Background: More than 90% of the cigarettes sold worldwide have a filter. Nearly all filters consist of a rod of numerous ( > 12 000) plastic-like cellulose acetate fibres. During high speed cigarette manufacturing procedures, fragments of cellulose acetate that form the mouthpiece of a filter rod become separated from the filter at the end face. The cut surface of the filter of nearly all cigarettes has these fragments. In smoking a cigarette in the usual manner, some of these fragments are released during puffing. In addition to the cellulose acetate fragments, carbon particles are released also from some cigarette brands that have a charcoal filter. Cigarettes with filters that release cellulose acetate or carbon particles during normal smoking conditions are defective.Objective: Specific goals were to review systematically the writings of tobacco companies to: (a) identify papers that would document the existence of defective filters; (b) characterise the extent of the defect; (c) establish when the defect became known; (d) determine whether the defect exists on cigarettes marketed currently; (e) assess the prevalence of the defect on cigarettes manufactured by different companies; (f) define whether the knowledge of the defect had been withheld by the tobacco company as confidential and not disclosed publicly; and (g) ascertain the feasibility of correcting or preventing the defect.Methods: Document searches utilised databases of the scientific literature, medical journals, chemical abstracts, US Patents, Tobacco Abstracts, papers presented at tobacco meetings and court documents.Results: Sixty one documents of Philip Morris, Inc were selected for study because they disclosed specifically the “fall-out” of cellulose acetate filter fibres and, for cigarettes with charcoal filters, carbon particles from cigarette filters. The term “fall-out” was defined in 1985 laboratory protocols of Philip Morris, Inc. as “loose fibers (or particles) that are drawn out of the filter during puffing of the cigarette”. As early as 1957, the health concern of inhaling cellulose acetate fibres released from cigarette filters was addressed by Philip Morris, Inc. A 1962 document reported the results of laboratory tests conducted by Phillip Morris, Inc that compared the “fall-out” of cellulose acetate fibres from the filters of their cigarettes (Marlboro) and cigarettes of their competitor (Liggett & Meyers). A 1997 overview by Phillip Morris of documents addressing the “fallout of carbon particles and cellulose acetate fibers from filters” stated that they were “essentially routine reports” of cigarette filter assays, and referenced a “Filter Fallout” memo written in 1961—more than 40 years ago. Most likely these tests are being conducted presently as illustrated by a 1999 report that details the revisions of the “fall-out” protocol of Phillip Morris, Inc and reports the results of tests that measured the discharge of cellulose acetate fibres and silica gel from beta cigarettes with a new type of filter. Our analysis of the “fall-out” tests results presented in the 61 “fall-out” documents showed that filter fibres and carbon particles were discharged from the filters of all types of cigarettes tested. These cigarette types (n = 130) included both coded cigarettes and popular brand name cigarettes. No publications were found in the scientific literature of the “fall-out” studies. Thus, the results of the “fall-out” studies are thought to have been withheld as confidential to Philip Morris, Inc. We have identified also other companies that have tested recently cigarettes for defective filters. In addition, our searches have shown that simple, expedient, and inexpensive technologies for decontaminating cigarette filters of loose cellulose acetate fibres and particles from the cut surface of the filter have been developed and described in 1997 and 1998 US patents. What is more important is that these patents also define methods for preventing or reducing the broken plastic-like fibres that arise during cigarette making. Many US patents (n = 607; 1957 to 2001) have been awarded for cigarette filters. Some of these inventions describe novel materials and unique filtration schemes that would eliminate or minimise the discharge of filter materials into mainstream smoke.Conclusions: We have shown that: (a) the filter of today's cigarette is defective; (b) Philip Morris, Inc has known of this filter defect for more than 40 years; (c) the existence of this filter defect has been confirmed by others in independent studies; (d) many methods exist to prevent and correct the filter defect, but have not been implemented; and (e) results of investigations substantiating defective filters have been concealed from the smoker and the health community. The tobacco industry has been negligent in not performing toxicological examinations and other studies to assess the human health risks associated with regularly ingesting and inhaling non-degradable, toxin coated cellulose acetate fragments and carbon microparticles and possibly other components that are released from conventional cigarette filters during normal smoking. The rationale for harm assessment is supported by the results of consumer surveys that have shown that the ingestion or inhalation of cigarette filter fibres are a health concern to nearly all smokers.
