Department of Neurosciences, University of Padua, Padua, Italy
Multiple sclerosis epidemiological trends in Italy highlight the environmental risk factors
Italy is definitely a high-risk country for multiple sclerosis (MS). Over the last 50 years, several epidemiological studies, including longitudinal surveys, have disclosed that MS incidence and prevalence in Italy mainland and Islands (Sardinia and Sicily) have progressively increased, picturing a semi-parabolic curve. Based on the comprehensive scrutiny of 58 papers, we conclude that the latitude risk gradient does not fit to the Italian map of MS. The genetic heterogeneity of the Italian ethnicities, that likely forms the basis of MS predisposition, does not account for the dramatic increase of MS incidence and prevalence observed in Italy over the last half century that, rather, seems better explained by the effect of environmental factors.
that is logical
Department of Occupational and Environmental Health Sciences, School of Public Health, Peking University, Beijing, China
Association between gaseous air pollutants and biomarkers of systemic inflammation: A systematic review and meta-analysis
Background: Studies have linked gaseous air pollutants to multiple health effects via inflammatory pathways. Several major inflammatory biomarkers, including C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) have also been considered as predictors of cardiovascular disease. However, there has been no meta-analysis to evaluate the associations between gaseous air pollutants and these typical biomarkers of inflammation to date.
Objectives: To evaluate the overall associations between short-term and long-term exposures to ambient ozone (O3), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon dioxide (CO) and inflammatory biomarkers including CRP, fibrinogen, IL-6 and TNF-α.
Methods: A meta-analysis was conducted for publications from PubMed, Web of Science, Scopus and EMBASE databases up to Feb 1st, 2021.
Results: The meta-analysis included 38 studies conducted among 201,459 participants. Generally, we only observed significant positive associations between short-term exposures to gaseous air pollutants and inflammatory biomarkers. For a 10 μg/m3 increase in short-term exposure to O3, NO2, and SO2, there were significant increases of 1.05% (95%CI: 0.09%, 2.02%), 1.60% (95%CI: 0.49%, 2.72%), and 10.44% (95%CI: 4.20%, 17.05%) in CRP, respectively. Meanwhile, a 10 μg/m3 increase in NO2 was also associated with a 4.85% (95%CI: 1.10%, 8.73%) increase in TNF-α. Long-term exposures to gaseous air pollutants were not statistically associated with these biomarkers, but the study numbers were relatively small. Subgroup analyses indicated that more apparent associations were found in studies with better study design, higher quality, and smaller sample size.
Conclusion: Short-term exposure to gaseous air pollutants is associated with increased levels of circulating inflammatory biomarkers, suggesting a systemic inflammatory state is activated. More studies on long-term exposure to gaseous air pollutants and inflammatory biomarkers are warranted to verify the associations.
Neurology Research Center, Kerman University of Medical Sciences, Kerman, Iran
Ambient air pollution and multiple sclerosis: a systematic review
Objectives: Some studies have shown that environmental risk factors, including air pollution, might be related to the incidence or recurrence of multiple sclerosis (MS). This systematic review was conducted to investigate the relation between air pollution and MS.
Methods: A systematic search was conducted in PubMed, Scopus, Science Direct, Embase, and Web of Science; until January 2020 with no restrictions. The search strategy was conducted with air pollution key words such as CO, PM2.5, PM10, SO2, and NO2, for exposure and the key word "Multiple sclerosis" as the outcome.
Results: Eventually, after applying the inclusion and exclusion criteria, 17 articles were included. The methodologies and outcomes reported were heterogeneous and different metrics had been used in the results; therefore conducting a meta-analysis was not possible. Eight studies had analyzed the relation between particulate matter (PM) and the prevalence or relapse of MS and had observed a significant relation. NO2 and NOx were associated with recurrence or prevalence of MS in three studies. But, in three cohort studies, no association was observed between air pollution and recurrence or occurrence of MS.
Conclusions: The results of this systematic review show that outdoor air pollution, especially PM and nitrogen oxides might be related to the prevalence or relapse of MS.
Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, Georgia
Low-Concentration Air Pollution and Mortality in American Older Adults: A National Cohort Analysis (2001-2017)
Mounting epidemiological evidence has documented the associations between long-term exposure to multiple air pollutants and increased mortality. There is a pressing need to determine whether risks persist at low concentrations including below current national standards. Air pollution levels have decreased in the United States, and better understanding of the health effects of low-level air pollution is essential for the amendment of National Ambient Air Quality Standards (NAAQS). A nationwide, population-based, open cohort study was conducted to estimate the association between long-term exposure to low-level PM2.5, NO2, O3, and all-cause mortality. The study population included all Medicare enrollees (ages 65 years or older) in the contiguous U.S. from 2001 to 2017. We further defined three low-exposure subcohorts comprised of Medicare enrollees who were always exposed to low-level PM2.5 (annual mean ≤12-μg/m3), NO2 (annual mean ≤53-ppb), and O3 (warm-season mean ≤50-ppb), respectively, over the study period. Of the 68.7-million Medicare enrollees, 33.1% (22.8-million, mean age 75.9 years), 93.8% (64.5-million, mean age 76.2 years), and 65.0% (44.7-million, mean age 75.6 years) were always exposed to low-level annual PM2.5, annual NO2, and warm-season O3 over the study period, respectively. Among the low-exposure cohorts, a 10-μg/m3 increase in PM2.5, 10-ppb increase in NO2, and 10-ppb increase in warm-season O3, were, respectively, associated with an increase in mortality rate ranging between 10 and 13%, 2 and 4%, and 12 and 14% in single-pollutant models, and between 6 and 8%, 1 and 3%, and 9 and 11% in tripollutant models, using three statistical approaches. There was strong evidence of linearity in concentration-response relationships for PM2.5 and NO2 at levels below the current NAAQS, suggesting that no safe threshold exists for health-harmful pollution levels. For O3, the concentration-response relationship shows an increasingly positive association at levels above 40-ppb. In conclusion, exposure to low levels of PM2.5, NO2, and warm-season O3 was associated with an increased risk of all-cause mortality.
Department of Medical, Surgical and Advanced Technologies "G.F. Ingrassia", University of Catania, Italy
Possible association between PM 2.5 and neurodegenerative diseases: A systematic review
Air pollution is one of the most serious environmental problems that afflict our planet and one of the greatest risk factors for human health. In particular, PM2.5 is able to cross the blood-alveolar and blood-brain barriers, thus increasing the onset of respiratory, cardiovascular and neurodegenerative diseases. Neurodegenerative disease is a progressive neuronal dysfunction that leads to neuronal lesions in both structure and function, and includes several diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), vascular dementia (VaD), multiple sclerosis (MS), and others. We carried out a systematic review using PRISMA approach to investigate on the possible association between exposure to PM2.5 and neurodegenerative diseases. The international databases (PubMed, Science Direct, Web of Sciences) were used to find published studies on the topic. The search period was between January 2011 and June 2021. About 2000 full research articles were selected, and finally, we included 20 full-research articles. Selected studies have highlighted how PM2.5 exposure can be associated with the onset of neurodegenerative diseases (AD, PD, MS, VaD). This association depends not only on age, PM2.5 levels and exposure time, but also on exposure to other air pollutants, proximity to areas with high vehicular traffic, and the presence of comorbidities. Exposure to PM2.5 promotes neuroinflammation processes, because through breathing the particles can reach the nasal epithelial mucosa and transferred to the brain through the olfactory bulb. Furthermore, exposure to PM2.5 has been associated with an increased expression of markers of neurodegenerative diseases (e.g. alpha-synuclein or beta-amyloid), which can contribute to the etiopathogenesis of neurodegenerative diseases. Although many studies have revealed the pathological relationship between PM2.5 exposure and cognitive impairment, the potential cellular and molecular mechanisms of PM2.5 leading to neurodegenerative disease remain not entirely clear, and then, further studies need to be carried out on the topic.
