Environmental Tobacco Smoke Links

Waltc sent me these useful links:

ENVIRONMENTAL TOBACCO SMOKE 

EXPOSURE: 

1) “Mainstream and Environmental Tobacco Smoke,” Gori, Mantel; Reg Toxicol Pharmacol, 1991 

Table 2 shows that from 1,170 to 1 million cigarettes would have to be simultaneously smoked in a small sealed unventilated chamber to reach OSHA’s level of possible harm if breathed for 10 straight hours. 

http://www.prevention.ch/20465909330950.pdf 

See also: “Toxic Toxicology,” Littlewood, Fennel, National Toxicology Program, 1999 

http://www.forces.org/evidence/download/ntp915c.pdf 

2) “Exposure to environmental tobacco smoke in sixteen cities in the United States as determined by personal breathing zone air sampling,” Jenkins et al, J. Expo Anal Environ Epid, 1996, 

” Exposures of typical [nonsmoking]subjects to nicotine in the workplace were 30-60% of those estimated by OSHA and 15-20% of those estimated by OSHA for the most highly exposed workers.” As confirmed by a biological marker (cotinine) “total daily nicotine exposure in smokers’ homes [16 hrs/day] was 6.8 ug/m3 and total daily exposure in workplaces where smoking was unrestricted [8 hrs/day] was 5.8 ug/m3.” [The OSHA PEL for nicotine is 500 ug/m3,] 

https://www.ncbi.nlm.nih.gov/pubmed/9087866 

3) “Assessment of air quality in Stockholm by personal monitoring of nonsmokers for respirable suspended particles and environmental tobacco smoke.” Scand J Work Environ, 1998 

“Over 70% of all nicotine measurements and 60% of all ETS particle measurements were below the level of quantification. When their median values were converted to cigarette equivalents, the [stay-at-home] nonsmoking spouses married to [stay-at-home] smokers would receive 6-9 CEs/year at home; working nonsmokers living with smokers would receive 0.6 to 0.7 CEs/year at home, and nonsmoking workers working with smokers would be exposed to 0.1 to 0.2 CEs/year [at work].” 

https://www.ncbi.nlm.nih.gov/pubmed/8817762?dopt=Abstract 

4) “Determination of exposure to environmental tobacco smoke in restaurant and tavern workers in one US city, ” Maskarinec et al, J Expos Anal Environ Epid, March 2000 

“Nicotine levels encountered by bartenders ranged from undetectable to more than 100 ug/m3… while RSP ranged from undetectable to 511 ug/m3 in bar areas. The maximumRSP–768 ug/m3 [ in a single-room bar where 246 cigarettes were smoked] was 6 1/2 times less than the OSHA-mandated [permissible] level of 5000 ug/m3.” 

https://www.nature.com/articles/7500069.pdf?origin=ppub 

5) “Exposure to Secondhand Smoke Lower Than Believed” Jenkins, Oak Ridge Nat’l Lab, Feb.00 

https://web.archive.org/web/20130510141506/http://www.ornl.gov/info/press_releases/get_press_release.cfm?ReleaseNumber=mr20000203-00 

6) “Environmental Tobacco Smoke and Respirable Suspended Particle Exposures for Non- Smokers in Beijing”, Keith Phillips, David A. Howard, Mark C. Bentley, Gunnar Alván; Sage, 1998 

“The highest exposures to ETS particles (SolPM) and nicotine were estimated for office workers living and working in smoking environments. These sub jects would potentially inhale between 5 and 11 cigarette equivalents per year.” 

https://journals.sagepub.com/doi/abs/10.1177/1420326X9800700503 

7) “Measured exposures by personal monitoring for respirable suspended particles and environmental tobacco smoke of housewives and office workers resident in Bremen, Germany,” Phillips et al, Int Arch Occup Environ Health, 1998 

“Overall, the levels were quite low, the majority of results below the limits of quantification. The most highly exposed, both living and working with smokers, would potentially inhale 20 cigarette equivalents (CE) per annum if based on the upper decile levels. Housewives living with smokers could inhale up to 11 CE per annum as based on the upper decile level.” 

