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BACKGROUND: Ambient air pollution, including particulate matter (such as PM10 and PM2·5) and nitrogen dioxide (NO2), has been linked to increases in mortality. Whether populations' vulnerability to these pollutants has changed over time is unclear, and studies on this topic do not include multicountry analysis. We evaluated whether changes in exposure to air pollutants were associated with changes in mortality effect estimates over time. METHODS: We extracted cause-specific mortality and air pollution data collected between 1995 and 2016 from the Multi-Country Multi-City (MCC) Collaborative Research Network database. We applied a two-stage approach to analyse the short-term effects of NO2, PM10, and PM2·5 on cause-specific mortality using city-specific time series regression analyses and multilevel random-effects meta-analysis. We assessed changes over time using a longitudinal meta-regression with time as a linear fixed term and explored potential sources of heterogeneity and two-pollutant models. FINDINGS: Over 21·6 million cardiovascular and 7·7 million respiratory deaths in 380 cities across 24 countries over the study period were included in the analysis. All three air pollutants showed decreasing concentrations over time. The pooled results suggested no significant temporal change in the effect estimates per unit exposure of PM10, PM2·5, or NO2 and mortality. However, the risk of cardiovascular mortality increased from 0·37% (95% CI -0·05 to 0·80) in 1998 to 0·85% (0·55 to 1·16) in 2012 with a 10 µg/m3 increase in PM2·5. Two-pollutant models generally showed similar results to single-pollutant models for PM fractions and indicated temporal differences for NO2. INTERPRETATION: Although air pollution levels decreased during the study period, the effect sizes per unit increase in air pollution concentration have not changed. This observation might be due to the composition, toxicity, and sources of air pollution, as well as other factors, such as socioeconomic determinants or changes in population distribution and susceptibility. FUNDING: None.

Asunto(s)

Contaminantes Atmosféricos , Contaminación del Aire , Enfermedades Cardiovasculares , Ciudades , Dióxido de Nitrógeno , Material Particulado , Enfermedades Respiratorias , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Humanos , Material Particulado/análisis , Material Particulado/efectos adversos , Enfermedades Cardiovasculares/mortalidad , Dióxido de Nitrógeno/análisis , Dióxido de Nitrógeno/efectos adversos , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Enfermedades Respiratorias/mortalidad , Enfermedades Respiratorias/inducido químicamente , Exposición a Riesgos Ambientales/efectos adversos

RESUMEN

INTRODUCTION: Traffic-related air and noise pollution are important public health issues. The aim of this study was to estimate their effects on allergic/respiratory outcomes in adult and elderly subjects. MATERIALS AND METHODS: Six hundred and forty-five subjects living in Pisa (Tuscany, Italy) were investigated through a questionnaire on allergic/respiratory symptoms and diseases. Traffic-related air pollution and noise exposures were assessed at residential address by questionnaire, modelled annual mean NO2 concentrations (1 km and 200 m resolution), and noise level over a 24-h period (Lden). Exposure effects were assessed through logistic regression models stratified by age group (18-64 years, ≥65 years), and adjusted for sex, educational level, occupational exposure, and smoking habits. RESULTS: 63.6% of the subjects reported traffic exposure near home. Mean exposure levels were: 28.24 (±3.26 SD) and 27.23 (±3.16 SD) µg/m3 for NO2 at 200 m and 1 km of resolution, respectively; 57.79 dB(A) (±6.12 SD) for Lden. Exposure to vehicular traffic (by questionnaire) and to high noise levels [Lden ≥ 60 dB(A)] were significantly associated with higher odds of allergic rhinitis (OR 2.01, 95%CI 1.09-3.70, and OR 1.99, 95%CI 1.18-3.36, respectively) and borderline with rhino-conjunctivitis (OR 2.20, 95%CI 0.95-5.10, and OR 1.76, 95%CI 0.91-3.42, respectively) only in the elderly. No significant result emerged for NO2. CONCLUSIONS: Our findings highlighted the need to better assess the effect of traffic-related exposure in the elderly, considering the increasing trend in the future global population's ageing.

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Global population is ageing.Allergic diseases are globally widespread even on adult population.The susceptibility due to ageing may increase the impact of air pollution on the elderly.Traffic-related air and noise pollution affects allergic status of the elderly.

Asunto(s)

Exposición a Riesgos Ambientales , Humanos , Persona de Mediana Edad , Masculino , Femenino , Anciano , Italia/epidemiología , Adulto , Adolescente , Exposición a Riesgos Ambientales/efectos adversos , Adulto Joven , Contaminación del Aire/efectos adversos , Contaminación por Tráfico Vehicular/efectos adversos , Encuestas y Cuestionarios , Emisiones de Vehículos , Ruido/efectos adversos , Rinitis Alérgica/epidemiología , Rinitis Alérgica/etiología , Hipersensibilidad/epidemiología , Hipersensibilidad/etiología , Modelos Logísticos , Dióxido de Nitrógeno/efectos adversos , Dióxido de Nitrógeno/análisis , Contaminantes Atmosféricos/efectos adversos , Ruido del Transporte/efectos adversos

RESUMEN

Importance: The role of air pollution in risk and progression of Parkinson disease (PD) is unclear. Objective: To assess whether air pollution is associated with increased risk of PD and clinical characteristics of PD. Design, Setting, and Participants: This population-based case-control study included patients with PD and matched controls from the Rochester Epidemiology Project from 1998 to 2015. Data were analyzed from January to June 2024. Exposures: Mean annual exposure to particulate matter with a diameter of 2.5 µm or less (PM2.5) from 1998 to 2015 and mean annual exposure to nitrogen dioxide (NO2) from 2000 to 2014. Main Outcomes and Measures: Outcomes of interest were PD risk, all-cause mortality, presence of tremor-predominant vs akinetic rigid PD, and development of dyskinesia. Models were adjusted for age, sex, race and ethnicity, year of index, and urban vs rural residence. Results: A total of 346 patients with PD (median [IQR] age 72 [65-80] years; 216 [62.4%] male) were identified and matched on age and sex with 4813 controls (median [IQR] age, 72 [65-79] years, 2946 [61.2%] male). Greater PM2.5 exposure was associated with increased PD risk, and this risk was greatest after restricting to populations within metropolitan cores (odds ratio [OR], 1.23; 95% CI, 1.11-1.35) for the top quintile of PM2.5 exposure compared with the bottom quintile. Greater NO2 exposure was also associated with increased PD risk when comparing the top quintile with the bottom quintile (OR, 1.13; 95% CI, 1.07-1.19). Air pollution was associated with a 36% increased risk of akinetic rigid presentation (OR per each 1-µg/m3 increase in PM2.5, 1.36; 95% CI, 1.02-1.80). In analyses among patients with PD only, higher PM2.5 exposure was associated with greater risk for developing dyskinesia (HR per 1-µg/m3 increase in PM2.5, 1.42; 95% CI, 1.17-1.73), as was increased NO2 exposure (HR per 1 µg/m3 increase in NO2, 1.13; 95% CI, 1.06-1.19). There was no association between PM2.5 and all-cause mortality among patients with PD. Conclusions and Relevance: In this case-control study of air pollution and PD, higher levels of PM2.5 and NO2 exposure were associated with increased risk of PD; also, higher levels of PM2.5 exposure were associated with increased risk of developing akinetic rigid PD and dyskinesia compared with patients with PD exposed to lower levels. These findings suggest that reducing air pollution may reduce risk of PD, modify the PD phenotype, and reduce risk of dyskinesia.

