I agree with the U.N. on one thing; there is not harm in secondhand smoke.
I suggest you read the following:
HEALTH CONSEQUENCES OF SECONDHAND SMOKE — Evidence of the health risks of secondhand smoking comes from epidemiological studies, which have directly assessed the associations of measures of SHS exposure with disease outcomes. Judgments about the causality of associations between SHS exposure and health outcomes are based not only upon this epidemiological evidence, but also upon the extensive evidence derived from epidemiological and toxicological investigation of the health consequences of active smoking. (See "Overview of smoking cessation", section on Benefits of cessation).
The literature on secondhand smoke and health has been periodically reviewed [7,11-14,19,20]. The most recent reviews were completed in 2005 by the California Environmental Protection Agency  and in 2006 by the office of the US Surgeon General . Causal conclusions were reached as early as 1986, when involuntary smoking was found to be a cause of lung cancer in nonsmokers by the International Agency for Research on Cancer , the US Surgeon General , and the US National Research Council . Each of these reports interpreted the available epidemiologic evidence in the context of the wider understanding of active smoking and lung cancer. In spite of somewhat differing approaches for reaching a conclusion, the findings of the three reports were identical: involuntary smoking is a cause of lung cancer in nonsmokers. This and subsequent causal conclusions have broad public health impact. (See "Cigarette smoking and other risk factors for lung cancer").
In 1986, the reports of the US Surgeon General and the National Research Council also addressed the then-mounting evidence of adverse respiratory effects of SHS exposure for children. Subsequent reports, including the 2006 Surgeon General's report, identified further effects of SHS exposure on children, and the more recent reports have classified SHS as causing a number of adverse effects for exposed children (show table 1) .
Annoyance and irritation, although not representing an illness or disease, are also firmly linked to exposure to SHS [7,21]. Surveys document discomfort involving the eye and upper airways; confirmatory evidence has been provided by studies involving exposures of volunteers to SHS in chambers.
Effects in children — There is an extensive list of adverse effects that various groups have concluded are causally associated with exposure of infants and children to SHS (show table 1). Exposure to SHS has been found to be a cause of slightly reduced birth weight, lower respiratory illnesses, chronic respiratory symptoms, middle ear disease, reduced lung function, ever having asthma among children of school age, and the onset of wheeze illness in early childhood . Maternal smoking has been characterized as a major cause of sudden infant death syndrome (SIDS), as has exposure to SHS generally. The conclusions of the other recent reports, including those from the California Environmental Protection Agency  and the United Kingdom's Scientific Committee on Tobacco  are similar.
Growth and development — Active smoking by pregnant women, resulting in secondhand smoke exposure for the developing fetus, increases risk for a variety of adverse health effects in children; these effects are hypothesized to result primarily from transplacental exposure of the fetus to tobacco smoke components. Maternal smoking during pregnancy reduces birth weight [5,14,22,23]. SHS exposure of nonsmoking mothers is associated with reduced birth weight as well, although the extent of the reduction is far less than for active maternal smoking during pregnancy. Summary estimates of the reduction of birth weight associated with paternal smoking range from 24 to 31 grams [24,25]. Adverse effects of in utero or postnatal exposure to SHS on neuropsychological development and physical growth have also been postulated. A number of components of SHS may produce these effects, including nicotine and carbon monoxide.
Other nonfatal perinatal health effects possibly associated with SHS exposure are growth retardation [26-28] and congenital malformations. The few studies conducted to assess the association between paternal smoking and congenital malformations have demonstrated risks ranging from 1.2 to 2.6 for exposed compared with nonexposed children [29-31].
Sudden infant death syndrome — Sudden infant death syndrome (SIDS) refers to the unexpected death of a seemingly healthy infant while asleep. Although maternal smoking during pregnancy has been causally associated with SIDS, these studies measured maternal smoking after pregnancy, along with paternal smoking and household smoking generally. (See "Sudden infant death syndrome", section on Maternal risk factors).
In the WHO consultation, the evidence on secondhand smoke (post-birth) and SIDS was considered inconclusive, although there was some indication of increased risk . Based on further evidence, the California EPA concluded that secondhand smoke is a cause of SIDS . The conclusions of both the 2004 and 2006 Surgeon General's reports state that the scientific evidence is insufficient to infer a causal relationship between exposure to secondhand smoke and sudden infant death syndrome [5,32]. The 2006 report goes on to state that tobacco smoke exposure is one of the major preventable risk factors for SIDS, and all measures should be taken to protect infants from exposure to secondhand smoke.
