Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 27  |  Issue : 1  |  Page : 23-27

Urinary cotinine level in passive smoker nondiabetic children of diabetic families


1 Department of Pediatrics, Faculty of Medicine, Menofiya University, Menufia, Egypt
2 Department of Clinical Pathology, Faculty of Medicine, Menofiya University, Menufia, Egypt

Date of Submission03-Oct-2013
Date of Acceptance06-Dec-2013
Date of Web Publication20-May-2014

Correspondence Address:
Mohamed I Yahia
11 Saad Mansour St. Cleopatra, 21562, Alexandria
Egypt
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-2098.132297

Rights and Permissions
  Abstract 

Objective
The aim of the study was to measure urinary cotinine level as a biomarker of passive smoking in children.
Background
Children's exposure to passive smoking is associated with a number of health hazards such as prenatal damage to the fetus, poor growth, respiratory illness, atopy and asthma, coronary heart disease, and sudden infant death syndrome.
Materials and methods
This study was conducted on 54 nondiabetic children from attendance of Genetic and Endocrine Units of Pediatric Department, Menofiya Faculty of Medicine.
They were divided into two groups: group A (34 children exposed to passive smoking) and group B (20 children not exposed to passive smoking).
The studied groups were subjected to detailed history taking, clinical examination, investigations (measurement of cotinine level by competitive enzyme immunoassay for the specific detection of cotinine in urine samples), and family counseling.
Results
There is significantly higher urinary cotinine levels among children with history of exposure to passive tobacco smoke (152.06 ± 106.92) in comparison with children with no history of exposure (3095.0 ± 1160.09; P ≤ 0.001). The urinary cotinine levels were found to be dependent on daily exposure to tobacco smoke as indicated by the number of cigarettes consumed by the smoker in the presence of the child.
Conclusion
Passive smoking is a risk factor for many health hazards, and cotinine is a valuable biomarker for assessing exposure to passive tobacco smoking especially in children.

Keywords: Biomarker, cotinine, passive smoking


How to cite this article:
Abou El-Ella SS, Tawfik MA, El Bassuoni MA, Yahia MI. Urinary cotinine level in passive smoker nondiabetic children of diabetic families. Menoufia Med J 2014;27:23-7

How to cite this URL:
Abou El-Ella SS, Tawfik MA, El Bassuoni MA, Yahia MI. Urinary cotinine level in passive smoker nondiabetic children of diabetic families. Menoufia Med J [serial online] 2014 [cited 2020 Feb 17];27:23-7. Available from: http://www.mmj.eg.net/text.asp?2014/27/1/23/132297


  Introduction Top


As a result of exposure to second-hand smoke (SHS), 600 000 people are estimated to die annually worldwide [1].

SHS, also known as environmental tobacco smoke (ETS), is a mixture of the smoke given off by the burning end of tobacco products (sidestream smoke) and the mainstream smoke exhaled by smokers. SHS occurs when a nonsmoker inhales ETS produced by smokers in the same vicinity [2].

In the mid 2000s, some researchers began focusing on 'third-hand smoke' - that is the odoriferous residue left on surfaces and clothing from smoking [3].

Children, in particular, seem to be the most susceptible population to the harmful effects of ETS, as children not only have higher metabolic rates, but also inhale much greater volumes of air per kilogram body weight than adults. In addition, their tendency to often sit closer to their parents, family members, or caregivers bring them closer to the source of pollutants than other passive smokers. Thus, the harmful effects of ETS on health are more severe in children than in adults. In addition, children are especially susceptible to third-hand smoke exposure because they breathe near, crawl and play on, touch, and mouth the contaminated surfaces [4].

Cigarette smoke is comprised of two main components: Mainstream and sidestream smoke. Mainstream smoke, an aerosol made up of a vapor phase and a particulate phase containing carcinogens (e.g. PAHs, aromatic amines, and aldehydes), is generated during inhalation through the butt end of a lit cigarette. Sidestream smoke is emitted from the burning end of a cigarette between puffs and is produced at generally lower temperatures, with a different airflow compared with mainstream smoke [5],[6].

Cigarette smoke contains more than 4000 compounds. Many of these compounds are known to be toxic, mutagenic, and carcinogenic [7].

