Why do cigarette filters have holes

Rates of adenocarcinoma of the lung, the lung cancer most associated with smoking, have more than quadrupled in men and increased eight-fold in women along with changes in the design and composition of cigarettes since the s, the researchers write.

Shields and his team review the evidence linking cigarette filter ventilation to these increased rates of lung cancer in a report online May 22nd in the Journal of the National Cancer Institute.

Filter ventilation reduces the amount of tar in the cigarette smoke when tested on smoking machines, but the increased ventilation and slower tobacco burn result in more puffs per cigarette and more toxic cancer-causing chemicals being inhaled by smokers, they write. The holes let them actually inhale more smoke with more cancer-causing agents. Increased filter ventilation also results in smaller particle size, allowing more smoke to reach vulnerable parts of the lung.

So, he will adapt his behaviour. The smoker will take more drags, inhale more deeply and partially block the filter holes with his lips or fingers. In the ISO method, every minute, a millilitre drag is taken. In the Canadian Intense protocol, every thirty seconds a millilitre drag is taken.

Ministry of Health, Welfare and Sport. The screen turns light blue and white. On-screen text: Want to learn more about filter ventilation in cigarettes? Surf to: rivm. An RIVM production, copyright Tomorrow's care begins today. Want to know more about filter ventilation in cigarettes? Nederlands English. RIVM Committed to health and sustainability.

Home Tobacco Filter ventilation Filter ventilation. Why do cigarette filters have holes? Text description On-screen title: Filter ventilation in cigarettes. In some cigarettes, the holes are visible to the naked eye. Our view is that those 10 percent ventilation-rate cigarettes are probably more dangerous than zero percent. Maybe the person ends up wired and anxious, and so desires only more wine, and ends up drinking three bottles of this horrible coffee-wine concoction.

But it has taken decades for the effects of these products to come to light. And the public-health community would endorse it—at least a step in the right direction—because they had a lower tar yield.

I asked some friends who smoke constantly if there is a belief in the young-smoker community that filtered cigarettes are healthier, and the consensus was nah.

By wet she was referring to the fact that filters are made to withstand dissolving in saliva—which means they linger on city streets and pile up on highways even while the rest of the cigarettes quickly dissolve and disintegrate. The global landscape would look dramatically different if cigarette filters fell out of use.

The money saved cleaning them up could be put to other use in bettering communities, the benefits of which are incalculable. Where was I? Oh yes. Even if the industry-generated health halo were totally dissolved by now, given the choice between smoking ten filtered cigarettes per day or ten unfiltered, Shields believes people would probably be better off with the filterless.

Nevertheless, consistent with the clinical trials, these studies Supplementary Table 6, available online demonstrate that exposure biomarkers are not statistically reduced when smoking cigarettes with differing tar yields and filter ventilation, except for perhaps some comparisons of the most extreme differences in tar yields 25 , 89 , , — This study showed few differences in biomarkers based on tar yields, and statistical differences were reported only for the most extreme comparisons of tar yields , , Tar yield was substantially less of a predictor for nicotine exposure compared with number of cigarettes per day, nicotine dependence, and puff topography.

Other studies, albeit smaller, show similar results 25 , , , , In summary, the consistency of the human clinical trials and cross-sectional studies demonstrates that lower machine tar yields do not predict lower exposures determined by biomarkers of exposure.

And actually, puff volumes increase for smokers of cigarettes with more ventilation, suggesting greater exposures in the lung. Reported results in cross-sectional studies of lower biomarkers for smokers of cigarettes with the most ventilation may be due to the characteristics of the smokers choosing these cigarettes rather than the tar yields affected by ventilation It can be noted that these studies do not support a causal relationship for filter ventilation and lung adenocarcinoma because they do not show increased levels of blood and urinary biomarkers.

