Occupational and Environmental Lung Diseases: Diseases from Work, Home, Outdoor and Other Exposures

Documents both environmental and work-related causes of lung disease

Unlike other books on the subject, this new volume approaches occupational and environmental lung disease from the starting point of the patient who comes to the physician with respiratory symptoms. The authors recognize that potentially harmful exposures occur not only in the work environment, but also as a result of hobbies or other leisure activities, or from outdoor air pollution, and it is up the physician to identify whether a particular job or hobby is the cause of the patient’s respiratory symptoms.
To help you arrive at a differential diagnosis, chapters in the book are arranged by job or exposure, and are divided into 5 sections:

• Personal environment
• Home environment
• Other indoor environments
• Work environment
• General environment

Each is written by an expert in the specific topic and provides pragmatic information for the practicing physician. This practical book is an invaluable resource that belongs close at hand for all physicians dealing with patients experiencing respiratory symptoms.

• Language: English
• Publisher: Wiley
• Release date: Jun 24, 2011
• ISBN: 9781119957225

Book preview

Part I

The personal environment

1

Cosmetics and personal care products in lung diseases

Howard M. Kipen

UMDNJ-Robert Wood Johnson Medical School, Piscataway, NJ, USA

1.1 Introduction: historical context of cosmetics and respiratory illness

Cosmetics may be associated with respiratory illness through two different but overlapping mechanisms. One is via causation of pathological disease, most prominently related to allergen-mediated mucosal and airway responses. The second mechanism is through symptoms and illness behavior associated with odors from the cosmetics. The extent to which these symptoms may also interact with mucosal irritant properties of the agents makes differentiation between airway pathology and symptoms unrelated to airway pathology at times problematic. This chapter will describe the data supporting different disease mechanisms and appropriate clinical and preventive responses.

A wide range of individuals, rather than typically ‘healthy workers’, regularly come into contact with personal care products such as soaps, perfumes and hair products. Many of these products are designed to announce their presence to those nearby (perfume odors), and they encompass a diverse array of chemical substances. Odordriven responses may be from the essential product, such as a perfume essence, or added material contained in a mix, such as fragrances added to a hairspray or after-shave. While behavioral effects of agents such as perfumes are intentional and legendary, the association of physical pulmonary conditions with cosmetic products was not reported until the late 1950s. Around 1960 a series of cases reporting a ‘storage disease’ (thesaurosis) or pneumonitis (‘hairspray lung’) were published. However a prevalent condition of the pulmonary parenchyma was never established (possibly due to various changes in hairspray formulations) and all subsequent concern with respiratory effects of cosmetic and personal care agents has centered on the airways, particularly asthma. The first report of allergic occupational asthma in hairdressers is attributed to Jack Pepys [1] in 1976. The remainder of this chapter will consider both allergic airway disease from cosmetics and personal products and the more complex nonallergic responses to odors.

1.2 Epidemiological context

1.2.1 Occupational exposure to cosmetics and personal care products

Data from the USA reveal the substantial size of the workforce involved in cosmetology. According to the US Bureau of Labor Statistics, barbers, cosmetologists and other personal appearance workers held about 790,000 US jobs in 2004. Of these, barbers, hairdressers, hairstylists and cosmetologists held 670,000 jobs; manicurists and pedicurists 60,000; skin care specialists 30,000; and shampooers 27,000. Because most of the relevant scientific literature pertains specifically to hairdressers, this term will be used for the remainder of the chapter. There is no available data on the number of individuals involved in the perfume industry.

Although methods for ascertainment differ greatly between countries, the burden of airway disease in hairdressers has been quantitiated in many different nations. Methodologies of varying rigor, including some that are population-based, have documented apparent excesses of asthma and respiratory symptoms relative to the general population among hairdressers working in Sweden, France, Germany, Belgium, Norway, Turkey and Italy.

A 2002 questionnaire study of all active Swedish hairdressers showed an asthma incidence rate ratio of 1.6 in never smokers, comparable to the effect of smoking alone in the same group. There was also a nonsignificant excess risk of asthma for self-reports of more frequent exposure to bleaching agents or hairsprays. Interestingly, there was no effect modification by reported atopy and no dose-response relationships for use of persulfates, at variance with much of the clinical data cited below that emphasize the role of persulfate exposure.

Iwatsubo and colleagues [2] found no increased respiratory symptoms among hairdressing apprentices compared with office apprentices, but there was a significant decline in FEV1 and FEF25-75 (forced expratory flow), not linked to any specific hairdressing activities. Other studies from France are based on the voluntary national physician reporting program for occupational asthma (Observatoire National des Asthmes Professionels). French asthma incidence rates for hairdressers are 308/million, placing hairdressers at the third highest risk for occupational asthma after bakers and pastry makers (683/million) and car painters (326/million).

In Belgium questionnaires completed by hairdressing students showed that 14.1% had already had asthma and 26.7% reported wheezing over the past 12 months. A 1996 study estimated that the burden of work-related asthma in Turkish hairdressers was 14.6%. In Italy about half of a group of hairdressers referred for work-related respiratory symptoms were found to have occupational asthma by specific inhalation challenge, along with a strong association with occupational rhinitis.

1.2.2 Non-occupational exposure to cosmetics and personal care products

In a Danish nonoccupational population-based study that included methacholine challenge and skin prick testing it was found that there was no relationship between perfume-associated significant symptoms and atopy, serum ECP or FEV1. However, 42% of subjects reported ocular or airway symptoms from exposure to fragrance, and these 42% were 2.3 times as likely to have bronchial hyperreactivity (BHR) as those without symptoms, suggesting a link between fragrance responses and this defined physiological vulnerability. The fact that 30-40% of those who reported respiratory symptoms in this population-based study had a positive BHR test suggests the possible import of fragrance-induced symptoms, although physiological studies in vulnerable or symptomatic individuals, discussed below, suggest that these relationships are quite complex.

Reported provocation of symptoms by environmental chemicals, prominently including perfumes and cosmetics, typically detected by odor, has been shown to be common, averaging about 10-20% of random samples with a range of 10-60% of more specific subpopulations, asthmatics being a prominent subgroup. A more extreme form of such reported sensitivity to chemicals is multiple chemical sensitivities (MCS) or idiopathic environmental intolerance (IEI). In this case the sensitivity to odors affects behavior and social interactions, becoming potentially disabling. No clear physiological abnormalities or explanations have been discovered. Although many clinicians and researchers favor psychological mechanisms for such odor-induced symptoms, there is substantial disagreement.

