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Living in areas with higher levels of surrounding greenness and access to urban green areas have been associated with beneficial health outcomes. Some studies suggested a beneficial influence on mortality, but the evidence is still controversial. We used longitudinal data from a large cohort to estimate associations of two measures of residential greenness exposure with cause-specific mortality and stroke incidence. We studied a population-based cohort of 1,263,721 residents in Rome aged [Formula: see text], followed from 2001 to 2013. As greenness exposure, we utilized the leaf area index (LAI), which expresses the tree canopy as the leaf area per unit ground surface area, and the normalized difference vegetation index (NDVI) within 300- and [Formula: see text] buffers around home addresses. We estimated the association between the two measures of residential greenness and the outcomes using Cox models, after controlling for relevant individual covariates and contextual characteristics, and explored potential mediation by air pollution [fine particulate matter with aerodynamic diameter [Formula: see text] [Formula: see text] and [Formula: see text]] and road traffic noise. We observed 198,704 deaths from nonaccidental causes, 81,269 from cardiovascular diseases [CVDs; 29,654 from ischemic heart disease (IHD)], 18,090 from cerebrovascular diseases, and 29,033 incident cases of stroke. Residential greenness, expressed as interquartile range (IQR) increase in LAI within [Formula: see text], was inversely associated with stroke incidence {hazard ratio (HR) 0.977 [95% confidence interval (CI): 0.961, 0.994]} and mortality for nonaccidental [HR 0.988 (95% CI: 0.981, 0.994)], cardiovascular [HR 0.984 (95% CI: 0.974, 0.994)] and cerebrovascular diseases [HR 0.964 (95% CI: 0.943, 0.985)]. Similar results were obtained using NDVI with 300- or [Formula: see text] buffers. Living in greener areas was associated with better health outcomes in our study, which could be partly due to reduced exposure to environmental hazards. Further research is required to understand the underlying mechanisms. https://doi.org/10.1289/EHP2854.

The role of chronic exposure to ambient air pollutants in increasing COVID-19 fatality is still unclear. The study aimed to investigate the association between long-term exposure to air pollutants and mortality among 4 million COVID-19 cases in Italy. We obtained individual records of all COVID-19 cases identified in Italy from February 2020 to June 2021. We assigned 2016-2019 mean concentrations of particulate matter (PM) with aerodynamic diameter ( ), PM with aerodynamic diameter ( ), and nitrogen dioxide ( ) to each municipality ( ) as estimates of chronic exposures. We applied a principal component analysis (PCA) and a generalized propensity score (GPS) approach to an extensive list of area-level covariates to account for major determinants of the spatial distribution of COVID-19 case-fatality rates. Then, we applied generalized negative binomial models matched on GPS, age, sex, province, and month. As additional analyses, we fit separate models by pandemic periods, age, and sex; we quantified the numbers of COVID-19 deaths attributable to exceedances in annual air pollutant concentrations above predefined thresholds; and we explored associations between air pollution and alternative outcomes of COVID-19 severity, namely hospitalizations or accesses to intensive care units. We analyzed 3,995,202 COVID-19 cases, which generated 124,346 deaths. Overall, case-fatality rates increased by 0.7% [95% confidence interval (CI): 0.5%, 0.9%], 0.3% (95% CI: 0.2%, 0.5%), and 0.6% (95% CI: 0.5%, 0.8%) per increment in , , and , respectively. Associations were higher among elderly subjects and during the first (February 2020-June 2020) and the third (December 2020-June 2021) pandemic waves. We estimated COVID-19 deaths were attributable to pollutant levels above the World Health Organization 2021 air quality guidelines. We found suggestive evidence of an association between long-term exposure to ambient air pollutants with mortality among 4 million COVID-19 cases in Italy. https://doi.org/10.1289/EHP11882.

