BACKGROUND: 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has a long half-life of 5-10 years in human beings as a result of its high lipophilicity, and little or no metabolism. We monitored TCDD, its form, distribution, and elimination in Victor Yushchenko after he presented with severe poisoning. METHODS: In late December, 2004, a patient presented with TCDD poisoning; the levels in his blood serum (108000 pg/g lipid weight) were more than 50 000-fold greater than those in the general population. We identified TCDD and its metabolites, and monitored their levels for 3 years using gas chromatography and high-resolution mass spectrometry in samples of blood serum, adipose tissue, faeces, skin, urine, and sweat, after they were extracted and cleaned with different organic solvents. FINDINGS: The amount of unmodified TCDD in the samples that were analysed accounted for about 60% of TCDD eliminated from the body during the same period. Two TCDD metabolites-2,3,7-trichloro-8-hydroxydibenzo-p-dioxin and 1,3,7,8-tetrachloro-2-hydroxydibenzo-p-dioxin-were identified in the faeces, blood serum, and urine. The faeces contained the highest concentration of TCDD metabolites, and were the main route of elimination. Altogether, the different routes of elimination of TCDD and its metabolites accounted for 98% of the loss of the toxin from the body. The half-life of TCDD in our patient was 15.4 months. INTERPRETATION: This case of poisoning with TCDD suggests that the design of methods for routine assessment of TCDD metabolites in human beings should be a main aim of TCDD research in the metabolomic era. FUNDING: University of Geneva Dermatology Fund, and Swiss Centre for Applied Human Toxicology.
Comment In: Lancet. 2009 Oct 3;374(9696):1131-219660808
Saguenay Lac-Saint-Jean, a geographically isolated region of northeastern Quebec has a high incidence of cystic fibrosis (CF) and three mutations only account for 94% of the CF chromosomes. The objective of the present study was to determine whether different mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene had different effects upon the sweat chloride concentration.
The sweat chloride concentration of 114 patients was measured by quantitative pilocarpine iontophoresis.
CF patients carrying the A455E mutation, usually associated with pancreatic sufficiency, had lower sweat chloride concentrations than those carrying mutations associated with pancreatic insufficiency (delta F508 and 621 + 1G-->T).
Our results confirm that mutations resulting in a reduction of the chloride current at the apical membrane of epithelial cells induce lower sweat chloride values. However, there are differences in the chloride current between genotypes, even if they are composed of mutations apparently having the same functional effect.
With the aid of gaschromatographic techniques a fatty-acid composition was studied of lipids of the expired air condensate and sweat of patients in uncomplicated/complicated course of acute myocardial infarction versus morphological changes in the blood-air barrier. The complicated course of the condition vs uncomplicated one has been found out to be accompanied by a significant increase in the lipid content of the polyunsaturated fatty acids--linoleic and arachidonic acids--in the studied biological objects, which fact can be used in diagnosis and prognostication of development of complications in the acute period of myocardial infarction.
Cystic fibrosis (CF) has a high incidence in the French-Canadian population of Saguenay Lac-Saint-Jean (Quebec). The A455E mutation accounts for 8.3% of the CF chromosomes. This mutation was shown to be associated with a milder lung disease in the Dutch population. Twenty two CF patients distributed in 17 families and compound heterozygotes for the A455E mutation have been followed at the Clinique de Fibrose Kystique de Chicoutimi. Fourteen patients also carried the delta F508 mutation while the remaining eight patients had the 621 + 1G-->T mutation. Each patient was matched by sex and age to a patient homozygous for the delta F508 mutation. The pairs were analyzed for several clinical and laboratory variables. The A455E compound heterozygotes were diagnosed at a later age (P = 0.003) and had chloride concentrations at the sweat test lower than those homozygous for the delta F508 mutation (P = 0.007). More patients were pancreatic sufficient (P = 0.004). They had a higher Shwachman score (P = 0.001) and better pulmonary function tests (P
Individual members of the phthalate family of chemical compounds are components of innumerable everyday consumer products, resulting in a high exposure scenario for some individuals and population groups. Multiple epidemiological studies have demonstrated statistically significant exposure-disease relationships involving phthalates and toxicological studies have shown estrogenic effects in vitro. Data is lacking in the medical literature, however, on effective means to facilitate phthalate excretion.
Blood, urine, and sweat were collected from 20 individuals (10 healthy participants and 10 participants with assorted health problems) and analyzed for parent phthalate compounds as well as phthalate metabolites using high performance liquid chromatography-tandem mass spectrometry.
Some parent phthalates as well as their metabolites were excreted into sweat. All patients had MEHP (mono(2-ethylhexyl) phthalate) in their blood, sweat, and urine samples, suggesting widespread phthalate exposure. In several individuals, DEHP (di (2-ethylhexl) phthalate) was found in sweat but not in serum, suggesting the possibility of phthalate retention and bioaccumulation. On average, MEHP concentration in sweat was more than twice as high as urine levels.
Induced perspiration may be useful to facilitate elimination of some potentially toxic phthalate compounds including DEHP and MEHP. Sweat analysis may be helpful in establishing the existence of accrued DEHP in the human body.
