Advantages and Disadvantages of Electronic Cigarettes

Electronic cigarettes (ECs) have been present on the consumer market for over a decade, and the number of related scientific publications in the PubMed database has now exceeded seven thousand. Despite the number of publications, there is still no consensus in the scientific community regarding their safety. However, it should be emphasized that a comparison of equivalent quantities of tobacco smoke and the aerosol produced from e-cigarettes showed that there was a significantly lower quantity of toxic compounds in the aerosol compared with the tobacco smoke. Therefore, the use of ECs could be seen as a way of reducing the health damage to cigarette smokers who cannot or are unwilling to quit using conventional methods. In addition, randomized studies are emerging suggesting that ECs could be useful in smoking cessation. On the other hand, ECs are now widely used among adolescents and may pose a serious risk of future nicotine dependence and health problems in this population, as they counteract their advantages in the population gained from smokers who quit using them. Therefore, as most authors stress, further research that will convincingly resolve the current controversies is needed. Clinicians urgently need evidence-based knowledge to better inform their patients about the use of these emerging tobacco products as a harm-reduction strategy, and regulators should regulate these products in ways that best serve public health, especially taking the youth population into account

Report of the Surgeon General

In 1964, the first Surgeon General's report on the effects of smoking on health was released. In the nearly 50 years since, extensive data from thousands of studies have consistently substantiated the devastating effects of smoking on the lives of millions of Americans. Yet today in the United States, tobacco use remains the single largest preventable cause of death and disease for both men and women. Now, this 2010 report of the Surgeon General explains beyond a shadow of a doubt how tobacco smoke causes disease, validates earlier findings, and expands and strengthens the science base. Armed with this irrefutable data, the time has come to mount a full-scale assault on the tobacco epidemic. More than 1,000 people are killed every day by cigarettes, and one-half of all long-term smokers are killed by smoking-related diseases. A large proportion of these deaths are from early heart attacks, chronic lung diseases, and cancers. For every person who dies from tobacco use, another 20 Americans continue to suffer with at least one serious tobacco-related illness. But the harmful effects of smoking do not end with the smoker. Every year, thousands of nonsmokers die from heart disease and lung cancer, and hundreds of thousands of children suffer from respiratory infections because of exposure to secondhand smoke. There is no risk-free level of exposure to tobacco smoke, and there is no safe tobacco product. This new Surgeon General's report describes in detail the ways tobacco smoke damages every organ in the body and causes disease and death. We must build on our successes and more effectively educate people about the health risks of tobacco use, prevent youth from ever using tobacco products, expand access to proven cessation treatments and services, and reduce exposure to secondhand smoke. Putting laws and other restrictions in place, including making tobacco products progressively less affordable, will ultimately lead to our goal of a healthier America by reducing the devastating effects of smoking. This 2010 Surgeon General's report represents another important step in the developing recognition, both in this nation and around the world, that tobacco use is devastating to public health. Past investments in research and in comprehensive tobacco control programs--combined with the findings presented by this new report--provide the foundation, evidence, and impetus to increase the urgency of our actions to end the epidemic of tobacco use.CDC-INFO Pub ID 220456220456U.S. Department of Health and Human Services. How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease: A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010.Chapter 1. Introduction, evaluation of evidence on mechanisms of disease production, and summary -- Chapter 2. The changing cigarette -- Chapter 3. Chemistry and toxicology of cigarette smoke and biomarkers of exposure and harm -- Chapter 4. Nicotine addiction: past and present -- Chapter 5. Cancer -- Chapter 6. Cardiovascular diseases -- Chapter 7. Pulmonary diseases -- Chapter 8. Reproductive and developmental effects -- Chapter 9. A vision for the future -- List of abbreviations -- List of tables and figures -- Definitions and alternative nomenclature of genetic symbols used in this report -- Index.2010704

Antioxidants in Health and Disease

Antioxidants in Health and Disease discusses the effects of dietary antioxidants and antioxidant supplementation in humans. It reviews the latest evidence-based research in the area, principally through prospective cohort studies and randomized controlled trials. The book assesses major dietary antioxidants and discusses their use in diseases such as cancer, diabetes, stroke, coronary heart disease, HIV/AIDS, and neurodegenerative and immune diseases. The use of antioxidants in health is also discussed along with common adverse effects associated with antioxidant use. Separating myth from fact, this book gives you insight into the true role of antioxidants in health and disease

