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. 2023 Jun 12:1–13. Online ahead of print. doi: 10.1007/s11356-023-28128-1

Secondhand and thirdhand smoke: a review on chemical contents, exposure routes, and protective strategies

Hossein Arfaeinia 1,2, Maryam Ghaemi 3, Anis Jahantigh 4, Farshid Soleimani 1,✉, Hassan Hashemi 5
PMCID: PMC10258487  PMID: 37306877

Abstract

Secondhand smoke (SHS: a mixture of sidestream and mainstream smoke) and thirdhand smoke (THS: made up of the pollutants that settle indoors after smoking in closed environments) are a significant public health concern. SHS and THS contain various chemicals which can be released into the air or settle on surfaces. At present, the hazards of SHS and THS are not as well documented. In this review, we describe the chemical contents of THS and SHS, exposure routes, vulnerable groups, health effects, and protective strategies. The literature search was conducted for published papers on September 2022 in Scopus, Web of Science, PubMed, and Google Scholar databases. This review could provide a comprehensive understanding of the chemical contents of THS and SHS, exposure routes, vulnerable groups, health effects, protective strategies, and future researches on environmental tobacco smoke.

Keywords: Secondhand smoke, Thirdhand smoke, Exposure routes, Vulnerable groups, Protective strategies

Introduction

Nearly 20% of the world smokes tobacco (Gowing et al. 2015; Roser 2019; Ritchie and Roser 2013), and global statistics predicted that the number of smokers will rise up to 1.6 billion by 2025 (James et al. 2022). Tobacco was associated with 8.71 million deaths globally in 2019 (WHO 2021) that contained 13.6% of all human deaths and 7.89% of all disability-adjusted life-years (DALYs) (GBD 2021; Reitsma et al. 2021). Tobacco smoke contains about 7000 chemicals (at least 69 carcinogenic chemicals) (Rodgman and Perfetti 2013; Services 2014), and smoking is a cause of about 30 percent of all cancer deaths (National Cancer Policy Forum 2013). During each smoking session, the accumulated chemicals are divided among different components, including mainstream smoke (MS: the smoke which the smoker breathes out during the puffs), sidestream smoke (SS: the smoke that is released from the end of a burning cigarette), secondhand smoke (SHS: made up of SS (~85%) and exhaled MS (~15%)) (Hang et al. 2020), and thirdhand smoke (THS: made up of the pollutants that settle indoors after smoking in closed environments) (Counts et al. 2005; Ding et al. 2006; Ajab et al. 2014; Jacob III et al. 2017; Hang et al. 2020; Vu et al. 2021; Soleimani et al. 2022a).

The health effects of firsthand smoke (MS) are well known, and research precedence has recently changed to identify the importance of SHS and THS (Bird and Staines-Orozco 2016; Lee et al. 2019). SHS is an important public health concern (Alzahrani 2020; Farrell et al. 2022; Schiavone et al. 2022). Exposure to tobacco smoke among passive/nonsmokers increases lung cancer risk (Weiss et al. 1983; Schwartz and Cote 2016; Mantzoros et al. 2017; Esdras et al. 2021; Mariano et al. 2022), and approximately one million people are estimated to die worldwide from passive smoking annually (Drope and Schluger 2018). SHS is estimated to cause more than 53,000 deaths in the United States annually (Jacobs et al. 2013). Also, exposure to SHS and THS in the home and/or closed environments is a risk factor for asthma in children (Al-Sayed and Ibrahim 2014; Xanthopoulou and Kousoulis 2014; den Dekker et al. 2015; Rajani et al. 2017; Butz et al. 2019).

Furthermore, THS has recently been recognized as a new threat. SHS refers to passive smoking in which nonsmokers are exposed to MS and SS due to smoking by another person (Sikorska-Jaroszynska et al. 2012; Mourino et al. 2022), and THS is mentioned to the exposure to smoke-related pollutants by entering an environment in a place in which someone has smoked and/or in contact with a smoker (Park and Sim 2022). The contaminants of tobacco smoke settle on the smoker’s body, as well as on different surfaces, including walls, carpets, curtains, and furniture, and can re-contaminate smokers and nonsmokers (Winickoff et al. 2009; Ferrante et al. 2013; Jacob III et al. 2017; Aquilina et al. 2022). THS exposure may happen long after SHS appears (Becquemin et al. 2010; Protano and Vitali 2011; Hang et al. 2018). Toxic substances remain on different surfaces even weeks and/or months after smoking (Matt et al. 2011a; Hang et al. 2018).

