Inhalation chemical exposures

Refer to the handbook s Glossary. The definitions provided are universally recognized. Many of these terms are not just pertinent to inhalation hazards. It would be remiss not to mention other risks beyond inhalation from chemical exposure in a work environment and to the general public. 

Inhaled gaseous compounds are absorbed in all parts of the respiratory system whereas particle size determines how deep into the airways the parti cles will he transported in the airstrearn. Shortness of breath is a typical sign of a chemical exposure that has affected the lungs, and it may be evoked through iminunological mechanisms (e.g., formaldehyde, ethyleneoxide), or through toxic irritation (formaldehyde, isocyanates, sulfur dioxide, nitrogen dioxide, Frequently the mechanism depends on the concentration ol the com... 

Symptoms of exposure Effects of exposure caused by inhalation of gases, ingestion of liquids or solids, contact with eyes or skin are provided. This information should only be used as a guide to identify potential effects of exposure. If exposure to a chemical is suspected or known, seek immediate medical attention. Additional information on the symptoms and effects of chemical exposure can be obtained from Patnaik (1992), Sax and Lewis (1987) and CHRIS (1984). 

As discussed in Section 2.2.1, most human exposure to 1,4-dichlorobenzene results from inhalation of vapors due to home use of mothballs and deodorizer blocks that contain this chemical. Exposure resulting from all other sources, including proximity to hazardous waste sites, is considered to be low. 

Hexanone has also been shown to potentiate the neurotoxic effects of some compounds. In hens, dermal or inhalation exposure to 2-hexanone in combination with dermal application of the pesticide O-ethyl-O-4-nitrophenyl phenylphosphonothioate (EPN) has resulted in earlier onset and far more severe clinical and histological manifestations of neurotoxic effects than with either chemical exposure alone (Abou-Donia et al. 1985a, 1985b). The authors speculated that this potentiation effect may have been due to induction of hepatic microsomal cytochrome P-450 by EPN, leading to increased metabolism of 2-hexanone to its neurotoxic metabolite, 2,5-hexanedione. An alternate explanation is that local trauma to the nervous tissue produced by 2-hexanone and EPN might increase vascular permeability and thus increase the entry of these compounds and their metabolites from circulation. 

The popular movie Erin Brockovich, although focusing on the power industry, is an example of how the popular media can simplify the public s perception of chemical exposure. In Erin Brockovich the chemical of concern was hexavalent chromium, Cr +. Hexavalent chromium is listed as a carcinogen by EPA, but complicated questions dealing with exposure (drinking, inhalation, absorption through skin), toxicity levels, and specific health effects were lost in Hollywood s version. 

Polybrominated Biphenyls. Hypothyroidism was diagnosed in 4 of 35 men who were occupationally exposed to unspecified PBBs and/or decaBDE (Bahn et al. 1980). The cohort consisted of workers (mean age 35.9 years) who had been employed at a production plant for at least 6 weeks during a 52-month period during which PBBs and decaBDE were the only chemicals manufactured and who had volunteered for a comprehensive medical evaluation performed 3 months after the end of the 52-month period. There was no further description of exposure, and it was assumed to have occurred by both inhalation and dermal routes. As detailed in Section 3.2.1.2, the results of this study suggest that occupational exposure to PBBs, decaBDE, and/or bromine affected the thyroid, but the mixed chemical exposure and a lack of data on serum or tissue levels of the chemicals preclude attributing effects solely to any particular congener or mixture of congeners. 

This is the process by which the chemical concentration in an aquatic organism achieves a level that exceeds that in the water, as a result of chemical uptake through all possible routes of chemical exposure (e.g., dietary absorption, transport across the respiratory surface, dermal absorption, inhalation). 

Finding chemicals in bodily fluids is evidence of contact with them through inhalation, dermal exposure, or ingestion, and it typically leads to two questions that pose important challenges in interpreting biomonitoring results and are the focus of this chapter ... 

Occupational exposure to chemical substances almost invariably involves multiple chemicals. That situation may result in PK interactions, which may affect the relationship between the atmospheric concentration of the parent chemical and the associated biomarker concentration (Viau 2002). For example, such an interaction is known to occur between ethylbenzene and the xylene isomers (Jang et al. 2001). Commercial xylene contains about 20% ethylbenzene, which modifies the slope of the relationship between urinary methylhippuric acid (MHA) and airborne xylene concentrations. That kind of interaction is unlikely at the subparts-per-million exposure concentrations seen in the general population. But because the BEI for MHA was obtained from the relationship observed after exposure to commercial xylene, thereby taking the interaction into account, the slope of the relationship cannot be extrapolated to the subparts-per-million range. Similar PK interactions have been observed for other mixtures but only at concentrations nearing or exceeding the occupational exposure limits (Viau 2002), so it would be a priori reasonable to consider extrapolation of the relationship between biomarker concentrations and those of their parent chemicals. For example, Tardif et al. (1991) demonstrated that, provided inhalation exposure to a mixture of toluene and xylene was kept below their airborne occupational exposure limits, there were no PK interactions between the compounds that affected the linear relationship between airborne parent-chemical exposure and urinary-metabolite concentrations. However, such an interaction was apparent at higher concentrations. 

