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Abstract

The objective of this paper was to review the epidemiological literature examining the association between secondhand smoke (SHS) and cardiovascular disease (CVD). Specifically, we examined the various screening methods available in assessing smoking behaviour and quantifying nicotine absorption. Further, we considered the natural history of those exposed to SHS and the associated risk of CVD. We reviewed routine methods used to assess exposure to SHS; evaluated the utility of subjective screening questions regarding smoking behaviour and examined the efficacy of nicotine and cotinine biomarkers used to quantify SHS exposure in epidemiological and clinical-based research. Self-reporting is practical and cost-effective in identifying smoking behaviour patterns, but is subject to recall bias and underestimation of exposure, especially in the presence of children. Nicotine and cotinine biomarkers have proven valuable in quantifying tobacco smoke absorption and establishing biological plausibility. A combination of SHS self-reported and biomarker evaluation provide the most stringent method of establishing exposure. Sufficient evidence is reported in epidemiological research to support a causal association between SHS exposure and increased risks of CVD morbidity and mortality among both men and women. The risk of developing an acute cardiac syndrome or chronic lifetime coronary events is at least 30%. Similarly, reduction in the incidence of a myocardial infarction decreases by nearly 50% in the absence of SHS. Considering the biological plausibility and dose-response relationship between SHS and CVD, effective interventions that incorporate a comprehensive screening method of behavioral and biological measures of exposure coupled with efficacious treatment should elicit favorable change for at-risk populations.
Inflammation & Allergy - Drug Targets, 2009, 8, 321-327 321
1871-5281/09 $55.00+.00 © 2009 Bentham Science Publishers Ltd.
Epidemiological Evidence Associating Secondhand Smoke Exposure with
Cardiovascular Disease
Brent E. Faught*,1, Andreas D. Flouris2 and John Cairney3
1Faculty of Applied Health Sciences, Brock University, Canada
2Institute of Human Performance and Rehabilitation, Centre for Research and Technology Thessaly, Greece
3Departments of Family Medicine, Psychiatry and Behavioural Neurosciences & Clinical Epidemiology and
Biostatistics, McMaster University, Canada
Abstract: The objective of this paper was to review the epidemiological literature examining the association between
secondhand smoke (SHS) and cardiovascular disease (CVD). Specifically, we examined the various screening methods
available in assessing smoking behaviour and quantifying nicotine absorption. Further, we considered the natural history
of those exposed to SHS and the associated risk of CVD. We reviewed routine methods used to assess exposure to SHS;
evaluated the utility of subjective screening questions regarding smoking behaviour and examined the efficacy of nicotine
and cotinine biomarkers used to quantify SHS exposure in epidemiological and clinical-based research. Self-reporting is
practical and cost-effective in identifying smoking behaviour patterns, but is subject to recall bias and underestimation of
exposure, especially in the presence of children. Nicotine and cotinine biomarkers have proven valuable in quantifying
tobacco smoke absorption and establishing biological plausibility. A combination of SHS self-reported and biomarker
evaluation provide the most stringent method of establishing exposure. Sufficient evidence is reported in epidemiological
research to support a causal association between SHS exposure and increased risks of CVD morbidity and mortality
among both men and women. The risk of developing an acute cardiac syndrome or chronic lifetime coronary events is at
least 30%. Similarly, reduction in the incidence of a myocardial infarction decreases by nearly 50% in the absence of
SHS. Considering the biological plausibility and dose-response relationship between SHS and CVD, effective
interventions that incorporate a comprehensive screening method of behavioral and biological measures of exposure
coupled with efficacious treatment should elicit favorable change for at-risk populations.
Keywords: Secondhand smoke, cardiovascular disease, epidemiology, screening, exposure, biomarkers, self-reporting,
morbidity, mortality.
1. INTRODUCTION
Secondhand smoke (SHS), previously known as passive
smoking is the involuntary breathing of other people's
tobacco smoke, Approximately 5000 chemicals are produced
from cigarette smoke; many poisonous [1]. Secondhand
smoke increases the risk of cardiovascular disease (CVD) by
30%, based on epidemiological and biological evidence [2].
A 30-minute SHS exposure was found to affect coronary
flow velocity reserve in non-smokers, suggesting endothelial
dysfunction in coronary circulation [3]. Evidence from
cohort [4, 5], case-control [6] designs and meta-analysis [7]
have all suggested a longitudinal association between CVD
and SHS exposure. Further, clinical-based and animal model
research has supported this association by suggested a
biological plausibility for prolonged exposure to SHS [8-10].
Nevertheless, controversial evidence also exists with regards
to the natural history of SHS exposure and risk of CVD in
non-smokers.
Lack of an accurate method of assessing SHS exposure
has been suggested as a probable reason for the
inconsistency in the literature. Exposure misclassification
appears to be attributed to proxy measures of exposure that
*Address correspondence to this author at the Faculty of Applied Health
Sciences, Brock University, St. Catharines, Ontario, L2S 3A1, Canada;
E-mail: bfaught@brocku.ca
do not account for spousal smoking status [11, 12], exposure
source including home and workplace [5, 11] and lack of
SHS normative data and/or recognition of quantifying
intolerable levels of nicotine differences in pediatric and
adult populations [13]. Valid and efficient means of
objectifying secondhand smoke exposure would lead to more
thorough surveillance techniques of estimating the risk of
cardiovascular disease. This epidemiological review will
address the current literature as it applies to quantifying SHS
exposure and the natural history of cardiovascular disease
among those exposed to secondhand smoke.
2. MEASURING SECONDHAND SMOKE EXPOSURE
Secondhand smoke is a controversial issue in public
health, particularly since laws governing the right to smoke
in community environments are felt to infringe the rights of
those who smoke, while protecting the health of non-
smokers. Public policy is, at times, established based on
epidemiological research. However, observational studies,
the mainstay of most epidemiological research, pose
significant methodological challenges, which in turn often
threaten both the internal and external validity of the results.
Specifically, validity of studies in cardiovascular disease and
SHS is the ability to accurately estimate tobacco smoke
exposure and absorption. Secondhand smoke exposure lacks
a true screening or reference standard and is an area of
research that requires specific attention when interpreting
322 Inflammation & Allergy - Drug Targets, 2009, Vol. 8, No. 5 Faught et al.
exposure and relative risk [14]. The inability to accurately
classify smokers and non-smokers makes establishing risk
challenging. Misclassification of smokers as non-smokers,
which is more likely due to recall bias and systematic error,
presents the opportunity for underestimating the causal
association between SHS exposure and cardiovascular
disease. An accurate assessment of the risks associated with
tobacco smoke exposure depends on a generalizable and
valid measurement. Self-reporting in conjunction with an
objective (biomarker) method of screening for SHS exposure
is well documented [15-19].
Subjective Measures
Self-administered questionnaires and interviews are an
attractive approach to establishing a measure of SHS
exposure and non-smokers because they are non-invasive
and demonstrate strong face validity [13]. Further, self-
report information provides important details regarding
source, duration of exposure and proximity of SHS exposure.
Matt and colleagues [20, 21] demonstrated that well
designed interviews can illicit information from parents
regarding SHS exposure in children, explaining 20-40% of
the variance from corresponding biomarker information.
Questionnaires are considered advantageous because of the
low costs and practicality of administering [22]. Nevertheless,
subjective measures are prone to recall bias in retrospective
epidemiologic studies. Further, self-report is always open to
question in specific populations such as pregnant mothers
and parents of young children to divulge their smoking status
or child’s exposure to SHS due to the social stigma of
smoking [14]. For example, Al-Delaimy and colleagues
(2001) showed that parents reported smoking outside the
home and never near their children to avoid SHS exposure
[23]. However, the results indicated higher levels of tobacco
smoke among the children of these parents compared to the
children of non-smoking parents. Nevertheless, subjective
measures including interview and questionnaire methods
provide necessary information on smoking patterns and
nicotine contamination.
