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Archives of Environmental Health: An International Journal Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/vzeh20
Exposure to Environmental Tobacco Smoke (ETS) and Serum Thiocyanate Level in Infants a
b
Yue Chen M.D, Ph.D. , Linda L. Pederson Ph.D. & Neville M. Lefcoe M.D.
c
a
Department of Epidemiology , School of Public Health Shanghai Medical University , People's Republic of China b
Department of Epidemiology and Biostatistics , University of Western Ontario London , London, Ontario, Canada c
Victoria Hospital University of Western Ontario , London, Ontario, Canada Published online: 03 Aug 2010.
To cite this article: Yue Chen M.D, Ph.D. , Linda L. Pederson Ph.D. & Neville M. Lefcoe M.D. (1990) Exposure to Environmental Tobacco Smoke (ETS) and Serum Thiocyanate Level in Infants, Archives of Environmental Health: An International Journal, 45:3, 163-167, DOI: 10.1080/00039896.1990.9936710 To link to this article: http://dx.doi.org/10.1080/00039896.1990.9936710
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http:// www.tandfonline.com/page/terms-and-conditions
Exposure to Environmental Tobacco Smoke (ETS) and
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Serum Thiocyanate Level in Infants
YUE CHEN, M.D., Ph.D.* Department of Epidemiology School of Public Health Shanghai Medical University People’s Republic of China LINDA 1. PEDERSON, Ph.D. Department of Epidemiology and Biostatistics University of Western Ontario London, Ontario, Canada NEVILLE M. LEFCOE, M.D. Victoria Hospital University of Western Ontario London, Ontario, Canada
ABSTRACT. The authors measured the concentrations of serum thiocyanate (SCN) of 80 infants in Chang-Ning District, Shanghai, People’s Republic of China. The infants were classified into one of three groups according to the total number of cigarettes family members collectively smoked per day: (1) unexposed, (2) lightly exposed (1-19 cigarettedd), and (3) heavily exposed (20+ cigarettes/d). The serum SCN levels (X f SO, pmol/l) were 27.7 f 10.72 for the unexposed group, 31.9 f 13.5 for the lightly exposed group, and 36.2 2 14.88 for the heavily exposed group. The concentrations in the heavily exposed group were significantly higher than those in the unexposed group (Z = 2.1 2, p < .05). Environmental exposure to tobacco smoke accounted for 5.3% of total variance of the SCN levels after adjusting the effects of father’s education level and type of feeding. It is concluded that passive exposure to cigarette smoke in the household results in higher levels of serum SCN in infants.
THE INFLUENCE of exposure to household environmental tobacco smoke (ETS) on the health of infants and children is an important public health concern.’ Environmental tobacco smoke increases incidences of acute respiratory illnesses and chronic respiratory symptoms and decreases pulmonary function in children.’ Chen et a1.2 reported a significant dose-response relationship between respiratory outcomes during a child’s first 18 mo of life and the level of exposure to ETS. The exposure data were Mayljune 1990 [Vol. 45 (No.3)]
obtained from responses to questions in an interview on daily cigarette consumption by all family members.* It has been argued that the level of individual exposure to ETS i s determined not only by the amount of cigarette consumption but also by many other fac‘Dr. Chen’s present address is Centre for Agricultural Medicine, Fifth Floor, Ellis Hall, University Hospital, Saskatoon, Saskatchewan, Canada S7N 0x0.
163
tors, e.g., specific toxic components in tobacco smoke, size of living space, ventilation, e t ~ . ’ Quan,~ tification of exposure by questionnaire i s difficult and has not been validated.’ This study reports an association between cigarette consumption by family members and serum thiocyanate (SCN) levels among babies selected randomly from the study population of the Chang-Ning Epidemiological Study.2 It has been suggested that SCN, a metabolic byproduct of tobacco smoke, is a better marker for long-term exposure because it has a longer half-life than carboxyhemoglobin and cotinine.4 Its measurement would help to confirm the real intake of cigarette smoke by passive smokers and possible provide a link between ETS and childrens health outcomes.
