This
was a B- paper. Comments by student
reviews follow the instructor's comments.
Grading
Mark each category 5 to 10:
10 = Yes, very well
9 = Yes
8 = Adequate
7 = Not quite adequate
6 = No
5 = Definitely no.
For comment:
Did the paper raise questions you would like answered? Name some.
What is the Dose?
What is the response at that dose?
Other comments:
It is difficult to find the risk assessment. You would assume that that legislation was a risk assessment, but it is not presented.
Student Review
For comment:
Did the paper raise questions you would like answered? Name some.
Was there any data used to assess
the risk?
Student Review
For comment:
Did the paper raise questions you would like answered? Name some.
Filter vs. non-filter cigarette comparison for SS.
Individual component analysis after short time elapse for SS.
Other comments:
Individual comments throughout paper with track changes.
Reference comments through paper so the reader knows where the data comes from.
Try not to use words like “thus”, “therefore”, and “hence” in scientific papers.
Do not start sentences with “because” and “it is”.
Avoid run-on sentences.
Delete all opinions. Opinions are too flowery and cause distractions. If opinions are necessary then put them into a discussion section.
You have a lot of good information. This paper is good but general. The paper would be better if you talked about only a few studies and argued from general to specific.
I enjoyed reading it. Thanks
Student Review
For comment:
Did the paper raise questions you would like answered? Name some.
No.
A lot of studies were referenced but no conclusions were drawn. Present
a summary of conclusions at the front of the paper and the supporting data
should follow.
Other comments: Most of the paper
seems to be direct quotes but no credit is given in the paper. Rum grammar and spelling check. Additional comments in the paper are in red.
Here I put the paper with the
comments. This is a good technical edit
of the paper. When I get a review like
this of my papers, I try to study the mistakes I made. Some are just matters of style, but most are
good suggestions.
Analysis of A Risk
Assessment on Respiratory Health
Effects of Passive Smoking:Lung Cancer and Other Disorders.
Tobacco smoking has long been recognized as a major cause of mortality and morbidity, responsible for an estimated 434,000 deaths per year in United States. Cigarette smoking is related to cancer at bladder, renal pelvis, pancreas, and upper respiratory and digestive tracts (IARC,1986). It also causes chronic obstructive pulmonary disease (COPD), cardiovascular diseases, influenza, bronchitis, pneumonia, lung function impairment, cough, phlegm, wheezing, and shortness of breadth (SPELLING). Low birth weight and increased risk of fetal and infant death result from maternal smoking during pregnancy (U.S.DHHS, 1989).
In recent years, there has been a lot (How much is a lot?) of concern and discussion that nonsmokers may also be at risk for some of these health effects as a result of their exposure to ETS (Environmental Tobacco Smoke) or Second Hand Smoke. Although this ETS is dilute compared with the mainstream smoke (MS) inhaled by active smokers, it is chemically similar, containing many of the same carcinogenic and toxic agents.
The U.S. Environmental Protection
Agency (EPA) has published a major assessment of the respiratory health risks
of passive smoking (Respiratory Health
Effects of Passive Smoking: Lung Cancer and other
(capitalize) Disorders; EPA/600/6-90/006F). The report concludes that exposure to ETS, commonly known as
second-hand smoke, is responsible for approximately 3000 lung cancer deaths
each year in non-smoking adults and impairs the respiratory health of hundreds
of thousands of children.
When a cigarette is smoked, approximately one-half of the smoke generated is Sidestream smoke (SS) emitted from the smoldering cigarette between puffs. This SS contains essentially all of the same carcinogenic and toxic agents that have been identified in the Mainstream smoke (MS) inhaled and exhaled by the smoker. SS and MS are the major components of ETS. ETS also contains contaminants emitted during the puff and contaminants that diffuse through the cigarette paper and mouth and between puffs. These emissions contain both vapor phase constituents and over half of the particulate matter. Overall, ETS is a complex mix of over 4,000 compounds (Guidelines for Health Risk Assessment of Chemical Mixtures (U.S. EPA, 1986b). This contains many known or suspended human carcinogens and toxic agents.
BACKGROUND: (Respiratory Health Effects of Passive Smoking: Lung Cancer and other Disorders)
The first epidemiological results associating passive smoking with lung cancer appeared in early 1980’s. In 1986, the National Research Council (NRC) and the Surgeon General of the U.S. Public Health Service independently assessed the health effects of exposure to ETS. Both of the 1986 reports conclude that ETS can cause lung cancer in adult nonsmokers and that children of parents who smoke have increased chances too.
