Pesticide exposure Occupational

Pesticides (occupational exposure) Pesticides (occupational exposure)... 

Hawthorne, A., et al. (1987) Models for estimating organic emissions from building materials formaldehyde example. Atmos. Environ. 21, No. 2. Lewis, R. G., et al. (1986) Monitoring for non-occupational exposure to pesticides in indoor and personal respiratory air. Presented at the 79th Annual Meeting of the Air Pollution Control Association, Minneapolis, MN. 

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. 

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. 

Substances hazardous to health include substances labelled as dangerous (i.e. very toxic, toxic, harmful, irritant or corrosive) under any other statutory requirements, agricultural pesticides and other chemicals used on farms, and substances with occupational exposure limits. They include harmful micro-organisms and substantial quantities of dust. Indeed any material, mixture or compound used at work, or arising from work activities, which can harm people s health is apparently covered. 

Pesticides, including insecticides, herbicides, and fungicides, are widely used in agriculture, and the potential for these residues to accumulate in food has led to concern for human safety. Pesticide residues may enter food animals from environmental sources or from treated or contaminated feeds. Immunoassay development for pesticides has had major impacts for pesticide registrations, analysis of residues in foods, monitoring environmental contamination, determination of occupational exposure, and integration of pest management. 

Besides alkylphosphates, OP metabolism gives rise to the production of other metabolites that can be used as exposure markers (Table 4). Unchanged OP compounds in blood or urine can also be measured to confirm exposure (Table 4), but this method is of limited use for routine biological monitoring of occupational exposure, as OP compounds are rapidly excreted in urine. Moreover, most OP pesticides are unstable, and, with a few exceptions, they are not detectable in biological specimens after a few hours. So far, the measurement of unchanged compounds in biological fluids has been performed primarily for research purposes and has limited practical applicability. 

Freed, V.H., Davies, J.E., Peters, L.J., and Parveen, F. (1980) Minimizing occupational exposure to pesticides repellency and penetrability of treated textiles to pesticide sprays, Res. Rev., 75 159-167. 

Franklin, C. (1985) Occupational exposure to pesticides and its role in risk assessment procedures used in Canada, in Dermal Exposure Related to Pesticide Use, Honeycutt, R., Zweig, G., and Ragsdale, N.N., Eds., ACS Symposium Series No. 273, American Chemical Society, Washington, D.C. 

Fenske, R.A. (1990) Nonuniform dermal deposition patterns during occupational exposure to pesticides, Arch. Environ. Contam. Toxicol., 19 332-337. 

Jongen, M.J.M, Engel, R., and Leenheers, L.H. (1991) High performance liquid chromatography method for the determination of occupational exposure to the pesticide abamectin, Am. Ind. Hygiene Assoc. ]., 52 433-437. 

Davis, J.E. (1980) Minimizing occupational exposure to pesticides personal monitoring, Residue Rev., 75 33-50. 

OCCUPATIONAL EXPOSURE 3.1. Occupational Exposure to Multiple Pesticides... 

Exposure Levels in Humans. Metabolism of endrin in humans is relatively rapid compared with other organochlorine pesticides. Thus, levels in human blood and tissue may not be reliable estimates of exposure except after very high occupational exposures or acute poisonings (Runhaar et al. 1985). Endrin was not found in adipose tissue samples of the general U.S. population (Stanley 1986), or in adipose breast tissue from breast cancer patients in the United States (Djordjevic et al. 1994). Endrin has been detected in the milk of lactating women (Alawi et al. 1992 Bordet et al. 1993 Dewailly et al. 1993), but no data from the United States could be located. Data on the concentrations of endrin in breast milk from U.S. women would be useful. No information was found on levels of endrin, endrin aldehyde, or endrin ketone in blood and other tissues of people near hazardous waste sites. This information is necessary for assessing the need to conduct health studies on these populations. 

Hunter J, Maxwell JD, Stewart DA, et al. 1972. Increased hepatic microsomal enzyme activity from occupational exposure to certain organochlorine pesticides. Nature 237 399-401. 

Mirex is no longer manufactured, formulated, or used in the United States. Therefore, there is currently no occupational exposure to this chemical associated with its production or application as a pesticide. Current occupational exposure is most likely to occur for workers employed at waste disposal sites or those engaged in remediation activities including removal of soils and sediments contaminated with mirex. There is a slight possibility of exposure for workers involved in dredging activities (e.g., sediment remediation work performed by the Corps of Engineers). 

Nervous system effects may occur in humans after occupational exposure to disulfoton (Wolfe et al. 1978). In this study, mean disulfoton concentrations of 0.460.633 mg/m caused a 22.8% depression in erythrocyte cholinesterase activity in workers at a pesticide-fertilizer mixing operation. The workers were exposed to disulfoton for 9 weeks, and there were no reports of adverse clinical signs due to disulfoton exposure. The study was limited in that baseline blood cholinesterase activities were obtained 2 weeks after the initial exposure and were compared with cholinesterase activities at 9 weeks. Therefore, the actual depression in cholinesterase activity over a 9-week period was probably >22.8%. In addition, these workers were also dermally exposed to disulfoton (see Section 2.2.3.4) therefore, the 22.8% depression in cholinesterase activity was probably due to both inhalation and dermal exposure. Despite these limitations, the study concluded that because this depression in cholinesterase activity was only associated with dry mixing operations, the wet mixing operations are less hazardous to workers. 

Humans can be exposed to POPs through diet, occupational exposures (for example, farmworkers may be exposed to POPs through pesticides), industrial accidents and the environment (including indoor exposure). Exposure to POPs, either acute or chronic, can be associated with a wide range of adverse health effects, including illness and death (L. Ritter et al., 1995). Laboratory animal studies and wildlife studies have associated POPs with endocrine disruption, reproductive and immune dysfunction, neurobehavioral disorders and cancer. More recently, some POPs have also been connected to reduced immunity in infants and children and a concomitant increase in infections. Other studies have linked POPS concentrations in humans with developmental abnormalities, neurobehavioral impairment and cancer and tumor induction or promotion.4... 

Two fatal cases of occupational exposure to 1,2-dibromoethane were reported by Letz et al. (1984). A worker collapsed shortly after entering a pesticide storage tank containing residues of 1,2-dibromoethane he remained in the tank for 45 minutes. A supervisor attempting to rescue the worker also collapsed and was exposed for 20-30 minutes prior to rescue. Both men died 12 and 64 hours after collapse, respectively. The primary route of exposure was postulated to be dermal, with inhalation also playing a potentially important role. Neither worker had been wearing protective clothing or respirators. 

There is very little information on dermal exposures in either humans or animals. Most occupational exposures to heptachlor and heptachlor epoxide are assumed to be some combination of inhalation and dermal exposure, but there are no data to quantitate the relative contribution of each route. The occupational studies on pesticide workers are discussed in Section 2.2.1. 

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