Health Education Research Advance Access originally published online on August 24, 2004
Health Education Research 2005 20(2):185-194; doi:10.1093/her/cyg117
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Health Education Research Vol.20 no.2, © Oxford University Press 2005; All rights reserved
Parental smoking and passive smoking in infants: fathers matter too
1 School of Health and Social Studies, University of Warwick, Coventry CV4 7AL, 2 Department of Health Sciences, University of Leicester, Leicester LE1 6TP and 3 Institute of Child Health, Birmingham Children's Hospital, Birmingham B4 6NH, UK
4 Correspondence to: C. M. Blackburn; E-mail: c.m.blackburn{at}warwick.ac.uk
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Abstract |
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This study examines mothers' and fathers' smoking patterns in different kinds of smoking households, and assesses their relative contribution to infants' exposure to environmental tobacco smoke. It uses data from a cross-sectional survey of 314 smoking households (infants: mean age 10 weeks) in Coventry and Birmingham, England, examining reported tobacco consumption and objective measures of exposure: the study infant's urinary cotinine:creatinine ratios and their mother's salivary cotinine. The study shows that both mothers' and fathers' tobacco smoke make substantial contributions to infant exposure to tobacco smoke. Households were more likely to contain a smoking father than mother, with over two-thirds of households including a smoking father. In households where both parents smoke, fathers' tobacco consumption was found to be significantly higher than in households where only the father smokes. This suggests that the interaction between parents needs to be considered rather than focusing on mothers' or fathers' smoking behaviour in isolation. The implications for health promotion programmes are discussed, particularly the need to place more emphasis on tackling fathers' smoking. Currently, fathers' smoking receives far less research or health promotion attention than mothers' smoking. Protecting infants from fathers' as well as mothers' smoking is key to reducing environmental tobacco exposure in early infancy, when the risk of Sudden Infant Death is highest.
This study examines mothers' and fathers' smoking patterns in different kinds of smoking households, and assesses their relative contribution to infants' exposure to environmental tobacco smoke. It uses data from a cross-sectional survey of 314 smoking households (infants: mean age 10 weeks) in Coventry and Birmingham, England, examining reported tobacco consumption and objective measures of exposure: the study infant's urinary cotinine:creatinine ratios and their mother's salivary cotinine. The study shows that both mothers' and fathers' tobacco smoke make substantial contributions to infant exposure to tobacco smoke. Households were more likely to contain a smoking father than mother, with over two-thirds of households including a smoking father. In households where both parents smoke, fathers' tobacco consumption was found to be significantly higher than in households where only the father smokes. This suggests that the interaction between parents needs to be considered rather than focusing on mothers' or fathers' smoking behaviour in isolation. The implications for health promotion programmes are discussed, particularly the need to place more emphasis on tackling fathers' smoking. Currently, fathers' smoking receives far less research or health promotion attention than mothers' smoking. Protecting infants from fathers' as well as mothers' smoking is key to reducing environmental tobacco exposure in early infancy, when the risk of Sudden Infant Death is highest.
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Introduction |
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Children's exposure to environmental tobacco smoke continues to be an area of public health concern. It is associated with a number of poor child health outcomes, including asthma and other respiratory conditions, otitis media, and conductive deafness (Etzel et al., 1992
; Chilmonczyk et al., 1993). Among infants, passive smoking is a risk factor for Sudden Infant Death Syndrome (Department of Health, 1996), although the evidence suggests that prenatal exposure is more important than exposure in the postnatal period (Sullivan and Barlow, 2001). Although health promotion campaigns to reduce the number of deaths from Sudden Infant Death Syndrome have been associated with improvements in some risk factors such as sleeping position and use of bed coverings, smoking behaviours in infant households appear to have been less influenced (Hiley and Morley, 1994). As a high proportion of Sudden Infant Deaths occur in smoking households (Blair et al., 1996), there is an imperative to understand smoking patterns and influences on smoking in infant households. Reducing exposure to environmental tobacco smoke, particularly exposure to parental tobacco smoke in infancy, is likely to bring about significant improvements in infant health (Nafstad et al., 1997; Margolis et al., 1998).