Objective Measures
Considering the biases associated with subjective
measures of SHS exposure, objective methods are necessary.
Biomarkers comprise the most recognizable objective means
of determining SHS exposure [24]. Furthermore, biomarkers
are critical in understanding the mechanisms responsible for
adverse health effects associated with SHS exposure.
Finally, biomarkers are necessary in establishing biological
plausibility in epidemiological research [25]. Nicotine and
cotinine measured in bodily fluids (blood, saliva and urine)
and hair are identified as the most recognized biomarkers of
tobacco smoke exposure. A recent investigation of men and
women of African-American and Caucasian ethnicity were
monitored for exposure to aged, diluted sidestream smoke
generated in a controlled environmental chamber with a
standard rate of air nicotine for 4 hours [26]. The results
indicated a consistent response from nicotine and cotinine
biomarkers in non-smokers, regardless of gender and race.
Nicotine is the main constituent of tobacco and secondhand
smoke exposure [27]. Ishiyama et al. (1983) first reported
nicotine in hair samples of humans [28]. Hair nicotine
concentration determined by gas chromatography/mass
spectrometry is traditionally considered superior in assessing
secondhand smoke exposure [29]. Nicotine assessed in
biological fluids has a short half-life of 2-3 hours, therefore
making these forms less discriminative in detecting absorption
[24]. Sorenson and colleagues (2007) reported a strong
association between nicotine in hair of one year old infants
exposed to low levels (10-99 days per year) of parental reported
secondhand smoke [17]. Further, nicotine extraction positively
correlates with the number of cigarettes smoked per day in the
household [15] and workplace [30]. The optimum method of
extracting nicotine in hair from children is using an isotope
dilution with spiked samples (3.3 ng/mg) with a 60 minute
shaking time. Man and colleagues (2009) reported that in order
to attain a high screening sensitivity, the amount of hair required
for nicotine extraction is minimal (5 mg) [15]. Despite the
proven validity and reliability of hair nicotine as a viable
biomarker for SHS exposure [29], controversial issues such as
hair treatment [31, 32], hair colour [29, 33] and ethnicity [34-
36] on nicotine levels in hair need to be examined in
epidemiological studies [22].
Cotinine is considered by some to be the most valid
biomarker of tobacco smoke exposure [37-39]. As a nicotine
metabolite, cotinine can be detected in bodily fluids (i.e.,
blood, urine, saliva) and hair. Cotinine is metabolized to 3’-
hydroxycotinine primarily through enzymatic activity of
CYP2A6, principally in the liver [13]. Renal excretion is the
main contributor to eliminating 3’-hydroxycotinine
accounting for 38% of all urinary nicotine metabolites in
humans [40] and has been shown to be present in urine 72
hours post-exposure [41]. Very little is known as to the value
of 3’-hydroxycotinine as a biomarker for SHS exposure,
suggesting more clinical-based research is required.
Nevertheless, urinalysis screening of nicotine and its’
metabolic constituents for SHS exposure has demonstrated
high utility. A recent comparative investigation of urinary
nicotine, cotinine and 3'-hydroxycotinine indicated a
consistently (90%) high detection rate suggesting these
chemicals can be used interchangeably as biomarkers of SHS
exposure [41].
Cotinine concentrations in urine have also been
positively correlated with blood cotinine levels [42]. Total
plasma cotinine is the principal assay used to quantify
smoking and exposure to secondhand smoke in
epidemiological research. However, cotinine is also
characterized into secondary biological metabolites,
including cotinine glucuronide, 3-hydroxycotinine, and 3-
hydroxycotinine glucuronide. De Leon and colleagues
(2002) investigated the stability of cotinine plasma and sub-
components as biomarkers for tobacco in smokers and non-
smokers [43]. Plasma total cotinine concentration was most
accurate in quantifying tobacco smoke followed by 3-
hydroxycotinine glucuronide and 3-hydroxycotinine plasma
concentrations. Cotinine glucuronide and its components of
glucuronidation were not effective biomarkers,
misclassifying 27% of non-smokers. Overall, the results
indicated that at least two plasma samples of total cotinine
are needed to accurately quantify SHS exposure in
epidemiological studies. Finally, urinary cotinine assessment
has demonstrated high utility in the surveillance of smoking
cessation programs after a clinical event or of smoking in
Epidemiological Evidence Associating Secondhand Smoke Exposure Inflammation & Allergy - Drug Targets, 2009, Vol. 8, No. 5 323
pregnant women. It also offers useful detection of SHS
exposure in children hospitalized for persistent respiratory
illnesses [44].
Cotinine measurements in saliva are receiving much
attention because of its non-invasive approach [39, 45].
Those exposed to low doses of secondhand smoke usually
have cotinine concentrations in saliva <5 ng/ml, while heavy
exposure to SHS in adults can result in levels >10 ng/ml
[37]. Murray and colleagues (1993) reported a higher cut-off
(20 ng/ml) for salivary cotinine in classifying smokers from
non-smokers [46]. Sensitivity and specificity were 99.0%
and 91.5%, respectively and were somewhat better than
carbon monoxide (sensitivity=93.7%; specificity=87.2%).
These results are also consistent with a lower saliva cotinine
cut-off of 13 ng/ml (sensitivity=86.5%; specificity=95.9%)
[47]. Saliva samples were also consistent with self-report
questionnaire, suggesting evidence of strong construct
validity for the screening of active and passive exposure to
tobacco smoke. Non-invasive saliva and urinary cotinine
sampling were superior to plasma cotinine in non-smoking
Italian females exposed and unexposed to SHS [48]. Finally,
commercial brand saliva cotinine test strips (i.e., NicAlert)
for smoking classification (10mg/ml) was found to be as
effective (sensitivity=93%; specificity=95%) and more time
and cost-effective than gas chromatography–nitrogen
phosphorous [49].
Cotinine fluid analysis from invasive and non-invasive
sources has proven effective, but has also posed unique
challenges. Specifically, cotinine in body fluids reflect SHS
exposure only a couple days preceding the study and do not
capture exposure in individuals that purposely abstain from
tobacco smoke several days prior to being assessed. As a
result, valid estimates of biomarkers are not time sensitive and
provoke the search for a more consistent and accurate
biomedical estimate of SHS exposure [24]. Cotinine hair
analysis is a noninvasive technique used to detect the presence
of nicotine metabolites in the hair shaft. Since cotinine collects
in the hair shaft during growth, it has the ability to measure
long-term and cumulative SHS exposure. Although cotinine
hair analysis addresses the issue of SHS duration of exposure,
a complete understanding of its’ overall utility is
undetermined at this point. Few studies have been published
that address this issue. Cotinine in the body is dependent on
nicotine metabolism, which in turn is influenced by factors
such as age and pregnancy. As a result, characterization of hair
cotinine should be population specific. A study by Groner and
colleagues (2004) examined cotinine hair levels in mother and
their children (<3 years old) exposed to active and passive
tobacco smoke. Both child and maternal hair cotinine levels
correlated with self-reported maternal smokers and self-
reported maternal non-smokers [50]. Overall, child hair
cotinine levels (1.18 ng/mg) were significantly higher than
maternal levels (.78 ng/mg). This was consistent among
children of non-smokers (.77 ng/mg) and their mothers (.35
ng/mg), while no difference was found in hair cotinine levels
of maternal smokers (1.91 ng/mg) and their children (1.92
ng/mg). Finally, child age, gender or race did not influence the
relationship between child and maternal hair cotinine. Further
research is necessary in understanding the utility of hair
cotinine in quantifying SHS exposure in young children and
adults.
