Air pollution may affect the assessment of smoking habits by exhaled carbon monoxide measurements
Introduction
The US EPA National Ambient Air Quality Standard (NAAQS) for carbon monoxide is set at the concentration of 9 ppm measured over 8 h (US Environmental Protection Agency, 2011). European Environmental Agency set a standard of 10 mg/m3 as the maximum daily 8-h mean (which translates to slightly over 8 ppm). A substantial body of legislation was adopted in EU countries to enforce these ambient air standards.
Tobacco smoking as a critical factor of low indoor concentration CO exposure (Krzych-Fałta et al., 2015; Sajid et al., 1993). The smoking and environmental exposure are inversely proportional regarding the time of exposure and peaks of CO concentrations, with one cigarette smoke delivering 5–22 mg of CO in the concentration of 460–575 mg/m3 (400–500 ppm)(Djulančić et al., 2013). Smoking in vehicles, offices, houses, public places may raise CO concentration in ambient air to 20–40 ppm.
Additional indoor and occupational source of CO exposure is related to unvented, faulty or improperly operated combustion equipment. Otherwise, exposure to carbon monoxide originates from commuting. However, it was shown that in general transport originated CO exposure declined over the years 1990–2015 (European Environment Agency, 2017a). Remaining environmental sources include industry (mostly burning fossil fuels), bush- and forest fires, etc.
Bruinen de Bruin et al. (2004) demonstrated in elegant simulation experiments based on EXPOLIS Milan microenvironment data that average exposure concentration of CO was attributed to ambient air (84%), residential indoor sources (4%), occupational indoor sources (3%), excess concentrations during transport (8%), and other sources (1%).
However, current EU ambient air carbon monoxide policies modify almost all of the total urban population exposure and reduce it by 100% of the ambient air concentration (WHO European Centre for Environment and Health, 2013). It was also shown for transportation-related CO exposure (Krzyzanowski et al., 2005). Consequently, in many European Union areas, current urban air carbon monoxide levels are well below the air quality limits (Braubach et al., 2013).
Conversely, in areas of high air pollution level, CO concentration was shown to correlate with cardiovascular mortality, some of the pulmonary emergency visits, etc. independently from particulate matter or NO2 pollutants (Li et al., 2018).
More than 100 years ago Douglas and Haldane (Douglas et al., 1912) provided first substantial scientific evidence for carbon monoxide (CO) toxicity mechanism. They showed differences in hemoglobin dissociation curves for both oxygen and CO. Although this initially suggested a mechanism of hypoxic tissue injury is still considered one of the critical factors of CO toxicity, we know much more about this phenomenon. They include but are not limited to reactive oxygen species formation, regulation of ion channels, affecting cytochrome C oxidase (Kajimura et al., 2010) and the cellular respiration as well as mitochondrial function, or nitric oxide release (Roderique et al., 2015).
But carbon monoxide role in the human organism is multifaceted. Except for toxicity in case of exposure, carbon monoxide is produced in small amounts in the human body by heme-oxygenase (Tenhunen et al., 1968). As a gaseous transmitter, CO serves an important protective and regulatory role at the cellular level (Dulak and Jozkowicz, 2014; Roderique et al., 2015). Releasing small and controlled amounts of CO might be one of the future therapeutic goals (Motterlini et al., 2005) in oncology, sepsis, and management of inflammatory reaction.
CO exposure is harmful not only in cases of acute intoxication with high amounts of CO inhaled (European Environment Agency, 2017b). Despite the methodological challenges, studies demonstrated that long-term exposure to low concentration of CO increases general risk and affects cardiovascular, nervous (Levy, 2015), respiratory (Evans et al., 2014; Pope et al., 2015) systems. Additionally, maternal exposure to CO was reported to be associated with reduced birth weight (Garrabou et al., 2016), placental pathology (Wylie et al., 2017), and hypertension in pregnancy (Mobasher et al., 2013). According to recent studies elevated CO plays role in oral mucosal lesions, which lead to oral cavity neoplasms (Gregorczyk-Maga et al., 2018).
CO may be measured adequately in exhaled air (Irving et al., 1988; Middleton and Morice, 2000). Exhaled CO levels indicate previous CO exposure both from smoking and from environmental sources (Deveci et al., 2004; Jones and Lam, 2006; Zhao et al., 2016).