Exposure of children to ETS in home increases the incidence of middle ear disease, asthma, wheeze, cough, bronchitis, bronchiolitis, pneumonia, and impaired pulmonary function. The link between exposure to ETS and children's morbidity and mortality is well established [8].

There is a growing body of evidence to suggest that smoking is an independent risk factor for diabetes [9].

Measurement of SHS-specific biomarkers can confirm exposure and may also contribute to an estimate of dose. A substantial number of compounds have been studied as potential biomarkers including carbon monoxide (in exhaled air or as carboxyhemoglobin), thiocyanate, nicotine and its metabolites (e.g. cotinine), and other compounds [10].

However, measurement of cotinine alone is sufficient for assessing exposures to SHS, especially in children [11].

The aim of this study was to measure urinary cotinine as a marker of exposure to passive smoking in nondiabetic children.


  Materials and methods Top


This study was conducted on 54 children selected from Menofiya University Hospital, Genetic and Endocrine Units, Pediatric Department, Egypt during the period from 2010 to 2012.

They were divided into two groups: Group A included 34 nondiabetic children exposed to passive smoking, 24 girls (70.5%) and 10 boys (29.5%).

Group A was further classified into two subgroups according to the number of cigarettes/day [12].

Group A1 included nine children mildly exposed to passive smoking (1-10 cigarettes/day or ≤ 0.5 pack) and group A2 included 25 children heavily exposed to passive smoking (>10 cigarettes/day or > 0.5 pack).

Group B included 20 nondiabetic children not exposed to passive smoking, six girls (30%) and 14 boys (70%).

Inclusion criteria

Nondiabetic children of age between 2 and 18 years, with positive history of exposure to passive smoking and positive family history of diabetes mellitus were included.

Exclusion criteria

Diabetic children of age less than 2 years or more than 18 years and active smokers were excluded.

All studied children were subjected to the following:

Detailed history taking with stress on history of exposure to passive smoking, thorough clinical examination, and cotinine assay by a competitive enzyme immunoassay for the specific detection of cotinine in urine samples. The wells of the microtiter strips are coated with anticotinine antibody. During the first incubation, the horseradish peroxidase-labeled cotinine competes with the free cotinine in the donors sample for the anticotinine antibody-binding sites on the microtiter strips.

The wells are washed to remove any excess enzyme material before the addition of the tetramethylbenzidine substrate solution. Addition of the stop solution terminates the reaction and absorbances are read spectrophotometrically at 450 nm.

Any sample with an absorbance less than or equal to the chosen cutoff calibrator (500 ng/ml calibrator) is considered positive, whereas any sample with an absorbance greater than the chosen cutoff calibrator is considered negative [13].

In addition, the smoker's families were given family counseling in two visits.

On the first visit, we made them aware about the hazards of both active and passive smoking and had discussion about the types of passive smoking (SHS and third-hand smoking).

On the second visit, we discussed about the results of urinary cotinine levels and its correlation with the frequency of infections (respiratory tract infections, otitis media) and the relationship between urinary cotinine level and the number of packs consumed by the smoker or the place of exposure. In addition, we discussed about how to quit smoking by explaining the health hazards of smoking on both active and passive smokers, the benefits of stopping smoking for the smoker, smoker's family, and community, and the ways to stop smoking including reduction in nicotine absorption (e.g. not hold smoke deeply).

Statistical methodology

The data collected were tabulated and analyzed by statistical package for the social science software (SPSS Inc. company, SPSS Ltd, Hong Kong), version 13 using a compatible computer. Quantitative data were expressed as mean and SD (X + SD) and were analyzed using the Student t-test for comparison of two groups of normally distributed variables and the Mann-Whitney U-test for non-normally distributed ones.

Qualitative data were expressed as number and percentage and were analyzed using the χ2 -test. All these tests were used as tests of significance at P value less than 0.05.


