The specific compounds that make ambient fine particulate matter (PM2.5) carcinogen remain poorly identified. Some metals contribute to ambient PM2.5 and possibly to its adverse effects. But the challenge of assessing exposure to airborne metals limits epidemiological studies. To analyze the relationships between several airborne metals and risk of cancer in a large population. We estimated the individual exposure to 12 airborne metals of ∼ 12,000 semi-urban and rural participants of the French population-based Gazel cohort using moss biomonitoring data from a 20-year national program. We used principal component analyses (PCA) to derive groups of metals, and focused on six single carcinogenic or toxic metals (arsenic, cadmium, chromium, lead, nickel, and vanadium). We used extended Cox models with attained age as time-scale and time-varying weighted average exposures, adjusted for individual and area-level covariables, to analyze the association between each exposure and all-site combined, bladder, lung, breast, and prostate cancer incidence. We identified 2,401 cases of all-site cancer between 2001 and 2015. Over the follow-up, median exposures varied from 0.22 (interquartile range (IQR): 0.18–0.28) to 8.68 (IQR: 6.62–11.79) µg.g−1 of dried moss for cadmium and lead, respectively. The PCA yielded three groups identified as "anthropogenic", "crustal", and "marine". Models yielded positive associations between most single and groups of metal and all-site cancer, with e.g. hazard ratios of 1.08 (95% CI: 1.03, 1.13) for cadmium or 1.06 (95% CI: 1.02,1.10) for lead, per interquartile range increase. These findings were consistent across supplementary analyses, albeit attenuated when accounting for total PM2.5. Regarding specific site cancers, we estimated positive associations mostly for bladder, and generally with large confidence intervals. Most single and groups of airborne metals, except vanadium, were associated with risk of cancer. These findings may help identify sources or components of PM2.5 that may be involved in its carcinogenicity.
BackgroundEmerging epidemiological evidence suggests a relationship between exposure to various air pollutants (AP) (fine particles (PM2.5), ozone (O3), nitrogen dioxide (NO2)) and dementia. However, most of existing studies relied on population-based health administrative databases to obtain a dementia diagnosis. In a large French population-based cohort (the Three-City Study), we aimed at assessing the effects of different AP on dementia risk using reliable diagnosis tools.MethodsParticipants aged ≥65 years were recruited between 1999-2001 and followed for 12 years. At baseline and every 2 years, dementia diagnoses were preliminary made using DSM-IV criteria and validated by an adjudication committee. NO2, O3, Black Carbon and PM2.5 levels were obtained at the residential addresses of participants using land-use regression models (ELAPSE project). For each year of follow-up (FU), we estimated a 10-year moving window of mean past exposure to each pollutant for each subject. We used Cox Proportional Hazard models where exposure was included as a time-varying variable. Analyses were adjusted for individual (age, sex, education, APOE4 genotype, vascular risk factors, respiratory diseases) and contextual (neighborhood's deprivation index) level confounders.ResultsThe mean (SD) age of the 8031 participants was 74.0 (5.4) years-old. Sixty-one percent of participants were women. The mean time of FU was 9.2 (3.6) years. The mean annual PM2.5 levels ranged from 15 to 33 µg/m3 and 920 participants developed dementia during the FU. We observed a positive association between PM2.5 levels and dementia risk [HR=1.16, 95%CI (1.03-1.32) for a 5µg/m3 increase in PM2.5]. We did not observe any relationship between the other AP exposures and dementia risk.ConclusionIn this large cohort with reliable diagnosis of dementia and individual estimates of AP exposure, long-term exposure to PM2.5 was associated with higher dementia incidence. These results suggest that PM2.5 exposure might be a modifiable risk factor of dementia.
