Indoor, outdoor, and regional summer and winter concentrations of PM10, PM2.5, SO4(2)-, H+, NH4+, NO3-, NH3, and nitrous acid in homes with and without kerosene space heaters. (9/8052)

Twenty-four-hour samples of PM10 (mass of particles with aerodynamic diameter < or = 10 microm), PM2.5, (mass of particles with aerodynamic diameter < or = 2.5 microm), particle strong acidity (H+), sulfate (SO42-), nitrate (NO3-), ammonia (NH3), nitrous acid (HONO), and sulfur dioxide were collected inside and outside of 281 homes during winter and summer periods. Measurements were also conducted during summer periods at a regional site. A total of 58 homes of nonsmokers were sampled during the summer periods and 223 homes were sampled during the winter periods. Seventy-four of the homes sampled during the winter reported the use of a kerosene heater. All homes sampled in the summer were located in southwest Virginia. All but 20 homes sampled in the winter were also located in southwest Virginia; the remainder of the homes were located in Connecticut. For homes without tobacco combustion, the regional air monitoring site (Vinton, VA) appeared to provide a reasonable estimate of concentrations of PM2.5 and SO42- during summer months outside and inside homes within the region, even when a substantial number of the homes used air conditioning. Average indoor/outdoor ratios for PM2.5 and SO42- during the summer period were 1.03 +/- 0.71 and 0.74 +/- 0.53, respectively. The indoor/outdoor mean ratio for sulfate suggests that on average approximately 75% of the fine aerosol indoors during the summer is associated with outdoor sources. Kerosene heater use during the winter months, in the absence of tobacco combustion, results in substantial increases in indoor concentrations of PM2.5, SO42-, and possibly H+, as compared to homes without kerosene heaters. During their use, we estimated that kerosene heaters added, on average, approximately 40 microg/m3 of PM2.5 and 15 microg/m3 of SO42- to background residential levels of 18 and 2 microg/m3, respectively. Results from using sulfuric acid-doped Teflon (E.I. Du Pont de Nemours & Co., Wilmington, DE) filters in homes with kerosene heaters suggest that acid particle concentrations may be substantially higher than those measured because of acid neutralization by ammonia. During the summer and winter periods indoor concentrations of ammonia are an order of magnitude higher indoors than outdoors and appear to result in lower indoor acid particle concentrations. Nitrous acid levels are higher indoors than outdoors during both winter and summer and are substantially higher in homes with unvented combustion sources.  (+info)

Cockroach allergy and asthma in a 30-year-old man. (10/8052)

A growing body of evidence has implicated allergens derived from cockroaches as an important environmental factor that may aggravate asthma in sensitized persons. We present the case of a 30-year-old man with asthma and a cockroach allergy. Allergy skin testing confirmed hypersensitivity to cockroach extract, and a home visit revealed visual evidence of infestation and the presence of Bla g 1 German cockroach allergen in vacuumed dust. As is typical of patients with a cockroach allergy and asthma, multiple factors in addition to cockroach allergen appeared to aggravate the patient's asthma. A multimodality therapeutic regimen, which included medications as well as cleaning of the home, integrated pest management, and professional application of chemical controls, resulted in substantial clinical improvement. The pathophysiology, epidemiology, and clinical features of cockroach-allergic asthma are reviewed, and an approach to diagnosis and management is suggested.  (+info)

Quantitative analysis of constitutive and 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced cytochrome P450 1B1 expression in human lymphocytes. (11/8052)

Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or dioxin) results in a broad spectrum of biological responses, including altered metabolism, disruption of normal hormone signaling pathways, reproductive and developmental effects, and cancer. Cytochrome P450 1B1 (CYP1B1) is a dioxin-inducible gene that is active in the formation of 4-hydroxyestradiol, a potentially genotoxic catechol estrogen. Therefore, the analysis of CYP1B1 in humans may be useful in establishing relationships between dioxin exposure and adverse health effects. In this study, we examined the expression of CYP1B1 in human peripheral blood lymphocytes of unexposed individuals using a quantitative reverse transcription-PCR method. Absolute CYP1B1 RNA levels varied more than 30-fold in uncultured mononuclear cells obtained from 10 individuals. In vitro treatment of mitogen-stimulated lymphocytes with TCDD for 1-5 days of culture resulted in a peak induction of CYP1B1 after 3 days. The induction of CYP1B1 RNA levels after 3 days of culture was dose-dependent, exhibited a maximum response above 10 nM TCDD, and varied greatly among different individuals. However, the half maximal dose required for this induction was similar between individuals and comparable to that observed in the MCF-7 and HepG2 human cell lines. These observations indicate that CYP1B1 exhibits variable constitutive expression and is inducible in vitro by TCDD in human lymphocytes and that the magnitude of induction varies within the population. These data define the suitability of CYP1B1 for use as a mechanistically based biomarker in ongoing molecular epidemiological studies of human populations exposed to dioxins and related chemicals that bind the aromatic hydrocarbon receptor.  (+info)