Of particular interest to pulmonologists, individuals fitting the description of MCS seem to have a high rate of pulmonary symptoms. Although data come from clinical series, when compared with age- and sex-matched controls, MCS individuals reported on questionnaires from 1.5 to over 10 times the rate of upper and lower respiratory symptoms, and as suggested above, individuals with asthma report higher rates of provocation by cosmetics and personal care products.

1.3 Description of exposures

1.3.1 Major work processes

Hairdressers, besides cutting and shampooing hair, are involved in permanent wave applications and rinsing, in applications of neutralizing agent, in preparing, applying and rinsing hair color, and in preparing, applying and rinsing hair bleaches. Mixing of bleaching powder takes 2-5 minutes per treatment, and it is thought that most exposure to persulfates occurs in this phase, often done in a back room of the salon, rather than during application in the salon per se.

1.3.2 Occupational exposures

Hair dressers have three main classes of workplace exposures:

1. para-phenylamine diamine based dyes, generally associated with delayed hyper-sensitivity contact dermatitis;

2. henna (vegetable dye), a rare cause of occupational asthma; and

3. lacquers and bleaching agents with persulfate salts, known to cause dermatitis, rhinitis and asthma.

We focus on the latter for this respiratory disease text.

There are three categories of hair-dye formulation used respectively for temporary, semi-permanent and permanent hair coloring. The latter are also known as oxidative dyes and are resistant to shampooing. The permanent dyes almost invariably contain ammonium, potassium and sodium persulfates. Persulfate salts are reactive, low-molecular weight compounds widely used in many industries, but particularly cosmetics. The persulfates (H2S2O8) are mixed with an oxidant (H2O2) immediately before use. Improved hair penetration is achieved with the addition of ammonia releasers such as ammonium chloride or ammonium phosphate. Permanent waving chemicals can be either alkaline or slightly acidic aqueous solutions. They contain thioglycolic acid or hydrogen peroxide, with ammonia added to enhance hair penetration. Thus, potent irritants/oxidants including ammonia, hydrogen peroxide (H2O2) and persulfates (H2S2O8) are commonly found in the hairdressing environment.

Hair bleaching agents are generally felt to be the most common cause of occupational asthma in hairdressers; however not all studies report that duration of exposure was significantly greater in those who became sensitized. They are the leading causes implicated in specific occupational asthma reports from France and Italy.

1.3.3 Perfumes and nonoccupational exposures

Perfumes are blends of odiferous ingredients made from a diluent (commonly ethanol) and mixtures of up to 3000 natural and synthetic fragrance ingredients including volatile oils and aldehydes, potential irritants and sensitizers. Because many of the ingredients are volatile, exposure is widespread, either intentionally or incidentally in proximity to users. Cleaning agents for home or commercial use are associated with asthma, and also contain perfume agents as well as cleaning agents that may be respiratory irritants or sensitizers.

1.3.4 Quantitation of exposures in hair salons

In a Swedish study exposures to persulfates during mixing were associated with personal exposures of 35-150 μg persulfates/m³ and mixing area exposures ranged from 23-50 μg persulfates/m³. In a study of exposure in French salons, H2O2 showed mean personal exposure levels of 51 μg/m³, NH3 was 900 μg/m³ and persulfate was 190 μg/m³. These values are below applicable workplace standards, although many deficiencies in ventilation were noted in this study and would seem to be common in the industry.

1.3.5 Exposure history: practical advice and pitfalls

It is important to understand the layout of a salon, including any separate rooms in which mixing of hair products takes place. Specific questions about windows or mechanical ventilation are important. Although ventilation in salons is often reported as substandard, in the rare instances when exposures have been measured, they have been typically less than applicable threshold limit values (TLV) (H2O2, NH3 and H2S2O8) on either side of the Atlantic. This may reflect that the salons studied were not completely representative of all salons. Of course, for individuals who have become sensitized, adherence to threshold limit values cannot be relied upon to prevent future reactions.

1.3.6 Documentation of exposure and biomonitoring

Exposure monitoring in salons is not commonly performed, and measures of persistent body burden do not exist and are probably not appropriate to the natural history of the relevant conditions. Moscato [3] reports that, although some hairdressers with asthma have positive skin tests to persulfate, it is not a reliable test of sensitization, because many individuals with disease and apparent exposure have negative tests. As with other prominent causes of occupational asthma, especially for low molecular weight antigens, the available skin test is not clearly immunologically (IgE) mediated. One caveat is that anaphylaxis to persulfate skin testing has been reported.

1.4 Respiratory diseases associated with exposure to cosmetics and personal care products

1.4.1 Occupational asthma

Occupational asthma in hairdressers is felt to arise most commonly from sensitization to persulfate salts, although there are case reports with henna as the sensitizer. Pulmonary function test changes and development of asthma are reported during apprenticeship, although latencies of up to 10-15 years appear in the literature. Most published descriptions of occupational asthma in hairdressers is of the allergic sensitization variant; however, there are a limited number of publications describing more immediate responses apparently independent of sensitization. The immunological basis of the sensitization has not been elucidated.

One provocative study implicated hairsprays as triggers of pre-existing asthma. Schleuter and colleagues [4] studied immediate responses to hairspray in 1979. They reported a 10-20% decrease in mid flows in eight asthmatics, with no response in 13 healthy subjects to a 20 second spray of two hairsprays. The investigators attributed this bronchoconstriction response to the perfume content of the hairspray rather than the plasticizer, diethyl phthalate. However, this and other phthalates in indoor air from building products have been subsequently epidemiologically implicated in asthma induction, and they are still prevalent in hairspray at concentrations of up to 3%. Further examination of a potential role for phthalates in respiratory irritation and asthma is warranted, in both occupational and nonoccupational settings. For more information on the use of phthalates in cosmetics see: http://www.safecosmetics.org/docUploads/NotTooPretty_r51.pdf

1.4.2 Responses to odors

Cone and Shusterman [5] discussed the health effects of indoor odors. They emphasized variability in the human odor response, and that perfumes are a commonly reported exacerbating agent for asthma. The citation supporting the relationship between perfume and asthma derives from a commonly cited convenience sample of 60 asthmatics specifically recruited by Shim and Williams [6] with sensitivity to odors in mind. They documented that physiological responses to odor provocation could occur; and that atropine, beta agonists and cromolyn abrogated responses in three out of four subjects tested. However, subjects were not blind to test exposures and thus the response could have been perceptual rather than irritant. In fact, they raised the possibility of behavioral sensitization to odorants. The differentiation between irritant/allergic airway effects as opposed to behaviorally or perceptually mediated effects is a recurring theme when considering the human (respiratory) response to cosmetics and personal care products. This differentiation is more frequently an issue in general environmental contexts rather than occupational contexts.