The majority of exposure to environmental tobacco smoke occurs within the home and the major source is parental smoking (Jarvis et al., 1992, 2000). Other people's tobacco smoke in the home and exposure outside of the home has been shown to be quantitatively less important in children (Cook et al., 1994; Jarvis et al., 2000). Mothers' smoking has been shown to be the most harmful (Cook et al., 1994), and has been the focus for research and of health promotion programmes to reduce passive smoking among infants and children. Fathers' smoking has received significantly less attention, but has also been linked with adverse health outcomes. Previous work has indicated that for respiratory illness in infancy, the effect of father's smoking in households where the mother does not smoke is statistically significant (Cook and Strachan, 1999).
Understanding smoking and infant exposure patterns in households with infants is central to the development of programmes that aim to reduce death rates from Sudden Infant Death Syndrome, promote smoking cessation and encourage the use of harm reduction strategies in households with infants. Yet, there are few data on smoking patterns and habits in households with infants. While a number of studies offer some indicative evidence, they lack the level of detail or generalizability to the wider population of infants. A number of studies report on smoking patterns in households with older children, of which a large proportion report on the link between children's exposure to tobacco smoke and poor health outcomes among children with specific health conditions such as asthma (Emerson et al., 1994; Strachan and Cook, 1997; Wakefield et al., 2000a). These studies are likely to be poor indicators of smoking patterns in the wider population, as there is evidence of lower household smoking levels and environmental tobacco exposure in children with these conditions (Berman et al., 2003). Although a number of studies have examined smoking patterns and environmental tobacco smoke exposure in households with age ranges which include infants, only a small number have studied infant households outside of the hospital setting (Nafstad et al., 1997; Erikson et al., 1996; Dwyer et al., 1999). These studies offer no insights into how tobacco consumption patterns may differ between different people in different types of smoking households with infants.
Few studies have estimated the proportion of infants living with fathers who smoke. While some studies of smoking patterns in households with children have recorded mothers' smoking habits in some detail, many have subsumed fathers' smoking habits within the category of ‘other’ household smoker. Although smoking rates vary internationally, a small number of studies from North America, the UK, Italy and Scandinavia that have recorded fathers' smoking status and habits indicated that between 50 and 80% of children in smoking households lived with a father who smoked (Dell'Orco et al., 1995; Erikson and Bruusgaard, 1995; Berman et al., 2003).
Detailed tobacco consumption data are key to understanding sources of exposure to tobacco smoke. The study we report here examined, in detail, tobacco smoked by mothers and fathers in infant homes and measured infant smoke exposure using a biologic measure (cotinine:creatinine ratios) in a sample of smoking households with infants. Studies of the validity of measures of environmental tobacco smoke indicate that parent-reported measures of tobacco consumption and sources of tobacco smoke are valid and reliable (Matt et al., 1997; Hovell et al., 2000). Estimation of how much nicotine is absorbed requires a biologic measure. Cotinine, a metabolite of nicotine, has been shown to be a valid quantitative measure of environmental tobacco smoke exposure and correlates well with daily tobacco consumption (Benowitz, 1996; Haufroid and Lison, 1998). We have found no other published studies that report, in detail, on differences in tobacco consumption between mothers and fathers in various types of smoking households, and examine how different categories of parental smokers contribute to the total amount of tobacco smoke infants are exposed to in early infancy.
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Methods |
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We used a cross-sectional survey design to collect data from a population-based sample of main carers of young infants living in smoking households. All main carers of all infants born to mothers living within the boundaries of two Community NHS Trusts in the West Midlands, England, over a 9-month period were asked to participate by their family health visitors at the first or second visit to the new baby. Parents of infants with a major perinatal illness were excluded. Trained nurse interviewers using a structured interview schedule interviewed participants, 98% of whom were the infant's mothers, at home. Participants whose first language was not English were given the opportunity to be interviewed with the assistance of an interpreter in their own language. Interviews took place when infants were between 4 and 24 weeks old.
