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1.
Artigo em Inglês | MEDLINE | ID: mdl-34587471

RESUMO

Rationale Infants born prematurely have impaired capacity to deal with oxidative stress shortly after birth. Objectives We hypothesize that the relative impact of exposure to air pollution on lung function is higher in preterm than in term infants. Methods In the prospective BILD-birth-cohort of 254 preterm and 517 term infants, we investigated associations of particulate matter (PM10) and nitrogen dioxide with lung function at 44 weeks postconceptional age and exhaled markers of inflammation and oxidative stress response (fraction of exhaled nitric oxide (FeNO)) in an explorative hypothesis-driven study design. Multilevel mixed-effects models were used and adjusted for known confounders. Measurements and Main Results Significant associations of PM10 during the second trimester of pregnancy with lung function and FeNO were found in term and preterm infants. Importantly, we observed stronger positive associations in preterm infants (born 32 - 36 weeks), with an increase of [184.9 (79.1, 290.7) mL/min] minute ventilation per 10 µg/m3 increase in PM10 than in term infants [75.3 (19.7, 130.8) mL/min] (pprematurity × PM10 interaction = 0.04, after multiple comparison adjustment padj = 0.09). Associations of PM10 and FeNO differed between moderate to late preterm [3.4 (-0.1, 6.8) ppb] and term [-0.3 (-1.5, 0.9) ppb] infants, the interaction with prematurity was significant (pprematurity × PM10 interaction = 0.006, padj = 0.036). Conclusion Preterm infants showed significant higher susceptibility even to low-to-moderate prenatal air pollution exposure than term infants, leading to increased impairment of postnatal lung function. FeNO results further elucidate differences in inflammatory/oxidative stress response comparing preterms to terms.

2.
Environ Pollut ; 291: 118066, 2021 Aug 30.
Artigo em Inglês | MEDLINE | ID: mdl-34536646

RESUMO

Ambient air pollution is the leading cause of environmental mortality and morbidity worldwide. However, the individual contributions to acute mortality of traffic-related air pollutants such as nitrogen dioxide (NO2) and fine particulate matter (PM2.5) are still debated. We conducted a time-stratified case-crossover study for a population located around Zurich airport in Switzerland, including 24,886 adult cardiovascular deaths from the Swiss National Cohort. We estimated the risk of cause-specific cardiovascular mortality associated with daily NO2 and PM2.5 concentrations at home using distributed lag models up to 7 days preceding death, adjusted for daily temperature, precipitation, acute night-time aircraft noise, firework celebrations, and holidays. Cardiovascular mortality was associated with NO2, whereas the association with PM2.5 disappeared upon adjustment for NO2. The strongest association was observed between NO2 and ischemic stroke mortality (odds ratio = 1.55 per 10 µg/m3, 95% confidence intervals = 1.20-2.00). Cause-specific mortality analyses showed differences in terms of delayed effect: odds ratios were highest at 1-3 days after exposure for most outcomes but at lags of 3-5 days for heart failure. Individual vulnerabilities to NO2 associated cardiovascular mortality also varied by cause of death, possibly highlighting the role of different behaviours and risk factors in the most susceptible groups. The risk of cardiovascular mortality was also increased on firework days and after public holidays, independent from NO2 and PM2.5 concentrations. This study confirms the association between ambient NO2, as a marker for primary emissions, and acute cardiovascular mortality in a specific setting around a major airport. Future research should clarify the role of additional air pollutants including ultra-fine particles on cardiovascular diseases to inform most efficient control measures.

3.
Sci Total Environ ; 804: 150091, 2021 Sep 04.
Artigo em Inglês | MEDLINE | ID: mdl-34517316

RESUMO

BACKGROUND: Ambient air pollution exposure has been associated with higher mortality risk in numerous studies. We assessed potential variability in the magnitude of this association for non-accidental, cardiovascular disease, respiratory disease, and lung cancer mortality in a country-wide administrative cohort by exposure assessment method and by adjustment for geographic subdivisions. METHODS: We used the Belgian 2001 census linked to population and mortality register including nearly 5.5 million adults aged ≥30 (mean follow-up: 9.97 years). Annual mean concentrations for fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and ozone (O3) were assessed at baseline residential address using two exposure methods; Europe-wide hybrid land use regression (LUR) models [100x100m], and Belgium-wide interpolation-dispersion (RIO-IFDM) models [25x25m]. We used Cox proportional hazards models with age as the underlying time scale and adjusted for various individual and area-level covariates. We further adjusted main models for two different area-levels following the European Nomenclature of Territorial Units for Statistics (NUTS); NUTS-1 (n = 3), or NUTS-3 (n = 43). RESULTS: We found no consistent differences between both exposure methods. We observed most robust associations with lung cancer mortality. Hazard Ratios (HRs) per 10 µg/m3 increase for NO2 were 1.060 (95%CI 1.042-1.078) [hybrid LUR] and 1.040 (95%CI 1.022-1.058) [RIO-IFDM]. Associations with non-accidental, respiratory disease and cardiovascular disease mortality were generally null in main models but were enhanced after further adjustment for NUTS-1 or NUTS-3. HRs for non-accidental mortality per 5 µg/m3 increase for PM2.5 for the main model using hybrid LUR exposure were 1.023 (95%CI 1.011-1.035). After including random effects HRs were 1.044 (95%CI 1.033-1.057) [NUTS-1] and 1.076 (95%CI 1.060-1.092) [NUTS-3]. CONCLUSION: Long-term air pollution exposure was associated with higher lung cancer mortality risk but not consistently with the other studied causes. Magnitude of associations varied by adjustment for geographic subdivisions, area-level socio-economic covariates and less by exposure assessment method.