8) “Airliner Cabin Environment: Contaminant Measurements, Health Risks and Mitigation Options” U.S.Dept of Transportation, DOT P-15-89-5, 1989 

Comparing air measurements on smoking vs no-smoking flights, DOT reported that by three rows beyond the smoking section, airborne nicotine was “undetectable on 82.6% ” of smoking flights; that, where detectable, it ranged from an average of 0.04 – 0.05 ug/m3 *; RSP averages, from 30.7-35.0 ug/m3 which compared favorably to no-smoking flights (34.8-40.0) **; CO averages, 0.7-0.8 ppm (smoking) vs 0.5-0.6 (no smoking) and CO2 was less on the smoking flights (1568 ppm) than on the no-smoking flights ( 1756) likely due to better air circulation. (Tables 4-14 to 4-23) 

* OSHA PEL (safe level) for nicotine is 500 ug/m3 ** for RSP, 5000 ug/m3 

http://inspirehep.net/record/289061?ln=en 

9) ” Assessment by Personal Monitoring of Respirable Suspended Particles and Environmental Tobacco Smoke Exposure for Non-Smokers in Sydney, Australia” Keith et al, Indoor and Built Environment Vol. 7, No. 4, 1998 – 

“Median annual exposure in smoking homes was less than smoking the equivalent of 4 cigarettes.” 

https://www.karger.com/article/Abstract/24582 

STUDIES ON HEALTH EFFECTS: 

LUNG CANCER 

10) “Environmental tobacco smoke and tobacco related mortality in a prospective study of Californians, 1960-98″ Enstrom, Kabat; BMJ, 2003 

“The results do not support a causal relation between environmental tobacco smoke and tobacco related mortality..” 

https://www.bmj.com/content/326/7398/1057.full 

11)-“Environmental Tobacco Smoke and Lung Cancer Risk,” Gravelle et al, Congressional Research Service, Nov 14, 1995 

“The statistical evidence does not appear to support a conclusion that there are substantial health effects of passive smoking…. Even at the greatest exposure levels….very few or even no deaths can be attributed to ETS.” 

12) “No Clear Link Between Passive Smoking and Lung Cancer,” Peres, Journal of the National Cancer Institute, 2013 

“Among women who reported never smoking, exposure to most categories of passive smoking did not increase the risk. Only those with 30 or more years of exposure showed a slightly increased risk that was not statistically significant, meaning it could be due to chance.”. 

https://academic.oup.com/jnci/article/105/24/1844/2517805 

See also: https://www.forbes.com/sites/geoffreykabat/2013/12/21/the-passive-smoking-issue-is-a-rorschach-test-for-the-ability-to-think-scientifically/#5dd767a52979 

13)“ Environmental Tobacco Smoke: Exposure Response Relationships in Epidemiologic Studies’ Wu-Williams – Risk Analysis, 1990 

This National Cancer Institute study found a statistically significant decreased risk of lung cancer among women married to smokers– RR: 0.7 (0.6- 0.9)– and similarly found no significant association with exposure from coworkers, cohabitants or parents 

https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1539-6924.1990.tb01018.x 

14) “Multicenter Case-Control Study of Exposure to ETS and Lung Cancer in Europe,” Boffetta et al, J. Natl Cancer Inst 90, 1998 

No risk at all from childhood exposure (RR 0.78) with “no trend in risk for number of smokers in the household and a decreasing risk with cumulative exposure.” For adults, no matter how it was sliced into sub-groups –by age, sex, diet, kind of cancer, kind of smoke, duration of exposure, place of exposure (home, work, car, bar, other public place) type of exposer ( roommate, spouse, kin) no risk could be found that was statistically significant. 

