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The occurrence of illicit drugs (cocaine, opioids, amphetamines and cannabis derivatives), some of their metabolites and 48 pharmaceuticals, was investigated in pool and source waters in ten Italian indoor swimming pools. The samples were analyzed by highperformance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS), after solid phase extraction (SPE). Cocaine and its metabolites were found in nine swimming pools, at concentrations from 0.3 to 4.2 ng/L for cocaine, 1.1 to 48.7 ng/L for norcocaine, 0.7 to 21.4 ng/L for benzoylecgonine and 0.1 to 7.3 ng/L for norbenzoylecgonine. Opioids, amphetamines and cannabis derivatives were never detected. The most frequent pharmaceuticals were anti-inflammatory drugs: ibuprofen was found in all the pool waters, with a maximum 197 ng/L and ketoprofen was detected in 9/10 samples (maximum 127 ng/L). Among anticonvulsants, carbamazepine and its metabolite, 10,11-dihydro-10,11dihydroxycarbamazepine, were frequent in swimming pool water (8/10 samples) at concentrations up to 62 ng/L. The cardiovascular drug valsartan was also found frequently (8/10 samples), but at lower concentrations (up to 9 ng/L). Other pharmaceuticals were detected occasionally and at lower concentrations (atenolol, enalapril, paracetamol, hydroclorothiazide, irbesartan and dehydro-erythromycin). Carbamazepine, irbesartan and dehydroerythromycin were detected at very low levels (up to 5 ng/L) in only one of the four source water samples. A quantitative risk assessment showed that the health risk for humans to these substance in swimming pool waters was generally negligible, even for vulnerable subpopulations such as children and adolescents., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Obesity has been linked to cognitive impairment, cognitive decline and dementia. Given that 38.5% of U.S. adults 60years and older are obese and these numbers are rapidly increasing, strategies to decouple obesity from cognitive decline are needed. Innovative lifestyle strategies that may postpone the onset of subclinical symptoms or even arrest the transition to overt dementia in at-risk individuals are critically needed. Poor diet is central to the development of obesity and diet may affect cognition. Adherence to a Mediterranean Diet (MedDiet) is associated with reduced risk of cognitive impairment and dementia. Furthermore, weight loss through caloric restriction improves cognitive function. This paper describes the Building Research in Diet and CoGnition (BRIDGE) study, a randomized trial examining the effect of the MedDiet, with and without weight loss, on cognitive functioning in obese older adults. Obese (BMI≥30 and ≤50kg/m 2 ) older adults (≥55years) (n=180) will be randomized in a 2:2:1 allocation scheme to: Typical Diet Control; MedDiet alone, without weight loss; or MedDiet lifestyle intervention to promote weight loss and weight loss maintenance. Both MedDiet intervention groups will meet for one individual session and 27 group sessions over an 8-month period. Individuals in the control group will not receive instruction on changing lifestyle habits. Outcomes will be assessed at baseline, 8 and 14months. The primary outcome is cognitive functioning; secondary outcomes will include changes in body weight, diet, cardiovascular, metabolic, and inflammatory biomarkers., (Copyright © 2017. Published by Elsevier Inc.)

