Epidemiology and prevention of domestic injuries among children in the Verona area (north-east Italy)

In the developed world, domestic injuries (DI) are an important cause of morbidity, temporary or permanent disability, and death in early life, the social and economic costs of which are often underestimated. To assess the epidemiology of this phenomenon in an area of north-eastern Italy, a retrospective investigation was performed with an anonymous questionnaire administered to the parents of approximately 3000 children aged between 3 and 15 years. More than 45% of the sample had suffered at least one DI in their lifetime. The most common involved falling, wounding and scalding, and particularly affected children above 4 years old. The various types of injury were analyzed and correlated with the parents' personal parameters, the circumstances and the location of the accident. The type of aid required (medical advice was sought in more than 70% of cases) and the outcome of the DI (26% cases of temporary disability and 2% of permanent disability) were also assessed. The majority of DI could be prevented by a capillary campaign on the prevention of domestic hazards in childhood, preferably as part of a holistic approach to the problem that also considers their living conditions in architectural and interior design terms.     

Needs, education and accreditation in occupational medicine in Italy

In Europe, continuing medical education is one of the main instruments for improving physicians performance and ensuring adequate health care for citizens. Recent regulations have made such continuing education compulsory in Italy. Considering the particular features of occupational medicine, the Italian Society of Industrial Medicine and Industrial Hygiene (S.I.M.L.I.I.) recently set up a specific education and accreditation programme for occupational physicians, called the Excellence Accreditation Scheme. The programme is based on the findings of a survey among occupational physicians, carried out in collaboration with the National Institute of Occupational Safety and Prevention (I.S.P.E.S.L.), which enquired into their training and continuing education needs. The programme started in 2003, and its first edition—presented here—involved more than 400 physicians specialising in occupational health.     

Risk of Respiratory Cancer around a Sewage Plant in Prato,Italy

In this study, the authors evaluated the risk of respiratory cancer related to environmental pollutants among a population that resided near a sewage plant in Prato, Italy. Subjects included lung cancer deaths (1987-1996) and incident cases of lung and laryngeal cancers (1987-1994) among residents of Prato. The authors used the mortality or incidence rates for the entire population of Prato (by gender and by 5-yr age group) to calculate the expected cases in each census unit. Data were analyzed and adjusted for an index of social deprivation (Stone test). Among males, the excess risk of lung cancer mortality decreased as distance from the plant increased for 2 time periods (1987-1996 [p = .008] and 1990-1996 [p = .030]) and for lung cancer incidence during 1987-1994 (p = .011). Similar results were obtained when sewage plant workers were excluded from the analysis. A similar, but not statistically significant, trend was observed among female incident lung cancer cases, as well as among male incident laryngeal cancer cases. Despite methodological limitations common to geographic studies, the results were consistent with those previously published on mortality excesses for lung cancer among plant workers under study. The role of environmental pollutants as a risk for respiratory cancer must be further clarified with additional epidemiological studies and an environmental monitoring program.     

Mimic of manganese superoxide dismutase to induce apoptosis of human non-Hodgkin lymphoma Raji cells through mitochondrial pathways

Increased reactive oxygen species (ROS) such as superoxide have been implicated as causal elements of oncogenesis. A variety of cancers have displayed changes in steady-state levels of key antioxidant enzymes, with the mitochondrial form of superoxide dismutase (MnSOD) being commonly implicated. Increasing MnSOD expression suppresses the malignant phenotype in various cancer cell lines and suppresses tumor formation in xenograft and transgenic mouse models. In this study, we examined the anti-proliferation effect of mimic of manganese superoxide dismutase (MnSODm) on human non-Hodgkin lymphoma Raji cells. The results showed that MnSODm significantly reduced the proliferation of Raji cells in a concentration and a time-dependent manner. By flow cytometric analysis, we found that MnSODm treatment resulted in an increased apoptosis in Raji cells. MnSODm also increased the production of ROS and the expression levels of cleaved caspase-9, caspase-3, poly (ADP-ribose) polymerase (PARP) and Bax in Raji cells. Moreover, the expression of Bcl-2 protein showed down-regulation in the MnSODm treatment group. In addition, MnSODm significantly elevated the level of cytochrome c in cytosol. These findings suggest that the activation of the mitochondrial pathway is involved in MnSODm-induced apoptosis in Raji cells.     

