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Several epidemiological studies have demonstrated that particulate matter (PM) in air pollution can be involved in the genesis or aggravation of different cardiovascular, respiratory, perinatal, and cancer diseases. This study assessed the in vitro effects of PM10 on the secretion of cytokines by a human monocytic cell line (THP-1). We compared the chemotactic, pro-inflammatory, and anti-inflammatory cytokines induced by PM10 collected for two years during three different seasons in five different Mexico City locations. MIP-1α, IP-10, MCP-1, TNF-α, and VEGF were the main secretion products after stimulation with 80 µg/mL of PM10 for 24 h. The THP-1 cells showed a differential response to PM10 obtained in the different sites of Mexico City. The PM10 from the north and the central city areas induced a higher pro-inflammatory cytokine response than those from the south. Seasonal pro-inflammatory cytokine secretion always exceeded anti-inflammatory secretion. The rainy-season-derived particles caused the lowest pro-inflammatory effects. We concluded that toxicological assessment of airborne particles provides evidence supporting their potential role in the chronic exacerbation of local or systemic inflammatory responses that may worsen the evolution of some chronic diseases.
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OBJECTIVE: To evaluate whether sleep duration, timing, and variability were associated with inflammatory cytokines in a cohort of Mexico City adolescents. METHODS: The analytic sample comprised >500 adolescents who were part of an ongoing longitudinal study in Mexico City. At two time points during mid-to-late puberty (average age 14, n = 391) and late-to-post puberty (average age 16, n = 345), adolescents completed a follow-up visit that included 7-day wrist actigraphy and clinical assessment of plasma inflammatory cytokines (high-sensitivity C-reactive protein, Interleukin 1ß, Interleukin 6, and Tumor Necrosis Factor É). Sleep characteristics included weekday and weekend sleep duration and midpoint (median of bed and wake time), as well as sleep variability (SD of sleep duration across 7 days) and social jetlag (midpoint difference from weekdays to weekends). At each time point, multivariable linear regression models were run with log inflammatory levels as the outcome and categories of sleep characteristics as predictors, while adjusting for potential confounders (specific to each model). Analyses were run unstratified and sex-stratified. RESULTS: In the mid-to-late pubertal visit, weekday sleep duration was inversely associated with natural log hs-CRP after adjustment (Q4 vs Q1: ß = -0.41, 95% Confidence Interval (CI) -0.81 to -0.01) and later sleep midpoint was positively associated with log hs-CRP (Q4 vs Q1: ß = 0.55, 95% CI 0.13 to 0.97). Sleep duration variability was associated with higher IL-1ß among boys, while in girls social jetlag was associated with higher IL-1ß and weekend sleep duration was inversely associated with IL-6. At the late-to-post pubertal visit, there were few associations except for a positive association between weekday sleep duration and hs-CRP among boys (ß = 0.60, 95% CI 0.04 to 1.16) and a non-linear positive association between social jetlag and hs-CRP among girls (ß = 0.80, 95% CI 0.22 to 1.37 comparing 2 to 3 h of social jetlag vs <1 h). CONCLUSION: Later timing, shorter duration, and inconsistency of sleep were related to higher levels of inflammatory biomarkers, but associations were more evident at the mid-to-late pubertal visit than the late-to-post pubertal visit.
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Proteína C-Reativa , Citocinas , Masculino , Feminino , Adolescente , Humanos , Estudos Longitudinais , México , Sono , Síndrome do Jet LagRESUMO
BACKGROUND: Particulate matter ≤10 µm in aerodynamic diameter (PM10) and diet quality are risk factors for systemic inflammation, which is associated with preterm birth (PTB). PM10 and a pro-inflammatory diet (assessed by the Dietary Inflammatory Index [DII®]) have been individually evaluated as causes of PTB and differences by offspring sex have been reported for the DII. However, additional studies are needed to evaluate joint effects of these associations to inform intervention efforts. OBJECTIVES: To evaluate the independent and joint effects of PM10 and energy-adjusted DII (E-DII) on PTB risks. METHODS: PM10 estimates were generated from daily citywide averages for 1216 pregnant women from three subcohorts of the Early Life Exposures in Mexico to Environmental Toxicants study using data from the Mexico City Outdoor Air Monitoring Network. Among a subset of participants (N = 620), E-DII scores were calculated using a validated food frequency questionnaire. Cox Proportional Hazards models were run for select periods during pregnancy and entire pregnancy averages for E-DII and PM10. We assessed for potential non-linear associations using natural splines. RESULTS: In adjusted models, PM10 exposure was associated with increased risks of PTB for a range of values (58-72 µg/m3) during the second trimester, while negative associations were seen during the second (≥74 µg/m3) and third trimesters (55-65 µg/m3). Analyses conducted using distributed lag models for periods closer to delivery (max lag = 90) did not show negative associations between PM10 exposure and preterm birth, and indeed positive significant associations were observed (estimates and figures). E-DII was not associated with PTB and there was no evidence of effect modification by infant sex. There was no evidence of interaction between PM10 and E-DII and the risk of preterm birth. DISCUSSION: Associations between PM10 and PTB in Mexico City varied over time and across levels of PM10. Our findings of negative associations in the second and third trimesters, which are contrary to the hypothesized relationship between PM10 and PTB, may be due to a number of factors, including live birth bias and the exposure period evaluated. Differences in results for the periods evaluated suggest that PM10 from shorter exposure windows may play a more proximal role in initiating preterm labor.