Communication among cells (also known as cross-talk) plays a prominent role in the current knowledge of the pathophysiology of cancer and of cancer-associated conditions such as paraneoplastic syndromes and cachexia that are responsible for much of cancer's morbidity and mortality. Yet, biomedical scientists lack an explicit unifying frame that places this exchange of molecular information at the core of their understanding of cancer as a systemic disease. Propaganda is a type of information that aims at misleading, a form of communication intended primarily to serve the messenger. The biased molecular cross-talk between cancer and non-cancer cells can be considered as a form of biological propaganda. I here propose cancer is a propagandist as a metaphor that may serve as a unifying frame to interpret both cancer and cancer-associated syndromes under the same communication-based concept and may thus serve to bring together research that is currently compartmentalized under separate disciplines., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Background: Our trial INTACT (Intensive Nutrition in Acute Lung Injury Trial) was designed to compare the impact of feeding from acute lung injury (ALI) diagnosis to hospital discharge, an interval that, to our knowledge, has not yet been explored. It was stopped early because participants who were randomly assigned to energy intakes at nationally recommended amounts via intensive medical nutrition therapy experienced significantly higher mortality hazards than did those assigned to standard nutrition support care that provided energy at 55% of recommended concentrations., Objective: We assessed the influence of dose and timing of feeding on hospital mortality., Design: Participants (n = 78) were dichotomized as died or discharged alive. Associations between the energy and protein received overall, early (days 1-7), and late (days ≥8) and the hazards of hospital mortality were evaluated between groups with multivariable analysis methods., Results: Higher overall energy intake predicted significantly higher mortality (OR: 1.14, 95% CI: 1.02, 1.27). Among participants enrolled for ≥8 d (n = 66), higher early energy intake significantly increased the HR for mortality (HR: 1.17, 95% CI: 1.07, 1.28), whereas higher late energy intake was significantly protective (HR: 0.91, 95% CI: 0.83, 1.0). Results were similar for early but not late protein (grams per kilogram) exposure (early-exposure HR: 8.9, 95% CI: 2.3, 34.3; late-exposure HR: 0.15, 95% CI: 0.02, 1.1). Threshold analyses indicated early mean intakes ≥18 kcal/kg significantly increased subsequent mortality., Conclusions: Providing kilocalories per kilogram or grams of protein per kilogram early post-ALI diagnosis at recommended levels was associated with significantly higher hazards for mortality, whereas higher late energy intakes reduced mortality hazards. This time-varying effect violated the Cox proportionality assumption, indicating that feeding trials in similar populations should extend beyond 7 d and use time-varying statistical methods. Future trials are required for corroboration. INTACT was registered at clinicaltrials.gov as NCT01921101., (© 2017 American Society for Nutrition.)