4.
BMJ ; 374: n1904, 2021 09 01.
Artigo em Inglês | MEDLINE | ID: mdl-34470785

RESUMO

OBJECTIVE: To investigate the associations between air pollution and mortality, focusing on associations below current European Union, United States, and World Health Organization standards and guidelines. DESIGN: Pooled analysis of eight cohorts. SETTING: Multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE) in six European countries. PARTICIPANTS: 325 367 adults from the general population recruited mostly in the 1990s or 2000s with detailed lifestyle data. Stratified Cox proportional hazard models were used to analyse the associations between air pollution and mortality. Western Europe-wide land use regression models were used to characterise residential air pollution concentrations of ambient fine particulate matter (PM2.5), nitrogen dioxide, ozone, and black carbon. MAIN OUTCOME MEASURES: Deaths due to natural causes and cause specific mortality. RESULTS: Of 325 367 adults followed-up for an average of 19.5 years, 47 131 deaths were observed. Higher exposure to PM2.5, nitrogen dioxide, and black carbon was associated with significantly increased risk of almost all outcomes. An increase of 5 µg/m3 in PM2.5 was associated with 13% (95% confidence interval 10.6% to 15.5%) increase in natural deaths; the corresponding figure for a 10 µg/m3 increase in nitrogen dioxide was 8.6% (7% to 10.2%). Associations with PM2.5, nitrogen dioxide, and black carbon remained significant at low concentrations. For participants with exposures below the US standard of 12 µg/m3 an increase of 5 µg/m3 in PM2.5 was associated with 29.6% (14% to 47.4%) increase in natural deaths. CONCLUSIONS: Our study contributes to the evidence that outdoor air pollution is associated with mortality even at low pollution levels below the current European and North American standards and WHO guideline values. These findings are therefore an important contribution to the debate about revision of air quality limits, guidelines, and standards, and future assessments by the Global Burden of Disease.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Poluição do Ar/efeitos adversos , Doenças Cardiovasculares/mortalidade , Exposição Ambiental/efeitos adversos , Doenças não Transmissíveis/mortalidade , Europa (Continente) , Humanos
5.
Lancet Planet Health ; 5(9): e620-e632, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34508683

RESUMO

BACKGROUND: Long-term exposure to outdoor air pollution increases the risk of cardiovascular disease, but evidence is unclear on the health effects of exposure to pollutant concentrations lower than current EU and US standards and WHO guideline limits. Within the multicentre study Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we investigated the associations of long-term exposures to fine particulate matter (PM2·5), nitrogen dioxide (NO2), black carbon, and warm-season ozone (O3) with the incidence of stroke and acute coronary heart disease. METHODS: We did a pooled analysis of individual data from six population-based cohort studies within ELAPSE, from Sweden, Denmark, the Netherlands, and Germany (recruited 1992-2004), and harmonised individual and area-level variables between cohorts. Participants (all adults) were followed up until migration from the study area, death, or incident stroke or coronary heart disease, or end of follow-up (2011-15). Mean 2010 air pollution concentrations from centrally developed European-wide land use regression models were assigned to participants' baseline residential addresses. We used Cox proportional hazards models with increasing levels of covariate adjustment to investigate the association of air pollution exposure with incidence of stroke and coronary heart disease. We assessed the shape of the concentration-response function and did subset analyses of participants living at pollutant concentrations lower than predefined values. FINDINGS: From the pooled ELAPSE cohorts, data on 137 148 participants were analysed in our fully adjusted model. During a median follow-up of 17·2 years (IQR 13·8-19·5), we observed 6950 incident events of stroke and 10 071 incident events of coronary heart disease. Incidence of stroke was associated with PM2·5 (hazard ratio 1·10 [95% CI 1·01-1·21] per 5 µg/m3 increase), NO2 (1·08 [1·04-1·12] per 10 µg/m3 increase), and black carbon (1·06 [1·02-1·10] per 0·5 10-5/m increase), whereas coronary heart disease incidence was only associated with NO2 (1·04 [1·01-1·07]). Warm-season O3 was not associated with an increase in either outcome. Concentration-response curves indicated no evidence of a threshold below which air pollutant concentrations are not harmful for cardiovascular health. Effect estimates for PM2·5 and NO2 remained elevated even when restricting analyses to participants exposed to pollutant concentrations lower than the EU limit values of 25 µg/m3 for PM2·5 and 40 µg/m3 for NO2. INTERPRETATION: Long-term air pollution exposure was associated with incidence of stroke and coronary heart disease, even at pollutant concentrations lower than current limit values. FUNDING: Health Effects Institute.