These toxic substances may be released into indoor air, react with atmospheric species (i.e., ozone and nitrous acid (HNO2)), and subsequently produce toxins that were not at first present in firsthand smoke (Sleiman et al. 2014; Collins et al. 2018). SHS and THS are considered as important sources of indoor exposure to tobacco-related chemicals (Sleiman et al. 2014; Tsai et al. 2018). However, the chemical contents and their concentration levels in environmental tobacco smoke (THS and SHS) are still poorly understood. To increase understanding of indoor environmental smoke as a source of health risks to humans, we conducted a narrative scientific review to investigate the chemical contents of THS and SHS, exposure routes, vulnerable groups, health effects, and protective strategies.

Materials and methods

The literature search was conducted for this narrative review in September 2022. Articles were recorded through a literature search in Scopus, Web of Science, PubMed, and Google Scholar databases. Articles (English language only) were only included if they investigated the chemical contents of SHS and THS and or discussed exposure routes, vulnerable groups, health effects, and control strategies of these environmental tobacco smokes. Search terms included (“Thirdhand smoke” OR “Third-hand smoke” OR “Secondhand smoke” OR “Second-hand smoke” OR “Side stream smoke” OR “Sidestream smoke” OR “Involuntary smoking” OR “Passive smoking”) AND (Chemical* OR “Chemical composition” OR “Chemical compound*” OR “Chemical constituents” OR “Environmental tobacco smoke”) AND (“Exposure routes”) AND (“Vulnerable groups”) AND (“Health effects”) AND (“Protective strategies”). These terms were used separately and combined to discover search results.

The initial search recorded 518 articles. Other language papers, duplicate papers, insufficient detail and not peer-reviewed papers, and papers that did not sufficiently discover our specific objectives were removed. After the application of these criteria, one hundred seventy-four scientific articles were nominated for full-text review. Also, we reviewed all the reference lists of the residual articles to find more related articles.

All remaining articles were revised to assure the claim of the last inclusion criteria and were additionally sieved by selecting only those meeting the following criteria: (1) research articles that measured at least one chemical constituent of SHS and/or THS and (2) articles that discussed at least one of the following issues: exposure routes, vulnerable groups, health effects, and protective strategies against SHS and/or THS chemical compositions. Lastly, after utilization of all criteria, 98 papers were involved in the current narrative review.

Results and discussion

The mean and/or range concentration levels of the chemical content of SHS are provided in Table 1. As shown, polycyclic aromatic hydrocarbons (PAHs) and nicotine were the most common chemicals measured in reviewed articles. Although heavy metals are known as one of the critical constituents of chemical components of MS and SS and cigarette butts (Soleimani et al. 2021; Soleimani et al. 2022), these chemicals have been less noticed in SHS. Despite limited studies on the chemical content of SHS, these reported that SHS might contain different chemicals that pose significant health and environmental worries. While numerous chemicals of concern have been recognized in SHS, there is still work to be done. Additional studies are essential to survey the chemical contents of SHS and parameters involved in the concentration levels of these chemicals. More researches are required to assess more strictly the range of chemicals found in SHS, mainly those largely ignored.

Table 1.