Background: Exposure to persistent organic pollutants (POPs) is associated with increased diabetes risk, although the mechanism of action is not well delineated., Methods: We investigated established diabetes biomarkers that could implicate potential mechanistic pathways, including C-reactive protein (CRP), a marker of systemic inflammation; gamma glutamyl transferase (GGT), a liver enzyme associated with oxidative stress; and adiponectin, an adipokine modulating glucose regulation and fatty acid oxidation. These biomarkers as well as hemoglobin A1c (HA1c), and POPs [polychlorinated biphenyls (PCBs), p,p-dichlorodiphenyldichloroethylene (DDE) and polybrominated diphenyl ethers (PBDEs)] were measured in a cohort of Great Lakes sport caught fish (GLSCF) consumers. We examined associations of POPs and fish consumption with HA1c and incident diabetes, and evaluated mediation and moderation by the diabetes biomarkers., Results: Odds of incident diabetes were elevated with exposure to DDE and PCBs. DDE and PCB 118 were positively, and fish meals were inversely, associated with HA1c. CRP was inversely associated with saltwater and total fish meals, particularly in persons with higher adiposity, but did not mediate the associations of fish meals with HA1c. There were few associations of POPs with adiponectin, CRP and GGT, with the exception of positive associations of PCB 118 with GGT, PBDEs with GGT in older persons, and PBDEs with adiponectin. Adiponectin, CRP and GGT did not mediate associations of DDE and PCBs with HA1c or incident diabetes. However, the association of DDE with HA1c was stronger in persons with higher CRP, GGT and BMI, and lower adiponectin, while the association of PCB 118 with HA1c was stronger in persons with higher GGT., Conclusions: These findings suggest that adiponectin, CRP and GGT did not mediate effects of POPs on diabetes or HA1c. However, POPs may have stronger effects on blood glucose in persons at higher risk for diabetes., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Acute pancreatitis (AP), although most often a mild and self-limiting inflammatory disease, worsens to a characteristically necrotic severe acute pancreatitis (SAP) in about 20% of cases. Obesity, affecting more than one-third of American adults, is a risk factor for the development of SAP, but the exact mechanism of this association has not been identified. Coincidental with chronic low-grade inflammation, activation of the nucleotide-binding domain, leucine-rich containing family, pyrin-domain containing 3 (NLRP3) inflammasome increases with obesity. Lean mice genetically deficient in specific components of the NLRP3 inflammasome are protected from experimentally induced AP, indicating a direct involvement of this pathway in AP pathophysiology. We hypothesized that inhibition of the NLRP3 inflammasome with the sulfonylurea drug glyburide would reduce disease severity in obese mice with cerulein-induced SAP. Treatment with glyburide led to significantly reduced relative pancreatic mass and water content and less pancreatic damage and cell death in genetically obese ob/ob mice with SAP compared with vehicle-treated obese SAP mice. Glyburide administration in ob/ob mice with cerulein-induced SAP also resulted in significantly reduced serum levels of interleukin 6, lipase, and amylase and led to lower production of lipopolysaccharide-stimulated interleukin 1β release in cultured peritoneal cells, compared with vehicle-treated ob/ob mice with SAP. Together, these data indicate involvement of the NLRP3 inflammasome in obesity-associated SAP and expose the possible utility of its inhibition in prevention or treatment of SAP in obese individuals., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Background: Epidemiological evidence of an association between disinfection by-products (DBPs) exposure via drinking water and reproductive outcomes is still inconclusive., Objective: The aim of this study was to investigate the association between trihalomethanes (THMs), chlorite and chlorate exposure and congenital anomalies., Methods: A case-control study was carried out in Emilia-Romagna Region (Italy). Data on 1917 different congenital anomalies (neural tube, cardiac, diaphragm and abdominal wall, oesophagus, cleft lip and palate, respiratory, urinary tract and chromosomal anomalies) observed in the period 2002-2005 were extracted from the Regional Malformation Registry. Four controls (newborns without anomalies) were randomly selected form the Regional Birth Register and frequency matched to cases according to pregnancy period. The network supplying water during the first trimester of pregnancy was identified on the basis of mother's address: DBPs data, technical and structural information were linked to each subject., Results: Overall, THMs exposure was very low (mean: 3.8±3.6 μg/l), and no risk excess was observed. Chlorite and chlorate values were fairly high (mean: 427±184 μg/l and 283±79 μg/l, respectively). Women exposed to chlorite level >700 μg/l were at higher risk of newborns with renal defects (OR: 3.30; 95% IC: 1.35-8.09), abdominal wall defects (OR: 6.88; 95% IC: 1.67-28.33) and cleft palate (OR: 4.1; 95% IC: 0.98-16.8); women exposed to chlorate level >200 μg/l were at higher risk of newborns with obstructive urinary defects (OR: 2.88; 95% IC: 1.09-7.63), cleft palate (OR: 9.60; 95% IC:1.04-88.9) and spina bifida (OR: 4.94; 95% IC:1.10-22)., Conclusions: This was the first study showing an excess risk of different congenital anomalies related to chlorite and chlorate exposure via drinking water: further research is needed to confirm the observed relationships in large datasets, specifically for chlorate, an unregulated DBP., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Adiponectin (APN) is an adipose tissue-derived cytokine that regulates insulin sensitivity and inflammation. It is also involved in modulation of cell proliferation by binding to various growth factors. Based on its known effects in modulating cell proliferation and oxidative stress, APN may potentially be involved in regulating tissue damage and repair following irradiation. Adiponectin KO mice and their WT littermates were exposed to a single whole-body dose of 3 or 6Gy gamma radiation. Radiation-induced alterations were studied in jejunum, blood, bone marrow and thymus at days 1 and 5 post-irradiation and compared with sham-irradiated groups. In WT mice, irradiation did not significantly alter serum APN levels while inducing a significant decrease in serum leptin. Irradiation caused a significant reduction in thymocyte cellularity, with concomitant decrease in CD4(+), CD8(+) and CD4(+)CD8(+) T cell populations, with no significant differences between WT and APN KO mice. Irradiation resulted in a significantly higher increase in the frequency of micronucleated reticulocytes in the blood of APN KO compared with WT mice, whereas frequency of micronucleated normochromatic erythrocytes in the bone marrow at day 5 was significantly higher in WT compared with APN KO mice. Finally, irradiation induced similar alterations in villus height and crypt cell proliferation in the jejunum of WT and APN KO mice. Jejunum explants from sham-irradiated APN KO mice produced higher levels of IL-6 compared with tissue from WT animals, but the difference was no longer apparent following irradiation. Our data indicate that APN deficiency does not play a significant role in modulating radiation-induced gastrointestinal injury in mice, while it may participate in regulation of damage to the hematopoietic system., (Copyright © 2009 Elsevier B.V. All rights reserved.)

