Lung Cancer Risk and Residential Exposure to Air Pollution: A Korean Population-Based Case-Control Study.
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ABSTRACT:
SUBMITTER: Lamichhane DK
PROVIDER: S-EPMC5653475 | biostudies-literature | 2017 Nov
REPOSITORIES: biostudies-literature
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Lung Cancer Risk and Residential Exposure to Air Pollution: A Korean Population-Based Case-Control Study.
Lamichhane Dirga Kumar DK Kim Hwan Cheol HC Choi Chang Min CM Shin Myung Hee MH Shim Young Mog YM Leem Jong Han JH Ryu Jeong Seon JS Nam Hae Seong HS Park Sung Min SM
Yonsei medical journal 20171101 6
<h4>Purpose</h4>To investigate the association between long-term exposure to ambient air pollution and lung cancer incidence in Koreans.<h4>Materials and methods</h4>This was a population-based case-control study covering 908 lung cancer patients and 908 controls selected from a random sample of people within each Korean province and matched according to age, sex, and smoking status. We developed land-use regression models to estimate annual residential exposure to particulate matter (PM₁₀) and ...[more]
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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 ?g/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.
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Project description:BACKGROUND:Some studies have supported an association between traffic-related air pollution exposure and breast cancer risk. However, few studies have considered exposures in early life, which may be a period of increased susceptibility. OBJECTIVES:To examine the association of childhood residential exposure to traffic-related air pollution with breast cancer development. METHODS:The Sister Study is a prospective cohort of 50,884 initially breast cancer-free women, of whom 42,934 provided information at enrollment about roads and traffic near their primary childhood residence before age 14 as well as relevant covariates. Adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs) for the association between traffic-related measures at childhood residence and adult incident breast cancer were estimated using Cox regression. RESULTS:During follow-up (mean = 6.3 years), 2,028 breast cancers were diagnosed. Traffic-related characteristics were not consistently associated with breast cancer risk. However, incidence was elevated among women who reported a median/barrier dividing either their primary childhood residential road (aHR = 1.2; 95% CI: 0.9-1.7) or the nearest cross-street (aHR = 1.3; 95% CI: 0.9-1.8, if the cross-street was within 100ft.), and among women whose nearest cross-street had the highest traffic, ?3 lanes, and/or a median/barrier (aHR = 1.4; 95% CI: 1.0-1.9). CONCLUSIONS:Measures of potential exposure to vehicular traffic were not consistently associated with breast cancer risk. However, living during childhood on or near a road with a median or other barrier, which may be a more easily remembered road characteristic than the others assessed, was associated with increased breast cancer risk.
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Project description:Air pollution exposure is a well-established risk factor for several adverse respiratory outcomes, including airways diseases and lung cancer. Few studies have investigated the relationship between air pollution and interstitial lung disease (ILD) despite many forms of ILD arising from environmental exposures. There are potential mechanisms by which air pollution could cause, exacerbate, or accelerate the progression of certain forms of ILD via pulmonary and systemic inflammation as well as oxidative stress. This article will review the current epidemiologic and translational data supporting the plausibility of this relationship and propose a new conceptual framework for characterizing novel environmental risk factors for these forms of lung disease.
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Project description:BackgroundRecently, there has been increasing evidence that exposure to air pollution is linked to neurodegenerative diseases, but little is known about the association with amyotrophic lateral sclerosis (ALS).ObjectivesWe investigated the association between long-term exposure to air pollution and risk of developing ALS.MethodsA population-based case-control study was conducted in Netherlands from 1 January 2006 to 1 January 2013. Data from 917 ALS patients and 2,662 controls were analyzed. Annual mean air pollution concentrations were assessed by land use regression (LUR) models developed as part of the European Study of Cohorts for Air Pollution Effects (ESCAPE). Exposure estimates included nitrogen oxides (NO2, NOx), particulate matter (PM) with diameters of <2.5 ?m (PM2.5), <10 ?m (PM10), between 10 ?m and 2.5 ?m (PMcoarse), and PM2.5 absorbance. We performed conditional logistic regression analysis using two different multivariate models (model 1 adjusted for age, gender, education, smoking status, alcohol use, body mass index, and socioeconomic status; model 2 additionally adjusted for urbanization degree).ResultsRisk of ALS was significantly increased for individuals in the upper exposure quartile of PM2.5 absorbance [OR=1.67; 95% confidence interval (CI): 1.27, 2.18], NO2 (OR=1.74; 95% CI: 1.32, 2.30), and NOx concentrations (OR=1.38; 95% CI: 1.07, 1.77). These results, except for NOx, remained significant after adjusting additionally for urbanization degree.ConclusionsBased on a large population-based case-control study, we report evidence for the association between long-term exposure to traffic-related air pollution and increased susceptibility to ALS. Our findings further support the necessity for regulatory public health interventions to combat air pollution levels and provide additional insight into the potential pathophysiology of ALS. https://doi.org/10.1289/EHP1115.
