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  • Andrea Ranzi1

  1. Arpa, Modena

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Ricerca bibliografica periodo dal 16 novembre 2013 – 31 gennaio 2014

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Stringa: (pollution[Title/Abstract] OR pollutant[Title/Abstract] OR pollutants[Title/Abstract] OR climate change[Title/Abstract] ) AND ("italy"[MeSH Terms] OR "italy"[All Fields]) AND ("2013/11/16"[PDAT] : "2014/01/31"[PDAT])
1. Candela S, Ranzi A, Bonvicini L, Baldacchini F, Marzaroli P, Evangelista A, Luberto F, Carretta E, Angelini P, Sterrantino AF, Broccoli S, Cordioli M, Ancona C, Forastiere F. Air pollution from incinerators and reproductive outcomes: a multisite study. Epidemiology. 2013 Nov;24(6):863-70. doi: 10.1097/EDE.0b013e3182a712f1.
From the aEpidemiology Unit, Local Health Authority, Reggio Emilia, Italy; bRegional Reference Centre on Environment and Health, ARPA Emilia-Romagna, Modena, Italy; cPublic Health Service, Emilia-Romagna Region, Italy; and dDepartment of Epidemiology, Lazio Region, Italy.

Abstract BACKGROUND: The few studies that have investigated the relationship between emissions from municipal solid-waste incinerators and adverse pregnancy outcomes have had conflicting results. We conducted a study to assess the effects of air emissions from the eight incinerators currently in operation in the Emilia-Romagna Region of Italy on reproductive outcomes (sex ratio, multiple births, preterm births, and small for gestational age [SGA] births). METHODS: We considered all births (n = 21,517) to women residing within a 4-km radius of an incinerator at the time of delivery during the period 2003-2010 who were successfully linked to the Delivery Certificate database. This source also provided information on maternal characteristics and deliveries. Each newborn was georeferenced and characterized by a specific level of exposure to incinerator emissions, categorized in quintiles of PM10, and other sources of pollution (NOx quartiles), evaluated by means of ADMS-Urban system dispersion models. We ran logistic regression models for each outcome, adjusting for exposure to other pollution sources and maternal covariates. RESULTS: Incinerator pollution was not associated with sex ratio, multiple births, or frequency of SGA. Preterm delivery increased with increasing exposure (test for trend, P < 0.001); for the highest versus the lowest quintile exposure, the odds ratio was 1.30 (95% confidence interval = 1.08-1.57). A similar trend was observed for very preterm babies. Several sensitivity analyses did not alter these results. CONCLUSIONS: Maternal exposure to incinerator emissions, even at very low levels, was associated with preterm delivery.

Breve commento a cura di Andrea Ranzi
L’articolo apparso su Epidemiology rappresenta il risultato principale, dal punto di vista delle indagini epidemiologiche, del progetto Moniter, che ha riguardato lo studio degli effetti sull’ambiente e sulla salute degli inceneritori di rifiuti solidi urbani presenti nella regione Emilia-Romagna. L’articolo riporta un aumento di rischio di parto pretermine per le donne che abitano in zone a maggior ricaduta degli inquinanti emessi dagli inceneritori di rifiuti solidi urbani della regione. Il risultato è frutto di due indagini ripetute nelle stesse aree su due periodi diversi (2003-2006 e 2007-2010), che avevano dato risultati positivi e comparabili (l’articolo presenta l’analisi completa). Il risultato più robusto dal punto di vista dell’analisi statistica di tutto il progetto arriva per eventi relativi ad esposizioni recenti. La discussione scientifica su questo risultato è importante: come è possibile che livelli di esposizione così bassi, inferiori anche di 3 ordini di grandezza rispetto a quelli di altri fattori di pressione esistenti nell’area, a livelli difficilmente rilevabili dagli strumenti di misura, possano portare effetti sulla salute riproduttiva? E’ così diversa la composizione di questi inquinanti, oppure il miglioramento nella qualità dei dati disponibili e delle metodologie di valutazione dell’esposizione permettono di osservare effetti precedentemente poco rilevati? Domande sicuramente aperte, che cominciano ad essere sollevate anche da altri studi.