Childhood cancers — Secondhand smoke, including maternal smoking during pregnancy, has been evaluated as a risk factor for the major childhood cancers. The evidence is limited and does not yet support conclusions about the causal nature of the observed associations. In a meta-analysis conducted for the WHO consultation, the pooled estimate of the relative risk for any childhood cancer associated with maternal smoking was 1.11 (95% CI 1.00-1.23) and that for leukemia was 1.14 (95% CI 0.97-1.33) .
Lower respiratory tract illnesses — Infants with smoking parents have an increased risk of lower respiratory tract illness, including a significantly increased frequency of bronchitis and pneumonia during the first year of life [5,33-36]. Presumably this association represents an increase in frequency or severity of illnesses that are infectious in etiology and not a direct response of the lung to the toxic components of SHS. Effects of exposure in utero on the airways may also play a role in the effect of postnatal exposure on risk for lower respiratory illnesses.
The approximate increase in lower respiratory illness risk is 50 percent if either parent smokes, with a somewhat greater increase for maternal smoking specifically (odds ratio 1.70 [95% CI 1.56-1.84]) . Although health outcome measures have varied somewhat among the various studies, the relative risks associated with involuntary smoking were similar, and dose-response relationships with the extent of parental smoking have been demonstrated.
Most studies have shown that maternal smoking rather than paternal smoking underlies the increased risk of parental smoking, although studies from China show that paternal smoking alone can increase the incidence of lower respiratory illness [36,37]. An effect of secondhand smoke has not been readily identified after the first few years of life; this finding may be explained by higher exposures because of the time-activity patterns of young infants, which place them in close proximity to cigarettes smoked by their mothers.
Respiratory symptoms and illness — Numerous surveys demonstrate a greater frequency of the most common respiratory symptoms: cough, phlegm, and wheeze, in the children of smokers [7,12,15,38]. In a meta-analysis prepared for the 2006 US Surgeon General's report of the relevant studies, including 45 of wheeze, 39 of chronic cough, 10 of chronic phlegm, and 6 of breathlessness, calculated pooled odds ratios for either parent smoking as 1.23 (95% CI 1.14-1.33) for asthma, 1.26 (95% CI 1.20-1.33) for wheeze, 1.35 (95% CI 1.27-1.43) for cough, 1.35 (95% CI 1.30-1.41) for phlegm, and 1.31 (95% CI 1.14-1.50) for breathlessness . Having both parents smoke was associated with the highest levels of risk (show table 2).
Participants in these studies have generally been school children. The less prominent effects of secondhand smoke in comparison with the studies of lower respiratory illness in infants may reflect lower exposures to SHS by older children who spend less time with their parents.
Asthma — Exposure to SHS may be a cause of asthma as a long-term consequence of the increased occurrence of lower respiratory infection in early childhood, or through other pathophysiological mechanisms including inflammation of the respiratory epithelium [5,39,40]. In utero exposures from maternal smoking may also affect lung development and increase the risk for asthma. As an example, assessment of airways responsiveness shortly after birth has shown that infants whose mothers smoked during pregnancy have increased airways responsiveness, a characteristic of asthma, compared with those whose mothers did not smoke . Maternal smoking during pregnancy also reduced ventilatory function measured shortly after birth .
While the underlying mechanisms remain to be identified, the epidemiologic evidence linking SHS exposure and childhood asthma is mounting [12,38]. There is a significant excess of childhood asthma if both parents or the mother smoke (show table 2) [5,38]. Exposure to secondhand smoke during childhood is also associated with increased prevalence of asthma in adults .
Involuntary smoking also appears to worsen the status of children with asthma, as demonstrated by the following observations:
In an evaluation of asthmatic children followed in a clinic, level of lung function, symptom frequency, and responsiveness to inhaled histamines were adversely affected by maternal smoking [44,45].
Population studies have also shown increased airways responsiveness for SHS-exposed children with asthma [46,47].
Exposure to smoking in the home increases the number of emergency department visits made by asthmatic children .
Asthmatic children with smoking mothers are more likely to use asthma medications .
Guidelines for the management of asthma all urge reduction of SHS exposure at home . (See "NAEPP Expert Panel Report II: (6) Control of factors contributing to asthma severity").