6.
Environ Int ; 157: 106805, 2021 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-34375941

RESUMO

BACKGROUND: The current evidence on health effects of long-term exposure to outdoor airborne black carbon (BC) exposure remains scarce. OBJECTIVES: To examine the association between long-term exposure to BC and mortality in a large population-based French cohort, with 28 years of follow-up. METHODS: Data from the GAZEL cohort were collected between 1989 and 2017. Land use regression model with temporal extrapolation wa used to estimate yearly BC and PM2.5 exposure at the residential addresses from 1989 until censoring for 19,906 participants. Time-varying Cox models with attained age as time-scale was used to estimate the associations between BC and all-cause and cardiovascular mortality, after adjusting for individual and area-level covariates. To handle confounding by PM2.5, we used the residual of BC regressed on PM2.5 as an alternate exposure variable. For all-cause mortality, we also examined effect modification by sex, smoking status, BMI and fruit/vegetable intake. RESULTS: The median of 20-year moving average of BC exposure was 2.02 10-5/m in study population. We found significant associations between BC exposure and all-cause mortality (n = 2357) using both 20-year moving average of BC and residual of BC, with corresponding hazard ratios (HR) of 1.14 (95 %CI: 1.07-1.22) and 1.17 (95 %CI: 1.10-1.24) for an inter-quartile range (IQR) increase (0.86 10-5/m for BC and 0.57 10-5/m for residual of BC). We found a similar association between BC and cardiovascular mortality (n = 277) with a HR of 1.15 (95 %CI: 0.95-1.38). The dose-response relationship between BC and all-cause mortality was monotonic but nonlinear with a steeper slope at high BC levels. In addition, the effect of BC was higher among never-smokers and among those having fruit/vegetables less than twice a week. CONCLUSIONS: There was a positive association between long-term exposure to BC and increased mortality risk, reinforcing the emerging evidence that BC is a harmful component of PM2.5.

7.
Environ Int ; 157: 106839, 2021 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-34454361

RESUMO

BACKGROUND: Rhinitis is one of the most common disease worldwide with a high and increasing prevalence. There is limited knowledge on the link between long-term exposure to air pollution and rhinitis. OBJECTIVES: We aim to study the associations between long-term exposure to air pollutants and self-reported current rhinitis among adults from Constances, a large French population-based cohort. METHODS: Current rhinitis was defined at inclusion from questionnaire by the presence of sneezing, runny or blocked nose in the last 12 months without a cold or the flu. Annual concentrations of nitrogen dioxide (NO2), particulate matter ≤ 2.5 µm (PM2.5) and black carbon (BC) were estimated at the participants' residential address by European land-use regression models. Cross-sectional associations between annual exposure to each air pollutant and current rhinitis were estimated using logistic models adjusted for age, sex, smoking, education level and French deprivation index. The health prevention centers were taken into account by marginal models with generalized estimating equations. Several supplementary analyses were performed. RESULTS: Analyses were performed on 127,108 participants (47 years old on average, 54% women, 19% current smokers). The prevalence of current rhinitis, allergic (AR) and non-allergic (NAR) rhinitis were 36%, 25% and 11% respectively. Adjusted ORs for current rhinitis were 1.13 (1.08, 1.17), 1.12 (1.07, 1.17), and 1.11 (1.06, 1.17) per one interquartile range increase of PM2.5 (4.85 µg/m3), BC (0.88 · 10-5 m-1) and NO2 (17.3 µg/m3) respectively. Significant and positive associations were also found for both AR and NAR. Results were similar in men and women, and in the different smoking strata, and were consistent with meta-analysis or after imputing missing covariates. DISCUSSION: An increase of modeled annual average residential exposure to PM2.5, BC, and NO2 was significantly associated with an increase of prevalence of current rhinitis in adults in the French general population. The results suggest that among air pollutants, BC may be of special interest.

8.
Int J Cancer ; 149(11): 1887-1897, 2021 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-34278567

RESUMO

Particulate matter air pollution and diesel engine exhaust have been classified as carcinogenic for lung cancer, yet few studies have explored associations with liver cancer. We used six European adult cohorts which were recruited between 1985 and 2005, pooled within the "Effects of low-level air pollution: A study in Europe" (ELAPSE) project, and followed for the incidence of liver cancer until 2011 to 2015. The annual average exposure to nitrogen dioxide (NO2 ), particulate matter with diameter <2.5 µm (PM2.5 ), black carbon (BC), warm-season ozone (O3 ), and eight elemental components of PM2.5 (copper, iron, zinc, sulfur, nickel, vanadium, silicon, and potassium) were estimated by European-wide hybrid land-use regression models at participants' residential addresses. We analyzed the association between air pollution and liver cancer incidence by Cox proportional hazards models adjusting for potential confounders. Of 330 064 cancer-free adults at baseline, 512 developed liver cancer during a mean follow-up of 18.1 years. We observed positive linear associations between NO2 (hazard ratio, 95% confidence interval: 1.17, 1.02-1.35 per 10 µg/m3 ), PM2.5 (1.12, 0.92-1.36 per 5 µg/m3 ), and BC (1.15, 1.00-1.33 per 0.5 10-5 /m) and liver cancer incidence. Associations with NO2 and BC persisted in two-pollutant models with PM2.5 . Most components of PM2.5 were associated with the risk of liver cancer, with the strongest associations for sulfur and vanadium, which were robust to adjustment for PM2.5 or NO2 . Our study suggests that ambient air pollution may increase the risk of liver cancer, even at concentrations below current EU standards.