The NRC report also concluded that (spacing) “household exposure to ETS is linked with increased rates of chronic ear infections and middle ear effusions in young children”.
The second major review, the Surgeon General report covers ETS chemistry, exposure, and various health effects, primarily lung cancer and childhood respiratory diseases. In 1987, a committee of the International Agency for Research on Cancer (IARC) issued a report on methods of analysis and exposure measurement related to passive smoking.
In 1988, EPA’s Indoor Air Division (now the Indoor Environments Division) requested EPA’S Office of Research and Development (ORD) undertake an assessment of the respiratory health effects of passive smoking. The document has been prepared under the authority of Title IV of Superfund (The Radon Gas and Indoor Air Quality Research Act 1986), which directs EPA to conduct research and disseminate information on all aspects of indoor air quality. A draft of this assessment was released for public review in June 1990. In December 1990, and in May 1992 EPA’s Science Advisory Board (SAB), a committee of independent scientists, conducted a review of the draft report. Following a July 1992 meeting, the SAB panel endorsed the conclusions of report.
EPA also
received and reviewed more than 100 comments from the public. (This whole
paragraph is irrelevant and can be deleted).
MAJOR CONCLUSIONS: (Fact Sheet: Respiratory Health Effects of Passive Smoking)
Based on available scientific evidence, EPA has concluded:
In Adults: “ETS is a human lung carcinogen, responsible for approximately 3,000 lung cancer deaths annually in U.S. nonsmokers. ETS has been classified as a Group A carcinogen”.
In Children: ETS exposure causes bronchitis and pneumonia amongst 150,000 and 300,000 annually in infants and children upto (spelling) 18 months of age. ETS exposure increases middle ear disease and increases severity in asthmatic children. ETS exposure is a risk factor for new cases of asthma in children who have not previously displayed symptoms.
ETS exposure irritates the upper respiratory tract and causes significant reduction in lung function.
EPA came to the conclusion that ETS is a human
carcinogen based on all the data that is available,
including more than 30 epidemiological studies concerning mainly
passive smoking and also active smoking, animal data, biological measurements
of human uptake of tobacco smoke. The conclusion was based on “total weight of
evidence” rather than on any one study. The conclusion that ETS is a human
carcinogen is based on the dose-related lung carcinogenicity of MS in active smokers and similarity in MS
and SS. The study is bolstered by exposure related increase in lung cancer in
nonsmoking spouses of smokers which is in turn found from 30 epidemiological
studies. The weight of evidence analysis for the non-cancer respiratory effects
in children is based primarily on review of more than 100 studies.
CLASSIFICATION OF ETS AS A GROUP A CARCINOGEN: (Setting the Record Straight: Secondhand Smoke is A Preventable Health Risk)
This is done by total weight of the available evidence and is not dependent on any single analysis. This evidence contains many facts. (Use a colon, not a period.)
1. Smoking tobacco causes lung cancer and there is no threshold.
2. Secondhand
smoke is chemically similar to the smoke
inhaled smoke
by smokers, and contains a number of
carcinogenic compounds.
3. A large no. (spell out) of people, all nonsmokers are exposed to, absorb, and metabolize secondhand smoke.
4. Evidence from
laboratory of the ability of secondhand smoke both to cause cancer in animals
and to damage DNA, which is instrumental in cancer development. (This sentence does not make sense?)
5. EPA did analysis on 30 epidemiological studies from eight different countries which associated secondhand smoke and lung cancer in women who were exposed to their husband’s smoke.
The most spectacular aspect is
the consistency of the results of the epidemiological studies that support a
causal association between secondhand smoke and lung cancer. These studies were a major source of information for EPA,
which looked into them closely before making any conclusions. (What were the conclusions and why is this
important?)
Since it is difficult to separate the individual compounds that make up ETS and then to assess exposures to those compounds, the assessment focuses on the characterization of the complex ETS mixture and exposure to it by nonsmokers. The physical and chemical properties of SS and MS are assessed to compare the potential for release of human carcinogens and toxic agents. Environmental and biological marker compounds are also analyzed carefully. The biomarker data points to the fact that levels of ETS contaminants encountered indoors by nonsmokers are of very high magnitude. MS, SS, and ETS are chemically similar and contain suspected human carcinogens and toxic compounds. The marker compounds for ETS are measurable in indoor environments. Exposure to ETS is extensive and nonsmokers take up a significant part of it.