Participants were asked about their own, their partner's and other household residents' tobacco consumption: usual total consumption, consumption in the house and in the house in the 48 hours prior to the interview. Data on tobacco consumption in the 48 hours prior to the interview were collected so that consumption data could be correlated with urinary cotinine:creatinine ratio data. Data were also collected on sociodemographic characteristics and material living conditions. If consent was obtained, a sample of the infant's urine for estimation of the urinary cotinine:creatinine ratio was collected. Urinary cotinine was estimated using ELISA, a competitive enzyme immunoassay method that has the specificity and sensitivity to detect urinary cotinine in infant urine, where cotinine levels may be very low. The ratio of cotinine (ng/ml) to creatinine (mmol/l) was measured to adjust for the effect of fluid dilution. Only bottle fed babies were included in this analysis as nicotine and cotinine are transmitted through breast milk (Mascola et al., 1998). The number of bottle-fed infants with urine samples in households where neither parent smoked but with another resident smoker was to small for meaningful analyses, thus urinary continine:creatinine ratios are not reported. Participants were asked to provide a sample of saliva for cotinine estimation so that reported consumption could be examined against a biologic measure of tobacco consumption.
For data analysis purposes, smoking households were defined as households with a resident who smoked tobacco (cigarettes, pipes or cigars). Frequencies and bivariate analyses were used to describe and assess differences in smoking patterns between households. As cigarette consumption, urinary cotinine:creatinine ratio and salivary cotinine data were not normally distributed, the median values were recorded and non-parametric tests (Mann–Whitney U) were used to examine differences. To test between-group differences in the frequency distribution of categorical variables we used the Pearson 
2 test, except in the case of 2 x 2 tables, when the Yates' Correction for Continuity was recorded (Pallet, 2001). The data reported in this paper are for cigarette consumption only (only 13 smoking households contained cigar smokers who smoked 1 or more cigars per month and two households contained a father who smoked pipe tobacco).
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Results |
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In total, 314 smoking households with young infants were recruited to the study. At the time of the interview, the mean age of the infants was 10 weeks. The sociodemographic characteristics of these households are reported in Table I. Compared to a representative sample of UK households with infants (Department of Health, 1997
), the study households were more likely to have left school age 16 or less and be from a manual or unclassified social class, reflecting the association between tobacco use and social disadvantage. The 236 households who declined to take part were more likely to be younger and from a black or minority ethnic group. The proportions of participants from black and minority ethnic groups were, however, similar to those in the communities from which they were recruited.
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We classified smoking households according to the smoking status of the study infant's parent(s) (Table II). The most prevalent type of smoking household was those where only the father smoked and the least prevalent was those where the study infant's parent(s) did not smoke, but where there was another resident smoker. A slightly greater percentage of infants (67.5%) lived with a father smoker than a mother smoker (60.8%) (Table II). The data for infants in households with no parent smokers, but where another smoker was resident, are not presented in the remaining sections of this paper as numbers were too small for meaningful analyses (n = 10).
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Table III examines mothers' and fathers' usual cigarette consumption. There were no significant differences between the median number of cigarettes mothers' and fathers' usually smoked in total. However, the median number of cigarettes usually smoked by mothers in the house was significantly higher than that of fathers. A significantly higher proportion of mothers smoked in the house than fathers.
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Table IV examines cigarette consumption for mothers and fathers according to whether they live with a partner who smoked. When cigarette consumption among mothers in mother-only smoking households was compared with those for mothers living in households where both parents smoked, there were no significant differences for any of the measures. A different pattern emerged among fathers. Fathers living in both-parent smoking households, when compared to those in father-only smoking households, were reported as having a higher median usual daily cigarette consumption in total, a higher median usual daily cigarette consumption in the house and a higher median cigarette consumption in the house during the 48 hours prior to the interview.
