Hazardous Cigarette Research Articles

Waste cigarette butt derived Carbon/Magnesium oxide nanocomposite as potential adsorbent for the removal of ciprofloxacin from waste water

The waste cigarette butts (CB) are intractable pollutant and poses severe threat to environmental health. In a quest to convert hazardous waste into valorization product, we prepared carbon from CB and synthesized carbon supported Magnesium oxide nanoparticle (C@MgO) using a microwave-assisted method. The prepared C@MgO possess high surface area (128 m2g−1) and strong adsorption property for CIP with high adsorption capacity of 556 mg/g. The adsorption experiment follows pseudo second-order kinetics and Langmuir isotherm. This work provide new insight into valorization of hazardous waste cigarette butts into useful product for environmental remediation.

Effects of cigarette butts on marine keystone species (Ulva lactuca L. and Mytilus edulis L.) and sediment microphytobenthos

Outdoor mesocosms with constantly flowing natural seawater were used to test the effects of littered cigarette butts on the filter feeder Mytilus edulis (blue mussel), the macroalga, Ulva lactuca (sea lettuce) and sediment microphytobenthos in a semi-natural marine setting. Either conventional, cellulose acetate, or biodegradable, cellulose, smoked cigarette butts were added at densities of 0.25 or 1 butt L−1. The clearance rates of mussels exposed to 1 butt L−1 of cellulose acetate butts were three times less than the controls. The growth of U. lactuca was not measurably affected by cigarette butts, however the sediment chlorophyll content was significantly less in mesocosms exposed to 0.25 and 1 butt L−1 of cellulose acetate butts. These effects occurred despite constant replacement of seawater indicating how hazardous conventional cigarette butts are to marine life. Biodegradable cellulose cigarette butts had minimal effects on the measured variables but should still not be discarded as litter.

A simple dilute-and-shoot method for screening and simultaneous quantification of nicotine and alkaloid impurities in electronic cigarette refills (e-liquids) by UHPLC-DAD

The electronic cigarette (e-cigarette) has emerged as a popular alternative to the traditional hazardous tobacco cigarette. The substantial increase in e-cigarette use also urgently calls for controlling the quality of e-cigarette refill liquid products (e-liquids). Currently, the most important quality indicator of e-liquid products is the quantification of nicotine and its related impurities. Although different methods have been published to measure nicotine and impurity levels, the majority of them use a targeted LC-MS/MS approach. There is, however, a need for more robust quantification methods that are easy to implement in most control (industrial and governmental) laboratories. Therefore, in this study, a simple dilute-and-shoot UHPLC-DAD method has been developed and validated for the simultaneous quantification of nicotine and its alkaloid impurities in electronic cigarette refills. An optimal separation of the alkaloids was achieved in a runtime of 11 min. The method was successfully validated using the “total error” approach in accordance with the validation requirements of ISO-17025. During this validation, interference between the target components and a number of popular flavouring compounds such as vanillin, maltol, ethylacetate, etc. could be excluded. In addition, small changes to the column temperature, pH and molar concentration of the mobile phase buffer were deliberately introduced in order to assess the robustness of the method. Only a slightly different outcome between the newly developed UV-detection method and the targeted MS approach was found, due to the sensitivity of the different detection techniques. However, in the context of quality control of nicotine related impurities, for which the European Pharmacopoeia limits are currently applied, the sensitivity of the UHPLC-DAD method was found to be within the acceptable range. Despite the somewhat lower selectivity of the newly developed UV-detection technique versus a targeted LC-MS/MS approach, it may be concluded that this method is a suitable alternative for quality control purposes.