In the case of MS, I say: O3 Petr
Department of Epidemiology, Lazio Region Health Service, Rome, Italy; Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
Long-term exposure to low ambient air pollution concentrations and mortality among 28 million people: results from seven large European cohorts within the ELAPSE project
https://pubmed.ncbi.nlm.nih.gov/3499846 ... /34998464/
Background: Long-term exposure to ambient air pollution has been associated with premature mortality, but associations at concentrations lower than current annual limit values are uncertain. We analysed associations between low-level air pollution and mortality within the multicentre study Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE).
Methods: In this multicentre longitudinal study, we analysed seven population-based cohorts of adults (age ≥30 years) within ELAPSE, from Belgium, Denmark, England, the Netherlands, Norway, Rome (Italy), and Switzerland (enrolled in 2000-11; follow-up until 2011-17). Mortality registries were used to extract the underlying cause of death for deceased individuals. Annual average concentrations of fine particulate matter (PM2·5), nitrogen dioxide (NO2), black carbon, and tropospheric warm-season ozone (O3) from Europe-wide land use regression models at 100 m spatial resolution were assigned to baseline residential addresses. We applied cohort-specific Cox proportional hazard models with adjustment for area-level and individual-level covariates to evaluate associations with non-accidental mortality, as the main outcome, and with cardiovascular, non-malignant respiratory, and lung cancer mortality. Subset analyses of participants living at low pollutant concentrations (as per predefined values) and natural splines were used to investigate the concentration-response function. Cohort-specific effect estimates were pooled in a random-effects meta-analysis.
Findings: We analysed 28 153 138 participants contributing 257 859 621 person-years of observation, during which 3 593 741 deaths from non-accidental causes occurred. We found significant positive associations between non-accidental mortality and PM2·5, NO2, and black carbon, with a hazard ratio (HR) of 1·053 (95% CI 1·021-1·085) per 5 μg/m3 increment in PM2·5, 1·044 (1·019-1·069) per 10 μg/m3 NO2, and 1·039 (1·018-1·059) per 0·5 × 10-5/m black carbon. Associations with PM2·5, NO2, and black carbon were slightly weaker for cardiovascular mortality, similar for non-malignant respiratory mortality, and stronger for lung cancer mortality. Warm-season O3 was negatively associated with both non-accidental and cause-specific mortality. Associations were stronger at low concentrations: HRs for non-accidental mortality at concentrations lower than the WHO 2005 air quality guideline values for PM2·5 (10 μg/m3) and NO2 (40 μg/m3) were 1·078 (1·046-1·111) per 5 μg/m3 PM2·5 and 1·049 (1·024-1·075) per 10 μg/m3 NO2. Similarly, the association between black carbon and non-accidental mortality was highest at low concentrations, with a HR of 1·061 (1·032-1·092) for exposure lower than 1·5× 10-5/m, and 1·081 (0·966-1·210) for exposure lower than 1·0× 10-5/m.
Interpretation: Long-term exposure to concentrations of PM2·5 and NO2 lower than current annual limit values was associated with non-accidental, cardiovascular, non-malignant respiratory, and lung cancer mortality in seven large European cohorts. Continuing research on the effects of low concentrations of air pollutants is expected to further inform the process of setting air quality standards in Europe and other global regions.
Section of Dermatology and Venereology, Department of Medicine, University of Verona, Verona, Italy
Association Between Short-term Exposure to Environmental Air Pollution and Psoriasis Flare
December 12, 2018
The connection between multiple sclerosis and psoriasis
https://www.dermatologytimes.com/view/c ... -psoriasis
..."By contrast," Chi et al. wrote, "we included more recent studies and separately analyzed data further according to different types of study design, thus providing robust evidence on the association of multiple sclerosis with psoriasis."