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Poluentes Atmosféricos , Poluição do Ar , Nascimento Prematuro , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Dieta/efeitos adversos , Exposição Dietética , Feminino , Humanos , Lactente , Recém-Nascido , Exposição Materna/efeitos adversos , México/epidemiologia , Material Particulado/análise , Material Particulado/toxicidade , Gravidez , Nascimento Prematuro/induzido quimicamente , Nascimento Prematuro/epidemiologiaRESUMO
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-1α, MIP-1ß, and TNFα 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-1ß and Eotaxin but inversely associated with cervico-vaginal cytokine TNFα, IP-10, MIP-1ß, MCP-1 and Eotaxin, controlling for false discovery rate. CO was inversely associated with cervico-vaginal TNFα, IL-6, MIP-1ß, 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.
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Poluição do Ar/estatística & dados numéricos , Citocinas/metabolismo , Monitoramento Ambiental , Exposição Materna/estatística & dados numéricos , Adulto , Biomarcadores/metabolismo , Exposição Ambiental , Feminino , Humanos , Inflamação , México , Gravidez , Adulto JovemRESUMO
Preterm birth is a public health issue of global significance, which may result in mortality during the perinatal period or may lead to major health and financial consequences due to lifelong impacts. Even though several risk factors for preterm birth have been identified, prevention efforts have failed to halt the increasing rates of preterm birth. Epidemiological studies have identified air pollution as an emerging potential risk factor for preterm birth. However, many studies were limited by study design and inadequate exposure assessment. Due to the ubiquitous nature of ambient air pollution and the potential public health significance of any role in causing preterm birth, a novel focus investigating possible causal mechanisms influenced by air pollution is therefore a global health priority. We hypothesize that air pollution may act together with other biological factors to induce systemic inflammation and influence the duration of pregnancy. Evaluation and testing of this hypothesis is currently being conducted in a prospective cohort study in Mexico City and will provide an understanding of the pathways that mediate the effects of air pollution on preterm birth. The important public health implication is that crucial steps in this mechanistic pathway can potentially be acted on early in pregnancy to reduce the risk of preterm birth.
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Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Exposição Materna/efeitos adversos , Complicações na Gravidez/diagnóstico , Citocinas/metabolismo , Dieta , Feminino , Humanos , Inflamação/complicações , México , Modelos Teóricos , Obesidade/complicações , Trabalho de Parto Prematuro/etiologia , Estresse Oxidativo , Material Particulado , Gravidez , Nascimento Prematuro , Fatores de RiscoRESUMO
Preterm birth is one of the leading causes of perinatal mortality and is associated with long-term adverse health consequences for surviving infants. Preterm birth rates are rising worldwide, and no effective means for prevention currently exists. Air pollution exposure may be a significant cause of prematurity, but many published studies lack the individual, clinical data needed to elucidate possible biological mechanisms mediating these epidemiological associations. This paper presents the design of a prospective study now underway to evaluate those mechanisms in a cohort of pregnant women residing in Mexico City. We address how air quality may act together with other factors to induce systemic inflammation and influence the duration of pregnancy. Data collection includes: biomarkers relevant to inflammation in cervico-vaginal exudate and peripheral blood, along with full clinical information, pro-inflammatory cytokine gene polymorphisms and air pollution data to evaluate spatial and temporal variability in air pollution exposure. Samples are collected on a monthly basis and participants are followed for the duration of pregnancy. The data will be used to evaluate whether ambient air pollution is associated with preterm birth, controlling for other risk factors. We will evaluate which time windows during pregnancy are most influential in the air pollution and preterm birth association. In addition, the epidemiological study will be complemented with a parallel toxicology invitro study, in which monocytic cells will be exposed to air particle samples to evaluate the expression of biomarkers of inflammation.