based our analyses on cross-sectional data that do not contain information about the temporal relations between studied variables, we used causal diagrams [directed acyclic graphs (DAGs)] to identify the minimal sufficient adjustment set. Based on prior biological and epidemiological knowledge, we specified the most likely temporal relations between variables (Figure 1). According to this DAG, short-term PM exposure, SES, and area of residence need to be adjusted for (model 1). Because of the difficulties inherent in adjusting for such a broad construct as SES, which increases the possibility of residual confounding, we additionally identified a sufficient adjustment set (model 2) that does not include SES but includes age, area of residence, and lifestyle-related factors [smoking behavior, ETS, body mass index (BMI), waist circumference, physical activity, alcohol consumption, low-density lipoprotein (LDL), and high-density lipoprotein (HDL)]. We performed analyses using both adjustment sets.


Chronic residential exposure to particulate matter air pollution and systemic inflammatory markers.

Hoffmann B, Moebus S, Dragano N, Stang A, Möhlenkamp S, Schmermund A, Memmesheimer M, Bröcker-Preuss M, Mann K, Erbel R, Jöckel KH - Environ. Health Perspect. (2009)

Causal diagram for the investigation of the relationship of residential air pollution exposure with inflammatory markers.
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2721876&req=5

f1-ehp-117-1302: Causal diagram for the investigation of the relationship of residential air pollution exposure with inflammatory markers.
Mentions: Although we based our analyses on cross-sectional data that do not contain information about the temporal relations between studied variables, we used causal diagrams [directed acyclic graphs (DAGs)] to identify the minimal sufficient adjustment set. Based on prior biological and epidemiological knowledge, we specified the most likely temporal relations between variables (Figure 1). According to this DAG, short-term PM exposure, SES, and area of residence need to be adjusted for (model 1). Because of the difficulties inherent in adjusting for such a broad construct as SES, which increases the possibility of residual confounding, we additionally identified a sufficient adjustment set (model 2) that does not include SES but includes age, area of residence, and lifestyle-related factors [smoking behavior, ETS, body mass index (BMI), waist circumference, physical activity, alcohol consumption, low-density lipoprotein (LDL), and high-density lipoprotein (HDL)]. We performed analyses using both adjustment sets.

Bottom Line: The induction of a low-grade systemic inflammatory state is a plausible mechanistic pathway.In the adjusted analysis, a cross-sectional exposure difference of 3.91 microg/m(3) in PM(2.5) (interdecile range) was associated with increases in hs-CRP of 23.9% [95% confidence interval (CI), 4.1 to 47.4%] and fibrinogen of 3.9% (95% CI, 0.3 to 7.7%) in men, whereas we found no association in women.This might provide a link between air pollution and coronary atherosclerosis.

View Article: PubMed Central - PubMed

Affiliation: Institute for Medical Informatics, Biometry, and Epidemiology, University of Duisburg-Essen, Essen, Germany. barbara.hoffmann@uk-essen.de

ABSTRACT

Background: Long-term exposure to urban air pollution may accelerate atherogenesis, but mechanisms are still unclear. The induction of a low-grade systemic inflammatory state is a plausible mechanistic pathway.

Objectives: We analyzed the association of residential long-term exposure to particulate matter (PM) and high traffic with systemic inflammatory markers.

Methods: We used baseline data from the German Heinz Nixdorf Recall Study, a population-based, prospective cohort study of 4,814 participants that started in 2000. Fine PM [aerodynamic diameter

Results: In the adjusted analysis, a cross-sectional exposure difference of 3.91 microg/m(3) in PM(2.5) (interdecile range) was associated with increases in hs-CRP of 23.9% [95% confidence interval (CI), 4.1 to 47.4%] and fibrinogen of 3.9% (95% CI, 0.3 to 7.7%) in men, whereas we found no association in women. Chronic traffic exposure was not associated with inflammatory markers. Short-term exposures to air pollutants and temperature did not influence the results markedly.

Conclusions: Our study indicates that long-term residential exposure to high levels of PM(2.5) is associated with systemic inflammatory markers in men. This might provide a link between air pollution and coronary atherosclerosis.

Show MeSH
Related in: MedlinePlus