Department of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China
Ambient air pollution, healthy diet and vegetable intakes, and mortality: a prospective UK Biobank study
Background: Recent studies suggest potential interactions of air pollutants with dietary factors and genetic susceptibility on mortality risk; however, evidence from prospective studies is still lacking. We aimed to assess the association between air pollution and mortality, and investigate the modification effects of a healthy diet and genetic susceptibility.
Methods: A total of 386 937 participants were enrolled from 2006 to 2010 and followed up to 2018 in the UK Biobank study. The annual average air pollutant concentrations of particulate matter (PM) with diameters ≤2.5 (PM2.5), ≤10 (PM10) and between 2.5 and 10 µm (PM2.5-10) and nitrogen oxides (NO2 and NOx) were calculated and linked to participants' residential addresses. Healthy dietary patterns were evaluated by a healthy diet score (HDS) based on intakes of vegetables, fruit, fish, unprocessed red meat and processed meat. We also calculated genetic risk score (GRS) of the lifespan. We examined potential interactions by setting variable cross-product terms of air pollutants with diets or GRS in the models.
Results: We identified 11 881 deaths [2426 from cardiovascular diseases (CVD), 1211 from coronary heart disease (CHD) and 466 from stroke] during a median follow-up of 8.9 years. We found that PM2.5 [hazard ratio (HR), 1.27; 95% CI, 1.05-1.55], PM10 (HR, 1.18; 95% CI, 1.04-1.34), NO2 (HR, 1.05; 95% CI, 1.01-1.08), and NOx (HR, 1.02; 95% CI, 1.01-1.03) were associated with all-cause mortality. PM2.5 was also associated with increased risks of CVD mortality (HR, 1.68; 95% CI, 1.10-2.56) and CHD mortality (HR, 2.08; 95% CI, 1.16-3.75). In addition, we found that adherence to healthy dietary patterns modified associations of PM2.5, NO2 and NOx with all-cause mortality (P-interaction = 0.006, 0.006 and 0.02, respectively). Among the individual dietary components, vegetable intakes showed interactions with PM2.5, NO2 and NOx (P-interaction = 0.007, 0.004 and 0.02, respectively). The associations between air pollutants and increased risks of all-cause mortality were attenuated among participants with higher vegetable intakes. We did not observe interactions between air pollutants and HDS on CVD, CHD or stroke mortality (P-interaction > 0.05). Besides, we did not find interactions between air pollutants and genetic risk for lifespan on mortality risk.
Conclusion: This study provides evidence linking long-term exposure to various air pollutants to the risk of all-cause, CVD and CHD mortality, and the potential attenuation of a healthy diet, especially high vegetable intakes, on such relations. Our findings highlight the importance of adherence to a healthy diet in lowering ambient air-pollution-related mortality risk.
Department of Family Planning, The Second Hospital of Tianjin Medical University, Tianjin, China
Ambient PM 2.5 exposures and systemic inflammation in women with early pregnancy
The association between ambient fine particulate matter (PM2.5) and systemic inflammation in women with early pregnancy is unclear. This study estimated the effects of PM2.5 exposures on inflammatory biomarkers in women with normal early pregnancy (NEP) or clinically recognized early pregnancy loss (CREPL). Serum interleukin-1beta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were measured in 228 early pregnant women recruited in Tianjin, China. Maternal PM2.5 exposures at lag 0 through lag 30 before blood collection were estimated using temporally-adjusted land use regression models. Daily exposures to ambient PM10, NO2, SO2, CO and 8-hours maximum ozone were estimated using city-level concentrations. Single-day lag effects at lag 0 through lag 7 were estimated using multivariable linear regression models. Distributed lag effects and cumulative effects over the preceding seven days and 30 days were estimated using distributed lag non-linear models. Serum IL-1β (8.0% increase at lag 3), IL-6 (33.9% increase at lag 5) and TNF-α (12.7% increase at lag 5) in early pregnant women were significantly increased with an interquartile range increase in PM2.5 exposures adjusted for temporal confounders and demographic characteristics. These effects were robust in several two-pollutant models. Distributed lag effects over the preceding 30 days also showed that the three cytokines were significantly increased with PM2.5 on some lag days. Among all cumulative effects of PM2.5 on the three cytokines in all subjects or in the two groups, only IL-6 was significantly increased in CREPL women over the preceding seven days and 30 days. No significant cumulative effect of PM2.5 was observed in NEP women. In conclusion, exposure to ambient PM2.5 may induce systemic inflammation in women in the first trimester of pregnancy. Whether the PM2.5-related cumulative increase in maternal IL-6 is involved in the pathogenic mechanisms of early pregnancy loss needs to be identified in future research.