The existence of decreased hypothalamic dopaminergic tone in HIV‐infected men has been suggested. In a cross‐sectional study, we determined 12 h nocturnal basal and pulsatile prolactin (PRL) release levels (by blood sampling every 10 min) and their correlation with CD4+ T cells in seven volunteer HIV‐negative, healthy men (group 1), and 21 normoprolactinemic, euthyroid, HIV‐infected men divided into 3 groups (each group = 7): (i) group 2, asymptomatic HIV‐infected stage A1 men, untreated; (ii) group 3, AIDS stage C3 without active opportunistic infections, untreated; and (iii) group 4, previously stage C3 after at least 6 months of successful highly active antiretroviral therapy. Serum PRL was measured by radioimmunoanalysis and the results were analysed by waveform‐independent deconvolution analysis. CD4+ T lymphocytes were measured by flow cytometry and viral load by a nucleic acid sequence‐based amplification assay. No differences were detected in the first two groups. In the third group, however, 100% of prolactin secretion was found to be pulsatile with a shorter secretory burst duration ( P = 0.04), and a greater circulating half‐life and pulse amplitude ( P ≤ 0.04). Group 4 had the greatest basal prolactin secretion ( P ≤ 0.04), and a shorter secretory burst duration ( P = 0.04 vs group 2), circulating half‐life ( P = 0.01 vs group 3) and intersecretory burst interval ( P = 0.06 vs group 1). PRL approximate entropy was similar among all groups. Linear correlations existed between CD4+ T cell counts and PRL secretory burst half duration ( r = 0.62, P = 0.002) and amplitude ( r = −0.63, P = 0.001), and in circulating serum half‐life ( r = − 0.61, P = 0.002) in HIV‐infected groups. Viral load showed no correlations. It is suggested that differential changes in nocturnal prolactin secretion among HIV‐infected men occurred while maintaining the normal coordinate feedback and/or feedforward control within the lactotropic axis. These changes may represent an adaptative mechanism to sustain, by different means, the maximal physiologic PRL production to stimulate the highest cellular immune response and/or reconstitution in attempting to survive.
Introduction: We have previously reported that outdoor levels of fine particles (PM2.5, diameter <2.5 μm) are associated with urinary CC16, a marker for lung damage, in Helsinki, Finland, but not in the other two ULTRA cities (Amsterdam, The Netherlands, and Erfurt, Germany). We here evaluated whether PM2.5 from specific source categories would be more strongly associated with CC16 than (total) PM2.5. In addition, we compared two source apportionment methods.Methods: We collected biweekly spot urinary samples over 6 months from 121 subjects with coronary heart disease for the determination of CC16 (n = 1251). Principal component analysis (PCA) was used to apportion daily outdoor PM2.5 between different source categories. In addition, the multilinear engine (ME) was used for the source apportionment in Amsterdam and Helsinki. We analyzed associations of source category-specific PM2.5 and PM2.5 absorbance, an indicator for combustion originating particles, with logarithmized values of CC16 adjusting for urinary creatinine using multivariate mixed models in STATA.Results: In the pooled analyses, CC16 was increased by 0.6% (standard error 0.3%) per 1 × 10−5 m−1 increase in the same-day levels of PM2.5 absorbance. Source category-specific PM2.5 concentrations were not consistently associated with the levels of CC16 in the three cities. Correlations between source category-specific PM2.5 determined using either PCA or ME were in general high. Associations of source category-specific PM2.5 with CC16 in Amsterdam and Helsinki were statistically less significant when ME was used.Conclusions: The present results suggest that PM2.5 from combustion sources increases epithelial barrier permeability in lungs.