3. SECONDHAND SMOKE AND CARDIOVASCULAR
DISEASE MORBIDITY AND MORTALITY
It is well known that secondhand smoke is a major threat to
public health due to its acknowledged adverse health effects
[51-55]. Exposure to SHS is related to the ever increasing
frequency of diseases among children and adults, such as
respiratory illness, asthma, otitis media, sudden infant death
syndrome, vascular dysfunction, and predisposition towards
cardiovascular disease and cancer [56]. The response of the
cardiovascular system in adults to secondhand smoke has been
well documented [51-55]. In the United States only, among
30,000 to 60,000 deaths from cardiovascular disease per year in
nonsmokers have been attributed to secondhand smoke [57].
The 2006 Surgeon General’s Report stated that evidence is
sufficient to infer a “causal relationship between exposure to
secondhand smoke and increased risks of coronary heart disease
morbidity and mortality among both men and women”, adding
that there is no risk-free level of exposure to secondhand smoke
[58]. Moreover, there is a confirmed link between chronic SHS
(lifestyle incorporating frequent SHS exposures) and various
types of cancer including lung cancer [59], leukemia [60, 61],
breast cancer [62], upper aero digestive tract carcinomas [63],
and nasal cancer [64].
A recent study demonstrated that the relative risk of
developing acute cardiac syndrome was found to be
increased by 50% among tobacco smoke exposed
nonsmokers [65]. Specifically, it was estimated that 34
coronary events per 134 subjects would occur as a result of
secondhand smoke exposure during their lifetime [65]. This
notion is in line with evidence showing a reduction in the
incidence of respiratory symptoms among hospitality
workers following the implementation of smoke-free laws in
different countries [66-68]. The latter is further supported in
a study where hospital admissions for myocardial infarctions
decreased by nearly 50% when a total smoking ban was
enforced and returned to baseline when the ban was repealed
[69]. Furthermore, a recent case control study [70]
examining the relationship of all types of tobacco exposure
(active smoking, past smoking, secondhand smoke exposure,
and chewing tobacco) and acute non-fatal myocardial
infarction demonstrated that secondhand smoke exposure
was associated with a graded increase in risk related to
exposure. In the same study, the odds ratio of acute
myocardial infarction was 1.24 in those exposed the least (1-
7 hours per week) and increased to 1.62 in those who were
most exposed (>21 hours per week) [70]. Epidemiological
evidence associating secondhand smoke with cardiovascular
disease morbidity and mortality based on evidence from the
2006 Report of the U.S. Surgeon General [58] are
summarized in Table 1. Based on the presented evidence, it
can be postulated that chronic exposures to secondhand
smoke generate significant adverse effects on several
systems of the human body and are associated with increased
morbidity and mortality.
The vast majority of published studies regarding the
effects of secondhand smoke have evaluated longitudinal
epidemiological data, while exposure studies assessing the
acute and short-term secondhand smoke effects are limited.
Yet, this knowledge is essential and of the utmost
importance for elucidating the underlying physiological
324 Inflammation & Allergy - Drug Targets, 2009, Vol. 8, No. 5 Faught et al.
mechanisms involved in the secondhand smoke-induced
system disruption [53]. The limited experimental studies that
assess the acute and short-term effects of exposure to
secondhand smoke include cellular, animal, and human
studies that indicate a number of pathophysiological
mechanisms through which the deleterious effects of
secondhand smoke may arise and have been recently
reviewed elsewhere [5]. In brief, data thus far have shown
that even brief exposures to secondhand smoke disrupt the
normal physiological functioning of the respiratory, the
cardiovascular, the immune and the endocrine systems
generating significant adverse effects [53].
4. SUMMARY
Numerous epidemiological studies indicate secondhand
smoke exposure increases the risk of cardiovascular disease
by an estimated 30%. The risk is substantially comparable to
mainstream smoking. Non-smokers appear to be more
sensitive to SHS than do smokers, possibly due to a hyper-
sensitive physiological system to small doses of SHS
compounds, as well as the physical adaptation typically
associated with smokers with years of prolonged tobacco
exposure. Nicotine and cotinine, the main metabolite of
nicotine, are the most useful biomarkers for quantifying
exposure to secondhand smoke. However, distinguishing
classification of smoking behaviour cannot be confirmed
using biomarkers alone. Despite biases reported with self-
report and interview questions; these subjective assessment
tools are valuable in establishing the source, frequency and
duration of secondhand smoke exposure. Combined self-
reporting and biomarker assessment is the most effective
means of establishing an accurate estimation of SHS
exposure in epidemiological research. In the presence of
Table 1. Epidemiological Evidence Associating Secondhand Smoke with Cardiovascular Disease Morbidity and Mortality Based
on Evidence from the 2006 Report of the U.S. Surgeon General [58]
Study/Location Design Exposure Population/Morbidity/Mortality Relative Risk (95% CI)
Ciruzzi [71]/ Argentina Case control SS & children smokers M: 336/ MI 1.68 (1.2-2.37)
Dobson [72]/ Australia Case control Work & home exposures M: 180, W: 160/ MI
or death from CVD M: 1.0 (0.5-1.8)
W: 2.5 (1.5-4.1)
Garland [73]/ U.S. Cohort SS W: 695/ death from CVD 2.7 (0.59-12.33)
He [74]/ China Case control SS & >5 yrs
workplace exposure W: 59/ CVD 2.36 (1.01-5.55)
He [75]/ China Case control SS W: 34/ death from CVD 1.5 (1.3-1.8)
Helsing [76]/ U.S. Cohort SS M: 3488, W: 12348/
death from CVD M: 1.31 (1.1-1.6)
W: 1.24 (1.1-1.4)
Humble [77]/ U.S. Cohort SS W: 513/ death from CVD 1.59 (0.99-2.57)
Kawachi [11]/ U.S. Cohort Home or workplace
exposures W: 32046/ MI or
death from CVD 1.73 (1.03-2.84)
La Vecchia [78]/ Italy Case control SS M: 69, W: 44 / MI 1.21 (0.57-2.52)
Layard [79]/ U.S. Case control SS M: 475, W: 914/
death from CVD M: 1.0 (0.7-1.3)
W: 1.0 (0.8-1.2)
Lee [80]/ UK Case control SS M: 41, W: 77/ CVD 1.03 (0.65-1.62)
LeVois [81]/ U.S. Cohort SS M: 88455, W: 247412/
death from CVD (0.97-1.04)
McElduff [82]/
Australia & New Zealand Case control Home & workplace
exposures combined M: 686, W: 267/
MI or death from MI 1.41 (0.73-2.71)
Muscat [83]/ U.S. Case control Home & workplace current
& childhood exposures M: 68, W: 46/ MI 2.4 (1.1-4.8)
Rosenlund [5]/ Sweden Case control SS M: 199, W: 135/ MI 1.37 (0.9-2.09)
Sandler [84]/ U.S. Cohort SS M: 4162, W: 14873/
death from CVD 1.22 (1.09-1.37)
Steenland [4]/ U.S Cohort Home or workplace
exposures M: 126500/ W: 353180/
death from CVD 1.21 (1.06-1.39)
Svendsen [85]/ U.S. Cohort SS M: 1245/ death from CVD 2.23 (0.72-6.92)
Teo [70]/ 52 countries Case control SS, friends, co-worker
smokers M & W: 12461/
acute non-fatal MI 1.24 (1.17 – 1.32)
1.62 (1.45-1.81)
Tunstall-Pedoe [86]/ Scotland Case control Any exposure 3 days
before survey M & W: 70/ CVD 1.5 (0.9-2.6)
Note: SS = s
p
ouse smoker; M = men; W = women; CVD = cardiovascular disease; MI = m
y
ocardial infarction.
Epidemiological Evidence Associating Secondhand Smoke Exposure Inflammation & Allergy - Drug Targets, 2009, Vol. 8, No. 5 325
error that is typically associated with biomarker
(measurement error) and self-report (bias) measures,
epidemiological studies should assume conservative results.
