National cohort and meteorological data based nested case–control study on the association between air pollution exposure and thyroid cancer
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ABSTRACT:
SUBMITTER: Park S
PROVIDER: S-EPMC8566463 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:This study aimed to evaluate the impact of weather conditions and air pollution on the onset of sudden sensorineural hearing loss (SSNHL). The Korean Health Insurance Review and Assessment Service - National Sample Cohort (HIRA-NSC) from 2002 through 2013 was used. A total of 5,200 participants with SSNHL were matched 1:4 for age, sex, income, region of residence, hypertension, diabetes, and dyslipidemia with 20,800 control participants. Meteorological data included daily mean temperature (°C), daily highest temperature (°C), daily lowest temperature (°C), daily temperature difference (°C), relative humidity (%), ambient atmospheric pressure (hPa), pressure, SO2 (ppm), NO2 (ppm), O3 (ppm), CO (ppm), and PM10 (μg/m3) of a mean of 60 days, 30 days, 14 days, 7 days, and 3 days before SSNHL were analyzed. Hourly measurements were taken from 94 places to assess the temperature, humidity, and atmospheric pressure and from 273 places to determine SO2, NO2, O3, CO, and PM10. Crude and adjusted odds ratios (ORs) and 95% confidence intervals (CIs) of meteorological data for SSNHL were analyzed using unconditional logistic regression analyses. Subgroup analyses were conducted by age and sex. The mean NO2 and O3 concentrations 14 days before the index date were different in the SSNHL group compared to those in the control group (P < 0.001 for NO2 and P = 0.021 for O3). The adjusted 14-day OR for NO2 (0.1 ppm) exposure was 3.12 in the SSNHL group compared to that in the control group (95% CI = 2.16-4.49, P < 0.001). The increased odds of NO2 exposure for 14 days in the SSNHL group persisted in the age group older than 30 years for both sexes. Other meteorological conditions did not show differences between the SSNHL and control groups. SSNHL was associated with high concentrations of NO2.
| S-EPMC6547844 | biostudies-literature
Project description:Previous studies revealed that chronic exposure to air pollution can significantly increase the risk of the development of Parkinson's disease (PD), but this relationship is inconclusive as large-scale prospective studies are limited and the results are inconsistent. Therefore, the purpose of this study was to ascertain the adverse health effects of air pollution exposure in a nationwide population using a longitudinal approach.We conducted a nested case-control study using the National Health Insurance Research Dataset (NHIRD), which consisted of 1,000,000 beneficiaries in the National Health Insurance Program (NHI) in the year 2000 and their medical records from 1995 to 2013 and using public data on air pollution concentrations from monitoring stations across Taiwan released from the Environmental Protection Administration to identify people with ages ≥ 40 years living in areas with monitoring stations during 1995-1999 as study subjects. Then, we excluded subjects with PD, dementia, stroke and diabetes diagnosed before Jan. 1, 2000 and obtained 54,524 subjects to follow until Dec. 31, 2013. In this observational period, 1060 newly diagnosed PD cases were identified. 4240 controls were randomly selected from those without PD using a matching strategy for age, sex, the year of PD diagnosis and the year of entering the NHI program at a ratio of 1:4. Ten elements of air pollution were examined, and multiple logistic regression models were used to measure their risks in subsequent PD development.The incidence of PD in adults aged ≥ 40 years was 1.9%, and the median duration for disease onset was 8.45 years. None of the chemical compounds (SO2, O3, CO, NOx, NO, NO2, THC, CH4, or NMHC) significantly affected the incidence of PD except for particulate matter. PM10 exposure showed significant effects on the likelihood of PD development (T3 level: > 65μg/m3 versus T1 level: ≤ 54μg/m3; OR = 1.35, 95% CI = 1.12-1.62, 0.001 ≤ P < 0.01). In addition, comorbid conditions such as dementia (ORs = 3.53-3.93, Ps < 0.001), stroke (ORs = 2.99-3.01, Ps < 0.001), depression (ORs = 2.51-2.64, Ps < 0.001), head injury (ORs = 1.24-1.29, 0.001 ≤ Ps < 0.01 or 0.01 ≤ Ps < 0.05), sleep disorder (OR = 1.23-1.26, 0.001 ≤ Ps < 0.01), and hypertension (ORs = 1.18-1.19, 0.01 ≤ Ps < 0.05) also significantly increased the risk for PD development.Although PM10 plays a significant role in PD development, the associated chemical/metal compounds that are capable of inducing adverse biological mechanisms still warrant further exploration. Because of a link between comorbid conditions and PM exposure, research on the causal relationship between long-term exposure to PM and the development of PD should be considered with caution because other possible modifiers or mediators, comorbid diseases in particular, may be involved.