9.
Environ Res ; 203: 111776, 2021 Jul 28.
Artigo em Inglês | MEDLINE | ID: mdl-34329637

RESUMO

STUDY OBJECTIVES: During infancy, adequate sleep is crucial for physical and neurocognitive development. In adults and children, night-time noise exposure is associated with sleep disturbances. However, whether and to what extent infants' sleep is affected, is unknown. Thus, this study investigated the relationship between nocturnal transportation noise and actimetry-derived habitual sleep behavior across the first year of life. METHODS: In 144 healthy infants (63 girls), nocturnal (23:00-7:00) transportation noise (i.e., road, railway, and aircraft) was modelled at the infants' individual places of residence. Using actimetry, we recorded movement patterns for 11 days in a longitudinal design at 3, 6, and 12 months of age and derived the recently proposed core sleep composites of night-time sleep duration, activity, and variability. Using linear mixed-effects models, we determined associations between noise exposure and sleep composites. Sex, gestational age, parents' highest educational level, infants' age, and the existence of siblings served as control variables. RESULTS: In models without interactions, night-time transportation noise was unrelated to sleep composites across the first year of life (p > .16). Exploratory analyses of an interaction between noise and the existence of siblings yielded an association between night-time transportation noise and sleep duration in infants without siblings only (p = .004). CONCLUSION: In our study, sleep in infants during the first year of life was relatively robust against external perturbation by night-time transportation noise. However, particularly in children without siblings increasing night-time transportation noise reduced sleep duration. This suggests that the habitual noise environment may modulate individual susceptibility to adverse effects of noise on sleep.

10.
Environ Res ; 202: 111633, 2021 Jul 10.
Artigo em Inglês | MEDLINE | ID: mdl-34256075

RESUMO

BACKGROUND: Air pollution and greenness are associated with short- and long-term respiratory health in children but the underlying mechanisms are only scarcely investigated. The nasal microbiota during the first year of life has been shown to be associated with respiratory tract infections and asthma development. Thus, an interplay between greenness, air pollution and the early nasal microbiota may contribute to short- and long-term respiratory health. We aimed to examine associations between fine particulate matter (PM2.5), nitrogen dioxide (NO2) and greenness with the nasal microbiota of healthy infants during the first year of life in a European context with low-to-moderate air pollution levels. METHODS: Microbiota characterization was performed using 16 S rRNA pyrosequencing of 846 nasal swabs collected fortnightly from 47 healthy infants of the prospective Basel-Bern Infant Lung Development (BILD) cohort. We investigated the association of satellite-based greenness and an 8-day-average exposure to air pollution (PM2.5, NO2) with the nasal microbiota during the first year of life. Exposures were individually estimated with novel spatial-temporal models incorporating satellite data. Generalized additive mixed models adjusted for known confounders and considering the autoregressive correlation structure of the data were used for analysis. RESULTS: Mean (SD) PM2.5 level was 17.1 (3.8 µg/m3) and mean (SD) NO2 level was 19.7 (7.9 µg/m3). Increased PM2.5 and increased NO2 were associated with reduced within-subject Ruzicka dissimilarity (PM2.5: per 1 µg/m3 -0.004, 95% CI -0.008, -0.001; NO2: per 1 µg/m3 -0.004, 95% CI -0.007, -0.001). Whole microbial community comparison with nonmetric multidimensional scaling revealed distinct microbiota profiles for different PM2.5 exposure levels. Increased NO2 was additionally associated with reduced abundance of Corynebacteriaceae (per 1 µg/m3: -0.027, 95% CI -0.053, -0.001). No associations were found between greenness and the nasal microbiota. CONCLUSION: Air pollution was associated with Ruzicka dissimilarity and relative abundance of Corynebacteriaceae. This suggests that even low-to-moderate exposure to air pollution may impact the nasal microbiota during the first year of life. Our results will be useful for future studies assessing the clinical relevance of air-pollution-induced alterations of the nasal microbiota with subsequent respiratory disease development.

