Exposure, occupational routes

As PCB production increased, more concerns were raised about the health and environmental effects of PCBs, which entered the environment through leakage, production processes, and improper disposal. The persistence and lipophilicity of PCBs resulted in its biomagnification in the environment (see DDT). Problems associated with PCB contamination in wildlife include deformities, tumors, disruption in the endocrine and reproduction systems, and death. Human exposure to PCBs occurs through environmental and occupational routes. The primary exposure... 

No quantitative data were located regarding absorption of CDDs in humans following inhalation exposure. However, based on data from studies with structurally related chemicals it is reasonable to assume that CDDs are absorbed by this route. Furthermore, data on levels of CDDs in blood from populations with above-background exposures (occupational, accidental) also suggest that transpulmonary absorption occurs in humans see Section 2.1 for more information. 

Dermal contact and inhalation are primary routes of exposure. Occupational exposure to TBHP may occur through these routes at workplaces. 

Inhalation, ingestion and dermal contact are all possible routes of exposure. Occupational exposure can occur during the use of carbamates produced from MIC. Small amounts of MIC are found in cigarette smoke. 

Humans may be exposed to DIDP by die oral, dermal, and inhalation routes of exposure. Occupational exposure occurs primarily through inhalation and dermal contact, while consumer exposure occurs primarily through oral and dermal routes. Exposure of children to DIDP through children s products is a public concern. 

Intermediate-Duration Exposure. Occupational exposure to 2,4-DNP resulted in death from pyrexia in some cases, and fatigue, elevation of body temperature, increased respiratory rate, profuse perspiration, and weight loss in some of the workers (Gisclard and Woodward 1946 Perkins 1919). Exposure occurred by the inhalation and also probably by the dermal route. Gastrointestinal symptoms (nausea, vomiting) were also noted (Perkins 1919). Autopsy of the fatal cases did not reveal any characteristic lesions, other than pulmonary edema, which was thought to be secondary to vasomotor effects. Hence many of the effects of 2,4-DNP in humans do not appear to be route-specific. No exposure levels were reported in these studies. 

For the general population, exposure to RDX is limited to areas around Army ammunition plants where it is manufactured, converted to munitions, packed, loaded, or released through the demilitarization of antiquated munitions. The most likely route of exposure is ingestion of contaminated drinking water. Inhalation exposure of contaminated particulate matter produced during incineration of RDX-containing waste material is also a possible route of exposure. Occupational exposure to RDX can occur when workers handle RDX at Army ammunition plants. According to the National Occupational Exposure Survey (NOES) of 1981-1983 conducted by NIOSH, the estimated number of workers potentially exposed to RDX in the United States was 488 (NOES 1990). 

EXPOSURE ROUTES air emissions aqueous effluent and solid waste products from manufacturing and processing plants incineration of DEP containing plastics ingestion of food inhalation and dermal exposure occupational exposure... 

Care must be exercised in handling carbon disulfide because of both health concerns and the danger of fire or explosions. Occupational exposure potentially may involve as many as 20,000 workers in the United States (136). Ingestion is rare, but a 10 mL dose can prove fatal (137). Contact usually occurs by inhalation of vapor. However, vapor and Hquid can be absorbed through intact skin and poisoning may occur by the dermal route (138). 

Human Health Effects. Any assessment of adverse human health effects from PCBs should consider the route(s) of and duration of exposure the composition of the commercial PCB products, ie, degree of chlorination and the levels of potentially toxic PCDF contaminants. As a result of these variables, it would not be surprising to observe significant differences in the effects of PCBs on different groups of occupationally-exposed workers. 

The toxicity of a substance is its capacity to cause injury once inside the body. The main modes of entry into the body by chemicals in industry are inhalation, ingestion and absorption through the skin. Gases, vapours, mists, dusts, fumes and aerosols can be inhaled and they can also affect the skin, eyes and mucous membranes. Ingestion is rare although possible as a result of poor personal hygiene, subconscious hand-to-mouth contact, or accidents. The skin can be affected directly by contact with the chemicals, even when intact, but its permeability to certain substances also offers a route into the body. Chemicals accorded a skin notation in the list of Occupational Exposure Limits (see Table 5.12) are listed in Table 5.2. Exposure may also arise via skin lesions. 