However, the above studies are somewhat limited in study design, do not measure exposure at the lung level, do not include validated biomarkers of harm, and the urine and blood studies might not be a surrogate for changes in lung exposure because of rapid absorption of carcinogens through the lung. As early as , filter ventilation was recognized by the tobacco industry to produce a smoke that is less strong, harsh, and irritating 58 , — This led smokers to believe that they are smoking a product that is less harmful , , Most smokers are unaware of the presence of filter ventilation leading to this effect , , although some might subconsciously partially block the holes with their fingers 23 , These perceptions were reinforced by implicit and explicit advertising claims about safer cigarettes 20 , 23 , 34 , , , — Although tar yield descriptors are currently prohibited, the messaging remains because the coloring and packaging has not changed , , and smokers retain their misperceptions about health effects based on the character and sensory effects of the smoke 20 , 23 , 34 , , , — Thus, an added adverse impact of filter ventilation is the fostering of a false belief that a lower-tar cigarette is a healthier cigarette.

The process of inhalation is separate from puffing for most smokers and is a multistep process of mouth-holding followed by inhalation — Filter ventilation allows smokers to have higher puff volumes and to take more frequent puffs 42 , making more toxicants available to be inhaled to deeper parts of the lungs and allowing for greater retention of nicotine and toxic chemicals 42 , — , To date, there are inconsistent results as to whether cigarettes with different tar yields directly influence inhalation, separate from allowing for more smoke to enter the lungs because of larger puff volumes, although the consensus within the academic community is that the depth of inhalation increases with greater filter ventilation 1 , 42 , 97 , , , , — There is no validated method to assess inhalation for smoking, and the inconsistencies may relate to variations in methodologies, use of unnatural environments eg, use of smoke chambers, constricting bands around the chest, and radiotracer studies , small study size, and inadequate study design eg, single use or limited use.

Importantly, many smoke constituents, such as nicotine, are rapidly absorbed through the lungs so that biomarker studies of the urine and blood might not reflect local lung exposures, and there is evidence for differential retention of particulate matter constituents such as TSNAs 97 , , , Smoke reaching the most distal parts of the lung, where air flow decreases, allows for easier sedimentation of the particles.

Also, particles may grow in size and water content in the lungs, allowing for more deposition and retention of particles with higher amounts of smoke toxicants due to filter ventilation , , To validate this in humans, smoke distribution and retention would need to be directly measured, but these methodologies do not exist.

There is some data for smoke distribution using experimental animal studies and modeling, but these are not developed based on actual smoking behavior data, which likely underestimate deposition , These models also do not account for flow of the gas phase chemicals or account for changes in filter ventilation.

In summary, there is conflicting data to conclude that filter ventilation increases depth of inhalation. Furthermore, how particles distribute in the lung generally is unclear, and this has not been studied with respect to filter ventilation specifically. However, a logical inference is that smokers with larger puff volumes due to cigarette elasticity will make more smoke available to travel deeper into the lungs.

Thus, greater depth of inhalation or a change in particle size do not necessarily need to occur to affect risk because more smoke is inhaled either way. The assumption of greater lung exposure to tobacco toxicants leading to an increased risk for lung adenocarcinomas due to filter ventilation is may not be in conflict with clinical trials and cross-sectional biomarker studies using blood and urine biomarkers because these studies do not provide information about lung exposure, distribution, or other local effects in the lung.

Small differences in exposure that are distributed widely in the body may not be measurable and subject to numerous factors related to innate characteristics of the smoker and rapid transfer from the lungs to the blood stream. However, we postulate that small differences in exposure concentrated on a per-puff basis might have a large impact localized in the lungs.

Experimental studies and limited human evidence indicate that the distal airways of the lung contain cells prone to the development of adenocarcinoma and that these regions may be more sensitive to TSNAs. It should be noted that most lung carcinogenesis studies in experimental animals focus on TSNAs and polycyclic aromatic hydrocarbons PAHs and are limited both in number and type of animal models; other smoke toxicants increased by filter ventilation also may contribute.

