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(1/1280) Double-blind intervention trial on modulation of ozone effects on pulmonary function by antioxidant supplements.

The aim of this study was to investigate whether the acute effects of ozone on lung function could be modulated by antioxidant vitamin supplementation in a placebo-controlled study. Lung function was measured in Dutch bicyclists (n = 38) before and after each training session on a number of occasions (n = 380) during the summer of 1996. The vitamin group (n = 20) received 100 mg of vitamin E and 500 mg of vitamin C daily for 15 weeks. The average ozone concentration during exercise was 77 microg/m3 (range, 14-186 microg/m3). After exclusion of subjects with insufficient compliance from the analysis, a difference in ozone exposure of 100 microg/m3 decreased forced expiratory volume in 1 second (FEV1) 95 ml (95% confidence interval (CI) -265 to -53) in the placebo group and 1 ml (95% CI -94 to 132) in the vitamin group; for forced vital capacity, the change was -125 ml (95% CI -384 to -36) in the placebo group and -42 ml (95% CI -130 to 35) in the vitamin group. The differences in ozone effect on lung function between the groups were statistically significant. The results suggest that supplementation with the antioxidant vitamins C and E confers partial protection against the acute effects of ozone on FEV1 and forced vital capacity in cyclists.  (+info)

(2/1280) Enrichment of enzyme activity on deformylation of 1-NFK-lysozyme.

The formamide linkage of an inactive lysozyme derivative (1-NFK-lysozyme), formed by selective ozonization of tryptophan 62 in hen egg-white lysozyme [EC 3.2.1.17] was hydrolyzed with dilute acid faster in the frozen state at about --10 degrees than at 20 degrees. On hydrolysis of 1-NFK-lysozyme the low lytic activity increased to approximately 80% of that of native lysozyme. It is suggested that the binding ability associated with kynurenine 62 in the lysozyme derivative formed by this hydrolysis may be responsible for increase in enzymatic activity.  (+info)

(3/1280) Airway inflammatory response to ozone in subjects with different asthma severity.

The aim of this study was to evaluate whether ozone exposure induces a similar airway inflammatory response in subjects with different degrees of asthma severity. Two groups of asthmatic subjects were studied: seven with intermittent mild asthma not requiring regular treatment (group A); and seven with persistent mild asthma requiring regular treatment with inhaled corticosteroids and long-acting beta2-agonists (group B). All subjects were exposed, in a randomized cross-over design, to air or O3 (0.26 parts per million (ppm) for 2 h with intermittent exercise); subjects in group B withdrew from regular treatment 72 h before each exposure. Before the exposure, and 1 and 2 h after the beginning of the exposure they performed a pulmonary function test, and a questionnaire was completed to obtain a total symptom score (TSS). Six hours after the end of the exposure, hypertonic saline (HS) sputum induction was conducted. Sputum cell percentages, eosinophil cationic protein (ECP) and interleukin (IL)-8 concentrations in the sputum supernatant were measured. TSS significantly increased and forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) significantly decreased after O3 exposure in comparison with air exposure in group A, whereas no changes were observed in group B except for a significant decrement of FEV1 2 h after the beginning of O3 exposure. Sputum neutrophil percentage was significantly higher after O3 exposure than after air exposure in both groups (Group A: 70.2% (28-87) versus 26.6% (8.6-73.2); Group B: 62.1% (25-82.4) versus 27.9% (14.4-54)). IL-8 was higher in sputum supernatant collected 6 h after O3 exposure than after air, only in group A. No change due to O3 has been found in sputum eosinophil percentage and ECP concentration in both groups. In conclusion, the degree of airway response to a short-term exposure to ozone is different in subjects with asthma of different severity. The available data do not allow elucidation of whether this difference depends on the severity of the disease or on the regular anti-inflammatory treatment.  (+info)

(4/1280) Capsaicin-sensitive C-fiber-mediated protective responses in ozone inhalation in rats.