The mean and/or range concentration levels of chemical content of SHS

Chemicals Matrix Duration after smoking (h) Mean and/or range concentrations References
Formaldehyde Indoor air 8 49 μg/m3 (Adlkofer et al. 1990)
Acetaldehyde Indoor air 8 1390 μg/m3
Propionaldehyde Indoor air 8 120 μg/m3
Benzo[A]pyrene 0.027 μg/m3
Pyrene 0.025 μg/m3
Chrysene 0.07 μg/m3
Toluene Indoor air 8 17.30 μg/m3
Ethylbenzene Indoor air 8 2 μg/m3
m,p-Xylene Indoor air 8 5.10 μg/m3
p-Xylene Indoor air 8 7 μg/m3
Benz[a]anthracene 0.32–1.7 ng/m3 (Grimmer et al. 1988, Chuang et al. 1991)
Benzo[a]pyrene 3.35 μg/m3 (Jenkins et al. 2000)
N-Nitrosodimethylamine (NDMA) 0.01–0.24 μg/m3
N-Nitrosodiethylamine (NDEA) 0.086 μg/m3
N-Nitrosopyrrolidine (NPYR) 0.013 μg/m3
N′-Nitrosonornicotine (NNN) ND–0.006 (Klus et al. 1992)
ND–0.023 (Brunnemann et al. 1992)
4.36 (Sleiman et al. 2009)
NNK (4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone) ND–0.013 (Brunnemann et al. 1992)
0.00–0.03
1.95 ng/m3 (Sleiman et al. 2009)
NNA (4-(methylnitrosamino)-4-(3-pyridyl)butanal) 0.58 ng/m3 (Sleiman et al. 2009)
NNAL (4-(methylnitrosamino)-4-(3-pyridyl)-1-butanol) <0.1 ng/m3 (Sleiman et al. 2009)
Benzene Indoor air 8 206 μg/m3 (Adlkofer et al. 1990)
4.2–63.7 μg/m3 (Scherer et al. 1995, Martin et al. 1997, Kim et al. 2001)
8–20 (Bolte et al. 2008)
3-Ethenylpyridine 3–24 (Bolte et al. 2008)
∑16 PAHs (polycyclic aromatic hydrocarbons) 0.12–0.84
43.43 to 155.11 ng/m3 (Adesina et al. 2021)
Dibenz[a, h]anthracene 1 ng/m3 (Vu-Duc and Huynh 1989)
5-Methylchrysene 35 ng/m3 (Vu-Duc and Huynh 1989)
Nicotine 2.20 (Leaderer and Hammond 1991)
3.30 (Emmons et al. 2001)
26.92 (Kraev et al. 2009)
0.021–0.047 (Matt et al. 2013)
3.7 μg/m3 (Wamboldt et al. 2008)
Restaurant 10 μg/m3 (Hammond 1999)
Bars 20 μg/m3
Discotheques 100 μg/m3
Indoor air 0.85 μg/m3 (Henderson et al. 2023)
Indoor air 8 71 μg/m3 (Adlkofer et al. 1990)
Isoprene 657 ng/m3 (Martin et al. 1997)
Acrolein 0.47 (Sleiman et al. 2014)
Catechol 1.24 ng/m3 (Sakuma et al. 1983, Martin et al. 1997)
Cd 4–38 ng/m3 (Wu et al. 1995)
0.00–0.01 (Bolte et al. 2008)
Ni 0.002–0.007
Cr 0.001–0.009
NO2 105–293 μg/m3 (Braun et al. 2021)
PM2.5 Primary smoking area 84 μg/m3 (Van Deusen et al. 2009)
Distal area from the primary smoking area 63 μg/m3
Nonsmoking homes 9 μg/m3
CO Pub indoor air 8 0–33.11 ppm (Goniewicz et al. 2009)
Aromatic amines Indoor air (without smokers) 5–11 ng/m3 (Palmiotto et al. 2001)
Indoor air (with smokers) 15–33 ng/m3
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The mean and/or range concentration levels of the chemical content of THS are provided in Table 2. As shown, nicotine and tobacco-specific nitrosamines (TSNAs: NNN and NNK) were the most frequent chemicals measured in included studies. Nicotine may persevere in indoor environments similar to some pesticides that persist outdoors. DDT, nitrosamines, nicotine, PAHs, phthalates, bisphenol A, and flame retardants in cigarette smoke are semi-volatile organic compounds. Once released indoors, they stuck to surfaces and desorb slowly back into the air or react to form other chemical mixtures (Weschler and Nazaroff 2008). Exposure of passive smokers to SHS causes a significant increase in urinary levels of metabolites of the tobacco-specific biomarkers (i.e., NNK). The presence of these metabolites links exposure to SHS with an increased risk for lung cancer (Services 2006).

