Maternal exposure to PM2.5 may increase the risk of congenital hypothyroidism in the offspring: a national database based study in China.
ABSTRACT: BACKGROUND:Maternal exposure to air pollution is related to fetal dysplasia. However, the association between maternal exposure to air pollution and the risk of congenital hypothyroidism (CH) in the offspring is largely unknown. METHODS:We conducted a national database based study in China to explore the association between these two parameters. The incidence of CH was collected from October 1, 2014 to October 1, 2015 from the Chinese Maternal and Child Health Surveillance Network. Considering that total period of pregnancy and consequently the total period of particle exposure is approximately 10?months, average exposure levels of PM2.5, PM10 and Air Quality Index (AQI) were collected from January 1, 2014 to January 1, 2015. Generalized additive model was used to evaluate the association between air pollution and the incidence of CH, and constructing receiver operating characteristic (ROC) curve was used to calculate the cut-off value. RESULTS:The overall incidence of CH was 4.31 per 10,000 screened newborns in China from October 1, 2014 to October 1, 2015. For every increase of 1??g/m3 in the PM2.5 exposure during gestation could increase the risk of CH (adjusted OR?=?1.016 per 1??g/m3 change, 95% CI, 1.001-1.031). But no significant associations were found with regard to PM10 (adjusted OR?=?1.009, 95% CI, 0.996-1.018) or AQI (adjusted OR?=?1.012, 95% CI,0.998-1.026) and the risk of CH in the offspring. The cut-off value of prenatal PM2.5 exposure for predicting the risk of CH in the offspring was 61.165??g/m3. CONCLUSIONS:The present study suggested that maternal exposure to PM2.5 may exhibit a positive association with increased risk of CH in the offspring. We also proposed a cut-off value of PM2.5 exposure that might determine reduction in the risk of CH in the offspring in highly polluted areas.
Project description:We investigated if greenness and air pollution exposure in parents' childhood affect offspring asthma and hay fever, and if effects were mediated through parental asthma, pregnancy greenness/pollution exposure, and offspring exposure. We analysed 1106 parents with 1949 offspring (mean age 35 and 6) from the Respiratory Health in Northern Europe, Spain and Australia (RHINESSA) generation study. Mean particulate matter (PM2.5 and PM10), nitrogen dioxide (NO2), black carbon (BC), ozone (O3) (µg/m3) and greenness (normalized difference vegetation index (NDVI)) were calculated for parents 0-18 years old and offspring 0-10 years old, and were categorised in tertiles. We performed logistic regression and mediation analyses for two-pollutant models (clustered by family and centre, stratified by parental lines, and adjusted for grandparental asthma and education). Maternal medium PM2.5 and PM10 exposure was associated with higher offspring asthma risk (odds ratio (OR) 2.23, 95%CI 1.32-3.78, OR 2.27, 95%CI 1.36-3.80), and paternal high BC exposure with lower asthma risk (OR 0.31, 95%CI 0.11-0.87). Hay fever risk increased for offspring of fathers with medium O3 exposure (OR 4.15, 95%CI 1.28-13.50) and mothers with high PM10 exposure (OR 2.66, 95%CI 1.19-5.91). The effect of maternal PM10 exposure on offspring asthma was direct, while for hay fever, it was mediated through exposures in pregnancy and offspring's own exposures. Paternal O3 exposure had a direct effect on offspring hay fever. To conclude, parental exposure to air pollution appears to influence the risk of asthma and allergies in future offspring.
