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Acute exacerbations and worsening of idiopathic pulmonary fibrosis (IPF) have been associated with exposure to ozone (O), nitrogen dioxide (NO) and particulate matter, but chronic exposure to air pollution might also affect the incidence of IPF. We investigated the association between chronic exposure to NO, O and particulate matter with an aerodynamic diameter <10 μm (PM) and IPF incidence in Northern Italy between 2005 and 2010.Daily predictions of PM concentrations were obtained from spatiotemporal models, and NO and O hourly concentrations from fixed monitoring stations. We identified areas with homogenous exposure to each pollutant. We built negative binomial models to assess the association between area-specific IPF incidence rate, estimated through administrative databases, and average overall and seasonal PM, NO, and 8-hour maximum O concentrations.Using unadjusted models, an increment of 10 µg·m in NO concentration was associated with an increase between 7.93% (95% CI 0.36-16.08%) and 8.41% (95% CI -0.23-17.80%) in IPF incidence rate, depending on the season. After adjustment for potential confounders, estimated effects were similar in magnitude, but with larger confidence intervals.Although confirmatory studies are needed, our results trace a potential association between exposure to traffic pollution and the development of IPF.

A total of 25 146 workers at 13 plants producing man made mineral fibres (MMMF) in seven European countries (Denmark, Finland, Federal Republic of Germany, Italy, Norway, Sweden, and United Kingdom) were studied in a historical cohort investigation. At 12 of the 13 plants an environmental survey was carried out to determine present day concentrations of airborne man made mineral fibres that showed levels of respirable fibres usually below 1 f/ml and most commonly in the range 0.01 to 0-1 f/ml. Workers were entered into the cohort at the moment of their first employment at one of the 13 factories (which started to operate between 1900 and 1955), and were followed up to at least 31 December 1977. Three per cent of the workers were lost to follow up. National death rates and national cancer incidence rates, where applicable, were used for each of the seven countries for comparison with the workers' cohort. A single death from mesothelioma was reported out of a total of 309 353 person-years of observation. No consistent differences (within and between plants) were noted between observed and expected numbers concerning individual causes of death or individual cancer sites, apart from lung cancer. For this cause a tendency was observed for the standardised mortality ratio (SMR) to increase with time from first employment. When the data from all the plants were pooled a statistically significant raised SMR of 192 (17 observed, 8-9 expected; 95% confidence interval 117-307) appeared in the group with 30 years or more since first employment. The relevance of this finding, to which different factors including uncontrolled confounders such as smoking habits may have contributed, cannot be established at present. The result is suggestive, however, of an increased risk associated with the man made mineral fibres working environment of 30 or more years ago.Man made vitreous fibres (MMVF), usually referred MMMF had reached an estimated world annual to as man made mineral fibres (MMMF), include total of 4-5m tons in 1973, thus being close to that different inorganic synthetic wool products (slag of asbestos.' Biologically, experiments in animal syswool, rock wool, glass wool) widely used as thermal tems have indicated that MMMF may have and acoustic insulation material and as filament pro-pathogenic actions2-4 (fibrogenic and carcinogenic), ducts used for textile manufacturing and for the while pertinent epidemiological observations on reinforcing of plastic materials. Production of pulmonary fibrosis (or more generally, chronic

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BACKGROUND: Inhalation of Particulate Matter (PM) and PM metal components has been associated with increased risk of lung cancer. MicroRNAs (miRNAs) are small, non-coding RNAs with an important role in biological activities and are linked to human diseases such as cancer. miRNA expression needs tight regulation, which also takes place at the epigenetic level. miRNAs undergo regulation by DNA methylation in miRNA coding genes, associate with silencing of miRNA expression. Increased expression of miR-21 has been implicated in various processes involved in carcinogenesis, including inhibition of apoptosis, promotion of cell proliferation and stimulation of tumor growth by targeting multiple tumor/metastasis suppressor genes. In cancer cells miR-222 promotes cell proliferation by targetting the cell cycle inhibitor and tumor suppressor p27. AIMS: We evaluated the effects of exposure to PM and PM metal components on candidate miRNAs methylation (miR-222 and miR-21) in 63 workers of an electric-furnace steel plant with well-characterized exposure. METHODS: We measured miR-222 and miR-21 methylation in blood leukocyte RNA obtained from 63 workers on the first day of a workweek (baseline) and after three days of work (post-exposure). Quantitative miRNA methylation analysis was performed through bisulfite PCR Pyrosequencing. We estimated individual exposures to PM1, PM10, coarse particles and PM metal components (chromium, lead, cadmium, arsenic, nickel, manganese) between the baseline and post-exposure measurements. RESULTS: miR-222 and miR-21 methylation was significantly decreased in post-exposure samples, compared with baseline (post-exposure=60.07±9.38, baseline=63.05±6.38; p=0.013 for miR-222; post-exposure=62.47±6.87, baseline=66.24±6.32; p=0.004 for miR-21). In post-exposure samples, miR-222 methylation was negatively associated with the average exposure to the levels of PM (βstd=-0.012, p=0.03 for PM10, βstd=-0.579, p=0.005 for PM1 and βstd=-0.013, p=0.032 for Coarse) and to the levels of PM metal components (βstd=-111.345, p=0.008 for Chromium and βstd=17.195, p=0.023 for Arsenic). CONCLUSIONS: Changes in miRNA methylation may represent a novel epigenetic mechanism mediating responses to PM and its metal components. Whether these modifications have a role in the initiation and progression of cancer needs to be evaluated in future studies. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4088.

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