Association between gaseous air pollutants and inflammatory, hemostatic and lipid markers in a cohort of midlife women

Xiangmei (May) Wu, Rupa Basu, Brian Malig, Rachel Broadwin, Keita Ebisu, Ellen B. Gold, Lihong Qi, Carol A. Derby, Rochelle S. Green

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Background Exposures to ambient gaseous pollutants have been linked to cardiovascular diseases (CVDs), but the biological mechanisms remain uncertain. Objectives This study examined the changes in CVD marker levels resulting from elevated exposure to ambient gaseous pollutants in midlife women. Methods Annual repeated measurements of several inflammatory, hemostatic and lipid makers were obtained from 2306 midlife women enrolled in the longitudinal Study of Women's Health Across the Nation (SWAN) between 1999 and 2004. Ambient carbon monoxide (CO), nitrogen dioxide (NO2), and sulfur dioxide (SO2) data were assigned to each woman based on proximity of the monitoring station to her residential address. Short- and long-term exposures were calculated, and their associations with markers were examined using linear mixed-effects regression models, adjusted for demographic, health and other factors. Results Short-term CO exposure was associated with increased fibrinogen, i.e., every interquartile increase of average prior one-week exposure to CO was associated with 1.3% (95% CI: 0.6%, 2.0%) increase in fibrinogen. Long-term exposures to NO2 and SO2 were associated with reduced high-density lipoproteins and apolipoprotein A1, e.g., 4.0% (1.7%, 6.3%) and 4.7% (2.8%, 6.6%) decrease per interquartile increment in prior one-year average NO2 concentration, respectively. Fine particle (PM2.5) exposure confounded associations between CO/NO2 and inflammatory/hemostatic markers, while associations with lipoproteins were generally robust to PM2.5 adjustment. Conclusions Exposures to these gas pollutants at current ambient levels may increase thrombotic potential and disrupt cholesterol metabolism, contributing to greater risk of CVDs in midlife women. Caution should be exercised in evaluating the confounding by PM2.5 exposure.

Original languageEnglish (US)
Pages (from-to)131-139
Number of pages9
JournalEnvironment International
Volume107
DOIs
StatePublished - Oct 1 2017

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lipid
carbon monoxide
cardiovascular disease
pollutant
womens health
woman
gaseous air pollutant
marker
exposure
nitrogen dioxide
sulfur dioxide
metabolism
gas

Keywords

  • Carbon monoxide
  • Cardiovascular
  • Coagulation
  • Fibrinolysis
  • Lipoprotein
  • Nitrogen dioxide
  • Sulfur dioxide

ASJC Scopus subject areas

  • Environmental Science(all)

Cite this

Association between gaseous air pollutants and inflammatory, hemostatic and lipid markers in a cohort of midlife women. / Wu, Xiangmei (May); Basu, Rupa; Malig, Brian; Broadwin, Rachel; Ebisu, Keita; Gold, Ellen B.; Qi, Lihong; Derby, Carol A.; Green, Rochelle S.

In: Environment International, Vol. 107, 01.10.2017, p. 131-139.

Research output: Contribution to journalArticle

Wu, Xiangmei (May) ; Basu, Rupa ; Malig, Brian ; Broadwin, Rachel ; Ebisu, Keita ; Gold, Ellen B. ; Qi, Lihong ; Derby, Carol A. ; Green, Rochelle S. / Association between gaseous air pollutants and inflammatory, hemostatic and lipid markers in a cohort of midlife women. In: Environment International. 2017 ; Vol. 107. pp. 131-139.
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abstract = "Background Exposures to ambient gaseous pollutants have been linked to cardiovascular diseases (CVDs), but the biological mechanisms remain uncertain. Objectives This study examined the changes in CVD marker levels resulting from elevated exposure to ambient gaseous pollutants in midlife women. Methods Annual repeated measurements of several inflammatory, hemostatic and lipid makers were obtained from 2306 midlife women enrolled in the longitudinal Study of Women's Health Across the Nation (SWAN) between 1999 and 2004. Ambient carbon monoxide (CO), nitrogen dioxide (NO2), and sulfur dioxide (SO2) data were assigned to each woman based on proximity of the monitoring station to her residential address. Short- and long-term exposures were calculated, and their associations with markers were examined using linear mixed-effects regression models, adjusted for demographic, health and other factors. Results Short-term CO exposure was associated with increased fibrinogen, i.e., every interquartile increase of average prior one-week exposure to CO was associated with 1.3{\%} (95{\%} CI: 0.6{\%}, 2.0{\%}) increase in fibrinogen. Long-term exposures to NO2 and SO2 were associated with reduced high-density lipoproteins and apolipoprotein A1, e.g., 4.0{\%} (1.7{\%}, 6.3{\%}) and 4.7{\%} (2.8{\%}, 6.6{\%}) decrease per interquartile increment in prior one-year average NO2 concentration, respectively. Fine particle (PM2.5) exposure confounded associations between CO/NO2 and inflammatory/hemostatic markers, while associations with lipoproteins were generally robust to PM2.5 adjustment. Conclusions Exposures to these gas pollutants at current ambient levels may increase thrombotic potential and disrupt cholesterol metabolism, contributing to greater risk of CVDs in midlife women. Caution should be exercised in evaluating the confounding by PM2.5 exposure.",
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T1 - Association between gaseous air pollutants and inflammatory, hemostatic and lipid markers in a cohort of midlife women

