Inner-city children are exposed to naphthalene, an understudied volatile Polycyclic Aromatic Hydrocarbon (PAH) and an IARC classified potential carcinogen, in indoor air from naphthalene containing household products such as mothballs, and from penetrating traffic emissions. Indoor air levels of naphthalene have been reported to be 5-10 fold those in outdoor air . Home use of naphthalene products varies culturally. In a NYC pediatric emergency room, 27% of African American and Caribbean families reported using moth- balls as air fresheners, while some Latin immigrants use them in traditional remedies[3,4]. Naphthalene expo- sure is associated with hemolytic anemia in infants  and with DNA damage in sperm, while in vitro exposure to naphthalene metabolites is toxic to colony forming units of human granulocyte precursors[5,6]. In the Columbia Center for Children's Environmental Health (CCCEH) birth cohort of Latino and African-American children in NYC, prenatal maternal exposure to airborne PAH is associated with infant chromosomal aberrations (CAs) measured in cord blood using Whole Chromosome Paints Fluorescent In Situ Hybridization (WCPFISH). CAs are an established marker of cancer risk and are a bio-dosimeter of clastogenic exposures in adults. Translocations, the most persistent subtype of CAs with half lives of 2-4 years [7,8], are considered the most meaningful cytogenetic endpoint for assessing cancer risk. Our preliminary data suggest that increasing levels of the naphthalene metabolites, 1- and 2-naphthol, measured in spot urine samples of 5 year olds in the CCCEH cohort, are associated with increased occurrence and frequency of CAs and translocations in peripheral blood lymphocytes drawn concurrently. Urinary naphthol levels in CCCEH 5 year olds are elevated compared to median levels in US children, though comparable to levels in Mexican Americans[10,11]. Urine levels of naphthol are a reliable measure of individual exposure but they have short half-lives and consequently vary significantly throughout the day. First-morning urine collections provide a more accurate measure of household exposure to naphthalene and collection at a uniform time maximizes detection of inter-subject differences. Age 9, the median US age for initiating puberty[12,13], is potentially significant for future cancer risk because it is an age of accelerated growth with increased cell division and opportunity for propagation of genetic damage. Our preliminary data suggests that naphthalene is a clastogen. In order to validate our initial data and to determine if naphthalene exposure predicts CAs and translocations in children, we propose to 1) measure 1- and 2- naphthol in first- morning urine samples, 2) score CAs and translocations using WCP FISH and 3) document home use of naphthalene-products in 158 nine year olds of the CCCEH, a cohort with documented exposure to varying and often high levels of ambient and indoor air PAH. We propose to measure the relationship between biomarkers of naphthalene exposure in childhood and CAs and translocations in order to document human response to a potentially myelotoxic and genotoxic exposure differentially affecting impoverished communities.
Chromosomal aberrations a marker of cancer risk are associated with exposure to naphthalene (a potential carcinogen) in 5 yr olds in our CCCEH cohort of poor Latino and African American children in NY. We propose to validate this preliminary finding by studying 158 nine yr olds in the CCCEH cohort by 1) measuring a marker of individual exposure to household sources of naphthalene, 2) documenting these sources, including ones more common in poor immigrant communities and 3) measuring their association with early genetic damage. This study aims to increase understanding of childhood exposure to an understudied indoor air pollutant.