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Immune biomarkers link air pollution exposure to blood pressure in adolescents.

ABSTRACT: BACKGROUND:Childhood exposure to air pollution contributes to cardiovascular disease in adulthood. Immune and oxidative stress disturbances might mediate the effects of air pollution on the cardiovascular system, but the underlying mechanisms are poorly understood in adolescents. Therefore, we aimed to identify immune biomarkers linking air pollution exposure and blood pressure levels in adolescents. METHODS:We randomly recruited 100 adolescents (mean age, 16?years) from Fresno, California. Using central-site data, spatial-temporal modeling, and distance weighting exposures to the participant's home, we estimated average pollutant levels [particulate matter (PM), polyaromatic hydrocarbons (PAH), ozone (O3), carbon monoxide (CO) and nitrogen oxides (NOx)]. We collected blood samples and vital signs on health visits. Using proteomic platforms, we quantitated markers of inflammation, oxidative stress, coagulation, and endothelial function. Immune cellular characterization was performed via mass cytometry (CyTOF). We investigated associations between pollutant levels, cytokines, immune cell types, and blood pressure (BP) using partial least squares (PLS) and linear regression, while adjusting for important confounders. RESULTS:Using PLS, biomarkers explaining most of the variance in air pollution exposure included markers of oxidative stress (GDF-15 and myeloperoxidase), acute inflammation (C-reactive protein), hemostasis (ADAMTS, D-dimer) and immune cell types such as monocytes. Most of these biomarkers were independently associated with the air pollution levels in fully adjusted regression models. In CyTOF analyses, monocytes were enriched in participants with the highest versus the lowest PM2.5 exposure. In both PLS and linear regression, diastolic BP was independently associated with PM2.5, NO, NO2, CO and PAH456 pollution levels (P ??0.009). Moreover, monocyte levels were independently related to both air pollution and diastolic BP levels (P ??0.010). In in vitro cell assays, plasma of participants with high PM2.5 exposure induced endothelial dysfunction as evaluated by eNOS and ICAM-1 expression and tube formation. CONCLUSIONS:For the first time in adolescents, we found that ambient air pollution levels were associated with oxidative stress, acute inflammation, altered hemostasis, endothelial dysfunction, monocyte enrichment and diastolic blood pressure. Our findings provide new insights on pollution-related immunological and cardiovascular disturbances and advocate preventative measures of air pollution exposure.

SUBMITTER: Prunicki M

PROVIDER: S-EPMC7566149 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Immune biomarkers link air pollution exposure to blood pressure in adolescents.

Prunicki Mary M Cauwenberghs Nicholas N Ataam Jennifer Arthur JA Movassagh Hesam H Kim Juyong Brian JB Kuznetsova Tatiana T Wu Joseph C JC Maecker Holden H Haddad Francois F Nadeau Kari K

Environmental health : a global access science source 20201016 1

<h4>Background</h4>Childhood exposure to air pollution contributes to cardiovascular disease in adulthood. Immune and oxidative stress disturbances might mediate the effects of air pollution on the cardiovascular system, but the underlying mechanisms are poorly understood in adolescents. Therefore, we aimed to identify immune biomarkers linking air pollution exposure and blood pressure levels in adolescents.<h4>Methods</h4>We randomly recruited 100 adolescents (mean age, 16 years) from Fresno, C ...[more]

