Association between Exposure to Ambient Air Pollution and Age-Related Cataract: A Nationwide Population-Based Retrospective Cohort Study.
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ABSTRACT:
SUBMITTER: Shin J
PROVIDER: S-EPMC7763970 | biostudies-literature | 2020 Dec
REPOSITORIES: biostudies-literature
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Association between Exposure to Ambient Air Pollution and Age-Related Cataract: A Nationwide Population-Based Retrospective Cohort Study.
Shin Jinyoung J Lee Hyungwoo H Kim Hyeongsu H
International journal of environmental research and public health 20201210 24
This study aimed to investigate the association between ambient air pollutants and cataracts in the general population aged 50 years or older using data from the Korean National Insurance Service-National Sample Cohort. Cataract patients were defined as those diagnosed by a physician and having undergone cataract surgery. After matching the average concentrations of PM<sub>2.5</sub>, PM<sub>10</sub>, NO<sub>2</sub>, CO, SO<sub>2</sub>, and O<sub>3</sub> in residential areas, the association betw ...[more]
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Project description:BackgroundThis study investigated the associations between exposure to ambient air pollutants and the incidence of osteoporosis using the Korean National Insurance Service-National Sample Cohort.MethodsThis nationwide, population-based, retrospective cohort study included 237,149 adults aged ≥40 years that did not have a diagnosis of osteoporosis at baseline between January 1, 2003, and December 31, 2015. Osteoporosis was defined as claim codes and prescriptions of bisphosphonates or selective estrogen receptor modulators at least twice annually. After matching values for PM10, NO2, CO, and SO2 during the 2002-2015 time period and PM2.5 in 2015 with residential areas, the incidence of osteoporosis was analyzed using a Cox proportional hazards regression model according to the quartile of average yearly concentrations of pollutants.ResultsOverall 22.2% of the study subjects, 52,601 (male: 5.6%, female: 37.6%) adults in total, were newly diagnosed with osteoporosis and treated. Exposure to PM10 was positively associated with incidence of osteoporosis (Q4: 1798 per 100,000 person-years vs. Q1: 1655 per 100,000 person-years). The adjusted hazard ratio (HR) with 95% confidence interval (CI) of Q4 in PM10 was 1.034 (1.009-1.062). The effect of PM10 on osteoporosis incidence was distinct in females (adjusted sub-HR: 1.065, 95% CI: 1.003-1.129), subjects aged < 65 years (adjusted sub-HR: 1.040, 95% CI: 1.010-1.072), and for residents in areas with low urbanization (adjusted sub-HR: 1.052, 95% CI: 1.019-1.087). However, there was no increase in osteoporosis based on exposure to NO2, CO, SO2, or PM2.5.ConclusionsLong-term exposure to PM10 was associated with newly diagnosed osteoporosis in Korean adults aged ≥40 years. This finding can aid in policy-making that is directed to control air pollution as a risk factor for bone health.
| S-EPMC8493748 | biostudies-literature
Project description:The evidence for the effects of environmental factors on COVID-19 case fatality remains controversial, and it is crucial to understand the role of preventable environmental factors in driving COVID-19 fatality. We thus conducted a nationwide cohort study to estimate the effects of environmental factors (temperature, particulate matter [PM2.5, PM10], sulfur dioxide [SO2], nitrogen dioxide [NO2], and ozone [O3]) on COVID-19 case fatality. A total of 71,808 confirmed COVID-19 cases were identified and followed up for their vital status through April 25, 2020. Exposures to ambient air pollution and temperature were estimated by linking the city- and county-level monitoring data to the residential community of each participant. For each participant, two windows were defined: the period from symptom onset to diagnosis (exposure window I) and the period from diagnosis date to date of death/recovery or end of the study period (exposure window II). Cox proportional hazards models were used to estimate the associations between these environmental factors and COVID-19 case fatality. COVID-19 case fatality increased in association with environmental factors for the two exposure windows. For example, each 10 μg/m3 increase in PM2.5, PM10, O3, and NO2 in window I was associated with a hazard ratio of 1.11 (95% CI 1.09, 1.13), 1.10 (95% CI 1.08, 1.13), 1.09 (95 CI 1.03, 1.14), and 1.27 (95% CI 1.19, 1.35) for COVID-19 fatality, respectively. A significant effect was also observed for low temperature, with a hazard ratio of 1.03 (95% CI 1.01, 1.04) for COVID-19 case fatality per 1°C decrease. Subgroup analysis indicated that these effects were stronger in the elderly, as well as in those with mild symptoms and living in Wuhan or Hubei. Overall, the sensitivity analyses also yielded consistent estimates. Short-term exposure to ambient air pollution and low temperature during the illness would play a nonnegligible part in causing case fatality due to COVID-19. Reduced exposures to high concentrations of PM2.5, PM10, O3, SO2, and NO2 and low temperature would help improve the prognosis and reduce public health burden.