birth weight, and type of feeding; residential area and household environmental exposure to cooking fuels; parental education; and the smoking habits of all family members. Analyses indicate that both the incidence density of hospitalization for respiratory illness and the cumulative incidence of bronchitis/ pneumonia increased significantly with a concommitant increase in cigarette consumption by family members during the infants’ first 18 mo of life.2 In the present study, a subsample of 80 infants was selected randomly from study subjects who were living at Tian-San Neighbourhood, one of eight neighborhoods at the Chang-Ning District. Information on smoking habits of parents and other family members, sociodemographic and educational status, infant’s characteristics, residential conditions, and fuels used for cooking was taken from the interview. There was little difference between this subsample of 80 babies and all others from the Chang-Ning survey with regard to sociodemographic characteristics and early experience (Table 1). A regular physical examination at the neighborhood hospital was conducted when the infants in this subgroup were between 1.5 to 2 y of age. A minimum of 3 ml of venous blood was drawn, and about 1.5 ml of serum was separated. All sera were frozen and stored at -20 “C for subsequent analysis. Measurement of SCN was completed by the method originally described by Pettigrew et al.5 and modified by Qian et a1.6 Optical absorption was determined at 520 nm on a 721 spectrophotometer. Spec-
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Methods
The Chang-Ning Epidemiological Study encompassed the entire area of the Chang-Ning District, Shanghai Municipality, and included 2 227 of 2 315 eligible infants born during the last quarter of 1983.2 The survey was conducted during March through June 1985, a time period when the children had reached the age of 1% y. Questionnaires were administered in the homes of the infants by trained interviewers from the health promotion sectors of each neighborhood hospital in the Chang-Ning District. The questionnaire included sociodemographic information; the infant’s characteristics, e.g., sex,
I
Table 1-Distribution of Characteristics of the Subsarnple, Compared with all Others of the Chang-Ning Survey Subsample (n = 80)
NO.
I I
1 ~
I
I
~
1 164
Sex Male Female Month of birth October November December Type of feeding Breast or mixed Artificial Day-care nursery Yes No Father’s education level University Secondary or primary Family smoking status Smoking families Nonsmoking families Birth weight (kg) Mother’s age at child‘s birth (y) Number of family members Living area per capita (m2)
(Yo)
All others (n = 2 147)
Mean
No. (%)
41 (51.3) 39(48.7)
1 114(51.9) 1 033(48.1)
31 (38.8) 24(30.0) 25(31.2)
711(33.1) 735(34.2) 701(32.7)
24(30.0) 56(70.0)
720(33.5) 1427(66.5)
lg(23.8) 61(76.2)
48W22.7) 1659(77.3)
lO(12.5) 70(87.5)
1 957(91.2)
60(75.O) 20(25.0)
1686(78.5) 461 (21.5)
Mean
190(8.8)
3.3
3.2
28.3 4.8 5.8
28.2 5.2 5.4
Archives of Environmental Health
imens were analyzed under conditions where the technician had no knowledge of the exposure status of the infants. The infants were classified into three groups according to total cigarette consumption by family members: (1) unexposed, (2) lightly exposed (1-19 cigarettedd), and (3) heavily exposed (20+ cigarettedd). Chi-square tests were used to analyze dichotomous variables, and the Mann-Whitney U test was used to test the significance of differences of serum SCN levels between the unexposed group and each of the exposed groups. A linear regression model was used for multivariate analysis to adjust for confounding factors.
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Results
A total of 60 (75.0%) children were living in families that included smokers. No mothers smoked during or after pregnancy. Exposure of the child to cigarette smoke was estimated from the total daily cigarette consumption of family members, who included the father and other family members, e.g., grandfather and grandmother who were living together with the child. Among these families who smoked, 34 included individuals who smoked a total of 1-19 cigarettes a day and 26 included individuals who smoked 20+ cigarettes. The average age of infants in these exposed groups was the same as the unexposed group, i.e., 1.8 y. Table 2 presents sociodemographic characteristics and outlines early experiences of babies by smoking status of family members. More exposed infants came from families in which the father was less educated (x2 = 12.40, p < .01). There were no other noticeable differences among these groups. Figure 1 details the results of serum SCN determinations, and it shows the marked variation in the values, particularly in the heavily exposed group. Otherwise, the average serum SCN level of the infants appears to increase as the total daily cigarette consumption by family members increases. The means and standard deviations of the serum SCN levels (micromoles per litre [pmol/l]) were 27.7 2 10.72 for the unexposed group, 31.9 rt 13.5 for the lightly exposed group, and 36.2 ? 