Leptin is a protein produced by adipocytes (and other cell types) that acts in the brain to regulate appetite and energy expenditure according to the amount of energy stored in adipose tissue. Leptin also exerts a variety of other functions, including important roles as a regulator of immune and inflammatory reactions. The present article is not meant to be a comprehensive review on leptin and immunity, but rather highlights a few controversial issues about leptin's place in the complex network of mediators regulating immune and inflammatory responses. Three issues are discussed: (1) Where am I going, or What is the cellular target of leptin for modulation of immune responses?; (2) Where am I coming from, or Is the cellular source important in determining leptin's effects on immune responses? and (3) What am I doing, or What are leptin's effects on immune and inflammatory responses?

A few epidemiologic studies have suggested that consumption of drinking water with high trihalomethane content increases the risk of cancer. We investigated the mortality of a cohort of 5144 residents in Guastalla, northern Italy, who were supplied tap water with high chloroform and trihalomethane content between 1965 and 1987. Using death rates of a nearby community as reference rates, the standardized mortality ratio from all cancers between 1987 and 1999 was slightly increased for both males (1.2, 95% confidence interval 1.1-1.4) and females (1.1, 95% confidence interval 1.0-1.3). This was mainly due to a higher mortality from stomach, liver, lung, prostate and bladder cancer in males and from stomach, pancreas, breast and ovarian cancer and lymphocytic leukemia in females. We also noted excess mortality from melanoma in both males and females. Overall, our findings were consistent with an association between trihalomethane exposure and increased cancer risk at some sites. However, the point estimates were statistically imprecise, due to the limited number of deaths for some site-specific cancers. In addition, we were unable to rule out the possibility of confounding due to smoking and other life-style factors with regard to some of the excess rates.

We studied four libraries in the University of Modena and Reggio Emilia (Northern Italy) to determine the presence of polluting agents such as total dusts, formaldehyde and other volatile organic compounds (VOCs) including benzene, toluene and xylenes and to assess the sense of well-being perceived by library users. This investigation was suggested by an increase in reported symptoms related to Sick Building Syndrome (SBS) observed in recent decades among people spending most of their time in various indoor environments, including libraries. The microclimatic conditions and the concentrations of pollutants indicated an acceptable situation on the whole, even though a wide range of total dust values (40-350 microg/m3) and total VOCs (203-749 microg/m3) was observed. However, the perception of the different environmental parameters by the 130 library users that were interviewed identified the existence of some discomfort mainly caused by the feeling of poor ventilation. Moreover, 78.5% of the subjects stated they had at least one of the 16 investigated symptoms potentially related to a SBS. The place of occurrence of the self-reported symptoms was also investigated, the symptoms arising during library attendance more frequently than elsewhere were only four, and in particular feeling hot, sore eyes, dry throat and breathing difficulties. Overall, our study has shown the existence of an association between microclimatic perceptions as reported by library users and subjective symptoms related to SBS, considering the four libraries separately, the highest prevalence of self-reported symptoms was found in the library where environmental discomfort as perceived by users was greatest. Nevertheless, an association between subjective self-reported symptoms and both microclimatic conditions as resulted by instrumental measurements and/or pollutants concentrations was not apparent.

The study evaluated occupational exposure to trihalomethanes (THMs) in indoor swimming pools. Thirty-two subjects, representing the whole workforce employed in the five public indoor swimming pools in the city of Modena (Northern Italy) were enrolled. Both environmental and biological monitoring of THMs exposure were performed. Environmental concentrations of THMs in different areas inside the swimming pools (at the poolside, in the reception area and in the engine-room) were measured as external exposure index, while individual exposure of swimming pool employees was estimated by THMs concentration in alveolar air. The levels of THMs observed in swimming pool water ranged from 17.8 to 70.8 microg/l; the mean levels of THMs in ambient air were 25.6+/-24.5 microg/m3 in the engine room, 26.1+/-24.3 microg/m3 in the reception area and 58.0+/-22.1 microg/m3 at the poolside. Among THMs, only chloroform and bromodichloromethane were always measured in ambient air, while dibromochloromethane was detected in ambient air rarely and bromoform only once. Biological monitoring results showed a THMs mean value of 20.9+/-15.6 microg/m3. Statistically significant differences were observed according to the main job activity: in pool attendants, THMs alveolar air were approximately double those observed in employees working in other areas of the swimming pools (25.1+/-16.5 microg/m3 vs. 14.8+/-12.3 microg/m3, P < 0.01). THMs in alveolar air samples were significantly correlated with THMs concentrations in ambient air (r = 0.57; P < 0.001). Indoor swimming pool employees are exposed to THMs at ambient air levels higher than the general population. The different environmental exposure inside the swimming pool can induce a different internal dose in exposed workers. The correlation found between ambient and alveolar air samples confirms that breath analysis is a good biological index of occupational exposure to these substances at low environmental levels.

