摘要:

The objective of this study was to investigate the spatial distribution of respiratory morbidity and asthma in children in relation to high levels of airborne dust pollution. A cross-sectional survey of 2035 children (aged 5-11 yr) by parent-completed questionnaire, with concurrent monitoring of dust deposition rates in the vicinity of children's homes, was performed in 15 primary schools (5 in each of 3 areas of Merseyside). The main outcome measures were (1) doctor-diagnosed asthma, (2) parent-reported respiratory symptoms of recent excess cough, wheeze, and breathlessness, and (3) school absenteeism due to respiratory ill health. Proximity to the source of dust pollution was associated with increased prevalence of excess cough, breathlessness, school absence due to respiratory ill health, and doctor-diagnosed asthma, after adjusting for a range of socioeconomic, environmental, and other confounding factors. The adjusted odds for excess cough and breathlessness for children living within 2 km of the source (dock area) are estimated to be almost twice those for children living more than 2 km away: excess cough 1.9 (95% CI 1.4-2.6); breathlessness 1.9 (1.3-2.7); school absence 1.5 (1.2-1.9); and doctor-diagnosed asthma 1.5 (1.1-2.0). Excess cough was significantly associated with the mean annual dust deposition recorded in the vicinity of the child's home. The adjusted odds ratio for excess cough corresponding to an increase in mean annual dust deposition of 50 mg/m2/d was 3.1 (95% CI 1.1-8.2). These results suggest that airborne dust was associated with respiratory morbidity in these children, which could relate to the high prevalence of childhood doctor-diagnosed asthma in this community.

ISSN:1528-7394    

DOI:10.1080/009841098158476

出版商:Informa UK Ltd    

年代:1998

数据来源: Taylor

摘要:

Recent research suggests that some cases of cardiovascular mortality may be related to carbon monoxide (CO) air pollution. Clinically based studies indicate the adverse effects of CO on the cardiopulmonary system. However, little attention has been paid to the question of hospital admissions for cardiovascular illness caused by ambient CO levels. The present study assesses the association between hospital admissions for cardiovascular system illnesses and the ambient levels of CO in the Reno-Sparks, NV, area over a 6-yr period (1989-1994). Daily admissions to all three hospitals in the region and daily ambient concentrations of CO, monitored at five sites, were included. There were 32,705 total cardiovascular (CV) admissions, including 13,108 with the diagnosis of ischemic heart disease (IHD) during the study period. The average daily 1-h maximum level of CO was 3.09 ppm. After adjusting for day-of-the-week and seasonal effects and controlling for the effects of autocorrelation errors, both weighted least squares (WLS) and autoregressive integrated moving average (ARIMA) methods showed consistently positive relationships between the ambient CO level and different groups of cardiovascular admissions, although the male gender and age older than 60 groups tended to be most affected. Data suggest a positive correlation between ambient CO levels and hospital admissions for CV diseases.

ISSN:1528-7394    

DOI:10.1080/009841098158485

出版商:Informa UK Ltd    

年代:1998

数据来源: Taylor

摘要:

Many harbor estuaries and their tributaries are contaminated with halogenated aromatic hydrocarbons (HAHs) and polycyclic aromatic hydrocarbons (PAHs). Planar congeners of these two classes initiate their toxic effects, including reproductive, developmental, and immunological dysfunction, primarily through the cytosolic arylhydrocabon receptor (Ahr). However, only rarely are aquatic environments contaminated with Ahr-binding contaminants alone. Instead, most are impacted by a variety of pollutants in mixture. Tributyltin (TBT), a common antifouling biocide, is also found in many harbor estuaries and their tributaries. Several reports indicate that TBT inhibits the cytochrome P-4501A system of fish, at least in vitro, and our recent studies with rodents indicate that TBT potentiates PCB-induced CYP1A. However, the effects of TBT on xenobiotic-induced CYP1A activity in aquatic organisms has been virtually unexplored. To this end, channel catfish, Ictalurus punctatus, were exposed to 3,3'4,4',5-pentachlorobiphenyl (PCB-126, PeCB), TBT, or both in combination, with corn oil (CO) serving as the carrier control. Immunoreactive CYP1A protein and ethoxyresorufin O -deethylase (EROD) activity were measured after (1) a single dose of 0.01, 0.1, or 1 mg/kg of each or both in combination, and (2) 6 injections of 0.017, 1.7, or 17 mug/kg of each (or in combination) given every 3 d over a 16-d period to yield a cumulative dose of 0.01, 0.1, or 1 mg/kg. As expected, PeCB alone, but not TBT, greatly induced these two CYP1A parameters. Low and middle doses of TBT (0.01 and 0.1 mg/ kg), but not the high dose, potentiated PeCBinduced activity at these same doses. This effect of TBT was even more pronounced in the repeated exposure study. Furthermore, EROD activity did not always reflect CYP1A protein induction; enzyme activity was inhibited by TBT at doses that potentiated protein induction (0.01 and 0.1 mg/ kg). In summary, TBT potentiates PeCB-induced CYP1A in channel catfish at doses that may be considered environmentally relevant.