The systematic error of biomarkers is quite possibly
distributed symmetrically across the normal distribution of
scores, while subjective human bias is more inclined to be
skewed toward a socially desirable response. Whenever
possible, epidemiological studies should be designed to
incorporate the most valid biomarkers available in an
environment whereby there exists’ little or no pressure to
give a socially desirable response by those exposed to both
active and passive tobacco smoke.
Large scale studies have demonstrated a significant dose-
response relationship, with greater exposure to secondhand
smoke associated with increased risk of cardiovascular
disease mortality. These epidemiological studies suggest that
both physiological and biochemical data point to SHS
adversely affecting platelet function and damage to arterial
endothelium as contributors to increasing the risk of
cardiovascular disease. The effects of secondhand smoke are
substantial and aggressive, which explains the relatively
large risks that have been reported in epidemiological
studies. Nevertheless, secondhand smoking exposure and
cardiovascular disease are at least partially reversible.
Finally, appropriate assessment of secondhand smoke
exposure in home and work environments are warranted, as
well as recommendations to avoid such exposure. Consistent
public health initiatives to eliminate secondhand smoke in
these environments are encouraged.
REFERENCES
[1] Randall, S. Children and secondhand smoke: not just a community
issue. Paediatr. Nurs., 2006, 18, 29-31.
[2] Tong, E.K.; Glantz, S.A. Tobacco industry efforts undermining
evidence linking secondhand smoke with cardiovascular disease.
Circulation, 2007, 116, 1845-54.
[3] Ahijevych, K.; Wewers, M.E. Passive smoking and vascular
disease. J. Cardiovasc. Nurs., 2003, 18, 69-74.
[4] Steenland, K.; Thun, M.; Lally, C.; Heath, C. Environmental
tobacco smoke and coronary heart disease in the American Cancer
Society CPS-II cohort. Circulation, 1996, 94, 622-8.
[5] Rosenlund, M.; Berglind, N.; Gustavsson, A.; Reuterwall, C.;
Hallqvist, J.; Nyberg, F.; Pershagen, G. Environmental tobacco
smoke and myocardial infarction among never-smokers in the
Stockholm Heart Epidemiology Program (SHEEP). Epidemiology,
2001, 12, 558-64.
[6] Pitsavos, C.; Panagiotakos, D.B.; Chrysohoou, C.; Skoumas, J.;
Tzioumis, K.; Stefanadis, C.; Toutouzas, P. Association between
exposure to environmental tobacco smoke and the development of
acute coronary syndromes: the CARDIO2000 case-control study.
Tob. Control, 2002, 11, 220-5.
[7] He, J.; Vupputuri, S.; Allen, K.; Prerost, M.R.; Hugues, J.;
Whelton, P.K. Passive smoking and the risk of coronary heart
disease – a meta-analysis of epidemiologic studies. N. Engl. J.
Med., 1999, 340, 920-6.
[8] Glantz, S.A.; Parmley, W.W. Passive smoking and heart disease:
epidemiology, physiology, and biochemistry. Circulation, 1991,
83, 1-12.
[9] Glantz, S.A.; Parmley, W.W. Passive smoking and heart disease:
mechanisms and risk. JAMA, 1995, 273, 1047-53.
[10] Celermajer, D.S.; Adams, M.R.; Clarkson, P.; Robinson, J.;
McCredie, R.; Donald, A.; Deanfield, J.E. Passive smoking and
impaired endothelium-dependent arterial dilatation in healthy
young adults. N. Engl. J. Med., 1996, 334, 150-4.
[11] Kawachi, I.; Colditz, G.A.; Speizer, F.E.; Manson, J.E.; Stampfer,
M.J.; Willett, W.C.; Hennekens, C.H. A prospective study of
passive smoke and coronary heart disease. Circulation, 1997, 95,
2374-9.
[12] Enstrom, J.E..; Kabat, G.C. Environmental tobacco smoke and
tobacco related mortality in a prospective study of Californians,
1960-98. BMJ, 1994, 309, 9901-11.
[13] Matt, G.E.; Bernert, J.T.; Hovell, M.F. Measuring secondhand
smoke exposure in children: an ecological measurement approach.
J. Pediatr. Psychol., 2008, 33, 156-75.
[14] Florescu, A.; Ferrence, R.; Einarson, T.; Selby, P.; Soldin, O.;
Koren, G. Methods for quantification of exposure to cigarette
smoking and environmental tobacco smoke: focus on
developmental toxicology. Ther. Drug Monit., 2009, 31, 14-30.
[15] Kim, S.R.; Wipfli, H.; Avila-Tang, E.; Samet, J.M.; Breysse, P.N.
Method validation for measurement of hair nicotine level in
nonsmokers. Biomed. Chromatogr., 2009, 23, 273-9.
[16] Man, C.N.; Ismail, S.; Harn, G.L.; Lajis, R.; Awang, R.
Determination of hair nicotine by gas chromatography-mass
spectrometry. J. Chromatogr. B. Analyt. Technol. Biomed. Life Sci.,
2009, 877, 339-42.
[17] Sorensen, M.; Bisgaard, H.; Stage, M.; Loft, S. Biomarkers of
exposure to environmental tobacco smoke in infants. Biomarkers,
2007, 12, 38-46.
[18] Bramer, S.L.; Kallungal, B.A. Clinical considerations in study
designs that use cotinine as a biomarker. Biomarkers, 2003, 8, 187-
203.
[19] Gilliland, F.; Berhane, K.; McConnell, R.; Gauderman, W.J.; Vora,
H.; Rappaport, E.B.; Avol, E.; Peters, J.M. Maternal smoking
during pregnancy, environmental tobacco smoke exposure and
childhood lung function. Thorax, 2000, 55, 271-6.
[20] Matt, G.E.; Hovell, M.F.; Zakarian, J.; Bernert, J.T.; Pirkle, J.L.;
Hammond, S.K. Measuring secondhand smoke exposure in babies:
the reliability and validity of mother reports in a sample of low-
income families. Health Psychol., 2000, 19, 232-41.
[21] Matt, G.E.; Wahlgren, D.R.; Hovell, M.F.; Zakarian, J.M.; Bernert,
J.T.; Meltzer, S.B.; Pirkle, J.L.; Caudill, S. Measuring
environmental tobacco smoke exposure in infants and young
children through urine cotinine and memory-based parental reports:
empirical findings and discussion. Tob. Control, 1999, 8, 282-9.
[22] Al-Delaimy, W.K. Hair as a biomarker for exposure to tobacco
smoke. Tob. Control, 2002, 11, 176-82.
[23] Al-Delaimy, W.K.; Crane, J.; Woodward, A. Exposure of children
to environmental tobacco smoke in the home: effect of avoidance
strategies as measured by hair nicotine levels. Arch Environ.
Health, 2001, 56, 117-22.
[24] Tutka, P.; Wielosz, M.; Zatoski, W. Exposure to environmental
tobacco smoke and children health. Int. J. Occup. Med. Environ.
Health, 2002, 15, 325-35.
[25] Husgafvel-Pursiainen, K. Biomarkers in the assessment of
exposure and the biological effects of environmental tobacco
smoke. Scand. J. Work Environ. Health, 2002, 28, 21-9.
[26] Bernert, J.T.; Gordon, S.M.; Jain, R.B.; Brinkman, M.C.; Sosnoff,
C.S.; Seyler, T.H.; Xia, Y.; McGuffey, J.E.; Ashley, D.L.; Pirkle,
J.L.; Sampson, E.J. Increases in tobacco exposure biomarkers
measured in non-smokers exposed to sidestream cigarette smoke
under controlled conditions. Biomarkers, 2009, 14, 82-93.
[27] Nilsen, T.; Nilsen, O.G. Accumulation of nicotine in human hair
during long-term controlled exposure toa low concentration of
nicotine vapour. Pharmacol. Toxicol., 1997, 81, 48-52.
[28] Ishiyama, I.; Nagai, T.; Toshida, S. Detection of basic drugs
(methamphetamine, antidepressants, and nicotine) from human
hair. J. Forensic Sci., 1983, 28, 380-5.