Experimental animal studies indicate that there are generally three types of epithelial cells in the lung, namely type I pneumocytes, type II pneumocytes primarily located in the alveolar space more distal airways—probably the progenitors of type I pneumocytes and Clara cells that are nonciliated and located in the terminal bronchioles now known as club cells or bronchiolar cells and located in the more proximal region of the lung , Although not well studied, there is evidence that type II pneumocytes are cells involved in inflammatory reactions , provide an inflammatory signal to recruit granulocytes and cause inflammation , and develop into adenocarcinoma — , while the Clara cell lineage secretes anti-inflammatory proteins and reduced with smoking, and may be the precursor to both squamous cell lung cancer and adenocarcinomas , , These cell types also have different carcinogen-metabolizing capacities , , — For example, more proximally located Clara cells have a greater ability to metabolize the carcinogen benzo a pyrene than type II pneumocytes, but the opposite occurs for TSNAs, although both cell types metabolize both carcinogens , — Further, suggestive experimental animal studies indicate that NNK induces peripheral lung adenomas , , while PAHs are more likely to induce central squamous cell tumors, although not exclusively — While there is some evidence that the Clara cells have more DNA damage than type II pneumocytes following exposure to NNK, the alveolar regions have more cell proliferation and tumors , There are two prospective human studies assessing TSNA exposure and lung cancer risk — Neither considers filter ventilation in its analysis, but each provides important support for the relationship of TSNAs and lung cancer risk.

When analyzed by lung cancer histology, the association of urinary NNAL with the risk of lung adenocarcinoma was statistically significant, but the results for other lung histologies combined were elevated, but not statistically significant.

The second study, using the Shanghai Cohort Study and the Singapore Chinese Study, also showed an overall increased lung cancer risk with higher levels of NNK exposure , ; data for specific cancer subtypes were not provided because histological confirmation was not done for many subjects. In summary, experimental animal studies indicate that the distal airways may be more sensitive to NNK than the proximal regions of the lung. Limited human cohort studies identify NNK as contributing to lung cancer risk, particularly for adenocarcinomas.

Given that filter ventilation increases NNK as do other factors and that larger puffs of smoke with higher NNK levels can reach the distal airways, along with other toxicants, these studies add to the biological plausibility for a relationship of filter ventilation to increased lung adenocarcinoma. This weight of evidence review broadly uses three groups of evidence, namely laboratory experimental data, human smoking behavior studies, and the epidemiology of lung cancer.

Table 1 and Figure 7 summarize our weight-of-evidence review in terms of the consistency of evidence, evidence of dose-response, temporality of exposure, strength of association, specificity of the evidence, and other causal criteria as they relate to the relationship of filter ventilation causing an increased risk of lung adenocarcinoma.

Table 1. Causation analysis for filter ventilation leading to lung adenocarcinomas. Evidence blocks for causation analysis.

Both IA and no relationship are treated as 0 and do not appear in blocks. Some criteria are weighted more heavily than others, as follows: Consistency and human intervention are adjusted for the greatest weight factor of 3 , dose response and biological plausibility are adjusted for a medium weight factor of 2 and the others are unadjusted.

A mode of action and human relevance framework also was applied, which is summarized in Supplementary Table 3 available online.

In addition to what is identified for Table 1 and Figure 7 , this framework also identifies what data may be inconsistent with a causal relationship and also what data are missing, for example a future research agenda.

There is consistency within evidence categories among the experimental data, human behavior studies, and lung cancer epidemiology with the exception of filter ventilation affecting inhalation and smoke distribution.

Numerous studies from the tobacco industry and academia indicate that filter ventilation, in spite of decreasing tar yields using standardized smoking machine methods on a per-cigarette basis, increases the generation of smoke toxicants, carcinogens, and mutagens on a per-mg-of-tar-and-nicotine basis.

Smoking behavior and exposures are clearly affected by smoking machine nicotine yields, such that smokers of low—nicotine yield cigarettes demonstrate an increase in puffing behavior due to the elasticity of the cigarette filter ventilation. This is borne out by both clinical trials and cross-sectional studies see Supplementary Tables 5 and 6 , available online.

