Cotinine

ENVIRONMENTAL TOBACCO SMOKE (ETS) in the home continues to be a major health risk for children in the United States. (1,2) Measuring ETS is a central feature of clinical and epidemiological studies, with children's exposure often assessed through parental estimates. Researchers have concerns about parents' ability or willingness to accurately report the extent of their children's ETS exposure in the home. (3-5) As a result, in most studies investigators use a combination of parental reports and a validation of these reports by using environmental measures (e.g., air nicotine monitors)in the home, or biomarkers of ETS exposure assessed among the children. One of the most widely used biomarkers is cotinine, a major metabolite of nicotine that can be measured in hair, plasma, saliva, and urine. (6,7) Studies have shown relatively consistent correspondence between parental reports and cotinine measures, suggesting that parents generally provide reliable estimates of their children's exposure. (3,8-14)

Cotinine levels provide objective validation of parental estimates of children's ETS exposure, but at a cost. Blood, hair, saliva, and urine sample collection can be intrusive and potentially distressing, especially for infants and young children. Cotinine levels exhibit intra-individual variation over time and inter-individual variation by dosage. (15,16) Analytical expense is relatively high, making the widespread application of cotinine measures costly, especially for observational and community-based epidemiological studies. Refining our understanding of relatively inexpensive parental reporting variables and their relation to cotinine measures is, therefore, desirable, particularly across population subgroups (e.g., by age of child, ethnicity, race, or socioeconomic status).

Studies vary by the parental report variables used for the estimation of children's ETS exposure, including reported number of cigarettes smoked daily, parental smoking status, amount of time spent smoking, estimated exposure hours for their children, indicators of room size, household crowding, and other similar measures. In several studies investigators have noted the particular importance of maternal smoking as a major covariate of cotinine concentration among children. (8-10,14,17-19)

The identification of specific parental report variables that correspond closely and consistently with cotinine measures could lead to the use of less burdensome questionnaires, or reduce the need for cotinine validation. In the current study, we examined data from a sample of urban, low-income, and largely ethnic minority children with asthma who live with at least 1 household member who smokes at home. Specifically, we assessed the relationship between ETS exposure of these children, as reported by their parents in a detailed ETS questionnaire, and cotinine concentrations measured in the children's urine.

Method

Data were obtained from a randomized controlled trial of an educational intervention, the purpose of which was the decrease of household ETS exposure among children with asthma and who live in households inhabited by 1 or more smokers. "Smoking households" were defined as homes in which any household member was a current smoker, and smoking had occurred at home either indoors or outdoors at least once in the previous month. The study, described elsewhere, (8) recruited 242 parent (or guardian) -child pairs through health facilities, schools and community agencies serving predominantly low-income, medically underserved populations. This study used a subsample of these parent-child pairs, as described later.

Cotinine measures. Urine samples for cotinine analyses were requested from all children [greater than or equal to] 7 yr of age (N = 184). Urine samples were obtained from 146 (79%) of the eligible children. Nonparticipants were accounted for primarily by subject refusals. There were no apparent differences between refusal cases and the remainder of the sample by age of the child or demographic characteristics of the parent, or in reported household smoking behaviors or ETS exposure. These 146 parent-child pairs constituted the sample for the current analysis (Table 1).

Urine samples were collected in sterile specimen cups at the recruitment sites, and the samples were transported in coolers for immediate freezing and storage (-20 [degrees]C) at the study office. The urine samples were analyzed at the Centers for Disease Control and Prevention, Division of Environmental Health Laboratory Sciences, with isotope dilution high-performance liquid chromatography/atmospheric pressure chemical ionization tandem mass spectrometry (Perkin-Elmer Sciex Instruments).

Survey measures. For each parent-child pair, an interview was conducted either in English or Spanish with the parent at the time of recruitment into the study. The survey gathered 4 types of information: (1) the number of household members and regular visitors who smoked in the home; (2) frequency and time (day, evening) of household smoking; (3) the extent to which the child with asthma was exposed to the smoking; and (4) particular practices or household regulations, if any, regarding smoking within the home and around the child with asthma.

Household smoking behaviors. We asked each parental respondent to create a household roster that included all people residing in the home, including family, friends, relatives, boarders, and any visitors who "spend time in your home and smoke on a regular basis, such as relatives, in-laws, other children, friends, babysitters or others, at least 4 days a week or more." The smoking status of each person on the household roster was determined. For each smoker, the parent was asked the following questions:

* On the days that (you smoke/PERSON smokes), about how many cigarettes (do you/does PERSON) usually smoke at home per day?

* When (you are/PERSON is) at home, where (do you/does PERSON) usually smoke? Would you say (you smoke/PERSON smokes) outdoors only, indoors only, both indoors and outdoors, or (do you/does PERSON) not smoke at home?