Hazardous Alcohol Drinking as Predictor of Smoking Relapse (3-, 6-, and 12-Months Follow-Up) by Gender

Diverse studies have found a relation between alcohol consumption and smoking relapse. Few studies have analyzed the relation of smoking relapse with pretreatment alcohol consumption and gender differences. The main purpose of this study is to analyze the influence of alcohol consumption in smoking relapse over 12 months (3-, 6-, and 12-months follow-up) and to determine possible gender differences. The sample included 374 smokers who quit smoking by participating in a psychological smoking cessation treatment. We assessed hazardous pretreatment alcohol drinking (AUDIT), cigarette consumption (FTND; number of cigarettes) and sociodemographic variables. Higher scores on hazardous pretreatment alcohol drinking predict smoking relapse at 3-, 6-, and 12-months after smoking cessation. In males, higher scores on hazardous pretreatment alcohol drinking predict relapse at 6 and at 12 months. In females, higher scores on hazardous pretreatment alcohol drinking predict tobacco relapse at 3 months. Hazardous pretreatment alcohol drinking predicts relapse at all intervals after smoking cessation (3-, 6-, and 12-months follow-up). However, the influence of hazardous pretreatment alcohol drinking on smoking relapse differs as a function of gender, as it is a short-term predictor in women (3 months) and a long-term predictor in men (6 and 12 months).

Longitudinal assessment of mental disorders, smoking, and hazardous drinking among a population-based cohort of US service members.

Combat exposure is known to increase the risk for mental disorders; however, less is known about the temporal relationship between mental disorders and alcohol misuse or smoking. To better understand these interrelationships, this study investigated mental disorders in association with hazardous drinking and cigarette smoking. Using data from a large population-based military cohort, standardized instruments were used to screen for posttraumatic stress disorder, depression, panic, and other anxiety syndromes. Self-reported use of cigarettes and hazardous drinking was also assessed. Subjects were classified as having "new-onset," "persistent," or "resolved" mental disorders and health risk behaviors on the basis of screening results from baseline to follow-up (n = 50,028). Multivariable logistic regression models were used to investigate temporal patterns between the development of mental disorders and the uptake of smoking or hazardous drinking. The strongest associations of new-onset mental disorders were among those who newly reported smoking or hazardous drinking (odds ratio [OR], 1.82; 95% confidence interval [CI], 1.28-2.59 and OR, 2.49; 95% CI, 2.15-2.89, respectively), even after adjustment for combat deployment experience. In addition, persistent smokers and hazardous drinkers had elevated odds for developing a mental disorder at follow-up. This study demonstrates a positive association between the onset of mental disorders with the uptake of smoking and hazardous drinking and the likelihood that multiple temporal sequence patterns exist to explain the relationship between mental disorders and hazardous drinking and smoking. Clinical approaches to mitigate deployment-related mental disorders should include alcohol and tobacco-related assessments and interventions.