Standardized testing procedures
for assessing physical and chemical
nature of SS do not exist, and there is not as much data on SS is not as much as on MS. The procedures for
collection of SS emissions are such that it can be directly compared with MS
and thus a
valuable information is got obtained regarding
into the physical and chemical nature of
ETS.
Results of laboratory tests have indicated that there are similarities and differences between MS and SS emissions from cigarettes. Differences between SS and MS are due to differences in temperature of combustion of the tobacco and degree of dilution with air. SS is generated at a low temperature (600 C between puffs) and at higher Ph (6.7-7.5) than MS (800-900 C and Ph 6.0-6.7). Being slightly more alkaline, SS contains more ammonia, less acids, greater quantities of organic bases, and less hydrogen cyanide than MS. Oxygen concentration in SS is 2% and in MS is 16%.
SS is rapidly diluted in air, which results in a SS particle size distribution smaller than that of MS and thus a change in phase distribution for several constituents.
Nicotine is found in particle phase in MS and in gas phase in ETS. The shift to gas phase is due to rapid dilution of SS. SS particle size is in the range of 0.01-1.0 micro m, while MS particle size is 0.1-1.0 micro m. The SS particle distribution shifts to small sizes with increasing dilution.
Despite quantitative differences and potential differences in phase distributions, the air contaminants emitted in MS and SS are qualitatively very similar in their chemical composition because they are produced by the same process. Part of the data available from studies MS and SS emissions are shown in Table 1.1. These data are for non-filtered cigarettes. It is evident from the table that SS emissions are considerably higher than MS emissions. Carcinogens, probable human carcinogens, and animal carcinogens are emitted at higher levels in SS than in MS. The enrichment of several known carcinogens in SS relative to MS suggests that SS might be even more carcinogenic than MS.
Because of the many potentially toxic agents in ETS it is neither feasible nor desirable to focus on any one contaminant. Rather the focus is made on gathering information on marker compounds or other indicators of ETS exposure. Both direct and indirect methods can be applied. Direct methods include personal monitoring and measurement of biological markers. Indirect ones employ models to estimate exposures.
Although ETS is a major source of indoor air contaminants but it is difficult to assess due to the background levels of contaminants from other indoor and outdoor sources. Little is known about the role of each individual component of ETS in eliciting the adverse health and nuisance effects observed. It is necessary then to identify a marker for ETS that will, when measured, accurately represent the frequency, duration, and magnitude of exposure to ETS. These markers can be chemicals measured in air, biomarkers, models, or simple questionnaires. Biomarkers of exposure are actually measures of dose or uptake and hence indicators that an exposure has taken place. Biomarkers for ETS are Thiocyanate, Carboxyhemoglobin etc.
Numerous epidemiological studies have conclusively established that the tobacco smoke inhaled from active smoking is a human carcinogen. A clear dose-response relationship exits between lung cancer and amount of exposure, without any evidence of a threshold level. It, is, therefore, reasonable to theorize that exposure to environmental tobacco smoke (ETS) might also increase the risk of lung cancer in both smokers and nonsmokers.
More than 50 independent studies have found a dose-related association between smoking and lung cancer. This is further enhanced by dose-response relationships. A gradient of increasing risk for lung cancer mortality with increasing numbers of cigarettes smoked per day was established. Lung cancer mortality ratios for male workers who smoked more than 20 cigarettes a daily were 15-25 times greater than those for nonsmokers. Smokers who smoked more than 10 cigarettes per day had lung cancer mortality ratios 3-10 times greater than those for nonsmokers.
In early 1960s, 50% of U.S. men and 30% of U.S. women smoked, although these proportions have been declining in recent years. In United States, deaths from lung cancer currently represent one-quarter of all cancer deaths. The uptake of tobacco smoke among adult population is upwards of 75% based on urinary cotinine / creatinine studies in non-smokers. The total number of U.S. cancer deaths in U.S. females from all causes is partitioned into compartments (non-tobacco causes, background ETS, spousal ETS, and ever-smoking). Calculations are made for the U.S. female population age 35 and over in 1985 based on parameter values from national statistics and estimates from epidemiological studies on ETS and lung cancer. These calculations prove that ETS does pose a considerable risk as a Group A carcinogen which causes lung cancer.
