159 research outputs found

    Pulmonary Epithelial Integrity in Children: Relationship to Ambient Ozone Exposure and Swimming Pool Attendance

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    Airway irritants such as ozone are known to impair lung function and induce airway inflammation. Clara cell protein (CC16) is a small anti-inflammatory protein secreted by the nonciliated bronchiolar Clara cells. CC16 in serum has been proposed as a noninvasive and sensitive marker of lung epithelial injury. In this study, we used lung function and serum CC16 concentration to examine the pulmonary responses to ambient O(3) exposure and swimming pool attendance. The measurements were made on 57 children 10–11 years of age before and after outdoor exercise for 2 hr. Individual O(3) exposure was estimated as the total exposure dose between 0700 hr until the second blood sample was obtained (mean O(3) concentration/m(3) × hours). The maximal 1-hr value was 118 μg/m(3) (59 ppb), and the individual exposure dose ranged between 352 and 914 μg/m(3)hr. These O(3) levels did not cause any significant changes in mean serum CC16 concentrations before or after outdoor exercise, nor was any decrease in lung function detected. However, children who regularly visited chlorinated indoor swimming pools had significantly lower CC16 levels in serum than did nonswimming children both before and after exercise (respectively, 57 ± 2.4 and 53 ± 1.7 μg/L vs. 8.2 ± 2.8 and 8.0 ± 2.6 μg/L; p < 0.002). These results indicate that repeated exposure to chlorination by-products in the air of indoor swimming pools has adverse effects on the Clara cell function in children. A possible relation between such damage to Clara cells and pulmonary morbidity (e.g., asthma) should be further investigated

    The Effects of On-site Measured Ozone Concentration on Pulmonary Function and Symptoms of Asthmatics

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    Most studies on the effects of ambient ozone on asthmatics have been based on ozone concentration measurements taken by air monitors in downtown areas. Using a passive ozone sampler, we investigated the effects of on-site ozone concentrations on the pulmonary function and symptoms of asthmatics. Twenty moderate to severe asthmatics who had been managed for at least 2 months without changes of their medication were enrolled from 3 June to 18 July 2005. Respiratory, nasal and ocular symptoms, peak expiratory flow (PEF), which was measured twice a day, and medication use were recorded on a daily basis during the study period. Data for 17 subjects were analyzed. The average ozone exposure level was 28.2±23.6 ppb (3.4-315.3 ppb). There was no significant correlation between PEF and ozone concentration (p>0.05) on the same day or 1-, 2-, or 3-day lags. Interestingly, the degree of asthma symptoms was influenced by the ozone concentration (ρ=0.303, p<0.001), even at concentrations less than 80 ppb (p=0.298, p<0.001), but the correlation between ozone exposure and the frequency of reliever medication use was not statistically significant (p=0.99). Our results suggest that exposure to relatively low concentrations of ozone influences the symptoms of moderate to severe asthmatics regardless of changes in pulmonary function or medication use

    Additive Effect of Diesel Exhaust Particulates and Ozone on Airway Hyperresponsiveness and Inflammation in a Mouse Model of Asthma

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    Allergic airway diseases are related to exposure to atmospheric pollutants, which have been suggested to be one factor in the increasing prevalence of asthma. Little is known about the effect of ozone and diesel exhaust particulates (DEP) on the development or aggravation of asthma. We have used a mouse asthma model to determine the effect of ozone and DEP on airway hyperresponsiveness and inflammation. Methacholine enhanced pause (Penh) was measured. Levels of IL-4 and IFN-γ were quantified in bronchoalveolar lavage fluids by enzyme immunoassays. The OVA-sensitized-challenged and ozone and DEP exposure group had higher Penh than the OVA-sensitized-challenged group and the OVA-sensitized-challenged and DEP exposure group, and the OVA-sensitized-challenged and ozone exposure group. Levels of IFN-γ were decreased in the OVA-sensitized-challenged and DEP exposure group and the OVA-sensitized-challenged and ozone and DEP exposure group compared to the OVA-sensitized-challenged and ozone exposure group. Levels of IL-4 were increased in the OVA-sensitized-challenged and ozone exposure group and the OVA-sensitized-challenged and DEP exposure group, and the OVA-sensitized-challenged and ozone and DEP exposure group compared to OVA-sensitized-challenged group. Co-exposure of ozone and DEP has additive effect on airway hyperresponsiveness by modulation of IL-4 and IFN-γ suggesting that DEP amplify Th2 immune response

    Changes in the expression of NO synthase isoforms after ozone: the effects of allergen exposure

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    BACKGROUND: The functional role of nitric oxide (NO) and various nitric oxide synthase (NOS) isoforms in asthma remains unclear. OBJECTIVE: This study investigated the effects of ozone and ovalbumin (OVA) exposure on NOS isoforms. METHODS: The expression of inducible NOS (iNOS), neuronal NOS (nNOS), and endothelial NOS (eNOS) in lung tissue was measured. Enhanced pause (P(enh)) was measured as a marker of airway obstruction. Nitrate and nitrite in bronchoalveolar lavage (BAL) fluid were measured using a modified Griess reaction. RESULTS: The nitrate concentration in BAL fluid from the OVA-sensitized/ozone-exposed/OVA-challenged group was greater than that of the OVA-sensitized/saline-challenged group. Methacholine-induced P(enh )was increased in the OVA-sensitized/ozone-exposed/OVA-challenged group, with a shift in the dose-response curve to the left, compared with the OVA-sensitized/saline-challenged group. The levels of nNOS and eNOS were increased significantly in the OVA-sensitized/ozone-exposed/OVA-challenged group and the iNOS levels were reduced compared with the OVA-sensitized/saline-challenged group. CONCLUSION: In mice, ozone is associated with increases in lung eNOS and nNOS, and decreases in iNOS. None of these enzymes are further affected by allergens, suggesting that the NOS isoforms play different roles in airway inflammation after ozone exposure