ANTIMUTAGENIC EFFECTS OF TANNIC ACID ON SOMATIC AND GERM CELLS OF RATS

There is increasing interest in identification of naturally occurring substances that may be capable in diminishing genotoxicity of the environmental carcinogens and still serve as leads for the development of novel pharmacological agents. Many such medicinal plants have hepatoprotective, neuroprotective, antiinflammatory and also antioxidant or radical-scavenging properties (Najmi et al., 2010; Zhang et al., 2010). Phenolic acids are secondary metabolites widely distributed in the plant kingdom and they come in the second priority after flavonoids in terms of their dominance. Tannic acid is a plant polyphenol which is found, along with other condensed tannins, in several beverages including red wine, beer, coffee, black tea, green tea, and many foodstuffs such as grapes, pears, bananas, sorghum, black-eyed peas, lentils and chocolate (Erexson, 2003; Bennett et al., 2010). Similar to many polyphenols, tannic acid has been shown to possess antioxidant (Ferguson, 2001; Wu et al., 2004; Andrade et al., 2005), antimutagenic (Ferguson, 2001; Chen and Chung, 2000) and anticarcinogenic properties (Huang et al., 2010; van der Logt et al., 2003). The antioxidant mechanism of tannic acid is still far from being fully understood; therefore, it requires further investigation. For example, in the presence of copper ions, tannic acid acts either as a prooxidant, promoting DNA damage (Ferguson, 2001; Khan et al., 2000), or as an antioxidant, suppressing hydroxyl radical formation (Andrade et al., 2005). Tannic acid is always used as a food additive. Its safe dosage ranges from 10 to 400 mg, depending on the type of food to which it is added (Chen and Chung, 2000). Also, several authors have demonstrated that tannic acid and other polyphenols have antimutagenic and anticarcinogenic activities (Ferguson, 2001; Andrade et al., 2005; Huang et al., 2010; van der Logt et al., 2003). Moreover, the consumption of polyphenol-rich fruits, vegetables, and beverages, such as tea and red wine, has been linked with inhibitory and preventive effects in various human cancers and cardiovascular diseases, which may be related-at least in part-with the antioxidant activity of polyphenols (Andrade et al., 2005). Phenolic acids have been shown to be anti-oxidant and it is a potent antagonist of the mutagenicity of polycyclic aromatic hydrocarbons (PAHs) such as benzo(a)pyrene (BaP) (Mansour et al., 2007). Benzo(a)pyrene is a semi-volatile, lipophilic, high molecular weight compound that belongs to the polycyclic aromatic hydrocarbon (PAH) family. Benzo(a)pyrene and other PAHs are products of combustion and can accumulate in crops via absorption from contaminated soils (ATSDR, 1995). Exclusive sources for BaP contamination of the environment and consequently human exposures include industrial and automobile emissions, hazardous waste sites, cigarette smoke, biomass burning, municipal incinerators, volcanic eruptions, home heating, and consumption of charcoal broiled and smoked foods (ATSDR, 1995; WHO, 1998). Food ingestion and inhalation are the major routes of entry into the human body for a large section of the general population exposed to PAHs (Ramesh et al., 2004). The previous experimental data has shown that PAHs must be metabolically activated by peroxy radical dependent pathway and the electrophilic bay-region diol-epoxides act as the ultimate carcinogenic metabolites of PAH (Li et al., 2004). This study aimed to investigate the multifunctional antioxidant properties of tannic acid on BaP-induced genotoxicity in somatic and germ cells of rats.

Cigarettes Butts and the Case for an Environmental Policy on Hazardous Cigarette Waste

Discarded cigarette butts are a form of non-biodegradable litter. Carried as runoff from streets to drains, to rivers, and ultimately to the ocean and its beaches, cigarette filters are the single most collected item in international beach cleanups each year. They are an environmental blight on streets, sidewalks, and other open areas. Rather than being a protective health device, cigarette filters are primarily a marketing tool to help sell ‘safe’ cigarettes. They are perceived by much of the public (especially current smokers) to reduce the health risks of smoking through technology. Filters have reduced the machine-measured yield of tar and nicotine from burning cigarettes, but there is controversy as to whether this has correspondingly reduced the disease burden of smoking to the population. Filters actually may serve to sustain smoking by making it seem less urgent for smokers to quit and easier for children to initiate smoking because of reduced irritation from early experimentation. Several options are available to reduce the environmental impact of cigarette butt waste, including developing biodegradable filters, increasing fines and penalties for littering butts, monetary deposits on filters, increasing availability of butt receptacles, and expanded public education. It may even be possible to ban the sale of filtered cigarettes altogether on the basis of their adverse environmental impact. This option may be attractive in coastal regions where beaches accumulate butt waste and where smoking indoors is increasingly prohibited. Additional research is needed on the various policy options, including behavioral research on the impact of banning the sale of filtered cigarettes altogether.