Table 2.

The mean and/or range concentration levels of chemical content of THS

Chemicals Matrix Mean and/or range concentrations (ng/m2) References
NNA (4-(methylnitrosamino)-4-(3-pyridyl)butanal) Furniture 37–256 (Matt et al. 2004, Sleiman et al. 2010b)
Household dust 3–15
Vehicle dashboard 17–30
Vehicle dust 41–68
Skin >280
2.2–220
Cotton 3500
Cellulose surface 60 ng/m2 (Sleiman et al. 2009)
NNK Furniture 5.3–36.5 (Matt et al. 2004, Sleiman et al. 2010b)
Household Dust 0.44–2.2
Vehicle dashboard 2.5–4.3
Vehicle dust 6.1–9.7
Skin >40
Skin 0.31–31
Cotton 500
Cellulose surface 990 ng/m2 (Sleiman et al. 2009)
Dust from nonsmoking homes 0.55 μg/g (Ramírez et al. 2012)
Dust from smoking homes 0.89 μg/g
Smokers’ homes 700 pg/100 cm2 (Thomas et al. 2014)
Nonsmokers’ homes 235 pg/100 cm2
NNA and NNK Indoor surfaces 2.2–3500 (Sleiman et al. 2010a)
NNN Cellulose surface <20 ng/m2 (Sleiman et al. 2010b)
Dust from nonsmoking homes 0.12 μg/g (Ramírez et al. 2012)
Dust from smoking homes 0.31 μg/g
N′-Nitrosoanatabine (NAT) Dust from nonsmoking homes 0.35 μg/g (Ramírez et al. 2012)
Dust from smoking homes 3.28 μg/g
N′-Nitrosoanabasine (NAB) Dust from nonsmoking homes 0.25 μg/g (Ramírez et al. 2012)
Dust from smoking homes 0.67 μg/g
NNAL (4-(methylnitrosamino)-4-(3-pyridyl)-1-butanol) Cellulose surface <70 ng/m2 (Sleiman et al. 2009)
Pb Window samples 82.8 (Matt et al. 2021)
Floor vacuum dust 31.4
Floor wipe samples
Cd Window samples 5
Floor vacuum dust 1.6
Floor wipe samples 0.7
Nicotine Floor 1.86
Surface wipe 6.3
Dust vacuum 1.63
0.70–1.9 μg/m2 (Matt et al. 2013)
Furniture 11–73 (Matt et al. 2004, Weschler and Nazaroff 2008, Destaillats et al. 2006)
Household dust 0.89–4.43
Vehicle dashboard 5–8.6
Vehicle dust 11.6–19.5
Skin >80
Skin 0.63–63
Cotton 1000
Dust 19.51 μg/g
Dashboards 8.61
Cellulose surface 16.5 mg/m2 (Sleiman et al. 2009)
Dust from nonsmoking homes 1.91 μg/g (Ramírez et al. 2012)
Dust from smoking homes 14.7 μg/g
Dust from nonsmoking homes 2.3 μg/g (Ramírez et al. 2014)
Dust from smoking homes 26 μg/g
Smoking residences 214 μg/m2 (Zhang et al. 2015)
Public places 1408 μg/m2
Transportations 1511 μg/m2
Surfaces 10.8–22.2 μg/m2 (Matt et al. 2011b)
Fingers of nonsmoking residents 9.1–29.1 μg/m2
Dust 5–9.3 μg/m2
Surface 4 μg/m2 (Kassem et al. 2014)
Air 0.00–2.18 μg/m3
N-Nitrosodimethylamine (NDMA) Dust from nonsmoking homes 0.45 μg/g (Ramírez et al. 2012)
Dust from smoking homes 0.29 μg/g
N-Nitrosomethylethylamine (NMEA) Dust from nonsmoking homes 0.77 μg/g (Ramírez et al. 2012)
Dust from smoking homes 0.35 μg/g
N-Nitrosodi-n-propylamine (NDPA) Dust from nonsmoking homes 0.26 μg/g (Ramírez et al. 2012)
Dust from smoking homes 0.67 μg/g
N-Nitrosodiethylamine (NDEA) Dust from nonsmoking homes 0.92 μg/g (Ramírez et al. 2012)
Dust from smoking homes 0.32 μg/g
N-Nitrosomorpholine (NMor), N-nitrosopyrrolidine (NPyr) Dust from nonsmoking homes 0.11 μg/g (Ramírez et al. 2012)
Dust from smoking homes 0.25 μg/g
N-Nitrosopiperidine (NPip) Dust from nonsmoking homes 0.67 μg/g (Ramírez et al. 2012)
Dust from smoking homes 0.54 μg/g
N-Nitrosodi-n-butylamine (NDBA) Dust from nonsmoking homes 0.11 μg/g (Ramírez et al. 2012)
Dust from smoking homes 1.22 μg/g
N-Nitrosodiphenylamine (NDPhA) Dust from nonsmoking homes 2.08 μg/g (Ramírez et al. 2012)
Dust from smoking homes 4.46 μg/g
4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) Dust from nonsmoking homes 2.02 μg/g (Ramírez et al. 2012)
Dust from smoking homes Non detect
Total tobacco-specific nitrosamines (TSNAs) Dust from nonsmoking homes 4 μg/g (Ramírez et al. 2014)
Dust from smoking homes 31 μg/g
Total PAHs Smoker homes (dust) 990 ng/g (Hoh et al. 2012)
Nonsmoker homes (dust) 756 ng/g
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Nicotine and other semi-volatile organic compounds are also found in human biological fluids (Control and Prevention 2009). Although THS is well known as a main source of indoor exposure to tobacco-related chemicals (Sleiman et al. 2014), the studies examining its chemical contents are limited. Therefore, the existing information is still unable to demonstrate a complete and dependable sight of the chemicals related to THS. Further studies are required to assess the possible health effects of THS. Although diverse chemicals have been known in THS, many toxic constituents have not been studied in recent investigations. Future experimental studies are necessary to assess the chemical contents focusing on those that are ignored in the previous researches. Also, there is a lack of scientific information on the reaction of the chemical content of THS with oxidants and the development of byproducts.