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Urinary cotinine:creatinine ratio data were available on 168 of the 239 bottle fed infants in the study. Missing data on the remaining 71 infants were due to some parents refusing consent to take a urine sample or to failure of the infant to produce sufficient urine for analysis at the time of the interview. To identify whether infants without urine samples were likely to be different in terms of exposure to tobacco smoke, respondents' own cigarette consumption in the house in the last 48 hours and reported total household tobacco consumption in the house in previous 48 hours was compared for infants with and without urine samples. There were no significant differences for either measure (respondent's cigarette consumption in the house in last 48 hours: Mann–Whitney U: z = –0.138, P = 0.890; total household consumption in the house in last 48 hours: Mann–Whitney U: z = –0.182, P = 0.856).
The range of infant urinary cotinine:creatinine ratios for different categories of smoking households is described in Table V. In smoking households, infant urinary cotinine:creatinine ratios were highest in households where both parents smoked and lowest in households with only father smokers. Differences in median urinary cotinine:creatinine ratios between the three types of smoking households were statistically significant (P < 0.001). Pair-wise comparisons indicated that median urinary cotinine:creatinine ratios were significantly higher in infants in mother-only smoking households than father-only smoking households (Mann–Whitney U: z = –5.170, P < 0.001), in infants in both-parent smoking households than mother-only smoking households (Mann–Whitney U: z = –2.133, P = 0.033) and in infants in both-parent households than father-only smoking households (Mann-Whitney U: z = –6.589, P < 0.001).
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Salivary cotinine data were available on 103 main carers, of which 100 were obtained from the infant's mother. As only three fathers were main carers, data presented here is for mothers only. Missing data resulted from some participants declining to give a saliva sample and from difficultly obtaining a sample from some participants who did agree to give a sample (some participants could not tolerate keeping the dental roll in their mouth for 5 minutes). Differences in median self-reported daily cigarette consumption between those with and without a saliva sample were not significant (Mann–Whitney U: z = –1.09, P = 0.276). Differences in median salivary cotinine levels between mothers in mother-only smoking households and those in both-parent smoking households were not significant (P = 0.086). This supports the findings based on self-reported consumption.
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Discussion |
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This paper uses data generated from parental reports of tobacco consumption and smoking habits to examine the relative contribution that mothers' and fathers' tobacco smoke makes to passive smoking among infants. It has generated detailed data on patterns of tobacco consumption and tobacco smoke exposure that raise a number of issues for health promotion. Our study points to the importance of carrying out more detailed analyses of parental tobacco consumption patterns and recording detailed data on fathers' as well as mothers' smoking. Tobacco consumption patterns are complex and vary across different categories of parental smokers. These consumption patterns offer important insights into why environmental tobacco smoke exposure levels vary among infants and are highest among children in households where two parents smoke, as found in this and other studies (Jarvis et al., 1992
; Dell'Orca et al., 1995).
As reported in other studies (Dell'Orca et al., 1995; Erikson and Bruusgaard, 1995), there was a higher prevalence of infants living in father-only smoking households than in mother-only or both-parent smoking households. Overall, infants were more likely to live in a household with a smoking father than a smoking mother. The overall pattern of tobacco consumption identified in this study was that fathers consumed less tobacco in the house than mothers. However, a more detailed examination of fathers' smoking behaviour indicated that in households where both parents smoked, fathers' tobacco consumption made a considerable contribution to the total amount of tobacco consumed in the house. Although as a group, fathers consumed less tobacco in the house than mothers, in households were both parents smoked, fathers' median cigarette consumption was higher than in father-only smoking households. For father smokers, but not mother smokers, living with a partner who smoked was associated with an increase in total tobacco consumption and an increase in tobacco consumption in the infant's home.
