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Association of Exposure to Ambient Air Pollution With Thyroid Function During Pregnancy.
ABSTRACT: Importance:Air pollutants interact with estrogen nuclear receptors, but their effect on thyroid signaling is less clear. Thyroid function is of particular importance for pregnant women because of the thyroid's role in fetal brain development. Objective:To determine the short-term association of exposure to air pollution in the first trimester with thyroid function throughout pregnancy. Design, Setting, and Participants:In this cohort study, 9931 pregnant women from 4 European cohorts (the Amsterdam Born Children and Their Development Study, the Generation R Study, Infancia y Medio Ambiente, and Rhea) and 1 US cohort (Project Viva) with data on air pollution exposure and thyroid function during pregnancy were included. The recruitment period for the Amsterdam Born Children and Their Development Study was January 2003 to March 2004; for Generation R, April 2002 to January 2006; for Infancia y Medio Ambiente, November 2003 to January 2008; for Rhea, February 2007 to February 2008; and for Project Viva, April 1999 to November 2002. Statistical analyses were conducted from January 2018 to April 2019. Main Outcomes and Measures:Residential air pollution concentrations (ie, nitrogen oxide and particulate matter [PM]) during the first trimester of pregnancy were estimated using land-use regression and satellite-derived aerosol optical depth models. Free thyroxine, thyrotropin, and thyroid peroxidase antibody levels were measured across gestation. Hypothyroxinemia was defined as free thyroxine below the fifth percentile of the cohort distribution with normal thyrotropin levels, following the American Thyroid Association guidelines. Results:Among 9931 participants, the mean (SD) age was 31.2 (4.8) years, 4853 (48.9%) had more than secondary educational levels, 5616 (56.6%) were nulliparous, 404 (4.2%) had hypothyroxinemia, and 506 (6.7%) tested positive for thyroid peroxidase antibodies. Concentrations of nitrogen dioxide and PM with an aerodynamic diameter of 2.5 μm or less (PM2.5) were lower and had less variation in women in the US cohort than those in European cohorts. No associations of nitrogen oxide with thyroid function were found. Higher exposures to PM2.5 were associated with higher odds of hypothyroxinemia in pregnant women (odds ratio per 5-μg/m3 change, 1.21; 95% CI, 1.00-1.47). Although exposure to PM with an aerodynamic diameter of 10 μm or less was not significantly associated with hypothyroxinemia, the coefficient was similar to that for the association of PM2.5 with hypothyroxinemia (odds ratio per 10-μg/m3 change, 1.18; 95% CI, 0.93-1.48). Absorbances of PM2.5 and PM with aerodynamic diameter from 2.5 to 10 μg and were not associated with hypothyroxinemia. There was substantial heterogeneity among cohorts with respect to thyroid peroxidase antibodies (P for heterogeneity, <.001), showing associations of nitrogen oxide and PM with thyroid autoimmunity only in the women in the Generation R Study. Conclusions and Relevance:The findings of this study suggest that first-trimester exposures to PM2.5 were associated with mild thyroid dysfunction throughout pregnancy. The association of PM2.5 exposure with thyroid function during pregnancy is of global health importance because air pollution exposure is widespread and hypothyroxinemia may adversely influence the brain development of offspring.
Project description:Exposure to air pollution particulate matter (PM) and tuberculosis (TB) are two of the leading global public health challenges affecting low and middle income countries. An estimated 4.26 million premature deaths are attributable to household air pollution and an additional 4.1 million to outdoor air pollution annually. Mycobacterium tuberculosis (M.tb) infects a large proportion of the world's population with the risk for TB development increasing during immunosuppressing conditions. There is strong evidence that such immunosuppressive conditions develop during household air pollution exposure, which increases rates of TB development. Exposure to urban air pollution has been shown to alter the outcome of TB therapy. Here we examined whether in vitro exposure to urban air pollution PM alters human immune responses to M.tb. PM2.5 and PM10 (aerodynamic diameters <2.5?m, <10?m) were collected monthly from rainy, cold-dry and warm-dry seasons in Iztapalapa, a highly populated TB-endemic municipality of Mexico City with elevated outdoor air pollution levels. We evaluated the effects of seasonality and size of PM on cytotoxicity and antimycobacterial host immunity in human peripheral blood mononuclear cells (PBMC) from interferon gamma (IFN-?) release assay (IGRA)+ and IGRA- healthy study subjects. PM10 from cold-dry and warm-dry seasons induced the highest cytotoxicity in PBMC. With the exception of PM2.5 from the cold-dry season, pre-exposure to all seasonal PM reduced M.tb phagocytosis by PBMC. Furthermore, M.tb-induced IFN-? production was suppressed in PM2.5 and PM10-pre-exposed PBMC from IGRA+ subjects. This observation coincides with the reduced expression of M.tb-induced T-bet, a transcription factor regulating IFN-? expression in T cells. Pre-exposure to PM10 compared to PM2.5 led to greater loss of M.tb growth control. Exposure to PM2.5 and PM10 collected in different seasons differentially impairs M.tb-induced human host immunity, suggesting biological mechanisms underlying altered M.tb infection and TB treatment outcomes during air pollution exposures.