Relationships have been documented in individuals among asthma symptoms, hay fever and chemical odorants. A number of well-controlled studies have shown that perfume stimuli induce respiratory symptoms in asthmatics but not always with accompanying physiological change. Millquist [7-9] exposed nonasthmatics, with a history of respiratory symptoms (but no airway obstruction) following nonspecific irritating stimuli, to perfume. She elicited respiratory symptoms (as well as hoarseness, eye irritation, headache and fatigue) without airway obstruction. The symptomatic responses persisted even after using a carbon filter to block odor. In a subsequent study of ocular exposure to perfume, she again elicited asthma symptoms, even in the absence of hyperventilation, as documented by stable end-tidal CO2. A sensory mechanism, possibly via the trigeminal nerve, was hypothesized, and this integrative approach is a promising avenue for further exploration of individual responses, as well as for therapy. Lastly, she exposed 10 asthmatics (all with provocative concentration for 20% fall in FEV1 < 2 mg/ml) to a commercial perfume and found no change in FEV1 compared with a saline exposure and no increase in symptoms.

Similarly Opiekun et al. [10] studied mild and moderate asthmatics following a 30 minute controlled exposure to a prototypical fragranced air-sanitizing product. They found increased nasal symptoms, but there were no explanatory physiological changes in nasal mucosal swelling (measured by acoustic rhinometry), no ocular hyperemia, and no significant changes in FEV1 (other spirometric values were not reported) at 5 or 30 minutes after exposure. These investigations document that both asthmatics and nonasthmatics can respond to perfumes with respiratory symptoms, yet no significant bronchoconstriction. Making this determination between physiological airway responses and perceived respiratory distress can be challenging for the clinician.

There are reports of those with immediate asthmatic (symptom) responses to perfume; however no analytic epidemiology addresses this issue per se. There is substantial literature on how professional cleaners/janitors and users of cleaning sprays have increased asthma morbidity; however this may be more associated with some of the cleaning agents as opposed to the scents and is addressed elsewhere in this book. Attempts to separate the effects of the alcohol vehicle from the active perfume ingredients have suggested that both may play a role in production of spirometric effects and symptoms, with more severe and atopic asthmatics showing greater responses to perfume challenge.

1.4.3 Unexplained symptoms and psychophysiological responses

As suggested in Millquist’s work above, many individuals suffer from episodic respiratory symptoms, sometimes triggered by environmental exposures, but do not meet diagnostic criteria for asthma or other conditions: they do not have bronchospasm. Prominent among reported triggering exposures are cosmetics, with frequently described exposures including cosmetic counters at department stores, churches and office or classroom environments where coworkers use perfumes and other cosmetics. The limited epidemiology has been described above, but there are a number of pertinent clinical studies that have been carried out and suggest the importance of odor-triggered neural mechanisms as explanations for these symptoms.

Van den Bergh suggested learned responses to odors of a Pavlovian nature that can be conditioned or deconditioned. A group in Toronto found that panic symptoms could be triggered by standardized stimuli much more readily in those with unexplained symptoms and suggested a relationship between unexplained symptoms, panic attacks and hyperventilation. Although this has not been studied in asthmatics, and does not directly concern perfume scents, it provides a potential mechanistic underpinning to understand individuals with complaints of respiratory distress attributed to scents, and suggests the design of behaviorally based therapeutic strategies where pathological pulmonary disease has been excluded.

1.5 Diagnosis and management of occupational asthma in hairdressers

There are no randomized trials to guide diagnosis or management of occupational asthma in hairdressers. Diagnosis of occupational asthma in hairdressers is not always straightforward due to the lack of reliable markers of sensitization to persulfate salts as discussed above, but general methods have been reviewed [11]. Both immediate and delayed symptom responses are reported. Because an underlying IgE mechanism is not reliably demonstrated, immunological tests by skin prick or serum-specific IgE lack both sensitivity and specificity. Thus, reliable confirmation of clinical suspicion relies on specific inhalation challenge testing. Various techniques have been described, although such challenges are not in widespread use in many areas of the world, particularly the USA.

Treatment of allergic occupational asthma is via standard protocols with avoidance of exposure at the top of the list. Once a diagnosis of occupational asthma in a hairdresser, usually to persulfate salts, has been made, exposure reduction or elimination is the most desirable therapeutic alternative. Use of respiratory protection is described but without apparent success, and improved hygiene of salons is often difficult to accomplish. In one study of eight cases, mean exposure duration prior to diagnosis was 15 years and mean duration of symptoms before diagnosis was 38 months, suggesting that improved surveillance could be a key to reducing morbidity.

1.5.1 Medical management of reactions to scented products

Once physiological responses to environmental or occupational exposures have been excluded, a more difficult set of management challenges faces the practitioner. Pulmonary medications have little relevance unless there is comorbid asthma. Speech therapy or behavioral approaches may be useful for upper airway (vocal cord) dysfunction, which may be triggered by irritants and possibly nonirritating odors.

Psychotherapy, anxiolytic medication, cognitive-behavioral therapy (CBT) and biofeedback have all been tried clinically, and have shown responses for individual cases in resolving respiratory and other symptoms associated with odiferous stimuli. More rigorous randomized trials have been conducted in broader groups of somatizing patients, and shown significant, 20-40%, improvement in symptoms and limitations, with courses of cognitive-behavioral therapy.

Blind referrals to mental health practitioners are often ineffective. The referring pulmonologist must clearly communicate that organic lung disease has been excluded, freeing the mental health practitioner to concentrate on reducing symptomatic responses, possibly even in the face of continued exposure to moderate levels of nonsensitizing cosmetics.

The ideal CBT takes place in the setting of a physician’s office, as some patients with these symptoms are reluctant to view their symptoms as psychological. It is sometimes useful to convey to the patient that they need to demonstrate the power of ‘mind over matter’, developing their mental strength to overcome as yet unidentified, but not lifethreatening, problems in their body.

1.5.2 Other illnesses

Upper extremity musculoskeletal complaints are associated with work as a hairdresser, and can largely be addressed through client chairs that are adjustable in height. Use of nail cosmetics in nail salons is gaining increasing popularity worldwide. Although a number of irritant compounds are used, there are no reports of respiratory disease in the literature. Ethyl methacrylate, formerly used in artificial nail processing, has been linked to asthma. Its use is largely discontinued.

