a b s t r a c tInhaled aerosol dose models play critical roles in medicine, the regulation of air pollutants and basic research. The models fall into several categories: traditional, computational fluid dynamical (CFD), physiologically based pharmacokinetic (PBPK), empirical, semi-empirical, and "reference". Each type of model has its strengths and weaknesses, so multiple models are commonly used for practical applications. Aerosol dose models combine information on aerosol behavior and the anatomy and physiology of exposed human and laboratory animal subjects. Similar models are used for in-vitro studies. Several notable advances have been made in aerosol dose modeling in the past 80 years. The pioneers include Walter Findeisen, who in 1935 published the first traditional model and established the structure of modern models. His model combined aerosol behavior with simplified respiratory tract structures. Ewald Weibel established morphometric techniques for the lung in 1963 that are still used to develop data for modeling today. Advances in scanning techniques have similarly contributed to the knowledge of respiratory tract structure and its use in aerosol dose modeling. Several scientists and research groups have developed and advanced traditional, CFD, and PBPK models. Current issues under study include understanding individual and species differences; examining localized particle deposition; modeling non-ideal aerosols and nanoparticle behavior; linking the regions of the respiratory tract airways from nasal-oral to alveolar; and developing sophisticated supporting software. Although a complete history of inhaled aerosol dose modeling is far too extensive to cover here, selected highlights are described in this paper.

Exposure to methyl mercury, a risk factor for neurodevelopmental toxicity, was assessed in U.S. Hair mercury levels were associated with age and fish consumption frequency.

The US Food and Drug Administration (FDA) has conducted the Total Diet Study (TDS) since 1961, which designed to monitor the US food supply for chemical contaminants, nutritional elements, and toxic elements. Recently, perchlorate was analyzed in TDS samples. Perchlorate is used as an oxidizing agent in rocket propellant, is found in other items (e.g., explosives, road flares, fireworks, and car airbags), occurs naturally in some fertilizers, and may be generated under certain climatic conditions. It has been detected in surface and groundwater and in food. Perchlorate at high (e.g., pharmacological) doses can interfere with iodide uptake into the thyroid gland, disrupting its function. The National Academy of Sciences (NAS) has identified that ''the fetuses of pregnant women who might have hypothyroidism or iodide deficiency as the most sensitive population.'' This study reports on intake estimates of perchlorate and iodine, a precursor to iodide, using the analytical results from the TDS. Estimated average perchlorate and iodine daily intakes as well as the contribution of specific food groups to total intakes were estimated for 14 age/sex subgroups of the US population. The estimated smallest lower bound to the largest upper bound average perchlorate intakes by the 14 age/sex groups range from 0.08 to 0.39 micrograms per kilogram body weight per day (mg/kg bw/day), compared with the US Environmental Protection Agency (EPA) reference dose (RfD) of 0.7 mg/kg bw/day. Infants and children demonstrated the highest estimated intakes of perchlorate on a body weight basis. The estimated average iodine intakes by the 14 age/sex groups reveal a lower bound (ND ¼ 0) and upper bound (ND ¼ LOD) range of average intakes from 138 to 353 mg/person/day. Estimated iodine intakes by infants 6-11 months exceed their adequate intake (AI), and intakes by children and adult age/sex groups exceed their relevant estimated average requirement (EAR).

ERCURY IS WIDESPREAD IN the environment, originating from both natural a n d a n t h r o p o g e n i c sources. [1][2][3] The general population may be exposed to 3 forms of mercury: elemental, inorganic, or organic (predominantly methyl). Elemental and inorganic mercury exposure can result from mercury spills, dental amalgams, exposure at the workplace, environmental exposure to natural weathering of mercury containing ores, and from the burning of coal and incineration of medical wastes. Methylmercury is formed through microbial action from inorganic mercury that has deposited in aquatic environments and bioaccumulates through the food chain so that concentrations are highest in large predatory fish. Exposure occurs primarily through consumption of seafood, freshwater fish, and shellfish. 1,[4][5][6] Methylmercury exposure is of particular concern because it is a wellestablished human neurotoxin and the developing fetus is most sensitive to its adverse effects. [1][2][3] Toxic effects of methylmercury exposure are known from past poisoning outbreaks, particularly those in Minamata, Niigata, and Kumomoto Prefecture, Japan, 7,8 and in Iraq. 9 Recent e p i d e m i o l o g i c a l s t u d i e s h a v e addressed neurodevelopmental effects in young children from in utero methylmercury exposure in populations in which fish or seafood is a substantial component of the diet and in which exposure levels may be comparable with those levels in high-end consumers in the United States. [10][11][12]

No abstract

The FDA has conducted the Total Dietary Study (TDS), a yearly market basket programme, since 1961. It is designed to monitor the levels of toxic chemical contaminants (pesticide residues, industrial and elemental contaminants) and essential nutrients in the US food supply. It also provides information on trends in dietary concentrations and exposures for the general population. Foods are collected from retail stores once a year from each of four geographic areas of the US and are analysed either after preparation/cooking or as ready-to-eat. The latest TDS (1991-1997) data show that arsenic (inorganic and organic, > or = 0.03 ppm) was found in 63 (24%) of the 261-264 foods/mixed dishes analysed. The highest concentration was found in seafood, followed by rice/rice cereal, mushrooms, and poultry. Based on the United States Department of Agriculture's 1987-1988 Nationwide Food Consumption Survey, the estimated daily total arsenic average intakes, in microgram/day, are: 2 for infants, 23 for toddlers, 20 for 6-year-old children, 13 for 10-year-old children, 15 for 14-16-year-old boys, 21 for 14-16-year-old girls, 57 for 25-30-year-old men, 28 for 25-30-year-old women, 47 for 40-45-year-old men, 37 for 40-45-year-old women, 92 for 60-65-year-old men, 72 for 60-65-year-old women, 69 for 70-year-old men, and 42 for 70-year-old women. Of the estimated total arsenic intakes for infants, 42% arise from seafood and 31% from rice/rice cereals. Of the estimated total arsenic intakes, seafood contributes 76-90% for children (2-10-year olds), 79-85% for 14-16-year olds, and 89-96% for adults (> or = 25-30-year olds); rice/rice cereals contributes 4-8% for children, 8% for 14-16-year olds, and 1-4% for adults (> or = 25-30-year olds).

No abstract

The US Food and Drug Administration's (FDA) Total Diet Study (TDS) has been conducted continuously since the early 1960s to measures levels of various pesticide residues, contaminants, and nutrients in foods and to estimate the dietary exposures to these compounds. Both the TDS food list and the consumption amounts used for estimating exposures are based on results of nationwide food consumption surveys, and they are updated periodically to reflect changes in food consumption patterns. The most recent update was completed in 2003 using the same methodology employed in the previous update (1990). The updated food list includes approximately the same number of foods (285) as the previous list (290). Although most (75%) foods are the same in both versions, the new list reflects trends in consumption of foods containing less fat. The updated diets reflect an increase in total food consumption, with most notable increases in consumption of grains and beverages. A case study comparing cadmium exposures calculated from both the 1990 and 2003 versions of the TDS demonstrated the potential impact of changes in both the food list and consumption amounts on TDS exposure estimates.