Asunto(s)

Contaminación del Aire , Exposición a Riesgos Ambientales , Dióxido de Nitrógeno , Enfermedad de Parkinson , Material Particulado , Humanos , Enfermedad de Parkinson/epidemiología , Enfermedad de Parkinson/etiología , Masculino , Femenino , Anciano , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Contaminación del Aire/estadística & datos numéricos , Estudios de Casos y Controles , Material Particulado/efectos adversos , Material Particulado/análisis , Anciano de 80 o más Años , Dióxido de Nitrógeno/efectos adversos , Dióxido de Nitrógeno/análisis , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/estadística & datos numéricos , Factores de Riesgo , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Persona de Mediana Edad

RESUMEN

BACKGROUND: Uncertainty remains about the long-term effects of air pollutants (AP) on multiple diseases, especially subtypes of cardiovascular disease (CVD). We aimed to assess the individual and joint associations of fine particulate matter (PM2.5), along with its chemical components, nitrogen dioxide (NO2) and ozone (O3), with risks of 32 health conditions. METHODS: A total of 17,566 participants in Sichuan Province, China, were included in 2018 and followed until 2022, with an average follow-up period of 4.2 years. The concentrations of AP were measured using a machine-learning approach. The Cox proportional hazards model and quantile g-computation were applied to assess the associations between AP and CVD. RESULTS: Per interquartile range (IQR) increase in PM2.5 mass, NO2, O3, nitrate, ammonium, organic matter (OM), black carbon (BC), chloride, and sulfate were significantly associated with increased risks of various conditions, with hazard ratios (HRs) ranging from 1.06 to 2.48. Exposure to multiple air pollutants was associated with total cardiovascular disease (HR 1.75, 95% confidence intervals (CIs) 1.62-1.89), hypertensive diseases (1.49, 1.38-1.62), cardiac arrests (1.52, 1.30-1.77), arrhythmia (1.76, 1.44-2.15), cerebrovascular diseases (1.86, 1.65-2.10), stroke (1.77, 1.54-2.03), ischemic stroke (1.85, 1.61-2.12), atherosclerosis (1.77, 1.57-1.99), diseases of veins, lymphatic vessels, and lymph nodes (1.32, 1.15-1.51), pneumonia (1.37, 1.16-1.61), inflammatory bowel diseases (1.34, 1.16-1.55), liver diseases (1.59, 1.43-1.77), type 2 diabetes (1.48, 1.26-1.73), lipoprotein metabolism disorders (2.20, 1.96-2.47), purine metabolism disorders (1.61, 1.38-1.88), anemia (1.29, 1.15-1.45), sleep disorders (1.54, 1.33-1.78), renal failure (1.44, 1.21-1.72), kidney stone (1.27, 1.13-1.43), osteoarthritis (2.18, 2.00-2.39), osteoporosis (1.36, 1.14-1.61). OM had max weights for joint effects of AP on many conditions. CONCLUSIONS: Long-term exposure to increased levels of multiple air pollutants was associated with risks of multiple health conditions. OM accounted for substantial weight for these increased risks, suggesting it may play an important role in these associations.

Asunto(s)

Contaminantes Atmosféricos , Contaminación del Aire , Enfermedades Cardiovasculares , Material Particulado , Humanos , China/epidemiología , Contaminación del Aire/efectos adversos , Masculino , Femenino , Persona de Mediana Edad , Estudios Prospectivos , Material Particulado/efectos adversos , Material Particulado/análisis , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Enfermedades Cardiovasculares/epidemiología , Adulto , Ozono/efectos adversos , Ozono/análisis , Anciano , Exposición a Riesgos Ambientales/efectos adversos , Factores de Riesgo , Dióxido de Nitrógeno/efectos adversos , Dióxido de Nitrógeno/análisis

RESUMEN

INTRODUCTION: Air pollution is a major health risk factor. Ports might be an understudied source of air pollution. METHODS: We conducted a spatial health impact assessment (HIA) of port-sourced air pollution for Barcelona for 2017 at the neighbourhood level. Total NO2 and PM10 and port-sourced NO2, PM10 and PM2.5 concentrations were available through the ADMS-Urban model. Population data, mortality and morbidity data, and risk estimates were obtained. We followed standard HIA methodologies and calculated relative risks and impact fractions for 1.35 million adults living in 73 neighbourhoods. RESULTS: The city-wide mean total NO2 and PM10 concentrations were 37.88 µg/m3 (range: 19.61-52.17 µg/m3) and 21.68 µg/m3 (range: 17.33-26.69 µg/m3), respectively, of which 7% (range: 2-36%) and 1% (range: 0-7%) were port-sourced, respectively. The mean port-sourced PM2.5 concentration was 0.19 µg/m3 (range: 0.06-1.38 µg/m3). We estimated that 1,123 (PI: 0-3,060) and 1,230 (95% CI: 0-2,566) premature deaths were attributable to total NO2 and PM10, respectively, of which 8.1% (91; PI: 0-264) and 1.1% (13; 95% CI 0-29) were attributable to port-sourced NO2 and PM10, respectively. 20 (95% CI: 15-26) premature deaths were attributable to port-sourced PM2.5. Additionally, a considerable morbidity burden and losses in life expectancy were attributable to port-sourced air pollution. Neighbourhoods closest to the port in the south-east were most adversely affected, gradually decreasing towards the north-west. CONCLUSIONS: The port is an understudied air pollution source in Barcelona with strong health impacts. Cities need local insight into health risk factors, their sources, attributable burdens and distributions for defining targeted policies.