ISSN:1528-7394    

DOI:10.1080/009841098158494

出版商:Informa UK Ltd    

年代:1998

数据来源: Taylor

摘要:

This study evaluated the effects of Ni2+ on testosterone (T) production of mouse Leydig cells in vitro following an in vivo or in vitro exposure. CFLP mice were subjected to repeated exposure (4 treatments, subcutaneously, every 3 d) to 10, 20 or 40 mg/ kg body weight of NiSO4 or 1.0 ml of 0.9% NaCl solution. Depressed human chorionic gonadotropin (hCG)-stimulated T response was seen over a 48-h culture of testicular interstitial cells obtained from the animals exposed to 20 mg/ kg or higher dose of NiSO4, while the basal T production remained unaltered. There were no Ni2+-related changes in the body weights or in the weights of testes, epididymides, adrenals, and kidneys. No histopathological alteration was found in the examined organs of NiSO4 treated groups except the dose-dependent tubular lesions in kidney as a result of a specific rather than a general cytotoxic action. To assess the direct effect of Ni2+ on Leydigcell T production, testicular interstitial cells were cultured with Ni2+ (62.5 to 1000 mu M) for 48 h in the presence or absence of maximally stimulating concentration of hCG. Dose-dependent depression in hCG-stimulated T production was seen at 125 mu M or higher dose of Ni2+, while basal T production was unaffected. In order to evaluate the time dependency of this effect the cells were cultured for various times in the presence or absence of 250 and 1000 mu M Ni2+. Decreased hCG-stimulated T production was found in the cultures maintained at least for 4 h in the presence of 1000 mu M Ni2+, whereas at 250 mu M at least 16 h was required to elicit the depression. Cell viability was assessed by a metabolic activity (MTT) assay. The viability of cells was unaltered by 250 mu M Ni2+, and only a slight decrease was found even at the end of the 48-h culture period in the presence of 1000 mu M Ni2+. Our results show a dose-related depression in stimulated T production of mouse Leydig cells in culture following either in vivo or in vitro Ni2+ treatment at a dose that does not induce any general toxic or significant cytotoxic action. The data of the time-course study indicate that the effect of Ni2+ on Leydigcell T production is both time and concentration dependent, and not due to cytotoxicity.

ISSN:1528-7394    

DOI:10.1080/009841098158502

出版商:Informa UK Ltd    

年代:1998

数据来源: Taylor

摘要:

This study examined differences in toxicity between 2- and 4-aminophenol using a renal cortical slice model. Renal cortical slice toxicity for 2- and 4-aminophenol was also monitored in tissue from Sprague-Dawley and Fischer 344 (F344) rats in order to determine potential strain differences for aminophenol toxicity. Renal cortical slices from Sprague-Dawley and F344 rats (age 50-65 d) were isolated and incubated for 15-120 min with 0-1 m M 2- or 4-aminophenol at 37 C under an oxygen atmosphere. Elevations in lactate dehydrogenase (LDH) leakage from renal cortical slices occurred at lower concentrations of 4-aminophenol than of 2-aminophenol from both strains of rats. Total glutathione levels were more markedly decreased by 4-aminophenol than by 2-aminophenol in renal slices from both strains. LDH release was elevated by 1 m M 2-aminophenol in renal slices from F344 rats, but values were comparable between control and treated in the renal slices from Sprague-Dawley rats. 4-Aminophenol was slightly more toxic to renal slices from F344 than from Sprague-Dawley rats. LDH release was increased, relative to controls, by 0.1 m M in the F344 rats group compared to 0.25 m M in the Sprague-Dawley group. Strain differences were not apparent when comparisons were made of total glutathione levels or rate-limiting substrates of gluconeogenesis. These results indicated that strain differences in toxicity were detected between SpragueDawley and F344 rat strains. Based on LDH release, renal cortical slices obtained from age-matched F344 rats were slightly more susceptible than Sprague-Dawley rats to toxicity by 2- and 4-aminophenol.

ISSN:1528-7394    

DOI:10.1080/009841098158511

出版商:Informa UK Ltd    

年代:1998

数据来源: Taylor