Regarding styrene, the variety of controlled human oral and inhalation studies that relate dose to urinary concentration and the existence of a pharmacokinetic model (Droz and Guillemin 1983) could facilitate interpretation of mandelic acid concentration in urine. A caveat in this regard is that other chemical exposures can produce mandelic acid in urine, such as ethyl benzene, acetophenone, and phenylglycine (ACGIH 1991). Those background sources would be more likely to confound low-level general-population biomarker results than workplace end-of-shift results. 

The Dow Fire and Explosion Index (FEI) (12) and the Dow Chemical Exposure Index (CEI) (14) are two commonly used tools that measure inherent safety characteristics. Gowland (25) reports on the use of the FEI and CEI in the development of safety improvements for a urethane plant. Tables 1 and 2 illustrate the application of the FEI and CEI in measuring inherent safety characteristics of process design options. These indices measure the inherent safety characteristics of processes in only two specific areas—fire and explosion hazards and acute chemical inhalation toxicity hazards. Other indices would be required to evaluate other types of hazards. 

For evaluating the toxic characteristics of an inhalable material (e.g., gas, volatile chemical, or aerosol/particulate material), animals are subjected to repeated exposures after initial information on material toxicity has been obtained by acute testing. It provides information on health hazards likely to arise from repeated exposure via the inhalation route over a limited period of time. Hazards of inhaled chemicals are influenced by inherent toxicity and physical factors, such as volatility and particulate size. 

Toxic effects of chemicals can range from mild and reversible (e.g., headache from inhaling petroleum naphtha vapors that disappears with fresh air) to serious and irreversible (e.g., liver or kidney damage from excessive exposures to chlorinated solvents). Toxic effects from chemical exposure depend on the severity of the exposures. Greater exposure and repeated exposure generally lead to more severe effects. 

Inhalation and direct skin contact are the most common routes of chemical exposure. The greatest exposure risk in handling potent compounds in an analytical laboratory therefore occurs when handling solid materials due to the potential to generate and inhale airborne dust particles of the compound. Once the potent material has been placed into solution, the airborne exposure risk is reduced and solutions of potent compounds may be handled in a manner similar to other nonpotent pharmaceutical compounds, assuming good laboratory practices are followed. Caution should be taken not to aerosolize the solutions since this could create an inhalation hazard. In addition, any sample solution spills should be adequately cleaned to prevent powder deposits of the compound from forming, which could potentially become airborne after the liquid has dried. 

Smoking is the main risk factor (about 1 in 4 smokers who smoke 40 cigarettes per day develop COPD if they continue to smoke) non-smokers very rarely suffer from COPD. Other environmental factors include exposure to occupational dusts, inhaled chemicals and air pollution. Some rare genetic conditions are risk... 

This chapter describes and illustrates probabilistic approaches to aggregate and cumulative assessments of exposure, dose and risk. Aggregate assessments account for multiple sources (e.g. food, water, residence and occupation) and multiple routes (ingestion, dermal and inhalation) of exposure for a single pesticide. Cumulative assessments combine exposures for chemicals that share a... 

The NAC/AEGL Committee estimates the range in variability of response to specific chemical exposures primarily on the basis of quantitative human data. Acceptable experimental data are more likely to be available for AEGL-1 and AEGL-2 endpoints than for AEGL-3 endpoints. For example, numerous studies have considered induction of bronchospasm after controlled exposmes to sulfur dioxide (SO2) in asthmatic and nonasthmatic individuals (see references below). There is marked individual variability in the severity of reaction to inhalation of low concentrations of SO2. Asthmatics, individuals with hyper-reactive airways, smokers, and those with chronic respiratory or cardiac disease respond at relatively lower concentrations (Aleksieva 1983 Simon 1986). Susceptibility may also be increased in people over 60 years of age, but reports have not been consistent (Rondinelli et al. 1987 Koenig et al. 1993). By contrast, comparable human data for AEGL-3 tier concentrations are limited to anecdotal case reports. 

The highest NOAEL values and all reliable LOAEL values in each species and duration category for systemic effects from chemical exposure to uranium by the inhalation route are presented in Table 2-1 and plotted in Figure 2-1. The radiation effect level values in each species and duration category for systemic effects from radiation exposure to uranium by the inhalation route are presented in Table 2-2 and plotted in Figure 2-2. 

Most BEIs are defined as concentrations of determinants or biomarkers anticipated in biological specimens collected from healthy workers whose exposure to certain chemicals by all routes is equivalent to that of workers with inhalation only exposure at the OEL. Others measure reversible effects on the body, and still others are those that are below the concentrations associated with health effects. However, other definitions are common. For example, the German biological tolerance values (BAT) can be defined as rates of excretion of the chemical or its metabolites, or the maximum possible deviation from the norm of biological parameters induced by these substances in exposed humans. BEIs for some chemicals use other criteria, such as direct comparison with a measurable toxic effect, like carboxyhemoglobin in blood for carbon monoxide. 

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