Asunto(s)

Contaminantes Atmosféricos , Contaminación del Aire , Evaluación del Impacto en la Salud , Material Particulado , España/epidemiología , Humanos , Contaminación del Aire/análisis , Contaminación del Aire/efectos adversos , Material Particulado/análisis , Material Particulado/efectos adversos , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/efectos adversos , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisis , Ciudades , Adulto , Monitoreo del Ambiente/métodos , Dióxido de Nitrógeno/análisis , Dióxido de Nitrógeno/efectos adversos

RESUMEN

The present study explores the modifications of cardiovascular autonomic control (CAC) during wake and sleep time and the systemic inflammatory profile associated with exposure to indoor air pollution (IAP) in a cohort of healthy subjects. Twenty healthy volunteers were enrolled. Indoor levels of fine particulate matter (PM2.5), nitrogen dioxide (NO2) and volatile organic compounds (VOCs) were monitored using a portable detector for 7 days. Together, a 7-day monitoring was performed through a wireless patch that continuously recorded electrocardiogram, respiratory activity and actigraphy. Indexes of CAC during wake and sleep time were derived from the biosignals: heart rate and low-frequency to high-frequency ratio (LF/HF), index of sympathovagal balance with higher values corresponding to a predominance of the sympathetic branch. Cyclic variation of heart rate index (CVHRI events/hour) during sleep, a proxy for the evaluation of sleep apnea, was assessed for each night. After the monitoring, blood samples were collected to assess the inflammatory profile. Regression and correlation analyses were performed. A positive association between VOC exposure and the CVHRI (Δ% = +0.2% for 1 µg/m3 VOCs, p = 0.008) was found. The CVHRI was also positively associated with LF/HF during sleep, thus higher CVHRI values corresponded to a shift of the sympathovagal balance towards a sympathetic predominance (r = 0.52; p = 0.018). NO2 exposure was positively associated with both the pro-inflammatory biomarker TREM-1 and the anti-inflammatory biomarker IL-10 (Δ% = +1.2% and Δ% = +2.4%, for 1 µg/m3 NO2; p = 0.005 and p = 0.022, respectively). The study highlights a possible causal relationship between IAP exposure and higher risk of sleep apnea events, associated with impaired CAC during sleep, and a pro-inflammatory state counterbalanced by an increased anti-inflammatory response in healthy subjects. This process may be disrupted in vulnerable populations, leading to a harmful chronic pro-inflammatory profile. Thus, IAP may emerge as a critical and often neglected risk factor for the public health that can be addressed through targeted preventive interventions.

Asunto(s)

Contaminación del Aire Interior , Sistema Nervioso Autónomo , Frecuencia Cardíaca , Sueño , Humanos , Masculino , Adulto , Contaminación del Aire Interior/efectos adversos , Contaminación del Aire Interior/análisis , Femenino , Sistema Nervioso Autónomo/efectos de los fármacos , Sistema Nervioso Autónomo/fisiopatología , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/efectos adversos , Inflamación/inducido químicamente , Material Particulado/análisis , Material Particulado/efectos adversos , Compuestos Orgánicos Volátiles/análisis , Dióxido de Nitrógeno/análisis , Dióxido de Nitrógeno/efectos adversos , Adulto Joven , Persona de Mediana Edad

RESUMEN

Objective: To investigate the association between exposure to atmospheric pollutants and preterm birth in a river valley-type city and its critical exposure windows. Methods: A retrospective cohort study was used to collect data from the medical records of preterm and full-term deliveries in two hospitals in urban areas of a typical river valley-type city from January 2018 to December 2019. A total of 7,288 cases were included in the study with general information such as pregnancy times, the number of cesarean sections, occupation, season of conception and regularity of the menstrual cycle. And confounding factors affecting preterm birth were inferred using the chi-square test. The effects of exposure to each pollutant, including particulate matter 2.5 (PM2.5), particulate matter 10 (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (CO) and ozone (O3), during pregnancy on preterm birth and the main exposure windows were explored by establishing a logistic regression model with pollutants introduced as continuous variables. Results: Maternal age, pregnancy times, number of births, number of cesarean sections, season of conception, complications diseases, comorbidities diseases, hypertension disorder of pregnancy and neonatal low birth weight of the newborn were significantly different between preterm and term pregnant women. Logistic regression analysis after adjusting for the above confounders showed that the risk of preterm birth increases by 0.9, 0.6, 2.4% in T2 and by 1.0, 0.9, 2.5% in T3 for each 10 µg/m3 increase in PM2.5, PM10, NO2 concentrations, respectively. The risk of preterm birth increases by 4.3% in T2 for each 10 µg/m3 increase in SO2 concentrations. The risk of preterm birth increases by 123.5% in T2 and increases by 188.5% in T3 for each 10 mg/m3 increase in CO concentrations. Conclusion: Maternal exposure to PM2.5, PM10, NO2, CO was associated with increased risk on preterm birth in mid-pregnancy (T2) and late pregnancy (T3), SO2 exposure was associated with increased risk on preterm birth in mid-pregnancy (T2).

Asunto(s)

Contaminantes Atmosféricos , Material Particulado , Nacimiento Prematuro , Humanos , Femenino , Nacimiento Prematuro/epidemiología , Estudios Retrospectivos , Embarazo , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Adulto , Material Particulado/efectos adversos , Material Particulado/análisis , Recién Nacido , Exposición Materna/efectos adversos , Exposición Materna/estadística & datos numéricos , China/epidemiología , Dióxido de Azufre/análisis , Dióxido de Azufre/efectos adversos , Dióxido de Nitrógeno/análisis , Dióxido de Nitrógeno/efectos adversos , Monóxido de Carbono/análisis , Monóxido de Carbono/efectos adversos , Contaminación del Aire/efectos adversos , Contaminación del Aire/estadística & datos numéricos , Factores de Riesgo , Ciudades