Lung growth and development — During childhood, measures of lung function increase are more or less parallel to increase in height. Parental smoking adversely affects growth of lung function during childhood [5,7,12,15,51-53]. In a study of 193 high school athletes, for example, there was a fourfold increase in incidence of low forced expiratory flow 25 to 75 percent (FEF25-75) and/or cough in athletes exposed to secondhand smoke compared with athletes not exposed . The WHO consultation noted the difficulty of separating effects of in utero exposure from those of childhood SHS exposure .
Middle ear disease — Positive associations between SHS and otitis media have been consistently demonstrated in prospective cohort studies, but not as consistently in case-control studies. This difference in findings may reflect the focus of the cohort studies on the first two years of life, the peak age of risk for middle ear disease. The case-control studies, on the other hand, have been directed at older children who are at lower risk for otitis media. Exposure to SHS has been most consistently associated with recurrent otitis media and not with incident or single episodes. The meta-analysis prepared for the 2006 US Surgeon General's report found a pooled odds ratio of 1.37 (95% CI 1.10-1.70) for recurrent otitis media if either parent smoked; a pooled odds ratio for prevalence of middle ear effusion of 1.33 (95% CI 1.12-1.58) if either parent smoked; and an odds ratio of 1.20 (95% CI .90-1.60) for clinical referrals or operative interventions for middle ear effusions if either parent smoked .
The US Surgeon General's Office [5,7], the National Research Council , and the US Environmental Protection Agency  have all reviewed the literature on SHS and otitis media and concluded that there is an association between SHS exposure and otitis media in children. The evidence to date supports a causal relationship [5,14].
Dental caries — Exposure to SHS may be associated with an increased risk of dental caries in children. A cross-sectional study of dental caries and serum cotinine levels in 3531 children ages 4 to 11 found that elevated cotinine levels were associated with caries in deciduous but not permanent teeth in a multivariate model .
Effects in adults
Lung cancer — The exposure to carcinogens with SHS is far less than the exposure that occurs with active smoking. On the other hand, exposure to SHS can begin in childhood and extend across the full lifespan. (See "Cigarette smoking and other risk factors for lung cancer").
An association between involuntary smoking and lung cancer is biologically plausible based upon the presence of carcinogens in sidestream smoke and the lack of a documented threshold dose for respiratory carcinogens in active smokers [10,55]. Furthermore, genotoxic activity, the ability to damage DNA, has been demonstrated for many components of SHS [56-58]. As mentioned above, experimental exposure of nonsmokers to SHS results in the urinary excretion of NNAL, a tobacco-specific carcinogen . Nonsmokers, including children, exposed to SHS also have increased concentrations of adducts of tobacco-related carcinogens [60,61].
A number of studies have shown that SHS is associated with lung cancer, and various review panels, including the 2006 Surgeon General's report, have concluded that SHS exposure causes lung cancer in nonsmokers [5,7-11,62,63]. There appears to be a dose-response relationship between intensity of exposure and relative risk.
Results of a meta-analysis including 52 studies and prepared for the 2006 Surgeon General's report showed that the relative risk of lung cancer among male and female nonsmokers who were ever exposed to secondhand smoke from the spouse was 1.21 (95% CI 1.13-1.30). The magnitude of the effect was comparable for men (odds ratio 1.37 [95% CI 1.05-1.79]) and women (odds ratio 1.22 [95% CI 1.13-1.31]), with no significant difference by geographic area .
A meta-analysis of 25 studies of lung cancer and exposure to secondhand smoke in the workplace prepared for the 2006 US Surgeon General's report estimated a pooled relative risk of 1.22 (95% CI 1.13-1.33) .
Another exposure of concern is that of adults exposed as children to smoking parents. A meta-analysis of 24 studies found that, for men and women exposed during childhood to smoking by either parent, the odds ratio of lung cancer was 1.11 (95% CI 0.94-1.31) . For maternal exposure only, the odds ratio was 1.15 (95% CI 0.86-1.52), while for paternal exposure only, the odds ratio was 1.10 (95% CI 0.89-1.36).
In a prospective cohort study of 91,540 nonsmoking women in Japan, standardized mortality ratios (SMRs) for lung cancer increased significantly with the amount smoked by the husbands . The findings could not be explained by confounding factors and were unchanged when follow-up of the study group was extended . There was also a significantly increased risk for nonsmoking men married to wives smoking one to 19 cigarettes and 20 or more cigarettes daily.
In a population based, case-control study, household exposure to 25 or more smoker-years during childhood and adolescence doubled the risk of lung cancer, whereas exposure to fewer than 25 smoker-years did not increase the risk . It was estimated that 17 percent of lung cancer in nonsmokers is attributable to high levels of environmental smoke exposure during childhood and adolescence.
