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Air pollution and inflammation: Findings from concurrent repeated measures of systemic and reproductive tract cytokines during term pregnancy in Mexico City.

ABSTRACT: BACKGROUND:Environmental exposures are associated with a number of outcomes including adverse pregnancy outcomes. Although inflammation is hypothesized to play a role, the mechanistic pathways between environmental exposures and adverse health outcomes, including associations between exposures and longitudinal measures of systemic and reproductive tract inflammation, need elucidation. OBJECTIVES:This study was conducted to evaluate whether exposure to air pollution is associated with immunologic responses in the systemic circulation and lower reproductive tract, and to evaluate whether systemic and reproductive tract immunologic responses are similar. METHODS:We quantified repeated measures of cytokines from cervico-vaginal exudates and serum obtained concurrently among 104 women with term pregnancies and estimated PM10 and CO exposure using the monitor nearest each participant's residence. Serum and cervico-vaginal cytokines were compared using Wilcoxon signed-ranks test and Spearman rank correlations for select gestational months. We used intraclass correlation coefficients (ICCs) to quantify reproducibility of cytokine measurements, and Tobit regression to estimate associations between air pollution and cytokines. RESULTS:Median cervico-vaginal levels of IL-6, Eotaxin, IP-10, MCP-1, MIP-1?, MIP-1?, and TNF? were higher than corresponding serum cytokines, significantly so for IL-6 and IP-10. Cervico-vaginal and serum cytokines were not correlated, but cytokines from the same fluid were correlated. ICCs for most serum cytokines were ?0.40, while ICCs were higher in cervico-vaginal cytokines (range 0.52-0.83). IP-10 and Eotaxin had the highest ICCs for both cytokine sources. In adjusted models, PM10 was positively associated with serum cytokines IL-6, IP-10, MIP-1? and Eotaxin but inversely associated with cervico-vaginal cytokine TNF?, IP-10, MIP-1?, MCP-1 and Eotaxin, controlling for false discovery rate. CO was inversely associated with cervico-vaginal TNF?, IL-6, MIP-1?, MCP-1 and Eotaxin. CONCLUSIONS:Inflammatory processes are compartment-specific. Systemic inflammatory markers may provide information on immunologic processes and response to environmental exposures, but are not proxies for lower reproductive tract inflammation.

SUBMITTER: Buxton MA

PROVIDER: S-EPMC6582973 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature

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Air pollution and inflammation: Findings from concurrent repeated measures of systemic and reproductive tract cytokines during term pregnancy in Mexico City.

Buxton Miatta A MA Meraz-Cruz Noemi N Sanchez Brisa N BN Gronlund Carina J CJ Foxman Betsy B Vadillo-Ortega Felipe F O'Neill Marie S MS

The Science of the total environment 20190505

<h4>Background</h4>Environmental exposures are associated with a number of outcomes including adverse pregnancy outcomes. Although inflammation is hypothesized to play a role, the mechanistic pathways between environmental exposures and adverse health outcomes, including associations between exposures and longitudinal measures of systemic and reproductive tract inflammation, need elucidation.<h4>Objectives</h4>This study was conducted to evaluate whether exposure to air pollution is associated w ...[more]