2. Parodi S, Santi I, Marani E, Casella C, Puppo A, Vercelli M, Stagnaro E. Risk of non-Hodgkin's lymphoma and residential exposure to air pollution in an industrial area in northern Italy: a case-control study. Arch Environ Occup Health. 2014;69(3):139-47. doi: 10.1080/19338244.2013.763756.
Author information: a Epidemiology, Biostatistics and Clinical Trials Unit, IRCCS AOU San Martino-IST, National Cancer Research Institute , Genoa , Italy.

Abstract The aim of this study was to evaluate the risk of non-Hodgkin's lymphoma (NHL) in an adult population residing in an area in northern Italy exposed to industrial air pollution from a big power plant, a coke oven, 2 chemical factories, and some minor plants. The design was a population-based case-control study and information about residential history and the main risk factors for NHL was obtained interviewing 133 cases and 279 controls using a structured questionnaire. Three exposure categories (heavy, moderate, and slight) were defined on the basis of the location of the major facilities with respect to the subject residence. NHL risk was not associated either with location or duration of residence in the heavily polluted area. However, the unavoidable limitations of this study prevent us from drawing definitive conclusions.

3. Cesaroni G1, Forastiere F, Stafoggia M, Andersen ZJ, Badaloni C, Beelen R, Caracciolo B, de Faire U, Erbel R, Eriksen KT, Fratiglioni L, Galassi C, Hampel R, Heier M, Hennig F, Hilding A, Hoffmann B, Houthuijs D, Jöckel KH, Korek M, Lanki T, Leander K, Magnusson PK, Migliore E, Ostenson CG, Overvad K, Pedersen NL, J JP, Penell J, Pershagen G, Pyko A, Raaschou-Nielsen O, Ranzi A, Ricceri F, Sacerdote C, Salomaa V, Swart W, Turunen AW, Vineis P, Weinmayr G, Wolf K, de Hoogh K, Hoek G, Brunekreef B, Peters A. Long term exposure to ambient air pollution and incidence of acute coronary events: prospective cohort study and meta-analysis in 11 European cohorts from the ESCAPE Project. BMJ. 2014 Jan 21;348:f7412. doi: 10.1136/bmj.f7412.

Abstract OBJECTIVES: To study the effect of long term exposure to airborne pollutants on the incidence of acute coronary events in 11 cohorts participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE). DESIGN: Prospective cohort studies and meta-analysis of the results. SETTING: Cohorts in Finland, Sweden, Denmark, Germany, and Italy. PARTICIPANTS: 100 166 people were enrolled from 1997 to 2007 and followed for an average of 11.5 years. Participants were free from previous coronary events at baseline. MAIN OUTCOME MEASURES: Modelled concentrations of particulate matter <2.5 μm (PM2.5), 2.5-10 μm (PMcoarse), and <10 μm (PM10) in aerodynamic diameter, soot (PM2.5 absorbance), nitrogen oxides, and traffic exposure at the home address based on measurements of air pollution conducted in 2008-12. Cohort specific hazard ratios for incidence of acute coronary events (myocardial infarction and unstable angina) per fixed increments of the pollutants with adjustment for sociodemographic and lifestyle risk factors, and pooled random effects meta-analytic hazard ratios. RESULTS: 5157 participants experienced incident events. A 5 μg/m(3) increase in estimated annual mean PM2.5 was associated with a 13% increased risk of coronary events (hazard ratio 1.13, 95% confidence interval 0.98 to 1.30), and a 10 μg/m(3) increase in estimated annual mean PM10 was associated with a 12% increased risk of coronary events (1.12, 1.01 to 1.25) with no evidence of heterogeneity between cohorts. Positive associations were detected below the current annual European limit value of 25 μg/m(3) for PM2.5 (1.18, 1.01 to 1.39, for 5 μg/m(3) increase in PM2.5) and below 40 μg/m(3) for PM10 (1.12, 1.00 to 1.27, for 10 μg/m(3) increase in PM10). Positive but non-significant associations were found with other pollutants. CONCLUSIONS: Long term exposure to particulate matter is associated with incidence of coronary events, and this association persists at levels of exposure below the current European limit values.