Objective To conduct a systematic review to evaluate the association between residential or occupational short- and long–term exposure to odour pollution from industrial sources and the health status of the exposed population. Methods The searches were conducted in Medline, EMBASE and Scopus in April 2021. Exposure to an environmental odour from industrial sources in population resident near the source or in workers was considered. We considered outcomes for which there was a biological plausibility, such as wheezing and asthma, cough, headache, nausea and vomiting (primary outcomes). We also included stress-related symptoms and novel outcomes (e.g. mood states). Risk of bias was evaluated using the OHAT tool. For primary outcomes, when at least 3 studies provided effect estimates by comparing exposed subjects versus not exposed, we pooled the study-specific estimates of odour-related effect using random effects models. Heterogeneity was evaluated with Higgins I 2 . Results Thirty studies were eligible for this review, mainly cross-sectional ( n  = 23). Only one study involved school-age children and two studies involved workers. Only five studies reported odour effects on objective laboratory or clinical outcomes. Animal Feeding Operations and waste were the most common industrial sources. The overall odds ratios in exposed versus not exposed population were 1.15 (95% CI 1.01 to 1.29) for headache (7 studies), 1.09 (95% CI 0.88 to 1.30) for nausea/vomiting (7 studies), and 1.27 (95% CI 1.10 to 1.44) for cough/phlegm (5 studies). Heterogeneity was a moderate concern. Overall, the body of evidence was affected by a definitely high risk of bias in exposure and outcome assessment since most studies used self-reported information. Conclusions Findings underline the public health importance of odour pollution for population living nearby industrial odour sources. The limited evidence for most outcomes supports the need for high quality epidemiological studies on the association between odour pollution and its effects on human health.

Background Municipal solid waste incinerators (MSWIs) are widely used for waste management. However, the health effects of their emissions remain uncertain, needing further investigation and monitoring of the potential risks associated with such exposure. The aim of this study is to update and synthesize evidence on the health effects of residential exposure to MSWIs. Methods A systematic review with meta-analysis was conducted following PRISMA guidelines. The systematic search in MEDLINE, EMBASE, and Web of Science (April 2025), using specific search strategies, identified observational studies reporting quantitative estimates on the association between long term residential exposure to MSWIs and health outcomes. Study quality was assessed using the Navigation Guide tool. A narrative synthesis was conducted for all outcomes. When possible, a random-effects meta-analysis was performed and Higgins I 2 was used to summarize heterogeneity. For the overall body of evidence, heatmaps were used to visually represent the direction of the associations (positive, negative or lack of association) stratified by study quality. Results Out of 3,273 records identified, 51 studies were included. The most frequently investigated outcomes were congenital anomalies, pregnancy outcomes, cardiovascular and respiratory diseases, and cancers. The narrative synthesis suggests a weak association for hospitalizations due to cardiovascular and respiratory diseases in high-quality studies and a potential increased risk for non-Hodgkin lymphoma, based on low-quality evidence. The meta-analysis confirms a slight increased risk for respiratory diseases (HR 1.02; 95% CI 0.94–1.11), particularly for COPD (HR 1.08; 95% CI 0.82–1.41) and asthma (HR 1.02; 95% CI 1.00–1.05). Moderate heterogeneity was observed for most outcomes (I 2  = 30%-60%). Conclusions This review highlights the current uncertainty surrounding the long-term health effects of MSWI exposure. While a slight indication of increased risk emerged for cardiovascular and respiratory hospitalizations, and a weak association with non-Hodgkin’s lymphoma was observed, overall evidence remains weak. Methodological limitations, heterogeneity across studies, and low exposure levels complicate risk assessment and comparability. Standardized, high-quality research is needed to clarify these associations and support evidence-based public health decisions and transparent communication with affected communities. Trial registration The protocol of this review was registered in PROSPERO on 02/06/2024 (CRD42024550168).