11.
Sci Total Environ ; 790: 147958, 2021 Oct 10.
Artigo em Inglês | MEDLINE | ID: mdl-34098271

RESUMO

Since the 2003 heatwave in Europe, evidence has been rapidly increasing on the association between extreme temperature and all-cause mortality. Little is known, however, about cause-specific cardiovascular mortality, effect modification by air pollution and aircraft noise, and which population groups are the most vulnerable to extreme temperature. We conducted a time-stratified case-crossover study in Zurich, Switzerland, including all adult cardiovascular deaths between 2000 and 2015 with precise individual exposure estimates at home location. We estimated the risk of 24,884 cardiovascular deaths associated with heat and cold using distributed non-linear lag models. We investigated potential effect modification of temperature-related mortality by fine particles, nitrogen dioxide, and night-time aircraft noise and performed stratified analyses across individual and social characteristics. We found increased risk of mortality for heat (odds ratio OR = 1.28 [95% confidence interval: 1.11-1.49] for 99th percentile of daily Tmean (24 °C) versus optimum temperature at 20 °C) and cold (OR = 1.15 [0.95-1.39], 5th percentile of daily Tmean (-3 °C) versus optimum temperature at 20 °C). Heat-related mortality was particularly strong for myocardial infarctions and hypertension related deaths, and among older women (>75 years). Analysis of effect modification also indicated that older women with lower socio-economic position and education are at higher risk for heat-related mortality. PM2.5 increased the risk of heat-related mortality for heart failure, but not all-cause cardiovascular mortality. This study provides useful information for preventing cause-specific cardiovascular temperature-related mortality in moderate climate zones comparable to Switzerland.


Assuntos
Poluição do Ar , Doenças Cardiovasculares , Adulto , Idoso , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Temperatura Baixa , Estudos Cross-Over , Feminino , Temperatura Alta , Humanos , Mortalidade , Suíça/epidemiologia , Temperatura
12.
Eur Respir J ; 57(6)2021 06.
Artigo em Inglês | MEDLINE | ID: mdl-34088754

RESUMO

BACKGROUND: Long-term exposure to ambient air pollution has been linked to childhood-onset asthma, although evidence is still insufficient. Within the multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we examined the associations of long-term exposures to particulate matter with a diameter <2.5 µm (PM2.5), nitrogen dioxide (NO2) and black carbon (BC) with asthma incidence in adults. METHODS: We pooled data from three cohorts in Denmark and Sweden with information on asthma hospital diagnoses. The average concentrations of air pollutants in 2010 were modelled by hybrid land-use regression models at participants' baseline residential addresses. Associations of air pollution exposures with asthma incidence were explored with Cox proportional hazard models, adjusting for potential confounders. RESULTS: Of 98 326 participants, 1965 developed asthma during a mean follow-up of 16.6 years. We observed associations in fully adjusted models with hazard ratios of 1.22 (95% CI 1.04-1.43) per 5 µg·m-3 for PM2.5, 1.17 (95% CI 1.10-1.25) per 10 µg·m-3 for NO2 and 1.15 (95% CI 1.08-1.23) per 0.5×10-5 m-1 for BC. Hazard ratios were larger in cohort subsets with exposure levels below the European Union and US limit values and possibly World Health Organization guidelines for PM2.5 and NO2. NO2 and BC estimates remained unchanged in two-pollutant models with PM2.5, whereas PM2.5 estimates were attenuated to unity. The concentration-response curves showed no evidence of a threshold. CONCLUSIONS: Long-term exposure to air pollution, especially from fossil fuel combustion sources such as motorised traffic, was associated with adult-onset asthma, even at levels below the current limit values.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Asma , Adulto , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Criança , Exposição Ambiental/análise , Europa (Continente) , Humanos , Incidência , Material Particulado/análise , Suécia
13.
Sci Total Environ ; 787: 147553, 2021 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-33989869

RESUMO

BACKGROUND: Greenspace exposure has been suggested to be associated with a range of health outcomes. The available evidence on the association of this exposure with cancer is still very scarce and inconsistent. OBJECTIVES: We aimed to study the association between greenspace exposure and all-site and site-specific (prostate, breast, colorectal, bladder, lung, and malignant melanoma of skin) cancer incidence in the GAZEL cohort. METHODS: This study was based on over 27 years of follow-up (1989-2016) of 19,408 participants across France. We assessed the residential greenspace exposure within several buffers as well as residential proximity to green spaces (agricultural, urban, and forests) in each follow-up. We used time-dependent Cox models, controlling for time-varying personal and area-level variables, with different lags between exposure and outcome. Additional analysis was conducted according to the urban-rural residence of the participants' over follow-up. RESULTS: Over the 294,645 person-years of follow-up, we registered 4075 incident cases of cancer. We found an increase in the risk for all-sites cancer with an inter-quartile range increase of Normalized Difference in Vegetation Index across different buffers (hazard ratio (HR) of 1.08; 95% CI: 1.02, 1.14 for the 100 m buffer). We found a positive association of all-sites cancer with proximity to agricultural lands (HR: 1.03; 95% CI: 1.00, 1.05), and forests (HR:1.04; 95% CI: 1.00, 1.07), but not with urban green spaces. The cancer site-specific analyses suggested a protective role of greenspace for breast, lung, and colorectal cancers (e.g. breast cancer HR at 100 m buffer: 0.82; 95% CI: 0.69, 0.99). Non-significant associations were observed for prostate, bladder, and skin cancer. Stratified analyses based on urban, semi-urban, and rural classification did not suggest any differential pattern. CONCLUSION: We identified an increased risk of all-site cancer with increased greenspace and proximity to agricultural lands and forests; whereas potential protective role of greenspace for breast cancer.


