Dietary exposure

Cohort study data on population dietary exposure, dietary data from case-control studies and food consumption surveys... 

Up to now, the TTC concept has only been developed and used for systemic effects following oral exposure (dietary uptake). For industrial chemicals, the predominant exposure is to workers and consumers via inhalation and/or by skin contact. Toxic endpoints of concern for industrial chemicals such as irritation and sensitization relevant for skin and lung are therefore not covered by the TTC concepts developed up to now. 

Human exposures to lead in the diet historically comprised a major fraction of overall lead exposures in the United States and elsewhere, especially for adults. However, in a number of instances, such as infant consumption of Pb in evaporated milk from lead-seamed cans, many children also sustained significant dietary Pb exposures. Dietary lead intakes, for purposes of this chapter, are separated from drinking beverages prepared from drinking water, but include foods cooked in tap water containing Pb. 

The reported incidence of hypercalcemia in sarcoidosis has varied from 2% to 63% in various series (180). These disparate findings may be attributable to differences in sunlight exposure, dietary calcium, skin color, and genetic factors of the populations studied. ACCESS found that a disorder in calcium metabolism from sarcoidosis was more common in men than women [17/268 (6.3%) versus 10/468 (2.1%), chi-square 7.38, p < 0.01], Caucasians compared to African Americans [20/393 (5.1%) versus 6/325 (1.8%), chi-square 223, p < 0.0001], and those diagnosed >age 40 years compared to <40 years [22/401 (5.5%) versus 5/335 (1.5%), chi-square 7.15, p < 0.01] (2). 

The treatment of sarcoidosis-related hypercalcemia includes (i) reduction of sunlight exposure, dietary calcium, oral calcium supplements, and vitamin D ... 

Eor high value food packaging appHcations, minimal migration of contaminants into food products is critical. Currently the PDA requirement is a maximum 0.5 parts per biUion (ppb) of noncarcinogenic compounds by dietary exposure (22). 

Exposure. The exposure of humans and animals to mercury from the general environment occurs mainly by inhalation and ingestion of terrestrial and aquatic food chain items. Pish generally rank the highest (10—300 ng/g) in food chain concentrations of mercury. Swordfish and pike may frequently exceed 1 p.g/g (27). Most of the mercury in fish is methyl mercury [593-74-8]. Worldwide, the estimated average intake of total dietary mercury is 5—10 p-g/d in Europe, Russia, and Canada, 20 pg/d in the United States, and 40—80 pg/d in Japan (27). 

In this period, the empirical healing of certain diseases by foods was estabUshed. Examples (3) were the treatment of night blindness (vitamin A deficiency) with hver ia many cultures over centuries, of beriberi (vitamin deficiency) by use of unpoHshed rice by the Japanese navy, of scurvy (vitamin C deficiency) by citms fmits ia the British navy or piae needle extracts by North American natives, and pellagra (niacia deficiency) by a dietary shift away from corn-based foods ia many countries. Other, nondietary empirical treatments iavolved, eg, exposure of children ia northern latitudes to sunlight to cute tickets (vitamin D deficiency) (4). 

Anorexia Anorexia is loss of appetite. You may be familiar with the eating disorder, anorexia nervosa, in which the victim restricts dietary intake to starvation levels. Anorexia may be a symptom of acute or chronic exposure to certain chemicals. If you have suffered an unexplained loss of appetite in conjunction with other unusual symptoms, you may want to explore the MSDSs for chemicals that... 

Routine gross and histopathological examinations revealed no treatment-related effects on the respiratory system of dogs exposed to 0.03, 0.1, or 0.3 mg/kg/day methyl parathion in the diet for 1 year (Suba 1981). Chronic dietary exposure to methyl parathion did not induce respiratory effects in mice fed 16.2 mg/kg/day or rats fed 2 mg/kg/day (NCI 1979). 

Some animal studies indicate that dietary exposure to methyl parathion causes decreased humoral and cellular responses (Shtenberg and Dzhunusova 1968 Street and Sharma 1975). A more recent, well-designed animal study that included a battery of immuno/lymphoreticular end points showed few effects at the nonneurotoxic doses tested (Crittenden et al. 1998). No adequate studies are available in humans to assess the immunotoxic potential of methyl parathion. Therefore, studies measuring specific immunologic parameters in occupationally exposed populations are needed to provide useful information. Further studies are also needed to investigate the mechanism for methyl parathion-induced immunotoxicity since this information would help to identify special populations at risk for such effects. 

Berry MR, Johnson LS, Jones JW, et al. 1997. Dietary characterizations in a study of human exposures in the lower Rio Grande Valley I. Foods and beverages. Environ Int 23 675-692. 

Juhler RK, Larsen SB, Meyer O, et al. 1999a. Human semen quality in relation to dietary pesticide exposure and organic diet. Arch Environ Contam Toxicol 37 415-423. 

Melnyk LJ, Berry MR, Sheldon LS. 1997. Dietary exposure from pesticide application on farms in the agricultural health pilot study. J Expo Anal Environ Epidemiol 7 61-80. 

Brock JW, Melynk LJ, Caudill SP, et al. 1998. Serum levels of several organochlorine pesticides in farmers correspond with dietary exposure and local use history. Toxicol Ind Health 14(l/2) 275-289. 

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