Human exposure manufacturing workers

Sources of human exposure to formaldehyde are engine exhaust, tobacco smoke, natural gas, fossil fuels, waste incineration, and oil refineries (129). It is found as a natural component in fmits, vegetables, meats, and fish and is a normal body metaboHte (130,131). FaciUties that manufacture or consume formaldehyde must control workers exposure in accordance with the following workplace exposure limits in ppm action level, 0.5 TWA, 0.75 STEL, 2 (132). In other environments such as residences, offices, and schools, levels may reach 0.1 ppm HCHO due to use of particle board and urea—formaldehyde foam insulation in constmction. 

There are no epidemiological or case reports of mirex-exposed individuals. The literature reviewed for the health effects of chlordecone in humans came from reports of one occupational cohort of workers exposed to chlordecone in a manufacturing plant. This exposure was classified as intermediate-to-chronic no precise duration or level of exposure to chlordecone could be quantified from these reports. A single route of exposure could not be established for this worker population poor hygiene in the plant made inhalation, oral, and dermal exposure routes likely to occur. The information on human exposure in this study is extremely limited because of the possible contamination with the precursor used to manufacture chlordecone, hexachloropentadiene. Therefore, information on human exposure to both mirex and chlordecone is limited. 

In contrast to animal studies, epidemiological studies of workers employed in the manufacture of aldrin provide no conclusive evidence of carcinogenicity in humans. " One study of a cohort having mixed exposure to aldrin, dieldrin, and endrin found 9 deaths from cancer versus 12 expected. The workers had been exposed to the pesticides for a mean of 11 years and followed a mean of 24 years. A more recent examination of 2384 manufacturing workers, employed between 1952 and 1982, with exposure to a number of pesticides including aldrin found no excess mortality rates attributable to occupational exposures. Similarly, a 2 3-year follow-up of 570 aldrin- and dieldrin-exposed workers found no increase in overall mortality rates or mortality from liver cancer."... 

Epidemiological studies examining cancer mortality in workers exposed to dieldrin showed no conclusive evidence of carcinogenicity in humans. A study of 870 men employed in the manufacture of aldrin, dieldrin, and endrin found no increase in mortality from all cancers there were apparent increases in mortality from cancers of the esophagus, rectum, and liver based on very small numbers. In another report, follow-up of 232 workers with similar exposures revealed 9 cancer deaths with 12 expected. Updated epidemiological studies of manufacturing workers have confirmed the earlier findings. A cohort... 

Worldwide production of chemicals has increased dramatically in recent decades, resulting in increased human exposure. This applies not only to workers who manufacture the chemicals and final products but also to those who use the products or are exposed through contamination of surface and ground water and air. 

The isocyanate-ketoxime is usually made in situ during the manufacture of the isocyanate, thereby minimizing environmental and worker exposure to the isocyanate. In ketoxime form, the isocyanate is no longer electrophilic and, therefore, not reactive. When ready to be used in coatings, the ketoxime moiety is removed thermally during application, thereby regenerating the isocyanate and enabling it to react with the intended nucleophile (usually an amine) without the risk of human exposure. 

Cardiovascular Effects. Information regarding cardiovascular effects in humans after inhalation exposure to chromium and its compounds is limited. In a survey of a facility engaged in chromate production in Italy, where exposure concentrations were 0.01 mg chromium(VI)/m3, electrocardiograms were recorded for 22 of the 65 workers who worked in the production of dichromate and chromium trioxide for at least 1 year. No abnormalities were found (Sassi 1956). An extensive survey to determine the health status of chromate workers in seven U.S. chromate production plants found no association between heart disease or effects on blood pressure and exposure to chromates. Various manufacturing processes in the plants resulted in exposure of workers to chromite ore (mean time-weighted concentration of 0-0.89 mg chromium(ni)/m3) water-soluble chromium(VI) compounds (0.005-0.17 mg chromium(VI)/m3) and acid-soluble/water-insoluble chromium compounds (including basic chromium sulfate), which may or may not entirely represent trivalent chromium (0-0.47 mg chromium/m3) (PHS 1953). No excess deaths were observed from cardiovascular diseases and ischemic heart disease in a cohort of 4,227 stainless steel production workers from 1968 to 1984 when compared to expected deaths based on national rates and matched for age, sex, and calender time (Moulin et al. 1993). No measurements of exposure were provided. In a cohort of 3,408 individuals who had worked in 4 facilities that produced chromium compounds from chromite ore in northern New Jersey sometime between 1937 and 1971, where the exposure durations of workers ranged from <1 to >20 years, and no increases in atherosclerotic heart disease were evident (Rosenman and Stanbury 1996). The proportionate mortality ratios for white and black men were 97 (confidence limits 88-107) and 90 (confidence limits 72-111), respectively. 

The most probable routes of human exposure to BPA are inhalation and dermal contact of workers involved in the manufacture, use, transport or packaging of this compound. Potential exposure to BPA can also be expected through oral intake, since BPA is... 

The most probable routes of human exposure to EDTA would be ingestion and dermal contact. Workers involved in the manufacture or use of EDTA may be exposed by inhalation and dermal contact. In chelation therapy, EDTA is administered via intravenous infusion. 

Limited epidemiology data exist for exposure to ethyl acrylate. Mortality from cancer of the colon and rectum was elevated in workers from plants manufacturing and polymerizing ethyl acrylate however, the findings were confounded by coexposure to other chemicals. Currently, there is inadequate evidence to link human exposures to ethyl acrylate with cancer. 

Thiram is a broad-spectrum fungicide and is found in most home-garden formulations whereby day-to-day human exposure can occur. Its use in various industries leads to multiple avenues for occupational exposures. The highest exposures occur in workers utilizing and/or manufacturing this compound. Exposure to thiram can occur via inhalation, ingestion, and eye or skin contact. 

To characterize the potential for human exposure and environmental release, the PMN submitter must describe occupational exposure, including the estimated number of workers exposed to the substance, the activities during which they would be exposed, and any protective equipment or engineering controls that would reduce exposure. Estimates of environmental release and exposme must include estimates of releases to air, surface water, land, incineration, or other media. The PMN form also requests optional pollution prevention information. The submitter may provide information on how the proposed manufacturing process or use of the new chemical substance contributes to source reduction, recycling achvities, and safer products or processes. The US EPA takes this informahon into account when assessing potential risks. 

There are no controlled, repeat dose studies in humans, but the exposure of workers to low doses of SM during its manufacture demonstrates that repeated exposures can produce serious long term toxic effects. 

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