Project description:Tuberculosis (TB) and air pollution both contribute significantly to the global burden of disease. Epidemiological studies show that exposure to household and urban air pollution increase the risk of new infections with Mycobacterium tuberculosis (M.tb) and the development of TB in persons infected with M.tb and alter treatment outcomes. There is increasing evidence that particulate matter (PM) exposure weakens protective antimycobacterial host immunity. Mechanisms by which exposure to urban PM may adversely affect M.tb-specific human T cell functions have not been studied. We, therefore, explored the effects of urban air pollution PM2.5 (aerodynamic diameters ?2.5µm) on M.tb-specific T cell functions in human peripheral blood mononuclear cells (PBMC). PM2.5 exposure decreased the capacity of PBMC to control the growth of M.tb and the M.tb-induced expression of CD69, an early surface activation marker expressed on CD3+ T cells. PM2.5 exposure also decreased the production of IFN-? in CD3+, TNF-? in CD3+ and CD14+ M.tb-infected PBMC, and the M.tb-induced expression of T-box transcription factor TBX21 (T-bet). In contrast, PM2.5 exposure increased the expression of anti-inflammatory cytokine IL-10 in CD3+ and CD14+ PBMC. Taken together, PM2.5 exposure of PBMC prior to infection with M.tb impairs critical antimycobacterial T cell immune functions.
Project description:Despite the importance of understanding the connection between air pollution exposure and diabetes, studies investigating links between air pollution and glucose metabolism in nondiabetic adults are limited.We aimed to estimate the association of medium-term air pollution exposures with blood glucose and glycated hemoglobin A1c (HbA1c) among nondiabetics.This study included observations from nondiabetic participants (nobs=7,108) of the population-based Heinz Nixdorf Recall study at baseline (2000–2003) and follow-up examination (2006–2008). Daily fine particulate matter (aerodynamic?diameter?2.5??m,?PM2.5; aerodynamic?diameter?10??m,?PM10), accumulation mode particle number (PNAM), and nitrogen dioxide (NO2) exposures were estimated at participants’ residences using the spatiotemporal European Air Pollution Dispersion (EURAD) chemistry transport model. We evaluated the associations between medium-term air pollution exposures (28- and 91-d means) and glucose metabolism measures using mixed linear regression and adjusting for season, meteorology, and personal characteristics. A range of other exposure windows (1-, 2-, 3-, 7-, 14-, 45-, 60-, 75-, 105-, 120-, and 182-d means) were also evaluated to identify potentially relevant biological windows.We observed positive associations between PM2.5 and PNAM exposures and blood glucose levels [e.g., 28-d PM2.5: 0.91 mg/dL (95% CI: 0.38, 1.44) per 5.7??g/m3]. PM2.5, PM10, and PNAM exposures were positively associated with HbA1c [e.g., 91-d PM2.5: 0.07 p.p. (95% CI: 0.04, 0.10) per 4.0??g/m3]. Mean exposures during longer exposure windows (75- to 105-d) were most strongly associated with HbA1c, whereas 7- to 45-d exposures were most strongly associated with blood glucose. NO2 exposure was not associated with blood glucose or with HbA1c.Medium-term PM and PNAM exposures were positively associated with glucose measures in nondiabetic adults. These findings indicate that reducing ambient air pollution levels may decrease the risk of diabetes. https://doi.org/10.1289/EHP2561.