https://www.ncbi.nlm.nih.gov/pubmed/9776409 

15) “Lung cancer and exposure to tobacco smoke in the household” Janerich et al, NEJM – 

“Household exposure of less than 25 smoker-years during childhood and adolescence did not increase the risk of lung cancer. Exposure to a spouse’s smoking, which constituted less than one third of total household exposure on average, was not associated with an increase in risk.” 

https://www.ncbi.nlm.nih.gov/pubmed/2385268?dopt=Abstract 

16) “Passive Smoking and Lung Cancer in Nonsmoking Women,” Brownson et al, Am J Public Health, 1992 

Though the study concludes that only for those with 40 years of household exposure is there “a small increased risk,” the tables themselves show a nonexistent risk for up to 40 years (RR 0.8) . It further declares that “ in our data set no elevated risk was noted for [spousal smoking],” that “in general, there was no elevated risk associated with passive smoke exposure in the workplace,” and “no evidence of excess lung cancer risk from passive smoke exposure in childhood.” 

https://www.ncbi.nlm.nih.gov/pubmed.1443304 

17) “Relation between exposure to environmental tobacco smoke and lung cancer in lifetime nonsmokers.” Kabat, Stellman, Am J Epidemiol, 1995 

“… [T]he pattern of odds ratios shows little indication of an association of environmental tobacco smoke with lung cancer in nonsmokers.” 

https://www.ncbi.nlm.nih.gov/pubmed/7598113?dopt=Abstract 

18) “Relation of exposure to environmental tobacco smoke and pulmonary adenocarcinoma in non- smoking women: a case control study” Shen et al, Oncol Rep 1998 

“Results show no statistical association between exposure to ETS and pulmonary adenocarcinoma. ” 

https://www.ncbi.nlm.nih.gov/pubmed/9683839 

19) “Meta-analysis of the potential relationship between exposure to environmental tobacco smoke and lung cancer in nonsmoking Chinese women, ” Wang et al, Lung Cancer, 1997. – 

“No statistically significant relationship was found between either the amount (cigarettes/day) or the duration (in years) of exposure to ETS and lung cancer. OR 0.9,” 

https://www.ncbi.nlm.nih.gov/pubmed/9152946 

20) “Time trends in lung cancer mortality among nonsmokers and a note on passive smoking,” Garfinkel, J. Natl Cancer Inst, Vol 66. – PubMed – NCBI 

“Compared to nonsmoking women married to nonsmoking husbands, nonsmokers married to smokers showed very little, if any, increase in risk of lung cancer” 

https://www.ncbi.nlm.nih.gov/pubmed/6941041 

21) “Exposure to environmental tobacco smoke and risk of adenocarcinoma of the lung” Bofetta et al, Int J Cancer, 1999, 

“Ever exposure to ETS from the parents during childhood was associated with a decreased risk (OR 0.6) … and there was a suggestion of a decreasing trend in risk with increasing duration of exposure. Ever exposure to ETS from the spouse was not associated with an increased risk. ” 

https://www.ncbi.nlm.nih.gov/pubmed/10521800 

22) “Smoking and other risk factors for lung cancer in Xuanwei, China,” Liu et al , Int J Epid 1991 

“Female’s results suggest an association of lung cancer with [other factors] but not with passive smoking. (OR 0.77).” 

https://www.ncbi.nlm.nih.gov/pubmed/2066232 

23) “Measurements of passive smoking and estimates of lung cancer risk among non-smoking Chinese females” Koo – 1987 – International Journal of Cancer 

“Relative risks based on the husband’s smoking habits, or lifetime estimates of total years, total hours, mean hours/day, or total cigarettes/day…did not show dose/response results. Similarly, when such categories… were combined… there were no apparent increases in relative risk.” 

https://onlinelibrary.wiley.com/doi/abs/10.1002/ijc.2910390207 

24) “Relationship of passive smoking to risk of lung cancer and other smoking-associated diseases” Lee; Br.J. Cancer, 1986. 