One of the popular and accepted methods of CO quantification in ambient air is an electrochemical measurement of CO oxidation to CO2 on the catalytic electrode.
Smokerlyzer is one of the analytical devices allowing CO measurement in exhaled air. It was validated in the clinical setting against carboxyhemoglobin (COHb) concentrations (Andersson and Møller, 2010) and other methods (Moscato et al., 2014) with good overall correlation. Additionally, there is a set of available clinical data on exhaled CO assessment in various healthy subject and patient populations (Champaneria et al., 2016; Dukellis et al., 2009; Krzych-Fałta et al., 2015; Moscato et al., 2014; Ohara et al., 2006; Sajid et al., 1993).
While exhaled CO measurements are fast, non-invasive and convenient, they are frequently used to confirm if the tobacco users refrained from smoking (Condoluci et al., 2016; Middleton and Morice, 2000; Pezzuto et al., 2013; Sajid et al., 1993). Findings are reliable and even used to substantiate declines in insurance claims. Additionally, these measurements were shown to differentiate active smokers and non-smokers as well as active and passive smokers (Krzych-Fałta et al., 2015). Attempts to distinguish passive smokers and non-smokers produced mixed final results (Deveci et al., 2004; Dukellis et al., 2009).
In the previous study (Maga et al., 2017) we were able to demonstrate that exhaled CO levels correlate well with tobacco use and exposure, but also depend on the environmental CO air exposure. Such exposure is a consequence of urban air pollution (primarily from the transportation, residential heating based on coal combustion and industrial sources). Thus, even non-smokers from polluted areas demonstrated higher exhaled CO levels. And a diagnostic concentration of 4 ppm CO in exhaled air was established to differentiate non-smoking inhabitants of large and small cities.
We took advantage of our previous study design (Maga et al., 2017) to plan and execute a new project. It should broaden the characterization of the possible influence of environmental pollution on exhaled CO measurements in subjects with variable smoking status.
Section snippets
Setting
Study was conducted in two large Polish cities with high level of air pollution (Warszawa (ca. 1 750,000 inhabitants) and Krakow (ca. 765,000 inhabitants, 11th most air-polluted city in European Union (European Environment Agency, 2017b; WHO European Centre for Environment and Health, 2013))), as well as a municipality with relatively low air pollution level (Kozienice ca. 18,000 inhabitants) – data extracted from Polish Inspectorate of Environmental Protection. Subject enrollment and
Results
Carbon monoxide monitoring data demonstrated the clear and statistically significant difference between Warszawa or Krakow and Kozienice regarding the mean monthly environmental concentrations of this component in the air (Table 1). The differences were equally significant both in the month covering the measurement in study subjects as well as during the three months preceding subject measurements.
Demography of the subject groups is shown in Table 2. Age, gender, BMI, education level
Summary of findings
Mean air concentrations of CO in metropolitan areas of Krakow and Warszawa were significantly higher than those in Kozienice and exceeded recommended EU limits.
Interestingly, exhaled CO measurements were also higher in a general population of highly polluted vs. low polluted areas of Poland, independent of smoking status.
Additionally, our measurements demonstrated significantly higher mean concentrations of exhaled CO in smoking vs. non-smoking subject groups.
Duration of smoking did not affect
Limitations
We are aware that our findings might apply only to the adult population. Dukellis et al. (2009) demonstrated negative results for passive smoking screening in children qualified for surgery. However, the main problem identified in this study was a difficulty in proper handling of a device and following instructions for use.
Exhaled CO levels are increased in some specific pathologies. Various disorders such as hemolytic anemia, type 1 and type 2 diabetes, asthma, chronic obstructive pulmonary
Funding
This work did not receive any significant financial support. Minor logistics and financial support were provided by the International Medical Students' Association IFMSA-Poland.
Declaration of Interest
All authors confirm that there are no known conflicts of interest associated with this publication
Ethics
Authors followed the rules on human research as described in Declaration of Helsinki (2015) and other applicable requirements. Institutional Review Board was notified, and waived a formal study approval considering non-interventional character of the study, and minimal risk involved. All subjects were adequately informed about the nature and design of study. All subjects signed informed consent forms formulated according to Institutional Review Board guidelines. Additionally personal data
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