Project description:The associations between ambient air pollutants and tuberculosis seasonality are unclear. We assessed the temporal cross-correlations between ambient air pollutants and tuberculosis seasonality. Monthly tuberculosis incidence data and ambient air pollutants (PM2.5, PM10, carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), sulfur dioxide (SO2)) and air quality index (AQI) from 2013 to 2017 in Shanghai were included. A cross-correlogram and generalized additive model were used. A 4-month delayed effect of PM2.5 (0.55), PM10 (0.52), SO2 (0.47), NO2 (0.40), CO (0.39), and AQI (0.45), and a 6-month delayed effect of O3 (-0.38) on the incidence of tuberculosis were found. The number of tuberculosis cases increased by 8%, 4%, 18%, and 14% for a 10 μg/m3 increment in PM2.5, PM10, SO2, and NO2; 4% for a 10 unit increment in AQI; 8% for a 0.1 mg/m3 increment in CO; and decreased by 4% for a 10 μg/m3 increment in O3. PM2.5 concentrations above 50 μg/m3, 70 μg/m3 for PM10, 16 μg/m3 for SO2, 47 μg/m3 for NO2, 0.85 mg/m3 for CO, and 85 for AQI, and O3 concentrations lower than 95 μg/m3 were positively associated with the incidence of tuberculosis. Ambient air pollutants were correlated with tuberculosis seasonality. However, this sort of study cannot prove causality.
Project description:While there is some evidence that maternal exposure to ambient air pollution is associated with orofacial clefts in offspring, the epidemiologic studies have been largely equivocal. We evaluated whether maternal exposure to elevated county-level ambient fine particulate matter with aerodynamic diameter ?2.5µm (PM2.5) and ozone during early gestation was associated with a higher prevalence of orofacial clefts.Birth data consisting of 4.7 million births from 2001 to 2007 were obtained from National Birth Defects Prevention Network for four states - Arizona, Florida, New York (excluding New York City), and Texas. The air pollution exposure assessment for gestational weeks 5-10 was based on county-level average concentrations of PM2.5 and ozone data generated using a Bayesian fusion model available through CDC's Environmental Public Health Tracking Network. Two outcomes were analyzed separately: cleft lip with or without cleft palate, cleft palate alone. In logistic regression analyses, we adjusted for factors that were suspected confounders or modifiers of the association between the prevalence of orofacial clefts and air pollution, i.e., infant sex, race-ethnicity, maternal education, smoking status during pregnancy, whether this was mother's first baby, maternal age.Each 10µg/m3 increase in PM2.5 concentration was significantly associated with cleft palate alone (OR =1.43, 95% CI: 1.11-1.86). There was no significant association between PM2.5 concentration and cleft lip with or without cleft palate. No associations were observed between ozone exposure and the two outcomes of orofacial clefts.Our study suggests that PM2.5 significantly increased the risk of cleft palate alone, but did not change the incidence of cleft lip with or without palate. Ozone levels did not correlate with incidence of orofacial clefts.
Project description:Active travel (cycling, walking) is beneficial for the health due to increased physical activity (PA). However, active travel may increase the intake of air pollution, leading to negative health consequences. We examined the risk-benefit balance between active travel related PA and exposure to air pollution across a range of air pollution and PA scenarios. The health effects of active travel and air pollution were estimated through changes in all-cause mortality for different levels of active travel and air pollution. Air pollution exposure was estimated through changes in background concentrations of fine particulate matter (PM2.5), ranging from 5 to 200?g/m3. For active travel exposure, we estimated cycling and walking from 0 up to 16h per day, respectively. These refer to long-term average levels of active travel and PM2.5 exposure. For the global average urban background PM2.5 concentration (22?g/m3) benefits of PA by far outweigh risks from air pollution even under the most extreme levels of active travel. In areas with PM2.5 concentrations of 100?g/m3, harms would exceed benefits after 1h 30min of cycling per day or more than 10h of walking per day. If the counterfactual was driving, rather than staying at home, the benefits of PA would exceed harms from air pollution up to 3h 30min of cycling per day. The results were sensitive to dose-response function (DRF) assumptions for PM2.5 and PA. PA benefits of active travel outweighed the harm caused by air pollution in all but the most extreme air pollution concentrations.