AU - Wu, Xiangmei (May)

AU - Basu, Rupa

AU - Malig, Brian

AU - Broadwin, Rachel

AU - Ebisu, Keita

AU - Gold, Ellen B.

AU - Qi, Lihong

AU - Derby, Carol A.

AU - Green, Rochelle S.

PY - 2017/10/1

Y1 - 2017/10/1

N2 - Background Exposures to ambient gaseous pollutants have been linked to cardiovascular diseases (CVDs), but the biological mechanisms remain uncertain. Objectives This study examined the changes in CVD marker levels resulting from elevated exposure to ambient gaseous pollutants in midlife women. Methods Annual repeated measurements of several inflammatory, hemostatic and lipid makers were obtained from 2306 midlife women enrolled in the longitudinal Study of Women's Health Across the Nation (SWAN) between 1999 and 2004. Ambient carbon monoxide (CO), nitrogen dioxide (NO2), and sulfur dioxide (SO2) data were assigned to each woman based on proximity of the monitoring station to her residential address. Short- and long-term exposures were calculated, and their associations with markers were examined using linear mixed-effects regression models, adjusted for demographic, health and other factors. Results Short-term CO exposure was associated with increased fibrinogen, i.e., every interquartile increase of average prior one-week exposure to CO was associated with 1.3% (95% CI: 0.6%, 2.0%) increase in fibrinogen. Long-term exposures to NO2 and SO2 were associated with reduced high-density lipoproteins and apolipoprotein A1, e.g., 4.0% (1.7%, 6.3%) and 4.7% (2.8%, 6.6%) decrease per interquartile increment in prior one-year average NO2 concentration, respectively. Fine particle (PM2.5) exposure confounded associations between CO/NO2 and inflammatory/hemostatic markers, while associations with lipoproteins were generally robust to PM2.5 adjustment. Conclusions Exposures to these gas pollutants at current ambient levels may increase thrombotic potential and disrupt cholesterol metabolism, contributing to greater risk of CVDs in midlife women. Caution should be exercised in evaluating the confounding by PM2.5 exposure.

AB - Background Exposures to ambient gaseous pollutants have been linked to cardiovascular diseases (CVDs), but the biological mechanisms remain uncertain. Objectives This study examined the changes in CVD marker levels resulting from elevated exposure to ambient gaseous pollutants in midlife women. Methods Annual repeated measurements of several inflammatory, hemostatic and lipid makers were obtained from 2306 midlife women enrolled in the longitudinal Study of Women's Health Across the Nation (SWAN) between 1999 and 2004. Ambient carbon monoxide (CO), nitrogen dioxide (NO2), and sulfur dioxide (SO2) data were assigned to each woman based on proximity of the monitoring station to her residential address. Short- and long-term exposures were calculated, and their associations with markers were examined using linear mixed-effects regression models, adjusted for demographic, health and other factors. Results Short-term CO exposure was associated with increased fibrinogen, i.e., every interquartile increase of average prior one-week exposure to CO was associated with 1.3% (95% CI: 0.6%, 2.0%) increase in fibrinogen. Long-term exposures to NO2 and SO2 were associated with reduced high-density lipoproteins and apolipoprotein A1, e.g., 4.0% (1.7%, 6.3%) and 4.7% (2.8%, 6.6%) decrease per interquartile increment in prior one-year average NO2 concentration, respectively. Fine particle (PM2.5) exposure confounded associations between CO/NO2 and inflammatory/hemostatic markers, while associations with lipoproteins were generally robust to PM2.5 adjustment. Conclusions Exposures to these gas pollutants at current ambient levels may increase thrombotic potential and disrupt cholesterol metabolism, contributing to greater risk of CVDs in midlife women. Caution should be exercised in evaluating the confounding by PM2.5 exposure.

KW - Carbon monoxide

KW - Cardiovascular

KW - Coagulation

KW - Fibrinolysis

KW - Lipoprotein

KW - Nitrogen dioxide

KW - Sulfur dioxide

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