| S-EPMC8226106 | biostudies-literature
Project description:BackgroundIt remains unclear whether in utero and childhood exposure to air pollution affects pubertal development, particularly age of menarche in girls.ObjectiveThe aim of this study was to determine whether residential ambient particulate matter (PM) exposure in utero and during childhood is associated with age of menarche.MethodsWe studied 5,201 girls in the Growing Up Today Study 2 (2004-present) who were 10-17 y of age at enrollment (47.7% premenarchal; 52.3% postmenarchal). Exposure to three size fractions of PM [fine PM with aerodynamic diameter ≤2.5μm (PM2.5), PM with aerodynamic diameters between 2.5μm and 10μm (PM2.5-10), and PM with aerodynamic diameter 10μm (PM10)] was assigned based on maternal residential address, updated every 2 y, using nationwide spatiotemporal models. We estimated average PM exposure in utero, and time-varying windows: annual average exposure in the prior 1 and 2 y and cumulative average from birth. Age of menarche was self-reported on three surveys administered in 2004, 2006, and 2008. We calculated hazard ratios (HR) for menarche for an interquartile range (IQR) increase in PM exposure using Cox proportional hazard models adjusting for potential confounders.ResultsGirls attained menarche at 12.3 y of age on average. In the adjusted model, higher residential exposure to ambient PM2.5 during all time windows was associated with earlier age of menarche. The HRs of menarche for each IQR (4 μg/m3) increase in exposure to PM2.5 during the in utero period, 1 y prior to menarche, and throughout childhood were 1.03 [95% confidence interval (CI): 1.00, 1.06], 1.06 (95% CI: 1.02, 1.10) and 1.06 (95% CI: 1.02, 1.10), respectively. Effect estimates for PM10 exposure were similar, albeit attenuated, for all time windows. PM2.5-10 exposure was not associated with age of menarche.DiscussionAmong a large, nationwide, prospective cohort of U.S. girls, higher exposure to PM2.5 and PM10 in utero and throughout childhood was associated with an earlier age of menarche. Our results suggest that PM2.5 and PM10 may have endocrine-disrupting properties that could lead to altered timing of menarche. https://doi.org/10.1289/EHP12110.
| S-EPMC10549984 | biostudies-literature
Project description:BackgroundEnvironmental factors may contribute to the development of Kawasaki disease in children, but prenatal environmental exposures are understudied.ObjectiveWe used a population-based cohort to investigate whether prenatal exposure to outdoor air pollution is associated with the incidence of Kawasaki disease in childhood.MethodsWe 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 ≤2.5μm 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).ResultsThe 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.DiscussionIn 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.
| S-EPMC7571626 | biostudies-literature
Project description:The aim of this study was to investigate the risk of developing preeclampsia (PE) associated with gestational exposure to ambient air pollutants in southern Sweden, a low-exposure area. We used a cohort of 43,688 singleton pregnancies and monthly mean exposure levels of black carbon (BC), local and total particulate matter (PM2.5 and PM10), and NOX at the maternal residential address estimated by Gaussian dispersion modeling from 2000 to 2009. Analyses were conducted using binary logistic regression. A subtype analysis for small-for-gestational age (SGA) was performed. All analyses were adjusted for obstetrical risk factors and socioeconomic predictors. There were 1286 (2.9%) PE cases in the analysis. An adjusted odds ratio (AOR) of 1.35 with a 95% confidence interval (CI) of 1.11-1.63 was found when comparing the lowest quartile of BC exposure to the highest quartile in the third trimester The AOR for PE associated with each 5 µg/m3 increase in locally emitted PM2.5 was 2.74 (95% CI: 1.68, 4.47) in the entire pregnancy. Similar patterns were observed for each 5 µg/m3 increment in locally emitted PM10. In pregnancies complicated by PE with SGA, the corresponding AOR for linear increases in BC was 3.48 (95% CI: 1.67, 7.27). In this low-level setting, maternal exposure to ambient air pollution during gestation was associated with the risk of developing PE. The associations seemed more pronounced in pregnancies with SGA complications, a finding that should be investigated further.