Vehicular traffic exposure to polycyclic aromatic hydrocarbons and breast cancer risk

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental pollutants, known human lung carcinogens, and potent mammary carcinogens in animal models. However, the association between PAHs and breast cancer in women is unclear. Vehicular traffic is a major source of ambient PAH exposure. This study evaluates the association between residential exposure to vehicular traffic-related PAHs and risk of breast cancer, overall and by tumor subtype, and within strata of nucleotide excision repair and base excision repair genotypes and fruit/vegetable intake. For this population-based study, residential histories, dietary intake, and other factors were assessed in 1996-1997 for 1,508 newly diagnosed breast cancer cases and 1,556 controls. Residential traffic exposure estimates were reconstructed using a validated model for the years 1960 through 1995. The following single nucleotide polymorphisms were genotyped: ERCC1 8092C/A, OGG1 Ser326Cys, XPA -4A/G, XPD Lys751Gln and Asp312Asn, XPF Arg415Gln, XPG Asp1104His, XRCC1 Arg194Trp and Arg399Gln. Medical records and archived tumor tissue were used to determine case tumor subtype. In spline figures, which were used to inform quantile cutpoints for regression models, breast cancer risk was increased among women with the top 1% of traffic PAH exposures. Odds ratios (and 95% confidence intervals) for breast cancer, estimated using unconditional logistic regression, were modestly elevated for the top 5% of long-term 1960-1990 traffic PAH exposure estimates, compared with below the median (1.44 (0.78, 2.68)). Associations between recent traffic exposure in 1995 (top 5% vs. below the median) and breast cancer were attenuated toward the null (1.14 (0.80, 1.64)), but were stronger among women with low fruit/vegetable intake (1.46 (0.89, 2.40)) and hormone-receptor negative tumors (1.67 (0.91, 3.05)). Associations were approximately two- to three-fold stronger among women with variant alleles for XPD (Lys751Gln) and XRCC1 (Arg194Trp), and wild-type alleles for XRCC1 (Arg399Gln) and OGG1 (Ser326Cys), when comparing the upper and lower tertiles of traffic exposure during 1995 or 1960-1990. This study reports positive associations between traffic-related PAH exposure and breast cancer risk among women with comparatively high long-term traffic exposures or among those with certain DNA repair genotypes, low fruit/vegetable intake or hormone receptor negative tumors, although confidence intervals were wide.Doctor of Philosoph