14.88 for the heavily exposed group. Because of the heterogeneity of variance in the groups, the Mann-Whitney U test was used to test the significance of the differences between the exposed groups and the nonexposed group. Table 3 illustrates the median values and ranges of these passive smoking groups. The heavily exposed group had significantly higher levels of serum SCN than did the unexposed group (Z = 2.12, p < .05). Although the mean of serum SCN among the lightly exposed group was greater than that for the nonexposed babies, the difference did not reach statistical significance (Z = 0.90, p > .05). Linear regression analysis revealed that household exposure to ETS accounted for 5.7% of the total variance in the infants' serum SCN levels. After adMay/June1990 [Vol. 45 (No. 3)]
j ust ing potentiaI conf o und e rs , inc Iud ing father's education level and type of feeding, 5.3% of the variance in the serum SCN levels was attributable to ETS in the household. Discussion Because people in Shanghai, especially young children, spend most of their time indoor^,^ the levels of indoor air pollution may be more important to an individual's health status than the levels of outdoor air pollutant^.^,^ Many epidemiological studies have shown that exposure to ETS is a risk factor for disease, including lung cancer, in healthy nonsmoke r ~ .Some ~ , ~ children who live among family members who smoke, when compared with children who live in nonsmoking families, have an increased frequency of respiratory infections, increased respiratory symtoms, and decreased lung f u n ~ t i o n , ~ - ~ , ' ~ - ~ ~ but other children exposed to ETS do not experience these health effects.13-15 In these epidemiological studies, individuals with different levels of exposure to ETS were usually identified by spousal, parental, and/or other family members' smoking status. But research on ETS must account for exposure that is quantified by type of ventilation, ambient environment, and duration of exposure to tobacco smoke. To enhance the validity of these epidemiologic studies, it i s important to include a biologic marker of chronic passive exposure reflecting the amount of tobacco smoke. Blood carboxyhemoglobin appears to be a useful biologic monitor of acute exposure to smoke, but it is not necessarily useful for chronic exposure because of its shorter half-life of about 4 h.4 The half-life of nicotine in the bloodsteam is even shorter; it ranges from 30 to 90 min.16,17Although it has been demonstrated that ETS is associated with higher levels of cotinine, its half-life i s only about 19-40 h, and day-to-day variation may influence its accuracy as an indicator of chronic exposure to tobacco smoke.lB Because of the stability of cotinine levels measured at different times during exposure, cotinine appears to be the short-term marker of choice in epidemiological studies.' Cyanide may be absorbed from cigarette smoke and i s detoxicated to SCN in the body. Poulton et aI.l9 suggested that measurement of serum SCN concentrations may be useful in estimating long-term passive smoking in children because it has a half-life of up to 2 wk. They also found that mean SCN levels in children exposed at home were significantly higher than those in unexposed children, 97.3 pmol/l v. 54.2 pmol/l (p = .02), respectively. Friedman et aI.*O found a mean SCN value of 40 pmol/l in unexposed adults, which rose significantly to 50 pmol/l in those who reported at least 40 h passive exposure to tobacco smoke per wk. Of particular interest i s a study by Botloms et a1.21that included 107 low-risk pregnancies; fetal SCN levels were increased in association with passive smoking even though the mothers were nonsmokers. The mean and standard deviation in the passive smoking 165
Table 2.-Characteristics Members
of Infants and Total Daily Cigarette Consumption by Family
Cigarettes smoked per day by family members None (n' = 20) No. (%) Mean
Characteristics of infants
1-19
20 t
( n = 34)
( n = 26)
No. (%)
Mean
Mean
No. (%) Q
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Sex Male Female Type of feeding Breast or mixed Artificial Day-care nursery Yes No Father's education level University Secondary Birth weight (kg) Mother's age at child's birth (y) Number of family members Living area per capita (m*)
13(65.0) 7(35.0)
lS(44.1) 19(59.9)
13(50.0) 13(50.0)
12(60.0) 8(40.0)
22(64.7) 12(35.3)
18(69.2) 8(30.8)
6(30.0) 14(70.0)
7(20.6) 27(79.4)
5(19.2) 21 (80.8)
7(35.0) 13(65.0)
2 (5.9) 32(94.1)
1 (3.8) 25(96.2)t
3.3
3.3
3.3
28.2 4.3 6.1
28.4 4.8 5.7
28.2 5.3
5.7
'Number of infants. + p < 0.01.
Table 3.-Medians and Ranges of Serum SCN Levels in Infants, by Total Number of Cigarettes Smoked per Day by Family Members
Serum SCN (Wmolil)
1
Cigarettes smoked daily Median None ( n = 20) 1-19 ( n = 34)
20-t ( n
..
..
.. ..
t
: 1
.
1.8
: a
.I'
..
1
.. i I
.. None (n = 20)
:
(n
1-19 = 34)
(n
20 + 26)
-
Number of cigarettes smoked per day Fig. 1. Serum SCN levels in infants according to number of cigarettes smoked per day by family members.