| S-EPMC7084298 | biostudies-literature
Project description:Study questionTo what extent are ambient concentrations of particulate matter <2.5 microns (PM2.5), nitrogen dioxide (NO2) and ozone (O3) associated with risk of self-reported physician-diagnosed uterine leiomyomata (UL)?Summary answerIn this large prospective cohort study of Black women, ambient concentrations of O3, but not PM2.5 or NO2, were associated with increased risk of UL.What is known alreadyUL are benign tumors of the myometrium that are the leading cause of gynecologic inpatient care among reproductive-aged women. Black women are clinically diagnosed at two to three times the rate of white women and tend to exhibit earlier onset and more severe disease. Two epidemiologic studies have found positive associations between air pollution exposure and UL risk, but neither included large numbers of Black women.Study design, size, durationWe conducted a prospective cohort study of 21 998 premenopausal Black women residing in 56 US metropolitan areas from 1997 to 2011.Participants/material, setting, methodsWomen reported incident UL diagnosis and method of confirmation (i.e. ultrasound, surgery) on biennial follow-up questionnaires. We modeled annual residential concentrations of PM2.5, NO2 and O3 throughout the study period. We used Cox proportional hazards regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for a one-interquartile range (IQR) increase in air pollutant concentrations, adjusting for confounders and co-pollutants.Main results and the role of chanceDuring 196 685 person-years of follow-up, 6238 participants (28.4%) reported physician-diagnosed UL confirmed by ultrasound or surgery. Although concentrations of PM2.5 and NO2 were not appreciably associated with UL (HRs for a one-IQR increase: 1.01 (95% CI: 0.93, 1.10) and 1.05 (95% CI: 0.95, 1.16), respectively), O3 concentrations were associated with increased UL risk (HR for a one-IQR increase: 1.19, 95% CI: 1.07, 1.32). The association was stronger among women age <35 years (HR: 1.26, 95% CI: 0.98, 1.62) and parous women (HR: 1.28, 95% CI: 1.11, 1.48).Limitations, reasons for cautionOur measurement of air pollution is subject to misclassification, as monitoring data are not equally spatially distributed and we did not account for time-activity patterns. Our outcome measure was based on self-report of a physician diagnosis, likely resulting in under-ascertainment of UL. Although we controlled for several individual- and neighborhood-level confounding variables, residual confounding remains a possibility.Wider implications of the findingsInequitable burden of air pollution exposure has important implications for racial health disparities, and may be related to disparities in UL. Our results emphasize the need for additional research focused on environmental causes of UL.Study funding/competing interest(s)This research was funded by the National Cancer Institute (U01-CAA164974) and the National Institute of Environmental Health Sciences (R01-ES019573). L.A.W. is a fibroid consultant for AbbVie, Inc. and accepts in-kind donations from Swiss Precision Diagnostics, Sandstone Diagnostics, FertilityFriend.com and Kindara.com for primary data collection in Pregnancy Study Online (PRESTO). M.J. declares consultancy fees from the Health Effects Institute (as a member of the review committee). The remaining authors declare they have no actual or potential competing financial interests.Trial registration numberN/A.
| S-EPMC8487660 | biostudies-literature
Project description:BackgroundAmbient air pollution exposure has been associated with childhood asthma, but previous studies have primarily focused on prevalence of asthma and asthma-related outcomes and urban traffic-related exposures.ObjectiveWe examined nationwide associations between pre- and postnatal exposure to ambient air pollution components and asthma incidence in children age 0-19 y.MethodsAsthma incidence was identified from hospital admission, emergency room, and outpatient contacts among all live-born singletons born in Denmark between 1998 and 2016. We linked registry data with monthly mean concentrations of particulate matter (PM) with aerodynamic diameter ≤2.5μm (PM2.5) and PM with aerodynamic diameter ≤10μm (PM10), nitrogen dioxide (NO2), nitrogen oxides, elemental carbon, and organic carbon (OC), sulfur dioxide, ozone, sulfate, nitrate, ammonium, secondary organic aerosols, and sea salt. Associations were estimated with Cox proportional hazard models using fixed prenatal exposure means and time-varying postnatal exposures.ResultsOf the 1,060,154 children included, 6.1% had asthma during the mean follow-up period of 8.8 y. The risk of asthma increased with increasing prenatal exposure to all pollutants except for O3 and sea salt. We also observed increased risk after restriction to asthma after age 4 y, after additional adjustment for area-specific socioeconomic status, and for postnatal exposure to most pollutants. The hazard ratio (HR) associated with an interquartile range increase of 2.4 and 8.7 μg/m3 in prenatal exposure was 1.06 [95% confidence interval (CI): 1.04, 1.08] for PM2.5 and 1.04 (95% CI: 1.02, 1.05) for NO2, respectively. This association with PM2.5 was stable after adjustment for NO2, whereas it attenuated for NO2 to 1.01 (95% CI: 0.99, 1.03) after adjustment for PM2.5. For a 0.5-μg/m3 increase in prenatal OC exposure, for which biomass is an important source, the HR was 1.08 (95% CI: 1.06, 1.10), irrespective of adjustment for PM2.5.DiscussionThese findings suggest that early-life exposure to ambient air pollution from multiple sources contributes to asthma development. https://doi.org/10.1289/EHP11539.