Lessons from the history of tobacco harm reduction: The National Cancer Institute's Smoking and Health Program and the “less hazardous cigarette”

Scientists and public health practitioners are sharply divided today over the risks and benefits of tobacco harm-reduction strategies. At the same time, a range of novel tobacco products is being marketed with claims of reduced exposure or risk. Current scientific efforts to study tobacco products and harm reduction should be informed by past experience. During the 1960s and 1970s, there was substantial support within government and academia, as well as among voluntary health organizations, for efforts to modify tobacco products to reduce harm. This paper analyzes the former National Cancer Institute (NCI) Smoking and Health Program, which, between 1968 and 1980, pursued the development of "less hazardous" cigarettes as its primary goal. During this period, the program spent over dollar 50 million on contract research, of which 74% went toward biological and chemical analysis of modified cigarettes, 9.6% to epidemiological studies of risk factors, and only 1.4% to studies evaluating smoking cessation or prevention programs. NCI officials predicted during the mid-1970s that new "low-tar" cigarette brands would substantially reduce smoking-related mortality, but by 1978 the research agenda began to change in response to a reorganization of NCI research activities, modification of government antismoking efforts, and an emerging understanding of nicotine addiction that challenged key scientific assumptions. In retrospect, the program suffered from significant weaknesses that severely limited the likelihood that it would generate knowledge beneficial to public health, including a research agenda that failed to include surveillance and behavioral research, tobacco industry influence of the research agenda, and a lack of access to information about the characteristics of products on the market. There exists today a need for a public health-oriented research agenda on tobacco products and harm reduction, but current efforts should include input from a diverse range of disciplines, collect data on users' behavior, and limit the involvement of industry scientists.

FAIRCHILD AND COLGROVE RESPOND

We appreciate the thoughtful comments and concerns of Giovino, who was intimately involved in the Institute of Medicine’s (IOM’s) assessment of the scientific basis for tobacco harm reduction. We did not state, nor did we intend to imply, that the IOM report was primarily about less hazardous cigarettes. Further, we took care to describe the report as “endorsing harm reduction only ‘as a component of a comprehensive national tobacco control program that emphasizes abstinence-oriented prevention and treatment.’ ” We recognize that the term “safer cigarette” is problematic. But our purpose in the article was to analyze the historical evolution of public health thinking about “safer” products. The belief that such products were possible was central to that history, as was the use of the term “safer cigarettes.” We believe that others who, like us, are interested in how broadly the public health community defines harm reduction in the coming years and what place tobacco products will occupy within that framework will appropriately read the IOM report as stating the need to face squarely the challenge of tobacco-based products.

The Institute of Medicine report on smoking: a blueprint for a renewed public health policy.

The Institute of Medicine report on smoking: a blueprint for a renewed public health policy.

Assessing underlying mechanisms of quinoid-induced hematopoietic cell toxicity.

Within the bone marrow are a number of cell populations that can serve as potential targets of xenobiotics and/or their metabolites (Trush et al., 1996). These include the hematopoietic and lymphopoietic stem cells, committed progenitors, mature functional blood cells and the cells that comprise the bone marrow stromal microenvironment. The altered function of different populations probably results in the manifestation of different toxicities. Two environmental chemicals that have been linked with toxicity to the bone marrow are benzene and benzo(a)pyrene (BP). There is continued concern about human exposure to benzene arising from a variety of sources including certain occupational settings, hazardous waste sites, automobiles and cigarette smoking. Exposure of humans to benzene is associated with the development of aplastic anemia and leukemia. Polycyclic aromatic hydrocarbons (PAHs), such as BP, have been shown to be myelotoxic in animals (Legraverend et. al., 1983). For example DBA/2 mice, with the Ahd/Ahdgenotype, develop an aplastic anemia-like condition and leukemia in response to orally administered benzo(a)pyrene. In this regard, diet is considered a major route of exposure to PAHs in humans (Buckley and Lioy, 1992). Whether dietary PAHs pose a risk to human bone marrow in poorly investigated from either an experimental or an epidemiologic perspective. The bone marrow toxicity of both benzene and BP has been linked to their biotransformation. Interestingly, both compounds are metabolized to quinone derivatives: benzene to hydroquinone; BP to 1,6-, 3,6-, and 6,12-quinone. Because of the importance of the bone marrow stromal microenvironment, we have studied the toxicity of hydroquinone and BP-derived quinones to stromal cells obtained from DBA/2 mice (Twerdok et al., 1992; Zhu et al., 1995).