4. Beelen R1, Raaschou-Nielsen O2, Stafoggia M3, Andersen ZJ4, Weinmayr G5, Hoffmann B6, Wolf K7, Samoli E8, Fischer P9, Nieuwenhuijsen M10, Vineis P11, Xun WW12, Katsouyanni K8, Dimakopoulou K8, Oudin A13, Forsberg B13, Modig L13, Havulinna AS14, Lanki T15, Turunen A15, Oftedal B16, Nystad W16, Nafstad P17, De Faire U18, Pedersen NL19, Östenson CG20, Fratiglioni L21, Penell J18, Korek M18, Pershagen G18, Eriksen KT2, Overvad K22, Ellermann T23, Eeftens M24, Peeters PH25, Meliefste K24, Wang M24, Bueno-de-Mesquita B9, Sugiri D6, Krämer U6, Heinrich J26, de Hoogh K11, Key T27, Peters A7, Hampel R7, Concin H28, Nagel G29, Ineichen A30, Schaffner E30, Probst-Hensch N30, Künzli N30, Schindler C30, Schikowski T30, Adam M30, Phuleria H30, Vilier A31, Clavel-Chapelon F31, Declercq C32, Grioni S33, Krogh V33, Tsai MY34, Ricceri F35, Sacerdote C36, Galassi C36, Migliore E36, Ranzi A37, Cesaroni G3, Badaloni C3, Forastiere F3, Tamayo I38, Amiano P38, Dorronsoro M38, Katsoulis M39, Trichopoulou A39, Brunekreef B40, Hoek G24. Effects of long-term exposure to air pollution on natural-cause mortality: an analysis of 22 European cohorts within the multicentre ESCAPE project. Lancet. 2014 Mar 1;383(9919):785-95. doi: 10.1016/S0140-6736(13)62158-3. Epub 2013 Dec 9.

Abstract BACKGROUND: Few studies on long-term exposure to air pollution and mortality have been reported from Europe. Within the multicentre European Study of Cohorts for Air Pollution Effects (ESCAPE), we aimed to investigate the association between natural-cause mortality and long-term exposure to several air pollutants. METHODS: We used data from 22 European cohort studies, which created a total study population of 367,251 participants. All cohorts were general population samples, although some were restricted to one sex only. With a strictly standardised protocol, we assessed residential exposure to air pollutants as annual average concentrations of particulate matter (PM) with diameters of less than 2.5 μm (PM2.5), less than 10 μm (PM10), and between 10 μm and 2.5 μm (PMcoarse), PM2.5 absorbance, and annual average concentrations of nitrogen oxides (NO2 and NOx), with land use regression models. We also investigated two traffic intensity variables-traffic intensity on the nearest road (vehicles per day) and total traffic load on all major roads within a 100 m buffer. We did cohort-specific statistical analyses using confounder models with increasing adjustment for confounder variables, and Cox proportional hazards models with a common protocol. We obtained pooled effect estimates through a random-effects meta-analysis. FINDINGS: The total study population consisted of 367,251 participants who contributed 5,118,039 person-years at risk (average follow-up 13.9 years), of whom 29,076 died from a natural cause during follow-up. A significantly increased hazard ratio (HR) for PM2.5 of 1.07 (95% CI 1.02-1.13) per 5 μg/m(3) was recorded. No heterogeneity was noted between individual cohort effect estimates (I(2) p value=0.95). HRs for PM2.5 remained significantly raised even when we included only participants exposed to pollutant concentrations lower than the European annual mean limit value of 25 μg/m(3) (HR 1.06, 95% CI 1.00-1.12) or below 20 μg/m(3) (1.07, 1.01-1.13). INTERPRETATION: Long-term exposure to fine particulate air pollution was associated with natural-cause mortality, even within concentration ranges well below the present European annual mean limit value.