RESPIRATORY DISORDERS OTHER THAN CANCER:
Previous studies (Surgeon General’s) as well as recent ones demonstrate that ETS also causes chronic phlegm and wheezing. Unlike active smoking, involuntary exposure to ETS affects individuals of all ages, particularly infants and children. Even small increases in risk due to passive exposure to ETS would considerably increase the absolute number of affected cases.
There is also evidence of relationship between exposure to ETS during childhood and acute respiratory illnesses, middle ear diseases, chronic respiratory symptoms, asthma, sudden infant death syndrome, and lung function impairment. Recent studies have shown that active smokers have increased prevalence of Bronchial Hyperresponsiveness when compared with nonsmokers.
Several sources of bias need to be considered in studies of the effects
of single exposure in subjects. Not considering active smoking or past smoking
significantly affects the results of tests. Adults are exposed to many harmful
substances during their lifetimes and it is not always possible to calculate
effects of these substances because they often are unknown or unmeasurable. The
influence of sources of bias, and irrregularity of effects together may explain
the inconsistent and sometimes contradictory results of the studies. Although
there is considerable uncertainty in the estimates from the resources but the outcomes provide some good gross
comparisons.
SECONDHAND SMOKE LEGISLATION:
President Clinton has signed into law, a legislation restricting smoking in
all places were where federal assistance is provided
to children.
The Clinton Administration
supportsed pending
(Use past tense; we have a new President.)
legislation (H.R. 3434, S.1680, S.262) that would protect nonsmokers, including
(spacing) children, from secondhand smoke in
most public places. These bills would not take away the smoker’s freedom to
choose to smoke, nor would it bring government regulation into the home. The
bills would also be good economically. EPA estimates that smoking restrictions
would result in saving $4 billion to $8 billion per year in housekeeping and
maintenance purposes.
The bill would prevent
thousands of premature deaths of nonsmokers per year and reduce the incidence
of respiratory illness in children. I think
tThis legislation was a great step towards forward in drawing the public attention towards the danger
posed by secondhand tobacco smoke.
Although EPA does not have any regulatory authority for controlling ETS, the Agency expects health professionals and policymakers to take appropriate steps to minimize exposure. In co-operation with other government agencies, EPA plans to continue to educate public and make programs to bring in more public participation.
|
Constituent |
Amount in MS |
Range in SS/MS |
|
Vapor Phase1: |
|
|
|
Carbon Monoxide |
10-23 mg |
2.5-4.7 |
|
Carbon Dioxide |
20-40 mg |
8-11 |
|
Benzene2 |
12-48 micro g |
5-10 |
|
Toluene |
100-200 micro g |
5.6-8.3 |
|
Hydrogen Cyanide |
400-500 micro g |
0.1-0.25 |
|
Ammonia |
50-130 micro g |
3.7-5.1 |
|
Nitrogen Oxides |
100-600 micro g |
4-10 |
|
Acetic Acid |
330-810 micro g |
1.9-3.6 |
|
Particulate Phase1: |
|
|
|
Particulate Matter3 |
15-40 mg |
1.3-1.9 |
|
Nicotine |
1-2.5 mg |
2.6-3.3 |
|
Phenol |
60-140 micro g |
1.6-3.0 |
|
Cholesterol |
22 micro g |
0.9 |
|
Quinoline |
0.5-2 micro g |
3-11 |
|
Aniline4 |
360 ng |
30 |
Table
1.1
Data in this table come from the National Research Council (NRC) report (1986).
1 Separation into vapor and particulate phases reflects conditions prevailing in MS and does not necessarily imply same separation in SS.
2 Known human carcinogen, according to U.S. EPA or IARC.
3 Contains di-and polycyclic aromatic hydrocarbons, some of which are known animal carcinogens.
4 Probable human carcinogen, according to U.S. EPA or IARC.
NOTE: The SS/MS ratios shown can be misleading because a no. (spell out) of
factors have impact on MS emissions. A filtered cigarette can reduce
MS of total mass content, thus resulting in higher SS/MS ratio. The lack of
variability in SS emissions is related to the fact that sidestream emissions
are related to weight of tobacco and paper consumed during the smoldering
period.