Objective~~-To inspect cigarettes with a triple granular filter for charcoal granules on the cut filter surface and, if present, to determine whether the charcoal granules on the filter are released during smoking. Design-400 Lark cigarettes in 20 packs were examined individually by each of three investigators for the presence of charcoal granules on the cut surface of the cellulose acetate filter. Without removing the cigarettes from the pack, the filters were examined with a stereo zoom microscope for charcoal granules. The percentage of cigarettes that had charcoal granules was defined, and charcoal granules on each filter were counted. Randomly selected cigarettes were then smoked by consenting adult smokers to assess whether the charcoal granules were released during smoking. Lark cigarettes were smoked with a conventional cigarette holder that had been configured to contain an in-line membrane. After smoking, the membrane was analysed microscopically for charcoal granules and other components of the filter that had been released during smoking.Results-Charcoal granules were observed in 79,8% (319/400) of the cigarettes examined. The number of granules per cigarette was 3.3 (SD 3.7). Gaps between the tipping papers-the wrapping papers that surround the filter-were often seen (70%? 242 (71); n = 400 cigarettes). Further, the charcoal cavity was about 60% empty. For all smokers (n ~ 8/8), charcoal granules were released during smoking. The number of charcoal granules captured on the membranes was 22,5 (16.2) per cigarette. Conclusions-Charcoal granules are incorporated into cigarette filters to aid in removing toxins in cigarette smoke. In studies of Lark, a popular American cigarette with a charcoal filter, charcoal granules were observed on the filter surface, and were released from the filter when the cigarettes were smoked. During smoking, the toxin-containing charcoal granules are inhaled or ingested, The specific adverse health effects of inhaling or ingesting carbon granules have not been addressed; nevertheless, the smoker, as an educated consumer, should be informed of the possible health risks. (Tobacco Control 1997;6:33-40)
A novel surface membrane nonglycosylated acidic polypeptide (34 kDa), encoded by a structural gene on chromosome 11, has been identified using murine monoclonal antibody (MoAb) 53.6 (IgG2a). MoAb 53.6, raised against uninduced cells of a human erythroleukemia line (HEL), recognizes a surface membrane antigen that is displayed on proliferating (cell cycle phase G1, S, and M + G2 phase) human leukocytes. The expression and redistribution (i.e., patching and capping) of the p34 kDa antigen on 27 different long-term human hematopoietic cell (HHC) lines was defined by fluorescence microscopy. These lines had been established from patients with leukemia or healthy donors and included phenotypically defined populations of T cells, B cells, and myelomonocytic cells. Almost all (greater than 95%) of the leukocytes of the 27 lines reacted strongly with MoAb 53.6. The majority of the leukocytes displayed p34 kDa antigen patching (26/27 lines; patched cells, 96-100%); moreover, 20 of 27 lines exhibited p34 kDa antigen capping (capped cells, 8-96%). Presentation of the p34 kDa antigen on surface membrane ultrastructures, imaged with immunogold using an indirect antibody labeling procedure, was illustrated by scanning electron microscopy, and endocytosis of the gold-tagged antigen-antibody complex was studied by transmission electron microscopy. The HHC lines are thought to represent immortalized populations of different human leukocyte subsets that are in different stages of maturation and/or differentiation; thus these lines should prove useful as models for further characterizing this unique p34 kDa proliferation-associated antigen and for defining the mechanisms and significance of surface membrane antigen redistribution and modulation that has been associated with leukocyte activation and propagation.
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