Hitherto, more than 50 toxic constituents have been recognized in THS (Sleiman et al. 2010a; Jacob III et al. 2017; Matt et al. 2021). In a study, the concentration levels of nicotine in the air of nonsmokers’ homes were 10 times lower than in those of smokers’ homes (Figueiró et al. 2016). In other studies, the acrolein concentrations in the air of smoker’s home were three times higher than outdoor air (Nazaroff and Singer 2004; Sleiman et al. 2014). Also, the level of nicotine in air samples ranged from 0.021 μg/m3 (nonsmoker local cars) to 0.047 μg/m3 (smoker local cars) (Matt et al. 2013). Also, the nicotine values in surface samples ranged from 0.7 μg/m2 (nonsmoker cars) to 1.9 μg/m2 in smoker cars (Matt et al. 2013). THS ingredients may settle on surfaces and air dust particles (Jacob III et al. 2017). Surface-attached THS constituents can be found in indoor air for days to months, and adequate time is provided for chemical changes in household air and surfaces (Jacob III et al. 2017). For instance, nicotine may react with nitrous acid and form carcinogenic TSNAs, subsequently (Sleiman et al. 2010b; Ramírez et al. 2014). The results of Tang et al.’s (Tang et al. 2022) study showed potential long-term health risks for passive/nonsmokers in homes contaminated with THS (Tang et al. 2022). Inhalation, direct dermal contact, gas-to-skin deposition, and epidermal nitrosation of nicotine are the main exposure routes of TSNAs (Tang et al. 2022). In addition, nicotine in indoor environment can be affected by the presence of ozone (Petrick et al. 2010). The reaction of ozone and absorbed nicotine causes the alarming THS and oxidation products including cotinine, myosmine, N-methyl formamide, and nicotine-1-oxide that these secondary byproducts may be back to the gas phase and affect indoor air quality over longer periods after smoking (Petrick et al. 2011a).