[29] Zahlsen, K.; Nilsen, O.G. Nicotine in hair of smokers and non-
smokers: sampling procedure and gas chromatographic/mass
spectrometric analysis. Pharmacol. Toxicol., 1994, 75, 143-9.
[30] Al-Delaimy, W.K.; Fraser, T.; Woodward, A. Nicotine in hair of
bar and restaurant staff. NZ Med. J., 2001, 114, 80-3.
[31] Baumgartner, W.; Berka, C. Hair analysis for drugs of abuse. Am.
Assoc. Clin. Chem., 1989, 10, 7-16.
[32] Welch, M.J.; Sniegoski, L.T.; Allgood, C.C.; Habram, M. Hair
analysis for drugs of abuse: evaluation of analytical methods,
environmental issues, and development of reference materials. J.
Anal. Toxicol., 1993, 17, 389-98.
[33] Uematsu, T.; Mizuno, A.; Nagashima, S.; Oshima, A.; Nakamura,
M. The axial distribution of nicotine content along hair shaft as an
indicator of changes in smoking behaviour: evaluation in a
smoking-cessation programme with or without the aid of nicotine
chewing gum. Br. J. Clin. Pharmacol., 1995, 39, 665-9.
326 Inflammation & Allergy - Drug Targets, 2009, Vol. 8, No. 5 Faught et al.
[34] Knight, J.M.; Eliopoulos, C.; Klein, J.; Greenwald, M.; Koren, G.
Passive smoking in children. Racial differences in systemic
exposure to cotinine by hair and urine analysis. Chest, 1996, 109,
446-50.
[35] Pérez-Stable, E.J.; Herrera, B.; Jacob, P.I.; Benowitz, N.L. Nicotine
metabolism and intake in black and white smokers. JAMA, 1998,
280, 152-6.
[36] Benowitz, N.L.; Pérez-Stable, E.J.; Fong, I.; Modin, G.; Herrera,
B.; Jacob, P. Ethnic differences in N-glucuronidation of nicotine
and cotinine. J. Pharmacol. Exp. Ther., 1999, 291, 1196-203.
[37] Etzel, R.A. A review of the use of saliva cotinine as a marker of
tobacco smoke exposure. Prev. Med., 1990, 19, 190-7.
[38] Phillips, K.; Bentley, M.C.; Abrar, M.; Howard, D.A.; Cook, J.
Low level saliva determination and its application as a biomarker
for environmental tobacco smoke exposure. Hum. Exp. Toxicol.,
1999, 18, 291-6.
[39] Chang, M.Y.; Hogan, A.D.; Rakes, G.P.; Ingram, J.M.; Hoover,
G.E.; Platts-Mills, T.A.; Heymann, P.W. Salivary cotinine levels in
children presenting with wheezing to an emergency department.
Pediatr. Pulmonol., 2000, 29, 257-63.
[40] Jacob, P.; Yu, L.; Wilson, M.; Benowitz, N.L. Selected ion
monitoring method for determination of nicotine, cotinine and
deuterium-labeled analogs: absence of an isotope effect in the
clearance of (S)-nicotine-3’,3’-d2 in humans. Biol. Mass Spectr.,
1991, 20, 247-52.
[41] Akiyama, Y.; Arashidani, K.; Kawano, W.; Kunugita, N. Urinary
nicotine and its metabolites as a biomarker of exposure to
environmental tobacco smoke. J. UOEH, 2006, 28, 245-252.
[42] Benowitz, N.L.; Jacob, P.; Fong, I.; Guota, S. Nicotine metabolic
profile in man: comparison of cigarette smoking and transdermal
nicotine. J. Pharmacol. Exp. Ther., 1994, 268, 296-303.
[43] de Leon, J.; Diaz, F.J.; Rogers, T.; Browne, D.; Dinsmore, L.;
Ghosheh, O.H.; Dwoskin, L.P.; Crooks, P.A. Total cotinine in
plasma: a stable biomarker for exposure to tobacco smoke. J. Clin.
Psychopharmacol., 2002, 22, 496-501.
[44] Berny, C.; Boyer, J.C.; Capolaghi, B.; De L'Homme, G.; Desch, G.;
Garelik, D.; Hayder, R.; Houdret, N.; Jacob, N.; Koskas, T.; Laine,
G.; Le Moel, G.; Moulsma, M.; Plantin-Carrenard, E.; Venembre,
P. Biomarkers of tobacco smoke exposure. Ann. Biol. Clin. (Paris),
2002, 60, 263-72.
[45] Willers, S.; Axmon, A.; Feyerabend, C.; Nielsen, J.; Skarping, G.;
Skerfving, S. Assessment of environmental tobacco smoke
exposure in children with asthmatic symptoms by questionnaire
and cotinine concentrations in plasma saliva, and urine. J. Clin.
Epidemiol., 2000, 53, 715-21.
[46] Murray, R.P.; Connett, J.E.; Lauger, G.G.; Voelker H.T. Error in
smoking measures: effects of intervention on relations of cotinine
and carbon monoxide to self-reported smoking. Am. J. Public
Health, 1993, 83, 1251-7.
[47] Etter, J.; Due, T.V.; Perneger, T.V. Saliva cotinine levels in
smokers and nonsmokers. Am. J. Epidemiol., 2000, 151, 251-8.
[48] Simoni, M.; Baldacci, S.; Puntoni, R.; Pistelli, F.; Farchi, S.; Lo
Presti, F.; Pistelli, R.; Corbo, G.; Agabiti, N.; Basso, S.; Matteelli,
G.; Di Pede, F.; Carrozzi, L.; Forastiere F.; Viegi, G. Plasma,
salivary and urinary cotinine in non-smoker Italian women exposed
and unexposed to environmental tobacco smoking (SEASD study).
Clin. Chem. Lab Med., 2006, 44, 632–8.
[49] Cooke, F.; Bullen, C.; Whittaker, R.; McRobbie, H.; Chen, Ml;
Walker, N. Diagnostic accuracy of NicAlert cotinine test strips in
saliva for verifying smoking status. Nicotine Tob. Res., 2008, 10,
607–12.
[50] Groner, J.; Wadwa, P.; Hoshaw-Woodard, S.; Hayes, J.; Klein, J.;
Koren, G.; Castile, R.G. Active and passive tobacco smoke
exposure: a comparison of maternal and child hair cotinine levels.
Nicotine Tob. Res., 2004, 6, 789-95.
[51] Flouris, A.D.; Faught, B.E.; Klentrou, P. Cardiovascular disease
risk in adolescent smokers: evidence of a ‘smoker lifestyle’. J.
Child Health Care, 2008, 12, 217-27.
[52] Flouris, A.D.; Metsios, G.S.; Carrillo, A.E.; Jamurtas, A.Z.;
Gourgoulianis, K.; Kiropoulos, T.; Tzatzarakis, M.N.; Tsatsakis,
A.M.; Koutedakis, Y. Acute and short-term effects of secondhand
smoke on lung function and cytokine production. Am. J. Respir.
Crit. Care Med., 2009, 179, 1029-33.
[53] Flouris, A.D.; Vardavas, C.I.; Metsios, G.S.; Tsatsakis, A.M.;
Koutedakis, Y. Biological evidence for the acute health effects of
secondhand smoke exposure. Am. J. Physiol. Lung Cell Mol.
Physiol., (in press, 2009).
[54] Flouris, A.D.; Metsios, G.S.; Jamurtas, A.Z.; Koutedakis, Y.
Sexual dimorphism in the acute effects of secondhand smoke on
thyroid hormone secretion, inflammatory markers and vascular
function. Am. J. Physiol. Endocrinol. Metab., 2008, 294, E456-462.