“Amongst lifelong non-smokers, passive smoking was not associated with any significant increase in risk of lung cancer, chronic bronchitis, ischaemic heart disease or stroke in any analysis.” 

https://www.ncbi.nlm.nih.gov/pubmed/3730259 

25) ” Selection, follow-up, and analysis in the American Cancer Society prospective studies” Garfinkel, National Cancer Inst Monograph 1985: 67:49-52 

No increased risk of lung cancer from exposure at work or other environments after either 5 years (RR 0.89) or 25 years (RR 0.93) 

https://www.ncbi.nlm.nih.gov/pubmed/4047150 

THE HEART 

26)-“Environmental Tobacco Smoke and Coronary Heart Syndromes: Absence of Association,” Gori, Regul Toxicol Pharmacol, April, 1995 

“By scientific standards, the weight of evidence continues to falsify the hypothesis that ETS exposure might be a CHD risk factor.” 

https://www.ncbi.nlm.nih.gov/pubmed/7644718 

27), “Publication Bias in the Environmental Tobacco Smoke/Coronary Heart Disease Epidemiologic Literature,” LeVois, Layard; Regul Toxicol Pharmacol, 1995; 21 

“The American Cancer Society Studies CPS-1 [with 1 million subjects] and CPS-2 [with 1.2 million] do not show an increased CHD risk associated with ETS. ” 

https://www.sciencedirect.com/science/article/pii/S0273230085710239 

28) Congressional Research Service Report-Discussion of Source of Claims of 50,000 Deaths from Passive Smoking,” Grevelle, Redhead, 3/94 

“In sum, this analysis suggests that Wells’ estimates are so high relative to measures of physical exposure that they seem implausible.” 

http://www.nycclash.com/Cabinet/CRSDiscusses_50000_Deaths.html 

29) “Environmental tobacco smoke and coronary heart disease mortality in the United States–a meta-analysis and critique,” Kabat, Enstrom; Inhal Toxicol, 2006, 

“[Never smokers’] exposure to ETS, as approximated by spousal smoking, is associated with roughly a 5% increased risk ..[with] no dose-response relationship and no elevated risk associated with the highest level of exposure in males or females….[T]he association of ETS with CHD death in U.S. never smokers is very weak. Previous assessments appear to have overestimated the strength of the association.” 

https://www.ncbi.nlm.nih.gov/pubmed/16399662 

30) ” Passive Smoking, Coronary Heart Disease and Meta-analysis,” Bailar, NEJM, March 1999 

“I regretfully conclude that we still do not know with any accuracy how much–or even if– exposure to environmental tobacco smoke increases the risk of coronary heart disease.” 

https://www.nejm.org/doi/full/10.1056/NEJM199903253401211 

31) “Changes in U.S. hospitalization and mortality rates following smoking bans” Shetty et al – Journal of Policy Analysis and Management, 2011 

This national study “in contrast with smaller regional studies, find[s] that smoking bans are not associated with statistically significant short-term declines in mortality or hospital admissions for myocardial infarction or other diseases. An analysis…reveals that large short-term increases in myocardial infarction incidence following a smoking ban are as common as the large decreases reported in the published literature.” 

https://onlinelibrary.wiley.com/doi/abs/10.1002/pam.20548 See also: https://reason.com/2010/12/20/first-nationwide-study-finds-n 

32) “Acute myocardial infarction mortality before and after state-wide smoking bans.” Rodu et al, J Community Health, 2012; 

The decline in 6 states with bans was not significantly different from that in 44 states without bans. In 3 of the 6, the declines were, in fact, less, and in one, South Dakota, the AMI rate actually rose by 8.9% in the wake of the state-wide ban. 

http://www.springerlink.com/content/prr81661082w4447/ 

33) “A Nationwide Assessment of the Association of Smoking Bans and Cigarette Taxes With Hospitalizations for Acute Myocardial Infarction, Heart Failure, and Pneumonia” Ho et al, Med Care Res Rev, 2017 

“Smoking bans were not associated with acute myocardial infarction or heart failure hospitalizations 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5665160/#!po=7.35294 

ASTHMA 

34) “Respiratory Effects in Children from Exposure to Secondhand Smoke,” 2006 Surgeon General’s Report, Chapter 6. 

