PubMed · 9766956
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1994. Cigarette secrets.. https://doi.org/10.1289/ehp.102-1567173
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Domestic coal combustion has had profound adverse effects on the health of millions of people worldwide. In China alone several hundred million people commonly burn raw coal in unvented stoves that permeate their homes with high levels of toxic metals and organic compounds. At least 3,000 people in Guizhou Province in southwest China are suffering from severe arsenic poisoning. The primary source of the arsenic appears to be consumption of chili peppers dried over fires fueled with high-arsenic coal. Coal samples in the region were found to contain up to 35,000 ppm arsenic. Chili peppers dried over high-arsenic coal fires adsorb 500 ppm arsenic on average. More than 10 million people in Guizhou Province and surrounding areas suffer from dental and skeletal fluorosis. The excess fluorine is caused by eating corn dried over burning briquettes made from high-fluorine coals and high-fluorine clay binders. Polycyclic aromatic hydrocarbons formed during coal combustion are believed to cause or contribute to the high incidence of esophageal and lung cancers in parts of China. Domestic coal combustion also has caused selenium poisoning and possibly mercury poisoning. Better knowledge of coal quality parameters may help to reduce some of these health problems. For example, information on concentrations and distributions of potentially toxic elements in coal may help delineate areas of a coal deposit to be avoided. Information on the modes of occurrence of these elements and the textural relations of the minerals and macerals in coal may help predict the behavior of the potentially toxic components during coal combustion.
The aim of the study was to investigate the influence of various environmental factors on occurrence of house dust mite allergens and the influence of allergen exposure on mite allergy. Ninety-two persons from a population study filled in a questionnaire, were skin prick and lung function tested and dust samples were collected from their mattresses for analyses. Two out of five patients with asthma had a positive skin reaction to house dust mite allergen in contrast to five out of 87 non-asthmatics. Fifty-nine per cent of the dust samples contained (group 1) mite allergen > 2 micrograms/g dust. Such mattresses were older (median 7 years, range 1-22) than mattresses with less allergen (median 4 years, range 1-20). In the six bedrooms reported to be humid or mouldy, mattresses contained high concentration of mite allergens. No other parameter investigated could predict the allergen contents. In almost all cases dust analyses are crucial to be able to advise patients with house dust mite allergy.
BACKGROUND: Epidemiological data indicate that in females cigarette smoking exerts antiestrogenic effects that manifest clinically in an increased incidence of osteoporosis, earlier menopause, increased spot bleeding, and decreased risk of endometrial cancer for female smokers. The molecular mechanism of this effect is unclear; however, decreased serum estrogen levels in female smokers have been correlated with increased concentrations of the metabolite 2-hydroxyestrogen in females who smoke. Induction of estrogen metabolizing enzymes, CYP1A1 and 1A2, is one mechanism by which increased 2-hydroxyestrogen concentrations may occur. It has also been suggested that the estrogen receptor (ER) may contribute to this anti-estrogenic effect by binding to antagonist(s) in cigarette smoke. METHODS: Gel retardation analysis was employed to determine if diluted mainstream cigarette smoke condensates (DMCSCs) could activate the aryl hydrocarbon receptor (AhR). AhR-regulated ethoxyresorufin-O-deethylase (EROD) activity and dioxin response element (DRE)-mediated luciferase induction were assessed in Hepa1c1c7 mouse hepatoma cells. A competitive ligand binding assay was utilized to determine if DMCSCs could bind to the ER. ER-dependent luciferase activity was assessed in MCF-7 cells. RESULTS: In gel retardation assays, DMCSCs induced a protein-DNA complex when incubated with a radiolabeled wild-type DRE oligonucleotide. The complex was effectively competed by excess unlabeled DRE but not by excess unlabeled mutant DRE. In Hepa1c1c7 mouse hepatoma cells transiently transfected with a DRE-regulated luciferase reporter gene, pGudluc1.1, treatment with DMCSCs resulted in a 23- and 25-fold increase in luciferase activity (P<0.01) and an 8.5- and 10.5-fold (P<0.01) induction in EROD activity, respectively. DMCSCs completely displaced bound tritiated E2 from the ER in a dose-dependent manner and induced ER-regulated luciferase activity significantly 6-fold (P<0.01), representing 86% of the maximal induction observed with E2. CONCLUSIONS: DMCSCs can bind to and transcriptionally activate the AhR and ER nuclear receptors and cause induction of DRE- and ER-regulated genes. Further study is required to identify the specific compound(s) responsible for these activities.