For discussion critical evaluation of smoking related discussions of health hazard estimates as presented by James Repace ET AL
that the predicted respirable smoke particulate (RSP) concentration during work hours
corresponding to this risk is 211 µg/m3. In fact, Repace (2004) measured an RSP
concentration of 205 µg/m3 in the Delaware Park Casino in the U.S., with a
corresponding carcinogenic particulate polycyclic aromatic hydrocarbon (PPAH)
concentration of 163 nanograms per cubic meter (ng/m3) before a Statewide smoking
ban, and corresponding RSP and PPAH concentrations after the smoking ban of 9 µg/m3
and 4 ng/m3 respectively.”
Repace estimates average environmental tobacco smoke [ETS] or [RSP] or [SHS] at 211 Micrograms per cubic meter of air in total. To state all ETS would be comprised of PM2.5 is erroneous as no research has been presented to establish this level truly exists. Nor can we assume all Particulate is present entirely in PM2.5. In identifying the particulate the reports are sloppy, in not more precisely defining the particulate, collection methods and sample duration, specific densities, origin and identification of PAH aerosols, Carbon type and source, Specific temperatures, humidity or age since formation in areas they are formed.
The general term Tobacco smoke is a vague description of a substantial variety of substances with ingredients which can vary among perhaps millions of possible combinations of what they may contain ventilation properties or the method of use.
Repace contends an average level of 250 micrograms per cubic meter of air the risk is 10,000 times his believed safe level. His statement from the Burswood casino offering of 225 deaths per year presents a 45 year risk of 10 in 1000 or 10,000 per million exposed. In measuring the toxic risk. a stretch which in relative risk terms exceeds even the risk of primary smoking by many times what was found in the most energetic of offerings.
When we look at the toxin described it is known to contain 3-5000 ingredients depending on who you choose to believe although a list seems to be a rare commodity. Which may be an enigma in itself. When assessing risk of a mixture, the total risk can not exceed the risk of its most dangerous component. Many as Repace seems to believe you may simply add up risk components to result the total risk unfortunately this is not the case. If as Repace demonstrates that would be particulate polycyclic aromatic hydrocarbon (PPAH)
which he simplistically compares to those PAHs produced by the spark ignition engine or diesel engine exhaust along a highway. His primary error is the sources are not similar nor the particulate or the PAHs produced. The burning of Oil products as compared to organic materials differ quite substantially and actually can be measured by instrumentation and differentiated if he so chose. Personally I would indicate the risk of Dioxin, as a more drastic reality in his advocacy. None the less we will proceed in his terms as presented. .
We are forced to deal with the sparse information base presented and generalized to evaluate what is being proposed in these amateurish adventures of ad agency style presentations of the most deceptive nature attempting to present as scientific knowledge. a seemingly impossible situation to unravel for any clear description or calculation in linear terms. to assess realistic risk. However I did not say this was impossible just very difficult to defend considering the source of the information available.
Perhaps to bring this into perspective we need to compare this study with a few professional reports dealing with similar toxins.
Quoting from; Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects (1983) http://newton.nap.edu/openbook.php?record_id=738&page=1
Commission on Life Sciences (CLS)
Aerosol Measurements.
“In all experiments, we measured aerosol surface properties using four pairs of a photoelectric aerosol sensor and a diffusion charger (PAS 2000 CE and DC 2000 CE, EcoChem), which quantify particulate PAHs (13–15) and aerosol active surface area (16), respectively. Aerosol active surface area affects condensation on particles, heterogeneous chemistry (e.g., reaction of gaseous species with particulate PAHs), and particle deposition (17). Normalizing the PAH concentration by active surface area provides information about the chemical composition of the particle (18) because particles from different combustion sources have different ratios of PAH concentration to surface area concentration. For example, the PAH concentration to surface area concentration ratio is nearly 3 times higher for candle soot versus diesel exhaust (16), and the ratio is much higher for diesel exhaust diluted at 24 versus 16 °C, due to the presence of nonphotoemitting nucleation mode particles at the lower temperature (19). We expect particles of noncombustion origin to have PAH concentration to surface area concentration ratios that are near zero.”