1.5.3 Medicolegal and compensation

Individual countries and states vary in their system of compensation and requirements. In those places where specific inhalation challenge is a component of compensation evaluation, this bodes well for specific identification of cases, allowing for appropriate compensation. In the USA, where specific challenge testing is not common, less direct evidence probably leads to less efficient, and likely more contentious, determinations.

1.5.4 Public health

Some of the epidemiology has indicated an increased prevalence of asthma among hairdressing apprentices. In one study of hairdressers there was a mean of 38 months between symptom onset and diagnosis, accounting for fairly poor outcomes with persistent symptoms and a decline in FEV1, despite cessation of exposure. This emphasizes the importance of surveillance and early recognition of occupational disease if there is to be any confidence of avoiding long-term impairment. Development of nonsensitizing products for hair bleaching is clearly a goal.

References

1. Pepys, J., Hutchcroft, B.J., Breslin, A.B. (1976) Asthma due to inhaled chemical agents persulphate salts and henna in hairdressers. Clin. Allergy 6(4): 399-404.

2. Iwatsubo, Y., Matrat, M., Brochard, P., Ameille, J., Choudat, D., Conso, F., Coulondre, D., Garnier, R., Hubert, C., Lauzier, F., Romano, M.C., Pairon, J.C. (2003) Healthy worker effect and changes in respiratory symptoms and lung function in hairdressing apprentices. Occup. Environ. Med. 60(11): 831-840.

3. Moscato, G., Pignatti, P., Yacoub, M.R., Romano, C., Spezia, S., Perfetti, L. (2005) Occupational asthma and occupational rhinitis in hairdressers. Chest 128(5): 3590-3598.

4. Schlueter, D.P., Soto, R.J., Baretta, E.D., Herrmann, A.A., Ostrander, L.E., Stewart, R.D. (1979) Airway response to hair spray in normal subjects and subjects with hyperreactive airways. Chest 75(5): 544-548.

5. Cone, J.E., Shusterman, D. (1991) Health effects of indoor odorants. Environ. Health Perspect. 95 53-59.

6. Shim, C., Williams, M.H. Jr. (1986) Effect of odors in asthma. Am. J. Med. 80(1): 18-22.

7. Millqvist, E., Bengtsson, U., Lowhagen, O. (1999) Provocations with perfume in the eyes induce airway symptoms in patients with sensory hyperreactivity. Allergy 54(5): 495-499.

8. Millqvist, E., Lowhagen, O. (1998) Methacholine provocations do not reveal sensitivity to strong scents. Ann. Allergy Asthma Immunol. 80(5): 381-384.

9. Millqvist, E., Lowhagen, O. (1996) Placebo-controlled challenges with perfume in patients with asthma-like symptoms. Allergy 51(6): 434-439.

10. Opiekun, R.E., Smeets, M., Sulewski, M., Rogers, R., Prasad, N., Vedula, U., Dalton, P. (2003) Assessment of ocular and nasal irritation in asthmatics resulting from fragrance exposure. Clin. Exp. Allergy 33(9): 1256-1265.

11. Moscato, G., Galdi, E. (2006) Asthma and hairdressers. Curr. Opin. Allergy Clin. Immunol. 6(2): 91-95.

Further reading

Albin, M., Rylander, L., Mikoczy, Z., Lillienberg, L., Dahlman Hoglund, A., Brisman, J., Toren, K., Meding, B., Kronholm Diab, K., Nielsen, J. (2002) Incidence of asthma in female Swedish hairdressers. Occup. Environ. Med. 59(2): 119-123.

Baur, X., Schneider, E.M., Wieners, D., Czuppon, A.B. (1999) Occupational asthma to perfume. Allergy 54(12): 1334-1335.

Bornehag, C.G., Sundell, J., Weschler, C.J., Sigsgaard, T., Lundgren, B., Hasselgren, M., HagerhedEngman, L. (2004) The association between asthma and allergic symptoms in children and phthalates in house dust: a nested case-control study. Environ. Health Perspect. 112(14): 1393-1397.

Committee on the Assessment of Asthma Indoor Air (2000) Clearing the Air: Asthma and Indoor Air Exposures. Division of Health Promotion and Disease Prevention, Institute of Medicine: Washington, DC.

Das-Munshi, J., Rubin, G.J., Wessely, S. (2007) Multiple chemical sensitivities: review. Curr. Opin. Otolaryngol. Head Neck Surg. 15(4): 274-280.

Elberling, J., Linneberg, A., Dirksen, A., Johansen, J.D., Frølund, L., Madsen, F., Nielsen, N.H., Mosbech, H. (2005) Mucosal symptoms elicited by fragrance products in a population-based sample in relation to atopy and bronchial hyper-reactivity. Clin. Exp. Allergy 35(1): 75-81.

Kipen, H.M., Fiedler, N., Lehrer, P. (1997) Multiple chemical sensitivity: a primer for pulmonologists. Clin. Pulmon. Med. 4(2): 76-83.

Kumar, P., Caradonna-Graham, V.M., Gupta, S., Cai, X., Rao, P.N., Thompson, J. (1995) Inhalation challenge effects of perfume scent strips in patients with asthma. Ann. Allergy Asthma Immunol. 75 (5): 429-433.

Muñoz, X., Cruz, M.J., Orriols, R., Torres, F., Espuga, M., Morell, F. (2004) Validation of specific inhalation challenge for the diagnosis of occupational asthma due to persulphate salts. Occup. Environ. Med. 61(10): 861-866.

Mounier-Geyssant, E., Oury, V., Mouchot, L., Paris, C., Zmirou-Navier, D. (2006) Exposure of hairdressing apprentices to airborne hazardous substances. Environ. Health 5: 23.

Tarlo, S.M., Poonai, N., Binkley, K., Antony, M.M., Swinson, R.P. (2002) Responses to panic induction procedures in subjects with multiple chemical sensitivity/idiopathic environmental intolerance: understanding the relationship with panic disorder. Environ Health Perspect. 110 (suppl. 4): 669-671.