RESUMEN

Although previous studies have suggested that meteorological factors and air pollutants can cause dry eye disease (DED), few clinical cohort studies have determined the individual and combined effects of these factors on DED. We investigated the effects of meteorological factors (humidity and temperature) and air pollutants [particles with a diameter ≤ 2.5 µ m (PM2.5), ozone (O3), nitrogen dioxide (NO2), and carbon monoxide (CO)] on DED. A retrospective cohort study was conducted on 53 DED patients. DED was evaluated by Symptom Assessment in Dry Eye (SANDE), tear secretion, tear film break-up time (TBUT), ocular staining score (OSS), and tear osmolarity. To explore the individual, non-linear, and joint associations between meteorological factors, air pollutants, and DED parameters, we used generalized linear mixed model (GLMM) and Bayesian kernel machine regression (BKMR). After adjusting for all covariates, lower relative humidity or temperature was associated with a higher SANDE (p < 0.05). Higher PM2.5, O3, and NO2 levels were associated with higher SANDE and tear osmolarity (p < 0.05). Higher O3 levels were associated with lower tear secretion and TBUT, whereas higher NO2 levels were associated with higher OSS (p < 0.05). BKMR analyses indicated that a mixture of meteorological factors and air pollutants was significantly associated with increased SANDE, OSS, tear osmolarity, and decreased tear secretion.

Asunto(s)

Contaminantes Atmosféricos , Síndromes de Ojo Seco , Humanos , Estudios Retrospectivos , Masculino , Femenino , Síndromes de Ojo Seco/etiología , Síndromes de Ojo Seco/epidemiología , Persona de Mediana Edad , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Anciano , Material Particulado/efectos adversos , Material Particulado/análisis , Adulto , Lágrimas/metabolismo , Dióxido de Nitrógeno/análisis , Dióxido de Nitrógeno/efectos adversos , Humedad/efectos adversos , Conceptos Meteorológicos , Ozono/efectos adversos , Ozono/análisis , Temperatura

RESUMEN

Air pollution stands as an environmental risk to child mental health, with proven relationships hitherto observed only in urban areas. Understanding the impact of pollution in rural settings is equally crucial. The novelty of this article lies in the study of the relationship between air pollution and behavioural and developmental disorders, attention deficit hyperactivity disorder (ADHD), anxiety, and eating disorders in children below 15 living in a rural area. The methodology combines spatio-temporal models, Bayesian inference and Compositional Data (CoDa), that make it possible to study areas with few pollution monitoring stations. Exposure to nitrogen dioxide (NO2), ozone (O3), and sulphur dioxide (SO2) is related to behavioural and development disorders, anxiety is related to particulate matter (PM10), O3 and SO2, and overall pollution is associated to ADHD and eating disorders. To sum up, like their urban counterparts, rural children are also subject to mental health risks related to air pollution, and the combination of spatio-temporal models, Bayesian inference and CoDa make it possible to relate mental health problems to pollutant concentrations in rural settings with few monitoring stations. Certain limitations persist related to misclassification of exposure to air pollutants and to the covariables available in the data sources used.

Asunto(s)

Contaminantes Atmosféricos , Contaminación del Aire , Teorema de Bayes , Salud Mental , Población Rural , Humanos , Niño , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Femenino , Masculino , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/efectos adversos , Exposición a Riesgos Ambientales/efectos adversos , Análisis Espacio-Temporal , Material Particulado/análisis , Material Particulado/efectos adversos , Adolescente , Preescolar , Trastorno por Déficit de Atención con Hiperactividad/epidemiología , Trastorno por Déficit de Atención con Hiperactividad/inducido químicamente , Trastorno por Déficit de Atención con Hiperactividad/etiología , Dióxido de Nitrógeno/análisis , Dióxido de Nitrógeno/efectos adversos , Ozono/análisis , Ozono/efectos adversos , Dióxido de Azufre/análisis , Dióxido de Azufre/efectos adversos , Ansiedad/epidemiología , Ansiedad/etiología

RESUMEN

BACKGROUND: Air pollution exposure has been linked with increased risk of preterm birth, which is one of the leading causes of infant mortality. Limited studies have attempted to explore these associations in low-polluted areas. In this study, we aimed to assess the association between short-term exposure to ambient air pollution and preterm birth in Sweden. METHOD: In this population-based study we included preterm births between 2014 and 2019 from the Swedish Pregnancy Register. We applied a spatiotemporal model to estimate daily levels of particulate matter <2.5 µm (PM2.5), PM < 10 µm (PM10), nitrogen dioxide (NO2), and ozone (O3) at the residential address of each participant. We applied a time-stratified case-crossover design with conditional logistic regression analysis to estimate odds ratios (OR) of preterm birth per 10 µg/m3 (PM10, NO2, O3) and 5 µg/m3 (PM2.5) increase in air pollution exposure at 0-6-day lag. Two-pollutant models were applied to evaluate the independent association of each exposure on preterm birth. We also stratified by maternal characteristics to identify potential effect modifiers. RESULTS: 28,216 (4.5%) preterm births were included. An increase in O3 exposure was associated with increased odds of preterm birth [OR = 1.06 per 10 µg/m3 (95% CI, 1.02; 1.10]. PM2.5 and PM10 were not significantly associated with preterm birth, and NO2 displayed a negative nonlinear association with preterm birth. We did not observe any notable effect modification, but we found suggestive larger associations between O3 and preterm birth when stratifying by male sex, spontaneous delivery, and spring season. CONCLUSIONS: Increased O3 exposure one week before delivery was associated with an increased risk of preterm birth in Sweden, a country with levels of air pollution below the current World Health Organization air quality guidelines. Increases in O3 levels with climate change make these findings especially concerning.