| S-EPMC5557354 | biostudies-other
Project description:There has been little study on the effect of traffic-related air pollution on the incidence and persistence of asthma in preschool children. We evaluated the association of exposure to traffic-related air pollution with the incidence/persistence of asthma during the first 3 years of life using a population-based study.A baseline survey was conducted in 1½-year-old children (n=63,266). A follow-up survey at 3 years of age (n=43,343) identified new-onset asthma cases (n=853) and persistence of asthma (n=214). In the prevalence/persistence study, the outdoor concentrations of nitrogen oxides (NOx) and elemental carbon (EC) at home during the first 1½ years of life were estimated by a dispersion model. In the nested case-control study, which regarded incidence of asthma as cases, the personal exposure levels were estimated by dispersion model including time-activity pattern.There was no statistically significant association between the incidence of asthma between age 1½ and 3 years and personal exposure levels to NOx nor EC. However, the persistence of asthmatic symptoms (between 1½ and 3 ears) was significantly associated with outdoor concentrations of NOx. ORs for the persistence of asthmatic symptoms were 6.02 (95% CI 1.51 to 23.92) for the comparison between the upper 5th and lower 25th centiles of NOx.While no statistically significant association was observed for the incidence of asthma, the persistence of asthmatic symptoms in preschool children was significantly associated with traffic-related air pollution. This supports its importance as a risk factor in childhood airway disease.
| S-EPMC4769392 | biostudies-other
Project description:Industrialization has been linked to the etiology of inflammatory bowel disease (IBD).We investigated the association between air pollution exposure and IBD.The European Prospective Investigation into Cancer and Nutrition cohort was used to identify cases with Crohn's disease (CD) (n = 38) and ulcerative colitis (UC) (n = 104) and controls (n = 568) from Denmark, France, the Netherlands, and the UK, matched for center, gender, age, and date of recruitment. Air pollution data were obtained from the European Study of Cohorts for Air Pollution Effects. Residential exposure was assessed with land-use regression models for particulate matter with diameters of <10 ?m (PM10), <2.5 ?m (PM2.5), and between 2.5 and 10 ?m (PMcoarse), soot (PM2.5 absorbance), nitrogen oxides, and two traffic indicators. Conditional logistic regression analyses were performed to calculate odds ratios (ORs) with 95 % confidence intervals (CIs).Although air pollution was not significantly associated with CD or UC separately, the associations were mostly similar. Individuals with IBD were less likely to have higher exposure levels of PM2.5 and PM10, with ORs of 0.24 (95 % CI 0.07-0.81) per 5 ?g/m(3) and 0.25 (95 % CI 0.08-0.78) per 10 ?g/m(3), respectively. There was an inverse but nonsignificant association for PMcoarse. A higher nearby traffic load was positively associated with IBD [OR 1.60 (95 % CI 1.04-2.46) per 4,000,000 motor vehicles × m per day]. Other air pollutants were positively but not significantly associated with IBD.Exposure to air pollution was not found to be consistently associated with IBD.