* In a typical week, what is your best estimate about the number of hours (you smoke/PERSON smokes) (inside your home/outside your home/in the car) in a week. Remember to think about both weekends and weekdays, evenings, and daytime.

* Thinking about the number of hours (you smoke/ PERSON smokes) (inside your home/outside your home/in the car) per week, about how many of these hours do you think your child was (in the same room/in the same place/in the car) when (you were/PERSON was) smoking?

We used the parental survey information to calculate several summary measures of household smoking, including total number of smokers in the home; paternal and maternal smoking status; total number of cigarettes smoked per day in the home, summed across all household smokers; total number of hours smoked per week (summed across ,all household smokers, at home indoors, at home outdoors, and in the car); and total number of hours the child with asthma was thought to be exposed to secondhand smoke in the home (indoors at home, outdoors at home, and in the car).

Household smoking regulations. Each parent was asked to read a series of statements and mark those that described how they handled smoking inside their homes: "People are allowed to smoke anywhere and anytime inside my home"; "People are allowed to smoke only in certain areas or rooms inside my home"; "People are allowed to smoke only at certain times inside my home"; "Smoking inside my home is allowed only for special guests or on special occasions"; and/or "No one is allowed to smoke at all inside my home." We used the responses to categorize households into 3 ordered categories: (1) those with absolute restrictions against smoking inside the home, (2) those with conditional restrictions on household smoking, and (3) those with no restrictions on household smoking.

Analyses. The parent-reported estimates of children's ETS exposure were compared with urinary cotinine concentrations measured among the children, on the underlying assumption that urine cotinine is a valid and reliable biochemical marker of ETS exposure. Cotinine concentrations were skewed right, so the variable was log-transformed to approximate a normal distribution of the values. Each self-reported measure was first examined with univariate linear regression, with the log-transformed cotinine concentration as the dependent variable. Multiple linear regression was then used for the examination of the significant predictors as a set of explanatory variables for the log-transformed cotinine concentration. Forward selection was used for the identification of a minimum set of parental report variables that best explained the variance in cotinine measures, and to rank these predictors by their explanatory power. List-wise deletion of missing values resulted in some reduction in sample size, depending on the variables in the regression equations. The ordered variable measuring level of household smoking restriction (1 = absolutely no smoking allowed indoors, 2 = conditional restrictions on smoking indoors, and 3 = no restrictions at all on smoking indoors) was treated as a continuous variable.

Results

The sample characteristics reflected the convenience sampling scheme by which the majority of participants in this study were recruited through asthma-related clinics or organizations serving low-income, largely minority populations. More than 70% of the adult respondents reported an annual household income of less than $20,000, and more than 80% classified their race/ethnicity as other than white. Mothers made up more than 90% of the adult respondents in the parentchild pairs. Approximately 29% of the respondents reported living in single-parent households (Table 1).

Although all study subjects came from smoking households, overall levels of smoking and ETS exposure reported by the parents were low, with more than half of the respondents reporting no hours of smoking indoors, and no hours of indoor ETS exposure among their children (Table 2). On average, more household smoking reportedly occurred outside the home than inside the home, and nearly half of the respondents reported that absolutely no smoking was allowed inside their home. The urine cotinine concentrations also indicated low levels of ETS exposure among the children, with measurements comparable to those found in other studies for households reporting low or no household ETS exposure. (10) Moreover, increasing restrictions placed on household smoking were significantly associated with lower urinary cotinine concentrations in children with asthma (Fig. 1).

[FIGURE 1 OMITTED]

In the simple linear-regression analyses, parent-reported level of household restriction on indoor smoking accounted for the greatest amount of variation in urine cotinine concentration (Table 3). Total number of cigarettes smoked by household members per day, presence of maternal smoking, total reported number of hours smoking indoors, and total reported number of hours of children's exposure to indoor smoking were all also significantly and positively associated with cotinine concentration. Presence of paternal smoking was associated negatively with urine cotinine concentration.

The multiple-regression analyses reflect similar findings (Table 4). Parent-reported level of restriction on household smoking was the first covariate to enter the regression, followed by presence of maternal smoking, total number of cigarettes smoked indoors per day, and presence of paternal smoking. The adjusted [R.sup.2] for the model as a whole was .448; the first 3 covariates collectively produced an [R.sup.2] of .423, with the final addition of the paternal smoking indicator adding only a modest amount (2%) to the predictive power of the overall model.

Discussion

In this sample of children with asthma living with smokers in low-income households, our data show that children's ETS exposure, as validated through urine cotinine measures, can be reasonably assessed with the use of relatively few items of information gathered from parental interviews. In particular, information on level of household smoking restriction, maternal smoking status, and number of cigarettes smoked per day accounted for approximately 43% of the variance in cotinine concentration. Information about paternal smoking added only modest additional information about the variance in the cotinine measure. Asking detailed questions about the duration of household smoking or children's ETS exposure, whether inside the home, outside the home, or in the car, added no additional significant information.