Asunto(s)

Contaminantes Atmosféricos , Contaminación del Aire , Dióxido de Nitrógeno , Ozono , Material Particulado , Nacimiento Prematuro , Humanos , Suecia/epidemiología , Nacimiento Prematuro/epidemiología , Femenino , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/efectos adversos , Embarazo , Material Particulado/análisis , Material Particulado/efectos adversos , Adulto , Ozono/análisis , Ozono/efectos adversos , Dióxido de Nitrógeno/análisis , Dióxido de Nitrógeno/efectos adversos , Recién Nacido , Adulto Joven , Masculino , Exposición Materna/efectos adversos , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisis

RESUMEN

The relationship between maternal peripheral blood mitochondrial DNA and adverse pregnancy outcomes, specifically preterm birth (PTB), remains uncertain. To investigate the effects of preconception mitochondrial DNA copy number (mtDNAcn) on the association between prenatal air pollutants exposure and PTB risk, a total of 1871 expectant mothers from six regions in Henan Province were recruited. Information regarding air pollutants was obtained from 151 environmental monitoring sites, and relative mtDNAcn was evaluated using real-time PCR analysis. After adjusting for potential confounding variables, it was determined that the risk of PTB increased with elevated levels of inhalable particulate matter (PM10), fine particulate matter (PM2.5), sulfur dioxide (SO2), carbon monoxide (CO) and ozone (O3) exposure (P < 0.05) but decreased with higher nitrogen dioxide (NO2) exposure (0.05 < P < 0.10) during the entire pregnancy. Additionally, the preconception relative mtDNAcn was lower in the PTB group (0.82 ± 0.23) compared to the term group (0.92 ± 0.29). Furthermore, for each 0.1-unit increase in preconception mtDNAcn, the risk of PTB decreased by 14.8%. Stratified analyses revealed that the risk of PTB rose with increasing O3 concentrations, regardless of the relative mtDNAcn. Moreover, the study found a significant association between PTB risk and prenatal exposure to elevated PM10, PM2.5, SO2, and CO, particularly in mothers with low mtDNAcn (≤0.88) (P < 0.05). Conversely, a decrease in the PTB risk was observed with elevated NO2 exposure in mothers with high mtDNAcn (>0.88). Interaction analysis revealed that exposure to PM10, PM2.5, SO2, NO2, and CO interacted with mtDNAcn, respectively, affecting PTB risk (P-interaction<0.05). These findings indicate a noteworthy association between PTB risk and prenatal air pollutants exposure, which is influenced by the preconception mtDNAcn.

Asunto(s)

Contaminantes Atmosféricos , Contaminación del Aire , Variaciones en el Número de Copia de ADN , ADN Mitocondrial , Material Particulado , Nacimiento Prematuro , Humanos , Femenino , Embarazo , Nacimiento Prematuro/epidemiología , Adulto , Contaminantes Atmosféricos/efectos adversos , Contaminación del Aire/efectos adversos , Material Particulado/efectos adversos , China/epidemiología , Exposición Materna/efectos adversos , Dióxido de Azufre/efectos adversos , Dióxido de Nitrógeno/efectos adversos , Adulto Joven , Ozono/efectos adversos

RESUMEN

OBJECTIVE: To evaluate the influence of environmental factors and prematurity relating to juvenile dermatomyositis (JDM), its course and refractoriness to treatment. METHODS: A case-control study with 35 patients followed up at a tertiary hospital and 124 healthy controls, all residents of São Paulo. Patients were classified according to monocyclic, polycyclic or chronic disease courses and refractoriness to treatment. The daily concentrations of pollutants (inhalable particulate matter-PM10, sulfur dioxide-SO2, nitrogen dioxide-NO2, ozone-O3 and carbon monoxide-CO) were provided by the Environmental Company of São Paulo. Data from the population were obtained through a questionnaire. RESULTS: Fifteen patients had monocyclic courses, and 19 polycyclic/chronic courses. Eighteen patients were refractory to treatment. Maternal occupational exposure to inhalable agents (OR = 17.88; IC 95% 2.15-148.16, p = 0.01) and exposure to O3 in the fifth year of life (third tertile > 86.28µg/m3; OR = 6.53, IC95% 1.60-26.77, p = 0.01) were risk factors for JDM in the multivariate logistic regression model. The presence of a factory/quarry at a distance farther than 200 meters from daycare/school (OR = 0.22; IC 95% 0.06-0.77; p = 0.02) was a protective factor in the same analysis. Prematurity, exposure to air pollutants/cigarette smoke/sources of inhalable pollutants in the mother's places of residence and work during the gestational period were not associated with JDM. Prematurity, maternal exposure to occupational pollutants during pregnancy as well as patient's exposure to ground-level pollutants up to the fifth year of life were not associated with disease course and treatment refractoriness. CONCLUSION: Risk factors for JDM were maternal occupational exposure and exposure to O3 in the fifth year of life.

Asunto(s)

Dermatomiositis , Exposición Profesional , Material Particulado , Humanos , Dermatomiositis/etiología , Femenino , Estudios de Casos y Controles , Masculino , Factores de Riesgo , Material Particulado/análisis , Material Particulado/efectos adversos , Niño , Brasil/epidemiología , Exposición Profesional/efectos adversos , Exposición Profesional/análisis , Embarazo , Ozono/análisis , Ozono/efectos adversos , Exposición Materna/efectos adversos , Monóxido de Carbono/análisis , Dióxido de Nitrógeno/análisis , Dióxido de Nitrógeno/efectos adversos , Dióxido de Azufre/análisis , Dióxido de Azufre/efectos adversos , Preescolar , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/efectos adversos , Exposición a Riesgos Ambientales/efectos adversos , Modelos Logísticos , Nacimiento Prematuro

RESUMEN

Background: There is mounting evidence that diabetic-related cardiac metabolism abnormalities with oxidative stress and inflammatory mechanism activation align with the functional impairments that result in atherosclerotic lesion formation. Among the possible non-traditional coronary lesion risk factors, environmental exposure may be significant, especially in diabetic patients. Methods: A total of 140 diabetic patients (115 (82%) males and 25 (18%) females) with a mean age of 65 (60-71) underwent surgical revascularization due to multivessel coronary disease. The possible all-cause mortality risk factors, including demographical and clinical factors followed by chronic air pollution exposure, were identified. Results: All patients were operated on using the off-pump technique and followed for 5.6 (5-6.1) years. The multivariable model for 5-year mortality prediction presented the nitrogen dioxide chronic exposure (HR: 3.99, 95% CI: 1.16-13.71, p = 0.028) and completeness of revascularization (HR: 0.19, 95% CI: 0.04-0.86, p = 0.031) as significant all-cause mortality risk factors. Conclusions: Ambient air pollutants such as an excessive chronic nitrogen dioxide concentration (>15 µg/m3) may increase 5-year all-cause mortality in diabetic patients following surgical revascularization.