2

Passive smoking

Maritta S. Jaakkola

University of Oulu and Oulu University Hospital, Oulu, Finland

2.1 Introduction

Passive smoking is defined as exposure of a (nonsmoking) person to tobacco combustion products from smoking by others. Several synonyms are used in the literature, including involuntary smoking, exposure to environmental tobacco smoke (ETS) and exposure to second-hand smoke (SHS). SHS exposure has been recently recommended as the term to be used, for example by the Tobacco Free Initiative of the World Health Organization [1]. The term ETS was previously used widely, but it seems to have been introduced originally by the tobacco industry and it is recommended to be used less, as it can obscure the preventable nature of this exposure. The term ‘involuntary’ could imply that voluntary smoking would not be as bad for the health, so this term will also be used less in the future.

Passive smoking is still common in homes, workplaces and public places in many countries, although in recent years there has been some progress, with increasing number of countries introducing smoke-free workplace legislation and other tobacco control measures. Some studies have suggested that smoke-free workplaces also reduce smoking at home, and thus lead to reduced passive smoking at home [2]. This may be explained by both increased awareness of the adverse health effects of passive smoking and the reduced active smoking detected in many studies as a consequence of the legislation. However, it is not possible to introduce legislation to protect directly those who are most vulnerable to the harmful effects of SHS exposure at home, i.e. infants, children and the elderly. To protect the health of these susceptible population groups, it is important to increase emphasis on educating people about the adverse effects of passive smoking, and to support smokers to quit or at least to behave in a way that does not expose others to tobacco smoke. In this work, healthcare personnel are among the key players.

This chapter will first introduce definitions related to passive smoking and describe exposure to tobacco smoke, then review the current knowledge on health effects of SHS exposure in children and adults, and finally discuss clinical applications and preventive measures.

In reviewing health effects, assessment of whether the relation between SHS exposure and the health condition is causal is based on the criteria usually used by the recent reviews. These include: (i) the number of studies that have been published on the topic and whether these studies come from different parts of the world; (ii) consistency of findings; (iii) validity of the studies, including control for confounding factors (i.e. other risk factors) and potential biases; (iv) evidence of an exposure-response relation (also called a dose-response relation); (v) evidence of biologically plausible mechanisms; and (vi) evidence of meaningful temporal relation. The best estimate of the effect is given based on recent meta-analyses, which have combined the results of studies published on the health outcome in question. If such a summary estimate is not available, the best effect estimate is given based on a recent, high-quality study.

2.2 Exposure to second-hand smoke

2.2.1 Definitions and constituents of tobacco smoke

Second-hand smoke is composed of sidestream smoke (SS), which is formed from the burning of tobacco products and emitted directly into the environment from the smouldering end of the cigarette between puffs, and exhaled mainstream smoke (MS), which is first inhaled by the smoker before being released into the environment. Other smaller contributors to SHS include smoke that diffuses through the wrapper of the cigarette and smoke that escapes while the smoker inhales. SS is the principal constituent of SHS.

Tobacco smoke is a mixture of thousands of chemicals released into the air as gases, vapors and particles [3]. Over 4000 individual constituents have been identified and these include more than 50 carcinogenic substances as well as many toxic and irritant compounds [4,5]. In addition, several compounds have adverse effects on reproduction. Many constituents are released in higher concentrations in SS than MS because of different burning conditions and less complete combustion of SS. Thus, SS contains higher concentrations of many harmful substances, but is usually then diluted into a larger volume (Table 2.1) [6]. The US National Toxicology Program estimated that at least 250 chemicals in SHS are known to be toxic or carcinogenic. In addition, it is possible that exposure to the mixture of different compounds in SHS is more harmful to health than exposure to any of the individual chemicals, as the compounds may have synergistic effects, i.e. they may have together a larger effect than would be expected from summing up the effects of individual compounds [7]. There is some evidence suggesting that evaporation of biologically less active components may cause aged sidestream smoke to be more toxic on a weight-for-weight basis.

Table 2.1 Emissions of selected tobacco smoke constituents in fresh, undiluted mainstream smoke (MS) and diluted sidestream smoke (SS) from nonfiltered cigarettes [6]

aIARC category 1 = carcinogenic to humans.

SHS exposure usually means passive smoking by nonsmokers. However, smokers are exposed to particularly high concentrations of sidestream smoke, because their own smoking is the major source of it and because they spend more time in smoky environments. Thus, SS may contribute to the adverse health effects detected in active smokers, but as this has not been studied much, this chapter will focus on the health effects of passive smoking in nonsmoking populations, which have been studied extensively. It should be noted that a fetus can be exposed to tobacco smoke by either the mother’s active smoking during pregnancy or a nonsmoking mother’s exposure to SHS. Both of these influence the development of the fetus, as tobacco smoke constituents are transferred across the placenta, so both of them result in fetal passive smoking. This chapter will focus on fetal passive smoking from the mother’s SHS exposure during pregnancy.

2.2.2 Sources of SHS exposure

For young children, smoking adults at home, especially the parents, form the principal source of SHS exposure. With increasing age, other places contribute as sources of SHS exposure: first day-care facilities and then school and many social environments. Among adults, home and workplace are the major sources of SHS exposure, because of the long time periods usually spent in these environments. However, some social environments, such as bars, restaurants and public transport, have been found to have particularly high concentrations of SHS. This chapter will focus on SHS exposure at home. It will briefly also mention SHS exposure at work, but other chapters will discuss SHS exposure in other environments.

2.2.3 Occurrence of SHS exposure

The prevalence of SHS exposure varies considerably between countries and is influenced by the prevalence of active smoking, the traditions and behavioral cultures, the tobacco control legislation and the healthcare and educational systems. Multicenter studies from North America and Europe have measured cotinine in body fluids as an indicator of passive smoking and found that, in the 1980s, more than 80% of the nonsmoking populations were exposed to SHS. They also showed an alarming trend for the highest exposures to be detected in children and young adults. Today there is more variability in SHS exposure within Europe and between different states of the USA, as some countries and states have adopted smoke-free workplace and other forms of stricter tobacco control legislation, while others have not yet taken these preventive steps. For example, estimates of the prevalence of passive smoking of children from Europe have ranged from 7-15% in Finland and Sweden to 70-75% in Bulgaria and Poland. SHS still remains the most important preventable indoor exposure even in many high-income countries. The smoking epidemic in low-income countries seems unfortunately to continue, meaning that a high proportion of children in such countries are exposed to SHS. These children may be especially vulnerable to the harmful effects of SHS, as they may suffer also from malnutrition and may be exposed to other harmful compounds, for example from use of solid fuels that may act synergistically with SHS. WHO has databases on smoking prevalences and tobacco control legislations across the world (http://www.who.int/tobacco/global_data/en/index.xhtml).