| S-EPMC5915195 | biostudies-literature
Project description:BackgroundPrenatal exposure to outdoor air pollution has been shown to have health effects in many studies; low birth weight, preterm delivery, small for gestational age, and stillbirth are the most often cited. However, exposure of pregnant women is difficult to quantify, especially with regard to their mobility, which is rarely taken into account in epidemiological studies. This study aimed to assess the impact of mobility of pregnant women living in Paris, France, on their exposure estimates to nitrogen dioxide (NO2).MethodsA total of 486 pregnant women were recruited in 5 maternity hospitals in Paris between January and April 2016. A questionnaire was used to collect mothers' characteristics (demography, education, etc.) and to assess their daily mobility during pregnancy (time spent at work, commuting time and mode used to move from residential to occupational places). Daily NO2 concentrations were estimated based on the combination of annual average concentrations modeled at the census block scale and daily concentrations measured from fixed monitoring stations. Different models were used to compare the exposure of pregnant women in residential and occupational places, also taking into account travel time and travel mode. The socioeconomic profile of the census blocks was characterized using a multi-component index.ResultsDuring the first trimester of pregnancy, women living in the least deprived census blocks were exposed to higher concentrations of NO2 than those living in the most deprived ones. Occupational mobility had a small impact on exposure levels (average increase after taking account of mobility: +?0.52 ?g/m3) which was not related to the socioeconomic profile of the women. The commuting mode made a greater difference (+?1.46 ?g/m3 on average), in particular among women living in the most deprived census blocks.ConclusionsOur study illustrates that air pollution exposure can be underestimated when ignoring occupational mobility and commuting mode of pregnant women. This effect might be differential according to the neighborhood deprivation profile.
| S-EPMC6194718 | biostudies-literature
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.
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Project description:BackgroundThe etiology of childhood cancer is poorly understood. The role of environmental factors, including air pollution (AP) exposure, has been addressed previously, but results so far have been inconclusive. In this study, we investigate the association between long-term AP exposures in relation to childhood cancer subtypes in Denmark (1981-2013).MethodsWe conducted a nationwide register-based case-control study. We identified 7745 incident cases of childhood cancers (<20 years) in the Danish Cancer Registry. Four randomly selected (cancer-free) controls were matched to each case according to sex and date of birth. We modelled concentrations of nitrogen dioxide (NO2), fine particles (PM2·5), and black carbon (BC) at all addresses and calculated a time-weighted average from birth to index-date with a state-of-the-art multiscale AP modelling system. We analyzed the risk of childhood cancer in conditional logistic regression models adjusted for socio-demographic variables obtained from registers at the individual and neighborhood level.FindingsThe main analyses included 5045 cases and 18,179 controls. For all cancers combined, we observed odds ratios (ORs) and 95% confidence intervals (95% CI) of 0·97 (0·94, 1·01) per 10 µg/m3 NO2, 0·89 (0·82, 0·98) per 5 µg/m3 PM2·5, and 0·94 (0·88, 1·01) per 1 µg/m3 BC, respectively. Most notably, we observed a higher risk of Non-Hodgkin Lymphoma (NHL) with higher childhood AP exposure with ORs and 95% CIs of 1·21 (0·94, 1·55) per 10 µg/m3 NO2, 2·11 (1·10, 4·01) per 5 µg/m3 PM2·5, and 1·68 (1·06, 2·66) per 1 µg/m3 BC, respectively. We observed indications of increased risks for other types of childhood cancer, however, with very wide CIs including 1.InterpretationsThe findings of this nation-wide study propose a role of AP in the development of childhood NHL, but more large-scale studies are needed.FundingNordForsk Project #75007.
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Project description:Prenatal air pollution exposure is frequently estimated using maternal residential location at the time of delivery as a proxy for residence during pregnancy. We describe residential mobility during pregnancy among 19,951 children from the Kaiser Air Pollution and Pediatric Asthma Study, quantify measurement error in spatially resolved estimates of prenatal exposure to mobile source fine particulate matter (PM2.5) due to ignoring this mobility, and simulate the impact of this error on estimates of epidemiologic associations. Two exposure estimates were compared, one calculated using complete residential histories during pregnancy (weighted average based on time spent at each address) and the second calculated using only residence at birth. Estimates were computed using annual averages of primary PM2.5 from traffic emissions modeled using a Research LINE-source dispersion model for near-surface releases (RLINE) at 250?m resolution. In this cohort, 18.6% of children were born to mothers who moved at least once during pregnancy. Mobile source PM2.5 exposure estimates calculated using complete residential histories during pregnancy and only residence at birth were highly correlated (rS>0.9). Simulations indicated that ignoring residential mobility resulted in modest bias of epidemiologic associations toward the null, but varied by maternal characteristics and prenatal exposure windows of interest (ranging from -2% to -10% bias).
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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.
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