Assuntos
Neoplasias , Parques Recreativos , Estudos de Coortes , Seguimentos , França/epidemiologia , Humanos , Incidência , Masculino , Neoplasias/induzido quimicamente , Neoplasias/epidemiologia
14.
Environ Health Perspect ; 129(4): 47009, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33844598

RESUMO

BACKGROUND: Inconsistent associations between long-term exposure to particles with an aerodynamic diameter ≤2.5 µm [fine particulate matter (PM2.5)] components and mortality have been reported, partly related to challenges in exposure assessment. OBJECTIVES: We investigated the associations between long-term exposure to PM2.5 elemental components and mortality in a large pooled European cohort; to compare health effects of PM2.5 components estimated with two exposure modeling approaches, namely, supervised linear regression (SLR) and random forest (RF) algorithms. METHODS: We pooled data from eight European cohorts with 323,782 participants, average age 49 y at baseline (1985-2005). Residential exposure to 2010 annual average concentration of eight PM2.5 components [copper (Cu), iron (Fe), potassium (K), nickel (Ni), sulfur (S), silicon (Si), vanadium (V), and zinc (Zn)] was estimated with Europe-wide SLR and RF models at a 100×100 m scale. We applied Cox proportional hazards models to investigate the associations between components and natural and cause-specific mortality. In addition, two-pollutant analyses were conducted by adjusting each component for PM2.5 mass and nitrogen dioxide (NO2) separately. RESULTS: We observed 46,640 natural-cause deaths with 6,317,235 person-years and an average follow-up of 19.5 y. All SLR-modeled components were statistically significantly associated with natural-cause mortality in single-pollutant models with hazard ratios (HRs) from 1.05 to 1.27. Similar HRs were observed for RF-modeled Cu, Fe, K, S, V, and Zn with wider confidence intervals (CIs). HRs for SLR-modeled Ni, S, Si, V, and Zn remained above unity and (almost) significant after adjustment for both PM2.5 and NO2. HRs only remained (almost) significant for RF-modeled K and V in two-pollutant models. The HRs for V were 1.03 (95% CI: 1.02, 1.05) and 1.06 (95% CI: 1.02, 1.10) for SLR- and RF-modeled exposures, respectively, per 2 ng/m3, adjusting for PM2.5 mass. Associations with cause-specific mortality were less consistent in two-pollutant models. CONCLUSION: Long-term exposure to V in PM2.5 was most consistently associated with increased mortality. Associations for the other components were weaker for exposure modeled with RF than SLR in two-pollutant models. https://doi.org/10.1289/EHP8368.

15.
Environ Health Perspect ; 129(3): 37005, 2021 03.
Artigo em Inglês | MEDLINE | ID: mdl-33759553

RESUMO

BACKGROUND: Black carbon (BC), a component of fine particulate matter [particles with an aerodynamic diameter ≤2.5 µm (PM2.5)], may contribute to carcinogenic effects of air pollution. Until recently however, there has been little evidence to evaluate this hypothesis. OBJECTIVE: This study aimed to estimate the associations between long-term exposure to BC and risk of cancer. This study was conducted within the French Gazel cohort of 20,625 subjects. METHODS: We assessed exposure to BC by linking subjects' histories of residential addresses to a map of European black carbon levels in 2010 with back- and forward-extrapolation between 1989 and 2015. We used extended Cox models, with attained age as time-scale and time-varying cumulative exposure to BC, adjusted for relevant sociodemographic and lifestyle variables. To consider latency between exposure and cancer diagnosis, we implemented a 10-y lag, and as a sensitivity analysis, a lag of 2 y. To isolate the effect of BC from that of total PM2.5, we regressed BC on PM2.5 and used the residuals as the exposure variable. RESULTS: During the 26-y follow-up period, there were 3,711 incident cancer cases (all sites combined) and 349 incident lung cancers. Median baseline exposure in 1989 was 2.65 10-5/m [interquartile range (IQR): 2.23-3.33], which generally slightly decreased over time. Using 10 y as a lag-time in our models, the adjusted hazard ratio per each IQR increase of the natural log-transformed cumulative BC was 1.17 (95% confidence interval: 1.06, 1.29) for all-sites cancer combined and 1.31 (0.93, 1.83) for lung cancer. Associations with BC residuals were also positive for both outcomes. Using 2 y as a lag-time, the results were similar. DISCUSSION: Our findings for a cohort of French adults suggest that BC may partly explain the association between PM2.5 and lung cancer. Additional studies are needed to confirm our results and further disentangle the effects of BC, total PM2.5, and other constituents. https://doi.org/10.1289/EHP8719.