Public Health Policies regarding Hazardous Waste Sites and Cigarette Smoking: An Argument by Analogy

Research ArticleOpen AccessPublic health policies regarding hazardous waste sites and cigarette smoking: an argument by analogy. M S Legator, and S F Strawn M S Legator Division of Environmental Toxicology, University of Texas Medical Branch, Galveston 77550. Search for more papers by this author and S F Strawn Division of Environmental Toxicology, University of Texas Medical Branch, Galveston 77550. Search for more papers by this author Published:22 April 1993https://doi.org/10.1289/ehp.931018AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit FiguresReferencesRelatedDetails Vol. 101, No. 1 April 1993Metrics About Article Metrics Publication History Originally published1 April 1993Published in print22 April 1993 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.

Yields of selected toxic agents in the smoke of Canadian cigarettes, 1969 and 1978. A decade of change?

Canadian sales-weighted averages of cigarette carbon monoxide (CO) and tar have been evaluated for the decade ending 1979. Virtually no change occurred up to 1976; between 1976 and 1979 the sales-weighted average CO dropped from 21 to 16 mg with a much smaller decrease in the corresponding values for tar (16.1 to 14.4 mg). Thus changes in CO deliveries did not take place at the same rate as changes in tar deliveries. If standardized smoking machine yields are related to the risk of smoking-related morbidity and mortality, the low correlation and the 8-year lag time in the curves describing the decrease in two of the major toxic constituents of cigarette smoke may be of importance in helping to explain a lower impact of less hazardous cigarettes on coronary heart disease (CHD) rates. Assuming that exposure to CO is a risk factor for CHD, the relatively recent reduction in sales-weighted CO yields might have the effect of decreasing CHD rates among smokers in the future. In addition to CO yields, HCN, acrolein, and total aldehyde yields of 25 brands of cigarettes manufactured in 1969 were compared with yields of the same cigarettes manufactured in 1978 in order to assess changes which may have occurred in other gas phase constituents. Significant decreases were noted in the yields of all constituents other than CO; the average decrease per brand was HCN, 69 μg; total aldehydes, 114 μg, and acrolein, 5.2 μg.

Estimating the hazards of less hazardous cigarettes. II. Study of cigarette yields of nicotine, carbon monoxide, and hydrogen cyanide in relation to levels of cotinine, carboxyhemoglobin, and thiocyanate in smokers.

Yields of chemical constituents such as tar, nicotine, CO, and HCN defined by smoking machines are commonly assumed to provide a reasonable indication of the relative hazard associated with smoking a given brand of cigarette. Results reported here suggest that this assumption should be carefully reexamined. A total of 240 subjects, representing a wide range of smoking and brand characteristics, were recruited for an investigation of possible relations between brand yields and exposure (levels of carboxyhemoglobin, breath CO, plasma cotinine, plasma thiocyanate, and saliva thiocyanate). Exposure was highly correlated with consumption (number of cigarettes per day), but their was no correlation between any estimate of exposure and brand yield when level of consumption was held constant. In addition, a comparison of levels of carboxyhemoglobin and plasma thiocyanate for 16 smokers of "low-hazard" and 15 smokers of "high-hazard" cigarette brands revealed little difference between the two groups, even though average cigarette yields differed as much as 2- to 3-fold. A possible explanation for the results may be that current values for average puff volume, duration, and interval differ significantly from those used in programming smoking machines, particularly in the case of brands with low nicotine delivery.