The effects of filter ventilation on depth of smoke inhalation are less clear for consistency or show no effect. However, the methodologies to assess depth of inhalation and particle deposition are not well developed, largely rely on methods that have not been validated, use statistical modeling that also is not validated, and do not consider gases and inhaling more smoke. Studies of smoke particle distribution consistently show increased size with ventilation see Supplementary Table 4 , available online.

It should be noted that increased depth of inhalation may not be required to alter regional distribution and adenocarcinoma risk because smokers either way are increasing the amount of smoke inhaled into the lungs because of larger puff volumes.

The research data indicating the shift from squamous cell cancers to adenocarcinomas have been replicated among studies, concurrent in time with lowering tar yields and the use of filter ventilation. Other data indicate that lung cancer risk from smoking more modern cigarettes has increased over time, by considering birth cohorts of men separately from women. It is not possible to directly assess the impact of cigarette design on lung cancer risk because almost all cigarettes on the market simultaneously decreased tar yields and increased filter ventilation, although, limited prospective data associate an increase in TSNA exposure with adenocarcinomas.

There is consistency among experimental studies for increasing filter ventilation, resulting in increased toxicant yields and mutagens.

Increasing filter ventilation affects smoking behavior and increases puff volumes, but the effects on inhalation are less clear and not studied based on levels of ventilation. Human studies of smoking behavior do not show increased biomarker levels with lower-tar cigarettes, and some biomarkers may decrease, but these do not assess regional lung exposure. Temporal trends of decreasing tar yields and decreasing cigarette smoking rates, concurrent with increasing risks based on birth cohorts that progressively imitate the use of ventilated filter cigarettes, are consistent with a dose-response effect, although studies directly assessing filter ventilation or risks by tar yields are not available.

These two criteria are met given the full range of studies from the laboratory to population-level surveillance, which provides important scientific support, although there is some uncertainty relating to human biomarker exposure studies.

How filter ventilation increases tobacco toxicant yield, mutagenicity, and particle size is understood. The elasticity of filter ventilation allows for increasing puffing behavior, allowing for more of the toxicants to enter the lungs, which then exposes distal airway lung cells that are more sensitive to NNK and the development of adenocarcinomas. Coherence comes from experimental studies of specific tobacco toxicants and animal tumorigenesis, as well as mutagenicity and other cell culture studies.

Human studies using biomarkers of exposure showing similar levels of exposure for smokers of cigarettes with different degrees of ventilation present some uncertainty, and while these studies are consistent with each other, they present an argument against coherence. The human studies indicate, however, that there is no difference rather than a beneficial effect. As noted above, the human studies using urine and blood biomarkers may not reflect exposures at the target organ level ie the lung where lung adenocarcinomas occur, and they do not use validated biomarkers of harm.

Thus, this area is an important research gap to address. While there is highly suggestive evidence to conclude that filter ventilation has increased the rates of lung adenocarcinoma, there are other potential causes. As noted in the SGR, in addition to filter ventilation, there is suggestive evidence that increased levels of TSNAs over time also could explain the increased adenocarcinoma risks. However, one mechanism does not preclude the other, and both may be contributing ; filter ventilation further increases NNK levels on a per-mg-of-tar-and-nicotine basis.

Higher levels of NNK and other TSNAs in cigarette smoke can be driven by their increases in tobacco filler as a result of changes in tobacco blend content eg increasing burley tobacco content , increase in nitrate content, and changes in microbial contamination 16 , 1 , 46 , — While most NNK yields in smoke happen as a direct transfer from tobacco, additional amounts may also be formed during tobacco burning, with nitrate-rich tobaccos potentially generating higher levels of NNK While filter ventilation influences NNK levels less than changing tobacco leaf blends filter ventilation also increases other toxicant exposures.