We found that among mothers, the median number of cigarettes smoked did not vary significantly according to whether they did or did not live with a partner who smoked. Other studies have found that women who lived with a partner who smoked were heavier smokers (Graham, 1993) or smoked more in the house (Erikson and Bruusgaard, 1995). A possible explanation for our finding could be that mothers misreported their tobacco consumption. However, salivary cotinine data, used as a biologic measure of mothers' tobacco consumption, also showed no significant differences in median tobacco consumption in the 48 hours prior to the interview between mothers. This confirms the finding, based on reported tobacco consumption data, that mothers' tobacco consumption did not vary significantly according to whether they lived in a mother-only or both-parent smoking household.
A biologic measure of infant smoke exposure, continine:creatinine ratios, enabled the relative contribution that mothers' and fathers' tobacco consumption makes to the total amount of smoke their infant absorbed to be examined. Confirming other studies, this study indicates that mothers' tobacco smoke makes an important contribution to the total amount of tobacco smoke that infants absorb in both mother-only and both-parent smoking households. Urinary cotinine:creatinine ratio values were highest in infants living in households where both parents smoked. As tobacco consumption data suggests that fathers, but not mothers, living in households with two parent smokers increased their tobacco consumption in the house, higher urinary cotinine:creatinine ratios in infants living in homes where both parents smoke can be explained, at least in part, by their father's tobacco consumption.
Methodological issues
Parent-reported tobacco consumption and a biologic measure of environmental tobacco exposure were utilized. Although some commentators have noted that tobacco consumption can be misreported (Cook et al., 1994; Ford et al., 1997) either intentionally or unintentionally, studies have found good agreement between parent reporting of smoking habits and biochemical measures of tobacco consumption in households with young children (Dell'Orca et al., 1997; Nafstad et al., 1997). It is possible that differences in cigarette consumption between fathers in father-only smoking households and fathers in both-parent smoking households may be due to inaccurate reporting of fathers' cigarette consumption patterns by the infant's mothers. However, the consistency of the data across measures of usual total consumption, usual consumption in the house and consumption in the previous 48 hours in the house suggest that this is unlikely to be the case. Furthermore, women's proxy reports of their partner's cigarette consumption have been shown to be in agreement with men's own self-reports and accurate enough to be used with confidence in epidemiological studies (Passaro et al., 1997).
A strength of this study was the use of salivary cotinine, which verified the accuracy of mothers' own reported tobacco consumption. Urinary cotinine, as a metabolite of nicotine, has been shown to be a valid quantitative measure of exposure to environmental tobacco smoke in infants (Benowitz, 1996). A limitation of the study may be that only single measures of urinary cotinine:creatinine ratio were made. Cotinine levels have been shown to vary over time and with the age of the child (Peterson et al., 1997). While multiple measurements have the advantage of establishing a profile of environmental tobacco smoke, single measures correlate well with reported parental tobacco consumption (Cook et al., 1994). In addition to usual cigarette consumption data, we also included a measure of cigarette consumption in the previous 48 hours. As cotinine has a half-life of about 20 hours and thus reflects smoke exposure in the previous 24–48 hours (Haufroid and Lison, 1998), inclusion of this reported measure is likely to have offset some of the problems associated with recording only a single measurement of cotinine.
In addition to the number of parental smokers in the home and total number of cigarettes consumed within the home, individual cotinine levels are affected by other factors including the consumption of other household smokers, proximity to smokers, the home, the size of the rooms and the use of harm reduction measures. A limitation of this study is that it did not report these data. A further limitation is the number of parent carers who declined to participate. In line with ethical requirements, parents were fully informed of the study's focus on smoking. This overt focus on smoking, at a time when public health policy depicts smoking near infants as irresponsible and health damaging, is likely to have had a negative effect on the recruitment process. However, participants' social and demographic profile, although more disadvantaged that that of the wider population of infant households, reflected the association between social disadvantage and tobacco use.