Asunto(s)

Dióxido de Nitrógeno , Humanos , Masculino , Femenino , Anciano , Persona de Mediana Edad , Estudios Retrospectivos , Factores de Riesgo , Dióxido de Nitrógeno/análisis , Dióxido de Nitrógeno/efectos adversos , Puente de Arteria Coronaria Off-Pump/efectos adversos , Puente de Arteria Coronaria Off-Pump/mortalidad , Diabetes Mellitus/mortalidad , Exposición a Riesgos Ambientales/efectos adversos , Enfermedad de la Arteria Coronaria/cirugía , Enfermedad de la Arteria Coronaria/mortalidad , Enfermedad de la Arteria Coronaria/complicaciones

RESUMEN

Background: Traditional observational studies exploring the association between air pollution and infections have been limited by small sample sizes and potential confounding factors. To address these limitations, we applied Mendelian randomization (MR) to investigate the potential causal relationships between particulate matter (PM2.5, PM2.5-10, and PM10), nitrogen dioxide, and nitrogen oxide and the risks of infections. Methods: Single nucleotide polymorphisms (SNPs) related to air pollution were selected from the genome-wide association study (GWAS) of the UK Biobank. Publicly available summary data for infections were obtained from the FinnGen Biobank and the COVID-19 Host Genetics Initiative. The inverse variance weighted (IVW) meta-analysis was used as the primary method for obtaining the Mendelian randomization (MR) estimates. Complementary analyses were performed using the weighted median method, MR-Egger method, and MR Pleiotropy Residual Sum and Outlier (MR-PRESSO) test. Results: The fixed-effect IVW estimate showed that PM2.5, PM2.5-10 and Nitrogen oxides were suggestively associated with COVID-19 [for PM2.5: IVW (fe): OR 3.573(1.218,5.288), PIVW(fe) = 0.021; for PM2.5-10: IVW (fe): OR 2.940(1.385,6.239), PIVW(fe) = 0.005; for Nitrogen oxides, IVW (fe): OR 1.898(1.318,2.472), PIVW(fe) = 0.010]. PM2.5, PM2.5-10, PM10, and Nitrogen oxides were suggestively associated with bacterial pneumonia [for PM2.5: IVW(fe): OR 1.720 (1.007, 2.937), PIVW(fe) = 0.047; for PM2.5-10: IVW(fe): OR 1.752 (1.111, 2.767), P IVW(fe) = 0.016; for PM10: IVW(fe): OR 2.097 (1.045, 4.208), PIVW(fe) = 0.037; for Nitrogen oxides, IVW(fe): OR 3.907 (1.209, 5.987), PIVW(fe) = 0.023]. Furthermore, Nitrogen dioxide was suggestively associated with the risk of acute upper respiratory infections, while all air pollution were not associated with intestinal infections. Conclusions: Our results support a role of related air pollution in the Corona Virus Disease 2019, bacterial pneumonia and acute upper respiratory infections. More work is need for policy formulation to reduce the air pollution and the emission of toxic and of harmful gas.

Asunto(s)

Contaminación del Aire , COVID-19 , Estudio de Asociación del Genoma Completo , Análisis de la Aleatorización Mendeliana , Material Particulado , Polimorfismo de Nucleótido Simple , Humanos , Contaminación del Aire/efectos adversos , Material Particulado/efectos adversos , COVID-19/epidemiología , Dióxido de Nitrógeno/efectos adversos , SARS-CoV-2/genética , Óxidos de Nitrógeno/efectos adversos , Contaminantes Atmosféricos/efectos adversos

RESUMEN

INTRODUCTION: This study investigates the association between maternal exposure to particulate matter (PM10) and nitric dioxide (NO2) during the first, second and third trimester and placental weight and birth weight/placental weight (BW/PW) ratio in twins at birth. METHODS: Cross-sectional data of 3340 twins from the East Flanders Prospective Twin Survey was used. Air pollutant exposure was estimated via spatial temporal interpolation. Univariable and multivariable mixed model analyses with a random intercept to account for the relatedness of newborns were conducted for twins with separate placentas. Twin pairs with one placental mass were studied with linear and logistic regression. RESULTS: In the third trimester, for each 10 µm/m3 increase in PM10 or NO2 placental weight decreased -19.7 g (95%-C.I. -35.1; -4.3) and -17.7 g (95%-C.I. -30.4; -0.5) respectively, in moderate to late preterm twins with separate placentas. Consequently, BW/PW ratio increased with higher air pollution exposure. PM10 exposure in the last week of pregnancy was associated with a higher odds ratio (OR) of 1.20 (95%-C.I. 1.00; 1.44) for a "small for gestational age placenta" (placental weight <10th percentile). Conversely, first trimester air pollutant exposure was associated with lower ORs of 0.55 (95%-C.I. 0.35; 0.88) and 0.60 (95%-C.I. 0.42; 0.84). DISCUSSION: The association of PM10 and NO2 on placental weight is trimester-specific, differs for twins with one versus two placentas and is most pronounced in moderate to late preterm twins. Longitudinal studies are needed to better understand the relationship between air pollutant exposure and placental weight evolution across different trimesters.

Asunto(s)

Contaminación del Aire , Exposición Materna , Placenta , Humanos , Femenino , Embarazo , Placenta/anatomía & histología , Placenta/patología , Placenta/efectos de los fármacos , Adulto , Exposición Materna/efectos adversos , Contaminación del Aire/efectos adversos , Tamaño de los Órganos/efectos de los fármacos , Estudios Transversales , Material Particulado/efectos adversos , Recién Nacido , Peso al Nacer/efectos de los fármacos , Trimestres del Embarazo , Gemelos , Estudios Prospectivos , Dióxido de Nitrógeno/efectos adversos , Dióxido de Nitrógeno/análisis , Embarazo Gemelar , Masculino , Contaminantes Atmosféricos/efectos adversos