Exposure routes to SHS and TSH

Exposure to tobacco smoke, well known as passive smoking, can accrue through direct exposure to tobacco smoke (SHS and THS) and is estimated to be the cause of nearly 1% of worldwide mortality (Torres et al. 2018). SHS may persist for hours indoors and become more toxic over time (Schick and Glantz 2007). Different parameters such as airflow patterns, ventilation, the distance between smokers and passive smokers, and smoking occurrence can affect human exposure (Services 2006). SHS exposure occurs when nonsmokers breathe the smoke exhaled by people who smoke and/or burn tobacco products. Homes are the main areas where residents are exposed to secondhand smoke (Walton et al. 2020). People are exposed to SHS in different places where they spend varying extents of time (Services 2006).

The burning of tobacco products as a source of SHS releases the resulting concentrations of secondhand smoke, contacting hazardous pollutants into the indoor air where people live. This concentration depends on diverse features, including the intensity of smoking, ventilation, design, and operation of a building and different methods that remove smoke from the air. Total exposure can be estimated by measuring SHS concentrations in prominent places and assessing the time spent in these environments (Council 1986; Services 2006). In Walton et al. (2020), nearly 25% of US students reported breathing SHS in their homes, and 23% stated breathing SHS in cars (Walton et al. 2020).

The existence and levels of THS can be measured through environmental matrix sampling (i.e., air, dust, and on different surfaces) (Jacob III et al. 2017). Nondietary ingestion and dermal absorption are the significant exposure routes to THS chemicals, which make children particularly vulnerable owing to their hand-to-mouth behavior and premature metabolism, among other reasons (Jacob III et al. 2017). Matt et al. reported high levels of nicotine on household surfaces and on the hands of smoking mothers (Matt et al. 2011a). They also reported THS levels in nonsmokers’ homes that had been lately where smokers dwelled (Matt et al. 2011b) and in used cars (Matt et al. 2008; Fortmann et al. 2010). Nicotine and other THS components have been observed in indoor environments in which tobacco has been smoked frequently and in nonsmoking indoor environments near commuted places by smokers (Jacob III et al. 2017). THS can be found even in areas where smoking bans are severely applied (i.e., neonatal intensive care units in hospitals). In a study, Northrup et al. reported that furniture had measurable surface nicotine, and both cotinine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone were identified in children urine samples (Northrup et al. 2016a). Therefore, it can be concluded that THS is ubiquitous, even in highly controlled and smoke-free environments, and humans are continuously exposed to its chemical content. In general, there are three usual exposure pathways for SHS and THS, including (1) inhalation of chemicals in the house dust, (2) dermal exposure by touching the polluted surfaces and direct absorption of toxins in the indoor air, and (3) oral exposure via hand-to-mouth transfer of surface remains after touching polluted items, mouthing of object dishes (Li et al. 2021; Yeh et al. 2022).

Health effects

SHS and THS have been shown to increase the risks of different health effects in nonsmokers exposed to normal environmental levels. Previous scientific reports have confirmed that exposure to SHS is a public health hazard (Singer et al. 2003; Petrick et al. 2011b; Jung et al. 2012; Northrup et al. 2016b). Repeated exposure to SHS may lead to several diseases, including asthma and pneumonia, sudden infant death syndrome, lung cancer, increased left ventricular mass, and heart attacks (Services 2006; Skipina et al. 2021). Also, it has been proved that chemicals in SHS can pass the placental barrier during pregnancy and affect the growth of infants’ brain structure by interfering with the breathing system (Liu et al. 2021). Lin et al. (2021) study also showed that early-life SHS exposure was associated with different sleep-related symptoms in 6–18-year-old children (Lin et al. 2021). Exposure to SHS during early life and following sleep problems in children have direct adverse effects on the heart and blood vessels and increase the risk for coronary heart disease and stroke (Services 2006; Services 2014).