2.2.4 Measuring exposure to SHS

Exposure to SHS can be assessed using different methods depending on the purposes of the measurements [7]. The most direct method to measure SHS exposure is to use personal monitors available for individual tobacco smoke components, such as nicotine or respirable suspended particles (RSP). However, this method requires a lot of labor, is rather expensive and only measures current exposure for a short interval. Individual tobacco smoke components can also be measured by fixed monitors in defined spaces. When combining the results of such measurements with information on time-activity patterns, an individual’s or a population’s exposure to SHS can be assessed. Again, this method only measures current exposure for a rather short interval, is expensive, and only measures exposure to specific compounds rather than to the entire mixture. However, such measurements may be useful, for example, when assessing the effectiveness of smoke-free workplace policy.

Studies of health effects have most commonly applied questionnaires or diaries to assess SHS exposure. These methods have the advantages of being cheap and providing the possibility to measure long-term exposure which may be more relevant for many health effects [8]. Questionnaires can also inquire into past exposures. This is the relevant exposure, for example, when investigating lung cancer, as the relevant exposure has taken place at least 10 years earlier because of the long lag time. A potential problem related to questionnaires and diaries is whether people remember and report their exposures correctly. Many studies that have compared questionnaires with other exposure assessment methods suggest that questionnaires provide valid information, i.e. the majority of people report correctly whether they have been or have not been exposed to SHS, but that the exact quantification of exposure may not be very precise. However, it is still likely that people are able to recall rather well whether they have been exposed heavily or lightly.

Another way to assess exposure to SHS is to measure biomarkers, i.e. compounds, their metabolites, hemoglobin or DNA adducts in biological samples, which are influenced by the uptake, metabolism and elimination mechanisms in addition to the exposure concentration. These may give relevant information about exposure to some target organs. The most commonly measured biomarker of tobacco smoke is cotinine in serum, saliva or urine. Cotinine is a major metabolite of nicotine. Its half-life is about 20 h, so it measures only recent exposure over the last 1-3 days. As a consequence of this, it may not be good assessment method for diseases for which long-term exposure is relevant. Hair nicotine concentration has been measured in some recent studies and seems to reflect exposure over the last 2 months. Some studies have also measured biomarkers of the carcinogenic substances, for example amino biphenyl hemoglobin adduct. Biomarkers are indicators for total exposure across different microenvironments, including home, workplace and social settings. For health effect studies, it has been recommended to use a combination of a questionnaire and some other method, if there are enough resources available.

2.3 Health effects of passive smoking in children

Children are more susceptible to the adverse effects of SHS than adults for several reasons. Their respiratory system is not fully mature at birth and continues to develop both immunologically and physiologically. Children have higher breathing rate and inhale more air per body volume than adults, which results in higher exposure with a similar SHS concentration. In addition, children’s liver metabolism and other clearing mechanisms are not yet fully developed, so the harmful substances remain longer in the body. Some studies have suggested that children who were exposed to tobacco smoke in utero through either active or passive smoking by the pregnant mother are at greater risk for developing SHS-related diseases later, so tobacco smoke exposure in the very early phases of lung development may also make children more vulnerable later in life.

This section will first discuss health effects related to SHS exposure from the mother’s passive smoking during pregnancy and then health effects related to the child’s passive smoking after birth. However, these exposures are highly correlated, as is maternal smoking during pregnancy and the child’s postnatal SHS exposure, so it has not been easy to disentangle the effects of these exposures.

2.3.1 Health effects of mother’s passive smoking during pregnancy

Health effects related to mothers’ SHS exposure during pregnancy are summarized in Table 2.2.

Table 2.2 Summary of health effects of mothers’ passive smoking during pregnancy

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a0 = no evidence of a relation between passive smoking and this condition; + = some evidence of a relation between passive smoking and condition; + + = strong but not definitive evidence of a causal relation between passive smoking and condition; + + + = established causal relation between passive smoking and condition.

Lung function impairment

Maternal smoking during pregnancy has been linked to reduced lung function in infants in many studies. According to recent reviews [5,9], there is also evidence of adverse effects of maternal passive smoking during pregnancy on the child’s lung function. However, as the number of studies looking at this question is limited, no definite conclusions concerning effects of mother’s SHS exposure during pregnancy on child’s lung function can be made.

Asthma

Maternal smoking during pregnancy has been strongly linked to the risk of childhood asthma [12], but again, the overall number of studies looking at the effects related to mother’s SHS exposure during pregnancy is limited [9].

Low birth weight

Active smoking by the mother is a well-known cause of low birth weight (LBW). There is increasing literature also on nonsmoking mothers’ exposure to SHS and low birth weight [9,13]. Low birth weight has usually been defined as birth weight <2500 g either preterm or at full term (≥ 37 weeks of gestation) birth. When LBW occurs at full term, it means that the fetal growth was reduced and the outcome is called small for gestational age (SGA). A review of this topic by US Surgeon General in 2006 [5] identified 43 cohort and three case-control studies on LBW or SGA. The most recent meta-analysis included 19 studies and gave a summary risk ratio of 1.2 (95% confidence interval, CI, 1.1-1.3), meaning a 20% excess risk in children of exposed mothers [10]. The average effect on birth weight was estimated as − 28 g (− 41 to − 16) in exposed infants compared with unexposed infants. The overall judgment based on recent reviews is that mothers’ passive smoking is causally linked to low birth weight of the infant [5,9,11,13]. This causal effect seems to be a consequence of reduced oxygen in the fetus, which is attributable to CO exposure from SHS and nicotine-induced vasoconstriction, leading to reduced blood flow of uterus, placenta and umbilical cord.

Preterm delivery and other developmental effects

The other pregnancy outcome that has been linked to mother’s passive smoking is preterm delivery, defined as <37 completed weeks of gestation [13]. The strongest evidence comes from a population-based Finnish study that found an OR of 1.30 (95% CI 0.30-5.58) for SHS exposure in the middle range and 6.12 (1.31-28.7) for the highest SHS exposure based on nonsmoking mother’s hair nicotine concentration [14]. The recent meta-analysis by California Environmental Protection Agency [11] gave a summary relative risk of 1.57 (1.35-1.84) for preterm delivery, meaning 57% excess risk in children of exposed mothers. However, not all studies have found consistent results, so more studies are needed before definite conclusions on causality of preterm delivery can be made.

Other developmental effects that have been linked to mothers’ passive smoking include spontaneous abortion and perinatal death, congenital malformations and impaired neuropsychological and physical development, but because of limited evidence, no definite conclusions can be made concerning the strength of these relations [5]. Maternal SHS exposure has also been linked to increased persistent pulmonary hypertension of the newborn.