BACKGROUND AND AIM: The main cause of female infertility after the age of 35 is diminished ovarian reserve (DOR). Several persistent organic pollutants (POPs) have been associated with an increased time-to-pregnancy but research on the effect of POPs on DOR is limited. METHODS: Our study included 139 cases and 153 controls from the AROPE case-control study. Study participants were women between the ages of 18 and 40 recruited amongst couples consulting for infertility in four fertility centres in western France. Cases were women with DOR (defined as anti-müllerian hormone levels 1.1 ng/ml and/or antral follicle count 7) and controls were women with normal evaluations, no malformations, and regular menstrual cycles. 41 POPs (including 15 organochlorine pesticides, 15 polychlorinated biphenyls and 9 polybromodiphenylethers) were measured in blood serum at inclusion. We conducted logistic regression adjusted on potential confounders to study the effect of each POP on DOR separately. In addition, we used Bayesian Kernel Machine Regression (BKMR) to measure the mixture effect of POPs on DOR. RESULTS:17 POPs were detected in over 20% of the serum samples. Individual multivariate logistic regressions showed that p,p'-DDE was associated with an increased risk of DOR (OR=1.50 [0.78 - 2.89] for the second tercile and OR=1.93 [1.00 - 3.73] for the third tercile) and Beta-HCH was associated with a decreased risk of DOR (OR=0.76 [0.42 - 1.40] for the second tercile and OR=0.45 [0.23 - 0.88] for the third tercile). BKMR showed similar associations for individual exposures but found no significant associations for the total mixture effect. In addition, BKMR results suggested an absence of interactions between POPs. CONCLUSIONS:Although BKMR indicated no interaction between POPs and no associations for POPs as a mixture, certain POPs could be individually associated with DOR. KEYWORDS: Reproductive outcomes, Female, Chemical exposures, Endocrine disrupting chemicals, Mixtures
The harmful effects of air pollution on asthma are recognized, but the underlying biological mechanisms are not yet well-known. Studying the associations between air pollution and asthma inflammatory phenotypes may bring new insights. Blood inflammatory phenotypes were identified as previously done among participants with current asthma in the French adult population-based cohort Constances (Tsiavia T, EBioMedicine, 2022). At inclusion, current asthma was defined by self-reporting asthma attacks, symptoms or treatments in the last 12 months. Blood eosinophil (0.25x109/L) and neutrophil (5x109/L) cut-offs defined paucigranulocytic, eosinophilic, neutrophilic and mixed asthma phenotypes. Annual concentrations of PM2.5, black carbon (BC) and NO2 at the participants9 residential addresses at inclusion were estimated using a land-use regression model. Multinomial logistic models adjusted for age, sex, smoking, education and French deprivation index were used. The ORs were expressed for one interquartile range increase of PM2.5 (4.16 µg/m3), BC (0.57 10-5/m) and NO2 (12.8 µg/m3). This study included 14873 participants with current asthma. The paucigranulocytic, neutrophilic, eosinophilic and mixed phenotype accounted for 57%, 6%, 33% and 4% respectively. Using paucigranulocytic phenotype as the reference, the neutrophilic phenotype had significantly higher odd for PM2.5 (OR: 1.11 (1.01-1.21)) and the eosinophilic phenotype had significantly lower odds for BC and NO2 (ORs: 0.95 (0.90-1.00) and 0.91 (0.87-0.96)). No association was evidenced for the mixed phenotype. These results showed that neutrophilic and eosinophilic phenotypes were differently associated with each air pollutant, suggesting different biological mechanisms.
Very few studies have examined whether a long-term beneficial effect of physical activity on lung function can be influenced by living in polluted urban areas.We assessed whether annual average residential concentrations of nitrogen dioxide (NO2) and particulate matter with aerodynamic diameters < 2.5 μm (PM2.5) and <10 μm (PM10) modify the effect of physical activity on lung function among never- (N = 2801) and current (N = 1719) smokers in the multi-center European Community Respiratory Health Survey.Associations between repeated assessments (at 27-57 and 39-67 years) of being physically active (physical activity: ≥2 times and ≥1 h per week) and forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) were evaluated using adjusted mixed linear regression models. Models were conducted separately for never- and current smokers and stratified by residential long-term NO2, PM2.5 mass and PM10 mass concentrations (≤75th percentile (low/medium) versus >75th percentile (high)).Among current smokers, physical activity and lung function were positively associated regardless of air pollution levels. Among never-smokers, physical activity was associated with lung function in areas with low/medium NO2, PM2.5 mass and PM10 mass concentrations (e.g. mean difference in FVC between active and non-active subjects was 43.0 mL (13.6, 72.5), 49.5 mL (20.1, 78.8) and 49.7 mL (18.6, 80.7), respectively), but these associations were attenuated in high air pollution areas. Only the interaction term of physical activity and PM10 mass for FEV1 among never-smokers was significant (p-value = 0.03).Physical activity has beneficial effects on adult lung function in current smokers, irrespective of residential air pollution levels in Western Europe. Trends among never-smokers living in high air pollution areas are less clear.