The burning of a candle produces 3 times the density of PAH as diesel exhaust a known class A carcinogen although few fear such a risk from a candle, exposure and duration may hold the truths in revealing why. First all respiratory particulate is not deadly the majority is inert. A very small component of the whole can be attributed to PAHs which is a bonded compound of aerosol attached to a carbon host which occurs as a result of burning Oil products and organic materials. The majority of which are expelled from the body in a few days through bowel movements and urination. It is believed a small amount of the toxins can stay within the body and may mutate at the cellular level to form cancers at various sites. The total risk of a collection of toxins can not exceed the maximum risk of any single component of the mixture unless it can be demonstrated a mixture forms a new toxin more deadly than either of it’s components. Such has never been demonstrated with PAHs. PAH is a range of components of varying degrees of toxicity. Among them benzo-[a]pyrene which is thought to be among the highest risk.
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1241432&blobtype=pdf
Health Risk.
The extremely high PAH concentrations found on Mexico City’s roadways may present an important health risk. Estimating the potential health risk is instructive, despite the large uncertainties involved in the calculations. We can estimate the approximate magnitude of risk from exposure to PAHs in vehicle exhaust in the MCMA by considering the lung cancer risk estimate for benzo[a]pyrene, measurements of TPAH concentrations on the MCMA roadways, and the speciation profiles of their exhaust. Among all roadway trips monitored in the diesel exposure, commuter, and mobile laboratory studies conducted in the MCMA in 2002, median TPAH concentrations range from 60 to 910 ng m−3, with an average of 310 ng m−3. Laboratory (38, 39) and on-road (31) studies suggest that benzo[a]pyrene accounts for 7% ± 5% (mean ± standard deviation) and 2% ± 3% of particulate PAHs in gasoline and diesel exhaust, respectively.
“On the basis of studies of lung cancer in coke oven workers, the World Health Organization suggests a lifetime risk estimate (24 h per day over 70 years) for humans of 9 × 10−5 per ng m−3 of benzo[a]pyrene as an indicator, and the risk refers to the total PAH mixture (40). Speciation profiles differ between coke ovens and vehicle exhaust; however, benzo-[a]pyrene’s high carcinogenic potency relative to other PAHs supports the use of it as an indicator of risk for other sources (30). Using a typical roadway TPAH concentration of 300 ng m−3 in the MCMA and a particulate PAH speciation for exhaust of 2% benzo[a]pyrene, we estimate roadway benzo-[a]pyrene concentrations to be 6 ng m−3. Such a concentration translates into a lung cancer risk level of approximately 5 × 10−4 for lifetime exposure to these PAH concentrations, or 2 × 10−5 if we assume that people are exposed for 2 h per day, 5 days per week, for 40 years while commuting on roadways in the MCMA. Professional drivers whose occupations require them to spend many hours per day on the road, street vendors, and city dwellers who live near roadways will face a higher risk due to their longer durations of exposure. Although many uncertainties exist in this risk assessment, the estimate suggests that exposure to PAHs on the MCMA’s roadways may be high enough to warrant concern. This analysis does not consider the other carcinogenic and cocarcinogenic compounds present in the atmosphere, which may amplify the risk”.
Supplied calculations;
Repace has provided some calculations which we can evaluate and asses the true nature of risk according to lifetime estimatesof the world health Organization as described previously. As we see from Burswood numbers presented; [Total RSP][ .08%] =[ total PAHs] =[211ug x .0008 = 168 Pico grams Total PAHsTo calculate benzo-[a]pyrene content of PAH from above is approx. 2% of total or 3.36 Pico grams
Epidemiology risk assessment from WHO figures;
For exposures of employees the WHO coincidentally determined lifetime risk of the same toxin.
