Exposure concentrations

However, if air sampling estabHshes that the lead exposure concentration is excessive, engineering controls (such as improved ventilation), adrninistrative controls (such as job rotation), and work practices (such as improved personal hygiene of workers) have to be appHed to comply with the permissible exposure limit (PEL) of the OSHA standard. 

Toxicity. Lethality is the primary ha2ard of phosphine exposure. Phosphine may be fatal if inhaled, swallowed, or absorbed through skin. AH phosphine-related effects seen at sublethal inhalation exposure concentrations are relatively small and completely reversible. The symptoms of sublethal phosphine inhalation exposure include headache, weakness, fatigue, di22iness, and tightness of the chest. Convulsions may be observed prior to death in response to high levels of phosphine inhalation. Some data are given in Table 2. 

Toxicity is the ability to cause biological injuiy. Toxicity is a property of all materials, even salt, sugar, and water. It is related to dose and the degree of hazard associated with a material. The amount of a dose is both time and duration dependent. Dose is a function of exposure (concentration) and duration and is sometimes expressed as dose = (concentration) X duration, where n can vaiy from 1 to 4. 

Toxicity is related to dose and degree of hazard associated with a material. Dose is time- and duration-dependent, in that dose is a function of exposure (concentration) times duration. 

Higher values can be used if standard is based on nuisance or odour and there are no known effects of the maximum exposure concentration measured. 

Health Hazards Information - Recommended Personal Protective Equipment Sel f-contained breathing apparatus for high concentrations of gas Symptoms Following Exposure Concentrations in air greater than 10% cause dizziness in a few minutes. 1 % concentrations give the same symptom in 10 min. High... 

Physical and Chemical Properties - Physical State at 15 C and I atm. Solid Molecular Weight 169.87 Boiling Point at 1 atm. Decomposes Freezing Point 414, 212,485 Critical Temperature Not pertinent Critical Pressure Not pertinent Specific Gravity 4.35 at 19 °C (solid) Veqtor (Gas) Density Not pertinent Ratio of Specific Heats of Vapor (Gas) Not pertinent Latent Heat of Vaporization Not pertinent Heat of Combustion Not pertinent Heat of Decomposition Not pertinent. Health Hazards I ormation - Recommended Persorial Protective Equipment Goggles or face shield rubber gloves Symptoms Following Exposure Concentrated solution will produce irritation, ulceration. 

TI8. Schlesinger, R. B. (1989). Factors affecting the response of lung clearance systems to acid aerosols role of exposure concentration. E.nviron. Health Perspect. 79, 121-126. 

The idea behind OELs is to identify the highest level of exposure concentration and the corresponding reference time period for which we can be confident that there will be no adverse effects on health. However, the concentrations and lengths of exposure at which the presence of airborne chemical agents could damage health have not been clear for many years, and even today there are many questions to be answered. 

The calculations that yield the occupational exposure concentration from the individual analytical values... 

Calculation of the occupational exposure concentration (OEC) depends on the type of OEL. For example, when the limit value has been set as an eight-hour time-weighted average, the cumulative exposure for an eight-hour work shift should be computed as follows ... 

When the limit value is a STEL type, usually based on a 15-minute period, the exposure concentration is... 

Comparison of the results of the occupational exposure concentration with the OEL leads to three different possibilities. 

In this step, the assessor qiuuitifies tlie magnitude, frequency and duration of exposure for each patliway identified in Step 2. Tliis step is most often conducted in two stages estimation of exposure concentrations and calculation of intakes. The later estimation is considered in Step 4. In tliis part of step 3. the exposure assessor determines the concentration of chemicals tliat will be contacted over the exposure period. E.xposure concentrations are estimated using monitoring data and/or chemical transport and environmental fate models. Modeling may be used to estimate future chemical concentrations in media tliat are currently contaminated or tliat may become contaminated, and current concentrations in media and/or at locations for which tliere are no monitoring data. The bulk of the material in tliis chapter is concerned witli tliis step. 

Thus, tlie focus of tliis subsection is on qualitative/semiquantitative approaches tliat can yield useful information to decision-makers for a limited resource investment. There are several categories of uncertainties associated with site risk assessments. One is tlie initial selection of substances used to characterize exposures and risk on tlie basis of the sampling data and available toxicity information. Oilier sources of uncertainty are inlierent in tlie toxicity values for each substance used to characterize risk. Additional micertainties are inlierent in tlie exposure assessment for individual substances and individual exposures. These uncertainties are usually driven by uncertainty in tlie chemical monitoring data and tlie models used to estimate exposure concentrations in tlie absence of monitoring data, but can also be driven by population intake parameters. As described earlier, additional micertainties are incorporated in tlie risk assessment when exposures to several substances across multiple patliways are suimned. 