[55] Metsios, G.S.; Flouris, A.D.; Jamurtas, A.Z.; Carrillo, A.E.;
Kouretas, D.; Germenis, A.E.; Gourgoulianis, K.; Kiropoulos, T.;
Tzatzarakis, M.N.; Tsatsakis, A.M.; Koutedakis, Y. A brief
exposure to moderate passive smoke increases metabolism and
thyroid hormone secretion. J. Clin. Endocrinol. Metab., 2007, 92,
208-11.
[56] Stranges, S.; Bonner, M.R.; Fucci, F.; Cummings, K.M.;
Freudenheim, J.L.; Dorn, J.M.; Muti, P.; Giovino, G.A.; Hyland,
A.; Trevisan, M. Lifetime cumulative exposure to secondhand
smoke and risk of myocardial infarction in never smokers. Results
from the Western New York health study. Arch. Intern. Med.,
2006, 166, 1961-7.
[57] Puranik, R.; Celermajer, D. Smoking and endothelial function.
Prog. Cardiovasc. Dis., 2003, 45, 443-58.
[58] U.S. Department of Health and Human Services. The health
consequences of involuntary exposure to tobacco smoke: A report
of the Surgeon General. Atlanta, GA: U.S. Department of Health
and Human Services, Centers of Disease Control and Prevention,
Coordinating Center for Health Promotion, National Center for
Chronic Disease Prevention and Health Promotion, Office on
Smoking and Health, 2006.
[59] Besaratinia, A.; Pfeifer, G.P. Second-hand smoke and human lung
cancer. Lancet Oncol., 2008, 9, 657-66.
[60] Chang, J.S. Parental smoking and childhood leukemia. Methods
Mol. Biol., 2009, 472, 103-37.
[61] Lee, K.M.; Ward, M.H.; Han, S.; Ahn, H.S.; Kang, H.J.; Choi,
H.S.; Shin, H.Y.; Koo, H.H.; Seo, J.J.; Choi, J.E.; Ahn, Y.O.;
Kang, D. Paternal smoking, genetic polymorphisms in CYP1A1
and childhood leukemia risk. Leuk. Res., 2009, 33, 250-8.
[62] Johnson, K.C. Accumulating evidence on passive and active
smoking and breast cancer risk. Int. J. Cancer, 2005, 117, 619-28.
[63] Sturgis, E.M.; Pytynia, K.B. After the smoke clears: environmental
and occupational risks for carcinoma of the upper aero digestive
tract. Cancer J., 2005, 11, 96-103.
[64] Rushton, L. Health impact of environmental tobacco smoke in the
home. Rev. Environ. Health, 2004, 19, 291-309.
[65] Pitsavos, C.; Panagiotakos, D.B.; Chrysohoou, C.; Tzioumis, K.;
Papaioannou, I.; Stefanadis, C.; Toutouzas, P. Association between
passive cigarette smoking and the risk of developing acute
coronary syndromes: the CARDIO 2000 study. Heart Vessels,
2002, 16, 127-30.
[66] Farrelly, M.C.; Nonnemaker, J.M.; Chou, R.; Hyland, A.; Peterson,
K.K.; Bauer, U.E. Changes in hospitality workers' exposure to
secondhand smoke following the implementation of New York's
smoke-free law. Tob. Control, 2005, 14, 236-41.
[67] Fernandez, E.; Fu, M.; Pascual, J.A.; Lopez, M.J.; Perez-Rios, M.;
Schiaffino, A.; Martinez-Sanchez, J.M.; Ariza, C.; Salto, E.; Nebot,
M. Impact of the Spanish smoking law on exposure to second-hand
smoke and respiratory health in hospitality workers: a cohort study.
PLoS One, 2009, 4, e4244.
[68] Larsson, M.; Boethius, G.; Axelsson, S.; Montgomery, S.M.
Exposure to environmental tobacco smoke and health effects
among hospitality workers in Sweden--before and after the
implementation of a smoke-free law. Scand. J. Work Environ.
Health, 2008, 34, 267-77.
[69] Sargent, R.P.; Shepard, R.M.; Glantz, S.A. Reduced incidence of
admissions for myocardial infarction associated with public
smoking ban: before and after study. BMJ, 2004, 328, 977-80.
[70] Teo, K.K.; Ounpuu, S.; Hawken, S.; Pandey, M.; Valentin, V.;
Hunt, D.; Diaz, R.; Rashed, W.; Freeman, R.; Jiang, L. Tobacco
use and risk of myocardial infarction in 52 countries in the
INTERHEART study: a case-control study. Lancet, 2006, 368,
647-58.
[71] Ciruzzi, M.; Pramparo, P.; Esteban, O.; Rozlosnik, J.; Tarteglione,
J.; Abescasis, B.; César, J.; De Rosa, J.; Paterno, C.; Schargrodsky,
H. Case-control study of passive smoking at home and risk of acute
myocardial infarction. J. Am. Col. Cardiol, 1998, 31, 797-803.
[72] Dobson, A.; Alexander, H.M.; Heller, R.F.; Lloyd, D.M. Passive
smoking and the risk of heart attack or coronary death. Med. J.
Aust., 1991, 154, 793-7.
Epidemiological Evidence Associating Secondhand Smoke Exposure Inflammation & Allergy - Drug Targets, 2009, Vol. 8, No. 5 327
[73] Garland, C.; Barretp-Connor, E.; Suarez, L.; Criqui, M.H.;
Wiingard, D.L. Effects of passive smoking on ischemic heart
disease mortality of nonsmokers. A prospective study. Am. J.
Epidemiol., 1985, 121, 645-50.
[74] He, Y.; Lam, T.H.; Li, L.S.; Li, L.S.; Du, R.Y.; Jia, G.L.; Huang,
J.Y.; Zheng, J.S. Passive smoking at work as a risk factor for
coronary heart disease in Chinese women who have never smoked.
Br. Med. J., 1994, 308, 380-84.
[75] He, Y. Women's passive smoking and coronary heart disease.
Chinese J. Prevent. Med., 1989, 23, 19-22.
[76] Helsing, K.; Sandler, D.P.; Comstock, G.W.; Chee, E. Heart
disease mortality in nonsmokers living with smokers. Am. J.
Epidemiol., 1988, 127, 915-22.
[77] Humble, C.; Croft, J.; Gerber, A.; Casper, M.; Hames, C.G.;
Tyroler, H.A. Passive smoking and 20-year cardiovascular disease
mortality among nonsmoking wives, Evans County, Georgia. Am.
J. Public Health, 1990, 80, 599-601.
[78] La Vecchia, C.; D’Avanzo, B.; Franzosi, M.G.; Tognoni, G.
Passive smoking and the risk of acute myocardial infarction.
Lancet, 1993, 341, 505-6.
[79] Layard, M.W. Ischemic heart disease and spousal smoking in the
National Mortality Followback Survey. Regul. Toxicol.
Pharmacol., 1995, 21, 180-3.
[80] Lee, P.; Chamberlain, J.; Alderson, M. Relationship of passive
smoking to risk of lung cancer and other smoking-associated
diseases. Br. J. Cancer, 1986, 54, 97-105.
[81] LeVois, M.; Layard, M. Publication bias in the environmental
tobacco smoke/coronary heart disease epidemiologic literature.
Regul. Toxicol. Pharmacol., 1995, 21, 184-91.
[82] McElduff, P.; Dobson, A.J.; Jackson, R.; Beaglehole, R.; Heller,
R.F.; Lay-Yee, R. Coronary events and exposure to environmental
tobacco smoke: a case-control study from Australia and New
Zealand. Tob. Control, 1998, 7, 41-6.
[83] Muscat, J.; Wynder, E. Exposure to environmental tobacco smoke
and the risk of heart attack. Int. J. Epidemiol., 1995, 24, 715-9.
[84] Sandler, D.; Comstock, G.W.; Helsing, K.J.; Shore, D.L. Deaths
from all causes in non-smokers who lived with smokers. Am. J.
Public Health, 1989, 79, 163-7.