In this article, exposure to trihalomethanes (THMs) in indoor swimming pools as a consequence of water chlorination is reported. Environmental and biological monitoring of THMs was performed in order to assess the uptake of these substances after a defined period in five competitive swimmers, regularly attending an indoor swimming pool to train for competition during four sampling sessions. Analyses were performed by gas-chromatography and the following THMs were detected: chloroform (CHC13), bromodichloromethane (CHBrC12), dibromochloromethane (CHBrsC1) and bromoform (CHBr3). CHC13 appeared the most represented compound both in water and in environmental air before and after swimming. CHBrC1w and CHBr2C1 were always present, even though at lower levels than CHC13, CHBr3, was rarely present. In relation to biological monitoring, CHC13, CHBrC12 and CHBr2C1 were detected in all alveolar air samples collected inside the swimming pool. Before swimming, after 1 h at rest at the pool edge, the mean values were 29.4 +/- 13.3, 2.7 +/- 1.2 and 0.8 +/- 0.8 micrograms/m3, respectively, while after spending 1 h swimming, higher levels were detected (75.6 +/- 18.6, 6.5 +/- 1.3 and 1.4 +/- 0.9 micrograms/m3, respectively). Only CHC13 was detected in all plasma samples (mean: 1.4 +/- 0.5 micrograms/1) while CHBrC1x and CHBr2C1 were observed only in few samples at a detection limit of 0.1 micrograms/1. After 1 h at rest, at an average environmental exposure of approx. 100 micrograms/m3, the THM uptake was approx. 30 micrograms/h (26 micrograms/h for CHC1c, 3 micrograms/h for CHBrC12 and 1.5 micrograms/h for CHBr2C1). After 1 h swimming, the THM uptake is approx. seven times higher than at rest: a THM mean uptake of 221 micrograms/h (177 micrograms/h, 26 micrograms/h and 18 micrograms/h for CHC13, CHBrC12 and CHBr2C1, respectively) was evaluated at an environmental concentration of approx. 200 micrograms/m3.

Interleukin-18 (IL-18) is a costimulatory factor for interferongamma (IFNgamma) production. Processing of pro-IL-18 by IL-1beta-converting enzyme (ICE) leads to the release of bioactive IL-18. Compared with wild-type (WT) mice, splenocytes from ICE-deficient mice produced low IFNgamma after lipopolysaccharide (LPS) or zymosan (50% and 80% reduction). In contrast, IFNgamma production was unimpaired in ICE-deficient mice using Concanavalin A (Con A). Comparable results were obtained when endogenous IL-18 was blocked with a neutralizing antibody. LPS-induced IFNgamma was also reduced by an ICE inhibitor. Exogenous IL-18 augmented zymosan-induced IFNgamma production in WT mice. In ICE-deficient cells, IFNgamma production was only partially restored by IL-18. The reduced levels of IFNgamma in ICE-deficient mice were not due to a lack of IL-12, because zymosan induced IL-12 equally in WT and in ICE-deficient mice. IFNgamma is an important regulator of cell proliferation. In accordance, splenocytes from ICE-deficient mice proliferated more when stimulated with LPS, but not with Con A. Furthermore, in ovalbumin-sensitized ICE-deficient mice, proliferation of lymph node cells in response to the specific antigen was not altered. Exogenous IFNgamma inhibited, whereas blockade of endogenous IFNgamma or IL-18 increased, LPS induced splenocyte proliferation both in WT and in ICE-deficient mice. Our results show that IL-18 is an IL-12-independent regulator of IFNgamma production and of cell proliferation induced by microbial stimuli. However, ICE-dependent processing of IL-18 is not needed for response to mitogens or antigens.