166
=
26)
Range
26.9 27.3
9.3-40.9 11.8-66.4
35.8
14.8-78.2
MannWhitnw U tesi'
I
Z = 0.90 p > .05 Z = 2.12 p < .05
group was 32.0 -C 16.3 pmol/l, compared with 24.3 + 11.5 pnol/l in the no-exposure group. The difference was still significant after controlling for possible effects of clinical characteristics. The results of these studies are similar to those reported herein to our findings for Chinese infants. The mean serum SCN level in the unexposed group was 27.7 pnol/l, compared with 31.9 pnol/l in the lightly exposed group and 36.2 pmol/l in the heavily exposed group. Aft e r adj ust ment for conf o unde rs , incl ud ing fat he r's education level and type of feeding, the association between ETS and serum SCN was still significant. The elevated serum SCN concentrations among the infants who lived in families where members smoke can be accounted for by exposure to cigarette smoke in the household. The extent of exposure may be estimated from the smoking history of family members. Archives of Environmental Health
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The subjects in this study were a part of the study population of the Chang-Ning Epidemiological Study2 Although this subsample was selected from only one of eight neighborhoods in the Chang-Ning District, there was no significant difference between the subsample and all others in the Chang-Ning survey with regard to sociodemographic characteristics and early experiences of the infants (Table 1). It is unlikely, therefore, that selection bias was operating. One possible problem is that the sample size might not have been sufficiently large to detect the possible difference between those exposed to low levels of ETS and the nonexposed group. However, as the number of cigarettes smoked per day by family members increased, there was a concomitant elevation of serum SCN observed in the infants. Thiocyanate is a metabolic product of cyanide, which may come from outdoor air pollution. But it is reasonable to assume that such pollution would exert almost the same effects on these children whether or not they were from families whose members smoked in this very limited area. In addition to tobacco smoke and other air pollutants, certain foods-particularly leafy vegetables and some nuts-are sources of cyanide.'J* Diets enriched in certain foods can produce thiocyanate levels as high as those found in habitual ~ m o k e r s . *In ~ this , ~ ~study, however, the type of feeding was not associated with the level of serum SCN in infants. Because the distributions of serum SCN concentrations overlapped considerably among the infants with and without exposure to tobacco smoke, and because only slightly more than 5% of the variance in SCN levels was accounted for by ETS in this study, it is important that future studies include measures of other sources of cyanide and more details about the diet.
2.
3. 4.
5. 6. 7.
8. 9. 10. 11. 12. 13. 14. 15. 16.
* * * * * * * * * *
17.
We thank the staffs of the Health and Anti-epidemic Station of Chang-Ning District and Tian-San Neighbourhood Hospital for collections of data and blood specimens. We acknowledge Drs. Yu Ming and Hua Jian-yifor their assistance. Submitted for publication April 19,1989; revised; accepted for publication February 2,1990. Requests for reprints should be sent to; Dr. Yue Chen, Centre for Agricultural Medicine, Fifth Floor, Ellis Hall, University Hospital, Saskatoon, Saskatchewan, Canada, S7N 0x0.
18.
* * * * * * * * * *
19. 20. 21. 22. 23.
References 1. U.S. Department of Health and Human Services. The health
consequences of involuntary smoking. A report of the Surgeon General. DHHS Pub. No. (CDC)87-8398. U.S. Depart-
May/june 1990 [Vol. 45 (No. 3)]
24.
ment of Health and Human Services, Public Health Service, Centers for Disease Control, Center for Health Promotion and Education, Office on Smoking and Health, 1986. Chen Y, Li WX, Yu SZ, Qian WH. Chang-Ning epidemiological study of children's health. I. Passive smoking and children's respiratory diseases. Int J Epidemiol1988;17:348-55. Weiss ST, Tager IB, Schenker M, Speizer FE. The health effects of involuntary smoking. Am Rev Respir Dis 1983;129:933-42. Cohen JD, Bartsch GE. A comparison between carboxyhemoglobin and serum thiocyanate determination as indicators of cigarette smoking. Am J Public Health 1980;70:284-86. Pettigrew AR, Fell GS. Simplified colorimetric determination of thiocyanate in biological fluids, and its application to investigation of the toxic amblyopias. Clin Chem 1972;18:996-1000. Qian GS, Xu LW, Xu HY, Zhang R, Gao YT. Measurement of thiocyanate level-a biological index of smoking. Cancer (in Chinese) 1985;5: 169-70. Department of Environmental Health. Shanghai survey of residential hygiene, 1985. Shanghai Medical University: School of Public Health. Binder RE, Mitchell CA, Housein HR, Roubuys A. Importance of the indoor environment in air pollution exposure. Arch Environ Health 1976;31:277-79. Zheng W, Gao M.A case-control study of women's lung cancer in Shanghai. Master's degree thesis, Shanghai Cancer Institute, 1986. Chen Y, Li WX, Yu SZ. Influence of passive smoking on admission for respiratory illness in early childhood. Br Med J 1986;293 :303-06. Chen Y, Li WX. The effect of passive smoking on children's pulmonary function in Shanghai. Am J Public Health 1986;76:515-18. Chen Y. Synergistic effect of passive smoking and artificial feeding on hospitalization for respiratory illness in early childhood. Chest 1989;95 :1004-07. Garfinkle L. Time trends in lung cancer mortality among nonsmokers and a note on passive smoking. J Nat Cancer SOC 1981;66 :1061-66. Dodge R. The effect of indoor air pollution on Arizona children. Arch Environ Health 1982;37:151-53. Speizer FE, Ferris BJ, Bishop YMM, Spengler J. Respiratorydisease rates and pulmonary function in children associated with NO, exposure. Am Rev Respir Dis 1980;121:2-10. Rosenberg J, Benowitz NL, Jacob P, Wilson KM. Disposition kinetics and effects of intravenous nicotine. Clin Pharmac Ther 1980;228:517-22. Isaac PG, Rand MJ.Cigarette smoking and plasma levels of nicotine. Nature 1972;236:308. Woodward A, Milles H, Grguriovich N. Nicotine in urine of smoker's infants. Lancet 1984;2:935. Poulton J, Rylance GW, Taylor AWJH, Edwards C. Serum thiocyanate levels as indicator of passive smoking in children. Lancet 1984;2 :1405. Friedman GD, Petitti DB, Bawol RD. Prevalence and correlates of passive smoking. Am J Public Health 1983;73:401-05. Botloms SF, Kuhnert BR, Kukert AM, Reese AL. Maternal passive smoking and fetal serum thiocyanate levels. Am J Obstet Gynecol1982;144:787-91. Stoa KF. Studies on thiocyanate in serum. Second Medical Yearbook, University of Pergen, 1957. Maleszewski TF, Boes DE. True and apparent thiocyanate in body fluids of smokers and non-smokers. J Appl Physiology 1955;8 :289-96. Haley NJ, Axelrad CM, Tilton KA. Validation of self-reported smoking behavior: Biochemical analysis of continine and thiocyanate. Am J Public Health 1983;73:1204-07.
167
Archives of Environmental Health: An International Journal Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/vzeh20
Exposure to Environmental Tobacco Smoke (ETS) and Serum Thiocyanate Level in Infants a
b
Yue Chen M.D, Ph.D. , Linda L. Pederson Ph.D. & Neville M. Lefcoe M.D.
c
a
Department of Epidemiology , School of Public Health Shanghai Medical University , People's Republic of China b
Department of Epidemiology and Biostatistics , University of Western Ontario London , London, Ontario, Canada c
Victoria Hospital University of Western Ontario , London, Ontario, Canada Published online: 03 Aug 2010.
To cite this article: Yue Chen M.D, Ph.D. , Linda L. Pederson Ph.D. & Neville M. Lefcoe M.D. (1990) Exposure to Environmental Tobacco Smoke (ETS) and Serum Thiocyanate Level in Infants, Archives of Environmental Health: An International Journal, 45:3, 163-167, DOI: 10.1080/00039896.1990.9936710 To link to this article: http://dx.doi.org/10.1080/00039896.1990.9936710
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http:// www.tandfonline.com/page/terms-and-conditions
Exposure to Environmental Tobacco Smoke (ETS) and
Downloaded by [UQ Library] at 15:16 31 October 2014
Serum Thiocyanate Level in Infants
YUE CHEN, M.D., Ph.D.* Department of Epidemiology School of Public Health Shanghai Medical University People’s Republic of China LINDA 1. PEDERSON, Ph.D. Department of Epidemiology and Biostatistics University of Western Ontario London, Ontario, Canada NEVILLE M. LEFCOE, M.D. Victoria Hospital University of Western Ontario London, Ontario, Canada
ABSTRACT. The authors measured the concentrations of serum thiocyanate (SCN) of 80 infants in Chang-Ning District, Shanghai, People’s Republic of China. The infants were classified into one of three groups according to the total number of cigarettes family members collectively smoked per day: (1) unexposed, (2) lightly exposed (1-19 cigarettedd), and (3) heavily exposed (20+ cigarettes/d). The serum SCN levels (X f SO, pmol/l) were 27.7 f 10.72 for the unexposed group, 31.9 f 13.5 for the lightly exposed group, and 36.2 2 14.88 for the heavily exposed group. The concentrations in the heavily exposed group were significantly higher than those in the unexposed group (Z = 2.1 2, p < .05). Environmental exposure to tobacco smoke accounted for 5.3% of total variance of the SCN levels after adjusting the effects of father’s education level and type of feeding. It is concluded that passive exposure to cigarette smoke in the household results in higher levels of serum SCN in infants.