Inhaling SHS causes lung cancer in nonsmokers (Wald et al. 1986; Melloni 2014). Some research also suggests that SHS may increase the risk of breast cancer (Lee and Hamling 2016; Kim et al. 2018), nasal sinus cavity cancer (Benninger 1999), and nasopharyngeal cancer (Rodenstein and Stănescu 1985) in adults; leukemia, lymphoma, and brain tumors in children (Boffetta et al. 2000; Hofhuis et al. 2003); and obesity in boys in early adolescence (Miyamura et al. 2023). Previous studies have confirmed that nonsmokers are at increased risk of death from ischemic heart disease (Helsing et al. 1988; Kawachi et al. 1997), lung cancer (Garfinkel 1981; Cardenas et al. 1997), and all causes (Svendsen et al. 1987; Sandler et al. 1989). In a study, Du et al. (2020) reported that nearly 16 percent of lung cancer cases among never smokers in China were probably attributable to passive smoking (Du et al. 2020). In another study, Kim et al. (2018) reported that SHS may increase the risk of lung and breast cancer for nonsmokers (Kim et al. 2018). Results of another meta-analysis revealed that a nonsmoking spouse has a higher risk for lung cancer when their spouse is a smoker (Taylor et al. 2007). In addition, passive smoking is harmful to mental health and a risk factor for dementia, as well as have a negative effect on depressive symptoms (Ling and Heffernan 2016; Lange et al. 2020; Park et al. 2021). Moreover, an animal study has shown that mice exposed to incredible levels of SHS have an increased level of carcinogen-DNA adducts, formed by covalent binding for carcinogen molecules to chemical moieties in DNA (Hackshaw et al. 1997). A study by Pirie et al. (2008) showed that the risk of breast cancer does not increase for passive smoker women who are regularly exposed to SHS at their home (Pirie et al. 2008). However, Gram et al. (2021) study results showed that 1 in 14 breast cancer cases is preventable in the lack of SHS exposure from parents within childhood in never-smoking women (Hori et al. 2016; Gram et al. 2021). Nitrosamines, as identified compounds in THS, can lead to cancer (Ramírez et al. 2014). In general, different effects such as damage in the liver and lungs, poor wound healing, oxidative stress and inflammation, insulin resistance, or hyperactivity were the primary health effects of THS exposure in mice (Jacob III et al. 2017). Also, SHS and THS exposure might have a significant role in the incidence, transmission, and development of COVID-19 in susceptible groups (Mahabee-Gittens et al. 2020). In a study, both active smoking and passive smoking were reported as risk factors for poor sleep quality (Zhou et al. 2018).

In addition, this finding that SHS causes different diseases such as lower respiratory illnesses in infancy and early childhood (Fergusson et al. 1980; Al-Delaimy et al. 2002; Services 2006), middle ear disease and adenotonsillectomy (Jones et al. 2012), cervical, breast, and lung cancer in nonsmokers (Winkelstein Jr 1990; Zhong et al. 2000; Terry et al. 2011) is vital not only from a public health perspective but also in the social and economic issues and active efforts by medical professionals and politicians to reduce exposure of the nonsmoking community to SHS. More actions are required to control the dangerous effects of passive smoking, particularly in women and infants, and public health actions should prioritize reducing levels of passive smoking at home. It seems that the most significant achievements can be attained with this action about the prevention of different diseases associated with passive smoking.

Vulnerable populations

Based on World Health Organization (WHO) statistics, approximately 40% of children are exposed to SHS (Öberg et al. 2011). In most countries, it has been estimated that 15–70 percent of the population is exposed to SHS (Wong et al. 2012). In a study, results showed that 37.8% of children were exposed to SHS at home in Chongqing (Huang et al. 2023). In another study, the prevalence of SHS exposure at home was 46.8% among the middle school students in Northern Thailand (Phetphum and Noosorn 2020). SHS and THS may be especially dangerous to vulnerable peoples. For instance, individuals with asthma might be more vulnerable to SHS and THS exposure (Barnoya and Navas-Acien 2012). Children, particularly infants, are probable to be among the most vulnerable populations regarding both exposure and health effects of THS (Matt et al. 2004; Sleiman et al. 2010b; Matt et al. 2011a). Infants and children may be highly exposed to THS via different dermally, orally, and inhalation routes in house dust and surface (WHO 2017). These groups are at high risk for exposure to THS than adults due to their behaviors, such as crawling and putting nonfood objects in their mouths, as well as tending to spend more time on floors (Jacob III et al. 2017). Tobacco smoke is also a known hazard for pregnant women, and SHS and THS pose a health risk for them (Sun et al. 2021). Exposure to THS may also be a risk factor for postpartum depression among pregnant women (Wang et al. 2018). There is also evidence that THS may reduce a mother’s breast milk (Northrup et al. 2021). Due to these adverse effects, it is vital that pregnant women must not be exposed to firsthand SHS or THS smoke. THS can also have a severe impact on lung development in infants (Rehan et al. 2011). Overall, children and pregnant women are predominantly susceptible to THS exposure because they could touch and/or breathe in the toxic substances from contaminated surfaces (Rehan et al. 2011).