| S-EPMC10171081 | biostudies-literature
Project description:Exposure to higher levels of ambient air pollution is a known risk factor for cardiovascular disease but long-term effects of pollution exposure on the pulmonary vessels are unknown.MethodsAmong 2428 Framingham Heart Study participants who underwent chest computed tomography (CT) between 2008 and 2011, pulmonary vascular volumes were calculated by image analysis, including the total vascular volume and small vessel volume (cross-sectional area <5 mm2; BV5 defined as small vessel volume). Using spatiotemporal models and participant home address, we assigned 1-year (2008) and 5-year (2004-2008) average concentrations of fine particulate matter (PM2.5), elemental carbon (EC), and ground-level ozone (O3), and distance to major roadway. We examined associations of 1- and 5-year exposures, and distance to road, with CT vascular volumes using multivariable linear regression models.ResultsThere was a consistent negative association of higher O3 with lower small vessel volumes, which persisted after adjustment for distance to road. Per interquartile range (IQR) of 2008 O3, BV5 was 0.34 mL lower (95% confidence intervals [CI], -0.61 to -0.06; P = 0.02), with similar results for 5-year exposure. One-year EC exposure and closer proximity to road were weakly associated with small vessel volumes; BV5 was 0.18 mL higher per IQR of 2008 EC (95% CI, -0.05 to 0.42; P = 0.13) and 0.40 mL higher per IQR closer proximity to road (95% CI: -0.10 to 0.89; P = 0.12). PM2.5 was not associated with small vascular volumes; BV5 was 0.26 mL lower per IQR of 2008 PM2.5 (95% CI: -0.68 to 0.16; P = 0.22).ConclusionsAmong community-dwelling adults living in the northeastern United States, higher exposure to O3 was associated with lower small pulmonary vessel volumes on CT.
| S-EPMC8043731 | biostudies-literature
Project description:ImportanceAir 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.ObjectiveTo 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 participantsPopulation-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.ExposuresWeekly 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 measuresCP cases were ascertained by a single inpatient hospitalization diagnosis or at least 2 outpatient diagnoses for children from birth to age 18 years.ResultsThe 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 relevanceIn 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.
| S-EPMC11234239 | biostudies-literature
Project description:Higher prenatal ambient air pollution exposure has been associated with impaired neurodevelopment in preschoolers and school-aged children. The purpose of this study was to explore the relationships between prenatal ambient air pollution exposure and neurodevelopment during infancy. This study examined 161 Latino mother-infant pairs from the Southern California Mother's Milk Study. Exposure assessments included prenatal nitrogen dioxide (NO2) and particulate matter smaller than 2.5 and 10 microns in diameter (PM2.5 and PM10, respectively). The pregnancy period was also examined as three windows, early, mid, and late, which describe the first, middle, and last three months of pregnancy. Infant neurodevelopmental outcomes at 2 years of age were measured using the Bayley-III Scales of Infant and Toddler Development. Multivariable linear models and distributed lag linear models (DLM) were used to examine relationships between prenatal exposures and neurodevelopmental scores, adjusting for socioeconomic status, breastfeeding frequency, time of delivery, pre-pregnancy body mass index, and infant birthweight and sex. Higher prenatal exposure to PM10 and PM2.5 was negatively associated with composite cognitive score (β = -2.01 [-3.89, -0.13] and β = -1.97 [-3.83, -0.10], respectively). In addition, higher average prenatal exposure to PM10 was negatively associated with composite motor (β = -2.35 [-3.95, -0.74]), scaled motor (β = -0.77 [-1.30, -0.24]), gross motor (β = -0.37 [-0.70, -0.04]), fine motor (β = -0.40 [-0.71, -0.09]), composite language (β = -1.87 [-3.52, -0.22]), scaled language (β = -0.61 [-1.18, -0.05]) and expressive communication scaled scores (β = -0.36 [-0.66, -0.05]). DLMs showed that higher prenatal air pollution exposure during mid and late pregnancy was inversely associated with motor, cognitive, and communication language scores. Higher exposure to air pollutants during pregnancy, particularly in the mid and late prenatal periods, was inversely associated with scaled and composite motor, cognitive, and language scores at 2 years. These results indicate that prenatal ambient air pollution may negatively impact neurodevelopment in early life.
| S-EPMC9872424 | biostudies-literature