16.
Environ Pollut ; 271: 116356, 2021 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-33387778

RESUMO

Residential radon exposure is a major public health issue in Switzerland due to the known association between inhaled radon progeny and lung cancer. To confirm recent findings of an association with skin cancer mortality, an updated national radon model is needed. The aim of this study was to derive the best possible residential radon prediction model for subsequent epidemiological analyses. Two different radon prediction models were developed (linear regression model vs. random forest) using ca. 80,000 measurements in the Swiss Radon Database (1994-2017). A range of geographic predictors and building specific predictors were considered in the 3-D models (x,y, floor of dwelling). A five-fold modelling strategy was used to evaluate the robustness of each approach, with models developed (80% measurement locations) and validated (20%) using standard diagnostics. Random forest consistently outperformed the linear regression model, with higher Spearman's rank correlation (51% vs. 36%), validation coefficient of determination (R2 31% vs. 15%), lower root mean square error (RMSE) and lower fractional bias. Applied to the population of 5.4 million adults in 2000, the random forest resulted in an arithmetic mean (standard deviation) of 75.5 (31.7) Bq/m3, and indicated a respective 16.1% and 0.1% adults with predicted radon concentrations exceeding the World Health Organization (100 Bq/m3) and Swiss (300 Bq/m3) reference values.


Assuntos
Poluentes Radioativos do Ar , Poluição do Ar em Ambientes Fechados , Neoplasias Pulmonares , Radônio , Poluentes Radioativos do Ar/análise , Poluição do Ar em Ambientes Fechados/análise , Exposição Ambiental/análise , Habitação , Humanos , Radônio/análise , Suíça
17.
Environ Int ; 146: 106306, 2021 01.
Artigo em Inglês | MEDLINE | ID: mdl-33395948

RESUMO

INTRODUCTION: To characterize air pollution exposure at a fine spatial scale, different exposure assessment methods have been applied. Comparison of associations with health from different exposure methods are scarce. The aim of this study was to evaluate associations of air pollution based on hybrid, land-use regression (LUR) and dispersion models with natural cause and cause-specific mortality. METHODS: We followed a Dutch national cohort of approximately 10.5 million adults aged 29+ years from 2008 until 2012. We used Cox proportional hazard models with age as underlying time scale and adjusted for several potential individual and area-level socio-economic status confounders to evaluate associations of annual average residential NO2, PM2.5 and BC exposure estimates based on two stochastic models (Dutch LUR, European-wide hybrid) and deterministic Dutch dispersion models. RESULTS: Spatial variability of PM2.5 and BC exposure was smaller for LUR compared to hybrid and dispersion models. NO2 exposure variability was similar for the three methods. Pearson correlations between hybrid, LUR and dispersion modeled NO2 and BC ranged from 0.72 to 0.83; correlations for PM2.5 were slightly lower (0.61-0.72). In general, all three models showed stronger associations of air pollutants with respiratory disease and lung cancer mortality than with natural cause and cardiovascular disease mortality. The strength of the associations differed between the three exposure models. Associations of air pollutants estimated by LUR were generally weaker compared to associations of air pollutants estimated by hybrid and dispersion models. For natural cause mortality, we found a hazard ratio (HR) of 1.030 (95% confidence interval (CI): 1.019, 1.041) per 10 µg/m3 for hybrid modeled NO2, a HR of 1.003 (95% CI: 0.993, 1.013) per 10 µg/m3 for LUR modeled NO2 and a HR of 1.015 (95% CI: 1.005, 1.024) per 10 µg/m3 for dispersion modeled NO2. CONCLUSION: Air pollution was positively associated with natural cause and cause-specific mortality, but the strength of the associations differed between the three exposure models. Our study documents that the selected exposure model may contribute to heterogeneity in effect estimates of associations between air pollution and health.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Doenças Respiratórias , Adulto , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Estudos de Coortes , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Humanos , Dióxido de Nitrogênio/análise , Dióxido de Nitrogênio/toxicidade , Material Particulado/efeitos adversos , Material Particulado/análise
18.
Environ Int ; 147: 106371, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33422970

RESUMO

BACKGROUND: We evaluated methods for the analysis of multi-level survival data using a pooled dataset of 14 cohorts participating in the ELAPSE project investigating associations between residential exposure to low levels of air pollution (PM2.5 and NO2) and health (natural-cause mortality and cerebrovascular, coronary and lung cancer incidence). METHODS: We applied five approaches in a multivariable Cox model to account for the first level of clustering corresponding to cohort specification: (1) not accounting for the cohort or using (2) indicator variables, (3) strata, (4) a frailty term in frailty Cox models, (5) a random intercept under a mixed Cox, for cohort identification. We accounted for the second level of clustering due to common characteristics in the residential area by (1) a random intercept per small area or (2) applying variance correction. We assessed the stratified, frailty and mixed Cox approach through simulations under different scenarios for heterogeneity in the underlying hazards and the air pollution effects. RESULTS: Effect estimates were stable under approaches used to adjust for cohort but substantially differed when no adjustment was applied. Further adjustment for the small area grouping increased the effect estimates' standard errors. Simulations confirmed identical results between the stratified and frailty models. In ELAPSE we selected a stratified multivariable Cox model to account for between-cohort heterogeneity without adjustment for small area level, due to the small number of subjects and events in the latter. CONCLUSIONS: Our study supports the need to account for between-cohort heterogeneity in multi-center collaborations using pooled individual level data.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Estudos de Coortes , Exposição Ambiental/análise , Humanos , Material Particulado/análise
19.
Environ Int ; 148: 106376, 2021 03.
Artigo em Inglês | MEDLINE | ID: mdl-33484961