To assess the role of lung sensory C fibers during and after inhalation of 1 part/million ozone for 8 h, we compared breathing pattern responses and epithelial injury-inflammation-repair in rats depleted of C fibers by systemic administration of capsaicin as neonates and in vehicle-treated control animals. Capsaicin-treated rats did not develop ozone-induced rapid, shallow breathing. Capsaicin-treated rats showed more severe necrosis in the nasal cavity and greater inflammation throughout the respiratory tract than did control rats exposed to ozone. Incorporation of 5-bromo-2'-deoxyuridine (a marker of DNA synthesis associated with proliferation) into terminal bronchiolar epithelial cells was not significantly affected by capsaicin treatment in rats exposed to ozone. However, when normalized to the degree of epithelial necrosis present in each rat studied, there was less 5-bromo-2'-deoxyuridine labeling in the terminal bronchioles of capsaicin-treated rats. These observations suggest that the ozone-induced release of neuropeptides does not measurably contribute to airway inflammation but may play a role in modulating basal and reparative airway epithelial cell proliferation.  (+info)

(5/1280) Air pollution, pollens, and daily admissions for asthma in London 1987-92.

BACKGROUND: A study was undertaken to investigate the relationship between daily hospital admissions for asthma and air pollution in London in 1987-92 and the possible confounding and modifying effects of airborne pollen. METHODS: For all ages together and the age groups 0-14, 15-64 and 65+ years, Poisson regression was used to estimate the relative risk of daily asthma admissions associated with changes in ozone, sulphur dioxide, nitrogen dioxide and particles (black smoke), controlling for time trends, seasonal factors, calendar effects, influenza epidemics, temperature, humidity, and autocorrelation. Independent effects of individual pollutants and interactions with aeroallergens were explored using two pollutant models and models including pollen counts (grass, oak and birch). RESULTS: In all-year analyses ozone was significantly associated with admissions in the 15-64 age group (10 ppb eight hour ozone, 3.93% increase), nitrogen dioxide in the 0-14 and 65+ age groups (10 ppb 24 hour nitrogen dioxide, 1.25% and 2.96%, respectively), sulphur dioxide in the 0-14 age group (10 micrograms/m3 24 hour sulphur dioxide, 1.64%), and black smoke in the 65% age group (10 micrograms/m3 black smoke, 5.60%). Significant seasonal differences were observed for ozone in the 0-14 and 15-64 age groups, and in the 0-14 age group there were negative associations with ozone in the cool season. In general, cumulative lags of up to three days tended to show stronger and more significant effects than single day lags. In two-pollutant models these associations were most robust for ozone and least for nitrogen dioxide. There was no evidence that the associations with air pollutants were due to confounding by any of the pollens, and little evidence of an interaction between pollens and pollution except for synergism of sulphur dioxide and grass pollen in children (p < 0.01). CONCLUSIONS: Ozone, sulphur dioxide, nitrogen dioxide, and particles were all found to have significant associations with daily hospital admissions for asthma, but there was a lack of consistency across the age groups in the specific pollutant. These associations were not explained by confounding by airborne pollens nor was there convincing evidence that the effects of air pollutants and airborne pollens interact in causing hospital admissions for asthma.  (+info)

(6/1280) Effect of insurance coverage on the relationship between asthma hospitalizations and exposure to air pollution.

OBJECTIVE: Based on the assumption that people without health insurance have limited access to the primary care services needed to prevent unnecessary hospitalizations for asthma, the authors hypothesized that insurance is a factor in the strength of the association between hospital admissions for asthma and exposure to air pollution. They tested this hypothesis with 1991-1994 data from central Los Angeles. METHODS: The authors analyzed the effect of insurance status on the association between asthma-related hospital admissions and exposure to atmospheric particulates (PM10) and ozone (O3) using hospital discharge and air quality data for 1991-1994 for central Los Angeles. They used regression techniques with weighted moving averages (simulating distributed lag structures) to measure the effects of exposure on overall hospital admissions, admissions of uninsured patients, admissions for which MediCal (California Medicaid) was the primary payer, and admissions for which the primary payer was another government or private health insurance program. RESULTS: No associations were found between asthma admissions and O3 exposure. An estimated increase from 1991 to 1994 of 50 micrograms per cubic meter in PM10 concentrations averaged over eight days was associated with an increase of 21.0% in the number of asthma admissions. An even stronger increase--27.4%--was noted among MediCal asthma admissions. CONCLUSIONS: The authors conclude that low family income, as indicated by MediCal coverage, is a better predictor of asthma exacerbations associated with air pollution than lack of insurance and, by implication, a better predictor of insufficient access to primary care.  (+info)

(7/1280) Public health consequences of global climate change in the United States--some regions may suffer disproportionately.