Dehydration can impair mental and on-field performance in soccer athletes; however, there is little data available from the female adolescent player. There is a lack of research investigating fluid and electrolyte losses in cool temperatures. Therefore, the purpose of this study was to investigate the pretraining hydration status, fluid balance, and sweat sodium loss in 34 female Canadian junior elite soccer athletes (mean age ± SD, 15.7 ± 0.7 years) in a cool environment. Data were collected during two 90 min on-field training sessions (9.8 ± 3.3 °C, 63% ± 12% relative humidity). Prepractice urine specific gravity (USG), sweat loss (pre- and post-training body mass), and sweat sodium concentration (regional sweat patch method) were measured at each session. Paired t tests were used to identify significant differences between training sessions and Pearson's product moment correlation analysis was used to assess any relationships between selected variables (p = 0.05). We found that 45% of players presented to practice in a hypohydrated state (USG > 1.020). Mean percent body mass loss was 0.84% ± 0.07% and sweat loss was 0.69 ± 0.54 L. Although available during each training session, fluid intake was low (63.6% of players consumed
Nickel exposure is the most common cause of contact allergy. The role of contact with nickel-containing coins has been controversial.
To compare the release of nickel from 1 and 2 EUR coins (both composed of two alloys: Cu 75%, Zn 20%, Ni 5% and Cu 75%, Ni 25%) and Swedish 1 SEK coin (alloy: Cu 75%, Ni 25%) and to assess the deposition of nickel onto skin by coin handling.
Nickel release was determined by immersion in artificial sweat (2 min, 1 hr, 24 hr, and 1 week). Deposition of nickel onto the skin was assessed in three subjects after 1-hr handling of 2 EUR and 1 SEK coins. Samples (n = 48) were taken from fingers and palms by acid wipe sampling and analysed by inductively coupled plasma mass spectrometry.
Amounts of nickel released by 1 week from 1 SEK, 1 EUR, and 2 EUR coins were 121, 86, and 99 microg/cm(2), respectively. Corresponding 2 min values were 0.11, 0.25, and 0.22 microg/cm(2). Nickel was deposited onto the skin by 1 hr coin handling (range 0.09-4.1 microg/cm(2)), the largest amounts were on fingers; similar amounts of nickel were deposited from 1 SEK and 2 EUR coins.
Nickel is released from 1 and 2 EUR and 1 SEK coins at similar amounts. Nickel is deposited onto skin at substantial and similar amounts by coin handling. Acid wipe sampling is suitable for studies of skin exposure to nickel and in risk assessment.
The goal of this study was to examine the ability of the current Canadian CF center network to conduct sweat testing, with a particular focus on testing in infants less than 3 months old.
Surveys were sent to the 37 CF centers in Canada supported by the Canadian CF Foundation, and results were interpreted with respect to their ability to obtain adequate sweat volumes in children less than 3 months and potential factors influencing these results.
Ten centers that care for adult patients referred patients to their local pediatric CF center for sweat testing; the remaining 27 centers conducted sweat tests and 26 responded. Insufficient sweat volume results in children 5% of insufficient tests in children 5% of insufficient sweat volumes in older children and adults.
Standardization of testing procedures is required to reduce the rates of insufficient sweat volumes in both infants less than 3 months old and children >3 months old. This will decrease the need for repeat testing and delay in diagnosis.
Previous research in many sports suggests that losing ~1%-2% body mass through sweating impairs athletic performance. Elite-level hockey involves high-intensity bursts of skating, arena temperatures are >10 degrees C, and players wear protective equipment, all of which promote sweating. This study examined the pre-practice hydration, on-ice fluid intake, and sweat and sodium losses of 44 candidates for Canada's junior men's hockey team (mean +/- SE age, 18.4 +/- 0.1 y; height, 184.8 +/- 0.9 cm; mass, 89.9 +/- 1.1 kg). Players were studied in groups of 10-12 during 4 intense 1 h practices (13.9 degrees C, 66% relative humidity) on 1 day. Hydration status was estimated by measuring urine specific gravity (USG). Sweat rate was calculated from body mass changes and fluid intake. Sweat sodium concentration ([Na]) was analyzed in forehead sweat patch samples and used with sweat rate to estimate sodium loss. Over 50% of players began practice mildly hypohydrated (USG > 1.020). Sweat rate during practice was 1.8 +/- 0.1 L.h(-1) and players replaced 58% (1.0 +/- 0.1 L.h(-1)) of the sweat lost. Body mass loss averaged 0.8% +/- 0.1%, but 1/3 of players lost more than 1%. Sweat [Na] was 54.2 +/- 2.4 mmol.L(-1) and sodium loss averaged 2.26 +/- 0.17 g during practice. Players drank only water during practice and replaced no sodium. In summary, elite junior hockey players incurred large sweat and sodium losses during an intense practice, but 2/3 of players drank enough to minimize body mass loss. However, 1/3 of players lost more than 1% body mass despite ready access to fluid and numerous drinking opportunities from the coaches.