Maternal smoking was linked significantly to urine cotinine concentration in the child and was more significant than paternal smoking status--echoing findings from other studies. (10,14,18,19) These results, however, must be interpreted with caution given the nature of the sample. Single-parent households accounted for 30% (44/146) of the sample, and the overwhelming majority of these (41/44, or 93%) were headed by mothers. Among the 2-parent households, both parents smoked in only 16% (16/102) of them. Inasmuch as the sample was restricted to smoking households, the absence of 1 smoking parent is strongly linked to the presence of smoking in the other.

The single variable that accounted for the greatest proportion of variance in urine cotinine was the level of restriction placed on smoking indoors at home. Biener et al. (21) also found that household restrictions on smoking were associated significantly with lower levels of ETS exposure among adolescents in a Massachusetts study, and Winkelstein et al. (22) found that urine cotinine concentrations among children with asthma were significantly lower in those whose parents reported smoking only outdoors. Cotinine levels were closely intertwined with the household structures of our sample, as well as the patterns of maternal and paternal smoking. Those who reported maternal smoking (and thus a greater likelihood of the absence of paternal smoking) appeared less likely to report absolute restrictions against smoking indoors than those reporting paternal smoking (Table 5). Given this study's small number of 2-parent households in which both parents smoke, these findings suggest that, for this sample, the children in households with a smoking father and nonsmoking mother had lower cotinine levels, perhaps through enforcement of restrictions against indoor smoking. Households with smoking mothers were less likely to report restrictions against indoor smoking, reported more hours of smoking indoors, and had children with higher urine cotinine concentrations.

This intertwining of maternal smoking, paternal smoking, and household smoking restrictions that characterized our study sample is most likely the reason for the relative lack of influence of paternal smoking in the multiple-regression analyses, and the somewhat counterintuitive finding that paternal smoking is linked to lower cotinine levels in the child with asthma.

The racial/ethnic distribution of our sample's adult respondents, in particular the majority Latino component (Table 1), raises the question of whether some of the household smoking characteristics found in this study were culturally mediated. The Latino respondents were more likely than their white or African American counterparts to report fewer cigarettes smoked per day in their homes, fewer hours of smoking and ETS exposure hours indoors, and having absolute restrictions against smoking inside their homes. (8) Whether these findings represent broader cultural factors needs to be explored in future studies with larger, more-diverse samples. Latinos overall are more likely to be occasional smokers than non-Hispanics. (23,24) Female Latinos in particular show a lower smoking prevalence than other women, (25) and the rate of maternal smoking in Mexican-American families is low, especially among the least acculturated. (26,27) Latinos are also more likely than whites or African Americans to report absolute restrictions against smoking inside the home.

The results of this study have shown that in households with low levels of smoking, parental reports remain a reasonably' reliable indicator of children's ETS exposure in the home. Moreover, the results suggest that in estimating ETS exposure for this particular sample, questionnaires that collect detailed information on smoking habits and ETS exposure would do no better than simpler surveys that inquire about smoking restrictions in the home, parental smoking status, and number of cigarettes smoked at home per day. It should be noted that these results were found in a sample that was largely made up of low-income and racial/ethnic minority households, and all the homes were habitated by children with asthma. These results may differ for populations of children without asthma, where parents may lack the external motivation to reduce or minimize their children's ETS exposure, or in households where parents are heavier smokers than encountered in our study.

Cotinine validation of parental reports of children's household ETS exposure is logistically difficult and costly, especially for epidemiological and community-based studies. Obtaining detailed information from parents about the extent of both smoking in the home and their children's exposure to ETS is also potentially time-consuming and burdensome for the respondent, and it may result in rough estimates at best. These issues point to the need for evaluation of ETS exposure results across studies to determine if simpler, more reliable parental report items can accurately and consistently assess level of ETS exposure among children. Such items would be useful not only in monitoring studies, but also in identifying children at risk in clinical situations as well.

The authors wish to thank Connie Sosnoff and Alberto Febo for their assistance in conducting the cotinine analyses; and Guadalupe Escobar, Claudia Huezo, Yanscy Flores, Melissa Aguayo, and Laura Hoyos--all of whom conducted the interviews. We gratefully acknowledge the contribution of Dr. K. Michael Cummings, as well as the support and assistance provided by the administrative and clinical staffs at our participating recruitment sites.

Support for this work was provided by Grant HL53957 from the National Heart, Lung and Blood Institute, Division of Lung Diseases.

Submitted for publication April 27, 2001; accepted for publication July 23, 2001.

Requests for reprints should be sent to Dr. Barbara Berman, Division of Cancer Prevention and Control Research, UCLA, Jonsson Comprehensive Cancer Center A2-125 CHS, Box 956900, Los Angeles, CA 90095-6900.

E-mail: bberman@ucla.edu

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