  Results Top


The results of this study were illustrated in [Table 1],[Table 2],[Table 3],[Table 4] and [Table 5].
Table 1: Demographic data of the studied groups

Click here to view
Table 2: Comparison of urinary cotinine levels between group A (exposed to passive smoking) and group B (the control group)

Click here to view
Table 3: Urinary cotinine levels between group A1 (mild ≤0.5 packs) and group A2 (heavy >0.5 packs)

Click here to view
Table 4: Urinary cotinine levels among group A with respect to the number of packs

Click here to view
Table 5: Comparison between urinary cotinine levels among subgroups A with respect to the type of smoking

Click here to view


[Figure 1] shows the difference in urinary cotinine level between group A and group B at a cutoff point of 500 ng/dl.{Figure 1}

[Table 1] shows significant difference among the studied groups regarding sex and the source of smoking and no significant difference regarding residence, birth order, consanguinity, and age.

[Table 2] shows a significantly higher urinary cotinine level among group A (exposed to passive smoking) when compared to group B (nonexposed to passive smoking).

[Table 3] shows significantly higher urinary cotinine levels among subgroup A2 (heavily exposed to passive smoking) when compared with subgroup A1 (mildly exposed to passive smoking).

[Table 4] shows significant correlation between urinary cotinine level among group A with respect to the number of packs.

[Table 5] shows significant difference in urinary cotinine level among subgroups A with respect to the type of smoking.

Results of family counseling

All families understood the hazards of smoking on the smokers and nonsmokers, especially children as they breathe faster than adults, stay at home for longer periods, and are exposed to both SHS and third-hand smoking.

Some families (22, 40.7%) agreed to quit smoking, other families (17, 31.48%) agreed to quit smoking at home only, and some other families (15, 27.77%) were not convinced to quit smoking.


  Discussion Top


Measurement of SHS-specific biomarkers can confirm the exposure and may also contribute to an estimate of dose of SHS. A substantial number of compounds have been studied as potential biomarkers including carbon monoxide (in exhaled air or as carboxyhemoglobin), thiocyanate, and nicotine and its metabolites (e.g. cotinine) [10].

However, measurement of cotinine alone is sufficient for assessing exposures to SHS, especially in children [11].

This study investigated cotinine level in passive smoking nondiabetic children of diabetic families by a competitive enzyme immunoassay for specific detection of cotinine in urine samples [13].

The study was conducted on 54 children at the Genetic and Endocrine Units, Pediatric Department, Menofiya University, Egypt.

The demographic data of the studied groups (group A exposed to passive smoking and group B control) show that the ages were between 2 and 17 years, with a mean age of 9.02 ± 4.63 years. There were 28 girls (51.9%) and 26 boys (48.1%), 26 of them from the rural areas (48.1%) and 28 of them from the urban areas (51.9%).

In this study, the mean age among group A (exposed to SHS) was 9.24 ± 4.69, whereas the mean age among group B (not exposed to SHS) was 8.30 ± 4.57.

In our study, the only current smoker in the exposed group was the father (70.6%), father and relatives (14.6%), father and teachers (5.9%), father and peers (2.9%), and father and others (5.8%). All mothers reported negative history of smoking. This would mean that mother is not an active smoking member in the Egyptian family, or there is a possibility of denying smoking by the mothers. These data are not consistent with a cross-sectional study conducted on children in Turkey in which father was a smoker in 50.7%, mother was a smoker in 13.2%, and both parents were smokers in 33.1% [14].

In contrast, another cross-sectional survey on tobacco use in the city of Alexandria, Egypt showed that the prevalence of current smoking was significantly higher among men (48.5%) than women (1.5%) [15].

In this study, there were 34 children with history of exposure to passive smoking, 30 children with history of exposure to passive cigarette, and four children with history of passive exposure to cigarette and sheesha, with significant difference between them (P < 0.001) and significant difference between group A (exposed to passive smoking) and group B (not exposed to passive smoking) with respect to the type of passive smoking exposure (P < 0.001).

The results of the present study demonstrated that there is significantly higher mean urinary cotinine levels among children with history of exposure to passive tobacco smoke (152.06 ± 106.92) in comparison with children with no history of exposure (3095.0 ± 1160.09; P ≤ 0.001).

These results are in agreement with that of Seifert et al. [16] who found that children with some form of reported ETS exposure had urinary cotinine levels 7.5 times higher than those who were not exposed.

