James Repace1, Wael K Al-Delaimy, John T Bernert. 1. Tufts University School of Medicine, and Repace Associates Inc., 101 Felicia Lane, Bowie, MD 20720, USA. repace@comcast.net
Abstract
OBJECTIVE: We sought to directly compare secondhand smoke (SHS) atmospheric markers to each other and to SHS dosimetric biomarkers, permitting intercomparison of clinical and atmospheric studies. METHODS: We used atmospheric and pharmacokinetic (PK) models for the quantitative estimation of SHS exposure and dose for infants, children, and adults, based on building smoker density and air exchange rate, and from exposure duration, default PK parameters, and respiration rates. RESULTS: We estimate the SHS serum cotinine doses for the typical and most-exposed individuals in the U.S. population; predictions compare well to measurements on a national probability sample. Using default respiration rates, we estimate serum cotinine dose from SHS nicotine exposure for 40 adults exposed to SHS in an environmental chamber; predictions agreed with observations. We correlate urine cotinine and hair nicotine levels for 127 infants exposed to parental smoking, and estimate corresponding atmospheric nicotine exposure via PK modeling. CONCLUSIONS: Our "Rosetta Stone" Equations allow the SHS atmospheric markers, respirable particles, nicotine, and carbon monoxide, to be related to the SHS biomarkers, cotinine in blood, urine, and saliva and nicotine in hair, permitting intercomparison of clinical and atmospheric studies of SHS for the first time.
OBJECTIVE: We sought to directly compare secondhand smoke (SHS) atmospheric markers to each other and to SHS dosimetric biomarkers, permitting intercomparison of clinical and atmospheric studies. METHODS: We used atmospheric and pharmacokinetic (PK) models for the quantitative estimation of SHS exposure and dose for infants, children, and adults, based on building smoker density and air exchange rate, and from exposure duration, default PK parameters, and respiration rates. RESULTS: We estimate the SHS serum cotinine doses for the typical and most-exposed individuals in the U.S. population; predictions compare well to measurements on a national probability sample. Using default respiration rates, we estimate serum cotinine dose from SHS nicotine exposure for 40 adults exposed to SHS in an environmental chamber; predictions agreed with observations. We correlate urine cotinine and hair nicotine levels for 127 infants exposed to parental smoking, and estimate corresponding atmospheric nicotine exposure via PK modeling. CONCLUSIONS: Our "Rosetta Stone" Equations allow the SHS atmospheric markers, respirable particles, nicotine, and carbon monoxide, to be related to the SHS biomarkers, cotinine in blood, urine, and saliva and nicotine in hair, permitting intercomparison of clinical and atmospheric studies of SHS for the first time.
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