Merkel cell carcinoma and melanoma: etiological similarities and differences. (12/8052)

Merkel cell carcinoma (MCC) of the skin and cutaneous malignant melanoma can now be compared epidemiologically through the use of population-based data not previously available for MCC. The results may provide new clues to etiology. In this study, United States data covered by the Surveillance, Epidemiology, and End Results (SEER) Program were from nine areas of the United States (approximately 10% of the population). In 1986-1994, 425 cases of MCC were registered. The annual age-adjusted incidence per 100,000 of MCC was 0.23 for whites and 0.01 for blacks; among whites, the ratio of melanoma to MCC was approximately 65 to 1. Only 5% of MCC occurred before age 50, unlike the lifelong risk of nodular and superficial spreading melanoma. Regional incidence rates of both cancers increased similarly with increasing sun exposure as measured by the UVB solar index. The most sun-exposed anatomical site, the face, was the location of 36% of MCC but only 14% of melanoma. Both cancers increased in frequency and aggressiveness after immunosuppression and organ transplantation (36 cases from the Cincinnati Transplant Tumor registry and 12 from published case reports) and after B-cell neoplasia (5 cases in this study; 13 from case series in the literature). The SEER data contained reports of six patients with both types of cancer; 5 melanomas before the diagnosis of MCC and 1 after diagnosis. MCC and melanoma are similarly related to sun exposure and immunosuppression, but they differ markedly from one another in their distributions by age, race, and anatomical site, especially the face.  (+info)

Five caffeine metabolite ratios to measure tobacco-induced CYP1A2 activity and their relationships with urinary mutagenicity and urine flow. (13/8052)

To choose a sensitive protocol to discriminate populations exposed and not exposed to inducers, five urinary metabolite ratios (MRs) [MR1 (17X + 17U)/137X, MR2 (5-acetylamino-6-formylamino-3-methyluracil [AFMU] + 1X + 1U)/17U, MR3 (17X/137X), MR4 (AFMU + 1X + 1U + 17X + 17U)/137X, and MR5 (AFMU + 1X + 1U)/17X] were calculated in 4-5 h and 0-24 h urine samples after caffeine intake. One hundred twenty-five healthy volunteers (59 nonsmokers and 66 smokers) were included in the study. All ratios showed a log-normal distribution. MR2 in the two time intervals was the only ratio nondependent on the urine flow. Differences between nonsmokers and smokers could be detected with all ratios at 4-5 h. However, only MR2 and, to a lesser extent, MR5 allowed the discrimination of higher cytochrome P450 1A2 (CYP1A2) activity in smokers in the 0-24 h sample. Although smokers had increased urinary mutagenicity in relation to nonsmokers, a significant association between MRs and urine mutagenicity was observed only with MR2 in the 4-5 h interval; this ratio/time schedule being that of higher association with tobacco consumption. The most flow-dependent ratios, MR1, MR3, and MR4, were closely correlated with each other at the two intervals. The flow dependency profile of each ratio may explain their different power to indicate both tobacco exposure and tobacco-derived mutagenicity. In conclusion, MR2 in the period of 4-5 h after caffeine intake seems preferable, especially at high urine flow rates.  (+info)

Passive smoking and the risk of coronary heart disease--a meta-analysis of epidemiologic studies. (14/8052)