THE INFLUENCE of exposure to household environmental tobacco smoke (ETS) on the health of infants and children is an important public health concern.’ Environmental tobacco smoke increases incidences of acute respiratory illnesses and chronic respiratory symptoms and decreases pulmonary function in children.’ Chen et a1.2 reported a significant dose-response relationship between respiratory outcomes during a child’s first 18 mo of life and the level of exposure to ETS. The exposure data were Mayljune 1990 [Vol. 45 (No.3)]
obtained from responses to questions in an interview on daily cigarette consumption by all family members.* It has been argued that the level of individual exposure to ETS i s determined not only by the amount of cigarette consumption but also by many other fac‘Dr. Chen’s present address is Centre for Agricultural Medicine, Fifth Floor, Ellis Hall, University Hospital, Saskatoon, Saskatchewan, Canada S7N 0x0.
163
tors, e.g., specific toxic components in tobacco smoke, size of living space, ventilation, e t ~ . ’ Quan,~ tification of exposure by questionnaire i s difficult and has not been validated.’ This study reports an association between cigarette consumption by family members and serum thiocyanate (SCN) levels among babies selected randomly from the study population of the Chang-Ning Epidemiological Study.2 It has been suggested that SCN, a metabolic byproduct of tobacco smoke, is a better marker for long-term exposure because it has a longer half-life than carboxyhemoglobin and cotinine.4 Its measurement would help to confirm the real intake of cigarette smoke by passive smokers and possible provide a link between ETS and childrens health outcomes.
birth weight, and type of feeding; residential area and household environmental exposure to cooking fuels; parental education; and the smoking habits of all family members. Analyses indicate that both the incidence density of hospitalization for respiratory illness and the cumulative incidence of bronchitis/ pneumonia increased significantly with a concommitant increase in cigarette consumption by family members during the infants’ first 18 mo of life.2 In the present study, a subsample of 80 infants was selected randomly from study subjects who were living at Tian-San Neighbourhood, one of eight neighborhoods at the Chang-Ning District. Information on smoking habits of parents and other family members, sociodemographic and educational status, infant’s characteristics, residential conditions, and fuels used for cooking was taken from the interview. There was little difference between this subsample of 80 babies and all others from the Chang-Ning survey with regard to sociodemographic characteristics and early experience (Table 1). A regular physical examination at the neighborhood hospital was conducted when the infants in this subgroup were between 1.5 to 2 y of age. A minimum of 3 ml of venous blood was drawn, and about 1.5 ml of serum was separated. All sera were frozen and stored at -20 “C for subsequent analysis. Measurement of SCN was completed by the method originally described by Pettigrew et al.5 and modified by Qian et a1.6 Optical absorption was determined at 520 nm on a 721 spectrophotometer. Spec-
Downloaded by [UQ Library] at 15:16 31 October 2014
Methods
The Chang-Ning Epidemiological Study encompassed the entire area of the Chang-Ning District, Shanghai Municipality, and included 2 227 of 2 315 eligible infants born during the last quarter of 1983.2 The survey was conducted during March through June 1985, a time period when the children had reached the age of 1% y. Questionnaires were administered in the homes of the infants by trained interviewers from the health promotion sectors of each neighborhood hospital in the Chang-Ning District. The questionnaire included sociodemographic information; the infant’s characteristics, e.g., sex,
I
Table 1-Distribution of Characteristics of the Subsarnple, Compared with all Others of the Chang-Ning Survey Subsample (n = 80)
NO.
I I
1 ~
I
I
~
1 164
Sex Male Female Month of birth October November December Type of feeding Breast or mixed Artificial Day-care nursery Yes No Father’s education level University Secondary or primary Family smoking status Smoking families Nonsmoking families Birth weight (kg) Mother’s age at child‘s birth (y) Number of family members Living area per capita (m2)
(Yo)
All others (n = 2 147)
Mean
No. (%)
41 (51.3) 39(48.7)
1 114(51.9) 1 033(48.1)
31 (38.8) 24(30.0) 25(31.2)
711(33.1) 735(34.2) 701(32.7)
24(30.0) 56(70.0)
720(33.5) 1427(66.5)
lg(23.8) 61(76.2)
48W22.7) 1659(77.3)
lO(12.5) 70(87.5)
1 957(91.2)
60(75.O) 20(25.0)
1686(78.5) 461 (21.5)
Mean
190(8.8)
3.3
3.2
28.3 4.8 5.8
28.2 5.2 5.4
Archives of Environmental Health
imens were analyzed under conditions where the technician had no knowledge of the exposure status of the infants. The infants were classified into three groups according to total cigarette consumption by family members: (1) unexposed, (2) lightly exposed (1-19 cigarettedd), and (3) heavily exposed (20+ cigarettedd). Chi-square tests were used to analyze dichotomous variables, and the Mann-Whitney U test was used to test the significance of differences of serum SCN levels between the unexposed group and each of the exposed groups. A linear regression model was used for multivariate analysis to adjust for confounding factors.