“The evidence is..not sufficient to infer a causal relationship between secondhand smoke from parental smoking and the onset of childhood asthma.” (P 375) 

https://www.ncbi.nlm.nih.gov/books/NBK44324/ 

35) “Internal Comments on the [1992 draft] EPA Report” Comment of Dr. Terry Harvey, EPA Director of Risk Assessment: 

“ETS must NOT [emphasis his] be portrayed as a public health risk to the general non- [genetically] predisposed [to asthma] public.” 

36) “Review of the Draft Passive Smoking Health Effects Document” EPA Science Advisory Board, Nov. 1992 (p. II 127-132) 

Drs James Woods and Howard Rockette condemned the Report’s misleading conclusion that ETS was a cause of asthma, citing “flawed methods and the failure to look at confounders [which were] simply implied away.” 

37) Congressional Record, July 21, 1993, Transcript of hearing on Environmental Tobacco Smoke to the House Subcommittee on Health and Environment, Serial No. 103-51, U.S. Govt Printing Office 

Testimony of SAB Chairman, Dr. Martin Lippman: “The data were insufficient to come to conclusions on causality [regarding] increased rates of cardiovascular mortality in adults, induction of asthma in previously asymptomatic children, increased risk of sudden infant death syndrome (SIDS) and increased rates of upper respiratory tract infections.” (P 135-136) 

38) “Does Civilization Cause Asthma?” The Atlantic, May 2000, 

Quoting Dr Fernando Martinez, author of the 1992-3 EPA Report’s chapters on asthma and other respiratory risks: “Like most people I assumed tobacco smoke and pollution were the problem–that was the politically correct way to think–but these factors turned out not to play a major role 

https://www.theatlantic.com/magazine/archive/2000/05/does-civilization-cause-asthma/378183/ 

39) “Risk factors associated with asthma and rhinoconjunctivitis among Swedish farmers.” Kronqvist et al, Allergy 54, 1999 

“[E]xposure to ETS [at any measure] in childhood or currently did not significantly affect the risk of airway disease in smokers, ex-smokers or nonsmokers.” 

https://www.ncbi.nlm.nih.gov/pubmed/10604549 

40) “An Epidemiologic Study of Bronchial Asthma and Smoking :” Flodin, Epidemiology 6, 1995 

“ETS exposure at home was not associated with a greater risk…workplace exposure indicated a slight but statistically insignificant risk.” 

https://journals.lww.com/epidem/Abstract/1995/09000/An_Epidemiologic_Study_of_Bronchial_Asthma_and.7.aspx 

BIRTH WEIGHT 

41) “Health Effects of Exposure to Environmental Tobacco Smoke,” Final draft, 1997, Office of Environmental Health Hazard Assessment/ California EPA. 

The report included the following previously published studies regarding the birth weight of infants born to nonsmoking mothers who were daily exposed to their husbands’ smoke. Keep in mind that 28.5 grams (g) is the equivalent of one (1) ounce. There are 453 grams to a pound. 