In the present study, the urinary cotinine levels were found to be dependent on daily exposure to tobacco smoke as indicated by the number of cigarettes consumed by the smoker in the presence of the child. We found significantly higher mean urinary cotinine levels among children with history of heavy exposure (109.80 ± 76.53) in comparison with children with history of mild exposure to tobacco smoke (269.44 ± 92.21; P ≤ 0.001).

These results are in agreement with that of Olivieri et al. [17] who found that the number of cigarettes smoked by parents correlates with the urinary cotinine levels.

Similarly, Reeves and Bernstein [18] stated a positive correlation between the reported amount of smoking and measurable levels of cotinine.

The results of the present study showed that there is highly significant difference in urinary cotinine absorbance among subgroups A (exposed to passive smoking) with respect to the number of packs (152.06 ± 106.92). Nine children were exposed to SHS up to 0.5 pack/day with mean cotinine level of 269.44 ± 92.21, 13 children were exposed to SHS (0.5-1 packs/day) with mean cotinine level of 155.85 ± 75.33, two children were exposed to SHS (1-1.5 packs/day) with mean cotinine level of 66.05 ± 5.66, eight children were exposed to SHS (1.5-2 packs/day) with mean cotinine level of 68.4 ± 38.49, and two children were exposed to SHS (0.5-1 packs/day) with mean cotinine level of 20.04 ± 28.28 (P < 0.001).

These results are in agreement with that of Kim et al. [19] who found that the cotinine level in adult passive smokers was significantly correlated with the number of cigarettes consumed daily at home (P < 0.05) in Korea.

These results are also in agreement with that of Seifert et al. [16] who found decreasing levels of cotinine as the reported exposure decreases.

In contrast, El-Sawy et al. [20] found no correlation between the cotinine values in children and the number of cigarettes smoked in their households (P > 0.05) in a case-control study on preschool children, Alexandria, Egypt.

Mannino et al. [21] found that 75.6% of children without any reported exposure had measurable cotinine levels.

As a result of family counseling, 22 families (40.7%) agreed to quit smoking and 17 families (31.48%) agreed to quit smoking at home only; however, 15 families (27.77%) were not convinced to quit smoking.

We can conclude that cotinine, the major proximate metabolite of nicotine, is important clinically because of its widespread use as a biomarker for nicotine exposure from smoking, as cotinine has an in-vivo half-life of ∼20 h, is detectable in urine, blood, saliva, and hair from several days to 1 week after the use of tobacco, and the level of cotinine is proportionate to the amount of exposure to tobacco smoke. Hence, it is a valuable indicator of tobacco smoke exposure, including secondary (passive) smoke.

We recommend the use of cotinine as a biomarker for ETS exposure, especially in children.

A smoke-free policy in which no one is allowed to smoke inside the house at any time under any circumstances is more effective in reducing smoking than partial restrictions. In addition, family counseling programs targeted to parents to help them quit smoking by explaining the health hazards of smoking on both active and passive smokers, especially children, are highly recommended.


  Acknowledgements Top


Conflicts of interest

None declared.

 
  References Top

1.WHO. Report on the global tobacco epidemic, implementing smoke-free environments. Geneva: World Health Organization; 2009.  Back to cited text no. 1
    
2.Pirkle JL, Bernert JT, Caudill SP, et al. Trends in the exposure of nonsmokers in the U.S. population to second hand smoke: 1988-2002. Environ Health Perspect 2006; 114 :853-858.  Back to cited text no. 2
    
3.Matt GE, Quintana P, Hovell MF, et al. Households contaminated by environmental tobacco smoke: Sources of infant exposures. Tob Control 2004; 13 :29-37.  Back to cited text no. 3
    
4.Cheraghi M, Salvi S. Environmental tobacco smoke (ETS) and respiratory health in children. Eur J Pediatr 2009; 168 :897-905.  Back to cited text no. 4
    
5.Spitz MR, Shi H, Yang F, et al. Case-control study of the D2 dopamine receptor gene and smoking status in lung cancer patients. J Natl Cancer Inst 1998; 90 :358-363.  Back to cited text no. 5
    
6.Guerin MR, Higgins CE, Jenkins RA. Measuring environmental emissions from tobacco combustion: Side stream cigarette smoke literature review. Atmos Environ 1987; 21 :291-297.  Back to cited text no. 6
    