RESUMEN

BACKGROUND: Air pollution has been classified as a human carcinogen based largely on findings for respiratory cancers. Emerging, but limited, evidence suggests that it increases the risk of breast cancer, particularly among younger women. We characterized associations between residential exposure to ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2) and breast cancer. Analyses were performed using data collected in the Ontario Environmental Health Study (OEHS). METHODS: The OEHS, a population-based case-control study, identified incident cases of breast cancer in Ontario, Canada among women aged 18-45 between 2013 and 2015. A total of 465 pathologically confirmed primary breast cancer cases were identified from the Ontario Cancer Registry, while 242 population-based controls were recruited using random-digit dialing. Self-reported questionnaires were used to collect risk factor data and residential histories. Land-use regression and remote-sensing estimates of NO2 and PM2.5, respectively, were assigned to the residential addresses at interview, five years earlier, and at menarche. Logistic regression was used to estimate odds ratios (OR) and their 95 % confidence intervals (CI) in relation to an interquartile range (IQR) increase in air pollution, adjusting for possible confounders. RESULTS: PM2.5 and NO2 were positively correlated with each other (r = 0.57). An IQR increase of PM2.5 (1.9 µg/m3) and NO2 (6.6 ppb) at interview residence were associated with higher odds of breast cancer and the adjusted ORs and 95 % CIs were 1.37 (95 % CI = 0.98-1.91) and 2.33 (95 % CI = 1.53-3.53), respectively. An increased odds of breast cancer was observed with an IQR increase in NO2 at residence five years earlier (OR = 2.16, 95 % CI: 1.41-3.31), while no association was observed with PM2.5 (OR = 0.96, 95 % CI 0.64-1.42). CONCLUSIONS: Our findings support the hypothesis that exposure to ambient air pollution, especially those from traffic sources (i.e., NO2), increases the risk of breast cancer in young women.

Asunto(s)

Contaminantes Atmosféricos , Neoplasias de la Mama , Exposición a Riesgos Ambientales , Dióxido de Nitrógeno , Material Particulado , Humanos , Femenino , Neoplasias de la Mama/epidemiología , Neoplasias de la Mama/etiología , Neoplasias de la Mama/inducido químicamente , Material Particulado/análisis , Material Particulado/efectos adversos , Dióxido de Nitrógeno/análisis , Dióxido de Nitrógeno/efectos adversos , Adulto , Ontario/epidemiología , Estudios de Casos y Controles , Adulto Joven , Exposición a Riesgos Ambientales/efectos adversos , Persona de Mediana Edad , Adolescente , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/efectos adversos , Incidencia , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Factores de Riesgo

RESUMEN

BACKGROUND: The world is becoming increasingly urbanised. As cities around the world continue to grow, it is important for urban planners and policy makers to understand how different urban configuration patterns affect the environment and human health. However, previous studies have provided mixed findings. We aimed to identify European urban configuration types, on the basis of the local climate zones categories and street design variables from Open Street Map, and evaluate their association with motorised traffic flows, surface urban heat island (SUHI) intensities, tropospheric NO2, CO2 per person emissions, and age-standardised mortality. METHODS: We considered 946 European cities from 31 countries for the analysis defined in the 2018 Urban Audit database, of which 919 European cities were analysed. Data were collected at a 250 m × 250 m grid cell resolution. We divided all cities into five concentric rings based on the Burgess concentric urban planning model and calculated the mean values of all variables for each ring. First, to identify distinct urban configuration types, we applied the Uniform Manifold Approximation and Projection for Dimension Reduction method, followed by the k-means clustering algorithm. Next, statistical differences in exposures (including SUHI) and mortality between the resulting urban configuration types were evaluated using a Kruskal-Wallis test followed by a post-hoc Dunn's test. FINDINGS: We identified four distinct urban configuration types characterising European cities: compact high density (n=246), open low-rise medium density (n=245), open low-rise low density (n=261), and green low density (n=167). Compact high density cities were a small size, had high population densities, and a low availability of natural areas. In contrast, green low density cities were a large size, had low population densities, and a high availability of natural areas and cycleways. The open low-rise medium and low density cities were a small to medium size with medium to low population densities and low to moderate availability of green areas. Motorised traffic flows and NO2 exposure were significantly higher in compact high density and open low-rise medium density cities when compared with green low density and open low-rise low density cities. Additionally, green low density cities had a significantly lower SUHI effect compared with all other urban configuration types. Per person CO2 emissions were significantly lower in compact high density cities compared with green low density cities. Lastly, green low density cities had significantly lower mortality rates when compared with all other urban configuration types. INTERPRETATION: Our findings indicate that, although the compact city model is more sustainable, European compact cities still face challenges related to poor environmental quality and health. Our results have notable implications for urban and transport planning policies in Europe and contribute to the ongoing discussion on which city models can bring the greatest benefits for the environment, climate, and health. FUNDING: Spanish Ministry of Science and Innovation, State Research Agency, Generalitat de Catalunya, Centro de Investigación Biomédica en red Epidemiología y Salud Pública, and Urban Burden of Disease Estimation for Policy Making as a Horizon Europe project.

Asunto(s)

Contaminación del Aire , Dióxido de Carbono , Ciudades , Mortalidad , Europa (Continente)/epidemiología , Contaminación del Aire/análisis , Contaminación del Aire/efectos adversos , Humanos , Dióxido de Carbono/análisis , Calor/efectos adversos , Planificación de Ciudades , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/efectos adversos , Dióxido de Nitrógeno/análisis , Dióxido de Nitrógeno/efectos adversos , Urbanización

RESUMEN

OBJECTIVES: To investigate the associations of traffic-related air pollution exposures in early pregnancy with birth outcomes and infant neurocognitive development. DESIGN: Cohort study. SETTING: Eligible women attended six visits in the maternity clinics of two centres, the First Affiliated Hospital of Chongqing Medical University and Chongqing Health Centre for Women and Children. PARTICIPANTS: Women who were between 20 and 40 years of age and were at 11-14 weeks gestation with a singleton pregnancy were eligible for participation. Women were excluded if they had a history of premature delivery before 32 weeks of gestation, maternal milk allergy or aversion or severe lactose intolerance. 1273 pregnant women enrolled in 2015-2016 and 1174 live births were included in this analysis. EXPOSURES: Air pollution concentrations at their home addresses, including particulate matter with diameter ≤2.5 µm (PM2.5) and nitrogen dioxide (NO2), during pre-conception and each trimester period were estimated using land-use regression models. OUTCOME MEASURES: Birth outcomes (ie, birth weight, birth length, preterm birth, low birth weight, large for gestational age and small for gestational age (SGA) status) and neurodevelopment outcomes measured by the Chinese version of Bayley Scales of Infant Development. RESULTS: An association between SGA and per-IQR increases in NO2 was found in the first trimester (OR: 1.57, 95% CI: 1.06 to 2.32) and during the whole pregnancy (OR: 1.33, 99% CI: 1.01 to 1.75). Both PM2.5 and NO2 exposure in the 90 days prior to conception were associated with lower Psychomotor Development Index scores (ß: -6.15, 95% CI: -8.84 to -3.46; ß: -2.83, 95% CI: -4.27 to -1.39, respectively). Increased NO2 exposure was associated with an increased risk of psychomotor development delay during different trimesters of pregnancy. CONCLUSIONS: Increased exposures to NO2 during pregnancy were associated with increased risks of SGA and psychomotor development delay, while increased exposures to both PM2.5 and NO2 pre-conception were associated with adverse psychomotor development outcomes at 12 months of age. TRIAL REGISTRATION NUMBER: ChiCTR-IOR-16007700.