In another similarly designed study, tobacco use by the spouse was associated with a 30 percent increase in risk of lung cancer . The risk rose with increasing levels of pack-year exposure from the spouse; 80 or more pack-years of exposure was associated with an 80 percent excess risk of lung cancer.
A meta-analysis of 37 published studies involving 4626 people with lung cancer found an excess risk of lung cancer of 24 percent (95% CI 13-36 percent) if an individual lived with a smoker . Adjustment for potential bias and confounding by diet did not alter the estimate. A significant dose-response relationship with the number of cigarettes smoked by the spouse and the duration of exposure was also documented. However, the absolute risk reduction from eliminating this exposure was small, with approximately 1250 persons required to stop smoking in order to prevent one case of lung cancer. Furthermore, it has been suggested that this analysis overestimated the carcinogenicity of secondhand smoke because of publication bias .
A cohort study subsequent to the above meta-analysis did not find an excess risk of lung cancer in spouses of smokers after 39 years of follow-up; however, the results of this study are weakened by its limited data on spousal smoking, which was only fully assessed at the start of the study without subsequent updating . Additionally, the author of the above meta-analysis reports that when the data from this later study were incorporated, there was little effect on the point estimate of the meta-analysis (excess risk reduced from 24 to 23 percent) .
Based upon the available data, the United Kingdom's Scientific Committee on Tobacco and Health concluded that exposure to secondhand smoke is a cause of lung cancer . The US Environmental Protection Agency has classified SHS as a Group A carcinogen, that is, a known human carcinogen . The International Agency for Research on Cancer (IARC) reached the same conclusion in 2002 .
The risk for the development of lung cancer in response to secondhand smoke may be influenced by genetics. One study found a significant increase in polymorphisms in the gene glutathione S-transferase M1 among 51 nonsmoking women with exposure to environmental tobacco smoke who developed lung cancer compared with 55 nonsmoking women with lung cancer who had no environmental tobacco smoke exposure . Glutathione S-transferase M1 is believed to play a role in detoxifying carcinogens in tobacco smoke; thus, mutations which decrease its activity could serve to promote tumorigenesis.
Cardiovascular disease — Causal associations between active smoking and fatal and nonfatal coronary heart disease (CHD) outcomes have long been demonstrated . The risk of CHD in active smokers increases with amount and duration of cigarette smoking and decreases quickly with cessation. Active cigarette smoking is considered to :
Increase the risk of cardiovascular disease by promoting atherosclerosis
Increase the tendency to thrombosis
Cause coronary artery spasm
Increase the likelihood of cardiac arrhythmias
Decrease the oxygen-carrying capacity of the blood
Affect vascular endothelial cell function
(See "Cardiovascular risk of smoking and benefits of smoking cessation").
It is biologically plausible that secondhand smoke could be associated with increased risk for CHD through the same mechanisms considered relevant for active smoking, although the lower exposures to smoke components of secondhand smoke have raised questions regarding the relevance of the mechanisms cited for active smoking [73,74]. One study found that 30 minutes of exposure to secondhand smoke in healthy young volunteers compromised coronary artery endothelial function in a manner that was indistinguishable from that of habitual smokers, suggesting that endothelial dysfunction may be an important mechanism by which secondhand smoke increases CHD risk . A cross-sectional study found that after controlling for some potential confounders, exposure to secondhand smoke was associated with increased inflammatory markers including higher white blood cell counts and levels of C-reactive protein, homocysteine, fibrinogen, and oxidized LDL cholesterol . Animal models also indicate adverse effects of SHS on the cardiovascular system.
A 1985 cohort study first raised concern that passive smoking may increase risk for CHD . There are now more than 20 studies on the association between SHS and cardiovascular disease. These studies assessed both fatal and nonfatal cardiovascular heart disease outcomes, and most used self-administered questionnaires to assess SHS exposure. They cover a wide range of racial and geographic populations. The majority of the studies measured the effect of SHS exposure due to spousal smoking; however, some studies also assessed exposures from smoking by other household members or occurring at work or in transit. Some studies have also included measurements of biomarkers.
While the risk estimates for SHS and CHD outcomes vary in these studies, they range mostly from null to modestly significant increases in risk, with the risk for fatal outcomes generally higher and more significant. The meta-analysis prepared for the 2006 US Surgeon General's report estimated the excess risk from SHS exposure as 27 percent (95% CI 19-36 percent) .