NRC- NATIONAL RESEARCH COUNCIL
IARC- INTERNATIONAL AGENCY FOR RESEARCH ON CANCER
U.S. DHHS- US DEPARTMENT OF HEALTH AND HUMAN SERVICES
ELECTRONIC REFERENCES:
1. Risk Assessment
“Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders”
EPA/600/6-90/006F
http://www.epa.gov/NCEA/ets/etsindex.htm
2. Fact Sheet
“Respiratory Health Effects of Passive Smoking”
Office of Research and Development
Office of Air and Radiation
January 1993
http://www.epa.gov/iaq/pubs/etsfs.html
3. Setting the Record Straight:
“Secondhand Smoke is A Preventable Health Risk”
EPA 402-F-94-005
June 1994
http://www.epa.gov/iaq/pubs/strsfs.html
4. Secondhand Smoke
“What you can do about Secondhand Smoke As Parents, Decision-Makers, And
Building Occupants”
EPA-402-F-93-004
July 1993
http://www.epa.gov/iaq/pubs/etsbro.html
1. Donald J. Ecobichon
Joseph M. Wu
“Environmental Tobacco Smoke”
Proceedings of the International Symposium at McGill University, Nov. (3-4) 1989
Montreal, Canada
Lexington Books Publication
1. United States Congress House Committee of Agriculture
“Review of the U.S. Environmental Protection Agency’s tobacco and smoke study”
Hearing before the Subcommittee on Speciality Crops and Natural Resources of the
Committee. (Washington: US. G.P.O. For sale by the U.S. G.P.O.)
Analysis
of A Risk Assessment on Respiratory Health Effects of Passive Smoking:Lung
Cancer and Other Disorders.
Tobacco smoking has long been recognized as a major cause of mortality and morbidity, responsible for an estimated 434,000 deaths per year in United States. Cigarette smoking is related to cancer at bladder, renal pelvis, pancreas, and upper respiratory and digestive tracts (IARC,1986). It also causes chronic obstructive pulmonary disease (COPD), cardiovascular diseases, influenza, bronchitis, pneumonia, lung function impairment, cough, phlegm, wheezing, and shortness of breadth. Low birth weight and increased risk of fetal and infant death result from maternal smoking during pregnancy (U.S.DHHS, 1989).
In recent years, there has been a lot of concern and discussion that nonsmokers may also be at risk for some of these health effects as a result of their exposure to ETS (Environmental Tobacco Smoke) or Second Hand Smoke. Although this ETS is dilute compared with the mainstream smoke (MS) inhaled by active smokers, it is chemically similar, containing many of the same carcinogenic and toxic agents.
The U.S. Environmental Protection
Agency (EPA) has published a major assessment of the respiratory health risks
of passive smoking (Respiratory Health Effects of Passive Smoking: Lung
Cancer and other Disorders; EPA/600/6-90/006F). The report concludes that exposure to ETS, commonly known as
second-hand smoke, is responsible for approximately 3000 lung cancer deaths
each year in non-smoking adults and impairs the respiratory health of hundreds
of thousands of children.
When a cigarette is smoked, approximately one-half of the smoke generated is Sidestream smoke (SS) emitted from the smoldering cigarette between puffs. This SS contains essentially all of the same carcinogenic and toxic agents that have been identified in the Mainstream smoke (MS) inhaled and exhaled by the smoker. SS and MS are the major components of ETS. ETS also contains contaminants emitted during the puff and contaminants that diffuse through the cigarette paper and mouth and between puffs. These emissions contain both vapor phase constituents and over half of the particulate matter. Overall, ETS is a complex mix of over 4,000 compounds (Guidelines for Health Risk Assessment of Chemical Mixtures (U.S. EPA, 1986b). This contains many known or suspended human carcinogens and toxic agents.
BACKGROUND: (Respiratory Health Effects of Passive Smoking: Lung Cancer and other Disorders)
The first epidemiological results associating passive smoking with lung cancer appeared in early 1980’s. In 1986, the National Research Council (NRC) and the Surgeon General of the U.S. Public Health Service independently assessed the health effects of exposure to ETS. Both of the 1986 reports conclude that ETS can cause lung cancer in adult nonsmokers and that children of parents who smoke have increased chances too.
The NRC report also concluded that “household exposure to ETS is linked with increased rates of chronic ear infections and middle ear effusions in young children”.
The second major review, the Surgeon General report covers ETS chemistry, exposure, and various health effects, primarily lung cancer and childhood respiratory diseases. In 1987, a committee of the International Agency for Research on Cancer (IARC) issued a report on methods of analysis and exposure measurement related to passive smoking.
