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

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 2,306 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.

Association between coarse particulate matter and inflammatory and hemostatic markers in a cohort of midlife women

“…Our previous studies have found that one-year exposures to PM 2.5 , NO 2 , and CO were positively associated with PAI-1 [ 18 , 19 ]. In two-pollutant models along with PM 10–2.5 , PM 2.5 , CO, and NO 2 were each still positively associated with PAI-1 levels, and the associations were stronger for PM 2.5 , CO, and NO 2 than PM 10–2.5 .…”

“…Site was included as a fixed effect because participants were nested within each site. First-order ante-dependence structure was specified for repeated measurements from each participant [ 19 ].…”

“…With longitudinal biomonitoring across years, this study offers a unique opportunity to study CVD risks associated with long-term PM 10–2.5 exposure. With previous work having shown associations between CVD markers and exposures to ambient PM 2.5 and gaseous pollutants [ 18 , 19 ], further research with respect to PM 10–2.5 exposure and CVD markers in the SWAN cohort would advance the understanding of whether PM 10–2.5 are associated with inflammation and coagulation. Moreover, with the ability to assess other air pollutants, this study could further evaluate confounding by co-pollutants and improve the understanding of the potential independent impact of PM 10–2.5 exposure on CVD.…”

Effects of ambient carbon monoxide on daily hospitalizations for cardiovascular disease: a time-stratified case-crossover study of 460,938 cases in Beijing, China from 2013 to 2017

“…However, the concentration of ambient CO is considered too low to induce the toxic effects of CO [ 51 ]. Several plausible biological mechanisms underlying the association between low concentrations of ambient CO with CVD have been proposed, including cardiac dysfunction [ 52 , 53 ], systemic inflammation [ 54 , 55 ], oxidative stress [ 56 , 57 ], and thrombotic reaction [ 55 ]. Both animal models and population-based cohort studies have demonstrated the cardiotoxicity of CO [ 48 , 52 , 53 ].…”

“…A recent longitudinal study confirmed that high-sensitivity C-reactive protein increased with short-term exposure to CO among 61 patients with cardiovascular disease [ 55 ]. Fibrinogen and D-dimer significantly also increased with ambient CO exposure, and these biomarkers are related to thrombotic reactions [ 54 , 55 ]. Overall, the scientific evidence supports that ambient CO exposure is associated with cardiovascular risk.…”