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Results
A total of 60 (75.0%) children were living in families that included smokers. No mothers smoked during or after pregnancy. Exposure of the child to cigarette smoke was estimated from the total daily cigarette consumption of family members, who included the father and other family members, e.g., grandfather and grandmother who were living together with the child. Among these families who smoked, 34 included individuals who smoked a total of 1-19 cigarettes a day and 26 included individuals who smoked 20+ cigarettes. The average age of infants in these exposed groups was the same as the unexposed group, i.e., 1.8 y. Table 2 presents sociodemographic characteristics and outlines early experiences of babies by smoking status of family members. More exposed infants came from families in which the father was less educated (x2 = 12.40, p < .01). There were no other noticeable differences among these groups. Figure 1 details the results of serum SCN determinations, and it shows the marked variation in the values, particularly in the heavily exposed group. Otherwise, the average serum SCN level of the infants appears to increase as the total daily cigarette consumption by family members increases. The means and standard deviations of the serum SCN levels (micromoles per litre [pmol/l]) were 27.7 2 10.72 for the unexposed group, 31.9 rt 13.5 for the lightly exposed group, and 36.2 ? 14.88 for the heavily exposed group. Because of the heterogeneity of variance in the groups, the Mann-Whitney U test was used to test the significance of the differences between the exposed groups and the nonexposed group. Table 3 illustrates the median values and ranges of these passive smoking groups. The heavily exposed group had significantly higher levels of serum SCN than did the unexposed group (Z = 2.12, p < .05). Although the mean of serum SCN among the lightly exposed group was greater than that for the nonexposed babies, the difference did not reach statistical significance (Z = 0.90, p > .05). Linear regression analysis revealed that household exposure to ETS accounted for 5.7% of the total variance in the infants' serum SCN levels. After adMay/June1990 [Vol. 45 (No. 3)]
j ust ing potentiaI conf o und e rs , inc Iud ing father's education level and type of feeding, 5.3% of the variance in the serum SCN levels was attributable to ETS in the household. Discussion Because people in Shanghai, especially young children, spend most of their time indoor^,^ the levels of indoor air pollution may be more important to an individual's health status than the levels of outdoor air pollutant^.^,^ Many epidemiological studies have shown that exposure to ETS is a risk factor for disease, including lung cancer, in healthy nonsmoke r ~ .Some ~ , ~ children who live among family members who smoke, when compared with children who live in nonsmoking families, have an increased frequency of respiratory infections, increased respiratory symtoms, and decreased lung f u n ~ t i o n , ~ - ~ , ' ~ - ~ ~ but other children exposed to ETS do not experience these health effects.13-15 In these epidemiological studies, individuals with different levels of exposure to ETS were usually identified by spousal, parental, and/or other family members' smoking status. But research on ETS must account for exposure that is quantified by type of ventilation, ambient environment, and duration of exposure to tobacco smoke. To enhance the validity of these epidemiologic studies, it i s important to include a biologic marker of chronic passive exposure reflecting the amount of tobacco smoke. Blood carboxyhemoglobin appears to be a useful biologic monitor of acute exposure to smoke, but it is not necessarily useful for chronic exposure because of its shorter half-life of about 4 h.4 The half-life of nicotine in the bloodsteam is even shorter; it ranges from 30 to 90 min.16,17Although it has been demonstrated that ETS is associated with higher levels of cotinine, its half-life i s only about 19-40 h, and day-to-day variation may influence its accuracy as an indicator of chronic exposure to tobacco smoke.lB Because of the stability of cotinine levels measured at different times during exposure, cotinine appears to be the short-term marker of choice in epidemiological studies.' Cyanide may be absorbed from cigarette smoke and i s detoxicated to SCN in the body. Poulton et aI.l9 suggested that measurement of serum SCN concentrations may be useful in estimating long-term passive smoking in children because it has a half-life of up to 2 wk. They also found that mean SCN levels in children exposed at home were significantly higher than those in unexposed children, 97.3 pmol/l v. 54.2 pmol/l (p = .02), respectively. Friedman et aI.*O found a mean SCN value of 40 pmol/l in unexposed adults, which rose significantly to 50 pmol/l in those who reported at least 40 h passive exposure to tobacco smoke per wk. Of particular interest i s a study by Botloms et a1.21that included 107 low-risk pregnancies; fetal SCN levels were increased in association with passive smoking even though the mothers were nonsmokers. The mean and standard deviation in the passive smoking 165
Table 2.-Characteristics Members
of Infants and Total Daily Cigarette Consumption by Family
Cigarettes smoked per day by family members None (n' = 20) No. (%) Mean
Characteristics of infants
1-19
20 t
( n = 34)
( n = 26)
No. (%)
Mean
Mean
No. (%) Q
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Sex Male Female Type of feeding Breast or mixed Artificial Day-care nursery Yes No Father's education level University Secondary Birth weight (kg) Mother's age at child's birth (y) Number of family members Living area per capita (m*)
13(65.0) 7(35.0)
lS(44.1) 19(59.9)
13(50.0) 13(50.0)
12(60.0) 8(40.0)
22(64.7) 12(35.3)
18(69.2) 8(30.8)
6(30.0) 14(70.0)
7(20.6) 27(79.4)
5(19.2) 21 (80.8)
7(35.0) 13(65.0)
2 (5.9) 32(94.1)
1 (3.8) 25(96.2)t
3.3
3.3
3.3
28.2 4.3 6.1
28.4 4.8 5.7
28.2 5.3
5.7
'Number of infants. + p < 0.01.