Current risk assessments of the likely regional health impacts of global climate change (GCC) are hindered by two factors. First, dose-response relationships between weather parameters and many of the likely health effects have not been developed, and second, reliable estimates of future regional climates across the United States are still beyond the scope of current modeling efforts. Consequently, probabilistic risk estimates of most of the likely regional health impacts of GCC have such a high degree of uncertainty that their usefulness to health officials dealing with regional issues is very limited. With the numerous pressures on today's health care systems, it is understandable that the possible consequences of GCC have received scant attention from regional health care decision makers. Indeed, the consensus among this community appears to be that any increases in health effects associated with GCC will be easily handled by the current health care system. However, such a position may be naive as the potential exists that an unequal distribution of such effects could overwhelm some regions, whereas others may feel little or no impact. This review of the likely regional impacts of GCC has been structured as a semianalytical look at this issue of distributional effects. Because of the lack of dose-response information and reliable estimates of future regional climates, however, it takes a historical perspective. That is, it assumes that the quality and quantity of health risks a region faces under GCC will be directly related to its recent history of health risks from warm weather/climate-related diseases as well as to the size, characteristics, and distribution of the sensitive subpopulations currently residing within its borders. The approach is semiquantitative; however, it uses national data gathered on a regional level and as such should only be used to generate a hypothesis rather than test it. When applied to the United States, its outcome leads to the hypothesis that if indeed history repeats itself, some states or regions may be more greatly affected by GCC than others, not only because historically they are more prone to summer weather/climate-related diseases, but also because they contain a greater proportion of the sensitive subpopulations in the United States.  (+info)

(8/1280) Drinking water disinfection byproducts: review and approach to toxicity evaluation.

There is widespread potential for human exposure to disinfection byproducts (DBPs) in drinking water because everyone drinks, bathes, cooks, and cleans with water. The need for clean and safe water led the U.S. Congress to pass the Safe Drinking Water Act more than 20 years ago in 1974. In 1976, chloroform, a trihalomethane (THM) and a principal DBP, was shown to be carcinogenic in rodents. This prompted the U.S. Environmental Protection Agency (U.S. EPA) in 1979 to develop a drinking water rule that would provide guidance on the levels of THMs allowed in drinking water. Further concern was raised by epidemiology studies suggesting a weak association between the consumption of chlorinated drinking water and the occurrence of bladder, colon, and rectal cancer. In 1992 the U.S. EPA initiated a negotiated rulemaking to evaluate the need for additional controls for microbial pathogens and DBPs. The goal was to develop an approach that would reduce the level of exposure from disinfectants and DBPs without undermining the control of microbial pathogens. The product of these deliberations was a proposed stage 1 DBP rule. It was agreed that additional information was necessary on how to optimize the use of disinfectants while maintaining control of pathogens before further controls to reduce exposure beyond stage 1 were warranted. In response to this need, the U.S. EPA developed a 5-year research plan to support the development of the longer term rules to control microbial pathogens and DBPs. A considerable body of toxicologic data has been developed on DBPs that occur in the drinking water, but the main emphasis has been on THMs. Given the complexity of the problem and the need for additional data to support the drinking water DBP rules, the U.S. EPA, the National Institute of Environmental Health Sciences, and the U.S. Army are working together to develop a comprehensive biologic and mechanistic DBP database. Selected DBPs will be tested using 2-year toxicity and carcinogenicity studies in standard rodent models; transgenic mouse models and small fish models; in vitro mechanistic and toxicokinetic studies; and reproductive, immunotoxicity, and developmental studies. The goal is to create a toxicity database that reflects a wide range of DBPs resulting from different disinfection practices. This paper describes the approach developed by these agencies to provide the information needed to make scientifically based regulatory decisions.  (+info)