    Prolonged ozone exposure in an allergic airway disease model: Adaptation of airway responsiveness and airway remodeling

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    BACKGROUND: Short-term exposure to high concentrations of ozone has been shown to increase airway hyper-responsiveness (AHR). Because the changes in AHR and airway inflammation and structure after chronic ozone exposure need to be determined, the goal of this study was to investigate these effects in a murine model of allergic airway disease. METHODS: We exposed BALB/c mice to 2 ppm ozone for 4, 8, and 12 weeks. We measured the enhanced pause (Penh) to methacholine and performed cell differentials in bronchoalveolar lavage fluid. We quantified the levels of IL-4 and IFN-γ in the supernatants of the bronchoalveolar lavage fluids using enzyme immunoassays, and examined the airway architecture under light and electron microscopy. RESULTS: The groups exposed to ozone for 4, 8, and 12 weeks demonstrated decreased Penh at methacholine concentrations of 12.5, 25, and 50 mg/ml, with a dose-response curve to the right of that for the filtered-air group. Neutrophils and eosinophils increased in the group exposed to ozone for 4 weeks compared to those in the filtered-air group. The ratio of IL-4 to INF-γ increased significantly after exposure to ozone for 8 and 12 weeks compared to the ratio for the filtered-air group. The numbers of goblet cells, myofibroblasts, and smooth muscle cells showed time-dependent increases in lung tissue sections from the groups exposed to ozone for 4, 8, and 12 weeks. CONCLUSION: These findings demonstrate that the increase in AHR associated with the allergic airway does not persist during chronic ozone exposure, indicating that airway remodeling and adaptation following repeated exposure to air pollutants can provide protection against AHR

    European Code against Cancer 4th Edition: Alcohol drinking and cancer.

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    Alcohol consumption is the third leading risk factor for disease and mortality in Europe. As evaluated by the International Agency for Research on Cancer (IARC) Monographs, a causal relationship is established for consumption of alcoholic beverages and cancers of the oral cavity, pharynx, larynx, oesophagus, liver, colorectum and female breast, even at low and moderate alcohol intakes. The higher the amount of alcohol consumed, the higher the risk of developing cancer. In Europe, an estimated 10% (95% CI: 7%-13%) of all cancer cases in men and 3% (95% CI: 1%-5%) of all cancer cases in women are attributable to alcohol consumption. Several biological mechanisms explain the carcinogenicity of alcohol; among them, ethanol and its genotoxic metabolite, acetaldehyde, play a major role. Taking all this evidence into account, a recommendation of the 4th edition of European Code against Cancer is: "If you drink alcohol of any type, limit your intake. Not drinking alcohol is better for cancer prevention.

    ‘Repeal the 8th’ in a Transnational Context: The Potential of SRHRs for Advancing Abortion Access in El Salvador

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    This article undertakes a discursive feminist reading of citizenship and human rights to understand, through the cases of Ireland and El Salvador, domestic abortion rights movements as part of a transnational women’s rights movement. While abortion has been partially decriminalised in Ireland, approximately 42 per cent of the world’s women1 of reproductive age still live in a country where abortion is prohibited entirely or only permitted to save a woman’s life or health (Singh et al., 2018, p. 4). In El Salvador, abortion is illegal and those suspected of having the procedure are prosecuted. As in Ireland, since 2012/2013 numerous controversies have brought the issue to wider public attention and have further galvanised the feminist movement to campaign for reform. Feminist abortion rights campaigns in both countries have connected important sites of activism and contestation: civil society, national parliaments, regional human rights systems and the United Nations

    From benzos to berries: treatment offered at an Aboriginal youth solvent abuse treatment centre relays the importance of culture.

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    First Nations and Inuit youth who abuse solvents are one of the most highly stigmatized substance-abusing groups in Canada. Drawing on a residential treatment response that is grounded in a culture-based model of resiliency, this article discusses the cultural implications for psychiatry's individualized approach to treating mental disorders. A systematic review of articles published in The Canadian Journal of Psychiatry during the past decade, augmented with a review of Canadian and international literature, revealed a gap in understanding and practice between Western psychiatric disorder-based and Aboriginal culture-based approaches to treatment and healing from substance abuse and mental disorders. Differing conceptualizations of mental health and substance abuse are discussed from Western psychiatric and Aboriginal worldviews, with a focus on connection to self, community, and political context. Applying an Aboriginal method of knowledge translation-storytelling-experiences from front-line workers in a youth solvent abuse treatment centre relay the difficulties with applying Western responses to Aboriginal healing. This lends to a discussion of how psychiatry can capitalize on the growing debate regarding the role of culture in the treatment of Aboriginal youth who abuse solvents. There is significant need for culturally competent psychiatric research specific to diagnosing and treating First Nations and Inuit youth who abuse substances, including solvents. Such understanding for front-line psychiatrists is necessary to improve practice. A health promotion perspective may be a valuable beginning point for attaining this understanding, as it situates psychiatry's approach to treating mental disorders within the etiology for Aboriginal Peoples
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