We carried out a survey in 16 libraries of the University of Modena, Northern Italy, to assess the indoor exposure to volatile organic compounds (VOCs), including formaldehyde, and total dusts. Data were collected on the main structural characteristics of the buildings; indoor microclimate parameters, such as temperature, relative humidity and ventilation rate were measured and air samples taken inside and outside the libraries. The mean value of total dusts was 190 +/- 130 microg/m3 with a wide range of values. Formaldehyde was found in only ten out of 16 libraries and the indoor concentrations ranged from 1.70 to 67.8 microg/m3 with an average value of 32.7 +/- 23.9 microg/m3. On the whole, VOCs were present in all the libraries investigated with an average value was 433 +/- 267 microg/m3 (range 102-936 microg/m3). No correlation was found among VOCs, formaldehyde and total dusts nor was a significant association observed with microclimatic parameters or the structural characteristics of the buildings. The general situation found in this study suggests no major problems related to indoor pollution. However, some of the pollutants investigated such as total dust and total VOCs deserve further investigation. It is important to identify the possible sources of contaminants and to define the relationship between indoor and outdoor levels of pollutants more accurately, taking into account the effects of air recycling due to natural ventilation systems.

Ciliary neurotrophic factor (CNTF) and interleukin-6 (IL-6) potentiate the elevation of serum corticosterone induced by suboptimal doses of interleukin-1 (IL-1). CNTF also potentiates IL-1-induced serum IL-6. Here, we report that four other cytokines (leukemia inhibitory factor [LIF], oncostatin M [OSM], interleukin-11 and cardiotrophin-1) also potentiated the elevation of serum corticosterone and IL-6 levels induced by IL-1. Furthermore, all the six cytokines studied induced the acute-phase protein serum amyloid A when administered alone. Because these cytokines differ both in structure and in function, but share gp130 as a subunit of their receptors, these results indicate that signaling through gp130 mediates potentiation of IL-1 activities. The potentiation of IL-1-induced serum corticosterone levels is not a consequence of the increased serum IL-6 observed after IL-1 administration. In fact, in IL-6 deficient mice, IL-1 increased serum corticosterone to a level comparable to that observed in wild-type mice. Thus, either endogenous IL-6 does not mediate IL-1-induced corticosterone increase, or its role may be fulfilled by other cytokines. To the extent that gp130-dependent cytokines may serve this role, they may be important feedback regulators of inflammation through the activation of the hypothalamus-pituitary-adrenal axis and the potentiation of acute-phase protein synthesis.

The presence of chloroform as the result of disinfection with sodium hypochlorite was demonstrated in the water and ambient air of indoor swimming pools. Environmental monitoring was performed in 12 indoor swimming pools in northern Italy and the level of human exposure was assessed. Biological monitoring performed by gas chromatography on human plasma and alveolar air samples evidenced that the uptake of chloroform in swimmers varies according to the intensity of the physical activity and age. The elimination of chloroform in alveolar air in one subject showed a very short half-life (from 20 to 27 min) and a complete clearance within 10 h after the end of exposure.

Dexamethasone (DEX) is a well-known inhibitor of tumor necrosis factor (TNF) production when given shortly before lipopolysaccharide (LPS). However, DEX (10 mg/kg, ip) potentiates TNF production when administered 24-48 hr before LPS (16 micrograms/kg, ip). We have found that this is probably due to DEX induction of cytochrome P450 3A, which is known to produce nitric oxide (NO). The upregulating effect of DEX on TNF production is associated with increased NO production. Both the upregulation of NO and of TNF production by DEX are inhibited by co-administration of the P450 3A inhibitor troleandomycin (TAO, 40 mg/kg, ip). These data suggest that P450 3A-generated NO might be involved in TNF induction.

Perchloroethylene (PCE) is the most widely used solvent in dry-cleaning; it is toxic to the liver, kidney and central nervous system and may be a human carcinogen. PCE levels in the ambient air of dry-cleaners' homes were measured, and samples of end-exhaled air (alveolar air) from subjects who were not themselves occupationally exposed, but who were members of the household of dry-cleaners were compared with samples from the general population. Thirty apartments were visited housing dry-cleaners and their families, and located well away from the dry-cleaning premises. Indoor air samples and alveolar air samples were collected contemporaneously from the dry-cleaners (36) and members of their household (34). The same sampling procedure was followed in 25 private homes where samples of alveolar air were collected from 41 subjects who were not occupationally exposed and who acted as control group. All the samples were analysed by direct-injection gas-chromatography. PCE levels in dry-cleaners' homes proved to be significantly higher than in control houses (geometric means: 265 vs. 2 micrograms/m3, P < 0.001). PCE levels in the alveolar air exhaled by dry-cleaners, their family members and control subjects were statistically different (geometric means: 5140, 225 and 3 micrograms/m3, respectively; P < 0.001). PCE is a ubiquitous substance in indoor air, but is present at higher concentrations in apartments where dry-cleaners and their families live. Biological monitoring of PCE in alveolar air confirms that family members of dry-cleaners are more exposed than the general population.