MacArthur & Knox (Lancet, 1987) 

“authors noted a 123g excess in [birth] weight if the father smoked.” (p 3: 4) 

42) Ibid. Zhang and Ratcliffe I, 1993 

“no dose-response trend by amount [husband] smoked with a greater adjusted weight decrement [-26g] for up to 19 cigarettes/day but an increase in birth weight at higher levels (20 or more cigarettes/ day).” ( p 3:7) 

43) Ibid. Underwood et al 

As compared to nonsmoking households, ” authors report little difference in rates of LBW or prematurity among births of nonsmoking mothers with smoking husbands.” [In fact the RR for the latter was 0.9.] (p 3:8) 

44) Ibid. Mathai et al, 1992 

With 52% of the sample exposed to spousal smoke, comparatively there was “no difference in the rates of LBW by mothers’ ETS exposure.” (p. 3:10) 

45) Ibid. Ogawa, 1991 

With 62% exposure to spousal smoke among 7000 Japanese women, there was ” an adjusted 10.8g decrement which was non-significant. Interestingly, the adjusted weight reduction associated with [the women’s own] active smoking of 10 cigarettes a day was only 5.6g.” (p 3:11) 

46) Ibid. Ahlborg & Bodin, 1991 

With 47% of Swedish nonsmoking mothers exposed to ETS, “the adjusted RR for lower birth weight for exposure in the home was 0.7 and for prematurity was 0.5. [In other words, the risk was less than for the unexposed group.] Workplace exposure was not associated with birthweight reduction.” (p 3:12) 

47) Zhang & Ratcliffe II 

“the rates [of birth weight] at term and IUGR were similar whether the father was a smoker or a nonsmoker. No consistent dose-response trend was seen with amount smoked.” (p 3:10) 

https://oehha.ca.gov/air/report/health-effects-exposure-environmental-tobacco-smoke 

FETAL AND INFANT HEALTH 

48) “Smoking habits, nicotine use and congenital malformations” Morales et al, Obstetrics & Gynecology, 2006 

“Our results showed no increase in [fetal] congenital malformations related to prenatal tobacco smoking. However, we identified a [60%] increase of malformations risk in nonsmokers using nicotine substitutes. ” 

https://www.ncbi.nlm.nih.gov/pubmed/16394039 

49) “High Infant Mortality in US Linked to Premature Births,” New York Times, 3/1/95, quoting Dr. Allan Wilcox, National Institute of Environmental Science: 

“Ounce for ounce, the babies of smoking mothers had a higher survival rate. Smoking may interfere with weight gain but does not shorten pregnancy.Thus, among smoking women, the smaller babies are more likely to be full term. [I]t’s prematurity not birth weight that explains higher mortality.” 

50 ) “Prepregnancy Weight and Pregnancy Outcome,” Goldenberg et al, Am J. Obs &Gyn, 1996: 

“White infants were heavier and born later than black infants [even though] the white women in this sample smoked more cigarettes” 

https://jamanetwork.com/journals/jama/article-abstract/400136 

51) “Disorders of the placenta, fetus and neonate: diagnosis and clinical significance” Naeye; Mosby, 1992 

“The respiratory distress syndrome had a lower frequency at every preterm gestational age in the neonates of smokers than of nonsmokers. The greater the number of cigarettes smoked, the lower were the frequency and the case fatality rate of the neonatal RDS. More than 56,000 pregnancies that produced offspring were analyzed” (p 84) 

https://www.researchgate.net/publication/44733561_Disorders_of_the_placenta_fetus_and_neonate_diagnosis_and_clinical_significance_Richard_L_Naeye

52) “Maternal smoking and infant respiratory distress syndrome,” White, Obst & Gyn, 1986 

“Infants of mothers who smoked had a reduced incidence of RDS [respiratory distress syndrome] for their gestation compared with infants of nonsmokers. The smoking effect was not explained by demographic differences between smokers and nonsmokers, nor by differences in the incidence of pregnancy complications between the two groups.” 

https://www.popline.org/node/343827 

53) “Association of intrauterine cigarette smoke exposure with indices of fetal lung maturation,” Lieberman et al, Obstetrics and Gynecology, 1992 

“Infants of smoking mothers were at a decreased risk of neonatal respiratory distress syndrome, a disease of lung immaturity.” 

