Pesticide occupational

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

Leng G, Lewalter J. 1999. Role of individual susceptibility in risk assessment of pesticides. Occup Environ Med 56 449-453. 

Zahm, S. etal. Pestiddes and Cancer. InKeffer, M. (ed.) Human Health Effects of Pesticides. Occupational Medicine State of the Art Reviews. Vol 12. No 2 (1997)... 

Beach, J.R., Spurgeon, A., Stephens, R. (1996). Ahnormalities on neurological examination among sheep farmers exposed to organophosphorus pesticides. Occup. Environ. Med. 53 520-6. 

Farahat, T.M., Abdefrasoul, G.M., Atnr, M.M., Shebl, M.M., Fareahat, F.M. and Anger, W.K. 2004. Neurobebavioral effects among workers occupationally exposed to organophosphorous pesticides. Occup. Environ. Med., 60 279-286. 

Beach JR, Spurgeon A, Stephens R, et al Abnormalities on neurological examination among sheep farmers exposed to organophosphorous pesticides. Occup Environ Med 53 520-525, 1996... 

Wesseling, C, van Wendel de Joode, B., Keifer, M., et al., 2010. Symptoms of psychological distress and suicidal ideation among banana workers with a history of poisoning by organophosphate or n-methyl carbamate pesticides. Occup. Environ. Med. 67, 778-784. 

C. Solomon, J. Poole, K. T. Palmer, R. Peveler and D. Coggon, Neuropsychiatric symptoms in past users of sheep dips and other pesticides, Occup. Environ. Med., 2001, 64, 259-266. 

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. 

Compounds Affecting Rq>roduction Compounds that can affect reproductive function include several drugs and occupationally important chemicals such as solvents and pesticides as well as a number of environmentally relevant com-fxrunds. A group of chemical compounds that has received much attention recently is endocrine disrupters, many of which are halogenated hydrocarbons, e.g., PCBs. These are known to induce feminization in fish and other animal species.1.5/ There is intense debate about the significance of these compounds to human health. Tobacco smoke and ethyl alcohol also have major effects on human reproduction, the effects of alcohol being especially important. Table 5.17 lists compounds that may disturb the functions of female and male reproductive functions. 

Hazard identification, step one, means identification of new chemicals or other factors that may cause harmful health effects. Previously, novel hazards were usually observed in case studies or after accidents or other excessive exposures, usually in occupational environments. Today, thorough toxicity studies are required on all pesticides, food additives, and drugs. New chemicals also have to be studied for their potential toxic effects. Thus, earlier hazards were in most cases identified after they had caused harmful effects in humans. Today, most chemical products have been evaluated for their toxicity with experimental animals. Therefore, hazard identification has become a preventive procedure based on safety studies conducted before a chemical compound or product reaches the market, and before individuals are exposed to it. ... 

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. 

Samples of the indoor and outdoor air at the homes of workers occupationally exposed to pesticides, farmers and pesticide formulators, were taken monthly and analyzed for methyl parathion. Methyl parathion was found in 13 of 52 indoor air samples of formulators homes at a mean concentration of 0.26 pg/m (range of 0.04-9.4 pg/m ). Outdoor air samples of formulators homes showed that 3 of 53 samples contained methyl parathion at concentrations ranging from 0.15 to 0.71 pg/m. Methyl parathion was not detected in the indoor and outdoor air samples from farmers homes (Tessari and Spencer 1971). 

Bason CW, Colbom T. 1998. U.S. application and distribution of pesticides and industrial chemicals capable of disrupting endocrine and immune systems. J Clean Technol Environ Toxicol Occup Med 7 147-156. 

Davies JE, Peterson JC. 1997. Surveillance of occupational, accidental, and incidental exposure to organophosphate pesticides using urine alkyl phosphate and phenolic metabolite measurements. Aim NY Acad Sci 837 257-268. 

De Vreede JAF, Brouwer DH, Stevenson H, et al. 1998. Exposure and risk estimation for pesticides in high-volume spraying. Ann Occup Hyg 42 151-157. 

He F. 1993. Biological monitoring of occupational pesticides exposure. Int Arch Occup Environ Health 93 S69-S76. 

Laurent C, Jadot P, Chabut C. 1996. Unexpected decrease in cytogenetic biomarkers frequencies observed after increased exposure to organophosphorus pesticides in a production plant. Int Arch Occup Environ Health 68 399-404. 

Sever EE, Arbuckle TE, Sweeney A. 1997. Reproductive and developmental effects of occupational pesticide exposure The epidemiologic evidence. Occup Med 12 305-325. 

Willis WO, de Peyster A, Molgaard CA, et al. 1993. Pregnancy outcome among women exposed to pesticides through work or residence in an agricultural area. J Occup Med 35 943-949. 

Wilson BW, Sanborn JR, OMalley MA, et al. 1997. Monitoring the pesticide-exposed worker. Occup Med 12 347-363. 

Zahm SH, Ward MH, Blair A. 1997. Pesticides and cancer. Occup Med 12 269-289. 

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