7.Polito J. Integrity of NRT studies in serious question. Rapid responses to West R, Sohal T catastrophic′pathways to smoking cessation: Findings from national survey. Br Med J 2006; 332 :458-460.  Back to cited text no. 7
    
8.Kitchens GG. Relationship of environmental tobacco smoke to otitis media in young children. Laryngoscope 1995; 105 :1-13.  Back to cited text no. 8
    
9.Ko G, Cockram C. Cause as well as effect: Smoking and diabetes. Diabetes Voice 2005; 50 :19-22.  Back to cited text no. 9
    
10.1Carmona R Kenneth P.Robert C, et al. U.S. Surgeon General Report, the health consequences of involuntary exposure to tobacco smoke executive summary. 2006; US Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health. Available at: http://www.surgeongeneral.gov/library/reports/secondhandsmoke/fullreport.pdf. [Accessed 1014 April 16].  Back to cited text no. 10
    
11.1Matt GE, Quintana PJ, Hovell MF, Bernert JT, Song S, Novianti N, et al. Households contaminated by environmental tobacco smoke: Sources of infant exposures. Tob Control 2004; 13 :29-37.  Back to cited text no. 11
    
12.1Nwhator SO, Winfunke-Savage K, Ayanbadejo P, Jeboda SO. Smokers′melanosis in a Nigerian population: A preliminary study. J Contemp Dent Pract 2007; 8 :68-75.  Back to cited text no. 12
    
13.1DRG Cotinine in urine (ELISA) Revised June 2012 RM (VERS. 4.1). Available at: http://www.surgeongeneral.gov/library/reports/secondhandsmoke/fullreport.pdf. [Accessed 1014 April 16].  Back to cited text no. 13
    
14.1Boyaci H, Etiler N, Duman C, et al. Environmental tobacco smoke exposure in school children: Parent report and urine cotinine measures. Pediatr Int 2004; 48 :382-389.  Back to cited text no. 14
    
15.1Youssef RM, Abou-Khatwa SA, Fouad HM. Prevalence of smoking and age of initiation in Alexandria, Egypt. East Mediterr Health J 2002; 8 :626-637.  Back to cited text no. 15
    
16.1Seifert JA, Ross CA, Norris JM. Validation of a five-question survey to assess a child′s exposure to environmental tobacco smoke. Ann Epidemiol 2002; 12 :273-277.  Back to cited text no. 16
    
17.1Olivieri M, Bodini A, Peroni DG, et al. Passive smoking in asthmatic children: Effect of a ′smoke-free house′ measured by urinary cotinine levels. Allergy Asthma Proc 2006; 27 :350-353.  Back to cited text no. 17
    
18.1Reeves S, Bernstein I. Effects of maternal tobacco-smoke exposure on fetal growth and neonatal size. Expert Rev Obstet Gynecol 2008; 3 :719-730.  Back to cited text no. 18
    
19.1Kim H, Lim Y, Lee S, et al. Relationship between environmental tobacco smoke and urinary cotinine levels in passive smokers at their residence. J Expo Anal Environ Epidemiol 2004; 14 :S65-S70.  Back to cited text no. 19
    
20.2El-Sawy IH, Nasr FM, Mowafy EW, Sharaki OA, Abdel Bakey AM. Passive smoking and lower respiratory tract illnesses in children. East Mediterr Health J 1997; 3 :425-434.  Back to cited text no. 20
    
21.2Mannino DM, Caraballo R, Benowitz N, et al. Predictors of cotinine levels in US children: Data from the Third National Health and Nutrition Examination Survey. Chest 2001; 120 :718-724.  Back to cited text no. 21
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]


This article has been cited by
1 The Relation between Exposure to Environmental Tobacco Smoke and the Quantity of Cotinine in the Urine of School Children in Taif City, Saudi Arabia
Dalia El Sayed Desouky,Gamal Elnemr,Ali Alnawawy,Azza Ali Taha
Asian Pacific Journal of Cancer Prevention. 2016; 17(1): 139
[Pubmed] | [DOI]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Materials and me...
Results
Discussion
Acknowledgements
References
Article Tables

 Article Access Statistics
    Viewed1150    
    Printed25    
    Emailed0    
    PDF Downloaded108    
    Comments [Add]    
    Cited by others 1    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]