Project description:Small for gestational age (SGA) is defined as intrauterine growth retardation or small sample, referring to the 10th percentile of birth weight lower or two standard deviations less than the average weight at the same gestational age. SGA infants bring great economic and psychological burdens to families and society. The association between exposure to air pollution and SGA in underdeveloped cities with poor air quality remains unclear. Thus, this study is conducted to estimate the effects of maternal exposure to air pollutants on SGA numbers. Birth information was collected from the Huangshi Maternity and Children's Health Hospital from January 1st to December 31st in 2017. Data of pregnancy exposure were accessed using stationary monitors. These data included particulate matter less than or equal to 10 ?m in aerodynamic diameter (PM10), particulate matter less than or equal to 2.5 ?m in aerodynamic diameter (PM2.5), nitrogen dioxide (NO2), and sulfur dioxide (SO2). Multivariate logistic regression models were performed to estimate the association between ambient air pollution and the risk of SGA during different exposure windows. It was found that a 1 ?g/m3 increase in air pollution concentrations during the entire pregnancy was associated with a higher risk of SGA, with an adjusted odds ratio (OR) and 95% confidence interval (CI) of 1.055 (1.035-1.076), 1.084 (1.053-1.116), 1.000 (0.953-1.049), and 1.051 (0.968-1.141) for PM10, PM2.5, NO2, and SO2, respectively. Thus, it is suggested that exposure to air pollution is associated with an increased risk of SGA. The effects of PM10 and PM2.5 were more stable than NO2 and SO2.
Project description:BACKGROUND:Environmental factors may contribute to the development of Kawasaki disease in children, but prenatal environmental exposures are understudied. OBJECTIVE:We used a population-based cohort to investigate whether prenatal exposure to outdoor air pollution is associated with the incidence of Kawasaki disease in childhood. METHODS:We performed a longitudinal cohort study of all children born in Quebec, Canada, between 2006 and 2012. Children were followed for Kawasaki disease from birth until 31 March 2018. We assigned prenatal air pollutant exposure according to the residential postal code at birth. The main exposure was annual average concentration of ambient fine particulate matter [PM ?2.5?m in aerodynamic diameter (PM2.5) and nitrogen dioxide (NO2) from satellite-based estimates and land-use regression models. As secondary exposures, we considered industrial PM2.5, NO2, and sulfur dioxide (SO2) emissions estimated from dispersion models. We estimated hazard ratios (HRs) using Cox proportional hazards models, adjusted for maternal age, parity, sex, multiple birth, maternal smoking during pregnancy, socioeconomic status, birth year, and rural residence. We considered single and multipollutant models. We performed several sensitivity analyses, including assessing modifying effects of maternal comorbidities (e.g., diabetes, preeclampsia). RESULTS:The cohort comprised 505,336 children, including 539 with Kawasaki disease. HRs for each interquartile range increase in ambient air pollution were 1.16 (95% CI: 0.96, 1.39) for PM2.5 and 1.12 (95% CI: 0.96, 1.31) for NO2. For industrial air pollution, HRs were 1.07 (95% CI: 1.01, 1.13) for SO2, 1.09 (95% CI: 0.99, 1.20) for NO2, and 1.01 (95% CI: 0.97, 1.05) for PM2.5. In multipollutant models, associations for ambient PM2.5 and NO2 (i.e., from all sources) were robust to adjustment for industrial pollution, and vice versa. DISCUSSION:In this population-based cohort study, both prenatal exposure to ambient and industrial air pollution were associated with the incidence of Kawasaki disease in childhood. Further studies are needed to consolidate the observed associations. https://doi.org/10.1289/EHP6920.