Less Hazardous Cigarette Debated

Less Hazardous Cigarette Debated

Toward Less Hazardous Cigarettes

To Editor.— In a recent issue ofThe Journal, Gio Gori, PhD, and Cornelius Lynch, PhD, report on [c]ritical levels of selected cigarette smoke constituents... expressed in terms of pre-1960 cigarettes that a smoker may consume without increasing his mortality risk substantially above that of a nonsmoker. These critical levels are translated into equivalent numbers of present-day low tar and nicotine cigarettes in order to provide information to help the smoker to wean himself to progressively less hazardous cigarettes. While authors' motivation is beyond reproach, their analysis is predicated on some highly questionable assumptions that, if wrong, challenge validity of their conclusion. Here I will note only two such assumptions. First, vast majority of current regular (eg, pack-a-day) smokers inhale. Hence, for a meaningful comparison between present-day low tar and nicotine cigarette smoking and pre-1960 ingestion of smoke constituents, latter must be associated with

Development of less hazardous cigarettes

To the Editor.— Our recent article inThe Journal(240:1255, 1978) on current advances in the development of less hazardous cigarettes resulted in scores of letters to us from physicians, scientists, and other concerned citizens. Two such letters, addressing the extremely important issues of the inhalation practices of smokers and of additives used in the manufacture of commercial brand cigarettes, are to be published inThe Journal, with our comments. We would like to take the opportunity here to clarify additional issues that were raised during the ensuing mass media coverage of our findings. It should be emphasized at the outset, however, that our article was intended to be evaluated on its merits by the readers ofThe Journaland was not intended for general mass media distribution. It was stated in the lay press that our analyses were statistical manipulations of data from short-term animal studies. However, neither animal

Development of Less Hazardous Cigarettes

<h3>To the Editor.—</h3> Our recent article inThe Journal(240:1255, 1978) on current advances in the development of less hazardous cigarettes resulted in scores of letters to us from physicians, scientists, and other concerned citizens. Two such letters, addressing the extremely important issues of the inhalation practices of smokers and of additives used in the manufacture of commercial brand cigarettes, are to be published inThe Journal, with our comments. We would like to take the opportunity here to clarify additional issues that were raised during the ensuing mass media coverage of our findings. It should be emphasized at the outset, however, that our article was intended to be evaluated on its merits by the readers ofThe Journaland was not intended for general mass media distribution. It was stated in the lay press that our analyses were statistical manipulations of data from short-term animal studies. However, neither animal

Conference on indications for tonsillectomy and adenoidectomy

<h3>To the Editor.—</h3> Our recent article inThe Journal(240:1255, 1978) on current advances in the development of less hazardous cigarettes resulted in scores of letters to us from physicians, scientists, and other concerned citizens. Two such letters, addressing the extremely important issues of the inhalation practices of smokers and of additives used in the manufacture of commercial brand cigarettes, are to be published inThe Journal, with our comments. We would like to take the opportunity here to clarify additional issues that were raised during the ensuing mass media coverage of our findings. It should be emphasized at the outset, however, that our article was intended to be evaluated on its merits by the readers ofThe Journaland was not intended for general mass media distribution. It was stated in the lay press that our analyses were statistical manipulations of data from short-term animal studies. However, neither animal

Threshold Theory vs Linear Theory

To the Editor.— Certainly inclusion of the article Toward Less Hazardous Cigarettes: Current Advances (240:1255, 1978) is appropriate for a publication such asThe Journal. I do not believe it necessary, therefore, to apologize for its inclusion. (Or was the editorial Smoke Screens an apology for its delay in inclusion?) Certainly the reminder of the tangled web that politics weaves with regard to this article is of interest. I doubt that this comes as a surprise to any of the readers and serves only to strengthen the wish that government and politics have as little to do in medicine as possible. Dr Barclay's comments (240:1271, 1978) with regard to the threshold theory vs linear theory of toxic action are interesting. I for one am not as certain that most scientists believe in the linear theory. Certainly our goals of environmental protection for various toxic substances are often thresholds for whatever