Breve commento a cura di Andrea Ranzi
Due importanti tasselli si aggiungono al mosaico dei risultati dello studio ESCAPE (European Study of Cohorts for Air Pollution Effects). Il lavoro di Giulia Cesaroni e colleghi, comparso sul BMJ, analizza il rischio di avere un primo evento coronarico acuto (infarto o angina instabile), rilevando aumenti del 12% in relazione a incrementi di 10 microgrammi per metro cubo di PM10. L’articolo di Beelen et al., pubblicato su Lancet, riguarda invece la mortalità per cause naturali in relazione all’esposizione all’inquinamento in ambito urbano. I risultati indicano un aumento del 7% della mortalità naturale per ogni aumento nell’esposizione media annua di 5 microgrammi per metro cubo di PM2,5 , e del 4% per ogni aumento di 10 microgrammi per metro cubo di PM10. Secondo gli autori della ricerca “I risultati suggeriscono un effetto del particolato anche per concentrazioni al di sotto dell’attuale limite annuale europeo di 25 µg/m3 per il PM2,5.” Sullo stesso numero di Lancet, l’editoriale di presentazione afferma: “Nonostante i grandi miglioramenti della qualità dell’aria negli ultimi 50 anni, i dati di Beelen e colleghi mostrano che gli effetti dell’inquinamento dell’aria sulla salute continuano. Questi dati, insieme ai risultati di altri grandi studi, suggeriscono quanto siano necessarie altre politiche per ridurre la mortalità in Europa. Come raccomandato dall’OMS, una priorità urgente dovrebbe essere quella di avviarsi verso i valori indicati dalle linee guida della qualità dell’aria dell’OMS che sono più restrittive.”

5. Gianicolo EA1, Mangia C2, Cervino M3, Bruni A4, Andreassi MG5, Latini G6. Congenital anomalies among live births in a high environmental risk area--a case-control study in Brindisi (southern Italy). Environ Res. 2014 Jan;128:9-14. doi: 10.1016/j.envres.2013.11.002. Epub 2013 Dec 17.

Abstract Maternal exposure to ambient pollution has been increasingly linked to the risk of congenital anomalies (CAs) in the fetus and newborns. Recently, a descriptive study in the high environmental risk city of Brindisi (Italy) revealed an increased prevalence of total CAs, especially congenital heart disease (CHD) and ventricular septal defects (VSDs), both at the local level and in comparison with the pool of EUROCAT registries. This paper concerns a population-based case control study to investigate the association between maternal exposure to air pollutants - sulfur dioxide (SO2) and total suspended particulate (TSP) matter - and the risk of CA. Cases were newborns up to 28 days of age, born to mothers resident in Brindisi between 2001 and 2010, and discharged with a diagnosis of CA. Cases and controls were individually matched according to sex, socio-economic status of the census area of residence of the mother, and year of beginning of pregnancy. Up to four controls were extracted for each case. Concentration data from monitoring stations were used to estimate air pollution exposure. Each case and control was assigned pollutant concentration values as mean and 90th percentile of the daily average values during weeks 3-8 of pregnancy. Exposure as both continuous and categorical variables was considered and a conditional logistic regression model was constructed to quantify the odds ratios of exposure to air pollutants and the occurrence of total CAs, CHDs and VSDs. We found exposure to the 90th percentile of SO2 to be associated with CHDs (p for trend =0.01) and VSDs (p for trend <0.05). Findings for TSP were less consistent. In conclusion, in the studied area, maternal exposure to sulfur dioxide increased risk of CHD.

6. Bind MA1, Lepeule J2, Zanobetti A2, Gasparrini A3, Baccarelli A2, Coull BA4, Tarantini L5, Vokonas PS6, Koutrakis P2, Schwartz J2. Air pollution and gene-specific methylation in the Normative Aging Study: Association, effect modification, and mediation analysis. Epigenetics. 2014 Jan 2;9(3). [Epub ahead of print]

Abstract The mechanisms by which air pollution has multiple systemic effects in humans are not fully elucidated, but appear to include inflammation and thrombosis. This study examines whether concentrations of ozone and components of fine particle mass are associated with changes in methylation on tissue factor (F3), interferon gamma (IFN-γ), interleukin 6 (IL-6), toll-like receptor 2 (TLR-2), and intercellular adhesion molecule 1 (ICAM-1). We investigated associations between air pollution exposure and gene-specific methylation in 777 elderly men participating in the Normative Aging Study (1999-2009). We repeatedly measured methylation at multiple CpG sites within each gene's promoter region and calculated the mean of the position-specific measurements. We examined intermediate-term associations between primary and secondary air pollutants and mean methylation and methylation at each position with distributed-lag models. Increase in air pollutants concentrations was significantly associated with F3, ICAM-1, and TLR-2 hypomethylation, and IFN-γ and IL-6 hypermethylation. An interquartile range increase in black carbon concentration averaged over the four weeks prior to assessment was associated with a 12% reduction in F3 methylation (95% CI: -17% to -6%). For some genes, the change in methylation was observed only at specific locations within the promoter region. DNA methylation may reflect biological impact of air pollution. We found some significant mediated effects of black carbon on fibrinogen through a decrease in F3 methylation, and of sulfate and ozone on ICAM-1 protein through a decrease in ICAM-1 methylation.