Background: Fine particulate matter (PM2.5) is associated with mortality, and recent evidence identified black carbon (BC) as one component of PM2.5 that may at least partly explain the health effects. Yet, this remains poorly documented. This study aimed to examine the association between long-term exposure to BC and mortality in a population-based French cohort. Methods: We used data from the Gazel cohort collected between 1989-2015, including geocoded residential address history. We used land use regression models with temporal extrapolation to estimate the exposure to BC and PM2.5 for 19,850 participants. We used extended Cox models with attained age as time-scale and time-varying average exposure to BC, adjusted for relevant covariates including sex, smoking status and cumulative pack-years, and including a 10-year lag, to estimate the association between long-term exposure to BC and all-cause and cardiovascular mortality. To handle confounding by PM2.5, we regressed BC against PM2.5 and used the residuals as the exposure variable in a sensitivity analysis. Separate analyses by sex and smoking status were also done to examine effect modification for all-cause mortality. Results: The median long-term BC exposure was 2.34 10-5/m (inter-quartile range (IQR): 1.09). We found a significant association between BC and all-cause mortality (n=1794) using long-term average BC and residuals, with respective hazard ratios (HR) of 1.10 (95%CI: 1.04-1.17) and 1.19 (1.11-1.26) per IQR increase. We found a similar association between BC and cardiovascular mortality (n=271) with a HR of 1.15 (0.99-1.35). The association with all-cause mortality slightly varied across population subsets with HRs of 1.10 (1.03-1.18) and 1.09 (0.96-1.24) for men and women, and 1.10 (0.97-1.25) and 1.14 (1.07-1.23) for never- and ever-smokers, respectively.Conclusions: We found positive associations between long-term exposure to BC and increased mortality, reinforcing the emerging evidence that BC is a harmful component of PM.
It is still unclear if air pollutants play a role in asthma development in adults. The aim was to assess the impact of long-term exposure to air pollution on adult onset asthma in 6 European cohorts (ECRHS, EGEA, E3N, NSHD, SALIA, SAPALDIA) using standardized ESCAPE exposure estimates.
Annual concentrations of NO2 and particulate matter (PM10 and PM2.5) at home addresses were estimated using land-use regression models. To assess incidence, asthma definition was developed being specific at baseline and sensitive at follow-up. Logistic regression models were adjusted for age, sex, BMI, education and smoking. Cohort-specific results were meta-analysed.
23701 subjects with NO2 and 16662 subjects with PM exposure estimates were included. Asthma incident cases were 1257. Incidence rates varied between 2.9 and 8.3/1000/year in SAPALDIA and EGEA respectively. The meta-analyses did not show significant associations between air pollution and asthma incidence (OR:1.05 (95%CI:0.97,1.14) per 10μg/m3 of NO2 and 1.04 (95%CI:0.88,1.22) per 10μg/m3 PM10). EGEA was the only cohort showing a significant positive association (OR:1.36 (95%CI:1.07,1.72) per 10μg/m3 of NO2).
![Figure][1]
The point estimates were lower than the ones previously published and the meta-analysis did not show statistically significant associations between air pollution and adult onset-asthma.
Funds: ESCAPE EC-FP7-GA 211250.
[1]: pending:yes
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