Skin is also important as an occupational exposure route. Lipid-soluble solvents often penetrate the skin, especially as a liquid. Not only solvents, but also many pesticides are, in fact, preferentially absorbed into the body through the skin. The ease of penetration depends on the molecular size of the compound, and the characteristics of the skin, in addition to the lipid solubility and polarity of the compounds. Absorption of chemicals is especially effective in such areas of the skin as the face and scrotum. Even though solid materials do not usually readily penetrate the skin, there are exceptions (e.g., benzo(Lt)pyrene and chlorophenols) to this rule. 

As stated earlier, inhalation is the main route of absorption for occupational exposure to chemicals. Absorption of gaseous substances depends on solubility ifi blood and tissues (as presented in Sections 2.3.3-2.3.5), blood flow, and pulmonary ventilation. Particle size has an important influence on the absorption of aerosols (see Sections 2.3.7 and 3.1.1). 

Polycyclic aromatic hydrocarbons have been classified as human carcinogens because they induce cancers in experimental animals and because smoking and exposure to mixtures of chemicals containing polycyclic aromatic hydrocarbons in the workplace increase the risk of lung cancer in exposed individuals. In experimental animals, benzo(a)pyrene induces cancer in different organs depending on the route of administration.Furthermore, exposure to polycyclic aromatic hydrocarbons commonly occurs in occupations related to traffic (use of diesel engines in transportation and railways). 

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. 

In a case-control study of pesticide factory workers in Brazil exposed to methyl parathion and formulating solvents, the incidence of chromosomal aberrations in lymphocytes was investigated (De Cassia Stocco et al. 1982). Though dichlorodiphenyltrichloroethane (DDT) was coformulated with methyl parathion, blood DDT levels in the methyl parathion-examined workers and "nonexposed" workers were not significantly different. These workers were presumably exposed to methyl parathion via both inhalation and dermal routes however, a dose level was not reported. The exposed workers showed blood cholinesterase depressions between 50 and 75%. However, the baseline blood cholinesterase levels in nonexposed workers were not reported. No increases in the percentage of lymphocytes with chromosome breaks were found in 15 of these workers who were exposed to methyl parathion from 1 week to up to 7 years as compared with controls. The controls consisted of 13 men who had not been occupationally exposed to any chemical and were of comparable age and socioeconomic level. This study is limited because of concomitant exposure to formulating solvents, the recent history of exposure for the workers was not reported, the selection of the control group was not described adequately, and the sample size was limited. 

Figure 3-5 graphically depicts the information that currently exists on the health effects of methyl parathion in humans and animals by various routes of exposure. The available literature reviewed concerning the health effects of methyl parathion in humans described case reports of longer-term studies of pesticide workers and case reports of accidental or intentional ingestion of methyl parathion. The occupational exposure is believed to be via the dermal and inhalation routes. The information on human exposure is limited in that the possibility of concurrent exposure to other pesticides or other toxic substances cannot be quantified. 

There are insufficient data to determine potential daily inhalation and dermal exposure levels. However, based on the information presented in Seetions 6.3 and 6.4, exposure levels for the general population are probably very low by these routes. Inhalation exposure is not important for the general population, with the possible exception of those individuals living near areas where methyl parathion is frequently sprayed. Since methyl parathion is readily adsorbed through the skin, dermal eontact may be the most relevant exposure pathway. Dermal eontaet is most likely to oeeur in people who are occupationally exposed. 

Where sufficient toxicologic information is available, we have derived minimal risk levels (MRLs) for inhalation and oral routes of entry at each duration of exposure (acute, intermediate, and chronic). These MRLs are not meant to support regulatory action but to acquaint health professionals with exposure levels at which adverse health effects are not expected to occur in humans. They should help physicians and public health officials determine the safety of a community living near a chemical emission, given the concentration of a contaminant in air or the estimated daily dose in water. MRLs are based largely on toxicological studies in animals and on reports of human occupational exposure. 

Information is available regarding excretion of endosulfan and metabolites in humans. Blanco-Coronado et al. (1992) measured total endosulfan in the urine of poisoned individuals shortly after poisoning occurred. However, it could not be ascertained whether the urine was a major or minor excretion route. a-Endosulfan, P-endosulfan, and/or metabolites were present in the urine of humans after intentional oral exposure (Boerebomm et al. 1998) and after occupational exposure either with (Arrebola et al. 1999) or without (Vidal et al. 1998) protective clothing. 

In occupational settings, exposure to endosulfan is mainly via the dermal and inhalation routes. Although workers involved in the manufacture and formulation of pesticide products containing endosulfan are potentially exposed to high concentrations of the compound, actual exposure is probably limited by the use of engineering controls and personal protection equipment. The highest documented dermal and inhalation exposures have been reported for agricultural workers involved in the spray... 

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