PMID: 33066786

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Project description:BackgroundThe association between prenatal household air pollution (HAP) exposure and childhood blood pressure (BP) is unknown.ObjectiveWithin the Ghana Randomized Air Pollution and Health Study (GRAPHS) we examined time-varying associations between a) maternal prenatal and b) first-year-of-life HAP exposure with BP at 4 years of age and, separately, whether a stove intervention delivered prenatally and continued through the first year of life could improve BP at 4 years of age.MethodsGRAPHS was a cluster-randomized cookstove intervention trial wherein n=1,414 pregnant women were randomized to one of two stove interventions: a) a liquefied petroleum gas (LPG) stove or improved biomass stove, or b) control (open fire cooking). Maternal HAP exposure over pregnancy and child HAP exposure over the first year of life was quantified by repeated carbon monoxide (CO) measurements; a subset of women (n=368) also performed one prenatal and one postnatal personal fine particulate matter (PM2.5) measurement. Systolic and diastolic BP (SBP and DBP) were measured in n=667 4-y-old children along with their PM2.5 exposure (n=692). We examined the effect of the intervention on resting BP z-scores. We also employed reverse distributed lag models to examine time-varying associations between a) maternal prenatal and b) first-year-of-life HAP exposure and resting BP z-scores. Among those with PM2.5 measures, we examined associations between PM2.5 and resting BP z-scores. Sex-specific effects were considered.ResultsIntention-to-treat analyses identified that DBP z-score at 4 years of age was lower among children born in the LPG arm (LPG β=-0.20; 95% CI: -0.36, -0.03) as compared with those in the control arm, and females were most susceptible to the intervention. Higher CO exposure in late gestation was associated with higher SBP and DBP z-score at 4 years of age, whereas higher late-first-year-of-life CO exposure was associated with higher DBP z-score. In the subset with PM2.5 measurements, higher maternal postnatal PM2.5 exposure was associated with higher SBP z-scores.DiscussionThese findings suggest that prenatal and first-year-of-life HAP exposure are associated with child BP and support the need for reductions in exposure to HAP, with interventions such as cleaner cooking beginning in pregnancy. https://doi.org/10.1289/EHP13225.

Project description:BACKGROUND: Traffic noise has been associated with prevalence of hypertension, but reports are inconsistent for blood pressure (BP). To ascertain noise effects and to disentangle them from those suspected to be from traffic-related air pollution, it may be essential to estimate people's noise exposure indoors in bedrooms. OBJECTIVES: We analyzed associations between long-term exposure to indoor traffic noise in bedrooms and prevalent hypertension and systolic (SBP) and diastolic (DBP) BP, considering long-term exposure to outdoor nitrogen dioxide (NO2). METHODS: We evaluated 1,926 cohort participants at baseline (years 2003-2006; Girona, Spain). Outdoor annual average levels of nighttime traffic noise (Lnight) and NO2 were estimated at postal addresses with a detailed traffic noise model and a land-use regression model, respectively. Individual indoor traffic Lnight levels were derived from outdoor Lnight with application of insulations provided by reported noise-reducing factors. We assessed associations for hypertension and BP with multi-exposure logistic and linear regression models, respectively. RESULTS: Median levels were 27.1 dB(A) (indoor Lnight), 56.7 dB(A) (outdoor Lnight), and 26.8 ?g/m3 (NO2). Spearman correlations between outdoor and indoor Lnight with NO2 were 0.75 and 0.23, respectively. Indoor Lnight was associated both with hypertension (OR = 1.06; 95% CI: 0.99, 1.13) and SBP (? = 0.72; 95% CI: 0.29, 1.15) per 5 dB(A); and NO2 was associated with hypertension (OR = 1.16; 95% CI: 0.99, 1.36), SBP (? = 1.23; 95% CI: 0.21, 2.25), and DBP (??= 0.56; 95% CI: -0.03, 1.14) per 10 ?g/m3. In the outdoor noise model, Lnight was associated only with hypertension and NO2 with BP only. The indoor noise-SBP association was stronger and statistically significant with a threshold at 30 dB(A). CONCLUSION: Long-term exposure to indoor traffic noise was associated with prevalent hypertension and SBP, independently of NO2. Associations were less consistent for outdoor traffic Lnight and likely affected by collinearity.

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Immune biomarkers link air pollution exposure to blood pressure in adolescents.

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Immune biomarkers link air pollution exposure to blood pressure in adolescents.

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