Several other causation criteria are met, although the emphasis of these is less, such as timing of exposure, where all the clinical trials and experimental studies demonstrate effects after exposure or lack of effects ; strength of association, which is inferred in some cases because the totality of the data indicates significant strength to cause a measurable change in adenocarcinoma rates and risks; and analogy, such as experimental animal studies using specific smoke constituents, such as NNK.

This weight of evidence review and causation analysis strongly suggests that the inclusion of ventilation in cigarette filters has contributed to increased lung adenocarcinomas among smokers.

There are some uncertainty and research gaps as noted below, including the potential lack of coherence between mechanistic smoking machine yields and human exposure biomarker studies the machine studies indicate the potential for increased exposure while the human studies indicate no difference.

Thus, it should not be concluded that there is sufficient evidence for causality, rather that this review leads to a conclusion that the data is highly suggestive. Importantly, the weight of evidence does not indicate a public health benefit for the inclusion of filter ventilation. The smoke from cigarettes with ventilated filters provides false perceptions to the smoker of reduced harmfulness.

Filter ventilation affects how the tobacco burns, smoking behavior, and how the lung is exposed to carcinogens, so that it plausibly contributes to the increased adenocarcinomas by a cigarette that the smoker falsely believes is less harmful. Epidemiologic data provide indirect evidence for filter ventilation as a contributing factor to the increased lung adenocarcinoma rates and risks.

Absent such clear and convincing evidence from any source, the FDA should consider adopting a standard to prohibit filter ventilation. While there may be other cigarette design features that have contributed to the risk of smoking and the rise of adenocarcinomas compared with squamous cell cancers , it is our belief, based on the evidence reviewed herein, that filter ventilation has contributed to at least some of the increased risk.

It should be noted that an FDA action regulating filter ventilation would not imply that filter ventilation is the only or most important cigarette design to impact lung cancer risk, and a filter ventilation standard could be adopted alone or in conjunction with other product standards, for example addressing NNK exposure or other aspects of cigarette design that contribute to addiction and disease risk.

If the FDA prohibits filter ventilation, it may issue complementary regulations that restrict other design methods that reduce exposures, for example using higher amounts of expanded tobaccos, decreasing rod length, using tobacco strains and curing methods to reduce TSNA formation, and using highly activated carbon filters, so long as the FDA has concluded that these other regulations would not adversely affect smoking behavior 16 , , Using the SEER 9 database, we calculated the yearly age-adjusted incidence rates for adenocarcinoma, squamous cell carcinoma, and total lung cancer cases for men between and We found an excess of 32 adenocarcinoma cases when compared with squamous cell carcinomas data not shown.

While this may not be solely attributable to filter ventilation, this represents an adverse public health impact. Equally important, there is no existing evidence that filter ventilation reduces lung cancer risk or has any other beneficial health effect that would argue against regulation. There are important research gaps that have been identified, including the reconciliation for coherence of human biomarker studies showing no increased exposure for smokers using cigarettes with higher degrees of ventilation and patterns of inhalation and smoke distribution in the lung.

These would need to be addressed by lung biomarker studies, including biomarkers of harm, for example, using bronchoscopy to collect biospecimens as smokers switch from ventilated cigarettes to unventilated cigarettes. Importantly, prior to the regulation of filter ventilation, the FDA also will need to assess possible unintended effects of regulating filter ventilation, including a ban, for example increasing smoking initiation, delaying cessation due to perceptions that these are safer cigarettes, and that these would not likely outweigh the benefits.

To date, there are no studies on the impact of removing filter ventilation on smoking behavior and perceptions, the addictiveness of unventilated cigarettes, and the resultant exposures and toxicity.

This and other data gaps are indicated in Supplementary Table 3 available online. If ventilation were removed from cigarette filters, we expect three possible results: 1 that toxic exposure will be decreased because the cigarette delivery is no longer elastic, limiting the ability of the smoker to compensate with larger puff volumes; 2 the greater amount of nicotine in smoke will result in the smoker decreasing the number of cigarettes per day and less smoke will enter the lungs; and 3 some smokers may quit smoking or transition to alternative nicotine delivery systems such as electronic cigarettes or nicotine replacement therapy because of the harshness of the cigarette smoke and perceptions of a more harmful smoke.