| S-EPMC5020109 | biostudies-literature
Project description:Ecologic analyses, case-case comparisons, and animal experiments suggest positive associations between air pollution and tuberculosis.We evaluated this hypothesis in a large sample, which yielded results that are applicable to the general population.We conducted a case-control study nested within a cohort of Kaiser Permanente of Northern California members. All active pulmonary tuberculosis (TB) cases newly diagnosed between 1996 and 2010 (n = 2,309) were matched to two controls (n = 4,604) by age, sex, and race/ethnicity on the index date corresponding with the case diagnosis date. Average individual-level concentrations of carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3), and particulate matter with aerodynamic diameter ? 2.5 ?m (PM2.5) and 10 ?m (PM10) for 2 years before diagnosis/entry into the study were estimated using measurements from the California Air Resources Board monitor closest to the participant's residence.In single-pollutant adjusted conditional logistic regression models, the pulmonary TB odds ratios (95% confidence intervals) for the highest quintile (vs. lowest) were 1.50 (95% CI: 1.15, 1.95) for CO and 1.42 (95% CI: 1.10, 1.84) for NO2. Corresponding estimates were higher among never [1.68 (95% CI: 1.26, 2.24)] than ever [1.19 (95% CI: 0.74, 1.92)] smokers for CO. In contrast, for NO2, estimates were higher among ever [1.81 (95% CI: 1.13, 2.91)] than never [1.29 (95% CI: 0.97, 1.71)] smokers. O3 was inversely associated for smokers [0.66 (95% CI: 0.43, 1.02)] and never smokers [0.65 (95% CI: 0.52, 0.81)]. No other consistent patterns were observed.In this first, to our knowledge, U.S. nested case-control study on air pollution and pulmonary TB, we observed positive associations with ambient CO and NO2, which require confirmation.Smith GS, Van Den Eeden SK, Garcia C, Shan J, Baxter R, Herring AH, Richardson DB, Van Rie A, Emch M, Gammon MD. 2016. Air pollution and pulmonary tuberculosis: a nested case-control study among members of a Northern California health plan. Environ Health Perspect 124:761-768;?http://dx.doi.org/10.1289/ehp.1408166.
| S-EPMC4892908 | biostudies-other
Project description:BackgroundFew epidemiological studies of air pollution have used residential histories to develop long-term retrospective exposure estimates for multiple ambient air pollutants and vehicle and industrial emissions. We present such an exposure assessment for a Canadian population-based lung cancer case-control study of 8353 individuals using self-reported residential histories from 1975 to 1994. We also examine the implications of disregarding and/or improperly accounting for residential mobility in long-term exposure assessments.MethodsNational spatial surfaces of ambient air pollution were compiled from recent satellite-based estimates (for PM2.5 and NO2) and a chemical transport model (for O3). The surfaces were adjusted with historical annual air pollution monitoring data, using either spatiotemporal interpolation or linear regression. Model evaluation was conducted using an independent ten percent subset of monitoring data per year. Proximity to major roads, incorporating a temporal weighting factor based on Canadian mobile-source emission estimates, was used to estimate exposure to vehicle emissions. A comprehensive inventory of geocoded industries was used to estimate proximity to major and minor industrial emissions.ResultsCalibration of the national PM2.5 surface using annual spatiotemporal interpolation predicted historical PM2.5 measurement data best (R2 = 0.51), while linear regression incorporating the national surfaces, a time-trend and population density best predicted historical concentrations of NO2 (R2 = 0.38) and O3 (R2 = 0.56). Applying the models to study participants residential histories between 1975 and 1994 resulted in mean PM2.5, NO2 and O3 exposures of 11.3 μg/m3 (SD = 2.6), 17.7 ppb (4.1), and 26.4 ppb (3.4) respectively. On average, individuals lived within 300 m of a highway for 2.9 years (15% of exposure-years) and within 3 km of a major industrial emitter for 6.4 years (32% of exposure-years). Approximately 50% of individuals were classified into a different PM2.5, NO2 and O3 exposure quintile when using study entry postal codes and spatial pollution surfaces, in comparison to exposures derived from residential histories and spatiotemporal air pollution models. Recall bias was also present for self-reported residential histories prior to 1975, with cases recalling older residences more often than controls.ConclusionsWe demonstrate a flexible exposure assessment approach for estimating historical air pollution concentrations over large geographical areas and time-periods. In addition, we highlight the importance of including residential histories in long-term exposure assessments. For submission to: Environmental Health.