BACKGROUND: The effect of passive smoking on the risk of coronary heart disease is controversial. We conducted a meta-analysis of the risk of coronary heart disease associated with passive smoking among nonsmokers. METHODS: We searched the Medline and Dissertation Abstracts Online data bases and reviewed citations in relevant articles to identify 18 epidemiologic (10 cohort and 8 case-control) studies that met prestated inclusion criteria. Information on the designs of the studies, the characteristics of the study subjects, exposure and outcome measures, control for potential confounding factors, and risk estimates was abstracted independently by three investigators using a standardized protocol. RESULTS: Overall, nonsmokers exposed to environmental smoke had a relative risk of coronary heart disease of 1.25 (95 percent confidence interval, 1.17 to 1.32) as compared with nonsmokers not exposed to smoke. Passive smoking was consistently associated with an increased relative risk of coronary heart disease in cohort studies (relative risk, 1.21; 95 percent confidence interval, 1.14 to 1.30), in case-control studies (relative risk, 1.51; 95 percent confidence interval, 1.26 to 1.81), in men (relative risk, 1.22; 95 percent confidence interval, 1.10 to 1.35), in women (relative risk, 1.24; 95 percent confidence interval, 1.15 to 1.34), and in those exposed to smoking at home (relative risk, 1.17; 95 percent confidence interval, 1.11 to 1.24) or in the workplace (relative risk, 1.11; 95 percent confidence interval, 1.00 to 1.23). A significant dose-response relation was identified, with respective relative risks of 1.23 and 1.31 for nonsmokers who were exposed to the smoke of 1 to 19 cigarettes per day and those who were exposed to the smoke of 20 or more cigarettes per day, as compared with nonsmokers not exposed to smoke (P=0.006 for linear trend). CONCLUSIONS: Passive smoking is associated with a small increase in the risk of coronary heart disease. Given the high prevalence of cigarette smoking, the public health consequences of passive smoking with regard to coronary heart disease may be important.  (+info)

Impact of diet on lead in blood and urine in female adults and relevance to mobilization of lead from bone stores. (15/8052)

We measured high precision lead isotope ratios and lead concentrations in blood, urine, and environmental samples to assess the significance of diet as a contributing factor to blood and urine lead levels in a cohort of 23 migrant women and 5 Australian-born women. We evaluated possible correlations between levels of dietary lead intake and changes observed in blood and urine lead levels and isotopic composition during pregnancy and postpartum. Mean blood lead concentrations for both groups were approximately 3 microg/dl. The concentration of lead in the diet was 5.8 +/- 3 microg Pb/kg [geometric mean (GM) 5.2] and mean daily dietary intake was 8.5 microg/kg/day (GM 7.4), with a range of 2-39 microg/kg/day. Analysis of 6-day duplicate dietary samples for individual subjects commonly showed major spikes in lead concentration and isotopic composition that were not reflected by associated changes in either blood lead concentration or isotopic composition. Changes in blood lead levels and isotopic composition observed during and after pregnancy could not be solely explained by dietary lead. These data are consistent with earlier conclusions that, in cases where levels of environmental lead exposure and dietary lead intake are low, skeletal contribution is the dominant contributor to blood lead, especially during pregnancy and postpartum.  (+info)

Tetrachloroethylene-contaminated drinking water in Massachusetts and the risk of colon-rectum, lung, and other cancers. (16/8052)

We conducted a population-based case-control study to evaluate the relationship between cancer of the colon-rectum (n = 326), lung (n = 252), brain (n = 37), and pancreas (n = 37), and exposure to tetrachloroethylene (PCE) from public drinking water. Subjects were exposed to PCE when it leached from the vinyl lining of drinking-water distribution pipes. Relative delivered dose of PCE was estimated using a model that took into account residential location, years of residence, water flow, and pipe characteristics. Adjusted odds ratios (ORs) for lung cancer were moderately elevated among subjects whose exposure level was above the 90th percentile whether or not a latent period was assumed [ORs and 95% confidence intervals (CIs), 3.7 (1.0-11.7), 3.3 (0.6-13.4), 6.2 (1.1-31.6), and 19.3 (2.5-141.7) for 0, 5, 7, and 9 years of latency, respectively]. The adjusted ORs for colon-rectum cancer were modestly elevated among ever-exposed subjects as more years of latency were assumed [OR and CI, 1.7 (0.8-3.8) and 2.0 (0.6-5.8) for 11 and 13 years of latency, respectively]. These elevated ORs stemmed mainly from associations with rectal cancer. Adjusted ORs for rectal cancer among ever-exposed subjects were more elevated [OR and CI, 2.6 (0. 8-6.7) and 3.1 (0.7-10.9) for 11 and 13 years of latency, respectively] than were corresponding estimates for colon cancer [OR and CI, 1.3 (0.5-3.5) and 1.5 (0.3-5.8) for 11 and 13 years of latency, respectively]. These results provide evidence for an association between PCE-contaminated public drinking water and cancer of the lung and, possibly, cancer of the colon-rectum.  (+info)