Document ID: chunk:federal_register_of_legislation:F2013C00288:reg:4:p19
Version: federal_register_of_legislation:F2013C00288
Segment Type: reg
Provision Reference: reg 4 (pt 19/24)
Character Range: 993027–996126

EPA (1989), Exhibit 6-16) should no longer be used when evaluating risk from the inhalation pathway". Hence for the quantification of exposures via inhalation of dust or vapours, it is appropriate that guidance available from US EPA (2009) is considered.

The equation for inhalation intakes of vapours and dust is published as follows and detailed in Table 3.
ECvapour (µg/m3)  =  CA  x ET x B x EF x ED
                                  AT

ECdust (µg/m3)  =  CA  x RF x ET x B x EF x ED
                                 AT

Table 3. Variables description for vapour inhalation intake calculation
Variable            Units      Description
B                   --         Bioavailability
ECvapour or ECdust  µg/m3      Exposure concentration (a time-weighted average concentration) relevant to chemicals present as a vapour or dust
CA                  µg/m3      Concentration in air (exposure point concentration which has been measured or modelled)
RF                  -          Lung retention factor relevant to the inhalation of dust and includes consideration of a deposition fraction and ciliary clearance
ET                  hours/day  Exposure time
EF                  days/year  Exposure frequency
ED                  years      Exposure duration
AT                  hours      Averaging time

For threshold chemicals the estimated exposure concentration (EC) is compared to the inhalation specific toxicity reference value for assessment of chronic or subchronic risks. For non-threshold chemicals, excess cancer risk is calculated by multiplying the URF by the EC. Note that a method for the assessment of acute exposure risk is also provided by US EPA (2009), in which the CA is compared directly to the appropriate toxicity reference value. When sourcing inhalation toxicity reference values using the hierarchy of data sources listed in Table 4, the inhalation value may be an air quality guideline.

4.8              Specific considerations in exposure modelling

    4.8.1          Blood lead modelling
There is a substantial body of evidence that links environmental exposure to lead to uptake into the blood stream. The impact of lead on cognitive processes, especially of children, is also well understood. Several studies have been undertaken at Port Pirie in South Australia showing the relationships between maternal blood lead and pregnancy outcome and children's abilities at various ages following environmental exposure to lead (e.g. Country Health SA 2007 at www.publications.health.sa.gov.au/envh). Studies suggest that an increase of 10 µg/dL of lead in blood (PbB) can lead to an IQ decrease of 1 to 5 points and recent studies show that there may be no lower threshold on the effect of lead in blood (ATSDR 2007).

A risk assessment technique has been developed to assess the uptake of lead into the blood, which effectively applies an a priori uptake factor to an estimated dose to estimate blood lead concentration. The US EPA integrated exposure uptake biokinetic model (IEUBK) for lead in children is widely known and used in this respect. In addition, the US