Background Air pollution is one of the main concerns for the health of European citizens, and cities are currently striving to accomplish EU air pollution regulation. The 2020 COVID-19 lockdown measures can be seen as an unintended but effective experiment to assess the impact of traffic restriction policies on air pollution. Our objective was to estimate the impact of the lockdown measures on NO 2 concentrations and health in the two largest Italian cities. Methods NO 2 concentration datasets were built using data deriving from a 1-month citizen science monitoring campaign that took place in Milan and Rome just before the Italian lockdown period. Annual mean NO 2 concentrations were estimated for a lockdown scenario (Scenario 1) and a scenario without lockdown (Scenario 2), by applying city-specific annual adjustment factors to the 1-month data. The latter were estimated deriving data from Air Quality Network stations and by applying a machine learning approach. NO 2 spatial distribution was estimated at a neighbourhood scale by applying Land Use Random Forest models for the two scenarios. Finally, the impact of lockdown on health was estimated by subtracting attributable deaths for Scenario 1 and those for Scenario 2, both estimated by applying literature-based dose–response function on the counterfactual concentrations of 10 μg/m 3 . Results The Land Use Random Forest models were able to capture 41–42% of the total NO 2 variability. Passing from Scenario 2 (annual NO 2 without lockdown) to Scenario 1 (annual NO 2 with lockdown), the population-weighted exposure to NO 2 for Milan and Rome decreased by 15.1% and 15.3% on an annual basis. Considering the 10 μg/m 3 counterfactual, prevented deaths were respectively 213 and 604. Conclusions Our results show that the lockdown had a beneficial impact on air quality and human health. However, compliance with the current EU legal limit is not enough to avoid a high number of NO 2 attributable deaths. This contribution reaffirms the potentiality of the citizen science approach and calls for more ambitious traffic calming policies and a re-evaluation of the legal annual limit value for NO 2 for the protection of human health.

Background and aimsResidents near industrial areas are exposed to several toxins from various sources and the assessment of the health effects is difficult. The area of Civitavecchia (Italy) has several sources of environmental contamination with potential health effects. We evaluated the association between exposure to pollutants from multiple sources and mortality in a cohort of people living in the area.MethodsAll residents of the area in 1996 were enrolled (from municipal registers) and followed until 2013. Long-term exposures to emissions from industrial sources (PM10) and traffic (NOx) at the residential addresses were assessed using a dispersion model. Residence close to the harbour was also considered. Cox survival analysis was conducted including a linear term for industrial PM10 and NOx exposure and a dichotomous variable to indicate residence within 500 m of the harbour. Age, sex, calendar period, occupation and area-based socioeconomic position (SEP) were considered (HRs, 95% CI).Results71 362 people were enrolled (52% female, 43% low SEP) and 14 844 died during the follow-up. We found an association between industrial PM10 and mortality from non-accidental causes (HR=1.06, 95% CI 1.01 to 1.12), all cancers (HR=1.11, 95% CI 1.01 to 1.21) and cardiac diseases (HR=1.12, 95% CI 1.01 to 1.23). We also found an association between NOx exposure from traffic and mortality from all cancers (HR=1.13, 95% CI 1.01 to 1.26) and neurological diseases (HR=1.50, 95% CI 1.01 to 2.20). Living near the harbour was associated with higher mortality from lung cancer (HR=1.31, 95% CI 1.04 to 1.66) and neurological diseases (HR=1.51, 95% CI 1.05 to 2.18).ConclusionsEstimated exposures to different pollution sources in this area were independently associated with several mortality outcomes while adjusting for occupation and socioeconomic status.

Outdoor air pollution —in particular particulate matter, nitrogen dioxide and ozone— can exert its effects on health after acute (short-term) and chronic (long-term) exposures. Short-term exposures increase the probability of the onset of acute diseases within a few days, such as myocardial infarction or stroke, or even death in the case of susceptible individuals. Long-term exposures are associated with decreased survival and incidence of several non-communicable diseases, including cardiorespiratory conditions and lung cancer. In Europe, the large ESCAPE project (European Study of Cohorts for Air Pollution Effects — www.escapeproject.eu ) evaluated the chronic effects of air pollution in the cohorts of adult subjects. The results of ESCAPE show an association between chronic exposure to air pollutants and natural mortality, cardiovascular events, lung, brain, breast and digestive tract cancer. The recent joint statement of the European Respiratory Society and the American Respiratory Society clarifies the wide spectrum of adverse effects of pollution, including “new” diseases such as neurological and metabolic syndrome previously not studied. The estimates by the Global Burden of Disease provide nowadays indications that air pollution causes illness and mortality, just after diet, smoking, hypertension and diabetes: 4.2 million premature deaths a year worldwide. Ischemic heart disease, stroke, chronic obstructive pulmonary disease, acute lower respiratory infections are the main conditions associated with air-pollution–related mortality.