https://www.ncbi.nlm.nih.gov/pubmed/1553178 

54) ” The effects of nicotine on the synthesis and secretion of surfactant in the rabbit fetal lung,”. Nakamura, 1988, PubMed – NCBI 

“The results of the present study might provide help to understand the clinical experiences reported by others, i.e. that in the [human] newborn from a smoking mother, respiratory distress occurred less frequently than in those from non-smokers” 

https://www.ncbi.nlm.nih.gov/m/pubmed/3235880/ 

55) “Effects of social and family factors on viral respiratory infection and illness in the first year of life.” Gardner, J. Epid Comm Health, 1984 PubMed – NCBI 

“No convincing differences for viral infection or respiratory illness were seen with parental smoking as a isolated factor.” 

https://www.ncbi.nlm.nih.gov/pubmed/6323611 

BREAST CANCER 

56) “A null association between active or passive cigarette smoking and breast cancer risk.” Lash,; Breast Cancer Res Treat, 2002 

Title says it. https://www.ncbi.nlm.nih.gov/pubmed/12243511 

57)”Passive smoking exposure and female breast cancer mortality” Wartenberg J Natl Cancer Inst 

“This [prospective] study found no association between exposure to ETS and female breast cancer mortality.” 

https://www.ncbi.nlm.nih.gov/pubmed/11036112 

58) “Passive smoking at home and cancer risk: a population-based prospective study in Japanese nonsmoking women” Nishino et al; Cancer Causes & Control 12, 2001 

“[A] significantly inverse association was observed for breast cancer (RR 0.58)” 

https://www.ncbi.nlm.nih.gov/pubmed/11714107 

59) “Active and passive smoking and the risk of breast cancer in women aged 36–45 years: a population based case–control study in the UK” Roddam, British Journal of Cancer 2007 

” Compared with women who were never active nor passive smokers, there was no significant association between passive smoking in the home and breast cancer risk in never smokers (RR 0.89) past smokers or current smokers (0.93).” 

https://www.nature.com/articles/6603859 

60) “Active and passive smoking in breast cancer: prospective results from the Nurses’ Health Study.” Egan, Epidemiology 13, 2002 

“The RR for regular passive smoking at work and at home was 0.90…Results suggest that passive smoking is unrelated to breast cancer.” 

https://www.ncbi.nlm.nih.gov/pubmed/11880753 

61) “Alcohol, Smoking, Passive Smoking and Caffeine in Relation to Breast Cancer in Young Women,” Smith, Brit J Cancer 70, 1994 

“The lack of effect of their own smoking and the fact that such smokers are also themselves exposed to the effects of passive smoking makes any relationship between exposure to others smoking and breast cancer risk implausible.” 

https://www.ncbi.nlm.nih.gov/pubmed/8018520 

PARKINSON’S AND ETS 

62) “Exploring causality of the association between smoking and Parkinson’s disease” Gillis et al, International Journal of Epidemiology, 2018 | Oxford Academic 

Former smokers had a 20% decreased risk and current smokers halved the risk of developing PD compared to never smokers (RR 0.70). A 30% reduced risk was also seen in people exposed to passive smoke compared to those who never smoked. Children of smokers also showed a lower risk of developing the disease. 

https://academic.oup.com/ije/advance-article/doi/10.1093/ije/dyy230/5184917 see also: https://parkinsonsnewstoday.com/2018/11/28/smoking-linked-reduced-parkinsons-risk-but-carries-caveat/ 

STUDIES ON STUDIES: GIGO 

63) “Deception Among Smokers,” Sillett, BMJ, 1978 

“Subjects in two different clinical trials who had been advised to stop smoking were asked if they had done so. 22% (11/51)in the first trial and 40% (33/83) in the second who said they had stopped were found to have raised carboxyhemoglobin concentration. Deception appears to be common in people trying to stop smoking.” 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1608315/ 