Project description:Ambient air pollution is a growing public health concern in major African cities, including Addis Ababa (Ethiopia), where little information is available on fine particulate matter (PM2.5, with aerodynamic diameter <2.5 µm) pollution. This paper aims to characterize annual PM2.5, including bulk composition and seasonal patterns, in Addis Ababa. We collected 24-h PM2.5 samples in the central city every 6 days from November 2015 to November 2016. The mean (±SD) daily PM2.5 concentration was 53.8 (±25.0) µg/m3, with 90% of sampled days exceeding the World Health Organization's guidelines. Principal components were organic matter (OM, 44.5%), elemental carbon (EC, 25.4%), soil dust (13.5%), and SNA (sulfate, nitrate, and ammonium ions, 8.2%). Higher PM2.5 concentrations were observed during the heavy rain season, while crustal dust concentrations ranged from 2.9 to 37.6%, with higher levels during dry months. Meteorological variables, vehicle emissions, biomass fuels, unpaved roads, and construction activity contribute to poor air quality. Compared to the Air Quality Index (AQI), 31% and 36% of observed days were unhealthy for everyone and unhealthy for sensitive groups, respectively. We recommend adopting effective prevention strategies and pursuing research on vehicle emissions, biomass burning, and dust control to curb air pollution in the city.
Project description:Indoor exposure to fine particulate matter (PM2.5) is a prominent health concern. However, few studies have examined the effectiveness of long-term use of indoor air filters for reduction of PM2.5 exposure and associated decrease in adverse health impacts in urban India. We conducted 20 simulations of yearlong personal exposure to PM2.5 in urban Delhi using the National Institute of Standards and Technology's CONTAM program (NIST, Gaithersburg, MD, USA). Simulation scenarios were developed to examine different air filter efficiencies, use schedules, and the influence of a smoker at home. We quantified associated mortality reductions with Household Air Pollution Intervention Tool (HAPIT, University of California, Berkeley, CA, USA). Without an air filter, we estimated an annual mean PM2.5 personal exposure of 103 µg/m3 (95% Confidence Interval (CI): 93, 112) and 137 µg/m3 (95% CI: 125, 149) for households without and with a smoker, respectively. All day use of a high-efficiency particle air (HEPA) filter would reduce personal PM2.5 exposure to 29 µg/m3 and 30 µg/m3, respectively. The reduced personal PM2.5 exposure from air filter use is associated with 8-37% reduction in mortality attributable to PM2.5 pollution in Delhi. The findings of this study indicate that air filter may provide significant improvements in indoor air quality and result in health benefits.
Project description:Over the last years, evidence has grown that exposure to air pollution, in addition to impairing lung function and health in individuals of all age, can be linked to negative effects in newborn when present during pregnancy. Data suggests that intrauterine exposure of fetuses (exposure of the mother to air pollution during pregnancy) in fact exerts a negative impact on lung development. However, the means by which exposure during pregnancy affects lung development, have not been studied in depth yet. In this study, we investigated alterations of the transcriptome of the developing lung in a mouse model of gestational and early-life postnatal exposure to urban PM2.5 (from Sao Paulo, Brazil). Overall design: Pregnant BALB/c mouse dams were randomly assigned to two study groups: one group exposed to a PM2.5 dose equivalent to 600µg/m3 for 1h daily (exposed group), the other group kept in filtered air during the whole study period (control group). Exposure to PM2.5 was started on embryonic day 5.5 (E5.5, time of placental implantation), dams from both groups were sacrificed and fetus lungs submitted to transcriptomic analysis at E14.5 (pseudoglandular stage of lung development, n=4 per group) and E18.5 (saccular stage, n=4 per group). The offspring of mice that carried out the whole pregnancy was furthermore exposed (and kept in filtered air, repectively) after birth until being sacrificed on the 40th day of life (P40, state of finished lung alveolarization, n=5 per group). This study included no cross-over, i.e. the offspring of PM2.5-expsosed dams was exposed until P40 alike and vice-versa.