Very few data are available on the effects of organotins in humans. Of the reported unintentional occupational exposures, none has an estimate of exposure concentration. Exposure was largely via the inhalation route, with some possibility of dermal exposure. Neurological effects were the most commonly reported, and these can persist for long periods. 

One of six workers died 12 days after exposure to a mixture of half dimethyltin dichloride and half trimeth-yltin chloride vapour during cleaning of a cauldron at a chemical plant in Germany in 1981. Maximum exposure time was 1.5 h over a 3-day period no estimates of exposure concentration were made. Symptoms preceding death included excretion of high levels of tin in the urine, respiratory depression, and coma (Rey et al.,... 

Time-Weighted Average (TWA)—An allowable exposure concentration averaged over a normal 8-hour... 

LSE figures graphically illustrate the data presented in the corresponding LSE tables. Figures help the reader quickly compare health effects according to exposure concentrations for particular exposure periods. 

Levels of Exposure concentrations or doses for each health effect in the LSE tables are graphically displayed in the LSE figures. Exposure concentration or dose is measured on the log scale "y" axis. Inhalation exposure is reported in mg/m or ppm and oral exposure is reported in mg/kg/day. 

PBPK/PD models refine our understanding of complex quantitative dose behaviors by helping to delineate and characterize the relationships between (1) the external/exposure concentration and target tissue dose of the toxic moiety, and (2) the target tissue dose and observed responses (Andersen et al. 1987 Andersen and Krishnan 1994). These models are biologically and mechanistically based and can be used to extrapolate the pharmacokinetic behavior of chemical substances from high to low dose, from route to route, between species, and between subpopulations within a species. The biological basis of... 

Although the likelihood for biologically harm has not been assessed fully, for most EDCs the exposure concentrations in ambient environments (away from hotspots of chemical discharges) would suggest that they are insufficient to do so. Exceptions to this inclnde the case studies detailed in the previous section. It should, however, also be emphasized that most studies on the effects of EDCs under controlled laboratory conditions have not considered long-term chronic exposures encompassing full life cycles, and some wildlife species are exposed lifelong to some of the EDCs described earlier. 

A study that examined the interaction between exposure concentration and time of exposure on nervous system function found that concentration, rather than time of exposure, was more important in determining effects (Bushnell 1997). Rats were trained to press two levers for food reward one lever when a light flashed, the second lever produced food when there was no signal. The trained rats were exposed to 0,400, 800, 1,200, 1,600,2,000, or 2,400 ppm trichloroethylene for 0.33, 0.67, or 1 hour. Response times were signiflcantly increased only at 2,400 ppm at 0.67 and 1 hour. Sensitivity was significantly decreased at 2,400 ppm at all exposure times. At 0.33 hour, sensitivity was not affected at the other concentrations. At 0.67 hour, sensitivity was significantly decreased at 2,000, and 1,200 ppm, and at 1 hour, sensitivity was... 

An update of a previous study (Axelson et al. 1978), Axelson (1986) evaluated an expanded cohort of 1,424 men (levels of trichloroethylene exposure inferred from measured urinary metabolite concentrations) and found a significant increase in incidences of bladder cancer and lymphomas, and a lower than expected incidence of total cancer mortality. A further update of this work (Axelson et al. 1994) expanded the cohort to include 249 women, tracking cancer morbidity over 30 years, and found no correlation between exposure concentration or exposure time and cancer incidence at any site. The highest standardized incidence ratio noted in this study was 1.56 (95% Cl of 0.51-3.64) for 5 cases of non-Hodgkin s lymphoma observed in men. Although four of these cases occurred in persons exposed for at least 2 years, and 3 cases had a latency of 10 years or more, urinary levels of TCA showed that 4 of the 5 cases were exposed to the lowest levels of trichloroethylene (urinary levels of TCA 0-49 mg/L). The study authors mentioned that a urinary TCA level below 50 mg/L corresponds to a trichloroethylene exposure concentration of about 20 ppm. The study authors concluded that "this study provides no evidence that trichloroethylene is a human carcinogen, i.e., when the exposure is as low as for this study population."... 

Additional studies of the Woburn population have been completed (MDPH 1994). The final report indicated that there was an increased prevalence in choanal atresia, a rare respiratory effect, and hypospadias/congenital chordee. A small increase in eye defects was observed, but there was no association between TCE exposure and heart defects. There was no statistically significant associations between exposure concentrations and birth defects, although analyses was limited by the small number of cases observed. Based on four cases in the Woburn population, a rate of 0.88 was observed in the exposed population, compared to rates of 0.11 and 0.13 in the Atlanta and California comparison populations, respectively. In a prospective study completed after well closure, the rate of choanal atresia was 0.88 (based on 1 case) in Woburn, 0.11 in the surrounding communities, and 0.2 and 0.13 in Atlanta and California, respectively. The study authors cautioned that their study did not rule out moderate increases in rates of the less common adverse reproductive outcomes. For these outcomes only large increases would have been detected. 

---