[85] Svendsen, K.H.; Kuller, L.H.; Martin, M.J.; Ockene, J.K. Effects of
passive smoking in the Multiple Risk Factor Intervention Trial. Am.
J. Epidemiol., 1987, 126, 783-95.
[86] Tunstall-Pedoe, H.; Brown, C.A.; Woodward, M.; Tavendale, R.
Passive smoking by self report and serum cotinine and the
prevalence of respiratory and coronary heart disease in the Scottish
Heart Health Study. J. Epidemiol. Commun. Health, 1995, 49, 139-
43.
Received: July 12, 2009 Revised: September 19, 2009 Accepted: September 30, 2009
... Products from cigarette burning released into the environment are associated with a greater risk of morbidity and mortality. (11) Hence, smoking affects the health of both active and passive smokers. Exposure to cigarette smoke (equivalent to 1% of 20 actively smoked cigarettes per day) is thought to impair endothelial vasodilator function, leading to atherosclerotic disease. ...
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... Exercise training is a physiological left ventricular hypertrophy adaptive response of the cardiomyocytes to physiological stresses which in response to increased workload [23,24]. Exercise training considers overlap exists between the mechanisms that control the pathological growth of the heart and the physiological growth of the heart [25]. Increased cardiomyocyte cell size and protein synthesis are properties of both physiological and pathological Left ventricular hypertrophy. ...
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... Furthermore, exposure to second-hand smoke contributes to health problems among women. Increased exposure to second-hand smoke is associated with an increased risk of death from cardiovascular disorders [13]. ...
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Context: It has been indicated that acute active and passive tobacco cigarette smoking may cause changes on redox status balance that may result in significant pathologies. However, no study has evaluated the effects of active and passive e-cigarette smoking on redox status of consumers. Objective: To examine the acute effects of active and passive e-cigarette and tobacco cigarette smoking on selected redox status markers. Methods: Using a randomized single-blind crossover design, 30 participants (15 smokers and 15 nonsmokers) were exposed to three different experimental conditions. Smokers underwent a control session, an active tobacco cigarette smoking session (smoked 2 cigarettes within 30-min) and an active e-cigarette smoking session (smoked a pre-determined number of puffs within 30-min using a liquid with 11 ng/ml nicotine). Similarly, nonsmokers underwent a control session, a passive tobacco cigarette smoking session (exposure of 1 h to 23 ± 1 ppm of CO in a 60 m3 environmental chamber) and a passive e-cigarette smoking session (exposure of 1 h to air enriched with pre- determined number of puffs in a 60 m3 environmental chamber). Total antioxidant capacity (TAC), catalase activity (CAT) and reduced glutathione (GSH) were assessed in participants’ blood prior to, immediately after, and 1-h post-exposure. Results: TAC, CAT and GSH remained similar to baseline levels immediately after and 1-h-post exposure (p > 0.05) in all trials. Conclusions: Tobacco and e-cigarette smoking exposure do not acutely alter the response of the antioxidant system, neither under active nor passive smoking conditions. Overall, there is not distinction between tobacco and e-cigarette active and passive smoking effects on specific redox status indices.
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Purpose: Exposure to secondhand smoke (SHS) has been associated with decreased heart rate variability (HRV). However, the time course of this association is unclear. Therefore, the objective of this study was to investigate the association between 15-240 minute SHS-related fine particulate matter (PM2.5) moving averages and indices of HRV. Methods: With a panel study design, we used personal monitors to continuously measure PM2.5 and HRV of 35 participants who were exposed to SHS for approximately 6 hours. Results: We observed negative, significant associations between 5-minute HRV indices and 15 minute PM2.5 moving averages and 240 minute PM2.5 moving averages: there was a significant (p<0.01) 7.5% decrease in the 5-minute square root of the mean squared differences of successive normal heart beats associated with (RMSSD), and a significant (p<0.01) 14.7% decrease in the 5-minute high frequency (HF) power associated with the 15 minute PM2.5 moving averages; there was also a significant (p<0.01) 46.9% decrease in the 5-minute RMSSD, and a significant (p<0.01) 77.7% decrease in the 5-minute high frequency (HF) power associated with the 240 minute PM2.5 moving averages. Conclusions: Our findings that exposure to SHS related PM2.5 was associated with HRV support the hypothesis that SHS can affect the cardiovascular system. The negative associations reported between short and longer term PM2.5 and HRV indicate adverse effects of SHS on the cardiovascular system.
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Com o intuito de aproximar os gestores estaduais e municipais de saúde com a gestão da Coordenação-Geral de Assistência Farmacêutica e Medicamentos Estratégicos (CGAFME), no sentido de qualificar a Assistência Farmacêutica, foi idealizado a realização do Seminário Nacional do Componente Estratégico. O primeiro “Seminário Nacional do Componente Estratégico da Assistência Farmacêutica”, que ocorreu em 2014, teve por objetivo discutir os principais desafios e perspectivas no âmbito do Componente Estratégico da Assistência Farmacêutica (Cesaf) e possibilitar a troca de experiências entre os gestores na busca da integralidade na assistência à saúde. Devido à importância da contribuição dos estados e dos municípios para a gestão participativa da CGAFME, em agosto de 2015 ocorreu a segunda edição do Seminário, que teve como objetivo contribuir com o avanço do processo de qualificação do Cesaf nas suas dimensões, oferecer garantia do acesso e da qualidade de medicamentos, assim como organizar os serviços farmacêuticos, com a atualização e a elaboração de Diretrizes Clínicas e Terapêuticas para o Cuidado Farmacêutico nas doenças e agravos que são de responsabilidade do Cesaf. O II Seminário foi constituído de mesas de debate com a participação dos gestores municipais, estaduais e federais. Além disso, foram apresentadas a experiência do planejamento da CGAFME e a organização da gestão do Cesaf por meio de relatos de experiência estaduais e municipais. O Seminário possibilitou o aprofundamento do debate para a qualificação do cuidado farmacêutico e do uso racional de medicamentos. Os avanços alcançados foram destacados e os desafios a serem superados, tais como o fortalecimento da relação interfederativa e a organização dos serviços farmacêuticos.
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Purpose: The purpose of this study was to identify the assertive behavior of asking smokers not to smoke and investigate the factors related to assertive behavior in patients with vascular diseases. Methods: Participants were 203 adult Korean patients with vascular diseases such as cerebral infarction and myocardial infarction. Data were collected using questionnaires that included the characteristics of secondhand smoke (SHS), secondhand smoke-related variables (Health belief model factors, health promotion model factors) and level of assertive behavior. Descriptive statistics, t-test, ANOVA and multiple regression using SPSS/WIN 18.0 were performed. Results: Participants who never ask smokers not to smoke was 39.9%, whereas participants who always ask was 7.4%. There was a weak positive relationship between assertive behavior and susceptibility to disease (r
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National surveys of the exposure of non-smokers to secondhand smoke based on serum cotinine analyses have consistently identified certain groups within the population including children, males and non-Hispanic Blacks as having relatively greater exposure. Although these differences in mean serum cotinine concentrations probably represent differences in exposure of individuals in their daily lives, it is also possible that metabolic or other differences in response might influence the results. To better define the nature of those findings, we have examined the response of 40 non-smokers including both men and women and African-Americans and whites to sidestream (SS) cigarette smoke generated by a smoking machine under controlled conditions. In this study, participants were exposed to aged, diluted SS smoke (ADSS) generated in an environmental chamber with a mean air nicotine concentration of 140 microg m(-3) and 8.6 ppm CO for 4 h. Salivary cotinine was measured every 30 min, and serum cotinine samples were taken prior to, and 2 h after exposure. Urinary nicotine metabolites and NNAL, a tobacco-specific nitrosamine, and 4-aminobiphenyl (4-AB) haemoglobin adducts were also measured prior to and 2 h following the exposure. Under these uniform, controlled conditions, we found a similar response to ADSS smoke exposure among all the participants. In all cases a significant increase in biomarker concentration was noted following exposure, and the short-term increases in salivary cotinine concentration were quite similar at approximately 12 pg ml(-1) min(-1) among the groups. In this small study, no significant differences by gender or race were seen in the mean increases observed in cotinine, NNAL or 4-AB adducts following 4 h of exposure. Thus, our results are most consistent with a relatively uniform response in tobacco biomarker concentrations following short-term exposure to ADSS tobacco smoke, and suggest that biomarker measurements are capable of effectively indicating increases in exposure among groups of non-smokers.