To assess this, a combination of human and experimental animal studies could be conducted in the context of the conceptual framework for tobacco product evaluation For example, clinical trials could assess smokers switching to filtered cigarettes without ventilation and with different packaging and study smoking topography, inhalation depth, and biomarkers of nicotine exposure and smoke toxicants. Studies would need to be done in ways to assess differing effects by race and ethnicity, gender, age, and vulnerable populations to inform the potential population-level effects.

Experimental animal studies that allow for manipulations in both adolescent and adult rodents would parallel the human trials to provide evidence for the impact on smoking initiation. Another research agenda item could focus on the impact of filter ventilation on the risk of other diseases eg chronic obstructive pulmonary disease , given shared etiologies due to tobacco toxicants.

Such research would provide additional support for an FDA regulatory action. In conclusion, the use of ventilation in the filters of cigarettes has failed to make cigarettes safer, and more than likely has made them more harmful. There is no demonstrated public health benefit, and smokers perceive these as less harmful, which in turn encourages smoking and causes harm.

The FDA now has the authority to require the elimination of filter ventilation because ventilation does not serve any public health purpose and instead provides a false promise of reduced risk. This single action for banning filter ventilation by the FDA is scientifically justified and within its mandate to improve the public health. Based on these weight-of-evidence reviews, the FDA should embark on a regulatory process of data evaluation and consider regulation s for the use of ventilation in filters, up to and including a ban on their use.

The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH or the FDA. Cummings has received grant funding from the Pfizer, Inc. Shields, Benowitz, Brasky, and Cummings have served as consultants and expert witnesses in litigation against tobacco companies.

The other authors declare no conflict of interest. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

The funders had no role in the writing of the review, data collection or analysis, conclusions, or decision to submit the review for publication. The authors appreciate the input and advice about this manuscript from Drs. Tobacco Smoke and Involuntary Smoking. Geneva: Who Press; The Massachusetts benchmark study; final report. Brown and Williamson Records. Lung cancer. Google Scholar. Jpn J Clin Oncol. Cigarette smoking and changes in the histopathology of lung cancer.

J Natl Cancer Inst. The increasing incidence of lung adenocarcinoma: Reality or artefact? A review of the epidemiology of lung adenocarcinoma. Int J Epidemiol. Percy C , Sobin L. Surveillance, Epidemiology, and End Results lung cancer data applied to the World Health Organization's classifications of lung tumors.

Cancer statistics, CA Cancer J Clin. N Engl J Med. Changes in mortality from smoking in two American Cancer Society prospective studies since Has the lung cancer risk from smoking increased over the last fifty years?

Cancer Causes Control. Do changes in cigarette design influence the rise in adenocarcinoma of the lung? Mortality in relation to smoking: 50 years' observations on male British doctors.

Monograph 7: The FTC cigarette test method for determining tar, nicotine, and carbon monoxide yields of U. Special report no. Hoffmann D , Hoffmann I.

The changing cigarette, J Toxicol Environ Health. How do different cigarette design features influence the standard tar yields of popular cigarette brands sold in different countries? Tob Control. Stephens WE. Dependence of tar, nicotine and carbon monoxide yields on physical parameters: Implications for exposure, emissions control and monitoring. Centers for Disease Control and Prevention. Filter ventilation and nicotine content of tobacco in cigarettes from Canada, the United Kingdom, and the United States.

The health consequences of smoking: A report of the Surgeon General. Nicotine yield from machine-smoked cigarettes and nicotine intakes in smokers: Evidence from a representative population survey. Clearing the smoke: The science base for tobacco harm reduction—executive summary. World Health Organization. Pollay RW , Dewhirst T. Kaufman N , Nichter M. The marketing of tobacco to women: Global perspectives.

Geneva: World Health Organization; Nicotine Tob Res. Cigarette pack labelling in 12 countries at different levels of economic development.