Project description:Importance:Thyroid hormones are critical for fetal growth and development. Prenatal particulate matter (PM) air pollution exposure has been associated with altered newborn thyroid function, but other air pollutants have not been evaluated, and critical windows of exposure are unknown. Objectives:To investigate the association of prenatal exposure to ambient and traffic-related air pollutants with newborn thyroid function and identify critical windows of exposure. Design, Setting, and Participants:This cohort study used data from 2050 participants in the Children's Health Study. Statistical analyses were conducted from 2017 to 2018 using pregnancy and birth data from 1994 to 1997 for a subset of participants recruited from schools in 13 southern California communities in 2002 to 2003 when participants were 5 to 7 years of age. Participants were included in statistical analyses if they could be linked to their newborn blood spot and had complete monthly exposure measures for at least 1 air pollutant across pregnancy. Exposures:Prenatal monthly averages of ambient (PM diameter <2.5 ?m [PM2.5] or <10 ?m [PM10], nitrogen dioxide, and ozone) and traffic-related (freeway, nonfreeway, and total nitrogen oxides) air pollutant exposures were determined using inverse distance-squared weighting of central monitoring data and the California Line Source Dispersion model, respectively. Main Outcomes and Measures:Newborn heel-stick blood spot total thyroxine (TT4) measures were acquired retrospectively from the California Department of Public Health. Results:Participants included 2050 newborns (50.5% male), with a median (interquartile range) age of 20 (15-29) hours. The majority of newborns were Hispanic white (1202 [58.6%]) or non-Hispanic white (638 [31.1%]). Sixty-six (3.2%) were black and 144 (7.0%) were from other racial/ethnic groups. The mean (SD) newborn TT4 measure was 16.2 (4.3) ?g/dL. A 2-SD increase in prenatal PM2.5 (16.3 ?g/m3) and PM10 (22.2 ?g/m3) was associated with a 1.2-?g/dL (95% CI, 0.5-1.8 ?g/dL) and 1.5-?g/dL (95% CI, 0.9-2.1 ?g/dL) higher TT4 measure, respectively, in covariate-adjusted linear regression models. Other pollutants were not consistently associated with newborn TT4. Distributed lag models revealed that PM2.5 exposure during months 3 to 7 of pregnancy and PM10 exposure during months 1 to 8 of pregnancy were associated with significantly higher newborn TT4 concentrations (P?<?.05). Conclusions and Relevance:Prenatal PM exposure, particularly in early pregnancy and midpregnancy, is associated with higher newborn TT4 concentrations. Future studies should assess the health implications of PM-associated differences in newborn TT4 concentrations.
Project description:Particulate matter mass (PM), trace gaseous pollutants, and select volatile organic compounds (VOCs) with meteorological variables were measured in Logan, Utah (Cache Valley), for >4 weeks during winter 2017 as part of the Utah Winter Fine Particle Study (UWFPS). Higher PM levels for short time periods and lower ozone (O3) levels were present due to meteorological and mountain valley conditions. Nitrogenous pollutants were relatively strongly correlated with PM variables. Diurnal cycles of NOx, O3, and fine PM(PM 2.5) (aerodynamic diameter <2.5 ?m [PM2.5]) suggested formation from NOx. O3 levels increased from early morning into midafternoon, and NOx and PM2.5 increased throughout the morning, followed by sharp decreases. Toluene/benzene and xylenes/benzene ratios and VOC correlations with nitrogenous and PM species were indicative of local traffic sources. Wind sector comparisons suggested that pollutant levels were lower when winds were from nearby mountains to the east versus winds from northerly or southerly origins. Implications: The Cache Valley in Idaho and Utah has been designated a PM2.5 nonattainment area that has been attributed to air pollution buildup during winter stagnation events. To inform state implementation plans for PM2.5 in Cache Valley and other PM2.5 nonattainment areas in Utah, a state and multiagency federal research effort known as the UWFPS was conducted in winter 2017. As part of the UWFPS, the U.S. Environmental Protection Agency (EPA) measured ground-based PM species and their precursors, VOCs, and meteorology in Logan, Utah. Results reported here from the EPA study in Logan provide additional understanding of wintertime air pollution conditions and possible sources of PM and gaseous pollutants as well as being useful for future PM control strategies in this area.
Project description:Limited information is available regarding long-term effects of air pollution on blood pressure (BP) and hypertension.We studied whether 1-year exposures to particulate matter (PM) and nitrogen oxides (NOx) were correlated with BP and hypertension in the elderly.We analyzed cross-sectional data from 27,752 Taipei City residents > 65 years of age who participated in a health examination program in 2009. Land-use regression models were used to estimate participants' 1-year exposures to particulate matter with aerodynamic diameter ? 10 ?m (PM10), coarse particles (PM2.5-10), fine particles (? 2.5 ?m; PM2.5), PM2.5 absorbance, NOx, and nitrogen dioxide (NO2). Generalized linear regressions and logistic regressions were used to examine the association between air pollution and BP and hypertension, respectively.Diastolic BP was associated with 1-year exposures to air pollution, with estimates of 0.73 [95% confidence interval (CI): 0.44, 1.03], 0.46 (95% CI: 0.30, 0.63), 0.62 (95% CI: 0.24, 0.99), 0.34 (95% CI: 0.19, 0.50), and 0.65 (95% CI: 0.44, 0.85) mmHg for PM10 (10 ?g/m3), PM2.5-10 (5 ?g/m3), PM2.5 absorbance (10-5/m), NOx (20 ?g/m3), and NO2 (10 ?g/m3), respectively. PM2.5 was not associated with diastolic BP, and none of the air pollutants was associated with systolic BP. Associations of diastolic BP with PM10 and PM2.5 absorbance were stronger among participants with hypertension, diabetes, or a body mass index ? 25 kg/m2 than among participants without these conditions. One-year air pollution exposures were not associated with hypertension.One-year exposures to PM10, PM2.5-10, PM2.5 absorbance, and NOx were associated with higher diastolic BP in elderly residents of Taipei.