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The acute effect of secondhand smoke (SHS) on lung function and the duration of system disruption remain unknown. To assess the SHS effects and their duration on lung function and inflammatory markers. In a randomized single-blind crossover experiment data were obtained from 16 (8 women) nonsmoking adults at baseline and at 0, 1, and 3 hours after a 1-hour SHS exposure set at bar/restaurant SHS levels. Serum and urine cotinine, lung function, and cytokines IL-4, IL-5, IL-6, tumor necrosis factor (TNF)-alpha, and IFN-gamma. At 0 hours most lung function parameters were significantly reduced (indicative: FEV(1), 4.3 +/- 0.4 vs. 3.8 +/- 0.3 L; FEV(1)/FVC, 0.9 +/- 0.1 vs. 0.8 +/- 0.1; P < 0.05) but at 3 hours they were at baseline levels. In contrast, cotinine (serum, 8.9 +/- 3.2 vs. 35.5 +/- 10.2 ng x ml(-1)), IL-4 (41.3 +/- 5.8 vs. 44.2 +/- 4.5 pg x ml(-1)), IL-5 (36.1 +/- 3.2 vs. 60.1 +/- 7.0 pg x ml(-1)), IL-6 (2.5 +/- 0.3 vs. 7.6 +/- 1.4 pg x ml(-1)) and IFN-gamma (0.3 +/- 0.2 vs. 0.6 +/- 0.2 IU x ml(-1)) at 3 hours were higher than at baseline (P < 0.05). IL-4 and TNF-alpha increased only in men, whereas IL-5, IL-6, and IFN-gamma were different between sexes after exposure (P < 0.05). Regression analyses revealed inverse associations of FEV(1) and FEV(1)/FVC ratio with IL-5 (P < 0.05) in men and with IL-5 (P = 0.01), IL-6 (P < 0.001), IFN-gamma (P = 0.034) and serum cotinine (P < 0.001) in women. We conclude that 1 hour of SHS exposure at bar/restaurant levels is accompanied by significant decrements on lung function and marked increases in inflammatory cytokines, particularly in men. More importantly, whereas most smoke-induced effects on lung function appear to recede within 60 minutes, inflammatory cytokines remain elevated for at least 3 hours after exposure to SHS.
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Both environmental and occupational exposures are associated with the development of carcinomas of the upper aerodigestive tract, although most squamous cell carcinomas of the upper aerodigestive tract are related to smoking and drinking. This review discusses environmental and occupational risk factors, other than tobacco and alcohol, for carcinoma of the upper aerodigestive tract and the difficulties encountered when attempts are made to study these environmental and occupational exposures. However, this is not an all-inclusive review; rather, it is designed to give the reader an understanding of the topic, to allow for appropriate counseling of patients, and perhaps to advance public health initiatives.
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We sought to study the relation between passive smoking at home and the risk of acute myocardial infarction (AMI). Previous epidemiologic studies have linked environmental tobacco smoke to an increased risk of coronary heart disease, but the evidence to support this view is not strong enough. To study this issue further, we analyzed the data from a case-control study conducted in Argentina between 1991 and 1994. Case patients included 336 never-smokers with AMI. Control patients were 446 never-smokers admitted to the same network of hospitals with a wide spectrum of acute disorders unrelated to smoking or to known or suspected risk factors for AMI. Data on the smoking habits of the participants' close relatives (spouse and children) were collected by trained interviewers using a structured questionnaire. Compared with subjects whose relatives had never smoked, the multivariate odds ratios for passive smokers, according to the smoking status of their relatives, were 1.68 (95% confidence interval [CI] 1.20 to 2.37) for one or more relatives who smoked; 1.59 (95% CI 0.85 to 2.96) for a spouse who smoked; 1.24 (95% CI 0.61 to 2.52) for a spouse who smoked 1 to 20 cigarettes/day; 4.03 (95% CI 0.99 to 16.32) for a spouse who smoked >20 cigarettes/day; and 1.80 (95% CI 1.20 to 2.68) for one or more children who smoked. There was a significant interaction between passive smoking and hypercholesterolemia (> or = 240 mg/dl), hypertension, diabetes and family history of MI. In never-smokers, passive smoking at home appeared to be associated with the risk of AMI, and approximately 14% of cases in men and 18% of cases in women in this Argentinian cohort are attributable to passive smoking.
Article
Human hair contains methamphetamine, amitriptyline, imipramine, nicotine, and their metabolites in some amount, which can be detected by routine toxicological methods. Sometimes, the level of drugs reaches over 100 micrograms/g. Animal experiments indicate that these drugs are found solely in sections of hair grown after administration of the drugs. The negative stage after the administration of drugs means that the hair section containing drugs has not come out of the hair follicle. Toxicological examination of the hairs may give some clue helping to identify the chronology of the intoxication.
Article
Active and passive smoking have been associated with an array of adverse effects on health. The development of valid and accurate scales of measurement for exposures associated with health risks constitutes an active area of research. Tobacco smoke exposure still lacks an ideal method of measurement. A valid estimation of the risks associated with tobacco exposure depends on accurate measurement. However, some groups of people are more reluctant than others to disclose their smoking status and exposure to tobacco. This is particularly true for pregnant women and parents of young children, whose smoking is often regarded as socially unacceptable. For others, recall of tobacco exposure may also prove difficult. Because relying on self-report and the various biases it introduces may lead to inaccurate measures of nicotine exposure, more objective solutions have been suggested. Biomarkers constitute the most commonly used objective method of ascertaining nicotine exposure. Of those available, cotinine has gained supremacy as the biomarker of choice. Traditionally, cotinine has been measured in blood, saliva, and urine. Cotinine collection and analysis from these sources has posed some difficulties, which have motivated the search for a more consistent and reliable source of this biomarker. Hair analysis is a novel, noninvasive technique used to detect the presence of drugs and metabolites in the hair shaft. Because cotinine accumulates in hair during hair growth, it is a unique measure of long-term, cumulative exposure to tobacco smoke. Although hair analysis of cotinine holds great promise, a detailed evaluation of its potential as a biomarker of nicotine exposure, is needed. No studies have been published that address this issue. Because the levels of cotinine in the body are dependent on nicotine metabolism, which in turn is affected by factors such as age and pregnancy, the characterization of hair cotinine should be population specific. This review aims at defining the sensitivity, specificity, and clinical utilization of different methods used to estimate exposure to cigarette smoking and environmental tobacco smoke.
Article
Hair nicotine is a known biomarker for monitoring long-term environmental tobacco smoke (ETS) exposure and smoking status. In general, hair nicotine assay involves alkaline digestion, extraction and instrumental analysis. The gas chromatography-mass spectrometry (GC-MS) assay currently developed has shown to be of high throughput with average approximately 100 hair samples being extracted and analyzed per day. This was achieved through simplified extraction procedure and shortened GC analysis time. The extraction was improved by using small volume (0.4 mL) of organic solvent that does not require further evaporation and salting steps prior to GC-MS analysis. Furthermore, the amount of hair utilized in the extraction was very little (5 mg) while the sensitivity and selectivity of the assay is equal, if not better than other established methods. The linearity of the assay (r(2)>0.995), limit of quantitation (0.04 ng/mg hair), within- and between-assays accuracies and precisions (<11.4%) and mean recovery (92.6%) were within the acceptable range.