“(24 h per day over 70 years) for humans of 9 × 10−5 per ng m−3 of benzo[a]pyrene”
9 per hundred thousand exposed for every nana gram per cubic meter measured in this case 3.36 x 9 or 30.24 excess risk per hundred thousand exposed. For an employee this represents a lifetime risk of 24 hours x 365days x 70years = 613200 hours if exposed 24 hours a day for 70 years clearly this is not the case.
We wish to compare the Repace definition of an employee exposure for a 45 year working lifetime at 40 hours a week. Assuming 5 day work weeks and no days off. 40 hours x 52 weeks x45 years = 93600 hours / 613200 = .153 or 15.3% of total maximum lifetime risk 24-7/-70 years exposure as above 15.3% of 30.24 per one hundred thousand is 4.6 per hundred thousand or a relative risk of .46 x 10 –4
Conclusions
For an average client in the bar/ Casino the attendance is only 10% of employee exposure assuming 4 hours per week or .046 x 10 –4 Epidemiology studies assess risk beginning at 1 x 10 –4 the risk to non smokers in a smoking allowed Casino .046 [CI 99.9% .045 -.047 ] Further to an employee working in a smoking environment, again a curative effect of.46 [CI 99.9% .45 -.47 ] Strangely; a conclusion common sense lead us to believe all along. In practical measures the following link augmented by numerous identical studies internationally, demonstrates;
This is normally the point one would post excusses while patting one self on the back with a wave to the crowd. To the publishers who will ignore this conspiracy nut theory; Get stuffed It's Thanks giving.Foot note;
In compliance with the first recommendation in dealing with class 1 carcinogens “replacing less hazardous materials”, an opportunity of simple regulation exists which would suit all affected in society as an inclusive measure Negating of course those seeking financial goals over the mortality incidence of others.
IARC
A Guide to the Classification of
Carcinogens, Mutagens and Teratogens under the Sixth Amendment,35 which is based
on the interpretation, for human exposure at the workplace, of the findings of the
International Agency for Research on Cancer on carcinogenesis. The most stringent of
the three categories, with the appropriate levels of control required, is described below.
-11-
(a) Category 1
Established human carcinogens are those substances known to be carcinogenic to
humans. There is sufficient evidence to establish a causal association between
human exposure to these substances and the development of cancer.
Under the circumstances where substitution of less hazardous materials is
technically not feasible, the use of these carcinogenic substances should be
controlled to the highest practicable standard by the application of effective
engineering control techniques and, where necessary, complemented by the use of
appropriate personal protective equipment. Routine monitoring of the workplace is
essential for indication of control performance. In some cases, health surveillance
and biological monitoring can indicate exposure and thus reveal the need for reassessment
of the control measures and work practices. For some substances,
specific control measures have been detailed in codes of practice.5,6,36
33. Doll, R. and Peto, R., The Causes of Cancer: Quantitative Estimates of Avoidable Risks of Cancer in
the United States Today, Oxford University Press, Oxford, United Kingdom, 1981.
34. Commission of the European Communities (EEC), Classification and Labeling of Dangerous
Substances, Council Directive 79/831/EEC, Sixth Amendment, Brussels, 1986.
35. European Chemical Industry Ecology and Toxicology Centre, A Guide to the Classification of
Carcinogens, Mutagens and Teratogens under the Sixth Amendment, technical report no. 21, Brussels,
February 1986.
5. National Occupational Health and Safety Commission, `Guide to the Control of Asbestos Hazards in
Buildings and Structures' [NOHSC:3001(1988)], in Asbestos: Code of Practice and Guidance Notes,
Australian Government Publishing Service, Canberra, 1988.
6. National Occupational Health and Safety Commission, `National Code of Practice for the Safe Removal
of Asbestos' [NOHSC:2002(1988)], in Asbestos: Code of Practice and Guidance Notes, Australian
Government Publishing Service, Canberra, 1988.`
36. National Occupational Health and Safety Commission, National Code of Practice for the Safe Use of
Vinyl Chloride [NOHSC:2004(1990)], Australian Government Publishing Service, Canberra, 1990.
