Abstract B89: Child second-hand and third-hand exposure to carcinogens and tobacco toxicants

Abstract

Exposure to secondhand tobacco smoke (SHS) is a recognized cause of cardiovascular disease and cancer in adults and respiratory disease in children. In spite of this, approximately one-third of children in the United States live in a home where cigarette smoking is permitted. Few limitations have been enacted on the primary source of SHS exposure in children, inhome exposure. We quantified 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and its glucoronidies (total NNAL) in the urine of 79 children who lived in homes with a parent(s) who smoked. Total NNAL is an accepted biomarker of uptake of the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone. Cotinine and nicotine and their glucuronides (total cotinine/nicotine) were also quantified. Children ranged in age from one month to 10 years (mean+ sd: 3.82+2.55); 49% were male. Among the parents, 56% were African American, 26% had < high school education, 67% were unemployed and 76% had a monthly income <$1800. Average number of cigarettes smoked per day (CPD) was 9.5+5.3; 64% reported smoking their first cigarette within 30 minutes of waking and average number of smokers living in home was 1.9+.96. 72% of parents reported that their child had been exposed to SHS in past week and 70.9% reported at least some home smoking bans in their home. Geometric mean levels of total NNAL were 0.08 pmol/mL (95% CI:0.06 — 0.10). Total cotinine and total nicotine 11.88 ng/mL (95% CI:8.42 — 16.77) and 6.90 ng/mL (95% CI:4.57 — 10.43), respectively. There were strong and significant correlations among all three biomarkers (.64 -.96, p<.001). Detectable total NNAL, cotinine and nicotine were found in 90%, 95% and 90% of children, respectively. Total NNAL was significantly different across: 1) ethnic groups (i.e., African American children > White and “Other” [.11, 95% CI:.08-.17 vs. .03, 95% CI:.02-.06 vs. .07, 95% CI: .03-.12, respectively], p<.01; 2) parental employment (i.e., children of unemployed parents > employed [i.e., .10, 95% CI:.07 — .14 vs. .05, 95% CI .03 — .05] p<.05) and 3) monthly income (i.e., lower income > higher income [.09, 95% CI .07 — .13 vs. .04, 95% CI: .02 — .09], p<.052). Nicotine and cotinine followed similar trends. Total NNAL was significantly different by parent level of nicotine dependence (< 30 minutes to first cigarette vs. > 30 minutes); parental endorsement of child exposure in home; and levels of home and car smoking restrictions. NNAL was also correlated with parent CO level (r=.29, p<.05); air quality (r=.28, p<.05); number of smokers residing in home (r=.23, p<.01); and CPD in home (r=.30, p<.01). Similar trends were observed in cotinine and nicotine. Although child age was not significantly correlated with NNAL or cotinine, a significant negative association was found for nicotine (r =-.27, p<.05), with younger age associated with higher nicotine values. Detection of NNAL but not iso-NNAL in our analyses indicates that the great majority of exposure is due to secondhand smoke exposure (via air) rather than thirdhand exposure (e.g. via residues on furniture, carpets). Our results suggest that children living with a smoking parent are exposed to detectable levels of carcinogens and nicotine. Interventions need to be designed to dramatically lower, or ideally eliminate, exposure to home SHS.

Citation Information: Cancer Prev Res 2010;3(12 Suppl):B89.