Protective strategies

Global efforts and regulations have been strengthened to prevent passive smoking (Park 2023). Since there is no risk-free level of exposure to SHS (Services 2006), the most essential way/method to protect against SHS and THS is to quit smoking and to support others to stop. Applying smoking bans in indoor environments is another practical approach to protect public health (Services 2006). Environmental conditions, such as opening windows, sitting in a separate area, ventilation, air conditioning, or a fan, cannot be safe against SHS and THS exposure. The only way to completely protect from the dangers of environmental tobacco smoke is through 100% smoke-free environments. Government and local authorities can keep children and/or other passive smokers from SHS and THS in the places they live, visit, and work by using confirmed methods to remove smoking in indoor environments of public places. Smoking in other places, using fans, or smoking in front of an open window does not prevent THS exposure. Disinfecting homes and/or cars that are used by a smoker may be costly because the smoke residue can stain surfaces. The smell of smoke also can remain in surfaces and building materials. Repairing services for homes and other buildings affected by tobacco smoke also may be effective for avoiding exposure and remediation (Jacob III et al. 2017). Also, removing severely affected materials (i.e., carpets and furniture) and/or using cleaners for washing also can be effective. Ammonia-based cleaners and ozone generators are suggested to remove tobacco odors (Jacob III et al. 2017). In a study, the nicotine and PAHs that adsorbed onto surfaces were effectively removed by the ozonation and reduced their concentration levels to initial levels (Tang et al. 2021). The results of the same study have shown that ozonation of THS-contaminated environment led to formation of secondary organic aerosol, as well as increased the concentration levels of VOCs, carbonyls, and particles (Tang et al. 2021). There is a lack of scientific reports on the efficiency and byproducts of these treatments that may be created. Several asthmagens have been found among the byproducts from the ozonation of nicotine (Sleiman et al. 2010a). Additional studies of the risks associated with the use of ozone in the remediation of THS, potential ozonation byproducts formed in these process, and possible advantages of ozonation are recommended.

Conclusion

Exposure to SHS and THS is a general health problem globally. Although public awareness and information of the dangers of THS exposure increase annually, it is still generally ignored in health and environmental strategies. To overcome this, research should pay attention to filling the gaps in our present understanding of SHS and THS chemicals content, long-term exposure effects, byproducts, toxicology, and particularly the mechanism of health effects of these exposures on susceptible populations. A comprehensive conception of human exposure to SHS and THS contaminants in different environments can supply intuitions for health policymakers to assess the throughout health effects of smoking at the population level, as well as for plans and apply appropriate policies for the protection of the health of vulnerable populations, and efficient methods for the clean-up these pollutants to decrease exposure to SHS and THS.

Author contributions

Hossein Arfaeinia: analysis, software, writing the first draft; Maryam Ghaemi: methodology, writing—review and editing; Anis Jahantigh: methodology, initial search; Farshid Soleimani: conceptualization, supervision, writing—review; Hassan Hashemi: writing—review and editing.

Funding

The authors would like to thank the financial support of this work by Bushehr University of Medical Sciences (Project No. 2377) and Iranian National Institute for Oceanography and Atmospheric Science (INIOAS) for their cooperation.

Data availability

Not applicable.

Declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

All authors have read the manuscript and have agreed to submit it in its current form for consideration for publication in the Journal.

Competing interests

The authors declare no competing interests.

Footnotes

Publisher’s note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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