Project description:Long-term exposure to particulate matter (PM) air pollution may increase blood pressure and the risk of hypertension. However, epidemiological evidence is scarce and inconsistent.We investigated the associations between long-term exposure to PM with an aerodynamic diameter <2.5?m (PM2.5), blood pressure, and incident hypertension in a large Taiwanese cohort.We studied 361,560 adults ?18y old from a large cohort who participated in a standard medical examination program during 2001 to 2014. Among this group, 125,913 nonhypertensive participants were followed up. A satellite-based spatiotemporal model was used to estimate the 2-y average PM2.5 concentrations at each participant's address. Multivariable linear regression was used in the cross-sectional data analysis with the 361,560 participants to investigate the associations between PM2.5 and systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse pressure (PP), and Cox proportional hazard regression was used in the cohort data analysis with the 125,913 participants to investigate the associations between PM2.5 and incident hypertension.Each 10-?g/m3 increment in the 2-y average PM2.5 concentration was associated with increases of 0.45?mmHg [95% confidence interval (CI): 0.40, 0.50], 0.07?mmHg (95% CI: 0.04, 0.11), and 0.38?mmHg (95% CI: 0.33, 0.42) in SBP, DBP, and PP, respectively, after adjusting for a wide range of covariates and possible confounders. Each 10-?g/m3 increment in the 2-y average PM2.5 concentration was associated with an increase of 3% in the risk of developing hypertension [hazard?ratio=1.03 (95% CI: 1.01, 1.05)]. Stratified and sensitivity analyses yielded similar results.Long-term exposure to PM2.5 air pollution is associated with higher blood pressure and an increased risk of hypertension. These findings reinforce the importance of air pollution mitigation strategies to reduce the risk of cardiovascular disease. https://doi.org/10.1289/EHP2466.
Project description:Importance:Telomere length is a marker of biological aging that may provide a cellular memory of exposures to oxidative stress and inflammation. Telomere length at birth has been related to life expectancy. An association between prenatal air pollution exposure and telomere length at birth could provide new insights in the environmental influence on molecular longevity. Objective:To assess the association of prenatal exposure to particulate matter (PM) with newborn telomere length as reflected by cord blood and placental telomere length. Design, Setting, and Participants:In a prospective birth cohort (ENVIRONAGE [Environmental Influence on Ageing in Early Life]), a total of 730 mother-newborn pairs were recruited in Flanders, Belgium between February 2010 and December 2014, all with a singleton full-term birth (?37 weeks of gestation). For statistical analysis, participants with full data on both cord blood and placental telomere lengths were included, resulting in a final study sample size of 641. Exposures:Maternal residential PM2.5 (particles with an aerodynamic diameter ?2.5 ?m) exposure during pregnancy. Main Outcomes and Measures:In the newborns, cord blood and placental tissue relative telomere length were measured. Maternal residential PM2.5 exposure during pregnancy was estimated using a high-resolution spatial-temporal interpolation method. In distributed lag models, both cord blood and placental telomere length were associated with average weekly exposures to PM2.5 during pregnancy, allowing the identification of critical sensitive exposure windows. Results:In 641 newborns, cord blood and placental telomere length were significantly and inversely associated with PM2.5 exposure during midgestation (weeks 12-25 for cord blood and weeks 15-27 for placenta). A 5-µg/m3 increment in PM2.5 exposure during the entire pregnancy was associated with 8.8% (95% CI, -14.1% to -3.1%) shorter cord blood leukocyte telomeres and 13.2% (95% CI, -19.3% to -6.7%) shorter placental telomere length. These associations were controlled for date of delivery, gestational age, maternal body mass index, maternal age, paternal age, newborn sex, newborn ethnicity, season of delivery, parity, maternal smoking status, maternal educational level, pregnancy complications, and ambient temperature. Conclusions and Relevance:Mothers who were exposed to higher levels of PM2.5 gave birth to newborns with shorter telomere length. The observed telomere loss in newborns by prenatal air pollution exposure indicates less buffer for postnatal influences of factors decreasing telomere length during life. Therefore, improvements in air quality may promote molecular longevity from birth onward.