Asunto(s)

Contaminación del Aire , Desarrollo Infantil , Exposición Materna , Material Particulado , Humanos , Femenino , Embarazo , China/epidemiología , Adulto , Recién Nacido , Estudios Prospectivos , Material Particulado/efectos adversos , Material Particulado/análisis , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Desarrollo Infantil/efectos de los fármacos , Exposición Materna/efectos adversos , Resultado del Embarazo/epidemiología , Adulto Joven , Dióxido de Nitrógeno/efectos adversos , Dióxido de Nitrógeno/análisis , Lactante , Peso al Nacer , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Efectos Tardíos de la Exposición Prenatal , Nacimiento Prematuro/epidemiología , Masculino

RESUMEN

Evidence regarding the link between long-term ambient ozone (O3) exposure and childhood sleep disorders is little. This study aims to examine the associations between long-term exposure to O3 and sleep disorders in children. We conducted a population-based cross-sectional survey, including 185,428 children aged 6-18 years in 173 schools across 14 Chinese cities during 2012 and 2018. Parents or guardians completed a checklist using Sleep Disturbance Scale for Children, and O3 exposure at residential and school addresses was estimated using a satellite-based spatiotemporal model. We used generalized linear mixed models to test the associations with adjustment for factors including socio-demographic variables, lifestyle, meteorology and multiple pollutants. Mean concentrations of O3, particulate matter with diameters ≤2.5 mm (PM2.5) and nitrogen dioxide (NO2) were 89.0 µg/m3, 42.5 µg/m3 and 34.4 µg/m3, respectively. O3 and NO2 concentrations were similar among provinces, while PM2.5 concentration varied significantly among provinces. Overall, 19.4% of children had at least one sleep disorder. Long-term exposure to O3 was positively associated with odds of sleep disorders for all subtypes. For example, each interquartile increment in home-school O3 concentrations was associated with a higher odds ratio for global sleep disorder, at 1.22 (95% confidence interval: 1.18, 1.26). Similar associations were observed for sleep disorder subtypes. The associations remained similar after adjustment for PM2.5 and NO2. Moreover, these associations were heterogeneous regionally, with more prominent associations among children residing in southeast region than in northeast and northwest regions in China. We concluded that long-term exposure to O3 is positively associated with risks of childhood sleep disorders. These associations varied by geographical region of China.

Asunto(s)

Contaminantes Atmosféricos , Exposición a Riesgos Ambientales , Ozono , Trastornos del Sueño-Vigilia , Humanos , Ozono/análisis , Ozono/efectos adversos , Niño , China/epidemiología , Adolescente , Masculino , Femenino , Contaminantes Atmosféricos/análisis , Exposición a Riesgos Ambientales/efectos adversos , Trastornos del Sueño-Vigilia/epidemiología , Trastornos del Sueño-Vigilia/inducido químicamente , Estudios Transversales , Material Particulado/análisis , Dióxido de Nitrógeno/análisis , Dióxido de Nitrógeno/efectos adversos , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis

RESUMEN

Importance: Air pollution is associated with structural brain changes, disruption of neurogenesis, and neurodevelopmental disorders. The association between prenatal exposure to ambient air pollution and risk of cerebral palsy (CP), which is the most common motor disability in childhood, has not been thoroughly investigated. Objective: To evaluate the associations between prenatal residential exposure to ambient air pollution and risk of CP among children born at term gestation in a population cohort in Ontario, Canada. Design, Setting, and Participants: Population-based cohort study in Ontario, Canada using linked, province-wide health administrative databases. Participants were singleton full term births (≥37 gestational weeks) born in Ontario hospitals between April 1, 2002, and March 31, 2017. Data were analyzed from January to December 2022. Exposures: Weekly average concentrations of ambient fine particulate matter with a diameter 2.5 µm (PM2.5) or smaller, nitrogen dioxide (NO2), and ozone (O3) during pregnancy assigned by maternal residence reported at delivery from satellite-based estimates and ground-level monitoring data. Main outcome and measures: CP cases were ascertained by a single inpatient hospitalization diagnosis or at least 2 outpatient diagnoses for children from birth to age 18 years. Results: The present study included 1 587 935 mother-child pairs who reached term gestation, among whom 3170 (0.2%) children were diagnosed with CP. The study population had a mean (SD) maternal age of 30.1 (5.6) years and 811 745 infants (51.1%) were male. A per IQR increase (2.7 µg/m3) in prenatal ambient PM2.5 concentration was associated with a cumulative hazard ratio (CHR) of 1.12 (95% CI, 1.03-1.21) for CP. The CHR in male infants (1.14; 95% CI, 1.02-1.26) was higher compared with the CHR in female infants (1.08; 95% CI, 0.96-1.22). No specific window of susceptibility was found for prenatal PM2.5 exposure and CP in the study population. No associations or windows of susceptibility were found for prenatal NO2 or O3 exposure and CP risk. Conclusions and relevance: In this large cohort study of singleton full term births in Canada, prenatal ambient PM2.5 exposure was associated with an increased risk of CP in offspring. Further studies are needed to explore this association and its potential biological pathways, which could advance the identification of environmental risk factors of CP in early life.

Asunto(s)

Contaminación del Aire , Parálisis Cerebral , Material Particulado , Efectos Tardíos de la Exposición Prenatal , Humanos , Embarazo , Femenino , Parálisis Cerebral/epidemiología , Parálisis Cerebral/etiología , Efectos Tardíos de la Exposición Prenatal/epidemiología , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Contaminación del Aire/estadística & datos numéricos , Masculino , Ontario/epidemiología , Adulto , Material Particulado/efectos adversos , Material Particulado/análisis , Lactante , Preescolar , Recién Nacido , Niño , Exposición Materna/efectos adversos , Exposición Materna/estadística & datos numéricos , Estudios de Cohortes , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Adolescente , Dióxido de Nitrógeno/efectos adversos , Dióxido de Nitrógeno/análisis