Implications for smoking intervention in households with infants
Our study findings raise a number of important issues for smoking intervention programmes. Current smoking cessation and tobacco harm reduction programmes predominantly target mothers who smoke. The greater health impact of mothers' than fathers' smoking behaviour on children's health (Cook et al., 1994; Brooke et al., 1997; Cook and Strachan, 1999) lends some legitimacy to this approach. In mother-only and both-parent smoking households, mothers' smoking makes a significant contribution to the total amount of environmental tobacco smoke infants are exposed to in the home. However, our data also indicate that failing to target actively fathers' smoking may be questionable for a number of reasons. First, estimates from this study suggest that health promotion interventions that only target households with mother smokers may fail to reach the significant proportion of households where only the father smokes. Although cigarette consumption in the house appears to be low generally in these households, it does not follow that they should not be targeted. In households where the mother does not smoke, fathers' smoking has been shown to be associated with illnesses of the lower respiratory tract in infants (Cook and Strachan, 1999). Our study, like a number of studies, identified that one-third of smoking households with young infants only contain fathers who smoke. This suggests that in the UK, only targeting mother smokers may capture less than two-thirds of all smoking households with infants.
Second, encouraging fathers to quit smoking, or where this is not possible, to not smoke in the house, may bring about reductions in infant exposure to tobacco smoke as well as making it easier for mothers to quit smoking. Studies suggest high concordance between long-term smoking cessation among women and the smoking status of their partners (Waterson et al., 1990; Wakefield et al., 1993; Nafstad et al., 1996). Failing to tackle fathers' smoking may have long-term consequences for smoking cessation rates among women. Women acknowledge their partner as being an important influence on their own smoking behaviour. Partners who smoke make cigarettes readily available and create the social opportunities to smoke, as well as acting as a constant source of temptation to women who are trying to quit or reduce their cigarette consumption.
Our study suggests that mothers may also shape the smoking behaviour of their partners. For fathers in this study, living with a partner who smoked appeared to be associated with higher total tobacco consumption and increased tobacco consumption in the house. This study did not examine why fathers' tobacco consumption in the house was significantly lower in households where fathers lived with a non-smoking partner but possible explanations may be that non-smoking mothers are more likely to insist on banning smoking from the home than mothers who smoke, and that for fathers living with a non-smoking partner there are less social opportunities to smoke at home and less temptations to light up a cigarette. How interactions between parents influence smoking patterns and harm-reduction behaviour should be considered in the design of health promotion programmes to reduce household smoking.
Although the sample of households in this study was broadly representative of infant households, the proportion of households from minority ethnic groups was too small to examine ethnic group differences despite active recruitment in areas with high proportions of minority ethnic groups and the use of interpreters. Recent studies of smoking patterns among Pakistani and Bangladeshi households (Nazroo, 1997; Johnson et al., 2000) suggest that among men the proportion of cigarette smokers is high and a high median number of cigarettes are consumed. In these households, the tobacco consumption of fathers and other male resident smokers may make a substantial contribution to the amount of tobacco smoke infants are exposed to. There are virtually no data on smoking patterns or use of harm reduction measures in minority ethnic households with infants and children, indicating a need for research in this area.
Reducing infant exposure to tobacco smoke, by encouraging parents to quit smoking or banning smoking in the home, is likely to bring about improved health outcomes for children. It may also reduce the likelihood of these infants becoming smokers themselves in later life (Wakefield et al., 2000b). Taken together, these findings suggest that the interaction between parents needs to be considered rather than focusing on mothers' or fathers' smoking behaviour in isolation. Although this study points to a need to focus health promotion programmes on fathers as well as mothers, there is little research to underpin such programmes. Unlike mothers' smoking, very few studies have examined the factors linked to fathers' smoking. Although men's smoking has received some research attention, this has generally focused on risk taking behaviour. Men as fathers have received no attention in the literature on smoking. Research efforts are needed in this area.
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Acknowledgments |
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We wish to thank the following for their assistance: parents who kindly agreed to participate; health visitors, their managers and staff in the child health departments of the NHS Trusts who helped with recruitment; and the nurse interviewers who undertook the data collection. We are grateful to the Foundation for the Study of Infant Deaths who awarded a grant (grant no. 266) for this project.
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Received on April 20, 2004; accepted on July 17, 2004
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