RESUMO

BACKGROUND: Emerging epidemiological evidence suggests a relationship between exposure to air pollution and dementia. However, most of the existing studies relied on health administrative databases for the diagnosis of dementia. In a large French population-based cohort (the 3C Study), we assessed the effects of particulate matter ≤2.5 µm (PM2.5), nitrogen dioxide (NO2) and black carbon (BC) on the risk of dementia diagnosed with reliable tools. METHODS: Participants aged ≥65 years were recruited between 1999 and 2001 and followed for 12 years. At baseline and every 2 years, dementia was suspected on the basis of the neuropsychological and neurological examination and confirmed by an independent committee of clinicians. Exposure to NO2, BC and PM2.5 at the participants' residential address was estimated using land use regression models. For each pollutant and year of follow-up, the 10-year moving average of past exposure was estimated. Multilevel spatial random-effects Cox proportional hazards models were used in which exposure was included as a time-varying variable. Analyses were adjusted for individual (age, sex, education, APOE4 genotype, health behaviours) and contextual (neighbourhood deprivation index) confounders. RESULTS: At baseline, the median age of the 7066 participants was 73.4 years, and 62% were women. The median follow-up duration was 10.0 years during which 791 participants developed dementia (n = 541 Alzheimer's disease (AD) and n = 155 vascular/mixed dementia (VaD)). The 10-year moving average of PM2.5 concentrations ranged from 14.6 to 31.3 µg/m3. PM2.5 concentration was positively associated with dementia risk: HR = 1.20, 95% CI (1.08-1.32) for all-cause dementia, 1.20 (1.09-1.32) for AD, and 1.33 (1.05-1.68) for VaD per 5 µg/m3 PM2.5 increase. No association was detected between NO2 or BC exposure and dementia risk. CONCLUSION: In this large cohort of older adults, long-term PM2.5 exposure was associated with increased dementia incidence. Reducing PM2.5 emissions might lessen the burden of dementia in aging populations.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Idoso , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Feminino , Humanos , Masculino , Material Particulado/efeitos adversos , Material Particulado/análise , Estudos Prospectivos
20.
Environ Res ; 193: 110568, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33278469

RESUMO

BACKGROUND: An association between long-term exposure to fine particulate matter (PM2.5) and lung cancer has been established in previous studies. PM2.5 is a complex mixture of chemical components from various sources and little is known about whether certain components contribute specifically to the associated lung cancer risk. The present study builds on recent findings from the "Effects of Low-level Air Pollution: A Study in Europe" (ELAPSE) collaboration and addresses the potential association between specific elemental components of PM2.5 and lung cancer incidence. METHODS: We pooled seven cohorts from across Europe and assigned exposure estimates for eight components of PM2.5 representing non-tail pipe emissions (copper (Cu), iron (Fe), and zinc (Zn)), long-range transport (sulfur (S)), oil burning/industry emissions (nickel (Ni), vanadium (V)), crustal material (silicon (Si)), and biomass burning (potassium (K)) to cohort participants' baseline residential address based on 100 m by 100 m grids from newly developed hybrid models combining air pollution monitoring, land use data, satellite observations, and dispersion model estimates. We applied stratified Cox proportional hazards models, adjusting for potential confounders (age, sex, calendar year, marital status, smoking, body mass index, employment status, and neighborhood-level socio-economic status). RESULTS: The pooled study population comprised 306,550 individuals with 3916 incident lung cancer events during 5,541,672 person-years of follow-up. We observed a positive association between exposure to all eight components and lung cancer incidence, with adjusted HRs of 1.10 (95% CI 1.05, 1.16) per 50 ng/m3 PM2.5 K, 1.09 (95% CI 1.02, 1.15) per 1 ng/m3 PM2.5 Ni, 1.22 (95% CI 1.11, 1.35) per 200 ng/m3 PM2.5 S, and 1.07 (95% CI 1.02, 1.12) per 200 ng/m3 PM2.5 V. Effect estimates were largely unaffected by adjustment for nitrogen dioxide (NO2). After adjustment for PM2.5 mass, effect estimates of K, Ni, S, and V were slightly attenuated, whereas effect estimates of Cu, Si, Fe, and Zn became null or negative. CONCLUSIONS: Our results point towards an increased risk of lung cancer in connection with sources of combustion particles from oil and biomass burning and secondary inorganic aerosols rather than non-exhaust traffic emissions. Specific limit values or guidelines targeting these specific PM2.5 components may prove helpful in future lung cancer prevention strategies.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Neoplasias Pulmonares , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Exposição Ambiental/análise , Europa (Continente)/epidemiologia , Humanos , Incidência , Neoplasias Pulmonares/induzido quimicamente , Neoplasias Pulmonares/epidemiologia , Material Particulado/análise
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