Suspected detrimental health effects associated with ultrafine particles (UFPs) are impressive. However, epidemiological evidence is still limited. This is potentially due to challenges related to UFP exposure assessment and the lack of consensus on a standard methodology for UFPs. It is imperative to focus future health studies on those UFP metrics more likely to represent health effects. This is the purpose of this paper, where we extend the results obtained during the CARE (“Carbonaceous Aerosol in Rome and Environs”) experiment started in 2017 in Rome. The major purpose is to investigate features of airborne UFPs associated with pro-inflammatory and oxidative responses. Aerosol chemical, microphysical, and optical properties were measured, together with the oxidative potential, at temporal scales relevant for UFPs (minutes to hours). The biological responses were obtained using both in-vivo and in-vitro tests carried out directly under environmental conditions. Findings indicate that caution should be taken when assessing health-relevant exposure to UFPs through the conventional metrics like total particle number concentration and PM2.5 and Black Carbon (BC) mass concentration. Conversely, we recommend adding to these, a UFP source apportionment analysis and indicators for both ultrafine black carbon and the size of particles providing most of the total surface area to available toxic molecules.

Urban air contains benzene and polycyclic aromatic hydrocarbons (PAHs) which have carcinogenic properties. The objective of this paper is to study the correlation of exposure biomarkers with biomarkers of nucleic acid oxidation also considering smoking. In 322 subjects, seven urinary dose biomarkers were analyzed for benzene, pyrene, nitropyrene, benzo[a]pyrene, and naphthalene exposure, and four effect biomarkers for nucleic acid and protein oxidative stress. Chemometrics was applied in order to investigate the existence of a synergistic effect for the exposure to the mixture and the contribution of active smoking. There is a significant difference between nicotine, benzene and PAH exposure biomarker concentrations of smokers and non-smokers, but the difference is not statistically significant for oxidative stress biomarkers. The PAH biomarkers are those which best correlate with all the oxidative stress biomarkers. Results suggest that 8-Oxo-7,8-dihydroguanine and protein nitro-oxidation 3-nitrotyrosine are the most sensitive biomarkers for the exposure to the urban pollutant mixtures and that a synergic effect of the mixtures exists. All the oxidative stress biomarkers studied drive the increase in the oxidative stress biomarkers in the subjects having higher exposures. Chemometrics proved to be a powerful method for the interpretation of human biomonitoring data.

Background: Benzene is an important component of cigarette smoke and car exhaust. Products containing benzene in concentrations greater than 0.1% are prohibited in Europe, but 1% of benzene is still allowed in gasoline. The purpose of the study was to assess the levels of urine benzene biomarkers in a sample of the general population not occupationally exposed to benzene, resident in the period 2013–2014 in Central Italy, compared to other groups. Methods: The urinary levels of the benzene metabolites S-phenyl-mercapturic acid (SPMA) and cotinine (nicotine metabolite) were determined by means of HPLC with mass spectrometric detection in 1076 subjects. Results: The median SPMA value in smokers was 1.132 µg/g of creatinine while in non-smokers it was 0.097 µg/g of creatinine, and the 95th percentile results were seven times higher. Conclusion: The main source of benzene exposure in the studied population was active smoking, however, non-smokers were also exposed to airborne benzene concentrations. The concentration ranges found in this study can be used as a background reference for occupational exposure assessment to benzene by means of SPMA biomonitoring.