A cohort study reported in 2003 did not find an excess risk of CHD in spouses of smokers after 39 years of follow-up; however, the results of this study are weakened by its limited data on spousal smoking, which was only fully assessed at the start of the study .
A prospective cohort study performed in 2004 measured serum cotinine levels . The study included 4729 men in the United Kingdom who provided baseline blood samples in 1978 to 1980. After 20 years of follow-up, among the 2105 men who were nonsmokers, the risk of CHD was increased in those with higher serum cotinine concentrations. Compared with men in the lowest quartile of serum cotinine concentration, after adjusting for established CHD risk factors, the risks in the second, third, and fourth quartiles were 1.45, 1.49, and 1.57, respectively. No consistent association was found between serum cotinine concentration and stroke.
A before-after study in Helena, Montana looked at the effect of a local law banning smoking in public and in workplaces; the law was in effect for six months, and then enforcement was suspended by a court order . Admissions of people living in Helena for acute myocardial infarction to the single hospital serving the area decreased significantly from an average of 40 admissions during the same six months in the years before and after the ban to 24 admissions during the ban; admissions of people not living in Helena showed no significant change. Although these and other data suggest acute effects of SHS on cardiovascular risk , the results in Helena could have been due to a decrease in exposure to SHS, to a decrease in active smoking caused by the ban, or both. The study does suggest, however, that laws that limit public and workplace smoking may result in rapid decreases in the risk of acute myocardial infarction within a community.
SHS may also be associated with noncardiac vascular disease. A large cross-sectional study of 60,377 women in China found an association between stroke in women and smoking by their husbands . The prevalence of stroke increased with greater duration of smoking and with an increasing number of cigarettes smoked daily.
In 1997, the California Environmental Protection Agency (CalEPA) concluded that there is "an overall risk of 30 percent" for CHD due to exposure from SHS . In 2005, the CalEPA established that 22,700 to 69,000 deaths from CHD were attributable to SHS in 2000 . The American Heart Association's Council on Cardiopulmonary and Critical Care concluded in 1992 that SHS both increases the risk of heart disease and is "a major preventable cause of cardiovascular disease and death" . This conclusion was subsequently echoed in 1998 by the Scientific Committee on Tobacco and Health in the United Kingdom , both CalEPA reports, and in the 2006 Surgeon General's report, which also stated that pooled relative risks from meta-analyses indicate a 25 to 30 percent increase in the risk of coronary heart disease from exposure to secondhand smoke .
Respiratory symptoms and illnesses — Only a few cross-sectional studies have investigated the association between respiratory symptoms in nonsmokers and involuntary exposure to tobacco smoke. These studies have primarily considered exposure outside the home. Consistent evidence of an effect of passive smoking on chronic respiratory symptoms in adults has not been found [83-89]. Several studies suggest that passive smoking may cause acute respiratory morbidity, ie, illnesses and symptoms [90-96].
Neither epidemiological nor experimental studies have established the role of SHS in exacerbating asthma in adults. The acute responses of asthmatics to SHS have been assessed by exposing persons with asthma to tobacco smoke in a chamber. This experimental approach cannot be readily controlled because of the impossibility of blinding subjects to exposure to SHS. However, suggestibility does not appear to underlie physiological responses of asthmatics of SHS . Of three studies involving exposure of unselected asthmatics to SHS, only one showed a definite adverse effect [44,98-100]. One study recruited 21 asthmatics who reported exacerbation with exposure to SHS . With challenge in an exposure chamber at concentrations much greater than typically encountered in indoor environments, seven of the subjects experienced a more than 20 percent decline in FEV1.
Lung function — Exposure to secondhand smoke has been associated in cross-sectional investigations with reduction of several lung function measures. However, the findings have not been consistent and methodologic issues constrain interpretation of the findings. Thus, a conclusion cannot yet be reached on the effects of SHS exposure on lung function in adults.
Diabetes — Some evidence suggests that active smoking may be a risk factor for diabetes, although the association between smoking and diabetes is not clearly causal. (See "Prediction and prevention of type 2 diabetes mellitus", section on Smoking.) A 15-year cohort study also found an increased incidence of glucose intolerance in young adults ages 18 to 30 exposed to SHS .
All-cause mortality — There are relatively few data on the association between all-cause mortality and SHS. Follow-up of never-smokers ages 45 to 74 years from the 1981 and 1996 censuses in New Zealand suggest that nonsmoking adults who lived with smokers had about a 15 percent increase in adjusted mortality compared with those living in a smoke-free household .