Project description:BACKGROUND:Maternal exposure to ambient air pollution has been associated with higher risk of preterm birth and reduced fetal growth, but heterogeneity among prior studies suggests that additional studies are needed in diverse populations and settings. We examined the associations between maternal ambient air pollution levels, risk of preterm birth and markers of fetal growth in an urban population with relatively low exposure to air pollution. METHODS:We linked 61?640 mother-infant pairs who delivered at a single hospital in Providence, Rhode Island, from 2002 to 2012 to birth certificate and hospital discharge data. We used spatial-temporal models and stationary monitors to estimate exposure to fine particulate matter (PM2.5) and black carbon (BC) during pregnancy. Using generalised linear models, we evaluated the association between pollutant levels, risk of preterm birth and markers of fetal growth. RESULTS:In adjusted models, an IQR (2.5?µg/m3) increase in pregnancy-average PM2.5 was associated with ORs of preterm birth of 1.04 (95% CI 0.94 to 1.15) and 0.86 (0.76 to 0.98) when considering modelled and monitored PM2.5, respectively. An IQR increase in modelled and monitored PM2.5 was associated with a 12.1?g (95%?CI -24.2 to -0.1) and 15.9?g (95%?CI -31.6 to -0.3) lower birth weight. Results for BC were highly sensitive to choice of exposure metric. CONCLUSION:In a population with relatively low exposures to ambient air pollutants, PM2.5 was associated with reduced birth weight but not with risk of preterm birth.
Project description:Exposure to fine ambient particulates (PM2.5) during gestation or neonatally has potent neurotoxic effects. While biological and behavioral data indicate a vulnerability to environmental pollutants across distinct neurodevelopmental windows, the behavioral consequences following exposure across the entire developmental period remain unknown. Moreover, several epidemiological studies support a link between developmental exposure to air pollution and an increased risk of later receiving a diagnosis of autism spectrum disorders (ASD), a neurodevelopmental disorder that persists throughout life. In the current study we sought to determine whether perinatal exposure to PM2.5 would reduce sociability and increase repetitive deficits in mice, two hallmark characteristics of ASD. Pregnant female B6C3F1 mice were exposed daily to concentrated ambient PM2.5 (CAPs) (135.8?g/m3) or filtered air (3.1?g/m3) throughout gestation followed by additional exposures to both dams and their litters from days 2-10 postpartum. Adult offspring were subsequently assessed for social and repetitive behaviors at 20 weeks of age. Daily perinatal exposure to CAPs significantly decreased sociability in male and female mice as measured by the social approach task; however, reductions in reciprocal social interaction and increased grooming behavior were only present in male offspring exposed to CAPs. These findings demonstrate that exposure to particulate air pollutants throughout early neurodevelopment induces long lasting behavioral deficits in a sex-dependent manner and may be an underlying cause of neurodevelopmental disorders such as ASD.
Project description:Associations between long-term exposure to air pollution and carotid intima-media thickness (CIMT) have inconsistent findings.In this study we aimed to evaluate association between 1-year average exposure to traffic-related air pollution and CIMT in middle-aged adults in Asia.CIMT was measured in Taipei, Taiwan, between 2009 and 2011 in 689 volunteers 35-65 years of age who were recruited as the control subjects of an acute coronary heart disease cohort study. We applied land-use regression models developed by the European Study of Cohorts for Air Pollution Effects (ESCAPE) to estimate each subject's 1-year average exposure to traffic-related air pollutants with particulate matter diameters ? 10 ?m (PM10) and ? 2.5 ?m (PM2.5) and the absorbance levels of PM2.5 (PM2.5abs), nitrogen dioxide (NO2), and nitrogen oxides (NOx) in the urban environment.One-year average air pollution exposures were 44.21 ± 4.19 ?g/m3 for PM10, 27.34 ± 5.12 ?g/m3 for PM2.5, and (1.97 ± 0.36) × 10-5/m for PM2.5abs. Multivariate regression analyses showed average percentage increases in maximum left CIMT of 4.23% (95% CI: 0.32, 8.13) per 1.0 × 10-5/m increase in PM2.5abs; 3.72% (95% CI: 0.32, 7.11) per 10-?g/m3 increase in PM10; 2.81% (95% CI: 0.32, 5.31) per 20-?g/m3 increase in NO2; and 0.74% (95% CI: 0.08, 1.41) per 10-?g/m3 increase in NOx. The associations were not evident for right CIMT, and PM2.5 mass concentration was not associated with the outcomes.Long-term exposures to traffic-related air pollution of PM2.5abs, PM10, NO2, and NOx were positively associated with subclinical atherosclerosis in middle-aged adults.