64) “Discrepancies between self-reported smoking and carboxyhemoglobin: an analysis of the second national health and nutrition survey.” Klesges, Am J Public Health 1992 

“Those with strong [physiological] evidence of cigarette consumption were 75% more likely to self-report as ex-smokers.” 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1694055/?page=4 

65) “Misclassification of smoking status by self-reported cigarette consumption” Perez ,Am Rev Respir Dis, 1992, 

When self-reports of nonsmoking status were compared with serum cotinine levels, the percentage of misrepresenters in each of three groups ranged from 4%-10.7%. 

https://www.ncbi.nlm.nih.gov/pubmed/1731599 

66) “Misclassification of smoking habits: An updated review of the literature” Hamling et al, World J Meta-anal 7, 2019 

“As percentages of true current smokers [based on cotinine levels] , 14.5% (12.36- 16.65%) claimed to be non-smokers; 5.70% (3.20-8.29%) claimed to be never-smokers ; and 8.93% (6.57-11.29%) claimed to be ex-smokers… There was considerable heterogeneity between misclassification rates. Rates of claiming never smoking were very high in Asian women smokers, the individual studies reporting rates of 12.5%, 22.4%, 33.3%, 54.2% and 66.3%. False claims of quitting were relatively high in pregnant women, in diseased individuals who may recently have been advised to quit, and in studies considering cigarette smoking rather than any smoking. False claims of smoking (3.6%) were higher in younger populations.” 

https://www.wjgnet.com/2308-3840/full/v7/i2/31.htm 

67) “Science, Policy, and Ethics: The Case of Environmental Tobacco Smoke,” Gori, J. Clin Epidemiol 47, 1994 

“Published reports indicate that between 2-10% (average 4.5%) of self-declared nonsmokers are in fact smokers. [Yet] the EPA used a 1.09% correction factor to reach a lung cancer risk estimate of 1.19% [for self-reported nonsmokers exposed to ETS]. Using a ….realistic factor of only 2.5% would nullify any excess risk estimates [for] spousal exposure.” 

https://eurekamag.com/research/044/274/044274441.php 

ON THE EFFECTS OF DENORMALIZING SMOKERS 

68) “Smoking, Stigma and Human Rights in Mental Health…” Warner, Social Policy and Society, 2009, Cambridge Univ. Press 

” The public health agenda on smoking involves the mobilization of stigma to persuade people to give up. …[this] risks adding to the process of ‘othering’ that many already experience and is unlikely to be effective in reducing smoking.” 

http://journals.cambridge.org/action/displayAbstract?aid=4571148 

69) “Tobacco Control, Stigma, and Public Health: Rethinking the Relations, ” Stuber, | AJPH | Vol. 96 Issue 1 2009 

“Wherever stigmatization occurred, the negative consequences were predictable.” 

https://ajph.aphapublications.org/doi/10.2105/AJPH.2005.071886 

70) “The Politics of Smoke: Why Anti-tobacco Policy and Legislation is a Diversity Issue.” Conrad; Habitat Intl. Coalition Conf., 2010 (p.400) 

“It is well within the scope of sociological analysis to examine the implications of the construction by society’s elites of a socially marginalized and financially exploitable pariah class in an effort to promote public health….[The] victories of the strategy have simply added to the misery of the disadvantaged who are disproportionately among the targeted group.” 

http://www.hicsocial.org/SOC2010.pdf (p 406)

71) “Outcasts: The Obese and other victims of denormalization,” Basham, Luik; Democracy Inst, London, Spring 2009 

“Denormalisation [as public health policy] cannot be successful separate from its success in generating the belief that being obese or a smoker is aberrant behavior. It is this artificially generated sense of aberrance and abhorrence which is outside the scope of moral government. To forget this is to forget that the 20th century’s experiments in denormalization ended with the gulag and the concentration camp.” 

http://www.democracyinstitute.org/pdfs/DI%20Denormalisation%20Study.pdf