Search

Simultaneous analysis here of urine data from both workers gave I f i SB r sb = 0.004, I s i SB s sb = 2 × 10 SP -4 sp d SP -1 sp , and assignment to Type S. (82) [553] assessed the airborne and internal aluminium exposure of 12 aluminium welders and fitters in a shipyard and five manufacturers of aluminium sulphate. Nevertheless, for each element, a default absorption type is recommended for use in the absence of information on which the exposure material can be assigned to Type F, M, or S. For most elements, Type M is recommended by default, including all of those in OIR Part 5 except the halogens (Type F) and aluminium (Type S). When comparing the bioavailability of orally gavaged aluminium citrate, nitrate, chloride, sulphate, and hydroxide in rats for 7 or 14 d, [528] noted few differences in blood and tissue concentrations, except for significantly higher aluminium content in rats gavaged with aluminium citrate. (90) As explained above, [471] monitored aluminium in urine and plasma, and airborne aluminium in the workplace of seven workers exposed to aluminium dust from polishing and shape cutting, or to aluminium welding fumes for 6 months. [Extracted from the article]

Recent epidemiological studies of the association between lung cancer and exposure to radon and its decay products are reviewed. Particular emphasis is given to pooled case-control studies of residential exposures, and to cohorts of underground miners exposed to relatively low levels of radon. The residential and miner epidemiological studies provide consistent estimates of the risk of lung cancer, with significant associations observed at average annual concentrations of approximately 200 Bq/m³ and cumulative occupational levels of approximately 50 working level months (WLM), respectively. Based on recent results from combined analyses of epidemiological studies of miners, a lifetime excess absolute risk of 5 × 10⁻⁴ per WLM [14 × 10⁻⁵ per (mJh/m³)] should now be used as the nominal probability coefficient for radon- and radon-progeny-induced lung cancer, replacing the previous Publication 65 (ICRP, 1993) value of 2.8 × 10⁻⁴ per WLM [8 × 10⁻⁵ per (mJh/m³)]. Current knowledge of radon-associated risks for organs other than the lungs does not justify the selection of a detriment coefficient different from the fatality coefficient for radon-induced lung cancer. Publication 65 (ICRP, 2003) recommended that doses from radon and its progeny should be calculated using a dose conversion convention based on epidemiological data. It is now concluded that radon and its progeny should be treated in the same way as other radionuclides within the ICRP system of protection; that is, doses from radon and its progeny should be calculated using ICRP biokinetic and dosimetric models. ICRP will provide dose coefficients per unit exposure to radon and its progeny for different reference conditions of domestic and occupational exposure, with specified equilibrium factors and aerosol characteristics.