Table 3.-Medians and Ranges of Serum SCN Levels in Infants, by Total Number of Cigarettes Smoked per Day by Family Members
Serum SCN (Wmolil)
1
Cigarettes smoked daily Median None ( n = 20) 1-19 ( n = 34)
20-t ( n
..
..
.. ..
t
: 1
.
1.8
: a
.I'
..
1
.. i I
.. None (n = 20)
:
(n
1-19 = 34)
(n
20 + 26)
-
Number of cigarettes smoked per day Fig. 1. Serum SCN levels in infants according to number of cigarettes smoked per day by family members.
166
=
26)
Range
26.9 27.3
9.3-40.9 11.8-66.4
35.8
14.8-78.2
MannWhitnw U tesi'
I
Z = 0.90 p > .05 Z = 2.12 p < .05
group was 32.0 -C 16.3 pmol/l, compared with 24.3 + 11.5 pnol/l in the no-exposure group. The difference was still significant after controlling for possible effects of clinical characteristics. The results of these studies are similar to those reported herein to our findings for Chinese infants. The mean serum SCN level in the unexposed group was 27.7 pnol/l, compared with 31.9 pnol/l in the lightly exposed group and 36.2 pmol/l in the heavily exposed group. Aft e r adj ust ment for conf o unde rs , incl ud ing fat he r's education level and type of feeding, the association between ETS and serum SCN was still significant. The elevated serum SCN concentrations among the infants who lived in families where members smoke can be accounted for by exposure to cigarette smoke in the household. The extent of exposure may be estimated from the smoking history of family members. Archives of Environmental Health
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The subjects in this study were a part of the study population of the Chang-Ning Epidemiological Study2 Although this subsample was selected from only one of eight neighborhoods in the Chang-Ning District, there was no significant difference between the subsample and all others in the Chang-Ning survey with regard to sociodemographic characteristics and early experiences of the infants (Table 1). It is unlikely, therefore, that selection bias was operating. One possible problem is that the sample size might not have been sufficiently large to detect the possible difference between those exposed to low levels of ETS and the nonexposed group. However, as the number of cigarettes smoked per day by family members increased, there was a concomitant elevation of serum SCN observed in the infants. Thiocyanate is a metabolic product of cyanide, which may come from outdoor air pollution. But it is reasonable to assume that such pollution would exert almost the same effects on these children whether or not they were from families whose members smoked in this very limited area. In addition to tobacco smoke and other air pollutants, certain foods-particularly leafy vegetables and some nuts-are sources of cyanide.'J* Diets enriched in certain foods can produce thiocyanate levels as high as those found in habitual ~ m o k e r s . *In ~ this , ~ ~study, however, the type of feeding was not associated with the level of serum SCN in infants. Because the distributions of serum SCN concentrations overlapped considerably among the infants with and without exposure to tobacco smoke, and because only slightly more than 5% of the variance in SCN levels was accounted for by ETS in this study, it is important that future studies include measures of other sources of cyanide and more details about the diet.
2.
3. 4.
5. 6. 7.
8. 9. 10. 11. 12. 13. 14. 15. 16.
* * * * * * * * * *
17.
We thank the staffs of the Health and Anti-epidemic Station of Chang-Ning District and Tian-San Neighbourhood Hospital for collections of data and blood specimens. We acknowledge Drs. Yu Ming and Hua Jian-yifor their assistance. Submitted for publication April 19,1989; revised; accepted for publication February 2,1990. Requests for reprints should be sent to; Dr. Yue Chen, Centre for Agricultural Medicine, Fifth Floor, Ellis Hall, University Hospital, Saskatoon, Saskatchewan, Canada, S7N 0x0.
18.
* * * * * * * * * *
19. 20. 21. 22. 23.
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