The results of a study on Zn, Cu, Ca and Mg content in whole saliva and supernatant of young adults in relation to caries prevalence are reported. A total of 225 university students were selected for the study on the basis of voluntary participation. The salivary electrolytes showed a high intersubjective variability and females had significantly lower levels than males. In whole saliva, the trace elements were highly correlated, whereas the correlations were weaker in the supernatant. The ratio supernatant/whole saliva varied between subjects and according to the examined electrolytes. No association could be found between the measured trace elements and DMFT. When we analysed the relation with recent caries experience in the subgroup of subjects undergoing oral examinations for at least 1 year, we found evidence that the Zn/Cu molar ratios in whole saliva were significantly decreased in subjects with more than three decayed teeth compared with those with no caries (1.54 vs. 1.11, P < 0.05). No significant association was found when supernatant was analysed. We conclude that the electrolytes' levels in whole saliva might be more adequate than the levels in supernatant to evaluate the relationship with caries.

We tested the effect of different inhibitors of cytochrome P450 on tumor necrosis factor (TNF) production. Metyrapone and SKF525A (100 and 50 mg/kg, ip, respectively) suppressed serum TNF induced by cotreatment with endotoxin (LPS), (2.5 micrograms/mouse). Inhibition was independent of endogenous corticosteroids since it was also observed in adrenalectomized mice. In vitro production of TNF by endotoxin-stimulated human monocytes was also inhibited by metyrapone and SKF525A. Since lipoxygenase (LO) inhibitors also block TNF production and metyrapone was reported to inhibit LO, we suggest that inhibition by metyrapone and SKF525A might be due to inhibition of either LO or a cytochrome P450 implicated in the oxidation of endogenous substrates involved in the inflammatory response.

We have measured the levels of zinc in serum (Zn-S) and in hair (Zn-H) in 391 adolescents, in good health, aged between 11 and 14 years. To evaluate the relationship between zinc status and sexual maturation we have analyzed, in the same subjects, the serum concentrations of the following hormones: luteinizing hormone (LH), follicle stimulating hormone (FSH), dehydroepiandrosterone-sulphate (DHA-S), testosterone (T) and estradiol (E2). No significant relationship between zinc in the biological samples and the hormones measured in all subjects was observed; only in prepuberal females was a positive correlation found between Zn-S and E2. A significant relationship between Zn-S and LH was observed only for males with short stature or low weight (less than 25th percentile) (r = 0.359, p = 0.010; r = 0.47, p = 0.008, respectively). When prepuberal males with short stature were considered, a significant association between Zn-S and T appeared (r = 0.399, p = 0.006). In females with short stature (less than 25th percentile), partial correlation coefficients showed a significant association between FSH and zinc in hair (r = 0.435, p = 0.004), while in girls with low weight, FSH appeared positively related to zinc in hair (r = 0.470, p = 0.003) and negatively related to zinc in serum (r = -0.320, p = 0.050). Our results suggest that zinc plays an important role in the metabolism of hormones linked to sexual maturation.

Zinc and copper status was evaluated in 63 early hypertensives and compared with that of 63 normotensives matched for sex, age, smoking habits and body mass index. Zinc and copper in serum, urine and hair were measured, and the serum activity of two zinc-dependent enzymes (AP and LDH) were analysed. Mean urinary copper concentration in patients was 14.11 micrograms g-1 creatinine compared with 9.16 micrograms g-1 creatinine in normotensive subjects (paired "t" = 3.94, p less than 0.001). Serum AP and LDH were significantly decreased (16 and 36%, respectively) in the patients compared with controls, although almost all values fell within the normal range of activities. Systolic and diastolic pressures were significantly and positively correlated to urinary copper excretion. These correlations were still apparent after correcting blood pressure values for other urinary measurements. Blood pressure levels (both systolic and diastolic) were also negatively correlated with the two zinc-dependent enzymes.