Particulate matter,air pollution,and blood pressure

A short-term increase in fine particulate matter air pollution (PM_2.5) concentration increases the risk for myocardial infarctions, strokes, and heart failure exacerbations. An important mechanism likely contributing to these associations is an elevation in arterial blood pressure (BP). Exposure to ambient PM_2.5 even at present-day concentrations can increase BP within a period of a few days while long-term exposure might also promote the development of chronic hypertension. Controlled human and animal experiments have corroborated the veracity of these findings and elucidated plausible biological mechanisms. PM_2.5 deposition within the pulmonary tree is capable of rapidly triggering autonomic nervous system imbalance, thereby increasing BP within minutes of inhalation. In addition, fine particles can instigate a systemic pro-inflammatory response over a more prolonged period of exposure. Higher circulating levels of activated immune cells and inflammatory cytokines could consequently cause vascular endothelial dysfunction leading to an imbalance in vascular homeostatic responses. Indeed, chronic PM_2.5 exposure augments pro-vasoconstrictive pathways while blunting vasodilator capacity. Finally, certain particle constituents (e.g., metals, organic compounds, and ultra-fine particles) might also be capable of reaching the systemic circulation upon inhalation and thereafter directly impair vascular function. At the molecular level, the generation of oxidative stress with the consequent up-regulation of redox sensitive pathways appears to be a common and fundamental mechanism involved in the instigation of these pro-hypertensive responses. Due to the ubiquitous, continuous and often involuntary nature of exposure, PM_2.5 may be an important and under-appreciated worldwide environmental risk factor for increased arterial BP.     

Association of CYP2E1, GST and mEH genetic polymorphisms with urinary acrylamide metabolites in workers exposed to acrylamide

This study elucidates the association of acrylamide metabolites, N-acetyl-S-(2-carbamoylethyl)-cysteine (AAMA), N-acetyl-S-(1-carbamoyl-2-hydroxyethyl)-cysteine (GAMA2), and N-acetyl-S-(2-carbamoyl-2-hydroxyethyl)-cysteine (GAMA3) in urine with genetic polymorphisms of the metabolic enzymes cytochrome P450 2E1 (CYP2E1), microsomal epoxide hydrolase (mEH) in exon 3 and exon 4, glutathione transferase theta (GSTT1) and mu (GSTM1), involved in the activation and detoxification of acrylamide (AA) in humans. Eighty-five workers were recruited, including 51 AA-exposed workers and 34 administrative staffs serve as controls. Personal air sampling was performed for the exposed workers. Each subject provided pre- and post-shift urine samples and blood samples. Urinary AAMA, GAMA2 and GAMA3 levels were simultaneously quantified using liquid chromatography-electronspray ionization/tandem mass spectrometry (LC-ESI-MS/MS). CYP2E1, mEH (in exon 3 and exon 4), GSTT1, and GSTM1 were analyzed using polymerase chain reaction (PCR). Our results reveal that AA personal exposures ranged from 4.37 × 10⁻³ to 113.61 μg/m³ with a mean at 15.36 μg/m³. The AAMA, GAMA2, and GAMA3 levels in the exposed group significantly exceeded those in controls. The GAMAs (the sum of GAMA2 and GAMA3)/AAMA ratios, potentially reflecting the proportion of AA metabolized to glycidamide (GA), varied from 0.003 to 0.456, and indicate high inter-individual variability in the metabolism of AA to GA in this study population. Multivariate regression analysis demonstrates that GSTM1 genotypes significantly modify the excretion of urinary AAMA and the GAMAs/AAMA ratio, exon 4 of mEH was significantly associated with the urinary GAMAs levels after adjustment for AA exposures. These results suggest that mEH and/or GSTM1 may be associated with the formation of urinary AAMA and GAMAs. Further study may be needed to shed light on the role of both enzymes in AA metabolism.     

p,p'-Dichlorodiphenoxydichloroethylene induced apoptosis of Sertoli cells through oxidative stress-mediated p38 MAPK and mitochondrial pathway

p,p′-DDE, the major metabolite of dichlorodiphenoxytrichloroethane (DDT), is a known persistent organic pollutant and male reproductive toxicant. However, the mechanism underlying its male reproductive toxicity remains limited. Our previous studies have demonstrated that p,p′-DDE could induce mitochondria-mediated apoptosis of cultured rat Sertoli cells. In the present study, we investigated mitogen-activated protein kinase pathways as well as other mitochondria-related molecules including Bax family members and cytochrome c. Results showed that p,p′-DDE could induce oxidative stress-mediated p38 and JNK phosphorylation. In addition, elevated mRNA levels of cytochrome c and ratios of bax/bcl-w and bak/bcl-w were induced by p,p′-DDE treatment, which could be inhibited by RNA synthesis inhibitor (actinomycin D). p,p′-DDE-induced apoptosis was blocked by NAC (N-acetyl-L-cystein) preincubation and attenuated by pretreatment with p38 inhibitor (SB202190) or actinomycin D, but not with JNK inhibitor (SP600125). All of the findings suggested that oxidative stress-mediated p38 MAPK pathway and the balance between pro- and anti-apoptotic bax-gene family might play critical roles in p,p′-DDE-induced apoptosis.