Department of Environmental and Biological Science, University of Eastern Finland, Finland; Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, China
Fine and ultrafine airborne PM influence inflammation response of young adults and toxicological responses in vitro
Little evidence is available regarding the impact of different sizes of inhaled particulate matter (PM) on inflammatory responses in healthy young adults in connection with toxicological responses. We conducted a five-time repeated measurement panel study on 88 healthy young college students in Guangzhou, China from December 2017 to January 2018. Blood samples were collected from each participant and tested for tumor necrosis factor alpha (TNF-α) levels every week for 5 consecutive weeks. Mass concentrations of ambient PM2.5, PM1, PM0.5 and number concentrations of ambient PM0.1 were measured. RAW 264.7 macrophages were exposed to PM (PM10-2.5, PM2.5-1, PM1-0.2, PM0.2) collected at the same time as the panel study. Cytotoxicity, oxidation and inflammatory parameters, cell cycle and genotoxicity were tested. Particles were characterized for their chemical composition. The trends of associations between PM2.5, PM1, PM0.5 and TNF-α level were consistent in lag 0 and 3 days, and the relative risk decreased as the particle size decreased. All the ambient air pollutants had the similar change trends in lag 1, 4 and 5 days. Similar results in RAW 264.7 macrophages were found; PM10-2.5 induced the greatest TNF-α and macrophage inflammatory protein 2 (MIP-2) productions and oxidative damage. PM1-0.2 and PM0.2 induced more significant dose-dependent increases of cell cycle and genotoxic response. In the component concentrations of PM samples, metal elements were PM10-2.5 > PM2.5-1 > PM0.2 ≥ PM1-0.2; ions and polycyclic aromatic hydrocarbons (PAHs) were PM0.2 > PM1-0.2 > PM2.5-1 > PM10-2.5. Our results suggested that exposure to all particle sizes was significantly associated with inflammation among healthy young adults and toxicological responses in RAW 264.7 macrophages. Different human and toxicological reactions caused by PM samples indicated the importance of investigating various particle sizes.
Department of Clinical Immunology, Institute of Pediatrics, Jagiellonian University Medical College, Krakow, Poland
Transcriptional Response of Blood Mononuclear Cells from Patients with Inflammatory and Autoimmune Disorders Exposed to "Krakow Smog"
Despite the general awareness of the need to reduce air pollution, the efforts were undertaken in Poland to eliminate the pollutants and their harmful effect on human health seem to be insufficient. Moreover, the latest data indicate that the city of Krakow is at the forefront of the most polluted cities worldwide. Hence, in this report, we investigated the impact of particulate matter isolated from the air of Krakow (PM KRK) on the gene expression profile of peripheral blood mononuclear cells (PBMCs) in healthy donors (HD) and patients with atherosclerosis (AS), rheumatoid arthritis (RA) and multiple sclerosis (MS), after in vitro exposure. Blood samples were collected in two seasons, differing in the concentration of PM in the air (below or above a daily limit of 50 µg/m3 for PM 10). Data show that PBMCs exposed in vitro to PM KRK upregulated the expression of genes involved, among others, in pro-inflammatory response, cell motility, and regulation of cell metabolism. The transcriptional effects were observed predominantly in the group of patients with AS and MS. The observed changes seem to be dependent on the seasonal concentration of PM in the air of Krakow and may suggest their important role in the progression of AS, MS, and RA in the residents of Krakow.