| S-EPMC3372423 | biostudies-literature
Project description:BACKGROUND:Preterm birth (PTB) has been associated with exposure to air pollution, but it is unclear whether effects might vary among air pollution sources and components. OBJECTIVES:We studied the relationships between PTB and exposure to different components of air pollution, including gases and particulate matter (PM) by size fraction, chemical composition, and sources. METHODS:Fine and ultrafine PM (respectively, PM2.5 and PM0.1) by source and composition were modeled across California over 2000-2008. Measured PM2.5, nitrogen dioxide, and ozone concentrations were spatially interpolated using empirical Bayesian kriging. Primary traffic emissions at fine scale were modeled using CALINE4 and traffic indices. Data on maternal characteristics, pregnancies, and birth outcomes were obtained from birth certificates. Associations between PTB (n = 442,314) and air pollution exposures defined according to the maternal residence at birth were examined using a nested matched case-control approach. Analyses were adjusted for maternal age, race/ethnicity, education and neighborhood income. RESULTS:Adjusted odds ratios for PTB in association with interquartile range (IQR) increases in average exposure during pregnancy were 1.133 (95% CI: 1.118, 1.148) for total PM2.5, 1.096 (95% CI: 1.085, 1.108) for ozone, and 1.079 (95% CI: 1.065, 1.093) for nitrogen dioxide. For primary PM, the strongest associations per IQR by source were estimated for onroad gasoline (9-11% increase), followed by onroad diesel (6-8%) and commercial meat cooking (4-7%). For PM2.5 composition, the strongest positive associations per IQR were estimated for nitrate, ammonium, and secondary organic aerosols (11-14%), followed by elemental and organic carbon (2-4%). Associations with local traffic emissions were positive only when analyses were restricted to births with residences geocoded at the tax parcel level. CONCLUSIONS:In our statewide nested case-control study population, exposures to both primary and secondary pollutants were associated with an increase in PTB. CITATION:Laurent O, Hu J, Li L, Kleeman MJ, Bartell SM, Cockburn M, Escobedo L, Wu J. 2016. A statewide nested case-control study of preterm birth and air pollution by source and composition: California, 2001-2008. Environ Health Perspect 124:1479-1486;?http://dx.doi.org/10.1289/ehp.1510133.
| S-EPMC5010414 | biostudies-literature
Project description:BACKGROUND:Thyroid hormones are critical for fetal development and growth. Whether prenatal exposure to fine particle air pollution (? 2.5 ?m; PM2.5) affects fetal thyroid function and what the impact is on birth weight in normal healthy pregnancies have not been studied yet. OBJECTIVES:We studied the impact of third-trimester PM2.5 exposure on fetal and maternal thyroid hormones and their mediating role on birth weight. METHODS:We measured the levels of free thyroid hormones (FT3, FT4) and thyroid-stimulating hormone (TSH) in cord blood (n = 499) and maternal blood (n = 431) collected after delivery from mother-child pairs enrolled between February 2010 and June 2014 in the ENVIRONAGE birth cohort with catchment area in the province of Limburg, Belgium. RESULTS:An interquartile range (IQR) increment (8.2 ?g/m3) in third-trimester PM2.5 exposure was inversely associated with cord blood TSH levels (-11.6%; 95% CI: -21.8, -0.1) and the FT4/FT3 ratio (-62.7%; 95% CI: -91.6, -33.8). A 10th-90th percentile decrease in cord blood FT4 levels was associated with a 56 g decrease in mean birth weight (95% CI: -90, -23). Assuming causality, we estimated that cord blood FT4 mediated 21% (-19 g; 95% CI: -37, -1) of the estimated effect of an IQR increment in third-trimester PM2.5 exposure on birth weight. Third-trimester PM2.5 exposure was inversely but not significantly associated with maternal blood FT4 levels collected 1 day after delivery (-4.0%, 95% CI: -8.0, 0.2 for an IQR increment in third-trimester PM2.5). CONCLUSIONS:In our study population of normal healthy pregnancies, third-trimester exposure to PM2.5 air pollution was associated with differences in fetal thyroid hormone levels that may contribute to reduced birth weight. Additional research is needed to confirm our findings in other populations and to evaluate potential consequences later in life.