In 1988, EPA’s Indoor Air Division (now the Indoor Environments Division) requested EPA’S Office of Research and Development (ORD) undertake an assessment of the respiratory health effects of passive smoking. The document has been prepared under the authority of Title IV of Superfund (The Radon Gas and Indoor Air Quality Research Act 1986), which directs EPA to conduct research and disseminate information on all aspects of indoor air quality. A draft of this assessment was released for public review in June 1990. In December 1990, and in May 1992 EPA’s Science Advisory Board (SAB), a committee of independent scientists, conducted a review of the draft report. Following a July 1992 meeting, the SAB panel endorsed the conclusions of report.
EPA also received and reviewed more than 100 comments from the public.
MAJOR CONCLUSIONS: (Fact Sheet: Respiratory Health Effects of Passive Smoking)
Based on available scientific evidence, EPA has concluded:
In Adults: “ETS is a human lung carcinogen, responsible for approximately 3,000 lung cancer deaths annually in U.S. nonsmokers. ETS has been classified as a Group A carcinogen”.
In Children: ETS exposure causes bronchitis and pneumonia amongst 150,000 and 300,000 annually in infants and children upto 18 months of age. ETS exposure increases middle ear disease and increases severity in asthmatic children. ETS exposure is a risk factor for new cases of asthma in children who have not previously displayed symptoms.
ETS exposure irritates the upper respiratory tract and causes significant reduction in lung function.
EPA came to the conclusion that ETS is a human carcinogen based on all the data that is available, including more than 30 epidemiological studies concerning mainly passive smoking and also active smoking, animal data, biological measurements of human uptake of tobacco smoke. The conclusion was based on “total weight of evidence” rather than on any one study. The conclusion that ETS is a human carcinogen is based on the dose-related lung carcinogenicity of MS in active smokers and similarity in MS and SS. The study is bolstered by exposure related increase in lung cancer in nonsmoking spouses of smokers which is in turn found from 30 epidemiological studies. The weight of evidence analysis for the non-cancer respiratory effects in children is based primarily on review of more than 100 studies.
CLASSIFICATION OF ETS AS A GROUP A CARCINOGEN: (Setting the Record Straight: Secondhand Smoke is A Preventable Health Risk)
This is done by total weight of the available evidence and is not dependent on any single analysis. This evidence contains many facts.
1. Smoking tobacco causes lung cancer and there is no threshold.
2. Secondhand smoke is chemically similar to the smoke inhaled by smokers, and contains a number of carcinogenic compounds.
3. A large no. of people, all nonsmokers are exposed to, absorb, and metabolize secondhand smoke.
4. Evidence from laboratory of the ability of secondhand smoke both to cause cancer in animals and to damage DNA, which is instrumental in cancer development.
5. EPA did analysis on 30 epidemiological studies from eight different countries which associated secondhand smoke and lung cancer in women who were exposed to their husband’s smoke.
The most spectacular aspect is the consistency of the results of the epidemiological studies that support a causal association between secondhand smoke and lung cancer. These studies were a major source of information for EPA, which looked into them closely before making any conclusions.
Since it is difficult to separate the individual compounds that make up ETS and then to assess exposures to those compounds, the assessment focuses on the characterization of the complex ETS mixture and exposure to it by nonsmokers. The physical and chemical properties of SS and MS are assessed to compare the potential for release of human carcinogens and toxic agents. Environmental and biological marker compounds are also analyzed carefully. The biomarker data points to the fact that levels of ETS contaminants encountered indoors by nonsmokers are of very high magnitude. MS, SS, and ETS are chemically similar and contain suspected human carcinogens and toxic compounds. The marker compounds for ETS are measurable in indoor environments. Exposure to ETS is extensive and nonsmokers take up a significant part of it.
Standardized testing procedures for assessing physical and chemical nature of SS do not exist, and data on SS is not as much as on MS. The procedures for collection of SS emissions are such that it can be directly compared with MS and thus a valuable information is got into the physical and chemical nature of ETS.
Results of laboratory tests have indicated that there are similarities and differences between MS and SS emissions from cigarettes. Differences between SS and MS are due to differences in temperature of combustion of the tobacco and degree of dilution with air. SS is generated at a low temperature (600 C between puffs) and at higher Ph (6.7-7.5) than MS (800-900 C and Ph 6.0-6.7). Being slightly more alkaline, SS contains more ammonia, less acids, greater quantities of organic bases, and less hydrogen cyanide than MS. Oxygen concentration in SS is 2% and in MS is 16%.
SS is rapidly diluted in air, which results in a SS particle size distribution smaller than that of MS and thus a change in phase distribution for several constituents.