2.3.2 Health effects of passive smoking in childhood

The first studies reporting a link between parental smoking and respiratory disease in children were published in the early 1970s. Since then abundant evidence on adverse health effects of SHS exposure in childhood has accumulated. This is summarized in Table 2.3.

Table 2.3 Summary of health effects of passive smoking in childhood

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a0 = no evidence of a relation between passive smoking and condition; + = some evidence of a relation between passive smoking and condition; + + = strong but not definitive evidence of a causal relation between passive smoking and condition; + + + = established causal relation between passive smoking and condition.

bPercentage difference of lung function in children exposed to SHS compared with unexposed children.

Acute lower respiratory illnesses

More than 100 studies from different parts of the world have been published on parental smoking in infancy and early childhood and the risk of the child’s acute lower respiratory illness. These have consistently shown an increased risk of acute lower respiratory illnesses, including respiratory infections such as acute bronchitis, bronchiolitis, respiratory syncytial virus infections and pneumonia, and in some studies also symptoms of the lower respiratory tract [5,9,11]. There is evidence of an exposure-response relation, meaning that the risk of the disease increases with increasing amount of exposure, measured as the number of smoking parents and other household members or the number of cigarettes smoked at home. The most recent meta-analysis of these studies was conducted by the US Surgeon General [5] and gave a summary odds ratio of 1.59 (95% CI 1.47-1.73), suggesting an excess risk of 59% among children exposed to parental smoking.

The risk related to mother’s smoking is higher (OR 1.72, 1.59-1.86) than that related to father’s smoking (OR 1.31, 1.19-1.43), but both maternal and paternal smoking increase significantly the child’s risk of getting lower respiratory illness. The higher risk from mother’s smoking could be explained by small children usually spending more time with their mother than with other adults, or by a synergistic effect between childhood maternal smoking and maternal smoking during pregnancy, as these often correlate. The risk from parental smoking seems to be highest in young children. For example in a meta-analysis by Li and co-workers [16], the summary RR was 1.71 (1.33-2.20) in children 0-2 years old. The smaller effect in older children has been explained by less time being spent in the presence of household smokers with increasing age as well as by maturation of the immune system of the child.

In terms of biologically plausible mechanisms for the relation between passive smoking and lower respiratory illness, tobacco smoke is known to impair the immunological defense mechanisms as well as the function of airway cilia, both of which are likely to lead to increased susceptibility to infections. In addition, SHS has been shown to enhance bacterial adherence and disrupt respiratory epithelium, which is an important host defense barrier. In conclusion, all recent reviews have concluded that parental smoking is causally linked to increased acute lower respiratory illnesses, especially in young children [5,9,11].

Otitis media

According to US Surgeon General’s Report in 2006 [5], 59 studies from different parts of the world have investigated the relation of parental smoking to middle ear disease in children. A causal association has been found with acute and recurrent otitis media as well as chronic middle ear effusion. The best estimates of relative risks from recent reviews are 1.38 (1.21-1.56) for acute otitis media and 1.37 (1.10-1.70) for recurrent otitis media in relation to either parent smoking, meaning 30-70% excess risk. The relative risk of chronic middle ear effusion is 1.33 (1.12-1.58). Potential mechanisms that underlie these relations include decreased mucociliary clearance leading to increased susceptibility to infections and Eustachian tube dysfunction due to mucosal swelling that can lead to accumulation of effusion in the middle ear [11].

Chronic respiratory symptoms

Since the first studies on parental smoking and chronic respiratory symptoms in children were published in the early 1970s, a large number of studies on this topic from different parts of the world have been reported. The recent report by the US Surgeon General [5] included 88 studies in their quantitative overview. The summary relative risks related to either of the parents smoking were 1.26 (95% CI 1.20-1.33) for wheeze, 1.35 (1.27-1.43) for cough, 1.35 (1.30-1.41) for phlegm and 1.31 (1.14-1.50) for breathlessness, meaning 26-35% excess risk in children of smoking parents. All symptoms showed increasing risk with increasing number of parents smoking at home, suggesting exposure-response relation. Generally the risk was higher in relation to mother’s smoking, but father’s smoking was also related to significantly increased risk. All recent reviews have concluded that parental smoking is causally related to chronic respiratory symptoms in children [5,9,11]. Tobacco smoke contains many substances that can induce irritation and chronic inflammation in the airways, and these mechanisms are likely to underlie the observed relations with respiratory symptoms. Wheeze is a symptom of both respiratory infections and asthma in children, and so reflects disease mechanisms of these conditions, as reviewed separately.

Asthma

Induction of asthma. About 85 studies from different parts of the world have addressed the risk of developing asthma in childhood in relation to parents’ smoking. The most updated meta-analysis of these was conducted by the California Environmental Protection Agency [11] in 2005. Its meta-analysis was based on 29 studies and gave a summary RR for new-onset asthma of 1.32 (95% CI 1.24-1.41), meaning 32% excess risk in children whose parent(s) smoke. The risk was higher in preschool children (1.44, 1.04-1.99), but remained significantly increased also in older children. When the child was exposed to parental smoking both during pregnancy and after birth the risk was strongest, but significant increase in the risk was detected also in association with postnatal SHS exposure only. The risk of asthma increased with increasing duration of passive smoking, suggesting an exposure-response relation: RR was 1.22 (1.16-1.34) for 5 years of postnatal SHS exposure and 1.42 (1.28-1.70) for 10 years of such exposure. In addition to mechanisms that will be discussed in connection with adult asthma, in infants other mechanisms may play a role. These include impaired airway development during pregnancy and in infancy in those exposed to passive smoking and the influence of SHS on development of immunological responses, for example the balance between Th1 and Th2 cells [5].

Exacerbation of asthma. Several studies have shown that parental smoking is a causal factor for exacerbation of asthma in children with a pre-existing disease [11], in addition to increasing the risk of new asthma in previously healthy children. Different types of outcomes related to exacerbation of asthma have been studied, including the frequency and severity of asthma symptoms, use of asthma medications, school absenteeism, use of healthcare services, hospitalization and changes in lung function parameters, such as peak expiratory flow (PEF). In longitudinal studies, the effects of passive smoking have been detected most consistently on increased asthmatic symptoms, more and prolonged use of medication, and increased school absenteeism.