7. Gatto MP1, Gariazzo C, Gordiani A, L'episcopo N, Gherardi M. Children and elders exposure assessment to particle-bound polycyclic aromatic hydrocarbons (PAHs) in the city of Rome, Italy. Environ Sci Pollut Res Int. 2013 Dec 28. [Epub ahead of print]

Abstract It has been amply demonstrated that exposure to fine particulate matter, containing polycyclic aromatic hydrocarbons (PAHs), may have adverse effects on human health, affecting especially the respiratory and cardiovascular systems. Among population, school-age children and elders present particular susceptibilities and unique exposures to environmental factors. The study presented in this paper belongs to the Project EXPAH, founded by the European (EU) LIFE+ instrument, and consists of the personal monitoring of five elementary school children and four elders during the spring and the summer/autumn of the year 2012 in the city of Rome, Italy. The average exposure, expressed as the sum of eight high-molecular-weight PAHs, resulted equal to 0.70 ng/m3 (SD = 0.37) for children and 0.59 ng/m3 (SD = 0.23) for the elderly people. The mean levels of gravimetric PM2.5 were equal to 23 μg/m3 (SD = 10) and 15 μg/m3 (SD = 4) for children and elders, respectively. During spring and summer seasons, personal BaPeq resulted well below the EU Air Quality reference value of 1 ng/m3. The personal monitoring average values were in the same order of magnitude with available indoor and outdoor environmental data in Rome during the same periods, for both PAHs and PM2.5. The results suggest that, during non-heating seasons, the personal exposure to PAHs in the city of Rome can be mainly ascribed to the urban background, especially traffic emissions and road dust resuspension; secondhand cigarette smoke can be also considered another possible source of PAHs personal exposure.

8. Bertazzi PA1, Cantone L, Pignatelli P, Angelici L, Bollati V, Bonzini M, Carugno M, Mannucci PM, Violi F. Does Enhancement of Oxidative Stress Markers Mediate Health Effects Of Ambient Air Particles? Antioxid Redox Signal. 2013 Dec 18. [Epub ahead of print]

Abstract Evidence indicates that oxidative stress generation may contribute to health effects associated with particulate matter (PM) exposure. We investigated oxidative stress markers in 113 workers exposed to metal-rich PM and 61 non-exposed comparable volunteers. The plasma levels of soluble NOX2-derived peptide (sNOX2-dp) and two oxidative stress markers, urinary 8-hydroxydeoxyguanosine (8OH-dG) and 8-iso-prostaglandinF2alpha (8-iso-PGF2), were analysed. The plasma levels of the antioxidant alpha-tocopherol were also evaluated. The workers' average exposure to PM with aerodynamic diameter <10 μm (PM10) was much higher at the workplace than in the city where the volunteers lived. Workers had significantly higher urinary 8-iso-PGF2 and 8-OHdG and plasma sNOX2-dp levels than non-exposed subjects. Alpha-tocopherol was much lower in workers compared to non-exposed subjects. In multivariable regression models adjusted for age, body mass index and smoking, 8-iso-PGF2α increased in workers in association with PM10 and metal exposure; 8-OHdG and sNOX2-dp were associated only with iron. Alpha-tocopherol was inversely associated with each of the oxidative stress markers. Our observation leads to the hypothesis that the enhancement of oxidative stress markers associated with exposure to high metal-rich PM levels represents a possible step in the pathways leading from particle exposure to systemic (e.g., cardiovascular) effects.