| S-EPMC5382000 | biostudies-literature
Project description:ObjectiveAnimal studies have indicated that perfluoroalkylated substances (PFAS) increase mammary fibroadenomas. A recent case-control study in Greenlandic Inuit women showed an association between the PFAS serum levels and breast cancer (BC) risk. The present study evaluates the association between serum levels of PFAS in pregnant Danish women and the risk of premenopausal BC during a follow-up period of 10-15 years using prospectively collected exposure data during the pregnancy.MethodsQuestionnaire and blood samples were taken during 1996-2002 and at the end of follow-up, all 250 BC cases and 233 frequency-matched controls were chosen for further analyses. Serum levels of ten perfluorocarboxylated acids, five perfluorosulfonated acids, and one sulfonamide (perflurooctane-sulfonamide, PFOSA) were determined by liquid chromatography-tandem mass spectrometry with electrospray ionization in negative mode. Computer-assisted telephone interviews taken during pregnancy provided data on potential confounders.ResultsWeak positive and negative insignificant associations were found between BC risk and levels of perfluorooctane sulfonamide (PFOSA) and perfluorohexanesulfonate (PFHxS), respectively. Grouped into quintile, the BC cases had a significant positive association with PFOSA at the highest quintiles and a negatively association for PFHxS. Sensitivity analyses excluding uncertain cases caused stronger data for PFOSA and weaker for PFHxS. No further significant associations were observed.ConclusionsThis study does not provide convincing evidence for a causal link between PFAS exposures and premenopausal BC risks 10-15 years later.
| S-EPMC4215104 | biostudies-literature
Project description:BackgroundPopulation exposure assessment methods that capture local-scale pollutant variability are needed for large-scale epidemiological studies and surveillance, policy, and regulatory purposes. Currently, such exposure methods are limited.MethodsWe created 2006 national pollutant models for fine particulate matter [PM with aerodynamic diameter ? 2.5 ?m (PM2.5)], nitrogen dioxide (NO2), benzene, ethylbenzene, and 1,3-butadiene from routinely collected fixed-site monitoring data in Canada. In multiple regression models, we incorporated satellite estimates and geographic predictor variables to capture background and regional pollutant variation and used deterministic gradients to capture local-scale variation. The national NO2 and benzene models are evaluated with independent measurements from previous land use regression models that were conducted in seven Canadian cities. National models are applied to census block-face points, each of which represents the location of approximately 89 individuals, to produce estimates of population exposure.ResultsThe national NO2 model explained 73% of the variability in fixed-site monitor concentrations, PM2.5 46%, benzene 62%, ethylbenzene 67%, and 1,3-butadiene 68%. The NO2 model predicted, on average, 43% of the within-city variability in the independent NO2 data compared with 18% when using inverse distance weighting of fixed-site monitoring data. Benzene models performed poorly in predicting within-city benzene variability. Based on our national models, we estimated Canadian ambient annual average population-weighted exposures (in micrograms per cubic meter) of 8.39 for PM2.5, 23.37 for NO2, 1.04 for benzene, 0.63 for ethylbenzene, and 0.09 for 1,3-butadiene.ConclusionsThe national pollutant models created here improve exposure assessment compared with traditional monitor-based approaches by capturing both regional and local-scale pollution variation. Applying national models to routinely collected population location data can extend land use modeling techniques to population exposure assessment and to informing surveillance, policy, and regulation.
| S-EPMC3237350 | biostudies-literature