PMID: 31103661

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Project description:UNLABELLED:Geostatistical interpolation methods to estimate individual exposure to outdoor air pollutants can be used in pregnancy cohorts where personal exposure data are not collected. Our objectives were to a) develop four assessment methods (citywide average (CWA); nearest monitor (NM); inverse distance weighting (IDW); and ordinary Kriging (OK)), and b) compare daily metrics and cross-validations of interpolation models. We obtained 2008 hourly data from Mexico City's outdoor air monitoring network for PM10, PM2.5, O3, CO, NO2, and SO2 and constructed daily exposure metrics for 1,000 simulated individual locations across five populated geographic zones. Descriptive statistics from all methods were calculated for dry and wet seasons, and by zone. We also evaluated IDW and OK methods' ability to predict measured concentrations at monitors using cross validation and a coefficient of variation (COV). All methods were performed using SAS 9.3, except ordinary Kriging which was modeled using R's gstat package. Overall, mean concentrations and standard deviations were similar among the different methods for each pollutant. Correlations between methods were generally high (r=0.77 to 0.99). However, ranges of estimated concentrations determined by NM, IDW, and OK were wider than the ranges for CWA. Root mean square errors for OK were consistently equal to or lower than for the IDW method. OK standard errors varied considerably between pollutants and the computed COVs ranged from 0.46 (least error) for SO2 and PM10 to 3.91 (most error) for PM2.5. OK predicted concentrations measured at the monitors better than IDW and NM. Given the similarity in results for the exposure methods, OK is preferred because this method alone provides predicted standard errors which can be incorporated in statistical models. The daily estimated exposures calculated using these different exposure methods provide flexibility to evaluate multiple windows of exposure during pregnancy, not just trimester or pregnancy-long exposures. IMPLICATIONS:Many studies evaluating associations between outdoor air pollution and adverse pregnancy outcomes rely on outdoor air pollution monitoring data linked to information gathered from large birth registries, and often lack residence location information needed to estimate individual exposure. This study simulated 1,000 residential locations to evaluate four air pollution exposure assessment methods, and describes possible exposure misclassification from using spatial averaging versus geostatistical interpolation models. An implication of this work is that policies to reduce air pollution and exposure among pregnant women based on epidemiologic literature should take into account possible error in estimates of effect when spatial averages alone are evaluated.

Project description:BackgroundTraffic-related air pollution has been associated to a range of adverse health impacts, including decreased heart rate variability (HRV). The association between traffic-related pollution and HRV, however, has varied by traffic-related or HRV marker as well as by study, suggesting the need for a more comprehensive and integrative approach to examining air pollution-mediated biological impacts on these outcomes. In a Bayesian framework, we examined the effect of traffic pollution on HRV using structural equation models (SEMs) and looked at effect modification by participant characteristics.MethodsWe studied measurements of 5 HRV markers [high frequency (HF), low frequency (LF), 5-min standard deviation of normal-to-normal intervals (SDNN), square root of the mean squared differences of successive normal-to-normal intervals (rMSSD), and LF/HF ratio (LF/HF)] for 700 elderly men from the Normative Aging Study. Using SEMs, we fit a latent variable for traffic pollution that is reflected by levels of carbon monoxide, nitrogen monoxide, nitrogen dioxide, and black carbon (BC) to estimate its effect on latent variable for parasympathetic tone that included HF, SDNN and rMSSD, and the sympathetic tone marker, LF/HF. Exposure periods were assessed using 4-, 24-, 48-, 72-hour moving average pre-visit. We compared our main effect findings using SEMs with those obtained using linear mixed models.ResultsTraffic pollution was not associated with mean parasympathetic tone and LF/HF for all examined moving averages. In Bayesian linear mixed models, however, BC was related to increased LF/HF, an inter quartile range (IQR) increase in BC was associated with a 6.5% (95% posterior interval (PI): -0.7%, 14.2%) increase in mean LF/HF 24-hours later. The strongest association observed was for the 4-hour moving average (10.1%; 95% PI: 3.0%, 17.6%). The effect of traffic on parasympathetic tone was stronger among diabetic as compared to non-diabetic participants. Specifically, an IQR increase in traffic pollution in the 48-hr prior to the clinic visit was associated with a 44.3% (95% PI: -67.7%, -4.2%) lower mean parasympathetic tone among diabetics, and a 7.7% (95% PI: -18.0%, 41.4%) higher mean parasympathetic tone among non-diabetics.ConclusionsBC was associated with adverse changes LF/HF in the elderly. Traffic pollution may decrease parasympathetic tone among diabetic elderly.

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Air pollution and inflammation: Findings from concurrent repeated measures of systemic and reproductive tract cytokines during term pregnancy in Mexico City.

Publications

Air pollution and inflammation: Findings from concurrent repeated measures of systemic and reproductive tract cytokines during term pregnancy in Mexico City.

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