9. Fossati S1, Baccarelli A, Zanobetti A, Hoxha M, Vokonas PS, Wright RO, Schwartz J. Ambient particulate air pollution and microRNAs in elderly men. Epidemiology. 2014 Jan;25(1):68-78. doi: 10.1097/EDE.0000000000000026.

Abstract BACKGROUND: Ambient particulate matter (PM) has been associated with mortality and morbidity for cardiovascular disease. MicroRNAs control gene expression at a posttranscriptional level. Altered microRNA expression has been reported in processes related to cardiovascular disease and PM exposure, such as systemic inflammation, endothelial dysfunction, and atherosclerosis. Polymorphisms in microRNA-related genes could influence response to PM. METHODS: We investigated the association of exposure to ambient particles in several time windows (4-hour to 28-day moving averages) and blood leukocyte expression changes in 14 candidate microRNAs in 153 elderly males from the Normative Aging Study (examined 2005-2009). Potential effect modification by six single nucleotide polymorphisms (SNPs) in three microRNA-related genes was investigated. Fine PM (PM2.5), black carbon, organic carbon, and sulfates were measured at a stationary ambient monitoring site. Linear regression models, adjusted for potential confounders, were used to assess effects of particles and SNP-by-pollutant interaction. An in silico pathway analysis was performed on target genes of microRNAs associated with the pollutants. RESULTS: We found a negative association for pollutants in all moving averages and miR-1, -126, -135a, -146a, -155, -21, -222, and -9. The strongest associations were observed with the 7-day moving averages for PM2.5 and black carbon and with the 48-hour moving averages for organic carbon. The association with sulfates was stable across the moving averages. The in silico pathway analysis identified 18 pathways related to immune response shared by at least two microRNAs; in particular, the "high-mobility group protein B1/advanced glycosylation end product-specific receptor signaling pathway" was shared by miR-126, -146a, -155, -21, and -222. No important associations were observed for miR-125a-5p, -125b, -128, -147, -218, and -96. We found significant SNP-by-pollutant interactions for rs7813, rs910925, and rs1062923 in GEMIN4 and black carbon and PM2.5 for miR-1, -126, -146a, -222, and -9, and for rs1640299 in DGCR8 and SO4 for miR-1 and -135a. CONCLUSIONS: Exposure to ambient particles could cause a downregulation of microRNAs involved in processes related to PM exposure. Polymorphisms in GEMIN4 and DGCR8 could modify these associations.
10. Marchetti P1, Marcon A, Pesce G, Paolo G, Guarda L, Pironi V, Fracasso ME, Ricci P, de Marco R. Children living near chipboard and wood industries are at an increased risk of hospitalization for respiratory diseases: a prospective study Int J Hyg Environ Health. 2014 Jan;217(1):95-101. doi: 10.1016/j.ijheh.2013.03.015. Epub 2013 Apr 6.

Abstract Pollutants emitted from wood processing factories may be harmful to the health of the population. The aim of this prospective cohort study was to evaluate whether proximity to wood factories was associated with the risk of hospital admissions in children living in the Viadana district (Italy), where two big chipboard industries and other smaller wood factories (sawmills, multi-strata layer manufacturing) are located. In 2006, children (3-14 years) living in the Viadana district were surveyed through a parental questionnaire (n=3854), their home/school addresses were geocoded and the distances to the wood industries were calculated. Hospital discharge records for the years 2007-2009 were obtained. Cox proportional hazard regression models were used to estimate the association between hospitalization rates and distance to the factories, adjusting for sex, age, nationality, parents' education, exposure to passive smoking and reported traffic near home. During the 3-year follow-up, the risk of hospitalization for all diagnoses (Hospitalization Hazard Ratio, HHR=1.55; 95% CI: 1.24-1.95) and for respiratory diseases (HHR=1.80; 95% CI: 1.14-2.86) was greater in the children living close (<2 km) to the chipboard industries, with respect to the children who lived at ≥2 km from any wood factory. The children living close to the smaller wood factories were also at increased risk of hospitalization for respiratory diseases (HHR=1.74; 95% CI: 1.06-2.85). This study highlights a health problem for the children living close to chipboard and wood factories in the Viadana district. Further research should develop accurate exposure models based on objective measurements of air pollution in order to confirm these findings.

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