Lung function impairment

There are numerous cross-sectional and some longitudinal studies showing that parental smoking is linked to lung function deficits as well as to reduced growth of lung function in children. As discussed above, exposure during pregnancy seems to be of importance, but postnatal SHS exposure has also been shown to have significant adverse effect on lung function of children. The recent review by US Surgeon General [5] included 26 studies and measured the summary effect as percentage differences of lung function in children exposed to SHS compared with unexposed children. The effects were −1.15% (95% CI − 1.56 to − 0.75) on forced expiratory volume in 1 second (FEV1), −0.32% (−0.71 to −0.08) on forced vital capacity (FVC), and −4.76% (−6.34 to −3.18) on mid-expiratory flow rate (MEFR).

Overall the results show small but significant adverse effect of childhood passive smoking on spirometric lung function, which is likely to persist into older ages. This effect has been judged by most recent reviews to be causal [5,11]. In addition, there is some evidence that passive smoking may lead to reduced diffusing capacity of the lungs [11].

Sudden infant death syndrome

Sudden infant death syndrome (SIDS) is a sudden, unexpected and unexplained death of an infant before one year of age. A review from 1997 identified 39 studies that had investigated the risk of SIDS in relation to passive smoking after birth and gave a summary relative risk of 1.94 (95% CI 1.55-2.43), meaning 94% excess risk in infants exposed to SHS [15]. Most studies assessed exposure from mother’s smoking after birth and one-third of them controlled for maternal smoking during pregnancy (i.e. prenatal exposure). Also father’s smoking has been significantly linked to increased risk of SIDS. Several studies have shown evidence of exposure-response relation with the amount of SHS exposure. All recent reviews have concluded that there is a causal relation between parental smoking and SIDS [5,11]. Exposure to nicotine and toxicants in tobacco smoke has been shown to have neurotoxic effects, affecting neuroregulation of breathing and apnoeic spells. SHS exposure has been found to be associated with a change in the ventilatory and cardiac responses to hypoxia [5,11].

Childhood cancers

Childhood cancers are relatively rare conditions. One cohort and some case-control studies have investigated the relations of childhood cancers to parental smoking. The strongest evidence links maternal smoking to overall childhood cancer risk. Of specific cancers, SHS exposure has been associated with leukemias, lymphomas and brain tumors. Few studies have distinguished the effects of postnatal exposure from exposure during pregnancy. Relevant exposure may have occurred already before conception, i.e. through mutations of male germ cells. In view of the rather small number of studies adjusting for other potentially important cancer risk factors, the relations between SHS exposure and childhood cancers have not been judged as causal and more studies on this topic are needed [5].

Neurobehavioral and other effects

There is some evidence that children’s cognition and behavior are adversely affected by passive smoking [5,11]. A large study based on the third US National Health and Nutrition Examination Survey (NHANES III) showed a significant inverse relation between child’s serum cotinine level and performance on cognitive tests: decrements in cognitive scores were detected at higher cotinine levels, i.e. among those with more exposure to SHS. A large British study showed that children whose mother smoked had lower scores in a vocabulary test. However, not all studies have found such effects and more studies are needed before any definite conclusions can be made.

Children’s passive smoking has also been linked in recent studies to significantly increased caries in young children and less favorable serum lipid profile in children up to 15 years of age, including significantly lower levels of high-density lipoprotein cholesterol (HDL).

2.4 Health effects of passive smoking in adults

The first studies linking passive smoking to adverse health effects in adults were from the early 1980s and focused mainly on lung cancer. More recently there has been increasing research also into nonmalignant effects of SHS exposure in adulthood. The evidence from adult studies is summarized in Table 2.4.

Table 2.4 Summary of health effects of passive smoking in adulthood

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a0 = no evidence of a relation between passive smoking and condition; + = some evidence of a relation between passive smoking and condition; + + = strong but not definitive evidence of a causal relation between passive smoking and condition; + + + = established causal relation between passive smoking and condition.

bPercentage difference of lung function in adults exposed to SHS compared with unexposed adults.

2.4.1 Lung cancer

Lung cancer is the leading cause of cancer deaths in many countries and its main cause is active smoking. The first studies that linked passive smoking to lung cancer were published in 1981 and studied nonsmoking women who were exposed to a spouse’s smoking. Since then more than 50 case-control and cohort studies from different parts of the world have addressed the risk of lung cancer in relation to SHS exposure. The most recent meta-analysis of these studies was conducted by the US Surgeon General in 2006 [5]. It concluded that SHS from the spouse’s smoking as well as from exposure at work are causally related to lung cancer in nonsmokers. Similar conclusions have been reached by earlier as well as two other recent reviews, one by the International Agency for Research on Cancer (IARC) [4] and the other by the California EPA [11]. The summary OR of lung cancer among nonsmokers ever exposed to spousal smoking was estimated at 1.29 (95% CI 1.13-1.49) among women and men combined, 1.22 (1.13-1.31) among women and 1.37 (1.05-1.79) among men [5]. The summary OR of lung cancer in relation to passive smoking at work was 1.22 (1.13-1.33). Thus, passive smoking at home and at work are both related to about 20-30% excess risk.

There is abundant evidence of exposure-response relation between increasing SHS exposure at home and/or at work (measured as amount or duration of passive smoking) and increasing lung cancer risk. Longitudinal studies have provided evidence of meaningful temporal relation, i.e. SHS exposure has preceded development of lung cancer. Tobacco smoke is known to contain many carcinogenic substances. Biomarker studies have shown that nonsmokers exposed to SHS take up and metabolize carcinogenic substances of tobacco smoke and experience increased mutation burden compared with unexposed nonsmokers [5]. Many recent studies have addressed potential methodological problems that were related to the early studies, such as misclassification of disease or passive smoking status and potential influence of other risk factors, and have still provided results consistent with a causal effect of passive smoking on lung cancer.

The effect of childhood passive smoking on lung cancer has also been investigated in some studies, but the results of these have been less consistent. A significant relation has been reported in studies from Asia, giving a summary relative risk of 1.59 (1.18-2.15) [5].

2.4.2 Breast and other cancers

Recently several studies have also addressed the relation between passive smoking and breast cancer. The results of these have been somewhat inconsistent and recent reviews on this topic have provided variable conclusions. US Surgeon General [5] concluded that the evidence on the relation between passive smoking and breast cancer is suggestive of causality, while California EPA concluded [11] that the evidence supports a causal relation. Both reports pointed out that the relation between SHS exposure and breast cancer is stronger in premenopausal women. The meta-analysis conducted by California EPA gave a summary risk ratio of 1.25 (95%