Research Topics
| N HarleySummaryAffiliation: New York University School of Medicine Country: USA Publications
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Detail Information
Publications
Attempted validation of ICRP 30 and ICRP 66 respiratory modelsN H Harley
Department of Environmental Medicine, New York University School of Medicine, New York, NY, USA
Radiat Prot Dosimetry 152:14-7. 2012..ICRP 66 was the exception and consistently overestimated the bronchial concentrations probably because of its assumption of an overly long 23-d clearance half-time in the bronchi and bronchioles...
Radon and leukemia in the Danish study: another source of doseNaomi H Harley
Department of Environmental Medicine, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
Health Phys 97:343-7. 2009..The relatively high dose estimate to lymphocytes circulating through the BE, potential precursor cells for ALL, provides a dose pathway for an association...
Measurement of the indoor and outdoor (220)Rn (thoron) equilibrium factor: application to lung doseN Harley
New York University School of Medicine, Department of Environmental Medicine, New York, NY 10016, USA
Radiat Prot Dosimetry 141:357-62. 2010..Thus, a long-term alpha track measurement of thoron multiplied by an appropriate indoor or outdoor equilibrium factor yields the EEC, which can be used to assess bronchial lung dose...
Residential radon remediation: performance over 17 yearsNaomi H Harley
Department of Environmental Medicine, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
Radiat Prot Dosimetry 145:194-7. 2011..1 Bq m(-3). The last measurement, 2007-2008, with a newer NYU detector measured both (222)Rn (radon) and (220)Rn (thoron). The basement thoron concentration was 1.5 ± 0.9 Bq m(-3) or about 8 % of the (222)Rn value...
Radon carcinogenesis: risk data and cellular hitsNaomi H Harley
Department of Environmental Medicine, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
Radiat Prot Dosimetry 130:107-9. 2008..The mechanism proposed is that the extensive prior DNA damage in smokers, followed by alpha particle damage to a critical site in checkpoint genes, accounts for the greater lung cancer response in smokers...