Nicotine is found in particle phase in MS and in gas phase in ETS. The shift to gas phase is due to rapid dilution of SS. SS particle size is in the range of 0.01-1.0 micro m, while MS particle size is 0.1-1.0 micro m. The SS particle distribution shifts to small sizes with increasing dilution.
Despite quantitative differences and potential differences in phase distributions, the air contaminants emitted in MS and SS are qualitatively very similar in their chemical composition because they are produced by the same process. Part of the data available from studies MS and SS emissions are shown in Table 1.1. The units of the table are not obvious. These data are for nonfilter cigarettes. It is evident from the table that SS emissions are considerably higher than MS emissions. Carcinogens, probable human carcinogens, and animal carcinogens are emitted at higher levels in SS than in MS. The enrichment of several known carcinogens in SS relative to MS suggests that SS might be even more carcinogenic than MS.
Because of the many potentially toxic agents in ETS it is neither feasible nor desirable to focus on any one contaminant. Rather the focus is made on gathering information on marker compounds or other indicators of ETS exposure. Both direct and indirect methods can be applied. Direct methods include personal monitoring and measurement of biological markers. Indirect ones employ models to estimate exposures.
Although ETS is a major source of indoor air contaminants but it is difficult to assess due to the background levels of contaminants from other indoor and outdoor sources. Little is known about the role of each individual component of ETS in eliciting the adverse health and nuisance effects observed. It is necessary then to identify a marker for ETS that will, when measured, accurately represent the frequency, duration, and magnitude of exposure to ETS. These markers can be chemicals measured in air, biomarkers, models, or simple questionnaires. Biomarkers of exposure are actually measures of dose or uptake and hence indicators that an exposure has taken place. Biomarkers for ETS are Thiocyanate, Carboxyhemoglobin etc.
Numerous epidemiological studies have conclusively established that the tobacco smoke inhaled from active smoking is a human carcinogen. A clear dose-response relationship exits between lung cancer and amount of exposure, without any evidence of a threshold level. It, is, therefore, reasonable to theorize that exposure to environmental tobacco smoke (ETS) might also increase the risk of lung cancer in both smokers and nonsmokers.
More than 50 independent studies have found a dose-related association between smoking and lung cancer. This is further enhanced by dose-response relationships. A gradient of increasing risk for lung cancer mortality with increasing numbers of cigarettes smoked per day was established. Lung cancer mortality ratios for male workers who smoked more than 20 cigarettes a daily were 15-25 times greater than those for nonsmokers. Smokers who smoked more than 10 cigarettes per day had lung cancer mortality ratios 3-10 times greater than those for nonsmokers.
In early 1960s, 50% of U.S. men and 30% of U.S. women smoked, although these proportions have been declining in recent years. In United States, deaths from lung cancer currently represent one-quarter of all cancer deaths. The uptake of tobacco smoke among adult population is upwards of 75% based on urinary cotinine / creatinine studies in non-smokers. The total number of U.S. cancer deaths in U.S. females from all causes is partitioned into compartments (non-tobacco causes, background ETS, spousal ETS, and ever-smoking). Calculations are made for the U.S. female population age 35 and over in 1985 based on parameter values from national statistics and estimates from epidemiological studies on ETS and lung cancer. These calculations prove that ETS does pose a considerable risk as a Group A carcinogen which causes lung cancer.
RESPIRATORY DISORDERS OTHER THAN CANCER:
Previous studies (Surgeon General’s) as well as recent ones demonstrate that ETS also causes chronic phlegm and wheezing. Unlike active smoking, involuntary exposure to ETS affects individuals of all ages, particularly infants and children. Even small increases in risk due to passive exposure to ETS would considerably increase the absolute number of affected cases.
There is also evidence of relationship between exposure to ETS during childhood and acute respiratory illnesses, middle ear diseases, chronic respiratory symptoms, asthma, sudden infant death syndrome, and lung function impairment. Recent studies have shown that active smokers have increased prevalence of Bronchial Hyperresponsiveness when compared with nonsmokers.
Several sources of bias need to be considered in studies of the effects of single exposure in subjects. Not considering active smoking or past smoking significantly affects the results of tests. Adults are exposed to many harmful substances during their lifetimes and it is not always possible to calculate effects of these substances because they often are unknown or unmeasurable. The influence of sources of bias, and irrregularity of effects together may explain the inconsistent and sometimes contradictory results of the studies. Although there is considerable uncertainty in the estimates from the resources but the outcomes provide some good gross comparisons.