Molecular Genetic Changes During Tumour Progression in Mouse Skin

This thesis describes the development of a model to analyse the genetic changes associated with tumour progression in mouse skin. Tumours were induced in F1 hybrid mice, thereby permitting the use of heterozygous DNA markers (restriction fragment length polymorphisms) to determine the role of allele loss in papilloma and carcinoma development. Frequently, initiation of mouse skin carcinogenesis involves H-ras activation. This gene is located on mouse chromosome 7. The F1 hybrid tumour model was used to demonstrate that tumours with this mutation also show loss of heterozygosity (LOH) or imbalance of alleles on chromosome 7 at a very high frequency. Thus LOH may indicate the presence of an oncogene, although it is often equated with tumour suppressor gene loss. Most frequently the alterations involved non-disjunction, but in some cases mitotic recombination or deletion was detected. These gross chromosome changes were not observed in mouse skin tumours lacking activated H-ras. Thus, it is clear that the initiation event can influence the type of alterations which occur at later stages of tumour progression. In the majority of cases, gross chromosome 7 changes result in an increased copy number of mutant H-ras and under-representation or loss of the normal allele, indicating that mutant H-ras is involved in both the initiation and progression of mouse skin tumours. It may be that elevation of the mutant signal is required to overcome a suppressive effect of the normal allele. In addition, because elevation of mutant H-ras gene copy number occurs by gross chromosomal mechanisms, it is possible that another chromosome 7 gene is also involved in tumour progression. In support of this, mitotic recombination or deletion was detected distal to H-ras in 4/26 of the chemically induced tumours with activated H-ras. In addition, a chromosome 7 alteration was detected in a v-H-ras initiated tumour, further evidence that a gene other than H-ras on this chromosome is involved in tumour progression. Human tumours frequently demonstrate LOH at the chromosomal region 11p 15.5, which is syntenic with the part of mouse chromosome 7 that encompasses the H-ras locus. Thus, the homologue of a tumour suppressor gene in this region of human chromosome 11 may be involved in mouse skin tumour development. The Wilms' tumour locus, also on human 11p, is on mouse chromosome 2. RFLP analyses provided no evidence that this gene has a role in mouse skin tumorigenesis. The non-random nature of chromosome 7 changes was supported by the low frequency of alterations on chromosomes 2 and 11. Two carcinomas did show LOH of a marker on the latter. Interestingly, this chromosome contains a region homologous to human chromosome 17p, which is involved in colorectal cancer. Minisatellite analysis also supported the non-random nature of chromosome 7 changes. Loss or rearrangement of minisatellite bands tended to involve hypervariable loci, suggesting that these were random rearrangements at unstable loci. In some human cancers genomic imprinting influences the direction of allele loss on 11p. However, this did not appear to be the case with LOH on chromosome 7 in mouse skin carcinomas. The parental strain also did not influence which alleles were under-represented in these tumours. Some important differences were detected between the genetic changes associated with carcinomas induced by initiation/promotion and those seen in carcinomas obtained by repeated carcinogen treatment. A similar proportion of MNNG/TPA and MNNG/MNNG carcinomas were positive for mutant H-ras. However, whereas non-disjunction of chromosome 7 had also occurred in the former, no chromosome 7 changes were detected in carcinomas induced by repeated MNNG treatment. This carcinogen may remove the need for additional chromosome 7 changes by mutating the gene(s) affected by these events in TPA-promoted tumours, or by altering entirely separate loci. In contrast, tumours induced with repeated DMBA treatment which were positive for activated H-ras also had chromosome 7 changes. However, the frequency of events such as mitotic recombination or deletion was much higher in these tumours than in carcinomas induced by an initiation/promotion regime. The major difference between DMBA/DMBA carcinomas and DMBA/TPA carcinomas was that the latter contained a much higher proportion of tumours which lacked activated H-ras. Thus it appears that repeated DMBA treatment stimulates the growth of initiated cells which are insensitive to TPA. Analysis of papillomas showed that gross chromosome 7 changes occur at a premalignant stage of tumorigenesis. This may suggest a tumour promoter-related genetic effect

Antioxidant and DPPH-Scavenging Activities of Compounds and Ethanolic Extract of the Leaf and Twigs of Caesalpinia bonduc L. Roxb.

Antioxidant effects of ethanolic extract of Caesalpinia bonduc and its isolated bioactive compounds were evaluated in vitro. The compounds included two new cassanediterpenes, 1α,7α-diacetoxy-5α,6β-dihydroxyl-cass-14(15)-epoxy-16,12-olide (1)and 12α-ethoxyl-1α,14β-diacetoxy-2α,5α-dihydroxyl cass-13(15)-en-16,12-olide(2); and others, bonducellin (3), 7,4’-dihydroxy-3,11-dehydrohomoisoflavanone (4), daucosterol (5), luteolin (6), quercetin-3-methyl ether (7) and kaempferol-3-O-α-L-rhamnopyranosyl-(1Ç2)-β-D-xylopyranoside (8). The antioxidant properties of the extract and compounds were assessed by the measurement of the total phenolic content, ascorbic acid content, total antioxidant capacity and 1-1-diphenyl-2-picryl hydrazyl (DPPH) and hydrogen peroxide radicals scavenging activities.Compounds 3, 6, 7 and ethanolic extract had DPPH scavenging activities with IC50 values of 186, 75, 17 and 102 μg/ml respectively when compared to vitamin C with 15 μg/ml. On the other hand, no significant results were obtained for hydrogen peroxide radical. In addition, compound 7 has the highest phenolic content of 0.81±0.01 mg/ml of gallic acid equivalent while compound 8 showed the highest total antioxidant capacity with 254.31±3.54 and 199.82±2.78 μg/ml gallic and ascorbic acid equivalent respectively. Compound 4 and ethanolic extract showed a high ascorbic acid content of 2.26±0.01 and 6.78±0.03 mg/ml respectively.The results obtained showed the antioxidant activity of the ethanolic extract of C. bonduc and deduced that this activity was mediated by its isolated bioactive compounds

Toxicological profile for chlorinated dibenzo-p-dioxins : (Update)

prepared by Research Triangle Institute ; prepared for U.S. Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry."Under Contract No. 205-93-0606."--T.b."December 1998."Also available via the World Wide Web (accessed 2009 September 30).Includes bibliographical references (p. 543-672)