SECONDHAND SMOKE LEGISLATION:
President Clinton has signed
into law, a legislation restricting what in
all places were federal assistance is provided to children.
The Clinton Administration supports pending legislation (H.R. 3434, S.1680, S.262) that would protect nonsmokers, including children, from secondhand smoke in most public places. ???? These bills would not take away the smoker’s freedom to choose to smoke, nor would it bring government regulation into the home. The bills would also be good economically. EPA estimates that smoking restrictions would result in saving $4 billion to $8 billion per year in housekeeping and maintenance purposes.
The bill would prevent thousands of premature deaths of nonsmokers per year and reduce the incidence of respiratory illness in children. I think this legislation was a great step towards drawing the public attention towards the danger posed by secondhand tobacco smoke.
Although EPA does not have any regulatory authority for controlling ETS, the Agency expects health professionals and policymakers to take appropriate steps to minimize exposure. In co-operation with other government agencies, EPA plans to continue to educate public and make programs to bring in more public participation.
|
Constituent |
Amount in MS |
Range in SS/MS |
|
Vapor Phase1: |
|
|
|
Carbon Monoxide |
10-23 mg |
2.5-4.7 |
|
Carbon Dioxide |
20-40 mg |
8-11 |
|
Benzene2 |
12-48 micro g |
5-10 |
|
Toluene |
100-200 micro g |
5.6-8.3 |
|
Hydrogen Cyanide |
400-500 micro g |
0.1-0.25 |
|
Ammonia |
50-130 micro g |
3.7-5.1 |
|
Nitrogen Oxides |
100-600 micro g |
4-10 |
|
Acetic Acid |
330-810 micro g |
1.9-3.6 |
|
Particulate Phase1: |
|
|
|
Particulate Matter3 |
15-40 mg |
1.3-1.9 |
|
Nicotine |
1-2.5 mg |
2.6-3.3 |
|
Phenol |
60-140 micro g |
1.6-3.0 |
|
Cholesterol |
22 micro g |
0.9 |
|
Quinoline |
0.5-2 micro g |
3-11 |
|
Aniline4 |
360 ng |
30 |
Table
1.1
Data in this table come from the National Research Council (NRC) report (1986).
1 Separation into vapor and particulate phases reflects conditions prevailing in MS and does not necessarily imply same separation in SS.
2 Known human carcinogen, according to U.S. EPA or IARC.
3 Contains di-and polycyclic aromatic hydrocarbons, some of which are known animal carcinogens.
4 Probable human carcinogen, according to U.S. EPA or IARC.
NOTE: The SS/MS ratios shown can be misleading because a no. factors have impact on MS emissions. A filtered cigarette can reduce MS of total mass content, thus resulting in higher SS/MS ratio. The lack of variability in SS emissions is related to the fact that sidestream emissions are related to weight of tobacco and paper consumed during the smoldering period.
NRC- NATIONAL RESEARCH COUNCIL
IARC- INTERNATIONAL AGENCY FOR RESEARCH ON CANCER
U.S. DHHS- US DEPARTMENT OF HEALTH AND HUMAN SERVICES
ELECTRONIC REFERENCES:
1. Risk Assessment
“Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders”
EPA/600/6-90/006F
http://www.epa.gov/NCEA/ets/etsindex.htm
2. Fact Sheet
“Respiratory Health Effects of Passive Smoking”
Office of Research and Development
Office of Air and Radiation
January 1993
http://www.epa.gov/iaq/pubs/etsfs.html
3. Setting the Record Straight:
“Secondhand Smoke is A Preventable Health Risk”
EPA 402-F-94-005
June 1994
http://www.epa.gov/iaq/pubs/strsfs.html
4. Secondhand Smoke
“What you can do about Secondhand Smoke As Parents, Decision-Makers, And
Building Occupants”
EPA-402-F-93-004
July 1993
http://www.epa.gov/iaq/pubs/etsbro.html
1. Donald J. Ecobichon
Joseph M. Wu
“Environmental Tobacco Smoke”
Proceedings of the International Symposium at McGill University, Nov. (3-4) 1989
Montreal, Canada
Lexington Books Publication
1. United States Congress House Committee of Agriculture
“Review of the U.S. Environmental Protection Agency’s tobacco and smoke study”
Hearing before the Subcommittee on Speciality Crops and Natural Resources of the
Committee. (Washington: US. G.P.O. For sale by the U.S. G.P.O.)